[Federal Register Volume 72, Number 132 (Wednesday, July 11, 2007)]
[Proposed Rules]
[Pages 37818-37919]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: E7-12416]
[[Page 37817]]
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Part II
Environmental Protection Agency
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40 CFR Part 50
National Ambient Air Quality Standards for Ozone; Proposed Rule
Federal Register / Vol. 72, No. 132 / Wednesday, July 11, 2007 /
Proposed Rules
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 50
[EPA-HQ-OAR-2005-0172; FRL-8331-5]
RIN 2060-AN24
National Ambient Air Quality Standards for Ozone
AGENCY: Environmental Protection Agency (EPA).
ACTION: Proposed rule.
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SUMMARY: Based on its review of the air quality criteria for ozone
(O3) and related photochemical oxidants and national ambient
air quality standards (NAAQS) for O3, EPA proposes to make
revisions to the primary and secondary NAAQS for O3 to
provide requisite protection of public health and welfare,
respectively, and to make corresponding revisions in data handling
conventions for O3.
With regard to the primary standard for O3, EPA proposes
to revise the level of the 8-hour standard to a level within the range
of 0.070 to 0.075 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 nonaccidental and
cardiopulmonary mortality. The EPA also proposes to specify the level
of the primary standard to the nearest thousandth ppm. The EPA solicits
comment on alternative levels down to 0.060 ppm and up to and including
retaining the current 8-hour standard of 0.08 ppm (effectively 0.084
ppm using current data rounding conventions).
With regard to the secondary standard for O3, EPA
proposes to revise the current 8-hour standard with one of two options
to provide increased protection against O3-related adverse
impacts on vegetation and forested ecosystems. One option is to replace
the current standard with a cumulative, seasonal standard expressed as
an index of the annual sum of weighted hourly concentrations, cumulated
over 12 hours per day (8 a.m. to 8:00 p.m.) 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 21 ppm-hours. The other
option is to make the secondary standard identical to the proposed
primary 8-hour standard. The EPA solicits comment on specifying a
cumulative, seasonal standard in terms of a 3-year average of the
annual sums of weighted hourly concentrations; on the range of
alternative 8-hour standard levels for which comment is being solicited
for the primary standard, including retaining the current secondary
standard, which is identical to the current primary standard; and on an
alternative approach to setting a cumulative, seasonal secondary
standard(s).
DATES: Written comments on this proposed rule must be received by
October 9, 2007.
ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2005-0172, by one of the following methods:
www.regulations.gov: Follow the on-line instructions for
submitting comments.
E-mail: [email protected].
Fax: 202-566-1741.
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.
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. For additional information about EPA's public docket, visit
the EPA Docket Center homepage at http://www.epa.gov/epahome/dockets.htm.
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.
Public Hearings: The EPA intends to hold public hearings around the
end of August to early September in several cities across the country,
and will announce in a separate Federal Register notice the dates,
times, and addresses of the public hearings on this proposed rule.
FOR FURTHER INFORMATION CONTACT: Dr. David J. McKee, 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: 919-541-5288; fax: 919-
541-0237; e-mail: [email protected].
SUPPLEMENTARY INFORMATION:
General Information
What Should I Consider as I Prepare My Comments for EPA?
1. Submitting CBI. Do not submit this information to EPA through
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
[[Page 37819]]
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.
If you estimate potential costs or burdens, explain how
you arrived at your estimate in sufficient detail to allow for it to be
reproduced.
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 (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.'' The 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 Staff Paper is available at http://www.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. EPA
will be making available corrected versions of the final Staff Paper
and human exposure and health risk assessment technical support
documents on these same EPA Web sites on or around July 16, 2007. These
and other related documents are also available for inspection and
copying in the EPA docket identified above.
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
II. Rationale for Proposed Decision on the Primary Standard
A. Health Effects Information
1. Mechanisms
2. Nature of Effects
3. Interpretation and Integration of the Health Evidence
4. O3-Related Impacts on Public Health
B. Human Exposure and Health Risk Assessments
1. Exposure Analyses
2. Quantitative Health Risk Assessment
C. Conclusions on the Adequacy of the Current Primary Standard
1. Background
2. Evidence- and Exposure/Risk-Based Considerations
3. CASAC Views
4. Administrator's Proposed Conclusions Concerning Adequacy of
Current Standard
D. Conclusions on the Elements of the Primary Standard
1. Indicator
2. Averaging Time
3. Form
4. Level
E. Proposed Decision on the Primary Standard
III. Communication of Public Health Information
IV. Rationale for Proposed Decision on the Secondary Standard
A. Vegetation Effects Information
1. Mechanisms Governing Plant Response to Ozone
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. Conclusions on the Adequacy of the Current Standard
1. Background
2. Evidence- and Exposure/Risk-Based Considerations
3. CASAC Views
4. Administrator's Proposed Conclusions Concerning Adequacy of
Current Standard
E. Conclusions on the Elements of the Secondary Standard
1. Indicator
2. Cumulative, Seasonal Standard
3. 8-Hour Average Standard
F. Proposed Decision on the Secondary Standard
V. Creation of Appendix P--Interpretation of the NAAQS for Ozone
A. Data Completeness
B. Data Handling and Rounding O3 Conventions
VI. Ambient Monitoring Related to Proposed Revised Standards
VII. Statutory and Executive Order Reviews
References
I. Background
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 his
judgment, may reasonably be anticipated to endanger public health and
welfare'' and 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 identifiable effects on public
health or welfare which may be expected from the presence of [a]
pollutant in ambient air * * *.''
Section 109 (42 U.S.C. 7409) directs the Administrator to propose
and promulgate ``primary'' and ``secondary'' NAAQS for pollutants
listed under section 108. 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 [the] 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 (D.C. 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 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) (Breyer, J., concurring
in part and concurring in judgment).
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. American 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. As discussed by Justice Breyer in Whitman v.
American Trucking Associations, however, ``this interpretation of Sec.
109 does not require the EPA to eliminate every health risk, however
slight, at any economic cost, however great, to the point of
``hurtling'' industry over ``the brink of ruin,'' or even forcing
``deindustrialization.'' Id. at 494 (Breyer J., concurring in part and
concurring in judgment) (citations omitted). Rather, as Justice Breyer
explained:
The statute, by its express terms, does not compel the
elimination of all risk; and it grants the Administrator sufficient
flexibility to avoid setting ambient air quality standards ruinous
to industry.
Section 109(b)(1) directs the Administrator to set standards
that are ``requisite to protect the public health'' with ``an
adequate margin of safety.'' But these words do not describe a world
that is free of all risk--an impossible and undesirable objective.
(citation omitted). Nor are the words ``requisite'' and ``public
health'' to be understood independent of context. We consider
football equipment ``safe'' even if its use entails a level of risk
that would make drinking water ``unsafe'' for consumption. And what
counts as ``requisite'' to protecting the public health will
similarly vary with background circumstances, such as the public's
ordinary tolerance of the particular health risk in the particular
context at issue. The Administrator can consider such background
circumstances when ``deciding what risks are acceptable in the world
in which we live.'' (citation omitted).
The statute also permits the Administrator to take account of
comparative health risks. That is to say, she may consider whether a
proposed rule promotes safety overall. A rule likely to cause more
harm to health than it prevents is not a rule that is ``requisite to
protect the public health.'' For example, as the Court of Appeals
held and the parties do not contest, the Administrator has the
authority to determine to what extent possible health risks stemming
from reductions in tropospheric ozone (which, it is claimed, helps
prevent cataracts and skin cancer) should be taken into account in
setting the ambient air quality standard for ozone. (citation
omitted).
The statute ultimately specifies that the standard set must be
``requisite to protect the public health'' ``in the judgment of the
Administrator,'' Sec. 109(b)(1), 84 Stat. 1680 (emphasis added), a
phrase that grants the Administrator considerable discretionary
standard-setting authority.
The statute's words, then, authorize the Administrator to
consider the severity of a pollutant's potential adverse health
effects, the number of those likely to be affected, the distribution
of the adverse effects, and the uncertainties surrounding each
estimate. (citation omitted). They permit the Administrator to take
account of comparative health consequences. They allow her to take
account of context when determining the acceptability of small risks
to health. And they give her considerable discretion when she does
so.
This discretion would seem sufficient to avoid the extreme
results that some of the industry parties fear. After all, the EPA,
in setting standards that ``protect the public health'' with ``an
adequate margin of safety,'' retains discretionary authority to
avoid regulating risks that it reasonably concludes are trivial in
context. Nor need regulation lead to deindustrialization.
Preindustrial society was not a very healthy society; hence a
standard demanding the return of the Stone Age would not prove
``requisite to protect the public health.''
Although I rely more heavily than does the Court upon
legislative history and alternative sources of statutory
flexibility, I reach the same ultimate conclusion. Section 109 does
not delegate to the EPA authority to base the national ambient air
quality standards, in whole or in part, upon the economic costs of
compliance.
Id. at 494-496.
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 NOX and 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
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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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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 current national
standards. Under the Federal Motor Vehicle Control Program (FMVCP, see
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. Recently
EPA proposed new standards for locomotive and marine diesel engines.
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. The EPA is currently working to
finalize new federal rules, or amendments to existing rules, that will
establish new nationwide VOC content limits for several categories of
consumer and commercial products, including aerosol coatings,
architectural and industrial maintenance coatings, and household and
institutional commercial products. These rules will take effect in
2009, and will yield significant new reductions in nationwide VOC
emissions--about 200,000 tons per year. Additionally, in O3
nonattainment areas, we anticipate reductions of an additional 25,000
tons per year following completion of control technique recommendations
for 3 additional consumer and commercial product categories. 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 and some large industrial boilers and
turbines. The EPA's landmark Clean Air Interstate Rule (CAIR), issued
on March 10, 2005, permanently caps power industry emissions of
NOX in the eastern United States. The first phase of the cap
begins in 2009, and a lower second phase cap begins in 2015. By 2015,
EPA projects that the CAIR and other programs in the Eastern U.S. will
reduce power industry O3 season NOX emissions in
that region by about 50 percent and annual NOX emissions by
about 60 percent from 2003 levels.
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
Tropospheric (ground-level) O3 is formed from biogenic
and anthropogenic precursor emissions. Naturally occurring
O3 in the troposphere can result from biogenic organic
precursors reacting with naturally occurring nitrogen oxides
(NOX) and by stratospheric O3 intrusion into the
troposphere. Anthropogenic precursors of O3, specifically
NOX and volatile organic compounds (VOC), originate from a
wide variety of stationary and mobile sources. Ambient O3
concentrations produced by these emissions are directly affected by
temperature, solar radiation, wind speed and other meteorological
factors.
The last review of the O3 NAAQS was completed on July
18, 1997, based on the 1996 O3 CD (U.S. EPA, 1996a) and 1996
O3 Staff Paper (U.S. EPA, 1996b). EPA revised the primary
and secondary O3 standards on the basis of the then latest
scientific evidence linking exposures to ambient O3 to
adverse health and welfare effects at levels allowed by the 1-hour
average standards (62 FR 38856). The O3 standards were
revised by replacing the existing primary 1-hour average standard with
an 8-hour average O3 standard set at a level of 0.08 ppm,
which is equivalent to 0.084 ppm using the standard rounding
conventions. The form of the primary standard was changed to the annual
fourth-highest daily maximum 8-hour average concentration, averaged
over three years. The secondary O3 standard was changed by
making it identical in all respects to the revised primary standard.
Following promulgation of the revised O3 NAAQS,
petitions for review were
[[Page 37822]]
filed addressing a broad range of issues. In May 1999, in response to
those challenges, the U.S. Court of Appeals for the District of
Columbia Circuit held that EPA's approach to establishing the level of
the standards in 1997, both for the O3 and for the
particulate matter (PM) NAAQS promulgated on the same day, effected
``an unconstitutional delegation of legislative authority.'' American
Trucking Associations v. EPA, 175 F.3d 1027 (DC Cir., 1999). Although
the D.C. Circuit stated that ``factors EPA uses in determining the
degree of public health concern associated with different levels of
O3 and PM are reasonable,'' it remanded the rule to EPA,
stating that when EPA considers these factors for potential non-
threshold pollutants ``what EPA lacks is any determinate criterion for
drawing lines'' to determine where the standards should be set. Id. at
1034. Consistent with EPA's long-standing interpretation and DC Circuit
precedent, the court also reaffirmed prior rulings holding that in
setting the NAAQS, it is ``not permitted to consider the cost of
implementing those standards.'' Id. at 1040-41. The DC Circuit further
directed EPA to consider on remand the potential indirect beneficial
health effects of O3 pollution in shielding the public from
the effects of solar ultraviolet (UV) radiation, as well as the direct
adverse health effects of O3 pollution.
Both sides filed cross appeals on the constitutional and cost
issues to the United States Supreme Court, and the Court granted
certiorari. On February 27, 2001, the U.S. Supreme Court issued a
unanimous decision upholding the EPA's position on both the
constitutional and the cost issues. Whitman v. American Trucking
Associations, 531 U.S. at 464, 475-76. On the constitutional issue, the
Court held that the statutory requirement that NAAQS be ``requisite''
to protect public health with an adequate margin of safety sufficiently
guided EPA's discretion, affirming EPA's approach of setting standards
that are neither more nor less stringent than necessary. The Supreme
Court remanded the case to the D.C. Circuit for resolution of any
remaining issues that had not been addressed by that Court's earlier
decisions. Id. at 475-76. On March 26, 2002, the D.C. Circuit Court
rejected all remaining challenges to the NAAQS, holding under
traditional standard of review that EPA ``engaged in reasoned decision-
making'' in setting the 1997 O3 NAAQS. Whitman v. American
Trucking Associations, 283 F.3d 355 (DC Cir. 2002).
In response to the DC Circuit Court's remand to consider the
potential indirect beneficial health effects of O3 in
shielding the public from the effects of solar (UV) radiation, on
November 14, 2001, EPA proposed to leave the 1997 8-hour NAAQS
unchanged (66 FR 57267). After considering public comment on the
proposed decision, EPA reaffirmed the 8-hour O3 NAAQS set in
1997 (68 FR 614). Finally, on April 30, 2004, EPA issued an 8-hour
implementation rule that, among other things, provided that the 1-hour
O3 NAAQS would no longer apply to areas one year after the
effective date of the designation of those areas for the 8-hour NAAQS
(69 FR 23966).\4\ For most areas, the date that the 1-hour NAAQS no
longer applied was June 15, 2005. (See 40 CFR 50.9 for details.)
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\4\ On December 22, 2006, the D.C. Circuit vacated the April 30,
2004 implementation rule. South Coast Air Quality Management
District v. EPA, 472 F.3d 882. In March 2007, EPA requested the
Court to reconsider its decision.
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The EPA initiated this current review in September 2000 with a call
for information (65 FR 57810) for the development of a revised Air
Quality Criteria Document for O3 and Other Photochemical
Oxidants (henceforth the ``Criteria Document''). A project work plan
(U.S. EPA, 2002) for the preparation of the Criteria Document was
released in November 2002 for CASAC and public review. 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, the CASAC offered
final comments on all chapters of the Criteria Document (Henderson,
2006a), and the final Criteria Document (EPA, 2006a) was released on
March 21, 2006. In a June 8, 2006 letter (Henderson, 2006b) to the
Administrator, the CASAC offered additional advice to the Agency
concerning chapter 8 of the final 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 and 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 Staff Paper (EPA, 2007) was released on
January 31, 2007. Around the time of the release of the final Staff
Paper in January 2007, EPA discovered a small error in the exposure
model that when corrected resulted in slight increases in the human
exposure estimates. 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.\5\ 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.
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\5\ EPA plans to make available corrected versions of the final
Staff Paper and the human exposure and health risk assessment
technical support documents on or around July 16, 2007 on the EPA
web site listed in the Availability of Related Information section
of this notice.
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The schedule for completion of this review is governed by a consent
decree resolving a lawsuit filed in March 2003 by a group of plaintiffs
representing national environmental and public health organizations,
alleging that EPA had failed to complete the current review within the
period provided by statute.\6\ The modified consent decree that governs
this review, entered by the court on December 16, 2004, provides 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. This 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.
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\6\ American Lung Association v. Whitman (No. 1:03CV00778,
D.D.C. 2003).
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This action presents the Administrator's proposed decisions on the
review of the current primary and secondary O3 standards.
Throughout this preamble a number of conclusions, findings, and
determinations proposed by the Administrator are noted. While
[[Page 37823]]
they identify the reasoning that supports this proposal, they are not
intended to be final or conclusive in nature. The EPA invites general,
specific, and/or technical comments on all issues involved with this
proposal, including all such proposed judgments, conclusions, findings,
and determinations.
II. Rationale for Proposed Decision on the Primary Standard
This section presents the rationale for the Administrator's
proposed decision to revise the existing 8-hour O3 primary
standard by lowering the level of the standard to within a range from
0.070 to 0.075 ppm, and to specify the standard to the nearest
thousandth ppm (i.e., to the nearest parts per billion). As discussed
more fully below, this rationale is based on a thorough review, in the
Criteria Document, of the latest scientific information on human health
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
Criteria Document and staff analyses of air quality, human exposure,
and health risks, presented in the Staff Paper, upon which staff
recommendations for revisions to the primary O3 standard are
based; (2) CASAC advice and recommendations, as reflected in
discussions of drafts of the Criteria Document and Staff Paper at
public meetings, in separate written comments, and in CASAC's letters
to the Administrator; and (3) public comments received during the
development of these documents, either in connection with CASAC
meetings or separately.
In developing this rationale, EPA has drawn upon an integrative
synthesis of the entire body of evidence, published 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.\7\ In considering
this evidence, EPA focuses on those health endpoints that have been
demonstrated to be caused by exposure to O3, or for which
the 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. Evidence- and exposure/
risk-based considerations that form the basis for the Administrator's
proposed decisions on the adequacy of the current standard and on the
elements of the range of proposed alternative standards are discussed
below in sections II.C and II.D, respectively.
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\7\ 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.
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Judgments made in the Criteria Document and 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 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
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 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
[[Page 37824]]
under varying air quality scenarios (e.g., just meeting the current or
alternative standards), as well as characterizations of the kind and
degree of uncertainties inherent in such estimates.
In this review, 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.\8\ EPA emphasizes
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. 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.
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\8\ Exposures of concern were also considered in the last 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)
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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 human clinical 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. 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 this review 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
current and various alternative O3 standards in a number of
example urban areas. There were two parts to this risk assessment: one
part was based on combining information from controlled human exposure
studies with modeled population exposure, and the other part was based
on combining information from community epidemiological studies with
either monitored or adjusted ambient concentrations levels. This
assessment not only provided 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 provided 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 has been
conducted since the last review of the O3 NAAQS, with
important new information coming from epidemiologic studies as well as
from controlled human exposure, toxicological, and dosimetric studies.
The newly available research studies evaluated in the Criteria Document
and the exposure and risk assessments presented in the 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, the review of this information has been extensive and
deliberate. In the judgment of the Administrator, this intensive
evaluation of the scientific evidence has provided an adequate basis
for regulatory decision making. This review also provides important
input to EPA's research plan for improving our future understanding of
the effects of ambient O3 at lower levels, especially in at-
risk population groups.
A. Health Effects Information
This section outlines key information contained in the Criteria
Document (chapters 4-8) and in the 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''
subpopulations.
The decision in the last 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
[[Page 37825]]
hospital admissions and emergency department (ED) visits for
respiratory causes. The Criteria Document prepared for this review
emphasizes a 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 emphasizes 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
exposure level that had been examined in the last 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), while
other studies have examined changes in host defense capability
following O3 exposure of healthy young adults and increased
airway responsiveness to allergens in subjects with allergic asthma and
allergic rhinitis exposed to O3.
(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 asthmatic subjects, as well as evidence on
new health endpoints, such as the relationships between ambient
O3 concentrations 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 respiratory diseases and
on 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 last
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 Criteria Document.\9\ Evidence from dosimetry,
toxicology, 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 last review an emerging body of
animal toxicology and human clinical 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.
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\9\ 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.
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With regard to the mechanisms related to short-term respiratory
effects, scientific evidence discussed in the 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 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 can become
apparent 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 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 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 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
[[Page 37826]]
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
\10\, as discussed more fully below in section II.A.4.b.
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\10\ 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 susceptible and population groups that are at
increased risk due to increased vulnerability or exposure. In this
notice, we use the phrase, ``at risk'' populations to include both
types of population groups.
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Based on new evidence from animal, human clinical and
epidemiological studies the Criteria Document concludes that people
with preexisting pulmonary disease 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 (CD, 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 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. These more serious responses in
asthmatics and others with lung disease provide biological plausibility
for the respiratory morbidity effects observed in epidemiological
studies.
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 Criteria Document concludes that the elderly population (>65 years
of age) appears 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 (EPA, 2006a, section 7.6.7.2).
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, p. 6-2). In human
clinical 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.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.
Clinical 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 clinical 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.
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
[[Page 37827]]
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 the highest common dose of
allergen.
2. Nature of Effects
The 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 Staff Paper, which is based on
scientific evidence critically reviewed in chapters 5, 6, and 7 of the
Criteria Document, as well as the Criteria Document's integration of
scientific evidence contained in chapter 8.\11\ 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 Criteria Document.
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\11\ Health effects discussions are also drawn from the more
detailed information and tables presented in the Criteria Document's
annexes.
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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 Criteria Document and chapter 3 of the 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 Criteria Document and
chapter 3 of the 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, 1996). In the last 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 >= 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 post-exposure,
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 hours to return to baseline. The majority of these
responses are attenuated after repeated consecutive exposures, but such
attenuation to O3 is lost one week post-exposure.
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 Staff Paper (Appendix 3C). As summarized in more detail in the
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 exercise and
typically using square-
[[Page 37828]]
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 toxicology.
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.\12\ 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, 2007, 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).\13\ In these studies, 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 >= 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, 2007, Figure 3-1B) and with 23 percent of subjects
(7 of 30) experiencing such effects when the results were corrected
(EPA, 2007, p. 3-6).\14\
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\12\ This study and other studies (Folinsbee et al., 1988;
Horstman et al., 1990; and McDonnell et al., 1991), conducted in
EPA's clinical research facility in Chapel Hill, NC, measured ozone
concentrations to within +/-5 percent or +/-0.004 ppm at the 0.080
ppm exposure level.
\13\ 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.
\14\ These distributional results presented in the Criteria
Document and Staff Paper for the Adams studies are based on study
data that were not included in the publication but were obtained
from the author.
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These studies by Adams (2002, 2006) are notable in that they are
the only available controlled exposure human 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 last 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 multiple comparisons of 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. 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, 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.\15\
Notably, these studies report a small percentage of subjects
experiencing lung function decrement (>= 10 percent) at the 0.060 ppm
exposure level.\16\
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\15\ Brown, J.S. (2007). EPA Office of Research and Development
memorandum to Ozone NAAQS Review Docket (OAR-2005-0172); Subject:
The effects of ozone on lung function at 0.06 ppm in healthy adults,
June 14, 2007.
\16\ 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, 2007, p. 3-6).
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(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 have 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 persons.
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 >= 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
[[Page 37829]]
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
(SD 80) in northern Mexico City to 0.196 ppm (SD 78) 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 effect 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 (SD 19.0) and 0.0513 ppm (SD 15.5), 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
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 provides 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. Even so, the evidence has continued to
expand since 1996 and now is considered to be much stronger than in the
previous review. The 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
previous 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. 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. 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 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.
[[Page 37830]]
(b) Increased Airway Responsiveness
As discussed in more detail in the Criteria Document (section 6.8)
and 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 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
inhalation of 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 current 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, p. 6-31).
The 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 responsiveness (Criteria Document, 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 previous 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
Criteria Document and section 3.3.1.3 of the 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 Criteria Document (pp. 8-21 to
8-24) consistent with the previous 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)\17\ 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.
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\17\ 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).
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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
[[Page 37831]]
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 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 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
(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 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. 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. Dysfunction 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 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 (EPA, 2006a, p. 8-
26). Integrating the recent animal study results with human exposure
evidence available in the 1996 Criteria Document, the 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 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
proliferation and fibrolitic changes in the CAR, these changes appear
to be transient with recovery time 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 of respiratory bronchiolitis, which have the
potential to progress to fibrotic lung disease (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 (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).
[[Page 37832]]
(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
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 last 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\18\ 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 prior 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 (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 last or the current
O3 NAAQS review.
---------------------------------------------------------------------------
\18\ 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 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. Among studies with
adequate controls for seasonal patterns, many reported at least one
significant positive association involving O3.
In reviewing evidence for associations between emergency department
visits for asthma and short-term O3 exposures, the Criteria
Document 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 (Figure 7-8, EPA, 2006a,
p. 7-68). 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. Thus, the Criteria Document has
concluded that stratified analyses by season generally supported a
positive association between O3 concentrations and emergency
department visits for asthma in the warm season.
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
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 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 human clinical, 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).
[[Page 37833]]
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 Criteria Document (p. 7-114) summarizes these studies
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 and that there is some limited, as yet uncertain,
evidence that seasonal O3 also may affect lung function 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 have 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 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
[[Page 37834]]
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 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 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 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 much needs to be done 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.
Epidemiologic 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,
ventricular arrhythmias, and incidence of heart attacks. 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 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.,
[[Page 37835]]
1997b). The results were robust to adjustment for various PM indices,
whereas the PM effects diminished when adjusting for gaseous
pollutants. Other studies stratified their analysis by temperature,
i.e., by warm 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./
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, human
controlled exposure, and epidemiologic studies, from the Criteria
Document 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 (EPA, 2006a, p. 8-77).
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 current Criteria Document includes 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
multi-city 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 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 multi-city 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 with 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
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 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
[[Page 37836]]
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 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. multi-city
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 Criteria Document
finds that the results from U.S. multi-city 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 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 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.\19\
---------------------------------------------------------------------------
\19\ 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).
---------------------------------------------------------------------------
ii. Mortality and Long-Term O3 Exposure
Little evidence was available in the last 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 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).\20\ 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 Staff Paper (section 3.3.2.2) but not in the Criteria
Document.
---------------------------------------------------------------------------
\20\ 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
[[Page 37837]]
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 Criteria Document discussed
concerns about the plausibility of the reported association with lung
cancer (EPA, 2006a, p. 7-130).
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 Criteria Document concludes that consistent
associations have not been reported between long-term O3
exposure and all-cause, cardiopulmonary or lung cancer mortality (EPA,
2006a, p. 7-130).
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
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 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 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 Criteria Document (section 10.2.3.6)
also discusses protective effects of UV-B radiation. Recent reports
indicate the necessity of UV-B in producing vitamin D, and that 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 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-
induced health outcomes cannot yet be critically assessed within
reasonable uncertainty (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 last review, the Administrator 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 in this review, the Criteria Document and 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-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.
EPA requests comment on available studies or data that would be
relevant to conducting a critical assessment with reasonable certainty
of UV-induced health outcomes and how evidence of UV-induced health
outcomes might inform the Agency's review of the primary O3
standard.
3. Interpretation and Integration of Health Evidence
As discussed below, in assessing the new health evidence, the
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
[[Page 37838]]
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 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 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
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 (EPA, 2006a, 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 Criteria
Document (sections 7.1.3 and 8.4.4.3) and 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 Criteria
Document (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; Xue 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 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
[[Page 37839]]
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 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
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 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 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 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 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 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 multi-city 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 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 Criteria Document
reports that results of available analyses indicate that such
associations generally were robust to adjustment for PM2.5
(EPA, 2006a, p. 7-154). For example, in a large multi-city 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 Criteria Document 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 (EPA, 2006a, p. 7-
154).''
The Criteria Document 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 (EPA, 2006a, p. 7-14). 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 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.
multi-city 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 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 multi-city 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
[[Page 37840]]
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 multi-city studies and single-city studies in
different areas, the 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 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 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.
Bell et al. (2006) found no difference in estimated effect even when
all days with 24-hour O3 concentrations <0.020 ppm were
excluded (EPA, 2006a, p. 8-43). 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 Criteria Document, one European
multi-city 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 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 Criteria Document finds that, taken together, the
available evidence from clinical 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 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
[[Page 37841]]
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 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 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 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 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 are 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 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
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 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.\21\ 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.
---------------------------------------------------------------------------
\21\ 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, chamber, and field
studies, the 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 (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
attenuation in functional responses
[[Page 37843]]
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 can become apparent within 3 hours after exposure in humans.
