[Federal Register Volume 75, Number 11 (Tuesday, January 19, 2010)]
[Proposed Rules]
[Pages 2938-3052]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2010-340]



  Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / 
Proposed Rules  

[[Page 2938]]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Parts 50 and 58

[EPA-HQ-OAR-2005-0172; FRL-9102-1]
RIN 2060-AP98


National Ambient Air Quality Standards for Ozone

AGENCY: Environmental Protection Agency (EPA).

ACTION: Proposed rule.

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SUMMARY: Based on its reconsideration of the primary and secondary 
national ambient air quality standards (NAAQS) for ozone 
(O3) set in March 2008, EPA proposes to set different 
primary and secondary standards than those set in 2008 to provide 
requisite protection of public health and welfare, respectively. With 
regard to the primary standard for O3, EPA proposes that the 
level of the 8-hour primary standard, which was set at 0.075 ppm in the 
2008 final rule, should instead be set at a lower level within the 
range of 0.060 to 0.070 parts per million (ppm), to provide increased 
protection for children and other ``at risk'' populations against an 
array of O3-related adverse health effects that range from 
decreased lung function and increased respiratory symptoms to serious 
indicators of respiratory morbidity including emergency department 
visits and hospital admissions for respiratory causes, and possibly 
cardiovascular-related morbidity as well as total non-accidental and 
cardiopulmonary mortality. With regard to the secondary standard for 
O3, EPA proposes that the secondary O3 standard, 
which was set identical to the revised primary standard in the 2008 
final rule, should instead be a new cumulative, seasonal standard 
expressed as an annual index of the sum of weighted hourly 
concentrations, cumulated over 12 hours per day (8 am to 8 pm) during 
the consecutive 3-month period within the O3 season with the 
maximum index value, set at a level within the range of 7 to 15 ppm-
hours, to provide increased protection against O3-related 
adverse impacts on vegetation and forested ecosystems.

DATES: Written comments on this proposed rule must be received by March 
22, 2010.
    Public Hearings: Three public hearings are scheduled for this 
proposed rule. Two of the public hearings will be held on February 2, 
2010 in Arlington, Virginia, and Houston, Texas. The third public 
hearing will be held on February 4, 2010 in Sacramento, California.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2005-0172, by one of the following methods:
     http://www.regulations.gov: Follow the on-line 
instructions for submitting comments.
     E-mail: [email protected].
     Fax: 202-566-9744.
     Mail: Docket No. EPA-HQ-OAR-2005-0172, Environmental 
Protection Agency, Mail code 6102T, 1200 Pennsylvania Ave., NW., 
Washington, DC 20460. Please include a total of two copies.
     Hand Delivery: Docket No. EPA-HQ-OAR-2005-0172, 
Environmental Protection Agency, EPA West, Room 3334, 1301 Constitution 
Ave., NW., Washington, DC. Such deliveries are only accepted during the 
Docket's normal hours of operation, and special arrangements should be 
made for deliveries of boxed information.
    Public Hearings: Three public hearings are scheduled for this 
proposed rule. Two of the public hearings will be held on February 2, 
2010 in Arlington, Virginia and Houston, Texas. The third public 
hearing will be held on February 4, 2010 in Sacramento, California. The 
hearings will be held at the following locations:

Arlington, Virginia--February 2, 2010

Hyatt Regency Crystal City @ Reagan National Airport, Washington Room 
(located on the Ballroom Level), 2799 Jefferson Davis Highway, 
Arlington, Virginia 22202, Telephone: 703-418-1234.

Houston, Texas--February 2, 2010

Hilton Houston Hobby Airport, Moody Ballroom (located on the ground 
floor), 8181 Airport Boulevard, Houston, Texas 77061, Telephone: 713-
645-3000.

Sacramento, California--February 4, 2010

Four Points by Sheraton Sacramento International Airport, Natomas 
Ballroom, 4900 Duckhorn Drive, Sacramento, California 95834, Telephone: 
916-263-9000.

    See the SUPPLEMENTARY INFORMATION under ``Public Hearings'' for 
further information.
    Instructions: Direct your comments to Docket ID No. EPA-HQ-OAR-
2005-0172. The EPA's policy is that all comments received will be 
included in the public docket without change and may be made available 
online at www.regulations.gov, including any personal information 
provided, unless the comment includes information claimed to be 
Confidential Business Information (CBI) or other information whose 
disclosure is restricted by statute. Do not submit information that you 
consider to be CBI or otherwise protected through www.regulations.gov 
or e-mail. The www.regulations.gov Web site is an ``anonymous access'' 
system, which means EPA will not know your identity or contact 
information unless you provide it in the body of your comment. If you 
send an e-mail comment directly to EPA without going through 
www.regulations.gov, your e-mail address will be automatically captured 
and included as part of the comment that is placed in the public docket 
and made available on the Internet. If you submit an electronic 
comment, EPA recommends that you include your name and other contact 
information in the body of your comment and with any disk or CD-ROM you 
submit. If EPA cannot read your comment due to technical difficulties 
and cannot contact you for clarification, EPA may not be able to 
consider your comment. Electronic files should avoid the use of special 
characters, any form of encryption, and be free of any defects or 
viruses.
    Docket: All documents in the docket are listed in the 
www.regulations.gov index. Although listed in the index, some 
information is not publicly available, e.g., CBI or other information 
whose disclosure is restricted by statute. Certain other material, such 
as copyrighted material, will be publicly available only in hard copy. 
Publicly available docket materials are available either electronically 
in www.regulations.gov or in hard copy at the Air and Radiation Docket 
and Information Center, EPA/DC, EPA West, Room 3334, 1301 Constitution 
Ave., NW., Washington, DC. The Public Reading Room is open from 8:30 
a.m. to 4:30 p.m., Monday through Friday, excluding legal holidays. The 
telephone number for the Public Reading Room is (202) 566-1744 and the 
telephone number for the Air and Radiation Docket and Information 
Center is (202) 566-1742.

FOR FURTHER INFORMATION CONTACT: Ms. Susan Lyon Stone, Health and 
Environmental Impacts Division, Office of Air Quality Planning and 
Standards, U.S. Environmental Protection Agency, Mail Code C504-06, 
Research Triangle Park, NC 27711; telephone: 919-541-1146; fax: 919-
541-0237; e-mail: [email protected].

SUPPLEMENTARY INFORMATION:

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General Information

What Should I Consider as I Prepare My Comments for EPA?

    1. Submitting CBI. Do not submit this information to EPA through 
http://www.regulations.gov or e-mail. Clearly mark the part or all of 
the information that you claim to be CBI. For CBI information in a disk 
or CD-ROM that you mail to EPA, mark the outside of the disk or CD-ROM 
as CBI and then identify electronically within the disk or CD-ROM the 
specific information that is claimed as CBI. In addition to one 
complete version of the comment that includes information claimed as 
CBI, a copy of the comment that does not contain the information 
claimed as CBI must be submitted for inclusion in the public docket. 
Information so marked will not be disclosed except in accordance with 
procedures set forth in 40 CFR part 2.
    2. Tips for Preparing Your Comments. When submitting comments, 
remember to:
     Identify the rulemaking by docket number and other 
identifying information (subject heading, Federal Register date and 
page number).
     Follow directions--The Agency may ask you to respond to 
specific questions or organize comments by referencing a Code of 
Federal Regulations (CFR) part or section number.
     Explain why you agree or disagree, suggest alternatives, 
and substitute language for your requested changes.
     Describe any assumptions and provide any technical 
information and/or data that you used.
     Provide specific examples to illustrate your concerns, and 
suggest alternatives.
     Explain your views as clearly as possible, avoiding the 
use of profanity or personal threats.
     Make sure to submit your comments by the comment period 
deadline identified.

Availability of Related Information

    A number of documents relevant to this rulemaking are available on 
EPA web sites. The Air Quality Criteria for Ozone and Related 
Photochemical Oxidants (2006 Criteria Document) (two volumes, EPA/and 
EPA/, date) is available on EPA's National Center for Environmental 
Assessment Web site. To obtain this document, go to http://www.epa.gov/ncea, and click on Ozone in the Quick Finder section. This will open a 
page with a link to the March 2006 Air Quality Criteria Document. The 
2007 Staff Paper, human exposure and health risk assessments, 
vegetation exposure and impact assessment, and other related technical 
documents are available on EPA's Office of Air Quality Planning and 
Standards (OAQPS) Technology Transfer Network (TTN) web site. The 
updated final 2007 Staff Paper is available at: http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html and the exposure and risk 
assessments and other related technical documents are available at 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html. The 
Response to Significant Comments Document is available at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_rc.html. These and 
other related documents are also available for inspection and copying 
in the EPA docket identified above.

Public Hearings

    The public hearings on February 2, 2010 and February 4, 2010 will 
provide interested parties the opportunity to present data, views, or 
arguments concerning the proposed rule. The EPA may ask clarifying 
questions during the oral presentations, but will not respond to the 
presentations at that time. Written statements and supporting 
information submitted during the comment period will be considered with 
the same weight as any oral comments and supporting information 
presented at the public hearing. Written comments must be received by 
the last day of the comment period, as specified in this proposed 
rulemaking.
    The public hearings will begin at 9:30 a.m. and continue until 7:30 
p.m. (local time) or later, if necessary, depending on the number of 
speakers wishing to participate. The EPA will make every effort to 
accommodate all speakers that arrive and register before 7:30 p.m. A 
lunch break is scheduled from 12:30 p.m. until 2 p.m.
    If you would like to present oral testimony at the hearings, please 
notify Ms. Tricia Crabtree (C504-02), U.S. EPA, Research Triangle Park, 
NC 27711. The preferred method for registering is by e-mail 
([email protected]). Ms. Crabtree may be reached by telephone at 
(919) 541-5688. She will arrange a general time slot for you to speak. 
The EPA will make every effort to follow the schedule as closely as 
possible on the day of the hearing.
    Oral testimony will be limited to five (5) minutes for each 
commenter to address the proposal. We will not be providing equipment 
for commenters to show overhead slides or make computerized slide 
presentations unless we receive special requests in advance. Commenters 
should notify Ms. Crabtree if they will need specific audiovisual (AV) 
equipment. Commenters should also notify Ms. Crabtree if they need 
specific translation services for non-English speaking commenters. The 
EPA encourages commenters to provide written versions of their oral 
testimonies either electronically on computer disk, CD-ROM, or in paper 
copy.
    The hearing schedules, including lists of speakers, will be posted 
on EPA's Web site for the proposal at http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_fr.html prior to the hearing. Verbatim 
transcripts of the hearings and written statements will be included in 
the rulemaking docket.

Children's Environmental Health

    Consideration of children's environmental health plays a central 
role in the reconsideration of the 2008 final decision on the 
O3 NAAQS and EPA's decision to propose to set the 8-hour 
primary O3 standard at a level within the range of 0.060 to 
0.070 ppm. Technical information that pertains to children, including 
the evaluation of scientific evidence, policy considerations, and 
exposure and risk assessments, is discussed in all of the documents 
listed above in the section on the availability of related information. 
These documents include: the Air Quality Criteria for Ozone and Other 
Related Photochemical Oxidants; the 2007 Staff Paper; exposure and risk 
assessments and other related documents; and the Response to 
Significant Comments. All of these documents are available on the Web, 
as described above, and are in the public docket for this rulemaking. 
The public is invited to submit comments or identify peer-reviewed 
studies and data that assess effects of early life exposure to 
O3.

Table of Contents

    The following topics are discussed in this preamble:

I. Background
    A. Legislative Requirements
    B. Related Control Requirements
    C. Review of Air Quality Criteria and Standards for 
O3
    D. Reconsideration of the 2008 O3 NAAQS Final Rule
    1. Decision to Initiate a Rulemaking to Reconsider
    2. Ongoing Litigation
II. Rationale for Proposed Decision on the Level of the Primary 
Standard
    A. Health Effects Information
    1. Overview of Mechanisms
    2. Nature of Effects
    3. Interpretation and Integration of Health Evidence
    4. O3-Related Impacts on Public Health
    B. Human Exposure and Health Risk Assessments

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    1. Exposure Analyses
    2. Quantitative Health Risk Assessment
    C. Reconsideration of the Level of the Primary Standard
    1. Evidence and Exposure/Risk-Based Considerations
    2. CASAC Views Prior to 2008 Decision
    3. Basis for 2008 Decision on the Primary Standard
    4. CASAC Advice Following 2008 Decision
    5. Administrator's Proposed Conclusions
    D. Proposed Decision on the Level of the Primary Standard
III. Communication of Public Health Information
IV. Rationale for Proposed Decision on the Secondary Standard
    A. Vegetation Effects Information
    1. Mechanisms
    2. Nature of Effects
    3. Adversity of Effects
    B. Biologically Relevant Exposure Indices
    C. Vegetation Exposure and Impact Assessment
    1. Exposure Characterization
    2. Assessment of Risks to Vegetation
    D. Reconsideration of Secondary Standard
    1. Considerations Regarding 2007 Proposed Cumulative Seasonal 
Standard
    2. Considerations Regarding 2007 Proposed 8-Hour Standard
    3. Basis for 2008 Decision on the Secondary Standard
    4. CASAC Views Following 2008 Decision
    5. Administrator's Proposed Conclusions
    E. Proposed Decision on the Secondary O3 Standard
V. Revision of Appendix P--Interpretation of the NAAQS for 
O3 and Proposed Revisions to the Exceptional Events Rule
    A. Background
    B. Interpretation of the Secondary O3 Standard
    C. Clarifications Related to the Primary Standard
    D. Revisions to Exceptions From Standard Data Completeness 
Requirements for the Primary Standard
    E. Elimination of the Requirement for 90 Percent Completeness of 
Daily Data Across Three Years
    F. Administrator Discretion To Use Incomplete Data
    G. Truncation Versus Rounding
    H. Data Selection
    I. Exceptional Events Information Submission Schedule
VI. Ambient Monitoring Related to Proposed O3 Standards
    A. Background
    B. Urban Monitoring Requirements
    C. Non-Urban Monitoring Requirements
    D. Revisions to the Length of the Required O3 
Monitoring Season
VII. Implementation of Proposed O3 Standards
    A. Designations
    B. State Implementation Plans
    C. Trans-boundary Emissions
VIII. Statutory and Executive Order Reviews
    A. Executive Order 12866: Regulatory Planning and Review
    B. Paperwork Reduction Act
    C. Regulatory Flexibility Act
    D. Unfunded Mandates Reform Act
    E. Executive Order 13132: Federalism
    F. Executive Order 13175: Consultation and Coordination With 
Indian Tribal Governments
    G. Executive Order 13045: Protection of Children From 
Environmental Health and Safety Risks
    H. Executive Order 13211: Actions That Significantly Affect 
Energy Supply, Distribution or Use
    I. National Technology Transfer and Advancement Act
    J. Executive Order 12898: Federal Actions To Address 
Environmental Justice in Minority Populations and Low-Income 
Populations
References

I. Background

    The proposed decisions presented in this notice are based on a 
reconsideration of the 2008 O3 NAAQS final rule (73 FR 
16436, March 27, 2008), which revised the level of the 8-hour primary 
O3 standard to 0.075 ppm and revised the secondary 
O3 standard by making it identical to the revised primary 
standard. This reconsideration is based on the scientific and technical 
information and analyses on which the March 2008 O3 NAAQS 
rulemaking was based. Therefore, much of the information included in 
this notice is drawn directly from information included in the 2007 
proposed rule (72 FR 37818, July 11, 2007) and the 2008 final rule (73 
FR 16436).

A. Legislative Requirements

    Two sections of the Clean Air Act (CAA) govern the establishment 
and revision of the NAAQS. Section 108 (42 U.S.C. 7408) directs the 
Administrator to identify and list ``air pollutants'' that in her 
``judgment, cause or contribute to air pollution which may reasonably 
be anticipated to endanger public health or welfare'' and satisfy two 
other criteria, including ``whose presence * * * in the ambient air 
results from numerous or diverse mobile or stationary sources'' and to 
issue air quality criteria for those that are listed. Air quality 
criteria are intended to ``accurately reflect the latest scientific 
knowledge useful in indicating the kind and extent of all identifiable 
effects on public health or welfare which may be expected from the 
presence of [a] pollutant in the ambient air. * * *''
    Section 109 (42 U.S.C. 7409) directs the Administrator to propose 
and promulgate ``primary'' and ``secondary'' NAAQS for pollutants for 
which air quality criteria are issued. Section 109(b)(1) defines a 
primary standard as one ``the attainment and maintenance of which in 
the judgment of the Administrator, based on such criteria and allowing 
an adequate margin of safety, are requisite to protect the public 
health.'' \1\ A secondary standard, as defined in section 109(b)(2), 
must ``specify a level of air quality the attainment and maintenance of 
which, in the judgment of the Administrator, based on such criteria, is 
requisite to protect the public welfare from any known or anticipated 
adverse effects associated with the presence of such air pollutant in 
the ambient air.'' \2\
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    \1\ The legislative history of section 109 indicates that a 
primary standard is to be set at ``the maximum permissible ambient 
air level * * * which will protect the health of any [sensitive] 
group of the population,'' and that for this purpose ``reference 
should be made to a representative sample of persons comprising the 
sensitive group rather than to a single person in such a group'' [S. 
Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970)].
    \2\ Welfare effects as defined in section 302(h) (42 U.S.C. 
7602(h)) include, but are not limited to, ``effects on soils, water, 
crops, vegetation, man-made materials, animals, wildlife, weather, 
visibility, and climate, damage to and deterioration of property, 
and hazards to transportation, as well as effects on economic values 
and on personal comfort and well-being.''
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    The requirement that primary standards include an adequate margin 
of safety was intended to address uncertainties associated with 
inconclusive scientific and technical information available at the time 
of standard setting. It was also intended to provide a reasonable 
degree of protection against hazards that research has not yet 
identified. Lead Industries Association v. EPA, 647 F.2d 1130, 1154 (DC 
Cir 1980), cert. denied, 449 U.S. 1042 (1980); American Petroleum 
Institute v. Costle, 665 F.2d 1176, 1186 (DC Cir. 1981), cert. denied, 
455 U.S. 1034 (1982). Both kinds of uncertainties are components of the 
risk associated with pollution at levels below those at which human 
health effects can be said to occur with reasonable scientific 
certainty. Thus, in selecting primary standards that include an 
adequate margin of safety, the Administrator is seeking not only to 
prevent pollution levels that have been demonstrated to be harmful but 
also to prevent lower pollutant levels that may pose an unacceptable 
risk of harm, even if the risk is not precisely identified as to nature 
or degree. The CAA does not require the Administrator to establish a 
primary NAAQS at a zero-risk level or at background concentration 
levels, see Lead Industries Association v. EPA, 647 F.2d at 1156 n. 51, 
but rather at a level that reduces risk sufficiently so as to protect 
public health with an adequate margin of safety.
    In addressing the requirement for an adequate margin of safety, EPA 
considers such factors as the nature and severity of the health effects 
involved, the size of the population(s) at risk, and the kind and 
degree of the uncertainties

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that must be addressed. The selection of any particular approach to 
providing an adequate margin of safety is a policy choice left 
specifically to the Administrator's judgment. Lead Industries 
Association v. EPA, 647 F.2d at 1161-62; Whitman v. American Trucking 
Associations, 531 U.S. 457, 495 (2001).
    In setting standards that are ``requisite'' to protect public 
health and welfare, as provided in section 109(b), EPA's task is to 
establish standards that are neither more nor less stringent than 
necessary for these purposes. Whitman v. America Trucking Associations, 
531 U.S. 457, 473. In establishing ``requisite'' primary and secondary 
standards, EPA may not consider the costs of implementing the 
standards. Id. at 471.
    Section 109(d)(1) of the CAA requires that ``not later than 
December 31, 1980, and at 5-year intervals thereafter, the 
Administrator shall complete a thorough review of the criteria 
published under section 108 and the national ambient air quality 
standards * * * and shall make such revisions in such criteria and 
standards and promulgate such new standards as may be appropriate. * * 
*'' Section 109(d)(2) requires that an independent scientific review 
committee ``shall complete a review of the criteria * * * and the 
national primary and secondary ambient air quality standards * * * and 
shall recommend to the Administrator any new * * * standards and 
revisions of existing criteria and standards as may be appropriate. * * 
*'' This independent review function is performed by the Clean Air 
Scientific Advisory Committee (CASAC) of EPA's Science Advisory Board.

B. Related Control Requirements

    States have primary responsibility for ensuring attainment and 
maintenance of ambient air quality standards once EPA has established 
them. Under section 110 of the Act (42 U.S.C. 7410) and related 
provisions, States are to submit, for EPA approval, State 
implementation plans (SIPs) that provide for the attainment and 
maintenance of such standards through control programs directed to 
emission sources.
    The majority of man-made nitrogen oxides (NOX) and 
volatile organic compounds (VOC) emissions that contribute to 
O3 formation in the United States come from three types of 
sources: Mobile sources, industrial processes (which include consumer 
and commercial products), and the electric power industry.\3\ Mobile 
sources and the electric power industry were responsible for 78 percent 
of annual NOX emissions in 2004. That same year, 99 percent 
of man-made VOC emissions came from industrial processes (including 
solvents) and mobile sources. Emissions from natural sources, such as 
trees, may also comprise a significant portion of total VOC emissions 
in certain regions of the country, especially during the O3 
season, which are considered natural background emissions.
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    \3\ See EPA report, Evaluating Ozone Control Programs in the 
Eastern United States: Focus on the NOX Budget Trading Program, 
2004.
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    The EPA has developed new emissions standards for many types of 
stationary sources and for nearly every class of mobile sources in the 
last decade to reduce O3 by decreasing emissions of 
NOX and VOC. These programs complement State and local 
efforts to improve O3 air quality and meet the 0.084 ppm 8-
hour national standards. Under title II of the CAA, 42 U.S.C. 7521-
7574), EPA has established new emissions standards for nearly every 
type of automobile, truck, bus, motorcycle, earth mover, and aircraft 
engine, and for the fuels used to power these engines. EPA also 
established new standards for the smaller engines used in small 
watercraft, lawn and garden equipment. In March 2008, EPA promulgated 
new standards for locomotive and marine diesel engines and in August 
2009, proposed to control emissions from ocean-going vessels.
    Benefits from engine standards increase modestly each year as 
older, more-polluting vehicles and engines are replaced with newer, 
cleaner models. In time, these programs will yield substantial emission 
reductions. Benefits from fuel programs generally begin as soon as a 
new fuel is available.
    The reduction of VOC emissions from industrial processes has been 
achieved either directly or indirectly through implementation of 
control technology standards, including maximum achievable control 
technology, reasonably available control technology, and best available 
control technology standards; or are anticipated due to proposed or 
upcoming proposals based on generally available control technology or 
best available controls under provisions related to consumer and 
commercial products. These standards have resulted in VOC emission 
reductions of almost a million tons per year accumulated starting in 
1997 from a variety of sources including combustion sources, coating 
categories, and chemical manufacturing. EPA has also finalized emission 
standards and fuel requirements for new stationary engines. In the area 
of consumer and commercial products, EPA has finalized new national VOC 
emission standards for aerosol coatings and is working toward amending 
existing rules to establish new nationwide VOC content limits for 
household and institutional consumer products and architectural and 
industrial maintenance coatings. The aerosol coatings rule took effect 
in July 2009; the compliance date for both the amended consumer product 
rule and architectural coatings rule is anticipated to be January 2011. 
These actions are expected to yield significant new VOC reductions--
about 200,000 tons per year. Additionally, in ozone nonattainment 
areas, we anticipate reductions of an additional 25,000 tons per year 
as States adopt rules this year implementing control techniques 
recommendations issued in 2008 for 4 additional categories of consumer 
and commercial products, typically surface coatings and adhesives used 
in industrial manufacturing operations. These emission reductions 
primarily result from solvent controls and typically occur where and 
when the solvent is used, such as during manufacturing processes.
    The power industry is one of the largest emitters of NOX 
in the United States. Power industry emission sources include large 
electric generating units (EGU) and some large industrial boilers and 
turbines. The EPA's landmark Clean Air Interstate Rule (CAIR), issued 
on March 10, 2005, was designed to permanently cap power industry 
emissions of NOX in the eastern United States. The first 
phase of the cap was to begin in 2009, and a lower second phase cap was 
to begin in 2015. The EPA had projected that by 2015, the CAIR and 
other programs would reduce NOX emissions during the 
O3 season by about 50 percent and annual NOX 
emissions by about 60 percent from 2003 levels in the Eastern U.S. 
However, on July 11, 2008 and December 23, 2008, the U.S. Court of 
Appeals for the DC Circuit issued decisions on petitions for review of 
the CAIR. In its July 11 opinion, the court found CAIR unlawful and 
decided to vacate CAIR and its associated Federal implementation plans 
(FIPs) in their entirety. On December 23, the court granted EPA's 
petition for rehearing to the extent that it remanded without vacatur 
for EPA to conduct further proceedings consistent with the Court's 
prior opinion. Under this decision, CAIR will remain in place only 
until replaced by EPA with a rule that is consistent with the Court's 
July

[[Page 2942]]

11 opinion. The EPA recognizes the need in our CAIR replacement effort 
to address the reconsidered ozone standard, and we are currently 
assessing our options for the best way to accomplish this. It should 
also be noted that new electric generating units (EGUs) are also 
subject to NOX limits under New Source Performance Standards 
(NSPS) under CAA section 111, as well as either nonattainment new 
source review or prevention of significant deterioration requirements.
    With respect to agricultural sources, the U.S. Department of 
Agriculture (USDA) has approved conservation systems and activities 
that reduce agricultural emissions of NOX and VOC. Current 
practices that may reduce emissions of NOX and VOC include 
engine replacement programs, diesel retrofit programs, manipulation of 
pesticide applications including timing of applications, and animal 
feeding operations waste management techniques. The EPA recognizes that 
USDA has been working with the agricultural community to develop 
conservation systems and activities to control emissions of 
O3 precursors.
    These conservation activities are voluntarily adopted through the 
use of incentives provided to the agricultural producer. In cases where 
the States need these measures to attain the standard, the measures 
could be adopted. The EPA will continue to work with USDA on these 
activities with efforts to identify and/or improve the control 
efficiencies, prioritize the adoption of these conservation systems and 
activities, and ensure that appropriate criteria are used for 
identifying the most effective application of conservation systems and 
activities.
    The EPA will work together with USDA and with States to identify 
appropriate measures to meet the primary and secondary standards, 
including site-specific conservation systems and activities. Based on 
prior experience identifying conservation measures and practices to 
meet the PM NAAQS requirements, the EPA will use a similar process to 
identify measures that could meet the O3 requirements. The 
EPA anticipates that certain USDA-approved conservation systems and 
activities that reduce agricultural emissions of NOX and VOC 
may be able to satisfy the requirements for applicable sources to 
implement reasonably available control measures for purposes of 
attaining the primary and secondary O3 NAAQS.

C. Review of Air Quality Criteria and Standards for O3

    In 1971, EPA first established primary and secondary NAAQS for 
photochemical oxidants (36 FR 8186). Both primary and secondary 
standards were set at a level of 0.08 parts per million (ppm), 1-hr 
average, total photochemical oxidants, not to be exceeded more than one 
hr per year. In 1977, EPA announced the first periodic review of the 
air quality criteria in accordance with section 109(d)(1) of the Act. 
The EPA published a final decision in 1979 (44 FR 8202). Both primary 
and secondary standard levels were revised from 0.08 to 0.12 ppm. The 
indicator was revised from photochemical oxidants to O3, and 
the form of the standards was revised from a deterministic to a 
statistical form, which defined attainment of the standards as 
occurring when the expected number of days per calendar year with 
maximum hourly average concentration greater than 0.12 ppm is equal to 
or less than one. In 1983, EPA announced that the second periodic 
review of the primary and secondary standards for O3 had 
been initiated. Following review and publication of air quality 
criteria and a supplement, EPA published a proposed decision (57 FR 
35542) in August 1992 that announced EPA's intention to proceed as 
rapidly as possible with the next review of the air quality criteria 
and standards for O3 in light of emerging evidence of health 
effects related to 6- to 8-hr O3 exposures. In March 1993, 
EPA concluded the review by deciding that revisions to the standards 
were not warranted at that time (58 FR 13008).
    In August 1992 (57 FR 35542), EPA announced plans to initiate the 
third periodic review of the air quality criteria and O3 
NAAQS. On the basis of the scientific evidence contained in the 1996 CD 
(U.S. EPA 1996a) and the 1996 Staff Paper (U.S. EPA, 1996b), and 
related technical support documents, linking exposures to ambient 
O3 to adverse health and welfare effects at levels allowed 
by the then existing standards, EPA proposed to revise the primary and 
secondary O3 standards in December 1996 (61 FR 65716). The 
EPA proposed to replace the then existing 1-hour primary and secondary 
standards with 8-hour average O3 standards set at a level of 
0.08 ppm (equivalent to 0.084 ppm using standard rounding conventions). 
The EPA also proposed, in the alternative, to establish a new distinct 
secondary standard using a biologically based cumulative seasonal form. 
The EPA completed the review in July 1997 (62 FR 38856) by setting the 
primary standard at a level of 0.08 ppm, based on the annual fourth-
highest daily maximum 8-hr average concentration, averaged over three 
years, and setting the secondary standard identical to the revised 
primary standard.
    The EPA initiated the most recent periodic review of the air 
quality criteria and standards for O3 in September 2000 with 
a call for information (65 FR 57810; September 26, 2000) for the 
development of a revised Air Quality Criteria Document for 
O3 and Other Photochemical Oxidants (henceforth the ``2006 
Criteria Document''). A project work plan (EPA, 2002) for the 
preparation of the Criteria Document was released in November 2002 for 
CASAC and public review. The EPA held a series of workshops in mid-2003 
on several draft chapters of the Criteria Document to obtain broad 
input from the relevant scientific communities. These workshops helped 
to inform the preparation of the first draft Criteria Document (EPA, 
2005a), which was released for CASAC and public review on January 31, 
2005; a CASAC meeting was held on May 4-5, 2005 to review the first 
draft Criteria Document. A second draft Criteria Document (EPA, 2005b) 
was released for CASAC and public review on August 31, 2005, and was 
discussed along with a first draft Staff Paper (EPA, 2005c) at a CASAC 
meeting held on December 6-8, 2005. In a February 16, 2006 letter to 
the Administrator, CASAC provided comments on the second draft Criteria 
Document (Henderson, 2006a), and the final 2006 Criteria Document (EPA, 
2006a) was released on March 21, 2006. In a June 8, 2006 letter to the 
Administrator (Henderson, 2006b), CASAC provided additional advice to 
the Agency concerning chapter 8 of the final 2006 Criteria Document 
(Integrative Synthesis) to help inform the second draft Staff Paper.
    A second draft Staff Paper (EPA, 2006b) was released on July 17, 
2006 and reviewed by CASAC on August 24-25, 2006. In an October 24, 
2006 letter to the Administrator, CASAC provided advice and 
recommendations to the Agency concerning the second draft Staff Paper 
(Henderson, 2006c). A final 2007 Staff Paper (EPA, 2007a) was released 
on January 31, 2007. In a March 26, 2007 letter (Henderson, 2007), 
CASAC offered additional advice to the Administrator with regard to 
recommendations and revisions to the primary and secondary 
O3 NAAQS.
    The schedule for completion of the 2008 rulemaking was governed by 
a consent decree resolving a lawsuit filed in March 2003 by a group of 
plaintiffs representing national environmental

[[Page 2943]]

and public health organizations, alleging that EPA had failed to 
complete the review within the period provided by statute.\4\ The 
modified consent decree that governed the 2008 rulemaking, entered by 
the court on December 16, 2004, provided that EPA sign for publication 
notices of proposed and final rulemaking concerning its review of the 
O3 NAAQS no later than March 28, 2007 and December 19, 2007, 
respectively. That consent decree was further modified in October 2006 
to change these proposed and final rulemaking dates to no later than 
May 30, 2007 and February 20, 2008, respectively. These dates for 
signing the publication notices of proposed and final rulemaking were 
further extended to no later than June 20, 2007 and March 12, 2008, 
respectively. The proposed decision was signed on June 20, 2007 and 
published in the Federal Register on July 11, 2007 (72 FR 37818).
---------------------------------------------------------------------------

    \4\ American Lung Association v. Whitman (No. 1:03CV00778, D.DC 
2003).
---------------------------------------------------------------------------

    Public hearings on the proposed decision were held on Thursday, 
August 30, 2007 in Philadelphia, PA and Los Angeles, CA. On Wednesday, 
September 5, 2007, hearings were held in Atlanta, GA, Chicago, IL, and 
Houston, TX. A large number of comments were received from various 
commenters on the 2007 proposed revisions to the O3 NAAQS. A 
comprehensive summary of all significant comments, along with EPA's 
responses (henceforth ``Response to Comments''), can be found in the 
docket for the 2008 rulemaking, which is also the docket for this 
reconsideration rulemaking.
    The EPA's final decision on the O3 NAAAQS was published 
in the Federal Register on March 27, 2008 (73 FR 16436). In the 2008 
rulemaking, EPA revised the level of the 8-hour primary standard for 
O3 to 0.075 parts per million (ppm), expressed to three 
decimal places. With regard to the secondary standard for 
O3, EPA revised the 8-hour standard by making it identical 
to the revised primary standard. The EPA also made conforming changes 
to the Air Quality Index (AQI) for O3, setting an AQI value 
of 100 equal to 0.075 ppm, 8-hour average, and making proportional 
changes to the AQI values of 50, 150 and 200.

D. Reconsideration of the 2008 O3 NAAQS Final Rule

    Consistent with a directive of the new Administration regarding the 
review of new and pending regulations (Emanuel memorandum, 74 FR 4435; 
January 26, 2009), the Administrator reviewed a number of actions that 
were taken in the last year by the previous Administration. The 2008 
final rule was included in this review in recognition of the central 
role that the NAAQS play in enabling EPA to fulfill its mission to 
protect the nation's public health and welfare. In her review, the 
Administrator was mindful of the need for judgments concerning the 
NAAQS to be based on a strong scientific foundation which is developed 
through a transparent and credible NAAQS review process, consistent 
with the core values highlighted in President Obama's memorandum on 
scientific integrity (March 9, 2009).
1. Decision To Initiate a Rulemaking To Reconsider
    In her review of the 2008 final rule, several aspects of the final 
rule related to the primary and secondary standards stood out to the 
Administrator. As an initial matter, the Administrator noted that the 
2008 final rule concluded that the 1997 primary and secondary 
O3 standards were not adequate to protect public health and 
public welfare, and that revisions were necessary to provide increased 
protection. With respect to revision of the primary standard, the 
Administrator noted that the revised level established in the 2008 
final rule was above the range that had been unanimously recommended by 
CASAC.\5\ She also noted that EPA received comments from a large number 
of commenters from the medical and public health communities, including 
EPA's Children's Health Protection Advisory Committee, all of which 
endorsed levels within CASAC's recommended range.
---------------------------------------------------------------------------

    \5\ The level of the 8-hour primary ozone standard was set at 
0.075 ppm, while CASAC unanimously recommended a range between 0.060 
and 0.070 ppm.
---------------------------------------------------------------------------

    With respect to revision of the secondary O3 standard, 
the Administrator noted that the 2008 final rule differed substantially 
from CASAC's recommendations that EPA adopt a new secondary 
O3 standard based on a cumulative, seasonal measure of 
exposure. The 2008 final rule revised the secondary standard to be 
identical to the revised primary standard, which is based on an 8-hour 
daily maximum measure of exposure. She also noted that EPA received 
comments from a number of commenters representing environmental 
interests, all of which endorsed CASAC;s recommendation for a new 
cumulative, seasonal secondary standard.\6\
---------------------------------------------------------------------------

    \6\ The Administrator also noted the exchange that had occurred 
between EPA and the Office of Management and Budget (OMB) with 
regard to the final decision on the secondary standard, as discussed 
in the 2008 final rule (73 FR 16497).
---------------------------------------------------------------------------

    Subsequent to issuance of the 2008 final rule, in April 2008, CASAC 
took the unusual step of sending EPA a letter expressing strong, 
unanimous disagreement with EPA's decisions on both the primary and 
secondary standards (Henderson, 2008). The CASAC explained that it did 
not endorse the revised primary O3 standard as being 
sufficiently protective of public health because it failed to satisfy 
the explicit stipulation of the Act to provide an adequate margin of 
safety. The CASAC also expressed the view that failing to revise the 
secondary standard to a cumulative, seasonal form was not supported by 
the available science. In addition to CASAC's letter, the Administrator 
noted a recent adverse ruling issued by the U.S. Court of Appeals for 
the District of Columbia Circuit on another NAAQS decision. In February 
2009, the DC Circuit remanded the Agency's decisions on the primary 
annual and secondary standards for fine particles (PM2.5). 
In so doing, the Court found that EPA had not adequately explained the 
basis for its decisions, including why CASAC's recommendations for a 
more health-protective primary annual standard and for secondary 
standards different from the primary standards were not accepted. 
American Farm Bureau v. EPA, 559 F.3d. 512 (DC Cir. 2009).
    Based on her review of the information described above, the 
Administrator is initiating a rulemaking to reconsider parts of the 
2008 final rule. Specifically, the Administrator is reconsidering the 
level of the primary standard to ensure that it is sufficiently 
protective of public health, as discussed in section II below, and is 
reconsidering all aspects of the secondary standard to ensure that it 
appropriately reflects the available science and is sufficiently 
protective of public welfare, as discussed in section IV below. Based 
on her review, the Administrator has serious cause for concern 
regarding whether the revisions to the primary and secondary 
O3 standards adopted in the 2008 final rule satisfy the 
requirements of the CAA, in light of the body of scientific evidence 
before the Agency. In addition, the importance of the O3 
NAAQS to public health and welfare weigh heavily in favor of 
reconsidering parts of the 2008 final rule as soon as possible, based 
on the scientific and technical information upon which the 2008 final 
rule was based.

[[Page 2944]]

    Also, EPA conducted a provisional assessment of ``new'' scientific 
papers (EPA, 2009) of scientific literature evaluating health and 
ecological effects of O3 exposure published since the close 
of the 2006 Criteria Document upon which the 2008 O3 NAAQS 
were based. The Administrator notes that the provisional assessment of 
``new'' science found that such studies did not materially change the 
conclusions in the 2006 Criteria Document. This provisional assessment 
is supportive of the Administrator's decision to reconsider parts of 
the 2008 final rule at this time, based on the scientific and technical 
information available for the 2008 final rule, as compared to foregoing 
such reconsideration and taking appropriate action in the future as 
part of the next periodic review of the air quality criteria and NAAQS, 
which will include such scientific and technical information.
    The reconsideration of parts of the 2008 final rule discussed in 
this notice is based on the scientific and technical record from the 
2008 rulemaking, including public comments and CASAC advice and 
recommendations. The information that was assessed during the 2008 
rulemaking includes information in the 2006 Criteria Document (EPA, 
2006a), the 2007 Policy Assessment of Scientific and Technical 
Information, referred to as the 2007 Staff Paper (EPA, 2007b), and 
related technical support documents including the 2007 REAs (U.S. EPA, 
2007c; Abt Associates, 2007a,b). Scientific and technical information 
developed since the 2006 Criteria Document will be considered in the 
next periodic review, instead of this reconsideration rulemaking, 
allowing the new information to receive careful and comprehensive 
review by CASAC and the public before it is used as a basis in a 
rulemaking that determines whether to revise the NAAQS.
2. Ongoing Litigation
    In May 2008, following publication of the 2008 final rule, numerous 
groups, including state, public health, environmental, and industry 
petitioners, challenged EPA's decisions in federal court. The 
challenges were consolidated as State of Mississippi, et al. v. EPA 
(No. 08-1200, DC Cir. 2008). On March 10, 2009, EPA filed an unopposed 
motion requesting that the Court vacate the briefing schedule and hold 
the consolidated cases in abeyance. The Agency stated its desire to 
allow time for appropriate officials from the new Administration to 
review the O3 standards to determine whether they should be 
maintained, modified or otherwise reconsidered. The EPA further 
requested that it be directed to notify the Court and all the parties 
of any actions it has taken or intends to take, if any, within 180 days 
of the Court vacating the briefing schedule. On March 19, 2009, the 
Court granted EPA's motion. Pursuant to the Court's order, on September 
16, 2009 EPA notified the Court and the parties of its decision to 
initiate a rulemaking to reconsider the primary and secondary 
O3 standards set in March 2008 to ensure they satisfy the 
requirements of the CAA.\7\ In its notice to the Court, EPA stated that 
this notice of proposed rulemaking would be signed by December 21, 
2009, and that the final rule will be signed by August 31, 2010.
---------------------------------------------------------------------------

    \7\ The EPA also separately announced that it will move quickly 
to implement any new standards that might result from this 
reconsideration. To reduce the workload for states during the 
interim period of reconsideration, the Agency intends to propose to 
defer compliance with the CAA requirement to designate areas as 
attainment or nonattainment. EPA will work with states, local 
governments and tribes to ensure that air quality is protected 
during that time.
---------------------------------------------------------------------------

II. Rationale for Proposed Decision on the Level of the Primary 
Standard

    As an initial matter, the Administrator notes that the 2008 final 
rule concluded that the 1997 primary O3 standard was ``not 
sufficient and thus not requisite to protect public health with an 
adequate margin of safety, and that revision is needed to provide 
increased public health protection'' (73 FR 16472). The Administrator 
is not reconsidering this aspect of the 2008 decision, which is based 
on the reasons discussed in section II.B of the 2008 final rule (73 FR 
16443-16472). The Administrator also notes that the 2008 final rule 
concluded that it was appropriate to retain the O3 
indicator, the 8-hour averaging time, and form of the primary 
O3 standard (specified as the annual fourth-highest daily 
maximum 8-hour concentration, averaged over 3 years), while concluding 
that revision of the standard level was appropriate.\8\ The 
Administrator is not reconsidering these aspects of the 2008 decision, 
which are based on the reasons discussed in sections II.C.1-3 of the 
2008 final rule, which address the indicator, averaging time, and form, 
respectively, of the primary O3 standard (73 FR 16472-
16475). For these reasons, the Administrator is not reopening the 2008 
decision with regard to the need to revise the 1997 primary 
O3 standard nor with regard to the indicator, averaging 
time, and form of the 2008 primary O3 standard. Thus, the 
information that follows in this section specifically focuses on a 
reconsideration of level of the primary O3 standard.
---------------------------------------------------------------------------

    \8\ The use of O3 as the indicator for photochemical 
oxidants was adopted in the 1979 final rule and retained in 
subsequent rulemaking. An 8-hour averaging time and a form based on 
the annual fourth-highest daily maximum 8-hour concentration, 
averaged over 3 years, were adopted in the 1997 final rule and 
retained in the 2008 rulemaking.
---------------------------------------------------------------------------

    This section presents the rationale for the Administrator's 
proposed decision that the O3 primary standard, which was 
set at a level of 0.075 ppm in the 2008 final rule, should instead be 
set at a lower level within the range from 0.060 to 0.070 ppm. As 
discussed more fully below, the rationale for the proposed range of 
standard levels is based on a thorough review of the latest scientific 
information on human health effects associated with the presence of 
O3 in the ambient air presented in the 2006 Criteria 
Document. This rationale also takes into account: (1) Staff assessments 
of the most policy-relevant information in the 2006 Criteria Document 
and staff analyses of air quality, human exposure, and health risks, 
presented in the 2007 Staff Paper, upon which staff recommendations for 
revisions to the primary O3 standard in the 2008 rulemaking 
were based; (2) CASAC advice and recommendations, as reflected in 
discussions of drafts of the 2006 Criteria Document and 2007 Staff 
Paper at public meetings, in separate written comments, and in CASAC's 
letters to the Administrator both before and after the 2008 rulemaking; 
and (3) public comments received during the development of these 
documents, either in connection with CASAC meetings or separately, and 
on the 2007 proposed rule.
    In developing this rationale, the Administrator recognizes that the 
CAA requires her to reach a public health policy judgment as to what 
standard would be requisite to protect public health with an adequate 
margin of safety, based on scientific evidence and technical 
assessments that have inherent uncertainties and limitations. This 
judgment requires making reasoned decisions as to what weight to place 
on various types of evidence and assessments, and on the related 
uncertainties and limitations. Thus, in selecting standard levels to 
propose, and subsequently in selecting a final level, the Administrator 
is seeking not only to prevent O3 levels that have been 
demonstrated to be harmful but also to prevent lower O3 
levels that may pose an unacceptable risk of harm, even if the risk is 
not precisely identified as to nature or degree.
    In this proposed rule, EPA has drawn upon an integrative synthesis 
of the entire body of evidence, published

[[Page 2945]]

through early 2006, on human health effects associated with the 
presence of O3 in the ambient air. As discussed below in 
section II.A, this body of evidence addresses a broad range of health 
endpoints associated with exposure to ambient levels of O3 
(EPA, 2006a, chapter 8), and includes over one hundred epidemiologic 
studies conducted in the U.S., Canada, and many countries around the 
world.\9\ In reconsidering this evidence, EPA focuses on those health 
endpoints that have been demonstrated to be caused by exposure to 
O3, or for which the 2006 Criteria Document judges 
associations with O3 to be causal, likely causal, or for 
which the evidence is highly suggestive that O3 contributes 
to the reported effects. This rationale also draws upon the results of 
quantitative exposure and risk assessments, discussed below in section 
II.B. Section II.C focuses on the considerations upon which the 
Administrator's proposed conclusions on the level of the primary 
standard are based. Policy-relevant evidence-based and exposure/risk-
based considerations are discussed, and the rationale for the 2008 
final rulemaking on the primary standard and CASAC advice, given both 
prior to the development of the 2007 proposed rule and following the 
2008 final rule, are summarized. Finally, the Administrator's proposed 
conclusions on the level of the primary standard are presented. Section 
II.D summarizes the proposed decision on the level of the primary 
O3 standard and the solicitation of public comments.
---------------------------------------------------------------------------

    \9\ In its assessment of the epidemiological evidence judged to 
be most relevant to making decisions on the level of the 
O3 primary standard, EPA has placed greater weight on 
U.S. and Canadian epidemiologic studies, since studies conducted in 
other countries may well reflect different demographic and air 
pollution characteristics.
---------------------------------------------------------------------------

    Judgments made in the 2006 Criteria Document and 2007 Staff Paper 
about the extent to which relationships between various health 
endpoints and short-term exposures to ambient O3 are likely 
causal have been informed by several factors. As discussed below in 
section II.A, these factors include the nature of the evidence (i.e., 
controlled human exposure, epidemiological, and/or toxicological 
studies) and the weight of evidence, which takes into account such 
considerations as biological plausibility, coherence of evidence, 
strength of association, and consistency of evidence.
    In assessing the health effects data base for O3, it is 
clear that human studies provide the most directly applicable 
information for determining causality because they are not limited by 
the uncertainties of dosimetry differences and species sensitivity 
differences, which would need to be addressed in extrapolating animal 
toxicology data to human health effects. Controlled human exposure 
studies provide data with the highest level of confidence since they 
provide human health effects data under closely monitored conditions 
and can provide exposure-response relationships. Epidemiological data 
provide evidence of associations between ambient O3 levels 
and more serious acute and chronic health effects (e.g., hospital 
admissions and mortality) that cannot be assessed in controlled human 
exposure studies. For these studies the degree of uncertainty 
introduced by potentially confounding variables (e.g., other 
pollutants, temperature) and other factors affects the level of 
confidence that the health effects being investigated are attributable 
to O3 exposures, alone and in combination with other 
copollutants.
    In using a weight of evidence approach to inform judgments about 
the degree of confidence that various health effects are likely to be 
caused by exposure to O3, confidence increases as the number 
of studies consistently reporting a particular health endpoint grows 
and as other factors, such as biological plausibility and strength, 
consistency, and coherence of evidence, increase. Conclusions regarding 
biological plausibility, consistency, and coherence of evidence of 
O3-related health effects are drawn from the integration of 
epidemiological studies with mechanistic information from controlled 
human exposure studies and animal toxicological studies. As discussed 
below, this type of mechanistic linkage has been firmly established for 
several respiratory endpoints (e.g., lung function decrements, lung 
inflammation) but remains far more equivocal for cardiovascular 
endpoints (e.g., cardiovascular-related hospital admissions). For 
epidemiological studies, strength of association refers to the 
magnitude of the association and its statistical strength, which 
includes assessment of both effects estimate size and precision. In 
general, when associations yield large relative risk estimates, it is 
less likely that the association could be completely accounted for by a 
potential confounder or some other bias. Consistency refers to the 
persistent finding of an association between exposure and outcome in 
multiple studies of adequate power in different persons, places, 
circumstances and times. For example, the magnitude of effect estimates 
is relatively consistent across recent studies showing association 
between short-term, but not long-term, O3 exposure and 
mortality.
    Based on the information discussed below in sections II.A.1-II.A.3, 
judgments concerning the extent to which relationships between various 
health endpoints and ambient O3 exposures are likely causal 
are summarized below in section II.A.3.c. These judgments reflect the 
nature of the evidence and the overall weight of the evidence, and are 
taken into consideration in the quantitative exposure and risk 
assessments, discussed below in section II.B.
    To put judgments about health effects that have been demonstrated 
to be caused by exposure to O3, or for which the 2006 
Criteria Document judges associations with O3 to be causal, 
likely causal, or for which the evidence is highly suggestive that 
O3 contributes to the reported effects into a broader public 
health context, EPA has drawn upon the results of the quantitative 
exposure and risk assessments. These assessments provide estimates of 
the likelihood that individuals in particular population groups that 
are at risk for various O3-related physiological health 
effects would experience ``exposures of concern'' and specific health 
endpoints under varying air quality scenarios (i.e., just meeting 
various standards \10\), as well as characterizations of the kind and 
degree of uncertainties inherent in such estimates.
---------------------------------------------------------------------------

    \10\ The exposure assessment done as part of the 2008 final 
rulemaking considered several air quality scenarios, including just 
meeting what was then the current standard set at a level of 0.084 
ppm, as well as just meeting alternative standards at levels of 
0.080, 0.074, 0.070, and 0.064 ppm.
---------------------------------------------------------------------------

    In the 2008 final rulemaking and in this reconsideration, the term 
``exposures of concern'' is defined as personal exposures while at 
moderate or greater exertion to 8-hour average ambient O3 
levels at and above specific benchmark levels which represent exposure 
levels at which O3-related health effects are known or can 
reasonably be inferred to occur in some individuals, as discussed below 
in section II.B.1.\11\ The EPA emphasizes

[[Page 2946]]

that although the analysis of ``exposures of concern'' was conducted 
using three discrete benchmark levels (i.e., 0.080, 0.070, and 0.060 
ppm), the concept is more appropriately viewed as a continuum with 
greater confidence and less uncertainty about the existence of health 
effects at the upper end and less confidence and greater uncertainty as 
one considers increasingly lower O3 exposure levels. The EPA 
recognizes that there is no sharp breakpoint within the continuum 
ranging from at and above 0.080 ppm down to 0.060 ppm. In considering 
the concept of exposures of concern, it is important to balance 
concerns about the potential for health effects and their severity with 
the increasing uncertainty associated with our understanding of the 
likelihood of such effects at lower O3 levels.
---------------------------------------------------------------------------

    \11\ Exposures of concern were also considered in the 1997 
review of the O3 NAAQS, and were judged by EPA to be an 
important indicator of the public health impacts of those 
O3-related effects for which information was too limited 
to develop quantitative estimates of risk but which had been 
observed in humans at and above the benchmark level of 0.08 ppm for 
6- to 8-hour exposures * * * including increased nonspecific 
bronchial responsiveness (for example, aggravation of asthma), 
decreased pulmonary defense mechanisms (suggestive of increased 
susceptibility to respiratory infection), and indicators of 
pulmonary inflammation (related to potential aggravation of chronic 
bronchitis or long-term damage to the lungs). (62 FR 38868)
---------------------------------------------------------------------------

    Within the context of this continuum, estimates of exposures of 
concern at discrete benchmark levels provide some perspective on the 
public health impacts of O3-related health effects that have 
been demonstrated in controlled human exposure and toxicological 
studies but cannot be evaluated in quantitative risk assessments, such 
as lung inflammation, increased airway responsiveness, and changes in 
host defenses. They also help in understanding the extent to which such 
impacts have the potential to be reduced by meeting various standards. 
These O3-related physiological effects are plausibly linked 
to the increased morbidity seen in epidemiological studies (e.g., as 
indicated by increased medication use in asthmatics, school absences in 
all children, and emergency department visits and hospital admissions 
in people with lung disease). Estimates of the number of people likely 
to experience exposures of concern cannot be directly translated into 
quantitative estimates of the number of people likely to experience 
specific health effects, since sufficient information to draw such 
comparisons is not available--if such information were available, these 
health outcomes would have been included in the quantitative risk 
assessment. Due to individual variability in responsiveness, only a 
subset of individuals who have exposures at and above a specific 
benchmark level can be expected to experience such adverse health 
effects, and susceptible subpopulations such as those with asthma are 
expected to be affected more by such exposures than healthy 
individuals. The amount of weight to place on the estimates of 
exposures of concern at any of these benchmark levels depends in part 
on the weight of the scientific evidence concerning health effects 
associated with O3 exposures at and above that benchmark 
level. It also depends on judgments about the importance from a public 
health perspective of the health effects that are known or can 
reasonably be inferred to occur as a result of exposures at and above 
the benchmark level. Such public health policy judgments are embodied 
in the NAAQS standard setting criteria (i.e., standards that, in the 
judgment of the Administrator, are requisite to protect public health 
with an adequate margin of safety).
    As discussed below in section II.B.2, the quantitative health risk 
assessment conducted as part of the 2008 final rulemaking includes 
estimates of risks of lung function decrements in asthmatic and all 
school age children, respiratory symptoms in asthmatic children, 
respiratory-related hospital admissions, and non-accidental and 
cardiorespiratory-related mortality associated with recent ambient 
O3 levels, as well as risk reductions and remaining risks 
associated with just meeting the then current 0.084 ppm standard and 
various alternative O3 standards in a number of example 
urban areas. There are two parts to this risk assessment: one part is 
based on combining information from controlled human exposure studies 
with modeled population exposure, and the other part is based on 
combining information from community epidemiological studies with 
either monitored or adjusted ambient concentrations levels. This 
assessment provides estimates of the potential magnitude of 
O3-related health effects, as well as a characterization of 
the uncertainties and variability inherent in such estimates. This 
assessment also provides insights into the distribution of risks and 
patterns of risk reductions associated with meeting alternative 
O3 standards.
    As discussed below, a substantial amount of new research conducted 
since the 1997 review of the O3 NAAQS was available to 
inform the 2008 final rulemaking, with important new information coming 
from epidemiologic studies as well as from controlled human exposure, 
toxicological, and dosimetric studies. The research studies newly 
available in the 2008 final rulemaking that were evaluated in the 2006 
Criteria Document and the exposure and risk assessments presented in 
the 2007 Staff Paper have undergone intensive scrutiny through multiple 
layers of peer review and many opportunities for public review and 
comment. While important uncertainties remain in the qualitative and 
quantitative characterizations of health effects attributable to 
exposure to ambient O3, and while different interpretations 
of these uncertainties can result in different public health policy 
judgments, the review of this information has been extensive and 
deliberate. In the judgment of the Administrator, this intensive 
evaluation of the scientific evidence provides an adequate basis for 
this reconsideration of the 2008 final rulemaking.

A. Health Effects Information

    This section outlines key information contained in the 2006 
Criteria Document (chapters 4-8) and in the 2007 Staff Paper (chapter 
3) on known or potential effects on public health which may be expected 
from the presence of O3 in ambient air. The information 
highlighted here summarizes: (1) New information available on potential 
mechanisms for health effects associated with exposure to 
O3; (2) the nature of effects that have been associated 
directly with exposure to O3 and indirectly with the 
presence of O3 in ambient air; (3) an integrative 
interpretation of the evidence, focusing on the biological plausibility 
and coherence of the evidence; and (4) considerations in characterizing 
the public health impact of O3, including the identification 
of ``at risk'' populations.
    The decision in the 1997 review focused primarily on evidence from 
short-term (e.g., 1 to 3 hours) and prolonged (6 to 8 hours) 
controlled-exposure studies reporting lung function decrements, 
respiratory symptoms, and respiratory inflammation in humans, as well 
as epidemiology studies reporting excess hospital admissions and 
emergency department (ED) visits for respiratory causes. The 2006 
Criteria Document prepared for the 2008 rulemaking emphasized the large 
number of epidemiological studies published since the last review with 
these and additional health endpoints, including the effects of acute 
(short-term and prolonged) and chronic exposures to O3 on 
lung function decrements and enhanced respiratory symptoms in asthmatic 
individuals, school absences, and premature mortality. It also 
emphasized important new information from toxicology, dosimetry, and 
controlled human exposure studies. Highlights of the evidence include:
    (1) Two new controlled human-exposure studies are now available 
that examine respiratory effects associated with prolonged 
O3 exposures at levels below 0.080 ppm, which was the lowest

[[Page 2947]]

exposure level that had been examined in the 1997 review.
    (2) Numerous controlled human-exposure studies have examined 
indicators of O3-induced inflammatory response in both the 
upper respiratory tract (URT) and lower respiratory tract (LRT), and 
increased airway responsiveness to allergens in subjects with allergic 
asthma and allergic rhinitis exposed to O3, while other 
studies have examined changes in host defense capability following 
O3 exposure of healthy young adults.
    (3) Animal toxicology studies provide new information regarding 
mechanisms of action, increased susceptibility to respiratory 
infection, and the biological plausibility of acute effects and 
chronic, irreversible respiratory damage.
    (4) Numerous acute exposure epidemiological studies published 
during the past decade offer added evidence of ambient O3-
related lung function decrements and respiratory symptoms in physically 
active healthy subjects and greater responses in asthmatic subjects, as 
well as evidence on new health endpoints, such as the relationships 
between ambient O3 concentrations and asthma medication use 
and school absenteeism, and between ambient O3 and cardiac-
related physiological endpoints.
    (5) Several additional studies have been published over the last 
decade examining the temporal associations between O3 
exposures and emergency department visits for asthma and other 
respiratory diseases and respiratory-related hospital admissions.
    (6) A large number of newly available epidemiological studies have 
examined the effects of acute exposure to PM and O3 on 
mortality, notably including large multicity studies that provide much 
more robust and credible information than was available in the 1997 
review, as well as recent meta-analyses that have evaluated potential 
sources of heterogeneity in O3-mortality associations.
1. Overview of Mechanisms
    Evidence on possible mechanisms by which exposure to O3 
may result in acute and chronic health effects is discussed in chapters 
5 and 6 of the 2006 Criteria Document.\12\ Evidence from dosimetry, 
toxicological, and human exposure studies has contributed to an 
understanding of the mechanisms that help to explain the biological 
plausibility and coherence of evidence for O3-induced 
respiratory health effects reported in epidemiological studies. More 
detailed information about the physiological mechanisms related to the 
respiratory effects of short- and long-term exposure to O3 
can be found in section II.A.3.b.i and II.A.3.b.iii, respectively. In 
the past, however, little information was available to help explain 
potential biological mechanisms which linked O3 exposure to 
premature mortality or cardiovascular effects. As discussed more fully 
in section II.A.3.b.ii below, since the 1997 review an emerging body of 
animal toxicology and controlled human exposure evidence is beginning 
to suggest mechanisms that may mediate acute O3 
cardiovascular effects. While much is known about mechanisms that play 
a role in O3-related respiratory effects, additional 
research is needed to more clearly understand the role that 
O3 may have in contributing to cardiovascular effects.
---------------------------------------------------------------------------

    \12\ While most of the available evidence addresses mechanisms 
for O3, O3 clearly serves as an indicator for 
the total photochemical oxidant mixture found in the ambient air. 
Some effects may be caused by one or more components in the overall 
pollutant mix, either separately or in combination with 
O3. However, O3 clearly dominates these other 
oxidants with their concentrations only being a few percent of the 
O3 concentration.
---------------------------------------------------------------------------

    With regard to the mechanisms related to short-term respiratory 
effects, scientific evidence discussed in the 2006 Criteria Document 
(section 5.2) indicates that reactions of O3 with lipids and 
antioxidants in the epithelial lining fluid and the epithelial cell 
membranes of the lung can be the initial step in mediating deleterious 
health effects of O3. This initial step activates a cascade 
of events that lead to oxidative stress, injury, inflammation, airway 
epithelial damage and increased alveolar permeability to vascular 
fluids. Inflammation can be accompanied by increased airway 
responsiveness, which is an increased bronchoconstrictive response to 
airway irritants and allergens. Continued respiratory inflammation also 
can alter the ability of the body to respond to infectious agents, 
allergens and toxins. Acute inflammatory responses to O3 in 
some healthy people are well documented, and precursors to lung injury 
are observed within 3 hours after exposure in humans. Repeated 
respiratory inflammation can lead to a chronic inflammatory state with 
altered lung structure and lung function and may lead to chronic 
respiratory diseases such as fibrosis and emphysema (EPA, 2006a, 
section 8.6.2). The severity of symptoms and magnitude of response to 
acute exposures depend on inhaled dose, as well as on individual 
susceptibility to O3, as discussed below. At the same 
O3 dose, individuals who are more susceptible to 
O3 will have a larger response than those who are less 
susceptible; among individuals with similar susceptibility, those who 
receive a larger dose will have a larger response to O3.
    The inhaled dose is the product of O3 concentration (C), 
minute ventilation or ventilation rate, and duration of exposure (T), 
or (C x ventilation rate x T). A large body of data regarding the 
interdependent effect of these components of inhaled dose on pulmonary 
responses was assessed in the 1986 and 1996 O3 Criteria 
Documents. In an attempt to describe O3 dose-response 
characteristics, acute responses were modeled as a function of total 
inhaled O3 dose, which was generally found to be a better 
predictor of response than O3 concentration, ventilation 
rate, or duration of exposure, alone, or as a combination of any two of 
these factors (EPA 2006a, section 6.2). Predicted O3-induced 
decrements in lung function have been shown to be a function of 
exposure concentration, duration and exercise level for healthy, young 
adults (McDonnell et al., 1997). A meta-analysis of 21 studies (Mudway 
and Kelly, 2004) showed that markers of inflammation and increased 
cellular permeability in healthy subjects are associated with total 
O3 dose.
    The 2006 Criteria Document summarizes information on potentially 
susceptible and vulnerable groups in section 8.7. As described there, 
the term susceptibility refers to innate (e.g., genetic or 
developmental) or acquired (e.g., personal risk factors, age) factors 
that make individuals more likely to experience effects with exposure 
to pollutants. A number of population groups and lifestages have been 
identified as potentially susceptible to health effects as a result of 
O3 exposure, including people with existing lung diseases, 
including asthma, children and older adults, and people who have larger 
than normal lung function responses that may be due to genetic 
susceptibility. In addition, some population groups and lifestages have 
been identified as having increased vulnerability to O3-
related effects due to increased likelihood of exposure while at 
elevated ventilation rates, including healthy children and adults who 
are active outdoors, for example, outdoor workers, and joggers. Taken 
together, the susceptible and vulnerable groups are more commonly 
referred to as ``at-risk'' groups,\13\ as discussed more fully below in 
section II.A.4.b.
---------------------------------------------------------------------------

    \13\ In previous Staff Papers and Federal Register notices 
announcing proposed and final decisions on the O3 and 
other NAAQS, EPA has used the phrase ``sensitive population groups'' 
to include both population groups that are at increased risk because 
they are more intrinsically susceptible and population groups that 
are more vulnerable due to an increased potential for exposure. In 
this notice, we use the phrase, ``at risk'' populations to include 
both types of population groups.

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[[Page 2948]]

    Based on a substantial body of new evidence from animal, controlled 
human exposure and epidemiological studies, the 2006 Criteria Document 
concludes that people with asthma and other preexisting pulmonary 
diseases are likely to be among those at increased risk from 
O3 exposure. Altered physiological, morphological and 
biochemical states typical of respiratory diseases like asthma, COPD 
and chronic bronchitis may render people sensitive to additional 
oxidative burden induced by O3 exposure (EPA 2006a, section 
8.7). Children and adults with asthma are the group that has been 
studied most extensively. Evidence from controlled human exposure 
studies indicates that asthmatics may exhibit larger lung function 
decrements in response to O3 exposure than healthy controls. 
As discussed more fully in section II.A.4.b.ii below, asthmatics 
present a differential response profile for cellular, molecular, and 
biochemical parameters (EPA, 2006a, section 8.7.1) that are altered in 
response to acute O3 exposure. They can have larger 
inflammatory responses, as manifested by larger increases in markers of 
inflammation such as white bloods cells (e.g., PMNs) or inflammatory 
cytokines. Asthmatics, and people with allergic rhinitis, are more 
likely to mount an allergic-type response upon exposure to 
O3, as manifested by increases in white blood cells 
associated with allergy (i.e., eosinophils) and related molecules, 
which increase inflammation in the airways. The increased inflammatory 
and allergic responses also may be associated with the larger late-
phase responses that asthmatics can experience, which can include 
increased bronchoconstrictor responses to irritant substances or 
allergens and additional inflammation. In addition to the experimental 
evidence of lung function decrements, respiratory symptoms, and other 
respiratory effects in asthmatic populations, two large U.S. 
epidemiological studies as well as several smaller U.S. and 
international studies, have reported fairly robust associations between 
ambient O3 concentrations and measures of lung function and 
daily symptoms (e.g., chest tightness, wheeze, shortness of breath) in 
children with moderate to severe asthma and between O3 and 
increased asthma medication use (EPA, 2007a, chapter 6). These 
responses in asthmatics and others with lung disease provide biological 
plausibility for the more serious respiratory morbidity effects 
observed in epidemiological studies, such as emergency department 
visits and hospital admissions.
    Children with and without asthma were found to be particularly 
susceptible to O3 effects on lung function and generally 
have greater lung function responses than older people. The American 
Academy of Pediatrics (2004) notes that children and infants are among 
the population groups most susceptible to many air pollutants, 
including O3. This is in part because their lungs are still 
developing. For example, eighty percent of alveoli are formed after 
birth, and changes in lung development continue through adolescence 
(Dietert et al., 2000). Moreover, children have high minute ventilation 
rates and relatively high levels of physical activity which also 
increases their O3 dose (Plunkett et al., 1992). Thus, 
children are at-risk due to both their susceptibility and 
vulnerability.
    Looking more broadly at age-related differences in susceptibility, 
several mortality studies have investigated age-related differences in 
O3 effects (EPA, 2006a, section 7.6.7.2), primarily in the 
older adult population. Among the studies that observed positive 
associations between O3 and mortality, a comparison of all 
age or younger age (65 years of age) O3-mortality effect 
estimates to that of the elderly population (>65 years) indicates that, 
in general, the elderly population is more susceptible to O3 
mortality effects. There is supporting evidence of age-related 
differences in susceptibility to O3 lung function effects. 
The 2006 Criteria Document (section 7.6.7.2) concludes that the elderly 
population (>65 years of age) appear to be at greater risk of 
O3-related mortality and hospitalizations compared to all 
ages or younger populations, and children (<18 years of age) experience 
other potentially adverse respiratory health outcomes with increased 
O3 exposure.
    Controlled human exposure studies have also indicated a high degree 
of interindividual variability in some of the pulmonary physiological 
parameters, such as lung function decrements. The variable effects in 
individuals have been found to be reproducible, in other words, a 
person who has a large lung function response after exposure to 
O3 will likely have about the same response if exposed again 
to the same dose of O3 (EPA 2006a, section 6.1). In 
controlled human exposure studies, group mean responses are not 
representative of this segment of the population that has much larger 
than average responses to O3. Recent studies, discussed in 
section II.A.4.b.iv below, reported a role for genetic polymorphism 
(i.e., the occurrence together in the same population of more than one 
allele or genetic marker at the same locus with the least frequent 
allele or marker occurring more frequently than can be accounted for by 
mutation alone) in observed differences in antioxidant enzymes and 
genes involved in inflammation to modulate pulmonary function and 
inflammatory responses to O3 exposure. These observations 
suggest a potential role for these markers in the innate susceptibility 
to O3, however, the validity of these markers and their 
relevance in the context of prediction to population studies needs 
additional experimentation.
    Controlled human exposure studies that provide information about 
mechanisms of the initial response to O3 (e.g., lung 
function decrements, inflammation, and injury to the lung) also inform 
the selection of appropriate lag times to analyze in epidemiological 
studies through elucidation of the time course of these responses (EPA 
2006a, section 8.4.3). Based on the results of these studies, it would 
be reasonable to expect that lung function decrements could be detected 
epidemiologically within lags of 0 (same day) or 1 to 2 days following 
O3 exposure, given the rapid onset of lung function changes 
and their persistence for 24 to 48 hours among more responsive human 
subjects in controlled human exposure studies. Other responses take 
longer to develop and can persist for longer periods of time. For 
example, although asthmatic individuals may begin to experience 
symptoms soon after O3 exposure, it may take anywhere from 1 
to 3 days after exposure for these subjects to seek medical attention 
as a result of increased airway responsiveness or inflammation that may 
persist for 2 to 3 days. This may be reflected by epidemiologic 
observations of significantly increased risk for asthma-related 
emergency department visits or hospital admissions with 1- to 3-day 
lags, or, perhaps, enhanced distributed lag risks (combined across 3 
days) for such morbidity indicators. Analogously, one might project 
increased mortality within 0- to 3-day lags as a possible consequence 
of O3-induced increases in clotting agents arising from the 
cascade of events, starting with cell injury described above, occurring 
within 12 to 24 hours of O3 exposure. The time course for 
many of these initial responses to O3 is highly variable.

[[Page 2949]]

Moreover these observations pertain only to the initial response to 
O3. Consequent responses can follow. For example, 
J[ouml]rres et al., (1996) found that in subjects with asthma and 
allergic rhinitis, a maximum percent fall in FEV1 of 27.9% 
and 7.8%, respectively, occurred 3 days after O3 exposure 
when they were challenged with of the highest common dose of allergen.
2. Nature of Effects
    The 2006 Criteria Document provides new evidence that notably 
enhances our understanding of short-term and prolonged exposure 
effects, including effects on lung function, symptoms, and inflammatory 
effects reported in controlled exposure studies. These studies support 
and extend the findings of the previous Criteria Document. There is 
also a significant body of new epidemiological evidence of associations 
between short-term and prolonged exposure to O3 and effects 
such as premature mortality, hospital admissions and emergency 
department visits for respiratory (e.g., asthma) causes. Key 
epidemiological and controlled human exposure studies are summarized 
below and discussed in chapter 3 of the 2007 Staff Paper, which is 
based on scientific evidence critically reviewed in chapters 5, 6, and 
7 of the 2006 Criteria Document, as well as the Criteria Document's 
integration of scientific evidence contained in chapter 8.\14\ 
Conclusions drawn about O3-related health effects are based 
upon the full body of evidence from controlled human exposure, 
epidemiological and toxicological data contained in the 2006 Criteria 
Document.
---------------------------------------------------------------------------

    \14\ Health effects discussions are also drawn from the more 
detailed information and tables presented in the Criteria Document's 
annexes.
---------------------------------------------------------------------------

a. Morbidity
    This section summarizes scientific information on the effects of 
inhalation of O3, including public health effects of short-
term, prolonged, and long-term exposures on respiratory morbidity and 
cardiovascular system effects, as discussed in chapters 6, 7 and 8 of 
the 2006 Criteria Document and chapter 3 of the 2007 Staff Paper. This 
section also summarizes the uncertainty about the potential indirect 
effects on public health associated with changes due to increases in 
UV-B radiation exposure, such as UV-B radiation-related skin cancers, 
that may be associated with reductions in ambient levels of ground-
level O3, as discussed in chapter 10 of the 2006 Criteria 
Document and chapter 3 of the 2007 Staff Paper.
i. Effects on the Respiratory System From Short-term and Prolonged 
O3 Exposures
    Controlled human exposure studies have shown that O3 
induces a variety of health effects, including: Lung function 
decrements, respiratory symptoms, increased airway responsiveness, 
respiratory inflammation and permeability, increased susceptibility to 
respiratory infection, and acute morphological effects. Epidemiology 
studies have reported associations between O3 exposures 
(i.e., 1-hour, 8-hour and 24-hour) and a wide range of respiratory-
related health effects including: pulmonary function decrements; 
respiratory symptoms; increased asthma medication use; increased school 
absences; increased emergency department visits and hospital 
admissions.
(a) Pulmonary Function Decrements, Respiratory Symptoms, and Asthma 
Medication Use
(i) Results From Controlled Human Exposure Studies
    A large number of studies published prior to 1996 that investigated 
short-term O3 exposure health effects on the respiratory 
system from short-term O3 exposures were reviewed in the 
1986 and 1996 Criteria Documents (EPA, 1986, 1996a). In the 1997 
review, 0.50 ppm was the lowest O3 concentration at which 
statistically significant reductions in forced vital capacity (FVC) and 
forced expiratory volume in 1 second (FEV1) were reported in 
sedentary subjects. During exercise, spirometric (lung function) and 
symptomatic responses were observed at much lower O3 
exposures. When minute ventilation was considerably increased by 
continuous exercise (CE) during O3 exposures lasting 2 hour 
or less at [gteqt] 0.12 ppm, healthy subjects generally experienced 
decreases in FEV1, FVC, and other measures of lung function; 
increases in specific airway resistance (sRaw), breathing frequency, 
and airway responsiveness; and symptoms such as cough, pain on deep 
inspiration, shortness of breath, throat irritation, and wheezing. When 
exposures were increased to 4- to 8-hours in duration, statistically 
significant lung function and symptom responses were reported at 
O3 concentrations as low as 0.08 ppm and at lower minute 
ventilation (i.e., moderate rather than high level exercise) than the 
shorter duration studies.
    The most important observations drawn from studies reviewed in the 
1996 Criteria Document were that: (1) Young healthy adults exposed to 
O3 concentrations = 0.080 ppm develop 
significant, reversible, transient decrements in pulmonary function if 
minute ventilation or duration of exposure is increased sufficiently; 
(2) children experience similar lung function responses but report 
lesser symptoms from O3 exposure relative to young adults; 
(3) O3-induced lung function responses are decreased in the 
elderly relative to young adults; (4) there is a large degree of 
intersubject variability in physiological and symptomatic responses to 
O3 but responses tend to be reproducible within a given 
individual over a period of several months; (5) subjects exposed 
repeatedly to O3 for several days show an attenuation of 
response upon successive exposures, but this attenuation is lost after 
about a week without exposure; and (6) acute O3 exposure 
initiates an inflammatory response which may persist for at least 18 to 
24 hours post exposure.
    The development of these respiratory effects is time-dependent 
during both exposure and recovery periods, with great overlap for 
development and disappearance of the effects. In healthy human subjects 
exposed to typical ambient O3 levels near 0.120 ppm, lung 
function responses largely resolve within 4 to 6 hours postexposure, 
but cellular effects persist for about 24 hours. In these healthy 
subjects, small residual lung function effects are almost completely 
gone within 24 hours, while in hyperresponsive subjects, recovery can 
take as much as 48 hour to return to baseline. The majority of these 
responses are attenuated after repeated consecutive exposures, but such 
attenuation to O3 is lost one week postexposure.
    Since 1996, there have been a number of studies published 
investigating lung function and symptomatic responses that generally 
support the observations previously drawn. Recent studies for acute 
exposures of 1 to 2 hours and 6 to 8 hours in duration are compiled in 
the 2007 Staff Paper (Appendix 3C). As summarized in more detail in the 
2007 Staff Paper (section 3.3.1.1), among the more important of the 
recent studies that examined changes in FEV1 in large 
numbers of subjects over a range of 1-2 hours at exposure levels of 
0.080 to 0.40 ppm were studies by McDonnell et al. (1997) and Ultman et 
al. (2004). These studies observed considerable intersubject 
variability in FEV1 decrements, which was consistent with 
findings in the 1996 Criteria Document.
    For prolonged exposures (4 to 8 hours) in the range of 0.080 to 
0.160 ppm O3 using moderate intermittent

[[Page 2950]]

exercise and typically using square-wave exposure patterns (i.e., a 
constant exposure level during time of exposure), several pre- and 
post-1996 studies (Folinsbee et al., 1988,1994; Horstman et al., 1990; 
Adams, 2002, 2003a, 2006) have reported statistically significant lung 
function responses and increased symptoms in healthy adults with 
increasing duration of exposure, O3 concentration, and 
minute ventilation. Studies that employed triangular exposure patterns 
(i.e., integrated exposures that begin at a low level, rise to a peak, 
and return to a low level during the exposure) (Hazucha et al., 1992; 
Adams 2003a, 2006) suggest that the triangular exposure pattern can 
potentially lead to greater FEV1 decrements and respiratory 
symptoms than square-wave exposures (when the overall O3 
doses are equal). These results suggest that peak exposures, reflective 
of the pattern of ambient O3 concentrations in some 
locations, are important in terms of O3 health effects.
    McDonnell (1996) used data from a series of studies to investigate 
the frequency distributions of FEV1 decrements following 6.6 
hour exposures and found statistically significant, but relatively 
small, group mean decreases in average FEV1 responses 
(between 5 and 10 percent) at 0.080 ppm O3.\15\ Notably, 
about 26 percent of the 60 exposed subjects had lung function 
decrements > 10 percent, including about 8 percent of the subjects that 
experienced large decrements (> 20 percent) (EPA, 2007b, Figure 3-1A). 
These results (which were not corrected for exercise in filtered air 
responses) demonstrate that while average responses may be relatively 
small at the 0.080 ppm exposure level, some individuals experience more 
severe effects that may be clinically significant. Similar results at 
the 0.080 ppm exposure level (for 6.6 hours during intermittent 
exercise) were seen in more recent studies of 30 healthy young adults 
by Adams (2002, 2006).\16\ In Adams (2006), relatively small but 
statistically significant lung function decrements and respiratory 
symptom responses were found (for both square-wave and triangular 
exposure patterns), with 17 percent of the subjects (5 of 30) 
experiencing [gteqt] 10 percent FEV1 decrements (comparing 
pre- and post-exposures) when the results were not corrected for the 
effects of exercise alone in filtered air (EPA, 2007b, Figure 3-1B) and 
with 23 percent of subjects (7 of 30) experiencing such effects when 
the results were corrected (EPA, 2007b, p. 3-6).\17\
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    \15\ This study and other studies (Folinsbee et al., 1988; 
Horstman et al., 1990; and McDonnell et al., 1991), conducted in 
EPA's human studies research facility in Chapel Hill, NC, measured 
ozone concentrations to within +/- 5 percent or +/- 0.004 ppm at the 
0.080 ppm exposure level.
    \16\ These studies, conducted at a facility at the University of 
California, in Davis, CA, reported O3 concentrations to 
be accurate within +/- 0.003 ppm over the range of concentrations 
included in these studies.
    \17\ These distributional results presented in the Criteria 
Document and Staff Paper for the Adams (2006) study are based on 
data for squate-wave exposures to 0.080 ppm that were not included 
in the publication but were obtained from the author.
---------------------------------------------------------------------------

    These studies by Adams (2002, 2006) were notable in that they were 
the only controlled exposure human studies available at the time of the 
2008 rulemaking that examined respiratory effects associated with 
prolonged O3 exposures at levels below 0.080 ppm, which was 
the lowest exposure level that had been examined in the 1997 review. 
The Adams (2006) study investigated a range of exposure levels (0.000, 
0.040, 0.060, and 0.080 ppm O3) using square-wave and 
triangular exposure patterns. The study was designed to examine hour-
by-hour changes in pulmonary function (FEV1) and respiratory 
symptom responses (total subjective symptoms (TSS) and pain on deep 
inspiration (PDI)) between these various exposure protocols at six 
different time points within the exposure periods to investigate the 
effects of different patterns of exposure. At the 0.060 ppm exposure 
level, the author reported no statistically significant differences for 
FEV1 decrements nor for most respiratory symptoms responses. 
Statistically significant responses were reported only for TSS for the 
triangular exposure pattern toward the end of the exposure period, with 
the PDI responses being noted as following a closely similar pattern 
(Adams, 2006, p. 131-132). EPA's reanalysis of the data from the Adams 
(2006) study addressed the more fundamental question of whether there 
were statistically significant differences in responses before and 
after the 6.6 hour exposure period (Brown, 2007), and used a standard 
statistical method appropriate for a simple before-and-after 
comparison. The statistical method used by EPA had been used previously 
by other researchers to address this same question. EPA's reanalysis of 
the data from the Adams (2006) study, comparing FEV1 
responses pre- and post-exposure at the 0.060 ppm exposure level, found 
small group mean differences from responses to filtered air that were 
statistically significant (Brown, 2007).\18\
---------------------------------------------------------------------------

    \18\ Dr. Adams submitted comments on EPA's reanalysis in which 
he concluded that the FEV1 response in healthy young 
adults at the 0.060 ppm exposure level in his study (Adams, 2006a) 
does not demonstrate a significant mean effect by ordinarily 
acceptable statistical analysis, but is rather in somewhat of a gray 
area, both in terms of a biologically meaningful response and a 
statistically significant response (Adams, 2007). The EPA responded 
to these comments in the 2008 final rule (73 FR 16455) and in the 
Response to Comments (EPA, 2008, pp. 26-28).
---------------------------------------------------------------------------

    Further examination of the post-exposure FEV1 data and 
mean data at other time points and concentrations also suggest a 
pattern of response at 0.06 ppm that is consistent with a dose-response 
relationship rather than random variability. For example, the response 
at 5.6 hours was similar to that of the post-exposure 6.6 hour response 
and appeared to also differ from the FA response. At the 0.08 ppm 
level, the subjects in this study did not appear to be more responsive 
to O3 than subjects in previous studies, as the observed 
response was similar to that of previous studies (Adams, 2003a,b; 
Horstman et al., 1990; McDonnell et al., 1991). Although of much 
smaller magnitude, the temporal pattern of the 0.06 ppm response was 
generally consistent with the temporal patterns of response to higher 
concentrations of O3 in this and other studies. These 
findings are not unexpected because the previously observed group mean 
FEV1 responses to 0.08 ppm were in the range of 6-9% 
suggesting that exposure to lower concentrations of O3 would 
result in smaller, but real group mean FEV1 decrements, 
i.e., the responses to 0.060 ppm O3 are consistent with the 
presence of a smooth exposure-response curve with responses that do not 
end abruptly below 0.080 ppm.
    Moreover, the Adams studies (2002, 2006) also report a small 
percentage of subjects experiencing moderate lung function decrements 
([gteqt] 10 percent) at the 0.060 ppm exposure level. Based on study 
data (Adams, 2006) provided by the author, 7 percent of the subjects (2 
of 30 subjects) experienced notable FEV1 decrements (>= 10 
percent) with the square wave exposure pattern at the 0.060 ppm 
exposure level (comparing pre- and post-exposures) when the results 
were corrected for the effects of exercise alone in filtered air (EPA, 
2007b, p. 3-6). Furthermore, in a prior publication (Adams, 2002), the 
author stated that, ``some sensitive subjects experience notable 
effects at 0.06 ppm,'' based on the observation that 20% of subjects 
exposed to 0.06 ppm O3 (in a face mask exposure study) had 
greater than a 10% decrement in FEV1 even though the group 
mean response was not statistically different from the filtered air 
response. The effects described by Adams (2002), along with

[[Page 2951]]

the reanalysis of the Adams (2006) data as described above, demonstrate 
considerable inter-individual variability in responses of healthy 
adults at the 0.060 ppm level with some individuals experiencing 
greater than 10% decrements in FEV1. The observation of 
statistically significant small group mean lung function decrements in 
healthy adults at 0.060 ppm O3 lowers the lowest-observed-
effects level found in controlled human exposure studies for lung 
function decrements and respiratory symptoms.
    Of potentially greater concern is the magnitude of the lung 
function decrements in the small group of healthy subjects who had the 
largest responses (i.e., FEV1 decrements [gteqt] 10%). This 
is a concern because for active healthy people, moderate levels of 
functional responses (e.g., FEV1 decrements of [gteqt] 10% 
but < 20%) and/or moderate symptomatic responses would likely interfere 
with normal activity for relatively few responsive individuals. 
However, for people with lung disease, even moderate functional or 
symptomatic responses would likely interfere with normal activity for 
many individuals, and would likely result in more frequent use of 
medication (see section II.A.4 below).
(ii) Results of Epidemiological and Field Studies
    A relatively large number of field studies investigating the 
effects of ambient O3 concentrations, in combination with 
other air pollutants, on lung function decrements and respiratory 
symptoms has been published over the last decade that support the major 
findings of the 1996 Criteria Document that lung function changes, as 
measured by decrements in FEV1 or peak expiratory flow 
(PEF), and respiratory symptoms in healthy adults and asthmatic 
children are closely correlated to ambient O3 
concentrations. Pre-1996 field studies focused primarily on children 
attending summer camps and found O3-related impacts on 
measures of lung function, but not respiratory symptoms, in healthy 
children. The newer studies have expanded to evaluate O3-
related effects on outdoor workers, athletes, the elderly, hikers, 
school children, and asthmatics. Collectively, these studies confirm 
and extend clinical observations that prolonged (i.e., 6-8 hour) 
exposure periods, combined with elevated levels of exertion or 
exercise, increase the dose of O3 to the lungs at a given 
ambient exposure level and result in larger lung function effects. The 
results of one large study of hikers (Korrick et al., 1998), which 
reported outcome measures stratified by several factors (e.g., gender, 
age, smoking status, presence of asthma) within a population capable of 
more than normal exertion, provide useful insight. In this study, lung 
function was measured before and after hiking, and individual 
O3 exposures were estimated by averaging hourly 
O3 concentrations from ambient monitors located at the base 
and summit. The mean 8-hour average O3 concentration was 
0.040 ppm (8-hour average concentration range of 0.021 ppm to 0.074 ppm 
O3). Decreased lung function was associated with 
O3 exposure, with the greatest effect estimates reported for 
the subgroup that reported having asthma or wheezing, and for those who 
hiked for longer periods of time.
    Asthma panel studies conducted both in the U.S. and in other 
countries have reported that decrements in PEF are associated with 
routine O3 exposures among asthmatic and healthy people. One 
large U.S. multicity study, the National Cooperative Inner City Asthma 
Study or NCICAS, (Mortimer et al., 2002) examined O3-related 
changes in PEF in 846 asthmatic children from 8 urban areas and 
reported that the incidence of [gteqt] 10 percent decrements in morning 
PEF are associated with increases in 8-hour average O3 for a 
5-day cumulative lag, suggesting that O3 exposure may be 
associated with clinically significant changes in PEF in asthmatic 
children; however, no associations were reported with evening PEF. The 
mean 8-hour average O3 was 0.048 ppm across the 8 cities. 
Excluding days when 8-hour average O3 was greater than 0.080 
ppm (less than 5 percent of days), the associations with morning PEF 
remained statistically significant. Mortimer et al. (2002) discussed 
potential biological mechanisms for delayed effects on pulmonary 
function in asthma, which included increased nonspecific airway 
responsiveness secondary to airway inflammation due to O3 
exposure. Two other panel studies (Romieu et al., 1996, 1997) carried 
out simultaneously in northern and southwestern Mexico City with mildly 
asthmatic school children reported statistically significant 
O3-related reductions in PEF, with variations in effect 
depending on lag time and time of day. Mean 1-hour maximum 
O3 concentrations in these locations ranged from 0.190 ppm 
in northern Mexico City to 0.196 ppm in southwestern Mexico City. While 
several studies report statistically significant associations between 
O3 exposure and reduced PEF in asthmatics, other studies did 
not, possibly due to low levels of O3 exposure. EPA 
concludes that these studies collectively indicate that O3 
may be associated with short-term declines in lung function in 
asthmatic individuals and that the Mortimer et al. (2002) study showed 
statistically significant effects at concentrations in the range below 
0.080 ppm O3.
    Most of the panel studies which have investigated associations 
between O3 exposure and respiratory symptoms or increased 
use of asthma medication are focused on asthmatic children. Two large 
U.S. studies (Mortimer et al., 2002; Gent et al., 2003) have reported 
associations between ambient O3 concentrations and daily 
symptoms/asthma medication use, even after adjustment for copollutants. 
Results were more mixed, meaning that a greater proportion of studies 
were not both positive and statistically significant, across smaller 
U.S. and international studies that focused on these health endpoints.
    The NCICAS reported morning symptoms in 846 asthmatic children from 
8 U.S. urban areas to be most strongly associated with a cumulative 1- 
to 4-day lag of O3 concentrations (Mortimer et al., 2002). 
The NCICAS used standard protocols that included instructing caretakers 
of the subjects to record symptoms (including cough, chest tightness, 
and wheeze) in the daily diary by observing or asking the child. While 
these associations were not statistically significant in several 
cities, when the individual data are pooled from all eight cities, 
statistically significant effects were observed for the incidence of 
symptoms. The authors also reported that the odds ratios remained 
essentially the same and statistically significant for the incidence of 
morning symptoms when days with 8-hour O3 concentrations 
above 0.080 ppm were excluded. These days represented less than 5 
percent of days in the study.
    Gent and colleagues (2003) followed 271 asthmatic children under 
age 12 and living in southern New England for 6 months (April through 
September) using a daily symptom diary. They found that mean 1-hour max 
O3 and 8-hour max O3 concentrations were 0.0586 
ppm and 0.0513 ppm, respectively. The data were analyzed for two 
separate groups of subjects, those who used maintenance asthma 
medications during the follow-up period and those who did not. The need 
for regular medication was considered to be a proxy for more severe 
asthma. Not taking any medication on a regular basis and not needing to 
use a bronchodilator would suggest the

[[Page 2952]]

presence of very mild asthma. Statistically significant effects of 1-
day lag O3 were observed on a variety of respiratory 
symptoms only in the medication user group. Both daily 1-hour max and 
8-hour max O3 concentrations were similarly related to 
symptoms such as chest tightness and shortness of breath. Effects of 
O3, but not PM2.5, remained significant and even 
increased in magnitude in two-pollutant models. Some of the 
associations were noted at 1-hour max O3 levels below 0.060 
ppm. In contrast, no effects were observed among asthmatics not using 
maintenance medication. In terms of person-days of follow-up, this is 
one of the larger studies currently available that address symptom 
outcomes in relation to O3 and provides supportive evidence 
for effects of O3 independent of PM2.5. Study 
limitations include the post-hoc nature of the population 
stratification by medication use. Also, the study did not account for 
all of the important meteorological factors that might influence these 
results, such as relative humidity or dew point.
    The multicity study by Mortimer et al. (2002), which examined an 
asthmatic population representative of the United States, and several 
single-city studies indicate a robust association of O3 
concentrations with respiratory symptoms and increased medication use 
in asthmatics. While there are a number of well-conducted, albeit 
relatively smaller, U.S. studies which showed only limited or a lack of 
evidence for symptom increases associated with O3 exposure, 
these studies had less statistical power and/or were conducted in areas 
with relatively low 1-hour maximum average O3 levels, in the 
range of 0.03 to 0.09 ppm. The 2006 Criteria Document concludes that 
the asthma panel studies, as a group, and the NCICAS in particular, 
indicate a positive association between ambient concentrations and 
respiratory symptoms and increased medication use in asthmatics. The 
evidence has continued to expand since 1996 and now is considered to be 
much stronger than in the 1997 review of the O3 primary 
standard.
    School absenteeism is another potential surrogate for the health 
implications of O3 exposure in children. The association 
between school absenteeism and ambient O3 concentrations was 
assessed in two relatively large field studies. The first study, Chen 
et al. (2000), examined total daily school absenteeism in about 28,000 
elementary school students in Nevada over a 2-year period (after 
adjusting for PM10 and CO concentrations) and found that 
ambient O3 concentrations with a distributed lag of 14 days 
were statistically significantly associated with an increased rate of 
school absences. The second study, Gilliland et al. (2001), studied 
O3-related absences among about 2,000 4th grade students in 
12 southern California communities and found statistically significant 
associations between 8-hour average O3 concentrations (with 
a distributed lag out to 30 days) and all absence categories, and 
particularly for respiratory causes. Neither PM10 nor 
NO2 were associated with any respiratory or nonrespiratory 
illness-related absences in single pollutant models. The 2006 Criteria 
Document concludes that these studies of school absences suggest that 
ambient O3 concentrations, accumulated over two to four 
weeks, may be associated with school absenteeism, and particularly 
illness-related absences, but further replication is needed before firm 
conclusions can be reached regarding the effect of O3 on 
school absences. In addition, more research is needed to help shed 
light on the implications of variation in the duration of the lag 
structures (i.e., 1 day, 5 days, 14 days, and 30 days) found both 
across studies and within data sets by health endpoint and exposure 
metric.
(b) Increased Airway Responsiveness
    As discussed in more detail in the 2006 Criteria Document (section 
6.8) and the 2007 Staff Paper (section 3.3.1.1.2), increased airway 
responsiveness, also known as airway hyperresponsiveness (AHR) or 
bronchial hyperreactivity, refers to a condition in which the 
propensity for the airways to bronchoconstrict due to a variety of 
stimuli (e.g., exposure to cold air, allergens, or exercise) becomes 
augmented. This condition is typically quantified by measuring the 
decrement in pulmonary function after inhalation exposure to specific 
(e.g., antigen, allergen) or nonspecific (e.g., methacholine, 
histamine) bronchoconstrictor stimuli. Exposure to O3 causes 
an increase in airway responsiveness as indicated by a reduction in the 
concentration of stimuli required to produce a given reduction in 
FEV1 or increase in airway obstruction. Increased airway 
responsiveness is an important consequence of exposure to O3 
because its presence means that the airways are predisposed to 
narrowing on exposure to various stimuli, such as specific allergens, 
cold air or SO2. Statistically significant and clinically 
relevant decreases in pulmonary function have been observed in early 
phase allergen response in subjects with allergic rhinitis after 
consecutive (4-day) 3-hour exposures to 0.125 ppm O3 (Holz 
et al., 2002). Similar increased airway responsiveness in asthmatics to 
house dust mite antigen 16 to 18 hours after exposure to a single dose 
of O3 (0.160 ppm for 7.6 hours) was observed. These 
observations, based on O3 exposures to levels much higher 
than the 0.084 ppm standard level suggest that O3 exposure 
may be a clinically important factor that can exacerbate the response 
to ambient bronchoconstrictor substances in individuals with 
preexisting allergic asthma or rhinitis. Further, O3 may 
have an immediate impact on the lung function of asthmatics as well as 
contribute to effects that persist for longer periods.
    Kreit et al. (1989) found that O3 can induce increased 
airway responsiveness in asthmatic subjects to O3, who 
typically have increased airway responsiveness at baseline. A 
subsequent study (J[ouml]rres et al., 1996) suggested an increase in 
specific (i.e., allergen-induced) airway reactivity in subjects with 
allergic asthma, and to a lesser extent in subjects with allergic 
rhinitis after short-term exposure to higher O3 levels; 
other studies reported similar results. According to one study 
(Folinsbee and Hazucha, 2000), changes in airway responsiveness after 
O3 exposure resolve more slowly than changes in 
FEV1 or respiratory symptoms. Other studies of repeated 
exposure to O3 suggest that changes in airway responsiveness 
tend to be somewhat less affected by attenuation with consecutive 
exposures than changes in FEV1 (EPA, 2006a, section 6.8).
    The 2006 Criteria Document (section 6.8) concludes that 
O3 exposure is linked with increased airway responsiveness. 
Both human and animal studies indicate that increased airway 
responsiveness is not mechanistically associated with inflammation, and 
does not appear to be strongly associated with initial decrements in 
lung function or increases in symptoms. As a result of increased airway 
responsiveness induced by O3 exposure, human airways may be 
more susceptible to a variety of stimuli, including antigens, 
chemicals, and particles. Because asthmatic subjects typically have 
increased airway responsiveness at baseline, enhanced bronchial 
response to antigens in asthmatics raises potential public health 
concerns as they could lead to increased morbidity (e.g., medication 
usage, school absences, emergency room visits, hospital admissions) or 
to more persistent alterations in airway

[[Page 2953]]

responsiveness (EPA 2006a, p. 8-21). As such, increased airway 
responsiveness after O3 exposure represents a plausible link 
between O3 exposure and increased hospital admissions.
(c) Respiratory Inflammation and Increased Permeability
    Based on evidence from the 1997 review, acute inflammatory 
responses in the lung have been observed subsequent to 6.6 hour 
O3 exposures to the lowest tested level--0.080 ppm--in 
healthy adults engaged in moderately high exercise (section 6.9 of the 
2006 Criteria Document and section 3.3.1.3 of the 2007 Staff Paper). 
Some of these prior studies suggest that inflammatory responses may be 
detected in some individuals following O3 exposures in the 
absence of O3-induced pulmonary decrements in those 
subjects. These studies also demonstrate that short-term exposures to 
O3 also can cause increased permeability in the lungs of 
humans and experimental animals. Inflammatory responses and epithelial 
permeability have been seen to be independent of spirometric responses. 
Not only are the newer lung inflammation and increased cellular 
permeability findings discussed in the 2006 Criteria Document (section 
8.4.2) consistent with the 1997 review, but they provide better 
characterization of the physiological mechanisms by which O3 
causes these effects.
    Lung inflammation and increased permeability, which are distinct 
events controlled by different mechanisms, are two commonly observed 
effects of O3 exposure observed in all of the species 
studied. Increased cellular permeability is a disruption of the lung 
barrier that leads to leakage of serum proteins, influx of 
polymorphonuclear leukocytes (neutrophils or PMNs), release of 
bioactive mediators, and movement of compounds from the airspaces into 
the blood.
    A number of controlled human exposure studies have analyzed 
bronchoalveolar lavage (BAL) and nasal lavage (NL) \19\ fluids and 
cells for markers of inflammation and lung damage (EPA, 2006a, Annex 
AX6). Increased lung inflammation is demonstrated by the presence of 
neutrophils found in BAL fluid in the lungs, which has long been 
accepted as a hallmark of inflammation. It is apparent, however, that 
inflammation within airway tissues may persist beyond the point that 
inflammatory cells are found in the BAL fluid. Soluble mediators of 
inflammation, such as cytokines and arachidonic acid metabolites have 
been measured in the BAL fluid of humans exposed to O3. In 
addition to their role in inflammation, many of these compounds have 
bronchoconstrictive properties and may be involved in increased airway 
responsiveness following O3 exposure. An in vitro study of 
epithelial cells from nonatopic and atopic asthmatics exposed to 0.010 
to 0.100 ppm O3 showed significantly increased permeability 
compared to cells from normal persons. This indicates a potentially 
inherent susceptibility of cells from asthmatic individuals for 
O3-induced permeability.
---------------------------------------------------------------------------

    \19\ Graham and Koren (1990) compared inflammatory mediators 
present in NL and BAL fluids of humans exposed to 0.4 ppm 
O3 for 2 hours and found similar increases in PMNs in 
both fluids, suggesting a qualitative correlation between 
inflammatory changes in the lower airways (BAL) and upper 
respiratory tract (NL).
---------------------------------------------------------------------------

    In the 1996 Criteria Document, assessment of controlled human 
exposure studies indicated that a single, acute (1 to 4 hours) 
O3 exposure (>= 0.080 to 0.100 ppm) of subjects engaged in 
moderate to heavy exercise could induce a number of cellular and 
biochemical changes suggestive of pulmonary inflammation and lung 
permeability (EPA, 2006a, p. 8-22). These changes persisted for at 
least 18 hours. Markers from BAL fluid following both 2-hour and 4-hour 
O3 exposures repeated up to 5 days indicate that there is 
ongoing cellular damage irrespective of attenuation of some cellular 
inflammatory responses of the airways, pulmonary function, and symptom 
scores (EPA, 2006a, p. 8-22). Acute airway inflammation was shown in 
Devlin et al. (1990) to occur among adults exposed to 0.080 ppm 
O3 for 6.6 hours with exercise. McBride et al. (1994) 
reported that asthmatic subjects were more sensitive than non-
asthmatics to upper airway inflammation for O3 exposures 
that did not affect pulmonary function (EPA, 2006a, p. 6-33). However, 
the public health significance of these changes is not entirely clear.
    The studies reporting inflammatory responses and markers of lung 
injury have clearly demonstrated that there is significant variation in 
response of subjects exposed, especially to 6.6 hours O3 
exposures at 0.080 and 0.100 ppm. To provide some perspective on the 
public health impact for these effects, the 2007 Staff Paper (section 
3.3.1.1.3) notes that one study (Devlin et al., 1991) showed that 
roughly 10 to 50 percent of the 18 young healthy adult subjects 
experienced notable increases (i.e., >= 2 fold increase) in most of the 
inflammatory and cellular injury indicators analyzed, associated with 
6.6-hour exposures at 0.080 ppm. Similar, although in some cases 
higher, fractions of the population of 10 healthy adults tested saw > 2 
fold increases associated with 6.6-hour exposures to 0.100 ppm. The 
authors of this study expressed the view that ``susceptible 
subpopulations such as the very young, elderly, and people with 
pulmonary impairment or disease may be even more affected'' (Devlin et 
al., 1991).
    Since 1996, a substantial number of human exposure studies have 
been published which have provided important new information on lung 
inflammation and epithelial permeability. Mudway and Kelly (2004) 
examined O3-induced inflammatory responses and epithelial 
permeability with a meta-analysis of 21 controlled human exposure 
studies and showed that an influx in neutrophils and protein in healthy 
subjects is associated with total O3 dose (product of 
O3 concentration, exposure duration, and minute ventilation) 
(EPA, 2006a, p. 6-34). Results of the analysis suggest that the time 
course for inflammatory responses (including recruitment of neutrophils 
and other soluble mediators) is not clearly established, but there is 
evidence that attenuation profiles for many of these parameters are 
different (EPA, 2006a, p. 8-22).
    The 2006 Criteria Document (chapter 8) concludes that interaction 
of O3 with lipid constituents of epithelial lining fluid 
(ELF) and cell membranes and the induction of oxidative stress is 
implicated in injury and inflammation. Alterations in the expression of 
cytokines, chemokines, and adhesion molecules, indicative of an ongoing 
oxidative stress response, as well as injury repair and regeneration 
processes, have been reported in animal toxicology and human in vitro 
studies evaluating biochemical mediators implicated in injury and 
inflammation. While antioxidants in ELF confer some protection, 
O3 reactivity is not eliminated at environmentally relevant 
exposures (2006 Criteria Document, p. 8-24). Further, antioxidant 
reactivity with O3 is both species-specific and dose-
dependent.
(d) Increased Susceptibility to Respiratory Infection
    As discussed in more detail in the 2006 Criteria Document (sections 
5.2.2, 6.9.6, and 8.4.2), short-term exposures to O3 have 
been shown to impair physiological defense capabilities in experimental 
animals by depressing alveolar macrophage (AM) functions and by 
altering the mucociliary clearance of inhaled particles and microbes 
resulting in increased susceptibility to respiratory infection.