Taken together, the 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, including 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.b, 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.b, 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 heart rate variability (HRV) and the other study
evaluated the association between O3 levels and the relative
risk of myocardial infarction (MI). 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 MI 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 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 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
Criteria Document finds that the overall evidence from these studies
remains inconclusive regarding the effect of O3 on
cardiovascular hospitalizations (EPA, 2006a, p. 7-83).
The Criteria Document notes that the suggestive positive
epidemiologic findings of O3 exposure on cardiac autonomic
control, including effects on HRV, ventricular arrhythmias and MI, 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 human clinical studies, which are indicative of plausible pathways
by which O3 may exert cardiovascular effects (EPA, 2006a,
section 8.6.1).
[[Page 37844]]
iii. Coherence and Plausibility of Effects Related to Long-Term
O3 Exposure
Human chamber studies can not 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 Criteria Document, previous epidemiological studies have
provided only inconclusive evidence for either mortality or morbidity
effects of long-term O3 exposure. The Criteria Document
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 (EPA, 2006a, p. 8-50).
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 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 pulmonary
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 Criteria Document (sections 7.4 and 8.6.3). These single- and
multi-city mortality studies coupled with 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. 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 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 Follow-up data
analysis indicates that about 20 percent of the adult population has
reduced FEV1 values, suggesting impaired lung function in
some 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.
Of much interest are several other types of newly available data
that 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 MI,
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
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).
c. Summary
Judgments concerning the extent to which relationships between
various health endpoints and ambient O3
[[Page 37845]]
exposures are likely causal are informed by the conclusions and
discussion in the Criteria Document as discussed above and summarized
in section 3.7.5 of the Staff Paper. These judgments reflect the nature
of the evidence and 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 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 symptoms have been reported in
epidemiology studies (EPA, 2006a, p. 8-75). Aggregate population time-
series studies showing robust associations with respiratory hospital
admissions and emergency department visits are strongly supported by
human clinical, animal toxicologic, and epidemiologic evidence for
O3-related lung function decrements, respiratory symptoms,
airway inflammation, and airway hyperreactivity. The 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 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 Criteria Document and section 3.6 of the Staff Paper to
characterize factors which modify responsiveness to O3,
subpopulations potentially at risk for O3-related health
effects, the adversity of O3-related effects, and the size
of the at-risk subpopulations 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 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 was estimated for 20 year old individuals exposed to
0.12 ppm O3, whereas similar exposure of 35 year old
individuals were estimated to have a 2.6% decrement. 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 tend to decrease with increasing age
(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. 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 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
[[Page 37846]]
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.\22\
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\22\ 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 human chamber studies have examined the
effects of O3 exposure in subjects performing continuous or
intermittent exercise for variable periods of time. Significant
O3-induced respiratory responses have been observed in
clinical studies of exercising individuals. 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 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. At the time of the last review, it was
concluded that this group was 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 pulmonary 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 subpopulation for
O3 health effects.
Several clinical studies reviewed in the 1996 Criteria Document on
atopic and asthmatic subjects had 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 Criteria Document indicate that asthmatics
are as sensitive as, if not more sensitive than, normal subjects in
manifesting O3-induced pulmonary 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 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 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 (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 cell 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., 1997a;
Michelson et al., 1999; Hiltermann et al., 1999; Holz et al., 2002;
Vagaggini et al., 2002). In asthma, the eosinophil, 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
[[Page 37847]]
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. (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 human clinical 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 may be 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
Criteria Document (section 7.6.7.1). Strong evidence from a large
multi-city study (Mortimer et al., 2002), along with support from
several single-city studies suggest that O3 exposure may be
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 in the 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
and other respiratory diseases, especially during the warm season.
Finally, from epidemiological studies that included assessment of
associations with specific causes of death, some studies have observed
larger effects estimates for respiratory mortality and others have
observed larger effects estimates for cardiovascular mortality. The
apparent inconsistency regarding the effect size of O3-
related respiratory mortality may be due to reduced statistical power
in this
[[Page 37848]]
subcategory of mortality (EPA, 2006a, p. 7-108).
Newly available reports from controlled human exposure studies (see
chapter 6 in the 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 changes 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 have such changes based on
their age. However, in section 8.7.1, the 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 COPD lung
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).
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 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 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 pulmonary 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% of the children, both with and without asthma, experienced a
greater than 10% change in FEV1, compared to only 5% of the
elderly population and athletes (Hoppe 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 being particularly susceptible to air
pollution. 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). (EPA 2006a, p. 8-60) 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 Criteria Document 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 (EPA, 2006a, p. 7-177).
The 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
[[Page 37849]]
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 human clinical 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 pulmonary function and
inflammatory responses to O3 exposure.\23\
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\23\ 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 needs additional experimentation.
---------------------------------------------------------------------------
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 and,
ultimately, can likely be integrated with epidemiological studies.
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 MI 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 Criteria Document 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 MI incidence
(EPA, 2006a, p. 7-65). In the 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 making judgments as to when various O3-related
effects become regarded as adverse to the health of individuals, the
Administrator has 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) \24\ 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 studies, which
could be extrapolated to humans only with a significant degree of
uncertainty, for the last two categories.
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\24\ 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.
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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 last 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 this 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 multi-city time-series epidemiology studies and meta-analyses of
these epidemiology 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
[[Page 37850]]
(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 Staff Paper.
For active healthy people, moderate levels of functional responses
(e.g., FEV1 decrements of >=10% but <20%, 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%, 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%
but <20%) 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% but <20%, 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%, 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%) is most appropriate for estimating potentially
adverse lung function decrements in active healthy people.
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.
d. Size of At-Risk Subpopulations
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 subpopulations
potentially at-risk for O3-related health effects discussed
above. For example, a population of concern includes people with
respiratory disease, including 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
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, subpopulations 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 age
groups include those most likely to have increased susceptibility to
the health effects of O3 and or those with the highest
ambient O3 exposures.
The 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 Criteria
[[Page 37851]]
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 Staff Paper 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
(Staff Paper, p. 6-20--6-21).
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 has changed
over time based on historical trends in monitored O3 air
quality data. As described in the Staff Paper (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.\25\
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\25\ 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.
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As noted in section I.C above, around the time of the release of
the final 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.\26\
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\26\ EPA plans to make available corrected versions of the final
Staff Paper, and human exposure and health risk assessment technical
support documents on or around July 16, 2007 on the EPA web site
listed in the Availability of Related Information section of this
notice.
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1. Exposure Analyses
a. Overview
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 current 8-hour O3 standard is not met. The
emphasis on children reflects the finding of the last 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 Staff Paper. The geographic extent of each
modeled area consists of the census tracts in the combined statistical
area (CSA) as defined by OMB (OMB, 2005).\27\
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\27\ 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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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 current NAAQS and various
alternative 8-hour standards based on the three year period 2002-
2004.\28\ This exposure assessment is more fully described and
presented in the Staff Paper and in a technical support document, Ozone
Population Exposure Analysis for Selected Urban Areas (US EPA, 2006b;
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.\29\
---------------------------------------------------------------------------
\28\ All 12 of the CSAs modeled did not meet the current
O3 NAAQS for the three year period examined.
\29\ The general approach used in the current exposure
assessment was described in the draft Health Assessment Plan (EPA,
2005a) 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
[[Page 37852]]
reductions associated with meeting alternative O3 standards.
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 Staff Paper (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 clinical 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 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 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. These are discussed fully in
the 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 (Tables 26 and 27 in Langstaff, 2007). 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
[[Page 37853]]
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,
2007, 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 include the 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.\30\ The
current standard uses 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, where the precision would extend to three
instead of two decimal places (in ppm).
---------------------------------------------------------------------------
\30\ The current O3 standard is 0.08 ppm, but the
current rounding convention specifies 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 the 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.
---------------------------------------------------------------------------
The 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 \31\ corresponding to the
standard being analyzed. The quadratic rollback technique reduces
higher concentrations more than lower concentrations near ambient
background levels.\32\ This procedure was considered in a sensitivity
analysis in the last 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.
---------------------------------------------------------------------------
\31\ 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
current 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.
\32\ 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 \33\ 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 health impacts of health
effects that we cannot currently evaluate 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 we know or can reasonably infer that specific
O3-related health effects are occurring. We refer to
exposures at and above these benchmark concentrations as ``exposures of
concern.''
---------------------------------------------------------------------------
\33\ As discussed above in Section II.A., O3 health
responses observed in human clinical 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.
---------------------------------------------------------------------------
EPA emphasizes 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. 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 human clinical 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, we first considered the exposure
level of 0.080 ppm, at which there is a substantial amount of clinical
evidence demonstrating a range of O3-related health effects
including lung inflammation and airway responsiveness in healthy
individuals. Thus, as in the last 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 epidemiology studies
indicates that people with asthma have larger and more serious effects
than healthy individuals, including lung function, respiratory
symptoms, increased airway
[[Page 37854]]
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 epidemiology 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. EPA has not included 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. 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 has chosen 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 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 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.\34\ 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 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 current
standard.
---------------------------------------------------------------------------
\34\ The full range of quantitative exposure estimates
associated with just meeting the current and alternative
O3 standards are presented in chapter 4 and Appendix 4A
of the 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 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 1 or more exposures of concern decline
from simulations of just meeting the current 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 current 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.
[[Page 37855]]
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 Data\1, 2\
----------------------------------------------------------------------------------------------------------------
All children, ages 5-18 aggregate for Asthmatic children, ages 5-18
8-Hour air 12 urban areas, number of children Aggregate for 12 urban areas, number
Benchmark levels of quality exposed (% of all) [%reduction from of children exposed (% of group) [%
exposures of standards\3\ current standard] reduction from current standard]
concern (ppm) (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%) 100,000 (1%) 330,000 (13%) 10,000 (0%) [75%]
[35%]. [62%]. [36%].
0.074 770,000 (4%) [77%] 20,000 (0%) [92%] 120,000 (5%) 0 (0%) [100%]
[77%].
0.070 270,000 (1%) [92%] 0 (0%) [100%].... 50,000 (2%) [90%] 0 (0%) [100%]
0.064 30,000 (0.2%) 0 (0%) [100%].... 10,000 (0.2%) 0 (0%) [100%]
[99%]. [98% ].
----------------------------------------------------------------------------------------------------------------
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%) 1,050,000 (6%) 1,020,000 (40%) 150,000 (6%)
[16%]. [42%]. [16%]. [44%]
0.074 4,550,000 (25%) 350,000 (2%) 700,000 (27%) 50,000 (2%) [81%]
[43%]. [80%]. [42%].
0.070 3,000,000 (16%) 110,000 (1%) 460,000 (18%) 10,000 (1%) [96%]
[62%]. [94%]. [62%].
0.064 950,000 (5%) [88%] 10,000 (0%) [99%] 150,000 (6%) 0 (0%) [100%]
[88%].
----------------------------------------------------------------------------------------------------------------
\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 current 8-hour standard 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 Staff Paper (section 4.5.8), recent O3 air quality
distributions have been statistically adjusted to simulate just meeting the current 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 the current
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 the current 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, 2007, Exhibit 2, p. 4-48). 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, 2007, Exhibit 8,
p. 4-60).
(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.
(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.\35\ As part of the last 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.\36\ The risk assessment for the last 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.
---------------------------------------------------------------------------
\35\ 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).
\36\ 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, Philadephia, St. Louis,
and Washington, DC.
---------------------------------------------------------------------------
a. Overview
The updated health risk assessment conducted as part of this review
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
[[Page 37856]]
risks associated with just meeting the current 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 the Staff Paper (EPA, 2007, chapter 5) and in a technical
support document (TSD), Ozone Health Risk Assessment for Selected Urban
Areas (Abt Associates, 2006, 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.\37\ 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.
---------------------------------------------------------------------------
\37\ The general approach used in the current risk assessment
was described in the draft Health Assessment Plan (EPA, 2005a) 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
current 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 Criteria Document and 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 the current 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 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.
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 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 the current
and selected 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, 2007, p. 6-20). With respect to
uncertainties about estimated background concentrations, as discussed
below and in the Staff Paper (EPA 2007b, section 5.4.3), alternative
assumptions about background levels have a variable impact depending on
the location, standard, and health endpoint analyzed.
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, 2007, pp.
6-20--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. EPA recognizes that these credible
intervals do not reflect all of the uncertainties noted above.
[[Page 37857]]
b. Scope and Key Components
The current health risk assessment is based on the information
evaluated in the final Criteria Document. The risk assessment includes
several categories of health effects and estimates risks associated
with just meeting the current 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.\38\ 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 do not meet the current 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.
---------------------------------------------------------------------------
\38\ 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 final Criteria Document and or 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 the
current and 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 current 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 Staff Paper (EPA, 2007, 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.\39\
---------------------------------------------------------------------------
\39\ 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 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).
Recognizing these complexities, EPA requests comments on the new
approach used in this review for estimating these levels as an input to
the health risk assessment.\40\
---------------------------------------------------------------------------
\40\ Recognizing the importance of this issue, EPA intends to
conduct additional sensitivity analyses related to policy-relevant
background and its implications for the risk assessment.
---------------------------------------------------------------------------
In the first part of the current 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 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, 2003, 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
Staff Paper (EPA, 2007, 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
[[Page 37858]]
to sample size in the combined data set that served as the basis for
the assessment. 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 current 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). 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 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 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 current 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.\41\ These 12 urban areas
include approximately 18.3 million school age children, of which 2.6
million are asthmatic school age children.\42\
---------------------------------------------------------------------------
\41\ 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.
\42\ 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 Staff Paper and in the Risk Assessment
TSD (Abt Associates, 2006).
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 Criteria Document and Staff Paper, as well as the
criteria discussed in chapter 5 of the 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 current risk assessment. With
respect to nonaccidental and cardiorespiratory mortality, the 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 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.\43\ 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.
---------------------------------------------------------------------------
\43\ 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 the current or alternative 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
[[Page 37859]]
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 multi-city and single-city
O3 concentration-response functions. While the Risk
Assessment TSD and chapter 5 of the Staff Paper present a more
comprehensive set of risk estimates, EPA has focused on estimates based
on multi-city studies where available. The advantages of relying more
heavily on concentration-response functions based on multi-city 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 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 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 Criteria Document finds that no definitive conclusion can be
reached with regard to the existence of population thresholds in
epidemiological studies (Criteria Document, pp. 8-44). 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 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
current 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 Staff Paper (chapter 5) and Risk Assessment TSD present risk
estimates associated with just meeting the current and several
alternative 8-hour standards, as well as three recent years of air
quality as represented by 2002, 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 has
chosen to include only the 8-hour moderate exertion exposures in the
current risk assessment for this health endpoint. Thus, the risk
estimates presented here and in the 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 current standard and several alternative 8-hour
standard levels with the same form as the current 8-hour standard. 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
[[Page 37860]]
across 5 urban areas \44\ 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 current 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 the current standard based on 2002 air quality data
compared to 230,000 (1.2 percent of children) associated with just
meeting the current standard based on 2004 air quality data.
---------------------------------------------------------------------------
\44\ 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.
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 1 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 \3\ [% reduction from current standard] of group) [% reduction from current
---------------------------------------- standard]
---------------------------------------
2002 2004 2002 2004]
----------------------------------------------------------------------------------------------------------------
0.084 ppm (Current standard).... 610,000 (3.3%).... 230,000 (1.2%).... 130,000 (7.8%).... 70,000 (4.2%).
0.080 ppm....................... 490,000 (2.7%) 180,000 (1.0%) NA \4\............ NA.
[20% reduction]. [22% reduction].
0.074 ppm....................... 340,000 (1.9%) 130,000 (0.7%) 90,000 (5.0%) [31 40,000 (2.7%) [43%
[44% reduction]. [43% reduction]. % reduction]. reduction].
0.070 ppm....................... 260,000 (1.5%) 100,000 (0.5%) NA................ NA.
[57% reduction]. [57% reduction].
0.064 ppm....................... 180,000 (1.0%) 70,000 (0.4%) [70% 50,000 (3.0%) [62% 20,000 (1.5%) [71%
[70% 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 current 8-hour standard 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
stated concentration level. As described in the Staff Paper (section 4.5.8), recent O3 air quality
distributions have been statistically adjusted to simulate just meeting the current 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.
As discussed in the Staff Paper, a child may experience multiple
occurrences of a lung function response during the O3
season. For example, upon meeting the current 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 the current 8-hour 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. 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 current and
alternative 8-hour standards are intermediate to the estimates
presented in Table 2 above in this notice and are presented in the
Staff Paper (chapter 5) and Risk Assessment TSD.
For just meeting the current 8-hour standard, Table 5-8 in the
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 Staff Paper and in the Risk Assessment
TSD.
For just meeting the current 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 attainment of the current 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
[[Page 37861]]
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 the current and
alternative 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 the current
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 the current
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 the current 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 the current 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 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 the current 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 the current 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 the
current 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 the current 8-hour standard to
3.0 cases per 100,000 under the 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. 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 the current standard (based on the 2002
simulation). The patterns for cardiorespiratory mortality are similar.
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 the current standard,
using simulated O3 concentrations that just meet the current
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 the
current 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 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
[[Page 37862]]
estimates upon just meeting the current and potential alternative 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 the current 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 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)\45\ 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 current
standard, was significantly less impacted.
---------------------------------------------------------------------------
\45\ 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. Conclusions on the Adequacy of the Current Primary Standard
1. Background
The initial issue to be addressed in the current review of the
primary O3 standard is whether, in view of the advances in
scientific knowledge and additional information, the existing standard
should be revised. In evaluating whether it is appropriate to retain or
revise the current standard, the Administrator builds upon the last
review and reflects the broader body of evidence and information now
available. The Administrator has taken into account both evidence-based
and quantitative exposure- and risk-based considerations in developing
conclusions on the adequacy of the current primary O3
standard. Evidence-based considerations include the assessment of
evidence from controlled human exposure, animal toxicological, field,
and epidemiological studies for a variety of health endpoints. For
those endpoints based on epidemiological studies, greater weight has
been placed on associations with health endpoints that are causal or
likely causal based on an integrative synthesis of the entire body of
evidence, including not only all available epidemiological evidence but
also evidence from animal toxicological and controlled human exposure
studies. Less weight has been placed on evidence of associations that
were judged to be only suggestive of possible causal relationships.
Consideration of quantitative exposure- and risk-based information
draws from the results of the exposure and risk assessments described
above. More specifically, estimates of the magnitude of O3-
related exposures and risks associated with recent air quality levels,
as well as the exposure and risk reductions likely to be associated
with just meeting the current 8-hour primary O3 NAAQS, have
been considered.
In this review, a series of general questions frames the approach
to reaching a decision on the adequacy of the current standard, such as
the following: (1) To what extent does newly available information
reinforce or call into question evidence of associations of
O3 exposures with effects identified in the last review?;
(2) to what extent has evidence of new effects and/or at-risk
populations become available since the last review?; (3) to what extent
have important uncertainties identified in the last review been reduced
and have new uncertainties emerged?; (4) to what extent does newly
available information reinforce or call into question any of the basic
elements of the current standards?
The question of whether the available evidence supports
consideration of a standard that is more protective than the current
standard includes consideration of: (1) Whether there is evidence that
associations, especially likely causal associations, extend to ambient
O3 concentration levels that are as low as or lower than had
previously been observed, and the important uncertainties associated
with that evidence; (2) the extent to which exposures of concern and
health risks are estimated to occur in areas upon meeting the current
standard and the important uncertainties associated with the estimated
exposures and risks; and (3) the extent to which the O3-
related health effects indicated by the evidence and the exposure and
risk assessments are considered important from a public health
perspective, taking into account the nature and severity of the health
effects, the size of the at-risk populations, and the kind and degree
of the uncertainties associated with these considerations.
The current primary O3 standard is an 8-hour standard,
which was set at a level of 0.08 ppm,\46\ with a form of the annual
fourth-highest daily maximum 8-hour average concentration, averaged
over three years. This standard was chosen to provide protection to the
public, especially children and other at-risk populations, against a
wide range of O3-induced health effects. As an introduction
to this discussion of the adequacy of the current O3
standard, it is useful to summarize the key factors that formed the
basis of the decision in the last review to revise the averaging time,
level, and form of the then current 1-hour standard.
---------------------------------------------------------------------------
\46\ If the standard were to be specified to the nearest
thousandth ppm, the current 0.08 ppm 8-hour standard would be
equivalent to a standard set at 0.084 ppm, reflecting the data
rounding conventions that are part of the definition of the current
8-hour standard.
---------------------------------------------------------------------------
In the last review, the key factor in deciding to revise the
averaging time of the primary standard was evidence from controlled
human exposure studies of healthy young adult subjects exposed for 1 to
8 hours to O3. The best documented health endpoints in these
studies were decrements in indices of lung function, such as forced
expiratory volume in 1 second (FEV1), and respiratory
symptoms, such as cough and chest pain on deep inspiration. For short-
term exposures of 1 to 3 hours, group mean FEV1 decrements were
statistically significant for O3 concentrations only at and
above 0.12 ppm, and only when subjects engaged in very heavy exertion.
By contrast, evidence available in the prior review showed that
prolonged exposures of 6 to 8 hours produced statistically significant
group mean FEV1 decrements at the lowest O3
concentrations evaluated in those studies, 0.080 ppm, even when
experimental subjects were engaged in more realistic intermittent
moderate exertion levels. The health significance of this newer
evidence led to the conclusion in the 1997 final decision that the 8-
hour averaging time is more directly associated with health effects of
concern at lower O3 concentrations than is the 1-hour
averaging time.
[[Page 37863]]
Based on the available evidence of O3-related health
effects, the following factors were of particular importance in the
last review in informing the selection of the level and form of a new
8-hour standard: (1) Quantitative estimates of O3-related
risks to active children, who were judged to be an at-risk subgroup of
concern, in terms of transient and reversible respiratory effects
judged to be adverse, including moderate to large decreases in lung
function and moderate to severe pain on deep inspiration, and the
uncertainty and variability in such estimates; (2) consideration of
both the estimated percentages, total numbers of children, and number
of times they were likely to experience such effects; (3)
epidemiological evidence of associations between ambient O3
and increased respiratory hospital admissions, and quantitative
estimates of percentages and total numbers of asthma-related admissions
in one example urban area that were judged to be indicative of a
pyramid of much larger effects, including respiratory-related hospital
admissions, emergency department visits, doctor visits, and asthma
attacks and related increased medication use; (4) quantitative
estimates of the number of ``exposures of concern\47\'' (defined as
exposures >= 0.080 ppm for 6 to 8 hour) that active children are likely
to experience, and the uncertainty and variability in such estimates;
(5) the judgment that such exposures are an important indicator of
public health impacts of O3-related effects for which
information is too limited to develop quantitative risk estimates,
including increased nonspecific bronchial responsiveness (e.g., related
to 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); (6) the
broader public health perspective of the number of people living in
areas that would breathe cleaner air as a result of the revised
standard; (7) consideration of the relative seriousness of various
health effects and the relative degree of certainty in both the
likelihood that people will experience various health effects and their
medical significance; (8) the relationship of a standard level to
estimated ``background'' levels associated with nonanthropogenic
sources of O3; and (9) CASAC's advice and recommendations.
Additional factors considered in selecting the form of the standard
included balancing the public health implications of the estimated
number of times in an O3 season that the standard level
might be exceeded in an area that is in attainment with the standard
with the year-to-year stability of the air quality statistic, which can
be particularly affected by years with unusual meteorology. A more
stable air quality statistic serves to avoid disruptions to ongoing
control programs that could result from moving into and out of
attainment, thereby interrupting the public health protection afforded
by such control programs.
---------------------------------------------------------------------------
\47\ In the last review, ``exposures of concern'' referred to
exposures at and above 0.08 ppm, 8-hour average, at which a range of
health effects have been observed in controlled human studies, but
for which data were too limited to allow for quantitative risk
assessment. (62 FR 38860, July 18, 1997).
---------------------------------------------------------------------------
In reaching a final decision in the last review, the Administrator
was mindful that O3 exhibits a continuum of effects, such
that there is no discernible threshold above which public health
protection requires that no exposures be allowed or below which all
risks to public health can be avoided. The final decision reflected a
recognition that important uncertainties remained, for example with
regard to interpreting the role of other pollutants co-occurring with
O3 in observed associations, understanding biological
mechanisms of O3-related health effects, and estimating
human exposures and quantitative risks to at-risk populations for these
health effects.
2. Evidence- and Exposure/Risk-Based Considerations in the Staff Paper
The Staff Paper (section 6.3.1) considers the evidence presented in
the Criteria Document as discussed above in section II.A as a basis for
evaluating the adequacy of the current O3 standard,
recognizing that important uncertainties remain. The extensive body of
human clinical, toxicological, and epidemiological evidence serves as
the basis for the judgments about O3-related health effects
discussed above, including judgments about causal relationships with a
range of respiratory morbidity effects, including lung function
decrements, increased respiratory symptoms, airway inflammation,
increased airway responsiveness, and respiratory-related
hospitalizations and emergency department visits in the warm season,
and about the evidence being highly suggestive that O3
directly or indirectly contributes to non-accidental and
cardiopulmonary-related mortality.
These judgments take into account important uncertainties that
remain in interpreting this evidence. For example, with regard to the
utility of time-series epidemiological studies to inform judgments
about a NAAQS for an individual pollutant, such as O3,
within a mix of highly correlated pollutants, such as the mix of
oxidants produced in photochemical reactions in the atmosphere, the
Staff Paper notes that there are limitations especially at ambient
O3 concentrations below levels at which O3-
related effects have been observed in controlled human exposure
studies. The Staff Paper (section 3.4.5) also recognizes that 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 variability in susceptibility to O3-related
effects in populations.
While noting these limitations in the interpretation of the
findings from the epidemiological studies, the Staff Paper (section
3.4.5) concludes that if a population threshold level does exist, it
would likely be well below the level of the current O3
standard and possibly within the range of background levels. As
discussed above in section II.A.3.a, this conclusion is supported by
several epidemiological studies that have explored the question of
potential thresholds directly, either using a statistical curve-fitting
approach to evaluate whether linear or non-linear models fit the data
better using sub-sets of the data, where days over or under a specific
cutpoint (e.g., 0.080 ppm or even lower O3 levels) were
excluded and then evaluating the association for statistical
significance. In addition to direct consideration of the
epidemiological studies, findings from controlled human exposure
studies discussed above in section II.A.2.a.i(a)(i) indicate that
prolonged exposures produced statistically significant group mean
FEV1 decrements and symptoms in healthy adult subjects at
levels down to at least 0.060 ppm, with a small percentage of subjects
experiencing notable effects (e.g., >10 percent FEV1
decrement, pain on deep inspiration). Controlled human exposure studies
evaluated in the last review also found significant responses in
indicators of lung inflammation and cell injury at 0.080 ppm in healthy
adult subjects. The effects in these controlled human exposure studies
were observed in healthy young adult subjects, and it is likely that
more serious responses, and
[[Page 37864]]
responses at lower levels, would occur in people with asthma and other
respiratory diseases. 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. The
observations provide additional support for the conclusion in the Staff
Paper that the associations observed in the epidemiological studies,
particularly for respiratory-related effects and potentially for
cardiovascular effects, extend down to O3 levels well below
the current standard (i.e., 0.084 ppm) (EPA, 2007, p. 6-7).
As discussed above in section II.A and in the Staff Paper (section
3.7), the newly available information reinforces the judgments about
the likelihood of causal relationships between O3 exposure
and respiratory effects observed in the last review and broadens the
evidence of O3-related associations to include additional
respiratory-related endpoints, newly identified cardiovascular-related
health endpoints, and mortality. Newly available evidence also has
shown that people with asthma are likely to experience more serious
effects than people who do not have asthma (section II.A.4.b.ii above).