[[Page 2954]]

Short-term O3 exposures also interfere with the clearance 
process by accelerating clearance for low doses and slowing clearance 
for high doses. Animal toxicological studies have reported that acute 
O3 exposures suppress alveolar phagocytosis and immune 
system functions. Impairment of host defenses and subsequent increased 
susceptibility to bacterial lung infection in laboratory animals has 
been induced by short-term exposures to O3 levels as low as 
0.080 ppm.
    A single controlled human exposure study reviewed in the 1996 
Criteria Document (p. 8-26) reported that exposure to 0.080 to 0.100 
ppm O3 for 6.6 hours (with moderate exercise) induced 
decrements in the ability of AMs to phagocytose microorganisms. 
Integrating the recent animal study results with human exposure 
evidence available in the 1996 Criteria Document, the 2006 Criteria 
Document concludes that available evidence indicates that short-term 
O3 exposures have the potential to impair host defenses in 
humans, primarily by interfering with AM function. Any impairment in AM 
function may lead to decreased clearance of microorganisms or nonviable 
particles. Compromised AM functions in asthmatics may increase their 
susceptibility to other O3 effects, the effects of 
particles, and respiratory infections (EPA, 2006a, p. 8-26).
(e) Morphological Effects
    The 1996 Criteria Document found that short-term O3 
exposures cause similar alterations in lung morphology in all 
laboratory animal species studied, including primates. As discussed in 
the 2007 Staff Paper (section 3.3.1.1.5), cells in the centriacinar 
region (CAR) of the lung (the segment between the last conducting 
airway and the gas exchange region) have been recognized as a primary 
target of O3-induced damage (epithelial cell necrosis and 
remodeling of respiratory bronchioles), possibly because epithelium in 
this region receives the greatest dose of O3 delivered to 
the lower respiratory tract. Following chronic O3 exposure, 
structural changes have been observed in the CAR, the region typically 
affected in most chronic airway diseases of the human lung (EPA, 2006a, 
p. 8-24).
    Ciliated cells in the nasal cavity and airways, as well as Type I 
cells in the gas-exchange region, are also identified as targets. While 
short-term O3 exposures can cause epithelial cell 
profileration and fibrolitic changes in the CAR, these changes appear 
to be transient with recovery occurring after exposure, depending on 
species and O3 dose. The potential impacts of repeated 
short-term and chronic morphological effects of O3 exposure 
are discussed below in the section on effects from long-term exposures. 
Long-term or prolonged exposure has been found to cause chronic lesions 
similar to early lesions found in individuals with respiratory 
bronchiolitis, which have the potential to progress to fibrotic lung 
disease (2006 Criteria Document, p. 8-25).
    Recent studies continue to show that short-term and sub-chronic 
exposures to O3 cause similar alterations in lung structure 
in a variety of experimental animal species. For example, a series of 
new studies that used infant rhesus monkeys and simulated seasonal 
ambient exposure (0.5 ppm 8 hours/day for 5 days, every 14 days for 11 
episodes) reported remodeling in the distal airways; abnormalities in 
tracheal basement membrane; eosinophil accumulation in conducting 
airways; and decrements in airway innervation (2006 Criteria Document, 
p. 8-25). Based on evidence from animal toxicological studies, short-
term and sub-chronic exposures to O3 can cause morphological 
changes in the respiratory systems, particularly in the CAR, of a 
number of laboratory animal species (EPA, 2006a, section 5.2.4).
(f) Emergency Department Visits/Hospital Admissions for Respiratory 
Causes
    Increased summertime emergency department visits and hospital 
admissions for respiratory causes have been associated with ambient 
exposures to O3. As discussed in section 3.3.1.1.6 of the 
2007 Staff Paper, numerous studies conducted in various locations in 
the U.S. and Canada consistently have shown a relationship between 
ambient O3 levels and increased incidence of emergency 
department visits and hospital admissions for respiratory causes, even 
after controlling for modifying factors, such as weather and 
copollutants. Such associations between elevated ambient O3 
during summer months and increased hospital admissions have a plausible 
biological basis in the human and animal evidence of functional, 
symptomatic, and physiologic effects discussed above and in the 
increased susceptibility to respiratory infections observed in 
laboratory animals.
    In the 1997 review of the O3 NAAQS, the Criteria 
Document evaluated emergency department visits and hospital admissions 
as possible outcomes following exposure to O3 (EPA, 2006a, 
section 7.3). The evidence was limited for emergency department visits, 
but results of several studies generally indicated that short-term 
exposures to O3 were associated with respiratory emergency 
department visits. The strongest and most consistent evidence, at both 
lower levels (i.e., below 0.120 ppm 1-hour max O3) and at 
higher levels (above 0.120 ppm 1-hour max O3), was found in 
the group of studies which investigated summertime \20\ daily hospital 
admissions for respiratory causes in different eastern North American 
cities. These studies consistently demonstrated that ambient 
O3 levels were associated with increased hospital admissions 
and accounted for about one to three excess respiratory hospital 
admissions per million persons with each 0.100 ppm increase in 1-hour 
max O3, after adjustment for possible confounding effects of 
temperature and copollutants. Overall, the 1996 Criteria Document 
concluded that there was strong evidence that ambient O3 
exposures can cause significant exacerbations of preexisting 
respiratory disease in the general public. Excess respiratory-related 
hospital admissions associated with O3 exposures for the New 
York City area (based on Thurston et al., 1992) were included in the 
quantitative risk assessment in the 1997 review and are included in the 
current assessment along with estimates for respiratory-related 
hospital admissions in Cleveland, Detroit, and Los Angeles based on 
more recent studies (2007 Staff Paper, chapter 5). Significant 
uncertainties and the difficulty of obtaining reliable baseline 
incidence numbers resulted in emergency department visits not being 
used in the quantitative risk assessment in either the 1997 or the 2008 
O3 NAAQS review.
---------------------------------------------------------------------------

    \20\ Discussion of the reasons for focusing on warm season 
studies is found in the section 2.A.3.a below.
---------------------------------------------------------------------------

    In the past decade, a number of studies have examined the temporal 
pattern associations between O3 exposures and emergency 
department visits for respiratory causes (EPA, 2006a, section 7.3.2). 
These studies are summarized in the 2006 Criteria Document (chapter 7 
Annex) and some are shown in Figure 1 (in section II.A.3). Respiratory 
causes for emergency department visits include asthma, bronchitis, 
emphysema, pneumonia, and other upper and lower respiratory infections, 
such as influenza, but asthma visits typically dominate the daily 
incidence counts. Most studies report positive associations with 
O3. Among studies with adequate controls for seasonal 
patterns, many reported at least one significant positive association 
involving O3.

[[Page 2955]]

    In reviewing evidence for associations between emergency department 
visits for asthma and short-term O3 exposures, the 2006 
Criteria Document (Figure 7-8, p. 7-68) notes that in general, 
O3 effect estimates from summer only analyses tended to be 
positive and larger compared to results from cool season or all year 
analyses. Several of the studies reported significant associations 
between O3 concentrations and emergency department visits 
for respiratory causes, in particular asthma. However, inconsistencies 
were observed which were at least partially attributable to differences 
in model specifications and analysis approach among various studies. 
For example, ambient O3 concentrations, length of the study 
period, and statistical methods used to control confounding by seasonal 
patterns and copollutants appear to affect the observed O3 
effect on emergency department visits.
    Hospital admissions studies focus specifically on unscheduled 
admissions because unscheduled hospital admissions occur in response to 
unanticipated disease exacerbations and are more likely than scheduled 
admissions to be affected by variations in environmental factors, such 
as daily O3 levels. Results of a fairly large number of 
these studies published during the past decade are summarized in 2006 
Criteria Document (chapter 7 Annex), and results of U.S. and Canadian 
studies are shown in Figure 1 below (in section II.A.3). As a group, 
these hospital admissions studies tend to be larger geographically and 
temporally than the emergency department visit studies and provide 
results that are generally more consistent. The strongest associations 
of respiratory hospital admissions with O3 concentrations 
were observed using short lag periods, in particular for a 0-day lag 
(same day exposure) and a 1-day lag (previous day exposure). Most 
studies in the United States and Canada indicated positive, 
statistically significant associations between ambient O3 
concentrations and respiratory hospital admissions in the warm season. 
However, not all studies found a statistically significant relationship 
with O3, possibly because of very low ambient O3 
levels. Analyses for confounding using multipollutant regression models 
suggest that copollutants generally do not confound the association 
between O3 and respiratory hospitalizations. Ozone effect 
estimates were robust to PM adjustment in all-year and warm-season only 
data.
    Overall, the 2006 Criteria Document concludes that positive and 
robust associations were found between ambient O3 
concentrations and various respiratory disease hospitalization 
outcomes, when focusing particularly on results of warm-season 
analyses. Recent studies also generally indicate a positive association 
between O3 concentrations and emergency department visits 
for asthma during the warm season (EPA, 2006a, p. 7-175). These 
positive and robust associations are supported by the controlled human 
exposure, animal toxicological, and epidemiological evidence for lung 
function decrements, increased respiratory symptoms, airway 
inflammation, and increased airway responsiveness. Taken together, the 
overall evidence supports a causal relationship between acute ambient 
O3 exposures and increased respiratory morbidity outcomes 
resulting in increased emergency department visits and hospitalizations 
during the warm season (EPA, 2006a, p. 8-77).
ii. Effects on the Respiratory System of Long-Term O3 
Exposures
    The 1996 Criteria Document concluded that there was insufficient 
evidence from the limited number of studies to determine whether long-
term O3 exposures resulted in chronic health effects at 
ambient levels observed in the U.S. However, the aggregate evidence 
suggested that O3 exposure, along with other environmental 
factors, could be responsible for health effects in exposed 
populations. Animal toxicological studies carried out in the 1980's and 
1990's demonstrated that long-term exposures can result in a variety of 
morphological effects, including permanent changes in the small airways 
of the lungs, including remodeling of the distal airways and CAR and 
deposition of collagen, possibly representing fibrotic changes. These 
changes result from the damage and repair processes that occur with 
repeated exposure. Fibrotic changes were also found to persist after 
months of exposure providing a potential pathophysiologic basis for 
changes in airway function observed in children in some recent 
epidemiological studies. It appears that variable seasonal ambient 
patterns of exposure may be of greater concern than continuous daily 
exposures.
    Several studies published since 1996 have investigated lung 
function changes over seasonal time periods (EPA, 2006a, section 
7.5.3). The 2006 Criteria Document (p. 7-114) summarizes these studies 
which collectively indicate that seasonal O3 exposure is 
associated with smaller growth-related increases in lung function in 
children than they would have experienced living in areas with lower 
O3 levels. There is some limited evidence that seasonal 
O3 also may affect lung function growth in young adults, 
although the uncertainty about the role of copollutants makes it 
difficult to attribute the effects to O3 alone.
    Lung capacity grows during childhood and adolescence as body size 
increases, reaches a maximum during the twenties, and then begins to 
decline steadily and progressively with age. Long-term exposure to air 
pollution has long been thought to contribute to slower growth in lung 
capacity, diminished maximally attained capacity, and/or more rapid 
decline in lung capacity with age (EPA, 2006a, section 7.5.4). 
Toxicological findings evaluated in the 1996 Criteria Document 
demonstrated that repeated daily exposure of rats to an episodic 
profile of O3 caused small, but significant, decrements in 
growth-related lung function that were consistent with early indicators 
of focal fibrogenesis in the proximal alveolar region, without overt 
fibrosis. Because O3 at sufficient concentrations is a 
strong respiratory irritant and has been shown to cause inflammation 
and restructuring of the respiratory airways, it is plausible that 
long-term O3 exposures might have a negative impact on 
baseline lung function, particularly during childhood when these 
exposures might be associated with long-term risks.
    Several epidemiological studies published since 1996 have examined 
the relationship between lung function development and long-term 
O3 exposure. The most extensive and robust study of 
respiratory effects in relation to long-term air pollution exposures 
among children in the U.S. is the Children's Health Study carried out 
in 12 communities of southern California starting in 1993. One analysis 
(Peters et al., 1999a) examined the relationship between long-term 
O3 exposures and self-reports of respiratory symptoms and 
asthma in a cross sectional analysis and found a limited relationship 
between outcomes of current asthma, bronchitis, cough and wheeze and a 
0.040 ppm increase in 1-hour max O3 (EPA, 2006a, p. 7-115). 
Another analysis (Peters et al., 1999b) examined the relationship 
between lung function at baseline and levels of air pollution in the 
community. They reported evidence that annual mean O3 levels 
were associated with decreases in FVC, FEV1, PEF and forced 
expiratory flow (FEF25-75) (the latter two being 
statistically significant) among females but not males. In a separate 
analysis (Gauderman et al., 2000) of 4th, 7th, and

[[Page 2956]]

10th grade students, a longitudinal analysis of lung function 
development over four years found no association with O3 
exposure. The Children's Health Study enrolled a second cohort of more 
than 1500 fourth graders in 1996 (Gauderman et al., 2002). While the 
strongest associations with negative lung function growth were observed 
with acid vapors in this cohort, children from communities with higher 
4-year average O3 levels also experienced smaller increases 
in various lung function parameters. The strongest relationship with 
O3 was with PEF. Specifically, children from the least-
polluted community had a small but statistically significant increase 
in PEF as compared to those from the most-polluted communities. In two-
pollutant models, only 8-hour average O3 and NO2 
were significant joint predictors of FEV1 and maximal 
midexpiratory flow (MMEF). Although results from the second cohort of 
children are supportive of a weak association, the definitive 8-year 
follow-up analysis of the first cohort (Gauderman et al., 2004a) 
provides little evidence that long-term exposure to ambient 
O3 at current levels is associated with significant deficits 
in the growth rate of lung function in children. Avol et al. (2001) 
examined children who had moved away from participating communities in 
southern California to other states with improved air quality. They 
found that a negative, but not statistically significant, association 
was observed between O3 and lung function parameters. 
Collectively, the results of these reports from the children's health 
cohorts provide little evidence to support an impact of long-term 
O3 exposures on lung function development.
    Evidence for a significant relationship between long-term 
O3 exposures and decrements in maximally attained lung 
function was reported in a nationwide study of first year Yale students 
(Kinney et al., 1998; Galizia and Kinney, 1999) (EPA, 2006a, p. 7-120). 
Males had much larger effect estimates than females, which might 
reflect higher outdoor activity levels and correspondingly higher 
O3 exposures during childhood. A similar study of college 
freshmen at University of California at Berkeley also reported 
significant effects of long-term O3 exposures on lung 
function (K[uuml]nzli et al., 1997; Tager et al., 1998). In a 
comparison of students whose city of origin was either Los Angeles or 
San Francisco, long-term O3 exposures were associated with 
significant changes in mid- and end-expiratory flow measures, which 
could be considered early indicators for pathologic changes that might 
progress to COPD.
    There have been a few studies that investigated associations 
between long-term O3 exposures and the onset of new cases of 
asthma (EPA, 2006a, section 7.5.6). The Adventist Health and Smog 
(AHSMOG) study cohort of about 4,000 was drawn from nonsmoking, non-
Hispanic white adult Seventh Day Adventists living in California (Greer 
et al., 1993; McDonnell et al., 1999). During the ten-year follow-up in 
1987, a statistically significant increased relative risk of asthma 
development was observed in males, compared to a nonsignificant 
relative risk in females (Greer et al., 1993). In the 15-year follow-up 
in 1992, it was reported that for males, there was a statistically 
significant increased relative risk of developing asthma associated 
with 8-hour average O3 exposures, but there was no evidence 
of an association in females. Consistency of results in the two studies 
with different follow-up times provides supportive evidence of the 
potential for an association between long-term O3 exposure 
and asthma incidence in adult males; however, representativeness of 
this cohort to the general U.S. population may be limited (EPA, 2006a, 
p. 7-125).
    In a similar study (McConnell et al., 2002) of incident asthma 
among children (ages 9 to 16 at enrollment), annual surveys of 3,535 
children initially without asthma were used to identify new-onset 
asthma cases as part of the Children's Health Study. Six high-
O3 and six low-O3 communities were identified 
where the children resided. There were 265 children who reported new-
onset asthma during the follow-up period. Although asthma risk was no 
higher for all residents of the six high-O3 communities 
versus the six low-O3 communities, asthma risk was 3.3 times 
greater for children who played three or more sports as compared with 
children who played no sports within the high-O3 
communities. This association was absent in the communities with lower 
O3 concentrations. No other pollutants were found to be 
associated with new-onset asthma (EPA, 2006a, p. 7-125). Playing sports 
may result in extended outdoor activity and exposure occurring during 
periods when O3 levels are higher. It should be noted, 
however, that the results of the Children's Health Study were based on 
a small number of new-onset asthma cases among children who played 
three or more sports. Future replication of these findings in other 
cohorts would help determine whether a causal interpretation is 
appropriate.
    In animal toxicology studies, the progression of morphological 
effects reported during and after a chronic exposure in the range of 
0.50 to 1.00 ppm O3 (well above current ambient levels) is 
complex, with inflammation peaking over the first few days of exposure, 
then dropping, then plateauing, and finally, largely disappearing (EPA, 
2006a, section 5.2.4.4). By contrast, fibrotic changes in the tissue 
increase very slowly over months of exposure, and, after exposure 
ceases, the changes sometimes persist or increase. Epithelial 
hyperplasia peaks soon after the inflammatory response but is usually 
maintained in both the nose and lungs with continuous exposure; it also 
does not return to pre-exposure levels after the end of exposure. 
Patterns of exposure in this same concentration range determine 
effects, with 18 months of daily exposure, causing less morphologic 
damage than exposures on alternating months. This is important as 
environmental O3 exposure is typically seasonal. Long-term 
studies by Plopper and colleagues (Evans et al., 2003; Schelegle et 
al., 2003; Chen et al., 2003; Plopper and Fanucchi, 2000) investigated 
infant rhesus monkeys exposed to simulated, seasonal O3 and 
demonstrated: (1) Remodeling in the distal airways, (2) abnormalities 
in tracheal basement membrane; (3) eosinophil accumulation in 
conducting airways; and (4) decrements in airway innervation (EPA, 
2006a, p. 5-45). These findings provide additional information 
regarding possible injury-repair processes occurring with long-term 
O3 exposures suggesting that these processes are only 
partially reversible and may progress following cessation of 
O3 exposure. Further, these processes may lead to 
nonreversible structural damage to lung tissue; however, there is still 
too much uncertainty to characterize the significance of these findings 
to human exposure profiles and effect levels (EPA, 2006a, p. 8-25).
    In summary, in the past decade, important new longitudinal studies 
have examined the effect of chronic O3 exposure on 
respiratory health outcomes. Limited evidence from recent long-term 
morbidity studies have suggested in some cases that chronic exposure to 
O3 may be associated with seasonal declines in lung function 
or reduced lung function development, increases in inflammation, and 
development of asthma in children and adults. Seasonal decrements or 
smaller increases in lung function measures have been reported in 
several studies; however, the extent to which these

[[Page 2957]]

changes are transient remains uncertain. While there is supportive 
evidence from animal studies involving effects from chronic exposures, 
large uncertainties still remain as to whether current ambient levels 
and exposure patterns might cause these same effects in human 
populations. The 2006 Criteria Document concludes that epidemiological 
studies of new asthma development and longer-term lung function 
declines remain inconclusive at present (EPA, 2006a, p. 7-134).
iii. Effects on the Cardiovascular System of O3 Exposure
    At the time of the 1997 review, the possibility of O3-
induced cardiovascular effects was largely unrecognized. Since then, a 
very limited body of evidence from animal, controlled human exposure, 
and epidemiologic studies has emerged that provides evidence for some 
potential plausible mechanisms for how O3 exposures might 
exert cardiovascular system effects, however further research is needed 
to substantiate these potential mechanisms. Possible mechanisms may 
involve O3-induced secretions of vasoconstrictive substances 
and/or effects on neuronal reflexes that may result in increased 
arterial blood pressure and/or altered electrophysiologic control of 
heart rate or rhythm. Some animal toxicology studies have shown 
O3-induced decreases in heart rate, mean arterial pressure, 
and core temperature. One controlled human exposure study that 
evaluated effects of O3 exposure on cardiovascular health 
outcomes found no significant O3-induced differences in ECG 
or blood pressure in healthy or hypertensive subjects but did observe a 
significant O3-induced increase the alveolar-to-arterial 
PO2 gradient and heart rate in both groups resulting in an 
overall increase in myocardial work and impairment in pulmonary gas 
exchange (Gong et al., 1998). In another controlled human exposure 
study, inhalation of a mixture of PM2.5 and O3 by 
healthy subjects increased brachial artery vasoconstriction and 
reactivity (Brook et al., 2002).
    The evidence from a few animal studies also includes potential 
direct effects such as O3-induced release from lung 
epithelial cells of platelet activating factor (PAF) that may 
contribute to blood clot formation that would have the potential to 
increase the risk of serious cardiovascular outcomes (e.g., heart 
attack, stroke, mortality). Also, interactions of O3 with 
surfactant components in epithelial lining fluid of the lung may result 
in production of oxysterols and reactive oxygen species that may 
exhibit PAF-like activity contributing to clotting and also may exert 
cytotoxic effects on lung and heart muscle cells.
    Epidemiological panel and field studies that examined associations 
between O3 and various cardiac physiologic endpoints have 
yielded limited evidence suggestive of a potential association between 
acute O3 exposure and altered heart rate variability (HRV), 
ventricular arrhythmias, and incidence of heart attacks (myocardial 
infarction or MI). A number of epidemiological studies have also 
reported associations between short-term exposures and hospitalization 
for cardiovascular diseases. As shown in Figure 7-13 of the 2006 
Criteria Document, many of the studies reported negative or 
inconsistent associations. Some other studies, especially those that 
examined the relationship when O3 exposures were higher, 
have found robust positive associations between O3 and 
cardiovascular hospital admissions (EPA, 2006a, p. 7-82). For example, 
one study reported a positive association between O3 and 
cardiovascular hospital admissions in Toronto, Canada in a summer-only 
analysis (Burnett et al., 1997b). The results were robust to adjustment 
for various PM indices, whereas the PM effects diminished when adjusted 
for gaseous pollutants. Other studies stratified their analysis by 
temperature (i.e., by warms days versus cool days). Several analyses 
using warm season days consistently produced positive associations.
    The epidemiologic evidence for cardiovascular morbidity is much 
weaker than for respiratory morbidity, with only one of several U.S. 
and Canadian studies showing statistically significant positive 
associations of cardiovascular hospitalizations with warm-season 
O3 concentrations. Most of the available European and 
Australian studies, all of which conducted all-year O3 
analyses, did not find an association between short-term O3 
concentrations and cardiovascular hospitalizations. Overall, the 
currently available evidence is inconclusive regarding an association 
between cardiovascular hospital admissions and ambient O3 
exposure (EPA, 2006a, p. 7-83).
    In summary, based on the evidence from animal toxicology, 
controlled human exposure, and epidemiological studies, from the 2006 
Criteria Document (p. 8-77) concludes that this generally limited body 
of evidence is suggestive that O3 can directly and/or 
indirectly contribute to cardiovascular-related morbidity, but that 
much needs to be done to more fully integrate links between ambient 
O3 exposures and adverse cardiovascular outcomes.
b. Mortality
i. Mortality and Short-term O3 Exposure
    The 1996 Criteria Document concluded that an association between 
daily mortality and O3 concentration for areas with high 
O3 levels (e.g., Los Angeles) was suggested. However, due to 
a very limited number of studies available at that time, there was 
insufficient evidence to conclude that the observed association was 
likely causal.
    The 2006 Criteria Document included results from numerous 
epidemiological analyses of the relationship between O3 and 
mortality. Additional single city analyses have also been conducted 
since 1996, however, the most pivotal studies in EPA's (and CASAC's) 
finding of increased support for the relationship between premature 
mortality and O3 is in part related to differences in study 
design--limiting analyses to warm seasons, better control for 
copollutants, particularly PM, and use of multicity designs (both time 
series and meta-analytic designs). Key findings are available from 
multicity time-series studies that report associations between 
O3 and mortality. These studies include analyses using data 
from 90 U.S. cities in the National Mortality, Morbidity and Air 
Pollution (NMMAPS) study (Dominici et al., 2003) and from 95 U.S. 
communities in an extension to the NMMAPS analyses (Bell et al., 2004).
    The original 90-city NMMAPS analysis, with data from 1987 to 1994, 
was primarily focused on investigating effects of PM10 on 
mortality. A significant association was reported between mortality and 
24-hour average O3 concentrations in analyses using all 
available data as well as in the warm season only analyses (Dominici et 
al., 2003). The estimate using all available data was about half that 
for the summer-only data at a lag of 1-day. The extended NMMAPS 
analysis included data from 95 U.S. cities and included an additional 6 
years of data, from 1987-2000 (Bell et al., 2004). Significant 
associations were reported between O3 and mortality in 
analyses using all available data. The effect estimate for increased 
mortality was approximately 0.5 percent per 0.020 ppm change in 24-hour 
average O3 measured on the same day, and approximately 1.04 
percent per 0.020 ppm change in 24-hour average O3 in a 7-
day distributed lag model (EPA, 2006a, p. 7-88). In analyses using only 
data from the warm season, the results were not significantly different 
from the full-year results. The authors also report

[[Page 2958]]

that O3-mortality associations were robust to adjustment for 
PM (EPA, 2006a, p. 7-100). Using a subset of the NMMAPS data set, Huang 
et al. (2005) focused on associations between cardiopulmonary mortality 
and O3 exposure (24-hour average) during the summer season 
only. The authors report an approximate 1.47 percent increase per 0.020 
ppm change in O3 concentration measured on the same day and 
an approximate 2.52 percent increase per 0.020 ppm change in 
O3 concentration using a 7-day distributed lag model. These 
findings suggest that the effect of O3 on mortality is 
immediate but also persists for several days.
    As discussed below in section II.A.3.a, confounding by weather, 
especially temperature, is complicated by the fact that higher 
temperatures are associated with the increased photochemical activities 
that are important for O3 formation. Using a case-crossover 
study design, Schwartz (2005) assessed associations between daily 
maximum concentrations and mortality, matching case and control periods 
by temperature, and using data only from the warm season. The reported 
effect estimate of approximately 0.92 percent change in mortality per 
0.040 ppm O3 (1-hour maximum) was similar to time-series 
analysis results with adjustment for temperature (approximately 0.76 
percent per 0.040 ppm O3), suggesting that associations 
between O3 and mortality were robust to the different 
adjustment methods for temperature.
    An initial publication from APHEA, a European multicity study, 
reported statistically significant associations between daily maximum 
O3 concentrations and mortality in four cities in a full 
year analysis (Toulomi et al., 1997). An extended analysis was done 
using data from 23 cities throughout Europe (Gryparis et al., 2004). In 
this report, a positive but not statistically significant association 
was found between mortality and 1-hour daily maximum O3 in a 
full year analysis. Gryparis et al. (2004) noted that there was a 
considerable seasonal difference in the O3 effect on 
mortality; thus, the small effect for the all-year data might be 
attributable to inadequate adjustment for confounding by seasonality. 
Focusing on analyses using summer measurements, the authors report 
statistically significant associations with total mortality, 
cardiovascular mortality and respiratory mortality (EPA, 2006a, p. 7-
93, 7-99).
    Numerous single-city analyses have also reported associations 
between mortality and short-term O3 exposure, especially for 
those analyses using warm season data. As shown in Figure 7-21 of the 
2006 Criteria Document, the results of recent publications show a 
pattern of positive, often statistically significant associations 
between short-term O3 exposure and mortality during the warm 
season. In considering results from year-round analyses, there remains 
a pattern of positive results but the findings are less consistent. In 
most single-city analyses, effect estimates were not substantially 
changed with adjustment for PM (EPA, 2006a, Figure 7-22).
    In addition, several meta-analyses have been conducted on the 
relationship between O3 and mortality. As described in 
section 7.4.4 of the 2006 Criteria Document, these analyses reported 
fairly consistent and positive combined effect estimates ranging from 
approximately 1.5 to 2.5 percent increase in mortality for a 
standardized change in O3 (EPA, 2006a, Figure 7-20). Three 
recent meta-analyses evaluated potential sources of heterogeneity in 
O3-mortality associations (Bell et al., 2005; Ito et al., 
2005; Levy et al., 2005). The 2006 Criteria Document (p. 7-96) observes 
common findings across all three analyses, in that all reported that 
effect estimates were larger in warm season analyses, reanalysis of 
results using default convergence criteria in generalized additive 
models (GAM) did not change the effect estimates, and there was no 
strong evidence of confounding by PM. Bell et al. (2005) and Ito et al. 
(2005) both provided suggestive evidence of publication bias, but 
O3-mortality associations remained after accounting for that 
potential bias. The 2006 Criteria Document concludes that the 
``positive O3 effects estimates, along with the sensitivity 
analyses in these three meta-analyses, provide evidence of a robust 
association between ambient O3 and mortality'' (EPA, 2006a, 
p. 7-97).
    Most of the single-pollutant model estimates from single-city 
studies range from 0.5 to 5 percent excess deaths per standardized 
increments. Corresponding summary estimates in large U.S. multicity 
studies ranged between 0.5 to 1 percent with some studies noting 
heterogeneity across cities and studies (EPA, 2006a, p. 7-110).
    Finally, from those studies that included assessment of 
associations with specific causes of death, it appears that effect 
estimates for associations with cardiovascular mortality are larger 
than those for total mortality. The meta-analysis by Bell et al. (2005) 
observed a slightly larger effect estimate for cardiovascular mortality 
compared to mortality from all causes. The effect estimate for 
respiratory mortality was approximately one-half that of cardiovascular 
mortality in the meta-analysis. However, other studies have observed 
larger effect estimates for respiratory mortality compared to 
cardiovascular mortality. The apparent inconsistency regarding the 
effect size of O3-related respiratory mortality may be due 
to reduced statistical power in this subcategory of mortality (EPA, 
2006a, p. 7-108).
    In summary, many single- and multi-city studies observed positive 
associations of ambient O3 concentrations with total 
nonaccidental and cardiopulmonary mortality. The 2006 Criteria Document 
finds that the results from U.S. multicity time-series studies provide 
the strongest evidence to date for O3 effects on acute 
mortality. Recent meta-analyses also indicate positive risk estimates 
that are unlikely to be confounded by PM; however, future work is 
needed to better understand the influence of model specifications on 
the risk coefficient (EPA, 2006a, p. 7-175). A meta-analysis that 
examined specific causes of mortality found that the cardiovascular 
mortality risk estimates were higher than those for total mortality. 
For cardiovascular mortality, the 2006 Criteria Document (Figure 7-25, 
p. 7-106) suggests that effect estimates are consistently positive and 
more likely to be larger and statistically significant in warm season 
analyses. The findings regarding the effect size for respiratory 
mortality have been less consistent, possibly because of lower 
statistical power in this subcategory of mortality. The 2006 Criteria 
Document (p. 8-78) concludes that these findings are highly suggestive 
that short-term O3 exposure directly or indirectly 
contribute to non-accidental and cardiopulmonary-related mortality, but 
additional research is needed to more fully establish underlying 
mechanisms by which such effects occur.\21\
---------------------------------------------------------------------------

    \21\ In commenting on the Criteria Document, the CASAC Ozone 
Panel raised questions about the implications of these time-series 
results in a policy context, emphasizing that ``* * * while the 
time-series study design is a powerful tool to detect very small 
effects that could not be detected using other designs, it is also a 
blunt tool'' (Henderson, 2006b). They note that ``* * * not only is 
the interpretation of these associations complicated by the fact 
that the day-to-day variation in concentrations of these pollutants 
is, to a varying degree, determined by meteorology, the pollutants 
are often part of a large and highly correlated mix of pollutants, 
only a very few of which are measured'' (Henderson, 2006b). Even 
with these uncertainties, the CASAC Ozone Panel, in its review of 
the Staff Paper, found ``* * * premature total non-accidental and 
cardiorespiratory mortality for inclusion in the quantitative risk 
assessment to be appropriate.'' (Henderson, 2006b)

---------------------------------------------------------------------------

[[Page 2959]]

ii. Mortality and Long-Term O3 Exposure
    Little evidence was available in the 1997 review on the potential 
for associations between mortality and long-term exposure to 
O3. In the Harvard Six City prospective cohort analysis, the 
authors report that mortality was not associated with long-term 
exposure to O3 (Dockery et al., 1993). The authors note that 
the range of O3 concentrations across the six cities was 
small, which may have limited the power of the study to detect 
associations between mortality and O3 levels (EPA, 2006a, p. 
7-127).
    As discussed in section 7.5.8 of the 2006 Criteria Document, in 
this review there are results available from three prospective cohort 
studies: the American Cancer Society (ACS) study (Pope et al., 2002), 
the Adventist Health and Smog (AHSMOG) study (Beeson et al., 1998; 
Abbey et al., 1999), and the U.S. Veterans Cohort study (Lipfert et 
al., 2000, 2003). In addition, a major reanalysis report includes 
evaluation of data from the Harvard Six City cohort study (Krewski et 
al., 2000).\22\ This reanalysis also includes additional evaluation of 
data from the initial ACS cohort study report that had only reported 
results of associations between mortality and long-term exposure to 
fine particles and sulfates (Pope et al., 1995). This reanalysis was 
discussed in the 2007 Staff Paper (section 3.3.2.2) but not in the 2006 
Criteria Document.
---------------------------------------------------------------------------

    \22\ This reanalysis report and the original prospective cohort 
study findings are discussed in more detail in section 8.2.3 of the 
Air Quality Criteria for Particulate Matter (EPA, 2004).
---------------------------------------------------------------------------

    In this reanalysis of data from the previous Harvard Six City 
prospective cohort study, the investigators replicated and validated 
the findings of the original studies, and the report included 
additional quantitative results beyond those available in the original 
report (Krewski et al., 2000). In the reanalysis of data from the 
Harvard Six Cities study, the effect estimate for the association 
between long-term O3 concentrations and mortality was 
negative and nearly statistically significant (relative risk = 0.87, 95 
percent CI: 0.76, 1.00).
    The ACS study is based on health data from a large prospective 
cohort of approximately 500,000 adults and air quality data from about 
150 U.S. cities. The initial report (Pope et al., 1995) focused on 
associations with fine particles and sulfates, for which significant 
associations had been reported in the earlier Harvard Six Cities study 
(Dockery et al., 1993). As part of the major reanalysis of these data, 
results for associations with other air pollutants were also reported, 
and the authors report that no significant associations were found 
between O3 and all-cause mortality. However, a significant 
association was reported for cardiopulmonary mortality in the warm 
season (Krewski et al., 2000). The ACS II study (Pope et al., 2002) 
reported results of associations with an extended data base; the 
mortality records for the cohort had been updated to include 16 years 
of follow-up (compared with 8 years in the first report) and more 
recent air quality data were included in the analyses. Similar to the 
earlier reanalysis, a marginally significant association was observed 
between long-term exposure to O3 and cardiopulmonary 
mortality in the warm season. No other associations with mortality were 
observed in both the full-year and warm season analyses.
    The Adventist Health and Smog (AHSMOG) cohort includes about 6,000 
adults living in California. In two studies from this cohort, a 
significant association has been reported between long-term 
O3 exposure and increased risk of lung cancer mortality 
among males only (Beeson et al., 1998; Abbey et al., 1999). No 
significant associations were reported between long-term O3 
exposure and mortality from all causes or cardiopulmonary causes. Due 
to the small numbers of lung cancer deaths (12 for males, 18 for 
females) and the precision of the effect estimate (i.e., the wide 
confidence intervals), the 2006 Criteria Document (p. 7-130) discussed 
concerns about the plausibility of the reported association with lung 
cancer.
    The U.S. Veterans Cohort study (Lipfert et al., 2000, 2003) of 
approximately 50,000 middle-aged males diagnosed with hypertension, 
reported some positive associations between mortality and peak 
O3 exposures (95th percentile level for several years of 
data). The study included numerous analyses using subsets of exposure 
and mortality follow-up periods which spanned the years 1960 to 1996. 
In the results of analyses using deaths and O3 exposure 
estimates concurrently across the study period, there were positive, 
statistically significant associations between peak O3 and 
mortality (EPA, 2006a, p. 7-129).
    Overall, the 2006 Criteria Document (p. 7-130) concludes that 
consistent associations have not been reported between long-term 
O3 exposure and all-cause, cardiopulmonary or lung cancer 
mortality.
c. Role of Ground-Level O3 in Solar Radiation-Related Human 
Health Effects
    Beyond the direct health effects attributable to inhalation 
exposure to O3 in the ambient air discussed above, the 2006 
Criteria Document also assesses potential indirect effects related to 
the presence of O3 in the ambient air by considering the 
role of ground-level O3 in mediating human health effects 
that may be directly attributable to exposure to solar ultraviolet 
radiation (UV-B). The 2006 Criteria Document (chapter 10) focuses this 
assessment on three key factors, including those factors that govern 
(1) UV-B radiation flux at the earth's surface, (2) human exposure to 
UV-B radiation, and (3) human health effects due to UV-B radiation. In 
so doing, the 2006 Criteria Document provides a thorough analysis of 
the current understanding of the relationship between reducing ground-
level O3 concentrations and the potential impact these 
reductions might have on increasing UV-B surface fluxes and indirectly 
contributing to UV-B related health effects.
    There are many factors that influence UV-B radiation penetration to 
the earth's surface, including latitude, altitude, cloud cover, surface 
albedo, PM concentration and composition, and gas phase pollution. Of 
these, only latitude and altitude can be defined with small uncertainty 
in any effort to assess the changes in UV-B flux that may be 
attributable to any changes in tropospheric O3 as a result 
of any revision to the O3 NAAQS. Such an assessment of UV-B 
related health effects would also need to take into account human 
habits, such as outdoor activities (including age- and occupation-
related exposure patterns), dress and skin care to adequately estimate 
UV-B exposure levels. However, little is known about the impact of 
these factors on individual exposure to UV-B.
    Moreover, detailed information does not exist regarding other 
factors that are relevant to assessing changes in disease incidence, 
including: Type (e.g., peak or cumulative) and time period (e.g., 
childhood, lifetime, current) of exposures related to various adverse 
health outcomes (e.g., damage to the skin, including skin cancer; 
damage to the eye, such as cataracts; and immune system suppression); 
wavelength dependency of biological responses; and interindividual 
variability in UV-B resistance to such health outcomes. Beyond these 
well recognized adverse health effects associated with various 
wavelengths of UV radiation, the 2006 Criteria Document (section 
10.2.3.6) also

[[Page 2960]]

discusses protective effects of UV-B radiation. Recent reports indicate 
the necessity of UV-B in producing vitamin D. Vitamin D deficiency can 
cause metabolic bone disease among children and adults, and may also 
increase the risk of many common chronic diseases (e.g., type I 
diabetes and rheumatoid arthritis) as well as the risk of various types 
of cancers. Thus, the 2006 Criteria Document concludes that any 
assessment that attempts to quantify the consequences of increased UV-B 
exposure on humans due to reduced ground-level O3 must 
include consideration of both negative and positive effects. However, 
as with other impacts of UV-B on human health, this beneficial effect 
of UV-B radiation has not been studied in sufficient detail to allow 
for a credible health benefits or risk assessment. In conclusion, the 
effect of changes in surface-level O3 concentrations on UV-
B-induced health outcomes cannot yet be critically assessed within 
reasonable uncertainty (2006 Criteria Document, p. 10-36).
    The Agency last considered indirect effects of O3 in the 
ambient air in its 2003 final response to a remand of the Agency's 1997 
decision to revise the O3 NAAQS. In so doing, based on the 
available information in the 1997 review, EPA determined that the 
information linking (a) changes in patterns of ground-level 
O3 concentrations likely to occur as a result of programs 
implemented to attain the 1997 O3 NAAQS to (b) changes in 
relevant exposures to UV-B radiation of concern to public health was 
too uncertain at that time to warrant any relaxation in the level of 
public health protection previously determined to be requisite to 
protect against the demonstrated direct adverse respiratory effects of 
exposure to O3 in the ambient air (68 FR 614). At that time, 
the more recent information on protective effects of UV-B radiation was 
not available, such that only adverse UV-B-related effects could be 
considered. Taking into consideration the more recent information 
available for the 2008 review, the 2006 Criteria Document and 2007 
Staff Paper conclude that the effect of changes in ground-level 
O3 concentrations, likely to occur as a result of revising 
the O3 NAAQS, on UV-B-induced health outcomes, including 
whether these changes would ultimately result in increased or decreased 
incidence of UV-B-related diseases, cannot yet be critically assessed.
3. Interpretation and Integration of Health Evidence
    As discussed below, in assessing the health evidence, the 2006 
Criteria Document integrates findings from experimental (e.g., 
toxicological, dosimetric and controlled human exposure) and 
epidemiological studies, to make judgments about the extent to which 
causal inferences can be made about observed associations between 
health endpoints and exposure to O3. In evaluating the 
evidence from epidemiological studies, the EPA focuses on well-
recognized criteria, including: The strength of reported associations, 
including the magnitude and precision of reported effect estimates and 
their statistical significance; the robustness of reported 
associations, or stability in the effect estimates after considering 
factors such as alternative models and model specification, potential 
confounding by co-pollutants, and issues related to the consequences of 
exposure measurement error; potential aggregation bias in pooling data; 
and the consistency of the effects associations as observed by looking 
across results of multiple- and single-city studies conducted by 
different investigators in different places and times. Consideration is 
also given to evaluating concentration-response relationships observed 
in epidemiological studies to inform judgments about the potential for 
threshold levels for O3-related effects. Integrating more 
broadly across epidemiological and experimental evidence, the 2006 
Criteria Document also focuses on the coherence and plausibility of 
observed O3-related health effects to reach judgments about 
the extent to which causal inferences can be made about observed 
associations between health endpoints and exposure to O3 in 
the ambient air.
a. Assessment of Evidence From Epidemiological Studies
    Key elements of the evaluation of epidemiological studies are 
briefly summarized below.
    (1) The strength of associations most directly refers to the 
magnitude of the reported relative risk estimates. Taking a broader 
view, the 2006 Criteria Document draws upon the criteria summarized in 
a recent report from the U.S. Surgeon General, which define strength of 
an association as ``the magnitude of the association and its 
statistical strength'' which includes assessment of both effect 
estimate size and precision, which is related to the statistical power 
of the study (CDC, 2004). In general, when associations are strong in 
terms of yielding large relative risk estimates, it is less likely that 
the association could be completely accounted for by a potential 
confounder or some other source of bias, whereas with associations that 
yield small relative risk estimates it is especially important to 
consider potential confounding and other factors in assessing 
causality. Effect estimates between O3 and some of the 
health outcomes are generally small in size and could thus be 
characterized as weak. For example, effect estimates for associations 
with mortality generally range from 0.5 to 5 percent increases per 
0.040 ppm increase in 1-hour maximum O3 or equivalent, 
whereas associations for hospitalization range up to 50 percent 
increases per standardized O3 increment. However, the 2006 
Criteria Document notes that there are large multicity studies that 
find small associations between short-term O3 exposure and 
mortality or morbidity and have done so with great precision due to the 
statistical power of the studies (p. 8-40). That is, the power of the 
studies allows the authors to reliably distinguish even weak 
relationships from the null hypothesis with statistical confidence.
    (2) In evaluating the robustness of associations, the 2006 Criteria 
Document (sections 7.1.3 and 8.4.4.3) and 2007 Staff Paper (section 
3.4.2) have primarily considered the impact of exposure error, 
potential confounding by copollutants, and alternative models and model 
specifications.
    In time-series and panel studies, the temporal (e.g., daily or 
hourly) changes in ambient O3 concentrations measured at 
centrally-located ambient monitoring stations are generally used to 
represent a community's exposure to ambient O3. In 
prospective cohort or cross-sectional studies, air quality data 
averaged over a period of months to years are used as indicators of a 
community's long-term exposure to ambient O3 and other 
pollutants. In both types of analyses, exposure error is an important 
consideration, as actual exposures to individuals in the population 
will vary across the community.
    Ozone concentrations measured at central ambient monitoring sites 
may explain, at least partially, the variance in individual exposures 
to ambient O3; however, this relationship is influenced by 
various factors related to building ventilation practices and personal 
behaviors. Further, the pattern of exposure misclassification error and 
the influence of confounders may differ across the outcomes of interest 
as well as in susceptible populations. As discussed in the 2006 
Criteria Document

[[Page 2961]]

(section 3.9), only a limited number of studies have examined the 
relationship between ambient O3 concentrations and personal 
exposures to ambient O3. One of the strongest predictors of 
the relationship between ambient concentrations and personal exposures 
appears to be time spent outdoors. The strongest relationships were 
observed in outdoor workers (Brauer and Brook, 1995, 1997; O'Neill et 
al., 2004). Statistically significant correlations between ambient 
concentrations and personal exposures were also observed for children, 
who likely spend more time outdoors in the warm season (Linn et al., 
1996; Xu et al., 2005). There is some concern about the extent to which 
ambient concentrations are representative of personal O3 
exposures of another particularly susceptible group of individuals, the 
debilitated elderly, since those who suffer from chronic cardiovascular 
or respiratory conditions may tend to protect themselves more than 
healthy individuals from environmental threats by reducing their 
exposure to both O3 and its confounders, such as high 
temperature and PM. Studies by Sarnat et al. (2001, 2005) that included 
this susceptible group reported mixed results for associations between 
ambient O3 concentrations and personal exposures to 
O3. Collectively, these studies observed that the daily 
averaged personal O3 exposures tend to be well correlated 
with ambient O3 concentrations despite the substantial 
variability that existed among the personal measurements. These studies 
provide supportive evidence that ambient O3 concentrations 
from central monitors may serve as valid surrogate measures for mean 
personal exposures experienced by the population, which is of most 
relevance for time-series studies. A better understanding of the 
relationship between ambient concentrations and personal exposures, as 
well as of the other factors that affect relationship will improve the 
interpretation of concentration-population health response associations 
observed.
    The 2006 Criteria Document (section 7.1.3.1) also discusses the 
potential influence of exposure error on epidemiologic study results. 
Zeger et al. (2000) outlined the components to exposure measurement 
error, finding that ambient exposure can be assumed to be the product 
of the ambient concentration and an attenuation factor (i.e., building 
filter) and that panel studies and time-series studies that use ambient 
concentrations instead of personal exposure measurements will estimate 
a health risk that is attenuated by that factor. Navidi et al. (1999) 
used data from a children's cohort study to compare effect estimates 
from a simulated ``true'' exposure level to results of analyses from 
O3 exposures determined by several methods, finding that 
O3 exposures based on the use of ambient monitoring data 
overestimate the individual's O3 exposure and thus generally 
result in O3 effect estimates that are biased downward (EPA, 
2006a, p. 7-8). Similarly, in a reanalysis of a study by Burnett et al. 
(1994) on the acute respiratory effects of ambient air pollution, Zidek 
et al. (1998) reported that accounting for measurement error, as well 
as making a few additional changes to the analysis, resulted in 
qualitatively similar conclusions, but the effects estimates were 
considerably larger in magnitude (EPA, 2006a, p. 7-8). A simulation 
study by Sheppard et al. (2005) also considered attenuation of the risk 
based on personal behavior, their microenvironment, and the qualities 
of the pollutant in time-series studies. Of particular interest is 
their finding that risk estimates were not further attenuated in time-
series studies even when the correlations between personal exposures 
and ambient concentrations were weak. In addition to overestimation of 
exposure and the resulting underestimation of effects, the use of 
ambient O3 concentrations may obscure the presence of 
thresholds in epidemiologic studies (EPA, 2006a, p. 7-9).
    As discussed in the 2006 Criteria Document (section 3.9), using 
ambient concentrations to determine exposure generally overestimates 
true personal O3 exposures by approximately 2- to 4-fold in 
available studies, resulting in attenuated risk estimates. The 
implication is that the effects being estimated occur at fairly low 
exposures and the potency of O3 is greater than these 
effects estimates indicate. As very few studies evaluating 
O3 health effects with personal O3 exposure 
measurements exist in the literature, effect estimates determined from 
ambient O3 concentrations must be evaluated and used with 
caution to assess the health risks of O3. In the absence of 
available data on personal O3 exposure, the use of routinely 
monitored ambient O3 concentrations as a surrogate for 
personal exposures is not generally expected to change the principal 
conclusions from O3 epidemiologic studies. Therefore, 
population health risk estimates derived using ambient O3 
levels from currently available observational studies, with appropriate 
caveats about personal exposure considerations, remain useful. The 2006 
Criteria Document recommends caution in the quantitative use of effect 
estimates calculated using ambient O3 concentrations as they 
may lead to underestimation of the potency of O3. However, 
the 2007 Staff Paper observes that the use of these risk estimates for 
comparing relative risk reductions between alternative ambient 
O3 standards considered in the risk assessment (discussed 
below in section II.B.2) is less likely to suffer from this concern.
    Confounding occurs when a health effect that is caused by one risk 
factor is attributed to another variable that is correlated with the 
causal risk factor; epidemiological analyses attempt to adjust or 
control for potential confounders. Copollutants (e.g., PM, CO, 
SO2 and NO2) can meet the criteria for potential 
confounding in O3-health associations if they are potential 
risk factors for the health effect under study and are correlated with 
O3. Effect modifiers include variables that may influence 
the health response to the pollutant exposure (e.g., co-pollutants, 
individual susceptibility, smoking or age). Both are important 
considerations for evaluating effects in a mixture of pollutants, but 
for confounding, the emphasis is on controlling or adjusting for 
potential confounders in estimating the effects of one pollutant, while 
the emphasis for effect modification is on identifying and assessing 
the effects for different modifiers.
    The 2006 Criteria Document (p. 7-148) observes that O3 
is generally not highly correlated with other criteria pollutants 
(e.g., PM10, CO, SO2 and NO2), but may 
be more highly correlated with secondary fine particles, especially 
during the summer months, and that the degree of correlation between 
O3 and other pollutants may vary across seasons. For 
example, positive associations are observed between O3 and 
pollutants such as fine particles during the warmer months, but 
negative correlations may be observed during the cooler months (EPA, 
2006a, p. 7-17). Thus, the 2006 Criteria Document (section 7.6.4) pays 
particular attention to the results of season-specific analyses and 
studies that assess effects of PM in potential confounding of 
O3-health relationships. The 2006 Criteria Document also 
discussed the limitations of commonly used multipollutant models that 
include the difficulty in interpreting results where the copollutants 
are highly colinear, or where correlations between pollutants change by 
season (EPA, 2006a, p. 7-150). This is particularly the situation where 
O3 and a copollutant, such as

[[Page 2962]]

sulfates, are formed under the same atmospheric condition; in such 
cases multipollutant models would produce unstable and possibly 
misleading results (EPA, 2006a, p. 7-152).
    For mortality, the results from numerous multicity and single-city 
studies indicate that O3-mortality associations do not 
appear to be substantially changed in multipollutant models including 
PM10 or PM2.5 (EPA, 2006a, p. 7-101; Figure 7-
22). Focusing on results of warm season analyses, effect estimates for 
O3-mortality associations are fairly robust to adjustment 
for PM in multipollutant models (EPA, 2006a, p. 7-102; Figure 7-23). 
The 2006 Criteria Document concludes that in the few multipollutant 
analyses conducted for these endpoints, copollutants generally do not 
confound the relationship between O3 and respiratory 
hospitalization (EPA, 2006a, p. 7-79 to 7-80; Figure 7-12). 
Multipollutant models were not used as commonly in studies of 
relationships between respiratory symptoms or lung function with 
O3, but the 2006 Criteria Document reports that results of 
available analyses indicate that such associations generally were 
robust to adjustment for PM2.5 (p. 7-154). For example, in a 
large multicity study of asthmatic children (Mortimer et al., 2002), 
the O3 effect was attenuated, but there was still a positive 
association; in Gent et al. (2003), effects of O3, but not 
PM2.5, remained statistically significant and even increased 
in magnitude in two-pollutant models (EPA, 2006a, p. 7-53). Considering 
this body of studies, the 2006 Criteria Document (p. 7-154) concludes: 
``Multipollultant regression analyses indicated that O3 risk 
estimates, in general, were not sensitive to the inclusion of 
copollutants, including PM2.5 and sulfate. These results 
suggest that the effects of O3 on respiratory health 
outcomes appear to be robust and independent of the effects of other 
copollutants.''
    The 2006 Criteria Document (p. 7-14) observes that another 
challenge of time-series epidemiological analysis is assessing the 
relationship between O3 and health outcomes while avoiding 
bias due to confounding by other time-varying factors, particularly 
seasonal trends and weather variables. These variables are of 
particular interest because O3 concentrations have a well-
characterized seasonal pattern and are also highly correlated with 
changes in temperature, such that it can be difficult to distinguish 
whether effects are associated with O3 or with seasonal or 
weather variables in statistical analyses.
    The 2006 Criteria Document (section 7.1.3.4) discusses statistical 
modeling approaches that have been used to adjust for time-varying 
factors, highlighting a series of analyses that were done in a Health 
Effects Institute-funded reanalysis of numerous time-series studies. 
While the focus of these reanalyses was on associations with PM, a 
number of investigators also examined the sensitivity of O3 
coefficients to the extent of adjustment for temporal trends and 
weather factors. In addition, several recent studies, including U.S. 
multicity studies (Bell et al., 2005; Huang et al., 2005; Schwartz et 
al., 2005) and a meta-analysis study (Ito et al., 2005), evaluated the 
effect of model specification on O3-mortality associations. 
As discussed in the 2006 Criteria Document (section 7.6.3.1), these 
studies generally report that associations reported with O3 
are not substantially changed with alternative modeling strategies for 
adjusting for temporal trends and meteorologic effects. In the meta-
analysis by Ito et al. (2005), a separate multicity analysis was 
presented that found that alternative adjustments for weather resulted 
in up to 2-fold difference in the O3 effect estimate. 
Significant confounding can occur when strong seasonal cycles are 
present, suggesting that season-specific results are more generally 
robust than year-round results in such cases. A number of 
epidemiological studies have conducted season-specific analyses, and 
have generally reported stronger and more precise effect estimates for 
O3 associations in the warm season than in analyses 
conducted in the cool seasons or over the full year.
    (3) Consistency refers to the persistent finding of an association 
between exposure and outcome in multiple studies of adequate power in 
different persons, places, circumstances and times (CDC, 2004). In 
considering results from multicity studies and single-city studies in 
different areas, the 2006 Criteria Document (p. 8-41) observes general 
consistency in effects of short-term O3 exposure on 
mortality, respiratory hospitalization and other respiratory health 
outcomes. The variations in effects that are observed may be 
attributable to differences in relative personal exposure to 
O3, as well as varying concentrations and composition of 
copollutants present in different regions. Thus, the 2006 Criteria 
Document (p. 8-41) concludes that ``consideration of consistency or 
heterogeneity of effects is appropriately understood as an evaluation 
of the similarity or general concordance of results, rather than an 
expectation of finding quantitative results with a very narrow range.''
    (4) The 2007 Staff Paper recognizes that it is likely that there 
are biological thresholds for different health effects in individuals 
or groups of individuals with similar innate characteristics and health 
status. For O3 exposure, individual thresholds would 
presumably vary substantially from person to person due to individual 
differences in genetic susceptibility, pre-existing disease conditions 
and possibly individual risk factors such as diet or exercise levels 
(and could even vary from one time to another for a given person). 
Thus, it would be difficult to detect a distinct threshold at the 
population level below which no individual would experience a given 
effect, especially if some members of a population are unusually 
sensitive even down to very low concentrations (EPA, 2004, p. 9-43, 9-
44).
    Some studies have tested associations between O3 and 
health outcomes after removal of days with higher O3 levels 
from the data set; such analyses do not necessarily indicate the 
presence or absence of a threshold, but provide some information on 
whether the relationship is found using only lower-concentration data. 
For example, using data from 95 U.S. cities, Bell et al. (2004) found 
that the effect estimate for an association between short-term 
O3 exposure and mortality was little changed when days 
exceeding 0.060 ppm (24-hour average) were excluded in the analysis. 
Using data from 8 U.S. cities, Mortimer and colleagues (2002) also 
reported that associations between O3 and both lung function 
and respiratory symptoms remained statistically significant and of the 
same or greater magnitude in effect size when concentrations greater 
than 0.080 ppm (8-hour average) were excluded (EPA, 2006a, p. 7-46). 
Several single-city studies also report similar findings of 
associations that remain or are increased in magnitude and statistical 
significance when data at the upper end of the concentration range are 
removed (EPA, 2006a, section 7.6.5).
    Other time-series epidemiological studies have used statistical 
modeling approaches to evaluate whether thresholds exist in 
associations between short-term O3 exposure and mortality. 
As discussed in section 7.6.5 of the 2006 Criteria Document, one 
European multicity study included evaluation of the shape of the 
concentration-response curve, and observed no deviation from a linear 
function across the range of O3 measurements from the study 
(Gryparis et al., 2004; EPA, 2006a p. 7-154). Several single-city 
studies also observed a monotonic increase in associations between 
O3 and morbidity that suggest

[[Page 2963]]

that no population threshold exists (EPA, 2006a, p. 7-159).
    On the other hand, a study in Korea used several different modeling 
approaches and reported that a threshold model provided the best fit 
for the data. The results suggested a potential threshold level of 
about 0.045 ppm (1-hour maximum concentration; < 0.035 ppm, 8-hour 
average) for an association between mortality and short-term 
O3 exposure during the summer months (Kim et al., 2004; EPA, 
2006a, p. 8-43). The authors reported larger effect estimates for the 
association for data above the potential threshold level, suggesting 
that an O3-mortality association might be underestimated in 
the non-threshold model. A threshold analysis recently reported by Bell 
et al. (2006) for 98 U.S. communities, including the same 95 
communities in Bell et al. (2004), indicated that if a population 
threshold existed for mortality, it would likely fall below a 24-hour 
average O3 concentration of 0.015 ppm (< 0.025 ppm, 8-hour 
average). In addition, Burnett and colleagues (1997a,b) plotted the 
relationships between air pollutant concentrations and both respiratory 
and cardiovascular hospitalization, and it appears in these results 
that the associations with O3 are found in the concentration 
range above about 0.030 ppm (1-hour maximum; < 0.025 ppm, 8-hour 
average). Vedal and colleagues (2003) reported a significant 
association between O3 and mortality in British Columbia 
where O3 concentrations were quite low (mean 1-hour maximum 
concentration of 0.0273 ppm). The authors did not specifically test for 
threshold levels, but the fact that the association was found in an 
area with such low O3 concentrations suggests that any 
potential threshold level would be quite low in this data set.
    In summary, the 2006 Criteria Document finds that, taken together, 
the available evidence from controlled human exposure and 
epidemiological studies suggests that no clear conclusion can now be 
reached with regard to possible threshold levels for O3-
related effects (EPA, 2006a, p. 8-44). Thus, the available 
epidemiological evidence neither supports nor refutes the existence of 
thresholds at the population level for effects such as increased 
hospital admissions and premature mortality. There are limitations in 
epidemiological studies that make discerning thresholds in populations 
difficult, including low data density in the lower concentration 
ranges, the possible influence of exposure measurement error, and 
interindividual differences in susceptibility to O3-related 
effects in populations. There is the possibility that thresholds for 
individuals may exist in reported associations at fairly low levels 
within the range of air quality observed in the studies but not be 
detectable as population thresholds in epidemiological analyses.
b. Biological Plausibility and Coherence of Evidence
    The body of epidemiological studies discussed in the 2007 Staff 
Paper emphasizes the role of O3 in association with a 
variety of adverse respiratory and cardiovascular effects. While 
recognizing a variety of plausible mechanisms, there exists a general 
consensus suggesting that O3, could either directly or 
through initiation, interfere with basic cellular oxidation processes 
responsible for inflammation, reduced antioxidant capacity, 
atherosclerosis and other effects. Reasoning that O3 
influences cellular chemistry through basic oxidative properties (as 
opposed to a unique chemical interaction), other reactive oxidizing 
species (ROS) in the atmosphere acting either independently or in 
combination with O3 may also contribute to a number of 
adverse respiratory and cardiovascular health effects. Consequently, 
the role of O3 should be considered more broadly as 
O3 behaves as a generator of numerous oxidative species in 
the atmosphere.
    In considering the biological plausibility of reported 
O3-related effects, the 2007 Staff Paper (section 3.4.6) 
considers this broader question of health effects of pollutant mixtures 
containing O3. The potential for O3-related 
enhancements of PM formation, particle uptake, and exacerbation of PM-
induced cardiovascular effects underscores the importance of 
considering contributions of O3 interactions with other 
often co-occurring air pollutants to health effects due to 
O3-containing pollutant mixes. The 2007 Staff Paper 
summarizes some examples of important pollutant mixture effects from 
studies that evaluate interactions of O3 with other co-
occurring pollutants, as discussed in chapters 4, 5, and 6 of the 2006 
Criteria Document.
    All of the types of interactive effects of O3 with other 
co-occurring gaseous and nongaseous viable and nonviable PM components 
of ambient air mixes noted above argue that O3 acts not only 
alone but that O3 also is a surrogate indicator for air 
pollution mixes which may enhance the risk of adverse effects due to 
O3 acting in combination with other pollutants. Viewed from 
this perspective, those epidemiologic findings of morbidity and 
mortality associations, with ambient O3 concentrations 
extending to quite low levels in many cases, become more understandable 
and plausible.
    The 2006 Criteria Document integrates epidemiological studies with 
mechanistic information from controlled human exposure studies and 
animal toxicological studies to draw conclusions regarding the 
coherence of evidence and biological plausibility of O3-
related health effects to reach judgments about the causal nature of 
observed associations. As summarized below, coherence and biological 
plausibility is discussed for each of the following types of 
O3-related effects: Short-term effects on the respiratory 
system, effects on the cardiovascular system, effects related to long-
term O3 exposure, and short-term mortality-related health 
endpoints.
i. Coherence and Plausibility of Short-Term Effects on the Respiratory 
System
    Acute respiratory morbidity effects that have been associated with 
short-term exposure to O3 include such health endpoints as 
decrements in lung function, increased respiratory symptoms, increased 
airway responsiveness, airway inflammation, increased permeability 
related to epithelial injury, immune system effects, emergency 
department visits for respiratory diseases, and hospitalization due to 
respiratory illness.
    Recent epidemiological studies have supported evidence available in 
the previous O3 NAAQS review on associations between ambient 
O3 exposure and decline in lung function for children. The 
2006 Criteria Document (p. 8-34) concludes that exposure to ambient 
O3 has a significant effect on lung function and is 
associated with increased respiratory symptoms and medication use, 
particularly in asthmatics. Short-term exposure to O3 has 
also been associated with more severe morbidity endpoints, such as 
emergency department visits and hospital admissions for respiratory 
cases, including specific respiratory illness (e.g., asthma) (EPA, 
2006a, sections 7.3.2 and 7.3.3). In addition, a few epidemiological 
studies have reported positive associations between short-term 
O3 exposure and respiratory mortality, though the 
associations are not generally statistically significant (EPA, 2006a, 
p. 7-108).
    Considering the evidence from epidemiological studies, the results 
described above provide evidence for coherence in O3-related 
effects on the respiratory system. Effect estimates from U.S. and 
Canadian studies are shown in

[[Page 2964]]

Figure 1, where it can be seen that mostly positive associations have 
been reported with respiratory effects ranging from respiratory 
symptoms, such as cough or wheeze, to hospitalization for various 
respiratory diseases, and there is suggestive evidence for associations 
with respiratory mortality. Many of the reported associations are 
statistically significant, particularly in the warm season. In Figure 
1, the central effect estimate is indicated by a square for each 
result, with the vertical bar representing the 95 percent confidence 
interval around the estimate. In the discussions that follow, an 
individual study result is considered to be statistically significant 
if the 95 percent confidence interval does not include zero.\23\ 
Positive effect estimates indicate increases in the health outcome with 
O3 exposure. In considering these results as a whole, it is 
important to consider not only whether statistical significance at the 
95 percent confidence level is reported in individual studies but also 
the general pattern of results, focusing in particular on studies with 
greater statistical power that report relatively more precise results.
---------------------------------------------------------------------------

    \23\ Results for studies of respiratory symptoms are presented 
as odds ratios; an odds ratio of 1.0 is equivalent to no effect, and 
thus is presented as equivalent to the zero effect estimate line.
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    Considering also evidence from toxicological, controlled human 
exposure, and field studies, the 2006 Criteria Document (section 8.6) 
discusses biological plausibility and coherence of evidence for acute 
O3-induced respiratory health effects. Inhalation of 
O3 for several hours while subjects are physically active 
can elicit both acute adverse pathophysiological changes and subjective 
respiratory tract symptoms (EPA, 2006a, section 8.4.2). Acute pulmonary 
responses observed in healthy humans exposed to O3 at 
ambient concentrations include: decreased inspiratory capacity; mild 
bronchoconstriction; rapid, shallow breathing during exercise; 
subjective symptoms of tracheobronchial airway irritation, including 
cough and pain on deep inspiration; decreases in measures of lung 
function; and increased airway resistance. The severity of symptoms and 
magnitude of response depends on inhaled dose, individual O3 
sensitivity, and the degree of attenuation or enhancement of response 
resulting from previous O3 exposures. Lung function studies 
of several animal species acutely exposed to relatively low 
O3 levels from a toxicological perspective (i.e., 0.25 to 
0.4 ppm) show responses similar to those observed in humans, including 
increased breathing frequency, decreased tidal volume, increased 
resistance, and decreased FVC. Alterations in breathing pattern return 
to normal within hours of exposure, and

[[Page 2966]]

attenuation in functional responses following repeated O3 
exposures is similar to those observed in humans.
    Physiological and biochemical alterations investigated in 
controlled human exposure and animal toxicology studies tend to support 
certain hypotheses of underlying pathological mechanisms which lead to 
the development of respiratory-related effects reported in epidemiology 
studies (e.g., increased hospitalization and medication use). Some of 
these are: (a) Decrements in lung function, (b) bronchoconstriction, 
(c) increased airway responsiveness, (d) airway inflammation, (e) 
epithelial injury, (f) immune system activation, (g) host defense 
impairment, and (h) sensitivity of individuals, which depends on at 
least a person's age, disease status, genetic susceptibility, and the 
degree of attenuation present due to prior exposures. The time 
sequence, magnitude, and overlap of these complex events, both in terms 
of development and recovery, illustrate the inherent difficulty of 
interpreting the biological plausibility of O3-induced 
cardiopulmonary health effects (EPA, 2006a, p. 8-48).
    The interaction of O3 with airway epithelial cell 
membranes and ELF to form lipid ozonation products and ROS is supported 
by numerous human, animal and in vitro studies. Ozonation products and 
ROS initiate a cascade of events that lead to oxidative stress, injury, 
inflammation, airway epithelial damage and increased epithelial damage 
and increased alveolar permeability to vascular fluids. Repeated 
respiratory inflammation can lead to a chronic inflammatory state with 
altered lung structure and lung function and may lead to chronic 
respiratory diseases such as fibrosis and emphysema (EPA, 2006a, 
section 8.6.2). Continued respiratory inflammation also can alter the 
ability to respond to infectious agents, allergens and toxins. Acute 
inflammatory responses to O3 are well documented, and lung 
injury appears within 3 hours after exposure in humans.
    Taken together, the 2006 Criteria Document concludes that the 
evidence from experimental human and animal toxicology studies 
indicates that acute O3 exposure is causally associated with 
respiratory system effects. These effects include O3-induced 
pulmonary function decrements; respiratory symptoms; lung inflammation 
and increased lung permeability; airway hyperresponsiveness; increased 
uptake of nonviable and viable particles; and consequent increased 
susceptibility to PM-related toxic effects and respiratory infections 
(EPA, 2006a, p. 8-48).
ii. Coherence and Plausibility of Effects on the Cardiovascular System
    There is very limited experimental evidence of animals and humans 
that has evaluated possible mechanisms or physiological pathways by 
which acute O3 exposures may induce cardiovascular system 
effects. Ozone induces lung injury, inflammation, and impaired 
mucociliary clearance, with a host of associated biochemical changes 
all leading to increased lung epithelial permeability. As noted above 
in section II.A.2.a, the generation of lipid ozonation products and ROS 
in lung tissues can influence pulmonary hemodynamics, and ultimately 
the cardiovascular system. Other potential mechanisms by which 
O3 exposure may be associated with cardiovascular disease 
outcomes have been described. Laboratory animals exposed to relatively 
high O3 concentrations (>= 0.5 ppm) demonstrate tissue edema 
in the heart and lungs. Ozone-induced changes in heart rate, edema of 
heart tissue, and increased tissue and serum levels of ANF found with 
8-hour 0.5 ppm O3 exposure in animal toxicology studies 
(Vesely et al., 1994a,b,c) also raise the possibility of potential 
cardiovascular effects of acute ambient O3 exposures.
    Animal toxicology studies have found both transient and persistent 
ventilatory responses with and without progressive decreases in heart 
rate (Arito et al., 1997). Observations of O3-induced 
vasoconstriction in a controlled human exposure study by Brook et al. 
(2002) suggests another possible mechanism for O3-related 
exacerbations of preexisting cardiovascular disease. One controlled 
human study (Gong et al., 1998) evaluated potential cardiovascular 
health effects of O3 exposure. The overall results did not 
indicate acute cardiovascular effects of O3 in either the 
hypertensive or control subjects. The authors observed an increase in 
rate-pressure product and heart rate, a decrement for FEV1, 
and a > 10 mm Hg increase in the alveolar/arterial pressure difference 
for O2 following O3 exposure. Foster et al. 
(1993) demonstrated that even in relatively young healthy adults, 
O3 exposure can cause ventilation to shift away from the 
well-perfused basal lung. This effect of O3 on ventilation 
distribution may persist beyond 24-hours post-exposure (Foster et al., 
1997). These findings suggest that O3 may exert 
cardiovascular effects indirectly by impairing alveolar-arterial 
O2 transfer and potentially reducing O2 supply to 
the myocardium. Ozone exposure may increase myocardial work and impair 
pulmonary gas exchange to a degree that could perhaps be clinically 
important in persons with significant preexisting cardiovascular 
impairment.
    As noted above in section II.A.2.a, a limited number of new 
epidemiological studies have reported associations between short-term 
O3 exposure and effects on the cardiovascular system. Among 
these studies, three were population-based and involved relatively 
large cohorts; two of these studies evaluated associations between 
O3 and HRV and the other study evaluated the association 
between O3 levels and the relative risk of MI or heart 
attack. Such studies may offer more informative results based on their 
large subject-pool and design. Results from these three studies were 
suggestive of an association between O3 exposure and the 
cardiovascular endpoints studied. In other recent studies on the 
incidence of heart attacks and some more subtle cardiovascular health 
endpoints, such as changes in HRV or cardiac arrhythmia, some but not 
all studies reported associations with short-term exposure to 
O3 (EPA, 2006a, section 7.2.7.1). From these studies, the 
2006 Criteria Document concludes that the ``current evidence is rather 
limited but suggestive of a potential effect on HRV, ventricular 
arrhythmias, and MI incidence'' (EPA, 2006a, p. 7-65).
    An increasing number of studies have evaluated the association 
between O3 exposure and cardiovascular hospital admissions. 
As discussed in section 7.3.4 of the 2006 Criteria Document, many 
reported negative or inconsistent associations, whereas other studies, 
especially those that examined the relationship when O3 
exposures were higher, have found positive and robust associations 
between O3 and cardiovascular hospital admissions. The 2006 
Criteria Document (p. 7-83) finds that the overall evidence from these 
studies remains inconclusive regarding the effect of O3 on 
cardiovascular hospitalizations. The 2006 Criteria Document notes that 
the suggestive positive epidemiologic findings of O3 
exposure on cardiac autonomic control, including effects on HRV, 
ventricular arrhythmias and heart attacks, and reported associations 
between O3 exposure and cardiovascular hospitalizations 
generally in the warm season gain credibility and scientific support 
from the results of experimental animal toxicology and controlled human 
exposure studies, which are indicative of plausible pathways by which 
O3 may exert cardiovascular effects (EPA, 2006a, section 
8.6.1).

[[Page 2967]]

iii. Coherence and Plausibility of Effects Related to Long-Term 
O3 Exposure
    Controlled human exposure studies cannot evaluate effects of long-
term exposures to O3; there is some evidence available from 
toxicological studies. While early animal toxicology studies of long-
term O3 exposures were conducted using continuous exposures, 
more recent studies have focused on exposures which mimic diurnal and 
seasonal patterns and more realistic O3 exposure levels 
(EPA, 2006a, p. 8-50). Studies of monkeys that compared these two 
exposure scenarios found increased airway pathology only with the 
latter design. Persistent and irreversible effects reported in chronic 
animal toxicology studies suggest that additional complementary human 
data are needed from epidemiologic studies (EPA, 2006a, p. 8-50).
    There is limited evidence from human studies for long-term 
O3-induced effects on lung function. As discussed in section 
8.6.2 of the 2006 Criteria Document, previous epidemiological studies 
have provided only inconclusive evidence for either mortality or 
morbidity effects of long-term O3 exposure. The 2006 
Criteria Document (p. 8-50) observes that the inconsistency in findings 
may be due to a lack of precise exposure information, the possibility 
of selection bias, and the difficulty of controlling for confounders. 
Several new longitudinal epidemiology studies have evaluated 
associations between long-term O3 exposures and morbidity 
and mortality and suggest that these long-term exposures may be related 
to changes in lung function in children; however, little evidence is 
available to support a relationship between chronic O3 
exposure and mortality or lung cancer incidence (EPA, 2006a, p. 8-50).
    The 2006 Criteria Document (p. 8-51) concludes that evidence from 
animal toxicology studies strongly suggests that chronic O3 
exposure is capable of damaging the distal airways and proximal 
alveoli, resulting in lung tissue remodeling leading to apparent 
irreversible changes. Such structural changes and compromised lung 
function caused by persistent inflammation may exacerbate the 
progression and development of chronic lung disease. Together with the 
limited evidence available from epidemiological studies, these findings 
offer some insight into potential biological mechanisms for suggested 
associations between long-term or seasonal exposures to O3 
and reduced lung function development in children which have been 
observed in epidemiologic studies (EPA, 2006a, p. 8-51).
iv. Coherence and Plausibility of Short-Term Mortality-Related Health 
Endpoints
    An extensive epidemiological literature on air pollution related 
mortality risk estimates from the U.S., Canada, and Europe is discussed 
in the 2006 Criteria Document (sections 7.4 and 8.6.3). These single- 
and multicity mortality studies coupled with results from meta-analyses 
generally indicate associations between acute O3 exposure 
and elevated risk for all-cause mortality, even after adjustment for 
the influence of season and PM exposure. Several single-city studies 
that specifically evaluated the relationship between O3 
exposure and cardiopulmonary mortality also reported results suggestive 
of a positive association (EPA, 2006a, p. 8-51). These mortality 
studies suggest a pattern of effects for causality that have 
biologically plausible explanations, but our knowledge regarding 
potential underlying mechanisms is very limited at this time and 
requires further research. Most of the physiological and biochemical 
parameters investigated in human and animal studies suggest that 
O3-induced biochemical effects are relatively transient and 
attenuate over time. The 2006 Criteria Document (p. 8-52) hypothesizes 
a generic pathway of O3-induced lung damage, potentially 
involving oxidative lung damage with subsequent inflammation and/or 
decline in lung function leading to respiratory distress in some 
sensitive population groups (e.g., asthmatics), or other plausible 
pathways noted below that may lead to O3-related 
contributions to cardiovascular effects that ultimately increase risk 
of mortality.
    The third National Health and Nutrition Examination Survey follow-
up data analysis indicates that about 20 percent of the adult 
population has reduced FEV1 values, suggesting impaired lung 
function in a significant portion of the population. Most of these 
individuals have COPD, asthma or fibrotic lung disease (Manino et al., 
2003), which are associated with persistent low-grade inflammation. 
Furthermore, patients with COPD are at increased risk for 
cardiovascular disease. Also, lung disease with underlying inflammation 
may be linked to low-grade systemic inflammation associated with 
atherosclerosis, independent of cigarette smoking (EPA, 2006a, p. 8-
52). Lung function decrements in persons with cardiopulmonary disease 
have been associated with inflammatory markers, such as C-reactive 
protein (CRP) in the blood. At a population level it has been found 
that individuals with the lowest FEV1 values have the 
highest levels of CRP, and those with the highest FEV1 
values have the lowest CRP levels (Manino et al., 2003; Sin and Man, 
2003). This complex series of physiological and biochemical reactions 
following O3 exposure may tilt the biological homeostasis 
mechanisms which could lead to adverse health effects in people with 
compromised cardiopulmonary systems.
    Several other types of newly available data also support reasonable 
hypotheses that may help to explain the findings of O3-
related increases in cardiovascular mortality observed in some 
epidemiological studies. These include the direct effect of 
O3 on increasing PAF in lung tissue that can then enter the 
general circulation and possibly contribute to increased risk of blood 
clot formation and the consequent increased risk of heart attacks, 
cerebrovascular events (stroke), or associated cardiovascular-related 
mortality. Ozone reactions with cholesterol in lung surfactant to form 
epoxides and oxysterols that are cytotoxic to lung and heart muscles 
and that contribute to atherosclerotic plaque formation in arterial 
walls represent another potential pathway. Stimulation of airway 
irritant receptors may lead to increases in tissue and serum levels of 
ANF, changes in heart rate, and edema of heart tissue. A few new field 
and panel studies of human adults have reported associations between 
ambient O3 concentrations and changes in cardiac autonomic 
control (e.g., HRV, ventricular arrhythmias, and MI). These represent 
plausible pathways that may lead to O3-related contributions 
to cardiovascular effects that ultimately increase the risk of 
mortality.
    In addition, O3-induced increases in lung permeability 
allow more ready entry for inhaled PM into the blood stream, and thus 
O3 exposure may increase the risk of PM-related 
cardiovascular effects. Furthermore, increased ambient O3 
levels contribute to ultrafine PM formation in the ambient air and 
indoor environments. Thus, the contributions of elevated ambient 
O3 concentrations to ultrafine PM formation and human 
exposure, along with the enhanced uptake of inhaled fine particles, 
consequently may contribute to exacerbation of PM-induced 
cardiovascular effects in addition to those more directly induced by 
O3 (EPA, 2006a, p. 8-53).