The Staff Paper also concludes that substantial progress has been made
since the last review in advancing the understanding of potential
mechanisms by which ambient O3, alone and in combination
with other pollutants, is causally linked to a range of respiratory-
related health endpoints, and may be causally linked to a range of
cardiovascular-related health endpoints. Thus, the Staff Paper (section
6.3.6) finds strong support in the evidence developed since the last
review, for consideration of an O3 standard that is at least
as protective as the current standard and finds no support for
consideration of an O3 standard that is less protective than
the current standard. This conclusion is consistent with the advice and
recommendations of CASAC and with the views expressed by all interested
parties who provided comments on drafts of the Staff Paper. While CASAC
and some commenters supported revising the current standard to provide
increased public health protection and other commenters supported
retaining the current standard, no one who provided comments supported
a standard that would be less protective than the current standard.
a. Evidence-Based Considerations
In looking more specifically at the controlled human exposure and
epidemiological evidence (which is summarized in chapter 3 and Appendix
3B of the Staff Paper), the Staff Paper first notes that controlled
human exposure studies provide the clearest and most compelling
evidence for an array of human health effects that are directly
attributable to acute exposures to O3 per se. Evidence from
such human studies, together with animal toxicological studies, help to
provide biological plausibility for health effects observed in
epidemiological studies. In considering the available evidence, the
Staff Paper focuses on studies that examined health effects that have
been demonstrated to be caused by exposure to O3, or for
which the Criteria Document judges associations with O3 to
be causal or likely causal, or for which the evidence is highly
suggestive that O3 contributes to the reported effects. In
considering the epidemiological evidence as a basis for reaching
conclusions about the adequacy of the current standard, the Staff Paper
focuses on studies reporting effects in the warm season, for which the
effect estimates are more consistently positive and statistically
significant than those from all-year studies. The Staff Paper (section
6.3.1.1) considers the extent to which such studies provide evidence of
associations that extend down to ambient O3 concentrations
below the level of the current standard, which would thereby call into
question the adequacy of the current standard. In so doing, the Staff
Paper notes, as discussed above, that if a population threshold level
does exist for an effect observed in such studies, it would likely be
at a level well below the level of the current standard. The Staff
Paper (section 6.3.1.1) also attempts to characterize whether the area
in which a study was conducted likely would or would not have met the
current standard during the time of the study, although it recognizes
that the confidence that would appropriately be placed on the
associations observed in any given study, or on the extent to which the
association would likely extend down to relatively low O3
concentrations, is not dependent on this distinction. Further, the
Staff Paper considered studies that examined subsets of data that
include only days with ambient O3 concentrations below the
level of the current O3 standard, or below even lower
O3 concentrations, and continue to report statistically
significant associations. The Staff Paper (section 6.3.1.1) judges that
such studies are directly relevant to considering the adequacy of the
current standard, particularly in light of reported responses to
O3 at levels below the current standard found in controlled
human exposure studies.
i. Lung Function, Respiratory Symptoms, and Other Respiratory Effects
Health effects for which the Criteria Document continues to find
clear evidence of causal associations with short-term O3
exposures include lung function decrements, respiratory symptoms,
pulmonary inflammation, and increased airway responsiveness. In the
last review, these O3-induced effects were demonstrated with
statistical significance down to the lowest level tested in controlled
human exposure studies at that time (i.e., 0.080 ppm). As discussed in
chapter 3 of the Staff Paper, and in section II.A.2.a.i.(a)(i) above,
two new studies are notable in that they are the only controlled human
exposure studies that examined respiratory effects, including lung
function decrements and respiratory symptoms, in healthy adults at
lower exposure levels than had previously been examined. EPA's
reanalysis of the data from the most recent study shows small group
mean decrements in lung function responses to be statistically
significant at the 0.060 ppm exposure level, while the author's
analysis did not yield statistically significant lung function
responses but did yield some statistically significant respiratory
symptom responses toward the end of the exposure period. Notably, these
studies report a small percentage of subjects experiencing lung
function decrements (>= 10 percent) at the 0.060 ppm exposure level.
These studies provide very limited evidence of O3-related
lung function decrements and respiratory symptoms at this lower
exposure level.
The Staff Paper (section 3.3.1.1.1) notes that evidence from
controlled human exposures studies indicates that people with moderate-
to-severe asthma have somewhat larger decreases in lung function in
response to O3 relative to healthy individuals and that lung
function responses in people with asthma appear to be affected by
baseline lung function (i.e., magnitude of responses increases with
increasing disease severity). As discussed in the Criteria Document
(p.8-80), this newer information expands our understanding of the
physiological basis for increased sensitivity in people with asthma and
other airway diseases, recognizing that
[[Page 37865]]
people with asthma present a different response profile for cellular,
molecular, and biochemical responses than people who do not have
asthma. New evidence indicates that some people with asthma have
increased occurrence and duration of nonspecific airway responsiveness,
which is an increased bronchoconstrictive response to airway irritants.
Controlled human exposure studies also indicate that some people with
allergic asthma and rhinitis have increased airway responsiveness to
allergens following O3 exposure. Exposures to O3
exacerbated lung function decrements in people with pre-existing
allergic airway disease, with and without asthma. 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.
The Staff Paper (p.6-10) also concludes that newly available human
exposure studies suggest that some people with asthma also have
increased inflammatory responses, relative to non-asthmatic subjects,
and that this inflammation may take longer to resolve. 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
qualitatively informs the Staff Paper's (pp.6-10 to 6-11) evaluation of
the adequacy of the current O3 standard in that it indicates
that human clinical 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 Staff Paper (p.6-11) notes that in addition to the experimental
evidence of lung function decrements, respiratory symptoms, and other
respiratory effects in healthy and asthmatic populations discussed
above, epidemiological studies have reported associations of lung
function decrements and respiratory symptoms in several locations
(Appendix 3B; also Figure 3-4 for respiratory symptoms). As discussed
in the Staff Paper (section 3.3.1.1.1) and above, two large U.S. panel
studies which together followed over 1000 asthmatic children on a daily
basis (Mortimer et al., 2002, the National Cooperative Inner-City
Asthma Study, or NCICAS; and Gent et al., 2003), as well as several
smaller U.S. and international studies, have reported 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. Overall, the
multi-city NCICAS (2002), Gent et al. (2003), and several other single-
city studies indicate a robust positive association between ambient
O3 concentrations and increased respiratory symptoms and
increased medication use in asthmatics.
In considering the large number of single-city epidemiological
studies reporting lung function or respiratory symptoms in healthy or
asthmatic populations (Staff Paper, Appendix 3B), the Staff Paper (p.6-
11) notes that most such studies that reported positive and often
statistically significant associations in the warm season were
conducted in areas that likely would not have met the current standard.
In considering the large multi-city NCICAS (Mortimer et al., 2002), the
Staff Paper notes that the 98th percentile 8-hour daily maximum
O3 concentrations at the monitor reporting the highest
O3 concentrations in each of the study areas ranged from
0.084 ppm to >0.10 ppm. However, the authors indicate that less than 5
percent of the days in the eight urban areas had 8-hour daily
O3 concentrations exceeding 0.080 ppm. Moreover, the authors
observed that when days with 8-hour average O3 levels
greater than 0.080 ppm were excluded, similar effect estimates were
seen compared to estimates which included all of the days. There are
also a few other studies in which the relevant air quality statistics
provide some indication that lung function and respiratory symptom
effects may be occurring in areas that likely would have met the
current standard (EPA, 2007, p.6-12).
ii. Respiratory Hospital Admissions and Emergency Department Visits
At the time of the last review, many time-series studies indicated
positive associations between ambient O3 and increased
respiratory hospital admissions and emergency room visits, providing
strong evidence for a relationship between O3 exposure and
increased exacerbations of preexisting lung disease at O3
levels below the level of the then current 1-hour standard (EPA 2007,
section 3.3.1.1.6). Analyses of data from studies conducted in the
northeastern U.S. indicated that O3 air pollution was
consistently and strongly associated with summertime respiratory
hospital admissions.
Since the last review, new epidemiological studies have evaluated
the association between short-term exposures to O3 and
unscheduled hospital admissions for respiratory causes. Large multi-
city studies, as well as many studies from individual cities, have
reported positive and often statistically significant O3
associations with total respiratory hospitalizations as well as asthma-
and COPD-related hospitalizations, especially in studies analyzing the
O3 effect during the summer or warm season. Analyses using
multipollutant regression models generally indicate that copollutants
do not confound the association between O3 and respiratory
hospitalizations and that the O3 effect estimates were
robust to PM adjustment in all-year and warm-season only data. The
Criteria Document (p.8-77) concludes that the evidence supports a
causal relationship between acute O3 exposures and increased
respiratory-related hospitalizations during the warm season.
In looking specifically at U.S. and Canadian respiratory
hospitalization studies that reported positive and often statistically
significant associations (and that either did not use GAM or were
reanalyzed to address GAM-related problems), the Staff Paper (p.6-12)
notes that many such studies were conducted in areas that likely would
not have met the current O3 standard, with many providing
only all-year effect estimates, and with some reporting a statistically
significant association in the warm season. Of the studies that provide
some indication that O3-related respiratory hospitalizations
may be occurring in areas that likely would have met the current
standard, the Staff Paper notes that some are all-year studies, whereas
others reported statistically significant warm-season associations.
Emergency department visits for respiratory causes have been the
focus of a number of new studies that have examined visits related to
asthma, COPD, bronchitis, pneumonia, and other upper and lower
respiratory infections, such as influenza, with asthma visits typically
dominating the daily incidence counts. Among studies with adequate
controls for seasonal patterns, many reported at least one significant
positive association involving O3. However, inconsistencies
were observed which were at least partially attributable to differences
in model specifications and analysis approach among various studies. 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. Almost all of the studies that reported
[[Page 37866]]
statistically significant effect estimates were conducted in areas that
likely would not have met the current standard. The Criteria Document
(section 7.3.2) concluded that analyses stratified by season generally
supported a positive association between O3 concentrations
and emergency department visits for asthma in the warm season. These
studies provide evidence of effects in areas that likely would not have
met the current standard and evidence of associations that likely
extend down to relatively low ambient O3 concentrations.
iii. Mortality
The 1996 Criteria Document concluded that an association between
daily mortality and O3 concentrations 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, and thus the possibility that O3 exposure may
be associated with mortality was not relied upon in the 1997 decision
on the O3 primary standard.
Since the last review, as described above, the body of evidence
with regard to O3-related health effects has been expanded
by animal, human clinical, and epidemiological studies and now includes
biologically plausible mechanisms by which O3 may affect the
cardiovascular system. In addition, there is stronger information
linking O3 to serious morbidity outcomes, such as
hospitalization, that are associated with increased mortality. Thus,
there is now a coherent body of evidence that describes a range of
health outcomes from lung function decrements to hospitalization and
premature mortality.
Newly available large multi-city studies (Bell et al., 2004; Huang
et al.,2005; and Schwartz 2005) designed specifically to examine the
effect of O3 and other pollutants on mortality have provided
much more robust and credible information. Together these studies have
reported significant associations between O3 and mortality
that were robust to adjustment for PM and different adjustment methods
for temperature and suggest that the effect of O3 on
mortality is immediate but also persists for several days. One recent
multi-city study (Bell et al., 2006) examined the shape of the
concentration-response function for the O3-mortality
relationship in 98 U.S. urban communities for the period 1987 to 2000
specifically to evaluate whether a ``safe'' threshold level exists.
Results from various analytic methods all indicated that any threshold,
if it exists, would likely occur at very low concentrations, far below
the level of the current O3 NAAQS and nearing background
levels.
New data are also available from several single-city studies
conducted world-wide, as well as from several meta-analyses that have
combined information from multiple studies. Three recent meta-analyses
evaluated potential sources of heterogeneity in O3-mortality
associations. All three analyses reported common findings, including
effect estimates that were statistically significant and larger in warm
season analyses. Reanalysis of results using default GAM criteria did
not change the effect estimates, and there was no strong evidence of
confounding by PM. The Criteria Document (p.7-175) finds that the
majority of these studies suggest that there is an elevated risk of
total nonaccidental mortality associated with acute exposure to
O3, especially in the summer or warm season when
O3 levels are typically high, with somewhat larger effect
estimate sizes for associations with cardiovascular mortality.
Overall, the Criteria Document (p.8-78) finds that the results from
U.S. multi-city time-series studies, along with the meta-analyses,
provide relatively strong evidence for associations between short-term
O3 exposure and all-cause mortality even after adjustment
for the influence of season and PM. The results of these analyses
indicate that copollutants generally do not appear to substantially
confound the association between O3 and mortality. In
addition, several single-city studies observed positive associations of
ambient O3 concentrations with total nonaccidental and
cardiopulmonary mortality.
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; effect estimates for respiratory
mortality are less consistent in size, possibly due to reduced
statistical power in this subcategory of mortality. For cardiovascular
mortality, the Criteria Document (p.7-106) suggests that effect
estimates are consistently positive and more likely to be larger and
statistically significant in warm season analyses. The Criteria
Document (p.8-78) concludes that these findings are highly suggestive
that short-term O3 exposure directly or indirectly
contributes to nonaccidental and cardiopulmonary-related mortality, but
additional research is needed to more fully establish underlying
mechanisms by which such effects occur.
b. Exposure- and Risk-Based Considerations
As discussed above in section II.B, the Staff Paper also estimated
quantitative exposures and health risks associated with recent air
quality levels and with air quality that meets the current standard to
help inform judgments about whether or not the current standard
provides adequate protection of public health. In so doing, it
presented the important uncertainties and limitations associated with
the exposure and risk assessments (discussed above in section II.B and
more fully in chapters 4 and 5 of the Staff Paper).
The 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
Staff Paper 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 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 recent air quality or air quality that just meets the
current 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.
As described above in section II.B, the Staff Paper estimated
exposures and risks for the three most recent years (2002-2004) for
which data were available at the time of the analyses. Within this 3-
year period, 2002 was a year with relatively higher O3
levels in most, but not all, areas and simulation of just meeting the
current standard based on 2002 air quality data provides a generally
more upper-end estimate of exposures and risks, while 2004 was a year
with relatively lower O3 levels in
[[Page 37867]]
most, but not all, areas and simulation of just meeting the current
standard using 2004 air quality data provides a generally more lower-
end estimate of exposures and risks.
i. Exposure Assessment Results
As discussed above in section II.B.1, the Staff Paper estimates
personal exposures to ambient O3 levels at and above
specific benchmark levels to 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 current air quality
levels, and the extent to which such impacts might be reduced by
meeting the current and alternative standards. As described in greater
detail in section II.B.1.c above, the Staff Paper refers to exposures
at and above these benchmark levels as ``exposures of concern.'' The
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
relevant public health concerns. Therefore, with the concurrence of the
CASAC, the Staff Paper estimated exposures of concern not only at 0.080
ppm O3, a level at which there are demonstrated effects, but
also at 0.070 and 0.060 ppm O3. The Staff Paper recognized
that there will be varying degrees of concern about exposures at each
of these levels, based in part on the population subgroups 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 O3 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 Staff Paper, and the discussion
below, focuses on exposures of concern at or above benchmark levels of
0.070 and 0.060 ppm O3 for purposes of evaluating the
adequacy of the current standard.
The exposure estimates presented in the Staff Paper are for the
number and percent of all school age children and asthmatic school age
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. As
shown in the Table 1 in this notice, the percent of population exposed
at any given level is very similar for all and asthmatic school age
children. Substantial year-to-year variability in exposure estimates is
observed, ranging to over an order of magnitude at the current standard
level, in estimates of the number of children and, as shown in Table 6-
1a and b of the Staff Paper, the number of occurrences of exposures of
concern at both of these benchmark levels. The Staff Paper states that
it is appropriate to consider not just the average estimates across all
years, but also to consider public health impacts in year with
relatively higher O3 levels. The 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 upon meeting
the current standard.
As discussed in the Staff Paper (EPA, 2007b, see section 6.3.1.2),
about 50 percent of asthmatic or all school age children, representing
nearly 1.3 million asthmatic children and about 8.5 million school age
children in the 12 urban areas examined, are estimated to experience
exposures of concern at or above the 0.070 ppm benchmark level (i.e.,
these individuals are estimated to experience 8-hour O3
exposures at or above 0.070 ppm while engaged in moderate or greater
exertion 1 or more times during the O3 season) associated
with 2002 O3 air quality levels. In contrast, about 17
percent of asthmatic and all school age children are estimated to
experience exposures of concern at or above the 0.070 ppm benchmark
level associated with 2004 O3 air quality levels. Just
meeting the current standard results in an aggregate estimate of about
20 percent of asthmatic or 18 percent or all school age children likely
to experience exposures of concern at or above the 0.070 ppm benchmark
level using the 2002 simulation. The exposure estimates for this
benchmark level range up to about 40 percent of asthmatic or all school
age children in the single city with the least degree of protection
from this standard. Just meeting the current standard based on the 2004
simulation, results in an aggregate estimate of about 1 percent of
asthmatic or all school age children experiencing exposures at the 0.07
ppm benchmark level.
At the benchmark level of 0.060 ppm, about 70 percent of all or
asthmatic school age children are estimated to experience exposures of
concern at this benchmark level for the aggregate of the 12 urban areas
associated with 2002 O3 levels. Just meeting the current
standard would result in an aggregate estimate of about 45 percent of
asthmatic or all school age children likely to experience exposures of
concern at or above the 0.060 ppm benchmark level using the 2002
simulation. The exposure estimates for this benchmark level range up to
nearly 70 percent of all or asthmatic school age children in the single
city with the least degree of protection associated with just meeting
the current standard using the 2002 simulation. The Staff Paper
indicates an aggregate estimate of about 10 percent of asthmatic or all
school age children would experience exposures at or above the 0.06 ppm
benchmark level associated with just meeting the current standard using
the 2004 simulation.
ii. Risk Assessment Results
As described in more detail in section II.B.2 above and in chapters
5 and 6 of the Staff Paper, risk estimates have been developed for
several important health endpoints, including: (1) Lung function
decrements (i.e., >=15 percent and >=20 percent reductions in
FEV1) in all school age children for 12 urban areas; (2)
lung function decrements (i.e., >=10 percent and >=20 percent
reductions in FEV1) in asthmatic school age children for 5
urban areas (a subset of the 12 urban areas); (3) respiratory symptoms
(i.e., chest tightness, shortness of breath, wheeze) in moderate to
severe asthmatic children for the Boston area; (4) respiratory-related
hospital admissions for 3 urban areas; and (5) nonaccidental and
cardiorespiratory mortality for 12 urban areas for three recent years
(2002 to 2004) and for just meeting the current standard using a 2002
simulation and a 2004 simulation.
With regard to estimates of moderate lung function decrements, as
shown in Tables 6-2 of the Staff Paper, meeting the current standard
substantially reduces the estimated number of school age children
experiencing one or more occurrences of FEV1 decrements >=15
percent for the 12 urban areas, going from about 1.3 million children
(7 percent of children) under 2002 air quality to about 610,000 (3
percent of children) based on the 2002 simulation, and from about
620,000 children (3 percent of children) to about 230,000 (1 percent of
children) using the 2004 simulation. In asthmatic children, the
estimated number of children experiencing one or more occurrences of
FEV1 decrements >=10 percent for the 5 urban areas goes from
about 250,000 children (16 percent of asthmatic children) under 2002
air quality to about 130,000 (8 percent of asthmatic children) using
the 2002 simulation, and from about 160,000 (10 percent of asthmatic
children) to about 70,000 (4 percent of asthmatic children) using the
2004 simulation. Thus, even when the
[[Page 37868]]
current standard is met, about 4 to 8 percent of asthmatic school age
children are estimated to experience one or more occurrences of
moderate lung function decrements, resulting in about 1 million
occurrences (using the 2002 simulation) and nearly 700,000 occurrence
(using the 2004 simulation) in just 5 urban areas. Moreover, the
estimated number of occurrences of moderate or greater lung function
decrements per child is on average approximately 6 to 7 in all children
and 8 to 10 in asthmatic children in an O3 season, even when
the current standard is met, depending on the year used to simulate
meeting the current standard. In the 1997 review of the O3
standard a general consensus view of the adversity of such moderate
responses emerged as the frequency of occurrences increases, with the
judgment that repeated occurrences of moderate responses, even in
otherwise healthy individuals, may be considered adverse since they may
well set the stage for more serious illness.
With regard to estimates of large lung function decrements, the
Staff Paper notes that FEV1 decrements 20 percent
would likely interfere with normal activities in many healthy
individuals, therefore single occurrences would be considered to be
adverse. In people with asthma, large lung function responses would
likely interfere with normal activities for most individuals and would
also increase the likelihood that these individuals would use
additional medication or seek medical treatment. Not only would single
occurrences be considered to be adverse to asthmatic individuals under
the ATS definition, but they also would be cause for medical concern.
While the current standard reduces the occurrences of large lung
function decrements in all children and asthmatic children from about
60 to 70%, in a year with relatively higher O3 levels
(2002), there are estimated to be about 500,000 occurrences in all
school children across the entire 12 urban areas, and about 40,000
occurrences in asthmatic children across just 5 urban areas. As noted
above, it is clear that even when the current standard is met over a
three-year period, O3 levels in each year can vary
considerably, as evidenced by relatively large differences between risk
estimates based on 2002 to 2004 air quality. The Staff Paper expressed
the view that it was appropriate to consider this yearly variation in
O3 levels allowed by the current standard in judging the
extent to which impacts on members of at-risk groups in a year with
relatively higher O3 levels remains of concern from a public
health perspective.
With regard to other O3-related health effects, as shown
in Tables 6-4 through 6-6 of the Staff Paper, the estimated risks of
respiratory symptom days in moderate to severe asthmatic children,
respiratory-related hospital admissions, and non-accidental and
cardiorespiratory mortality, respectively, are not reduced to as great
an extent by meeting the current standard as are lung function
decrements. For example, just meeting the current standard reduces the
estimated average incidence of chest tightness in moderate to severe
asthmatic children living in the Boston urban area by 11 to 15%, based
on 2002 and 2004 simulations, respectively, resulting in an estimated
incidence of about 23,000 to 31,000 per 100,000 children attributable
to O3 exposure (Table 6-4). Just meeting the current
standard is estimated to reduce the incidence of respiratory-related
hospital admissions in the New York City urban area by about 16 to 18%,
based on 2002 and 2004 simulations, respectively, resulting in an
estimated incidence per 100,000 population of 4.6 to 6.4, respectively
(Table 6-5). Across the 12 urban areas, the estimates of non-accidental
mortality incidence per 100,000 relevant population range from 0.4 to
2.6 (for 2002) and 0.5 to 1.5 (for 2004) (Table 6-6). Meeting the
current standard results in a reduction of the estimated incidence per
100,000 population to a range of 0.3 to 2.4 based on the 2002
simulation and a range of 0.3 to 1.2 based on the 2004 simulation.
Estimates for cardiorespiratory mortality show similar patterns.
In considering the estimates of the proportion of population
affected and the number of occurrences of the health effects that are
included in the risk assessment, the Staff Paper notes that these
limited estimates are indicative of a much broader array of
O3-related health endpoints 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, emergency department visits) and which primarily affect
members of at-risk groups. While the Staff Paper had sufficient
information to estimate and consider the number of symptom days in
children with moderate to severe asthma, it recognized that there are
many other effects that may be associated with symptom days, such as
increased medication use, school and work absences, or visits to
doctors' offices, for which there was not sufficient information to
estimate risks but which are important to consider in assessing the
adequacy of the current standard. The same is true for more serious,
but less frequent effects. The Staff Paper estimated hospital
admissions, but there was not sufficient information to estimate
emergency department visits in a quantitative risk assessment.
Consideration of such unquantified risks in the Staff Paper reinforces
the Staff Paper conclusion that consideration should be given to
revising the standard so as to provide increased public health
protection, especially for at-risk groups such as people with asthma or
other lung diseases, as well as children and older adults, particularly
those active outdoors, and outdoor workers.
c. Summary
Based on the available information and taking into account the
views of CASAC and public comments, the Staff Paper initially notes
that all parties commenting on the NAAQS review agree that the standard
should be at least as protective as the current standard, as no party
suggested it should be revised to provide less protection. The Staff
Paper concludes that the overall body of evidence clearly calls into
question the adequacy of the current standard in protecting at-risk
groups, notably including asthmatic children and other people with lung
disease, as well as all children and older adults, especially those
active outdoors, and outdoor workers,\48\ against an array of adverse
health effects that range from decreased lung function to serious
indicators of respiratory morbidity including emergency department
visits and hospital admissions for respiratory causes, nonaccidental
mortality, and possibly cardiovascular effects. The available
information provides strong support for consideration of an
O3 standard that would provide increased health protection
for these at-risk groups. The Staff Paper also concludes that risks
projected to remain upon meeting the current standard, based on the
exposure and risk estimates discussed above and in more detail in the
Staff Paper, are indicative of risks to at-risk groups that can be
judged to be important from a public health perspective, which
reinforces the Staff Paper conclusion that consideration should be
given to revising the level of the standard so as to provide increased
[[Page 37869]]
public health protection (EPA, 2007, section 6.3.6).
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\48\ In defining at-risk groups this way we are including both
groups with greater inherent sensitivity and those more likely to be
exposed.
---------------------------------------------------------------------------
3. CASAC Views
In its letter to the Administrator, the CASAC O3 Panel,
with full endorsement of the chartered CASAC, unanimously concluded
that there is ``no scientific justification for retaining'' the current
primary O3 standard, and the current standard ``needs to be
substantially reduced to protect human health, particularly in
sensitive subpopulations'' (Henderson, 2006c, pp. 1-2). In its
rationale for this conclusion, the CASAC Panel concluded that ``new
evidence supports and build-upon key, health-related conclusions drawn
in the 1997 Ozone NAAQS review'' (id., p. 3). The Panel points to
studies discussed in chapter 3 and Appendix 3B of the Staff Paper in
noting that several new single-city studies and large multi-city
studies have provided more evidence for adverse health effects at
concentrations lower than the current standard, and that these
epidemiological studies are backed-up by evidence from controlled human
exposure studies. The Panel specifically noted evidence from the recent
Adams (2006) study that reported statistically significant decrements
in the lung function of healthy, moderately exercising adults at a
0.080 ppm exposure level, and importantly, also reported adverse lung
function effects in some healthy individuals at 0.060 ppm. The Panel
concluded that these results indicate that the current standard ``is
not sufficiently health-protective with an adequate margin of safety,''
noting that that while similar studies in sensitive groups such as
asthmatics have yet to be conducted, ``people with asthma, and
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 volunteers (Mortimer et al.,
2002)'' (Henderson, 2006c, p. 4).
The CASAC Panel also highlighted a number of O3-related
adverse health effects, that are associated with exposure to ambient
O3, below the level of the current standard, based on a
broad range of epidemiological studies (Henderson, 2006c). These
adverse health effects include increases in school absenteeism,
respiratory hospital emergency department visits among asthmatics and
patients with other respiratory diseases, hospitalizations for
respiratory illnesses, symptoms associated with adverse health effects
(including chest tightness and medication usage), and premature
mortality (nonaccidental, cardiorespiratory deaths) reported at
exposure levels well below the current standard. ``The CASAC considers
each of these findings to be an important indicator of adverse health
effects'' (Henderson, 2006c).
The CASAC Panel expressed the view that more emphasis should be
placed on the subjects in controlled human exposure studies with
FEV1 decrements greater than 10 percent, which can be
clinically significant, rather than on the relatively small average
decrements. The Panel also emphasized significant O3-related
inflammatory responses and markers of injury to the epithelial lining
of the lung that are independent of spirometric responses. Further, the
Panel expressed the view that the Staff Paper did not place enough
emphasis on serious morbidity (e.g., hospital admissions) and mortality
observed in epidemiology studies. On the basis of the large amount of
recent data evaluating adverse health effects at levels at and below
the current O3 standard, it was the unanimous opinion of the
CASAC Panel that the current primary O3 standard is not
adequate to protect human health, that the relevant scientific data do
not support consideration of retaining the current standard, and that
the current standard needs to be substantially reduced to be protective
of human health, particularly in sensitive subpopulations (Henderson,
2006c, pp. 4-5).
Further, the CASAC letter noted that ``there is no longer
significant scientific uncertainty regarding the CASAC's conclusion
that the current 8-hour primary NAAQS must be lowered'' (Henderson,
2006c, p. 5). The Panel noted that a ``large body of data clearly
demonstrates adverse human health effects at the current level'' of the
standard, such that ``[R]etaining this standard would continue to put
large numbers of individuals at risk for respiratory effects and/or
significant impact on quality of life including asthma exacerbations,
emergency room visits, hospital admissions and mortality'' (Henderson,
2006c). The Panel also noted that ``scientific uncertainty does exist
with regard to the lower level of O3 exposure that would be
fully protective of human health,'' concluding that ``it is possible
that there is no threshold for an O3-induced impact on human
health and that some adverse events may occur at policy-relevant
background'' (Henderson, 2006c, p.5).