[[Page 2968]]

c. Summary
    Judgments concerning the extent to which relationships between 
various health endpoints and ambient O3 exposures are likely 
to be causal are informed by the conclusions and discussion in the 2006 
Criteria Document as discussed above and summarized in section 3.7.5 of 
the 2007 Staff Paper. These judgments reflect the nature of the 
evidence and the overall weight of the evidence, and are taken into 
consideration in the quantitative risk assessment discussed below in 
section II.B.2.
    For example, there is a very high level of confidence that 
O3 induces lung function decrements in healthy adults and 
children due in part to the dozens of controlled human exposure and 
epidemiological studies consistently showing such effects. The 2006 
Criteria Document (p. 8-74) states that these studies provide clear 
evidence of causality for associations between short-term O3 
exposures and statistically significant declines in lung function in 
children, asthmatics and adults who exercise outdoors. An increase in 
respiratory symptoms (e.g., cough, shortness of breath) has been 
observed in controlled human exposure studies of short-term 
O3 exposures, and significant associations between ambient 
O3 exposures and a wide variety of respiratory symptoms have 
been reported in epidemiology studies (EPA, 2006a, p. 8-75). Population 
time-series studies showing robust associations between O3 
exposures and respiratory hospital admissions and emergency department 
visits are strongly supported by controlled human exposure, animal 
toxicological, and epidemiological evidence for O3-related 
lung function decrements, respiratory symptoms, airway inflammation, 
and airway hyperreactivity. The 2006 Criteria Document (p. 8-77) 
concludes that, taken together, the overall evidence supports the 
inference of a causal relationship between acute ambient O3 
exposures and increased respiratory morbidity outcomes resulting in 
increased emergency department visits and hospitalizations during the 
warm season. Further, recent epidemiologic evidence has been 
characterized in the 2006 Criteria Document (p. 8-78) as highly 
suggestive that O3 directly or indirectly contributes to 
non-accidental and cardiopulmonary-related mortality.
4. O3-Related Impacts on Public Health
    The following discussion draws from chapters 6 and 7 and section 
8.7 of the 2006 Criteria Document and section 3.6 of the 2007 Staff 
Paper to characterize factors which modify responsiveness to 
O3, populations potentially at risk for O3-
related health effects, the adversity of O3-related effects, 
and the size of the at-risk populations in the U.S. These 
considerations are all important elements in characterizing the 
potential public health impacts associated with exposure to ambient 
O3.
a. Factors That Modify Responsiveness to Ozone
    There are numerous factors that can modify individual 
responsiveness to O3. These include: influence of physical 
activity; age; gender and hormonal influences; racial, ethnic and 
socioeconomic status (SES) factors; environmental factors; and oxidant-
antioxidant balance. These factors are discussed in more detail in 
section 6.5 of the 2006 Criteria Document.
    It is well established that physical activity increases an 
individual's minute ventilation and will thus increase the dose of 
O3 inhaled (EPA, 2006a, section 6.5.4). Increased physical 
activity results in deeper penetration of O3 into more 
distal regions of the lungs, which are more sensitive to acute 
O3 response and injury. This will result in greater lung 
function decrements for acute exposures of individuals during increased 
physical activity. Research has shown that respiratory effects are 
observed at lower O3 concentrations if the level of exertion 
is increased and/or duration of exposure and exertion are extended. 
Predicted O3-induced decrements in lung function have been 
shown to be a function of exposure concentration, duration and exercise 
level for healthy, young adults (McDonnell et al., 1997).
    Most of the studies investigating the influence of age have used 
lung function decrements and symptoms as measures of response. For 
healthy adults, lung function and symptom responses to O3 
decline as age increases. The rate of decline in O3 
responsiveness appears greater in those 18 to 35 years old compared to 
those 35 to 55 years old, while there is very little change after age 
55. In one study (Seal et al., 1996) analyzing a large data set, a 5.4% 
decrement in FEV1 on average was estimated for 20-year-old 
individuals exposed to 0.12 ppm O3 for 2.3 hours, whereas 
similar exposure of 35-year-old individuals resulted in a 2.6% 
decrement on average. While healthy children tend not to report 
respiratory symptoms when exposed to low levels of O3, for 
subjects 18 to 36 years old symptom responses induced by O3 
are observed but tend to decrease with increasing age within this range 
(McDonnell et al., 1999).
    Limited evidence of gender differences in response to O3 
exposure has suggested that females may be predisposed to a greater 
susceptibility to O3. Lower plasma and NL fluid levels of 
the most prevalent antioxidant, uric acid, in females relative to males 
may be a contributing factor. Consequently, reduced removal of 
O3 in the upper airways may promote deeper penetration. 
However, most of the evidence on gender differences appears to be 
equivocal, with one study (Hazucha et al., 2003) suggesting that 
physiological responses of young healthy males and females may be 
comparable (EPA, 2006a, section 6.5.2).
    A few studies have suggested that ethnic minorities might be more 
responsive to O3 than Caucasian population groups (EPA, 
2006a, section 6.5.3). This may be more the result of a lack of 
adequate health care and socioeconomic status (SES) than any 
differences in sensitivity to O3. The limited data 
available, which have investigated the influence of race, ethnic or 
other related factors on responsiveness to O3, prevent 
drawing any clear conclusions at this time.
    Few human studies have examined the potential influence of 
environmental factors such as the sensitivity of individuals who 
voluntarily smoke tobacco (i.e., smokers) and the effect of high 
temperatures on O3 responsiveness. New controlled human 
exposure studies have confirmed that smokers are less responsive to 
O3 than nonsmokers; however, time course of development and 
recovery of these effects, as well as reproducibility, was not 
different from nonsmokers (EPA, 2006a, section 6.5.5). Influence of 
ambient temperature on pulmonary effects induced by O3 has 
been studied very little, but additive effects of heat and 
O3 exposure have been reported.
    Antioxidants, which scavenge free radicals and limit lipid 
peroxidation in the ELF, are the first line of defense against 
oxidative stress. Ozone exposure leads to absorption of O3 
in the ELF with subsequent depletion of antioxidant in the nasal ELF, 
but concentration and antioxidant enzyme activity in ELF or plasma do 
not appear related to O3 responsiveness (EPA 2006a, section 
6.5.6). Controlled studies of dietary antioxidant supplements have 
shown some protective effects on lung function decrements but not on 
symptoms and airway inflammatory responses. Dietary antioxidant 
supplements have provided some protection to asthmatics by attenuating 
post-exposure airway hyperresponsiveness. Animal studies

[[Page 2969]]

have also supported the protective effects of ELF antioxidants.
b. At-Risk Subgroups for O3-Related Effects
    Several characteristics may increase the extent to which a 
population group shows increased susceptibility or vulnerability. 
Information on potentially susceptible and vulnerable groups is 
summarized in section 8.7 of the 2006 Criteria Document. As described 
there, the term susceptibility refers to innate (e.g., genetic or 
developmental) or acquired (e.g., personal risk factors, age) factors 
that make individuals more likely to experience effects with exposure 
to pollutants. A number of population groups have been identified as 
potentially susceptible to health effects as a result of O3 
exposure, including people with existing lung diseases, including 
asthma, children and older adults, and people who have larger than 
normal lung function responses that may be due to genetic 
susceptibility. In addition, some population groups have been 
identified as having increased vulnerability to O3-related 
effects due to increased likelihood of exposure while at elevated 
ventilation rates, including healthy children and adults who are active 
outdoors, for example, outdoor workers and joggers. Taken together, the 
susceptible and vulnerable groups make up ``at-risk'' groups.\24\
---------------------------------------------------------------------------

    \24\ In the Staff Paper and documents from previous 
O3 NAAQS reviews, ``at-risk'' groups have also been 
called ``sensitive'' groups, to mean both groups with greater 
inherent susceptibility and those more likely to be exposed.
---------------------------------------------------------------------------

i. Active People
    A large group of individuals at risk from O3 exposure 
consists of outdoor workers and children, adolescents, and adults who 
engage in outdoor activities involving exertion or exercise during 
summer daylight hours when ambient O3 concentrations tend to 
be higher. This conclusion is based on a large number of controlled-
human exposure studies and several epidemiologic field/panel studies 
which have been conducted with healthy children and adults and those 
with preexisting respiratory diseases (EPA 2006a, sections 6.2, 6.3, 
7.2, and 8.4.4). The controlled human exposure studies show a clear 
O3 exposure-response relationship with increasing 
spirometric and symptomatic response as exercise level increases. 
Furthermore, O3-induced response increases as time of 
exposure increases. Studies of outdoor workers and others who 
participate in outdoor activities indicate that extended exposures to 
O3 at elevated exertion levels can produce marked effects on 
lung function, as discussed above in section IIA.2 (Brauer et al., 
1996; H[ouml]ppe et al., 1995; Korrick et al., 1998; McConnell et al., 
2002).
    These field studies with subjects at elevated exertion levels 
support the extensive evidence derived from controlled human exposure 
studies. The majority of controlled human exposure studies has examined 
the effects of O3 exposure in subjects performing continuous 
or intermittent exercise for variable periods of time and has reported 
significant O3-induced respiratory responses. The 
epidemiologic studies discussed above also indicate that prolonged 
exposure periods, combined with elevated levels of exertion or 
exercise, may magnify O3 effects on lung function. Thus, 
outdoor workers and others who participate in higher exertion 
activities outdoors during the time of day when high peak O3 
concentrations occur appear to be particularly vulnerable to 
O3 effects on respiratory health. Although these studies 
show a wide variability of response and sensitivity among subjects and 
the factors contributing to this variability continue to be 
incompletely understood, the effect of increased exertion is 
consistent. It should be noted that this wide variability of response 
and sensitivity among subjects may be in part due to the wide range of 
other highly reactive photochemical oxidants coexisting with 
O3 in the ambient air.
ii. People With Lung Disease
    People with preexisting pulmonary disease are among those at 
increased risk from O3 exposure. Altered physiological, 
morphological, and biochemical states typical of respiratory diseases 
like asthma, COPD, and chronic bronchitis may render people sensitive 
to additional oxidative burden induced by O3 exposure. At 
the time of the 1997 review, it was concluded that these groups were at 
greater risk because the impact of O3-induced responses on 
already-compromised respiratory systems would noticeably impair an 
individual's ability to engage in normal activity or would be more 
likely to result in increased self-medication or medical treatment. At 
that time there was little evidence that people with pre-existing 
disease were more responsive than healthy individuals in terms of the 
magnitude of lung function decrements or symptomatic responses. The new 
results from controlled exposure and epidemiologic studies continue to 
indicate that individuals with preexisting pulmonary disease are a 
sensitive population for O3-related health effects.
    Several controlled human exposure studies reviewed in the 1996 
Criteria Document on atopic and asthmatic subjects have suggested but 
not clearly demonstrated enhanced responsiveness to acute O3 
exposure compared to healthy subjects. The majority of the newer 
studies reviewed in Chapter 6 of the 2006 Criteria Document indicate 
that asthmatics are more sensitive than normal subjects in manifesting 
O3-induced lung function decrements. In one key study 
(Horstman et al., 1995), the FEV1 decrement observed in the 
asthmatics was significantly larger than in the healthy subjects (19% 
versus 10%, respectively). There was also a notable tendency for a 
greater group mean O3-induced decrease in 
FEF25-75 in asthmatics relative to the healthy subjects (24% 
versus 15%, respectively). A significant positive correlation in 
asthmatics was also reported between the magnitude of O3-
induced spirometric responses and baseline lung function, i.e., 
responses increased with severity of disease.
    Asthmatics present a differential response profile for cellular, 
molecular, and biochemical parameters (2006 Criteria Document, Figure 
8-1) that are altered in response to acute O3 exposure. 
Ozone-induced increases in neutrophils, IL-8 and protein were found to 
be significantly higher in the BAL fluid from asthmatics compared to 
healthy subjects, suggesting mechanisms for the increased sensitivity 
of asthmatics (Basha et al., 1994; McBride et al., 1994; Scannell et 
al., 1996; Hiltermann et al., 1999; Holz et al., 1999; Bosson et al., 
2003). Neutrophils, or PMNs, are the white blood cells most associated 
with inflammation. IL-8 is an inflammatory cytokine with a number of 
biological effects, primarily on neutrophils. The major role of this 
cytokine is to attract and activate neutrophils. Protein in the airways 
is leaked from the circulatory system, and is a marker for increased 
cellular permeability.
    Bronchial constriction following provocation with O3 
and/or allergens presents a two-phase response. The early response is 
mediated by release of histamine and leukotrienes that leads to 
contraction of smooth muscle cells in the bronchi, narrowing the lumen 
and decreasing the airflow. In people with allergic airway disease, 
including people with rhinitis and asthma, these mediators also cause 
accumulation of eosinophils in the airways (Bascom et al., 1990; Jorres 
et al., 1996; Peden et al., 1995 and 1997; Frampton et al., 1997; 
Michelson et al., 1999; Hiltermann et al., 1999; Holz et al., 2002; 
Vagaggini et al., 2002). In asthma, the eosinophil,

[[Page 2970]]

which increases inflammation and allergic responses, is the cell most 
frequently associated with exacerbations of the disease. A study by 
Bosson et al. (2003) evaluated the difference in O3-induced 
bronchial epithelial cytokine expression between healthy and asthmatic 
subjects. After O3 exposure the epithelial expression of IL-
5 and GM-CSF increased significantly in asthmatics, compared to healthy 
subjects. Asthma is associated with Th2-related airway response 
(allergic response), and IL-5 is an important Th2-related cytokine. The 
O3-induced increase in IL-5, and also in GM-CSF, which 
affects the growth, activation and survival of eosinophils, may 
indicate an effect on the Th2-related airway response and on airway 
eosinophils. The authors reported that the O3-induced Th2-
related cytokine responses that were found within the asthmatic group 
may indicate a worsening of their asthmatic airway inflammation and 
thus suggest a plausible link to epidemiological data indicating 
O3-associated increases in bronchial reactivity and hospital 
admissions.
    The accumulation of eosinophils in the airways of asthmatics is 
followed by production of mucus and a late-phase bronchial constriction 
and reduced airflow. In a study of 16 intermittent asthmatics, 
Hiltermann et al. (1999) found that there was a significant inverse 
correlation between the O3-induced change in the percentage 
of eosinophils in induced sputum and the change in PC20, the 
concentration of methacholine causing a 20% decrease in 
FEV1. Characteristic O3-induced inflammatory 
airway neutrophilia at one time was considered a leading mechanism of 
airway hyperresponsiveness. However, Hiltermann et al. (1999) 
determined that the O3-induced change in percentage 
neutrophils in sputum was not significantly related to the change in 
PC20. These results are consistent with the results of Zhang 
et al. (1995), which found neutrophilia in a murine model to be only 
coincidentally associated with airway hyperresponsiveness, i.e., there 
was no cause and effect relationship. (2006 Criteria Document, AX 6-
26). Hiltermann et al. (1999) concluded that the results point to the 
role of eosinophils in O3-induced airway 
hyperresponsiveness. Increases in O3-induced nonspecific 
airway responsiveness incidence and duration could have important 
clinical implications for asthmatics.
    Two studies (J[ouml]rres et al., 1996; Holz et al., 2002) observed 
increased airway responsiveness to O3 exposure with 
bronchial allergen challenge in subjects with preexisting allergic 
airway disease. J[ouml]rres et al. (1996) found that O3 
causes an increased response to bronchial allergen challenge in 
subjects with allergic rhinitis and mild allergic asthma. The subjects 
were exposed to 0.25 ppm O3 for 3 hours with IE. Airway 
responsiveness to methacholine was determined 1 hour before and after 
exposure; responsiveness to allergen was determined 3 hours after 
exposure. Statistically significant decreases in FEV1 
occurred in subjects with allergic rhinitis (13.8%) and allergic asthma 
(10.6%), and in healthy controls (7.3%). Methacholine responsiveness 
was statistically increased in asthmatics, but not in subjects with 
allergic rhinitis or healthy controls. Airway responsiveness to an 
individual's historical allergen (either grass and birch pollen, house 
dust mite, or animal dander) was significantly increased after 
O3 exposure when compared to FA exposure. In subjects with 
asthma and allergic rhinitis, a maximum percent fall in FEV1 
of 27.9% and 7.8%, respectively, occurred 3 days after O3 
exposure when they were challenged with of the highest common dose of 
allergen. The authors concluded that subjects with asthma or allergic 
rhinitis, without asthma, could be at risk if a high O3 
exposure is followed by a high dose of allergen. Holz et al. (2002) 
reported an early phase lung function response in subjects with 
rhinitis after a consecutive 4-day exposure to 0.125 ppm O3 
that resulted in a clinically relevant (>20%) decrease in 
FEV1. Ozone-induced exacerbation of airway responsiveness 
persists longer and attenuates more slowly than O3-induced 
lung function decrements and respiratory symptom responses and can have 
important clinical implications for asthmatics.
    A small number of in vitro studies corroborate the differences in 
the responses of asthmatic and healthy subject generally found in 
controlled human exposure studies. In vitro studies (Schierhorn et al., 
1999) of nasal mucosal biopsies from atopic and nonatopic subjects 
exposed to 0.1 ppm O3 found significant differences in 
release of IL-4, IL-6, IL-8, and TNF-[alpha]. Another study by 
Schierhorn et al. (2002) found significant differences in the 
O3-induced release of the neuropeptides neurokinin A and 
substance P for allergic patients in comparison to nonallergic 
controls, suggesting increased activation of sensory nerves by 
O3 in the allergic tissues. Another study by Bayram et al. 
(2002) using in vitro culture of bronchial epithelial cells recovered 
from atopic and nonatopic asthmatics also found significant increases 
in epithelial permeability in response to O3 exposure.
    The new data on airway responsiveness, inflammation, and various 
molecular markers of inflammation and bronchoconstriction indicate that 
people with asthma and allergic rhinitis (with or without asthma) 
comprise susceptible groups for O3-induced adverse effects. 
This body of evidence indicates that controlled human exposure and 
epidemiological panel studies of lung function decrements and 
respiratory symptoms that evaluate only healthy, non-asthmatic subjects 
likely underestimate the effects of O3 exposure on 
asthmatics and other susceptible populations. The effects of 
O3 on lung function, inflammation, and increased airway 
responsiveness demonstrated in subjects with asthma and other allergic 
airway diseases, provide plausible mechanisms underlying the more 
serious respiratory morbidity effects, such as emergency department 
visits and hospital admissions, and respiratory mortality effects.
    A number of epidemiological studies have been conducted using 
asthmatic study populations. The majority of epidemiological panel 
studies that evaluated respiratory symptoms and medication use related 
to O3 exposures focused on children. These studies suggest 
that O3 exposure is associated with increased respiratory 
symptoms and medication use in children with asthma. Other reported 
effects include respiratory symptoms, lung function decrements, and 
emergency department visits, as discussed in the 2006 Criteria Document 
(section 7.6.7.1). Strong evidence from a large multicity study 
(Mortimer et al., 2002), along with support from several single-city 
studies indicate that O3 exposure is associated with 
increased respiratory symptoms and medication use in children with 
asthma. With regard to ambient O3 levels and increased 
hospital admissions and emergency department visits for asthma and 
other respiratory causes, strong and consistent evidence establishes a 
correlation between O3 exposure and increased exacerbations 
of preexisting respiratory disease for 1-hour maximum O3 
concentrations <0.12 ppm. As discussed above and in the 2006 Criteria 
Document, section 7.3, several hospital admission and emergency 
department visit studies in the U.S., Canada, and Europe have reported 
positive associations between increase in O3 and increased 
risk of emergency department visits and hospital admissions for asthma 
other

[[Page 2971]]

respiratory diseases, especially during the warm season.
    In summary, based on a substantial new body of evidence from 
animal, controlled human exposure and epidemiological studies the 2006 
Criteria Document (section x.x) concludes that people with asthma and 
other preexisting pulmonary diseases are among those at increased risk 
from O3 exposure. Evidence from controlled human exposure 
studies indicates that asthmatics may exhibit larger lung function 
decrements and can have larger inflammatory responses in response to 
O3 exposure than healthy controls. Asthmatics present a 
different response profile for cellular, molecular, and biochemical 
parameters that are altered in response to acute O3 
exposure. Asthmatics, and people with allergic rhinitis, are more 
likely to mount an allergic-type response upon exposure to 
O3, as manifested by increases in white blood cells 
associated with allergy and related molecules, which increase 
inflammation in the airways. The increased inflammatory and allergic 
responses also may be associated with the larger late-phase responses 
that asthmatics can experience, which can include increased 
bronchoconstrictor responses to irritant substances or allergens and 
additional inflammation. Epidemiological studies have reported fairly 
robust associations between ambient O3 concentrations and 
measures of lung function and daily respiratory symptoms (e.g., chest 
tightness, wheeze, shortness of breath) in children with moderate to 
severe asthma and between O3 and increased asthma medication 
use. These more serious responses in asthmatics and others with lung 
disease provide biological plausibility for the respiratory morbidity 
effects observed in epidemiological studies, such as emergency 
department visits and hospital admissions. The body of evidence from 
controlled human exposure and epidemiological studies, which includes 
asthmatic as well as non-asthmatic subjects, indicates that controlled 
human exposure studies of lung function decrements and respiratory 
symptoms that evaluate only healthy, non-asthmatic subjects likely 
underestimate the effects of O3 exposure on asthmatics and 
other susceptible populations.
    Newly available reports from controlled human exposure studies (see 
chapter 6 in the 2006 Criteria Document) utilized subjects with 
preexisting cardiopulmonary diseases such as COPD, asthma, allergic 
rhinitis, and hypertension. The data generated from these studies that 
evaluated changes in spirometry did not find clear differences between 
filtered air and O3 exposure in COPD subjects. However, the 
new data on airway responsiveness, inflammation, and various molecular 
markers of inflammation and bronchoconstriction indicate that people 
with atopic asthma and allergic rhinitis comprise susceptible groups 
for O3-induced adverse health effects.
    Although controlled human exposure studies have not found evidence 
of larger spirometric responses to O3 in people with COPD 
relative to healthy subjects, this may be due to the fact that most 
people with COPD are older adults who would not be expected to be as 
responsive based on their age. However, in section 8.7.1, the 2006 
Criteria Document notes that new epidemiological evidence indicates 
that people with COPD may be more likely to experience other effects, 
including emergency room visits, hospital admissions, or premature 
mortality. For example, results from an analysis of five European 
cities indicated strong and consistent O3 effects on 
unscheduled respiratory hospital admissions, including COPD (Anderson 
et al., 1997). Also, an analysis of a 9-year data set for the whole 
population of the Netherlands provided risk estimates for more specific 
causes of mortality, including COPD (Hoek et al., 2000, 2001; 
reanalysis Hoek, 2003); a positive, but nonsignificant, excess risk of 
COPD-related mortality was found to be associated with short-term 
O3 concentrations. Moreover, as indicated by Gong et al. 
(1998), the effects of O3 exposure on alveolar-arterial 
oxygen gradients may be more pronounced in patients with preexisting 
obstructive lung diseases. Relative to healthy elderly subjects, COPD 
patients have reduced gas exchange and low SaO2. Any 
inflammatory or edematous responses due to O3 delivered to 
the well-ventilated regions of the lung in COPD subjects could further 
inhibit gas exchange and reduce oxygen saturation. In addition, 
O3-induced vasoconstriction could also acutely induce 
pulmonary hypertension. Inducing pulmonary vasoconstriction and 
hypertension in these patients would perhaps worsen their condition, 
especially if their right ventricular function was already compromised 
(EPA, 2006a, section 6.10). These controlled human exposure and 
epidemiological studies indicate that people with pre-existing lung 
diseases other than asthma are also at greater risk from O3 
exposure than people without lung disease.
iii. Children and Older Adults
    Supporting evidence exists for heterogeneity in the effects of 
O3 by age. As discussed in section 6.5.1 of the 2006 
Criteria Document, children, adolescents, and young adults (<18 yrs of 
age) appear, on average, to have nearly equivalent spirometric 
responses to O3, but have greater responses than middle-aged 
and older adults when exposed to comparable O3 doses. 
Symptomatic responses to O3 exposure, however, do not appear 
to occur in healthy children, but are observed in asthmatic children, 
particularly those who use maintenance medications. For adults (>17 yrs 
of age) symptoms gradually decrease with increasing age. In contrast to 
young adults, the diminished symptomatic responses in children and the 
diminished symptomatic and spirometric responses in older adults 
increases the likelihood that these groups continue outdoor activities 
leading to greater O3 exposure and dose.
    As described in the section 7.6.7.2 of the 2006 Criteria Document, 
many epidemiological field studies focused on the effect of 
O3 on the respiratory health of school children. In general, 
children experienced decrements in lung function parameters, including 
PEF, FEV1, and FVC. Increases in respiratory symptoms and 
asthma medication use were also observed in asthmatic children. In one 
German study, children with and without asthma were found to be 
particularly susceptible to O3 effects on lung function. 
Approximately 20 percent of the children, both with and without asthma, 
experienced a greater than 10 percent change in FEV1, 
compared to only 5 percent of the elderly population and athletes 
(H[ouml]ppe et al., 2003).
    The American Academy of Pediatrics (2004) notes that children and 
infants are among the population groups most susceptible to many air 
pollutants, including O3. This is in part because their 
lungs are still developing. For example, eighty percent of alveoli are 
formed after birth, and changes in lung development continue through 
adolescence (Dietert et al., 2000). Children are also likely to spend 
more time outdoors than adults, which results in increased exposure to 
air pollutants (Wiley et al., 1991a,b). Moreover, children have high 
minute ventilation rates and high levels of physical activity which 
also increases their dose (Plunkett et al., 1992).
    Several mortality studies have investigated age-related differences 
in O3 effects (EPA, 2006a, section 7.6.7.2). Older adults 
are also often classified as

[[Page 2972]]

being particularly susceptible to air pollution. The 2006 Criteria 
Document (p. 8-60) concludes that the basis for increased O3 
sensitivity among the elderly is not known, but one hypothesis is that 
it may be related to changes in the respiratory tract lining fluid 
antioxidant defense network (Kelly et al., 2003). Older adults have 
lower baseline lung function than younger people, and are also more 
likely to have preexisting lung and heart disease. Increased 
susceptibility of older adults to O3 health effects is most 
clearly indicated in the newer mortality studies. Among the studies 
that observed positive associations between O3 and 
mortality, a comparison of all age or younger age (<= 65 years of age) 
O3-mortality effect estimates to that of the elderly 
population (> 65 years) indicates that, in general, the elderly 
population is more susceptible to O3 mortality effects. The 
meta-analysis by Bell et al. (2005) found a larger mortality effect 
estimate for the elderly than for all ages. In the large U.S. 95 
communities study (Bell et al., 2004), mortality effect estimates were 
slightly higher for those aged 65 to 74 years, compared to individuals 
less than 65 years and 75 years or greater. The absolute effect of 
O3 on premature mortality may be substantially greater in 
the elderly population because of higher rates of preexisting 
respiratory and cardiac diseases. The 2006 Criteria Document (p. 7-177) 
concludes that the elderly population (>65 years of age) appear to be 
at greater risk of O3-related mortality and hospitalizations 
compared to all ages or younger populations.
    The 2006 Criteria Document notes that, collectively, there is 
supporting evidence of age-related differences in susceptibility to 
O3 lung function effects. The elderly population (> 65 years 
of age) appear to be at increased risk of O3-related 
mortality and hospitalizations, and children (< 18 years of age) 
experience other potentially adverse respiratory health outcomes with 
increased O3 exposure (EPA, 2006a, section 7.6.7.2).
iv. People With Increased Responsiveness to Ozone
    New animal toxicology studies using various strains of mice and 
rats have identified O3-sensitive and resistant strains and 
illustrated the importance of genetic background in determining 
O3 susceptibility (EPA, 2006a, section 8.7.4). Controlled 
human exposure studies have also indicated a high degree of variability 
in some of the pulmonary physiological parameters. The variable effects 
in individuals have been found to be reproducible, in other words, a 
person who has a large lung function response after exposure to 
O3 will likely have about the same response if exposed again 
to the same dose of O3. In controlled human exposure 
studies, group mean responses are not representative of this segment of 
the population that has much larger than average responses to 
O3. Recent studies of asthmatics by David et al. (2003) and 
Romieu et al. (2004) reported a role for genetic polymorphism in 
observed differences in antioxidant enzymes and genes involved in 
inflammation to modulate lung function and inflammatory responses to 
O3 exposure.\25\
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    \25\ Similar to animal toxicology studies referred above, a 
polymorphism in a specific proinflammatory cytokine gene has been 
implicated in O3-induced lung function changes in 
healthy, mild asthmatics and individuals with rhinitis. These 
observations suggest a potential role for these markers in the 
innate susceptibility to O3, however, the validity of 
these markers and their relevance in the context of prediction to 
population studies requires additional research.
---------------------------------------------------------------------------

    Biochemical and molecular parameters extensively evaluated in these 
experiments were used to identify specific loci on chromosomes and, in 
some cases, to relate the differential expression of specific genes to 
biochemical and physiological differences observed among these species. 
Utilizing O3-sensitive and O3-resistant species, 
it has been possible to identify the involvement of increased airway 
reactivity and inflammation processes in O3 susceptibility. 
However, most of these studies were carried out using relatively high 
doses of O3, making the relevance of these studies 
questionable in human health effects assessment. The genes and genetic 
loci identified in these studies may serve as useful biomarkers in the 
future.
v. Other Population Groups
    There is limited, new evidence supporting associations between 
short-term O3 exposures and a range of effects on the 
cardiovascular system. Some but not all, epidemiological studies have 
reported associations between short-term O3 exposures and 
the incidence of heart attacks and more subtle cardiovascular health 
endpoints, such as changes in HRV and cardiac arrhythmia. Others have 
reported associations with hospitalization or emergency department 
visits for cardiovascular diseases, although the results across the 
studies are not consistent. Studies also report associations between 
short-term O3 exposure and mortality from cardiovascular or 
cardiopulmonary causes. The 2006 Criteria Document (p. 7-65) concludes 
that current cardiovascular effects evidence from some field studies is 
rather limited but supportive of a potential effect of short-term 
O3 exposure and HRV, cardiac arrhythmia, and heart attack 
incidence. In the 2006 Criteria Document's evaluation of studies of 
hospital admissions for cardiovascular disease (EPA 2006a, section 
7.3.4), it is concluded that evidence from this growing group of 
studies is generally inconclusive regarding an association with 
O3 in studies conducted during the warm season (EPA 2006a, 
p. 7-83). This body of evidence suggests that people with heart disease 
may be at increased risk from short-term exposures to O3; 
however, more evidence is needed to conclude that people with heart 
disease are a susceptible population.
    Other groups that might have enhanced sensitivity to O3, 
but for which there is currently very little evidence, include groups 
based on race, gender and SES, and those with nutritional deficiencies, 
which presents factors which modify responsiveness to O3.
c. Adversity of Effects
    In the 2008 rulemaking, in making judgments as to when various 
O3-related effects become regarded as adverse to the health 
of individuals, EPA looked to guidelines published by the American 
Thoracic Society (ATS) and the advice of CASAC. While recognizing that 
perceptions of ``medical significance'' and ``normal activity'' may 
differ among physicians, lung physiologists and experimental subjects, 
the ATS (1985) \26\ defined adverse respiratory health effects as 
``medically significant physiologic changes generally evidenced by one 
or more of the following: (1) Interference with the normal activity of 
the affected person or persons, (2) episodic respiratory illness, (3) 
incapacitating illness, (4) permanent respiratory injury, and/or (5) 
progressive respiratory dysfunction.'' During the 1997 review, it was 
concluded that there was evidence of causal associations from 
controlled human exposure studies for effects in the first of these 
five ATS-defined categories, evidence of statistically significant 
associations from epidemiological studies for effects in the second and 
third categories, and evidence from animal toxicology

[[Page 2973]]

studies, which could be extrapolated to humans only with a significant 
degree of uncertainty, for the last two categories.
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    \26\ In 2000, the American Thoracic Society (ATS) published an 
official statement on ``What Constitutes an Adverse Health Effect of 
Air Pollution?'' (ATS, 2000), which updated its earlier guidance 
(ATS, 1985). Overall, the new guidance does not fundamentally change 
the approach previously taken to define adversity, nor does it 
suggest a need at this time to change the structure or content of 
the tables describing gradation of severity and adversity of effects 
described below.
---------------------------------------------------------------------------

    For ethical reasons, clear causal evidence from controlled human 
exposure studies still covers only effects in the first category. 
However, for this review there are results from epidemiological 
studies, upon which to base judgments about adversity, for effects in 
all of the categories. Statistically significant and robust 
associations have been reported in epidemiology studies falling into 
the second and third categories. These more serious effects include 
respiratory events (e.g., triggering asthma attacks) that may require 
medication (e.g., asthma), but not necessarily hospitalization, as well 
as respiratory hospital admissions and emergency department visits for 
respiratory causes. Less conclusive, but still positive associations 
have been reported for school absences and cardiovascular hospital 
admissions. Human health effects for which associations have been 
suggested through evidence from epidemiological and animal toxicology 
studies, but have not been conclusively demonstrated still fall 
primarily into the last two categories. In the 1997 review of the 
O3 standard, evidence for these more serious effects came 
from studies of effects in laboratory animals. Evidence from animal 
studies evaluated in the 2006 Criteria Document strongly suggests that 
O3 is capable of damaging the distal airways and proximal 
alveoli, resulting in lung tissue remodeling leading to apparently 
irreversible changes. Recent advancements of dosimetry modeling also 
provide a better basis for extrapolation from animals to humans. 
Information from epidemiological studies provides supporting, but 
limited evidence of irreversible respiratory effects in humans than was 
available in the prior review. Moreover, the findings from single-city 
and multicity time-series epidemiology studies and meta-analyses of 
these epidemiological studies are highly suggestive of an association 
between short-term O3 exposure and mortality particularly in 
the warm season.
    While O3 has been associated with effects that are 
clearly adverse, application of these guidelines, in particular to the 
least serious category of effects related to ambient O3 
exposures, involves judgments about which medical experts on the CASAC 
panel and public commenters have expressed diverse views in the past. 
To help frame such judgments, EPA staff have defined specific ranges of 
functional responses (e.g., decrements in FEV1 and airway 
responsiveness) and symptomatic responses (e.g., cough, chest pain, 
wheeze), together with judgments as to the potential impact on 
individuals experiencing varying degrees of severity of these 
responses, that have been used in previous NAAQS reviews. These ranges 
of pulmonary responses and their associated potential impacts are 
summarized in Tables 3-2 and 3-3 of the 2007 Staff Paper.
    For active healthy people, moderate levels of functional responses 
(e.g., FEV1 decrements of >= 10 percent but < 20 percent, 
lasting up to 24 hours) and/or moderate symptomatic responses (e.g., 
frequent spontaneous cough, marked discomfort on exercise or deep 
breath, lasting up to 24 hours) would likely interfere with normal 
activity for relatively few responsive individuals. On the other hand, 
EPA staff determined that large functional responses (e.g., 
FEV1 decrements >= 20 percent, lasting longer than 24 hours) 
and/or severe symptomatic responses (e.g., persistent uncontrollable 
cough, severe discomfort on exercise or deep breath, lasting longer 
than 24 hours) would likely interfere with normal activities for many 
responsive individuals. EPA staff determined that these would be 
considered adverse under ATS guidelines. In the context of standard 
setting, CASAC indicated that a focus on the mid to upper end of the 
range of moderate levels of functional responses (e.g., FEV1 
decrements >= 15 percent but < 20 percent) is appropriate for 
estimating potentially adverse lung function decrements in active 
healthy people. However, for people with lung disease, even moderate 
functional (e.g., FEV1 decrements >= 10 percent but < 20 
percent, lasting up to 24 hours) or symptomatic responses (e.g., 
frequent spontaneous cough, marked discomfort on exercise or with deep 
breath, wheeze accompanied by shortness of breath, lasting up to 24 
hours) would likely interfere with normal activity for many 
individuals, and would likely result in more frequent use of 
medication. For people with lung disease, large functional responses 
(e.g., FEV1 decrements >= 20 percent, lasting longer than 24 
hours) and/or severe symptomatic responses (e.g., persistent 
uncontrollable cough, severe discomfort on exercise or deep breath, 
persistent wheeze accompanied by shortness of breath, lasting longer 
than 24 hours) would likely interfere with normal activity for most 
individuals and would increase the likelihood that these individuals 
would seek medical treatment. In the context of standard setting, the 
CASAC indicated (Henderson, 2006c) that a focus on the lower end of the 
range of moderate levels of functional responses (e.g., FEV1 
decrements >= 10 percent) is most appropriate for estimating 
potentially adverse lung function decrements in people with lung 
disease.
    In judging the extent to which these impacts represent effects that 
should be regarded as adverse to the health status of individuals, an 
additional factor that has been considered in previous NAAQS reviews is 
whether such effects are experienced repeatedly during the course of a 
year or only on a single occasion. While some experts would judge 
single occurrences of moderate responses to be a ``nuisance,'' 
especially for healthy individuals, a more general consensus view of 
the adversity of such moderate responses emerges as the frequency of 
occurrence increases.
    The new guidance builds upon and expands the 1985 definition of 
adversity in several ways. There is an increased focus on quality of 
life measures as indicators of adversity. There is also a more specific 
consideration of population risk. Exposure to air pollution that 
increases the risk of an adverse effect to the entire population is 
adverse, even though it may not increase the risk of any individual to 
an unacceptable level. For example, a population of asthmatics could 
have a distribution of lung function such that no individual has a 
level associated with significant impairment. Exposure to air pollution 
could shift the distribution to lower levels that still do not bring 
any individual to a level that is associated with clinically relevant 
effects. However, this would be considered to be adverse because 
individuals within the population would have diminished reserve 
function, and therefore would be at increased risk if affected by 
another agent.
    Of the various effects of O3 exposure that have been 
studied, many would meet the ATS definition of adversity. Such effects 
include, for example, any detectible level of permanent lung function 
loss attributable to air pollution, including both reductions in lung 
growth or acceleration of the age-related decline of lung function; 
exacerbations of disease in individuals with chronic cardiopulmonary 
diseases; reversible loss of lung function in combination with the 
presence of symptoms; as well as more serious effects such as those 
requiring medical care including hospitalization and, obviously, 
mortality.

[[Page 2974]]

d. Size of At-Risk Populations
    Although O3-related health risk estimates may appear to 
be small, their significance from an overall public health perspective 
is determined by the large numbers of individuals in the population 
groups potentially at risk for O3-related health effects 
discussed above. For example, a population of concern includes people 
with respiratory disease, which includes approximately 11 percent of 
U.S. adults and 13 percent of children who have been diagnosed with 
asthma and 6 percent of adults with chronic obstructive pulmonary 
disease (chronic bronchitis and/or emphysema) in 2002 and 2003 (Table 
8-4 in the 2006 Criteria Document, section 8.7.5.2). More broadly, 
individuals with preexisting cardiopulmonary disease may constitute an 
additional population of concern, with potentially tens of millions of 
people included in each disease category. In addition, populations 
based on age group also comprise substantial segments of the population 
that may be potentially at risk for O3-related health 
impacts. Based on U.S. census data from 2003, about 26 percent of the 
U.S. population are under 18 years of age and 12 percent are 65 years 
of age or older. Hence, large proportions of the U.S. population are 
included in life stages that are most likely to have increased 
susceptibility to the health effects of O3 and/or those with 
the highest ambient O3 exposures.
    The 2006 Criteria Document (section 8.7.5.2) notes that the health 
statistics data illustrate what is known as the ``pyramid'' of effects. 
At the top of the pyramid, there are approximately 2.5 millions deaths 
from all causes per year in the U.S. population, with about 100,000 
deaths from chronic lower respiratory diseases. For respiratory health 
diseases, there are nearly 4 million hospital discharges per year, 14 
million emergency department visits, 112 million ambulatory care 
visits, and an estimated 700 million restricted activity days per year 
due to respiratory conditions from all causes per year. Applying small 
risk estimates for the O3-related contribution to such 
health effects with relatively large baseline levels of health outcomes 
can result in quite large public health impacts related to ambient 
O3 exposure. Thus, even a small percentage reduction in 
O3 health impacts on cardiopulmonary diseases would reflect 
a large number of avoided cases. In considering this information 
together with the concentration-response relationships that have been 
observed between exposure to O3 and various health 
endpoints, the 2006 Criteria Document (section 8.7.5.2) concludes that 
exposure to ambient O3 likely has a significant impact on 
public health in the U.S.

B. Human Exposure and Health Risk Assessments

    To put judgments about health effects that are adverse for 
individuals into a broader public health context, EPA has developed and 
applied models to estimate human exposures and health risks. This 
broader context includes consideration of the size of particular 
population groups at risk for various effects, the likelihood that 
exposures of concern will occur for individuals in such groups under 
varying air quality scenarios, estimates of the number of people likely 
to experience O3-related effects, the variability in 
estimated exposures and risks, and the kind and degree of uncertainties 
inherent in assessing the exposures and risks involved.
    As discussed below there are a number of important uncertainties 
that affect the exposure and health risk estimates. It is also 
important to note that there have been significant improvements in both 
the exposure and health risk model. CASAC expressed the view that the 
exposure analysis represents a state-of-the-art modeling approach and 
that the health risk assessment was ``well done, balanced and 
reasonably communicated (Henderson, 2006c). While recognizing and 
considering the kind and degree of uncertainties in both the exposure 
and health risk estimates, the 2007 Staff Paper (pp. 6-20 to 6-21) 
judged that the quality of the estimates is such that they are suitable 
to be used as an input to the Administrator's decisions on the 
O3 primary standard.
    In modeling exposures and health risks associated with just meeting 
the current and alternative O3 standards, EPA has simulated 
air quality to represent conditions just meeting these standards based 
on O3 air quality patterns in several recent years and on 
how the shape of the O3 air quality distribution have 
changed over time based on historical trends in monitored O3 
air quality data. As described in the 2007 Staff Paper (EPA, 2007b, 
section 4.5.8) and discussed below, recent O3 air quality 
distributions have been statistically adjusted to simulate just meeting 
the current and selected alternative standards. These simulations do 
not reflect any consideration of specific control programs or 
strategies designed to achieve the reductions in emissions required to 
meet the specified standards. Further, these simulations do not 
represent predictions of when, whether, or how areas might meet the 
specified standards.\27\
---------------------------------------------------------------------------

    \27\ Modeling that projects whether and how areas might attain 
alternative standards in a future year is presented in the 
Regulatory Impact Analysis being prepared in connection with this 
rulemaking.
---------------------------------------------------------------------------

    As noted in section I.C above, around the time of the release of 
the final 2007 Staff Paper in January 2007, EPA discovered a small 
error in the exposure model that when corrected resulted in slight 
increases in the simulated exposures. Since the exposure estimates are 
an input to the lung function portion of the health risk assessment, 
this correction also resulted in slight increases in the lung function 
risk estimates as well. The exposure and risk estimates discussed in 
this notice reflect the corrected estimates, and thus are slightly 
different than the exposure and risk estimates cited in the January 31, 
2007 Staff Paper.\28\
---------------------------------------------------------------------------

    \28\ EPA made available corrected versions of the final 2007 
Staff Paper, and human exposure and health risk assessment technical 
support documents in July 2007 on the EPA Web site listed in the 
Availability of Related Information section of this notice.
---------------------------------------------------------------------------

1. Exposure Analyses
a. Overview
    As part of the 2008 rulemaking, the EPA conducted exposure analyses 
using a simulation model to estimate O3 exposures for the 
general population, school age children (ages 5-18), and school age 
children with asthma living in 12 U.S. metropolitan areas representing 
different regions of the country where the then current 8-hour 
O3 standard is not met. The emphasis on children reflects 
the finding of the 1997 O3 NAAQS review that children are an 
important at-risk group. The 12 modeled areas combined represent a 
significant fraction of the U.S. urban population, 89 million people, 
including 18 million school age children of whom approximately 2.6 
million have asthma. The selection of urban areas to include in the 
exposure analysis took into consideration the location of O3 
epidemiological studies, the availability of ambient O3 
data, and the desire to represent a range of geographic areas, 
population demographics, and O3 climatology. These selection 
criteria are discussed further in chapter 5 of the 2007 Staff Paper 
(EPA, 2007b). The geographic extent of each modeled area consists of 
the census tracts in the combined statistical area (CSA) as defined by 
OMB (OMB, 2005).\29\
---------------------------------------------------------------------------

    \29\ The 12 CSAs modeled are: Atlanta-Sandy Springs-Gainesville, 
GA-AL; Boston-Worcester-Manchester, MA-NH; Chicago-Naperville-
Michigan City, IL-IN-WI; Cleveland-Akron-Elyria, OH; Detroit-Warren-
Flint, MI; Houston-Baytown-Huntsville, TX; Los Angeles-Long Beach-
Riverside, CA; New York-Newark-Bridgeport, NY-NJ-CT-PA; 
Philadelphia-Camden-Vineland, PA-NJ-DE-MD; Sacramento--Arden-
Arcade--Truckee, CA-NV; St. Louis-St. Charles-Farmington, MO-IL; 
Washington-Baltimore-N. Virginia, DC-MD-VA-WV.

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[[Page 2975]]

    Exposure estimates were developed using a probabilistic exposure 
model that is designed to explicitly model the numerous sources of 
variability that affect people's exposures. As discussed below, the 
model estimates population exposures by simulating human activity 
patterns, air conditioning prevalence, air exchange rates, and other 
factors. The modeled exposure estimates were developed for three recent 
years of ambient O3 concentrations (2002, 2003, and 2004), 
as well as for O3 concentrations adjusted to simulate 
conditions associated with just meeting the then current NAAQS and 
various alternative 8-hour standards based on the three year period 
2002-2004.\30\ This exposure assessment is more fully described and 
presented in the 2007 Staff Paper and in a technical support document, 
Ozone Population Exposure Analysis for Selected Urban Areas (EPA, 
2007c; hereafter Exposure Analysis TSD). The scope and methodology for 
this exposure assessment were developed over the last few years with 
considerable input from the CASAC Ozone Panel and the public.\31\
---------------------------------------------------------------------------

    \30\ All 12 of the CSAs modeled did not meet the 0.084 ppm 
O3 NAAQS for the three year period examined.
    \31\ The general approach used in the human exposure assessment 
was described in the draft Health Assessment Plan (EPA, 2005d) that 
was released to the CASAC and general public in April 2005 and was 
the subject of a consultation with the CASAC O3 Panel on 
May 5, 2005. In October 2005, OAQPS released the first draft of the 
Staff Paper containing a chapter discussing the exposure analyses 
and first draft of the Exposure Analyses TSD for CASAC consultation 
and public review on December 8, 2005. In July 2006, OAQPS released 
the second draft of the Staff Paper and second draft of the Exposure 
Analyses TSD for CASAC review and public comment which was held by 
the CASAC O3 Panel on August 24-25, 2006.
---------------------------------------------------------------------------

    The goals of the O3 exposure assessment were: (1) To 
provide estimates of the size of at-risk populations exposed to various 
levels associated with recent O3 concentrations, and with 
just meeting the current O3 NAAQS and alternative 
O3 standards, in specific urban areas; (2) to provide 
distributions of exposure estimates over the entire range of ambient 
O3 concentrations as an important input to the lung function 
risk assessment summarized below in section II.B.2; (3) to develop a 
better understanding of the influence of various inputs and assumptions 
on the exposure estimates; and (4) to gain insight into the 
distribution of exposures and patterns of exposure reductions 
associated with meeting alternative O3 standards.
    The EPA recognizes that there are many sources of variability and 
uncertainty inherent in the inputs to this assessment and that there is 
uncertainty in the resulting O3 exposure estimates. With 
respect to variability, the exposure modeling approach accounts for 
variability in ambient O3 levels, demographic 
characteristics, physiological attributes, activity patterns, and 
factors affecting microenvironmental (e.g., indoor) concentrations. In 
EPA's judgment, the most important uncertainties affecting the exposure 
estimates are related to the modeling of human activity patterns over 
an O3 season, the modeling of variations in ambient 
concentrations near roadways, and the modeling of air exchange rates 
that affect the amount of O3 that penetrates indoors. 
Another important uncertainty that affects the estimation of how many 
exposures are associated with moderate or greater exertion is the 
characterization of energy expenditure for children engaged in various 
activities. As discussed in more detail in the 2007 Staff Paper (EPA, 
2007b, section 4.3.4.7), the uncertainty in energy expenditure values 
carries over to the uncertainty of the modeled breathing rates, which 
are important since they are used to classify exposures occurring at 
moderate or greater exertion which are the relevant exposures since 
O3-related effects observed in controlled human exposure 
studies only are observed when individuals are engaged in some form of 
exercise. The uncertainties in the exposure model inputs and the 
estimated exposures have been assessed using quantitative uncertainty 
and sensitivity analyses. Details are discussed in the 2007 Staff Paper 
(section 4.6) and in a technical memorandum describing the exposure 
modeling uncertainty analysis (Langstaff, 2007).
b. Scope and Key Components
    Population exposures to O3 are primarily driven by 
ambient outdoor concentrations, which vary by time of day, location, 
and peoples' activities. Outdoor O3 concentration estimates 
used in the exposure assessment are provided by measurements and 
statistical adjustments to the measured concentrations. The current 
exposure analysis allows comparisons of population exposures to 
O3 within each urban area, associated with current 
O3 levels and with O3 levels just meeting several 
potential alternative air quality standards or scenarios. Human 
exposure, regardless of the pollutant, depends on where individuals are 
located and what they are doing. Inhalation exposure models are useful 
in realistically estimating personal exposures to O3 based 
on activity-specific breathing rates, particularly when recognizing 
that large scale population exposure measurement studies have not been 
conducted that are representative of the overall population or at risk 
subpopulations.
    The model EPA used to simulate O3 population exposure is 
the Air Pollutants Exposure Model (APEX), the human inhalation exposure 
model within the Total Risk Integrated Methodology (TRIM) framework 
(EPA, 2006c,d). APEX is conceptually based on the probabilistic NAAQS 
exposure model for O3 (pNEM/O3) used in the last 
O3 NAAQS review. Since that time the model has been 
restructured, improved, and expanded to reflect conceptual advances in 
the science of exposure modeling and newer input data available for the 
model. Key improvements to algorithms include replacement of the cohort 
approach with a probabilistic sampling approach focused on individuals, 
accounting for fatigue and oxygen debt after exercise in the 
calculation of breathing rates, and a new approach for construction of 
longitudinal activity patterns for simulated persons. Major 
improvements to data input to the model include updated air exchange 
rates, more recent census and commuting data, and a greatly expanded 
daily time-activities database.
    APEX is a probabilistic model designed to explicitly model the 
numerous sources of variability that affect people's exposures. APEX 
simulates the movement of individuals through time and space and 
estimates their exposures to O3 in indoor, outdoor, and in-
vehicle microenvironments. The exposure model takes into account the 
most significant factors contributing to total human O3 
exposure, including the temporal and spatial distribution of people and 
O3 concentrations throughout an urban area, the variation of 
O3 levels within each microenvironment, and the effects of 
exertion on breathing rate in exposed individuals. A more detailed 
description of APEX and its application is presented in chapter 4 of 
the 2007 Staff Paper and associated technical documents (EPA, 
2006b,c,d).
    Several methods have been used to evaluate the APEX model and to 
characterize the uncertainty of the model estimates. These include 
conducting model evaluation, sensitivity analyses, and a detailed 
uncertainty analysis for one urban area.

[[Page 2976]]

These are discussed fully in the 2007 Staff Paper (section 4.6) and in 
Langstaff (2007). The uncertainty of model structure was judged to be 
of lesser importance than the uncertainties of the model inputs and 
parameters. Model structure refers to the algorithms in APEX designed 
to simulate the processes that result in people's exposures, for 
example, the way that APEX models exposures to individuals when they 
are near roads. The uncertainties in the model input data (e.g., 
measurement error, ambient concentrations, air exchange rates, and 
activity pattern data) have been assessed individually, and their 
impact on the uncertainty in the modeled exposure estimates was 
assessed in a unified quantitative analysis with results expressed in 
the form of estimated confidence ranges around the estimated measures 
of exposure. This uncertainty analysis was conducted for one urban area 
(Boston) using the observed 2002 O3 concentrations and 2002 
concentrations adjusted to simulate just meeting the current standard, 
with the expectation that the results would be similar for other cities 
and years. One significant source of uncertainty, due to limitations in 
the database used to model peoples' daily activities, was not included 
in the unified analysis, and was assessed through separate sensitivity 
analyses. This analysis indicates that the uncertainty of the exposure 
results is relatively small. For example, 95 percent uncertainty 
intervals were calculated for the APEX estimates of the percent of 
children or asthmatic children with exposures above 0.060, 0.070, or 
0.080 ppm under moderate exertion, for two air quality scenarios 
(current 2002 and 2002 adjusted to simulate just meeting the current 
standard) in Boston (Langstaff, 2007, Tables 26 and 27). The 95 percent 
uncertainty intervals for this set of 12 exposure estimates indicate 
the possibility of underpredictions of the exposure estimates ranging 
from 3 to 25 percent of the modeled estimates, and overpredictions 
ranging from 4 to 11 percent of the estimates. For example, APEX 
estimates the percent of asthmatic children with exposures above 0.070 
ppm under moderate exertion to be 24 percent, for Boston 2002 
O3 concentrations adjusted to simulate just meeting the 
current standard. The 95 percent uncertainty interval for this estimate 
is 23-30 percent, or -4 to +25 percent of the estimate. These 
uncertainty intervals do not include the uncertainty engendered by 
limitations of the activity database, which is in the range of one to 
ten percent.
    The exposure periods modeled here are the O3 seasons in 
2002, 2003, and 2004. The O3 season in each area includes 
the period of the year where elevated O3 levels tend to be 
observed and for which routine hourly O3 monitoring data are 
available. Typically this period spans from March or April through 
September or October, or in some areas, spanning the entire year. Three 
years were modeled to reflect the substantial year-to-year variability 
that occurs in O3 levels and related meteorological 
conditions, and because the standard is specified in terms of a three-
year period. The year-to-year variability observed in O3 
levels is due to a combination of different weather patterns and the 
variation in emissions of O3 precursors. Nationally, 2002 
was a relatively high year with respect to the 4th highest daily 
maximum 8-hour O3 levels observed in urban areas across the 
U.S. (EPA, 2007b, Figure 2-16), with the mean of the distribution of 
O3 levels for the urban monitors being in the upper third 
among the years 1990 through 2006. In contrast, on a national basis, 
2004 is the lowest year on record through 2006 for this same air 
quality statistic, and 8-hour daily maximum O3 levels 
observed in most, but not all of the 12 urban areas included in the 
exposure and risk analyses were relatively low compared to other recent 
years. The 4th highest daily maximum 8-hour O3 levels 
observed in 2003 in the 12 urban areas and nationally generally were 
between those observed in 2002 and 2004.
    Regulatory scenarios examined in the 2008 rulemaking include the 
then current 0.08 ppm, average of the 4th daily maximum 8-hour averages 
over a three year period standard; standards with the same form but 
with alternative levels of 0.080, 0.074, 0.070, and 0.064 ppm; 
standards specified as the average of the 3rd highest daily maximum 8-
hour averages over a three year period with alternative levels of 0.084 
and 0.074 ppm; and a standard specified as the average of the 5th 
highest daily maximum 8-hour averages over a three year period with a 
level of 0.074 ppm.\32\ The then current standard used a rounding 
convention that allows areas to have an average of the 4th daily 
maximum 8-hour averages as high as 0.084 ppm and still meet the 
standard. All alternative standards analyzed were intended to reflect 
improved precision in the measurement of ambient concentrations (in 
ppm), where the precision would extend to three instead of two decimal 
places.
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    \32\ The 8-hour O3 standard established in 1997 was 
0.08 ppm, but the rounding convention specified that the average of 
the 4th daily maximum 8-hour average concentrations over a three-
year period must be at 0.084 ppm or lower to be in attainment of 
this standard. When EPA staff selected alternative standards to 
analyze, it was presumed that the same type of rounding convention 
would be used, and thus alternative standards of 0.084, 0.074, 0.064 
ppm were chosen.
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    The then current standard and all alternative standards were 
modeled using a quadratic rollback approach to adjust the hourly 
concentrations observed in 2002-2004 to yield a design value \33\ 
corresponding to the standard being analyzed. The quadratic rollback 
technique reduces higher concentrations more than lower concentrations 
near ambient background levels.\34\ This procedure was considered in a 
sensitivity analysis in the 1997 review of the O3 standard 
and has been shown to be more realistic than a linear, proportional 
rollback method, where all of the ambient concentrations are reduced by 
the same factor.
---------------------------------------------------------------------------

    \33\ A design value is a statistic that describes the air 
quality status of a given area relative to the level of the NAAQS. 
Design values are often based on multiple years of data, consistent 
with specification of the NAAQS in Part 50 of the CFR. For the 8-
hour O3 NAAQS, the 3-year average of the annual 4th-
highest daily maximum 8-hour average concentrations, based on the 
monitor within (or downwind of) an urban area yielding the highest 
3-year average, is the design value.
    \34\ The quadratic rollback approach and evaluation of this 
approach are described by Johnson (1997), Duff et al. (1998) and 
Rizzo (2005, 2006).
---------------------------------------------------------------------------

c. Exposure Estimates and Key Observations
    The exposure assessment, which provides estimates of the number of 
people exposed to different levels of ambient O3 while at 
specified exertion levels,\35\ serve two purposes. First, the entire 
range of modeled personal exposures to ambient O3 is an 
essential input to the portion of the health risk assessment based on 
exposure-response functions from controlled human exposure studies, 
discussed in the next section. Second, estimates of personal exposures 
to ambient O3 concentrations at and above specific benchmark 
levels provide some perspective on the public

[[Page 2977]]

health impacts of health effects that cannot currently be evaluated in 
quantitative risk assessments that may occur at current air quality 
levels, and the extent to which such impacts might be reduced by 
meeting the current and alternative standards. This is especially true 
when there are exposure levels at which it is known or can reasonably 
be inferred that specific O3-related health effects are 
occurring. In this notice, exposures at and above these benchmark 
concentrations are referred to as ``exposures of concern.''
---------------------------------------------------------------------------

    \35\ As discussed above in Section II.A, O3 health 
responses observed in controlled human exposure studies are 
associated with exposures while engaged in moderate or greater 
exertion and, therefore, these are the exposure measures of 
interest. The level of exertion of individuals engaged in particular 
activities is measured by an equivalent ventilation rate (EVR), 
ventilation normalized by body surface area (BSA, in m\2\), which is 
calculated as VE/BSA, where VE is the ventilation rate (liters/
minute). Moderate and greater exertion levels were defined as EVR > 
13 liters/min-m\2\ (Whitfield et al., 1996) to correspond to the 
exertion levels measured in most subjects studied in the controlled 
human exposure studies that reported health effects associated with 
6.6 hour O3 exposures.
---------------------------------------------------------------------------

    It is important to note that although the analysis of ``exposures 
of concern'' was conducted using three discrete benchmark levels (i.e., 
0.080, 0.070, and 0.060 ppm), the concept is more appropriately viewed 
as a continuum with greater confidence and less uncertainty about the 
existence of health effects at the upper end and less confidence and 
greater uncertainty as one considers increasingly lower O3 
exposure levels. The EPA recognizes that there is no sharp breakpoint 
within the continuum ranging from at and above 0.080 ppm down to 0.060 
ppm. In considering the concept of exposures of concern, it is 
important to balance concerns about the potential for health effects 
and their severity with the increasing uncertainty associated with our 
understanding of the likelihood of such effects at lower O3 
levels.
    Within the context of this continuum, estimates of exposures of 
concern at discrete benchmark levels provide some perspective on the 
public health impacts of O3-related health effects that have 
been demonstrated in controlled human exposure and toxicological 
studies but cannot be evaluated in quantitative risk assessments, such 
as lung inflammation, increased airway responsiveness, and changes in 
host defenses. They also help in understanding the extent to which such 
impacts have the potential to be reduced by meeting the current and 
alternative standards. In the selection of specific benchmark 
concentrations for this analysis, staff first considered the exposure 
level of 0.080 ppm, at which there is a substantial amount of 
controlled human exposure evidence demonstrating a range of 
O3-related health effects including lung inflammation and 
airway responsiveness in healthy individuals. Thus, as in the 1997 
review, this level was selected as a benchmark level for this 
assessment of exposures of concern. Evidence newly available in this 
review is the basis for identifying additional, lower benchmark levels 
of 0.070 and 0.060 ppm for this assessment.
    More specifically, as discussed above in section II.A.2, evidence 
available from controlled human exposure and epidemiological studies 
indicates that people with asthma have larger and more serious effects 
than healthy individuals, including lung function, respiratory 
symptoms, increased airway responsiveness, and pulmonary inflammation, 
which has been shown to be a more sensitive marker than lung function 
responses. Further, a substantial new body of evidence from 
epidemiological studies shows associations with serious respiratory 
morbidity and cardiopulmonary mortality effects at O3 levels 
that extend below 0.080 ppm. Additional, but very limited new evidence 
from controlled human exposure studies shows lung function decrements 
and respiratory symptoms in healthy subjects at an O3 
exposure level of 0.060 ppm. The selected benchmark level of 0.070 ppm 
reflects the new information that asthmatics have larger and more 
serious effects than healthy people and therefore controlled human 
exposure studies done with healthy subjects may underestimate effects 
in this group, as well as the substantial body of epidemiological 
evidence of associations with O3 levels below 0.080 ppm. The 
selected benchmark level of 0.060 ppm additionally reflects the very 
limited new evidence from controlled human exposure studies that show 
lung function decrements and respiratory symptoms in some healthy 
subjects at the 0.060 ppm exposure level, recognizing that asthmatics 
are likely to have more serious responses and that lung function is not 
likely to be as sensitive a marker for O3 effects as is lung 
inflammation.
    The estimates of exposures of concern were reported in terms of 
both ``people exposed'' (the number and percent of people who 
experience a given level of O3 concentrations, or higher, at 
least one time during the O3 season in a given year) and 
``occurrences of exposure'' (the number of times a given level of 
pollution is experienced by the population of interest, expressed in 
terms of person-days of occurrences). Estimating exposures of concern 
is important because it provides some indication of the potential 
public health impacts of a range of O3-related health 
outcomes, such as lung inflammation, increased airway responsiveness, 
and changes in host defenses. These particular health effects have been 
demonstrated in controlled human exposure studies of healthy 
individuals to occur at levels as low as 0.080 ppm O3, but 
have not been evaluated at lower levels in controlled human exposure 
studies. The EPA did not include these effects in the quantitative risk 
assessment due to a lack of adequate information on the exposure-
response relationships.
    The 1997 O3 NAAQS review estimated exposures associated 
with 1-hour heavy exertion, 1-hour moderate exertion, and 8-hour 
moderate exertion for children, outdoor workers, and the general 
population. The EPA's analysis in the 1997 Staff Paper showed that 
exposure estimates based on the 8-hour moderate exertion scenario for 
children yielded the largest number of children experiencing exposures 
at or above exposures of concern. Consequently, EPA chose to focus on 
the 8-hour moderate and greater exertion exposures in all and asthmatic 
school age children in the current exposure assessment. While outdoor 
workers and other adults who engage in moderate or greater exertion for 
prolonged durations while outdoors during the day in areas experiencing 
elevated O3 concentrations also are at risk for experiencing 
exposures associated with O3-related health effects, EPA did 
not focus on quantitative estimates for these populations due to the 
lack of information about the number of individuals who regularly work 
or exercise outdoors. Thus, the exposure estimates presented here and 
in the 2007 Staff Paper are most useful for making relative comparisons 
across alternative air quality scenarios and do not represent the total 
exposures in all children or other groups within the general population 
associated with the air quality scenarios.
    Population exposures to O3 were estimated in 12 urban 
areas for 2002, 2003, and 2004 air quality, and also using 
O3 concentrations adjusted to just meet the then current and 
several alternative standards. The estimates of 8-hour exposures of 
concern at and above benchmark levels of 0.080, 0.070, and 0.060 ppm 
aggregated across all 12 areas are shown in Table 1 for air quality 
scenarios just meeting the current and four alternative 8-hour average 
standards.\36\ Table 1 provides estimates of the number and percent of 
school age children and asthmatic school age children exposed, with 
daily 8-hour maximum exposures at or above each O3 benchmark 
level of exposures of concern, while at intermittent moderate or 
greater exertion and based on O3 concentrations observed in 
2002 and

[[Page 2978]]

2004. Table 1 summarizes estimates for 2002 and 2004 because these 
years reflect years that bracket relatively higher and lower 
O3 levels, with year 2003 generally containing O3 
levels in between when considering the 12 urban areas modeled. This 
table also reports the percent change in the number of persons exposed 
when a given alternative standard is compared with the then current 
standard.
---------------------------------------------------------------------------

    \36\ The full range of quantitative exposure estimates 
associated with just meeting the 0.084 ppm and alternative 
O3 standards are presented in chapter 4 and Appendix 4A 
of the 2007 Staff Paper.
---------------------------------------------------------------------------

    Key observations important in comparing exposure estimates 
associated with just meeting the current NAAQS and alternative 
standards under consideration include:
    (1) As shown in Table 6-1 of the 2007 Staff Paper, the patterns of 
exposure in terms of percentages of the population exceeding a given 
exposure level are very similar for the general population and for 
asthmatic and all school age (5-18) children, although children are 
about twice as likely to be exposed, based on the percent of the 
population exposed, at any given level.
    (2) As shown in Table 1 below, the number and percentage of 
asthmatic and all school-age children aggregated across the 12 urban 
areas estimated to experience one or more exposures of concern decline 
from simulations of just meeting the then current 0.084 ppm standard to 
simulations of alternative 8-hour standards by varying amounts 
depending on the benchmark level, the population subgroup considered, 
and the year chosen. For example, the estimated percentage of school 
age children experiencing one or more exposures >= 0.070 ppm, while 
engaged in moderate or greater exertion, during an O3 season 
is about 18 percent of this population when the 0.084 ppm standard is 
met using the 2002 simulation; this is reduced to about 12, 4, 1, and 
0.2 percent of children upon meeting alternative standards of 0.080, 
0.074, 0.070, and 0.064 ppm, respectively (all specified in terms of 
the 4th highest daily maximum 8-hour average), using the 2002 
simulation.

    Table 1--Number and Percent of All and Asthmatic School Age Children in 12 Urban Areas Estimated To Experience 8-Hour Ozone Exposures Above 0.080,
  0.070, and 0.060 ppm While at Moderate or Greater Exertion, One or More Times per Season, and the Number of Occurrences Associated With Just Meeting
                                    Alternative 8-Hour Standards Based on Adjusting 2002 and 2004 Air Quality Data1 2
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                       All children, ages 5-18 Aggregate for 12 urban    Asthmatic children, ages 5-18 Aggregate for 12
                                       8-Hour air      areas Number of children exposed (% of all) [%     urban areas Number of children exposed (% of
  Benchmark levels of exposures of       quality             reduction from 0.084 ppm standard]           group) [% reduction from 0.084 ppm standard]
           concern (ppm)              standards \3\ ----------------------------------------------------------------------------------------------------
                                          (ppm)                2002                     2004                      2002                     2004
--------------------------------------------------------------------------------------------------------------------------------------------------------
0.080..............................           0.084             700,000 (4%)              30,000 (0%)              110,000 (4%)                   0 (0%)
                                              0.080       290,000 (2%) [70%]        10,000 (0%) [67%]         50,000 (2%) [54%]                   0 (0%)
                                              0.074        60,000 (0%) [91%]            0 (0%) [100%]         10,000 (0%) [91%]                   0 (0%)
                                              0.070        10,000 (0%) [98%]            0 (0%) [100%]             0 (0%) [100%]                   0 (0%)
                                              0.064            0 (0%) [100%]            0 (0%) [100%]             0 (0%) [100%]                   0 (0%)
--------------------------------------------------------------------------------------------------------------------------------------------------------
0.070..............................           0.084          3,340,000 (18%)             260,000 (1%)             520,000 (20%)              40,000 (1%)
                                              0.080    2,160,000 (12%) [35%]       100,000 (1%) [62%]       330,000 (13%) [36%]        10,000 (0%) [75%]
                                              0.074       770,000 (4%) [77%]        20,000 (0%) [92%]       120,000 (5%) [77% ]            0 (0%) [100%]
                                              0.070       270,000 (1%) [92%]            0 (0%) [100%]         50,000 (2%) [90%]            0 (0%) [100%]
                                              0.064      30,000 (0.2%) [99%]            0 (0%) [100%]      10,000 (0.2%) [98% ]            0 (0%) [100%]
--------------------------------------------------------------------------------------------------------------------------------------------------------
0.060..............................           0.084          7,970,000 (44%)          1,800,000 (10%)           1,210,000 (47%)            270,000 (11%)
                                              0.080    6,730,000 (37%) [16%]     1,050,000 (6%) [42%]     1,020,000 (40%) [16%]       150,000 (6%) [44%]
                                              0.074    4,550,000 (25%) [43%]       350,000 (2%) [80%]       700,000 (27%) [42%]        50,000 (2%) [81%]
                                              0.070    3,000,000 (16%) [62%]       110,000 (1%) [94%]       460,000 (18%) [62%]        10,000 (1%) [96%]
                                              0.064       950,000 (5%) [88%]        10,000 (0%) [99%]        150,000 (6%) [88%]            0 (0%) [100%]
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Moderate or greater exertion is defined as having an 8-hour average equivalent ventilation rate = 13 l-min/m\2\.
\2\ Estimates are the aggregate results based on 12 combined statistical areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, Los Angeles, New
  York, Philadelphia, Sacramento, St. Louis, and Washington, DC). Estimates are for the ozone season which is all year in Houston, Los Angeles and
  Sacramento and March or April to September or October for the remaining urban areas.
\3\ All standards summarized here have the same form as the 8-hour standard established in 1997 which is specified as the 3-year average of the annual
  4th highest daily maximum 8-hour average concentrations must be at or below the concentration level specified. As described in the 2007 Staff Paper
  (EPA, 2007b, section 4.5.8), recent O3 air quality distributions have been statistically adjusted to simulate just meeting the 0.084 ppm standard and
  selected alternative standards. These simulations do not represent predictions of when, whether, or how areas might meet the specified standards.

    (3) Substantial year-to-year variability in exposure estimates is 
observed over the three-year modeling period. For example, the 
estimated number of school age children experiencing one or more 
exposures >= 0.070 ppm during an O3 season when a 0.084 ppm 
standard is met in the 12 urban areas included in the analysis is 3.3, 
1.0, or 0.3 million for the 2002, 2003, and 2004 simulations, 
respectively.
    (4) There is substantial variability observed across the 12 urban 
areas in the percent of the population subgroups estimated to 
experience exposures of concern. For example, when 2002 O3 
concentrations are simulated to just meet a 0.084 ppm standard, the 
aggregate 12 urban area estimate is 18 percent of all school age 
children are estimated to experience O3 exposures >= 0.070 
ppm (Table 1 below), while the range of exposure estimates in the 12 
urban areas considered separately for all children range from 1 to 38 
percent (EPA, 2007b, p. 4-48, Exhibit 2). There was also variability in 
exposure estimates among the modeled areas when using the 2004 air 
quality simulation for the same scenario; however it was reduced and 
ranged from 0 to 7 percent in the 12 urban areas (EPA, 2007b, p. 4-60, 
Exhibit 8).
    (5) Of particular note, as discussed above in section II.A of this 
notice, high inter-individual variability in responsiveness means that 
only a subset of individuals in these groups who are exposed at and 
above a given benchmark level would actually be expected to experience 
such adverse health effects.

[[Page 2979]]

    (6) In considering these observations, it is important to take into 
account the variability, uncertainties, and limitations associated with 
this assessment, including the degree of uncertainty associated with a 
number of model inputs and uncertainty in the model itself, as 
discussed above.
2. Quantitative Health Risk Assessment
    This section discusses the approach used to develop quantitative 
health risk estimates associated with exposures to O3 
building upon a more limited risk assessment that was conducted during 
the last review.\37\ As part of the 1997 review, EPA conducted a health 
risk assessment that produced risk estimates for the number and percent 
of children and outdoor workers experiencing lung function and 
respiratory symptoms associated with O3 exposures for 9 
urban areas.\38\ The risk assessment for the 1997 review also included 
risk estimates for excess respiratory-related hospital admissions 
related to O3 concentrations for New York City. In the last 
review, the risk estimates played a significant role in both the staff 
recommendations and in the proposed and final decisions to revise the 
O3 standards. The health risk assessment conducted for the 
current review builds upon the methodology and lessons learned from the 
prior review.
---------------------------------------------------------------------------

    \37\ The methodology, scope, and results from the risk 
assessment conducted in the last review are described in Chapter 6 
of the 1996 Staff Paper (EPA, 1996) and in several technical reports 
(Whitfield et al., 1996; Whitfield, 1997) and publication (Whitfield 
et al., 1998).
    \38\ The 9 urban study areas included in the exposure and risk 
analyses conducted during the last review were: Chicago, Denver, 
Houston, Los Angeles, Miami, New York City, Philadelphia, St. Louis, 
and Washington, DC.
---------------------------------------------------------------------------

a. Overview
    The updated health risk assessment conducted as part of the 2008 
rulemaking includes estimates of (1) risks of lung function decrements 
in all and asthmatic school age children, respiratory symptoms in 
asthmatic children, respiratory-related hospital admissions, and non-
accidental and cardiorespiratory-related mortality associated with 
recent ambient O3 levels; (2) risk reductions and remaining 
risks associated with just meeting the then current 0.084 ppm 8-hour 
O3 NAAQS; and (3) risk reductions and remaining risks 
associated with just meeting various alternative 8-hour O3 
NAAQS in a number of example urban areas. This risk assessment is more 
fully described and presented in chapter 5 of the 2007 Staff Paper and 
in a technical support document (TSD), Ozone Health Risk Assessment for 
Selected Urban Areas (Abt Associates, 2007a, hereafter referred to as 
``Risk Assessment TSD''). The scope and methodology for this risk 
assessment were developed over the last few years with considerable 
input from the CASAC O3 Panel and the public.\39\ The 
information contained in these documents included specific criteria for 
the selection of health endpoints, studies, and locations to include in 
the assessment. In a peer review letter sent by CASAC to the 
Administrator documenting its advice in October 2006 (Henderson, 
2006c), the CASAC O3 Panel concluded that the risk 
assessment was ``well done, balanced, and reasonably communicated'' and 
that the selection of health endpoints for inclusion in the 
quantitative risk assessment was appropriate.
---------------------------------------------------------------------------

    \39\ The general approach used in the health risk assessment was 
described in the draft Health Assessment Plan (EPA, 2005d) that was 
released to the CASAC and general public in April 2005 and was the 
subject of a consultation with the CASAC O3 Panel on May 
5, 2005. In October 2005, OAQPS released the first draft of the 
Staff Paper containing a chapter discussing the risk assessment and 
first draft of the Risk Assessment TSD for CASAC consultation and 
public review on December 8, 2005. In July 2006, OAQPS released the 
second draft of the Staff Paper and second draft of the Risk 
Assessment TSD for CASAC review and public comment which was held by 
the CASAC O3 Panel on August 24-25, 2006.
---------------------------------------------------------------------------

    The goals of the risk assessment are: (1) To provide estimates of 
the potential magnitude of several morbidity effects and mortality 
associated with current O3 levels, and with meeting the then 
current 0.084 ppm standard and alternative 8-hour O3 
standards in specific urban areas; (2) to develop a better 
understanding of the influence of various inputs and assumptions on the 
risk estimates; and (3) to gain insights into the distribution of risks 
and patterns of risk reductions associated with meeting alternative 
O3 standards. The health risk assessment is intended to be 
dependent on and reflect the overall weight and nature of the health 
effects evidence discussed above in section II.A and in more detail in 
the 2006 Criteria Document and 2007 Staff Paper. While not independent 
of the overall evaluation of the health effects evidence, the 
quantitative health risk assessment provides additional insights 
regarding the relative public health implications associated with just 
meeting a 0.084 ppm standard and several alternative 8-hour standards.
    The risk assessment covers a variety of health effects for which 
there is adequate information to develop quantitative risk estimates. 
However, as noted by CASAC (Henderson, 2007) and in the 2007 Staff 
Paper, there are a number of health endpoints (e.g., increased lung 
inflammation, increased airway responsiveness, impaired host defenses, 
increased medication usage for asthmatics, increased emergency 
department visits for respiratory causes, and increased school 
absences) for which there currently is insufficient information to 
develop quantitative risk estimates, but which are important to 
consider in assessing the overall public health impacts associated with 
exposures to O3. These additional health endpoints are 
discussed above in section II.A.2 and are also taken into account in 
considering the level of exposures of concern in populations 
particularly at risk, discussed above in this notice.
    There are two parts to the health risk assessment: One based on 
combining information from controlled human exposure studies with 
modeled population exposure and the other based on combining 
information from community epidemiological studies with either 
monitored or adjusted ambient concentrations levels. Both parts of the 
risk assessment were implemented within a new probabilistic version of 
TRIM.Risk, the component of EPA's Total Risk Integrated Methodology 
(TRIM) model framework that estimates human health risks.
    The EPA recognizes that there are many sources of uncertainty and 
variability in the inputs to this assessment and that there is 
significant variability and uncertainty in the resulting O3 
risk estimates. As discussed in chapters 2, 5, and 6 of the 2007 Staff 
Paper, there is significant year-to-year and city-to-city variability 
related to the air quality data that affects both the controlled human 
exposure studies-based and epidemiological studies-based parts of the 
risk assessment. There are also uncertainties associated with the air 
quality adjustment procedure used to simulate just meeting various 
alternative standards. In the prior review, different statistical 
approaches using alternative functional forms (i.e., quadratic, 
proportional, Weibull) were used to reflect how O3 air 
quality concentrations have historically changed. Based on sensitivity 
analyses conducted in the prior review, the choice of alternative air 
quality adjustment procedures had only a modest impact on the risk 
estimates (EPA, 2007b, p. 6-20). With respect to uncertainties about 
estimated background concentrations, as discussed below and in the 2007 
Staff Paper (section 5.4.3), alternative assumptions about background 
levels have a variable impact depending on the location, standard, and 
health endpoint analyzed.

[[Page 2980]]

    With respect to the lung function part of the health risk 
assessment, key uncertainties include uncertainties in the exposure 
estimates, discussed above, and uncertainties associated with the shape 
of the exposure-response relationship, especially at levels below 0.08 
ppm, 8-hour average, where only very limited data are available down to 
0.04 ppm and there is an absence of data below 0.04 ppm (EPA, 2007b, 
pp. 6-20 to 6-21). Concerning the part of the risk assessment based on 
effects reported in epidemiological studies, important uncertainties 
include uncertainties (1) surrounding estimates of the O3 
coefficients for concentration-response relationships used in the 
assessment, (2) involving the shape of the concentration-response 
relationship and whether or not a population threshold or non-linear 
relationship exists within the range of concentrations examined in the 
studies, (3) related to the extent to which concentration-response 
relationships derived from studies in a given location and time when 
O3 levels were higher or behavior and/or housing conditions 
were different provide accurate representations of the relationships 
for the same locations with lower air quality distributions and/or 
different behavior and/or housing conditions, and (4) concerning the 
possible role of co-pollutants which also may have varied between the 
time of the studies and the current assessment period. An important 
additional uncertainty for the mortality risk estimates is the extent 
to which the associations reported between O3 and non-
accidental and cardiorespiratory mortality actually reflect causal 
relationships.
    As discussed below, some of these uncertainties have been addressed 
quantitatively in the form of estimated confidence ranges around 
central risk estimates; others are addressed through separate 
sensitivity analyses (e.g., the influence of alternative estimates for 
policy-relevant background levels) or are characterized qualitatively. 
For both parts of the health risk assessment, statistical uncertainty 
due to sampling error has been characterized and is expressed in terms 
of 95 percent credible intervals. The EPA recognizes that these 
credible intervals do not reflect all of the uncertainties noted above.
b. Scope and Key Components
    The health risk assessment is based on the information evaluated in 
the 2006 Criteria Document. The risk assessment includes several 
categories of health effects and estimates risks associated with just 
meeting a 0.084 ppm standard and alternative 8-hour O3 NAAQS 
and with several individual recent years of air quality (i.e., 2002, 
2003, and 2004). The risk assessment considers the same alternative air 
quality scenarios that were examined in the human exposure analyses 
described above. Risk estimates were developed for up to 12 urban areas 
selected to illustrate the public health impacts associated with these 
air quality scenarios.\40\ As discussed above in section II.B.1, the 
selection of urban areas was largely determined by identifying areas in 
the U.S. which represented a range of geographic areas, population 
demographics, and climatology; with an emphasis on areas that did not 
meet the then current 0.084 ppm 8-hour O3 NAAQS and which 
included the largest areas with O3 nonattainment problems. 
The selection criteria also included whether or not there were 
acceptable epidemiological studies available that reported 
concentration-response relationships for the health endpoints selected 
for inclusion in the assessment.
---------------------------------------------------------------------------

    \40\ The 12 urban areas are the same urban areas evaluated in 
the exposure analysis discussed in the prior section. However, for 
most of the health endpoints based on findings from epidemiological 
studies, the geographic areas and populations examined in the health 
risk assessment were limited to those counties included in the 
original epidemiological studies that served as the basis for the 
concentration-response relationships.
---------------------------------------------------------------------------

    The short-term exposure related health endpoints selected for 
inclusion in the quantitative risk assessment include those for which 
the 2006 Criteria Document or the 2007 Staff Paper concluded that the 
evidence as a whole supports the general conclusion that O3, 
acting alone and/or in combination with other components in the ambient 
air pollution mix, is either clearly causal or is judged to be likely 
causal. Some health effects met this criterion of likely causality, but 
were not included in the risk assessment for other reasons, such as 
insufficient exposure-response data or lack of baseline incidence data.
    As discussed in the section above describing the exposure analysis, 
in order to estimate the health risks associated with just meeting 
various alternative 8-hour O3 NAAQS, it is necessary to 
estimate the distribution of hourly O3 concentrations that 
would occur under any given standard. Since compliance is based on a 3-
year average, the amount of control has been applied to each year of 
data (i.e., 2002 to 2004) to estimate risks for a single O3 
season or single warm O3 season, depending on the health 
effect, based on a simulation that adjusted each of these individual 
years so that the three year period would just meet the specified 
standard.
    Consistent with the risk assessment approach used in the last 
review, the risk estimates developed for both recent air quality levels 
and just meeting the then current 0.084 ppm standard and selected 
alternative 8-hour standards represent risks associated with 
O3 levels attributable to anthropogenic sources and 
activities (i.e., risk associated with concentrations above ``policy-
relevant background''). Policy-relevant background O3 
concentrations used in the O3 risk assessment were defined 
in chapter 2 of the 2007 Staff Paper (pp. 2-48--2-55) as the 
O3 concentrations that would be observed in the U.S. in the 
absence of anthropogenic emissions of precursors (e.g., VOC, 
NOX, and CO) in the U.S., Canada, and Mexico. The results of 
a global tropospheric O3 model (GEOS-CHEM) have been used to 
estimate monthly background daily diurnal profiles for each of the 12 
urban areas for each month of the O3 season using 
meteorology for the year 2001. Based on the results of the GEOS-CHEM 
model, the Criteria Document indicates that background O3 
concentrations are generally predicted to be in the range of 0.015 to 
0.035 ppm in the afternoon, and they are generally lower under 
conditions conducive to man-made O3 episodes.\41\
---------------------------------------------------------------------------

    \41\ EPA notes that the estimated level of policy-relevant 
background O3 used in the prior risk assessment was a 
single concentration of 0.04 ppm, which was the midpoint of the 
range of levels for policy-relevant background that was provided in 
the 1996 Criteria Document.
---------------------------------------------------------------------------

    This approach of estimating risks in excess of background is judged 
to be more relevant to policy decisions regarding ambient air quality 
standards than risk estimates that include effects potentially 
attributable to uncontrollable background O3 concentrations. 
Sensitivity analyses examining the impact of alternative estimates for 
background on lung function and mortality risk estimates have been 
developed and are included in the 2007 Staff Paper and Risk Assessment 
TSD and key observations are discussed below. Further, CASAC noted the 
difficulties and complexities associated with available approaches to 
estimating policy-relevant background concentrations (Henderson, 2007).
    In the first part of the risk assessment, lung function decrement, 
as measured by FEV1, is the only health response that is 
based on data from controlled human exposure studies. As discussed 
above, there is clear evidence of a causal relationship between lung 
function decrements and O3 exposures for school age children 
engaged in moderate

[[Page 2981]]

exertion based on numerous controlled human exposure and summer camp 
field studies conducted by various investigators. Risk estimates have 
been developed for O3-related lung function decrements 
(measured as changes in FEV1) for all school age children 
(ages 5 to 18) and a subset of this group, asthmatic school age 
children (ages 5 to 18), whose average exertion over an 8-hour period 
was moderate or greater. The exposure period and exertion level were 
chosen to generally match the exposure period and exertion level used 
in the controlled human exposure studies that were the basis for the 
exposure-response relationships. A combined data set including 
individual level data from the Folinsbee et al. (1988), Horstman et al. 
(1990), and McDonnell et al. (1991) studies, used in the previous risk 
assessment, and more recent data from Adams (2002, 2003a, 2006) have 
been used to estimate probabilistic exposure-response relationships for 
8-hour exposures under different definitions of lung function response 
(i.e., >= 10, 15, and 20 percent decrements in FEV1). As 
discussed in the 2007 Staff Paper (p. 5-27), while these specific 
controlled human exposure studies only included healthy adults aged 18-
35, findings from other controlled human exposure studies and summer 
camp field studies involving school age children in at least six 
different locations in the northeastern United States, Canada, and 
Southern California indicated changes in lung function in healthy 
children similar to those observed in healthy adults exposed to 
O3 under controlled chamber conditions.
    Consistent with advice from CASAC (Henderson, 2006c), EPA has 
considered both linear and logistic functional forms in estimating the 
probabilistic exposure-response relationships for lung function 
responses. A Bayesian Markov Chain Monte Carlo approach, described in 
more detail in the Risk Assessment TSD, has been used that incorporates 
both model uncertainty and uncertainty due to sample size in the 
combined data set that served as the basis for the assessment. The EPA 
has chosen a model reflecting a 90 percent weighting on a logistic form 
and a 10 percent weighting on a linear form as the base case for the 
risk assessment. The basis for this choice is that the logistic form 
provides a very good fit to the combined data set, but a linear model 
cannot be entirely ruled out since there are only very limited data 
(i.e., 30 subjects) at the two lowest exposure levels (i.e., 0.040 and 
0.060 ppm). The EPA has conducted a sensitivity analysis which examines 
the impact on the lung function risk estimates of two alternative 
choices, an 80 percent logistic/20 percent linear split and a 50 
percent logistic/50 percent linear split.
    As noted above, risk estimates have been developed for three 
measures of lung function response (i.e., >= 10, 15, and 20 percent 
decrements in FEV1). However, the 2007 Staff Paper and risk 
estimates summarized below focus on FEV1 decrements >= 15 
percent for all school age children and >= 10 percent for asthmatic 
school age children, consistent with the advice from CASAC (Henderson, 
2006c) that these levels of response represent indicators of adverse 
health effects in these populations. The Risk Assessment TSD and 2007 
Staff Paper present the broader range of risk estimates including all 
three measures of lung function response.
    Developing risk estimates for lung function decrements involved 
combining probabilistic exposure-response relationships based on the 
combined data set from several controlled human exposure studies with 
population exposure distributions for all and asthmatic school age 
children associated with recent air quality and air quality simulated 
to just meet the then current 0.084 ppm standard and alternative 8-hour 
O3 NAAQS based on the results from the exposure analysis 
described in the previous section. The risk estimates have been 
developed for 12 large urban areas for the O3 season.\42\ 
These 12 urban areas include approximately 18.3 million school age 
children, of which 2.6 million are asthmatic school age children.\43\
---------------------------------------------------------------------------

    \42\ As discussed above in section II.B.1, the urban areas were 
defined using the consolidated statistical areas definition and the 
total population residing in the 12 urban areas was approximately 
88.5 million people.
    \43\ For 9 of the 12 urban areas, the O3 season is 
defined as a period running from March or April to September or 
October. In 3 of the urban areas (Houston, Los Angeles, and 
Sacramento), the O3 season is defined as the entire year.
---------------------------------------------------------------------------

    In addition to uncertainties arising from sample size 
considerations, which are quantitatively characterized and presented as 
95 percentile credible intervals, there are additional uncertainties 
and caveats associated with the lung function risk estimates. These 
include uncertainties about the shape of the exposure-response 
relationship, particularly at levels below 0.080 ppm, and about policy-
relevant background levels, for which sensitivity analyses have been 
conducted. Additional important caveats and uncertainties concerning 
the lung function portion of the health risk assessment include: (1) 
The uncertainties and limitations associated with the exposure 
estimates discussed above and (2) the inability to account for some 
factors which are known to affect the exposure-response relationships 
(e.g., assigning healthy and asthmatic children the same responses as 
observed in healthy adult subjects and not adjusting response rates to 
reflect the increase and attenuation of responses that have been 
observed in studies of lung function responses upon repeated 
exposures). A more complete discussion of assumptions and uncertainties 
is contained in chapter 5 of the 2007 Staff Paper and in the Risk 
Assessment TSD.
    The second part of the risk assessment is based on health effects 
observed in epidemiological studies. Based on a review of the evidence 
evaluated in the 2006 Criteria Document and 2007 Staff Paper, as well 
as the criteria discussed in chapter 5 of the 2007 Staff Paper, the 
following categories of health endpoints associated with short-term 
exposures to ambient O3 concentrations were included in the 
risk assessment: respiratory symptoms in moderate to severe asthmatic 
children, hospital admissions for respiratory causes, and non-
accidental and cardiorespiratory mortality. As discussed above, there 
is strong evidence of a causal relationship for the respiratory 
morbidity endpoints included in the risk assessment. With respect to 
nonaccidental and cardiorespiratory mortality, the 2006 Criteria 
Document concludes that there is strong evidence which is highly 
suggestive of a causal relationship between nonaccidental and 
cardiorespiratory-related mortality and O3 exposures during 
the warm O3 season. As discussed in the 2007 Staff Paper 
(chapter 5), EPA also recognizes that for some of the effects observed 
in epidemiological studies, such as increased respiratory-related 
hospital admissions and nonaccidental and cardiorespiratory mortality, 
O3 may be serving as an indicator for reactive oxidant 
species in the overall photochemical oxidant mix and that these other 
constituents may be responsible in whole or part for the observed 
effects.
    Risk estimates for each health endpoint category were only 
developed for areas that were the same or close to the location where 
at least one concentration-response function for the health endpoint 
had been estimated.\44\

[[Page 2982]]

Thus, for respiratory symptoms in moderate to severe asthmatic children 
only the Boston urban area was included and four urban areas were 
included for respiratory-related hospital admissions. Nonaccidental 
mortality risk estimates were developed for 12 urban areas and 8 urban 
areas were included for cardiorespiratory mortality.
---------------------------------------------------------------------------

    \44\ The geographic boundaries for the urban areas included in 
this portion of the risk assessment were generally matched to the 
geographic boundaries used in the epidemiological studies that 
served as the basis for the concentration-response functions. In 
most cases, the urban areas were defined as either a single county 
or a few counties for this portion of the risk assessment.
---------------------------------------------------------------------------

    The concentration-response relationships used in the assessment are 
based on findings from human epidemiological studies that have relied 
on fixed-site ambient monitors as a surrogate for actual ambient 
O3 exposures. In order to estimate the incidence of a 
particular health effect associated with recent air quality in a 
specific county or set of counties attributable to ambient 
O3 exposures in excess of background, as well as the change 
in incidence corresponding to a given change in O3 levels 
resulting from just meeting various 8-hour O3 standards, 
three elements are required for this part of the risk assessment. These 
elements are: (1) Air quality information (including recent air quality 
data for O3 from ambient monitors for the selected location, 
estimates of background O3 concentrations appropriate for 
that location, and a method for adjusting the recent data to reflect 
patterns of air quality estimated to occur when the area just meets a 
given O3 standard); (2) relative risk-based concentration-
response functions that provide an estimate of the relationship between 
the health endpoints of interest and ambient O3 
concentration; and (3) annual or seasonal baseline health effects 
incidence rates and population data, which are needed to provide an 
estimate of the seasonal baseline incidence of health effects in an 
area before any changes in O3 air quality.
    A key component in the portion of the risk assessment based on 
epidemiological studies is the set of concentration-response functions 
which provide estimates of the relationships between each health 
endpoint of interest and changes in ambient O3 
concentrations. Studies often report more than one estimated 
concentration-response function for the same location and health 
endpoint. Sometimes models include different sets of co-pollutants and/
or different lag periods between the ambient concentrations and 
reported health responses. For some health endpoints, there are studies 
that estimated multicity and single-city O3 concentration-
response functions. While the Risk Assessment TSD and chapter 5 of the 
2007 Staff Paper present a more comprehensive set of risk estimates, 
EPA has focused on estimates based on multicity studies where 
available. As discussed in chapter 5 of the 2007 Staff Paper, the 
advantages of relying more heavily on concentration-response functions 
based on multicity studies include: (1) More precise effect estimates 
due to larger data sets, reducing the uncertainty around the estimated 
coefficient; (2) greater consistency in data handling and model 
specification that can eliminate city-to-city variation due to study 
design; and (3) less likelihood of publication bias or exclusion of 
reporting of negative or nonsignificant findings. Where studies 
reported different effect estimates for varying lag periods, consistent 
with the 2006 Criteria Document, single day lag periods of 0 to 1 days 
were used for associations with respiratory hospital admissions and 
mortality. For mortality associated with exposure to O3 
which may result over a several day period after exposure, distributed 
lag models, which take into account the contribution to mortality 
effects over several days, were used where available
    One of the most important elements affecting uncertainties in the 
epidemiological-based portion of the risk assessment is the 
concentration-response relationships used in the assessment. The 
uncertainty resulting from the statistical uncertainty associated with 
the estimate of the O3 coefficient in the concentration-
response function was characterized either by confidence intervals or 
by Bayesian credible intervals around the corresponding point estimates 
of risk. Confidence and credible intervals express the range within 
which the true risk is likely to fall if the only uncertainty 
surrounding the O3 coefficient involved sampling error. 
Other uncertainties, such as differences in study location, time period 
(i.e., the years in which the study was conducted), and model 
uncertainties are not represented by the confidence or credible 
intervals presented, but were addressed by presenting estimates for 
different urban areas, by including risk estimates based on studies 
using different time periods and models, where available, and/or are 
discussed throughout section 5.3 of the 2007 Staff Paper. Because 
O3 effects observed in the epidemiological studies have been 
more clearly and consistently shown for warm season analyses, all 
analyses for this portion of the risk assessment were carried out for 
the same time period, April through September.
    The 2006 Criteria Document (p. 8-44) finds that no definitive 
conclusion can be reached with regard to the existence of population 
thresholds in epidemiological studies. The EPA recognizes, however, the 
possibility that thresholds for individuals may exist for reported 
associations at fairly low levels within the range of air quality 
observed in the studies, but not be detectable as population thresholds 
in epidemiological analyses. Based on the 2006 Criteria Document's 
conclusions, EPA judged and CASAC concurred, that there is insufficient 
evidence to support use of potential population threshold levels in the 
quantitative risk assessment. However, EPA recognizes that there is 
increasing uncertainty about the concentration-response relationship at 
lower concentrations which is not captured by the characterization of 
the statistical uncertainty due to sampling error. Therefore, the risk 
estimates for respiratory symptoms in moderate to severe asthmatic 
children, respiratory-related hospital admissions, and premature 
mortality associated with exposure to O3 must be considered 
in light of uncertainties about whether or not these O3-
related effects occur in these populations at very low O3 
concentrations.
    With respect to variability within this portion of the risk 
assessment, there is variability among concentration-response functions 
describing the relation between O3 and both respiratory-
related hospital admissions and nonaccidental and cardiorespiratory 
mortality across urban areas. This variability is likely due to 
differences in population (e.g., age distribution), population 
activities that affect exposure to O3 (e.g., use of air 
conditioning), levels and composition of co-pollutants, baseline 
incidence rates, and/or other factors that vary across urban areas. The 
risk assessment incorporates some of the variability in key inputs to 
the analysis by using location-specific inputs (e.g., location-specific 
concentration-response functions, baseline incidence rates, and air 
quality data). Although spatial variability in these key inputs across 
all U.S. locations has not been fully characterized, variability across 
the selected locations is imbedded in the analysis by using, to the 
extent possible, inputs specific to each urban area.
c. Risk Estimates and Key Observations
    The 2007 Staff Paper (chapter 5) and Risk Assessment TSD present 
risk estimates associated with just meeting the then current 0.084 ppm 
standard and several alternative 8-hour standards, as well as three 
recent years of air quality as represented by 2002,

[[Page 2983]]

2003, and 2004 monitoring data. As discussed in the exposure analysis 
section above, there is considerable city-to-city and year-to-year 
variability in the O3 levels during this period, which 
results in significant variability in both portions of the health risk 
assessment.
    In the 1997 risk assessment, risks for lung function decrements 
associated with 1-hour heavy exertion, 1-hour moderate exertion, and 8-
hour moderate exertion exposures were estimated. Since the 8-hour 
moderate exertion exposure scenario for children clearly resulted in 
the greatest health risks in terms of lung function decrements, EPA 
chose to include only the 8-hour moderate exertion exposures in the 
risk assessment for this health endpoint. Thus, the risk estimates 
presented here and in the 2007 Staff Paper are most useful for making 
relative comparisons across alternative air quality scenarios and do 
not represent the total risks for lung function decrements in children 
or other groups within the general population associated with any of 
the air quality scenarios. Thus, some outdoor workers and adults 
engaged in moderate exertion over multi-hour periods (e.g., 6-8 hour 
exposures) also would be expected to experience similar lung function 
decrements. However, the percentage of each of these other 
subpopulations expected to experience these effects is expected to be 
smaller than all school age children who tend to spend more hours 
outdoors while active based on the exposure analyses conducted during 
the prior review.
    Table 2 presents a summary of the risk estimates for lung function 
decrements for the 0.084 ppm standard set in 1997 and several 
alternative 8-hour standard levels with the same form.