4. Administrator's Proposed Conclusions Concerning Adequacy of Current
Standard
Based on the large body of evidence concerning the public health
impacts of O3 pollution, including significant new evidence
concerning effects at O3 concentrations below the level of
the current standard, the Administrator proposes that the current
standard does not protect public health with an adequate margin of
safety and should be revised to provide additional public health
protection. In considering whether the primary standard should be
revised, the Administrator has carefully considered the conclusions
contained in the Criteria Document, the rationale and recommendations
contained in the Staff Paper, the advice and recommendations from the
CASAC, and public comments to date. The Administrator notes that
evidence of a range of respiratory-related morbidity effects seen in
the last review has been considerably strengthened, both through
toxicological and controlled human exposure studies as well as through
many new panel and epidemiological studies.
In addition, new evidence from controlled human exposure and
epidemiological studies identifies people with asthma as an important
susceptible population for which estimates of respiratory effects in
the general population likely underestimate the magnitude or importance
of these effects. New evidence about mechanisms of toxicity more
completely explains the biological plausibility of O3-
induced respiratory effects and is beginning to suggest mechanisms that
may link O3 exposure to cardiovascular effects. Further,
there is now relatively strong evidence for associations between
O3 and total nonaccidental and cardiopulmonary mortality,
even after adjustment for the influence of season and PM. Relative to
the information that was available to inform the Agency's 1997 decision
to set the current standard, the newly available evidence increases the
Administrator's confidence that respiratory morbidity effects such as
lung function decrements and respiratory symptoms are causally related
to O3 exposures, that indicators of respiratory morbidity
such as emergency department visits and hospital admissions are
causally related to O3 exposures, and that the evidence is
highly suggestive that O3 exposures during the O3
season contribute to premature mortality.
The Administrator judges that there is important new evidence
demonstrating that exposures to O3 at levels below the level
of the current standard are associated with a broad array of adverse
health effects, especially in at-risk populations. These at-risk
populations include people with asthma or other lung diseases who are
likely to experience more serious effects from
[[Page 37870]]
exposure to O3. As discussed in section II.A.4 above, these
groups also include children and older adults with increased
susceptibility, as well as those who are likely to be vulnerable as a
result of spending a lot of time outdoors engaged in physical activity,
especially active children and outdoor workers.
Examples of this important new evidence include demonstration of
O3-induced lung function effects and respiratory symptoms in
some healthy individuals down to the previously observed exposure level
of 0.080 ppm, as well as very limited new evidence at exposure levels
well below the level of the current standard. In addition, there is now
epidemiological evidence of statistically significant O3-
related associations with lung function and respiratory symptom
effects, respiratory-related emergency department visits and hospital
admissions, and increased mortality, in areas that likely would have
met the current standard. There are also many epidemiological studies
done in areas that likely would not have met the current standard but
which nonetheless report statistically significant associations that
generally extend down to ambient O3 concentrations that are
below the level of the current standard. Further, there are a few
studies that have examined subsets of data that include only days with
ambient O3 concentrations below the level of the current
standard, or below even much lower O3 concentrations, and
continue to report statistically significant associations with
respiratory morbidity outcomes and mortality. The Administrator
recognizes that the evidence from controlled human exposure studies,
together with animal toxicological studies, provides considerable
support for the biological plausibility of the respiratory morbidity
associations observed in the epidemiological studies and for concluding
that the associations extend below the level of the current standard.
Based on the strength of the currently available evidence of
adverse health effects, and on the extent to which the evidence
indicates that such effects result from exposures to ambient
O3 concentrations below the level of the current standard,
the Administrator judges that the current standard does not protect
public health with an adequate margin of safety and that the standard
should be revised to provide such protection, especially for at-risk
groups, against a broad array of adverse health effects.
In reaching this judgment, the Administrator has also considered
the results of both the exposure and risk assessments conducted for
this review, to provide some perspective on the extent to which at-risk
groups would likely experience ``exposures of concern'' \49\ and on the
potential magnitude of the risk of experiencing various adverse health
effects when recent air quality data (from 2002 to 2004) are used to
simulate meeting the current standard and alternative standards in a
number of urban areas in the U.S.\50\ In considering the exposure
assessment results, the Administrator is relying on analyses that
define exposures of concern by three benchmark exposure levels: 0.080,
0.070, and 0.060 ppm. Estimates of exposures of concern in at-risk
groups at and above these benchmark levels, using O3 air
quality data in 2002 and 2004, provide some indication of the potential
magnitude of the incidence of health outcomes that cannot currently be
evaluated in a quantitative risk assessment, such as increased airway
responsiveness, increased pulmonary inflammation, including increased
cellular permeability, and decreased pulmonary defense mechanisms.
These physiological effects have been demonstrated to occur in healthy
people at O3 exposures as low as 0.080 ppm, the lowest level
tested. They are associated with aggravation of asthma, increased
medication use, increased school and work absences, increased
susceptibility to respiratory infection, increased visits to doctors'
offices and emergency departments, increased admissions to hospitals,
and possibly to cardiovascular system effects and chronic effects such
as chronic bronchitis or long-term damage to the lungs that can lead to
reduced quality of life.
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\49\ As discussed in section II.B.1.c above, ``exposures of
concern'' are estimates of 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 with
varying degrees of certainty be inferred to occur in some
individuals. Estimates of exposures of concern provide some
perspective on the public health impacts of health effects that may
occur in some individuals at recent air quality levels but cannot be
evaluated in quantitative risk assessments, and the extent to which
such impacts might be reduced by meeting the current and alternative
standards.
\50\ As described in the Staff Paper (section 4.5.8) and
discussed above, recent O3 air quality distributions have
been statistically adjusted to simulate just meeting the current and
selected alternative standards. These simulations do not represent
predictions of when, whether, or how areas might meet the specified
standards.
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In considering these various benchmark levels for exposures of
concern, the Administrator has focused primarily on estimated exposures
at and above the 0.070 ppm benchmark level as an important surrogate
measure for potentially more serious health effects in at-risk groups
such as people with asthma. This judgment is based on the strong
evidence of effects in healthy people at the 0.080 ppm exposure level
and the new evidence that people with asthma are likely to experience
larger and more serious effects than healthy people at the same level
of exposure. In the Administrator's view, this evidence does not
support a focus on exposures at and above the benchmark level of 0.080
ppm O3, as it would not adequately account for the increased
risk of harm from exposure for members of at-risk groups, especially
people with asthma. The Administrator also judges that the evidence of
demonstrated effects is too limited to support a primary focus on
exposures down to the lowest benchmark level considered of 0.060 ppm.
The Administrator particularly notes that although the analysis of
``exposures of concern'' was conducted to estimate exposures at and
above three discrete benchmark levels (0.080, 0.070, and 0.060 ppm),
the concept is appropriately viewed as a continuum. As discussed at the
outset in section II.A above, the Administrator strives to balance
concern 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 exposure levels.
The Administrator observes that based on the aggregate exposure
estimates for the 2002 simulation summarized above in Table 1 (section
II.B.1) and in the Staff Paper (EPA, 2007b, Table 6-7) for the 12 U.S.
urban areas included in the exposure analysis, upon just meeting the
current standard up to about 20 percent of asthmatic or all school age
children are likely to experience one or more exposures of concern at
and above the 0.070 ppm benchmark level; the 2004 simulation yielded an
estimate of about 1 percent of such children. The Administrator notes
from this comparison that there is substantial year-to-year
variability, ranging up to an order of magnitude or more in estimates
of the number of people and the number of occurrences of exposures of
concern at and above this benchmark level. Moreover, within any given
year, the exposure assessment indicates that there is substantial city-
to-city variability in the estimates of the children exposed or the
number of occurrences of exposure at and above this benchmark level.
For example, city-specific estimates of the percent of asthmatic or all
school age children likely to experience exposures at and above the
benchmark level of 0.070 ppm
[[Page 37871]]
ranges from about 1 percent up to about 40 percent across the 12 urban
areas upon just meeting the current standard based on the 2002
simulation; the 2004 simulation yielded estimates that range from about
0 up to about 7 percent. The Administrator judges it is important to
recognize the substantial year-to-year and city-to-city variability in
considering these estimates.
With regard to the results of the risk assessment, as discussed
above, the Administrator recognizes that a simulation of just meeting
the current standard in the cities included in the assessment indicate
that the estimated risk is lower for all of the health endpoints
evaluated. In considering the adequacy of the current standard, the
Administrator has focused on the risks estimated to remain upon just
meeting the current standard. Based on the aggregate risk estimates
summarized above in Table 2 (section II.B.2 of this notice), the
Administrator observes that upon just meeting the current standard
based on the 2002 simulation, approximately 8 percent of asthmatic
school age children across 5 urban areas (ranging up to about 11
percent in the city that receives relatively less protection) and
approximately 3 percent of all school age children across 12 urban
areas (ranging up to over 5 percent in the city that receives
relatively less protection) would still be estimated to experience
moderate or greater lung function decrements one or more times within
an O3 season. The Administrator recognizes that, as with the
estimates of exposures of concern, there is substantial year-to-year
and city-to-city variability in these risk estimates.
In addition to the percentage of asthmatic or all children
estimated to experience 1 or more occurrences of an effect, the
Administrator recognizes that some individuals are estimated to have
multiple occurrences. For example, across all the cities in the
assessment, approximately 6 to 7 occurrences of moderate or greater
lung function decrements per child are estimated to occur in all
children and approximately 8 to 10 occurrences are estimated to occur
in asthmatic children in an O3 season, even upon just
meeting the current standard. In the last review, a general consensus
view of the adversity of such responses emerged as the frequency of
occurrences increases, with the judgment that repeated occurrences of
moderate responses, even in otherwise healthy individuals, may be
considered adverse since they may well set the stage for more serious
illness. The Administrator continues to support this view.
Large lung function decrements (i.e., >=20 percent FEV1
decrement) would likely interfere with normal activities in many
healthy individuals, therefore single occurrences would be considered
to be adverse. In people with asthma, large lung function responses
(i.e., >= 20 percent FEV1 decrement), would likely interfere
with normal activities for most individuals and would also increase the
likelihood that these individuals would use additional medication or
seek medical treatment. Not only would single occurrences be considered
to be adverse to asthmatic individuals under the ATS definition, but
they also would be cause for medical concern for some individuals. Upon
just meeting the current standard based on the 2002 simulation, close
to 1 percent of asthmatic and all school age children are estimated to
experience one or more occurrences of large lung function decrements in
the aggregate across 5 and 12 urban areas, respectively, with close to
2 percent of both asthmatic and all school age children estimated to
experience such effects in the city that receives relatively less
protection from this standard. These estimates translate into
approximately 500,000 occurrences of large lung function decrements in
all children across 12 urban areas, and about 40,000 occurrences in
asthmatic children across just 5 urban areas upon just meeting the
current standard based on the 2002 simulation; the 2004 simulation
yielded estimates that translate into approximately 160,000 and 10,000
such occurrences in all children and asthmatic children, respectively.
Upon just meeting the current standard based on the 2002
simulation, the estimate of the O3-related risk of
respiratory symptom days in moderate to severe asthmatic children in
the Boston area is about 8,000 symptom days; the 2004 simulation
yielded an estimate of about 6,000 such symptoms days. These estimates
translate into as many as one symptom day in 6, and one symptom day in
8, respectively, that are attributable to O3 exposure during
the O3 season of the total number of symptom days associated
with all causes of respiratory symptoms in asthmatic children during
those years.
The estimated O3-related risk of respiratory-related
hospital admissions upon just meeting the current standard based on the
2002 simulation is greater than 500 hospital admissions in the New York
City area alone, or about 1.5 percent of the total incidence of
respiratory-related admissions associated with all causes; the 2004
simulation yielded an estimate of approximately 400 such hospital
admissions. For nonaccidental mortality, just meeting the current
standard based on the 2002 simulation results in an estimated incidence
of from 0.3 to 2.4 per 100,000 population; the 2004 simulation resulted
in an estimated incidence of from 0.3 to 1.2 per 100,000 population.
Estimates for cardiorespiratory mortality show similar patterns. (Abt
Associates, 2007, Table 4-26).
The Administrator recognizes that in considering the estimates of
the proportion of population affected and the number of occurrences of
those specific health effects that are included in the risk assessment,
these limited estimates based on 2002 and 2004 simulations are
indicative of a much broader array of O3-related health
endpoints that are part of a ``pyramid of effects'' (discussed above in
section II.A.4.d) that include various indicators of morbidity that
could not be included in the risk assessment (e.g., school absences,
increased medication use, emergency department visits) and which
primarily affect members of at-risk groups. Moreover, the Administrator
notes that the CASAC Panel supported a qualitative consideration of the
much broader array of O3-related health endpoints, and
specifically referred to respiratory emergency department visits in
asthmatics and people with other lung diseases, increased medication
use, and increased respiratory symptoms reported at exposure levels
well below the current standard.
The Administrator believes the exposure and risk estimates
discussed in the Staff Paper and summarized above are important from a
public health perspective and are indicative of potential exposures and
risks to at-risk groups. In reaching this proposed judgment, the
Administrator considered the following factors: (1) The estimates of
numbers of persons exposed at and above the 0.070 ppm benchmark level;
(2) the risk estimates of the proportion of the population and number
of occurrences of various health effects in areas upon just meeting the
current standard; (3) the year-to-year and city-to-city variability in
both the exposure and risk estimates; (4) the uncertainties in these
estimates; and (5) recognition that there is a broader array of
O3-related adverse health outcomes for which risk estimates
could not be quantified (that are part of a broader ``pyramid of
effects'') and that the scope of the assessment was limited to just a
sample of urban areas and to some but not all at-risk populations,
leading to an incomplete estimation of public health impacts associated
with O3 exposures
[[Page 37872]]
across the country. The Administrator also notes that it was the
unanimous conclusion of the CASAC Panel that there is no scientific
justification for retaining the current primary O3 standard,
that the current standard is not sufficiently health-protective with an
adequate margin of safety, and that the standard needs to be
substantially reduced to protect human health, particularly in at-risk
subpopulations.
Based on all of these considerations, the Administrator proposes
that the current O3 standard is not requisite to protect
public health with an adequate margin of safety because it does not
provide sufficient protection and that revision would result in
increased public health protection, especially for members of at-risk
groups.
D. Conclusions on the Elements of the Primary Standard
1. Indicator
In the last review EPA focused on a standard for O3 as
the most appropriate surrogate for ambient photochemical oxidants. In
this review, while the complex atmospheric chemistry in which
O3 plays a key role has been highlighted, no alternative to
O3 has been advanced as being a more appropriate surrogate
for ambient photochemical oxidants.
The Staff Paper (section 2.2.2) notes that it is generally
recognized that control of ambient O3 levels provides the
best means of controlling photochemical oxidants. Among the
photochemical oxidants, the acute exposure chamber, panel, and field
epidemiological human health database provides specific evidence for
O3 at levels commonly reported in the ambient air, in part
because few other photochemical oxidants are routinely measured.
However, recent investigations on copollutant interactions have used
simulated urban photochemical oxidant mixes. These investigations
suggest the need for similar studies to help in understanding the
biological basis for effects observed in epidemiological studies that
are associated with air pollutant mixtures, where O3 is used
as the surrogate for the mix of photochemical oxidants. Meeting the
O3 standard can be expected to provide some degree of
protection against potential health effects that may be independently
associated with other photochemical oxidants but which are not
discernable from currently available studies indexed by O3
alone. Since the precursor emissions that lead to the formation of
O3 generally also lead to the formation of other
photochemical oxidants, measures leading to reductions in population
exposures to O3 can generally be expected to lead to
reductions in population exposures to other photochemical oxidants.
The Staff Paper notes that while the new body of time-series
epidemiological evidence cannot resolve questions about the relative
contribution of other photochemical oxidant species to the range of
morbidity and mortality effects associated with O3 in these
types of studies, control of ambient O3 levels is generally
understood to provide the best means of controlling photochemical
oxidants in general, and thus of protecting against effects that may be
associated with individual species and/or the broader mix of
photochemical oxidants, independent of effects specifically related to
O3.
In its letter to the Administrator, the CASAC O3 Panel
noted that O3 is ``the key indicator of the extent of
oxidative chemistry and serves to integrate multiple pollutants.''
CASAC also stated that ``although O3 itself has direct
effects on human health and ecosystems, it can also be considered as an
indicator of the mixture of photochemical oxidants and of the oxidizing
potency of the atmosphere'' (Henderson, 2006c, p. 9).
Based on the available information, and consistent with the views
of EPA staff and the CASAC, the Administrator proposes to continue to
use O3 as the indicator for a standard that is intended to
address effects associated with exposure to O3, alone or in
combination with related photochemical oxidants. In so doing, the
Administrator recognizes that measures leading to reductions in
population exposures to O3 will also reduce exposures to
other photochemical oxidants.
2. Averaging Time
a. Short-Term and Prolonged (1 to 8 Hours)
The current 8-hour averaging time for the primary O3
NAAQS was set in 1997. At that time, the decision to revise the
averaging time of the primary standard from 1 to 8 hours was supported
by the following key observations and conclusions:
(1) The 1-hour averaging time of the previous NAAQS was originally
selected primarily on the basis of health effects associated with
short-term (i.e., 1- to 3-hour) exposures.
(2) Substantial health effects information was available for the
1997 review that demonstrated associations between a wide range of
health effects (e.g., moderate to large lung function decrements,
moderate to severe symptoms and pulmonary inflammation) and prolonged
(i.e., 6- to 8-hour) exposures below the level of the then current 1-
hour NAAQS.
(3) Results of the quantitative risk analyses showed that
reductions in risks from both short-term and prolonged exposures could
be achieved through a primary standard with an averaging period of
either 1 or 8 hours. Thus establishing both a 1-hour and an 8-hour
standard would not be necessary to reduce risks associated with the
full range of observed health effects.
(4) The 8-hour averaging time is more directly associated with
health effects of concern at lower O3 concentrations than
the 1-hour averaging time. It was thus the consensus of CASAC ``that an
8-hour standard was more appropriate for a human health-based standard
than a 1-hour standard.'' (Wolff, 1995)
(5) An 8-hour averaging results in a significantly more uniformly
protective national standard than the then current 1-hour standard.
(6) An 8-hour averaging time effectively limits both 1- and 8-hour
exposures of concern.
In looking at the new information that is discussed in section
7.6.2 of the current Criteria Document, the Staff Paper noted that
epidemiological studies have used various averaging periods for
O3 concentrations, most commonly 1-hour, 8-hour and 24-hour
averages. As described more specifically in sections 3.3 and 3.4 of the
Staff Paper, in general the results presented from U.S. and Canadian
studies show no consistent difference for various averaging times in
different studies. Because the 8-hour averaging time continues to be
more directly associated with health effects of concern from controlled
human exposure studies at lower concentrations than do shorter
averaging periods, the Staff Paper did not evaluate alternative
averaging times in this review and did not conduct exposure or risk
assessments for standards with averaging times other than 8 hours.
The Staff Paper discusses an analysis of a recent three-year period
of air quality data (2002 to 2004) which was conducted to determine
whether the comparative 1- and 8-hour air quality patterns that were
observed in the last review continue to be observed based on more
recent air quality data. This updated air quality analysis (McCluney,
2007) is very consistent with the analysis done in the last review in
that it indicates that only two urban areas of the U.S. have such
``peaky'' air quality patterns such that the ratio of 1-hour to 8-hour
design values is greater than 1.5. This suggests that, based on recent
air quality data, it is reasonable to again conclude that an 8-hour
average
[[Page 37873]]
standard at or below the current level would generally be expected to
provide protection equal to or greater than the previous 1-hour
standard of 0.12 ppm in almost all urban areas. Thus, the Staff Paper
again concluded that setting a standard with an 8-hour averaging time
can effectively limit both 1- and 8-hour exposures of concern and is
appropriate to provide adequate and more uniform protection of public
health from both short-term and prolonged exposures to O3 in
the ambient air.
In its letter to the Administrator, the CASAC O3 Panel
supported the continued use of an 8-hour averaging time for the primary
O3 standard (Henderson, 2006c, p. 2), as did many
commenters. Some other commenters expressed the view that consideration
should be given to setting or reinstating a 1-hour standard, in
addition to maintaining the use of an 8-hour averaging time, to protect
people in those parts of the country with relatively more ``peaky''
exposure profiles. These commenters point out that when controlled
exposure studies using triangular exposure patterns (with relatively
higher 1-hour peaks) have been compared to constant exposure patterns
with the same aggregate O3 dose (in terms of concentration x
time), ``peaky'' exposure patterns are seen to lead to higher risks.
The California Air Resources Board made particular note of this point,
expressing the view that a 1-hour standard would more closely represent
actual exposures, in that many people spend only 1 to 2 hours a day
outdoors, and that it would be better matched to O3
concentration profiles along the coasts where O3 levels are
typically high for shorter averaging periods than 8 hours.
b. Long-term
During the last review, there was a large animal toxicological
database for consideration that provided clear evidence of associations
between long-term (e.g., from several months to years) exposures and
lung tissue damage, with additional evidence of reduced lung elasticity
and accelerated loss of lung function. However, there was no
corresponding evidence for humans, and the state of the science had not
progressed sufficiently to allow quantitative extrapolation of the
animal study findings to humans. For these reasons, consideration of a
separate long-term primary O3 standard was not judged to be
appropriate at that time, recognizing that the 8-hour standard would
act to limit long-term exposures as well as short-term and prolonged
exposures.
Taking into consideration the currently available evidence on long-
term O3 exposures, discussed above in section II.A.2.a.ii,
the Staff Paper concludes that a health-based standard with a longer-
term averaging time than 8 hours is not warranted at this time. The
Staff Paper notes that, while potentially more serious health effects
have been identified as being associated with longer-term exposure
studies of laboratory animals and in epidemiology studies, there
remains substantial uncertainty regarding how these data could be used
quantitatively to develop a basis for setting a long-term health
standard. Because long-term air quality patterns would be improved in
areas coming into attainment with an 8-hour standard, the potential
risk of health effects associated with long-term exposures would be
reduced in any area meeting an 8-hour standard. Thus, the Staff Paper
did not recommend consideration of a long-term, health-based standard
at this time.
In its final letter to the Administrator, the CASAC O3
Panel offered no views on the long-term exposure evidence, nor did it
suggest that consideration of a primary O3 standard with a
long-term averaging time was appropriate. In fact, the CASAC
O3 Panel agreed with the choice of an 8-hour averaging time
for the primary O3 NAAQS suggested by Agency staff
(Henderson, 2007). Similarly, no commenters expressed support for
considering such a long-term standard.
c. Administrator's Conclusions on Averaging Time
In considering the information discussed above, CASAC views and
public comments, the Administrator concludes that a standard with an 8-
hour averaging time can effectively limit both 1- and 8-hour exposures
of concern and that an 8-hour averaging time is appropriate to provide
adequate and more uniform protection of public health from both short-
term (1- to 3-hour) and prolonged (6- to 8-hour) exposures to
O3 in the ambient air. This conclusion is based on the
observations summarized above, particularly: (1) The fact that the 8-
hour averaging time is more directly associated with health effects of
concern at lower O3 concentrations than are averaging times
of shorter duration and (2) results from quantitative risk analyses
showing that attaining an 8-hour standard reduces the risk of
experiencing health effects associated with both 8-hour and shorter
duration exposures. Furthermore, the Administrator observes that the
CASAC O3 Panel agreed with the choice of averaging time
(Henderson, 2007). Therefore, the Administrator proposes to retain the
8-hour averaging time and is not proposing a separate 1-hour standard.
The Administrator also concludes that a standard with a long-term
averaging time is not warranted at this time.
3. Form
In 1997, the primary O3 NAAQS was changed from a ``1-
expected-exceedance'' form per year over three years \51\ to a
concentration-based statistic, specifically the 3-year average of the
annual fourth-highest daily maximum 8-hour concentrations. The
principal advantage of the concentration-based form is that it is more
directly related to the ambient O3 concentrations that are
associated with the health effects. With a concentration-based form,
days on which higher O3 concentrations occur would weigh
proportionally more than days with lower concentrations, since the
actual concentrations are used in determining whether the standard is
attained. That is, given that there is a continuum of effects
associated with exposures to varying levels of O3, the
extent to which public health is affected by exposure to ambient
O3 is related to the actual magnitude of the O3
concentration, not just whether the concentration is above a specified
level.
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\51\ The 1-expected-exceedance form essentially requires that
the fourth-highest air quality value in 3 years, based on
adjustments for missing data, be less than or equal to the level of
the standard for the standard to be met at an air quality monitoring
site.
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During the 1997 review, consideration was given to a range of
alternative forms, including the second-, third-, fourth- and fifth-
highest daily maximum 8-hour concentrations in an O3 season,
recognizing that the public health risks associated with exposure to a
pollutant without a clear, discernable threshold can be appropriately
addressed through a standard that allows for multiple exceedances to
provide increased stability, but that also significantly limits the
number of days on which the level may be exceeded and the magnitude of
such exceedances. Consideration was given to setting a standard with a
form that would provide a margin of safety against possible, but
uncertain chronic effects, and would also provide greater stability to
ongoing control programs. The fourth-highest daily maximum was selected
because it was decided that the differences in the degree of protection
against potential chronic effects afforded by the alternatives within
the range were not well enough understood to use any such differences
as a basis for
[[Page 37874]]
choosing the most restrictive forms. On the other hand, the relatively
large percentage of sites that would experience O3 peaks
well above 0.080 ppm and the number of days on which the level of the
standard may be exceeded, even when attaining a fifth-highest 0.080 ppm
concentration-based standard, argued against choosing that form.
As an initial matter, the Staff Paper considered whether it is
appropriate to continue to specify the level of the O3
standard to the nearest hundredth (two decimal places) ppm, or whether
the precision with which ambient O3 concentrations are
measured supports specifying the standard level to the thousandth ppm
(i.e., to the part per billion (ppb)). The Staff Paper discusses an
analysis conducted by EPA staff to determine the impact of ambient
O3 measurement error on calculated 8-hour average
O3 design value concentrations, which are compared to the
level of the standard to determine whether the standard is attained
(Cox and Camalier, 2006). The results of this analysis suggest that
instrument measurement error, or possible instrument bias, contribute
very little to the uncertainty in design values. More specifically,
measurement imprecision was determined to contribute less than 1 ppb to
design value uncertainty, and a simulation study indicated that
randomly occurring instrument bias could contribute approximately 1
ppb. EPA staff interpreted this analysis as being supportive of
specifying the level of the standard to the nearest thousandth ppm. If
the current standard were to be specified to this degree of precision,
the current standard would effectively be at a level of 0.084 ppm,
reflecting the data rounding conventions that are part of the
definition of the current 0.080 ppm 8-hour standard. This information
was provided to the CASAC O3 Panel and made available to the
public.
In evaluating alternative forms for the primary standard in
conjunction with specific standard levels, the Staff Paper considered
the adequacy of the public health protection provided by the
combination of the level and form to be the foremost consideration. In
addition, the Staff Paper recognized that it is important to have a
form of the standard that is stable and insulated from the impacts of
extreme meteorological events that are conducive to O3
formation. Such instability can have the effect of reducing public
health protection, because frequent shifting in and out of attainment
due to meteorological conditions can disrupt an area's ongoing
implementation plans and associated control programs. Providing more
stability is one of the reasons that EPA moved to a concentration-based
form in 1997.
The Staff Paper considered two concentration-based forms of the
standard: the nth-highest maximum concentration and a percentile-based
form. A percentile-based statistic is useful for comparing datasets of
varying length because it samples approximately the same place in the
distribution of air quality values, whether the dataset is several
months or several years long. However, a percentile-based form would
allow more days with higher air quality values in locations with longer
O3 seasons relative to places with shorter O3
seasons. An nth-highest maximum concentration form would more
effectively ensure that people who live in areas with different length
O3 seasons receive the same degree of public health
protection. For this reason, the exposure and risk analyses were based
on a form specified in terms of an nth-highest concentration, with n
ranging from 3 to 5.
The results of some of these analyses are shown in the Staff Paper
(Figures 6-1 through 6-4) and specifically discussed in chapter 6.
These figures illustrate the estimated percent change in risk estimates
for the incidence of moderate or greater decrements in lung function
(>=15 percent FEV1) in all school age children and moderate
or greater lung function decrements (>=10 percent FEV1) in
asthmatic school age children, associated with going from meeting the
current standard to meeting alternative standards with alternative
forms based on the 2002 and 2004 simulations. Figures 6-5 and 6-6
illustrate the estimated percent of change in the estimated incidence
of non-accidental mortality, associated with going from meeting the
current standard to meeting alternative standards, based on the 2002
and 2004 simulations. These results are generally representative of the
patterns found in all of the analyses. The estimated reductions in risk
associated with different forms of the standard, ranging from third- to
fourth-highest daily maximum concentrations at 0.084 ppm, and from
third- to fifth-highest daily maximum concentrations at 0.074 ppm, are
generally less than the estimated reductions associated with the
different levels that were analyzed. As seen in these figures, there is
much city-to-city variability, particularly in the percent changes
associated with going from a fourth-highest to third-highest form at
the current level of 0.084 ppm, and with estimated reductions
associated with the fifth-highest form at a 0.074 ppm level. In most
cities, there are generally only small differences in the estimated
reductions in risks associated with the third- to fifth-highest forms
at a level of 0.074 ppm simulated using 2002 and 2004 O3
monitoring data.
The Staff Paper noted that there is not a clear health-based
threshold for selecting a particular nth-highest daily maximum form of
the standard from among the ones analyzed. It also noted that the
changes in the form considered in the analyses result in only small
differences in the estimated reductions in risks in most cities,
although in some cities larger differences are estimated. The Staff
Paper concluded that a range of concentration-based forms from the
third- to the fifth-highest daily maximum 8-hour average concentration
is appropriate for consideration in setting the standard. Given that
there is a continuum of effects associated with exposures to varying
levels of O3, the extent to which public health is affected
by exposure to ambient O3 is related to the actual magnitude
of the O3 concentration, not just whether the concentration
is above a specified level. The principal advantage of a concentration-
based form is that it is more directly related to the ambient
O3 concentrations that are associated with health effects.
Robust, concentration-based forms, in the range of the third- to fifth-
highest daily maximum 8-hour average concentration, including the
current 4th-highest daily maximum form, minimize the inherent lack of
year-to-year stability of exceedance-based forms and provide insulation
from the impacts of extreme meteorological events. Such instability can
have the effect of reducing public health protection by disrupting
ongoing implementation plans and associated control programs.
With regard to the precision of the standard, in their letter to
the Administrator, the CASAC concluded that current monitoring
technology ``allows accurate measurement of O3
concentrations with a precision of parts per billion'' (Henderson,
2006c). The CASAC recommended that the specification of the level of
the O3 standard should reflect this degree of precision
(Henderson, 2006c). Some public comments supported specifying the
standard in terms of parts per billion, or to three decimal places if
specified in terms of parts per million.\52\ Other public commenters
stated that the
[[Page 37875]]
basis for changing the current rounding procedures is not supported by
a complete analysis of the O3 compliance monitoring
procedures, including consideration of uncertainty related to humidity
effects and interferences from aromatic compounds in the monitoring of
O3 levels.
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\52\ The Staff Paper notes that the 8-hour O3
standard adopted by the State of California in 2006 is specified to
the nearest thousandth part per million (at a level of 0.070 ppm)
(http://www.arb.ca.gov/research/aaqs/ozone-rs/ozone-rs.htm).
---------------------------------------------------------------------------
With regard to the form of the standard, in their letter to the
Administrator, CASAC recommended that ``a range of concentration-based
forms from the third-to the fifth-highest daily maximum 8-hour average
concentration'' be considered (Henderson, 2006c, p. 5). Some public
commenters that expressed the view that the current primary
O3 standard is not adequate also submitted comments that
supported a more health-protective form of the standard than the
current form (e.g., a second-or third-highest daily maximum form).
Commenters who expressed the view that the current standard is adequate
did not provide any views on alternative forms that would be
appropriate for consideration should the Administrator consider
revisions to the standard.
The Administrator proposes that the level of the standard be
specified to the nearest thousandth ppm, based on the staff's analysis
and conclusions discussed in the Staff Paper that current monitoring
technology allows accurate measurement of O3 to support
specifying the 8-hour standard to this degree of precision, and on
CASAC's recommendation with respect to this aspect of the standard. The
Administrator invites comment on this proposal to specify the standard
to the thousandth ppm.
The Administrator recognizes that there is not a clear health-based
threshold for selecting a particular nth-highest daily maximum form of
the standard from among the ones analyzed in the Staff Paper, and that
the current form of the standard provides a stable target for
implementing programs to improve air quality. The Administrator also
agrees that the adequacy of the public health protection provided by
the combination of the level and form is a foremost consideration.
Based on this, the Administrator proposes to retain the form of the
current standard, 4th-highest daily maximum 8-hour average
concentration, recognizing that the public health protection that would
be provided by the standard is based on combining this form with the
level discussed below. Mindful of the recommendation of the
O3 CASAC Panel and the view expressed by commenters, the
Administrator also invites comment on two alternative forms of the
standard, the third- and the fifth-highest daily maximum 8-hour average
concentrations.
4. Level
a. Evidence and Exposure/Risk Based Considerations in the Staff Paper
The approach used in the Staff Paper as a basis for staff
recommendations on standard levels builds upon and broadens the general
approach used by EPA in the last review. This approach reflects the
more extensive and stronger body of evidence now available 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. multi-city 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) evidence of
increased susceptibility in people with asthma and other lung diseases.
In evaluating evidence-based and exposure/risk-based considerations,
the 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.
In taking into account evidence-based considerations, the 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.
In considering the available controlled human exposure studies, as
discussed above in section II.A.2.a.i(a)(i), two new studies are
notable in that they are the only controlled human exposure studies
that examined respiratory effects, including lung function decrements
and respiratory symptoms, in healthy adults at lower exposure levels
than had previously been examined. EPA's reanalysis of the data from
the most recent study shows small group mean decrements in lung
function responses to be statistically significant at the 0.060 ppm
exposure level, while the author's analysis did not yield statistically
significant lung function responses (but did yield some statistically
significant respiratory symptom responses toward the end of the
exposure period). Notably, these studies report a small percentage of
subjects experiencing lung function decrements (> 10 percent) at the
0.060 ppm exposure level. These studies provide very limited evidence
of O3-related lung function decrements and respiratory
symptoms at this lower exposure level.
In considering controlled human exposure studies of pulmonary
inflammation, airway responsiveness, and impaired host defense
capabilities, the Staff Paper notes 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. 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.
In considering epidemiological studies, the Staff Paper first
recognizes 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 current
O3 standard and
[[Page 37876]]
possibly within the range of background levels. As discussed above (and
more fully in the Staff Paper in chapter 3 and the Criteria Document in
chapter 7), a number of 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 up to approximately 0.050
ppm. Other studies, however, observe linear concentration-response
functions suggesting no effect threshold. The Staff Paper concludes
that the statistically significant associations between ambient
O3 concentrations and lung function decrements, respiratory
symptoms, indicators of respiratory morbidity including increased
emergency department visits and hospitals 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 current standard (EPA, 2007, p. 6-60). Toward the lower end of the
range of O3 concentrations observed in such studies, ranging
down to background levels, however, the Staff paper states 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 Staff Paper also considered studies that did subset analyses
that include only days with ambient O3 concentrations below
the level of the 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
associations even when only days with a maximum 8-hour average
O3 concentration below a value of approximately 0.061 ppm
were included.\53\ Also of note is the large multi-city 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).
---------------------------------------------------------------------------
\53\ Bell et al. (2006) referred to this level as being
approximately equivalent to 120 [mu]g/m3, daily 8-hour
maximum, the World Health Organization guideline and European
Commission target value for O3.
---------------------------------------------------------------------------
Being mindful of the uncertainties and limitations inherent in
interpreting the available evidence, the Staff Paper states 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 Staff Paper also concludes that the lower end to 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.
In addition to the evidence-based considerations informing staff
recommendations on alternative levels, the Staff Paper also evaluated
quantitative exposures and health risks estimated to occur upon meeting
the current and alternative standards.\54\ In so doing, it presented
the important uncertainties and limitations associated with these
exposure and risk assessments. For example, the Staff Paper noted
important uncertainties affecting the exposure estimates are related to
modeling human activity patterns over an O3 season
(especially repetitive exposures), modeling ambient concentrations near
roadways and modeling building air exchange rates which impact
estimates of indoor O3 concentrations. With regard to the
risk assessment, important uncertainties include, for example, those
related to exposure estimates for children engaged in moderate or
greater exertion, as well as those related to estimation of
concentration-response functions, specification of concentration-
response models, the possible role of copollutants in interpreting
reported associations with O3, and inferences of a likely
causal relationship between O3 exposure and nonaccidental
mortality (for risk estimates based on epidemiological studies).
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\54\ As described in the Staff Paper (section 4.5.8) and
discussed above, recent O3 air quality distributions have
been statistically adjusted to simulate just meeting the current 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.
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Beyond these uncertainties, the Staff Paper also recognized
important limitations to the exposure and risk analyses. For example,
the Staff Paper 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 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 risk analyses. The Staff Paper notes that 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 current or alternative standards. On the other hand, due to
individual variability in responsiveness, only a subset of individuals
who are estimated to experience exposures of concern at and above a
specific benchmark level can be expected to experience certain adverse
health effects, although susceptible subpopulations such as those with
asthma are expected to be affected more by such exposures than healthy
individuals. In taking these limitations into account, the Staff Paper
reflected CASAC's advice 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 Staff Paper focused on alternative standards with the same form
as the current O3 standard (i.e. the 0.074/4, 0.070/4 and
0.064/4 scenarios).\55\ Having concluded in the 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 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
[[Page 37877]]
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.
---------------------------------------------------------------------------
\55\ The abbreviated notation used to identify the current 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 current standard is
identified as ``0.084/4.''
---------------------------------------------------------------------------
As discussed in section II.B.1 of this notice, the exposure
estimates presented in the 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. For reasons discussed above in section
II.C.2, the Staff Paper focused on exposures of concern at the 0.070
and 0.060 ppm benchmark levels for the purpose of evaluating
alternative standard levels. As shown in the Table 1 in this notice,
the percent of population exposed at any given level is very similar
for all and asthmatic school age children. Substantial year-to-year
variability in exposure estimates 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 of these benchmark levels. The 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 discussed in the Staff Paper, a standard set at the upper part
of the range recommended by EPA staff (e.g., the 0.074/4 scenario)
would result in an aggregate estimate of about 4 percent of all or
asthmatic school age children likely to experience exposures of concern
at the >=0.070 ppm benchmark level based on the 2002 simulation, a year
with relatively high O3 levels, while the estimates range up
to 12 percent of all or asthmatic school age children in the single
city with the least degree of protection from this standard. Using the
2004 simulation, a year with relatively low O3 levels,
exposures of concern at this level are essentially eliminated. At the
benchmark level of >=0.060 ppm, in aggregate using the 2002 simulation
about 22 percent of all or asthmatic school age children are estimated
to experience exposures of concern; this estimate ranges up to about 46
percent of all or asthmatic school age children in the single city with
the least degree of protection from this standard. Using the 2004
simulation, exposures of concern at this level are estimated to be
substantially lower. A standard set at this level is estimated to
reduce the number of all and asthmatic school age children estimated to
experience one or more moderate lung function decrements by about 30 to
50 percent relative to the current standard, with city-to-city
differences accounting for most of the variability in estimates. A
standard set at this level is estimated to reduce non-accidental
mortality by about 10 to 40 percent, with most of the variability
occurring across the 12 city estimates.
Using the 2002 simulation, a standard set at this level (the 0.074/
4 scenario) is estimated to reduce the incidence of symptom days in
children with moderate to severe asthma in the Boston area by about
1,000 days, a 15 percent reduction relative to the current 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. Estimated incidence of respiratory-related
hospital admissions was reduced by 14 to 17 percent by a standard set
at this level relative to the current standard, in the year with
relatively high and relatively low O3 air quality levels
respectively.
The Staff Paper notes that a standard set at the middle part of the
staff-recommended range, as indicated by the estimates for the 0.070/4
scenario, would reduce the exposures of concern at the 0.070 ppm level
substantially over the current standard, resulting in an aggregate
estimate of about 1.5 to nearly 2 percent of all or asthmatic school
age children likely to experience exposures of concern even using the
2002 simulation, and leaving approximately 5 percent or less of
children likely to experience exposures of concern in the city with the
least degree of protection. Using the 2004 simulation, it essentially
eliminates exposures of concern at this level. It reduces exposures of
concern at the 0.060 ppm benchmark level less so, leaving larger
percentages of all school age children unprotected using the 2002
simulation (about 15 percent in aggregate) or in the city with the
least protection from this standard (about 33 percent). However, using
the 2004 simulation, it is estimated to reduce exposures of concern at
this benchmark level to approximately 5 percent or less of children
even in the city with the least degree of protection. It provides
considerable additional protection for members of at-risk groups, over
the current O3 standard, against respiratory morbidity
effects such as lung function decrements, respiratory symptom days and
hospital admissions, as well as non-accidental mortality.
A standard set at lower part of the staff-recommended range (e.g.,
the 0.064/4 scenario), would result in an aggregate estimate of less
than 0.5 percent of all and asthmatic school age children likely to
experience exposures of concern at the 0.070 ppm benchmark level using
the 2002 simulation and only about 1 percent of all and asthmatic
school age children in the city with the least degree of protection
from this standard. At the benchmark level of 0.060 ppm, in aggregate
using the 2002 simulation about 5 percent of all and asthmatic school
age children are estimated to experience exposures of concern; this
number ranges up to 15 percent of all and asthmatic school age children
in the city with the least degree of protection from this standard. A
standard set at this level is estimated to reduce the number of all and
asthmatic school age children estimated to experience one or more
moderate lung function decrements by about 40 to 75 percent over the
current standard, and non-accidental mortality by about 25 to 75
percent, with most of the variability occurring across the 12 city
estimates.
A standard set at the 0.064/4 scenario 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 1,900 days,
about a 25 to 30 percent reduction over the current 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. Estimated incidence of respiratory-related hospital
admissions would be reduced by 30 to 35 percent over the current
standard, a reduction of 125 to 150 hospital admissions in the New York
City area alone, using the 2002 and 2004 simulations, respectively.
b. CASAC Views
As 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 follows from its more general recommendation, discussed
above, that the current standard of 0.084 ppm needs 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)
[[Page 37878]]
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 to the
Administrator, 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 Criteria Document and 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.).
c. Administrator's Proposed Conclusions on Level
For the reasons discussed below, and taking into account
information and assessments presented in the Criteria Document and
Staff Paper, the advice and recommendations of CASAC, and the public
comments to date, the Administrator proposes to revise the existing 8-
hour primary O3 standard. Specifically, the Administrator
proposes to revise (1) The level of the primary O3 standard
to within a range from 0.070 to 0.075 ppm and (2) the degree of
precision to which the level of the standard is specified to the
thousandth ppm.
However, in recognition of alternative views of the science, the
exposure and risk assessments and the uncertainties inherent in these
assessments, and the appropriate policy responses based on the
currently available information, the Administrator also solicits
comments on whether to proceed instead with: (1) Alternative levels of
the 8-hour primary O3 standard, within ranges of below 0.070
ppm down to 0.060 ppm and above 0.075 ppm up to and including retaining
the current standard; (2) alternative forms of the standard, including
the 3-year average of the annual third- and fifth-highest daily maximum
8-hour average O3 concentrations; and (3) retaining the
degree of precision of the current standard (to the nearest hundredth
ppm). Based on the comments received and the accompanying rationales,
the Administrator may adopt other standards within the range of the
alternative levels and forms identified above in lieu of the standards
he is proposing today.
The Administrator's consideration of alternative levels of the
primary O3 standard builds on his proposal, discussed above,
that the overall body of evidence indicates that the current 8-hour
O3 standard is not requisite to protect public health with
an adequate margin of safety because it does not provide sufficient
protection and that revision would result in increased public health
protection, especially for members of at-risk groups, notably including
asthmatic children and other people with lung disease, as well as all
children and older adults, especially those active outdoors, and
outdoor workers, against an array of adverse health effects. These
effects range from health outcomes that could be quantified in the risk
assessment, including decreased lung function, respiratory symptoms,
serious indicators of respiratory morbidity such as hospital admissions
for respiratory causes, and nonaccidental mortality, to health outcomes
that could not be directly estimated, including pulmonary inflammation,
increased medication use, emergency department visits, and possibly
cardiovascular-related morbidity effects. In reaching a proposed
decision about the level of the O3 primary standard, the
Administrator has considered: the evidence-based considerations from
the Criteria Document and the Staff Paper; the results of the exposure
and risk assessments discussed above and in the Staff Paper, giving
weight to the exposure and risk assessments as judged appropriate;
CASAC advice and recommendations, as reflected in discussions of drafts
of the Criteria Document and Staff Paper at public meetings, in
separate written comments, and in 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 8-hour standard is
requisite to protect public health with an adequate margin of safety,
the Administrator is mindful that this choice requires judgment based
on an interpretation of the evidence and other information that neither
overstates nor understates the strength and limitations of the evidence
and information nor the appropriate inferences to be drawn.
The Administrator notes that the most certain evidence of adverse
health effects from exposure to O3 comes from the clinical
studies, and that the large bulk of this evidence derives from studies
of exposures at levels of 0.080 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. Moreover there is no
evidence that the 0.080 ppm level is a threshold for these effects.
Although the Administrator takes note of the very limited new evidence
of lung function decrements and respiratory symptoms in some healthy
individuals at the 0.060 ppm exposure level, he judges this evidence
too limited to support a primary focus at this level. The Administrator
also notes that clinical studies, supported by epidemiological studies,
provide important new evidence that people with asthma are likely to
experience larger and more serious effects than healthy people from
exposure to O3. There are also epidemiological studies that
provide evidence of statistically significant associations between
short-term O3 exposures and more serious health effects such
as emergency department visits and hospital admissions, and premature
mortality, in areas that likely would have met the current standard.
There are also many epidemiological studies done in areas that likely
would not have met the current standard but which nonetheless report
statistically significant associations that generally extend down to
ambient O3 concentrations that are below the level of the
current standard. Further, there are a few studies that have examined
subsets of data that include only days with ambient O3
concentrations below the level of the current standard, or below even
much lower O3 concentrations, and continue to report
statistically significant associations with respiratory morbidity
outcomes and mortality. In considering this evidence, the Administrator
notes that the extent to which these studies provide evidence of causal
relationships with exposures to O3 alone down to the lowest
levels observed remains uncertain. To further inform the interpretation
of this evidence, EPA seeks comment on the degree to which associations
observed in epidemiological studies reflect causal relationships
between important health endpoints and exposure to O3 alone
at ambient O3 levels below the current standard.
Therefore, the Administrator judges that revising the current
standard to protect public health with an adequate margin of safety is
warranted, and
[[Page 37879]]
would reduce risk to public health, based on: (1) The strong body of
clinical evidence in healthy people at exposure levels of 0.080 and
above of lung function decrements, respiratory symptoms, pulmonary
inflammation, and other medically significant airway responses, as well
as some indication of lung function decrements and respiratory symptoms
at lower levels; (2) the substantial body of clinical and
epidemiological evidence indicating that people with asthma are likely
to experience larger and more serious effects than healthy people; and
(3) the body of epidemiological evidence indicating associations are
observed for a wide range of serious health effects, including
respiratory emergency department visits and hospital admissions, and
premature mortality, at and below 0.080 ppm. The Administrator also
judges that the estimates of exposures of concern and risks remaining
upon just meeting the current standard or a standard at the 0.080 ppm
level provide additional support for this view. For the same reasons,
and the reasons discussed above in section II.C on the adequacy of the
current standard, the Administrator judges that the standard should be
set below 0.080 ppm, a level at which the evidence provides a high
degree of certainty about the adverse effects of O3 exposure
even in healthy people.
The Administrator next considered what standard level below 0.080
ppm would be requisite to protect public health with an adequate margin
of safety, that is sufficient but not more than necessary to achieve
that result, recognizing that such a standard would result in increased
public health protection. The assessment of a standard level calls for
consideration of both the degree of additional protection that
alternative levels of the standard might be expected to provide as well
as the certainty that any specific level will in fact provide such
protection. In the circumstances present in this review, 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 holistically in making this
public health policy judgment, and selecting a standard level from a
range of reasonable values.
The Administrator notes that at exposure levels below 0.080 ppm
there is only a very limited amount of evidence from clinical studies
indicating effects in some healthy individuals at levels as low as
0.060 ppm. The great majority of the evidence concerning effects below
0.080 ppm is from epidemiological studies. The epidemiological studies
do not identify any bright-line threshold level for effects. At the
same time, the epidemiological studies are not themselves direct
evidence of a causal link between exposure to O3 and the
occurrence of the effects. The Administrator considers these studies in
the context of all the other available evidence in evaluating the
degree of certainty that O3-related adverse health effects
would occur at various ambient levels below 0.080 ppm, including the
strong human clinical studies and the toxicological studies that
demonstrate the biological plausibility and mechanisms for the effects
of O3 on airway inflammation and increased airway
responsiveness at exposure levels of 0.080 ppm and above.
Based on consideration of the entire body of evidence and
information available at this time, as well as the recommendations of
CASAC, the Administrator proposes that a standard within the range of
0.070 to 0.075 ppm would be requisite to protect public health with an
adequate margin of safety. 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 clinical studies, and the emergency
department visits, hospital admissions and mortality effects indicated
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.
The Administrator considered the degree of improvements in public
health that potentially could be achieved by a standard of 0.070 to
0.075 ppm, giving weight to the exposure and risk assessments as he
judged appropriate, as discussed below. In considering the results of
the exposure assessment, as discussed above (section II.C.4), the
Administrator has primarily focused on exposures at and above the 0.070
ppm benchmark level as an important surrogate measure for potentially
more serious health effects for at-risk groups, including people with
asthma. In so doing, the Administrator particularly notes that although
the analysis of ``exposures of concern'' was conducted to estimate
exposures at and above three discrete benchmark levels, the concept is
appropriately viewed as a continuum. As discussed above, the
Administrator strives to balance concern 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 exposure levels. In focusing on this benchmark, the
Administrator notes that upon just meeting a standard within the range
of 0.070 to 0.075 ppm based on the 2002 simulation, the number of
school age children likely to experience exposures at and above this
benchmark level in aggregate (for the 12 cities in the assessment), is
estimated to be approximately 2 to 4 percent of all and asthmatic
children, and generally less than 10 percent of children even in cities
that receive the least degree of protection from such a standard in a
recent year with relatively high O3 levels. A standard
within the 0.070 to 0.075 ppm range would thus substantially reduce
exposures of concern by about 90 to 80 percent, respectively, from
those estimated to occur upon just meeting the current standard. While
placing less weight on the results of the risk assessment, in light of
the important uncertainties inherent in the assessment, the
Administrator notes that the results indicate that a standard set
within this range would likely reduce risks to at-risk groups from the
O3-related health effects considered in the risk assessment,
and by inference across the much broader array of O3-related
health effects that can only be considered qualitatively, relative to
the level of protection afforded by the current standard. This lends
support to the proposed range.
The Administrator judges that a standard set within the range of
0.070 to 0.075 ppm would provide a degree of reduction in risk that is
important from a public health perspective, and that a standard within
this range would be requisite to protect public health, including the
health of at-risk groups, with an adequate margin of safety. EPA's
evaluation of the body of scientific evidence and quantitative
estimates of exposures and risks indicates that substantial reductions
in public health risks would occur throughout this range. Because there
is no bright line clearly directing the choice of level within this
reasonable range, the choice of what is appropriate, considering the
strengths and limitations of the evidence, and the appropriate
inferences to be drawn from the evidence and the exposure and risk
assessments, is a public health policy judgment. To further inform this
judgment, EPA seeks comment on the extent to which the epidemiological
and clinical evidence provides guidance as to the level of a standard
that would be requisite to protect public health with
[[Page 37880]]
an adequate margin of safety, especially for at-risk groups.
In considering the available information, the Administrator also
judges that a standard level below 0.070 ppm would not be appropriate.
In reaching this judgment, the Administrator notes that there is only
quite limited evidence from clinical studies at exposure levels below
0.080 ppm O3. Moreover, the Administrator recognizes that in
the body of epidemiological evidence, many studies report positive and
statistically significant associations, while others report positive
results that are not statistically significant, and a few do not report
any positive O3-related associations. In addition, the
Administrator judges that evidence of a causal relationship between
adverse health outcomes and O3 exposures becomes
increasingly uncertain at lower levels of exposure.
The Administrator also has considered the results of the exposure
assessments in reaching his judgment that a standard level below 0.070
ppm would not be appropriate. The Administrator notes that in
considering the results from the exposure assessment, a standard set at
the 0.070 ppm level, with the same form as the current standard, is
estimated to provide substantial reductions in exposures of concern
(i.e., approximately 90 to 92 percent reductions in the numbers of
school age children and 94 percent reduction in the total number of
occurrences) for both all and asthmatic school age children relative to
just meeting the current standard based on a simulation of a recent
year with relatively high O3 levels (2002). Thus, a 0.070
ppm standard would be expected to provide protection from the exposures
of concern that the Administrator has primarily focused on for over 98
percent of all and asthmatic school age children even in a year with
relatively high O3 levels, increasing to over 99.9 percent
of children in a year with relatively low O3 levels (2004).
In considering the results of the health risk assessment, as
discussed in section II.B above, the Administrator notes that there are
important uncertainties and assumptions inherent in the risk assessment
and that this assessment is most appropriately used to simulate trends
and patterns that can be expected as well as providing informed but
still imprecise estimates of the potential magnitude of risks. The
Administrator particularly notes that as lower standard levels are
modeled, including a standard set at a level below 0.070 ppm, the risk
assessment continues to assume a causal link between O3
exposures and the occurrence of the health effects examined, such that
the assessment continues to indicate reductions in O3-
related risks upon meeting a lower standard level. As discussed above,
however, the Administrator recognizes that evidence of a causal
relationship between adverse health effects and O3 exposures
becomes increasingly uncertain at lower levels of exposure. Given all
of the information available to him at this time, the Administrator
judges that the increasing uncertainty of the existence and magnitude
of additional public health protection that standards below 0.070 ppm
might provide suggests that such lower standard levels would likely be
below what is necessary to protect public health with an adequate
margin of safety.
In addition, the Administrator judges that a standard level higher
than 0.075 ppm would also not be appropriate. This judgment takes into
consideration the information discussed above in section II.B, and is
based on the strong body of clinical evidence in healthy people at
exposure levels of 0.080 ppm and above, the substantial body of
clinical and epidemiological evidence indicating that people with
asthma are likely to experience larger and more serious effects than
healthy people, the body of epidemiological evidence indicating that
associations are observed for a wide range of more serious health
effects at levels below 0.080 ppm, and the estimates of exposure and
risk remaining upon just meeting a standard set at 0.080 ppm. The much
greater certainty of the existence and magnitude of additional public
health protection that such levels would forego provides the basis for
judging that levels above 0.075 ppm would be higher than what is
requisite to protect public health, including the health of at-risk
groups, with an adequate margin of safety.
For the reasons discussed above, the Administrator proposes to
revise the level of the primary O3 standard to within the
range of 0.070 to 0.075 ppm.
Having reached this decision based on the approach to interpreting
the evidence described above, the Administrator recognizes that other
approaches to selecting a standard level have been presented to the
Agency. As described above, the CASAC has stated in two letters to the
Administrator (Henderson, 2006c; Henderson, 2007) its unanimous
recommendation that the current primary O3 NAAQS be revised
to within the range from 0.060 to 0.070 ppm. The CASAC Panel noted that
while data exist that adverse health effects may occur at levels lower
than 0.060 ppm, these data are less certain and that achievable gains
in protecting human health can be accomplished through lowering the
O3 NAAQS to a level between 0.060 and 0.070 ppm. In addition
to the views of CASAC described above, the Agency received the public
comments described below.