    Table 2--Number and Percent of All and Asthmatic School Age Children in Several Urban Areas Estimated To
Experience Moderate or Greater Lung Function Responses One or More Times per Season Associated With 8-Hour Ozone
Exposures Associated With Just Meeting Alternative 8-Hour Standards Based on Adjusting 2002 and 2004 Air Quality
                                                    Data 1 2
----------------------------------------------------------------------------------------------------------------
                                    All children, ages 5-18 FEV1 >= 15     Asthmatic Children, ages 5-18 FEV1 >=
                                  percent  Aggregate for 12 urban areas      10 percent  Aggregate for 5 urban
                                  Number of children affected (% of all)   areas  Number of children affected (%
  8-Hour air quality standards    [% reduction from 0.084 ppm standard]   of group)  [% reduction from 0.084 ppm
              \3\               -----------------------------------------                standard]
                                                                         ---------------------------------------
                                         2002                2004                2002                2004
----------------------------------------------------------------------------------------------------------------
0.084 ppm (Standard set in       610,000 (3.3%)       230,000 (1.2%)      130,000 (7.8%)      70,000 (4.2%)
 1997).
0.080 ppm......................  490,000 (2.7%) [20%  180,000 (1.0%)      NA \4\              NA
                                  reduction]           [22% reduction]
0.074 ppm......................  340,000 (1.9%) [44%  130,000 (0.7%)      90,000 (5.0%) [31%  40,000 (2.7%) [43%
                                  reduction]           [43% reduction]     reduction]          reduction]
0.070 ppm......................  260,000 (1.5%) [57%  100,000 (0.5%)      NA                  NA
                                  reduction]           [57% reduction]
0.064 ppm......................  180,000 (1.0%) [70%  70,000 (0.4%) [70%  50,000 (3.0%) [62%  20,000 (1.5%) [71%
                                  reduction]           reduction]          reduction]          reduction]
----------------------------------------------------------------------------------------------------------------
\1\ Associated with exposures while engaged in moderate or greater exertion, which is defined as having an 8-
  hour average equivalent ventilation rate >= 13 l-min/m \2\.
\2\ Estimates are the aggregate central tendency results based on either 12 urban areas (Atlanta, Boston,
  Chicago, Cleveland, Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and
  Washington, DC) or 5 urban areas (Atlanta, Chicago, Houston, Los Angeles, New York). Estimates are for the O3
  season which is all year in Houston, Los Angeles and Sacramento and March or April to September or October for
  the remaining urban areas.
\3\ All standards summarized here have the same form as the 8-hour standard set in 1997, which is specified as
  the 3-year average of the annual 4th highest daily maximum 8-hour average concentrations. As described in the
  2007 Staff Paper (section 4.5.8), recent O3 air quality distributions have been statistically adjusted to
  simulate just meeting the 0.084 ppm standard set in 1997 and selected alternative standards. These simulations
  do not represent predictions of when, whether, or how areas might meet the specified standards
\4\ NA (not available) indicates that EPA did not develop risk estimates for these scenarios for the asthmatic
  school age children population.

    The estimates are for the aggregate number and percent of all 
school age children across 12 urban areas and the aggregate number and 
percent of asthmatic school age children across 5 urban areas \45\ who 
are estimated to have at least 1 moderate or greater lung function 
response (defined as FEV1 >= 15 percent in all children and 
>= 10 percent in asthmatic children) associated with 8-hour exposures 
to O3 while engaged in moderate or greater exertion on 
average over the 8-hour period. The lung function risk estimates 
summarized in Table 2 illustrate the year-to-year variability in both 
remaining risk associated with a relatively high year (i.e., based on 
adjusting 2002 O3 air quality data) and relatively low year 
(based on adjusting 2004 O3 air quality data) as well as the 
year-to-year variability in the risk reduction estimated to occur 
associated with various alternative standards relative to just meeting 
the then current 0.084 ppm standard. For example, it is estimated that 
about 610,000 school age children (3.2 percent of school age children) 
would experience 1 or more moderate lung function decrements for the 12 
urban areas associated with O3 levels just meeting a 0.084 
ppm standard based on 2002 air quality data compared to 230,000 (1.2 
percent of children) associated with just meeting a 0.084 ppm standard 
based on 2004 air quality data.
---------------------------------------------------------------------------

    \45\ Due to time constraints, lung function risk estimates for 
asthmatic school age children were developed for only 5 of the 12 
urban areas, and the areas were selected to represent different 
geographic regions. The 5 areas were: Atlanta, Chicago, Houston, Los 
Angeles, and New York City.
---------------------------------------------------------------------------

    As discussed in the 2007 Staff Paper, a child may experience 
multiple occurrences of a lung function response during the 
O3 season. For example, upon meeting a 0.084 ppm 8-hour 
standard, the median estimates are that about 610,000 children would 
experience a moderate or greater lung function response 1 or more times 
for the aggregate of the 12 urban areas over a single O3 
season (based on the 2002 simulation), and that there would be almost 
3.2 million total occurrences. Thus, on average it is estimated that 
there would be about 5 occurrences per O3 season per 
responding child for air quality just meeting a 0.084 ppm 8-hour

[[Page 2984]]

standard across the 12 urban areas. While the estimated number of 
occurrences per O3 season is lower when based on the 2004 
simulation than for the 2002 simulation, the estimated number of 
occurrences per responding child is similar. The EPA recognizes that 
some children in the population might have only 1 or 2 occurrences 
while others may have 6 or more occurrences per O3 season. 
Risk estimates based on adjusting 2003 air quality to simulate just 
meeting the a 0.084 ppm standard and alternative 8-hour standards are 
intermediate to the estimates presented in Table 2 above in this notice 
and are presented in the 2007 Staff Paper (chapter 5) and Risk 
Assessment TSD.
    For just meeting a 0.084 ppm 8-hour standard, Table 5-8 in the 2007 
Staff Paper shows that median estimates across the 12 urban areas for 
all school age children experiencing 1 or more moderate lung function 
decrements ranges from 0.9 to 5.4 percent based on the 2002 simulation 
and from 0.8 to 2.2 percent based on the 2004 simulation. Risk 
estimates for each urban area included in the assessment, for each of 
the three years analyzed, and for additional alternative standards are 
presented in chapter 5 of the 2007 Staff Paper and in the Risk 
Assessment TSD.
    For just meeting a 0.084 ppm 8-hour standard, the median estimates 
across the 5 urban areas for asthmatic school age children range from 
3.4 to 10.9 percent based on the 2002 simulation and from 3.2 to 6.9 
percent based on the 2004 simulation.
    Key observations important in comparing estimated lung function 
risks associated with just meeting the 0.084 ppm NAAQS and alternative 
standards under consideration include:
    (1) As discussed above, there is significant year to year 
variability in the range of median estimates of the number of school 
age children (ages 5-18) estimated to experience at least one 
FEV1 decrement >= 15 percent due to 8-hour O3 
exposures across the 12 urban areas analyzed, and similarly across the 
5 urban areas analyzed for asthmatic school age children (ages 5-18) 
estimated to experience at least one FEV1 decrement >= 10 
percent, when various 8-hour standards are just met.
    (2) For asthmatic school age children, the median estimates of 
occurrences of FEV1 decrements >= 10% range from 52,000 to 
nearly 510,000 responses associated with just meeting a 0.084 ppm 
standard (based on the 2002 simulation) and range from 61,000 to about 
240,000 occurrences (based on the 2004 simulation). These risk 
estimates would be reduced to a range of 14,000 to about 275,000 
occurrences (2002 simulation) and to about 18,000 to nearly 125,000 
occurrences (2004 simulation) upon just meeting the most stringent 
alternative 8-hour standard (0.064 ppm, 4th highest). The average 
number of occurrences per asthmatic child in an O3 season 
ranged from about 6 to 11 associated with just meeting a 0.084 ppm 
standard (2002 simulation). The average number of occurrences per 
asthmatic child ranged from 4 to 12 upon meeting the most stringent 
alternative examined (0.064 ppm, 4th-highest) based on the 2002 
simulation. The number of occurrences per asthmatic child is similar 
for the scenarios based on the 2004 simulation.
    As discussed above, several epidemiological studies have reported 
increased respiratory morbidity outcomes (e.g., respiratory symptoms in 
moderate to severe asthmatic children, respiratory-related hospital 
admissions) and increased nonaccidental and cardiorespiratory mortality 
associated with exposure to ambient O3 concentrations. The 
results and key observations from this portion of the risk assessment 
are presented below:
    (1) Estimates for increased respiratory symptoms (i.e., chest 
tightness, shortness of breath, and wheeze) in moderate/severe 
asthmatic children (ages 0-12) were developed for the Boston urban area 
only. The median estimated number of days involving chest tightness 
(using the concentration-response relationship with only O3 
in the model) is about 6,100 (based on the 2002 simulation) and about 
4,500 (based on the 2004 simulation) upon meeting a 0.084 ppm 8-hour 
standard and this is reduced to about 4,600 days (2002 simulation) and 
3,100 days (2004 simulation) upon meeting the most stringent 
alternative examined (0.064 ppm, 4th-highest daily maximum 8-hour 
average). This corresponds to 11 percent (2002 simulation) and 8 
percent (2004 simulation) of total incidence of chest tightness upon 
meeting a 0.084 ppm 8-hour standard and to about 8 percent (2002 
simulation) and 5.5 percent (2004 simulation) of total incidence of 
chest tightness upon meeting a 0.064 ppm, 4th-highest daily maximum 8-
hour average standard. Similar patterns of effects and reductions in 
effects are observed for each of the respiratory symptoms examined.
    (2) The 2007 Staff Paper and Risk Assessment TSD present 
unscheduled hospital admission risk estimates for respiratory illness 
and asthma in New York City associated with short-term exposures to 
O3 concentrations in excess of background levels from April 
through September for several recent years (2002, 2003, and 2004) and 
upon just meeting a 0.084 ppm standard and alternative 8-hour standards 
based on simulating O3 levels using 2002-2004 O3 
air quality data. For total respiratory illness, EPA estimates about 
6.4 cases per 100,000 relevant population (2002 simulation) and about 
4.6 cases per 100,000 relevant population (2004 simulation), which 
represents 1.5 percent (2002 simulation) and 1.0 percent (2004 
simulation) of total incidence or about 510 cases (2002 simulation) and 
about 370 cases (2004 simulation) upon just meeting a 0.084 ppm 8-hour 
standard. For asthma-related hospital admissions, which are a subset of 
total respiratory illness admissions, the estimates are about 5.5 cases 
per 100,000 relevant population (2002 simulation) and about 3.9 cases 
per 100,000 relevant population (2004 simulation), which represents 
about 3.3 percent (2002 simulation) and 2.4 percent (2004 simulation) 
of total incidence or about 440 cases (2002) and about 310 cases (2004) 
for this same air quality scenario.
    For increasingly more stringent alternative 8-hour standards, there 
is a gradual reduction in respiratory illness cases per 100,000 
relevant population from 6.4 cases per 100,000 upon just meeting a 
0.084 ppm 8-hour standard to 4.6 cases per 100,000 under the most 
stringent 8-hour standard (i.e., 0.064 ppm, average 4th-highest daily 
maximum) analyzed based on the 2002 simulation. Similarly, based on the 
2004 simulation there is a gradual reduction from 4.6 cases per 100,000 
relevant population upon just meeting a 0.084 ppm 8-hour standard to 
3.0 cases per 100,000 under a 0.064 ppm, average 4th-highest daily 
maximum standard.
    Additional respiratory-related hospital admission estimates for 
three other locations are provided in the Risk Assessment TSD. The EPA 
notes that the concentration-response functions for each of these 
locations examined different outcomes in different age groups (e.g., > 
age 30 in Los Angeles, > age 64 in Cleveland and Detroit, vs. all ages 
in New York City), making comparison of the risk estimates across the 
areas very difficult.
    (3) Based on the median estimates for incidence for nonaccidental 
mortality (based on the Bell et al. (2004) 95 cities concentration-
response function), meeting the most stringent standard (0.064 ppm) is 
estimated to reduce mortality by 40 percent of what it would be 
associated with just meeting a 0.084 ppm standard (based on the 2002 
simulation). The patterns for cardiorespiratory mortality are similar.

[[Page 2985]]

The aggregate O3-related cardiorespiratory mortality upon 
just meeting the most stringent standard shown is estimated to be about 
42 percent of what it would be upon just meeting a 0.084 ppm standard, 
using simulated O3 concentrations that just meet a 0.084 ppm 
standard and alternative 8-hour standards based on the 2002 simulation. 
Using the 2004 simulation, the corresponding reductions show a similar 
pattern but are somewhat greater.
    (4) Much of the contribution to the risk estimates for non-
accidental and cardiorespiratory mortality upon just meeting a 0.084 
ppm 8-hour standard is associated with 24-hour O3 
concentrations between background and 0.040 ppm. Based on examining 
relationships between 24-hour concentrations averaged across the 
monitors within an urban area and 8-hour daily maximum concentrations, 
8-hour daily maximum levels at the highest monitor in an urban area 
associated with these averaged 24-hour levels are generally about twice 
as high as the 24-hour levels. Thus, most O3-related 
nonaccidental mortality is estimated to occur when O3 
concentrations are between background and when the highest monitor in 
the urban area is at or below 0.080 ppm, 8-hour average concentration.
    The discussion below highlights additional observations and 
insights from the O3 risk assessment, together with 
important uncertainties and limitations.
    (1) As discussed in the 2007 Staff Paper (section 5.4.5), EPA has 
greater confidence in relative comparisons in risk estimates between 
alternative standards than in the absolute magnitude of risk estimates 
associated with any particular standard.
    (2) Significant year-to-year variability in O3 
concentrations combined with the use of a 3-year design value to 
determine the amount of air quality adjustment to be applied to each 
year analyzed, results in significant year-to-year variability in the 
annual health risk estimates upon just meeting various 8-hour 
standards.
    (3) There is noticeable city-to-city variability in estimated 
O3-related incidence of morbidity and mortality across the 
12 urban areas analyzed for both recent years of air quality and for 
air quality adjusted to simulate just meeting a 0.084 ppm standard and 
selected potential alternative standards. This variability is likely 
due to differences in air quality distributions, differences in 
exposure related to many factors including varying activity patterns 
and air exchange rates, differences in baseline incidence rates, and 
differences in susceptible populations and age distributions across the 
12 urban areas.
    (4) With respect to the uncertainties about estimated policy-
relevant background concentrations, as discussed in the 2007 Staff 
Paper (section 5.4.3), alternative assumptions about background levels 
had a variable impact depending on the health effect considered and the 
location and standard analyzed in terms of the absolute magnitude and 
relative changes in the risk estimates. There was relatively little 
impact on either absolute magnitude or relative changes in lung 
function risk estimates due to alternative assumptions about background 
levels. With respect to O3-related non-accidental mortality, 
while notable differences (i.e., greater than 50 percent) \46\ were 
observed for nonaccidental mortality in some areas, particularly for 
more stringent standards, the overall pattern of estimated reductions, 
expressed in terms of percentage reduction relative to the 0.084 ppm 
standard, was significantly less impacted.
---------------------------------------------------------------------------

    \46\ For example, assuming lower background levels resulted in 
increased estimates of non-accidental mortality incidence per 
100,000 that were often 50 to 100 percent greater than the base case 
estimates; assuming higher background levels resulted in decreased 
estimates of non-accidental mortality incidence per 100,000 that 
were less than the base case estimates by 50 percent or more in many 
of the areas.
---------------------------------------------------------------------------

C. Reconsideration of the Level of the Primary Standard

1. Evidence and Exposure/Risk-Based Considerations
    The approach used in the 2007 Staff Paper as a basis for staff 
recommendations on standard levels builds upon and broadens the general 
approach used by EPA in the 1997 review. This approach reflects the 
more extensive and stronger body of evidence available for the 2008 
rulemaking on a broader range of health effects associated with 
exposure to O3, including: (1) Additional respiratory-
related endpoints; (2) new information about the mechanisms underlying 
respiratory morbidity effects supporting a judgment that the link 
between O3 exposure and these effects is causal; (3) newly 
identified cardiovascular-related health endpoints from animal 
toxicology and controlled human exposures studies that are highly 
suggestive that O3 can directly or indirectly contribute to 
cardiovascular morbidity, and (4) new U.S. multicity time series 
studies, single city studies, and several meta-analyses of these 
studies that provide relatively strong evidence for associations 
between short-term O3 exposures and all-cause 
(nonaccidental) mortality, at levels below the current primary 
standard: As well as (5) a substantial body of new evidence of 
increased susceptibility in people with asthma and other lung diseases. 
In evaluating evidence-based and exposure/risk-based considerations, 
the 2007 Staff Paper considered: (1) The ranges of levels of 
alternative standards that are supported by the evidence, and the 
uncertainties and limitations in that evidence and (2) the extent to 
which specific levels of alternative standards reduce the estimated 
exposures of concern and risks attributable to O3 and other 
photochemical oxidants, and the uncertainties associated with the 
estimated exposure and risk reductions.
a. Evidence-Based Considerations
    In taking into account evidence-based considerations, the 2007 
Staff Paper evaluated available evidence from controlled human exposure 
studies and epidemiological studies, as well as the uncertainties and 
limitations in that evidence. In particular, it focused on the extent 
to which controlled human exposure studies provide evidence of lowest-
observed-effects levels and the extent to which epidemiological studies 
provide evidence of associations that extend down to the lower levels 
of O3 concentrations observed in the studies or some 
indication of potential effect thresholds in terms of 8-hour average 
O3 concentrations.
    The most certain evidence of adverse health effects from exposure 
to O3 comes from the controlled human exposure studies, as 
discussed above in section II.A.2, and the large bulk of this evidence 
derives from studies of exposures at levels of 0.080 ppm and above. At 
those levels, there is consistent evidence of lung function decrements 
and respiratory symptoms in healthy young adults, as well as evidence 
of inflammation and other medically significant airway responses.
    Two studies by Adams (2002, 2006), newly available for 
consideration in the 2008 rulemaking, are the only available controlled 
human exposure studies that examine respiratory effects associated with 
prolonged O3 exposures at levels below 0.080 ppm, which was 
the lowest exposure level that had been examined in the 1997 review. As 
discussed above in section II.A.2.a.i.(a)(i), the Adams (2006) study 
investigated a range of exposure levels, including 0.060 and 0.080 ppm 
O3, and analyzed hour-by-hour changes in responses, 
including lung function (measured in term of decrements in 
FEV1) and respiratory

[[Page 2986]]

symptoms, to investigate the effects of different patterns of exposure. 
At the 0.060 ppm exposure level, the author reported no statistically 
significant differences for lung function decrements; statistically 
significant responses were reported for total subjective respiratory 
symptoms toward the end of the exposure period for one exposure 
pattern. The EPA's reanalysis (Brown, 2007) of the data from the Adams 
(2006) study addressed the more fundamental question of whether there 
were statistically significant changes in lung function from a 6.6-hour 
exposure to 0.060 ppm O3 versus filtered air and used a 
standard statistical method appropriate for a simple paired comparison. 
This reanalysis found small group mean lung function decrements in 
healthy adults at the 0.060 ppm exposure level to be statistically 
significantly different from responses associated with filtered air 
exposure.
    Moreover, the Adams' studies also report a small percentage of 
subjects (7 to 20 percent) experienced lung function decrements (> 10 
percent) at the 0.060 ppm exposure level. This is a concern because, 
for active healthy people, moderate levels of functional responses 
(e.g., FEV1 decrements of > 10% but < 20%) and/or moderate 
respiratory symptom responses would likely interfere with normal 
activity for relatively few responsive individuals. However, for people 
with lung disease, even moderate functional or symptomatic responses 
would likely interfere with normal activity for many individuals, and 
would likely result in more frequent use of medication. In the context 
of standard setting, the CASAC indicated (Henderson, 2006c) that a 
focus on the lower end of the range of moderate levels of functional 
responses (e.g., FEV1 decrements >= 10%) is most appropriate 
for estimating potentially adverse lung function decrements in people 
with lung disease. Therefore, the results of the Adams studies which 
indicate that a small percentage of healthy, non-asthmatic subjects are 
likely to experience FEV1 decrements >= 10% when exposed to 
0.060 ppm O3 have implications for setting a standard that 
protects public health, including the health of sensitive populations 
such as asthmatics, with an adequate margin of safety.
    In considering these most recent controlled human exposure studies, 
the 2007 Staff Paper concluded that these studies provide evidence of a 
lowest-observed-effects level of 0.060 ppm for potentially adverse lung 
function decrements and respiratory symptoms in some healthy adults 
while at prolonged moderate exertion. It further concluded that since 
people with asthma, particularly children, have been found to be more 
sensitive and to experience larger decrements in lung function in 
response to O3 exposures than would healthy adults, the 
0.060 ppm exposure level also can be interpreted as representing a 
level likely to cause adverse lung function decrements and respiratory 
symptoms in children with asthma and more generally in people with 
respiratory disease.
    In considering controlled human exposure studies of pulmonary 
inflammation, airway responsiveness, and impaired host defense 
capabilities, discussed above in section II.A.2.a.i, the 2007 Staff 
Paper noted that these studies provide evidence of a lowest-observed-
effects level for such effects in healthy adults at prolonged moderate 
exertion of 0.080 ppm, the lowest level tested. Moreover there is no 
evidence that the 0.080 ppm level is a threshold for these effects. 
Studies reporting inflammatory responses and markers of lung injury 
have clearly demonstrated that there is significant variation in 
response of subjects exposed, even to O3 exposures at 0.080 
ppm. One study showed notable interindividual variability in young 
healthy adult subjects in most of the inflammatory and cellular injury 
indicators analyzed at 0.080 ppm. This inter-individual variability 
suggests that some portion of the population would likely experience 
such effects at exposure levels extending well below 0.080 ppm.
    As discussed above, these physiological effects have been linked to 
aggravation of asthma and increased susceptibility to respiratory 
infection, potentially leading to increased medication use, increased 
school and work absences, increased visits to doctors' offices and 
emergency departments, and increased hospital admissions. Further, 
pulmonary inflammation is related to increased cellular permeability in 
the lung, which may be a mechanism by which O3 exposure can 
lead to cardiovascular system effects, and to potential chronic effects 
such as chronic bronchitis or long-term damage to the lungs that can 
lead to reduced quality of life. These are all indicators of adverse 
O3-related morbidity effects, which are consistent with and 
lend plausibility to the adverse morbidity effects and mortality 
effects observed in epidemiological studies.
    Significant associations between ambient O3 exposures 
and a wide variety of respiratory symptoms and other morbidity outcomes 
(e.g., asthma medication use, school absences, emergency department 
visits, and hospital admissions) have been reported in epidemiological 
studies, as discussed above in section II.A.2.a.i. Overall, the 2006 
Criteria Document concludes that positive and robust associations were 
found between ambient O3 concentrations and various 
respiratory disease hospitalization outcomes, when focusing 
particularly on results of warm-season analyses. Recent studies also 
generally indicate a positive association between O3 
concentrations and emergency department visits for asthma during the 
warm season. These positive and robust associations are supported by 
the controlled human exposure, animal toxicological, and 
epidemiological evidence for lung function decrements, increased 
respiratory symptoms, airway inflammation, and increased airway 
responsiveness. Taken together, the overall evidence supports a causal 
relationship between acute ambient O3 exposures and 
increased respiratory morbidity outcomes resulting in increased 
emergency department visits and hospitalizations during the warm season 
(EPA, 2006a, p. 8-77).
    Moreover, many single- and multicity epidemiological studies 
observed positive associations of ambient O3 concentrations 
with total nonaccidental and cardiopulmonary mortality. As discussed 
above in section II.A.2.b.i, the 2006 Criteria Document finds that the 
results from U.S. multicity time-series studies provide the strongest 
evidence to date for O3 effects on acute mortality. Recent 
meta-analyses also indicate positive risk estimates that are unlikely 
to be confounded by PM; however, future work is needed to better 
understand the influence of model specifications on the magnitude of 
risk. The 2006 Criteria Document concludes that the ``positive 
O3 effects estimates, along with the sensitivity analyses in 
these three meta-analyses, provide evidence of a robust association 
between ambient O3 and mortality'' (EPA, 2006a, p. 7-97). In 
summary, the 2006 Criteria Document (p. 8-78) concludes that these 
findings are highly suggestive that short-term O3 exposure 
directly or indirectly contribute to non-accidental and 
cardiopulmonary-related mortality, but additional research is needed to 
more fully establish underlying mechanisms by which such effects occur.
    The 2007 Staff Paper considered the epidemiological studies to 
evaluate evidence related to potential effects thresholds at the 
population level for morbidity and mortality effects. As discussed 
above in section II.A.3.a (and more fully in the 2007 Staff Paper in 
chapter 3 and the 2006 Criteria

[[Page 2987]]

Document in chapter 7), a number of time-series studies have used 
statistical modeling approaches to evaluate potential thresholds at the 
population level. A few such studies reported some suggestive evidence 
of possible thresholds for morbidity and mortality outcomes in terms of 
24-hour, 8-hour, and 1-hour averaging times. These results, taken 
together, provide some indication of possible 8-hour average threshold 
levels from below about 0.025 to 0.035 ppm (within the range of 
background concentrations) up to approximately 0.050 ppm. Other 
studies, however, observe linear concentration-response functions 
suggesting no effect threshold. The 2007 Staff Paper (p.6-60) concluded 
that the statistically significant associations between ambient 
O3 concentrations and lung function decrements, respiratory 
symptoms, indicators of respiratory morbidity including increase 
emergency department visits and hospital admissions, and possibly 
mortality reported in a large number of studies likely extend down to 
ambient O3 concentrations that are well below the level of 
the then current standard (0.084 ppm). These associations also extend 
well below the level of the standard set in 2008 (0.075 ppm) in that 
the highest level at which there is any indication of a threshold is 
approximately 0.050 ppm. Toward the lower end of the range of 
O3 concentrations observed in such studies, ranging down to 
background levels (i.e., 0.035 to 0.015 ppm), however, the 2007 Staff 
Paper stated that there is increasing uncertainty as to whether the 
observed associations remain plausibly related to exposures to ambient 
O3, rather than to the broader mix of air pollutants present 
in the ambient atmosphere.
    The 2007 Staff Paper also considered studies that did subset 
analyses, which included only days with ambient O3 
concentrations below the level of the then current standard, or below 
even lower O3 concentrations, and continue to report 
statistically significant associations. Notably, as discussed above, 
Bell et al. (2006) conducted a subset analysis that continued to show 
statistically significant mortality associations even when only days 
with a maximum 8-hour average O3 concentration below a value 
of approximately 0.061 ppm were included.\47\ Also of note is the large 
multicity NCICAS (Mortimer et al., 2002) that reported statistically 
significant associations between ambient O3 concentrations 
and lung function decrements even when days with 8-hour average 
O3 levels greater than 0.080 ppm were excluded (which 
consisted of less than 5 percent of the days in the eight urban areas 
in the study).
---------------------------------------------------------------------------

    \47\ Bell et al. (2006) referred to this level as being 
approximately equivalent to 120 [micro]g/m\3\, daily 8-hour maximum, 
the World Health Organization guideline and European Commission 
target value for O3.
---------------------------------------------------------------------------

    Further, as discussed above in section II.A.3.a, there are 
limitations in epidemiological studies that make discerning thresholds 
in populations difficult, including low data density in the lower 
concentration ranges, the possible influence of exposure measurement 
error, and interindividual differences in susceptibility to 
O3-related effects in populations. There is the possibility 
that thresholds for individuals may exist in reported associations at 
fairly low levels within the range of air quality observed in the 
studies but not be detectable as population thresholds in 
epidemiological analyses.
    Based on the above considerations, the 2007 Staff Paper recognized 
that the available evidence neither supports nor refutes the existence 
of effect thresholds at the population level for morbidity and 
mortality effects, and that if a population threshold level does exist, 
it would likely be well below the level of the then current standard 
and possibly within the range of background levels. Taken together, 
these considerations also support the conclusion that if a population 
threshold level does exist, it would likely be well below the level of 
the 0.075 ppm, 8-hour average, standard set in 2008.
    In looking more broadly at evidence from animal toxicological, 
controlled human exposure, and epidemiological studies, the 2006 
Criteria Document found substantial evidence, newly available in the 
2008 rulemaking, that people with asthma and other preexisting 
pulmonary diseases are among those at increased risk from O3 
exposure. Altered physiological, morphological, and biochemical states 
typical of respiratory diseases like asthma, COPD, and chronic 
bronchitis may render people sensitive to additional oxidative burden 
induced by O3 exposure (EPA, 2006a, section 8.7). Children 
and adults with asthma are the groups that have been studied most 
extensively. Evidence from controlled human exposure studies indicates 
that asthmatics may exhibit larger lung function decrements in response 
to O3 exposure than healthy controls. As discussed more 
fully in section II.A.4 above, asthmatics present a different response 
profile for cellular, molecular, and biochemical parameters (EPA, 
2006a, Figure 8-1) that are altered in response to acute O3 
exposure. They can have larger inflammatory responses, as manifested by 
larger increases in markers of inflammation such as white bloods cells 
(e.g., PMNs) or inflammatory cytokines. Asthmatics, and people with 
allergic rhinitis, are more likely to have an allergic-type response 
upon exposure to O3, as manifested by increases in white 
blood cells associated with allergy (i.e., eosinophils) and related 
molecules, which increase inflammation in the airways. The increased 
inflammatory and allergic responses also may be associated with the 
larger late-phase responses that asthmatics can experience, which can 
include increased bronchoconstrictor responses to irritant substances 
or allergens and additional inflammation.
    In addition to the experimental evidence of lung function 
decrements, respiratory symptoms, and other respiratory effects in 
asthmatic populations, two large U.S. epidemiological studies as well 
as several smaller U.S. and international studies, have reported fairly 
robust associations between ambient O3 concentrations and 
measures of lung function and daily respiratory symptoms (e.g., chest 
tightness, wheeze, shortness of breath) in children with moderate to 
severe asthma and between O3 and increased asthma medication 
use (EPA, 2007a, chapter 6). These more serious responses in asthmatics 
and others with lung disease provide biological plausibility for the 
respiratory morbidity effects observed in epidemiological studies, such 
as emergency department visits and hospital admissions.
    The body of evidence from controlled human exposure and 
epidemiological studies, which includes asthmatic as well as non-
asthmatic subjects, indicates that controlled human exposure studies of 
lung function decrements and respiratory symptoms that evaluate only 
healthy, non-asthmatic subjects likely underestimate the effects of 
O3 exposure on asthmatics and other susceptible populations. 
Therefore, relative to the healthy, non-asthmatic subjects used in most 
controlled human exposure studies, including the Adams (2002, 2006) 
studies, a greater proportion of people with asthma may be affected, 
and those who are affected may have as large or larger lung function 
and symptomatic responses at ambient exposures to 0.060 ppm 
O3. This indicates that the lowest-observed-effects levels 
demonstrated in controlled human exposure studies that use only healthy 
subjects may not

[[Page 2988]]

reflect the lowest levels at which people with asthma or other lung 
diseases may respond.
    Being mindful of the uncertainties and limitations inherent in 
interpreting the available evidence, the 2007 Staff Paper stated the 
view that the range of alternative O3 standards for 
consideration should take into account information on lowest-observed-
effects levels in controlled human exposure studies as well as 
indications of possible effects thresholds reported in some 
epidemiological studies and questions of biological plausibility in 
attributing associations observed down to background levels to 
O3 exposures alone. Based on the evidence and these 
considerations, it concluded that the upper end of the range of 
consideration should be somewhat below 0.080 ppm, the lowest-observed-
effects level for effects such as pulmonary inflammation, increased 
airway responsiveness and impaired host-defense capabilities in healthy 
adults while at prolonged moderate exertion. The 2007 Staff Paper also 
concluded that the lower end of the range of alternative O3 
standards appropriate for consideration should be the lowest-observed-
effects level for potentially adverse lung function decrements and 
respiratory symptoms in some healthy adults, 0.060 ppm.
b. Exposure and Risk-Based Considerations
    In addition to the evidence-based considerations informing staff 
recommendations on alternative levels, as discussed above in section 
II.B, the 2007 Staff Paper also evaluated quantitative exposures and 
health risks estimated to occur upon meeting the then current 0.084 ppm 
standard and alternative standards.\48\ In so doing, it presented the 
important uncertainties and limitations associated with these exposure 
and risk assessments (discussed above in section II.B and more fully in 
chapters 4 and 5 of the 2007 Staff Paper).
---------------------------------------------------------------------------

    \48\ As described in the 2007 Staff Paper (section 4.5.8) and 
discussed above in section II.B, recent O3 air quality 
distributions have been statistically adjusted to simulate just 
meeting the then current 0.084 ppm standard and selected alternative 
standards. These simulations do not represent predictions of when, 
whether, or how areas might meet the specified standards. Modeling 
that projects whether and how areas might attain alternative 
standards in a future year is presented in the Regulatory Impact 
Analysis being prepared in connection with this rulemaking.
---------------------------------------------------------------------------

    The 2007 Staff Paper (and the CASAC) also recognized that the 
exposure and risk analyses could not provide a full picture of the 
O3 exposures and O3-related health risks posed 
nationally. The EPA did not have sufficient information to evaluate all 
relevant at-risk groups (e.g., outdoor workers) or all O3-
related health outcomes (e.g., increased medication use, school 
absences, and emergency department visits that are part of the broader 
pyramid of effects discussed above in section II.A.4.d), and the scope 
of the 2007 Staff Paper analyses was generally limited to estimating 
exposures and risks in 12 urban areas across the U.S., and to only five 
or just one area for some health effects included in the risk 
assessment. Thus, national-scale public health impacts of ambient 
O3 exposures are clearly much larger than the quantitative 
estimates of O3-related incidences of adverse health effects 
and the numbers of children likely to experience exposures of concern 
associated with meeting the 0.084 ppm standard or alternative 
standards. On the other hand, inter-individual variability in 
responsiveness means that only a subset of individuals in each group 
estimated to experience exposures exceeding a given benchmark exposure 
of concern level would actually be expected to experience such adverse 
health effects.
    The 2007 Staff Paper focused on alternative standards with the same 
form as the then current 0.084 ppm O3 standard (i.e. the 
0.074/4, 0.070/4 and 0.064/4 scenarios).\49\ Having concluded in the 
2007 Staff Paper that it was appropriate to consider a range of 
standard levels from somewhat below 0.080 ppm down to as low as 0.060 
ppm, the 2007 Staff Paper looked to results of the analyses of exposure 
and risk for the 0.074/4 scenario to represent the public health 
impacts of selecting a standard in the upper part of the range, the 
results of analyses of the 0.070/4 scenario to represent the impacts in 
the middle part of the range, and the results of the analyses of the 
0.064/4 scenario to represent the lower part of the range.
---------------------------------------------------------------------------

    \49\ The abbreviated notation used to identify the then current 
0.084 ppm standard and alternative standards in this section and in 
the risk assessment section of the Staff Paper is in terms of ppm 
and the nth highest daily maximum 8-hour average. For example, the 
8-hour standard established in 1997 is identified as ``0.084/4.''
---------------------------------------------------------------------------

    As discussed in section II.B.1 of this notice, the exposure 
estimates presented in the 2007 Staff Paper are for the number and 
percent of all children and asthmatic children exposed, and the number 
of person-days (occurrences) of exposures, with daily 8-hour maximum 
exposures at or above several benchmark levels while at intermittent 
moderate or greater exertion. Exposures above selected benchmark levels 
provide some perspective on the public health impacts of health effects 
that cannot currently be evaluated in quantitative risk assessments but 
that may occur at existing air quality levels, and the extent to which 
such impacts might be reduced by meeting alternative standard levels. 
As described in section II.B.1.c above, the 2007 Staff Paper refers to 
exposures at and above these benchmark levels as ``exposures of 
concern.'' The 2007 Staff Paper notes that exposures of concern, and 
the health outcomes they represent, likely occur across a range of 
O3 exposure levels, such that there is no one exposure level 
that addresses all public health concerns. As noted above in section 
II.B., EPA also has acknowledged that the concept is more appropriately 
viewed as a continuum with greater confidence and less uncertainty 
about the existence of health effects at the upper end and less 
confidence and greater uncertainty as one considers increasingly lower 
O3 exposure levels.
    Consistent with advice from CASAC, the 2007 Staff Paper estimates 
exposures of concern not only at 0.080 ppm O3, a level at 
which there are clearly demonstrated effects, but also at 0.070 and 
0.060 ppm O3 levels where there is some evidence that health 
effects are likely to occur in some individuals. The 2007 Staff Paper 
recognizes that there will be varying degrees of concern about 
exposures at each of these levels, based in part on the population 
groups experiencing them. Given that there is clear evidence of 
inflammation, increased airway responsiveness, and changes in host 
defenses in healthy people exposed to 0.080 ppm and reason to infer 
that such effects will continue at lower exposure levels, but with 
increasing uncertainty about the extent to which such effects occur at 
lower O3 concentrations, the 2007 Staff Paper and discussion 
below, focus on exposures of concern at or above benchmark levels of 
0.070 and 0.060 ppm O3 for purposes of evaluating 
alternative standards. The focus on these two benchmark levels reflects 
the following evidence-based considerations, discussed above in section 
II.C.1, that raise concerns about adverse health effects likely 
occurring at levels below 0.080 ppm: (1) That there is limited, but 
important, new evidence from controlled human exposure studies showing 
lung function decrements and respiratory symptoms in some healthy 
subjects at 0.060 ppm; (2) that asthmatics are likely to have more 
serious responses than healthy individuals; (3) that lung function is 
not likely to be as sensitive a marker for O3

[[Page 2989]]

effects as lung inflammation; and (4) that there is epidemiological 
evidence which reports associations with O3 levels that 
extend well below 0.080 ppm.
    Table 3 below summarizes the exposure estimates for all children 
and asthmatic children for the 0.060 and 0.070 ppm health effect 
benchmark levels associated with O3 levels adjusted to just 
meet 0.074/4, 0.070/4, and 0.064/4 alternative 8-hour standards based 
on a generally poorer year of air quality (2002) and based on a 
generally better year of air quality (2004). This table includes 
exposure estimates reflecting the aggregate estimate for the 12 urban 
areas as well as the range across these same 12 areas. As shown in 
Table 3 below, the percent of population exposed over the selected 
benchmark levels is very similar for all and asthmatic school age 
children. Thus, the following discussion focuses primarily on the 
exposure estimates for asthmatic children, recognizing that the pattern 
of exposure estimates is similar for all children when expressed in 
terms of percentage of the population.
    As noted in section II.B.2 and shown in Tables 1 and 3 of this 
notice, substantial year-to-year variability is observed, ranging to 
over an order of magnitude at the higher alternative standard levels, 
in estimates of the number of children and the number of occurrences of 
exposures of concern at both the 0.060 and 0.070 ppm benchmark levels. 
As shown in Table 3, and discussed more fully below, aggregate 
estimates of exposures of concern for the 12 urban areas included in 
the assessment are considerably larger for the benchmark level of >= 
0.060 ppm O3, compared to the 0.070 ppm benchmark, while the 
pattern of year-to-year variability is fairly similar.
    As shown in Table 3, aggregate estimates of exposures of concern 
for a 0.060 ppm benchmark level vary considerably among the three 
alternative standards included in this table, particularly for the 2002 
simulations (a year with generally poorer air quality in most, but not 
all areas). For air quality just meeting a 0.074/4 standard 
approximately 27% of asthmatic children, based on the 2002 simulation, 
and approximately 2% of asthmatic children based on the 2004 simulation 
(a year with better air quality in most but not all areas), are 
estimated to experience one or more exposures of concern at the 
benchmark level of >= 0.060 ppm O3. Considering a 0.070/4 
standard using the same benchmark level (0.060 ppm), about 18% of 
asthmatic children are estimated to experience one or more exposures of 
concern, in a year with poorer air quality (2002), and only about 1% in 
a year with better air quality (2004). For the most stringent standard 
examined (a 0.064/4 standard), about 6% of asthmatic children are 
estimated to experience one or more exposures of concern in the 
simulation based on the year with poorer air quality (2002), and 
exposures of concern at the 0.060 ppm benchmark level are essentially 
eliminated based on a year with better air quality (2004).
    Table 3 also provides aggregate exposure estimates for the 12 urban 
areas where a benchmark level of >= 0.070 ppm is used. Based on the 
year with poorer air quality (2002), the estimate of the percent of 
asthmatic children exposed one or more times is about 5% when a 0.074/4 
standard is just met; based on a year with better air quality (2004), 
exposures of concern are essentially eliminated. For this same 
benchmark (0.070 ppm), when a 0.070/4 standard is just met, estimates 
range from about 2% of asthmatic children exposed one or more times 
over this benchmark based on a year with poorer air quality (2002), and 
exposures of concern are essentially eliminated based on a year with 
better air quality (2004). At the 0.070 ppm benchmark, just meeting a 
0.064/4 standard essentially eliminates exposures of concern regardless 
of the year that is used as the basis for the analysis.
    The 2007 Staff Paper also notes that there is substantial city-to-
city variability in these estimates, and notes that it is appropriate 
to consider not just the aggregate estimates across all cities, but 
also to consider the public health impacts in cities that receive 
relatively less protection from the alternative standards. As shown in 
Table 3, in considering the benchmark level of >= 0.060 ppm, while the 
aggregate percentage of asthmatic children estimated to experience one 
or more exposures of concern across all 12 cities for a 0.074/4 
standard is about 27% based on the year with poorer air quality (2002), 
it ranges up to approximately 51% for asthmatic children in the city 
with the least degree of protection from that alternative standard. 
Similarly, for air quality just meeting a 0.070/4 standard, the 
aggregate percentage of asthmatic children estimated to experience one 
or more exposures of concern across all 12 cities is 18% based on the 
year with poorer air quality, but it ranges up to about 41% in the city 
with the least degree of protection associated with just meeting that 
alternative standard. For just meeting a 0.064/4 standard, the 
aggregate estimate of asthmatic children experiencing exposures of 
concern for the 0.060 ppm benchmark is about 6% based on the year with 
poorer air quality and ranges up to 16% in the city with the least 
degree of protection.
    This pattern of city-to-city variability also occurs at the 
benchmark level of >= 0.070 ppm associated with air quality just 
meeting these same three alternative standards (i.e., 0.074/4, 0.070/4, 
and 0.064/4). While the aggregate percentage of asthmatic children 
estimated to experience such exposures of concern across all 12 cities 
is about 5% based on the year with poorer air quality for just meeting 
the 0.074/4 standard, it ranges up to 14% in the city with the least 
degree of protection associated with that alternative standard. For 
just meeting a 0.070/4 standard the aggregate estimate is 2% of 
asthmatic children experiencing exposures of concern for the 0.070 ppm 
benchmark based on the year with poorer air quality and ranges up to 6% 
in the city with the least degree of protection. The aggregate estimate 
for exposures of concern is further reduced to 0.2% of asthmatic 
children for this same benchmark level for air quality just meeting a 
0.064/4 standard based on the year with poorer air quality and ranges 
up to 1% in the city with the least degree of protection.
    In addition to observing the fraction of the population estimated 
to experience exposures of concern associated with just meeting 
alternative standards, EPA also took into consideration in the 2007 
Staff Paper the percent reduction in exposures of concern and health 
risks associated with alternative standards relative to just meeting 
the then current 0.084/4 standards. For the current decision it is also 
informative to consider the incremental reductions in exposures of 
concern associated with more stringent alternative standards relative 
to the 0.075 ppm standard. As shown in Table 1 above, at the >= 0.060 
ppm benchmark level based on a year with poorer air quality, the 
reduction in exposures of concern for asthmatic children in going from 
the 0.074/4 standard (which approximates the 0.075 ppm standard adopted 
in 2008) down to a 0.064/4 standard is observed to be very similar to 
the reduction estimated to occur in going from then current 0.084/4 
standard down to a 0.074/4 standard. More specifically, the estimates 
for asthmatic children are reduced from 47% (about 1.2 million 
children) associated with meeting a 0.084/4 standard down to 27% (about 
700,000 children) for just meeting a 0.074/4 standard and the estimates 
are reduced further to about 6% (about 150,000 children) associated 
with just meeting a

[[Page 2990]]

0.064/4 standard in the 12 urban areas included in the assessment. In a 
year with better air quality (2004), exposures estimated to exceed the 
0.060 ppm benchmark in asthmatic children one or more times in a year 
are reduced from 11% associated with just meeting a 0.084/4 standard 
down to about 2% for a 0.074/4 standard and are essentially eliminated 
when a 0.064/4 standard is just met.
    Turning to consideration of the risk assessment estimates, Table 2 
above summarizes the risk estimates for moderate lung function 
decrements in both all school age children and asthmatic school age 
children associated with just meeting several alternative standards 
based on simulations involving a year with relatively poorer air 
quality (2002) and a year with relatively better air quality (2004). As 
shown in Table 2, for the 2002 simulation the reduction in the number 
of asthmatic children estimated to experience one or more moderate lung 
function decrements going from a 0.074/4 standard down to a 0.064/4 
standard is roughly equivalent to the additional health protection 
afforded associated with just meeting a 0.074/4 standard relative to 
then current 0.084/4 standard. More specifically, for just 5 urban 
areas, it is estimated that nearly 8% of asthmatic children (130,000 
children) would experience one or more occurrences of moderate lung 
function decrements per year at a 0.084/4 standard and this would be 
reduced to about 5% (90,000 children) at a 0.074/4 standard and further 
reduced down to about 3% (50,000 children) at a 0.064/4 standard. Based 
on the 2002 simulations, the percent reduction associated with just 
meeting a 0.064/4 standard relative to then current 0.084/4 standard is 
about 62% which is about twice the reduction in risk compared to the 
estimated 31% reduction associated with just meeting a 0.074/4 
standard. As shown in Table 2 above, similar patterns were observed in 
reductions in lung function risk for all school age children in 12 
urban areas associated with these alternative standards.
    Figures 6-5 and 6-6 in the 2007 Staff Paper (EPA, 2007b) show the 
percent reduction in non-accidental mortality risk estimates associated 
with just meeting the same alternative standards discussed above 
relative to just meeting the then current 0.084/4 standard for 12 urban 
areas, based on adjusting 2002 and 2004 air quality data. These figures 
also provide perspective on the extent to which the risks in these 
years (i.e., 2002 and 2004) are greater than those estimated to occur 
upon meeting the then current 0.084/4 standard (in terms of a negative 
percent reduction relative to a 0.084/4 standard). Based on the 2002 
simulations (EPA, 2007b, Figure 6-5), the estimated reduction in non-
accidental mortality is about 30 to 70% across the 12 urban areas for 
just meeting a 0.064/4 standard relative to the then current 0.084/4 
standard. This reduction is roughly twice the 15 to 30% estimated 
reduction across the 12 urban areas associated with just meeting a 
0.074/4 standard relative to a 0.084/4 standard. While the estimated 
incidence is lower based on the 2004 simulations (EPA, 2007b, Figure 6-
6), the pattern of risk reductions among alternative standards is 
roughly similar to that observed for the 2002 simulations.
    In addition to the risk estimates for lung function decrements in 
all school age children and non-accidental mortality that were 
estimated for 12 urban areas and lung function decrements in asthmatic 
children for 5 urban areas, a similar pattern of incremental reductions 
in health risks was shown for two health outcomes where risks were 
estimated in one city only for each of these outcomes. These included 
reductions in respiratory symptoms in asthmatic children (EPA, 2007b; 
Boston, Table 6-9) and respiratory-related hospital admissions (EPA, 
2007a; New York City, Table 6-10) associated with just meeting 
alternative 8-hour standards set at 0.074 ppm, 0.070 ppm, and 0.064 ppm 
relative to just meeting the then current 0.084 ppm standard. Using the 
2002 simulation, a standard set at 0.074/4 is estimated to reduce the 
incidence of symptom days in children with moderate to severe asthma in 
the Boston area by about 15 percent relative to a 0.084/4 standard. 
With this reduction, it is estimated that about 1 respiratory symptom 
day in 8 during the O3 season would be attributable to 
O3 exposure. A standard set at 0.064/4 is estimated, based 
on the 2002 simulation, to reduce the incidence of symptom days in 
children with moderate to severe asthma in the Boston area by about a 
25 to 30 percent reduction relative to a 0.084 ppm standard, which is 
roughly twice the reduction compared to that provided by a 0.074/4 
standard. But even with this reduction, it is estimated that 1 
respiratory symptom day in 10 during the O3 season is 
attributable to O3 exposure.
    As shown in Table 6-10 (EPA, 2007b) estimated incidence of 
respiratory-related hospital admissions in one urban area (New York 
City) was reduced by 14 to 17 percent by a standard set at 0.074/4 
relative to then current 0.084/4 standard, in the year with relatively 
high and relatively low O3 air quality levels, respectively. 
Similar to the pattern observed for the other health outcomes discussed 
above, the reduction in incidence of respiratory-related hospital 
admissions for a 0.064/4 standard relative to a 0.084/4 standard is 
about twice that associated with a 0.074/4 standard relative to a 
0.084/4 standard.

  Table 3--Number and Percent of All and Asthmatic School Age Children in 12 Urban Areas Estimated to Experience 8-Hour Ozone Exposures Above 0.060 and
    0.070 ppm While at Moderate or Greater Exertion, One or More Times per Season Associated With Just Meeting Alternative 8-Hour Standards Based on
                                                       Adjusting 2002 and 2004 Air Quality Data1 2
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                          All children, ages 5-18  Aggregate for       Asthmatic children, ages 5-18
                                                                            12 urban areas  Number of children     Aggregate for 12 urban areas  Number
                                                      8-Hour air quality   exposed  (% of all children)  [Range      of children exposed  (% of group)
   Benchmark levels of exposures of concern (ppm)        standards \3\     across 12 cities, % of all children]    [Range across 12 cities, % of group]
                                                             (ppm)       -------------------------------------------------------------------------------
                                                                                 2002                2004                2002                2004
--------------------------------------------------------------------------------------------------------------------------------------------------------
0.070...............................................               0.074        770,000 (4%)         20,000 (0%)        120,000 (5%)              0 (0%)
                                                                                     [0-13%]              [0-1%]             [0-14%]              [0-1%]
                                                                   0.070        270,000 (1%)              0 (0%)         50,000 (2%)              0 (0%)
                                                                                      [0-5%]                [0%]              [0-6%]                [0%]
                                                                   0.064       30,000 (0.2%)              0 (0%)       10,000 (0.2%)              0 (0%)
                                                                                      [0-1%]                [0%]             [0-1% ]                [0%]

[[Page 2991]]

 
0.060...............................................               0.074     4,550,000 (25%)        350,000 (2%)       700,000 (27%)         50,000 (2%)
                                                                                     [1-48%]              [0-9%]             [1-51%]              [0-9%]
                                                                   0.070     3,000,000 (16%)        110,000 (1%)       460,000 (18%)         10,000 (1%)
                                                                                     [1-36%]              [0-4%]             [0-41%]              [0-3%]
                                                                   0.064        950,000 (5%)         10,000 (0%)        150,000 (6%)              0 (0%)
                                                                                     [0-17%]              [0-1%]             [0-16%]              [0-1%]
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Moderate or greater exertion is defined as having an 8-hour average equivalent ventilation rate >= 13 1-min/m\2\.
\2\ Estimates are the aggregate results based on 12 combined statistical areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, Los Angeles, New
  York, Philadelphia, Sacramento, St. Louis, and Washington, DC). Estimates are for the ozone season which is all year in Houston, Los Angeles and
  Sacramento and March or April to September or October for the remaining urban areas.
\3\ All standards summarized here have the same form as the 8-hour standard established in 1997 which is specified as the 3-year average of the annual
  4th highest daily maximum 8-hour average concentrations must be at or below the concentration level specified. As described in the 2007 Staff Paper
  (EPA, 2007b, section 4.5.8), recent O3 air quality distributions have been statistically adjusted to simulate just meeting the 0.084 ppm standard and
  selected alternative standards. These simulations do not represent predictions of when, whether, or how areas might meet the specified standards.

2. CASAC Views Prior to 2008 Decision
    In comments on the second draft Staff Paper, CASAC stated in its 
letter to the Administrator, ``the CASAC unanimously recommends that 
the current primary ozone NAAQS be revised and that the level that 
should be considered for the revised standard be from 0.060 to 0.070 
ppm'' (Henderson, 2006c, p. 5). This recommendation followed from its 
more general recommendation that the 0.084 ppm standard needed to be 
substantially reduced to be protective of human health, particularly in 
at-risk subpopulations.
    The CASAC Panel noted that beneficial reductions in some adverse 
health effects were estimated to occur upon meeting the lowest standard 
level (0.064 ppm) considered in the risk assessment (Henderson, 2006c, 
p. 4). The lower end of this range reflects CASAC's views that 
``[w]hile data exist that adverse health effects may occur at levels 
lower than 0.060 ppm, these data are less certain and achievable gains 
in protecting human health can be accomplished through lowering the 
ozone NAAQS to a level between 0.060 and 0.070 ppm.'' (id.).
    In a subsequent letter sent specifically to offer advice to aid the 
Administrator and Agency staff in developing the O3 
proposal, the CASAC reiterated that the Panel members ``were unanimous 
in recommending that the level of the current primary ozone standard 
should be lowered from 0.08 ppm to no greater than 0.070 ppm'' 
(Henderson, 2007, p. 2). Further, the CASAC Panel expressed the view 
that the 2006 Criteria Document and 2007 Staff Paper, together with the 
information in its earlier letter, provide ``overwhelming scientific 
evidence for this recommendation,'' and emphasized the Clean Air Act 
requirement that the primary standard must be set to protect the public 
health with an adequate margin of safety (id.).
3. Basis for 2008 Decision on the Primary Standard
    This section presents the rationale for the 2008 final decision on 
the primary O3 standard as presented in the 2008 final rule 
(73 FR 16475). The EPA's conclusions on the level of the standard began 
by noting that, having carefully considered the public comments on the 
appropriate level of the O3 standard, EPA concluded that the 
fundamental scientific conclusions on the effects of O3 
reached in the 2006 Criteria Document and 2007 Staff Paper remained 
valid. In considering the level at which the primary O3 
standard should be set, EPA placed primary consideration on the body of 
scientific evidence available in the 2008 final rulemaking on the 
health effects associated with O3 exposure, while viewing 
the results of exposure and risk assessments as providing information 
in support of the decision. In considering the available scientific 
evidence, EPA concluded that a focus on the proposed range of 0.070 to 
0.075 ppm was appropriate in light of the large body of controlled 
human exposure and epidemiological and other scientific evidence. The 
notice stated that this body of evidence did not support retaining the 
then current 0.084 ppm 8-hour O3 standard, as suggested by 
some commenters, nor did it support setting a level just below 0.080 
ppm, because, based on the entire body of evidence, such a level would 
not provide a significant increase in protection compared to the 0.084 
ppm standard. Further, such a level would not be appreciably below the 
level in controlled human exposure studies at which adverse effects 
have been demonstrated (i.e., 0.080 ppm). The notice also stated that 
the body of evidence did not support setting a level of 0.060 ppm or 
below, as suggested by other commenters. In evaluating the information 
from the exposure assessment and the risk assessment, EPA judged that 
this information did not provide a clear enough basis for choosing a 
specific level within the range of 0.075 to 0.070 ppm.
    In making a final judgment about the level of the primary 
O3 standard, EPA noted that the level of 0.075 ppm is above 
the range recommended by the CASAC (i.e., 0.070 to 0.060 ppm). The 
notice stated that in placing great weight on the views of CASAC, 
careful consideration had been given to CASAC's stated views and the 
scientific basis and policy views for the range it recommended. In so 
doing, EPA fully agreed that the scientific evidence supports the 
conclusion that the current standard was not adequate and must be 
revised.

[[Page 2992]]

    With respect to CASAC's recommended range of standard levels, EPA 
observed that the basis for CASAC's recommendation appeared to be a 
mixture of scientific and policy considerations. While in general 
agreement with CASAC's views concerning the interpretation of the 
scientific evidence, EPA noted that there was no bright line clearly 
directing the choice of level, and the choice of what was appropriate 
was clearly a public health policy judgment entrusted to the EPA 
Administrator. This judgment must include consideration of the 
strengths and limitations of the evidence and the appropriate 
inferences to be drawn from the evidence and the exposure and risk 
assessments. In reviewing the basis for the CASAC Panel's 
recommendation for the range of the O3 standard, EPA 
observed that it reached a different policy judgment than the CASAC 
Panel based on apparently placing different weight in two areas: The 
role of the evidence from the Adams studies and the relative weight 
placed on the results from the exposure and risk assessments. While EPA 
found the evidence reporting effects at the 0.060 ppm level from the 
Adams studies to be too limited to support a primary focus at this 
level, EPA observed that the CASAC Panel appeared to place greater 
weight on this evidence, as indicated by its recommendation of a range 
down to 0.060 ppm. It was noted that while the CASAC Panel supported a 
level of 0.060 ppm, they also supported a level above 0.060, which 
indicated that they did not believe that the results of Adams studies 
meant that the level of the standard had to be set at 0.060 ppm. The 
EPA also observed that the CASAC Panel appeared to place greater weight 
on the results of the risk assessment as a basis for its recommended 
range. In referring to the risk assessment results for lung function, 
respiratory symptoms, hospital admissions and mortality, the CASAC 
Panel concluded that: ``beneficial effects in terms of reduction of 
adverse health effects were calculated to occur at the lowest 
concentration considered (i.e., 0.064 ppm)'' (Henderson, 2006c, p. 4). 
However, EPA more heavily weighed the implications of the uncertainties 
associated with the Agency's quantitative human exposure and health 
risk assessments. Given these uncertainties, EPA did not agree that 
these assessment results appropriately served as a primary basis for 
concluding that levels at or below 0.070 ppm were required for the 8-
hour O3 standard.
    The notice stated that after carefully taking the above comments 
and considerations into account, and fully considering the scientific 
and policy views of the CASAC, EPA decided to revise the level of the 
primary 8-hour O3 standard to 0.075 ppm. The EPA judged, 
based on the available evidence, that a standard set at this level 
would be requisite to protect public health with an adequate margin of 
safety, including the health of sensitive subpopulations, from serious 
health effects including respiratory morbidity, that were judged to be 
causally associated with short-term and prolonged exposures to 
O3, and premature mortality. The EPA also judged that a 
standard set at this level provides a significant increase in 
protection compared to the 0.084 ppm standard, and is appreciably below 
0.080 ppm, the level in controlled human exposure studies at which 
adverse effects have been demonstrated. At a level of 0.075 ppm, 
exposures at and above the benchmark of 0.080 ppm are essentially 
eliminated, and exposures at and above the benchmark of 0.070 are 
substantially reduced or eliminated for the vast majority of people in 
at-risk groups. A standard set at a level lower than 0.075 would only 
result in significant further public health protection if, in fact, 
there is a continuum of health risks in areas with 8-hour average 
O3 concentrations that are well below the concentrations 
observed in the key controlled human exposure studies and if the 
reported associations observed in epidemiological studies are, in fact, 
causally related to O3 at those lower levels. Based on the 
available evidence, EPA was not prepared to make these assumptions. 
Taking into account the uncertainties that remained in interpreting the 
evidence from available controlled human exposure and epidemiological 
studies at very low levels, EPA noted that the likelihood of obtaining 
benefits to public health decreased with a standard set below 0.075 ppm 
O3, while the likelihood of requiring reductions in ambient 
concentrations that go beyond those that are needed to protect public 
health increased. The EPA judged that the appropriate balance to be 
drawn, based on the entire body of evidence and information available 
in the 2008 final rulemaking, was to set the 8-hour primary standard at 
0.075 ppm. The EPA expressed the belief that a standard set at 0.075 
ppm would be sufficient to protect public health with an adequate 
margin of safety, and did not believe that a lower standard was needed 
to provide this degree of protection. The EPA further asserted that 
this judgment appropriately considered the requirement for a standard 
that was neither more nor less stringent than necessary for this 
purpose and recognized that the CAA does not require that primary 
standards be set at a zero-risk level, but rather at a level that 
reduces risk sufficiently so as to protect public health with an 
adequate margin of safety.
4. CASAC Advice Following 2008 Decision
    Following the 2008 decision on the O3 standard, serious 
questions were raised as to whether the standard met the requirements 
of the CAA. In April 2008, the members of the CASAC Ozone Review Panel 
sent a letter to EPA stating ``In our most-recent letters to you on 
this subject--dated October 2006 and March 2007--the CASAC unanimously 
recommended selection of an 8-hour average Ozone NAAQS within the range 
of 0.060 to 0.070 parts per million for the primary (human health-
based) Ozone NAAQS'' (Henderson, 2008). The letter continued: ``The 
CASAC now wishes to convey, by means of this letter, its additional, 
unsolicited advice with regard to the primary and secondary Ozone 
NAAQS. In doing so, the participating members of the CASAC Ozone Review 
Panel are unanimous in strongly urging you or your successor as EPA 
Administrator to ensure that these recommendations be considered during 
the next review cycle for the Ozone NAAQS that will begin next year'' 
(id.). Moreover, the CASAC Panel noted that ``numerous medical 
organizations and public health groups have also expressed their 
support of these CASAC recommendations.'' (id.) The letter further 
stated the following strong, unanimous view:

    [the CASAC did] ``not endorse the new primary ozone standard as 
being sufficient protective of public health. The CASAC--as the 
Agency's statutorily-established science advisory committee for 
advising you on the national ambient air quality standards--unanimously 
recommended decreasing the primary standard to within the range of 
0.060-0.070 ppm. It is the Committee's consensus scientific opinion 
that your decision to set the primary ozone standard above this range 
fails to satisfy the explicit stipulations of the Clean Air Act that 
you ensure an adequate margin of safety for all individuals, including 
sensitive populations'' (Henderson, 2008).
5. Administrator's Proposed Conclusions
    For the reasons discussed below, the Administrator proposes to set 
a new level for the 8-hour primary O3 within

[[Page 2993]]

the range from 0.060 to 0.070 ppm.\50\ In reaching this proposed 
decision, the Administrator has considered: the evidence-based 
considerations from the 2006 Criteria Document and the 2007 Staff 
Paper; the results of the exposure and risk assessments discussed above 
and in the 2007 Staff Paper; CASAC advice and recommendations provided 
in CASAC's letters to the Administrator both during and following the 
2008 rulemaking; EPA staff recommendations; and public comments 
received in conjunction with review of drafts of these documents and on 
the 2007 proposed rule. In considering what level of an 8-hour 
O3 standard is requisite to protect public health with an 
adequate margin of safety, the Administrator is mindful that this 
choice requires judgments based on an interpretation of the evidence 
and other information that neither overstates nor understates the 
strength and limitations of the evidence and information.
---------------------------------------------------------------------------

    \50\ As discussed above at the beginning of section II, the 
Administrator has focused her reconsideration of the primary 
O3 standard set in the 2008 final rule on the level of 
the standard, having decided not to reopen the 2008 final rule with 
regard to the need to revise the 1997 primary O3 standard 
to provide increased public health protection nor with regard to the 
indicator, averaging period, and form of the 2008 standard.
---------------------------------------------------------------------------

    The Administrator notes that the most certain evidence of adverse 
health effects from exposure to O3 comes from the controlled 
human exposure studies, and that the large bulk of this evidence 
derives from studies of exposures at levels of 0.080 ppm and above. At 
those levels, there is consistent evidence of lung function decrements 
and respiratory symptoms in healthy young adults, as well as evidence 
of O3-induced pulmonary inflammation, airway responsiveness, 
impaired host defense capabilities, and other medically significant 
airway responses. Moreover, there is no evidence that the 0.080 ppm 
exposure level is a threshold for any of these types of respiratory 
effects. Rather, there is now controlled human exposure evidence, 
including studies of lung function decrements and respiratory symptoms 
at the 0.060 ppm exposure level, that strengthens our previous 
understanding that this array of respiratory responses are likely to 
occur in some healthy adults at such lower levels.
    In particular, the Administrator notes two studies by Adams (2002, 
2006), newly available in the 2008 rulemaking, that examined lung 
function and respiratory symptom effects associated with prolonged 
O3 exposures at levels below 0.080 ppm, as well as EPA's 
reanalysis of the data from the Adams (2006) study at a 0.060 ppm 
exposure level. As discussed above, while the author's analysis focused 
on hour-by-hour comparisons of effects, for the purpose of exploring 
responses associated with different patterns of exposure, EPA's 
reanalysis focused on addressing the more fundamental question of 
whether the pre- to post-exposure change in lung function differed 
between a 6.6-hour exposure to 0.060 ppm O3 versus a 6.6 
hour exposure to clean filtered air. The Administrator notes that this 
reanalysis found small, but statistically significant group mean 
differences in lung function decrements in healthy adults at the 0.060 
ppm exposure level, which is now the lowest-observed-effects level for 
these effects. Moreover, these studies also report a small percentage 
of subjects (7 to 20 percent) experienced moderate lung function 
decrements (>= 10 percent) at the 0.060 ppm exposure level. While for 
active healthy people, moderate levels of functional responses (e.g., 
FEV1 decrements of >= 10% but < 20%) and/or moderate 
respiratory symptom responses would likely interfere with normal 
activity for relatively few responsive individuals, the Administrator 
notes that for people with lung disease, even moderate functional or 
symptomatic responses would likely interfere with normal activity for 
many individuals, and would likely result in more frequent use of 
medication. Further, she notes that CASAC indicated that a focus on the 
lower end of the range of moderate levels of functional responses 
(e.g., FEV1 decrements >= 10%) is most appropriate for 
estimating potentially adverse lung function decrements in people with 
lung disease (Henderson, 2006c).
    The Administrator also notes that many public commenters on the 
2007 proposed rule raised a number of questions about the weight that 
should be placed on the Adams studies and EPA's reanalysis of data from 
the Adams (2006) study. Some commenters expressed the view that the 
results of these studies and EPA's reanalysis provided support for 
setting a standard level below the proposed range, while others raised 
questions about EPA's reanalysis and generally expressed the view that 
the study results were not robust enough to reach conclusions about 
respiratory effects at the 0.060 ppm exposure level.\51\
---------------------------------------------------------------------------

    \51\ The EPA responded to these comments in the 2008 final rule 
(73 FR 16454-5).
---------------------------------------------------------------------------

    Based on all the above considerations, the Administrator concludes 
that the Adams studies provide limited but important evidence which 
adds to the overall body of evidence that informs her proposed decision 
on the range of levels within which a standard could be set that would 
be requisite to protect public health with an adequate margin of 
safety, including the health of at-risk populations such as people with 
lung disease.
    In considering controlled human exposure studies reporting 
O3-induced pulmonary inflammation, airway responsiveness, 
and impaired host defense capabilities at exposure levels down to 0.080 
ppm, the lowest level at which these effects have been tested, the 
Administrator notes that these physiological effects have been linked 
to aggravation of asthma and increased susceptibility to respiratory 
infection, potentially leading to increased medication use, increased 
school and work absences, increased visits to doctors' offices and 
emergency departments, and increased hospital admissions, especially in 
people with lung disease. These physiological effects are all 
indicators of potential adverse O3-related morbidity 
effects, which are consistent with and lend plausibility to the 
associations observed between O3 and adverse morbidity 
effects and mortality effects in epidemiological studies.
    With regard to epidemiological studies, the Administrator observes 
that statistically significant associations between ambient 
O3 levels and a wide array of respiratory symptoms and other 
morbidity outcomes including school absences, emergency department 
visits, and hospital admissions have been reported in a large number of 
studies. More specifically, positive and robust associations were found 
between ambient O3 concentrations and respiratory hospital 
admissions and emergency department visits, when focusing particularly 
on the results of warm season analyses. Taken together, the overall 
body of evidence from controlled human exposure, toxicological, and 
epidemiological studies supports the inference of a causal relationship 
between acute ambient O3 exposures and increased respiratory 
morbidity outcomes resulting in increased emergency department visits 
and hospitalizations during the warm season. Further, the Administrator 
notes that recent epidemiological evidence is highly suggestive that 
O3 directly or indirectly contributes to non-accidental and 
cardiopulmonary-related mortality.
    The Administrator also considered the epidemiological evidence with 
regard to considering potential effects thresholds at the population 
level for

[[Page 2994]]

morbidity and mortality effects. As discussed above, while some studies 
provide some indication of possible 8-hour average threshold levels 
from below about 0.025 to 0.035 ppm (within the range of background 
concentrations) up to approximately 0.050 ppm, other studies observe 
linear concentration-response functions suggesting that there may be no 
effects thresholds at the population level above background 
concentrations. In addition, other studies conducted subset analyses 
that included only days with ambient O3 concentrations below 
the level of the then current standard, or below even lower 
O3 concentrations, including a level as low as 0.061 ppm, 
and continue to report statistically significant associations. The 
Administrator notes that the relationships between ambient 
O3 concentrations and lung function decrements, respiratory 
symptoms, indicators of respiratory morbidity including increased 
respiratory-related emergency department visits and hospital 
admissions, and possibly mortality reported in a large number of 
studies likely extend down to ambient O3 concentrations well 
below the level of the standard set in 2008 (0.075 ppm), in that the 
highest level at which there is any indication of a threshold is 
approximately 0.050 ppm. The Administrator notes as well that toward 
the lower end of the range of O3 concentrations observed in 
such studies, ranging down to background levels (i.e., 0.035 to 0.015 
ppm), there is increasing uncertainty as to whether the observed 
associations remain plausibly related to exposures to ambient 
O3, rather than to the broader mix of air pollutants present 
in the ambient atmosphere. She also notes that there are limitations in 
epidemiological studies that make discerning population thresholds 
difficult, as discussed above, such that there is the possibility that 
thresholds for individuals may exist in reported associations at fairly 
low levels within the range of air quality observed in the studies but 
not be detectable as population thresholds in epidemiological analyses.
    In looking more broadly at evidence from animal toxicological, 
controlled human exposure, and epidemiological studies, the 
Administrator finds substantial evidence, newly available for 
consideration in the 2008 rulemaking, that people with asthma and other 
preexisting pulmonary diseases are among those at increased risk from 
O3 exposure. As discussed above, altered physiological, 
morphological, and biochemical states typical of respiratory diseases 
like asthma, COPD, and chronic bronchitis may render people sensitive 
to additional oxidative burden induced by O3 exposure. 
Children and adults with asthma are the group that has been studied 
most extensively. Evidence from controlled human exposure studies 
indicates that asthmatics and people with allergic rhinitis may exhibit 
larger lung function decrements in response to O3 exposure 
than healthy subjects and that they can have larger inflammatory 
responses. The Administrator also notes that two large U.S. 
epidemiological studies, as well as several smaller U.S. and 
international studies, have reported fairly robust associations between 
ambient O3 concentrations and measures of lung function and 
daily symptoms (e.g., chest tightness, wheeze, shortness of breath) in 
children with moderate to severe asthma and between O3 and 
increased asthma medication use. These more serious responses in 
asthmatics and others with lung disease provide biological plausibility 
for the respiratory morbidity effects observed in epidemiological 
studies, such as respiratory-related emergency department visits and 
hospital admissions.
    The Administrator also observes that a substantial body of evidence 
from controlled human exposure and epidemiological studies indicates 
that relative to the healthy, non-asthmatic subjects used in most 
controlled human exposure studies, a greater proportion of people with 
asthma may be affected, and those who are affected may have as large or 
larger lung function and symptomatic responses to O3 
exposures. Thus, the Administrator concludes that controlled human 
exposure studies of lung function decrements and respiratory symptoms 
that evaluate only healthy, non-asthmatic subjects likely underestimate 
the effects of O3 exposure on asthmatics and other 
susceptible populations.
    In addition to the evidence-based considerations discussed above, 
the Administrator also considered quantitative exposures and health 
risks estimated to occur associated with air quality simulated to just 
meet various standard levels to help inform judgments about a range of 
standard levels for consideration that could provide an appropriate 
degree of public health protection. In so doing, she is mindful of the 
important uncertainties and limitations that are associated with the 
exposure and risk assessments, as discussed in more detail in the 2007 
Staff Paper, and above in sections II.B and II.C.1.b. Beyond these 
uncertainties, the Administrator also recognized important limitations 
related to the exposure and risk analyses. For example, EPA did not 
have sufficient information to evaluate all relevant at-risk groups 
(e.g., outdoor workers) or all O3-related health outcomes 
(e.g., increased medication use, school absences, emergency department 
visits), and the scope of the analyses was generally limited to 
estimating exposures and risks in 12 urban areas across the U.S., and 
to only five or just one area for some health effects. Thus, it is 
clear that national-scale public health impacts of ambient 
O3 exposures are much larger than the quantitative estimates 
of O3-related incidences of adverse health effects and the 
numbers of children likely to experience exposures of concern 
associated with meeting the then current standard or alternative 
standards. Taking these limitations into account, the CASAC advised EPA 
not to rely solely on the results of the exposure and risk assessments 
in considering alternative standards, but also to place significant 
weight on the body of evidence of O3-related health effects 
in drawing conclusions about an appropriate range of levels for 
consideration. The Administrator agrees with this advice.
    Turning first to the results of the exposure assessment, the 
Administrator focused on the extent to which alternative standard 
levels, approximately at and below the 0.075 ppm O3 standard 
set in the 2008 final rule, are estimated to reduce exposures over the 
0.060 and 0.070 ppm health effects benchmark levels, for all and 
asthmatic school age children in the 12 urban areas included in the 
assessment.\52\ The Administrator also took note that the lowest 
standard level included in the exposure and health risk assessments was 
0.064 ppm and that additional reductions in exposures over the selected 
health benchmark levels would be anticipated for just meeting a 0.060 
ppm standard.
---------------------------------------------------------------------------

    \52\ As noted in section II.C.1.b.above, the Administrator 
focused on alternative standards with different levels but the same 
form and averaging time as the primary standard set in 2008.
---------------------------------------------------------------------------

    As an initial matter, the Administrator recognized that the concept 
of ``exposures of concern'' is more appropriately viewed as a 
continuum, with greater confidence and less uncertainty about the 
existence of health effects at the upper end and less confidence and 
greater uncertainty as one considers increasingly lower O3 
exposure levels. In considering the concept of exposures of concern, 
the Administrator also noted that it is important to balance concerns 
about the potential for health effects and their

[[Page 2995]]

severity with the increasing uncertainty associated with our 
understanding of the likelihood of such effects at lower O3 
levels. Within the context of this continuum, estimates of exposures of 
concern at discrete benchmark levels provide some perspective on the 
public health impacts of O3-related physiological effects 
that have been demonstrated in controlled human exposure and 
toxicological studies but cannot be evaluated in quantitative risk 
assessments, such as lung inflammation, increased airway 
responsiveness, and changes in host defenses. They also help in 
understanding the extent to which such impacts have the potential to be 
reduced by meeting alternative standards. As discussed in II.C.1.a 
above, these O3-related physiological effects are plausibly 
linked to the increased morbidity seen in epidemiological studies 
(e.g., as indicated by increased medication use in asthmatics, school 
absences in all children, and emergency department visits and hospital 
admissions in people with lung disease).
    Estimates of the number of people likely to experience exposures of 
concern cannot be directly translated into quantitative estimates of 
the number of people likely to experience specific health effects, 
since sufficient information to draw such comparisons is not 
available--if such information were available, these health outcomes 
would have been included in the quantitative risk assessment. Due to 
individual variability in responsiveness, only a subset of individuals 
who have exposures at and above a specific benchmark level are expected 
to experience such adverse health effects, and susceptible population 
groups such as those with asthma are expected to be affected more by 
such exposures than healthy individuals.
    For the reasons discussed in section II.C.1.b above, the 
Administrator has concluded that it is appropriate to focus on both the 
0.060 and 0.070 ppm health effect benchmarks for her decision on the 
primary standard. In summary, the focus on these two benchmark levels 
reflects the following evidence-based considerations, discussed above 
in section II.C.1.a, that raise concerns about adverse health effects 
likely occurring at levels below 0.080 ppm: (1) That there is limited, 
but important, new evidence from controlled human exposure studies 
showing lung function decrements and respiratory symptoms in some 
healthy subjects at 0.060 ppm; (2) that asthmatics are likely to have 
more serious responses than healthy individuals; (3) that lung function 
is not likely to be as sensitive a marker for O3 effects as 
lung inflammation; and (4) that there is epidemiological evidence which 
reports associations between ambient O3 concentrations and 
respiratory symptoms, ED visits, hospital admissions, and premature 
mortality in areas with O3 levels that extend well below 
0.080 ppm.
    Based on the exposure and risk considerations discussed in detail 
in the 2007 Staff Paper and presented in sections II.B and II.C.1.b 
above, the Administrator notes the following important observations 
from these assessments: (1) There is a similar pattern for all children 
and asthmatic school age children in terms of exposures of concern over 
selected benchmark levels when estimates are expressed in terms of 
percentage of the population; (2) the aggregate estimates of exposures 
of concern reflecting estimates for the 12 urban areas included in the 
assessment are considerably larger for the benchmark level of 0.060 ppm 
compared to the 0.070 ppm benchmark; (3) there is notable year-to-year 
variability in exposure and risk estimates with higher exposure and 
risk estimates occurring in simulations involving a year with generally 
poorer air quality in most areas (2002) compared to a year with 
generally better air quality (2004); and (4) there is significant city-
to-city variability in exposure and risk estimates, with some cities 
receiving considerably less protection associated with air quality just 
meeting the same standard. As discussed above, the Administrator 
believes that it is appropriate to consider not just the aggregate 
estimates across all cities, but also to consider the public health 
impacts in cities that receive relatively less protection from 
alternative standards under consideration. Similarly, the Administrator 
believes that year-to-year variability should also be considered in 
making judgments about which standards will protect public health with 
an adequate margin of safety.
    In addition, significant reductions in exposures of concern and 
risk have been estimated to occur across standard levels analyzed. The 
magnitudes of exposure and risk reductions estimated to occur in going 
from a 0.074 ppm standard to a 0.064 ppm standard are as large as those 
estimated to occur in going from the then current 0.084 ppm standard to 
a 0.074 ppm standard. Consequently, the reduction in risk that can be 
achieved by going from a standard of 0.074 ppm to a standard of 0.064 
ppm is comparable to the risk reduction that can be achieved by moving 
from the 1997 O3 standard, effectively a 0.084 ppm standard, 
to a standard very close to the 2008 standard of 0.075 ppm.
    The Administrator also observes that estimates of exposures of 
concern associated with air quality just meeting the alternative 
standards below 0.080 ppm (i.e., 0.074, 0.070, and 0.064 ppm, the 
levels included in the assessment) are notably lower than estimates for 
alternative standards set at and above 0.080 ppm. As shown in Table 6-8 
in the 2007 Staff Paper, just meeting a 0.080 ppm standard is 
associated with an aggregate estimate of exposures of concern of about 
13% of asthmatic children at the 0.070 ppm benchmark level, ranging up 
to 31% in the city with the least degree of protection in a year with 
generally poorer air quality, and an aggregate estimate of exposures of 
concern of about 40% of asthmatic children, ranging up to 63% in the 
city with the least degree of protection at the 0.060 ppm benchmark 
level. Based on the exposure estimates presented in Table 3 in this 
notice, she observes that standards included in the assessment below 
0.080 ppm (i.e., 0.074, 0.070, and 0.064 ppm), are estimated to have 
substantially lower estimates of exposures of concern at the 0.070 ppm 
benchmark level. Similarly, she notes that exposures of concern at the 
0.060 ppm benchmark associated with alternative standards below 0.080 
ppm are appreciably lower than exposures associated with standards at 
or above 0.080 ppm, especially for standards set at 0.064 and 0.070 
ppm.
    As noted previously, the Administrator also recognizes that the 
risk estimates for health outcomes included in the risk assessment are 
limited and that the overall health effects evidence is indicative of a 
much broader array of O3-related health effects that are 
part of a ``pyramid of effects'' that include various indicators of 
morbidity that could not be included in the risk assessment (e.g., 
school absences, increased medication use, doctor's visits, and 
emergency department visits), some of which have a greater impact on 
at-risk groups. Consideration of such unquantified risks for this array 
of health effects, taken together with the estimates of exposures of 
concern and the quantified health risks discussed above, supports the 
Administrator's evidence-based conclusion that revising the standard 
level to a level well below 0.080 ppm will provide important increased 
public health protection, especially for at-risk groups such as people 
with asthma or other lung disease, as well as children and older 
adults, particularly those active outdoors, and outdoor workers.

[[Page 2996]]

    Based on the evidence- and exposure/risk-based considerations 
discussed above, the Administrator concludes that it is appropriate to 
set the level of the primary O3 standard to a level well 
below 0.080 ppm, a level at which the evidence provides a high degree 
of certainty about the adverse effects of O3 exposure in 
healthy people, to provide an adequate margin of safety for at-risk 
groups. In selecting a proposed range of levels, the Administrator 
believes it is appropriate to consider the following information: (1) 
The strong body of evidence from controlled human exposure studies 
evaluating healthy people at exposure levels of 0.080 ppm and above 
that demonstrated lung function decrements, respiratory symptoms, 
pulmonary inflammation, and other medically significant airway 
responses, as well as limited but important evidence of lung function 
decrements and respiratory symptoms in healthy people down to 
O3 exposure levels of 0.060 ppm; (2) the substantial body of 
evidence from controlled human exposure and epidemiological studies 
indicating that people with asthma are likely to experience larger and 
more serious effects than healthy people; (3) the body of 
epidemiological evidence indicating associations are observed for a 
wide range of serious health effects, including respiratory-related 
emergency department visits and hospital admissions and premature 
mortality, across distributions of ambient O3 concentrations 
that extend below the current standard level of 0.075 ppm, as well as 
questions of biological plausibility in attributing the observed 
effects to O3 alone at the lower end of the concentration 
ranges extending down to background levels; and (4) the estimates of 
exposures of concern and risks for a range of health effects that 
indicate that important improvements in public health are very likely 
associated with O3 levels just meeting alternative 
standards, especially for standards set at 0.070 and 0.064 ppm (the 
lowest levels included in the assessment), relative to standards set at 
and above 0.080 ppm.
    The Administrator next considered what standard level well below 
0.080 ppm would be requisite to protect public health, including the 
health of at-risk groups, with an adequate margin of safety that is 
sufficient but not more than necessary to achieve that result. The 
assessment of a standard level calls for consideration of both the 
degree of risk to public health at alternative levels of the standard 
as well as the certainty that such risk will occur at any specific 
level. Based on the information available in the 2008 rulemaking, there 
is no evidence-based bright line that indicates a single appropriate 
level. Instead there is a combination of scientific evidence and other 
information that needs to be considered as a whole in making this 
public health policy judgment, and selecting a standard level from a 
range of potentially reasonable values.
    As an initial matter, the Administrator considered whether the 
standard level of 0.075 ppm set in the 2008 final rule is sufficiently 
below 0.080 ppm to be requisite to protect public health with an 
adequate margin of safety. In considering this standard level, the 
Administrator looked to the rationale for selecting this level 
presented in the 2008 final rule, as summarized above in section 
II.C.3. In that rationale, EPA observed that a level of 0.075 ppm is 
above the range of 0.060 to 0.070 ppm recommended by CASAC, and that 
the CASAC Panel appeared to place greater weight on the evidence from 
the Adams studies and on the results of the exposure and risk 
assessments, whereas EPA placed greater weight on the limitations and 
uncertainties associated with that evidence and the quantitative 
exposure and risk assessments. Additionally, EPA's rationale did not 
discuss and thus placed no weight on exposures of concern relative to 
the 0.060 ppm benchmark. Further, EPA concluded that ``[a] standard set 
at a lower level than 0.075 ppm would only result in significant 
further public health protection if, in fact, there is a continuum of 
health risks in areas with 8-hour average O3 concentrations 
that are well below the concentrations observed in the key controlled 
human exposure studies and if the reported associations observed in 
epidemiological studies are, in fact, causally related to O3 
at those lower levels. Based on the available evidence, [EPA] is not 
prepared to make these assumptions'' (73 FR 16483).
    In reconsidering the entire body of evidence available in the 2008 
rulemaking, including the Agency's own assessment of the 
epidemiological evidence in the 2006 Criteria Document, and placing 
significant weight on the views of CASAC, the Administrator now 
concludes that important and significant risks to public health are 
likely to occur at a standard level of 0.075 ppm. She judges that a 
standard level of 0.075 ppm is not sufficient to provide protection 
with an adequate margin of safety. In support of this conclusion, the 
Administrator finds that setting a standard that would protect public 
health, including the health of at-risk populations, with an adequate 
margin of safety should reasonably depend upon giving some weight to 
the results of the Adams studies and EPA's reanalysis of the Adams's 
data, and to how effectively alternative standard levels would serve to 
limit exposures of concern relative to the 0.060 ppm benchmark level as 
well as to the 0.070 ppm benchmark level. The Administrator notes that 
EPA's risk assessment estimates comparable risk reductions in going 
from a 0.074 ppm standard to a 0.064 ppm standard as were estimated in 
going from the then current 0.084 ppm standard down to a 0.074 ppm 
standard for an array of health effects analyzed. These estimates 
include reductions in risk for lung function decrements in all and 
asthmatic school age children, respiratory symptoms in asthmatic 
children, respiratory-related hospital admissions, and non-accidental 
mortality.
    Further, based on the exposure assessment estimates discussed 
above, the Administrator notes that for air quality just meeting a 
0.074 ppm standard, approximately 27% of asthmatic school age children 
and 25% of all school age children are estimated to experience one or 
more exposures of concern over the 0.060 ppm benchmark level based on 
simulations for a year with generally poorer air quality; this estimate 
increases to about 50% of asthmatic and all children in the city with 
the least degree of protection. The Administrator judges that these 
estimates are large and strongly suggest significant public health 
impacts would likely remain in many areas with air quality just meeting 
a 0.075 ppm O3 standard.
    In light of these estimates and the available evidence, the 
Administrator agrees with CASAC's conclusion that important public 
health protections can be achieved by a standard set below 0.075 ppm, 
within the range of 0.060 to 0.070 ppm. In addition, based on both the 
evidence- and exposure/risk-based considerations summarized above, the 
Administrator concludes that a standard set as high as 0.075 would not 
be considered requisite to protect public health with an adequate 
margin of safety, and that consideration of lower levels is warranted. 
In considering such lower levels, the Administrator recognizes that the 
CAA requires her to reach a public health policy judgment as to what 
standard would be requisite to protect public health with an adequate 
margin of safety, based on scientific evidence and technical 
assessments that have inherent uncertainties and limitations. This 
judgment requires making reasoned decisions as to what weight to place 
on various types of

[[Page 2997]]

evidence and assessments and on the related uncertainties and 
limitations.
    In selecting a level below 0.075 ppm that would serve as an 
appropriate upper end for a range of levels to propose, the 
Administrator has considered a more cautious approach to interpreting 
the available evidence and exposure/risk-based information--that is, an 
approach that places significant weight on uncertainties and 
limitations in the information so as to avoid potentially 
overestimating public health risks and protection likely to be 
associated with just meeting a particular standard level. In so doing, 
she notes that the most certain evidence of adverse health effects from 
exposure to O3 comes from the controlled human exposure 
studies, and that the large bulk of this evidence derives from studies 
of exposures at levels of 0.080 ppm and above. At those levels, there 
is consistent evidence of lung function decrements and respiratory 
symptoms in healthy young adults, as well as evidence of inflammation 
and other medically significant airway responses. Further, she takes 
note of the limited but important evidence from controlled human 
exposure studies indicating that lung function decrements and symptoms 
can occur in healthy people at levels as low as 0.060 ppm, while also 
recognizing the limitations in that evidence, as discussed above in 
sections II.A.1 and II.C.1.a. She also notes that some people with 
asthma are likely to experience larger and more serious effects than 
the healthy subjects evaluated in the controlled exposure studies, 
while recognizing that there is uncertainty about the magnitude of such 
differences. In considering the available epidemiological studies, she 
recognizes that they provide evidence of serious respiratory morbidity 
effects, including respiratory-related emergency department visits and 
hospital admissions, and non-accidental mortality at levels well below 
0.080 ppm, while also recognizing that there is increasing uncertainty 
associated with the likelihood that such effects occur at decreasing 
O3 levels down to background levels. Considering the 
exposure/risk information, as shown in Table 3, the Administrator 
observes that a standard set at 0.070 ppm would likely substantially 
limit exposures of concern relative to the 0.070 ppm benchmark level, 
while affording far less protection against exposures of concern 
relative to the 0.060 ppm benchmark level. To the extent that more 
weight is placed on protection relative to the higher benchmark level, 
and more weight is placed on the uncertainties associated with the 
epidemiological evidence, a standard set at 0.070 ppm might be 
considered to be adequately protective. Taken together, this type of 
cautious approach to interpreting the evidence and the exposure/risk 
information serves as the basis for the Administrator's conclusion that 
the upper end of the proposed range should be set at 0.070 ppm 
O3.
    In selecting a level that would serve as an appropriate lower end 
for a range of levels to propose, the Administrator has considered a 
more precautionary approach to interpreting the available evidence and 
exposure/risk-based information--that is, an approach that places less 
weight on uncertainties and limitations in the information so as to 
avoid potentially underestimating public health improvements likely to 
be associated with just meeting a particular standard level. In so 
doing, the Administrator notes the limited, but important evidence of a 
lowest-observed-effects level at 0.060 ppm O3 from 
controlled human exposure studies reporting lung function decrements 
and respiratory symptoms in healthy subjects. Notably, these studies 
also report that a small percentage of subjects (7 to 20 percent) 
experienced moderate lung function decrements (>= 10 percent) at the 
0.060 ppm exposure level, recognizing that for people with lung 
disease, such moderate functional or symptomatic responses would likely 
interfere with normal activity for many individuals, and would likely 
result in more frequent use of medication. In addition, a substantial 
body of evidence indicates that people with asthma are likely to 
experience larger and more serious effects than healthy people and 
therefore controlled human exposure studies done with healthy subjects 
likely underestimate effects in this at-risk population.
    Moreover, epidemiological studies provide evidence of serious 
respiratory morbidity effects, including respiratory-related emergency 
department visits and hospital admissions, and non-accidental mortality 
at O3 levels that may plausibly extend down to at least 
0.060 ppm even when considering the uncertainties inherent in such 
studies. The Administrator notes that the controlled human exposure 
studies conducted at 0.060 ppm provide some biological plausibility for 
associations between respiratory morbidity and mortality effects found 
in epidemiological studies and O3 exposures down to 0.060 
ppm. Considering the exposure information, as shown in Table 3, the 
Administrator observes that a standard set at 0.064 ppm would likely 
essentially eliminate exposures of concern relative to the 0.070 ppm 
benchmark level, while appreciably limiting exposures of concern 
relative to the 0.060 ppm benchmark level to approximately 6 percent of 
asthmatic children in the aggregate across 12 cities and up to 16 
percent in the city that would receive the least protection. While not 
addressed in the exposure assessment done as part of the 2008 
rulemaking, a standard set at 0.060 ppm would be expected to provide 
somewhat greater protection from such exposures, which is important to 
the extent that more weight is placed on providing protection relative 
to the lower benchmark level. Taken together, the Administrator 
concludes that this precautionary approach to interpreting the evidence 
and the exposure/risk information supports a level of 0.060 ppm as the 
lower end of the proposed range.
    The Administrator has also concluded that the lower end of the 
proposed range should not extend below 0.060 ppm O3. In 
reaching this conclusion, she gives significant weight to the 
recommendation of the CASAC panel that 0.060 ppm should be the lower 
end of the range for consideration (Henderson, 2006c). In the 
Administrator's view, the evidence from controlled human exposure 
studies at the 0.060 ppm exposure level, the lowest level tested, is 
not robust enough to support consideration of a lower level. While some 
epidemiological studies provide evidence of serious respiratory 
morbidity effects and non-accidental mortality with no evidence of a 
threshold, the Administrator notes that other studies provide evidence 
of a potential threshold somewhat below 0.060 ppm. Moreover, there are 
limitations in epidemiological studies that make discerning population 
thresholds difficult, including fewer observations in the range of 
lower concentrations, concerns related to exposure measurement error, 
the possible role of copollutants and effects modifiers, and 
interindividual differences in susceptibility to O3-related 
effects. In the Administrator's judgment, these limitations in 
epidemiological studies, including the limitations in judging the 
causality of observed associations at lower O3 levels, and 
the lack of robust controlled human exposure data at 0.060 ppm make it 
difficult to interpret this evidence as a basis for a standard level 
set below 0.060 ppm. Thus, in selecting 0.060 ppm as the lower end of 
the range for the proposed level of the O3 standard, the 
Administrator has taken into

[[Page 2998]]

account information on the lowest-observed-effects levels in controlled 
human exposure studies, indications of possible thresholds reported in 
some epidemiological studies, the increasing uncertainty in the 
epidemiological evidence at even lower levels, as well as evidence 
about increased susceptibility of people with asthma and also other 
lung diseases. In so doing, she concludes that a primary O3 
standard set below 0.060 ppm would be more than is necessary to protect 
public health with an adequate margin of safety for at-risk groups.
    In reaching her proposed decision, the Administrator has also 
considered the public comments that were received on the 2007 proposed 
rule (72 FR 37818). The Administrator notes that there were sharply 
divergent views expressed by two general sets of commenters with regard 
to considering the health effects evidence, results of exposure and 
risk assessments, and the advice of the CASAC panel. On one hand, 
medical groups, health effects researchers, public health 
organizations, environmental groups, and some state, tribal and local 
air pollution control agencies strongly supported a standard set within 
the range recommended by the CASAC. These commenters generally placed 
significant weight on the more recent evidence from controlled human 
exposure studies, down to the 0.060 ppm exposure level, as well as on 
the epidemiological studies and the results of the exposure and risk 
assessment conducted for the 2008 rulemaking. Many of these commenters 
took a more precautionary view and supported a standard set at 0.060 
ppm O3, the lower end of the CASAC recommended range. The 
Administrator notes that these views are generally consistent with her 
proposed conclusions. On the other hand, another group of commenters 
primarily representing industry associations and businesses and some 
state environmental agencies, primarily expressed the view that the 
more recent evidence from controlled human exposure, the 
epidemiological studies, and the results of exposure and human health 
risk assessments were so uncertain that they did not provide a basis 
for making any changes to the then current 0.084 ppm O3 
standard set in 1997. This group of commenters generally argued that 
the health effects evidence newly available in the 2008 rulemaking, the 
results of the exposure and health risk assessments, and the advice of 
the CASAC were flawed. For the reasons discussed above, the 
Administrator does not agree with the later group of commenters that 
essentially no weight should be placed on any of the new evidence or 
assessments that were available for consideration in the 2008 
rulemaking.
    Based on consideration of the entire body of evidence and 
information available in the 2008 rulemaking, including exposure and 
risk estimates, as well as the recommendations of CASAC, the 
Administrator proposes to set the level of the primary 8-hour 
O3 standard to a level within the range of 0.060 to 0.070 
ppm. A standard level within this range would reduce the risk of a 
variety of health effects associated with exposure to O3, 
including the respiratory symptoms and lung function effects 
demonstrated in the controlled human exposure studies, and the 
respiratory-related emergency department visits, hospital admissions 
and mortality effects observed in the epidemiological studies. All of 
these effects are indicative of a much broader array of O3-
related health endpoints, such as school absences and increased 
medication use, that are plausibly linked to these observed effects. 
Depending on the weight placed on the evidence and information 
available in the 2008 rulemaking, as well as the uncertainties and 
limitations in the evidence and information, a standard could be set 
within this range at a level that would be requisite to protect public 
health with an adequate margin of safety.
    In reaching this proposed decision, as discussed above, the 
Administrator has focused on the nature of the increased public health 
protection that would be afforded by a standard set within the proposed 
range of levels relative to the protection afforded by the standard set 
in 2008. Having considered the public comments received on the 2007 
proposed rule in reaching this proposed decision that reconsiders the 
2008 final rule, the Administrator is interested in again receiving 
public comment on the benefits to public health associated with a 
standard set at specific levels within the proposed range relative to 
the benefits associated with the standard set in 2008.