One group of commenters submitted comments that supported revising
the level of the primary O3 standard from 0.070 ppm down to
or even below 0.060 ppm, consistent with or below the range recommended
by CASAC. In considering the available evidence as a basis for their
views, these commenters generally noted that the controlled human
exposure studies, showing statistically significant declines in lung
function, and increases in respiratory symptoms, airway inflammation
and airway responsiveness at a 0.080 ppm exposure level, were conducted
with healthy adults, not members of at-risk groups including people
with asthma and active children generally. Further, recognizing the
substantial variability in response between subjects, some of these
commenters felt that the number of subjects included in these studies
was too small to ascertain the full range of responses, especially for
at-risk groups. Such considerations in part were the basis for these
commenters' view that an O3 standard set at 0.080 ppm is not
protective of public health and has no margin of safety for at-risk
groups. In addition, some of these commenters also noted that the World
Health Organization's guidelines for O3 air quality are in
the range of 0.061 to 0.051 ppm.
In considering the results of the human exposure and health risk
assessment, this group of commenters generally expressed the view that
these assessments substantially underestimate the public health impacts
of exposure to O3. For example, several commenters noted
that the assessments are done for a limited number of cities, they do
not address risks to important at-risk subpopulations (e.g., outdoor
workers, active people who spend their summers outdoors, children up to
5 years of age), and they do not include many health effects that are
important from a public health perspective (e.g., school absences,
restricted activity days). Further, some of these commenters expressed
the view that the primary O3 standard should be set to
protect the most exposed and most vulnerable groups, and the fact that
some children are frequently indoors, and thus at lower risk, should
not weigh against setting a standard to protect those children who are
active outdoors. To the extent the exposure and risk estimates
[[Page 37881]]
are considered, some of these commenters felt that primary
consideration should be given to the estimates based on 2002 air
quality, for which most areas had relatively higher O3
levels than in 2004, so as to ensure public health protection even in
years with relatively worse O3 air quality levels. Some
commenters also felt that the exposure analysis should focus on a
benchmark concentration for exposures of concern at the 0.060 ppm
level, the lower end of the range of alternative standards advocated by
the CASAC Panel.
In sharp contrast to the views discussed above, other public
commenters supported retaining the current standard. In considering the
available evidence as a basis for their views, these commenters
challenged a number of aspects of the interpretation of the evidence
presented in the Criteria Document. For example, some of these
commenters asserted that EPA generally overestimates the magnitude and
consistency of the results of short-term exposure epidemiological
studies (e.g., for respiratory symptoms, school absences, hospital
admissions, mortality), mistakenly links statistical significance and
consistency with strength of associations, and underestimates the
uncertainties in interpreting the results of such studies. Further,
these commenters generally express the view that there is significant
uncertainty related to the reliability of estimates from time-series
studies, in that ambient monitors do not provide reliable estimates of
personal exposures, such that the small reported morbidity and
mortality risks are unlikely to be attributable to people's exposures
to O3. Rather, these commenters variously attribute the
reported risks to the inability of time series studies to account for
key model specification factors such as smoothing for time-varying
parameters, meteorological factors, and removal of O3 by
building ventilation systems, and confounding by co-pollutants. In
particular, these commenters generally asserted that reported
associations between short-term O3 exposure and mortality
are not causal, in that the reported relative risks are too small to
provide a basis for inferring causality and the associations are most
likely due to confounding, inappropriately specified statistical
models, or publication bias.
In considering the results of the human exposure and health risk
assessment, this group of commenters generally expressed the view that
these assessments are based on a number of studies that should not be
used in quantitative risk assessment. For example, some commenters
asserted that the results of time-series studies should not be used at
all in quantitative risk assessments, that risk estimates from single
city time-series studies should not be used since they are highly
heterogeneous and influenced by publication bias, and that risk
estimates from multi-city studies should not be used in estimating risk
for individual cities. This group of commenters also generally
expressed the view that the assessments generally overestimate the
public health impacts of exposure to O3. Noting that the
risk assessment used a nonlinear exposure-response function to estimate
decreased lung function risks, some commenters expressed the view that
a nonlinear approach should also be used to assess other acute
morbidity effects and mortality. This view was in part based on
judgments that it is not possible to determine if thresholds exist
using time-series analyses and that the lack of association of
O3 to mortality in the winter season is highly supportive of
the likelihood of the existence of an effect threshold. With regard to
the risk assessment based on controlled human exposure studies of lung
function decrements, some commenters expressed the view that the
assessment should not rely on what they characterized as ``outlier''
information to define exposure-response relationships, with reference
to the data in the Adams (2006) study at the 0.060 and 0.040 ppm
exposure levels, but rather should focus on group central tendency
response levels. Further, some commenters expressed the view that the
air quality rollback algorithm used introduces significant uncertainty,
especially when applied to areas requiring very large reductions in air
quality to meet the alternative standards examined, and may result in
overestimates in benefits from emission reductions. Some commenters
noted that potential beneficial effects of O3 in shielding
from UV-B radiation are not quantified in the assessment, and that the
assessment should discuss the evidence for both adverse and beneficial
effects with the same objectivity. Finally, some of these commenters
asserted that since estimates of exposures of concern (which they
defined as the benchmark concentration of 0.080 ppm) and lung function
decrements are substantially below the estimates available when the
current O3 standard was set in 1997, retaining the current
standard is the most appropriate policy alternative.
Some commenters also have raised concerns about potential
uncertainties with regard to estimating policy-relevant background
O3 levels including: (1) Stratospheric O3
contributions to the mid- and upper troposphere, which are relatively
long-lived (1 to 2 months), and are transported downward to the surface
over time; (2) potential trends in stratospheric O3 levels
due to changes in stratospheric circulation or to reduction of
O3 depleting chemicals; (3) O3 levels due to
lightning strikes in estimating policy-relevant background
concentrations; and (4) potential uncertainty with regard to policy-
relevant background O3 levels having to do with increases in
O3 precursors elsewhere in the world. EPA asks for comments
on these issues and on how they may relate to the estimation and
consideration of policy-relevant background levels in setting the
O3 standards.
Several Governors, State Legislators, and other local officials
have expressed concerns related to a more stringent standard. These
officials recognize that State and local governments have important
roles in developing and implementing policy that improve air quality
while at the same time achieving economic and quality of life
objectives. In addition, these officials note that States are just
beginning to implement current air quality standards and raise concern
with moving forward on revised standards without first realizing the
results from the last revision.
As a related concern, a number of areas--including some of the
cities involved in the risk assessment--will have difficulty in
complying with the current 8-hour standard within the next decade. As a
result, the full public health gains in these areas from a more
stringent 8-hour standard are unlikely to be realized for a number of
years. In light of the fact that these public health gains may not
fully materialize within the attainment date structure set forth in the
Clean Air Act, some commenters question whether the Agency can or
should consider these projected gains as a health based criterion for
its decisionmaking. EPA requests comment on this view.
The Administrator is mindful that the country has important goals
related to the increased production and use of renewable energy, and
that these new energy sources can have important public health,
environmental and other benefits, such as national security benefits.
In some contexts and situations, however, the use of renewable fuels
may impact compliance with a lowered ozone NAAQS standard. For example,
the Agency recently promulgated final regulations pursuant to section
211(o) of the Clean Air Act,
[[Page 37882]]
which was enacted as part of the Energy Policy Act of 2005. This
provision requires the use of 7.5 billion gallons of renewable fuel by
2012, a level which will be greatly exceeded in practice. In the
Regulatory Impact Analysis which accompanied the renewable fuel
regulations, the Agency recognized the impact of this program on
emissions related to ozone, toxics and greenhouse gases and otherwise
reviewed the impacts on energy security. The Administrator requests
comment on such factors and any relationship to this rulemaking,
including the extent of EPA's discretion under the Clean Air Act to
take such factors into account (see section I.A).
In general, these commenters' concerns are consistent with the view
that adopting a more stringent 8-hour standard now, without a better
understanding of the health effects associated with O3
exposure at lower levels, would have an uncertain public health
benefit. The Administrator recognizes that commenters have raised
numerous concerns regarding various types of uncertainties in the
available information, including for example uncertainties in (1) The
assessment of exposures, (2) the estimation of concentration-response
associations in the epidemiological studies, (3) the potential role of
co-pollutants in interpreting the reported associations in
epidemiological studies, and (4) the estimation of background
concentrations. The Administrator has heard these concerns from
Governors and other commenters and invites comment on whether it would
be appropriate to retain the existing standard and delay considering
modification of the 8-hour standard until the next NAAQS review, when a
more complete body of information is expected to be available.
Consistent with the goal of soliciting comment on a wide array of
views, the Administrator also solicits comments on these alternative
approaches and views, and on related standard levels, including levels
down to 0.060 ppm and up to retaining the level of the current 8-hour
standard (i.e., effectively 0.084 ppm with the current rounding
convention). The Administrator recognizes that these sharply divergent
views on the appropriate level of the standard are based on very
different interpretations of the science itself, including its relative
strengths and limitations, very different judgments as to how such
scientific evidence should be used in making policy decisions on
proposed standards, and very different public health policy judgments.
E. Proposed Decision on the Primary Standard
For the reasons discussed above, and taking into account
information and assessments presented in the Criteria Document and
Staff Paper, the advice and recommendations of CASAC, and the public
comments to date, the Administrator proposes to revise the existing 8-
hour primary O3 standard. Specifically, the Administrator
proposes to revise: (1) The level of the primary O3 standard
to within a range from 0.070 to 0.075 ppm and (2) the degree of
precision to which the level of the standard is specified to the
thousandth ppm. The proposed 8-hour primary standard, with a level in
the range of 0.070 to 0.075 ppm, would be met at an ambient air
monitoring site when the 3-year average of the annual forth-highest
daily maximum 8-hour average O3 concentration is less than
or equal to the level of the standard that is promulgated. Data
handling conventions are specified in the proposed creation of Appendix
P, as discussed in section V below.
However, in recognition of alternative views of the science, the
exposure and risk assessments and the uncertainties inherent in these
assessments, and the appropriate policy responses based on the
currently available information, the Administrator also solicits
comments on whether to proceed instead with: (1) Alternative levels of
the 8-hour primary O3 standard, within ranges of below 0.070
ppm down to 0.060 ppm and above 0.075 ppm up to and including retaining
the current standard; (2) alternative forms of the standard, including
the 3-year average of the annual third- and fifth-highest daily maximum
8-hour average O3 concentrations; and (3) retaining the
degree of precision of the current standard (to the nearest hundredth
ppm). Based on the comments received and the accompanying rationales,
the Administrator may adopt other standards within the range of the
alternative levels and forms identified above in lieu of the standards
he is proposing today.
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. For the current O3 NAAQS, an 8-hour average
concentration of 0.084 ppm corresponds to an AQI value of 100. 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; 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.
The Agency recognizes the importance of revising the AQI in a
timely manner to be consistent with any revisions to the NAAQS.
Therefore EPA proposes to finalize conforming changes to the AQI, in
connection with the Agency's final decision on the O3 NAAQS
if revisions to the primary standard are promulgated. These conforming
changes would include setting the 100 level of the AQI at the same
level as the revised primary O3 NAAQS, 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 review does not
inform decisions about breakpoints at those higher levels.
IV. Rationale for Proposed Decision on the Secondary Standard
This section presents the rationale for the Administrator's
proposed decision to revise the existing 0.08 ppm, 8-hour O3
secondary NAAQS. The Administrator proposes to revise the current
secondary standard by replacing it with one of two standard options.
One
[[Page 37883]]
option is to adopt a new cumulative, seasonal concentration-weighted
form, set at an annual level in the range of 7 to 21 ppm-hours. This
standard would be expressed as a sum of weighted hourly concentrations,
cumulated over the 12-hour daylight period (8 a.m. to 8 p.m.) during
the consecutive 3-month period within the O3 monitoring
season with the maximum index value. This concentration-weighted form
is commonly called W126, and is defined as the sum of sigmoidally
weighted hourly O3 concentrations over a specified period,
where the daily sigmoidal weighting function is defined as:
[GRAPHIC] [TIFF OMITTED] TP11JY07.001
The other option is to revise the current secondary standard by making
it identical to the proposed 8-hour primary standard, within the
proposed range of 0.070 to 0.075 ppm. For this option, EPA also
solicits comment on a wider range of 8-hour secondary standard levels,
including down to 0.060 ppm and up to and including retaining the
current 8-hour secondary standard of 0.08 ppm. The Administrator has
also considered and solicits comment on an alternative approach to
setting a cumulative, seasonal standard(s).
As discussed more fully below, the rationale for these proposed
options is based on a thorough review of the latest scientific
information on vegetation effects associated with exposure to ambient
levels of O3, as assessed in the Criteria Document. This
rationale also takes into account: (1) Staff assessments of the most
policy-relevant information in the Criteria Document regarding the
evidence of adverse effects of O3 to vegetation and
ecosystems, information on biologically-relevant exposure metrics, and
staff analyses of air quality, vegetation exposure and risks, presented
in the Staff Paper and described in greater detail in the associated
Technical Report on Ozone Exposure, Risk, and Impact Assessments for
Vegetation (Abt, 2007), upon which staff recommendations for revisions
to the secondary O3 standard are based; (2) CASAC advice and
recommendations as reflected in discussion of drafts of the Criteria
Document and Staff Paper at public meetings, in separate written
comments, and in CASAC's letters to the Administrator (Henderson,
2006a, b, c; 2007); (3) public comments received during development of
these documents either in conjunction with CASAC meetings or
separately; and (4) consideration of the degree of protection to
vegetation potentially afforded by the proposed 8-hour primary
standard.
In developing this rationale, EPA has again focused on direct
O3 effects on vegetation, specifically drawing upon an
integrative synthesis of the entire body of evidence, published through
early 2006, on the broad array of vegetation effects associated with
exposure to ambient levels of O3 (EPA, 2006a, chapter 9). 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 included, though these effects are not quantifiable at this time.
As was concluded in the 1997 review, and based on the body of
scientific literature assessed in the current Criteria Document, the
Administrator believes that it is reasonable to conclude that a
secondary standard protecting the public welfare from known or
anticipated adverse effects to trees, native vegetation and crops would
also afford increased protection from adverse effects to other
environmental components relevant to the public welfare, including
ecosystem services and function. The peer-reviewed literature includes
studies conducted in the U.S., Canada, Europe, and many other countries
around the world. 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 last review provides important
information coming from field-based exposure studies, including free
air, gradient and biomonitoring surveys, in addition to the more
traditional controlled open top chamber (OTC) studies. Moreover, the
newly available studies evaluated in the 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 in this review has provided an adequate basis for
regulatory decision-making at this time. This review also provides
important input to EPA's research plan for improving our future
understanding of the effects of ambient O3 at lower levels.
A. Vegetation Effects Information
This section outlines key information contained in the Criteria
Document (chapter 9) and in the Staff Paper (chapter 7) on known or
potential effects on public welfare 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 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 last 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 OTC exposure method, found
cumulative, seasonal O3 exposures were most strongly
associated with observed vegetation response. The Criteria Document
prepared for this review 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 subcellular, cellular,
and whole
[[Page 37884]]
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. These non-chambered, field-based
study results begin to address one of the key data gaps cited by the
Administrator in the last 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
Criteria Document (chapter 9) and the Staff Paper (chapter 7).
1. Mechanisms Governing Plant Response to Ozone
The interpretation of predictions of risk associated with
vegetation response at ambient O3 exposure levels can be
informed by scientific understanding regarding O3 impacts at
the genetic, physiological, and mechanistic 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 last
review (EPA, 1996a, 2006a). In addition, during the last decade
understanding of the cellular processes within plants has been further
clarified and enhanced. Therefore, this section reviews the key
scientific conclusions identified in 1996 Criteria Document (EPA,
1996a), and incorporates new information from the current 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 penetrate the leaf's cuticle, it
must reach the stomatal openings in the leaf for absorption to occur.
The 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 and water
status, and in some cases the presence of air pollutants, including
O3. These modifying factors produce stomatal conductance
that vary between leaves of the same plant, individuals and genotypes
within a species and 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. Having entered 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. An early step in a series of O3-induced events
that leads to leaf injury seems to involve alteration in cell membrane
function, including membrane transport properties (EPA, 2006a). 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). A few studies have documented direct stomatal
closure or restriction in the presence of O3 in some
species. 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, subcellular 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 Criteria Document concludes that scientific
understanding of the detoxification mechanisms is not yet complete and
requires further investigation (EPA, 2006a).
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 or degree of tolerance, nor are all
stages of a plant's development 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
[[Page 37885]]
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 the 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.
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 exposures to low
O3 concentrations. These 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 O3 affects long-term growth and resistance to
other biotic and abiotic 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, when it has accumulated
sufficiently, will be propagated to the level of the 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 last review. Recent studies 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
will be 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 last 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 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 yield loss at various exposure
levels in terms of a 12-hour W126. For example, 50 percent of the
[[Page 37886]]
tree seedling cases would be protected from greater than 10 percent
biomass loss at a 3-month, 12-hour W126 of approximately 24 ppm-hrs,
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-hrs.
Since the 1996 review, only a few studies have developed C-R
functions for additional tree seedling species (EPA, 2006a). One such
study is of particular importance in that it documented growth effects
from O3 exposure in the field without the use of chambers or
other fumigation methods that were as great as those seen in OTC
studies (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 was selected because it is fast growing, O3
sensitive and important ecologically, along stream banks, 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 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 has been 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
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 did 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 Staff Paper thus concluded that the combined evidence from the
AspenFACE \56\ 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 in the
weight of evidence available in this review and provide additional
evidence that O3-induced effects observed in chambers also
occur in the field.
---------------------------------------------------------------------------
\56\ Only a few northern forest types in the U.S. have been well
studied with respect to O3 exposures using the FACE
method, though these systems are being used to expose numerous other
ecosystem types to elevated levels of CO2. Additional
FACE studies with O3 on other U.S. forest types would
provide a better understanding of whether these results can be
extrapolated to other forest types and mature forest stands.
---------------------------------------------------------------------------
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 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
[[Page 37887]]
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, 1993). 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 1996 NAAQS 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).
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 a few 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
may include increased susceptibility to freezing temperatures, pest
infestations and/or root disease, and compromised ability to compete
for available resources. For example, when species with differing
O3-sensitivities occur together, the resulting decrease in
growth in O3-sensitive species may lead to an increase in
growth of more O3-tolerant species, which are now able to
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 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) include 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 Criteria Document (EPA, 2006a) 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
[[Page 37888]]
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. The composition of lichens was
significantly reduced. 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.
One of the best-documented studies of population and community
response 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 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
[[Page 37889]]
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
1980's to early 1990's. 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 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 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 last review and again in the current Criteria
Document and Staff Paper, the National Crop Loss Assessment Network
(NCLAN) studies undertaken in the early to mid-1980's 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 and increased
O3 above ambient (i.e., modified ambient). 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\57\.
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 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.
---------------------------------------------------------------------------
\57\ Given the usefulness of generating robust C-R functions
such as have been developed under NCLAN, it would be beneficial to
employ a similar protocol to update and expand this research to
include more recent and additional crop species and varieties, such
as fruit and vegetable species, as well as recent O3 air
quality.
---------------------------------------------------------------------------
In addition to the effects described on annual crop species,
several studies published since the last 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 Staff Paper recognized that the statute requires that a
secondary standard be protective against ``adverse'' O3
effects, not all identifiable effects. In considering what constitutes
a vegetation effect that is adverse to the public welfare, the 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
[[Page 37890]]
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 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 Criteria Document concluded that O3 exposure indices
that cumulate differentially weighted hourly concentrations are the
best candidates for relating exposure to plant growth responses (EPA,
2006a). 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
(EPA, 2006a). The following selections, taken from section 5.5 the 1996
Criteria Document (EPA, 1996a), 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 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 last review, the biological basis for a
cumulative, seasonal form was not in dispute. There was general
agreement between the EPA staff, CASAC, and the Administrator, 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 seasonal cumulative 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 \58\ and W126, in the absence of biological evidence
to distinguish between them, the Administrator based her 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, the Administrator chose the SUM06 as the most
appropriate cumulative, seasonal form to consider when proposing an
alternative secondary standard form (61 FR 65716).
---------------------------------------------------------------------------
\58\ SUM06: 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 last 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 notice of proposed
rulemaking, the Administrator 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, the Administrator decided to make the
secondary standard identical to the primary standard. She acknowledged,
[[Page 37891]]
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, chapter 7 of the current Staff Paper
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 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 are lower than in the last review. The W126 form, also
evaluated in the last review, was again selected for comparison with
the SUM06 form. Regarding the first consideration, the Staff Paper
noted that 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 to concentrations in this range
are very small. 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 Staff Paper concludes that the W126
form is the most biologically-relevant cumulative, seasonal form
appropriate to consider in the context of the secondary standard
review.
C. Vegetation Exposure and Impact Assessment
The vegetation exposure and impact assessment conducted for the
current review and described in the Staff paper, consisted of exposure,
risk and benefits analyses and improves and builds upon similar
analyses performed in the last 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 recent monitored O3 air quality for the years 2001-2004;
(2) estimates of seedling growth loss under 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 current and alternative 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 final O3 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 last 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 are afforded a higher level of
protection. 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 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,
[[Page 37892]]
however, the 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 Staff Paper
therefore investigated the appropriateness of using the O3
outputs from the EPA/NOAA Community Multi-scale Air Quality (CMAQ) \59\
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 this review, 2001 outputs
from CMAQ version 4.5 were the most recent available.
---------------------------------------------------------------------------
\59\ The CMAQ model is a multi-pollutant, multiscale air quality
model that contains state-of-the-science techniques for simulating
all 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 Staff Paper concluded that it
was appropriate to use separate interpolation techniques in these two
regions. AQS and CASTNET monitoring data were solely 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., 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 uncertainty in 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 Staff Paper utilized adjusted 2001 base year
O3 air quality distributions with a rollback method (Horst
and Duff, 1995; Rizzo, 2005 & 2006) to reflect meeting the current and
alternative secondary standard options. This technique combines both
linear and quadratic elements to reduce higher O3
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 current standard) and 0.070 ppm
levels; (2) 3-month, 12-hour. SUM06: 25 ppm-hour (proposed in the 1996
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 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 is rolled back to meet the current 8-hour
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
current 0.08 ppm, 8-hour standard. Most areas were predicted to have
O3 levels below the W126 level of 21 ppm-hr, 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 proposed 0.070 ppm, 8-hour
secondary standard would provide substantially improved protection in
some areas for vegetation from seasonal O3 exposures of
concern. The 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.
[[Page 37893]]
To further characterize O3 air quality in terms of
current and alternative secondary standard forms, an analysis was
performed in the 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
Staff Paper presented this analysis using recent (2002-2004) \60\
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 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.
---------------------------------------------------------------------------
\60\ 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 the 0.08
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-
hours, 135 counties with air quality meeting the 3-year average form of
the 0.08 ppm, 8-hour average standard, would be above this W126 level.
In addition, when the 3-year average of the 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-hour average and a cumulative, seasonal form at these
sites. The Staff Paper concludes 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 Criteria Document (EPA, 2006a), 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) stratospheric
intrusions might occasionally elevate O3 at high-altitude
sites, however, these events are rare. Therefore, the Staff Paper
concludes that springtime PRB levels in the range identified above and
rare stratospheric intrusions of O3 are unlikely to
influence 3 month cumulative seasonal W126 values significantly.
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 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 an 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 Risk to Vegetation
The Staff Paper presents results from quantitative and qualitative
risk assessments of O3 risks to vegetation (EPA, 2007). In
the last 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 currently faced by seedling, sapling and mature
tree species growing in field settings, and indirectly, forested
ecosystems. Specifically, new research 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 earlier (Section A), recent systematic injury surveys
continue to document visible foliar injury symptoms diagnostic of
phytotoxic O3 exposures on sensitive bioindicator plants.
These surveys produced more expansive evidence than that available at
the time of the last review that visible foliar injury is occurring in
many areas of the U.S. under current ambient conditions. The 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 the current 0.08 8-hour standard. Of the counties that met an
8-hour level of 0.07 ppm in those years, 11 to 30 percent still had
incidence of visible foliar
[[Page 37894]]
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 the current secondary standard
or alternative 0.07 ppm 8-hour standard. Additionally, the data show
that visible foliar injury occurrence is geographically widespread and
is 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 last review (EPA, 1996b), 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, tulip poplar were found to
be sensitive to cumulative seasonal O3 exposures. Work done
since the 1996 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 analysis, C-R functions for
biomass loss for available seedling tree species taken from the CD 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 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 Staff Paper. For example, quaking aspen had a wide range of
O3 exposure across its growing range and therefore, showed
significant variability in 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 current 8-hour standard. For instance, black
cherry, ponderosa pine, eastern white pine, and aspen had estimated
median seedling biomass losses over portions of their growing range as
high as 24, 11, 6, and 6 percent, respectively, when O3 air
quality was rolled back to just meet the current 8-hour standard. The
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, a consensus workshop on O3 effects
reported 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 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 scenarios from just meeting alternative
O3 standards on the growth of mature trees. TREGRO is a
process-based, individual tree growth simulation model (Weinstein et
al., 1991) and has been used to evaluate the effects of a variety of
O3 scenarios and linked with concurrent climate data to
account for O3 and climate/meteorology interactions on
several species of trees in different regions of the U.S. (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 Staff Paper analyses found that just meeting the current
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 the current 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
[[Page 37895]]
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
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 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 Staff Paper
analysis accounted for 69 percent of 2004 principal crop acreage
planted in the U.S. in 2004.\61\ 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 last review (Abt 1995). The 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.
---------------------------------------------------------------------------
\61\ 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 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. 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 current 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 the current 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
current standard (0-4 percent).
The Staff Paper also presented estimates of monetized benefits for
crops associated with the current 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 current and
alternative standard levels were met. Meeting the various alternative
standards did show some significant benefits beyond the current 8-hour
standard. However, the Staff Paper recognized the AGSIM modeled
economic benefits had many uncertainties: For example, much of the
economic benefits were from the fruits and vegetables which had
uncertain C-R relationships, there was uncertainty in assumptions about
the treatment and effect of government farm payment programs, and there
was also uncertainty about near-term changes in 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, the uncertainties limited the utility of the
absolute numbers.
D. Conclusions on the Adequacy of the Current Standard
1. Background
The initial issue to be addressed in the current review of the
secondary O3 standard is whether, in view of the advances in
scientific knowledge reflected in the Criteria Document and additional
information on exposure and risk discussed in the Staff Paper, the
existing standard should be revised. The current secondary standard is
a 3-year average of the annual 4th-highest maximum 8-hour average
O3 concentration set at a level of 0.08 ppm. In evaluating
whether it is appropriate to retain or revise the current secondary
O3 standard, the Administrator adopts an approach in this
review that builds upon the general approach used in the last review
and reflects the broader body of evidence now available.
In developing proposed conclusions on the adequacy of the current
secondary O3 standard, the Administrator has considered a
weight-of-evidence approach that evaluated information across the
variety of vegetation-related research areas described in the Criteria
Document (e.g., seedling, sapling and mature forest tree species growth
stages and commodity, fruit, vegetable and forage crop species), and
included the assessments of air quality, exposures, and qualitative and
quantitative risks associated with alternative air quality scenarios.
Evidence-based considerations included assessment of vegetation effects
evidence obtained from chamber, free air, gradient, model and field-
based observation studies across an array of vegetation effects
endpoints. Exposure- and risk-based considerations were drawn from
exposure and risk assessments that relied upon both monitored and
interpolated O3 exposures as described in the Staff Paper.
These assessments reflect the availability of new tools and assessment
methods, as well as the larger and more diverse body of evidence
available since the last review. Specifically, estimates of exposures
and risks associated with recent O3 air quality levels, as
well as estimates of the relative magnitude of exposure and risk
reductions potentially associated with meeting the current 8-hour
secondary O3 NAAQS and alternative standards, have also been
considered, along with all known associated uncertainties.
In this review, a series of general questions frames the approach
to reaching a proposed decision on the adequacy of the current
standard, beginning with: (1) To what extent does newly available
information reinforce or call into question evidence of associations of
O3 exposures with effects identified in the last review?;
(2) to what extent does newly available information reinforce or call
into question any of the basic elements of the current standard?;
[[Page 37896]]
and (3) to what extent have important uncertainties identified in the
last review been reduced and have new uncertainties emerged? To the
extent the available information suggests that revision of the current
standard may be appropriate, the question of whether the available
information supports consideration of a standard that is either more or
less protective than the current standard is addressed, including: (1)
Whether there is evidence that vegetation effects extend to ambient
O3 concentration levels that are as low as or lower than had
previously been observed, and what are the important uncertainties
associated with that evidence?; (2) whether vegetation exposures and
risks of concern estimated to occur in areas upon meeting the current
standard are considered important from a public welfare perspective;
and (3) what are the important uncertainties associated with the
estimated risks?
The current secondary standard was selected to provide protection
to the public welfare against a range of O3-induced
vegetation effects, particularly yield loss in agricultural crops and
biomass loss in tree seedlings. As an introduction to the discussion in
this section of the adequacy of the current O3 standard, it
is useful to summarize the key factors that formed the basis of the
decision in the last review to revise the averaging time, level and
form of the then current 1-hour secondary standard.
In the 1996 proposal notice (61 FR 65716), the Administrator
proposed to replace the then existing 1-hour O3 secondary
NAAQS with one of two alternative new standards: a standard identical
to the proposed and now current 0.08 ppm, 8-hour primary standard
(described above), or alternatively, a new seasonal standard, SUM06,
expressed as a sum of hourly concentrations greater than or equal to
0.06 ppm, cumulated daily over a 12 hour daylight window (8 am to 8 pm)
during the maximum consecutive 3-month period (e.g., the consecutive 3
month period with the highest SUM06 index value) during the
O3 monitoring season, set at a level of 25 ppm-hours. The
latter form and level were selected to provide protection to vegetation
on the basis of annual, rather than 3-year average, exposures.
In the final rule for the O3 NAAQS published in July
1997 (62 FR 38877), the Administrator decided to replace the then
current 1-hour, 0.12-ppm secondary NAAQS with a standard that was
identical in every way to the new revised primary standard of an 0.08
ppm annual 4th-highest maximum 8-hour average standard averaged over 3
years. Her decision was based on: (1) Her judgment that the then
existing secondary standard did not provide adequate protection for
vegetation against the adverse welfare effects of O3; (2)
CASAC advice ``that a secondary NAAQS, more stringent than the present
primary standard, was necessary to protect vegetation from
O3'' (Wolff, 1996); (3) her judgment that the new 8-hour
average standard would provide substantially improved protection for
vegetation from O3-related adverse effects as compared to
the level of protection provided by the then current 1-hour, 0.12-ppm
secondary standard; (4) recognition that significant uncertainties
remained with respect to exposure dynamics, air quality relationships,
and the exposure, risk, and monetized valuation analyses presented in
the proposal, resulting in only rough estimates of the increased public
welfare likely to be afforded by each of the proposed alternative
standards; (5) her judgment that there was value in allowing more time
to obtain additional information to better characterize O3-
related vegetation effects under field conditions from additional
research and to develop a more complete rural monitoring network and
air quality database from which to evaluate the elements of an
appropriate seasonal secondary standard; and (6) her judgment that
there was value in allowing more time to evaluate more specifically the
improvement in rural air quality and in O3-related
vegetation effects resulting from measures designed to attain the new
primary standard (62 FR 38877-78).
The Administrator further concluded (62 FR 38877-78) that continued
research on the effects of O3 on vegetation under field
conditions and on better characterizing the relationship between
O3 exposure dynamics and plant response would be important
in the next review because: (1) The available biological database
highlighted the importance of cumulative, seasonal exposures as a
primary determinant of plant responses; (2) the association between
daily maximum 8-hour O3 concentrations and plant responses
had not been specifically examined in field tests; (3) the impacts of
attaining an 8-hour, 0.08 ppm primary standard in upwind urban areas on
rural air quality distributions could not be characterized with
confidence due to limited monitoring data and air quality modeling in
rural and remote areas.
2. Evidence- and Exposure/Risk-Based Considerations
The new evidence available in this review as described in the
Criteria Document continues to support and strengthen key policy-
relevant conclusions drawn in the previous review (EPA, 2006a). Based
on this new evidence, the current Criteria Document once more concludes
that: (1) A plant's response to O3 depends upon the
cumulative nature of ambient exposure as well as the temporal dynamics
of those concentrations; (2) current ambient concentrations in many
areas of the country are sufficient to impair growth of numerous common
and economically valuable plant and tree species; (3) the entrance of
O3 into the leaf through the stomata is the critical step in
O3 effects; (4) effects can occur with only a few hourly
concentrations above 0.08 ppm; (5) other environmental biotic and
abiotic factors are also influential to the overall impact of
O3 on plants and trees; and (6) a high degree of uncertainty
remains in our ability to assess the impact of O3 on
ecosystem services.
In light of the new evidence, as described in the Criteria
Document, the Staff Paper evaluates the adequacy of the current
standard based on assessments of both the most policy-relevant
vegetation effects evidence and exposure and risk-based information, as
summarized above in sections IV.A and IV.C, respectively. In evaluating
the strength of this information, the Staff Paper takes into account
the uncertainties and limitations in the scientific evidence and
analyses as well as the views of CASAC. The Staff Paper concludes that
progress has been made since the last review and generally finds
support in the available effects- and exposure/risk-based information
for consideration of an O3 standard that is more protective
than the current standard. The Staff Paper further concludes that there
is no support for consideration of an O3 standard that is
less protective than the current standard. This general conclusion is
consistent with the advice and recommendations of CASAC.
a. Evidence-Based Considerations
In the last review, crop yield and tree seedling biomass loss data
obtained in OTC studies provided the basis for the Administrator's
judgment that the then current 1-hour, 0.12 ppm secondary standard was
inadequate (EPA, 1996b). Since then, several additional lines of
evidence have progressed sufficiently to provide a more complete and
coherent picture of the scope of O3-related
[[Page 37897]]
vegetation risks, especially those currently faced by sensitive
seedling, sapling and mature growth stage tree species growing in field
settings, and their associated forested ecosystems. Specifically, new
research reflects an increased emphasis on field-based exposure methods
(e.g., free air, ambient gradient, and biomonitoring surveys). In
reaching conclusions regarding the adequacy of the current standard,
the Staff Paper has considered the combined information from all these
areas together, along with associated uncertainties, in an integrated,
weight-of-evidence approach.
Regarding the O3-induced effect of visible foliar
injury, observations for the years 2001 to 2004 at USDA FIA
biomonitoring sites showed widespread O3-induced leaf injury
occurring in the field, including in forested ecosystems, under current
ambient O3 conditions. For a few studied species, it has
been shown that the presence of visible foliar injury is further linked
to the presence of other vegetation effects (e.g., reduced plant growth
and impaired below ground root development) (EPA, 2006), though for
most species, this linkage has not been specifically studied or where
studied, has not been found. Nevertheless, when visible foliar injury
is present, the possibility that other O3-induced vegetation
effects could also be present for some species should be considered.
Likewise, the absence of visible foliar injury should not be construed
to demonstrate the absence of other O3-induced vegetation
effects. The Staff Paper concludes that it is not possible at this time
to quantitatively assess the degree of visible foliar injury that
should be judged adverse in all settings and across all species, and
that other environmental factors can mitigate or exacerbate the degree
of O3-induced visible foliar injury expressed at any given
concentration of O3. However, the Staff Paper also concludes
that the presence of visible foliar injury alone can be adverse to the
public welfare, especially when it occurs in protected areas such as
national parks and wilderness areas. Thus, on the basis of the
available information on the widespread distribution of O3-
sensitive species within the U.S. including in areas, such as national
parks, which are afforded a higher degree of protection, the Staff
Paper concludes that the current standard continues to allow levels of
visible foliar injury in some locations that could reasonably be
considered to be adverse from a public welfare perspective. Additional
monitoring of both O3 air quality and foliar injury levels
are needed in these areas of national significance to more fully
characterize the spatial extent of this public welfare impact.
With respect to O3-induced biomass loss in trees, the
Staff Paper concludes that the significant new body of field-based
research on trees strengthens the conclusions drawn on tree seedling
biomass loss from earlier OTC work by documenting similar seedling
responses in the field. For example, recent empirical studies conducted
on quaking aspen at the AspenFACE site in Wisconsin have confirmed the
detrimental effects of O3 exposure on tree growth in a field
setting without chambers (Isebrands et al., 2000, 2001). In addition,
results from an ambient gradient study (Gregg et al., 2003), which
evaluated biomass loss in cottonwood along an urban-to-rural gradient
at several locations, found that conditions in the field were
sufficient to produce substantial biomass loss in cottonwood, with
larger impacts observed in downwind rural areas due to the presence of
higher O3 concentrations. These gradients from low urban to
higher rural O3 concentrations occur when O3
precursors generated in urban areas are transported to downwind sites
and are transformed into O3. In addition,O3
concentrations typically fall to near 0 ppm at night in urban areas due
to scavenging of O3 by NOX and other compounds.
In contrast, rural areas, due to a lack of nighttime scavenging, tend
to maintain elevated O3 concentrations for longer periods.
On the basis of such key studies, the Staff Paper concludes that the
expanded body of field-based evidence, in combination with the
substantial corroborating evidence from OTC data, provides stronger
evidence than that available in the last review that ambient levels of
O3 are sufficient to produce visible foliar injury symptoms
and biomass loss in sensitive vegetative species growing in natural
environments. Further, the Staff Paper judges that the consistency in
response in studied species/genotypes to O3 under a variety
of exposure conditions and methodologies demonstrates that these
sensitive genotypes and populations of plants are susceptible to
adverse impacts from O3 exposures at levels known to occur
in the ambient air. Due to the potential for compounded risks from
repeated insults over multiple years in perennial species, the Staff
Paper concludes that these sensitive subpopulations are not afforded
adequate protection under the current secondary O3 standard.
Despite the fact that only a relatively small portion of U.S. plant
species have been studied with respect to O3 sensitivity,
those species/genotypes shown to have O3 sensitivity span a
broad range of vegetation types and public use categories, including
direct-use categories like food production for human and domestic
animal consumption; fiber, materials, and medicinal production; urban/
private landscaping. Many of these species also contribute to the
structure and functioning of natural ecosystems (e.g., the EEAs) and
thus, to the goods and services those ecosystems provide (Young and
Sanzone, 2002), including non-use categories such as relevance to
public welfare based on their aesthetic, existence or wildlife habitat
value.
The Staff Paper therefore concludes that the current secondary
standard is inadequate to protect the public welfare against the
occurrence of known adverse levels of visible foliar injury and tree
seedling biomass loss occurring in tree species (e.g., ponderosa pine,
aspen, black cherry, cottonwood) that are sensitive and clearly
important to the public welfare.
b. Exposure- and Risk-Based Considerations
The Staff Paper also presents the results of exposure and risk
assessments. Due to multiple sources of uncertainty, both known and
unknown, that continue to be associated with these analyses, the Staff
Paper put less weight on this information in drawing conclusions on the
adequacy of the current standard. However, the Staff Paper also
recognizes that some progress has been made since the last review in
better characterizing some of these associated uncertainties and,
therefore concluded that the results of the exposure and risk
assessments continue to provide information useful to informing
judgments as to the relative changes in risks predicted to occur under
exposure scenarios associated with the different standard alternatives
considered. Importantly, with respect to two key uncertainties, the
uncertainty associated with continued reliance on C-R functions
developed from OTC exposure systems to predict plant response in the
field and the potential for changes in tree seedling and crop
sensitivities in the intervening period since the C-R functions were
developed, the Staff Paper concluded that recent research has provided
information useful in judging how much weight to put on these concerns.
Specifically, new field-based studies, conducted on a limited number of
tree seedling and crop species to date, demonstrate plant growth and
visible foliar injury responses in the field that
[[Page 37898]]
are similar in nature and magnitude to those observed previously under
OTC exposure conditions, lending qualitative support to the conclusion
that OTC conditions do not fundamentally alter the nature of the
O3-plant response. Second, nothing in the recent literature
suggests that the O3 sensitivity of crop or tree species
studied in the last review and for which C-R functions were developed
has changed significantly in the intervening period. Indeed, in the few
recent studies where this is examined, O3 sensitivities were
found to be as great as or greater than those observed in the last
review.
i. Seedling and Mature Tree Biomass Loss
Biomass loss in sensitive tree seedlings is predicted to occur
under O3 exposures that meet the level of the current
secondary standard. For instance, black cherry, ponderosa pine, eastern
white pine, and aspen had estimated median seedling biomass losses as
high as 24, 11, 6, and 6 percent, respectively, over some portions of
their growing ranges when air quality was rolled back to meet the
current 8-hr standard with the 10 percent downward adjustment for the
potential O3 gradient between monitor height and short plant
canopies applied. The Staff Paper notes 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. Decreased root growth
associated with biomass loss has the potential to indirectly affect the
vigor and survivability of tree seedlings. If such effects occur on a
sufficient number of seedlings within a stand, overall stand health and
composition can be affected in the long term. Thus, the Staff Paper
concludes that these levels of estimated tree seedling growth reduction
should be considered significant and potentially adverse, given that
they are well above the 2 percent level of concern identified by the
1997 consensus workshop (Heck and Cowling, 1997).
Though there is significant uncertainty associated with this
analysis, the Staff Paper recommends that this information should be
given careful consideration in light of several other pieces of
evidence. Specifically, limited evidence from experimental studies that
go beyond the seedling growth stage continues to show decreased growth
under elevated O3 levels (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). The potential for effects to ``carry over'' to
the following year or cumulate over multiple years, including the
potential for compounding, must be considered. The accumulation of such
``carry-over'' effects over time may affect long-term survival and
reproduction of individual trees and ultimately the abundance of
sensitive tree species in forest stands.
ii. Qualitative Ecosystem Risks
In addition to the quantifiable risk categories discussed above,
the Staff Paper presents qualitative discussions on a number of other
public welfare effects categories. In so doing, the Staff Paper
concludes that the quantified risks to vegetation estimated to be
occurring under current air quality or upon meeting the current
secondary standard likely represent only a portion of actual risks that
may be occurring for a number of reasons.
First, as mentioned above, out of the over 43,000 plant species
catalogued as growing within the U.S. (USDA PLANTS database, USDA,
NRCS, 2006), only a small percentage have been studied with respect to
O3 sensitivity. Most of the studied species were selected
because of their commercial importance or observed O3-
induced visible foliar injury in the field. Given that O3
impacts to vegetation also include less obvious but often more
significant impacts, such as reduced annual growth rates and below
ground root loss, the paucity of information on other species means the
number of O3-sensitive species that exists within U.S.,
could be greater than what is now known. Since no state in the lower 48
states has less than seven known O3-sensitive plant species,
with the majority of states having between 11 and 30 (see Appendix 7J-2
in Staff Paper), protecting O3 sensitive vegetation is
clearly important to the public welfare at the national scale.
Second, the Staff Paper also takes into consideration the
possibility that more subtle and hidden risks to ecosystems are
potentially occurring in areas where vegetation is being significantly
impacted. Given the importance of these qualitative and anticipated
risks to important public welfare effects categories such as ecosystem
impacts leading to potential losses or shifts in ecosystem goods and
services (e.g., carbon sequestration, hydrology, and fire disturbance
regimes), the Staff Paper concludes that any secondary standard set to
protect against the known and quantifiable adverse effects to
vegetation should also consider the anticipated, but currently
unquantifiable, potential effects on natural ecosystems.
iii. Crop Yield Loss
Exposure and risk assessments in the Staff Paper estimated that
meeting the current 8-hour standard would still allow O3-
related yield loss to occur in several fruit and vegetable and
commodity crop species currently grown in the U.S. These estimates of
crop yield loss are substantially lower than those estimated in the
last review as a result of several factors, including adjusted exposure
levels to reflect the presence of a variable O3 gradient
between monitor height and crop canopies, and use of a different
econometric agricultural benefits model updated to reflect more recent
agricultural policies (EPA, 2006b). Though these sources of uncertainty
associated with the crop risk and benefits assessments were better
documented in this review, the Staff Paper concludes that the presence
of these uncertainties make the risk estimates suitable only as a basis
for understanding potential trends in relative yield loss and economic
benefits. The Staff Paper further recognizes that actual conditions in
the field and management practices vary from farm to farm, that
agricultural systems are heavily managed, and that adverse impacts from
a variety of other factors (e.g., weather, insects, disease) can be
orders of magnitude greater than that of yield impacts predicted for a
given O3 exposure. Thus, the relevance of such estimated
impacts on crop yields to the public welfare are considered highly
uncertain and less useful as a basis for assessing the adequacy of the
current standard. The Staff Paper notes, however, that in some
experimental cases, exposure to O3 has made plants more
sensitive or vulnerable to some of these other important stressors,
including disease, insect pests, and harsh weather (EPA, 2006a). The
Staff Paper therefore concluded that this remains an important area of
uncertainty and that additional research to better characterize the
nature and significance of these interactions between O3 and
other plant stressors would be useful.
c. Summary
In summary, the Staff Paper concludes that the current secondary
O3 standard is inadequate. This conclusion is based on the
extensive vegetation effects evidence, in particular the recent
empirical field-based evidence on biomass loss in seedlings, saplings
and mature trees, and foliar injury incidence that has become available
in this review, which demonstrates the occurrence of adverse vegetation
effects at ambient
[[Page 37899]]
levels of recent O3 air quality, as well as evidence and
exposure- and risk-based analyses indicating that adverse effects would
be predicted to occur under air quality scenarios that meet the current
standard.
3. CASAC Views
In a letter to the Administrator (Henderson, 2006c), the CASAC
O3 Panel, with full endorsement of the chartered CASAC,
unanimously concluded that ``despite limited recent research, it has
become clear since the last review that adverse effects on a wide range
of vegetation including visible foliar injury are to be expected and
have been observed in areas that are below the level of the current 8-
hour primary and secondary ozone standards.'' Therefore, ``based on the
Ozone Panel's review of Chapters 7 and 8 [of the Staff Paper], the
CASAC unanimously agrees that it is not appropriate to try to protect
vegetation from the substantial, known or anticipated, direct and/or
indirect, adverse effects of ambient O3 by continuing to
promulgate identical primary and secondary standards for O3.
Moreover, the members of the Committee and a substantial majority of
the Ozone Panel agree with EPA staff conclusions and encourage the
Administrator 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 currently existing
or potentially revised 8-hour primary standard'' (Henderson,
2006c).\62\
---------------------------------------------------------------------------
\62\ One CASAC Panel member reached different conclusions from
those of the broader Panel regarding certain aspects of the
vegetation effects information and the appropriate degree of
emphasis that should be placed on the associated uncertainties.
These concerns related to how the results of O3/
vegetation exposure experiments carried out in OTC can be
extrapolated to the ambient environment and how C-R functions
developed in the 1980's can be used today given that he did not
expect that current crop species/cultivars in use in 2002 would have
the same O3 sensitivity as those studied in NCLAN
(Henderson, 2007, pg. C-18).
---------------------------------------------------------------------------
4. Administrator's Proposed Conclusions Concerning Adequacy of Current
Standard
The Administrator recognizes that the secondary standard is to
protect against ``adverse'' O3 effects, discussed above in
section IV.A.3. In considering what constitutes a vegetation effect
that is also adverse to the public welfare, the Administrator took into
account the Staff Paper conclusions regarding the nature and strength
of the vegetation effects evidence, the exposure and risk assessment
results, the degree to which the associated uncertainties should be
considered in interpreting the results, and the views of CASAC and
members of the public. On these bases, the Administrator proposes that
the current secondary standard is inadequate to protect the public
welfare from known and anticipated adverse O3-related
effects on vegetation and ecosystems. Ozone levels that would be
expected to remain after meeting the current secondary standard are
sufficient to cause visible foliar injury, seedling and mature tree
biomass loss, and crop yield reductions to degrees that could be
considered adverse depending on the intended use of the plant and its
significance to the public welfare, and the current secondary standard
does not provide adequate protection from such effects. Other
O3-induced effects described in the literature, including an
impaired ability of many sensitive species and genotypes within species
to adapt to or withstand other environmental stresses, such as freezing
temperatures, pest infestations and/or disease, and to compete for
available resources, would also be anticipated to occur. In the long
run, the result of these impairments (e.g., loss in vigor) could lead
to premature plant death in O3 sensitive species. Though
effects on other ecosystem components have only been examined in
isolated cases, effects such as those described above could have
significant implications for plant community and associated species
biodiversity and the structure and function of whole ecosystems. These
considerations also support the proposed conclusion that the current
secondary standard is not adequate and that revision is needed to
provide additional public welfare protection.
E. Conclusions on the Elements of the Secondary Standard
Given his proposed conclusion that the current secondary standard
is inadequate, the Administrator then considered what revisions to the
standard are appropriate. In so doing, the Administrator has focused on
revisions to the key standard elements of indicator, form, averaging
time, and level. On the basis of the strength and coherence of the
vegetation effects evidence suggesting that a biologically-based
standard for vegetation, at a minimum, should cumulate exposures and
differentially-weight higher O3 concentrations, the
Administrator judges that it is appropriate to consider revisions to
the secondary standard that reflect this understanding. In addition,
the Administrator also judges that the current 8-hour average form,
though not based on the most biologically relevant and coherent
vegetation effects literature, can also provide substantially improved
protection to vegetation when set at an appropriate level. Therefore,
the Administrator also considered whether revision to the level of the
current 8-hour secondary standard might provide the requisite level of
public welfare protection. In light of these considerations, as
discussed below, the Administrator is proposing two options for
revising the current secondary standard: one option is a cumulative
seasonal standard (section IV.E.2) and the other option is an 8-hour
average standard consistent with the revised 8-hour average standard
proposed above for the primary standard (section IV.E.3). The
Administrator has also considered an alternative approach to setting a
cumulative, seasonal standard(s) as described below in section IV.E.2.
1. Indicator
In the last review, EPA focused on a standard for O3 as
the most appropriate surrogate for ambient photochemical oxidants. In
this review, while the complex atmospheric chemistry in which
O3 plays a key role has been highlighted, no alternatives to
O3 have been advanced as being a more appropriate surrogate
for ambient photochemical oxidants. Thus, as is the case for the
primary standard, (discussed above in section II.D.1.), the
Administrator proposes to continue to use O3 as the
indicator for a standard that is intended to address effects associated
with exposure to O3, alone and in combination with related
photochemical oxidants. In so doing, the Administrator recognizes that
measures leading to reductions in vegetation exposures to O3
will also reduce exposures to other photochemical oxidants.
2. Cumulative, Seasonal Standard
The Administrator proposes to replace the current secondary
standard with a new cumulative, seasonal standard expressed as an index
of the annual sum of weighted hourly concentrations (using the W126
form), set at a level in the range of 7 to 21 ppm-hours. The index
would be cumulated over the 12-hour daylight period (8 a.m. to 8 p.m.)
during the consecutive 3-month period within the O3 season
with the maximum index value. In addition, as discussed below, the
Administrator is considering an alternative approach to setting a
cumulative, seasonal standard(s) that would afford differing degrees of
protection for O3-related impacts on different types of
vegetation with different intended uses.
[[Page 37900]]
a. Form
The current Criteria Document and Staff Paper concluded that the
recent vegetation effects literature evaluated in this review
strengthens and reaffirms conclusions made in the last 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 1996 review focused in particular on two of these
cumulative forms, the SUM06 and W126. As described in the last review
(EPA, 1996a, b) it was concluded that, based on statistical reanalysis
of the NCLAN data, these different cumulative forms performed equally
well in predicting crop yield loss response to O3 exposure.
Given that the data available at that time were unable to distinguish
between these forms, the Administrator, based on the policy
consideration of not including O3 concentrations considered
to be within the PRB, concluded that the SUM06 form was the more
appropriate choice for a secondary standard.
In this review, the Staff Paper evaluated the continued
appropriateness of the SUM06 form in light of two key pieces of
information: new estimates of PRB that are lower than in the last
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 Staff Paper concluded that the W126 form was more
appropriate in the context of this review. 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.
The CASAC, based on its assessment of the same vegetation effects
science, agreed with the Criteria Document and 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 CASAC
and a substantial majority of the CASAC O3 Panel agreed with
Staff Paper conclusions and encouraged the Administrator 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).\63\
---------------------------------------------------------------------------
\63\ One CASAC Panel member expressed the view that the
O3 exposure indices, SUM06 and W126, are simply
mathematical expressions of exposure and, thus, cannot be said to
have a biological basis (Henderson, 2007, pg. C-18).
---------------------------------------------------------------------------
The Administrator agrees with the conclusions drawn in the Criteria
Document, Staff Paper and by CASAC that the scientific evidence
available in the current review 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 seasonal secondary standard to protect against the effects of
O3 on vegetation. The Administrator further agrees with both
the Staff Paper and CASAC that the most appropriate cumulative,
concentration-weighted form to consider in this review is the
sigmoidally weighted W126 form, due to his 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 review. Thus,
the Administrator proposes as one option to replace the current 8-hour
average secondary standard form with the cumulative, seasonal W126
form.
b. Averaging Times \64\
---------------------------------------------------------------------------
\64\ While the term ``averaging time'' is used, for the
cumulative, seasonal standard the time period at issue is one over
which exposures during a specified period of time are cumulated, not
averaged.
---------------------------------------------------------------------------
The Staff Paper, in addition to form, also considers what
``averaging'' periods or exposure 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. Exposure
periods are discussed below in terms of a seasonal window, a diurnal
window, and an annual versus 3-year average standard.
(1) In considering an appropriate seasonal window, the Staff Paper
recognizes 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 Staff Paper notes 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 Staff Paper further concludes
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 Staff Paper again
concludes, as it did in 1996, 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
recognizes 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
[[Page 37901]]
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 do not take up O3 at
night or occur in areas with elevated nighttime O3
concentrations.
In light of a recent work on this topic conducted by Musselman and
Minnick (2000), the Staff Paper again revisited the issue of what
diurnal period is of most relevance in influencing O3-
induced effects on vegetation. This work reports 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 Staff Paper concludes 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 Staff Paper concludes that this information continues to
be preliminary, and does not provide a basis for reaching a different
conclusion at this time. The Staff Paper further notes 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 last review, the Staff
Paper again concludes 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 an annual or 3-year averaging period is
more appropriate, the 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 averaging period for purposes of standard stability.
However, the 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, while for
other welfare effects (e.g., mature tree biomass loss), a 3-year
averaging period may also be appropriate. Thus, the Staff Paper
concludes that it is appropriate to consider both an annual and a 3-
year averaging period. Further, the Staff Paper concludes that should a
3-year average of the 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 CASAC, in considering what seasonal and diurnal time periods
are most appropriate when combined with a cumulative, concentration-
weighted form to protect vegetation from exposures of concern, agreed
that the Staff Paper conclusion regarding the 3-month seasonal period
and 12-hour daylight window was appropriate, with the distinction that
both time designations 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 maximum 8-hour concentrations. CASAC 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 determining which seasonal and diurnal time
periods are most appropriate to propose, took into account Staff Paper
and CASAC views. The Administrator, in being careful to consider what
is needed to provide the requisite degree of protection, no more and no
less, proposes that the 3-month seasonal period and 12-hour daylight
period are appropriate. Based on the Staff Paper conclusions discussed
above, the Administrator is 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, the Administrator also recognizes 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, the Administrator
agrees with the 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 Administrator 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 Administrator further proposes that the maximum 3-
month period is sufficient and appropriate to characterize
O3 exposure levels associated with known levels of plant
response. Therefore, the Administrator proposes 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 Administrator also proposes an annual rather than a multi-year
cumulative, seasonal standard. In proposing this alternative, the
Administrator also believes that it is appropriate to consider the
benefits to the public welfare that would accrue from establishing a 3-
year average secondary standard, and solicits comment on this
alternative. In so doing, the Administrator also agrees with 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.
[[Page 37902]]
c. Level
The 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, considers
what information from the array of vegetation effects evidence and
exposure and risk assessment results was most useful. In regards to the
vegetation effects evidence, the Staff Paper finds stronger support
than what was available at the time of the last 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
Staff Paper concludes that just meeting the 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 air
quality 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 Staff Paper also considers 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 Staff Paper concludes 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 Staff Paper also recognizes that in the last
review, the Administrator took into account the results of a 1996
consensus-building workshop as described in a January 1997 report (Heck
and Cowling, 1997). 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 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 range of 10 to 15 (7 to 13) ppm-hours would be
protective. For growth effects to tree seedlings and saplings in
plantations, the consensus range was 12 to 16 (9 to 14) ppm-hours. For
visible foliar injury to natural ecosystems, the consensus range was 8
to 12 (5 to 9) ppm-hours (Heck and Cowling, 1997).