D. Proposed Decision on the Level of the Primary Standard

    For the reasons discussed above, and taking into account 
information and assessments presented in the 2006 Criteria Document and 
2007 Staff Paper, the advice and recommendations of CASAC, and public 
comments received during the 2008 rulemaking, the Administrator 
proposes to set a new level for the 8-hour primary O3 
standard. Specifically, the Administrator proposes to set the level of 
the 8-hour primary O3 standard to within a range of 0.060 to 
0.070 ppm. The proposed 8-hour primary standard would be met at an 
ambient air monitoring site when the 3-year average of the annual 
fourth-highest daily maximum 8-hour average O3 concentration 
is less than or equal to the level of the standard that is promulgated. 
Thus, the Administrator proposes to set a standard with a level within 
this range. She solicits comment on this range and on the appropriate 
weight to place on the various types of available evidence, the 
exposure and risk assessment results, and the uncertainties and 
limitations related to this information, as well as on the benefits to 
public health associated with a standard set within this range relative 
to the benefits associated with the standard set in 2008.

III. Communication of Public Health Information

    Information on the public health implications of ambient 
concentrations of criteria pollutants is currently made available 
primarily through EPA's Air Quality Index (AQI) program. The current 
Air Quality Index has been in use since its inception in 1999 (64 FR 
42530). It provides accurate, timely, and easily understandable 
information about daily levels of pollution (40 CFR 58.50). The AQI 
establishes a nationally uniform system of indexing pollution levels 
for O3, carbon monoxide, nitrogen dioxide, particulate 
matter and sulfur dioxide. The AQI converts pollutant concentrations in 
a community's air to a number on a scale from 0 to 500. Reported AQI 
values enable the public to know whether air pollution levels in a 
particular location are characterized as good (0-50), moderate (51-
100), unhealthy for sensitive groups (101-150), unhealthy (151-200), 
very unhealthy (201-300), or hazardous (300-500). The AQI index value 
of 100 typically corresponds to the level of the short-term NAAQS for 
each pollutant. An AQI value greater than 100 means that a pollutant is 
in one of the unhealthy categories (i.e., unhealthy for sensitive 
groups, unhealthy, very unhealthy, or hazardous) on a given day; 
whereas an AQI value at or below 100 means that a pollutant 
concentration is in one of the satisfactory categories (i.e., moderate 
or good). Decisions about the pollutant concentrations at which to set 
the various AQI breakpoints, that delineate the various AQI categories, 
draw directly from the underlying health information that supports the 
NAAQS review.

[[Page 2999]]

    In the 2008 rulemaking, the AQI for O3 was revised by 
setting an AQI value of 100 equal to 0.075 ppm, 8-hour average, the 
level of the revised primary O3 standard. The other AQI 
breakpoints were also revised as follows: An AQI value of 50 is set at 
0.059 ppm; an AQI value of 150 was set at 0.095 ppm; and an AQI value 
of 200 was set at 0.115 ppm. All these levels are averaged over 8 
hours. These levels were developed by making proportional adjustments 
to the other AQI breakpoints (i.e., AQI values of 50, 150 and 200).
    The Agency recognizes the importance of revising the AQI in a 
timely manner to be consistent with any revisions to the NAAQS. 
Therefore, having proposed to set a new level for the 2008 primary 8-
hour O3 standard in this action, EPA also proposes to 
finalize conforming changes to the AQI in connection with the Agency's 
final decision on the level of the primary O3 standard. 
These conforming changes would include setting the 100 level of the AQI 
at the same level as that set for the primary O3 standard 
resulting from this rulemaking, and also making proportional 
adjustments to AQI breakpoints at the lower end of the range (i.e., AQI 
values of 50, 150 and 200). EPA does not propose to change breakpoints 
at the higher end of the range (from 300 to 500), which would apply to 
state contingency plans or the Significant Harm Level (40 CFR 51.16), 
because the information from this reconsideration of the 2008 final 
rule does not inform decisions about breakpoints at those higher 
levels.
    With respect to reporting requirements (40 CFR Part 58, Sec.  
58.50), EPA proposes to require that the AQI be reported in all 
metropolitan and micropolitan statistical areas where O3 
monitoring is required, as discussed below in section VI. The Agency 
solicits comments on our proposed approach to AQI reporting 
requirements. We are also revising 40 CFR Part 58, Sec.  58.50(c) to 
require the reporting requirements to be based on the latest available 
census figures, rather than the most recent decennial U.S. census. This 
change is consistent with our current practice of using the latest 
population figures to make monitoring requirements more responsive to 
changes in population.

IV. Rationale for Proposed Decision on the Secondary Standard

    As an initial matter, the Administrator notes that the 2008 final 
rule concluded that (1) the protection afforded by the 1997 secondary 
O3 standard was ``not sufficient and that the standard needs 
to be revised to provide additional protection from known and 
anticipated adverse effects on sensitive natural vegetation and 
sensitive ecosystems, and that such a revised standard could also be 
expected to provide additional protection to sensitive ornamental 
vegetation'' and (2) ``that there is not adequate information to 
establish a separate secondary standard based on other effects of 
O3 on public welfare'' (73 FR 16497). The Administrator is 
not reconsidering these aspects of the 2008 decision, which are based 
on the reasons discussed in section IV.B of the 2008 final rule (73 FR 
16489-16497). The Administrator also notes that the 2008 final rule 
concluded that it was appropriate to retain the O3 indicator 
for the secondary O3 standard. The Administrator is not 
reconsidering this aspect of the 2008 decision, which was based on the 
reasons discussed in sections IV.B and IV.C of the 2008 final rule (73 
FR 16489-16497). For these reasons, the Administrator is not reopening 
the 2008 decision with regard to the need to revise the 1997 secondary 
O3 standard to provide additional protection from known and 
anticipated adverse effects on sensitive natural vegetation and 
sensitive ecosystems, nor with regard to the appropriate indicator for 
the secondary standard. Thus, the information that follows in this 
section specifically focuses on a reconsideration of the 8-hour 
secondary O3 standard set in the 2008 final rule for the 
purpose of determining whether and, if so, how to revise the form, 
averaging time, and level of the standard to provide appropriate 
protection from known and anticipated adverse effects on sensitive 
natural vegetation and sensitive ecosystems.
    This section presents the rationale for the Administrator's 
proposed decision that the secondary O3 standard, which was 
set identical to the revised primary standard in the 2008 final rule, 
should instead be a new cumulative, seasonal standard. This standard is 
expressed in terms of a concentration-weighted form commonly called 
W126, which uses a sigmoidal weighting function to assign a weight to 
each hourly O3 concentration within the 12-hour daylight 
period (8 am to 8 pm). This daily ozone index is defined as follows:
[GRAPHIC] [TIFF OMITTED] TP19JA10.000

    The daily index values are then summed over each month within the 
O3 season, and the annual highest consecutive three month 
sum is determined. The proposed standard consists of the three-year 
average of this highest three-month statistic, set at a level within 
the range of 7 to 15 ppm-hours.
    As discussed more fully below, the rationale for this proposed new 
standard is based on a thorough review, in the 2006 Criteria Document, 
of the latest scientific information on vegetation, ecological and 
other public welfare effects associated with the presence of 
O3 in the ambient air. This rationale also takes into 
account and is consistent with: (1) Staff assessments of the most 
policy-relevant information in the 2006 Criteria Document and staff 
analyses of air quality, vegetation effects evidence, exposure, and 
risks, presented in the 2007 Staff Paper, upon which staff 
recommendations for revisions to the secondary O3 standard 
are based; (2) CASAC advice and recommendations as reflected in 
discussions of drafts of the 2006 Criteria Document and 2007 Staff 
Paper at public meetings, in separate written comments, and in CASAC's 
letters to the Administrator, both before and after the 2008 
rulemaking, and (3) public comments received during development of 
these documents, either in conjunction with CASAC meetings or 
separately; and on the 2007 proposed rule, and (4) consideration of the 
degree of protection to vegetation potentially afforded by the 2008 8-
hour standard.
    In developing this rationale, the Administrator has again focused 
on direct O3 effects on vegetation, specifically drawing 
upon an integrative synthesis of the entire body of evidence (EPA, 
2006a, chapter 9), published through early 2006, on the broad array of 
vegetation effects associated with the presence of O3 in the 
ambient air. In addition, because O3 can also indirectly 
affect other ecosystem components such as soils, water, and wildlife, 
and their associated ecosystem goods and services, through its effects 
on vegetation, a qualitative discussion of these other indirect impacts 
is also

[[Page 3000]]

included, though these effects were not quantifiable at the time of the 
2008 rulemaking. As discussed below in section IV.A, the peer-reviewed 
literature includes studies conducted in the U.S., Canada, Europe, and 
many other countries around the world.\53\ In reconsidering this 
evidence, as was concluded in the 2008 rulemaking, and based on the 
body of scientific literature assessed in the 2006 Criteria Document, 
the Administrator continues to believe that it is reasonable to 
conclude that a secondary standard protecting the public welfare from 
known or anticipated adverse effects to trees and native vegetation 
would also afford increased protection from adverse effects to other 
environmental components relevant to the public welfare, including 
ecosystem services and function. Section IV.B focuses on considerations 
related to biologically relevant exposure indices. This rationale also 
draws upon the results of quantitative exposure and risk assessments, 
discussed below in section IV.C. Section IV.D focuses on the 
considerations upon which the Administrator's proposed conclusions are 
based. Considerations regarding a cumulative seasonal standard as well 
as an 8-hour standard are discussed, and the rationale for the 2008 
decision on the secondary standard and CASAC advice, given both prior 
to the development of the 2007 proposed rule and following the 2008 
final rule, are summarized. Finally, the Administrator's proposed 
conclusions on the secondary standard are presented. Section IV.E 
summarizes the proposed decision on the secondary O3 
standard and the solicitation of public comments.
---------------------------------------------------------------------------

    \53\ In its assessment of the evidence judged to be most 
relevant to making decisions on the level of the O3 
secondary standard, however, EPA has placed greater weight on U.S. 
studies, due to the often species-, site- and climate-specific 
nature of O3-related vegetation response.
---------------------------------------------------------------------------

    As with virtually any policy-relevant vegetation effects research, 
there is uncertainty in the characterization of vegetation effects 
attributable to exposure to ambient O3. As discussed below, 
however, research conducted since the 1997 review provides important 
information coming from field-based exposure studies, including free 
air, gradient, and biomonitoring surveys, in addition to the more 
traditional open top chamber (OTC) studies. Moreover, the newly 
available studies evaluated in the 2006 Criteria Document have 
undergone intensive scrutiny through multiple layers of peer review and 
many opportunities for public review and comment. While important 
uncertainties remain, the review of the vegetation effects information 
has been extensive and deliberate. In the judgment of the 
Administrator, the intensive evaluation of the scientific evidence that 
has occurred provides an adequate basis for this reconsideration of the 
2008 rulemaking.

A. Vegetation Effects Information

    This section outlines key information contained in the 2006 
Criteria Document (chapter 9) and in the 2007 Staff Paper (chapter 7) 
on known or anticipated effects on public welfare associated with the 
presence of O3 in ambient air. The information highlighted 
here summarizes: (1) New information available in the 2008 rulemaking 
on potential mechanisms for vegetation effects associated with exposure 
to O3; (2) the nature of effects on vegetation that have 
been associated with exposure to O3 and consequent potential 
impacts on ecosystems; and (3) considerations in characterizing what 
constitutes an adverse welfare impact of O3.
    Exposures to O3 have been associated quantitatively and 
qualitatively with a wide range of vegetation effects. The decision in 
the 1997 review to set a more protective secondary standard primarily 
reflected consideration of the quantitative information on vegetation 
effects available at that time, particularly growth impairment (e.g., 
biomass loss) in sensitive forest tree species during the seedling 
growth stage and yield loss in important commercial crops. This 
information, derived mainly using the open top chamber (OTC) exposure 
method, found cumulative, seasonal O3 exposures were most 
strongly associated with observed vegetation response. The 2006 
Criteria Document discusses a number of additional studies that support 
and strengthen key conclusions regarding O3 effects on 
vegetation and ecosystems found in the previous Criteria Document (EPA, 
1996a, 2006a), including further clarification of the underlying 
mechanistic and physiological processes at the sub-cellular, cellular, 
and whole system levels within the plant. More importantly, however, in 
the context of this review, new quantitative information is now 
available across a broader array of vegetation effects (e.g., growth 
impairment during seedlings, saplings and mature tree growth stages, 
visible foliar injury, and yield loss in annual crops) and across a 
more diverse set of exposure methods, including chamber, free air, 
gradient, model, and field-based observation. The non-chambered, field-
based study results begin to address one of the key data gaps cited by 
EPA in the 1997 review.
    The following discussion of the policy-relevant science regarding 
vegetation effects associated with cumulative, seasonal exposures to 
ambient levels of O3 integrates information from the 2006 
Criteria Document (chapter 9) and the 2007 Staff Paper (chapter 7).
1. Mechanisms
    Scientific understanding regarding O3 impacts at the 
genetic, physiological, and mechanistic levels helps to explain the 
biological plausibility and coherence of the evidence for 
O3-induced vegetation effects and informs the interpretation 
of predictions of risk associated with vegetation response at ambient 
O3 exposure levels. In most cases, the mechanisms of 
response are similar regardless of the degree of sensitivity of the 
species. The evidence assessed in the 2006 Criteria Document (EPA, 
2006a) regarding the O3-induced changes in physiology 
continues to support the information discussed in the 1997 review (EPA, 
1996a, 2006a). In addition, during the last decade understanding of the 
cellular processes within plants has been further clarified and 
enhanced. This section reviews the key scientific conclusions 
identified in 1996 Criteria Document (EPA, 1996a), and incorporates 
recent information from the Criteria Document (EPA, 2006a). This 
section describes: (1) Plant uptake of O3, (2) 
O3-induced cellular to systemic response, (3) plant 
compensation and detoxification mechanisms, (4) O3-induced 
changes to plant metabolism, and (5) plant response to chronic 
O3 exposures.
a. Plant Uptake of Ozone
    To cause injury, O3 must first enter the plant through 
openings in the leaves called stomata. Leaves exist in a three 
dimensional environment called the plant canopy, where each leaf has a 
unique orientation and receives a different exposure to ambient air, 
microclimatological conditions, and sunlight. In addition, a plant may 
be located within a stand of other plants which further modifies 
ambient air exchange with individual leaves. Not all O3 
entering a plant canopy is absorbed into the leaf stomata, but may be 
adsorbed to other surfaces e.g., leaf cuticles, stems, and soil (termed 
non-stomatal deposition) or scavenged by reactions with intra-canopy 
biogenic VOCs and naturally occurring NOx emissions from soils. Because 
O3 does not typically penetrate the leaf's cuticle, it must 
reach the stomatal openings in the leaf for absorption to occur. The

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movement of O3 and other gases such as CO2 into 
and out of leaves is controlled by stomatal guard cells that regulate 
the size of the stomatal apertures. These guard cells respond to a 
variety of internal species-specific factors as well as external site 
specific environmental factors such as light, temperature, humidity, 
CO2 concentration, soil fertility, water status, and in some 
cases, the presence of air pollutants, including O3. These 
modifying factors produce stomatal conductances that vary between 
leaves of the same plant, individuals and genotypes within a species as 
well as diurnally and seasonally.
b. Cellular to Systemic Response
    Once inside the leaf, O3 can react with a variety of 
biochemical compounds that are exposed to the air spaces within the 
leaf or it can be dissolved into the water lining the cell wall of the 
air spaces. Once in the aqueous phase, O3 can be rapidly 
altered to form oxidative products that can diffuse more readily into 
and through the cell and react with many biochemical compounds. Early 
steps in a series of O3-induced events that can lead to leaf 
injury seems to involve alteration in cell membrane function, including 
membrane transport properties (EPA, 2006a) and/or reactions with 
organic molecules that in certain circumstances result in the 
generation of signaling compounds. The generation of such signaling 
compounds can lead to a cascade of events. One such signaling molecule 
is hydrogen peroxide (H2O2). The presence of 
higher-than-normal levels of H2O2 within the leaf 
is a potential trigger for a set of metabolic reactions that include 
those typical of the well documented ``wounding'' response or pathogen 
defense pathway generated by cutting of the leaf or by pathogen/insect 
attack. Ethylene is another compound produced when plants are subjected 
to biotic or abiotic stressors. Increased ethylene production by plants 
exposed to O3 stress was identified as a consistent marker 
for O3 exposure in studies conducted decades ago (Tingey et 
al., 1976).
c. Compensation and Detoxification
    Ozone injury will not occur if (1) the rate and amount of 
O3 uptake is small enough for the plant to detoxify or 
metabolize O3 or its metabolites or (2) the plant is able to 
repair or compensate for the O3 impacts (Tingey and Taylor, 
1982; U.S. EPA, 1996a). With regard to the first, a few studies have 
documented direct stomatal closure or restriction in the presence of 
O3 in some species, which limits O3 uptake and 
potential subsequent injury. This response may be initiated ranging 
from within minutes to hours or days of exposure (Moldau et al., 1990; 
Dann and Pell, 1989; Weber et al., 1993). However, exclusion of 
O3 simultaneously restricts the uptake of CO2, 
which also limits photosynthesis and growth. In addition, antioxidants 
present in plants can effectively protect tissue against damage from 
low levels of oxidants by dissipating excess oxidizing power. Since 
1996, the role of detoxification in providing a level of resistance to 
O3 has been further investigated. A number of antioxidants 
have been found in plants. However, the pattern of changes in the 
amounts of these antioxidants varies greatly among different species 
and conditions. Most recent reports indicate that ascorbate within the 
cell wall provides the first significant opportunity for detoxification 
to occur. In spite of the new research, however, it is still not clear 
as to what extent detoxification protects against O3 injury. 
Specifically, data are needed on potential rates of antioxidant 
production, sub-cellular location(s) of antioxidants, and whether 
generation of these antioxidants in response to O3-induced 
stress potentially diverts resources and energy away from other vital 
uses. Thus, the 2006 Criteria Document concludes that scientific 
understanding of the detoxification mechanisms is not yet complete and 
requires further investigation (EPA, 2006a).
    Regarding the second, once O3 injury has occurred in 
leaf tissue, some plants are able to repair or compensate for the 
impacts. In general, plants have a variety of compensatory mechanisms 
for low levels of stress including reallocation of resources, changes 
in root/shoot ratio, production of new tissue, and/or biochemical 
shifts, such as increased photosynthetic capacity in new foliage and 
changes in respiration rates, indicating possible repair or replacement 
of damaged membranes or enzymes. Since these mechanisms are genetically 
determined, not all plants have the same complement of compensatory 
mechanisms or degree of tolerance, and these may vary over the life of 
the plant as not all stages of a plant's development are equally 
sensitive to O3. At higher levels or over longer periods of 
O3 stress, some of these compensatory mechanisms, such as a 
reallocation of resources away from storage in the roots in favor of 
leaves or shoots, could occur at a cost to the overall health of the 
plant. However, it is not yet clear to what degree or how the use of 
plant resources for repair or compensatory processes affects the 
overall carbohydrate budget or subsequent plant response to 
O3 or other stresses (EPA, 1996a, EPA, 2006a).
d. Changes to Plant Metabolism
    Ozone inhibits photosynthesis, the process by which plants produce 
energy rich compounds (e.g., carbohydrates) in the leaves. This 
impairment can result from direct impact to chloroplast function and/or 
O3-induced stomatal closure resulting in reduced uptake of 
CO2. A large body of literature published since 1996 has 
further elucidated the mechanism of effect of O3 within the 
chloroplast. Pell et al. (1997) showed that O3 exposure 
results in a loss of the central carboxylating enzyme that plays an 
important role in the production of carbohydrates. Due to its central 
importance, any decrease in this enzyme may have severe consequences 
for the plant's productivity. Several recent studies have found that 
O3 has a greater effect as leaves age, with the greatest 
impact of O3 occurring on the oldest leaves (Fiscus et al., 
1997; Reid and Fiscus, 1998; Noormets et al., 2001; Morgan et al., 
2004). The loss of this key enzyme as a function of increasing 
O3 exposure is also linked to an early senescence or a 
speeding up of normal development leading to senescence. If total plant 
photosynthesis is sufficiently reduced, the plant will respond by 
reallocating the remaining carbohydrate at the level of the whole 
organism (EPA, 1996a, 2006a). This reallocation of carbohydrate away 
from the roots into above ground vegetative components can have serious 
implications for perennial species, as discussed below.
e. Plant Response to Chronic Ozone Exposures
    Though many changes that occur with O3 exposure can be 
observed within hours, or perhaps days, of the exposure, including 
those connected with wounding, other effects take longer to occur and 
tend to become most obvious after chronic seasonal exposures to low 
O3 concentrations. These lower chronic exposures have been 
linked to senescence or some other physiological response very closely 
linked to senescence. In perennial plant species, a reduction in 
carbohydrate storage in one year may result in the limitation of growth 
the following year (Andersen et al., 1997). Such ``carry-over'' effects 
have been documented in the growth of tree seedlings (Hogsett et al., 
1989; Sasek et al., 1991; Temple et al., 1993; EPA, 1996a) and in roots 
(Andersen et al., 1991; EPA, 1996a). Though it is not fully understood 
how chronic seasonal O3 exposure affects long-term growth 
and resistance to other biotic and abiotic

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insults in long-lived trees, accumulation of these carry-over effects 
over time could affect survival and reproduction.
2. Nature of Effects
    Ozone injury at the cellular level can accumulate sufficiently to 
induce effects at the level of a whole leaf or plant. These larger 
scale effects can include: Reduced carbohydrate production and/or 
reallocation; reduced growth and/or reproduction; visible foliar injury 
and/or premature senescence; and reduced plant vigor. Much of what is 
now known about these O3-related effects, as summarized 
below, is based on research that was available in the 1997 review. 
Studies available in the 2008 rulemaking continue to support and expand 
this knowledge (EPA, 2006a).
a. Carbohydrate Production and Allocation
    When total plant photosynthesis is sufficiently reduced, the plant 
will respond by reallocating the remaining carbohydrate at the level of 
the whole organism. Many studies have demonstrated that root growth is 
more sensitive to O3 exposure than stem or leaf growth (EPA, 
2006a). When fewer carbohydrates are present in the roots, less energy 
is available for root-related functions such as acquisition of water 
and nutrients. In addition, by inhibiting photosynthesis and the amount 
of carbohydrates available for transfer to the roots, O3 can 
disrupt the association between soil fungi and host plants. Fungi in 
the soil form a symbiotic relationship with many terrestrial plants. 
For host plants, these fungi improve the uptake of nutrients, protect 
the roots against pathogens, produce plant growth hormones, and may 
transport carbohydrates from one plant to another (EPA, 1996a). These 
below ground effects have recently been documented in the field (Grulke 
et al., 1998; Grulke and Balduman, 1999). Data from a long-studied 
pollution gradient in the San Bernardino Mountains of southern 
California suggest that O3 substantially reduces root growth 
in natural stands of Ponderosa pine (Pinus ponderosa). Root growth in 
mature trees was decreased at least 87 percent in a high-pollution site 
as compared to a low-pollution site (Grulke et al., 1998), and a 
similar pattern was found in a separate study with whole-tree harvest 
along this gradient (Grulke and Balduman, 1999). Though effects on 
other ecosystem components were not examined, a reduction of root 
growth of this magnitude could have significant implications for the 
below-ground communities at those sites. Because effects on leaf and 
needle carbohydrate content under O3 stress can range from a 
reduction (Barnes et al., 1990; Miller et al., 1989), to no effect 
(Alscher et al., 1989), to an increase (Luethy-Krause and Landolt, 
1990), studies that examine only above-ground vegetative components may 
miss important O3-induced changes below ground. These below-
ground changes could signal a shift in nutrient cycling with 
significance at the ecosystem level (Young and Sanzone, 2002).
b. Growth Effects on Trees
    Studies comparing the O3-related growth response of 
different vegetation types (coniferous and deciduous) and growth stages 
(e.g., seedling and mature) have established that on average, 
individual coniferous trees are less sensitive than deciduous trees, 
and deciduous trees are generally less sensitive to O3 than 
most annual plants, with the exception of a few fast growing deciduous 
tree species (e.g., quaking aspen, black cherry, and cottonwood), which 
are highly sensitive and, in some cases, as much or more sensitive to 
O3 than sensitive annual plants. In addition, studies have 
shown that the relationship between O3 sensitivity in 
seedling and mature growth stages of trees can vary widely, with 
seedling growth being more sensitive to O3 exposures in some 
species, while in others, the mature growth stage is the more 
O3 sensitive. In general, mature deciduous trees are likely 
to be more sensitive to O3 than deciduous seedlings, and 
mature evergreen trees are likely to be less sensitive to O3 
than their seedling counterparts. Based on these results, stomatal 
conductance, O3 uptake, and O3 effects cannot be 
assumed to be equivalent in seedlings and mature trees.
    In the 1997 review (EPA, 1996b), analyses of the effects of 
O3 on trees were limited to 11 tree species for which 
concentration-response (C-R) functions for the seedling growth stage 
had been developed from OTC studies conducted by the National Health 
and Environmental Effects Research Lab, Western Ecology Division 
(NHEERL-WED). A number of replicate studies were conducted on these 
species, leading to a total of 49 experimental cases. The 2007 Staff 
Paper presented a graph of the composite regression equation that 
combines the results of the C-R functions developed for each of the 49 
cases. The NHEERL-WED study predicted relative biomass loss at various 
exposure levels in terms of a 12-hour W126. For example, 50 percent of 
the tree seedling cases would be protected from greater than 10 percent 
biomass loss at a 3-month, 12-hour W126 of approximately 24 ppm-hour, 
while 75 percent of cases would be protected from 10 percent biomass 
loss at a 3-month, 12-hour W126 level of approximately 16 ppm-hour.
    Since the 1997 review, only a few studies have developed C-R 
functions for additional tree seedling species (EPA, 2006a). One such 
study is of particular importance because it documented growth effects 
in the field of a similar magnitude as those previously seen in OTC 
studies but without the use of chambers or other fumigation methods 
(Gregg et al., 2003). This study placed eastern cottonwood (Populus 
deltoides) saplings at sites along a continuum of ambient O3 
exposures that gradually increased from urban to rural areas in the New 
York City area (Gregg et al., 2003). Eastern cottonwood is a fast 
growing O3 sensitive tree species that is important 
ecologically along streams and commercially for pulpwood, furniture 
manufacturing, and as a possible new source for energy biomass (Burns 
and Hankola, 1990). Gregg et al. (2003) found that the cottonwood 
saplings grown in urban New York City grew faster than saplings grown 
in downwind rural areas. Because these saplings were grown in pots with 
carefully controlled soil nutrient and moisture levels, the authors 
were able to control for most of the differences between sites. After 
carefully considering these and other factors, the authors concluded 
the primary explanation for the difference in growth was the gradient 
of cumulative O3 exposures that increased as one moved 
downwind from urban to less urban and more rural sites. It was 
determined that the lower O3 exposure within the city center 
was due to NOX titration reactions which removed 
O3 from the ambient air. The authors were able to reproduce 
the growth responses observed in the field in a companion OTC 
experiment, confirming O3 as the stressor inducing the 
growth loss response (Gregg et al., 2003).
    Another recent set of studies employed a modified Free Air 
CO2 Enrichment (FACE) methodology to expose vegetation to 
elevated O3 without the use of chambers. This exposure 
method was originally developed to expose vegetation to elevated levels 
of CO2, but was later modified to include O3 
exposure in Illinois (SoyFACE) and Wisconsin (AspenFACE) for soybean 
and deciduous trees, respectively (Dickson et al., 2000; Morgan et al., 
2004). The FACE method releases gas (e.g., CO2, 
O3) from a series of orifices placed along the length of the 
vertical pipes surrounding a circular field plot and uses the

[[Page 3003]]

prevailing wind to distribute it. This exposure method has many 
characteristics that differ from those associated with the OTC. Most 
significantly, this exposure method more closely replicates conditions 
in the field than do OTCs. This is because, except for O3 
levels which are varied across co-located plots, plants are exposed to 
the same ambient growing conditions that occur naturally in the field 
(e.g., location-specific pollutant mixtures; climate conditions such as 
light, temperature and precipitation; insect pests, pathogens). By 
using one of several co-located plots as a control (e.g., receives no 
additional O3), and by exposing the other rings to differing 
levels of elevated O3, the growth response signal that is 
due solely to the change in O3 exposure can be clearly 
determined. Furthermore, the FACE system can expand vertically with the 
growth of trees, allowing for exposure experiments to span numerous 
years, an especially useful capability in forest research.
    On the other hand, the FACE methodology also has the undesirable 
characteristic of potentially creating hotspots near O3 gas 
release orifices or gradients of exposure in the outer ring of trees 
within the plots, such that averaging results across the entire ring 
potentially overestimates the response. In recognition of this 
possibility, researchers at the AspenFACE experimental site only 
measured trees in the center core of each ring, (e.g., at least 5-6 
meters away from the emission sites of O3) (Dickson et al., 
2000, Karnosky et al., 2005). By taking this precaution, it is unlikely 
that their measurements were influenced by any potential hotspots or 
gradients of exposure within the FACE rings. Taking all of the above 
into account, results from the Wisconsin FACE site on quaking aspen 
appear to demonstrate that the detrimental effects of O3 
exposure seen on tree growth and symptom expression in OTCs can be 
observed in the field using this exposure method (Karnosky et al., 
1999; 2005).
    The 2007 Staff Paper thus concluded that the combined evidence from 
the AspenFACE and Gregg et al. (2003) field studies provide compelling 
and important support for the appropriateness of continued use of the 
C-R functions derived using OTC from the NHEERL-WED studies to estimate 
risk to these tree seedlings under ambient field exposure conditions. 
These studies make a significant contribution to the coherence of the 
weight of evidence available in this review and provide additional 
evidence that O3-induced effects observed in chambers also 
occur in the field.
    Trees and other perennials, in addition to cumulating the effects 
of O3 exposures over the annual growing season, can also 
cumulate effects across multiple years. It has been reported that 
effects can ``carry over'' from one year to another (EPA, 2006a). 
Growth affected by a reduction in carbohydrate storage in one year may 
result in the limitation of growth in the following year (Andersen et 
al., 1997). Carry-over effects have been documented in the growth of 
some tree seedlings (Hogsett et al., 1989; Simini et al., 1992; Temple 
et al., 1993) and in roots (Andersen et al., 1991; EPA, 1996a). On the 
basis of past and recent OTC and field study data, ambient 
O3 exposures that occur during the growing season in the 
United States are sufficient to potentially affect the annual growth of 
a number of sensitive seedling tree species. However, because most 
studies do not take into account the possibility of carry over effects 
on growth in subsequent years, the true implication of these annual 
biomass losses may be missed. It is likely that under ambient exposure 
conditions, some sensitive trees and perennial plants could experience 
compounded impacts that result from multiple year exposures.
c. Visible Foliar Injury
    Cellular injury to leaves due to exposure to O3 can and 
often does become visible. Acute injury usually appears within 24 hours 
after exposure to O3 and, depending on species, can occur 
under a range of exposures and durations from 0.040 ppm for a period of 
4 hours to 0.410 ppm for 0.5 hours for crops and 0.060 ppm for 4 hours 
to 0.510 ppm for 1 hour for trees and shrubs (Jacobson, 1977). Chronic 
injury may be mild to severe. In some cases, cell death or premature 
leaf senescence may occur. The significance of O3 injury at 
the leaf and whole plant levels depends on how much of the total leaf 
area of the plant has been affected, as well as the plant's age, size, 
developmental stage, and degree of functional redundancy among the 
existing leaf area. As a result, it is not presently possible to 
determine, with consistency across species and environments, what 
degree of injury at the leaf level has significance to the vigor of the 
whole plant.
    The presence of visible symptoms due to O3 exposures 
can, however, by itself, represent an adverse impact to the public 
welfare. Specifically, it can reduce the market value of certain leafy 
crops (such as spinach, lettuce), impact the aesthetic value of 
ornamentals (such as petunia, geranium, and poinsettia) in urban 
landscapes, and affect the aesthetic value of scenic vistas in 
protected natural areas such as national parks and wilderness areas. 
Many businesses rely on healthy looking vegetation for their 
livelihoods (e.g., horticulturalists, landscapers, Christmas tree 
growers, farmers of leafy crops) and a variety of ornamental species 
have been listed as sensitive to O3 (Abt Associates Inc., 
1995). Though not quantified, there is likely some level of economic 
impact to businesses and homeowners from O3-related injury 
on sensitive ornamental species due to the cost associated with more 
frequent replacement and/or increased maintenance (fertilizer or 
pesticide application). In addition, because O3 not only 
results in discoloration of leaves but can lead to more rapid 
senescence (early shedding of leaves) there potentially could be some 
lost tourist dollars at sites where fall foliage is less available or 
attractive.
    The use of sensitive plants as biological indicators to detect 
phytotoxic levels of O3 is a longstanding and effective 
methodology (Chappelka and Samuelson, 1998; Manning and Krupa, 1992). 
Each bioindicator exhibits typical O3 injury symptoms when 
exposed under appropriate conditions. These symptoms are considered 
diagnostic as they have been verified in exposure-response studies 
under experimental conditions. In recent years, field surveys of 
visible foliar injury symptoms have become more common, with greater 
attention to the standardization of methods and the use of reliable 
indicator species (Campbell et al., 2000; Smith et al., 2003). 
Specifically, the United States Forest Service (USFS) through the 
Forest Health Monitoring Program (FHM) (1990-2001) and currently the 
Forest Inventory and Analysis (FIA) Program collects data regarding the 
incidence and severity of visible foliar injury on a variety of 
O3 sensitive plant species throughout the U.S. (Coulston et 
al., 2003, 2004; Smith et al., 2003).
    Since the conclusion of the 1997 review, the FIA monitoring program 
network and database has continued to expand. This network continues to 
document foliar injury symptoms in the field under ambient exposure 
conditions. Recent survey results show that O3-induced 
foliar injury incidence is widespread across the country. The visible 
foliar injury indicator has been identified as a means to track 
O3 exposure stress trends in the nation's natural plant 
communities as highlighted in EPA's most recent Report on the 
Environment (EPA, 2003a; http://www.epa.gov/indicators/roe).

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    Previous Criteria Documents have noted the difficulty in relating 
visible foliar injury symptoms to other vegetation effects such as 
individual tree growth, stand growth, or ecosystem characteristics 
(EPA, 1996a) and this difficulty remains to the present day (EPA, 
2006a). It is important to note that direct links between O3 
induced visible foliar injury symptoms and other adverse effects are 
not always found. Therefore, visible foliar injury cannot serve as a 
reliable surrogate measure for other O3-related vegetation 
effects because other effects (e.g., biomass loss) have been reported 
with and without visible injury. In some cases, visible foliar symptoms 
have been correlated with decreased vegetative growth (Karnosky et al., 
1996; Peterson et al., 1987; Somers et al., 1998) and with impaired 
reproductive function (Black et al., 2000; Chappelka, 2002). Therefore, 
the lack of visible injury should not be construed to indicate a lack 
of phytotoxic concentrations of O3 nor absence of other non-
visible O3 effects.
d. Reduced Plant Vigor
    Though O3 levels over most of the U.S. are not high 
enough to kill vegetation directly, current levels have been shown to 
reduce the ability of many sensitive species and genotypes within 
species to adapt to or withstand other environmental stresses. These 
O3 effects may include increased susceptibility to freezing 
temperatures, increased vulnerability to pest infestations and/or root 
disease, and compromised ability to compete for available resources. As 
an example of the latter, when species with differing O3-
sensitivities occur together, O3-sensitive species may 
experience a greater reduction in growth than more O3-
tolerant species, which then can better compete for available 
resources. The result of such above effects can produce a loss in plant 
vigor in O3-sensitive species that over time may lead to 
premature plant death.
e. Ecosystems
    Ecosystems are comprised of complex assemblages of organisms and 
the physical environment with which they interact. Each level of 
organization within an ecosystem has functional and structural 
characteristics. At the ecosystem level, functional characteristics 
include, but are not limited to, energy flow; nutrient, hydrologic, and 
biogeochemical cycling; and maintenance of food chains. The sum of the 
functions carried out by ecosystem components provides many benefits to 
humankind, as in the case of forest ecosystems (Smith, 1992). Some of 
these benefits, also termed ``ecosystem goods and services'', include 
food, fiber production, aesthetics, genetic diversity, maintenance of 
water quality, air quality, and climate, and energy exchange. A 
conceptual framework for discussing the effects of stressors, including 
air pollutants such as O3, on ecosystems was developed by 
the EPA Science Advisory Board (Young and Sanzone, 2002). In this 
report, the authors identify six essential ecological attributes (EEAs) 
of ecosystems including landscape condition, biotic condition, 
chemical/physical condition, ecological processes, hydrology/
geomorphology, and natural disturbance regime. Each EEA is depicted as 
one of six triangles that together build a hexagon. On the outside of 
each triangle is a list of stressors that can act on the EEA. 
Tropospheric O3 is listed as a stressor of both biotic 
condition and the chemical/physical condition of ecosystems. As each 
EEA is linked to all the others, it is clearly envisioned in this 
framework that O3 could either directly or indirectly impact 
all of the EEAs associated with an ecosystem that is being stressed by 
O3.
    Vegetation often plays an influential role in defining the 
structure and function of an ecosystem, as evidenced by the use of 
dominant vegetation forms to classify many types of natural ecosystems, 
e.g., tundra, wetland, deciduous forest, and conifer forest. Plants 
simultaneously inhabit both above-and below-ground environments, 
integrating and influencing key ecosystem cycles of energy, water, and 
nutrients. When a sufficient number of individual plants within a 
community have been affected, O3-related effects can be 
propagated up to ecosystem-level effects. Thus, through its impact on 
vegetation, O3 can be an important ecosystem stressor.
i. Potential Ozone Alteration of Ecosystem Structure and Function
    The 2006 Criteria Document outlines seven case studies where 
O3 effects on ecosystems have either been documented or are 
suspected. The oldest and clearest example involves the San Bernardino 
Mountain forest ecosystem in California. This system experienced 
chronic high O3 exposures over a period of 50 or more years. 
The O3-sensitive and co-dominant species of ponderosa and 
Jeffrey pine demonstrated severe levels of foliar injury, premature 
senescence, and needle fall that decreased the photosynthetic capacity 
of stressed pines and reduced the production of carbohydrates resulting 
in a decrease in radial growth and in the height of stressed trees. It 
was also observed that ponderosa and Jeffrey pines with slight to 
severe crown injury lost basal area in relation to competing species 
that are more tolerant to O3. Due to a loss of vigor, these 
trees eventually succumbed to the bark beetle, leading to elevated 
levels of tree death. Increased mortality of susceptible trees shifted 
the community composition towards white fir and incense cedar, 
effectively reversing the development of the normal fire climax mixture 
dominated by ponderosa and Jeffrey pines, and leading to increased fire 
susceptibility. At the same time, numerous other organisms and 
processes were also affected either directly or indirectly, including 
successional patterns of fungal microflora and their relationship to 
the decomposer community. Nutrient availability was influenced by the 
heavy litter and thick needle layer under stands with the most severe 
needle injury and defoliation. In this example, O3 appeared 
to be a predisposing factor that led to increased drought stress, 
windthrow, root diseases, and insect infestation (Takemoto et al., 
2001). Thus, through its effects on tree water balance, cold hardiness, 
tolerance to wind, and susceptibility to insect and disease pests, 
O3 potentially impacted the ecosystem-related EEA of natural 
disturbance regime (e.g., fire, erosion). Although the role of 
O3 was extremely difficult to separate from other 
confounding factors, such as high nitrogen deposition, there is 
evidence that this shift in species composition has altered the 
structure and dynamics of associated food webs (Pronos et al., 1999) 
and carbon (C) and nitrogen (N) cycling (Arbaugh et al., 2003). Ongoing 
and new research in this important ecosystem is needed to reveal the 
extent to which ecosystem services have been affected and to what 
extent strong causal linkages between historic and/or current ambient 
O3 exposures and observed ecosystem-level effects can be 
made.
    Ozone has also been reported to be a selective pressure among 
sensitive tree species (e.g., eastern white pine) in the east. The 
nature of community dynamics in eastern forests is different, however, 
than in the west, consisting of a wider diversity of species and uneven 
aged stands, and the O3 levels are less severe. Therefore, 
lower level chronic O3 stress in the east is more likely to 
produce subtle long-term forest responses such as shifts in species 
composition, rather than wide-spread community degradation.
    Some of the best-documented studies of population and community 
response

[[Page 3005]]

to O3 effects are the long-term studies of common plantain 
(Plantago major) in native plant communities in the United Kingdom 
(Davison and Reiling, 1995; Lyons et al., 1997; Reiling and Davison, 
1992c). Elevated O3 significantly decreased the growth of 
sensitive populations of common plantain (Pearson et al., 1996; Reiling 
and Davison, 1992a, b; Whitfield et al., 1997) and reduced its fitness 
as determined by decreased reproductive success (Pearson et al., 1996; 
Reiling and Davison, 1992a). While spatial comparisons of population 
responses to O3 are complicated by other environmental 
factors, rapid changes in O3 resistance were imposed by 
ambient levels and variations in O3 exposure (Davison and 
Reiling, 1995). Specifically, in this case study, it appeared that 
O3-sensitive individuals are being removed by O3 
stress and the genetic variation represented in the population could be 
declining. If genetic diversity and variation is lost in ecosystems, 
there may be increased vulnerability of the system to other biotic and 
abiotic stressors, and ultimately a change in the EEAs and associated 
services provided by those ecosystems.
    Recent free-air exposure experiments have also provided new insight 
into how O3 may be altering ecosystem structure and function 
(Karnosky et al., 2005). For example, a field O3 exposure 
experiment at the AspenFACE site in Wisconsin (described in section 
IV.A.2.b. above) was designed to examine the effects of both elevated 
CO2 and O3 on mixed stands of aspen (Populus 
tremuloides), birch (Betula papyrifera), and sugar maple (Acer 
saccharum) that are characteristic of Great Lakes aspen-dominated 
forests (Karnosky et al., 2003; Karnosky et al., 1999). They found 
evidence that the effects on above- and below-ground growth and 
physiological processes have cascaded through the ecosystem, even 
affecting microbial communities (Larson et al., 2002; Phillips et al., 
2002). This study also confirmed earlier observations of O3-
induced changes in trophic interactions involving keystone tree 
species, as well as important insect pests and their natural enemies 
(Awmack et al., 2004; Holton et al., 2003; Percy et al., 2002).
    Collectively these examples suggest that O3 is an 
important stressor in natural ecosystems, but it is difficult to 
quantify the contribution of O3 due to the combination of 
other stresses present in ecosystems. In most cases, because only a few 
components in each of these ecosystems have been examined and 
characterized for O3 effects, the full extent of ecosystem 
changes in these example ecosystems is not fully understood. Clearly, 
there is a need for highly integrated ecosystem studies that 
specifically investigate the effect of O3 on ecosystem 
structure and function in order to fully determine the extent to which 
O3 is altering ecosystem services. Continued research, 
employing new approaches, will be necessary to fully understand the 
extent to which O3 is affecting ecosystem services.
ii. Effects on Ecosystem Services and Carbon Sequestration
    Since it has been established that O3 affects 
photosynthesis and growth of plants, O3 is most likely 
affecting the productivity of forest ecosystems. Therefore, it is 
desirable to link effects on growth and productivity to essential 
ecosystem services. However, it is very difficult to quantify 
ecosystem-level productivity losses because of the amount of complexity 
in scaling from the leaf-level or individual plant to the ecosystem 
level, and because not all organisms in an ecosystem are equally 
affected by O3.
    Terrestrial ecosystems are important in the Earth's carbon (C) 
balance and could help offset emissions of CO2 by humans if 
anthropogenic C is sequestered in vegetation and soils. The annual 
increase in atmospheric CO2 is less than the total inputs 
from fossil fuel burning and land use changes (Prentice et al., 2001), 
and much of this discrepancy is thought to be attributable to 
CO2 uptake by plant photosynthesis (Tans & White, 1998). 
Temperate forests of the northern hemisphere have been estimated to be 
a net sink of about 0.6 to 0.7 petagrams (Pg) C per year (Goodale et 
al. 2002). Ozone interferes with photosynthesis, causes some plants to 
senesce leaves prematurely, and in some cases, reduces allocation to 
stem and root tissue. Thus, O3 decreases the potential for C 
sequestration. For the purposes of this discussion, C sequestration is 
defined as the net exchange of carbon by the terrestrial biosphere. 
However, long-term storage in the soil organic matter is considered to 
be the most stable form of C storage in ecosystems.
    In a study including all ecosystem types, Felzer et al. (2004), 
estimated that U.S. net primary production (net flux of C into an 
ecosystem) was decreased by 2.6-6.8 percent due to O3 
pollution in the late 1980s to early 1990s. Ozone not only reduces C 
sequestration in existing forests, it can also affect reforestation 
projects (Beedlow et al. 2004). This effect, in turn, has been found to 
ultimately inhibit C sequestration in forest soils which act as long-
term C storage (Loya et al., 2003; Beedlow et al. 2004). The 
interaction of rising O3 pollution and rising CO2 
concentrations in the coming decades complicates predictions of future 
sequestration potential. Models generally predict that, in the future, 
C sequestration will increase with increasing CO2, but often 
do not account for the decrease in productivity due to the local 
effects of current or potentially increasing levels of tropospheric 
O3. In the presence of high O3 levels, the 
stimulatory effect of rising CO2 concentrations on forest 
productivity has been estimated to be reduced by more that 20 percent 
(Tingey et al., 2001; Ollinger et al. 2002; Karnosky et al., 2003).
    In summary, it would be anticipated that meeting lower 
O3 standards would increase the amount of CO2 
uptake by many ecosystems in the U.S. However, the amount of this 
improvement would be heavily dependent on the species composition of 
those ecosystems. Many ecosystems in the U.S. do have O3 
sensitive plants. For example, forest ecosystems with dominant species 
such as aspen or ponderosa pine would be expected to increase 
CO2 uptake more with lower O3 than forests with 
more O3 tolerant species.
    A recent critique of the secondary NAAQS review process published 
in the report by the National Academy of Sciences on Air Quality 
Management in the United States (NRC, 2004) stated that ``EPA's current 
practice for setting secondary standards for most criteria pollutants 
does not appear to be sufficiently protective of sensitive crops and 
ecosystems * * *'' This report made several specific recommendations 
for improving the secondary NAAQS process and concluded that ``There is 
growing evidence that tighter standards to protect sensitive ecosystems 
in the United States are needed. * * *'' An effort has been recently 
initiated within the Agency to identify indicators of ecological 
condition whose responses can be clearly linked to changes in air 
quality that are attributable to Agency environmental programs. Using a 
single indicator to represent the complex linkages and dynamic cycles 
that define ecosystem condition will always have limitations. With 
respect to O3-related impacts on ecosystem condition, only 
two candidate indicators, foliar injury (as described above) and radial 
growth in trees, have been suggested. Thus, while at the present time, 
most O3-related effects on ecosystems must be inferred from 
observed or predicted O3-related effects on individual 
plants, additional research at the ecosystem level could identify new 
indicators and/or establish stronger causal linkages

[[Page 3006]]

between O3-induced plant effects and ecosystem condition.
f. Yield Reductions in Crops
    Ozone can interfere with carbon gain (photosynthesis) and 
allocation of carbon with or without the presence of visible foliar 
injury. As a result of decreased carbohydrate availability, fewer 
carbohydrates are available for plant growth, reproduction, and/or 
yield. Recent studies have further confirmed and demonstrated 
O3 effects on different stages of plant reproduction, 
including pollen germination, pollen tube growth, fertilization, and 
abortion of reproductive structures, as reviewed by Black et al. 
(2000). For seed-bearing plants, these reproductive effects will 
culminate in reduced seed production or yield.
    As described in the 1997 review and again in the 2006 Criteria 
Document and 2007 Staff Paper, the National Crop Loss Assessment 
Network (NCLAN) studies undertaken in the early to mid-1980s provide 
the largest, most uniform database on the effects of O3 on 
agricultural crop yields. The NCLAN protocol was designed to produce 
crop exposure-response data representative of the areas in the U.S. 
where the crops were typically grown. In total, 15 species (e.g., corn, 
soybean, winter wheat, tobacco, sorghum, cotton, barley, peanuts, dry 
beans, potato, lettuce, turnip, and hay [alfalfa, clover, and fescue]), 
accounting for greater than 85 percent of U.S. agricultural acreage 
planted at that time, were studied. Of these 15 species, 13 species 
including 38 different cultivars were combined in 54 cases representing 
unique combinations of cultivars, sites, water regimes, and exposure 
conditions. Crops were grown under typical farm conditions and exposed 
in open-top chambers to ambient O3, sub-ambient 
O3, and above ambient O3. Robust C-R functions 
were developed for each of these crop species. These results showed 
that 50 percent of the studied cases would be protected from greater 
than 10 percent yield loss at a W126 level of 21 ppm-hour, while a W126 
of 13 ppm-hour would provide protection for 75 percent of the cases 
studied from greater than 10 percent yield loss.
    Recent studies continue to find yield loss levels in crop species 
studied previously under NCLAN that reflect the earlier findings. In 
other words, there has been no evidence that crops are becoming more 
tolerant of O3 (EPA, 2006a). For cotton, some newer 
varieties have been found to have higher yield loss due to 
O3 compared to older varieties (Olszyk et al., 1993, Grantz 
and McCool, 1992). In a meta-analysis of 53 studies, Morgan et al. 
(2003) found consistent deleterious effects of O3 exposures 
on soybean from studies published between 1973 and 2001. Further, early 
results from the field-based exposure experiment SoyFACE in Illinois 
indicate a lack of any apparent difference in the O3 
tolerance of old and recent cultivars of soybean in a study of 22 
soybean varieties (Long et al., 2002). Thus, the 2007 Staff Paper 
concluded that the recent scientific literature continues to support 
the conclusions of the 1996 Criteria Document that ambient 
O3 concentrations are reducing the yield of major crops in 
the U.S.
    In addition to the effects described on annual crop species, 
several studies published since the 1997 review have focused on 
perennial forage crops (EPA, 2006a). These recent results confirm that 
O3 is also impacting yields and quality of multiple-year 
forage crops at sufficient magnitude to have nutritional and possibly 
economic implications to their use as ruminant animal feed at 
O3 exposures that occur in some years over large areas of 
the U.S.
3. Adversity of Effects
    The 2007 Staff Paper recognized that the statute requires that a 
secondary standard be protective against ``adverse'' O3 
effects, not all identifiable O3-induced effects. In 
considering what constitutes a vegetation effect that is adverse to the 
public welfare, the 2007 Staff Paper recognizes that O3 can 
cause a variety of vegetation effects, beginning at the level of the 
individual cell and accumulating up to the level of whole leaves, 
plants, plant populations, communities and whole ecosystems, not all of 
which have been classified in past reviews as ``adverse'' to public 
welfare.
    Previous reviews have classified O3 vegetation effects 
as either ``injury'' or ``damage'' to help in determining adversity. 
Specifically, ``injury'' is defined as encompassing all plant 
reactions, including reversible changes or changes in plant metabolism 
(e.g., altered photosynthetic rate), altered plant quality, or reduced 
growth, that does not impair the intended use or value of the plant 
(Guderian, 1977). In contrast, ``damage'' has been defined to include 
those injury effects that reach sufficient magnitude as to also reduce 
or impair the intended use or value of the plant. Examples of effects 
that are classified as damage include reductions in aesthetic values 
(e.g., foliar injury in ornamental species) as well as losses in terms 
of weight, number, or size of the plant part that is harvested (reduced 
yield or biomass production). Yield loss also may include changes in 
crop quality, i.e., physical appearance, chemical composition, or the 
ability to withstand storage, while biomass loss includes slower growth 
in species harvested for timber or other fiber uses. While this 
construct has proved useful in the past, it appears to be most useful 
in the context of evaluating effects on single plants or species grown 
in monocultures such as agricultural crops or managed forests. It is 
less clear how it might apply to potential effects on natural forests 
or entire ecosystems when O3-induced species level impacts 
lead to shifts in species composition and/or associated ecosystem 
services such as nutrient cycling or hydrologic cycles, where the 
intended use or value of the system has not been specifically 
identified.
    A more recent construct for assessing risks to forests described in 
Hogsett et al. (1997) suggests that ``adverse effects could be 
classified into one or more of the following categories: (1) Economic 
production, (2) ecological structure, (3) genetic resources, and (4) 
cultural values.'' This approach expands the context for evaluating the 
adversity of O3-related effects beyond the species level. 
Another recent publication, A Framework for Assessing and Reporting on 
Ecological Condition: An SAB report (Young and Sanzone, 2002), provides 
additional support for expanding the consideration of adversity beyond 
the species level by making explicit the linkages between stress-
related effects (e.g., O3 exposure) at the species level and 
at higher levels within an ecosystem hierarchy. Taking this recent 
literature into account, the 2007 Staff Paper concludes that a 
determination of what constitutes an ``adverse'' welfare effect in the 
context of the secondary NAAQS review can appropriately occur within 
this broader paradigm.

B. Biologically Relevant Exposure Indices

    The 2006 Criteria Document concluded that O3 exposure 
indices that cumulate differentially weighted hourly concentrations are 
the best candidates for relating exposure to plant growth responses. 
This conclusion follows from the extensive evaluation of the relevant 
studies in the 1996 Criteria Document (EPA, 1996a) and the recent 
evaluation of studies that have been published since that time. The 
following selections, taken from the 1996 Criteria Document (EPA, 
1996a, section 5.5), further elucidate the depth and strength of these 
conclusions. Specifically, with respect to the importance of taking 
into account exposure duration, the 1996 Criteria Document stated, 
``when O3 effects are the primary cause of variation

[[Page 3007]]

in plant response, plants from replicate studies of varying duration 
showed greater reductions in yield or growth when exposed for the 
longer duration'' and ``the mean exposure index of unspecified duration 
could not account for the year-to-year variation in response'' (EPA, 
1996a, pg. 5-96). Further, ``because the mean exposure index treats all 
concentrations equally and does not specifically include an exposure 
duration component, the use of a mean exposure index for characterizing 
plant exposures appears inappropriate for relating exposure with 
vegetation effects'' (EPA, 1996a, pg. 5-88). Regarding the relative 
importance of higher concentrations than lower in determining plant 
response, the 1996 Criteria Document concluded that ``the ultimate 
impact of long-term exposures to O3 on crops and seedling 
biomass response depends on the integration of repeated peak 
concentrations during the growth of the plant'' (EPA, 1996a, pg. 5-
104). Further, ``at this time, exposure indices that weight the hourly 
O3 concentrations differentially appear to be the best 
candidates for relating exposure with predicted plant response'' (EPA, 
1996a, pgs. 5-136).
    At the conclusion of the 1997 review, the biological basis for a 
cumulative, seasonal form was not in dispute. There was general 
agreement between EPA and CASAC, based on their review of the air 
quality criteria, that a cumulative, seasonal form was more 
biologically based than the then current 1-hour and newly proposed 8-
hour average form. However, in selecting a specific form appropriate 
for a secondary standard, there was less agreement. An evaluation of 
the performance of several cumulative seasonal forms in predicting 
plant response data taken from OTC experiments had found that all 
performed about equally well and was unable to distinguish between them 
(EPA, 1996a). In selecting between two of these cumulative forms, the 
SUM06 \54\ and W126, in the absence of biological evidence to 
distinguish between them, EPA based its decision on both science and 
policy considerations. Specifically, these were: (1) All cumulative, 
peak-weighted exposure indices considered, including W126 and SUM06, 
were about equally good as exposure measures to predict exposure-
response relationships reported in the NCLAN crop studies; and (2) the 
SUM06 form would not be influenced by PRB O3 concentrations 
(defined at the time as 0.03 to 0.05 ppm) under many typical air 
quality distributions. On the basis of these considerations, EPA chose 
the SUM06 as the most appropriate cumulative, seasonal form to consider 
when proposing an alternative secondary standard form (61 FR 65716).
---------------------------------------------------------------------------

    \54\ The SUM06 index is defined as the sum of all hourly 
O3 concentrations greater or equal to 0.06 ppm over a 
specified time.
---------------------------------------------------------------------------

    Though the scientific justification for a cumulative, seasonal form 
was generally accepted in the 1997 review, an analysis undertaken by 
EPA at that time had shown that there was considerable overlap between 
areas that would be expected not to meet the range of alternative 8-
hour standards being considered for the primary NAAQS and those 
expected not to meet the range of values (expressed in terms of the 
seasonal SUM06 index) of concern for vegetation. This result suggested 
that improvements in national air quality expected to result from 
attaining an 8-hour primary standard within the recommended range of 
levels would also be expected to significantly reduce levels of concern 
for vegetation in those same areas. Thus, in the 1996 proposed rule, 
EPA proposed two alternatives for consideration: one alternative was to 
make the secondary standard equal in every way to the proposed 8-hour, 
0.08 ppm primary standard; and the second was to establish a 
cumulative, seasonal secondary standard in terms of a SUM06 form as 
also appropriate to protect public welfare from known or anticipated 
adverse effects given the available scientific knowledge and that such 
a seasonal standard ``* * * is more biologically relevant * * *'' (61 
FR 65716).
    In the 1997 final rule, EPA decided to make the secondary standard 
identical to the primary standard. The EPA acknowledged, however, that 
``it remained uncertain as to the extent to which air quality 
improvements designed to reduce 8-hr average O3 
concentrations averaged over a 3-year period would reduce O3 
exposures measured by a seasonal SUM06 index.'' (62 FR 38876) In other 
words, it was uncertain as to whether the 8-hour average form would, in 
practice, provide sufficient protection for vegetation from the 
cumulative, seasonal and concentration-weighted exposures described in 
the scientific literature as of concern.
    On the basis of that history, the 2007 Staff Paper (chapter 7) 
revisited the issue of whether the SUM06 was still the most appropriate 
choice of cumulative, seasonal form for a secondary standard to protect 
the public welfare from known and anticipated adverse vegetation 
effects in light of the new information available in this review. 
Specifically, the 2007 Staff Paper considered: (1) The continued lack 
of evidence within the vegetation effects literature of a biological 
threshold for vegetation exposures of concern; and (2) new estimates of 
PRB that were lower than in the 1997 review. The W126 form, also 
evaluated in the 1997 review, was again selected for comparison with 
the SUM06 form. Regarding the first consideration, the 2007 Staff Paper 
noted that the W126 form, by its incorporation of a continuous 
sigmoidal weighting scheme, does not create an artificially imposed 
concentration threshold, yet also gives proportionally more weight to 
the higher and typically more biologically potent concentrations, as 
supported by the scientific evidence. Second, the index value is not 
significantly influenced by O3 concentrations within the 
range of estimated PRB, as the weights assigned by the sigmoidal 
weighting scheme to concentrations in this range are near zero. Thus, 
it would also provide a more appropriate target for air quality 
management programs designed to reduce emissions from anthropogenic 
sources contributing to O3 formation. On the basis of these 
considerations, the 2007 Staff Paper concluded that the W126 form was 
the most biologically-relevant cumulative, seasonal form appropriate to 
consider in the context of the 2008 rulemaking.

C. Vegetation Exposure and Impact Assessment

    The vegetation exposure and impact assessment conducted for the 
2008 rulemaking and described in the 2007 Staff paper, consisted of 
exposure, risk and benefits analyses and improved and built upon 
similar analyses performed in the 1997 review (EPA 1996b). The 
vegetation exposure assessment was performed using interpolation and 
included information from ambient monitoring networks and results from 
air quality modeling. The vegetation risk assessment included both tree 
and crop analyses. The tree risk analysis includes three distinct lines 
of evidence: (1) Observations of visible foliar injury in the field 
linked to monitored O3 air quality for the years 2001-2004; 
(2) estimates of seedling growth loss under then current and 
alternative O3 exposure conditions; and (3) simulated mature 
tree growth reductions using the TREGRO model to simulate the effect of 
meeting alternative air quality standards on the predicted annual 
growth of a single western species (ponderosa pine) and two eastern 
species (red maple and tulip poplar). The crop analysis includes 
estimates of the risks to crop yields from then current and alternative

[[Page 3008]]

O3 exposure conditions and the associated change in economic 
benefits expected to accrue in the agriculture sector upon meeting the 
levels of various alternative standards. Each element of the assessment 
is described below, including discussions of known sources and ranges 
of uncertainties associated with the elements of this assessment.
1. Exposure Characterization
    Though numerous effects of O3 on vegetation have been 
documented as discussed above, it is important in considering risk to 
examine O3 air quality patterns in the U.S. relative to the 
location of O3 sensitive species that have a known 
concentration-response in order to predict whether adverse effects are 
occurring at current levels of air quality, and whether they are likely 
to occur under alternative standard forms and levels.
    The most important information about exposure to vegetation comes 
from the O3 monitoring data that are available from two 
national networks: (1) Air Quality System (AQS; http://www.epa.gov/ttn/airs/airsaqs) and (2) Clean Air Status and Trends Network (CASTNET; 
http://www.epa.gov/castnet/). The AQS monitoring network currently has 
over 1100 active O3 monitors which are generally sited near 
population centers. However, this network also includes approximately 
36 monitors located in national parks. CASTNET is the nation's primary 
source for data on dry acidic deposition and rural, ground-level 
O3. It consists of over 80 sites across the eastern and 
western U.S. and is cooperatively operated and funded with the National 
Park Service. In the 1997 O3 NAAQS final rule, it was 
acknowledged that because the national air quality surveillance network 
for O3 was designed principally to monitor O3 
exposure in populated areas, there was limited measured data available 
to characterize O3 air quality in rural and remote sites. 
Since the 1997 review, there has been a small increase in the number of 
CASTNET sites (from approximately 52 sites in 1992 to 84 sites in 
2004), however these monitors are not used for attainment designations.
    National parks represent areas of nationally recognized ecological 
and public welfare significance, which have been afforded a high level 
of protection by Congress. Two recent reports presented some discussion 
of O3 trends in a subset of national parks: The Ozone 
Report: Measuring Progress Through 2003 (EPA, 2004), and 2005 Annual 
Performance and Progress Report: Air Quality in National Parks (NPS, 
2005). Unfortunately, much of this information is presented only in 
terms of the current 8-hr average form. The 2007 Staff Paper analyzed 
available air quality data in terms of the cumulative 12-hour W126 form 
from 2001 to 2005 for a subset of national parks and other significant 
natural areas representing 4 general regions of the U.S. Many of these 
national parks and natural areas have monitored O3 levels 
above concentrations that have been shown to decrease plant growth and 
above the 12-hour W126 levels analyzed in this review. For example, the 
Great Smokey Mountain, Rocky Mountain, Grand Canyon, Yosemite and 
Sequoia National Parks all had more than one year within the 2001-2005 
period with a 12-hour W126 above 21 ppm-hour. This level of exposure 
has been associated with approximately no more than 10 percent biomass 
loss in 50 percent of the 49 tree seedling cases studied in the NHEERL-
WED experiments (Lee and Hogsett, 1996). Black cherry (Prunus 
serotina), an important O3-sensitive tree species in the 
eastern U.S., occurs in the Great Smoky Mountain National Park and is 
estimated to have O3-related seedling biomass loss of 
approximately 40 percent when exposed to a 3 month, 12-hour W126 
O3 level greater than 21 ppm-hour. Ponderosa pine (Pinus 
ponderosa) which occurs in the Grand Canyon, Yosemite and Sequoia 
National Parks has been reported to have approximately 10 percent 
biomass losses at 3 month, 12 hour W126 O3 levels as low as 
17 ppm-hour (Lee and Hogsett, 1996). Impacts on seedlings may 
potentially affect long-term tree growth and survival, ultimately 
affecting the competitiveness of O3-sensitive tree species 
and genotypes within forest stands.
    In order to characterize exposures to vegetation at the national 
scale, however, the 2007 Staff Paper concluded that it could not rely 
solely on limited site-specific monitoring data, and that it was 
necessary to select an interpolation method that could be used to 
characterize O3 air quality over broad geographic areas. The 
2007 Staff Paper therefore investigated the appropriateness of using 
the O3 outputs from the EPA/NOAA Community Multi-scale Air 
Quality (CMAQ) \55\ model system (http://www.epa.gov/asmdnerl/CMAQ, 
Byun and Ching, 1999; Arnold et al. 2003, Eder and Yu, 2005) to improve 
spatial interpolations based solely on existing monitoring networks. 
Due to the significant resources required to run CMAQ, model outputs 
were only available for a limited number of years. For the 2008 
rulemaking, the most recent outputs available at the time from CMAQ 
version 4.5 were for the year 2001.
---------------------------------------------------------------------------

    \55\ The CMAQ model is a multi-pollutant, multiscale air quality 
model that contains state-of-the-science techniques for simulating 
atmospheric and land processes that affect the transport, 
transformation, and deposition of atmospheric pollutants and/or 
their precursors on both regional and urban scales. It is designed 
as a science-based modeling tool for handling many major pollutants 
(including photochemical oxidants/O3, particulate matter, 
and nutrient deposition) holistically. The CMAQ model can generate 
estimates of hourly O3 concentrations for the contiguous 
U.S., making it possible to express model outputs in terms of a 
variety of exposure indices (e.g., W126, 8-hour average).
---------------------------------------------------------------------------

    Based on the significant difference in monitor network density 
between the eastern and western U.S., the 2007 Staff Paper concluded 
that it was appropriate to use separate interpolation techniques in 
these two regions. Only AQS and CASTNET monitoring data were used for 
the eastern interpolation, since it was determined that enhancing the 
interpolation with CMAQ data did not add much information to the 
eastern U.S. interpolation. In the western U.S., however, where rural 
monitoring is more sparse, O3 values generated by the CMAQ 
model were used to develop scaling factors to augment the 
interpolation.
    In order to characterize uncertainties associated with the 
interpolation method, monitored O3 concentrations were 
systematically compared to interpolated O3 concentrations in 
areas where monitors were located. In general, the interpolation method 
used in the current review performed well in many areas in the U.S., 
although it under-predicted higher 12-hour W126 exposures in rural 
areas. Due to the important influence of higher exposures in 
determining risks to plants, this feature of the interpolated surface 
could result in an under-estimation of risks to vegetation in some 
areas. Taking these uncertainties into account, and given the absence 
of more complete rural monitoring data, this approach was used in 
developing national vegetation exposure and risk assessments that 
estimate relative changes in risk for the various alternative standards 
analyzed.
    To evaluate changing vegetation exposures and risks under selected 
air quality scenarios, the 2007 Staff Paper utilized 2001 base year 
O3 air quality distributions that had been adjusted with a 
rollback method (Horst and Duff, 1995; Rizzo, 2005, 2006) to reflect 
meeting the then current and alternative secondary standard options. 
This technique combines both linear and quadratic elements to reduce 
higher O3

[[Page 3009]]

concentrations more than lower ones. In this regard, the rollback 
method attempts to account for reductions in emissions without greatly 
affecting lower concentrations. The following O3 air quality 
scenarios were analyzed: (1) 4th-highest daily maximum 8-hour average: 
0.084 ppm (the effective level of the then current standard) and 0.070 
ppm levels; (2) 3-month, 12-hour. SUM06: 25 ppm-hour (proposed in the 
1997 review) and 15 ppm-hour levels; and (3) 3-month, 12-hour W126: 21 
ppm-hour and 13 ppm-hour levels.
    The two 8-hour average levels were chosen as possible alternatives 
of the then current form for comparison with the cumulative, seasonal 
alternative forms. The SUM06 scenarios were very similar to the W126 
scenarios. Since the W126 was judged to be the more biologically-
relevant cumulative, seasonal form, only the results for the W126 
scenarios are summarized below. For the W126 form, the two levels were 
selected on the basis of the associated levels of tree seedling biomass 
loss and crop yield loss protection identified in the NHEERL-WED and 
NCLAN studies, respectively. Specifically, the upper level of W126 (21 
ppm-hour) was associated with a level of tree and crop protection of 
approximately no more than 10 percent growth or yield loss in 50 
percent of cases studied. Alternatively, the lower level of W126 (13 
ppm-hour) was associated with a level of tree seedling and crop 
protection of approximately no more than 10 percent growth or yield 
loss in 75 percent of studied cases.
    The following discussion highlights key observations drawn from 
comparing predicted changes in interpolated air quality under each 
alternative standard form and level scenario for the base year, 2001:
    (1) Under the base year (2001) ``as is'' air quality, a large 
portion of California had 12-hr W126 O3 levels above 31 ppm-
hour, which has been associated with approximately no more than 14 
percent biomass loss in 50 percent of tree seedling cases studies. 
Broader multi-state regions in the east (NC, TN, KY, IN, OH, PA, NJ, 
NY, DE, MD, VA) and west (CA, NV, AZ, OK, TX) are predicted to have 
levels of air quality above the W126 level of 21 ppm-hour, which is 
approximately equal to the secondary standard proposed in 1996 and is 
associated with approximately no more than 10 percent biomass loss in 
50 percent of tree seedling cases studied. Much of the east and Arizona 
and California have 12-hour W126 O3 levels above 13 ppm-
hour, which has been associated with approximately no more than 10 
percent biomass loss in 75 percent of tree seedling cases studied. The 
results of the exposure assessment indicate that current air quality 
levels could result in significant impacts to vegetation in some areas.
    (2) When 2001 air quality was rolled back to meet the then current 
8-hour, 0.084 ppm secondary standard, the overall 3-month 12-hour W126 
O3 levels were somewhat improved, but not substantially. 
Under this scenario, there were still many areas in California with 12-
hour W126 O3 levels above 31 ppm-hour. A broad multi-state 
region in the east (NC, TN, KY, IN, OH, PA, MD) and west (CA, NV, AZ, 
OK, TX) were still predicted to have O3 levels above the 
W126 level of 21 ppm-hour.
    (3) Exposures generated for just meeting a 0.070 ppm, 4th-highest 
maximum 8-hour average alternative standard showed substantially 
improved O3 air quality when compared to just meeting the 
then current 8-hour standard. Most areas were predicted to have 
O3 levels below the W126 level of 21 ppm-hour, although some 
areas in the east (KY, TN, MI, AR, MO, IL) and west (CA, NV, AZ, UT, 
NM, CO, OK, TX) were still predicted to have O3 levels above 
the W126 level of 13 ppm-hour.
    These results suggest that meeting a 0.070 ppm, 8-hour secondary 
standard would provide substantially improved protection in some areas 
for vegetation from seasonal O3 exposures of concern. The 
2007 Staff Paper recognizes, however, that some areas meeting a 0.070 
ppm 8-hour standard could continue to have elevated seasonal exposures, 
including forested park lands and other natural areas, and Class I 
areas which are federally mandated to preserve certain air quality 
related values. This is especially important in the high elevation 
forests in the Western U.S. where there are few O3 monitors. 
This is because the air quality patterns in remote areas can result in 
relatively low 8-hour averages while still experiencing relatively high 
cumulative exposures.
    To further characterize O3 air quality in terms of 
various secondary standard forms, an analysis was performed in the 2007 
Staff Paper to evaluate the extent to which county-level O3 
air quality measured in terms of various levels of the current 8-hour 
average form overlapped with that measured in terms of various levels 
of the 12-hour W126 cumulative, seasonal form. The 2007 Staff Paper 
presented this analysis using 2002-2004 \56\ county-level O3 
air quality data from AQS sites and the subset of CASTNET sites having 
the highest O3 levels for the counties in which they are 
located. Since the current 8-hour average secondary form is a 3-year 
average, the analysis initially compared the 3-year averages of both 
the 8-hour and W126 forms. In addition, recognizing that some 
vegetation effects (e.g. crop yield loss and foliar injury) are driven 
solely by annual O3 exposures and are typically evaluated 
with respect to exposures within the annual growing season, the 2007 
Staff Paper also presented a comparison of the current 3-year average 
8-hour form to the annual W126 form for the individual years, 2002 and 
2004.
---------------------------------------------------------------------------

    \56\ This analysis was updated using 2003-2005 air quality as it 
became available, finding similar results.
---------------------------------------------------------------------------

    Results of the 3-year average comparisons showed that of the 
counties with air quality meeting the 3-year average form of a 0.084 
ppm, 8-hour average standard, 7 counties showed 3-year average W126 
values above the 21 ppm-hour level. At the lower W126 level of 13 ppm-
hour, 135 counties with air quality meeting the 3-year average form of 
a 0.084 ppm, 8-hour average standard, would be above this W126 level. 
In addition, when the 3-year average of an 8-hour form was compared to 
annual W126 values, further variability in the degree of overlap 
between the 8-hour form and W126 form became apparent. For example, the 
relatively high 2002 O3 air quality year showed a greater 
degree of overlap between those areas that would meet the levels 
analyzed for the current 8-hour and alternative levels of the W126 form 
than did the relatively low O3 2004 air quality year. This 
lack of a consistent degree of overlap between the two forms in 
different air quality years demonstrates that annual vegetation would 
be expected to receive widely differing degrees of protection from 
cumulative seasonal exposures in some areas from year to year, even 
when the 3-year average of the 8-hour form was consistently met.
    It is clear that this analysis is limited by the lack of monitoring 
in rural areas where important vegetation and ecosystems are located, 
especially at higher elevation sites. This is because O3 air 
quality distributions at high elevation sites often do not reflect the 
typical urban and near-urban pattern of low morning and evening 
O3 concentrations with a high mid-day peak, but instead 
maintain relatively flat patterns with many concentrations in the mid-
range (e.g., 0.05-0.09 ppm) for extended periods. These conditions can 
lead to relatively low daily maximum 8-hour averages concurrently with 
high cumulative values so that there is potentially less overlap 
between an 8-

[[Page 3010]]

hour average and a cumulative, seasonal form at these sites. The 2007 
Staff Paper concluded that it is reasonable to anticipate that 
additional unmonitored rural high elevation areas important for 
vegetation may not be adequately protected even with a lower level of 
the 8-hour form.
    The 2006 Criteria Document discusses policy relevant background 
(PRB) levels for high elevation sites and makes the following 
observations: (1) PRB concentrations of 0.04 to 0.05 ppm occur 
occasionally at high-elevation sites (e.g., > 1.5 km) in the spring due 
to the free-tropospheric influence, including some limited contribution 
from hemispheric pollution (O3 produced from anthropogenic 
emissions outside North America); and (2) while stratospheric 
intrusions might occasionally elevate O3 at high-altitude 
sites, these events are rare at surface sites. Therefore, the 2007 
Staff Paper concluded that springtime PRB levels in the range 
identified above and rare stratospheric intrusions of O3 are 
unlikely to be a major influence on 3-month cumulative seasonal W126 
values.
    It further remains uncertain as to the extent to which air quality 
improvements designed to reduce 8-hour O3 average 
concentrations would reduce O3 exposures measured by a 
seasonal, cumulative W126 index. The 2007 Staff Paper indicated this to 
be an important consideration because: (1) The biological database 
stresses the importance of cumulative, seasonal exposures in 
determining plant response; (2) plants have not been specifically 
tested for the importance of daily maximum 8-hour O3 
concentrations in relation to plant response; and (3) the effects of 
attainment of a 8-hour standard in upwind urban areas on rural air 
quality distributions cannot be characterized with confidence due to 
the lack of monitoring data in rural and remote areas. These factors 
are important considerations in determining whether the current 8-hour 
form can appropriately provide requisite protection for vegetation.
2. Assessment of Risks to Vegetation
    The 2007 Staff Paper presents results from quantitative and 
qualitative risk assessments of O3 risks to vegetation (EPA, 
2007). In the 1997 review, crop yield and seedling biomass loss OTC 
data provided the basis for staff analyses, conclusions, and 
recommendations (EPA, 1996b). Since then, several additional lines of 
evidence have progressed sufficiently to provide staff with a more 
complete and coherent picture of the scope of O3-related 
vegetation risks, especially those faced by seedling, sapling and 
mature tree species growing in field settings, and indirectly, forested 
ecosystems. Specifically, research published after the 1997 review 
reflects an increased emphasis on field-based exposure methods (e.g., 
free air exposure and ambient gradient), improved field survey 
biomonitoring techniques, and mechanistic tree process models. Findings 
from each of these research areas are discussed separately below. In 
conducting these assessments, the Staff Paper analyses relied on both 
measured and modeled air quality information. For some effects, like 
visible foliar injury and modeled mature tree growth response, only 
monitored air quality information was used. For other effects 
categories (e.g., crop yield and tree seedling growth), staff relied on 
interpolated O3 exposures.
a. Visible Foliar Injury
    As discussed above (section IV.A.2.c), systematic injury surveys 
have documented visible foliar injury symptoms diagnostic of phytotoxic 
O3 exposures on sensitive bioindicator plants. These surveys 
have produced more expansive evidence than that available at the time 
of the 1997 review that visible foliar injury is occurring in many 
areas of the U.S. under current ambient conditions. The 2007 Staff 
Paper presents an assessment combining recent U.S. Forest Service 
Forest Inventory and Analysis (FIA) biomonitoring site data with the 
county level air quality data for those counties containing the FIA 
biomonitoring sites. This assessment showed that incidence of visible 
foliar injury ranged from 21 to 39 percent during the four-year period 
(2001-2004) across all counties with air quality levels at or below 
that of a 0.084 ppm, 8-hour standard. Of the counties that met an 8-
hour level of 0.070 ppm in those years, 11 to 30 percent still had 
incidence of visible foliar injury. The magnitude of these percentages 
suggests that phytotoxic exposures sufficient to induce visible foliar 
injury would still occur in many areas after meeting the level of a 
0.084 ppm secondary standard or alternative 0.070 ppm 8-hour standard. 
Additionally, the data showed that visible foliar injury occurrence was 
geographically widespread and occurring on a variety of plant species 
in forested and other natural systems. Linking visible foliar injury to 
other plant effects is still problematic. However, its presence 
indicates that other O3-related vegetation effects could 
also be present.
b. Seedling and Mature Tree Biomass Loss
    In the 1997 review, analyses of the effects of O3 on 
trees were limited to 11 tree species for which C-R functions for the 
seedling growth stage had been developed from OTC studies conducted by 
the NHEERL-WED. Important tree species such as quaking aspen, ponderosa 
pine, black cherry, and tulip poplar were found to be sensitive to 
cumulative seasonal O3 exposures. Work done since the 1997 
review at the AspenFACE site in Wisconsin on quaking aspen (Karnosky et 
al., 2005) and a gradient study performed in the New York City area 
(Gregg et al. 2003) has confirmed the detrimental effects of 
O3 exposure on tree growth in field studies without chambers 
and beyond the seedling stage (King et al. 2005). These field studies 
are discussed above in section IV.A.
    To update the seedling biomass loss risk analysis, C-R functions 
for biomass loss for available seedling tree species taken from the 
2006 Criteria Document and information on tree growing regions derived 
from the U.S. Department of Agriculture's Atlas of United States Trees 
were combined with projections of O3 air quality based on 
2001 interpolated exposures, to produce estimated biomass loss for each 
of the seedling tree species individually. Maps of these biomass loss 
projections are presented in the 2007 Staff Paper. For example, quaking 
aspen had a wide range of O3 exposures across its growing 
range and therefore, showed significant variability in percentages of 
projected seedling biomass loss across its range. Quaking aspen 
seedling biomass loss was projected to be greater than 4 percent over 
much of its geographic range, though it can reach above 10 percent in 
areas of Ohio, Pennsylvania, New York, New Jersey and California. 
Biomass loss for black cherry was projected to be greater than 20 
percent in approximately half its range. Greater than 30 percent 
biomass loss for black cherry was projected in North Carolina, 
Tennessee, Indiana, Ohio, Pennsylvania, Arizona, Michigan, New York, 
New Jersey, Maryland and Delaware. For ponderosa pine, an important 
tree species in the western U.S., biomass loss was projected to be 
above 10 percent in much of its range in California. Biomass loss still 
occurred in many tree species when O3 air quality was 
adjusted to meet the then current 8-hour standard of 0.084 ppm. For 
instance, black cherry, ponderosa pine, eastern white pine, and aspen 
had estimated median seedling biomass losses over portions of their 
growing

[[Page 3011]]

range as high as 24, 11, 6, and 6 percent, respectively, when 
O3 air quality was rolled back to just meet a 0.084 ppm, 8-
hour standard. The 2007 Staff Paper noted that these results are for 
tree seedlings and that mature trees of the same species may have more 
or less of a response to O3 exposure. Due to the potential 
for compounding effects over multiple years, experts at a consensus 
workshop on O3 vegetation effects and secondary standards, 
hereinafter referred to as the 1996 Consensus Workshop, reported in a 
subsequent 1997 Workshop Report, that a biomass loss greater than 2 
percent annually can be significant (Heck and Cowling, 1997). Decreased 
seedling root growth and survivability could affect overall stand 
health and composition in the long term.
    In addition to the estimation of O3 effects on seedling 
growth, recent work available in the 2008 rulemaking has enhanced our 
understanding of risks beyond the seedling stage. In order to better 
characterize the potential O3 effects on mature tree growth, 
a tree growth model (TREGRO) was used as a tool to evaluate the effect 
of changing O3 air quality under just meet scenarios for 
selected alternative O3 standards on the growth of mature 
trees. TREGRO is a process-based, individual tree growth simulation 
model (Weinstein et al, 1991). This model has been used to evaluate the 
effects of a variety of O3 exposure scenarios on several 
species of trees by incorporating concurrent climate data in different 
regions of the U.S. to account for O3 and climate/
meteorology interactions (Tingey et al., 2001; Weinstein et al., 1991; 
Retzlaff et al., 2000; Laurence et al., 1993; Laurence et al., 2001; 
Weinstein et al., 2005). The model provides an analytical framework 
that accounts for the nonlinear relationship between O3 
exposure and response. The interactions between O3 exposure, 
precipitation and temperature are integrated as they affect vegetation, 
thus providing an internal consistency for comparing effects in trees 
under different exposure scenarios and climatic conditions. An earlier 
assessment of the effectiveness of national ambient air quality 
standards in place since the early 1970s took advantage of 40 years of 
air quality and climate data for the Crestline site in the San 
Bernardino Mountains of California to simulate ponderosa pine growth 
over time with the improving air quality using TREGRO (Tingey et al., 
2004).
    The TREGRO model was used to assess growth of Ponderosa pine in the 
San Bernardino Mountains of California (Crestline) and the growth of 
yellow poplar and red maple in the Appalachian mountains of Virginia 
and North Carolina, Shenandoah National Park (Big Meadows) and Linville 
Gorge Wilderness Area (Cranberry), respectively. Total tree growth 
associated with ``as is'' air quality, and air quality adjusted to just 
meet alternative O3 standards was assessed. Ponderosa pine 
is one of the most widely distributed pines in western North America, a 
major source of timber, important as wildlife habitat, and valued for 
aesthetics (Burns and Honkala, 1990). Red maple is one of the most 
abundant species in the eastern U.S. and is important for its brilliant 
fall foliage and highly desirable wildlife browse food (Burns and 
Honkala, 1990). Yellow poplar is an abundant species in the southern 
Appalachian forest. It is 10 percent of the cove hardwood stands in 
southern Appalachians which are widely viewed as some of the country's 
most treasured forests because the protected, rich, moist set of 
conditions permit trees to grow the largest in the eastern U.S. The 
wood has high commercial value because of its versatility and as a 
substitute for increasingly scarce softwoods in furniture and framing 
construction. Yellow poplar is also valued as a honey tree, a source of 
wildlife food, and a shade tree for large areas (Burns and Honkala, 
1990).
    The 2007 Staff Paper analyses found that just meeting a 0.084 ppm 
standard would likely continue to allow O3-related 
reductions in annual net biomass gain in these species. This is based 
on model outputs that estimate that as O3 levels are reduced 
below those of a 0.084 ppm standard, significant improvements in growth 
would occur. For instance, estimated growth in red maple increased by 4 
and 3 percent at Big Meadows and Cranberry sites, respectively, when 
air quality was rolled back to just met a W126 value of 13 ppm-hour. 
Yellow poplar was projected to have a growth increase between 0.6 and 8 
percent under the same scenario at the two eastern sites.
    Though there is uncertainty associated with the above analyses, 
this information should be given careful consideration in light of 
several other pieces of evidence. Specifically, new evidence from 
experimental studies that go beyond the seedling growth stage continues 
to show decreased growth under elevated O3 (King et al. 
2005). Some mature trees such as red oak have shown an even greater 
sensitivity of photosynthesis to O3 than seedlings of the 
same species (Hanson et al., 1994). As indicated above, smaller growth 
loss increments may be significant for perennial species. The potential 
for cumulative ``carry over'' effects as well as compounding also must 
be considered. The accumulation of such ``carry-over'' effects over 
time may affect long-term survival and reproduction of individuals and 
ultimately the abundance of sensitive tree species in forest stands.
c. Crops
    As discussed in the 2007 Staff Paper, risk of O3 
exposure and associated monetized benefits were estimated for commodity 
crops, fruits and vegetables. Similar to the tree seedling analysis, 
this analysis combined C-R information on crops, crop growing regions 
and interpolated exposures during each crop growing season. NCLAN crop 
functions were used for commodity crops. According to USDA National 
Agricultural Statistical Survey (NASS) data, the 9 commodity crop 
species (e.g., cotton, field corn, grain sorghum, peanut, soybean, 
winter wheat, lettuce, kidney bean, potato) included in the 2007 Staff 
Paper analysis accounted for 69 percent of 2004 principal crop acreage 
planted in the U.S. in 2004.\57\ The C-R functions for six fruit and 
vegetable species (tomatoes-processing, grapes, onions, rice, 
cantaloupes, Valencia oranges) were identified from the California 
fruit and vegetable analysis from the 1997 review (Abt Associates Inc, 
1995). The 2007 Staff Paper noted that fruit and vegetable studies were 
not part of the NCLAN program and C-R functions were available only in 
terms of seasonal 7-hour or 12-hour mean index. This index form is 
considered less effective in predicting plant response for a given 
change in air quality than the cumulative form used with other crops. 
Therefore, the fruit and vegetable C-R functions were considered more 
uncertain than those for commodity crops.
---------------------------------------------------------------------------

    \57\ Principal crops as defined by the USDA include corn, 
sorghum, oats, barley, winter wheat, rye, Durum wheat, other spring 
wheat, rice, soybeans, peanuts, sunflower, cotton, dry edible beans, 
potatoes, sugar beets, canola, proso millet, hay, tobacco, and 
sugarcane. Acreage data for the principal crops were taken from the 
USDA NASS 2005 Acreage Report (http://usda.mannlib.cornell.edu/reports/nassr/field/pcp-bba/acrg0605.pdf).
---------------------------------------------------------------------------

    Analyses in the 2007 Staff Paper showed that some of the most 
important commodity crops such as soybean, winter wheat and cotton had 
some projected losses under the 2001 base year air quality. Soybean 
yield losses were projected to be 2-4 percent in parts of Pennsylvania, 
New Jersey, Maryland and Texas. Winter wheat was projected to have 
yield losses of 2-6 percent in parts of California.

[[Page 3012]]

Additionally, cotton was projected to have yield losses of above 6 
percent in parts of California, Texas and North Carolina in 2001. The 
risk assessment estimated that just meeting the then current 0.084 ppm, 
8-hour standard would still allow O3=related yield loss to 
occur in some commodity crop species and fruit and vegetable species 
currently grown in the U.S. For example, based on median C-R function 
response, in counties with the highest O3 levels, potatoes 
and cotton had estimated yield losses of 9-15 percent and 5-10 percent, 
respectively, when O3 air quality just met the level of a 
0.084 ppm, 8-hour standard. Estimated yield improved in these counties 
when the alternative W126 standard levels were met. The very important 
soybean crop had generally small yield losses throughout the country 
under just meeting the then current standard (0-4 percent).
    The 2007 Staff Paper also presented estimates of monetized benefits 
for crops associated with a 0.084 ppm, 8-hour and alternative 
standards. The Agriculture Simulation Model (AGSIM) (Taylor, 1994; 
Taylor, 1993) was used to calculate annual average changes in total 
undiscounted economic surplus for commodity crops and fruits and 
vegetables when the then current and alternative standard levels were 
met. Meeting the various alternative standards did show some 
significant benefits beyond a 0.084 ppm, 8-hour standard. However, the 
2007 Staff Paper recognized that the AGSIM economic benefits estimates 
also incorporate several sources of uncertainty, including: (1) 
Estimates of economic benefits derived from use of the more uncertain 
C-R relationships for fruits and vegetables; (2) uncertain assumptions 
about the treatment and effect of government farm payment programs; and 
(3) uncertain assumptions about near-term changes in the agriculture 
sector due to the increased use of crops as biofuels. Although the 
AGSIM model results provided a relative comparison of agricultural 
benefits between alternative standards, these uncertainties limited the 
utility of the absolute numbers.

D. Reconsideration of Secondary Standard

    As discussed above at the beginning of section IV, this 
reconsideration of the secondary O3 standard set in the 2008 
rulemaking focuses on reconsidering certain elements of the standard, 
the form, averaging times, and level. The general approach for setting 
a secondary O3 standard used in the 2008 rulemaking, and in 
the previous 1997 rulemaking, was to consider two basic policy options: 
Setting a distinct secondary standard with a biologically relevant form 
and averaging times, or setting a secondary standard identical to the 
primary standard. In the 2007 proposed rule, both such options were 
evaluated, commented on by CASAC and the public, and proposed, as 
discussed below in sections IV.D.1 and IV.D.2, respectively. In the 
2008 final rule, EPA decided to set the secondary standard identical to 
the revised 8-hour primary standard, as discussed below in section 
IV.D.3. Section IV.D.4 summarizes comments received from CASAC 
following the 2008 decision. The Administrator's proposed conclusions 
based on this reconsideration are presented in section IV.D.5.
1. Considerations Regarding the 2007 Proposed Cumulative Seasonal 
Standard
a. Form
    The 2006 Criteria Document and 2007 Staff Paper concluded that the 
recent vegetation effects literature evaluated in the 2008 rulemaking 
strengthened and reaffirmed conclusions made in the 1997 review that 
the use of a cumulative exposure index that differentially weights 
ambient concentrations is best able to relate ambient exposures to 
vegetation response at this time (EPA, 2006a, b; see also discussion in 
IV.B above). The 1997 review focused in particular on two of these 
cumulative forms, the SUM06 and W126. In the 2008 rulemaking, the 2007 
Staff Paper again evaluated these two forms in light of two key pieces 
of then recent information: Estimates of PRB that were lower than in 
the 1997 review, and continued lack of evidence within the vegetation 
effects literature of a biological threshold for vegetation exposures 
of concern. On the basis of those policy and science-related 
considerations, the 2007 Staff Paper concluded that the W126 form was 
more appropriate in the context of the 2008 rulemaking. Specifically, 
the W126 form, by its incorporation of a sigmoidal weighting scheme, 
does not create an artificially imposed concentration threshold, gives 
proportionally more weight to the higher and typically more 
biologically potent concentrations, and is not significantly influenced 
by O3 concentrations within the range of estimated PRB. The 
Staff Paper further concluded that ``it is not appropriate to continue 
to use an 8-hour averaging time for the secondary standard'' and that 
``the 8-hour average form should be replaced with a cumulative, 
seasonal, concentration weighted form'' (EPA, 2007b; pg. 8-25).
    The CASAC, based on its assessment of the same vegetation effects 
science, agreed with the 2006 Criteria Document and 2007 Staff Paper 
and unanimously concluded that it is not appropriate to try to protect 
vegetation from the known or anticipated adverse effects of ambient 
O3 by continuing to promulgate identical primary and 
secondary standards for O3. Moreover, the members of the 
CASAC and a substantial majority of the CASAC O3 Panel 
agreed with 2007 Staff Paper conclusions and encouraged EPA to 
establish an alternative cumulative secondary standard for 
O3 and related photochemical oxidants that is distinctly 
different in averaging time, form and level from the current or 
potentially revised 8-hour primary standard. The CASAC also stated that 
``the recommended metric for the secondary ozone standard is the 
(sigmoidally-weighted) W126 index'' (Henderson, 2007).
    The EPA agreed with the conclusions drawn in the 2006 Criteria 
Document, 2007 Staff Paper and by CASAC that the scientific evidence 
available in the 2008 rulemaking continued to demonstrate the 
cumulative nature of O3-induced plant effects and the need 
to give greater weight to higher concentrations. Thus, EPA concluded 
that a cumulative exposure index that differentially weights 
O3 concentrations represents a reasonable policy choice for 
a seasonal secondary standard to protect against the effects of 
O3 on vegetation. The EPA further agreed with both the 2007 
Staff Paper and CASAC that the most appropriate cumulative, 
concentration-weighted form to consider in the 2008 rulemaking was the 
sigmoidally weighted W126 form, due to EPA's recognition that there is 
no evidence in the literature for an exposure threshold that would be 
appropriate across all O3-sensitive vegetation and that this 
form is unlikely to be significantly influenced by O3 air 
quality within the range of PRB levels identified in this rulemaking. 
Thus, in 2007 EPA proposed as one option to replace the then current 
0.084 ppm, 8-hour average secondary standard with a standard defined in 
terms of the cumulative, seasonal W126 form. The EPA also proposed the 
option of making the secondary identical to the proposed revised 
primary standard.
b. Averaging Times \58\
---------------------------------------------------------------------------

    \58\ While the term ``averaging time'' is used, for the 
cumulative, seasonal standard the seasonal and diurnal time periods 
at issue are those over which exposures during a specified period of 
time are cumulated, not averaged.
---------------------------------------------------------------------------

    The 2007 Staff Paper, in addition to form, also considered what 
exposure

[[Page 3013]]

periods or durations are most relevant for vegetation, which, unlike 
people, is exposed to ambient air continuously throughout its lifespan. 
For annual species, this lifespan encompasses a period of only one year 
or less; while for perennials, lifespans can range from a few years to 
decades or centuries. However, because O3 levels are not 
continuously elevated and plants are not equally sensitive to 
O3 over the course of a day, season or lifetime, it becomes 
necessary to identify periods of exposure that have the most relevance 
for plant response. The 2007 Staff Paper discussed exposure periods 
relevant for vegetation in terms of a seasonal window and a diurnal 
window, and it also discussed defining the standard in terms of an 
annual index value versus a 3-year average of annual index values. The 
numbered paragraphs below present the 2007 Staff Paper discussions on 
these exposure periods, and the annual versus 3-year average index 
value, followed by a discussion of CASAC views and EPA proposed 
conclusions.
    (1) In considering an appropriate seasonal window, the 2007 Staff 
Paper recognized that, in general, many annual crops are grown for 
periods of a few months before being harvested. In contrast, other 
annual and perennial species may be photosynthetically active longer, 
and for some species and locations, throughout the entire year. In 
general, the period of maximum physiological activity and thus, maximum 
potential O3 uptake for annual crops, herbaceous species, 
and deciduous trees and shrubs coincides with some or all of the intra-
annual period defined as the O3 season, which varies on a 
state-by-state basis. This is because the high temperature and high 
light conditions that promote the formation of tropospheric 
O3 also promote physiological activity in vegetation.
    The 2007 Staff Paper noted that the selection of any single 
seasonal exposure period for a national standard would represent a 
compromise, given the significant variability in growth patterns and 
lengths of growing seasons among the wide range of vegetation species 
occurring within the U.S. that may experience adverse effects 
associated with O3 exposures. However, the 2007 Staff Paper 
further concluded that the consecutive 3-month period within the 
O3 season with the highest W126 index value (e.g., maximum 
3-month period) would, in most cases, likely coincide with the period 
of greatest plant sensitivity on an annual basis. Therefore, the 2007 
Staff Paper again concluded, as it did in the 1997 review, that the 
annual maximum consecutive 3-month period is a reasonable seasonal time 
period, when combined with a cumulative, concentration weighted form, 
for protection of sensitive vegetation.
    (2) In considering an appropriate diurnal window, the Staff Paper 
recognized that over the course of the 24-hour diurnal period, plant 
stomatal conductance varies in response to changes in light level, soil 
moisture and other environmentally and genetically controlled factors. 
In general, stomata are most open during daylight hours in order to 
allow sufficient CO2 uptake for use in carbohydrate 
production through the light-driven process of photosynthesis. At most 
locations, O3 concentrations are also highest during the 
daytime, and thus, most likely to coincide with maximum stomatal 
uptake. It is also known however, that in some species, stomata may 
remain open sufficiently at night to allow for some nocturnal uptake to 
occur. In addition, at some rural, high elevation sites, the 
O3 concentrations remain relatively flat over the course of 
the day, often at levels above estimated PRB. At these sites, nighttime 
W126 values can be of similar magnitude as daytime values, though the 
significance of these exposures is much less certain. This is because 
O3 uptake during daylight hours is known to impair the 
light-driven process of photosynthesis, which can then lead to impacts 
on carbohydrate production, plant growth, reproduction (yield) and root 
function. It is less clear at this time to what extent and by what 
mechanisms O3 uptake at night adversely impacts plant 
function. In addition, many species have not been shown to take up 
O3 at night and/or do not occur in areas with elevated 
nighttime O3 concentrations.
    In reviewing the information on this topic that became available 
after the 1997 review, the 2007 Staff Paper considered the information 
compiled in a summary report by Musselman and Minnick (2000). This work 
reported that some species take up O3 at night, but that the 
degree of nocturnal stomatal conductance varies widely between species 
and its relevance to overall O3-induced vegetation effects 
remain unclear. In considering this information, the 2007 Staff Paper 
concluded that for the vast majority of studied species, daytime 
exposures represent the majority of diurnal plant O3 uptake 
and are responsible for inducing the plant response of most 
significance to the health and productivity of the plant (e.g., reduced 
carbohydrate production). Until additional information is available 
about the extent to which co-occurrence of sensitive species and 
elevated nocturnal O3 exposures exists, and what levels of 
nighttime uptake are adverse to affected species, the 2007 Staff Paper 
concluded that this information continues to be preliminary, and does 
not provide a basis for reaching a different conclusion regarding the 
diurnal window at this time. The 2007 Staff Paper further noted that 
additional research is needed to address the degree to which a 12-hour 
diurnal window may be under-protective in areas where elevated 
nighttime levels of O3 co-occur with sensitive species with 
a high degree of nocturnal stomatal conductance. Thus, as in the 1997 
review, the 2007 Staff Paper again concluded that based on the 
available science, the daytime 12-hour window (8 a.m. to 8 p.m.) is the 
most appropriate period over which to cumulate diurnal O3 
exposures, specifically those most relevant to plant growth and yield 
responses.
    (3) In considering whether the standard should be defined in terms 
of an annual index value or a 3-year average of annual index values, 
the 2007 Staff Paper recognized that though most cumulative seasonal 
exposure levels of concern for vegetation have been expressed in terms 
of the annual timeframe, it may be appropriate to consider a 3-year 
average for purposes of standard stability. However, the 2007 Staff 
Paper noted that for certain welfare effects of concern (e.g., foliar 
injury, yield loss for annual crops, growth effects on other annual 
vegetation and potentially tree seedlings), an annual time frame may be 
a more appropriate period in which to assess what level would provide 
the requisite degree of protection, while for other welfare effects 
(e.g., mature tree biomass loss), a 3-year average may also be 
appropriate. Thus, the 2007 Staff Paper concluded that it is 
appropriate to consider both an annual and a 3-year average. Further, 
the 2007 Staff Paper concluded that should a 3-year average of the 12-
hour W126 form be selected, a lower standard level should be considered 
to reduce the potential of adverse impacts to annual species from a 
single high O3 year that could still occur while attaining a 
standard on average over 3 years.
    The CASAC, in considering what seasonal, diurnal, and annual or 
multiyear time periods are most appropriate when combined with a 
cumulative, seasonal form to protect vegetation from exposures of 
concern, agreed that the 2007 Staff Paper

[[Page 3014]]

conclusion regarding the 3-month seasonal period and 12-hour daylight 
window was appropriate, with the distinction that both of these time 
periods likely represents the minimum time periods of importance. In 
particular, one O3 Panel member commented that for some 
species, additional O3 exposures of importance were 
occurring outside the 3-month seasonal and 12-hour diurnal windows. 
Further, the CASAC concluded that multi-year averaging to promote a 
``stable'' secondary standard is less appropriate for a cumulative, 
seasonal secondary standard than for a primary standard based on daily 
maximum 8-hour concentrations. The CASAC further concluded that if 
multi-year averaging is employed to afford greater stability of the 
secondary standard, the level of the standard should be revised 
downward to assure that the desired degree of protection is not 
exceeded in individual years.
    The EPA, in determining which seasonal and diurnal time periods are 
most appropriate to propose, took into account the 2007 Staff Paper and 
CASAC views. In being careful to consider what is needed to provide the 
requisite degree of protection, no more and no less, in 2007 EPA 
proposed that the 3-month seasonal period and 12-hour daylight period 
are appropriate. Based on the 2007 Staff Paper conclusions discussed 
above, EPA was mindful that there is the potential for under-protection 
with a 12-hour diurnal window in areas with sufficiently elevated 
nighttime levels of O3 where sensitive species with a high 
degree of nocturnal stomatal conductance occur. On the other hand, EPA 
also recognized that a longer diurnal window (e.g., 24-hour) has the 
possibility of over-protecting vegetation in areas where nighttime 
O3 levels remain relatively high but where no species having 
significant nocturnal uptake exist. In weighing these considerations, 
EPA agreed with the 2007 Staff Paper conclusion that until additional 
information is available about the extent to which this co-occurrence 
of sensitive species and elevated nocturnal O3 exposures 
exists, and what levels of nighttime uptake are adverse to affected 
species, this information does not provide a basis for reaching a 
different conclusion at this time. The EPA also considered to what 
extent the 3-month period within the O3 season was 
appropriate, recognizing that many species of vegetation have longer 
growing seasons. The EPA further proposed that the maximum 3-month 
period is sufficient and appropriate to characterize O3 
exposure levels associated with known levels of plant response. 
Therefore, EPA proposed that the most appropriate exposure periods for 
a cumulative, seasonal form is the daytime 12-hour window (8 a.m. to 8 
p.m.) during the consecutive 3-month period within the O3 
monitoring season with the maximum W126 index value.
    The EPA also proposed an annual rather than a multi-year 
cumulative, seasonal standard. In proposing this option, EPA also 
believed that it was appropriate to consider the benefits to the public 
welfare that would accrue from establishing a 3-year average secondary 
standard, and solicited comment on this alternative. In so doing, EPA 
also agreed with 2007 Staff Paper and CASAC conclusions that should a 
3-year standard be finalized, the level of the standard should be set 
so as to provide the requisite degree of protection for those 
vegetation effects judged to be adverse to the public welfare within a 
single annual period.
c. Level
    The 2007 Staff Paper, in identifying a range of levels for a 3-
month, 12-hour W126 annual form appropriate to protect the public 
welfare from adverse impacts to vegetation from O3 
exposures, considered what information from the array of vegetation 
effects evidence and exposure and risk assessment results was most 
useful. Regarding the vegetation effects evidence, the 2007 Staff Paper 
found stronger support than what was available at the time of the 1997 
review for an increased level of protection for trees and ecosystems. 
Specifically, this expanded body of support includes: (1) Additional 
field based data from free air, gradient and biomonitoring surveys 
demonstrating adverse levels of O3-induced above and/or 
below-ground growth reductions on trees at the seedling, sapling and 
mature growth stages and incidence of visible foliar injury occurring 
at biomonitoring sites in the field at ambient levels of exposure; (2) 
qualitative support from free air (e.g., AspenFACE) and gradient 
studies on a limited number of tree species for the continued 
appropriateness of using OTC-derived C-R functions to predict tree 
seedling response in the field; (3) studies that continue to document 
below-ground effects on root growth and ``carry-over'' effects 
occurring in subsequent years from O3 exposures; and (4) 
increased recognition and understanding of the structure and function 
of ecosystems and the complex linkages through which O3, and 
other stressors, acting at the organism and species level can influence 
higher levels within the ecosystem hierarchy and disrupt essential 
ecological attributes critical to the maintenance of ecosystem goods 
and services important to the public welfare.
    Based on the above observations and on the vegetation effects and 
the results of the exposure and impact assessment summarized above, the 
2007 Staff Paper concluded that just meeting the then current standard 
would still allow adverse levels of tree seedling biomass loss in 
sensitive commercially and ecologically important tree species in many 
regions of the country. Seedling risk assessment results showed that 
some tree seedling species are extremely sensitive (e.g., cottonwood, 
black cherry and aspen), with annual biomass losses occurring in the 
field of the same or greater magnitude that that of annual crops. Such 
information from the tree seedling risk assessment suggests that 
O3 levels would need to be substantially reduced to protect 
sensitive tree seedlings like black cherry from growth and foliar 
injury effects.
    In addition to the currently quantifiable risks to trees from 
ambient exposures, the 2007 Staff Paper also considered the more subtle 
impacts of O3 acting in synergy with other natural and man-
made stressors to adversely affect individual plants, populations and 
whole systems. By disrupting the photosynthetic process, decreasing 
carbon storage in the roots, increasing early senescence of leaves and 
affecting water use efficiency in trees, O3 exposures could 
potentially disrupt or change the nutrient and water flow of an entire 
system. Weakened trees can become more susceptible to other 
environmental stresses such as pest and pathogen outbreaks or harsh 
weather conditions. Though it is not possible to quantify all the 
ecological and societal benefits associated with varying levels of 
alternative secondary standards, the 2007 Staff Paper concluded that 
this information should be weighed in considering the extent to which a 
secondary standard should be set so as to provide potential protection 
against effects that are anticipated to occur.
    In addition, the 2007 Staff Paper also recognized that in the 1997 
review, EPA took into account the results of a 1996 Consensus Workshop. 
At this workshop, a group of independent scientists expressed their 
judgments on what standard form(s) and level(s) would provide 
vegetation with adequate protection from O3-related adverse 
effects. Consensus was reached with respect to selecting appropriate 
ranges of levels in terms of a cumulative, seasonal 3-month, 12-hr 
SUM06

[[Page 3015]]

standard for a number of vegetation effects endpoints. These ranges are 
identified below, with the estimated approximate equivalent W126 
standard values shown in parentheses. For growth effects to tree 
seedlings in natural forest stands, a consensus was reached that a 
SUM06 range of 10 to 15 (W126 range of 7 to 13) ppm-hour would be 
protective. For growth effects to tree seedlings and saplings in 
plantations, the consensus SUM06 range was 12 to 16 (W126 range of 9 to 
14) ppm-hour. For visible foliar injury to natural ecosystems, the 
consensus SUM06 range was 8 to 12 (W126 range of 5 to 9) ppm-hour.
    Taking these consensus statements into account, EPA stated in the 
1997 final rule (62 FR 38856) that ``the report lends important support 
to the view that the current secondary standard is not adequately 
protective of vegetation * * * [and] * * * foreshadows the direction of 
future scientific research in this area, the results of which could be 
important in future reviews of the O3 secondary standard'' 
(62 FR 38856).
    Given the importance EPA put on the consensus report in the 1997 
review, the 2007 Staff Paper considered to what extent research 
published after 1997 provided empirical support for the ranges of 
levels identified by the experts as protective of different types of 
O3-induced effects. With regard to O3-induced 
biomass loss in sensitive tree seedlings/saplings growing in natural 
forest stands, the information discussed in the 2007 Staff Paper, 
including the evidence from free air and gradient studies, provides 
additional direct support for the conclusion that the 1996 Consensus 
Workshop approximate W126 range of 7-13 ppm-hour was an appropriate 
range to consider in selecting a protective level. With regard to 
visible foliar injury, the available evidence, including the 2007 Staff 
Paper analysis of incidence in counties with FIA monitoring sites and 
air quality data, showed significant levels of county-level visible 
foliar injury incidence at the W126 level of 13 ppm-hour. However, 
because this analysis did not address risks of this effect at lower 
levels of O3 air quality, and because there is a significant 
uncertainty in predicting the degree of visible foliar injury symptoms 
expected for lower levels of O3 air quality, the evidence 
provides less certain but qualitative directional support for the 1996 
Consensus Workshop range of 5 to 9 ppm-hour to protect against this 
effect. With regard to O3-induced effects on plantation 
trees, there is far less direct information available. Though some 
forest plantation trees are O3-sensitive, the monoculture 
nature of these stands makes uncertain the degree to which competition 
for resources might play a role and to what degree the variety of 
management practices applied would be expected to mitigate the 
O3-induced effects. Thus, it is difficult to distinguish a 
protective range of levels for plantation trees from a range of levels 
that would be protective of O3-sensitive tree seedlings and 
saplings in natural forest stands. Therefore, on the basis of the 
strength of the evidence available, the 2007 Staff Paper concluded that 
it was appropriate to consider a range for a 3-month, 12-hour, W126 
standard that included the 1996 consensus recommendations for growth 
effects in tree seedlings in natural forest stands (i.e., 7-13 ppm-hour 
in terms of a W126 form).
    In considering the available information on O3-related 
effects on crops in the 2008 rulemaking, the 2007 Staff Paper observed 
the following regarding the strength of the underlying crop science: 
(1) Nothing in the recent literature points to a change in the 
relationship between O3 exposure and crop response across 
the range of species and/or cultivars of commodity crops currently 
grown in the U.S. that could be construed to make less appropriate the 
use of commodity crop C-R functions developed in the NCLAN program; (2) 
new field-based studies (e.g., SoyFACE) provide qualitative support in 
a few limited cases for the appropriateness of using OTC-derived C-R 
functions to predict crop response in the field; and (3) refinements in 
the exposure, risk and benefits assessments in this review reduce some 
of the uncertainties present in the 1997 review. On the basis of these 
observations, the 2007 Staff Paper concluded that nothing in the newly 
assessed information called into question the strength of the 
underlying science upon which EPA based its proposed decision in the 
1997 review to select a level of a cumulative, seasonal form associated 
with protecting 50 percent of crop cases from no more than 10 percent 
yield loss as providing the requisite degree of protection for 
commodity crops.
    The 2007 Staff Paper then considered whether any additional 
information is available to inform judgments as to the adversity of 
various O3-induced levels of crop yield loss to the public 
welfare. As noted above, the 2007 Staff Paper observed that 
agricultural systems are heavily managed, and that in addition to 
stress from O3, the annual productivity of agricultural 
systems is vulnerable to disruption from many other stressors (e.g., 
weather, insects, disease), whose impact in any given year can greatly 
outweigh the direct reduction in annual productivity resulting from 
elevated O3 exposures. On the other hand, O3 can 
also more subtly impact crop and forage nutritive quality and 
indirectly exacerbate the severity of the impact from other stressors. 
Though these latter effects currently cannot be quantified, they should 
be considered in judging to what extent a level of protection selected 
to protect commodity crops should be precautionary.
    Based on the above considerations, the 2007 Staff Paper concluded 
that the level of protection (no more than 10% yield or biomass loss in 
50% of studied cases) judged requisite in the 1997 review to protect 
the public welfare from adverse levels of O3-induced 
reductions in crop yields and tree seedling biomass loss, as provided 
by a W126 level of 21 ppm-hour, remains appropriate for consideration 
as an upper bound of a range of appropriate levels.
    Thus, the 2007 Staff Paper concluded, based on all the above 
considerations, that an appropriate range of 3-month, 12-hour W126 
levels was 7 to 21 ppm-hour, recognizing that the level selected is 
largely a policy judgment as to the requisite level of protection 
needed. In determining the requisite level of protection for crops and 
trees, and indirectly, ecosystems, the 2007 Staff Paper recognized that 
it is appropriate to weigh the importance of the predicted risks of 
these effects in the overall context of public welfare protection, 
along with a determination as to the appropriate weight to place on the 
associated uncertainties and limitations of this information.
    The CASAC, in its final letter to the Administrator (Henderson, 
2007), agreed with the 2007 Staff Paper recommendations that the lower 
bound of the range within which a seasonal W126 welfare-based 
(secondary) O3 standard should be considered is 
approximately 7 ppm-hour; however, it did not agree with staff's 
recommendation that the upper bound of the range for consideration 
should be as high as 21 ppm-hour. Rather, CASAC recommended that the 
upper bound of the range considered should be no higher than 15 ppm-
hour, which is just above the upper ends of the ranges identified in 
the 1996 Consensus Workshop as being protective of tree seedlings and 
saplings grown in natural forest stands and in plantations. The lower 
end of this range (7 ppm-hour) is the same as the lower end of the 
range identified in the 1996 Consensus Workshop as protective of tree 
seedlings

[[Page 3016]]

in natural forest stands from growth effects.
    In the 2007 proposed rule, taking 2007 Staff Paper and CASAC views 
into account, EPA proposed a range of levels for a cumulative, seasonal 
secondary standard as expressed in terms of the maximum 3 month, 12-
hour W126 form, in the range of 7 to 21 ppm-hour. This range 
encompasses the range of levels recommended by CASAC, and also includes 
a higher level as recommended for consideration in the 2007 Staff 
Paper. Given the uncertainty in determining the risk attributable to 
various levels of exposure to O3, EPA believed, as a public 
welfare policy judgment, that this was a reasonable range to propose.
2. Considerations Regarding the 2007 Proposed 8-Hour Standard
    In the 1997 review, the 1996 Staff Paper included an analysis to 
compare the degree of overlap between areas that would be expected not 
to meet the range of alternative 8-hour standards being considered for 
the primary NAAQS and those expected not to meet the range of values 
(expressed in terms of the seasonal SUM06 index) of concern for 
vegetation. This result suggested that improvements in national air 
quality expected to result from attaining an 8-hour primary standard 
within the recommended range of levels would also be expected to reduce 
levels of concern for vegetation in those same areas. In the 1997 final 
rule, the decision was made, on the basis of both science and policy 
considerations, to make the secondary identical to the primary 
standard. It acknowledged, however, that uncertainties remained ``as to 
the extent to which air quality improvements designed to reduce 8-hour 
average O3 concentrations averaged over a 3-year period 
would reduce O3 exposures measured by a seasonal SUM06 
index'' (62 FR 38876).
    On the basis of that history, the 2007 Staff Paper analyzed the 
degree of overlap expected between alternative 8-hour and cumulative 
seasonal secondary standards (as discussed above in section IV.C.1) 
using then recent air quality. Based on the results, the 2007 Staff 
Paper concluded that the degree to which the then current 8-hour 
standard form and level would overlap with areas of concern for 
vegetation expressed in terms of the 12-hour W126 standard is 
inconsistent from year to year and would depend greatly on the level of 
the 12-hour W126 and 8-hour standards selected and the distribution of 
hourly O3 concentrations within the annual and/or 3-year 
average period.
    Thus, though the 2007 Staff Paper recognized again that meeting the 
current or alternative levels of the 8-hour average standard could 
result in air quality improvements that would potentially benefit 
vegetation in some areas, it urged caution be used in evaluating the 
likely vegetation impacts associated with a given level of air quality 
expressed in terms of the 8-hour average form in the absence of 
parallel W126 information. This caution was due to the concern that the 
analysis in the 2007 Staff Paper may not be an accurate reflection of 
the true situation in non-monitored, rural counties due to the lack of 
more complete monitor coverage in many rural areas. Further, of the 
counties that did not show overlap between the two standard forms, most 
were located in rural/remote high elevation areas which have 
O3 air quality patterns that are typically different from 
those associated with urban and near urban sites at lower elevations. 
Because the majority of such areas are currently not monitored, it is 
believed there are likely to be additional areas that have similar air 
quality distributions that would lead to the same disconnect between 
forms. Thus, the 2007 Staff Paper concluded that it remained 
problematic to determine the appropriate level of protection for 
vegetation using an 8-hour average form.
    The CASAC recognized that an important difference between the 
effects of acute exposures to O3 on human health and the 
effects of O3 exposures on welfare is that vegetation 
effects are more dependent on the cumulative exposure to, and uptake 
of, O3 over the course of the entire growing season 
(Henderson, 2006c). The CASAC O3 Panel members were 
unanimous in concluding the protection of natural terrestrial 
ecosystems and managed agricultural crops requires a secondary 
O3 standard that is substantially different from the primary 
O3 standard in averaging time, level, and form (Henderson, 
2007).
    In considering the appropriateness of proposing a revised secondary 
standard that would be identical to the proposed primary standard, EPA 
took into account the approach used by the Agency in the 1997 review, 
the conclusions of the 2007 Staff Paper, CASAC advice, and the views of 
public commenters. The EPA first considered the 2007 Staff Paper 
analysis of the projected degree of overlap between counties with air 
quality expected to meet various alternative levels of an 8-hour 
standard and alternative levels of a W126 standard based on monitored 
air quality data. This analysis showed significant overlap within the 
proposed range of the primary 8-hour form and selected levels of the 
W126 standard form being considered, with the degree of overlap between 
these two forms depending greatly on the levels selected and the 
distribution of hourly O3 concentrations within the annual 
and/or 3-year average period. On this basis, EPA concluded that a 
secondary standard set identical to the proposed primary standard would 
provide a significant degree of additional protection for vegetation as 
compared to that provided by the current secondary standard. The EPA 
also recognized that lack of rural monitoring data made uncertain the 
degree to which the proposed 8-hour or W126 alternatives would be 
protective, and that there would be the potential for not providing the 
appropriate degree of protection for vegetation in areas with air 
quality distributions that result in a high cumulative, seasonal 
exposure but do not result in high 8-hour average exposures. While this 
potential for under-protection using an 8-hour standard was clear, the 
number and size of areas at issue and the degree of risk was hard to 
determine. On the other hand, EPA also considered at that time that 
there was a potential risk of over-protection with a cumulative, 
seasonal standard given the inherent uncertainties associated with 
moving to a new form for the secondary standard, in particular those 
associated with predicting exposure and risk patterns based on a 
limited rural monitoring network.
    The EPA also considered the views and recommendations of CASAC, and 
agreed that a cumulative, seasonal standard is the most biologically 
relevant way to relate exposure to plant growth response. However, as 
reflected in the public comments, EPA also recognized that there 
remained significant uncertainties in determining or quantifying the 
degree of risk attributable to varying levels of O3 
exposure, the degree of protection that any specific cumulative, 
seasonal standard would produce, and the associated potential for error 
in determining the standard that will provide a requisite degree of 
protection--i.e., sufficient but not more than what is necessary. Given 
this uncertainty, EPA also believed it was appropriate to consider the 
degree of protection that would be afforded by a secondary standard 
that was identical to the then proposed primary standard. Based on its 
consideration of the full range of views as described above, and in the 
2007 proposed rule, EPA proposed as a second option to revise

[[Page 3017]]

the secondary standard to be identical in every way to the then 
proposed primary standard.
3. Basis for 2008 Decision on the Secondary Standard
    In the 2008 final rule, EPA noted that deciding on the appropriate 
secondary standard involved making a choice between two possible 
alternatives, each with their strengths and weaknesses. The 2008 final 
rule reported that within the Administration at that time there had 
been a robust discussion of the same strengths and weaknesses 
associated with each option that were identified earlier. The process 
by which EPA reached its final conclusion is described in the final 
rule (73 FR 16497). The rationale for the 2008 decision presented in 
the final rule (73 FR 16499-16500) is described below.
    In considering the appropriateness of establishing a new standard 
defined in terms of a cumulative, seasonal form, or revising the then 
current secondary standard by making it identical to the revised 
primary standard, EPA took into account the approach used by the Agency 
in the 1997 review, the conclusions of the 2007 Staff Paper, CASAC 
advice, and the views of public commenters. In giving consideration to 
the approach taken in the 1997 review, EPA first considered the 2007 
Staff Paper analysis of the projected degree of overlap between 
counties with air quality expected to meet the revised 8-hour primary 
standard, set at a level of 0.075 ppm, and alternative levels of a W126 
standard based on currently monitored air quality data. This analysis 
showed significant overlap between the revised 8-hour primary standard 
and selected levels of the W126 standard form being considered, with 
the degree of overlap between these alternative standards depending 
greatly on the W126 level selected and the distribution of hourly 
O3 concentrations within the annual and/or 3-year average 
period.\59\ On this basis, as an initial matter, EPA concluded that a 
secondary standard set identical to the proposed primary standard would 
provide a significant degree of additional protection for vegetation as 
compared to that provided by the then current 0.084 ppm secondary 
standard. In further considering the significant uncertainties that 
remain in the available body of evidence of O3-related 
vegetation effects and in the exposure and risk analyses conducted for 
the 2008 rulemaking, and the difficulty in determining at what point 
various types of vegetation effects become adverse for sensitive 
vegetation and ecosystems, EPA focused its consideration on a level for 
an alternative W126 standard at the upper end of the proposed range 
(i.e., 21 ppm-hour). The 2007 Staff Paper analysis showed that at that 
W126 standard level, there would be essentially no counties with air 
quality that would be expected both to exceed such an alternative W126 
standard and to meet the revised 8-hour primary standard--that is, 
based on this analysis of currently monitored counties, a W126 standard 
would be unlikely to provide additional protection in any monitored 
areas beyond that likely to be provided by the revised primary 
standard.
---------------------------------------------------------------------------

    \59\ Prior to publication of the 2008 final rule, EPA did 
further analysis of the degree of overlap to extend the 2007 Staff 
Paper analyses, and that analysis was available in the docket.
---------------------------------------------------------------------------

    The EPA also recognized that the general lack of rural monitoring 
data made uncertain the degree to which the revised 8-hour standard or 
an alternative W126 standard would be protective in those areas, and 
that there would be the potential for not providing the appropriate 
degree of protection for vegetation in areas with air quality 
distributions that result in a high cumulative, seasonal exposure but 
do not result in high 8-hour average exposures. While this potential 
for under-protection using an 8-hour standard was clear, the number and 
size of areas at issue and the degree of risk was hard to determine. 
However, EPA concluded at that time that an 8-hour standard would also 
tend to avoid the potential for providing more protection than is 
necessary, a risk that EPA concluded would arise from moving to a new 
form for the secondary standard despite significant uncertainty in 
determining the degree of risk for any exposure level and the 
appropriate level of protection, as well as uncertainty in predicting 
exposure and risk patterns.
    The EPA also considered the views and recommendations of CASAC, and 
agreed that a cumulative, seasonal standard was the most biologically 
relevant way to relate exposure to plant growth response. However, as 
reflected in some public comments, EPA also judged that there remained 
significant uncertainties in determining or quantifying the degree of 
risk attributable to varying levels of O3 exposure, the 
degree of protection that any specific cumulative, seasonal standard 
would produce, and the associated potential for error in determining 
the standard that will provide a requisite degree of protection--i.e., 
sufficient but not more than what is necessary. Given these significant 
uncertainties, EPA concluded at that time that establishing a new 
secondary standard with a cumulative, seasonal form would result in 
uncertain benefits beyond those afforded by the revised primary 
standard and therefore may be more than necessary to provide the 
requisite degree of protection.
    Based on its consideration of the views discussed above, EPA judged 
in the 2008 rulemaking that the appropriate balance to be drawn was to 
revise the secondary standard to be identical in every way to the 
revised primary standard. The EPA believed that such a standard would 
be sufficient to protect public welfare from known or anticipated 
adverse effects, and did not believe that an alternative cumulative, 
seasonal standard was needed to provide this degree of protection. The 
EPA believed that this judgment appropriately considered the 
requirement for a standard that is neither more nor less stringent than 
necessary for this purpose.
    For the reasons discussed above, and taking into account 
information and assessments presented in the 2006 Criteria Document and 
2007 Staff Paper, the advice and recommendations of the CASAC Panel, 
and the public comments to date, EPA decided to revise the existing 8-
hour secondary standard. Specifically, EPA revised the then current 8-
hour average 0.084 ppm secondary standard by making it identical to the 
revised 8-hour primary standard set at a level of 0.075 ppm.
4. CASAC Views Following 2008 Decision
    Following the 2008 decision on the O3 standards, serious 
questions were raised as to whether the standards met the requirements 
of the CAA. In April 2008, the members of the CASAC Ozone Review Panel 
sent a letter to EPA stating ``In our most-recent letters to you on 
this subject--dated October 2006 and March 2007--* * * the Committee 
recommended an alternative secondary standard of cumulative form that 
is substantially different from the primary Ozone NAAQS in averaging 
time, level and form--specifically, the W126 index within the range of 
7 to 15 ppm-hour, accumulated over at least the 12 ``daylight'' hours 
and the three maximum ozone months of the summer growing season'' 
(Henderson, 2008). The letter continued: ``The CASAC now wishes to 
convey, by means of this letter, its additional, unsolicited advice 
with regard to the primary and secondary Ozone NAAQS. In doing so, the 
participating members of the CASAC Ozone Review Panel are unanimous in 
strongly urging you or your successor as EPA Administrator to

[[Page 3018]]

ensure that these recommendations be considered during the next review 
cycle for the Ozone NAAQS that will begin next year'' (id.). The letter 
further stated the following views:
    The CASAC was * * * greatly disappointed that you failed to 
change the form of the secondary standard to make it different from 
the primary standard. As stated in the preamble to the Final Rule, 
even in the previous 1996 ozone review, ``there was general 
agreement between the EPA staff, CASAC, and the Administrator, * * * 
that a cumulative, seasonal form was more biologically relevant than 
the previous 1-hour and new 8-hour average forms (61 FR 65716)'' for 
the secondary standard. Therefore, in both the previous review and 
in this review, the Agency staff and its advisors agreed that a 
change in the form of the secondary standard was scientifically 
well-justified.
* * * * *
    Unfortunately, this scientifically-sound approach of using a 
cumulative exposure index for welfare effects was not adopted, and 
the default position of using the primary standard for the secondary 
standard was once again instituted. Keeping the same form for the 
secondary Ozone NAAQS as for the primary standard is not supported 
by current scientific knowledge indicating that different indicator 
variables are needed to protect vegetation compared to public 
health. The CASAC was further disappointed that a secondary standard 
of the W126 form was not considered from within the Committee's 
previously-recommended range of 7 to 15 ppm-hour. The CASAC 
sincerely hopes that, in the next round of Ozone NAAQS review, the 
Agency will be able to support and establish a reasonable and 
scientifically-defensible cumulative form for the secondary 
standard. (Henderson, 2008)
5. Administrator's Proposed Conclusions
    For the reasons discussed below, the Administrator proposes to set 
a cumulative seasonal standard expressed as an annual index of the sum 
of weighted hourly concentrations (i.e., the W126 form), cumulated over 
12 hours per day (8 am to 8 pm) during the consecutive 3-month period 
within the O3 season with the maximum index value, set at a 
level within the range of 7 to 15 ppm-hour. This proposed decision 
takes into account the information and assessments presented in the 
2006 Criteria Document and the 2007 Staff Paper and related technical 
support documents, the advice and recommendations of CASAC both during 
and following the 2008 rulemaking, and public comments received in 
conjunction with review of drafts of these documents and on the 2007 
proposed rule.
a. Form
    As discussed above in section IV.B, the 2006 Criteria Document and 
2007 Staff Paper concluded that the recent vegetation effects 
literature evaluated in the 2008 rulemaking strengthens and reaffirms 
conclusions made in the 1997 review that the use of a cumulative 
exposure index that differentially weights ambient concentrations is 
best able to relate ambient exposures to vegetation response. The 1997 
review focused in particular on two of these cumulative forms, the 
SUM06 and W126 (EPA, 1996). Given that the data available at that time 
were unable to distinguish between these forms, the EPA, based on the 
policy consideration of not including O3 concentrations 
considered to be within the PRB, estimated at that time to be between 
0.03 and 0.05 ppm, concluded that the SUM06 form would be the more 
appropriate choice for a cumulative, exposure index for a secondary 
standard.
    In the 2008 rulemaking, the 2007 Staff Paper evaluated the 
continued appropriateness of the SUM06 form in light of new estimates 
of PRB that were lower than in the 1997 review, and the continued lack 
of evidence within the vegetation effects literature of a biological 
threshold for vegetation exposures of concern. On the basis of these 
policy and science-related considerations, the 2007 Staff Paper 
concluded that the W126 form was the more appropriate cumulative, 
concentration-weighted form. Specifically, the W126, by its 
incorporation of a sigmoidal weighting scheme, does not create an 
artificially imposed concentration threshold, gives proportionally more 
weight to the higher and typically more biologically potent 
concentrations, and is not significantly influenced by O3 
concentrations within the range of estimated PRB.
    As discussed above, the CASAC, based on its assessment of the same 
vegetation effects science, agreed with the 2006 Criteria Document and 
2007 Staff Paper and unanimously concluded that protection of 
vegetation from the known or anticipated adverse effects of ambient 
O3 ``requires a secondary standard that is substantially 
different from the primary standard in averaging time, level, and 
form,'' i.e. not identical to the primary standard for O3 
(Henderson, 2007). Moreover, the members of CASAC and a substantial 
majority of the other CASAC Panel members agreed with 2007 Staff Paper 
conclusions and encouraged EPA to establish an alternative cumulative 
secondary standard for O3 and related photochemical oxidants 
that is distinctly different in averaging time, form and level from the 
then current or potentially revised 8-hour primary standard (Henderson, 
2006c). The CASAC Panel also stated that ``the recommended metric for 
the secondary ozone standard is the (sigmoidally weighted) W126 index'' 
(Henderson, 2007).
    In reconsidering the 2008 final rule, the Administrator agrees with 
the conclusions drawn in the 2006 Criteria Document, 2007 Staff Paper 
and by CASAC that the scientific evidence available in the 2008 
rulemaking continues to demonstrate the cumulative nature of 
O3-induced plant effects and the need to give greater weight 
to higher concentrations. Thus, the Administrator concludes that a 
cumulative exposure index that differentially weights O3 
concentrations represents a reasonable policy choice for a secondary 
standard to protect against the effects of O3 on vegetation. 
The Administrator further agrees with both the 2007 Staff Paper and 
CASAC that the most appropriate cumulative, concentration-weighted form 
to consider is the sigmoidally weighted W126 form.
    The Administrator notes that in the 2007 proposed rule, EPA 
proposed a second option of revising the then current 8-hour average 
secondary standard by making it identical to the proposed 8-hour 
primary standard. The 2007 Staff Paper analyzed the degree of overlap 
expected between alternative 8-hour and cumulative seasonal secondary 
standards using recent air quality monitoring data. Based on the 
results, the 2007 Staff Paper concluded that the degree to which the 
current 8-hour standard form and level would overlap with areas of 
concern for vegetation expressed in terms of the 12-hour W126 standard 
is inconsistent from year to year and would depend greatly on the level 
of the 12-hour W126 and 8-hour standards selected and the distribution 
of hourly O3 concentrations within the annual and/or 3-year 
average period. The 2007 Staff Paper also recognized that meeting the 
then current or alternative levels of the 8-hour average standard could 
result in air quality improvements that would potentially benefit 
vegetation in some areas, but urged caution be used in evaluating the 
likely vegetation impacts associated with a given level of air quality 
expressed in terms of the 8-hour average form in the absence of 
parallel W126 information. This caution was due to the concern that the 
analysis in the 2007 Staff Paper may not be an accurate reflection of 
the true situation in non-monitored, rural counties due to the lack of 
more complete monitor coverage in many rural areas. Further, of

[[Page 3019]]

the counties that did not show overlap between the two standard forms, 
most were located in rural/remote high elevation areas which have 
O3 air quality patterns that are typically different from 
those associated with urban and near urban sites at lower elevations. 
Because the majority of such areas are currently not monitored, there 
are likely to be additional areas that have similar air quality 
distributions that would lead to the same disconnect between forms. 
Thus, the 2007 Staff Paper concluded that it remains problematic to 
determine the appropriate level of protection for vegetation using an 
8-hour average form.
    The Administrator also notes that CASAC recognized that an 
important difference between the effects of acute exposures to 
O3 on human health and the effects of O3 
exposures on welfare is that vegetation effects are more dependent on 
the cumulative exposure to, and uptake of, O3 over the 
course of the entire growing season (Henderson, 2006c). The CASAC 
O3 Panel members were unanimous in concluding the protection 
of natural terrestrial ecosystems and managed agricultural crops 
requires a secondary O3 standard that is substantially 
different from the primary O3 standard in form, averaging 
time, and level (Henderson, 2007).
    In reaching her proposed decision in this reconsideration of the 
2008 final rule, the Administrator has considered the comments received 
on the 2007 proposed rule regarding revising the secondary standard 
either to reflect a new, cumulative form or by remaining equal to a 
revised primary standard. The commenters generally fell into two 
groups.
    One group of commenters, including environmental organizations, 
strongly supported the proposed option of moving to a cumulative, 
seasonal standard, generally based on the reasoning explained in the 
2007 proposal. Commenters in this group also expressed serious concerns 
with the other proposed option of setting a secondary O3 
standard in terms of the same form and averaging time (i.e., daily 
maximum 8-hour average O3 concentration) as the primary 
standard. These commenters expressed the view that such a standard 
would fail to protect public welfare because the maximum daily 8-hour 
average O3 concentration failed to adequately characterize 
harmful O3 exposures to vegetation. This view was generally 
based on the observation that there is no consistent relationship in 
areas across the U.S. between 8-hour peak O3 concentrations 
and the longer-term cumulative exposures aggregated over a growing 
season that are biologically relevant in characterizing O3-
related effects on sensitive vegetation. Thus, as EPA noted in the 2007 
proposed rule, there is a lack of a rational connection between the 
level of an 8-hour standard and the requisite degree of protection 
required for a secondary O3 NAAQS.
    Another group of commenters, including industry organizations, 
agreed that a cumulative form of the standard may better match the 
underlying data, but expressed the view that remaining uncertainties 
associated with the vegetation effects evidence and/or EPA's exposure, 
risk and benefits assessments were so great that the available 
information did not provide an adequate basis to adopt a standard with 
a level based on a cumulative, seasonal form. These commenters asserted 
that because of the substantial uncertainties remaining at the time of 
the 2008 rulemaking, the benefits of changing to a W126 form were too 
uncertain to warrant revising the form of the standard at that time.
    The Administrator notes that in both the 1997 and the 2008 
decisions, EPA recognized that the risk to vegetation from 
O3 exposures comes from cumulative exposures over a season 
or seasons. The CASAC has fully endorsed this view based on the 
available scientific evidence and assessments, and there is no 
significant disagreement on this issue by commenters. Thus, it is clear 
that the purpose of the secondary O3 NAAQS should be to 
provide an appropriate degree of protection against cumulative, 
seasonal exposures to O3 that are known or anticipated to 
harm sensitive vegetation or ecosystems. In reconsidering the 2008 
final rule, the Administrator recognizes that the issue before the 
Agency is what form of the standard is most appropriate to perform that 
function.
    Within this framework, the Administrator recognizes that it is 
clear that a cumulative, seasonal form has a distinct advantage in 
protecting against cumulative, seasonal exposures. Such a form is 
specifically designed to measure directly the kind of O3 
exposures that can cause harm to vegetation. In contrast, an 8-hour 
standard does not measure cumulative, seasonal exposures directly, and 
can only indirectly afford some degree of protection against such 
exposures. To the extent that clear relationships exist between 8-hour 
daily peak O3 concentrations and cumulative, seasonal 
exposures, the 8-hour form and averaging time would have the potential 
to be effective as an indirect surrogate. However, as discussed in the 
2007 proposed rule and the 2008 final rule, the evidence shows that 
there are known types of O3 air quality patterns that can 
lead to high levels of cumulative, seasonal O3 exposures 
without the occurrence of high daily 8-hour peak O3 
concentrations. An 8-hour form and averaging time is an indirect way to 
measure biologically relevant exposure patterns, is poorly correlated 
with such exposure patterns, and therefore is less likely to identify 
and protect against the kind of cumulative, seasonal exposure patterns 
that have been determined to be harmful.
    Past arguments or reasons for not moving to a cumulative, seasonal 
form, with appropriate exposure periods, have not been based on 
disagreement over the biological relevance of the cumulative, seasonal 
form, or the recognized disadvantages of an 8-hour standard in 
measuring and identifying a specified cumulative, seasonal exposure 
pattern. The reasons for not moving to such a form have been based on 
concerns over whether EPA has an adequate basis to identify the nature 
and magnitude of cumulative, seasonal exposure patterns that the 
standard should be designed to protect against, given the various 
uncertainties in the evidence and the lack of rural O3 
monitoring data. This most directly translates into a concern over 
whether EPA has an adequate basis to determine an appropriate level for 
a cumulative, seasonal secondary standard.
    The Administrator has also considered issues associated with 
selection of the W126 cumulative form, as reflected in the following 
assertions made by some commenters on the 2007 proposed rule: (1) The 
W126 form lacks a biological basis, since it is merely a mathematical 
expression of exposure that has been fit to specific responses in OTC 
studies, such that its relevance for real world biological responses is 
unclear; (2) a flux-based model would be a better choice than a 
cumulative metric because it is an improvement over the many 
limitations and simplifications associated with the cumulative form; 
however, there is insufficient data to apply such a model at present; 
(3) the European experience with cumulative O3 metrics has 
been disappointing and now Europeans are working on their second level 
approach, which will be flux-based; and (4) a second index that 
reflects the accumulation of peaks at or above 0.10 ppm (called N100) 
should be added to a W126 index to achieve appropriate protection.
    With regard to whether the W126 index lacks a biological basis, the 
Administrator finds no basis for reaching such a conclusion. As 
discussed above in section IV.B, the

[[Page 3020]]

vegetation effects science is clear that exposures of concern to plants 
are not based on one discrete 8-hour period but on the repeated 
occurrence of elevated O3 levels throughout the plant's 
growing season. The cumulative nature of the W126 is supported by the 
basic biological understanding that plants in the U.S. are generally 
most biologically active during the warm season and are exposed to 
ambient O3 throughout this biologically active period. In 
addition, it has been shown in the scientific literature that all else 
being equal, plants respond more to higher O3 
concentrations, with no evidence of an exposure threshold for 
vegetation effects. The W126 sigmoidal weighting function reflects both 
of these understandings, by not including a threshold below which 
concentrations are not included, and by differentially weighting 
concentrations to give greater weight to higher concentrations and less 
weight to lower ones.
    With regard to whether a flux-based model would be a better choice, 
the 2007 Staff Paper acknowledged that flux models may produce a more 
accurate calculation of dose to a specific plant species in a specific 
area. However, dose-response relationships have not been developed for 
these flux calculations for plants growing in the U.S. Further, flux 
calculations require large amounts of data for the physiology of each 
plant species and the local conditions for the growing range of each 
plant species. These exercises may be useful for limited small-scale 
risk assessments, but do not provide an appropriate basis for a 
national standard at this time.
    With regard to dissatisfaction with the performance of a particular 
cumulative index in use in Europe,\60\ and growing interest in 
development of flux-based models, the 2007 Staff Paper (Appendix 7A) 
noted that ``because of a lack of flux-response data, a cumulative, 
cutoff concentration based (e.g., AOT40) exposure index will remain in 
use in Europe for the near future for most crops and for forests and 
semi-natural herbaceous vegetation (Ashmore et al., 2004a).'' Further, 
like the SUM06 index, the AOT40 index incorporates a threshold below 
which concentrations are not considered. Though the AOT40 threshold is 
lower than the threshold value in SUM06, the 2007 Staff Paper concluded 
that the vegetation effects information does not provide evidence of an 
effects threshold that applies to all species. Thus, the Administrator 
concludes neither of these forms is as biologically relevant as the 
W126 form.
---------------------------------------------------------------------------

    \60\ The AOT40 index used in Europe is a cumulative index that 
incorporates a threshold at 0.04 ppm (40 ppb). This index is 
calculated as the area over the threshold (AOT) by subtracting 40 
ppb from the value of each hourly concentration above that threshold 
and then cumulating each hourly difference over a specified window.
---------------------------------------------------------------------------

    With regard to consideration of coupling a W126 form with a 
separate N100 index, there was very little research on the N100 index 
or a coupled approach to be evaluated in the 2008 rulemaking. The 
CASAC, after reviewing all the information in the 2006 Criteria 
Document and the 2007 Staff Paper, did not recommend an additional N100 
index for consideration. Therefore, there is no basis at this time to 
judge the extent to which such a coupled W126-N100 form would be a 
better choice than the proposed W126 form. Further, the W126 form 
incorporates a weighting scheme that places greater weight on 
increasing concentrations and gives every concentration of 0.10 ppm and 
above an equal weight of 1, which is the highest weight in this 
sigmoidal weighting function.
    In summary, having considered the scientific information and 
assessment results available in the 2008 rulemaking as discussed above 
in this proposal notice, as well as the recommendations of the staff 
and CASAC, and having taken into consideration issues raised in public 
comments received as part of the 2008 rulemaking, and recognizing the 
determinations made below in section IV.D.5.c on level, the 
Administrator concludes that it is appropriate to set the secondary 
standard using a cumulative, seasonal form. The Administrator also 
concludes that the W126 form is best suited to reflect the biological 
impacts of O3 exposure on vegetation, and that there is 
adequate certainty in the information available in the 2008 rulemaking 
to support such a change in form. Thus, the Administrator proposes to 
set the secondary standard using a cumulative, seasonal W126 form.
b. Averaging Times \61\
---------------------------------------------------------------------------

    \61\ While the term ``averaging time'' is used, for the 
cumulative, seasonal standard the seasonal and diurnal time periods 
at issue are those over which exposures during a specified period of 
time are cumulated, not averaged.
---------------------------------------------------------------------------

    The Administrator, in addition to reconsidering what form of a 
secondary standard is most appropriate for protecting vegetation, is 
also reconsidering what exposure periods (e.g., seasonal window, 
diurnal window), and what standard index, in terms of an annual index 
value versus a 3-year average of annual index values, are most 
appropriate when used in conjunction with the W126 cumulative seasonal 
form. Based on the information set forth in the 2007 Staff Paper, as 
well as CASAC views, as discussed above in section IV.D.1.b, the 
Administrator has reached conclusions regarding exposure periods, and 
the annual versus 3-year average index, that have the most biological 
relevance for plant response, as discussed below.
    In considering an appropriate seasonal window, the Administrator 
notes that the 2007 Staff Paper concluded that the consecutive 3-month 
period within the O3 season with the highest W126 index 
value (e.g., maximum 3-month period) was a reasonable seasonal time 
period to consider. The Administrator further notes that the 2007 Staff 
Paper acknowledged that the selection of any single seasonal exposure 
period for a national standard would necessarily represent a 
compromise, given the significant variability in growth patterns and 
lengths of growing seasons among the wide range of sensitive vegetation 
species occurring within the U.S. However, the Administrator also 
considered the Staff Paper conclusion that the period of maximum 
potential plant uptake of O3 would also likely coincide with 
the period of highest O3 occurring within the intra-annual 
period defined as the O3 season, since the high temperature 
and light conditions conducive to O3 formation are also 
conducive for plant activity. The Administrator also observes that the 
CASAC panel was supportive of the Staff Paper views, while recognizing 
that 3 months likely represented the minimum timeframe appropriate to 
consider. Therefore, the Administrator concludes, on these bases, that 
the consecutive 3-month period within the O3 season with the 
highest W126 index value (e.g., maximum 3-month period) remains an 
appropriate seasonal window to propose for the protection of sensitive 
vegetation.
    With regard to consideration of an appropriate diurnal window, the 
Administrator has taken into account the 2007 Staff Paper conclusion 
that for the vast majority of studied species, daytime exposures 
represent the majority of diurnal plant O3 uptake and are 
responsible for inducing the plant response of most significance to the 
health and productivity of the plant (e.g., reduced carbohydrate 
production). The Administrator is also aware, based on discussions in 
the 2007 Staff Paper that there are some number of species that show 
non-negligible amounts of O3 uptake at night due to 
incomplete stomatal closure. In reaching her conclusion that the 2007 
Staff Paper recommendation of a 12-hour daytime

[[Page 3021]]

window (8 a.m. to 8 p.m.) remains the most appropriate period over 
which to cumulate diurnal O3 exposures, specifically those 
most relevant to plant growth and yield responses, the Administrator 
places weight on the fact that the CASAC comments were also supportive 
of this diurnal window, recognizing again that it likely represents a 
minimum period over which plants can be vulnerable to O3 
uptake. Therefore, the Administrator is again proposing the 12-hour 
daytime window (8 a.m. to 8 p.m.) as an appropriate diurnal window to 
protect against O3-induced plant effects.
    Lastly, in considering whether an annual or a 3-year average index 
is more appropriate, the Administrator notes that in addition to the 
available scientific evidence regarding plant effects that can be 
brought to bear, there are also other public welfare considerations 
that may be appropriate to consider. In taking this view, the 
Administrator notes that the 2007 Staff Paper recognized that though 
most cumulative seasonal exposure levels of concern for vegetation have 
been expressed in terms of the annual timeframe, it may be appropriate 
to consider a 3-year average for purposes of standard stability. The 
Administrator has considered that while the 2007 Staff Paper notes that 
for certain welfare effects of concern (e.g., foliar injury, yield loss 
for annual crops, growth effects on other annual vegetation and 
potentially tree seedlings), an annual time frame may be a more 
appropriate period in which to assess what level would provide the 
requisite degree of protection, for other welfare effects (e.g., mature 
tree biomass loss), it also points out that a 3-year average may also 
be appropriate. The Administrator further observes that in concluding 
that it was appropriate to consider both an annual and a 3-year 
average, the 2007 Staff Paper also concluded that should a 3-year 
average of the 3-month, 12-hour W126 form be selected, a potentially 
lower level should be considered to reduce the potential of adverse 
impacts to annual species from a single high O3 year that 
could still occur while attaining a standard on average over 3-years. 
The Administrator also took note that the CASAC Panel, in addressing 
this issue of annual versus 3-year average concluded that multi-year 
averaging to promote a ``stable'' secondary standard is less 
appropriate for a cumulative, seasonal secondary standard than for a 
primary standard based on maximum 8-hour concentrations, and further 
concluded that if multi-year averaging is employed to increase the 
stability of the secondary standard, the level of the standard should 
be revised downward to assure that the desired degree of protection is 
not exceeded in individual years. The Administrator, in considering the 
merits of both the annual and 3-year average, and taking into account 
both the 2007 Staff Paper and CASAC views, concludes that it is 
important to place more weight on the public welfare benefit in having 
a stable standard, and that appropriate protection for vegetation can 
be achieved using a 3-year average form. The Administrator is thus 
proposing a 3-year average. However, given the uncertain nature of the 
evidence and potential concerns with using a 3-year average form, the 
Administrator is proposing to take comment on the appropriateness of 
the specific seasonal and diurnal exposure periods proposed, as well as 
the use of a 3-year average, and, as discussed below, the impact that 
selection of these proposed seasonal and diurnal exposure periods would 
have, in conjunction with a 3-year average form, on the appropriateness 
of the proposed range of levels.
c. Level
i. Considerations Regarding 2007 Proposed Range of Levels
    The 2007 Staff Paper, in identifying a range of levels for a 3-
month, 12-hour (daytime) W126 standard appropriate for the 
Administrator to consider in protecting the public welfare from known 
or anticipated adverse effects to vegetation from O3 
exposures, considered what information from the array of vegetation 
effects evidence and exposure and risk assessment results was most 
useful. With respect to the vegetation effects evidence, the 2007 Staff 
Paper found stronger support than what was available at the time of the 
1997 review for an increased level of protection for trees and forested 
ecosystems. Specifically, the expanded body of evidence included: (1) 
Additional field based data from free air, gradient and biomonitoring 
surveys demonstrating adverse levels of O3-induced growth 
reductions on trees at the seedling, sapling and mature growth stages 
and incidence of visible foliar injury occurring at biomonitoring sites 
in the field at ambient levels of exposure; (2) qualitative support 
from free air (e.g., AspenFACE) and gradient studies on a limited 
number of tree species for the continued appropriateness of using OTC-
derived C-R functions to predict tree seedling response in the field; 
(3) studies that continued to document below-ground effects on root 
growth and ``carry-over'' effects occurring in subsequent years from 
O3 exposures; and (4) increased recognition and 
understanding of the structure and function of ecosystems and the 
complex linkages through which O3, and other stressors, 
acting at the organism and species level can influence higher levels 
within the ecosystem hierarchy and disrupt essential ecological 
attributes critical to the maintenance of ecosystem goods and services 
important to the public welfare.
    Based on the above sources of vegetation effects information and 
the results of the exposure and risk assessments summarized above, the 
2007 Staff Paper concluded that just meeting the then current 0.084 
ppm, 8-hour average standard would continue to allow adverse levels of 
O3-induced effects to occur in sensitive commercially and 
ecologically important tree species in many regions of the country. The 
2007 Staff Paper further concluded that air quality levels would need 
to be substantially reduced to protect sensitive tree seedlings, such 
as black cherry, aspen, and cottonwood, from these growth and foliar 
injury effects.
    In addition to the currently quantifiable risks to trees from 
ambient exposures, the 2007 Staff Paper also considered the more subtle 
impacts of O3 acting in synergy with other natural and man-
made stressors to adversely affect individual plants, populations and 
whole systems. By disrupting the photosynthetic process, decreasing 
carbon storage in the roots, increasing early senescence of leaves and 
affecting water use efficiency in trees, O3 exposures could 
potentially disrupt or change the nutrient and water flow of an entire 
system. Weakened trees can become more susceptible to other 
environmental stresses such as pest and pathogen outbreaks or harsh 
weather conditions. Though it is not possible to quantify all the 
ecological and societal benefits associated with varying levels of 
alternative secondary standards, the 2007 Staff Paper concluded that 
this information should be weighed in considering the extent to which a 
secondary standard should be set so as to provide potential protection 
against effects that are anticipated to occur.
    The 2007 Staff Paper also recognized that in the 1997 review, EPA 
took into account the results of a 1996 Consensus Workshop. At this 
workshop, a group of independent scientists expressed their judgments 
on what standard form(s) and level(s) would provide vegetation with 
adequate protection from O3-related adverse effects. 
Consensus was reached

[[Page 3022]]

on protective ranges of levels in terms of a cumulative, seasonal 3-
month, 12-hr SUM06 standard for a number of vegetation effects 
endpoints. These ranges are identified below, with the estimated 
approximate equivalent W126 standard levels shown in parentheses. For 
growth effects to tree seedlings in natural forest stands, a consensus 
was reached that a SUM06 range of 10 to 15 (W126 range of 7 to 13) ppm-
hour would be protective. For growth effects to tree seedlings and 
saplings in plantations, the consensus SUM06 range was 12 to 16 (W126 
range of 9 to 14) ppm-hour. For visible foliar injury to natural 
ecosystems, the consensus SUM06 range was 8 to 12 (W126 range of 5 to 
9) ppm-hour.
    The 2007 Staff Paper then considered to what extent recent research 
provided empirical support for the ranges of levels identified by the 
experts as protective of different types of O3-induced 
effects. As discussed above in section IV.D.1.c, the 2007 Staff Paper 
concluded on the basis of the available evidence that it was 
appropriate to consider a range for a 3-month, 12-hour, W126 standard 
level that included the 1996 Consensus Workshop recommendations 
regarding a range of levels protective against O3-induced 
growth effects in tree seedlings in natural forest stands (i.e., 7-13 
ppm-hour in terms of a W126 form).
    In considering the newly available information on O3-
related effects on crops in this review, the 2007 Staff Paper observed 
the following regarding the strength of the underlying crop science: 
(1) Nothing in the recent literature points to a change in the 
relationship between O3 exposure and crop response across 
the range of species and/or cultivars of commodity crops currently 
grown in the U.S. that could be construed to make less appropriate the 
use of commodity crop C-R functions developed in the NCLAN program; (2) 
new field-based studies (e.g., SoyFACE) provide qualitative support in 
a few limited cases for the appropriateness of using OTC-derived C-R 
functions to predict crop response in the field; and (3) refinements in 
the exposure, risk and benefits assessments in this review reduce some 
of the uncertainties present in 1996. On the basis of these 
observations, the 2007 Staff Paper concluded that nothing in the newly 
assessed information calls into question the strength of the underlying 
science upon which EPA based its proposed decision in the last review 
to select a level of a cumulative, seasonal form associated with 
protecting 50 percent of crop cases from no more than 10 percent yield 
loss as providing the requisite degree of protection for commodity 
crops.
    The 2007 Staff Paper then considered whether any additional 
information was available to inform judgments as to the adversity of 
various O3-induced levels of crop yield loss to the public 
welfare. As noted above, the 2007 Staff Paper observed that 
agricultural systems are heavily managed, and that in addition to 
stress from O3, the annual productivity of agricultural 
systems is vulnerable to disruption from many other stressors (e.g., 
weather, insects, disease), whose impact in any given year can greatly 
outweigh the direct reduction in annual productivity resulting from 
elevated O3 exposures. On the other hand, O3 can 
also more subtly impact crop and forage nutritive quality and 
indirectly exacerbate the severity of the impact from other stressors. 
Since these latter effects could not be quantified at that time, they 
could only be considered qualitatively in reaching judgments about an 
appropriate degree of protection for commodity crops from 
O3-related effects.
    Based on the above considerations, the 2007 Staff Paper concluded 
that the level of protection judged requisite in the 1997 review to 
protect the public welfare from adverse levels of O3-induced 
reductions in crop yields and tree seedling biomass loss, as 
approximately provided by a W126 level of 21 ppm-hour, remained 
appropriate for consideration as an upper bound of a range of 
appropriate levels. The 2007 Staff Paper also recognized that a 
standard set at this level would not protect the most sensitive species 
or individuals within a species from all potential effects related to 
O3 exposures and further, that this level derives from the 
extensive and quantitative historic and recent crop effects database, 
as well as current staff exposure and risk analyses (EPA, 2007, pg. 8-
22).
    In identifying a lower bound for the range of alternative standard 
levels appropriate for consideration, staff concluded that several 
lines of evidence pointed to the need for greater protection for tree 
seedlings, mature trees, and associated forested ecosystems. Staff 
believed that tree growth was an important endpoint to consider because 
it is related to other aspects of societal welfare such as sustainable 
production of timber and related goods, recreation, and carbon 
(CO2) sequestration. Impacts on tree growth can also affect 
ecosystems through shifts in species composition and the loss of 
genetic diversity due to the loss of O3 sensitive 
individuals or species. In selecting an appropriate level of protection 
for trees, staff considered the results of the 1996 Consensus Workshop 
which identified the SUM06 range of 10 to 15 (W126 of 7 to 13) ppm-hour 
for growth effects to tree seedlings in natural forest stands.
    Because staff believed that O3-related effects on forest 
tree species are important public welfare effects of concern, it 
therefore concluded, based on the above, that it was appropriate to 
include 7 ppm-hour as the lower bound of the recommended range, the 
lower end of the approximate range recommended by CASAC (Henderson, 
2006c) and identified by the 1996 Consensus Workshop participants as 
protective of forest trees. At this lower end of the range, staff 
anticipated, based on its analyses of risks of tree seedling biomass 
loss and mature tree growth reductions and on the basis of the 
scientific effects literature, that adverse effects of O3 on 
forested ecosystems would be substantially reduced. Further, staff 
anticipated that the lower end of this range would provide increased 
protection from the more subtle impacts of O3 acting in 
synergy with other natural and man-made stressors to adversely affect 
individual plants, populations and whole systems. Staff also noted that 
by disrupting the photosynthetic process, decreasing carbon storage in 
the roots, increasing early senescence of leaves and affecting water 
use efficiency in trees, O3 exposure could potentially 
disrupt or change the nutrient and water flow of an entire system. Such 
weakened trees can become more susceptible to other environmental 
stresses such as pest and pathogen outbreaks or harsh weather 
conditions. While recognizing that it is not possible to quantify all 
the ecological and societal benefits associated with varying levels of 
alternative secondary standards, staff believed that this information 
should be weighed in considering the extent to which a secondary 
standard should be precautionary in nature in protecting against 
effects that have not yet been adequately studied and evaluated.
    Thus, the 2007 Staff Paper concluded, based on all the above 
considerations, that an appropriate range of levels, for an annual 
standard using a 3-month, 12-hour W126 form, for the Administrator to 
consider was 7 to 21 ppm-hour, recognizing that the level selected is 
largely a policy judgment as to the requisite level of protection 
needed. In determining the requisite level of protection for crops and 
trees, the 2007 Staff Paper recognized that it was appropriate to weigh 
the importance of the predicted risks of these effects in the overall 
context of

[[Page 3023]]

public welfare protection, along with a determination as to the 
appropriate weight to place on the associated uncertainties and 
limitations of this information.
ii. CASAC and Public Comments Prior to 2008 Decision
    In considering the evidence described in both the 2006 Criteria 
Document and 2006 draft Staff Paper, CASAC, in its October 24, 2006 
letter to the Administrator, expressed its view regarding the 
appropriate form and range of levels for the Administrator to consider. 
The CASAC preferred a seasonal 3-month W126 standard in a range that is 
the approximate equivalent of the SUM06 at 10 to 20 ppm-hour. Following 
the 2007 proposal, EPA received additional CASAC and public comments 
regarding an appropriate range of levels of a W126 form for the 
Administrator to consider in finalizing a revised secondary NAAQS for 
O3. The CASAC, in its final letter to the Administrator 
(Henderson, 2007), agreed with the 2007 Staff Paper recommendations 
that the lower bound of the range within which a seasonal W126 
secondary O3 standard should be considered is approximately 
7 ppm-hour; however, it did not agree with staff's recommendation that 
the upper bound of the range should be as high as 21 ppm-hour. Rather, 
as discussed above in section IV.D.1.c, the CASAC Panel recommended 
that the upper bound of the range considered should be no higher than a 
W126 of 15 ppm-hour for an annual standard.
    The comments received from the public fell into two groups. One 
group of commenters supported the CASAC recommended range of 7-15 ppm-
hour for a W126 standard. Many of these same commenters further 
emphasized the lower end of the proposed range as necessary to provide 
adequate protection for sensitive species. These commenters based their 
recommendation primarily on four sources of information: (1) Field-
based evidence of foliar injury occurring on sensitive species at air 
quality levels well below that of the current standard; (2) the 1996 
Consensus Workshop recommendations for protective levels in terms of 
cumulative exposures for different vegetation types; (3) CASAC advice 
and recommendations; and (4) studies published after the close of the 
2006 Criteria Document that potentially strengthen the link between 
species level impacts and ecosystem response.
    The other group of commenters did not support revising the current 
secondary standard. These commenters primarily focused on uncertainties 
regarding the sources of information relied upon by the first group of 
commenters as support for a level within the range of levels 
recommended by CASAC. These uncertainties included: (1) potential 
confounders, such as soil moisture, on visible foliar injury and the 
lack of a clear relationship between visible foliar injury symptoms and 
other vegetation effects; (2) lack of documentation of the basis for 
the recommendations from the 1996 Consensus Workshop in selecting a 
range of levels, indicating that these recommendations should be used 
with great caution; (3) failure of CASAC and EPA to take into account 
the monitor height measurement gradient when making their 
recommendations concerning the level of the secondary standard; and (4) 
inability to quantitatively estimate ecosystem effects of O3 
or to extrapolate meaningfully from effects on individual plants to 
ecosystem effects due to inadequate data.
iii. Conclusions on Level
    The Administrator is proposing to set a cumulative, seasonal 
standard expressed in terms of the maximum 3-month, 12-hour W126 form, 
in the range of 7 to 15 ppm-hour. In reaching this proposed decision 
about an appropriate range of levels for the secondary standard, the 
Administrator has considered the following: the evidence described in 
the 2006 Criteria Document and the 2007 Staff Paper; the results of the 
vegetation exposure and risk assessments discussed above and in the 
2007 Staff Paper, giving weight to the assessments as judged 
appropriate; the CASAC Panel's advice and recommendations in the 
CASAC's letters to the Administrator; EPA staff recommendations; and 
public comments received during the development of these documents, 
either in connection with CASAC meetings or separately. In considering 
what range of levels of a cumulative 3-month standard to propose, the 
Administrator notes that this choice requires judgment as to what 
standard will protect the public welfare from any known or anticipated 
adverse effects. This choice must be based on an interpretation of the 
evidence and other information, such as the exposure and risk 
assessments, that neither overstates nor understates the strength and 
limitations of the evidence and information nor the appropriate 
inferences to be drawn. In taking all of the above into consideration, 
the Administrator also notes that there is no bright line clearly 
directing the choice of level for any of the effects of concern, and 
the choice of what is appropriate is clearly a public welfare policy 
judgment entrusted to the Administrator.
    In particular, the Administrator has given careful consideration to 
the following: (1) The nature and degree of effects of O3 to 
the public welfare, including what constitutes an adverse effect; (2) 
the strengths and limitations of the evidence that is available 
regarding known or anticipated adverse effects from cumulative, 
seasonal exposures, and its usefulness in informing selection of a 
proposed range; and (3) CASAC's views regarding the strength of the 
evidence and its adequacy to inform a range of levels. Each of these 
topics is discussed in turn below.
    In determining the nature and degree of effects of O3 on 
the public welfare, the Administrator recognizes that the significance 
to the public welfare of O3-induced effects on sensitive 
vegetation growing within the U.S. can vary, depending on the nature of 
the effect, the intended use of the sensitive plants or ecosystems, and 
the types of environments in which the sensitive vegetation and 
ecosystems are located. Any given O3-related effect on 
vegetation and ecosystems (e.g., biomass loss, foliar injury), 
therefore, may be judged to have a different degree of impact on the 
public depending, for example, on whether that effect occurs in a Class 
I area, a city park, or commercial cropland. In her judgment, it is 
appropriate that this variation in the significance of O3-
related vegetation effects should be taken into consideration in 
judging the level of ambient O3 that is requisite to protect 
the public welfare from any known or anticipated adverse effects. In 
this regard, the Administrator agrees with the definition of adversity 
as described above in section IV.A.3 and in the 2008 rulemaking. As a 
result, the Administrator concludes that of those known and anticipated 
O3-related vegetation and ecosystem effects identified and 
discussed in this reconsideration, the highest priority and 
significance should be given to those that occur on sensitive species 
that are known to or are likely to occur in federally protected areas 
such as Class I areas \62\ or on lands set aside by States, Tribes and 
public interest groups to provide similar benefits to the public

[[Page 3024]]

welfare, for residents on those lands, as well as visitors to those 
areas.
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    \62\ For example, the level of protection granted by Congress 
under the Wilderness Act of 1964 for designated ``wilderness areas'' 
requires that these areas ``shall be administered for the use and 
enjoyment of the American people in such manner as will leave them 
unimpaired for future use as wilderness, and so as to provide for 
the protection of these areas, the preservation of their wilderness 
character'' (The Wilderness Act, 1964).
---------------------------------------------------------------------------

    Likewise, the Administrator also notes that the same known or 
anticipated O3-induced effects, occurring in other areas may 
call for less protection. For example, the maintenance of adequate 
agricultural crop yields is extremely important to the public welfare 
and is currently achieved through the application of intensive 
management practices, including in some cases, genetic engineering. 
These management practices, in conjunction with market forces and 
government programs, assure an appropriate balance is reached between 
costs of production and market availability. Thus, while research on 
agricultural crop species remains useful in illuminating mechanisms of 
action and physiological processes, information from this sector on 
O3-induced effects is considered less useful in informing 
judgments on what level(s) would be sufficient but not more than 
necessary to protect the public welfare. With respect to commercial 
production of commodities, the Administrator notes that judgments about 
the extent to which O3-related effects on commercially 
managed vegetation are adverse from a public welfare perspective are 
particularly difficult to reach, given that what is known about the 
relationship between O3 exposures and agricultural crop 
yield response derives largely from data generated almost 20 years ago. 
The Administrator recognizes that there is substantial uncertainty at 
this time as to whether these data remain relevant to the majority of 
species and cultivars of crops being grown in the field today. In 
addition, the extensive management of such vegetation may to some 
degree mitigate potential O3-related effects. The management 
practices used on these lands are highly variable and are designed to 
achieve optimal yields, taking into consideration various environmental 
conditions. Thus, the Administrator concludes there is no need for such 
additional protection for agricultural crops through the NAAQS.
    The Administrator also recognizes that O3-related 
effects on sensitive vegetation can occur in other areas that have not 
been afforded special Federal protections, ranging from effects on 
vegetation growing in residential or commercial settings, such as 
ornamentals used in urban/suburban landscaping, to vegetation grown in 
land use categories that are heavily managed for commercial production 
of commodities such as timber. For vegetation used for residential or 
commercial ornamental purposes, such as urban/suburban landscaping, the 
Administrator believes that there is not adequate information at this 
time to establish a secondary standard based specifically on impairment 
of urban/suburban landscaping and other uses of ornamental vegetation, 
but notes that a secondary standard revised to provide protection for 
sensitive natural vegetation and ecosystems would likely also provide 
some degree of protection for such ornamental vegetation.
    Based on the above, the Administrator finds that the types of 
information most useful in informing the selection of an appropriate 
range of protective levels is appropriately focused on information 
regarding exposures and responses of sensitive trees and other native 
species known or anticipated to occur in protected areas such as Class 
I areas or on lands set aside by States, Tribes and public interest 
groups to provide similar benefits to the public welfare, for residents 
on those lands, as well as visitors to those areas.
    With regard to the available evidence, the Administrator finds the 
coherence and strength of the weight of evidence from the large body of 
available literature compelling. This evidence addresses a broad array 
of O3-induced effects on a variety of tree species across a 
range of growth stages (i.e., seedlings, saplings and mature trees) 
using diverse field-based (e.g. free air, gradient and ambient) and OTC 
exposure methods. It demonstrates that significant numbers of forest 
tree species are potentially experiencing O3-induced stress 
under levels of ambient air quality, both at and below the level of the 
1997 standard.
    In particular, the Administrator notes the evidence from recent 
field-based studies and a gradient study of eastern cottonwood saplings 
(Gregg et al., 2003). She observes that this study found that 
cottonwood saplings grown in urban New York City grew faster than 
saplings grown in downwind rural areas where cumulative O3 
exposures were higher, and the difference in biomass production between 
the urban site with the lowest cumulative exposure and the rural site 
with the highest cumulative exposure is dramatic (Figure 7-17 in the 
2007 Staff Paper). The Administrator further notes that cottonwood is 
one of the most sensitive tree species studied to date and it is also 
important both from an ecological and public welfare perspective, as 
discussed above in section IV.A.2.b and in the 2007 Staff Paper.
    The Administrator also notes the evidence related to the 
O3-induced effect of visible foliar injury. The 
Administrator observes that the visible foliar injury database created 
from the ambient field-based monitoring network managed by the Unites 
States Forest Service (USFS) Forest Inventory and Analysis (FIA) 
Program has continued to expand since the conclusion of the 1997 
review. In utilizing this dataset, EPA staff collaborated with FIA 
staff to compare the incidence of visible foliar injury at different 
levels of air quality by county throughout the U.S. in counties with 
FIA monitoring sites. In considering the results of this analysis, 
depicted in Table 7-4 of the 2007 Staff Paper, the Administrator notes 
that for the 2001-2004 period, the percent of counties with documented 
foliar injury at a level approximately equivalent to the W126 of 21 
ppm-hour, was 26 to 49 percent, while at the lower level approximately 
equivalent to a W126 of 13 ppm-hour, incidence values ranged from 12 to 
35 percent. The Administrator believes it likely that some sensitive 
species occurring in specially protected areas would also exhibit 
visible foliar injury symptoms to a similar degree at these exposure 
levels. She further notes that while direct links between O3 
induced visible foliar injury symptoms and other adverse effects (e.g., 
biomass loss) are not always found, visible foliar injury in itself is 
considered by the National Park Service (NPS) to affect adversely air 
quality related values (AQRV) in Class I areas.
    The Administrator places significant weight on the judgments of 
CASAC. In so doing, the Administrator has carefully considered its 
stated views and the basis for the range of levels the CASAC 
O3 Panel recommended. In its 2007 letter to the 
Administrator, the CASAC O3 Panel agreed with EPA staff 
recommendations that the lower bound of the range within which a 
seasonal W126 O3 standard should be considered is 
approximately 7 ppm-hour. However, ``it does not agree with Staff's 
recommendations that the upper bound of the range should be as high as 
21 ppm-hour. Rather, the Panel recommends that the upper bound of the 
range considered should be no higher than 15 ppm-hour, which the Panel 
estimates is approximately equivalent to a seasonal 12-hour SUM06 level 
of 20 ppm-hour'' (Henderson, 2007). The Administrator notes that CASAC 
views concerning an appropriate range of levels for the Administrator 
to consider were presented after CASAC had considered the entire body 
of evidence presented in both the 2006 Criteria Document and 2007 Staff 
Paper, and are generally consistent with the 1996 Consensus Workshop 
recommendations.

[[Page 3025]]

    In considering the issues raised by commenters on the 2007 proposed 
rule, the Administrator noted that many public commenters supported the 
range of levels recommended by CASAC. The Administrator also considered 
the views expressed by the NPS as to what range of levels it identified 
as useful in helping it achieve its mandate to protect AQRVs in 
national parks and wilderness areas and to provide a level of 
protection for its resources in keeping with the Congressional mandate 
set forth in The Wilderness Act of 1964. In so doing, the Administrator 
notes that the NPS supported the range recommended by CASAC, while 
emphasizing that the lower end of the range was more appropriate. The 
NPS notes that though some visible foliar injury would still be 
expected to occur above the lower end of the CASAC recommended range 
(i.e. 7 ppm-hour), the potential for growth impacts at that level would 
be very low. It further notes that most of these parks contain aspen, 
black cherry, or ponderosa pine, all sensitive species predicted to 
have significant growth effects at current W126 levels.
    The Administrator also considered those comments that highlighted 
sources of uncertainty in the evidence and risk assessments (summarized 
above in section IV.D.5.c.ii) to inform her judgments on how much 
weight to place on these associated uncertainties, as discussed below.
    With regard to the issue of possible confounders of foliar injury 
information, the Administrator recognizes that visible foliar injury, 
like other O3-induced plant effects, is moderated by 
environmental factors other than O3 exposure. However, the 
Administrator also notes that the O3-related visible foliar 
injury effect persisted across a four year period (2001-2004), despite 
year-to-year variability in meteorology and other environmental factors 
(see Table 7-4 in the 2007 Staff Paper). She also notes that 
approximately 26 to 49 percent of counties had visible foliar injury 
incidence at the approximate W126 level of 21 ppm-hour, while at a W126 
level of 13 ppm-hour, this range of percentages dropped to 
approximately 12 to 23 percent. In an area such as a national park, 
where visitors come in part for the aesthetic quality of the landscape, 
the Administrator recognizes that visible foliar injury incidence is an 
important welfare effect which should be considered in determining an 
appropriately protective standard level.
    With regard to the issues of what weight to place on the 
recommendations from the 1996 Consensus Workshop in selecting a range 
of levels, as the 1997 Workshop Report did not clearly document the 
basis for its recommendations, the Administrator recognizes that the 
absence of such documentation does call for care in placing weight on 
such recommendations. However, the Administrator notes that the 
workshop participants were asked to review both the 1996 O3 
Criteria Document and Staff Paper, representing the most up to date 
compilation of the state of the science available at that time, in 
order to ensure that their expert judgments made were also informed by 
the latest science. She also notes that another group of experts, the 
CASAC O3 Panel, reached a similar consensus based upon an 
expanded body of scientific evidence. In addition, the 2007 Staff Paper 
evaluated the same recommendations in the context of subsequent 
empirical evidence, and reached similar views, with the exception of 
the upper end of the recommended range, which in the 2007 Staff Paper 
was based on effects on commercial crops that had been considered in 
the 1997 review. While it would always be more useful to have 
documentation of the reasoning and basis for an expert's advice, in 
this case the Administrator judges that the 1996 Consensus Workshop 
recommendations should be given substantial weight.
    With regard to other issues raised by some commenters related to 
uncertainties in the technical evidence and analyses, the Administrator 
notes that such issues had been addressed in the 2007 Staff Paper that 
reflected CASAC's advice on such issues. For example, while the 
Administrator recognizes that uncertainty remains as to what level of 
annual tree seedling biomass loss when compounded over multiple years 
should be judged adverse to the public welfare, she believes that the 
potential for such anticipated effects should be considered in judging 
to what degree a standard should be precautionary.
    In considering all of the issues discussed above, the Administrator 
has decided to propose a range of 7-15 ppm-hour. In selecting as an 
upper bound a level of 15 ppm-hour, the Administrator notes that this 
level was specifically supported by the CASAC O3 Panel and 
is just above the range identified in the 1996 Consensus Workshop 
report as needed to provide adequate protection for trees growing in 
natural areas. In addition, the NPS, along with many public commenters, 
were in support of the CASAC range, including the upper bound of 15 
ppm-hour, and indicated that lower values within this range would be 
more protective for sensitive trees in protected areas from biomass 
loss and visible foliar injury symptoms.
    While the upper end of this range is lower than the upper end of 21 
ppm-hour recommended in the 2007 Staff Paper, this upper level of 21 
ppm-hour was originally put forward in the 1997 review in terms of a 
SUM06 of 25 ppm-hour (W126 of 21 ppm-hour) and was justified on the 
basis that it was predicted to allow up to 10% biomass loss annually in 
50% of studied commercial crops and tree seedling species. Recognizing 
the significant uncertainties that are associated with evaluating 
effects on commercial crops from a public welfare perspective, the 
Administrator now concludes that commercial crop data are no longer 
useful for setting the upper level of the range for proposal.
    With regard to her selection of a proposed range, the Administrator 
has considered that the direction from Congress to provide a high 
degree of protection in Class I areas creates a clearer target for 
gauging what types and magnitudes of effects would be known or 
anticipated to affect the intended use of these and other similarly 
protected areas, that would thus be considered adverse to the public 
welfare. Such similar areas include lands set aside by States, Tribes 
and public interest groups to provide similar benefits to the public 
welfare, for residents on those lands, as well as visitors to those 
areas. The Administrator also believes that in order to preserve 
wilderness areas in an unimpaired state for future generations, she 
must consider a level that affords substantial protection from known 
adverse O3-related effects of biomass loss and foliar injury 
on sensitive tree species, as well as a level that takes into account 
potential ``anticipated'' adverse O3-related effects, 
including effects that result in continued impairment in the year 
following O3 exposure (i.e., carry-over effects), below 
ground impacts, ecosystem level impacts, and reduced CO2 
sequestration
    While the Administrator acknowledges that growth effects and 
visible foliar injury can still occur in sensitive species at levels 
below the upper bound of the proposed range, the Administrator also 
recognizes that some significant uncertainties remain regarding the 
risk of these effects, as discussed above. For example, the 
Administrator concludes that remaining uncertainties make it difficult 
to judge the point at which visible foliar injury becomes adverse to 
the public welfare in various types of specially protected areas. 
Uncertainties associated with monitoring ambient exposures must be

[[Page 3026]]

considered in evaluating the strength of predictions regarding the 
degree of tree seedling growth impairment estimated to occur at varying 
ambient exposures. These uncertainties add to the challenge of judging 
which exposure levels are expected to be associated with levels of tree 
seedling growth effects considered adverse to public welfare The 
Administrator believes that it is important to consider these 
uncertainties, and the weight to place on such uncertainties, in 
selecting a range of standard levels to propose. Establishing 15 ppm-
hour as the upper end of the proposed range reflects her judgment 
regarding the appropriate weight to place on these uncertainties in 
determining the degree of protection that is warranted for known and 
anticipated adverse effects.
    With regard to her selection of a lower bound for the proposed 
range, the Administrator believes that if weight is placed on taking a 
more precautionary approach, recognizing that the real world impacts on 
trees and ecosystems could, in some cases, be greater than predicted, 
then the lower end of the range of 7 ppm-hour could be warranted. There 
is clear evidence that higher cumulative exposures can occur in rural 
areas downwind of urban areas and potentially in Class I areas. 
Unmonitored high elevation sites would also likely have higher 
cumulative exposures than lower elevation sites that are currently 
monitored. All of these considerations lead the Administrator to 
propose 7 ppm-hour as the low end of the proposed range.
    As discussed above in section IV.D.5.a, the main opposition to 
changing to a secondary standard with a cumulative, seasonal form has 
been the view that EPA does not have an adequate basis to identify the 
kinds and types of cumulative, seasonal exposure patterns that the 
standard should be designed to protect against, given the various 
uncertainties in the evidence, and whether EPA has an adequate basis to 
determine an appropriate level for a cumulative, seasonal secondary 
standard. While EPA agreed with this position in the 1997 review, the 
Administrator believes that the evidence before her appropriately 
supports a secondary standard that is distinctly different in form and 
averaging time from the 8-hour primary standard, and that such a 
standard is necessary to provide sufficient protection from cumulative, 
seasonal exposures to O3.
    While a different conclusion on this issue was reached in the 1997 
review, the current conclusion that an exposure index that is 
cumulative and seasonal in nature, and therefore that setting a 
standard based on such a form is necessary and appropriate, is based on 
information newly available in the 2008 rulemaking, which strengthens 
the information available in the 1997 review and reduces remaining 
uncertainties.
    Such newly available information includes quantitative information 
for a broader array of vegetation effects (extending to sapling and 
mature tree growth stages) obtained using a more diverse set of field-
based research study designs and improved analytical methods for 
assessing O3-related exposures and risks as discussed above 
in sections IV.A-C.
    These newly available studies also provide important support to the 
quantitative estimates of impaired tree growth based on earlier studies 
available in the 1997 review and address one of the key data gaps cited 
in the 1997 review. Additional qualitative information is also 
available regarding improved understanding of linkages between stress-
related effects of O3 exposures at the species level and 
those at higher levels within ecosystems. Finally, this information 
includes the use of new analytical methods, including a new multi-
pollutant, multi-scale air quality model used to characterize exposures 
of O3-sensitive tree and crop species further address 
uncertainties in the assessments done in the 1997 review. In total, 
this newly available information increases the Administrator's 
confidence in important aspects of this rulemaking
    The decision in 2008 to set the secondary O3 standard 
identical to the 8-hour primary standard largely mirrored the decision 
in 1997, but failed to account for this significant increase in the 
body of knowledge available to support the 2008 rulemaking. This body 
of knowledge, while continuing to reflect significant uncertainties, 
provides an appropriate basis for determining a level of a cumulative, 
seasonal standard that, in the judgment of the Administrator, provides 
sufficient but not more than necessary protection from cumulative, 
seasonal exposures to O3. This is clearly so when compared 
to a standard that uses an indirect form that is not biologically 
relevant, an 8-hour average standard aimed at peak daily exposures. 
This judgment is fully consistent with the advice provided by CASAC.
    After carefully taking the above considerations into account, and 
giving significant weight to the views of CASAC, the Administrator has 
decided to propose a range of levels of 7-15 ppm-hour for a cumulative, 
seasonal secondary O3 standard expressed as an index of the 
annual sum of weighted hourly concentrations (i.e., the W126 form), 
cumulated over 12 hours per day during the consecutive 3-month period 
within the O3 season with the maximum index value, averaged 
over three years. In the Administrator's judgment, based on the 
information available in the 2008 rulemaking, a standard could be set 
within this range that would be requisite to protect public welfare 
from known or anticipated adverse effects to O3-sensitive 
vegetation and ecosystems. In the Administrator's judgment, a standard 
set at a level below the lower end of the range is not now supported by 
the weight of evidence and would not give sufficient weight to the 
important uncertainties and limitations inherent in the available 
scientific evidence and in the quantitative assessments conducted for 
the 2008 rulemaking. A standard set at a level above the upper end of 
the range is also not now supported by the weight of evidence and would 
not give sufficient weight to the credible inferences that the Agency 
has drawn from the scientific evidence nor to the quantitative 
assessments conducted for the 2008 rulemaking. The Administrator judges 
that the appropriate balance to be drawn, based on the entire body of 
evidence and information available in the 2008 rulemaking, is a range 
between 7 and 15 ppm-hour. On balance, the Administrator believes that 
a standard could be set within this range that would be sufficient but 
not more than necessary to protect public welfare from known or 
anticipated adverse effects due to O3.
    In reaching this proposed decision, as discussed above, the 
Administrator has focused on the nature of the benefits associated with 
setting a distinct secondary standard with a cumulative, seasonal form 
relative to a standard with a peak daily 8-hour average form, as well 
as on assessments that quantify the degree of protection likely to be 
afforded by such standards. In so doing, the Administrator has 
acknowledged limitations in quantifying the expected benefits 
associated with the proposed cumulative seasonal standard relative to 
the secondary standard set in 2008. Having considered the public 
comments received on the 2007 proposed rule in reaching this proposed 
decision, the Administrator is interested in again receiving public 
comment on the benefits to public welfare associated with the proposed 
cumulative seasonal standard set at specific levels within the proposed 
range relative to the standard set in 2008.

[[Page 3027]]

E. Proposed Decision on the Secondary O3 Standard

    For the reasons discussed above, and taking into account 
information and assessments presented in the 2006 Criteria Document and 
2007 Staff Paper, the advice and recommendations of CASAC, and the 
public comments received in conjunction with the 2008 rulemaking, the 
Administrator has decided to propose to set a new cumulative, seasonal 
secondary O3 standard with a form expressed as an index of 
the annual sum of weighted hourly concentrations (i.e., the W126 form), 
cumulated over 12 hours per day (8 a.m. to 8 p.m.) during the 
consecutive 3-month period within the O3 season with the 
maximum index value, averaged over three years, set within a range of 7 
to 15 ppm-hour. The Administrator solicits comment on the weight that 
is appropriately placed on the various types of evidence and analyses 
upon which this proposed standard is based, and on the appropriate 
weight to be placed on the uncertainties in this information, as well 
as on the benefits to public welfare associated with the proposed 
standard relative to the benefits associated with the standard set in 
2008.
    Data handling conventions for the proposed new secondary 
O3 standard are specified in the proposed addition of a new 
section to 40 CFR 50 Appendix P, as discussed in section V below. 
Issues related to monitoring requirements for the proposed new 
secondary O3 standard are discussed below in section VI.

V. Interpretation of the NAAQS for O3 and Proposed Revisions 
to the Exceptional Events Rule

    Appendix P to 40 CFR part 50, Interpretation of the Primary and 
Secondary National Ambient Air Quality Standards for Ozone, addresses 
data completeness requirements, data reporting, handling, and rounding 
conventions, and example calculations. The current Appendix P explains 
the computations necessary for determining when the current identical 
primary and secondary standards are met. The EPA is proposing to revise 
Appendix P to reflect the proposed revisions to the primary and 
secondary O3 NAAQS discussed above and to make other changes 
described below.
    As discussed below, the proposed revisions to Appendix P include 
the following: The addition of data interpretation procedures 
applicable to the proposed cumulative, seasonal secondary NAAQS (see 
section V.B); clarification of certain language in the current 
provisions applicable to the primary NAAQS to reduce potential 
confusion (section V.C); revisions to the provisions regarding the use 
of incomplete data sets for purposes of the primary NAAQS and the data 
completeness requirements across three years (sections V.D and V.E); 
the addition of a provision providing the Administrator discretion to 
use incomplete data as if it were complete, for the purpose of the 
primary NAAQS (section V.F); a change from truncation to rounding of 
multi-hour and multi-year average O3 concentrations for the 
purposes of the primary standard (section V.G); and the addition of 
provisions addressing data to be used in making comparisons to the 
NAAQS (section V.H). The proposed revisions also include changes in 
organization for greater clarity and consistency with other data 
interpretation appendices to 40 CFR part 50, which are not further 
described in this preamble.
    The EPA is also proposing changes to the O3-specific 
deadlines, in 40 CFR 50.14, by which states must flag ambient air data 
that they believe have been affected by exceptional events and submit 
initial descriptions of those events, and the deadlines by which states 
must submit detailed justifications to support the exclusion of that 
data from EPA determinations of attainment or nonattainment with the 
NAAQS. The O3-specific deadlines in the current 40 CFR 50.14 
would not be appropriate given the anticipated schedule for the 
designations of areas under the proposed revised O3 NAAQS.

A. Background

    The purpose of a data interpretation appendix in general is to 
provide the practical details on how to make a comparison between 
multi-day and possibly multi-monitor ambient air concentration data and 
the level of the NAAQS, so that determinations of compliance and 
violation are as objective as possible. Data interpretation guidelines 
also provide criteria for determining whether there are sufficient data 
to make a NAAQS level comparison at all. Appendix P was promulgated in 
March 2008 along with the most recent revisions to the primary and 
secondary O3 NAAQS. It is very similar to Appendix I, 
Interpretation of the 8-Hour Primary and Secondary National Ambient Air 
Quality Standards for Ozone, which was adopted in 1997 when the 
O3 NAAQS were first revised to have an 8-hour averaging 
period rather than the earlier 1-hour averaging period, along with 
other changes in form and level. The only substantive difference 
between Appendix I and the current version of Appendix P is that 
Appendix P contains truncation procedures consistent with the 
additional decimal digit used to express the level of the 2008 NAAQS in 
parts per million (0.075 ppm) compared to the 1997 NAAQS (0.08 ppm). In 
July 2007, EPA had also proposed to include in Appendix P data 
interpretation procedures for the proposed cumulative, seasonal 
secondary O3 NAAQS, but these procedures were not finalized 
given that the final secondary NAAQS was identical in all respects to 
the final primary NAAQS.
    An exceptional event is defined in 40 CFR 50.1 as an event that 
affects air quality, is not reasonably controllable or preventable, is 
an event caused by human activity that is unlikely to recur at a 
particular location or a natural event, and is determined by the 
Administrator in accordance with 40 CFR 50.14 to be an exceptional 
event. Air quality data that are determined to have been affected by an 
exceptional event under the procedural steps and substantive criteria 
specified in section 50.14 may be excluded from consideration when EPA 
makes a determination that an area is meeting or violating the 
associated NAAQS. The key procedural deadlines in section 50.14 are 
that a state must notify EPA that data have been affected by an event, 
i.e., ``flag'' the data in the Air Quality Systems (AQS) database, and 
provide an initial description of the event by July 1 of the year after 
the data are collected, and that the State must submit the full 
justification for exclusion within 3 years after the quarter in which 
the data were collected. However, if a regulatory decision based on the 
data, for example a designation action, is anticipated, the schedule is 
shortened and all information must be submitted to EPA no later than a 
year before the decision is to be made. This generic schedule presents 
problems when a NAAQS has been recently revised, as discussed in 
section V.I below. On May 15, 2009, EPA finalized a set of 
O3-specific deadlines that corrected these problems at the 
time with respect to the 2008 NAAQS revisions (74 FR 23307). However, 
because of the anticipated effect of the current reconsideration on the 
schedule for O3 designations, the schedule problems will 
resurface unless the deadlines are adjusted again.

B. Interpretation of the Secondary O3 Standard

    The EPA is proposing data interpretation procedures for the 
proposed secondary O3 NAAQS, which is defined in terms of a 
specific cumulative, seasonal form, commonly

[[Page 3028]]

referred to as the W126 form, as described above in section IV. The 
proposed new section 4 of Appendix P on data interpretation for the 
secondary standard contains the following main features.
    The ``design value'' for the secondary standard, the statistic for 
a monitoring site which would be compared to the level of the secondary 
standard to determine if the site meets the standard, would be the 
average of the annual maximum values of the three-month index value 
from three calendar years.
    The new section would provide clear directions and examples for the 
calculation of the daily index value, the monthly cumulative index 
value, the annual maximum index value for a year, and the design value 
itself.
    Only the data from the required O3 monitoring season 
would be examined to determine the annual maximum index value; any 
additional period of monitoring undertaken voluntarily by a state would 
not be considered. The EPA believes that because of the recently 
proposed extension of the required monitoring seasons in many states 
(74 FR 34525, July 16, 2009), as discussed below in section VI, such a 
period of voluntary monitoring would be unlikely to have such high 
index values as to affect the annual maximum index value. Moreover, the 
proposed required monitoring season may encompass the most active 
growing season in many areas. The EPA invites comment on whether 
instead the entire actual O3 monitoring period should be 
considered, to eliminate any possibility that the highest cumulative 
index value that can be determined with available data might be missed.
    For each month in a three-month period, O3 data would 
have to be available for at least 75 percent of daylight hours (defined 
for this purpose as 8 a.m.-7:59 p.m. LST). If data are available for at 
least 75 percent but fewer than 100 percent of these daylight hours in 
a month, the cumulative index value calculated from the available 
daylight hours in the month would be increased to compensate for the 
missing hours, based on an assumption that the missing hours would have 
the same distribution of O3 concentrations as the available 
hours. A substitution test is also proposed, by which months in which 
fewer than 75 percent of daylight hours have O3 
concentration data might also be useable for calculating a valid 
cumulative index value. Such months would be used if the available 
O3 concentrations are so high that even substituting low 
concentration values for enough missing data to meet the 75 percent 
requirement would result in a design value greater than the level of 
the standard. The low value that would be substituted would be the 
lowest 1-hour O3 concentration observed at the monitoring 
site during daylight hours during the required O3 monitoring 
season, in that calendar year, or one-half the method detection limit 
(MDL) of the ozone instrument, whichever is higher.\63\
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    \63\ Because only enough missing 1-hour ozone values would be 
substituted as needed to meet the 75 percent completeness 
requirement, to avoid unreasonable underestimation of the true W126 
index, tying the the selection of the substitution value to the hour 
of the missing value, as is proposed for data substitution for the 
purpose of the primary standard (see section V.D), would introduce 
considerable complexity by requiring an algorithm for determining 
which specific missing values would be substituted. Therfore, EPA is 
proposing this simpler substitution approach for the secondary 
standard.
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    The EPA notes that while this proposed approach to identifying the 
substitution value for the secondary standard is technically 
appropriate, it would necessitate data processing efforts during 
implementation that might be avoidable via some other approach that is 
also technically reasonable. We therefore invite comment on such 
alternative approaches, and we may adopt another approach in the final 
rule. For example, for simplicity the substituted 1-hour O3 
concentration value could instead simply always be zero or one-half the 
MDL of the O3 instrument, noting that because of the 
sigmoidal weighting factor the exact magnitude of the low substitution 
value may typically make very little difference to the annual index 
value. Also, using the previous calendar year as the source of the 
substitution value instead of the current calendar year would have the 
advantage of allowing all parties to know early in each year what the 
substitution value will be.
    The EPA is proposing that all decimal digits be retained in 
intermediate steps of the calculation of the cumulative index, with the 
result rounded to have no decimal digits when expressed in ppm-hours 
before comparison the level of the secondary NAAQS.
    EPA expects that the three months over which the cumulative 
weighted index value is highest will generally occur in the middle of 
each year. Therefore, the proposed new section 4 of Appendix P presumes 
this, and does not address a situation in which the three months of 
maximum cumulative index spans two calendar years, for example December 
to February. The EPA invites comment on whether a provision addressing 
such a remote possibility is needed and what its terms should be. For 
example, the process of checking each three month period in a calendar 
year to determine which gives the highest index value could include the 
combinations of December/January/February and November/December/January 
within one calendar year.

C. Clarifications Related to the Primary Standard

    The EPA is proposing two clarifying changes to Appendix P to make 
unambiguous two aspects of data interpretation for the primary 8-hour 
standard. The first change clarifies that the standard data 
completeness requirement that valid daily maximum 8-hour values exist 
for 75 percent of all days refers to days within the required 
O3 monitoring season only. The current wording of Appendix P 
is somewhat open to a reading that the requirement applies to all days 
in the actual monitoring record for the site in question, which could 
be longer than the required season if a state voluntarily monitors on 
additional days, or shorter than the required season if a monitor has 
started or ceased operation sometime during the required season. The 
O3 data completeness requirement is intended to avoid a 
determination that an area has met the NAAQS when in fact more than a 
reasonable number of days with high O3 potential were not 
successfully monitored. This purpose can be served if the data within 
the required O3 monitoring season only are reasonably 
complete, because as mentioned above EPA has proposed to revise the 
required O3 seasons so that they encompass all days with 
potential for an exceedance of even the lowest proposed level for the 
primary standard. Unsuccessful monitoring outside the required season 
should not be an obstacle to a finding of attainment. However, if an 
O3 monitor has missed more than 25 percent of the required 
O3 monitoring season, for example because it started or 
stopped operation mid-season, this should prevent a finding of 
attainment based on a three-year period that includes that season. The 
proposed clarifying language reflects EPA's actual intention and our 
past practice in applying Appendix P for regulatory purposes, and 
Appendix I as well.\64\
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    \64\ At present, EPA's Air Quality System (AQS) for storing and 
reporting air quality data provides a completeness report that is 
based on yet a third approach, in which the period for reporting 
data completeness is the required monitoring season plus any 
extension needed to encompass any exceedances that may have occurred 
outside the required season. However, EPA's practice for regulatory 
purposes has been to consider completeness only over the required 
ozone monitoring season.

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[[Page 3029]]

    The second proposed clarifying change would make it clear that when 
determining the fourth-highest daily maximum 8-hour O3 
concentration for a year, all days with monitoring data are to be 
considered, not just days within the required O3 monitoring 
season. This proposed clarifying language also reflects EPA's actual 
intention and our past practice in applying Appendix P, and Appendix I 
as well. While EPA believes it to be quite unlikely that an exceedance 
will occur outside the proposed revised required O3 
monitoring seasons and have a high enough concentration to affect the 
selection of the fourth-highest concentration for the year, when and if 
such an occurrence does happen, the data should not be ignored.

D. Revision to Exceptions From Standard Data Completeness Requirements 
for the Primary Standard

    The EPA is proposing to revise portions of Appendix P that describe 
certain exceptions to the standard data completeness requirements, 
under which a monitoring site can in some cases be determined to be 
meeting or violating the primary NAAQS despite not meeting the standard 
data completeness requirements. These changes would make Appendix P 
more logical in certain types of cases with incomplete data. While the 
particular types of cases whose outcome would be different with these 
changes have been rare historically, there may be more such affected 
cases in the future in conjunction with a primary O3 
standard revised to a level within the range of levels proposed in this 
action.
    The standard data completeness requirements in Appendix P for the 
primary O3 NAAQS apply a 75 percent requirement at each of 
three stages of data completeness testing. As discussed below, for each 
stage, there is an existing exception to the 75 percent requirement.
    In the first stage, an 8-hour period can be considered to have a 
valid 8-hour average O3 concentration only if at least 75 
percent of the hours, i.e., 6 or more hours, have a valid hourly 
O3 value. The provided exception is that if there are 5 or 
fewer hours but if substituting a very low value (specifically, one-
half the MDL of the O3 instrument) for all the missing hours 
results in a hypothetical 8-hour average that is above the level of the 
primary standard, the 8-hour period is considered valid and is assigned 
the hypothetical level resulting from the data substitution.\65\ For 
example, if the O3 concentration was 0.125 ppm for 5 hours, 
substituting a typical MDL/2 value of 0.0025 ppm for three missing 
hours would result in an 8-hour average of 0.079 ppm, which is an 
exceedance of the current primary standard, so the valid 8-hour average 
for the period would be taken to be 0.079 ppm. If this value is higher 
than one or more of the highest four daily maximum 8-hour 
concentrations otherwise calculated for the year, considering it to be 
valid affects the value identified as the fourth-highest for the year 
and thus also affects the final design value. The logical problem with 
this approach is that it is possible for a hypothetical 8-hour average 
with such substitution to be below the level of the NAAQS, thus not 
meeting the current condition for the exception, but for it to still 
make a critical difference in making the three-year design value be 
above the level of the NAAQS, because a three-year design value can 
include (and be sensitive to the exact value of) an annual fourth-
highest daily maximum that is not above the level of the NAAQS. This 
could be the case if the hypothetical 8-hour average with substitution 
is the maximum concentration 8-hour period for its day, and the day is 
one of the highest four O3 days of the year. Whether it 
actually is the case would further depend on the value of the 8-hour 
average itself, the values of the next highest daily maximum 8-hour 
average concentration in the year, and the values of the annual fourth-
highest daily maximum 8-hour concentration from the other two years. If 
the substituted 8-hour average would make a critical difference, it 
should be treated as valid and used in the calculation of the three-
year design value, even if it is not itself above the level of the 
standard. Another problem is that one-half of the MDL, which typically 
is about 0.0025 ppm, is very likely to be considerably lower than the 
actual O3 concentrations that were not successfully 
measured. Thus, while the one-half-MDL-substituted value is prevented 
from being an overestimate of the actual 8-hour average concentration, 
it is an unreasonably low estimate of that concentration which may have 
the effect of allowing a site with actual O3 levels above 
the standard to be found to meet the standard. The condition in the 
exception requiring a one-half-MDL-substituted ``8-hour'' average to be 
above the level of the NAAQS is therefore inappropriate.
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    \65\ Actually, it is an interpretation of the text of Appendix 
P, section 2.1, that the average resulting from the data 
substitution is to be taken as the ``8-hour'' average, rather than 
the average of the available 5 or fewer hours of data, which would 
be higher. The text is not entirely clear on this point.
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    In the second stage of data completeness testing, 75 percent of the 
24 possible 8-hour time blocks, which is 18 or more, must have valid 8-
hour average concentrations values. The intent of this requirement is 
to make sure that most of the day was actually monitored, such that the 
highest concentration 8-hour period was likely to be captured in the 
data. When this is not the case, the day is not considered in selecting 
the annual fourth-highest daily maximum 8-hour concentration and no 
credit for the day's monitoring is given towards the third stage of 
data interpretation (see below). The provided exception in the current 
Appendix P is that a day is considered valid if at least one 8-hour 
period has an average concentration above the level of the standard. 
However, as in the first stage, it is possible for an 8-hour period 
with an average concentration at or below the level of the NAAQS to 
play a critical role in whether the three-year design value meets the 
standard. Invalidating the day could have the effect of causing a lower 
value to be selected as the annual fourth-highest daily maximum 8-hour 
concentration, leading to a three-year design value that does not 
exceed the NAAQS while it would have exceeded if the day and the 8-hour 
average value had been treated as valid. The condition in the exception 
requiring at least one 8-hour average during the day to be above the 
level of the NAAQS is therefore inappropriate.
    In the third stage of data completeness testing, a completeness 
criterion is applied for the number of days in the required 
O3 season that have a valid maximum 8-hour average, i.e., 
days that have met the completeness conditions in the first two stages 
or have met the condition for an exception. Specifically, for each of 
the three years being used in the design value calculation, the number 
of valid days within the required O3 monitoring season (with 
no credit for extra days outside the season) must be at least 75 
percent of the days in the required O3 season, and the 
number of valid days across all three years must be 90 percent of the 
days in the three seasons.\66\ The provided exception to the 75/90 
percent requirement is that data from a year with less than 75 percent 
of seasonal days can nevertheless be used if during the year at least 
one day's maximum 8-hour average O3 concentration was

[[Page 3030]]

above the level of the standard and if the three-year design value is 
also above the standard.\67\ The problem with this exception, similar 
to the problems with the exceptions in the first and second stages of 
data completeness testing, is that a daily maximum 8-hour concentration 
that is at or below the level of the NAAQS can nevertheless make a 
critical difference in making the three-year design value be above the 
level of the NAAQS. When it does, an incorrect final result will be 
reached if the year of data is not granted an exception to the 75/90 
percent requirement. Specifically, there would be no valid three-year 
design value and no conclusion would be reached as to attainment or 
nonattainment, despite it being clear that the actual situation is 
nonattainment, in the sense that successful collection of additional 
hours and days of monitoring data could not possibly have resulted in a 
passing three-year design value. Moreover, since the three-year design 
value is the average of the fourth-highest daily maximum 8-hour 
concentration from each year, there is no logical connection between 
the design value and the existence of a single daily maximum 
concentration greater than the level of the standard, which is the 
current condition for the exception for this stage of testing for data 
incompleteness.
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    \66\ EPA also is proposing eliminate this 90 percent 
requirement, see section V.E. The point made in this paragraph 
applies with or without the 90 percent requirement in place.
    \67\ EPA notes that in the current versions of Appendix I and P, 
it is not explicit that this provided exception also applies in the 
case of three years which each have 75 percent or more of days with 
valid data but less than 90 percent across three years. Because EPA 
is proposing to remove the 90 percent requirement (see section V.E) 
this ambiguity does not need correction.
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    EPA proposes to remedy this situation by replacing the three 
separate statements of the exceptions to the three standard 
completeness requirements with a new data substitution step that 
addresses the root cause of the data incompleteness situation: missing 
hourly concentrations which make it doubtful whether actual maximum 
daily 8-hour concentrations were measured on a reasonably large 
percentage of the days during the required O3 monitoring 
season of each year. In the event that only 1, 2, 3, 4, or 5 hourly 
averages are available for an 8-hour period, a partially substituted 8-
hour average would be computed by substituting for all the hours 
without hourly averages a low hourly average value selected as follows, 
and then using 8 as the divisor.\68\ For days within the required 
O3 monitoring season, the substitution value would be the 
lowest hourly average O3 concentration observed for that 
hour of the day (local standard time) on any day during the required 
O3 monitoring season of that year, or one-half the MDL, 
whichever is higher. Using this value makes it highly unlikely that the 
resulting partially substituted 8-hour average concentration is higher 
than the actual concentration. Therefore, using the partially 
substituted 8-hour average in the design value calculation procedure is 
highly unlikely to result in an incorrect finding that a site does not 
meet the standard, but it may lead to a correct finding that a site 
does not meet the standard in some cases in which there would be no 
finding possible or an incorrect finding under the current version of 
Appendix P. However, the use of the higher of the lowest observed same-
hour concentration or one-half the MDL could be problematic if a robust 
set of hourly measurements is not available for the year, for example 
if a monitor began operation late in an ozone season. In such a case, 
the lowest observed same-hour concentration might not be low enough to 
eliminate all possibility that the value used for substitution is 
higher than the missing concentration value. To reduce this likelihood 
to essentially zero, we are proposing that if the number of same-hour 
concentration values available for the required O3 
monitoring season for the year is less than 50 percent of the number of 
days during the required O3 monitoring season, one-half the 
MDL of the O3 instrument would be used in the substitution 
instead of the lowest observed concentration. We invite comment on 
whether another percentage should be used for this purpose instead of 
50 percent.
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    \68\ Appendix P now provides that in the event that only 6 or 7 
hourly averages are available, the valid 8-hour average shall be 
computed on the basis of the hours available, using 6 or 7 as the 
divisor. We are not proposing to change this provision.
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    The EPA notes that while this proposed approach to identifying the 
substitution value for the primary standard is technically appropriate, 
it would necessitate new data processing efforts during implementation 
that might be avoidable via some other approach that is also 
technically reasonable. There may also be approaches which are more 
technically appropriate. We therefore invite comment on such 
alternative approaches, and we may adopt another approach in the final 
rule. Examples of simpler approaches would be to identify in the final 
rule a fixed substitution value other than one-half the MDL, to accept 
as valid 8-hour periods with only five measured hourly concentrations, 
to interpret between two hourly concentrations to obtain a substitute 
for a single missing hourly concentration, or to use the previous 
calendar year as the source of the substitution value instead of the 
current calendar year (thereby allowing all parties to know early in 
each year what the substitution value will be). Examples of more 
complex approaches that might be more technically appropriate include 
selecting a low percentile of the available same-hour concentration 
data rather than the lowest value to be the substitution value, or 
selecting the lowest same-hour value from the same calendar quarter or 
month (of the current year or the most recent year) rather than from 
the entire required ozone monitoring season. We also invite comment on 
whether the proposed approach to substitution should be used at all and 
if not what other approach should be used to address the potential 
problem just described.
    We propose that for simplicity and to further reduce any risk of a 
false finding that a site does not meet the standard, for days outside 
the required O3 monitoring season, the substitution value 
would always be one-half the MDL of the O3 instrument. We 
similarly invite comment on this aspect.
    There would be no condition that a partially substituted 8-hour 
average exceed the level of the standard for it be used in calculating 
the design value, unlike is now the case. An 8-hour period with no 
available hourly averages at all would not have a valid 8-hour average, 
as is now the case.
    In addition, to complete the solution to the problems described 
above, we are proposing that a design value that is greater than the 
level of the primary standard would be valid provided that in each year 
there were at least four days with at least one valid 8-hour 
concentration.\69\ One or more of these 8-hour average concentrations 
could be the partially substituted 8-hour average concentration 
resulting from the above described substitution procedure. In such a 
case, there is essentially no possibility that more complete monitoring 
data would have shown the site to be meeting the NAAQS. It is 
appropriate to include all 8-hour averages including those involving 
substitution when testing for an exceedance of the standard, because 
those averages are extremely unlike to

[[Page 3031]]

be overestimates of actual concentrations.
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    \69\ The requirement that there be at least four days with at 
least one hourly measurement is actually redundant and is stated 
only for ease of understanding, since there would be no annual 
fourth-highest daily maximum 8-hour concentration unless there are 
at least four days with monitoring data, and a single hourly data 
point is necessary and sufficient (with the proposed substitution 
step) to generate a daily maximum 8-hour concentration.
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    Finally, a design value equal to or less than the level of the 
standard would be valid only if at least 75 percent of the days in the 
required O3 monitoring season of each year have daily 
maximum 8-hour concentrations that are based on at least 18 periods 
with at least 6 hourly concentrations. This ensures that a site will be 
found to meet the standard only when a reasonably high percentage of 
the days in the required O3 monitoring season have 
reasonably complete hourly data. In this situation, it would be 
inappropriate to count the 8-hour periods with five or fewer actual 
hourly measurement values towards the 75 percent requirement when 
testing for whether a site meets the standard, because those 8-hour 
averages will be based on substitution of low values and therefore will 
be underestimates of actual concentrations. The only way to be 
reasonably certain that no 8-hour period had a high enough 
concentration so as to contribute to a design value over the level of 
the standard is to have at least 18 periods in which substitution for 
missing O3 values was not needed. This provision has the 
same effect as several elements of the current Appendix P considered 
together, and thus is not a substantive change.

E. Elimination of the Requirement for 90 Percent Completeness of Daily 
Data Across Three Years

    As stated above in section VI.D, Appendix P currently requires that 
in order for a design value equal to or less than the standard to be 
valid, at least 75 percent of days in each of three years must have a 
valid daily maximum 8-hour average concentration value, i.e., that many 
days must have at least 18 8-hour periods with at least 6 reported 
hourly concentrations each. Appendix P also requires that the average 
of the percentages from three consecutive years be at least 90 percent. 
The EPA is proposing to eliminate this 90 percent requirement for the 
average of three years and to retain only the requirement that each 
individual year have a percentage of at least 75 percent.
    The 90 percent requirement was incorporated into Appendix I (the 
data interpretation appendix for the 0.08 ppm O3 NAAQS) in 
1997 with an explanation that EPA had observed that 90 percent of 
O3 monitoring sites routinely achieved 90 percent data 
capture. The EPA now notes, however, that while the majority of 
monitoring sites do achieve 90 percent or better data capture in any 
given year, there are exceptions every year. The 90 percent requirement 
applied to the average percentage over three years is quite unforgiving 
if there has been one year with relatively low data completeness. For 
example, if one year just met the 75 percent requirement, the remaining 
two years would have to achieve a 97.5 percent data capture rate in 
order for the three years to meet the 90 percent requirement. This 
would allow only 4 missed hours of measurements per week, which would 
be challenging. The consequences for states could be important, under 
the current requirement. One possible result could be that an area 
actually in nonattainment with the NAAQS might have to be designated 
unclassifiable, although the substitution procedure proposed for cases 
of incomplete data, as described above in section VI.D, provides a path 
to an appropriate nonattainment finding in at least some cases. Another 
possible result is that a nonattainment area which had actually come 
into attainment could be unable to receive an attainment determination 
until three more years of sufficiently complete data are collected. 
This might, for example, result in an area which has achieved needed 
emissions reductions by its attainment deadline nevertheless being 
bumped up to a higher classification.
    The 90 percent requirement over three years has the potential to 
treat two areas disparately, for no obvious logical reason. Consider 
two areas with identical air quality. Suppose the first area has annual 
completeness percentages of 75, 95, and 95 percent (averaging to 85 
percent and thus failing the 90 percent requirement) and the second 
area has annual completeness percentages of 75, 98, and 98 percent 
(averaging to 90 percent). Suppose that the three-year design values in 
both areas are below the level of the NAAQS. Practically speaking, the 
most important uncertainty about whether each area actually meets the 
NAAQS is the low data capture rate in the first year. There is no 
obvious logic why the fact that the second area achieves marginally 
better data capture in the second and third year should permit it to 
receive an attainment finding despite this uncertainty, while the first 
area may not.
    The EPA also notes that for the other gaseous criteria pollutants--
sulfur dioxide, carbon monoxide and nitrogen dioxide--the completeness 
requirement is for 75 percent completeness of hourly measurements in an 
individual year.\70\
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    \70\ EPA has recently proposed to amend the completeness 
requirements for sulfur dioxide and nitrogen dioxide to add 
quarterly 75 percent completeness requirements in connection with 
proposals to establish 1-hour primary NAAQS for these pollutants, 
still with no requirement for 90 percent completeness across three 
years.
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    For these reasons, EPA proposes to eliminate the 90 percent 
requirement across three years of data but to retain the 75 percent 
requirement for individual years. The EPA notes that as a practical 
matter, the current 90 percent requirement in effect requires a minimum 
data capture rate somewhat above 75 percent in each year, because if 
data capture in any one year were as low as 75 percent the required 
data capture in the other years would be very hard to achieve. The 
minimum annual data capture rate is effectively somewhere in the range 
of 80 percent (implying a requirement to achieve 95 percent data 
capture in the two remaining years in order to meet the 90 percent 
requirement across three years) and 85 percent (implying a requirement 
to achieve 92.5 percent data capture in the two remaining years). The 
EPA invites comment on whether instead of retaining the 75 percent 
completeness requirement in each individual year, the requirement 
should be 80 percent or 85 percent.

F. Administrator Discretion To Use Incomplete Data

    The EPA is proposing that the Administrator have general discretion 
to use incomplete data to calculate design values that would be treated 
as valid for comparison to the NAAQS despite the incompleteness, either 
at the request of a state or at her own initiative. Similar provisions 
exist already for the PM2.5 and lead NAAQS, and EPA has 
recently proposed such provisions to accompany the proposed 1-hour 
NO2 and SO2 primary NAAQS. The Administrator 
would consider monitoring site closures/moves, monitoring diligence, 
and nearby concentrations in determining whether to use such data.

G. Truncation Versus Rounding

    Almost all State agencies now report hourly O3 
concentrations in parts per million to three decimal places, since the 
typical incremental sensitivity of currently used O3 
monitors is 0.001 ppm. In the current Appendix P approach, in 
calculating 8-hour average O3 concentrations from such 
hourly data any calculated digits past the third decimal place are 
truncated rather than retained or rounded back to three decimal places. 
Also, in calculating 3-year averages of the fourth-highest daily 
maximum 8-hour average concentrations, Appendix P currently requires 
the result to be reported to the

[[Page 3032]]

third decimal place with digits to the right of the third decimal place 
truncated. In this regard, Appendix P follows the precedent of Appendix 
I, except that Appendix P is based on a NAAQS level specified to three 
decimal places (0.075 ppm) while Appendix I addressed the case of a 
NAAQS level specified to only two decimal places (0.08 ppm). In the 
rulemaking that concluded in 2008 by establishing the 0.075 ppm level, 
EPA noted that the 2007 Staff Paper demonstrated that taking into 
account the precision and bias in 1-hour O3 measurements, 
the 8-hour design value had an uncertainty of approximately 0.001 ppm. 
Thus, EPA considered any value less than 0.001 ppm to be highly 
uncertain and, therefore, proposed and adopted truncation to the third 
decimal place for reporting 1-hour O3 concentrations and for 
both the individual 8-hour averages used to determine the annual fourth 
maximum and the 3-year average of the fourth maxima.
    The effect of this repeated truncation is that there is a 
consistent downward bias in the calculation of the three-year design 
value. The size of this bias can be notable. For example, seven hours 
with O3 concentrations of 0.076 ppm plus one hour of 0.075 
ppm results in an 8-hour average of 0.075 ppm after truncation, nearly 
a full 0.001 ppm below the actual 8-hour average of 0.075875 ppm. Seven 
hours with O3 concentrations of 0.077 ppm plus one hour of 
0.076 ppm results in an 8-hour average of 0.076 ppm after truncation. 
One year with the first pattern plus two years with the second pattern 
would give a three-year design value of 0.075 ppm, meeting the NAAQS, 
even though 23 of the 24 individual 1-hour concentrations involved in 
the calculation of the design value were above 0.075 ppm.
    The EPA has decided to reconsider this aspect of O3 data 
interpretation. Specifically, we are proposing that (1) 1-hour 
concentrations continue to be reported to only three decimal places, 
the same as is now specified in Appendix P, i.e., that the current 
practice of truncation of the 1-hour data to the nearest 0.001 ppm be 
retained; (2) all digits resulting from the calculation of 8-hour 
averages be retained; and (3) the three-year average of annual fourth-
highest daily maximum 8-hour concentrations be rounded to three decimal 
places before comparison to the NAAQS. The EPA continues to believe 
that given the uncertainty in individual 1-hour O3 
concentration measurements it is appropriate to truncate those 
measurements at three decimal places (many O3 instruments 
are programmed to only report three digits anyway). However, the 
calculations of 8-hour averages and three-year averages are 
mathematical steps, not a measurement process subject to uncertainties, 
and EPA perceives no logic in having a consistent downward bias by 
truncating the results of these mathematical steps. The EPA notes that 
the O3 NAAQS is the only NAAQS for which multi-hour, multi-
day, or multi-year averages of concentrations are truncated rather than 
rounded. The proposed change will make this aspect of O3 
data interpretation consistent with data interpretation procedures for 
the other criteria pollutants.

H. Data Selection

    The current version of Appendix P does not explicitly address the 
issue of what ambient monitoring data for O3 can and must be 
compared to the O3 NAAQS. The EPA proposes to add to 
Appendix P language addressing this issue. This language is similar to 
provisions recently proposed to be included in new data interpretation 
appendices for nitrogen dioxide and sulfur dioxide. The new section of 
Appendix P would clarify that all quality assured data collected with 
approved monitoring methods and known to EPA shall be compared to the 
NAAQS, even if not submitted to EPA's Air Quality System. The section 
also addresses the question of what O3 data should be used 
when two or more O3 monitors have been operating and have 
reported data for the same period at one monitoring site.

I. Exceptional Events Information Submission Schedule

    States are responsible for identifying air quality data that they 
believe warrant special consideration, including data affected by 
exceptional events. States identify such data by flagging (making a 
notation in a designated field in the electronic data record) specific 
values in the Air Quality System (AQS) database. States must flag the 
data and submit a justification that the data are affected by 
exceptional events if they wish EPA to consider excluding the data in 
determining whether or not an area is attaining the new O3 
NAAQS.
    All states that include areas that could exceed the O3 
NAAQS and could therefore be designated as nonattainment for the 
O3 NAAQS have the potential to be affected by this 
rulemaking. Therefore, this action applies to all states; to local air 
quality agencies to which a state has delegated relevant 
responsibilities for air quality management including air quality 
monitoring and data analysis; and to Tribal air quality agencies where 
appropriate. The Exceptional Events Rule preamble describes in greater 
detail to whom the rule applies (72 FR 13562-13563, March 22, 2007).
    The CAA Section 319(b)(2) authorizes EPA to promulgate regulations 
that govern the review and handling of air quality monitoring data 
influenced by exceptional events. Under this authority, EPA promulgated 
the Exceptional Events Rule (Treatment of Data Influenced by 
Exceptional Events (72 FR 13560, March 22, 2007) which sets a schedule 
for states to flag monitored data affected by exceptional events in AQS 
and for them to submit documentation to demonstrate that the flagged 
data values were caused by an exceptional event. Under this schedule, a 
state must initially notify EPA that data have been affected by an 
exceptional event by July 1 of the year after the data are collected; 
this is accomplished by flagging the data in AQS. The state must also 
include an initial description of the event when flagging the data. In 
addition, the state is required to submit a full demonstration to 
justify exclusion of such data within three years after the quarter in 
which the data were collected, or if a regulatory decision based on the 
data (such as a designation action) is anticipated, the demonstration 
must be submitted to EPA no later than one year before the decision is 
to be made.
    The rule also authorizes EPA to revise data flagging and 
documentation schedules for data used in the initial designation of 
areas under a new NAAQS. The generic schedule, while appropriate for 
the period after initial designations have been made under a NAAQS, may 
need adjustment when a new NAAQS is promulgated because until the level 
and form of the NAAQS have been promulgated, a state would not have 
complete knowledge of the criteria for excluding data. In these cases, 
the generic schedule may preclude states from submitting timely flags 
and associated documentation for otherwise approvable exceptional 
events. This could, if not modified, result in some areas receiving a 
nonattainment designation when the NAAQS violations were legitimately 
due to exceptional events.
    As a result of the Administrator's decision to reconsider the 2008 
O3 NAAQS, EPA is proposing to revise the exceptional events 
flagging and documentation schedule to correspond to the designations 
schedules that EPA is considering for the proposed revisions to the 
primary and secondary O3 NAAQS. The designation schedules

[[Page 3033]]

under consideration are discussed in greater detail below in section 
VII.A and summarized here. The CAA requires EPA to promulgate the 
initial designations for all areas no later than 2 years from the 
promulgation of a new NAAQS. Such period may be extended for up to one 
year if EPA has insufficient information. (See CAA section 107(d).) For 
a new primary O3 standard, EPA intends to issue designations 
on an accelerated schedule. For a new seasonal secondary O3 
standard, EPA is considering two alternative schedules for initial area 
designations.
    Primary Standard: If, as a result of the reconsideration, EPA 
promulgates a new primary O3 standard on August 31, 2010, 
EPA is proposing that state Governors would need to submit their 
initial designation recommendations to EPA by January 7, 2011. EPA 
would promulgate the final designations in July 2011 to allow 
sufficient time for the designations to be published and effective by 
August 31, 2011. EPA expects to base the final designations for the 
primary O3 standard on three consecutive years of certified 
air quality monitoring data from the years 2007-2009 or 2008-2010, if 
available. EPA is proposing that for exceptional event claims made for 
data years 2007-2009, states must flag and provide an initial 
description and detailed documentation by November 1, 2010. For data 
collected during data year 2010, EPA is proposing that exceptional 
event data that states want EPA to exclude from consideration in the 
designations process must be flagged with an initial description and 
fully documented by March 1, 2011 or 60 days after the end of the 
quarter when the event occurred, whichever date is first. To meet this 
proposed 60-day deadline, a state would also have to submit the 
O3 concentration data to AQS sooner than the normal deadline 
for such submission, which is 90 days after the end of the calendar 
quarter. EPA believes this is a reasonable expectation given that most 
states currently submit O3 data earlier than the 90-day 
deadline.
    Secondary Standard: If, as a result of the reconsideration, EPA 
promulgates a new seasonal secondary O3 standard by August 
31, 2010, EPA is taking comment on two alternative designations 
schedules. Under the first alternative, EPA would designate areas for 
the secondary standard on the same accelerated schedule discussed above 
for the primary standard. Under the second alternative, EPA would 
designate areas for the secondary standard on the maximum 2-year 
schedule provided under the CAA. Accelerated Schedule: Under the 
accelerated schedule for a seasonal secondary O3 NAAQS, EPA 
is proposing that for exceptional event claims made for data years 
2007-2009, states must flag and provide an initial description and 
detailed documentation by November 1, 2010. For data collected during 
data year 2010, EPA is proposing that exceptional event data that 
states want EPA to exclude from consideration in the designations 
process must be flagged with an initial description and fully 
documented by March 1, 2011 or 60 days after the end of the quarter 
when the event occurred, whichever date is first.
    2-year Schedule: Under the 2-year schedule, states would have 1 
year, or by August 2011, to submit their designations recommendations 
and EPA would finalize designations under the new secondary standard by 
August 2012. EPA expects to base final designations for a new seasonal 
secondary standard on the most recent three years of certified air 
quality monitoring data, which would typically be from the years 2009-
2011 in this case. Exceptional event data claims used from years 2008-
2010 must be flagged with an initial description included in AQS and 
submitted with complete documentation supporting such claims by July 1, 
2011. Exceptional event data claims from data year 2011 must be flagged 
with an initial description and submitted with complete documentation 
supporting such claims 60 days after the end of the calendar quarter 
when the event occurred or March 1, 2012, whichever occurs first.
    Therefore, using the authority provided in CAA section 319(b)(2) 
and in the Exceptional Events Rule at 40 CFR 50.14(c)(2)(vi), EPA is 
proposing to modify the schedule for data flagging and submission of 
demonstrations for exceptional events data considered for initial 
designations under the proposed reconsidered O3 primary and 
secondary NAAQS, as follows:

      Table 1--Schedule for Exceptional Event Flagging and Documentation Submission for Data To Be Used in
                                      Designations Decisions for New NAAQS
----------------------------------------------------------------------------------------------------------------
                                            Air quality
    NAAQS Pollutant/standard/(level)/     data collected   Event flagging & initial     Detailed documentation
            promulgation date              for calendar      description deadline         submission deadline
                                               year
----------------------------------------------------------------------------------------------------------------
Primary Ozone/8-Hr Standard (Level TBD)/       2007-2009  November 1, 2010 \b\......  November 1, 2010.\b\
 promulgated by August 31, 2010.
                                                    2010  60 Days after the end of    60 Days after the end of
                                                           the calendar quarter in     the calendar quarter in
                                                           which the event occurred    which the event occurred
                                                           or March 1, 2011,           or March 1, 2011,
                                                           whichever date occurs       whichever date occurs
                                                           first.\b\                   first.\b\
Secondary Ozone/(Level TBD) Alternative             2008  July 1, 2011\b\...........  July 1, 2011.\a\
 2-year Schedule--to be promulgated by
 August 31, 2010.
                                               2009-2010  July 1, 2011\b\...........  July 1, 2011.\b\
                                                    2011  60 Days after the end of    60 Days after the end of
                                                           the calendar quarter in     the calendar quarter in
                                                           which the event occurred    which the event occurred
                                                           or March 1, 2012,           or March 1, 2012,
                                                           whichever occurs            whichever occurs
                                                           first.\b\                   first.\b\
Secondary Ozone/(Level TBD)--Alternative       2007-2009  November 1, 2010 \b\......  November 1, 2010.\b\
 Accelerated Schedule--to be promulgated
 by August 31, 2010.
                                                    2010  60 Days after the end of    60 Days after the end of
                                                           the calendar quarter in     the calendar quarter in
                                                           which the event occurred    which the event occurred
                                                           or March 1, 2011,           or March 1, 2011,
                                                           whichever date occurs       whichever date occurs
                                                           first.\b\                   first.\b\
----------------------------------------------------------------------------------------------------------------
\a\ These dates are unchanged from those published in the original rulemaking.

[[Page 3034]]

 
\b\ Indicates change from general schedule in 40 CFR 50.14.
Note: EPA notes that the table of revised deadlines only applies to data EPA will use to establish the final
  initial designations for new NAAQS. The general schedule applies for all other purposes, most notably, for
  data used by EPA for redesignations to attainment.

VI. Ambient Monitoring Related to Proposed O3 Standards

    Presently, States (including the District of Columbia, Puerto Rico, 
and the Virgin Islands, and including local agencies when so delegated 
by the State) are required to operate minimum numbers of EPA-approved 
O3 monitors based on the population of each of their 
Metropolitan Statistical Areas (MSA) and the most recently measured 
O3 levels in each area. Each State (or in some cases 
portions of a State) also has a required O3 monitoring 
season based on historical experience on when O3 levels are 
high enough to be of regulatory or public health concern. These 
requirements are contained in 40 CFR part 58 Appendix D, Network Design 
Criteria for Ambient Air Quality Monitoring. See section 4.1, 
especially Tables D-2 and D-3. These requirements were last revised on 
October 17, 2006 as part of a comprehensive review of ambient 
monitoring requirements for all criteria pollutants (71 FR 61236).

A. Background

    In the 2007 proposed rule for the O3 NAAQS (72 FR 
37818), EPA did not propose specific changes to monitoring requirements 
to support the proposed NAAQS revisions, but instead solicited comment 
on several key matters that were expected to be important issues 
affecting the potential redesign of monitoring networks if revisions to 
the NAAQS were finalized. These matters included O3 
monitoring requirements in urban areas, the potential need for 
monitoring to support multiple objectives important to characterization 
in non-urban areas including the support of the secondary O3 
NAAQS, and the length of the required O3 monitoring seasons. 
Comments on these monitoring issues were received during the ensuing 
public comment period, and these comments were summarized in the 2008 
final rule for the O3 NAAQS (73 FR 16501). As noted in that 
action, EPA stated its intention to propose, in a separate rulemaking, 
the specific changes to O3 monitoring requirements that were 
deemed necessary to support the revised 2008 O3 NAAQS which 
set the level of the primary 8-hour O3 standard to 0.075 ppm 
and set the secondary standard identical in all respects to the primary 
standard. EPA published these proposed changes to O3 
monitoring requirements in a proposal dated July 16, 2009, Ambient 
Ozone Monitoring Regulations: Revisions to Network Design Requirements 
(74 FR 34525). The EPA currently plans to finalize these changes in a 
final O3 monitoring rule in 2010, either before or in 
conjunction with the final rule on the O3 NAAQS.
    In the following sections, the specific provisions of the 2009 
O3 monitoring proposal are briefly reviewed, and then 
discussed in the context of the proposed revisions of the 2008 
O3 NAAQS that have been discussed earlier in this notice.

B. Urban Monitoring Requirements

    As noted earlier, current O3 monitoring requirements for 
urban areas are based on two factors: MSA population and the most 
recent 3-year design value concentrations within each MSA. There are 
higher minimum monitoring requirements for areas that have most recent 
design values greater than or equal to 85 percent of the NAAQS (i.e., 
design value concentrations that are greater than or equal to 85 
percent of the level of the NAAQS), and lower requirements for areas 
that have design values less than 85 percent of the NAAQS. These 
minimum monitoring requirements for O3 were revised during 
the 2006 monitoring rulemaking to ensure that additional monitors would 
be required in areas with higher design values and to also ensure that 
these requirements would remain applicable through future NAAQS reviews 
and potential revisions of the standards. Accordingly, these 
requirements do not need to be updated with the revisions of the 
O3 NAAQS proposed in this action since the 85 percent 
threshold will be applied to the standard levels that are finalized for 
the primary and secondary standards.\71\ For example, given the range 
of levels of the primary standard being proposed, the level of the 85 
percent threshold that requires greater minimum monitoring requirements 
ranges from 0.051 ppm (85 percent of 0.060 ppm) to 0.060 ppm (85 
percent of 0.070 ppm).
---------------------------------------------------------------------------

    \71\ The requirements specified in Table D-2 of Appendix D to 
part 58, as noted in the third footnote of Table D-2, are applicable 
to the levels of the O3 NAAQS as defined in 40 CFR part 
50. Accordingly, the 85 percent threshold for requiring higher 
minimum monitoring requirements within MSAs would apply to the 
proposed levels for the cumulative, seasonal secondary standard as 
well as to the proposed levels of the 8-hour primary standard.
---------------------------------------------------------------------------

    EPA did propose one change to urban monitoring requirements in the 
2009 O3 monitoring proposal. Specifically, EPA proposed to 
modify the minimum O3 monitoring requirements to require one 
monitor to be placed in MSAs of populations ranging from 50,000 to less 
than 350,000 in situations where there is no current monitor and no 
history of O3 monitoring within the previous 5 years 
indicating a design value of less than 85 percent of the revised 
NAAQS.\72\ Since this proposed change to minimum requirements is also 
subject to the 85 percent threshold, EPA believes that the proposed 
change remains appropriate to support the revisions to the primary and 
secondary O3 NAAQS proposed in this action.
---------------------------------------------------------------------------

    \72\ These MSAs are not currently required to monitor for 
O3.
---------------------------------------------------------------------------

C. Non-Urban Monitoring Requirements

    In the 2007 proposed rule for the O3 NAAQS, EPA 
solicited comment on the status of monitoring requirements for non-
urban areas, specifically whether non-urban areas with sensitive 
vegetation that are only currently sparsely monitored for O3 
could experience undetected violations of the secondary NAAQS as a 
result of transport from urban areas with high precursor emissions and/
or O3 concentrations or from formation of additional 
O3 from precursors emitted from sources outside urban areas.
    Comments that were received in response to the 2009 O3 
NAAQS monitoring proposal noted the voluntary nature of most non-urban 
O3 monitoring and the resulting relative lack of non-urban 
O3 monitors in some areas. These commenters stated that EPA 
should consider adding monitoring requirements to support the secondary 
NAAQS by requiring O3 monitors in locations that contain 
O3-sensitive plants or ecosystems. These commenters also 
noted that the placement of current O3 monitors may not be 
appropriate for evaluating issues such as vegetation exposure since 
many of these monitors were likely located to meet other objectives.
    Based on these comments as well as analyses of O3 
concentrations from discretionary non-urban monitors located across the 
U.S, EPA included new proposed non-urban O3 monitoring 
requirements in the 2009 O3 monitoring proposal. These 
proposed requirements are intended to satisfy several important 
objectives including: (1) Better characterization of O3 
concentrations to which O3-sensitive vegetation and

[[Page 3035]]

ecosystems are exposed in rural/remote areas to ensure that potential 
secondary NAAQS violations are measured; (2) assessment of 
O3 concentrations in smaller communities located outside of 
the larger urban MSAs covered by urban monitoring requirements; and (3) 
the assessment of the location and severity of maximum O3 
concentrations that occur in non-urban areas and may be attributable to 
upwind urban sources. For reasons noted below, EPA believes that these 
proposed O3 monitoring requirements are sufficient to 
support the revisions to the O3 NAAQS proposed in this 
action.
    With regard to the first objective, we note uncertainties will 
remain about the O3 concentrations to which sensitive 
natural vegetation and ecosystems are exposed until additional monitors 
are sited in National Parks, State and/or tribal areas, wilderness 
areas, and other similar locations with sensitive ecosystems that are 
set aside to provide similar public welfare benefits. These monitors 
would support evaluation of the secondary NAAQS with a more robust data 
set than is now available. As noted in the 2009 O3 
monitoring proposal, EPA proposed that States operate at least one 
monitor to be located in areas such as some Federal, State, Tribal, or 
private lands, including wilderness areas that have O3-
sensitive natural vegetation and/or ecosystems. If EPA finalizes a 
cumulative, seasonal secondary standard at the lower end of the 
proposed range, then it is plausible that additional O3 
monitors, above the number required by the monitoring proposal, may be 
needed in such areas to provide adequate coverage of locations likely 
to experience violations of the revised secondary NAAQS. These 
additional monitors could be established through discretionary State 
initiatives to supplement minimum monitoring requirements, negotiated 
agreements between States and EPA Regional Administrators, or through a 
future rulemaking that addresses potential increased O3 
monitoring requirements to specifically address the need for additional 
monitoring to ensure detection of secondary standard violations.
    With regard to the second objective of characterizing elevated 
ambient O3 levels to which people are exposed in smaller 
communities located outside of the larger urban MSAs, the likelihood of 
measuring concentrations that approach or exceed the levels of the 
NAAQS due to the transport of O3 from upwind areas and/or 
the formation of O3 due to precursor emissions from 
industrial sources outside of urban areas is clearly increased due to 
the revised NAAQS proposed in this action. Given that the analyses 
described in the 2009 O3 monitoring proposal demonstrated 
that 50 percent of existing monitors located in such Micropolitan 
Statistical Areas \73\ exceeded the current NAAQS and nearly all 
monitors recorded design values greater than or equal to 85 percent of 
the current NAAQS, the potential for violations in such areas can only 
be increased with the NAAQS revisions proposed in this action. As noted 
for the first non-urban monitoring objective, it is plausible that 
additional O3 monitors, above the number required by the 
2009 monitoring proposal may be needed in Micropolitan Statistical 
Areas to provide adequate coverage of locations likely to experience 
violations of the proposed lower primary NAAQS levels. These additional 
monitors could be established through discretionary State initiatives 
to supplement minimum monitoring requirements, negotiated requirements 
between States and EPA Regional Administrators, or through a future 
rulemaking that addresses potential increased O3 monitoring 
requirements to specifically address the need for additional monitoring 
to ensure detection of primary standard violations in smaller 
communities.
---------------------------------------------------------------------------

    \73\ Defined as areas having at least one urban cluster of at 
least 10,000 but less than a population of 50,000.
---------------------------------------------------------------------------

    The third proposed non-urban monitoring objective, requiring 
O3 monitors to be located in the area of expected maximum 
O3 concentration outside of any MSA, potentially including 
the far downwind transport zones of currently well-monitored urban 
areas, is not directly related to the level of the O3 NAAQS. 
It is instead intended to ensure that all parts of a State meet the 
NAAQS and that all necessary emission control strategies have been 
included in State Implementation Plans. Accordingly, this proposed 
monitoring objective remains applicable independent of revisions to the 
O3 NAAQS proposed in this action.

D. Revisions to the Length of the Required O3 Monitoring Seasons

    Ozone monitoring is only required during the seasons of the year 
that are conducive to O3 formation. These seasons vary in 
length as the conditions that determine the likely O3 
formation (i.e., seasonally-dependent factors such as ambient 
temperature, strength of solar insolation, and length of day) differ by 
location. In some locations, conditions conducive to O3 
formation are limited to a few summer months of the year while in other 
locations these conditions occur year-round. As a result, the length of 
currently required O3 monitoring seasons can vary from a 
length of 4 months in colder climates to a length of 12 months in 
warmer climates.
    The 2009 O3 monitoring proposal also addressed the issue 
of whether in some areas the required O3 monitoring season 
should be made longer. The proposal also addressed the status of any 
currently effective Regional Administrator-granted waiver approvals to 
O3 monitoring seasons, and the impact of proposed changes to 
monitoring requirements on such waiver approvals.
    The EPA performed several analyses in support of proposed changes 
to the required O3 monitoring seasons. The first analysis 
determined the number of observed exceedances of the 0.075 ppm level of 
the current 8-hour NAAQS in the months falling outside the currently 
required local O3 monitoring season using monitors in areas 
that collected O3 data year-round in 2004-2006. The second 
analysis examined observed occurrences of daily maximum 8-hour 
O3 averages of at least 0.060 ppm. This threshold was chosen 
because it represented 80 percent of the current 0.075 ppm NAAQS level 
and provides an indicator of ambient conditions that may be conducive 
to the formation of O3 concentrations that approach or 
exceed the NAAQS. While proposals for revising each State's required 
monitoring season were based on observed data in and surrounding each 
State, statistically predicted exceedances were also used to validate 
conclusions for each State.
    The aforementioned analyses provided several results. The analysis 
of observed exceedances of the 0.075 ppm level of the current 
O3 NAAQS indicated occurrences in eight States during months 
outside of the current required monitoring season. The eight States 
were Maine, Massachusetts, New Hampshire, New Jersey, New York, South 
Carolina, Vermont, and Wyoming. With the exception of Wyoming, these 
exceedances occurred in a very limited manner and timeframe, just 
before the beginning of these States' required O3 monitoring 
season (beginning in these States on April 1). The frequency of 
observed occurrences of maximum 8-hour average O3 levels of 
at least 0.060 ppm was quite high across the country in months outside 
of the current required monitoring season. A total of 32 States 
experienced such occurrences; 22 States had such levels only before the 
required monitoring season; 9 States had such levels both before and 
after the required monitoring

[[Page 3036]]

season; and 1 State had such levels only after the required monitoring 
season. In a number of cases, the frequency of such ambient 
concentrations was high, with some States experiencing between 31 to 46 
out-of-season days during 2004 to 2006 at a high percentage of all 
operating year-round O3 monitors.
    Based on these analyses, EPA proposed a lengthening of the 
O3 monitoring season requirements in many areas. The 2009 
proposed changes were based not only on the goal of monitoring out-of-
season O3 NAAQS violations but also on the goal of ensuring 
monitoring when ambient O3 levels reach 80 percent of the 
NAAQS so that persons unusually sensitive to O3 would be 
alerted to potential NAAQS exceedances.
    The EPA believes that the factors used to support the 2009 proposed 
changes to O3 monitoring seasons are appropriate to support 
the revisions of the O3 NAAQS proposed in this action. With 
regard to the primary standard, we note that the lower end of the range 
being proposed is an 8-hour level of 0.060 ppm, which is identical to 
the ambient O3 level that was utilized in one of the 
analyses discussed above. Although that level was chosen to provide an 
indicator of ambient levels that were below but approaching the level 
of the NAAQS and hence to serve as an alert to potential exceedances, 
we note that EPA's traditional practice had been to base the length of 
required O3 monitoring seasons on the likelihood of 
measuring exceedances of the level of the NAAQS. Therefore, if EPA 
finalizes the level of the primary standard at the lower end of the 
proposed range, the O3 monitoring seasons that have been 
proposed as part of the 2009 O3 monitoring proposal would 
provide sufficient monitoring coverage to ensure the goal of measuring 
potential violations of the primary standard.
    One O3 monitoring season issue that was not considered 
in the 2009 O3 monitoring proposal was the question of 
whether analyses of ambient data based on 8-hour average statistics 
would also indicate whether the resulting proposed monitoring seasons 
would capture the cumulative maximum consecutive 3-month O3 
levels necessary to compute design values based on the secondary NAAQS 
proposed in this action, which is defined in terms of a W126 cumulative 
peak-weighted index, as discussed above in section IV. If areas 
experienced high cumulative index values during months outside of the 
required O3 monitoring seasons (based on 8-hour statistics), 
then further revisions to the required monitoring seasons might be 
necessary to ensure monitoring during all months important to the 
calculation of design values for the revised form proposed for the 
secondary NAAQS. A related issue is whether such high cumulative 
O3 values also occurred during time periods that are 
biologically relevant for O3-sensitive vegetation.
    The EPA is not proposing additional revisions to O3 
monitoring seasons at this time. Additional analyses of the 
distribution of elevated cumulative W126 index values will be 
conducted, and the biologically relevant seasonal issue will be further 
reviewed. Based on the results of these analyses, EPA may consider 
proposing further revisions to the O3 monitoring season as 
related to the secondary O3 NAAQS.

VII. Implementation of Proposed O3 Standards

A. Designations

    After EPA establishes or revises a NAAQS, the CAA directs EPA and 
the states to take steps to ensure that the new or revised NAAQS are 
met. The first step is to identify areas of the country that do not 
meet the new or revised NAAQS. This step is known as the initial area 
designations.
    The CAA provides that, ``By such date as the Administrator may 
reasonably require, but not later than 1 year after promulgation of a 
new or revised national ambient air quality standard for any pollutant 
under section 109, the Governor of each state shall * * * submit to the 
Administrator a list of all areas (or portions thereof) in the state'' 
that designates those areas as nonattainment, attainment, or 
unclassifiable. The CAA specifies that, ``The Administrator may not 
require the Governor to submit the required list sooner than 120 days 
after promulgating a new or revised national ambient air quality 
standard.'' The CAA defines an area as nonattainment if it is violating 
the NAAQS or if it is contributing to a violation in a nearby area. 
(See CAA section 107(d)(1).)
    The CAA further provides, ``Upon promulgation or revision of a 
national ambient air quality standard, the Administrator shall 
promulgate the designations of all areas (or portions thereof) * * * as 
expeditiously as practicable, but in no case later than 2 years from 
the date of promulgation of the new or revised national ambient air 
quality standard. Such period may be extended for up to one year in the 
event the Administrator has insufficient information to promulgate the 
designations.'' EPA is required to notify states of any intended 
modifications to their recommendations that EPA may deem necessary no 
later than 120 days prior to promulgating designations. States then 
have an opportunity to demonstrate why any such proposed modification 
is inappropriate. Whether or not a state provides a recommendation, EPA 
must promulgate the designation that the Agency deems appropriate. (See 
CAA section 107(d)(1)(B).)
    On September 16, 2009, when the Administrator announced her 
decision to reconsider the 2008 O3 NAAQS, she also indicated 
that the Agency would work with states to accelerate implementation of 
the standards adopted after reconsideration, including the initial area 
designations process. Acceleration of designations for the primary 
standard would help limit any delays in health protections associated 
with the reconsideration of the standards. If a secondary standard 
different from the primary standard is adopted, this would be the first 
time different primary and secondary standards would be in place for 
the O3 standards. While welfare protection is also 
important, for the reasons provided below, we are providing alternative 
schedules for designating areas for the secondary standard.
    If, as a result of the reconsideration, EPA determines that the 
record supports a primary standard different from that promulgated in 
2008 and promulgates such different primary O3 NAAQS in 
2010, EPA intends to promulgate final designations on an accelerated 
schedule to allow the designations to be effective in 1 year. In order 
to meet such a schedule, EPA is proposing that the deadline for states 
to submit their designations recommendations for the revised 2010 
primary standard be 129 days after promulgation of that primary 
standard. EPA recognizes that the proposed deadline would be an 
ambitious schedule. Therefore, EPA intends to provide technical 
information and guidance for states as early as possible to facilitate 
the development of their recommendations. Many of the areas that would 
be violating the proposed primary ozone standard are also violating the 
2008 ozone standards. State Governors have provided recommendations on 
these areas pursuant to the 2008 standards and recommendations may not 
need much further evaluation.
    Based on this proposed schedule, if EPA promulgates a new primary 
standard on August 31, 2010, state Governors would need to submit their 
initial designation recommendations to EPA by January 7, 2011. If the 
Administrator intends to modify any state recommendation, EPA would

[[Page 3037]]

notify the Governor no later than March 2011, 120 days prior to 
promulgating the final designations. States would then have an 
opportunity to comment on EPA's intended designations before EPA 
promulgates the final designations. EPA would promulgate the final 
designations in July 2011 to allow sufficient time for the designations 
to be published and effective by August 31, 2011. EPA expects to base 
the final designations for the primary O3 standard on three 
consecutive years of certified air quality monitoring data from the 
years 2007-2009 or from 2008-2010, if available.
    If, as a result of the reconsideration, EPA promulgates a distinct 
secondary standard that differs from that promulgated in 2008 and also 
differs from the 2010 primary standard, as proposed above, EPA is 
proposing two alternative deadlines for states to submit their 
designations recommendations. Under the first alternative, EPA would 
designate areas for the secondary standard on the same accelerated 
schedule discussed above for the primary standard. In order to meet 
that schedule, EPA is proposing that states submit their 
recommendations for the revised 2010 secondary standard 129 days after 
promulgation of that secondary standard. Accordingly, if EPA 
promulgates the new secondary standard on August 31, 2010, state 
Governors would need to submit their initial designation 
recommendations to EPA by January 7, 2011.
    Weighing in favor of designating areas for the secondary standard 
at the same time as designations for the primary standard is that 
planning for both standards would occur on the same schedule. Our 
examination of current air quality data from the existing monitoring 
network indicates that for levels of the primary and secondary 
standards proposed in this action, it is likely that the vast majority 
of areas violating the secondary standard would overlap with areas 
violating the primary standard. In this case, implementing requirements 
for the primary and secondary standards on different schedules could 
present resource challenges to state and local agencies by requiring 
duplication of effort and hindering consideration of all factors when 
deciding which control strategies to adopt for each standard. For 
example, if designations for the secondary standard were delayed by a 
certain period (e.g., a year) beyond the designations for the primary 
standard, then EPA would likely delay submission of attainment SIPs for 
the secondary standard for a similar period beyond the proposed date 
for submission of the attainment SIPs for the primary standard. In this 
case, the initial transportation conformity determination for the 
secondary standard would be required later than the initial 
determination for the primary standard by the difference in time 
between the effective dates of the two designations.
    Under the second alternative, EPA would designate areas for the 
secondary standard on the maximum 2-year schedule provided under the 
CAA. To meet that 2-year schedule, EPA is proposing that states submit 
their recommendations for the revised secondary standard no later than 
1 year after promulgation of the 2010 secondary standard. Accordingly, 
if EPA promulgates a secondary standard on August 31, 2010, that 
differs from the primary standard, as proposed, under the alternative 
2-year designations schedule, state Governors would need to submit 
their initial designation recommendations to EPA by August 31, 2011. If 
the Administrator intends to modify any state recommendation, EPA would 
notify the Governor no later than May 2012, 120 days prior to the 2-
year deadline for promulgating the final designations. States would 
then have an opportunity to comment on EPA's intended designations 
before EPA promulgates the final designations. EPA would promulgate the 
final designations for the secondary standard by August 31, 2012. EPA 
expects to base the final designations in August 2012 for a different 
secondary standard on the most recent three consecutive years of 
certified air quality monitoring data, which would be from the years 
2009-2011.
    In the past, EPA has always set the secondary O3 
standard to be identical to the primary O3 standard and the 
standards have embodied relatively short-term average concentrations 
(e.g., 1-hour or 8-hour). In this action, EPA is proposing a 
cumulative, seasonal secondary standard that differs from the proposed 
primary standard. EPA has not previously set a seasonal secondary 
standard for O3. Therefore, EPA and states do not have 
experience in implementing this type of secondary O3 
standard or in determining what area boundaries would be appropriate. 
As we further explore implementation considerations for the secondary 
standard, we may encounter unanticipated issues that may require 
additional time to address. Thus, EPA is considering whether an 
accelerated schedule for a seasonal secondary standard would provide 
adequate time for resolving issues that we cannot now anticipate. If 
EPA designates areas for the secondary standard on a 2-year schedule, 
we note that we expect that accelerated implementation of the health-
based primary standard would also result in accelerated welfare 
benefits. EPA requests comment on factors affecting the efficient and 
effective implementation of a secondary standard that differs from the 
primary standard in the context of establishing designations schedules.
    EPA notes, as discussed in greater detail above in section VI, that 
it has proposed a monitoring rule that would increase the density of 
monitoring in National Parks and other non-urban and lesser populated 
areas (July 16, 2009; 74 FR 34525). The proposed requirements are 
intended to satisfy several important objectives, including better 
characterization of O3 exposures to O3-sensitive 
vegetation and ecosystems in rural/remote areas to ensure that 
potential secondary NAAQS violations are measured. As proposed, the new 
monitors would not be deployed until 2012 or 2013. Therefore, data from 
these monitors would not be available for use within the statutory 
timeframe for EPA to complete designations for a 2010 secondary 
standard regardless of which schedule EPA follows.
    While CAA section 107 specifically addresses states, EPA intends to 
follow the same process for tribes to the extent practicable, pursuant 
to section 301(d) of the CAA regarding tribal authority, and the Tribal 
Authority Rule (63 FR 7254; February 12, 1998).
    In a separate notice elsewhere in today's Federal Register, EPA is 
announcing that it is using its authority under the CAA to extend by 1 
year the deadline for promulgating initial area designations for the 
O3 NAAQS that were promulgated in March 2008. The new 
deadline is March 12, 2011. That notice explains the basis for the 
deadline extension. As mentioned above, on September 16, 2009, EPA 
notified the Court of its decision to initiate a rulemaking to 
reconsider the primary and secondary O3 NAAQS set in March 
2008 to ensure they satisfy the requirements of the CAA. In its notice 
to the Court, EPA stated that the final rule would be signed by August 
31, 2010. Extending the deadline for promulgating designations for the 
2008 O3 NAAQS until March 12, 2011 will allow EPA to 
complete the reconsideration rulemaking for the 2008 O3 
NAAQS before determining whether it is necessary to finalize 
designations for those NAAQS or, instead, whether it is necessary to 
begin the designation process for different NAAQS promulgated pursuant 
to the reconsideration.

[[Page 3038]]

B. State Implementation Plans

    The CAA section 110 provides the general requirements for SIPs. 
Within 3 years after the promulgation of new or revised NAAQS (or such 
shorter period as the Administrator may prescribe) each State must 
adopt and submit ``infrastructure'' SIPs to EPA to address the 
requirements of section 110(a)(1). Thus, States should submit these 
SIPs no later than August 21, 2013, three years after promulgation of 
the reconsidered ozone standard in 2010. These ``infrastructure SIPs'' 
provide assurances of State resources and authorities, and establish 
the basic State programs, to implement, maintain, and enforce new or 
revised standards.
    In addition to the infrastructure SIPs, which apply to all States, 
CAA title I, part D outlines the State requirements for achieving clean 
air in designated nonattainment areas. These requirements include 
timelines for when designated nonattainment areas must attain the 
standards, deadlines for developing SIPs that demonstrate how the State 
will ensure attainment of the standards, and specific emissions control 
requirements. EPA plans to address how these requirements, such as 
attainment demonstrations and attainment dates, reasonable further 
progress, new source review, conformity, and other implementation 
requirements, apply to the O3 NAAQS promulgated pursuant to 
the reconsideration in a subsequent rulemaking. Also in that rulemaking 
EPA will establish deadlines for submission of nonattainment area SIPs 
but anticipates that the deadlines will be no later than the end of 
December 2013, or 28 months after final designations.

C. Trans-Boundary Emissions

    Cross border O3 contributions from within North America 
(Canada and Mexico) entering the U.S. are generally thought to be 
small. Section 179B of the Clean Air Act allows designated 
nonattainment areas to petition EPA to consider whether such a locality 
might have met a clean air standard ``but for'' cross border 
contributions. To date, few areas have petitioned EPA under this 
authority. The impact of foreign emissions on domestic air quality in 
the United States is a challenging and complex problem to assess. EPA 
is engaged in a number of activities to improve our understanding of 
international transport. As work progresses on these activities, EPA 
will be able to better address the uncertainties associated with trans-
boundary flows of air pollution and their impacts.

VIII. Statutory and Executive Order Reviews

A. Executive Order 12866: Regulatory Planning and Review

    Under section 3(f)(1) of Executive Order (EO) 12866 (58 FR 51735, 
October 4, 1993), the O3 NAAQS action is an ``economically 
significant regulatory action'' because it is likely to have an annual 
effect on the economy of $100 million or more. Accordingly, EPA 
submitted this action to the Office of Management and Budget (OMB) for 
review under EO 12866 and any changes made in response to OMB 
recommendations have been documented in the docket for this action. In 
addition, EPA prepared this regulatory impact analysis (RIA) of the 
potential costs and benefits associated with this action. This analysis 
is contained in the Regulatory Impact Analysis for the Ozone NAAQS 
Reconsideration, October 2009 (henceforth, ``RIA''). A copy of the 
analysis is available in the RIA docket (EPA-HQ-OAR-2007-0225) and the 
analysis is briefly summarized here. The RIA estimates the costs and 
monetized human health and welfare benefits of attaining five 
alternative O3 NAAQS nationwide. Specifically, the RIA 
examines the alternatives of 0.079 ppm, 0.075 ppm, 0.070 ppm, 0.065 
ppm, and 0.060 ppm. The RIA contains illustrative analyses that 
consider a limited number of emissions control scenarios that States 
and Regional Planning Organizations might implement to achieve these 
alternative O3 NAAQS. However, the Clean Air Act (CAA) and 
judicial decisions make clear that the economic and technical 
feasibility of attaining ambient standards are not to be considered in 
setting or revising NAAQS, although such factors may be considered in 
the development of State plans to implement the standards. Accordingly, 
although an RIA has been prepared, the results of the RIA have not been 
considered in issuing this proposed rule.

B. Paperwork Reduction Act

    This action does not impose an information collection burden under 
the provisions of the Paperwork Reduction Act, 44 U.S.C. 3501 et seq. 
There are no information collection requirements directly associated 
with the establishment of a NAAQS under section 109 of the CAA.
    Burden means the total time, effort, or financial resources 
expended by persons to generate, maintain, retain, or disclose or 
provide information to or for a Federal agency. This includes the time 
needed to review instructions; develop, acquire, install, and utilize 
technology and systems for the purposes of collecting, validating, and 
verifying information, processing and maintaining information, and 
disclosing and providing information; adjust the existing ways to 
comply with any previously applicable instructions and requirements; 
train personnel to be able to respond to a collection of information; 
search data sources; complete and review the collection of information; 
and transmit or otherwise disclose the information.
    An agency may not conduct or sponsor, and a person is not required 
to respond to a collection of information unless it displays a 
currently valid OMB control number. The OMB control numbers for EPA's 
regulations in 40 CFR are listed in 40 CFR part 9.

C. Regulatory Flexibility Act

    The Regulatory Flexibility Act (RFA) generally requires an agency 
to prepare a regulatory flexibility analysis of any rule subject to 
notice and comment rulemaking requirements under the Administrative 
Procedure Act or any other statute unless the agency certifies that the 
rule will not have a significant economic impact on a substantial 
number of small entities. Small entities include small businesses, 
small organizations, and small governmental jurisdictions.
    For purposes of assessing the impacts of today's proposed rule on 
small entities, small entity is defined as: (1) A small business that 
is a small industrial entity as defined by the Small Business 
Administration's (SBA) regulations at 13 CFR 121.201; (2) a small 
governmental jurisdiction that is a government of a city, county, town, 
school district or special district with a population of less than 
50,000; and (3) a small organization that is any not-for-profit 
enterprise which is independently owned and operated and is not 
dominant in its field.
    After considering the economic impacts of today's proposed rule on 
small entities, I certify that this action will not have a significant 
economic impact on a substantial number of small entities. This 
proposed rule will not impose any requirements on small entities. 
Rather, this rule establishes national standards for allowable 
concentrations of O3 in ambient air as required by section 
109 of the CAA. See also American Trucking Associations v. EPA. 175 F. 
3d at 1044-45 (NAAQS do not have significant impacts upon small

[[Page 3039]]

entities because NAAQS themselves impose no regulations upon small 
entities). We continue to be interested in the potential impacts of the 
proposed rule on small entities and welcome comments on issues related 
to such impacts

D. Unfunded Mandates Reform Act

    Title II of the Unfunded Mandates Reform Act of 1995 (UMRA), Public 
Law 104-4, establishes requirements for Federal agencies to assess the 
effects of their regulatory actions on State, local, and Tribal 
governments and the private sector. Under section 202 of the UMRA, EPA 
generally must prepare a written statement, including a cost-benefit 
analysis, for proposed and final rules with ``Federal mandates'' that 
may result in expenditures to State, local, and Tribal governments, in 
the aggregate, or to the private sector, of $100 million or more in any 
1 year. Before promulgating an EPA rule for which a written statement 
is needed, section 205 of the UMRA generally requires EPA to identify 
and consider a reasonable number of regulatory alternatives and to 
adopt the least costly, most cost-effective or least burdensome 
alternative that achieves the objectives of the rule. The provisions of 
section 205 do not apply when they are inconsistent with applicable 
law. Moreover, section 205 allows EPA to adopt an alternative other 
than the least costly, most cost-effective or least burdensome 
alternative if the Administrator publishes with the final rule an 
explanation why that alternative was not adopted. Before EPA 
establishes any regulatory requirements that may significantly or 
uniquely affect small governments, including Tribal governments, it 
must have developed under section 203 of the UMRA a small government 
agency plan. The plan must provide for notifying potentially affected 
small governments, enabling officials of affected small governments to 
have meaningful and timely input in the development of EPA regulatory 
proposals with significant Federal intergovernmental mandates, and 
informing, educating, and advising small governments on compliance with 
the regulatory requirements.
    Today's proposed rule contains no Federal mandates (under the 
regulatory provisions of Title II of the UMRA) for State, local, or 
Tribal governments or the private sector. The proposed rule imposes no 
new expenditure or enforceable duty on any State, local or Tribal 
governments or the private sector, and EPA has determined that this 
proposed rule contains no regulatory requirements that might 
significantly or uniquely affect small governments. Furthermore, as 
indicated previously, in setting a NAAQS EPA cannot consider the 
economic or technological feasibility of attaining ambient air quality 
standards, although such factors may be considered to a degree in the 
development of State plans to implement the standards. See also 
American Trucking Associations v. EPA, 175 F. 3d at 1043 (noting that 
because EPA is precluded from considering costs of implementation in 
establishing NAAQS, preparation of a Regulatory Impact Analysis 
pursuant to the Unfunded Mandates Reform Act would not furnish any 
information which the court could consider in reviewing the NAAQS). 
Accordingly, EPA has determined that the provisions of sections 202, 
203, and 205 of the UMRA do not apply to this proposed decision. The 
EPA acknowledges, however, that any corresponding revisions to 
associated SIP requirements and air quality surveillance requirements, 
40 CFR part 51 and 40 CFR part 58, respectively, might result in such 
effects. Accordingly, EPA will address, as appropriate, unfunded 
mandates if and when it proposes any revisions to 40 CFR parts 51 or 
58.

E. Executive Order 13132: Federalism

    Executive Order 13132, entitled ``Federalism'' (64 FR 43255, August 
10, 1999), requires EPA to develop an accountable process to ensure 
``meaningful and timely input by State and local officials in the 
development of regulatory policies that have federalism implications.'' 
``Policies that have federalism implications'' is defined in the 
Executive Order to include regulations that have ``substantial direct 
effects on the States, on the relationship between the national 
government and the States, or on the distribution of power and 
responsibilities among the various levels of government.''
    This proposed rule does not have federalism implications. It will 
not have substantial direct effects on the States, on the relationship 
between the national government and the States, or on the distribution 
of power and responsibilities among the various levels of government, 
as specified in Executive Order 13132. The rule does not alter the 
relationship between the Federal government and the States regarding 
the establishment and implementation of air quality improvement 
programs as codified in the CAA. Under section 109 of the CAA, EPA is 
mandated to establish NAAQS; however, CAA section 116 preserves the 
rights of States to establish more stringent requirements if deemed 
necessary by a State. Furthermore, this proposed rule does not impact 
CAA section 107 which establishes that the States have primary 
responsibility for implementation of the NAAQS. Finally, as noted in 
section E (above) on UMRA, this rule does not impose significant costs 
on State, local, or Tribal governments or the private sector. Thus, 
Executive Order 13132 does not apply to this rule.
    However, as also noted in section D (above) on UMRA, EPA recognizes 
that States will have a substantial interest in this rule and any 
corresponding revisions to associated SIP requirements and air quality 
surveillance requirements, 40 CFR part 51 and 40 CFR part 58, 
respectively. Therefore, in the spirit of Executive Order 13132, and 
consistent with EPA policy to promote communications between EPA and 
State and local governments, EPA specifically solicits comment on this 
proposed rule from State and local officials.

F. Executive Order 13175: Consultation and Coordination With Indian 
Tribal Governments

    Executive Order 13175, entitled ``Consultation and Coordination 
with Indian Tribal Governments'' (65 FR 67249, November 9, 2000), 
requires EPA to develop an accountable process to ensure ``meaningful 
and timely input by tribal officials in the development of regulatory 
policies that have tribal implications.'' This rule concerns the 
establishment of O3 NAAQS. The Tribal Authority Rule gives 
Tribes the opportunity to develop and implement CAA programs such as 
the O3 NAAQS, but it leaves to the discretion of the Tribe 
whether to develop these programs and which programs, or appropriate 
elements of a program, they will adopt.
    This proposed rule does not have Tribal implications, as specified 
in Executive Order 13175. It does not have a substantial direct effect 
on one or more Indian Tribes, since Tribes are not obligated to adopt 
or implement any NAAQS. Thus, Executive Order 13175 does not apply to 
this rule.
    Although Executive Order 13175 does not apply to this rule, EPA 
contacted tribal environmental professionals during the development of 
the March 2008 rule. The EPA staff participated in the regularly 
scheduled Tribal Air call sponsored by the National Tribal Air 
Association during the spring of 2007 as the proposal was under 
development. EPA specifically solicits additional comment on this 
proposed rule from Tribal officials.

[[Page 3040]]

G. Executive Order 13045: Protection of Children From Environmental 
Health and Safety Risks

    Executive Order 13045, ``Protection of Children from Environmental 
Health Risks and Safety Risks'' (62 FR 19885, April 23, 1997) applies 
to any rule that: (1) Is determined to be ``economically significant'' 
as defined under Executive Order 12866, and (2) concerns an 
environmental health or safety risk that EPA has reason to believe may 
have a disproportionate effect on children. If the regulatory action 
meets both criteria, the Agency must evaluate the environmental health 
or safety effects of the planned rule on children, and explain why the 
planned regulation is preferable to other potentially effective and 
reasonably feasible alternatives considered by the Agency.
    This proposed rule is subject to Executive Order 13045 because it 
is an economically significant regulatory action as defined by 
Executive Order 12866, and we believe that the environmental health 
risk addressed by this action may have a disproportionate effect on 
children. The proposed rule will establish uniform national ambient air 
quality standards for O3; these standards are designed to 
protect public health with an adequate margin of safety, as required by 
CAA section 109. However, the protection offered by these standards may 
be especially important for children because children, especially 
children with asthma, along with other sensitive population subgroups 
such as all people with lung disease and people active outdoors, are 
potentially susceptible to health effects resulting from O3 
exposure. Because children are considered a potentially susceptible 
population, we have carefully evaluated the environmental health 
effects of exposure to O3 pollution among children. 
Discussions of the results of the evaluation of the scientific 
evidence, policy considerations, and the exposure and risk assessments 
pertaining to children are contained in sections II.B and II.C of this 
preamble. A listing of the documents that contain the evaluation of 
scientific evidence, policy considerations, and exposure and risk 
assessments that pertain to children is found in the section on 
Children's Environmental Health in the Supplementary Information 
section of this preamble, and a copy of all documents have been placed 
in the public docket for this action. The public is invited to submit 
comments or identify peer-reviewed studies and data that assess effects 
of early life exposure to O3.

H. Executive Order 13211: Actions That Significantly Affect Energy 
Supply, Distribution or Use

    This proposed rule is not a ``significant energy action'' as 
defined in Executive Order 13211, ``Actions Concerning Regulations That 
Significantly Affect Energy Supply, Distribution, or Use'' (66 FR 28355 
(May 22, 2001)) because in the Agency's judgment it is not likely to 
have a significant adverse effect on the supply, distribution, or use 
of energy. The purpose of this rule is to establish revised NAAQS for 
O3. The rule does not prescribe specific pollution control 
strategies by which these ambient standards will be met. Such 
strategies will be developed by States on a case-by-case basis, and EPA 
cannot predict whether the control options selected by States will 
include regulations on energy suppliers, distributors, or users. Thus, 
EPA concludes that this rule is not likely to have any adverse energy 
effects and does not constitute a significant energy action as defined 
in Executive Order 13211.

I. National Technology Transfer and Advancement Act

    Section 12(d) of the National Technology Transfer and Advancement 
Act of 1995 (NTTAA), Public Law 104-113, section 12(d) (15 U.S.C. 272 
note) directs EPA to use voluntary consensus standards in its 
regulatory activities unless to do so would be inconsistent with 
applicable law or otherwise impractical. Voluntary consensus standards 
are technical standards (e.g., materials specifications, test methods, 
sampling procedures, and business practices) that are developed or 
adopted by voluntary consensus standards bodies. The NTTAA directs EPA 
to provide Congress, through OMB, explanations when the Agency decides 
not to use available and applicable voluntary consensus standards.
    This proposed rulemaking does not involve technical standards. 
Therefore, EPA is not considering the use of any voluntary consensus 
standards.

J. Executive Order 12898: Federal Actions To Address Environmental 
Justice in Minority Populations and Low-Income Populations

    Executive Order 12898 (59 FR 7629 (Feb. 16, 1994)) establishes 
federal executive policy on environmental justice. Its main provision 
directs federal agencies, to the greatest extent practicable and 
permitted by law, to make environmental justice part of their mission 
by identifying and addressing, as appropriate, disproportionately high 
and adverse human health or environmental effects of their programs, 
policies, and activities on minority populations and low-income 
populations in the United States.
    EPA has determined that this proposed rule will not have 
disproportionately high and adverse human health or environmental 
effects on minority or low-income populations because it increases the 
level of environmental protection for all affected populations without 
having any disproportionately high and adverse human health or 
environmental effects on any population, including any minority or low-
income population. The proposed rule will establish uniform national 
standards for O3 air pollution.

References

Abbey, D. E.; Nishino, N.; McDonnell, W. F.; Burchette, R. J.; 
Knutsen, S. F.; Beeson, W. L.; Yang, J. X. (1999) Long-term 
inhalable particles and other air pollutants related to mortality in 
nonsmokers. Am. J. Respir. Crit. Care Med. 159: 373-382.
Abt Associates Inc. (1995) Ozone NAAQS benefits analysis: California 
crops. Report to U.S. EPA, July 1995. EPA Docket No. A-95-58 Item 
II-I-3.
Abt Associates Inc. (2007a) Ozone Health Risk Assessment for 
Selected Urban Areas. Prepared for Office of Air Quality Planning 
and Standards, U.S. Environmental Protection Agency, Research 
Triangle Park, NC. July 2007; EPA report no. EPA-452/R-07-009. 
Available online at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html.
Abt Associates Inc. (2007b) Technical Report on Ozone Exposure, 
Risk, and Impacts Assessments for Vegetation: Final Report. Prepared 
for Office of Air Quality Planning and Standards, U.S. Environmental 
Protection Agency, Research Triangle Park, NC. January 2007; EPA 
report no. EPA-452/R-07-002. Available online at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html.
Adams, W. C. (2002) Comparison of chamber and face-mask 6.6-hour 
exposures to ozone on pulmonary function and symptoms responses. 
Inhalation Toxicol. 14: 745-764.
Adams, W. C. (2003a) Comparison of chamber and face mask 6.6-hour 
exposure to 0.08 ppm ozone via square-wave and triangular profiles 
on pulmonary responses. Inhalation Toxicol. 15: 265-281.
Adams, W. C. (2003b) Relation of pulmonary responses induced by 6.6 
hour exposures to 0.08 ppm ozone and 2-hour exposures to 0.30 ppm 
via chamber and face-mask inhalation. Inhalation Toxicol. 15: 745-
759.
Adams, W. C. (2006) Comparison of chamber 6.6 hour exposures to 
0.04-0.08 ppm ozone via square-wave and triangular

[[Page 3041]]

profiles on pulmonary responses. Inhalation Toxicol. 18: 127-136.
Adams, W.C. (2007) Comment on EPA memorandum: The effects of ozone 
on lung function at 0.06 ppm in healthy adults. October 9. EPA-HQ-
OAR-2005-0172-4783.
American Academy of Pediatrics, Committee on Environmental Health. 
(2004) Ambient air pollution: health hazards to children. Pediatrics 
114: 1699-1707.
American Thoracic Society. (1985) Guidelines as to what constitutes 
an adverse respiratory health effect, with special reference to 
epidemiologic studies of air pollution. Am. Rev. Respir. Dis. 131: 
666-668.
American Thoracic Society (2000) What constitutes an adverse effect 
of air pollution? Am. J. Respir. Crit. Care Med. 161: pp. 665-673.
Andersen, C. P.; Hogsett, W. E.; Wessling, R.; Plocher, M. (1991) 
Ozone decreases spring root growth and root carbohydrate content in 
ponderosa pine the year following exposure. Can. J. For. Res. 21: 
1288-1291.
Anderson, H. R.; Spix, C.; Medina, S.; Schouten, J. P.; 
Castellsague, J.; Rossi, G.; Zmirou, D.; Touloumi, G.; Wojtyniak, 
B.; Ponka, A.; Bacharova, L.; Schwartz, J.; Katsouyanni, K. (1997) 
Air pollution and daily admissions for chronic obstructive pulmonary 
disease in 6 European cities: results from the APHEA project. Eur. 
Respir. J. 10: 1064-1071.
Arbaugh, M.; Bytnerowicz, A.; Grulke, N.; Fenn, M.; Poth, M.; 
Temple, P.; Miller, P. (2003) Photochemical smog effects in mixed 
conifer forests along a natural gradient of ozone and nitrogen 
deposition in the San Bernardino Mountains. Environ. Int. 29: 401-
406.
Arnold J.R.; R. L. Dennis; G. S. Tonnesen, (2003) Diagnostic 
evaluation of numerical air quality models with specialized ambient 
observations: testing the Community Multiscale Air Quality modeling 
system (CMAQ) at selected SOS 95 ground sites, Atmos. Environ. 37: 
1185-1198.
Ashmore, M.; Emberson, L.; Karlsson, P. E.; Pleijel, H. (2004) New 
directions: a new generation of ozone critical levels for the 
protection of vegetation in Europe (correspondence). Atmos. Environ. 
38: 2213-2214.
Arito, H.; Takahashi, M.; Iwasaki, T.; Uchiyama, I. (1997) Age-
related changes in ventilatory and heart rate responses to acute 
ozone exposure in the conscious rat. Ind. Health 35: 78-86.
Avol, E. L.; Gauderman, W. J.; Tan, S. M.; London, S. J.; Peters, J. 
M. (2001) Respiratory effects of relocating to areas of differing 
air pollution levels. Am. J. Respir. Crit. Care Med. 164: 2067-2072.
Awmack, C. S.; Harrington, R.; Lindroth, R. L. (2004) Aphid 
individual performance may not predict population responses to 
elevated CO2 or O3. Global Change Biol. 10: 1414-1423.
Barnes, J. D.; Eamus, D.; Brown, K. A. (1990) The influence of 
ozone, acid mist and soilnutrient status on Norway spruce [Picea 
abies (L.) Karst.]: II. photosynthesis, dark respiration and soluble 
carbohydrates of trees during late autumn. New Phytol. 115: 149-156.
Bascom, R.; Naclerio, R. M.; Fitzgerald, T. K.; Kagey-Sobotka, A.; 
Proud, D. (1990) Effect of ozone inhalation on the response to nasal 
challenge with antigen of allergic subjects. Am. Rev. Respir. Dis. 
142: 594-601.
Basha, M. A.; Gross, K. B.; Gwizdala, C. J.; Haidar, A. H.; 
Popovich, J., Jr. (1994) Bronchoalveolar lavage neutrophilia in 
asthmatic and healthy volunteers after controlled exposure to ozone 
and filtered purified air. Chest 106: 1757-1765.
Beedlow P.A., Tingey D.T., Phillips D.L., Hogsett W.E. & Olszyk D.M. 
(2004) Rising atmospheric CO2 and carbon sequestration in forests. 
Frontiers in Ecology and the Environment 2, 315-322.
Beeson, W. L.; Abbey, D. E.; Knutsen, S. F. (1998) Long-term 
concentrations of ambient air pollutants and incident lung cancer in 
California adults: results from the AHSMOG study. Environ. Health 
Perspect. 106: 813-823.
Bell, M. L.; McDermott, A.; Zeger, S. L.; Samet, J. M.; Dominici, F. 
(2004) Ozone and short-term mortality in 95 US urban communities, 
1987-2000. JAMA J. Am. Med. Assoc. 292: 2372-2378.
Bell, M. L.; Dominici, F.; Samet, J. M. (2005) A meta-analysis of 
time-series studies of ozone and mortality with comparison to the 
national morbidity, mortality, and air pollution study. Epidemiology 
16: 436-445.
Bell, M. L.; Peng, R. D.; Dominici, F. (2006) The exposure-response 
curve for ozone and risk of mortality and the adequacy of current 
ozone regulations. Environ. Health Perspect.: doi:10.1289/ehp.8816. 
Available online at: http://dx.doi.org/ [23 January, 2006].
Bosson, J.; Stenfors, N.; Bucht, A.; Helleday, R.; Pourazar, J.; 
Holgate, S. T.; Kelly, F. J.; Sandstr[ouml]m, T.; Wilson, S.; Frew, 
A. J.; Blomberg, A. (2003) Ozone-induced bronchial epithelial 
cytokine expression differs between healthy and asthmatic subjects. 
Clin. Exp. Allergy 33: 777-782.
Brauer, M.; Blair, J.; Vedal, S. (1995) Effect of ambient ozone 
exposure on lung function in farm workers. Am. J. Respir. Crit. Care 
Med. 154: 981-987.
Brauer, M.; Blair, J.; Vedal, S. (1996) Effect of ambient ozone 
exposure on lung function in farm workers. Am. J. Respir. Crit. Care 
Med. 154: 981-987.
Brauer, M.; Brook, J. R. (1997) Ozone personal exposures and health 
effects for selected groups residing in the Fraser Valley. In: 
Steyn, D. G.; Bottenheim, J. W., eds. The Lower Fraser Valley 
Oxidants/Pacific '93 Field Study. Atmos. Environ. 31: 2113-2121.
Black, V. J.; Black, C. R.; Roberts, J. A.; Stewart, C. A. (2000) 
Impact of ozone on the reproductive development of plants. New 
Phytol. 147: 421-447.
Brook, R. D.; Brook, J. R.; Urch, B.; Vincent, R.; Rajagopalan, S.; 
Silverman, F. (2002) Inhalation of fine particulate air pollution 
and ozone causes acute arterial vasoconstriction in healthy adults. 
Circulation 105: 1534-1536.
Brown, J. S. The effects of ozone on lung function at 0.06 ppm in 
healthy adults. June 14, 2007. Memo to the Ozone NAAQS Review 
Docket. EPA-HQ-OAR-2005-0172-0175. Available online at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html.
Burnett, R. T.; Dales, R. E.; Raizenne, M. E.; Krewski, D.; Summers, 
P. W.; Roberts, G. R.; Raad-Young, M.; Dann, T.; Brook, J. (1994) 
Effects of low ambient levels of ozone and sulfates on the frequency 
of respiratory admissions to Ontario hospitals. Environ. Res. 65: 
172-194.
Burnett, R. T.; Brook, J. R.; Yung, W. T.; Dales, R. E.; Krewski, D. 
(1997a) Association between ozone and hospitalization for 
respiratory diseases in 16 Canadian cities. Environ. Res. 72: 24-31.
Burnett, R. T.; Cakmak, S.; Brook, J. R.; Krewski, D. (1997b) The 
role of particulate size and chemistry in the association between 
summertime ambient air pollution and hospitalization for 
cardiorespiratory diseases. Environ. Health Perspect. 105: 614-620.
Burns, R. M., Honkala, B. H., tech. coords. (1990) Silvics of North 
America: 1. Conifers; 2. Hardwoods. Agriculture Handbook 654. U.S. 
Department of Agriculture, Forest Service, Washington, DC. vol.2, p. 
877.
Byun, D.W., Ching, J.K.S. (Eds.), 1999. Science Algorithms of the 
EPA Models-3 Community Multiscale Air Quality Model (CMAQ) Modeling 
System. EPA/600/R-99/030, U.S. Environmental Protection Agency, 
Office of Research and Development, Washington, DC 20460.
Campbell, S.; Temple, P.; Pronos, J.; Rochefort, R.; Andersen, C. 
(2000) Monitoring for ozone injury in west coast (Oregon, 
Washington, California) forests in 1998. Portland, OR: U.S. 
Department of Agriculture, Forest Service, Pacific Northwest 
Research Station; general technical report no. PNW-GTR-495. 
Available: http://www.fs.fed.us/pnw/gtrs.htm [11 April, 2003].
Centers for Disease Control and Prevention. (2004) The health 
consequences of smoking: a report of the Surgeon General. Atlanta, 
GA: U.S. Department of Health and Human Services, National Center 
for Chronic Disease Prevention and Health Promotion, Office on 
Smoking and Health. Available: http://www.cdc.gov/tobacco/sgr/sgr_2004/chapters.htm (18 August, 2004).
Chappelka, A. H. (2002) Reproductive development of blackberry 
(Rubus cuneifolius) as influenced by ozone. New Phytol. 155: 249-
255.
Chappelka, A. H.; Samuelson, L. J. (1998) Ambient ozone effects on 
forest trees of the eastern United States: a review. New Phytol. 
139: 91-108.
Chen, L.; Jennison, B. L.; Yang, W.; Omaye, S. T. (2000) Elementary 
school absenteeism and air pollution. Inhalation Toxicol. 12: 997-
101.
Chen, C.-Y.; Bonham, A. C.; Plopper, C. G.; Joad, J. P. (2003) 
Plasticity in respiratory motor control: selected contribution:

[[Page 3042]]

neuroplasticity in nucleus tractus solitarius neurons following 
episodic ozone exposure in infant primates. J. Appl. Physiol. 94: 
819-827.
Clean Air Scientific Advisory Committee (CASAC) (2006) Transcript of 
Public Meeting Held in Research Triangle Park, N.C. on August 24, 
2006.
Cox, W. M.; Camalier, L. (2006) The effect of measurement error on 
8-hour ozone design concentrations. Memo to the Ozone NAAQS Review 
Docket. EPA-HQ-OAR-2005-0172-0026. Available online at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html.
Coulston, J. W., Smith, G. C. and Smith, W. D. (2003) ``Regional 
assessment of ozone sensitive tree species using bioindicator 
plants.'' Environmental Monitoring and Assessment 83: 113-127.
Coulston, J. W., K. H. Riitters and G. C. Smith (2004) A Preliminary 
Assessment of the Montr[eacute]al Process Indicators of Air 
Pollution for the United States. Environmental Monitoring and 
Assessment 95: 57-74.
Dann, M. S.; Pell, E. J. (1989) Decline of activity and quantity of 
ribulose bisphosphatecarboxylase/oxygenase and net photosynthesis in 
ozone-treated potato foliage. PlantPhysiol. 91: 427-432.
David, G. L.; Romieu, I.; Sienra-Monge, J. J.; Collins, W. J.; 
Ramirez-Aguilar, M.; Del Rio-Navarro, B. E.; Reyes-Ruiz, N. I.; 
Morris, R. W.; Marzec, J. M.; London, S. J. (2003) Nicotinamide 
adenine dinucleotide (phosphate) reduced:quinone oxidoreductase and 
glutathione s-transferase m1 polymorphism and childhood asthma. Am. 
J. Respir. Crit. Care Med. 168: 1199-1204.
Davison, A. W.; Reiling, K. (1995) A rapid change in ozone 
resistance of Plantago major after summers with high ozone 
concentrations. New Phytol. 131: 337-344.
Devlin, R. B.; McDonnell, W. F.; Koren, H. S.; Becker, S. (1990) 
Prolonged exposure of humans to 0.10 and 0.08 ppm ozone results in 
inflammation in the lung. Presented at: 83rd annual meeting of the 
Air & Waste Management Association; June; Pittsburgh, PA. 
Pittsburgh, PA: Air & Waste Management Association; paper no. 90-
150.2.
Devlin, R. B.; McDonnell, W. F.; Mann, R.; Becker, S.; House, D. E.; 
Schreinemachers, D.; Koren, H. S. (1991) Exposure of humans to 
ambient levels of ozone for 6.6 hrs causes cellular and biochemical 
changes in the lung. Am. J. Respir. Cell Mol. Biol. 4: 72-81.
Dickson, R. E., Lewin K. F., Isebrands J. G., Coleman M. D., Heilman 
W. E., Riemenschneider D. E., Sober J., Host G. E., Zak D. F., 
Hendrey G. R., Pregitzer K. S. and Karnosky D. F. (2000) Forest 
atmosphere carbon transfer storage-II (FACTS II)--The aspen free-air 
CO2 and O3 enrichment (FACE) project in an 
overview. USDA Forest Service North Central Research Station. 
General Tech. Rep. NC-214. 68pp.
Dietert, R. R.; Etzel, R. A.; Chen, D.; Halonen, M.; Holladay, S. 
D.; Jarabek, A. M.; Landreth, K.; Peden, D. B.; Pinkerton, K.; 
Smialowicz, R. J.; Zoetis, T. (2000) Workshop to identify critical 
window of exposure for children's health: immune and respiratory 
systems work group summary. Environ. Health Perspect. Suppl. 108(3): 
483-490.
Dockery, D. W.; Pope, C. A., III; Xu, X.; Spengler, J. D.; Ware, J. 
H.; Fay, M. E.; Ferris, B. G., Jr.; Speizer, F. E. (1993) An 
association between air pollution and mortality in six U.S. cities. 
N. Engl. J. Med. 329: 1753-1759.
Dominici, F.; McDermott, A.; Daniels, M.; Zeger, S. L.; Samet, J. M. 
(2003) Mortality among residents of 90 cities. In: Revised analyses 
of time-series studies of air pollution and health. Special report. 
Boston, MA: Health Effects Institute; pp. 9-24. Available: http://www.healtheffects.org/Pubs/TimeSeries.pdf [12 May, 2004].
Duff, M., Horst, R. L., Johnson, T. R. (1998) ``Quadratic Rollback: 
A Technique to Model Ambient Concentrations Due to Undefined 
Emission Controls.'' Presented at the Air and Waste Management 
Annual Meeting. San Diego, California. June 14-18, 1998.
Eder, B. and S. Yu, 2006: A performance evaluation of the 2004 
release of Models-3 CMAQ, Atmos. Environ. 40: 4811-4824. Special 
issue on Model Evaluation: Evaluation of Urban and Regional Eulerian 
Air Quality Models.
Environmental Protection Agency (1986) Air quality criteria for 
ozone and other photochemical oxidants. Research Triangle Park, NC: 
Office of Health and Environmental Assessment, Environmental 
Criteria and Assessment Office; report nos. EPA-600/8-84-020aF-eF. 
5v. Available from: NTIS, Springfield, VA; PB87-142949.
Environmental Protection Agency (1996a) Air quality criteria for 
ozone and related photochemical oxidants. Research Triangle Park, 
NC: Office of Research and Development; EPA report no. EPA/600/AP-
93/004aF-cF. 3v. Available from: NTIS, Springfield, VA; PB96-185582, 
PB96-185590, and PB96-185608. Available online at: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=2831.
Environmental Protection Agency (1996b) Review of National Ambient 
Air Quality Standards for Ozone: Assessment of Scientific and 
Technical Information. OAQPS Staff Paper (Final) Research Triangle 
Park, NC: Office of Air Quality Planning and Standards; EPA report 
no. EPA/452/R-96-007. Available online at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_pr_sp.html.
Environmental Protection Agency (2002) Project Work Plan for Revised 
Air Quality Criteria for Ozone and Related Photochemical Oxidants. 
Research Triangle Park, NC: National Center for Environmental 
Assessment; EPA report no. NCEA-R-1068.
Environmental Protection Agency (2004) The Ozone Report: Measuring 
Progress through 2003. EPA/454/K-04-001. Office of Air Quality 
Planning and Standards, Research Triangle Park, NC.
Environmental Protection Agency (2005a) Air Quality Criteria for 
Ozone and Related Photochemical Oxidants (First External Review 
Draft). Washington, DC: National Center for Environmental 
Assessment; EPA report no. EPA/600/R-05/004aA-cA. Available online 
at: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=114523.
Environmental Protection Agency (2005b) Air Quality Criteria for 
Ozone and Related Photochemical Oxidants (Second External Review 
Draft) Washington, DC: National Center for Environmental Assessment; 
EPA report no. EPA/600/R-05/004aB-cB. Available online at: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=137307.
Environmental Protection Agency (2005c) Review of the national 
ambient air quality standards for ozone: assessment of scientific 
and technical information. OAQPS staff paper (First Draft). Research 
Triangle Park, NC: Office of Air Quality Planning and Standards; EPA 
report no. EPA-452/D-05-002. Available online at: http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html.
Environmental Protection Agency (2005d) Health Assessment Plan for 
Review of the National Ambient Air Quality Standards for Ozone. 
Office of Air Quality Planning and Standards, Research Triangle 
Park, NC. April 2005. Available electronically on the internet at: 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_pd.html.
Environmental Protection Agency (2006a) Air Quality Criteria for 
Ozone and Related Photochemical Oxidants. (Final) Washington, DC: 
National Center for Environmental Assessment; EPA report no. EPA/
600/R-05/004aB-cB. Available online at: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=149923.
Environmental Protection Agency (2006b) Review of the national 
ambient air quality standards for ozone: assessment of scientific 
and technical information. OAQPS staff paper. (Second Draft). 
Research Triangle Park, NC: Office of Air Quality Planning and 
Standards; EPA report no. EPA-452/D-05-002. Available online at: 
http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html.
Environmental Protection Agency (2007a) Review of the national 
ambient air quality standards for ozone: assessment of scientific 
and technical information. OAQPS staff paper. (Final) January 2007. 
Research Triangle Park, NC: Office of Air Quality Planning and 
Standards; EPA report no. EPA-452/R-07-003. Available online at: 
http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html.
Environmental Protection Agency (2007b) Review of the national 
ambient air quality standards for ozone: assessment of scientific 
and technical information. OAQPS staff paper. (Updated Final) July 
2007. Research Triangle Park, NC: Office of Air Quality Planning and 
Standards; EPA report no. EPA-452/R-07-007. Available online at: 
http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html.
Environmental Protection Agency (2007c) Ozone Population Exposure 
Analysis for

[[Page 3043]]

Selected Urban Areas. (Updated Final) July 2007. Research Triangle 
Park, NC: Office of Air Quality Planning and Standards; EPA report 
no. EPA-452/R-07-010. Available online at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html.
Environmental Protection Agency (2008) Responses to Significant 
Comments on the 2007 Proposed Rule on the National Ambient Air 
Quality Standards for Ozone (July 11, 2007; 72 FR 37818). March 
2008. Research Triangle Park, NC; Office of Air Quality Planning and 
Standards. Available online at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_rc.html.
Environmental Protection Agency (2009) Provisional Assessment of 
Recent Studies on Health and Ecological Effects of Ozone Exposure. 
September 2009. Research Triangle Park: National Center for 
Environmental Assessment; EPA report no. EPA/600/R-09/101.
Evans, M. J.; Fanucchi, M. V.; Baker, G. L.; Van Winkle, L. S.; 
Pantle, L. M.; Nishio, S. J.; Schelegle, E. S.; Gershwhin, L. J.; 
Miller, L. A.; Hyde, D. M.; Sannes, P. L.; Plopper, C. G. (2003) 
Atypical development of the tracheal basement membrane zone of 
infant rhesus monkeys exposed to ozone and allergen. Am. J. Physiol. 
285: L931-L939.
Felzer, B.; Kickligher, D.; Melillo, J.; Wang, C.; Zhuang, Q.; 
Prinn, R. (2004) Effects of ozone on net primary production and 
carbon sequestration in the conterminous United States using a 
biogeochemistry model. Tellus B 56 (3), 230-248.
Fiore, A. M.; Jacob, D. J.; Bey, I.; Yantosca, R. M.; Field, B. D.; 
Fusco, A. C.; Wilkinson, J. G. (2002) Background ozone over the 
United States in summer: origin, trend, and contribution to 
pollution episodes. J. Geophys. Res. (Atmos.) 107(D15): 10.1029/
2001JD000982.
Fiore, A. M.; Jacob, D. J.; Liu, H.; Yantosca, R. M.; Fairlie, T. 
D.; Fusco, A. C.; Li, Q. (2003) Variability in surface ozone 
background over the United States: implications for Air Quality 
Policy. J. of Geophysical Research, 108(D24)19-1-19-12.
Fiscus, E. L.; Reid, C. D.; Miller, J. E.; Heagle, A. S. (1997) 
Elevated CO2 reduces O3 flux and 
O3-induced yield losses in soybeans: possible 
implications for elevated CO2 studies. J. Exp. Bot. 48: 
307-313.
Folinsbee, L. J.; McDonnell, W. F.; Horstman, D. H. (1988) Pulmonary 
function and symptom responses after 6.6-hour exposure to 0.12 ppm 
ozone with moderate exercise. JAPCA 38: 28-35.
Folinsbee, L. J.; Horstman, D. H.; Kehrl, H. R.; Harder, S.; Abdul-
Salaam, S.; Ives, P. J. (1994) Respiratory responses to repeated 
prolonged exposure to 0.12 ppm ozone. Am. J. Respir. Crit. Care Med. 
149: 98-105.
Folinsbee, L. J.; Hazucha, M. J. (2000) Time course of response to 
ozone exposure in healthy adult females. Inhalation Toxicol. 12: 
151-167.
Foster, W. M.; Silver, J. A.; Groth, M. L. (1993) Exposure to ozone 
alters regional function and particle dosimetry in the human lung. 
J. Appl. Physiol. 75: 1938-1945.
Foster, W. M.; Weinmann, G. G.; Menkes, E.; Macri, K. (1997) Acute 
exposure of humans to ozone impairs small airway function. Ann. 
Occup. Hyg. 41(suppl. 1): 659-666.
Frampton, M. W.; Morrow, P. E.; Torres, A.; Cox, C.; Voter, K. Z.; 
Utell, M. J.; Gibb, F. R.; Speers, D. M. (1997) Ozone responsiveness 
in smokers and nonsmokers. Am. J. Respir. Crit. Care Med. 155: 116-
121.
Galizia, A.; Kinney, P. L. (1999) Long-term residence in areas of 
high ozone: associations with respiratory health in a nationwide 
sample of nonsmoking young adults. Environ. Health Perspect. 107: 
675-679.
Gauderman, W. J.; McConnell, R.; Gilliland, F.; London, S.; Thomas, 
D.; Avol, E.; Vora, H.; Berhane, K.; Rappaport, E. B.; Lurmann, F.; 
Margolis, H. G.; Peters, J. (2000) Association between air pollution 
and lung function growth in southern California children. Am. J. 
Respir. Crit. Care Med. 162: 1383-1390.
Gauderman, W. J.; Gilliland, G. F.; Vora, H.; Avol, E.; Stram, D.; 
McConnell, R.; Thomas, D.; Lurmann, F.; Margolis, H. G.; Rappaport, 
E. B.; Berhane, K.; Peters, J. M. (2002) Association between air 
pollution and lung function growth in southern California children: 
results from a second cohort. Am. J. Respir. Crit. Care Med. 166: 
76-84.
Gauderman, W. J.; Avol, E.; Gilliland, F.; Vora, H.; Thomas, D.; 
Berhane, K.; McConnell, R.; Kuenzli, N.; Lurmann, F.; Rappaport, E.; 
Margolis, H.; Bates, D.; Peters, J. (2004a) The effect of air 
pollution on lung development from 10 to 18 years of age. N. Engl. 
J. Med. 351: 1057-1067.
Gauderman, W. J.; Avol, E.; Gilliland, F. (2004b) Air pollution and 
lung function [reply letter]. N. Engl. J. Med. 351: 2653.
Gent, J. F.; Triche, E. W.; Holford, T. R.; Belanger, K.; Bracken, 
M. B.; Beckett, W. S.; Leaderer, B. P. (2003) Association of low-
level ozone and fine particles with respiratory symptoms in children 
with asthma. JAMA J. Am. Med. Assoc. 290: 1859-1867.
Gilliland, F. D.; Berhane, K.; Rappaport, E. B.; Thomas, D. C.; 
Avol, E.; Gauderman, W. J.; London, S. J.; Margolis, H. G.; 
McConnell, R.; Islam, K. T.; Peters, J. M. (2001) The effects of 
ambient air pollution on school absenteeism due to respiratory 
illnesses. Epidemiology 12: 43-54.
Goldstein, A. H.; Millet, D. B.; McKay, M.; Jaegle, L.; Horowitz, 
L.; Cooper, O.; Hudman, R.; Jacob, D; Oltmans, S; Clarke, A. (2004) 
Impact of Asian emissions on observations at Trinidad Head, 
California, during ITCT 2K2. J. of Geophysical Research, 
109(D23S17), doi: 10.1029/2003JD004406.
Gong, H., Jr.; Wong, R.; Sarma, R. J.; Linn, W. S.; Sullivan, E. D.; 
Shamoo, D. A.; Anderson, K. R.; Prasad, S. B. (1998) Cardiovascular 
effects of ozone exposure in human volunteers. Am. J. Respir. Crit. 
Care Med. 158: 538-546.
Goodale, C. L., Apps, M. J., Birdsey, R. A., Field, C. B., Heath, L. 
S., Houghton, R. A., Jenkins, J. C., Kohlmaier, G. H., Kurz, W., 
Liu, S., Nabuurs, G.-J., Nilsson, S. and Shvidenko, A. Z. (2002) 
Forest carbon sinks in the northern hemisphere. Ecol. Appl. 12, 891-
899.
Grantz, D.A., McCool, P.H. (1992) Effect of ozone on Pima and Acala 
cottons in the San Joaquin Valley. In: Herber, D.J., Richter, D.A. 
(Eds.), Proceedings 1992 Beltwide Cotton Conferences, vol. 3. 
National Cotton Council of America, Memphis, TN, pp. 1082-1084.
Greer, J.R.; Abbey, D.E.; Burchette, R.J. (1993) Asthma related to 
occupational and ambient air pollutants in nonsmokers. J. Occup. 
Med. 35: 909-915.
Gregg, J.W.; Jones, C.G.; Dawson, T.E. (2003) Urbanization effects 
on tree growth in the vicinity of New York City. Nature 424: 183-
187.
Grulke, N.E.; Andersen, C.P.; Fenn, M.E.; Miller, P.R. (1998) Ozone 
exposure and nitrogen deposition lowers root biomass of ponderosa 
pine in the San Bernardino Mountains, California. Environ. Pollut. 
103: 63-73.
Grulke, N.E.; Balduman, L. (1999) Deciduous conifers: high N 
deposition and O3 exposure effects on growth and biomass 
allocation in ponderosa pine. Water Air Soil Pollut. 116: 235-248.
Gryparis, A.; Forsberg, B.; Katsouyanni, K.; Analitis, A.; Touloumi, 
G.; Schwartz, J.; Samoli, E.; Medina, S.; Anderson, H.R.; Niciu, E. 
M.; Wichmann, H.-E.; Kriz, B.; Kosnik, M.; Skorkovsky, J.; Vonk, 
J.M.; D[ouml]rtbudak, Z. (2004) Acute effects of ozone on mortality 
from the ``air pollution and health: a European approach'' project. 
Am. J. Respir. Crit. Care Med. 170: 1080-1087.
Guderian, R. (1977) Discussion of the suitability of plant responses 
as a basis for air pollution control measures. In: Billings, W.D.; 
Golley, F.; Lange, O.L.; Olson, J.S., eds. Air pollution: 
phytotoxicity of acidic gases and its significance in air pollution 
control. Berlin, Federal Republic of Germany: Springer Verlag; pp. 
75-97.
Hanson, P., Samuelson, L., Wullschleger, S., Tabberer, T.; Edwards, 
G. (1994) ``Seasonal patterns of light-saturated photosynthesis and 
leaf conductance for mature and seedling Quercus rubra L. foliage: 
differential sensitivity to ozone exposure.'' Tree Physiology 
14:1351-1366.
Hazucha, M.J.; Folinsbee, L.J.; Seal, E., Jr. (1992) Effects of 
steady-state and variable ozone concentration profiles on pulmonary 
function. Am. Rev. Respir. Dis. 146: 1487-1493.
Hazucha, M.J.; Folinsbee, L.J.; Bromberg, P. A. (2003) Distribution 
and reproducibility of spirometric response to ozone by gender and 
age. J. Appl. Physiol. 95: 1917-1925.
Heck, W.W.; Cowling, E.B. (1997) The need for a long term cumulative 
secondary ozone standard--an ecological perspective. EM (January): 
23-33.

[[Page 3044]]

Henderson, R. (2006a) Letter from CASAC Chairman Rogene Henderson to 
EPA Administrator Stephen Johnson. February 16, 2006, EPA-CASAC-06-
003.
Henderson, R. (2006b) Letter from CASAC Chairman Rogene Henderson to 
EPA Administrator Stephen Johnson. June 5, 2006, EPA-CASAC-06-007.
Henderson, R. (2006c) Letter from CASAC Chairman Rogene Henderson to 
EPA Administrator Stephen Johnson. October 24, 2006, EPA-CASAC-07-
001.
Henderson, R. (2007) Letter from CASAC Chairman Rogene Henderson to 
EPA Administrator Stephen Johnson. March 26, 2007, EPA-CASAC-07-002.
Henderson, R. (2008) Letter from CASAC Chairman Rogene Henderson to 
EPA Administrator Stephen Johnson. April 7, 2008, EPA-CASAC-08-009.
Hill, A.B. (1965) The environment and disease: association or 
causation? Proc. R. Soc. Med. 58: 295-300.
Hiltermann, J.T.N.; Lapperre, T.S.; Van Bree, L.; Steerenberg, P.A.; 
Brahim, J.J.; Sont, J.K.; Sterk, P.J.; Hiemstra, P.S.; Stolk, J. 
(1999) Ozone-induced inflammation assessed in sputum and bronchial 
lavage fluid from asthmatics: a new noninvasive tool in 
epidemiologic studies on air pollution and asthma. Free Radical 
Biol. Med. 27: 1448-1454.
Hoek, G. (2003) Daily mortality and air pollution in The 
Netherlands. In: Revised analyses of time-series studies of air 
pollution and health. Special report. Boston, MA: Health Effects 
Institute; pp. 133-142. Available: http://www.healtheffects.org/Pubs/TimeSeries.pdf [12 May, 2004].
Hoek, G.; Brunekreef, B.; Verhoeff, A.; Van Wijnen, J.; Fischer, P. 
(2000) Daily mortality and air pollution in the Netherlands. J. Air 
Waste Manage. Assoc. 50: 1380-1389.
Hoek, G.; Brunekreef, B.; Fischer, P.; Van Wijnen, J. (2001) The 
association between air pollution and heart failure, arrhythmia, 
embolism, thrombosis, and other cardiovascular causes of death in a 
time series study. Epidemiology 12: 355-357.
Hogsett, W.E.; Tingey, D.T.; Hendricks, C.; Rossi, D. (1989) 
Sensitivity of western conifers to SO2 and seasonal interaction of 
acid fog and ozone. In: Olson, R.K.; Lefohn, A.S., eds. Effects of 
air pollution on western forests [an A&WMA symposium; June; Anaheim, 
CA]. Air Pollution Control Association; pp. 469-491 (APCA 
transactions series: no. 16).
Holton, M.K.; Lindroth, R.L.; Nordheim, E.V. (2003) Foliar quality 
influences tree-herbivore-parisitoid interactions: effects of 
elevated CO2, O3, and plant genotype. Oecologia 137: 233-
244.
Holz, O.; M[uuml]cke, M.; Paasch, K.; B[ouml]hme, S.; Timm, P.; 
Richter, K.; Magnussen, H.; J[ouml]rres, R.A. (2002) Repeated ozone 
exposures enhance bronchial allergen responses in subjects with 
rhinitis or asthma. Clin. Exp. Allergy. 32: 681-689.
H[ouml]ppe, P.; Praml, G.; Rabe, G.; Lindner, J.; Fruhmann, G.; 
Kessel, R. (1995) Environmental ozone field study on pulmonary and 
subjective responses of assumed risk groups. Environ. Res. 71: 109-
121.
Horst, R.; Duff, M. (1995). Concentration data transformation and 
the quadratic rollback methodology (Round 2, Revised). Unpublished 
memorandum to R. Rodr[iacute]guez, U.S. EPA, June 8.
Horstman, D.H.; Folinsbee, L.J.; Ives, P.J.; Abdul-Salaam, S.; 
McDonnell, W.F. (1990) Ozone concentration and pulmonary response 
relationships for 6.6-hr exposures with five hours of moderate 
exercise to 0.08, 0.10, and 0.12 ppm. Am. Rev. Respir. Dis. 142: 
1158-1163.
Horstman, D.H.; Ball, B.A.; Brown, J.; Gerrity, T.; Folinsbee, L.J. 
(1995) Comparison of pulmonary responses of asthmatic and 
nonasthmatic subjects performing light exercise while exposed to a 
low level of ozone. Toxicol. Ind. Health 11: 369-385.
Huang, Y.; Dominici, F.; Bell, M.L. (2005) Bayesian hierarchical 
distributed lag models for summer ozone exposure and cardio-
respiratory mortality. Environmetrics 16: 547-562.
Isebrands, J.G.; Dickson, R.E.; Rebbeck, J.; Karnosky, D.F. (2000) 
Interacting effects of multiple stresses on growth and physiological 
processes in northern forest trees. In: Mickler, R.A.; Birsdey, 
R.A.; Hom, J., eds. Responses of northern U.S. forests to 
environmental change. New York, NY: Springer-Verlag; pp. 149-180. 
(Ecological studies: v. 139).
Isebrands, J.G.; McDonald, E.P.; Kruger, E.; Hendrey, G.; Percy, K.; 
Pregitzer, K.; Sober, J.; Karnosky, D.F. (2001) Growth responses of 
Populus tremuloides clones to interacting carbon dioxide and 
tropospheric ozone. Environ. Pollut. 115: 359-371.
Ito, K.; De Leon, S.F.; Lippmann, M. (2005) Associations between 
ozone and daily mortality, analysis and meta-analysis. Epidemiology 
16: 446-457.
Jacobson, J.S. (1977) The effects of photochemical oxidants on 
vegetation. In: Ozon und Begleitsubstanzen im photochemischen Smog: 
das Kolloquium [Ozone and related substances in photochemical smog: 
the colloquium]; September 1976; Dusseldorf, Federal Republic of 
Germany. Dusseldorf, Federal Republic of Germany: VDI-Verlag GmbH; 
pp. 163-173. (VDI-Berichte nr. 270).
Johnson, T. (1997) ``Sensitivity of Exposure Estimates to Air 
Quality Adjustment Procedure,'' Letter to Harvey Richmond, Office of 
Air Quality Planning and Standards, U.S. Environmental Protection 
Agency, Research Triangle Park, North Carolina.
J[ouml]rres, R.; Nowak, D.; Magnussen, H.; Speckin, P.; Koschyk, S. 
(1996) The effect of ozone exposure on allergen responsiveness in 
subjects with asthma or rhinitis. Am. J. Respir. Crit. Care Med. 
153: 56-64.
Karnosky, D.F., Z.E. Gagnon, R.E. Dickson, M.D. Coleman, E.H. Lee, 
J.G. Isebrands, (1996) ``Changes in growth, leaf abscission, biomass 
associated with seasonal tropospheric ozone exposures of Populus 
tremuloides clones and seedlings.'' Can. J. For. Res. 26: 23-37.
Karnosky, D.F., B. Mankovska, K. Percy, R.E. Dickson, G.K. Podila, 
J. Sober, A. Noormets, G. Hendrey, M.D. Coleman, M. Kubiske, K.S. 
Pregitzer, and J.G. Isebrands (1999) ``Effects of tropospheric 
O3 on trembling aspen and interaction with 
CO2: Results from an O3-gradient and a FACE 
experiment.'' J. Water, Air and Soil Pollut. 116: 311-322.
Karnosky, D.F.; Zak, D.R.; Pregitzer, K. S.; Awmack, C.S.; Bockheim, 
J.G.; Dickson, R.E.; Hendrey, G.R.; Host, G.E.; King, J.S.; Kopper, 
B.J.; Kruger, E.L.; Kubiske, M.E.; Lindroth, R. L.; Mattson, W.J.; 
McDonald, E.P. (2003) Tropospheric O3 moderates responses 
of temperate hardwood forests to elevated CO2: A 
synthesis of molecular to ecosystem results from the Aspen FACE 
project. Funct. Ecol. 17: 289-304.
Karnosky, D.F., Pregitzer, K.S., Zak, D.R., Kubiske, M.E., Hendrey, 
G.R., Weinstein, D., Nosal, M. & Percy, K.E. (2005) Scaling ozone 
responses of forest trees to the ecosystem level in a changing 
climate. Plant Cell Environ.28, 965-981.
Kelly, F.J.; Dunster, C.; Mudway, I. (2003) Air pollution and the 
elderly: oxidant/antioxidant issues worth consideration. Eur. 
Respir. J. Suppl. 40: 70S-75S.
Kim, S.-Y.; Lee, J.-T.; Hong, Y.-C.; Ahn, K.-J.; Kim, H. (2004) 
Determining the threshold effect of ozone on daily mortality: an 
analysis of ozone and mortality in Seoul, Korea, 1995-1999. Environ. 
Res. 94: 113-119.
King, J.S., M.E. Kubiske, K.S. Pregitzer, G.R. Hendrey, E.P. 
McDonald, C.P. Giardina, V.S. Quinn, D.F. Karnosky. (2005) 
Tropospheric O3 compromises net primary production in 
young stands of trembling aspen, paper birch and sugar maple in 
response to elevated atmospheric CO2. New Phytologist. 
168:623-636.
Kinney, P.L.; Aggarwal, M.; Nikiforov, S.V.; Nadas, A. (1998) 
Methods development for epidemiologic investigations of the health 
effects of prolonged ozone exposure. Part III: an approach to 
retrospective estimation of lifetime ozone exposure using a 
questionnaire and ambient monitoring data (U.S. sites). Cambridge, 
MA: Health Effects Institute; research report no. 81; pp. 79-108.
Korrick, S.A.; Neas, L.M.; Dockery, D.W.; Gold, D.R.; Allen, G.A.; 
Hill, L.B.; Kimball, K.D.; Rosner, B.A.; Speizer, F.E. (1998) 
Effects of ozone and other pollutants on the pulmonary function of 
adult hikers. Environ. Health Perspect. 106: 93-99.
Koutrakis, P.; Suh, H.H.; Sarnat, J.A.; Brown, K.W.; Coull, B.A; 
Schwartz, J. (2005) Characterization of particulate and gas 
exposures of sensitive subpopulations living in Baltimore and 
Boston. HEI Research Report 131.
Kreit, J.W.; Gross, K.B.; Moore, T.B.; Lorenzen, T.J.; D'Arcy, J.; 
Eschenbacher, W.L. (1989) Ozone-induced changes in pulmonary 
function and bronchial responsiveness in asthmatics. J. Appl. 
Physiol. 66: 217-222.

[[Page 3045]]

Krewski, D.; Burnett, R.T.; Goldberg, M.S.; Hoover, K.; Siemiatycki, 
J,; Jerrett, M.; Abrahamowicz, M.; White, W.H. (2000) Reanalysis of 
the Harvard Six Cities Study and the American Cancer Society Study 
of particulate air pollution and mortality. A special report of the 
Institute's particle epidemiology reanalysis project. Cambridge, MA: 
Health Effects Institute.
K[uuml]nzli, N.; Lurmann, F.; Segal, M.; Ngo, L.; Balmes, J.; Tager, 
I.B. (1997) Association between lifetime ambient ozone exposure and 
pulmonary function in college freshmen--results of a pilot study. 
Environ. Res. 72: 8-23.
Langstaff, J. (2007) Analysis of Uncertainty in Ozone Population 
Exposure Modeling. January 31, 2007. Memo to the Ozone NAAQS Review 
Docket. EPA-HQ-OAR-2005-0172-0174. Available online at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html.
Larson, J.L.; Zak, D.R.; Sinsabaugh, R.L. (2002) Extracellular 
enzyme activity beneath temperate trees growing under elevated 
carbon dioxide and ozone. Soil Sci. Soc. Am. J. 66: 1848-1856.
Laurence, J.A.,Kohut, R.J., Amundson, R.G., (1993). Use of TREGRO to 
simulate the effects of ozone on the growth of red spruce seedlings. 
Forest Science. 39: 453-464.
Laurence, J.A.; Retzlaff, W.A.; Kern, J.S.; Lee, E.H.; Hogsett, 
W.E.; Weinstein, D.A. (2001) Predicting the regional impact of ozone 
and precipitation on the growth of loblolly pine and yellow poplar 
using linked TREGRO and ZELG models. For. Ecol. Manage. 146: 247-
263.
Lee, E. H.; Hogsett, W. E. (1996) Methodology for calculating inputs 
for ozone secondary standard benefits analysis: part II. Report 
prepared for Office of Air Quality Planning and Standards, Air 
Quality Strategies and Standards Division, U.S. Environmental 
Protection Agency, Research Triangle Park, N.C., March. EPA Docket 
No. A-95-58 Item II-I-265.
Lefohn, A.S.; Runeckles, V.C.; Krupa, S.V.; Shadwick, D.S. (1989) 
Important considerations for establishing a secondary ozone standard 
to protect vegetation. JAPCA 39, pp. 1039-1045.
Levy, J.I.; Chemerynski, S.M.; Sarnat, J.A. (2005) Ozone exposure 
and mortality, an empiric Bayes metaregression analysis. 
Epidemiology 16: 458-468.
Linn, W.S.; Shamoo, D.A.; Anderson, K.R.; Peng, R.-C.; Avol, E.L.; 
Hackney, J.D.; Gong, H., Jr. (1996) Short-term air pollution 
exposures and responses in Los Angeles area schoolchildren. J. 
Exposure Anal. Environ. Epidemiol. 6: 449-472.
Lipfert, F.W.; Perry, H.M., Jr.; Miller, J.P.; Baty, J.D.; Wyzga, 
R.E.; Carmody, S.E. (2000) The Washington University-EPRI veterans' 
cohort mortality study: preliminary results. In: Grant, L.D., ed. 
PM2000: particulate matter and health. Inhalation Toxicol. 12(suppl. 
4): 41-73.
Lipfert, F.W.; Perry, H.M., Jr.; Miller, J.P.; Baty, J.D.; Wyzga, 
R.E.; Carmody, S.E. (2003) Air pollution, blood pressure, and their 
long-term associations with mortality. Inhalation Toxicol. 15: 493-
512.
Long, S., Nelson, R.L., Ainsworth, L., Hollis, K., Mies, T., Morgan, 
P., Naidu, S., Ort, D.R., Webster, R., Zhu, X. Adapting Soybean To 
Current And Future Change In Atmospheric Composition. Do We Need 
More Than Field Selection Under Current Conditions. Cellular and 
Molecular Biology of Soybean Biennial Conference. (2002) p. 401. 
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=142752
Loya W.M., Pregitzer K.S., Karberg N.J., King J.S. & Giardina C.P. 
(2003) Reduction of soil carbon formation by tropospheric ozone 
under elevated carbon dioxide. Nature 425, 705-707.
Luethy-Krause, B.; Landolt, W. (1990) Effects of ozone on starch 
accumulation in Norway spruce (Picea abies). Trees 4: 107-110.
Lyons, T.M.; Barnes, J.D.; Davison, A.W. (1997) Relationships 
between ozone resistance and climate in European populations of 
Plantago major. New Phytol. 136: 503-510.
Manning, W.J.; Krupa, S.V. (1992) Experimental methodology for 
studying the effects of ozone on crops and trees. In: Lefohn, A.S., 
ed. Surface level ozone exposures and their effects on vegetation. 
Chelsea, MI: Lewis Publishers, Inc.; pp. 93-156.
Mannino, D.M.; Ford, E.S.; Redd, S.C. (2003) Obstructive and 
restrictive lung disease and markers of inflammation: data from the 
Third National Health and Nutrition Examination. Am. J. Med. 114: 
758-762.
Marty, M. (2007a) Letter from CHPAC Chair to the Administrator. 
March 23. EPA-HQ-OAR-2005-0172-0105.
Marty, M. (2007b) Letter from CHPAC Chair to the Administrator. 
September 4. EPA-HQ-OAR-2005-0172-2031.
McBride, D.E.; Koenig, J.Q.; Luchtel, D.L.; Williams, P.V.; 
Henderson, W.R., Jr. (1994) Inflammatory effects of ozone in the 
upper airways of subjects with asthma. Am. J. Respir. Crit. Care 
Med. 149: 1192-1197.
McCluney, L. (2007) Ozone 1-Hour to 8-Hour Ratios for the 2002-2004 
Design Value Period. January 18, 2007. Memo to the Ozone NAAQS 
Review Docket. EPA-HQ-OAR-0172-0073.
McConnell, R.; Berhane, K.; Gilliland, F.; London, S.J.; Islam, T.; 
Gauderman, W.J.; Avol, E.; Margolis, H.G.; Peters, J.M. (2002) 
Asthma in exercising children exposed to ozone: a cohort study. 
Lancet 359: 386-391.
McDonnell, W.F.; Kehrl, H.R.; Abdul-Salaam, S.; Ives, P.J.; 
Folinsbee, L.J.; Devlin, R.B.; O'Neil, J.J.; Horstman, D.H. (1991) 
Respiratory response of humans exposed to low levels of ozone for 
6.6 hours. Arch. Environ. Health 46: 145-150.
McDonnell, W.F. (1996) Individual variability in human lung function 
responses to ozone exposure. Environ. Toxicol. Pharmacol. 2: 171-
175.
McDonnell, W.F.; Stewart, P.W.; Andreoni, S.; Seal, E., Jr.; Kehrl, 
H.R.; Horstman, D.H.; Folinsbee, L.J.; Smith, M.V. (1997) Prediction 
of ozone-induced FEV1 changes: effects of concentration, duration, 
and ventilation. Am. J. Respir. Crit. Care Med. 156: 715-722.
McDonnell, W.F.; Abbey, D.E.; Nishino, N.; Lebowitz, M.D. (1999) 
Long-term ambient ozone concentration and the incidence of asthma in 
nonsmoking adults: the ahsmog study. Environ. Res. 80: 110-121.
McLaughlin, S.B., Nosal, M., Wullschleger, S.D., Sun, G. (2007a) 
Interactive effects of ozone and climate on tree growth and water 
use in a southern Appalachian forest in the USA. New Phytologist 
174: 109-124.
McLaughlin, S.B., Wullschleger, S.D., Sun, G. and Nosal, M. (2007b) 
Interactive effects of ozone and climate on water use, soil moisture 
content and streamflow in a southern Appalachian forest in the USA. 
New Phytologist 174: 125-136.
Michelson, P.H.; Dailey, L.; Devlin, R.B.; Peden, D.B. (1999) Ozone 
effects on the immediate-phase response to allergen in the nasal 
airways of allergic asthmatic subjects. Otolaryngol. Head Neck Surg. 
120: 225-232.
Miller, P.R.; McBride, J.R.; Schilling, S.L.; Gomez, A.P. (1989) 
Trend of ozone damage to conifer forests between 1974 and 1988 in 
the San Bernardino Mountains of southern California. In: Olson, 
R.K.; Lefohn, A.S., eds. Effects of air pollution on western forests 
[an A&WMA symposium; June; Anaheim, CA]. Air and Waste Management 
Association; pp. 309-323. (APCA transactions series, no. 16).
Moldau, H.; S[ouml]ber, J.; S[ouml]ber, A. (1990) Differential 
sensitivity of stomata and mesophyll tosudden exposure of bean 
shoots to ozone. Photosynthetica 24: 446-458.
Morgan, P.B.; Ainsworth, E.A.; Long, S.P. (2003) How does elevated 
ozone impact soybean? A meta-analysis of photosynthesis, growth and 
yield. Plant Cell Environ. 26: 1317-1328.
Morgan, P.B., Bernacchi, C.J., Ort, D.R., Long, S.P. (2004) An in 
vivo analysis of the effect of season-long open-air elevation of 
ozone to anticipated 2050 levels on photosynthesis in soybean. Plant 
Physiology 135: 2348-2357.
Mortimer, K.M.; Neas, L.M.; Dockery, D.W.; Redline, S.; Tager, I.B. 
(2002) The effect of air pollution on inner-city children with 
asthma. Eur. Respir. J. 19: 699-705.
Mudway, I.S.; Kelly, F.J. (2004) An investigation of inhaled ozone 
dose and the magnitude of airway inflammation in healthy adults. Am. 
J. Respir. Crit. Care Med. 169: 1089-1095.
Musselman, R.C.; Lefohn, A.S.; Massman, W.J.; Heath, R.L. (2006) A 
critical review and analysis of the use of exposure- and flux-based 
ozone indices for predicting vegetation effects. Atmos. Environ. 40: 
1869-1888.
National Association of Clean Air Agencies (NACAA) (2007) Letter and 
Comments Sent to Docket No. OAR-2005-0172 re: Proposed Rule--
National Ambient Air Quality Standards for Ozone. Docket No. OAR-
2005-0172-4274. October 9, 2007.

[[Page 3046]]

NPS (2005) 2005 Annual Performance & Progress Report: Air Quality in 
National Parks. National Park Service. http://www2.nature.nps.gov/air/Pubs/pdf/gpra/Gpra2005_Report_03202006_Final.pdf
National Park Service (NPS) Letter and Comments Sent to Docket No. 
OAR-2005-0172 re: Proposed Rule--National Ambient Air Quality 
Standards for Ozone. Docket No. OAR-2005-0172-4934. September 27, 
2007.
Navidi, W.; Thomas, D.; Langholz, B.; Stram, D. (1999) Statistical 
methods for epidemiologic studies of the health effects of air 
pollution. Cambridge, MA: Health Effects Institute; research report 
no. 86.
Noormets, A.; Sober, A.; Pell, E.J.; Dickson, R.E.; Posila, G.K.; 
Sober, J.; Isebrands, J.G.; Karnosky, D.F. (2001) Stomatal and non-
stomatal limitation to photosynthesis in two trembling aspen 
(Populus tremuloides Michx) clones exposed to elevated 
CO2 and/or O3. Plant Cell Environ. 24: 327-
336.
Ollinger, S.V., Aber, J.D., Reich, P.B. and Freuder, R.J. (2002) 
Interactive effects of nitrogen deposition, tropospheric ozone, 
elevated CO2 and land use history on the carbon dynamics 
of northern hardwood forests. Glob. Change Biol. 8(6), 545-562.
Olszyk, D., Bytnerowlez, A., Kats, G., Reagan, C., Hake, S., Kerby, 
T., Millhouse, D., Roberts, B., Anderson, C., Lee, H. (1993) Cotton 
yield losses and ambient ozone concentrations in California's San 
Joaquin Valley. Journal of Environmental Quality 22, 602-611.
OMB (2005). Update of Statistical Area Definitions and Guidance on 
Their Uses. U.S. Office of Management and Budget, Bulletin No. 05-
02. February 22, 2005.
O'Neill, M.S.; Loomis, D.; Borja-Aburto, V.H. (2004) Ozone, area 
social conditions, and mortality in Mexico City. Environ. Res. 94: 
234-242.
Pearson, S.; Davison, A.W.; Reiling, K.; Ashenden, T.; Ollerenshaw, 
J.H. (1996) The effects of different ozone exposures on three 
contrasting populations of Plantago major. New Phytol. 132: 493-502.
Peden, D.B.; Setzer, R.W., Jr.; Devlin, R.B. (1995) Ozone exposure 
has both a priming effect on allergen-induced responses and an 
intrinsic inflammatory action in the nasal airways of perennially 
allergic asthmatics. Am. J. Respir. Crit. Care Med. 151: 1336-1345.
Peden, D.B.; Boehlecke, B.; Horstman, D.; Devlin, R. (1997) 
Prolonged acute exposure to 0.16 ppm ozone induces eosinophilic 
airway inflammation in asthmatic subjects with allergies. J. Allergy 
Clin. Immunol. 100: 802-808.
Pell, E.J.; Schlagnhaufer, C.D.; Arteca, R.N. (1997) Ozone-induced 
oxidative stress: mechanisms of action and reaction. Physiol. Plant. 
100: 264-273.
Percy, K.E.; Awmack, C.S.; Lindroth, R.L.; Kubiske, M.E.; Kopper, 
B.J.; Isebrands, J.G.; Pregitzer, K.S.; Hendry, G.R.; Dickson, R.E.; 
Zak, D.R.; Oksanen, E.; Sober, J.; Harrington, R.; Karnosky, D.F. 
(2002) Altered performance of forest pests under atmospheres 
enriched with CO2 and O3. Nature (London) 420: 
403-407.
Percy, K. E.; Nosal, M.; Heilman, W.; Dann, T; Sober, J.; Legge, A. 
H.; Karnosky, D. F. (2007) New exposure-based metric approach for 
evaluating O3 risk to North American aspen forests. Environmental 
Pollution 147:3 554-566.
Peters, J. M.; Avol, E.; Navidi, W.; London, S. J.; Gauderman, W. 
J.; Lurmann, F.; Linn, W. S.; Margolis, H.; Rappaport, E.; Gong, H., 
Jr.; Thomas, D. C. (1999a) A study of twelve southern California 
communities with differing levels and types of air pollution. I. 
Prevalence of respiratory morbidity. Am. J. Respir. Crit. Care Med. 
159: 760-767.
Peters, J. M.; Avol, E.; Gauderman, W. J.; Linn, W. S.; Navidi, W.; 
London, S. J.; Margolis, H.; Rappaport, E.; Vora, H.; Gong, H., Jr.; 
Thomas, D. C. (1999b) A study of twelve southern California 
communities with differing levels and types of air pollution. II. 
Effects on pulmonary function. Am. J. Respir. Crit. Care Med. 159: 
768-775.
Peterson, D. L.; Arbaugh, M. J.; Wakefield, V. A.; Miller, P. R. 
(1987) Evidence of growth reduction in ozone-injured Jeffrey pine 
(Pinus jeffreyi Grev and Balf) in Sequoia and Kings Canyon National 
Parks. JAPCA 37: 906-912.
Phillips, R. L.; Zak, D. R.; Holmes, W. E.; White, D. C. (2002) 
Microbial community composition and function beneath temperate trees 
exposed to elevated atmospheric carbon dioxide and ozone. Oecologia 
131: 236-244.
Plopper, C. G.; Fanucchi, M. V. (2000) Do urban environmental 
pollutants exacerbate childhood lung diseases? Environ. Health 
Perspect. 108: A252-A253.
Plunkett, L. M.; Turnbull, D.; Rodricks, J. V. (1992) Differences 
between adults and children affecting exposure assessment. In: 
Guzelian, P. S.; Henry, D. J.; Olin, S. S., eds. Similarities and 
differences between children and adults: implications for risk 
assessment. Washington, DC: ILSI Press, pp. 79-96.
Pope, C. A., III; Thun, M. J.; Namboodiri, M. M.; Dockery, D. W.; 
Evans, J. S.; Speizer, F. E.; Heath, C. W., Jr. (1995) Particulate 
air pollution as a predictor of mortality in a prospective study of 
U.S. adults. Am. J. Respir. Crit. Care Med. 151: 669-674.
Pope, C. A., III; Burnett, R. T.; Thun, M. J.; Calle, E. E.; 
Krewski, D.; Ito, K.; Thurston, G. D. (2002) Lung cancer, 
cardiopulmonary mortality, and long-term exposure to fine 
particulate air pollution. JAMA J. Am. Med. Assoc. 287: 1132-1141.
Prentice IC, Farquhar GD, Fasham MJR, et al. (2001) The Carbon Cycle 
and Atmospheric Carbon Dioxide. In Climate Change 2001: The 
Scientific Basis. Contribution of Working Group I to the Third 
Assessment Report of the Intergovernmental Panel on Climate Change. 
(ed J. T. Houghton YD, D. J. Griggs, M. Noguer, P. J. van der 
Linder, X. Dai, K. Maskell, and C. A. Johnson), pp. 241-280. 
Cambridge University Press, Cambridge, United Kingdom and New York, 
NY, USA.
Pronos, J.; Merrill, L.; Dahlsten, D. (1999) Insects and pathogens 
in a pollution-stressed forest. In: Miller, P. R.; McBride, J. R., 
eds. Oxidant air pollution impacts in the montane forests of 
southern California. Springer, pp. 317-337.
Reid, C. D.; Fiscus, E. L. (1998) Effects of elevated [CO2] and/or 
ozone on limitations to CO2 assimilation in soybean (Glycine max). 
J. Exp. Bot. 49: 885-895.
Reiling, K.; Davison, A. W. (1992a) Effects of a short ozone 
exposure given at different stages in the development of Plantago 
major L. New Phytol. 121: 643-647.
Reiling, K.; Davison, A. W. (1992b) The response of native, 
herbaceous species to ozone: growth and fluorescence screening. New 
Phytol. 120: 29-37.
Retzlaff, W. A.; Arthur, M. A.; Grulke, N. E.; Weinstein, D. A.; 
Gollands, B. (2000) Use of a single-tree simulation model to predict 
effects of ozone and drought on growth of a white fir tree. Tree 
Physiol. 20: 195-202.
Rizzo, M (2005). Evaluation of a quadratic approach for adjusting 
distributions of hourly ozone concentrations to meet air quality 
standards. November 7, 2005. Available online at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html.
Rizzo, M. (2006). A distributional comparison between different 
rollback methodologies applied to ambient ozone concentrations. 
August 23, 2006. Available online at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html.
Romieu, I.; Meneses, F.; Ruiz, S.; Sienra, J. J.; Huerta, J.; White, 
M. C.; Etzel, R. A. (1996) Effects of air pollution on the 
respiratory health of asthmatic children living in Mexico City. Am. 
J. Respir. Crit. Care Med. 154: 300-307.
Romieu, I.; Meneses, F.; Ruiz, S.; Huerta, J.; Sienra, J. J.; White, 
M.; Etzel, R.; Hernandez, M. (1997) Effects of intermittent ozone 
exposure on peak expiratory flow and respiratory symptoms among 
asthmatic children in Mexico City. Arch. Environ. Health 52: 368-
376.
Romieu, I.; Sienra-Monge, J. J.; Ram[iacute]rez-Aguilar, M.; Moreno-
Macias, H.; Reyes-Ruiz, N. I.; Estela del Rio-Navarro, B.; 
Hern[aacute]ndez-Avila, M.; London, S. J. (2004) Genetic 
polymorphism of GSTM1 and antioxidant supplementation influence lung 
function in relation to ozone exposure in asthmatic children in 
Mexico City. Thorax 59: 8-10.
Sarnat, J. A.; Schwartz, J.; Catalano, P. J.; Suh, H. H. (2001) 
Gaseous pollutants in particulate matter epidemiology: confounders 
or surrogates? Environ. Health Perspect. 109: 1053-1061.
Sarnat, J. A.; Brown, K. W.; Schwartz, J.; Coull, B. A.; Koutrakis, 
P. (2005) Ambient gas concentrations and personal particulate matter 
exposures: implications for studying the health effects of 
particles. Epidemiology 16: 385-395.

[[Page 3047]]

Sarnat, J. A.; Coull, B. A.; Schwartz, J; Gold, D. R.; Suh, H. H. 
(2006) Factors affecting the association between ambient 
concentrations and personal exposure to particles and gases. 
Environ. Health Perspect. 114(5): 649-654.
Sasek, T. W.; Richardson, C. J.; Fendick, E. A.; Bevington, S. R.; 
Kress, L. W. (1991) Carryover effects of acid rain and ozone on the 
physiology of multiple flushes of loblolly pine seedlings. For. Sci. 
37: 1078-1098.
Scannell, C.; Chen, L.; Aris, R. M.; Tager, I.; Christian, D.; 
Ferrando, R.; Welch, B.; Kelly, T.; Balmes, J. R. (1996) Greater 
ozone-induced inflammatory responses in subjects with asthma. Am. J. 
Respir. Crit. Care Med. 154: 24-29.
Schwartz, J. (2005) How sensitive is the association between ozone 
and daily deaths to control for temperature? Am. J. Respir. Crit. 
Care Med. 171: 627-631.
Schildcrout, J. S.; Sheppard, L.; Lumley, T.; Slaughter, J. C.; 
Koenig, J. Q.; Shapiro, G. G. (2006) Ambient air pollution and 
asthma exacerbations in children: an eight city analysis. Am. J. 
Epidemiol. 164(5): 505-517.
Schierhorn, K.; Hanf, G.; Fischer, A.; Umland, B.; Olze, H.; Kunkel, 
G. (2002) Ozone-induced release of neuropeptides from human nasal 
mucosa cells. Int. Arch. Allergy Immunol. 129: 145-151.
Sheppard, L.; Slaughter, J. C.; Schildcrout, J.; Liu, L.-J. S.; 
Lumley, T. (2005) Exposure and measurement contributions to 
estimates of acute air pollution effects. J. Exposure Anal. Environ. 
Epidemiol. 15: 366-376.
Simini, M.; Skelly, J. M.; Davis, D. D.; Savage, J. E.; Comrie, A. 
C. (1992) Sensitivity of four hardwood species to ambient ozone in 
north central Pennsylvania. Can. J. For. Res. 22: 1789-1799.
Sin, D. D.; Man, S. F. P. (2003) Why are patients with chronic 
obstructive pulmonary disease at increased risk of cardiovascular 
diseases? Circulation 107: 1514-1519.
Sitch, S.; Cox, P. M.; Collins, W. J.; Huntingford, C. (2007) 
Indirect radiative forcing of climate change through ozone effects 
on the land-carbon sink. Nature (London, U.K.) 448: 791-794.
Smith, W. H. (1992) Air pollution effects on ecosystem processes. 
In: Barker, J. R.; Tingey, D. T., eds. Air pollution effects on 
biodiversity. Van Nostrand Reinhold; pp. 234-260.
Smith, G., Coulston J., Jepsen, J. and Prichard, T. (2003) ``A 
national ozone biomonitoring program: Results from field surveys of 
ozone sensitive plants in northeastern forest (1994-2000)'' 
Environmental Monitoring and Assessment 87(3): 271-291.
Somers, G. L.; Chappelka, A. H.; Rosseau, P.; Renfro, J. R. (1998) 
Empirical evidence of growth decline related to visible ozone 
injury. For. Ecol. Manage. 104: 129-137.
Tager, I. B.; K[uuml]nzli, N.; Lurmann, F.; Ngo, L.; Segal, M.; 
Balmes, J. (1998) Methods development for epidemiologic 
investigations of the health effects of prolonged ozone exposure. 
Part II: an approach to retrospective estimation of lifetime ozone 
exposure using a questionnaire and ambient monitoring data 
(California sites). Cambridge, MA: Health Effects Institute; 
research report no. 81; pp. 27-78.
Takemoto, B. K.; Bytnerowicz, A.; Fenn, M. E. (2001) Current and 
future effects of ozone and atmospheric nitrogen deposition on 
California's mixed conifer forests. For. Ecol. Manage. 144: 159-173.
Tans P.P., White J.W.C. (1998) In balance, with a little help from 
the plants. Science, 281, 183-184.
Taylor, C.R. ``AGSIM: Model Description and Documentation.'' 
Agricultural Sector Models for the United States. C.R. Taylor, K.H. 
Reichelderfer, and S.R. Johnson, eds. Ames IA: Iowa State University 
Press, (1993).
Taylor R. (1994) ``Deterministic versus stochastic evaluation of the 
aggregate economic effects of price support programs'' Agricultural 
Systems 44: 461-473.
Temple, P. J.; Riechers, G. H.; Miller, P. R.; Lennox, R. W. (1993) 
Growth responses of ponderosa pine to longterm exposure to ozone, 
wet and dry acidic deposition, and drought. Can. J. For. Res. 23: 
59-66.
Thurston, G.D.; Ito, K.; Kinney, P.L.; Lippmann, M. (1992) A multi-
year study of air pollution and respiratory hospital admissions in 
three New York State metropolitan areas: results for 1988 and 1989 
summers. J. Exposure Anal. Environ. Epidemiol. 2:429-450.
Tingey, D. T.; Standley, C.; Field, R. W. (1976) Stress ethylene 
evolution: a measure of ozone effects on plants. Atmos. Environ. 10: 
969-974.
Tingey, D. T.; Taylor, G. E., Jr. (1982) Variation in plant response 
to ozone: a conceptual model of physiological events. In: Unsworth, 
M. H.; Ormrod, D. P., eds. Effects of gaseous air pollution in 
agriculture and horticulture. London, United Kingdom: Butterworth 
Scientific; pp. 113-138.
Tingey, D. T.; Laurence, J. A.; Weber, J. A.; Greene, J.; Hogsett, 
W. E.; Brown, S.; Lee, E. H. (2001) Elevated CO2 and temperature 
alter the response of Pinus ponderosa to ozone: A simulation 
analysis. Ecol. Appl.11: 1412-1424.
Tingey, D. T.; Hogsett, W. E.; Lee, E. H.; Laurence, J. A. (2004) 
Stricter ozone ambient air quality standard has beneficial effect on 
Ponderosa pine in California. Environ. Manage. 34: 397-405.
Touloumi, G.; Katsouyanni, K.; Zmirou, D.; Schwartz, J.; Spix, C.; 
Ponce de Leon, A.; Tobias, A.; Quennel, P.; Rabczenko, D.; 
Bacharova, L.; Bisanti, L.; Vonk, J. M.; Ponka, A. (1997) Short-term 
effects of ambient oxidant exposure on mortality: a combined 
analysis within the APHEA project. Am. J. Epidemiol. 146: 177-185.
U.S. Department of Agriculture, 2006. The PLANTS Database (http://plants.usda.gov, December 2006). National Plant Data Center, Baton 
Rouge, LA.
Ultman, J. S.; Ben-Jebria, A.; Arnold, S. F. (2004) Uptake 
distribution of ozone in human lungs: intersubject variability in 
physiologic response. Boston, MA: Health Effects Institute.
Vagaggini, B.; Taccola, M.; Clanchetti, S.; Carnevali, S.; Bartoli, 
M. L.; Bacci, E.; Dente, F. L.; Di Franco, A.; Giannini, D.; 
Paggiaro, P. L. (2002) Ozone exposure increases eosinophilic airway 
response induced by previous allergen challenge. Am. J. Respir. 
Crit. Care Med. 166: 1073-1077.
Vedal, S.; Brauer, M.; White, R.; Petkau, J. (2003) Air pollution 
and daily mortality in a city with low levels of pollution. Environ. 
Health Perspect. 111: 45-51.
Vesely, D. L.; Giordano, A. T.; Raska-Emery, P.; Montgomery, M. R. 
(1994a) Ozone increases amino- and carboxy-terminal atrial 
natriuretic factor prohormone peptides in lung, heart, and 
circulation. J. Biochem. Toxicol. 9: 107-112.
Vesely, D. L.; Giordano, A. T.; Raska-Emery, P.; Montgomery, M. R. 
(1994b) Increase in atrial natriuretic factor in the lungs, heart, 
and circulatory system owing to ozone. Chest 105: 1551-1554.
Vesely, D. L.; Giordano, A. T.; Raska-Emery, P.; Montgomery, M. R. 
(1994c) Ozone increases atrial natriuretic peptides in heart, lung 
and circulation of aged vs. adult animals. Gerontology (Basel) 40: 
227-236.
Weber, J. A.; Clark, C. S.; Hogsett, W. E. (1993) Analysis of the 
relationship(s) among O3 uptake, conductance, and 
photosynthesis in needles of Pinus ponderosa. Tree Physiol. 13: 157-
172.
Weinstein, D.A., Beloin, R.M., R.D. Yanai (1991) ``Modeling changes 
in red spruce carbon balance and allocation in response to 
interacting ozone and nutrient stress.'' Tree Physiology 9: 127-146.
Weinstein, D.A., J.A. Laurence, W.A. Retzlaff, J.S. Kern, E.H. Lee, 
W.E. Hogsett, J. Weber (2005) Predicting the effects of tropospheric 
ozone on regional productivity of ponderosa pine and white fir. 
Forest Ecology and Management 205: 73-89.
Whitfield, R.; Biller, W.; Jusko, M.; and Keisler, J. (1996) A 
Probabilistic Assessment of Health Risks Associated with Short- and 
Long-Term Exposure to Tropospheric Ozone. Argonne National 
Laboratory, Argonne, IL.
Whitfield, R. (1997) A Probabilistic Assessment of Health Risks 
Associated with Short-term Exposure to Tropospheric Ozone: A 
Supplement. Argonne National Laboratory, Argonne, IL.
Whitfield, C. P.; Davison, A. W.; Ashenden, T. W. (1997) Artificial 
selection and heritability of ozone resistance in two populations of 
Plantago major. New Phytol. 137: 645-655.
Whitfield, R.G.; Richmond, H.M.; and Johnson, T.R. (1998) ``Overview 
of Ozone Human Exposure and Health Risk Analyses Used in the U.S. 
EPA's Review of the Ozone Air Quality Standard,'' pp.483-516 in: T. 
Schneider, ed. Air Pollution in the 21st Century: Priority Issues 
and Policy Elsevier; Amsterdam.
Wolff, G.T. (1995) Letter from Chairman of Clean Air Scientific 
Advisory Committee

[[Page 3048]]

to the EPA Administrator, dated November 30, 1995. EPA-SAB-CASAC-
LTR-96-002.
Wolff, G.T. (1996) Letter from Chairman of Clean Air Scientific 
Advisory Committee to the EPA Administrator, dated April 4, 1996. 
EPA-SAB-CASAC-LTR-96-006.
Xu, X.; Ding, H.; Wang, X. (1995) Acute effects of total suspended 
particles and sulfur dioxides on preterm delivery: a community-based 
cohort study. Arch. Environ. Health 50: 407-415.
Young, T. F.; Sanzone, S., eds. (2002) A framework for assessing and 
reporting on ecological condition: an SAB report. Washington, DC: 
U.S. Environmental Protection Agency, Science Advisory Board; report 
no. EPA-SAB-EPEC-02-009. Available online at: http://
yosemite.epa.gov/sab/sabproduct.nsf/
C3F89E598D843B58852570CA0075717E/$File/epec02009a.pdf.
Zeger, S. L.; Thomas, D.; Dominici, F.; Samet, J. M.; Schwartz, J.; 
Dockery, D.; Cohen, A. (2000) Exposure measurement error in time-
series studies of air pollution: concepts and consequences. Environ. 
Health Perspect. 108: 419-426.
Zhang, L.-Y.; Levitt, R. C.; Kleeberger, S. R. (1995) Differential 
susceptibility to ozone-induced airways hyperreactivity in inbred 
strains of mice. Exp. Lung Res. 21: 503-518.
Zidek, J. V.; White, R.; Le, N. D.; Sun, W.; Burnett, R. T. (1998) 
Imputing unmeasured explanatory variables in environmental 
epidemiology with application to health impact analysis of air 
pollution. Environ. Ecol. Stat. 5: 99-115.

List of Subjects in 40 CFR Parts 50 and 58

    Environmental protection, Air pollution control, Carbon monoxide, 
Lead, Nitrogen dioxide, Ozone, Particulate matter, Sulfur oxides.

    Dated: January 6, 2010.
Lisa P. Jackson,
Administrator.

    For the reasons set forth in the preamble, parts 50 and 58 of 
chapter 1 of title 40 of the code of Federal regulations are proposed 
to be amended as follows:

PART 50--NATIONAL PRIMARY AND SECONDARY AMBIENT AIR QUALITY 
STANDARDS

    1. The authority citation for part 50 continues to read as follows:

    Authority:  42 U.S.C. 7401 et seq.

    2. Section 50.15 is revised to read as follows:


Sec.  50.15  National primary and secondary ambient air quality 
standards for ozone.

    (a) The level of the national 8-hour primary ambient air quality 
standard for O3 is (0.060-0.070) parts per million (ppm), 
daily maximum 8-hour average, measured by a reference method based on 
Appendix D to this part and designated in accordance with part 53 of 
this chapter or an equivalent method designated in accordance with part 
53 of this chapter.
    (b) The 8-hour primary O3 ambient air quality standard 
is met at an ambient air quality monitoring site when the average of 
the annual fourth-highest daily maximum 8-hour average O3 
concentration is less than or equal to (0.060-0.070) ppm, as determined 
in accordance with appendix P to this part.
    (c) The level of the national secondary ambient air quality 
standard for O3 is a cumulative index value of (7-15) ppm-
hours, measured by a reference method based on Appendix D to this part 
and designated in accordance with part 53 of this chapter or an 
equivalent method designated in accordance with part 53 of this 
chapter.
    (d) The secondary O3 ambient air quality standard is a 
seasonal standard expressed as a sum of weighted hourly concentrations, 
cumulated over the 12 hour daylight period from 8 a.m. to 8 p.m. local 
standard time, during the consecutive 3-month period within the 
O3 monitoring season with the maximum index value. The 
secondary O3 standard is met at an ambient air quality 
monitoring site when the annual maximum consecutive 3-month cumulative 
index value (W126) is less than or equal to (7-15) ppm-hours, as 
determined in accordance with appendix P to this part.
    3. Section 50.14 is amended by adding entries for primary and 
secondary ozone standards to the end of Table 1 in paragraph (c)(2)(vi) 
to read as follows:


Sec.  50.14  Treatment of air quality monitoring data influenced by 
exceptional events.

* * * * *
    (c) * * *
    (2) * * *
    (vi) * * *

      Table 1--Schedule for Exceptional Event Flagging and Documentation Submission for Data To Be Used in
                                      Designations Decisions for New NAAQS
----------------------------------------------------------------------------------------------------------------
                                            Air quality
   NAAQS pollutant/ standard/(level)/     data collected   Event flagging & initial     Detailed documentation
            promulgation date              for calendar      description deadline         submission deadline
                                               year
----------------------------------------------------------------------------------------------------------------
 
                                                  * * * * * * *
Primary Ozone/8-Hr......................       2007-2009  November 1, 2010 \b\......  November 1, 2010.\b\
Standard (Level TBD)/promulgated by                 2010  60 Days after the end of    60 Days after the end of
 August 31, 2010.                                          the calendar quarter in     the calendar quarter in
                                                           which the event occurred    which the event occurred
                                                           or March 1, 2011,           or March 1, 2011,
                                                           whichever date occurs       whichever date occurs
                                                           first.\b\                   first.\b\
Secondary Ozone/(Level TBD) Alternative             2008  July 1, 2011 \b\..........  July 1, 2011.\a\
 2-year Schedule--to be Promulgated by
 August 31, 2010.
                                               2009-2010  July 1, 2011 \b\..........  July 1, 2011.\b\
                                                    2011  60 Days after the end of    60 Days after the end of
                                                           the calendar quarter in     the calendar quarter in
                                                           which the event occurred    which the event occurred
                                                           or March 1, 2012,           or March 1, 2012,
                                                           whichever occurs            whichever occurs
                                                           first.\b\                   first.\b\
Secondary Ozone/(Level TBD)--Alternative       2007-2009  November 1, 2010 \b\......  November 1, 2010.\b\
 Accelerated Schedule--to be promulgated
 by August 31, 2010.
                                                    2010  60 Days after the end of    60 Days after the end of
                                                           the calendar quarter in     the calendar quarter in
                                                           which the event occurred    which the event occurred
                                                           or March 1, 2011,           or March 1, 2011,
                                                           whichever date occurs       whichever date occurs
                                                           first.\b\                   first.\b\
 

[[Page 3049]]

 
                                                  * * * * * * *
----------------------------------------------------------------------------------------------------------------
\a\ These dates are unchanged from those published in the original rulemaking.
\b\ Indicates change from general schedule in 40 CFR 50.14.
Note: EPA notes that the table of revised deadlines only applies to data EPA will use to establish the final
  initial designations for new NAAQS. The general schedule applies for all other purposes, most notably, for
  data used by EPA for redesignations to attainment.

    4. Appendix P to part 50 is revised to read as follows:

Appendix P to Part 50--Interpretation of the Primary and Secondary 
National Ambient Air Quality Standards for Ozone

1. General

    (a) This appendix explains the data handling conventions and 
computations necessary for determining whether the 8-hour primary 
and secondary national ambient air quality standards for ozone 
specified in Sec.  50.15 are met at an ambient ozone air quality 
monitoring site. Ozone is measured in the ambient air by a reference 
method based on Appendix D of this part, as applicable, and 
designated in accordance with part 53 of this chapter, or by an 
equivalent method designated in accordance with part 53 of this 
chapter. Data reporting, data handling, and computation procedures 
to be used in making comparisons between reported ozone 
concentrations and the levels of the ozone standards are specified 
in the following sections.
    (b) Whether to exclude, retain, or make adjustments to the data 
affected by exceptional events, including stratospheric ozone 
intrusion and other natural events, is determined by the 
requirements under Sec. Sec.  50.1, 50.14 and 51.930.
    (c) The terms used in this appendix are defined as follows:
    8-hour average is the rolling average of eight hourly ozone 
concentrations as explained in section 3 of this appendix.
    Annual fourth-highest daily maximum refers to the fourth-highest 
value measured at a monitoring site during a particular year.
    Annual Cumulative W126 Index is the maximum sum over three 
consecutive calendar months of the monthly W126 index in a year, as 
explained in section 4 of this appendix.
    Daily maximum 8-hour average concentration refers to the maximum 
calculated 8-hour average for a particular day as explained in 
section 3 of this appendix.
    Daily W126 Index is the sum of the sigmoidally weighted hourly 
ozone concentrations during the 12-hour daylight period, 8 a.m. to 
7:59 p.m. local standard time (LST).
    Design values are the metrics (i.e., statistics) that are 
compared to the primary and secondary NAAQS levels to determine 
compliance, calculated as shown in sections 3 and 4 of this 
appendix.
    Monthly W126 Index is the sum of the daily W126 index over one 
calendar month during the required ozone monitoring season, adjusted 
for incomplete data if appropriate, as explained in section 4 of 
this appendix.
    Required ozone monitoring season refers to the span of time 
within a calendar year when individual States are required to 
measure ambient ozone concentrations as listed in part 58 Appendix D 
to this chapter.
    Year refers to calendar year.

2. Requirements for Data Used for Comparisons With the Ozone NAAQS

    (a) All valid FRM/FEM ozone data submitted to EPA's Air Quality 
System (AQS), or otherwise available to EPA, meeting the 
requirements of part 58 of this chapter including appendices A, C, 
and E shall be used in design value calculations.
    (b) When two or more ozone monitors are operated at a site, the 
state may in advance designate one of them as the primary monitor. 
If the state has not made this designation, the Administrator will 
make the designation, either in advance or retrospectively. Design 
values will be developed using only the data from the primary 
monitor, if this results in a valid design value. If data from the 
primary monitor do not allow the development of a valid design 
value, data solely from the other monitor(s) will be used in turn to 
develop a valid design value, if this results in a valid design 
value. If there are three or more monitors, the order for such 
comparison of the other monitors will be determined by the 
Administrator. The Administrator may combine data from different 
monitors in different years for the purpose of developing a valid 
primary or secondary standard design value, if a valid design value 
cannot be developed solely with the data from a single monitor. 
However, data from two or more monitors in the same year at the same 
site will not be combined in an attempt to meet data completeness 
requirements, except if one monitor has physically replaced another 
instrument permanently, in which case the two instruments will be 
considered to be the same monitor, or if the state has switched the 
designation of the primary monitor from one instrument to another 
during the year.
    (c) Hourly average concentrations shall be reported in parts per 
million (ppm) to the third decimal place, with additional digits to 
the right of the third decimal place truncated. The start of each 
hour shall be identified in local standard time (LST).

3. Comparison to the Primary Standard for Ozone

(a) Computing 8-Hour Averages

    Running 8-hour averages shall be computed from the hourly ozone 
concentration data for each hour of the year and shall be stored in 
the first, or start, hour of the 8-hour period. In the event that 
only 6 or 7 hourly averages are available, the valid 8-hour average 
shall be computed on the basis of the hours available, using 6 or 7 
as the divisor. In the event that only 1, 2, 3, 4, or 5 hourly 
averages are available, the 8-hour average shall be computed on the 
basis of substituting for all the hours without hourly averages a 
low hourly average value selected as follows, using 8 as the 
divisor. For days within the required ozone monitoring season, the 
substitution value shall be the lowest hourly average ozone 
concentration observed during the same hour (local standard time) of 
any day in the required ozone monitoring season of that year, or 
one-half of the method detection limit of the ozone instrument, 
whichever is higher. However, if the number of same-hour 
concentration values available for the required ozone monitoring 
season for the year, from which the lowest observed hourly 
concentration would be identified for purposes of this substitution, 
is less than 50% of the number of days during the required ozone 
monitoring season, one-half the method detection limit of the ozone 
instrument shall be used in the substitution. For days outside the 
required ozone monitoring season, the substitution value shall be 
one-half the method detection limit of the ozone instrument. An 8-
hour period with no available hourly averages does not have a valid 
8-hour average. The computed 8-hour average ozone concentrations are 
not rounded or truncated.

(b) Daily Maximum 8-Hour Average Concentrations

    There are 24 8-hour periods in each calendar day. Some of these 
may not have valid 8-hour averages, under section 3(a). The daily 
maximum 8-hour concentration for a given calendar day is the highest 
of the valid 8-hour average concentrations computed for that day. 
This process is repeated, yielding a daily maximum 8-hour average 
ozone concentration for each day with ambient ozone monitoring data, 
including days outside the required ozone monitoring season if data 
are available. The daily maximum 8-hour concentrations from two 
consecutive days may have some hourly concentrations in common. 
Generally, overlapping daily maximum 8-hour averages are not likely,

[[Page 3050]]

except in those non-urban monitoring locations with less pronounced 
diurnal variation in hourly concentrations. In these cases, the 
maximum 8-hour average concentration from each day is used, even if 
the two averages have some hours in common.
    (c) Primary Standard Design Value
    The primary standard design value is the annual fourth-highest 
daily maximum 8-hour ozone concentration considering all days with 
monitoring data including any days outside the required ozone 
monitoring season, expressed in parts per million, averaged over 
three years. The 3-year average shall be computed using the three 
most recent, consecutive years of monitoring data that can yield a 
valid design value. For a design value to be valid for comparison to 
the standard, the monitoring data set on which it is based must meet 
the data completeness requirements described in section 3(d). The 
computed 3-year average of the annual fourth-highest daily maximum 
8-hour average ozone concentrations shall be rounded to three 
decimal places. Values equal to or greater than 0.xxx5 ppm shall 
round up.

(d) Data Completeness Requirements for a Valid Design Value

    (i) A design value greater than the standard is valid if in each 
of the three years there are at least four days with a daily maximum 
8-hour average concentration. Under sections 3(a) and 3(b), there 
will be a daily maximum 8-hour average concentration on any day with 
at least one hourly concentration. One or more of these four days 
may be outside the required ozone monitoring season.
    (ii) A design value less than or equal to the standard is valid 
if for at least 75% of the days in the required ozone monitoring 
season in each of the three years there are at least 18 8-hour 
averages in the day that are based on at least 6 measured hourly 
average concentrations.
    (iii) When computing whether the minimum data completeness 
requirement in section 3(d)(ii) has been met for the purpose of 
showing that a design value equal to or less than the standard is 
valid, meteorological or ambient data may be sufficient to 
demonstrate that ozone levels on days with missing data would not 
have affected the design value. At the request of the state, the 
Regional Administrator may consider demonstrations that 
meteorological conditions on one or more days in the required ozone 
monitoring season which do not have at least 18 8-hour averages in 
the day that are based on at least 6 measured hourly average 
concentrations could not have caused a daily maximum 8-hour 
concentration high enough to have been one of the four highest daily 
maximum 8-hour concentrations for the year. At the request of the 
state, days so demonstrated may be counted towards the 75% 
requirement for the purpose of validating the design value, subject 
to the approval of the Regional Administrator.
    (vi) Years that do not meet the completeness criteria stated in 
3(d)(ii) may nevertheless be used to calculate a design value that 
will be deemed valid with the approval of, or at the initiative of, 
the Administrator, who may consider factors such as monitoring site 
closures/moves, monitoring diligence, the consistency and levels of 
the valid concentration measurements that are available, and nearby 
concentrations in determining whether to use such data.

(e) Comparison With the Primary Ozone Standard

    (i) The primary ozone ambient air quality standard is met at an 
ambient air quality monitoring site when the design value is less 
than or equal to [0.075] ppm.
    (ii) Comparison with the primary ozone standard is demonstrated 
by examples 1 and 2 as follows:

    Example 1.  Ambient monitoring site attaining the primary ozone 
standard.

--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                           Percent valid
                                                           days (within     1st Highest     2nd Highest     3rd Highest     4th Highest     5th Highest
                          Year                             the required    daily max 8-    daily max 8-    daily max 8-    daily max 8-    daily max 8-
                                                            monitoring      hour conc.      hour conc.      hour conc.      hour conc.      hour conc.
                                                              season)          (ppm)           (ppm)           (ppm)           (ppm)           (ppm)
--------------------------------------------------------------------------------------------------------------------------------------------------------
2006....................................................              80        0.092500        0.090375        0.085125        0.078375        0.078125
2007....................................................              96        0.084750        0.083500        0.075375        0.071875        0.070625
2008....................................................              98        0.080875        0.079750        0.077625        0.075500        0.060375
                                                         -----------------------------------------------------------------------------------------------
    Average.............................................  ..............  ..............  ..............  ..............        0.075250  ..............
                                                         -----------------------------------------------------------------------------------------------
    Rounded.............................................  ..............  ..............  ..............  ..............        0.075     ..............
--------------------------------------------------------------------------------------------------------------------------------------------------------

    As shown in Example 1, this monitoring site meets the primary 
ozone standard because the 3-year average of the annual fourth-
highest daily maximum 8-hour average ozone concentrations (i.e., 
0.075256 ppm, rounded to 0.075 ppm) is less than or equal to [0.075] 
ppm. The data completeness requirement is also met because no single 
year has less than 75% data completeness. In Example 1, the 
individual 8-hour averages and the 3-year average are shown with six 
decimal digits. In actual calculations, all digits supported by the 
calculator or calculation software must be retained.
    Example 2. Ambient monitoring site failing to meet the primary 
ozone standard.

--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                           Percent valid
                                                           days (within    1st  Highest    2nd  Highest    3rd  Highest    4th  Highest    5th  Highest
                                                           the required    daily max  8-   daily max  8-   daily max  8-   daily max  8-   daily max  8-
                          Year                              monitoring      hour conc.      hour conc.      hour conc.      hour conc.      hour conc.
                                                              season)          (ppm)           (ppm)           (ppm)           (ppm)           (ppm)
                                                             (percent)
--------------------------------------------------------------------------------------------------------------------------------------------------------
2006....................................................              96        0.105125        0.103500        0.101125        0.078625        0.072375
2007....................................................              74        0.104250        0.103625        0.093000        0.080250        0.069500
2008....................................................              98        0.103125        0.101875        0.101750        0.075375        0.074625
                                                         -----------------------------------------------------------------------------------------------
    Average.............................................  ..............  ..............  ..............  ..............        0.078083  ..............
                                                         -----------------------------------------------------------------------------------------------
    Rounded.............................................  ..............  ..............  ..............  ..............        0.078     ..............
--------------------------------------------------------------------------------------------------------------------------------------------------------

    As shown in Example 2, the data capture in 2007 is less than 
75%. The primary ozone standard is not met for this monitoring site 
because the 3-year average of the fourth-highest daily maximum 8-
hour average ozone concentrations (i.e., 0.078083 ppm, rounded to 
0.078 ppm) is greater than [0.075] ppm and is therefore valid 
despite this incompleteness. In Example 2, the individual 8-hour 
averages and the 3-year average are shown with six decimal digits. 
In actual calculations, all digits supported by the

[[Page 3051]]

calculator or calculation software must be retained.

4. Secondary Ambient Air Quality Standard for Ozone

    (a) Computing the daily W126 index value.
    The secondary ozone ambient air quality standard is a seasonal 
standard expressed as a sum of weighted hourly concentrations, 
cumulated over the 12 hour daylight period from 8 a.m. to 8 p.m. 
local standard time, during the consecutive 3-month period within 
the ozone monitoring season with the maximum index value. The first 
step in determining whether the standard is met at a monitoring site 
is to compute the daily W126 index value for each day by applying 
the sigmoidal weighting function in Equation 1 to each reported 
measurement of hourly average concentration.
[GRAPHIC] [TIFF OMITTED] TP19JA10.001

Where:

Ci = hourly O3 at hour i, and
[GRAPHIC] [TIFF OMITTED] TP19JA10.002

    The computed value of the sigmoidally weighted hourly 
concentration is not rounded or truncated. The daily W126 index is 
formed by summing the twelve computed hourly values, retaining all 
decimal places. An illustration of computing a daily W126 index 
value is below:

    Example 3.  Daily W126 index value calculation for an ambient 
ozone monitoring site.

------------------------------------------------------------------------
                                                            Weighted
           Start of hour              Concentration      concentration
                                          (ppm)              (ppm)
------------------------------------------------------------------------
8:00 a.m..........................              0.045           0.002781
9:00 a.m..........................              0.060           0.018218
10:00 a.m.........................              0.075           0.055701
11:00 a.m.........................              0.080           0.067537
12:00 p.m.........................              0.079           0.065327
1:00 p.m..........................              0.082           0.071715
2:00 p.m..........................              0.085           0.077394
3:00 p.m..........................              0.088           0.082448
4:00 p.m..........................              0.083           0.073683
5:00 p.m..........................              0.081           0.069667
6:00 p.m..........................              0.065           0.029260
7:00 p.m..........................              0.056           0.011676
                                   -------------------------------------
    Sum=Daily W126 index value....  .................         * 0.625406
------------------------------------------------------------------------
* ppm-hours.

    In Example 3, the individual weighted concentrations and their 
sum are shown with six decimal digits. In actual calculations, all 
digits supported by the calculator or calculation software must be 
retained. There are no data completeness requirements for the daily 
index. If fewer than 12 hourly values are available, only the 
available hours are weighted and summed. However, there are data 
completeness requirements for the monthly W126 index values and a 
required adjustment for incomplete data, as describe in the next 
section.
    (b) Computing the Monthly W126 Index
    As described in section 4(a), the daily index value is computed 
at each monitoring site for each calendar day in each month during 
the required ozone monitoring season with no rounding or truncation. 
The monthly W126 index is the sum of the daily index values over one 
calendar month. At an individual monitoring site, a monthly W126 
index is valid if hourly average ozone concentrations are available 
for at least 75% of the possible daylight hours in the month. For 
months with more than 75% but less than 100% data completeness, the 
monthly W126 value shall be adjusted for incomplete data by 
multiplying the unadjusted monthly W126 index value by the ratio of 
the number of possible reporting hours to the number of hours with 
reported ambient hourly concentrations using Equation 2 in this 
appendix:
[GRAPHIC] [TIFF OMITTED] TP19JA10.003

where

M.I. = the adjusted monthly W126 index,
D.I. = daily W126 index (i.e., the daily sum of the sigmoidally 
weighted daylight hourly concentrations),
n = the number of days in the calendar month,
v = the number of daylight reporting hours (8 a.m.-7:59 p.m. LST) in 
the month with reported valid hourly ozone concentrations.

    The resulting adjusted value of the monthly W126 index shall not 
be rounded or truncated.

(c) Secondary Standard Design Value

    The secondary standard design value is the 3-year average of the 
annual maximum consecutive 3-month sum of adjusted monthly W126 
index values expressed in ppm-hours. Specifically, the annual W126 
index value is computed on a calendar year basis using the three 
highest, consecutive adjusted monthly W126 index values. The 3-year 
average shall be computed using the most recent, consecutive three 
calendar years of monitoring data meeting the data completeness 
requirements described in section 4(c). The computed 3-year average 
of the annual maximum consecutive 3-month sum of adjusted monthly 
W126 index values in ppm-hours shall be rounded to a whole number 
with decimal values equal to or greater than 0.500 rounding up.

(c) Data Completeness Requirement

    (i) The annual W126 index is valid for purposes of calculating a 
3-year design value if each full calendar month in the required 
ozone monitoring season has at least 75% data completeness for 
daylight hours.
    (ii) If one or more months during the ozone monitoring seasons 
of three successive years has less than 75% data completeness, the 
three years shall nevertheless be used in the computation of a valid 
design value for the site if substituting the lowest hourly ozone 
concentration observed during daylight hours in the required ozone 
monitoring season of each year, or one-half of the method detection 
limit of the ozone instrument, whichever is higher, for enough of 
the missing hourly concentrations within each incomplete month to 
make the month 75% complete, and then adjusting for the remaining 
missing data using Equation 2, above results in a design value 
greater than the level of the standard.

(d) Comparisons With the Secondary Ozone Standard

    (i) The secondary ambient ozone air quality standard is met at 
an ambient air quality monitoring site when the design value is less 
than or equal to [15] ppm-hours.
    (ii) Comparison with the secondary ozone standard is 
demonstrated by example 4 as follows:

    Example 4.  Ambient Monitoring Site Failing to Meet the 
Secondary Ozone Standard

[[Page 3052]]



--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                  April       May        June       July      August    September   October     Overall
--------------------------------------------------------------------------------------------------------------------------------------------------------
                             2006
 
Adjusted monthly W126 index...................................      4.442      9.124     12.983     16.153     13.555       4.364      1.302  ..........
3-Month sum...................................................         na         na     26.549     38.260     42.691      34.072     19.221  ..........
2006 Maximum..................................................  .........  .........  .........  .........     42.691  ..........  .........      42.691
--------------------------------------------------------------------------------------------------------------------------------------------------------
                             2007
 
Adjusted monthly W126 index...................................      3.114      7.214      8.214      8.111      7.455       7.331      5.115  ..........
3-Month sum...................................................         na         na     18.542     23.539     23.780      22.897     19.901  ..........
2007 Maximum..................................................  .........  .........  .........  .........     23.780  ..........  .........      23.780
--------------------------------------------------------------------------------------------------------------------------------------------------------
                             2008
 
Adjusted monthly W126 index...................................      4.574      5.978      6.786      8.214      5.579       4.331      2.115  ..........
3-Month sum...................................................         na         na     17.338     20.978     20.579      18.124     12.025  ..........
2008 Maximum..................................................  .........  .........  .........     20.978  .........  ..........  .........      20.978
3-Year average W126 index.....................................  .........  .........  .........  .........  .........  ..........  .........   29.149666
                                                               -----------------------------------------------------------------------------------------
    Rounded...................................................  .........  .........  .........  .........  .........  ..........  .........          29
--------------------------------------------------------------------------------------------------------------------------------------------------------

    As shown in example 4, the secondary ozone standard is not met 
for this monitoring site because the 3-year average of the annual 
W126 index value for this site is greater than [15] ppm-hours:

3-year average W126 index = (42.691 + 23.780 + 20.978)/3 = 
29.149666, which rounds to 29 ppm-hours.

    In Example 4, the adjusted monthly W126 index values and the 3-
month sums of the adjusted monthly W126 index values are shown with 
three decimal digits. In actual calculations, all digits supported 
by the calculator or calculation software must be retained.

PART 58--AMBIENT AIR QUALITY SURVEILLANCE

    5. The authority citation for part 58 continues to read as follows:

    Authority:  42 U.S.C. 7410 7403, 7410, 7601(a), 7611, and 7619.

    6. Section 58.50 is amended by revising paragraph (c) and adding 
paragraph (d) to read as follows:


Sec.  58.50  Index reporting.

* * * * *
    (c) The population of a metropolitan statistical area for purposes 
of index reporting is the latest available U.S. census population.
    (d) For O3, reporting is required in metropolitan and 
micropolitan statistical areas wherever monitoring is required under 
Appendix D to Part 58--SLAMS Minimum O3 Monitoring 
Requirements.
    7. Appendix G of Part 58 is amended by revising section 3. to read 
as follows:

Appendix G to Part 58--Uniform Air Quality Index (AQI) and Daily 
Reporting

* * * * *

3. Must I Report the AQI?

    You must report the AQI daily if yours is a metropolitan 
statistical area (MSA) with a population over 350,000. For 
O3, reporting is required in metropolitan and 
micropolitan statistical areas wherever monitoring is required under 
Appendix D to Part 58--SLAMS Minimum O3 Monitoring 
Requirements.
* * * * *
[FR Doc. 2010-340 Filed 1-15-10; 8:45 am]
BILLING CODE 6560-50-P