Taking these consensus statements into account, the Administrator
stated in the 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 the Administrator put on the consensus report
in the last review, the Staff Paper considered to what extent new
research provided empirical support for the ranges of levels identified
by the experts as protective of different types of O3-
induced effects. On the basis of new field-based tree seedling growth
loss and foliar injury data, and including both the above quantitative
and qualitative information regarding O3-induced effects on
sensitive trees and forested ecosystems, the Staff Paper concludes that
it is appropriate to consider a range for a 3-month, 12-hour, W126
standard that includes the consensus recommendations for growth effects
in tree seedlings in natural forest stands.
In considering the newly available information on O3-
related effects on crops in this review, the Staff Paper observes 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 Staff Paper concludes that nothing in the newly assessed
information calls into question the strength of the underlying science
upon which the Administrator based her 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 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 Staff Paper observes that agricultural systems are
heavily managed, and that in addition to stress from O3, the
annual productivity of agricultural systems is vulnerable to
[[Page 37903]]
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 Staff Paper concludes that
the level of protection judged requisite in the last review to protect
the public welfare from adverse levels of O3-induced
reductions in crop yields, as provided by a W126 level of 21 ppm-hours,
remains appropriate for consideration as an upper bound of a range of
appropriate levels.
Thus, the Staff Paper concludes, based on all the above
considerations, that an appropriate range of 3-month, 12-hour W126
levels is 7 to 21 ppm-hours, 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 Staff Paper recognizes 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 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-
hours; however, it did not agree with Staff's recommendation that the
upper bound of the range should be as high as 21 ppm-hours. Rather,
CASAC recommended that the upper bound of the range considered should
be no higher than 15 ppm-hours, which the Panel estimates is
approximately equivalent to a seasonal 12-hour SUM06 level of 20 ppm-
hours. The lower end of this range (7 ppm-hours) is the same as the
lower end of the range identified in the 1997 Consensus Workshop as
protective of tree seedlings in natural forest stands from growth
effects (Heck and Cowling, 1997).
The Administrator, taking Staff Paper and CASAC views into account,
proposes 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-hours. This range encompasses the
range of levels recommended by CASAC, and also includes a higher level
as recommended in the Staff Paper. Given the uncertainty in determining
the risk attributable to various levels of exposure to O3,
the Administrator believes as a public welfare policy judgment that
this is a reasonable range to propose.
In taking into account the uncertainty associated with the above,
the Administrator has also considered an alternative approach to
establishing a secondary standard(s). This alternative approach would
establish a cumulative, seasonal standard(s) that would afford
differing degrees of protection for O3-related impacts on
different types of vegetation with different intended uses.
The Administrator recognizes that known O3-sensitive
plant species growing within the U.S experience a variety of
O3-induced effects, including visible foliar injury, biomass
loss and yield loss, and that the public welfare significance of each
of these effects can vary significantly, depending on the nature of the
effect, the intended use of the plant, and/or the type of environment
or location in which the plant grows. Any given O3-related
effect on vegetation (e.g., biomass loss, or foliar injury) may be
judged to have a different degree of impact on public welfare
depending, for example, on whether that effect occurs in a Class I
area, commercial cropland, or a city park. This variation in the
significance of O3-related vegetation effects from a public
welfare perspective across type of effect, intended plant use, and area
grown means that the level of ambient O3 that is requisite
to protect the public welfare may also vary. The level of ambient
O3 that is requisite in a federally designated Class I area
may be lower than the level that is requisite in a cropland area. EPA
is therefore considering and soliciting comment on an alternative
approach for the secondary O3 standard, with the aim of
reasonably reflecting these variations.
Specifically, the Administrator seeks comment on an alternative
approach that would establish a suite of secondary standards. The suite
of standards would contain different ambient levels, with each standard
at a level that is requisite to protect public welfare for that
variation in plant effect, use, and/or location. For example, a
secondary standard intended to provide protection to natural systems
valued for their aesthetic beauty and/or important ecological functions
they might serve could be set at a lower, more protective level to
provide the requisite degree of protection against a broad array of
O3-related effects on important sensitive species in such
areas. In contrast, while negative impacts on yield production in
sensitive agricultural crops is also an important public welfare
effect, O3-related reductions in yield may be considered
less significant or adverse to the public welfare, depending on the
degree of impact, since the intended use of such land is to produce
optimum yields and croplands are already heavily managed to achieve
that goal. Thus, a secondary standard set to provide the requisite
degree of crop protection for such an area could be set at a higher
level.
The Administrator recognizes that variation in vegetation type and
location, intended use, and impacts related to O3 exposure
can be diverse, and believes that it is appropriate to consider whether
it is appropriate and feasible to establish a suite of standards that
accounts more broadly for such variation. EPA recognizes that this
approach is unique with regard to secondary standards and will pose
unique challenges, including how to classify areas according to
intended use. Some geographic areas have already been identified for
specific uses, such as Federal Class I areas,\65\ which are intended to
conserve unimpaired natural ecosystems and their associated species for
the enjoyment of future generations. Likewise, the USDA has classified
cultivated areas in the U.S. into certain categories of intended use
(such as cropland, rangeland, timberland) that could help inform the
setting of a suite of standards.
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\65\ The Clean Air Act defines Class I areas as national parks
over 6,000 acres, national wilderness areas and national memorial
parks over 5,000 acres, and international parks. The National Park
Service was created in 1916 by Congress through the National Park
Service Organic Act in order to ``conserve the scenery and the
natural and historic objects and the wild life therein and to
provide for the enjoyment of the same in such manner and by such
means as will leave them unimpaired for the enjoyment of future
generations.''
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EPA is taking comment on all aspects of this alternative approach,
including whether it is appropriate to set a suite of secondary
standards that varies depending on use, location, and type of effect on
vegetation. EPA invites comment on the appropriateness of this
approach, from the scientific, legal, and policy perspectives, and on
other factors that should be considered in determining the
applicability of any one level within a suite of standards.
[[Page 37904]]
3. 8-Hour Average Standard
The Administrator is also proposing to revise the current secondary
standard by making it identical to the proposed 8-hour primary
standard, which is proposed to be within the range of 0.070 to 0.075
ppm. For this option, EPA also solicits comment on a wider range of 8-
hour standard levels, including levels down to 0.060 ppm and up to the
current standard (i.e., effectively 0.084 ppm with the current rounding
convention).
In the last review, the 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 current 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 recent air quality. Based on the results, the 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.
Thus, though the 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 urges 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 is due to the concern that the
analysis in the 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 Staff Paper concluded that it remains 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).
A number of public commenters also presented views for the
Administrator's consideration regarding the adequacy of the current
standard and whether or not revisions to that standard were warranted.
These commenters did not support adopting an alternative, cumulative
form for the secondary standard. These commenters stated that ``though
directionally a cumulative form of the standard may better match the
underlying data,'' they believed further work is needed to determine
whether a cumulative exposure index for the form of the secondary
standard is necessary. These commenters identified a number of key
concerns regarding the available evidence that, in their view, make it
inappropriate to revise the secondary standard at this time. In
particular they assert that (1) The key uncertainties, cited by the
Administrator in the 1997 review as reasons for deciding it was not
appropriate to move forward with a seasonal secondary, have not been
materially reduced in the current review; and (2) the exposure
assessment is inaccurate and too uncertain due to the use of low
estimates of PRB, an arbitrary rollback method that is uninformed by
atmospheric chemistry from photochemical models, and the use of the
CMAQ model in the west, whose biases and uncertainties are
insufficiently characterized and evaluated.
In considering the appropriateness of proposing a revised secondary
standard that would be identical to the proposed primary standard, the
Administrator took into account the approach used by the Agency in the
last review, the conclusions of the Staff Paper, CASAC advice, and the
views of public commenters. The Administrator first considered the
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, the
Administrator recognizes 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 Administrator also recognizes that
lack of rural monitoring data makes 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 is clear, the number and size of areas at issue and the
degree of risk is hard to determine. However, such a standard would
also tend to avoid the potential for providing more protection than is
necessary, a risk that 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 Administrator also considered the views and recommendations of
[[Page 37905]]
CASAC, and agrees 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, the Administrator also
recognizes that there remain 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, the Administrator also believes
it is appropriate to consider the degree of protection that would be
afforded by a secondary standard that is identical to the proposed
primary standard. Based on his consideration of the full range of views
as described above, the Administrator proposes as a second option to
revise the secondary standard to be identical in every way to the
proposed primary standard.
F. Proposed Decision on the Secondary Standard
The Administrator proposes to replace the current secondary
standard with one of two options. One option is a new cumulative,
seasonal standard expressed as an index of the annual sum of weighted
hourly concentrations (using the W126 form), set at a level in the
range of 7 to 21 ppm-hours. The index would be cumulated over the 12-
hour daylight period (8 a.m. to 8 p.m.) during the consecutive 3-month
period within the O3 season with the maximum index value.
The other option is to revise the current secondary standard by making
it identical to the proposed 8-hour primary standard, which is proposed
to be within the range of 0.070 to 0.075 ppm. For this option, EPA also
solicits comment on a wider range of 8-hour standard levels, including
levels down to 0.060 ppm and up to the current standard (i.e.,
effectively 0.084 ppm with the current rounding convention. The
Administrator is also soliciting comment on an alternative approach for
a setting cumulative, seasonal standard(s) that would afford differing
degrees of protection for O3-related impacts on different
types of vegetation with different intended uses.
V. Creation of Appendix P--Interpretation of the NAAQS for Ozone
The EPA is proposing to create Appendix P to 40 CFR part 50 to
reflect the proposed revisions to the primary and secondary standards
discussed above. This Appendix would explain the computations necessary
for determining when the proposed primary and secondary standards are
met. More specifically, Appendix P addresses data completeness
requirements, data reporting, handling, and rounding conventions, and
example calculations. Although EPA is proposing two alternative
secondary standards, the proposed Appendix has been written to address
a seasonal secondary standard expressed in the W126 form. If EPA adopts
a secondary standard identical to the primary standard, Appendix P will
be modified accordingly. The proposed Appendix also reflects the final
rule promulgated on March 22, 2007 for the treatment of data influenced
by exceptional events (72 FR 13560).
Key elements of the proposed revisions to Appendix P are outlined
below.
A. Data Completeness
The data completeness requirements in Appendix P proposed here for
the proposed 8-hr primary standard secondary standards are the same as
those in Appendix I to 40 CFR part 50 required for the current
standard. To satisfy the date completeness requirement, Appendix P
would require 90% data completeness, on average, for the 3-year period
at a monitoring site, with no single year within the period having less
than 75% data completeness. This data completeness requirement would
have to be satisfied in order to determine that the standard(s) have
been met at a monitoring site. A site could be found not to have met
the standard(s) with less than complete data. EPA concluded in adopting
these same data completeness requirements in Appendix I in 1997 that
these proposed requirements are reasonable based on its earlier
analysis of available air quality data that showed that 90% of all
monitoring sites that are operated on a continuous basis routinely meet
this objective. The EPA is seeking comment, however, on whether
meteorological data would provide an objective basis for determining,
on a day for which there is missing data, that the meteorological
conditions were not conducive to high O3 concentrations, and
therefore, that the day could be assumed to have an O3
concentration less than 0.070 to 0.075 ppm.
We are proposing separate data completeness requirements for the
proposed seasonal secondary standard expressed in the W126 form. For
such a standard, Appendix P would require a site to have 75% data
completeness in a given month. Appendix P would also provide a
mechanism for adjusting for missing data. Because this alternative is a
seasonal cumulative index, representing a distribution of O3
values under a range of meteorological conditions, rather than a peak
statistic, the EPA is proposing a missing data procedure that would
require the monthly total index to be adjusted for incomplete data by
multiplying the unadjusted W126 value by the ratio of the number of
possible daylight hours (8:00 a.m. to 8:00 p.m.) to the number of hours
with valid ambient hourly concentrations. This adjustment is analogous
to calculating an estimated number of exceedances contained within part
50 Appendix I for the one hour O3 standard.
B. Data Handling and Rounding Conventions
Almost all State agencies now report hourly O3
concentrations to three decimal places, in ppm, since the typical
incremental sensitivity of currently used O3 monitors is
0.001 ppm. Consistent with the current approach for computing 8-hr
averages, in calculating 8-hr average O3 concentrations from
such hourly data, any calculated digits past the third decimal place
would be truncated to preserve the number of significant digits in the
reported data. In calculating 3-year averages of the fourth highest
maximum 8-hr average concentrations, EPA is proposing to require the
result to be reported to the third decimal place with digits to the
right of the third decimal place truncated to preserve the number of
significant digits in the reported data, as prescribed by the current
standard. Analyses discussed in the 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 considers any value less than 0.001
ppm to be highly uncertain and, therefore, proposes truncating both the
individual 8-hour averages used to determine the annual fourth maximum
as well as the 3-year average of the fourth maxima to the third decimal
place. Nevertheless, EPA solicits comment on the appropriateness of
rounding to the third decimal place as well as the policy reasons
behind either truncating or rounding the 3-year average to the third
decimal place (with 0.0005 and greater rounding up). EPA is also
seeking comment on the scientific validity of truncating the three year
average as opposed to rounding it as well as the policy reasons behind
either truncating or rounding the average to the third decimal place.
[[Page 37906]]
To determine whether the proposed standard is met, the calculated
value of the fourth highest maximum 8-hour average concentrations,
averaged over three years, would be compared to the level of the
standard. As discussed in section II, the EPA is proposing to issue an
8-hr standard extending to three decimal places, based on the staff's
analysis and conclusions discussed in the Staff paper that expressing
the proposed standard to the third decimal place is consistent with the
precision requirements of the current O3 monitoring
technology. Given that both the proposed standard and the calculated
value of the 3-year average of the fourth highest maximum 8-hr
O3 concentration are expressed to three decimal places, the
two values can be compared directly. This is different than the
approach for determining compliance with the current standard
O3 standard. In comparing the calculated 3-year average
(which is expressed to three decimal places) to the current standard
O3 standard (which is expressed to only two decimal places),
Appendix I requires the calculated 3-year average to be rounded to two
decimal places. This additional step would not be necessary for the
proposed standard given that the standard and the 3-year average are
each expressed to three decimal places.
For the proposed seasonal secondary standard, the annual maximum 3-
month W126 value computed on a calendar year basis using the three
highest, consecutive monthly W126 values would be used as the summary
statistic. The resulting value would then be compared to the level of
the secondary O3 standard. The Agency is also interested in
receiving comments regarding a 3-year average form summary statistic.
VI. Ambient Monitoring Related to Proposed Revised O3
Standards
The EPA is not proposing any specific changes to existing
requirements for monitoring of O3 in the ambient air.
However, we invite comment on a number of issues which naturally arise
in connection with the proposed revision of the O3 NAAQS.
The EPA may propose changes to some of the existing requirements at a
later date.
Current requirements regarding EPA-approved measurement methods for
ambient O3 are stated in 40 CFR part 50 Appendix D,
Measurement Principle and Calibration Procedure for the Measurement of
Ozone in the Atmosphere, and in 40 CFR part 53, Ambient Air Monitoring
Reference and Equivalent Methods. The EPA does not intend to propose
any changes to these requirements, because we believe these
requirements would continue to be appropriate to support implementation
of a revised O3 NAAQS.
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)
Certain deviations including minimum monitoring requirements and/or
monitoring season requirements may be approved by the EPA Regional
Administrator on a case-by-case basis.
Required O3 monitoring seasons range from four to 12
months. The minimum number of monitors in an MSA ranges from zero (for
an area with population under 350,000 and no recent history of an
O3 design value greater than 85 percent of the NAAQS) to
four (for an area with population greater than 10 million and an
O3 design value greater than 85 percent of the NAAQS).
Because these requirements apply at the MSA level, large urban areas
consisting of multiple MSAs can require more than four monitors. For
example, the New York-Newark-Bristol NY-NJ-CT-PA combined statistical
area requires about 14 monitors. In total, about 400 monitors are
required in MSAs, but about 1100 are actually operating in MSAs because
most States operate more than the minimum required number of monitors.
There are no EPA requirements for O3 monitoring in less
populated areas outside of MSA boundaries (e.g., Metropolitan
Statistical Areas) or in rural areas. However, there are about 250
O3 monitors in counties that are not part of MSAs. Some
required State monitors are placed downwind of the urban center of the
MSA of interest in locations that are in some cases in a county outside
the MSA itself; some States also operate a few rural monitors for
research purposes. The EPA operates a network of about 56 O3
monitors as part of its Clean Air Status and Trends Network (CASTNET).
The National Park Service (NPS) operates about 27 monitors at other
CASTNET sites. The NPS also has O3 monitoring stations in
parks that are not part of the CASTNET dry deposition monitoring effort
including multiple O3 stations in Great Smoky Mountains,
Sequoia, Yosemite, and Joshua Tree National Parks.
Required quality assurance procedures for O3 monitoring
are given in 40 CFR Part 58 Appendix A, Quality Assurance Requirements
for State and local air monitoring stations (SLAMS), special purpose
monitors (SPM), and prevention of significant deterioration (PSD) Air
Monitoring. The EPA does not intend to propose any changes to these
quality assurance requirements, because we believe that the current
measurement uncertainty goals and related procedures for assessing
precision and bias as documented in paragraph 2.3.1.2 of Appendix A are
appropriate to support the implementation of a revised O3
NAAQS.
States are required to report O3 data quarterly to EPA's
Air Quality System (AQS), and most also voluntarily report their pre-
validated O3 data on an hourly basis to EPA's real time
AirNow data system, where the data are used to forecast O3
concentrations and to provide public advisories. The National Park
Service and many other organizations also report their O3
data to AQS and/or AirNow. The locations of currently operating
O3 monitors which report data to EPA's Air Quality System
are available through the EPA AirData Web site http://www.epa.gov/air/data/index.html.
Data from O3 monitors at CASTNET stations are currently
kept in a separate national data base.\66\
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\66\ At present, not all ozone monitors at CASTNET sites are
operated in full compliance with the quality assurance requirements
of 40 CFR Part 58 Appendix D, as they have not been primarily
intended for regulatory use. The EPA is working towards such
compliance in the near future and towards making CASTNET ozone data
available through AQS.
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The EPA invites comments on O3 monitoring issues (other
than O3 monitoring methods and quality assurance
requirements), including the following:
(1) Ozone monitoring network requirements in urban areas. Table D-2
of 40 CFR Part 58 Appendix D is based on the percentage of the
O3 NAAQS, with a break point at 85 percent of the NAAQS.
Therefore, a revision of the NAAQS would automatically increase the
required number of O3 monitors. For example, assuming a
final NAAQS of
[[Page 37907]]
0.070 ppm for purposes of illustration only, about 70 MSAs with current
O3 design values in the range of about 0.060 ppm (about 85
percent of the current NAAQS) to 0.070 ppm (about 85 percent of 0.070
ppm) would be affected, with most changing from no required monitors to
one, or from one required monitor to two. Because most of these areas
already are operating at least as many monitors as the possible new
requirement, the number of monitors which would need to be initiated
(or moved from a location of excess monitors) would be only about five
monitors. About 100 MSAs with populations less than 350,000 presently
are without any O3 monitors, and hence they do not have an
O3 design value for use with Table D-2. If for the purpose
of applying Table D-2, these areas are treated as if they have
O3 concentrations below 85 percent of the revised NAAQS,
then a NAAQS revision would not automatically result in a requirement
for O3 monitoring in these MSAs.\67\ EPA invites comments on
the appropriateness of the existing minimum monitoring requirements for
purposes of implementing the proposed revised NAAQS, including the
automatic changes to minimum monitoring requirements that would be
triggered by a NAAQS revision.
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\67\ EPA might instead treat one or more of these counties as
having a design value based on a monitor in a nearby monitored
county, in which case ozone monitoring might become required in
certain currently unmonitored MSAs and the number of new required
monitors would increase in the illustrative NAAQS example stated
above.
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(2) Ozone monitoring seasons. As mentioned, the currently required
O3 monitoring seasons range from four to 12 months of the
year. In some cases, O3 monitoring may start a couple of
weeks before and may end a couple of weeks after the required season.
With a lower O3 NAAQS, the issue arises of whether in some
areas the required O3 monitoring season should be made
longer. The EPA notes that under the existing regulations, the Regional
Administrator may approve State-requested deviations from the
established O3 monitoring season but EPA may not increase
the length of the season for an area at EPA's own initiative other than
by notice and comment rulemaking.
(3) Monitoring to support implementation of a secondary
O3 NAAQS. It is fair to say that the existing O3
monitoring requirements and current State monitoring practices are
primarily oriented towards protecting against health effects in people,
i.e., towards implementation of the primary NAAQS. This accounts for
the focus on urban areas, which can combine large populations, large
emissions of O3-forming precursors, and O3
concentrations of concern. The purpose of the secondary NAAQS is to
protect against vegetation damage and other welfare effects, which can
occur in both urban and rural areas. States have largely been given
discretion on whether to add additional monitors aimed specifically at
achieving the objectives of the previous and current secondary NAAQS.
In urban areas, EPA in general believes that an O3
monitoring network (and monitoring season) appropriate to support
implementation of the primary NAAQS will also be appropriate for
implementing the secondary NAAQS. However, rural areas are presently
only sparsely monitored for O3 so violations of the
secondary NAAQS in areas with sensitive vegetation may occur
undetected, 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. It is conceivable that rural violations of
a secondary NAAQS could occur in areas with sensitive vegetation even
though urban monitoring networks are showing compliance with the
primary NAAQS, whether the forms and levels of the two standards are
the same or different. The EPA invites comment on the likelihood of
this occurring under the possible combinations of primary and secondary
standards proposed in this notice, and on whether, where, and how EPA
should require monitoring in rural areas specifically aimed at
implementation of the secondary NAAQS (and/or promote more voluntary
monitoring or conduct monitoring itself in rural areas).
VII. 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
prepared this regulatory impact analysis (RIA) of the potential costs
and benefits associated with this action. The RIA estimates the costs
and monetized human health and welfare benefits of attaining three
alternative O3 NAAQS nationwide. Specifically, the RIA
examines the alternatives of 0.075 ppm, 0.070 ppm, and 0.065 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 final 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.
[[Page 37908]]
For purposes of assessing the impacts of today's 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
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 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 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 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 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 E (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
[[Page 37909]]
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
this 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 this proposal was under development. EPA specifically
solicits additional comment on this proposed rule from Tribal
officials.
G. Executive Order 13045: Protection of Children From Environmental
Health & 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. These
effects and the size of the population affected are summarized in
section 8.7 of the Criteria Document and section 3.6 of the Staff
Paper, and the results of our evaluation of the effects of
O3 pollution on children are discussed in sections II.A-C of
this preamble.
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 No. 104-113, Sec. 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.
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List of Subjects in 40 CFR Part 50
Environmental protection, Air pollution control, Carbon monoxide,
Lead, Nitrogen dioxide, Ozone, Particulate matter, Sulfur oxides.
Dated: June 20, 2007.
Stephen L. Johnson,
Administrator.
For the reasons stated in the preamble, title 40, chapter I of the
code of Federal regulations is 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 added 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 (0.070-0.075) 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.
(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 (0.070-0.075) 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 (7-21) ppm-
hours, measured by a reference method based on Appendix D to this part
and 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 (7-21) ppm-hours, as
[[Page 37917]]
determined in accordance with appendix P to this part.
3. Appendix P is added 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 national 8-hour
primary and secondary ambient air quality standards for
O3 specified in Sec. 50.14 are met at an ambient
O3 air quality monitoring site. Ozone is measured in the
ambient air by a Federal reference method (FRM) based on appendix D
of this part, as applicable, and designated in accordance with part
53 of this chapter, or by a Federal equivalent method (FEM)
designated in accordance with part 53 of this chapter, or by an
Approved Regional Method (ARM) designated in accordance with part 58
of this chapter. Data reporting, data handling, and computation
procedures to be used in making comparisons between reported
O3 concentrations and the level of the O3
standard are specified in the following sections. Whether to
exclude, retain, or make adjustments to the data affected by
exceptional events, including stratospheric O3 intrusion
and other natural events, is subject to the requirements under Sec.
50.1, Sec. 50.14 and Sec. 51.930.
(b) The terms used in this appendix are defined as follows:
8-hour average is the rolling average of hourly O3
concentrations as explained in section 2 of this appendix.
Annual fourth highest daily maximum refers to the fourth highest
value measured at a monitoring location during the O3
season for a particular year.
Daily maximum 8-hour average concentration refers to the maximum
calculated 8 hour average for a particular day as explained in
section 2 of this appendix.
Design values are the metrics (i.e., statistics) that are
compared to the NAAQS levels to determine compliance, calculated as
shown in sections 3 and 4 of this appendix.
Ozone monitoring season refers to the span of time within a
calendar year when individual States are required to measure ambient
O3 concentrations as listed in part 58 appendix D to this
chapter.
W126 is the weighted hourly O3 concentrations based
on seasonal measurements as explained in section 4 of this appendix.
Year refers to calendar year.
2. Primary Ambient Air Quality Standard for Ozone
2.1 Data Reporting and Handling Conventions
Computing 8-hour averages. Hourly average concentrations shall
be reported in parts per million (ppm) to the third decimal place,
with additional digits to the right being truncated. Running 8-hour
averages shall be computed from the hourly O3
concentration data for each hour of the year and the result shall be
stored in the first, or start, hour of the 8-hour period. An 8-hour
average shall be considered valid if at least 75% of the hourly
averages for the 8-hour period are available. In the event that only
6 (or 7) hourly averages are available, the 8-hour average shall be
computed on the basis of the hours available using 6 (or 7) as the
divisor (8-hour periods with three or more missing hours shall not
be ignored if, after substituting one-half the minimum detectable
limit for the missing hourly concentrations, the 8-hour average
concentration is greater than the level of the standard). The
computed 8-hour average O3 concentrations shall be
reported to three decimal places (the insignificant digits to the
right of the third decimal place are truncated, consistent with the
data handling procedures for the reported data).
Daily maximum 8-hour average concentrations. (a) There are 24
possible running 8-hour average O3 concentrations for
each calendar day during the O3 monitoring season. The
daily maximum 8-hour concentration for a given calendar day is the
highest of the 24 possible 8-hour average concentrations computed
for that day. This process is repeated, yielding a daily maximum 8-
hour average O3 concentration for each calendar day with
ambient O3 monitoring data. Because the 8-hour averages
are recorded in the start hour, 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, except in those non-urban monitoring
locations with less pronounced diurnal variation in hourly
concentrations.
(b) An O3 monitoring day shall be counted as a valid
day if valid 8-hour averages are available for at least 75% of
possible hours in the day (i.e., at least 18 of the 24 averages). In
the event that less than 75% of the 8-hour averages are available, a
day shall also be counted as a valid day if the daily maximum 8-hour
average concentration for that day is greater than the level of the
ambient standard.
2.2 Primary Standard-Related Summary Statistic
The standard-related summary statistic is the annual fourth-
highest daily maximum 8-hour O3 concentration, expressed
in parts per million, averaged over three years. The 3-year average
shall be computed using the three most recent, consecutive calendar
years of monitoring data meeting the data completeness requirements
described in this appendix. The computed 3-year average of the
annual fourth-highest daily maximum 8-hour average O3
concentrations shall be reported to three decimal places (the
insignificant digits to the right of the third decimal place are
truncated, consistent with the data handling procedures for the
reported data).
2.3 Comparisons With the Primary Ozone Standard
(a) The primary O3 ambient air quality standard is
met at an ambient air quality 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 [0.070 to
0.075] ppm.
(b) This comparison shall be based on three consecutive,
complete calendar years of air quality monitoring data. This
requirement is met for the three year period at a monitoring site if
daily maximum 8-hour average concentrations are available for at
least 90%, on average, of the days during the designated
O3 monitoring season, with a minimum data completeness in
any one year of at least 75% of the designated sampling days. When
computing whether the minimum data completeness requirements have
been met, meteorological or ambient data may be sufficient to
demonstrate that meteorological conditions on missing days were not
conducive to concentrations above the level of the standard. Missing
days assumed less than the level of the standard are counted for the
purpose of meeting the data completeness requirement, subject to the
approval of the appropriate Regional Administrator.
(c) Years with concentrations greater than the level of the
standard shall not be ignored on the ground that they have less than
complete data. Thus, in computing the 3-year average fourth maximum
concentration, calendar years with less than 75% data completeness
shall be included in the computation if the average annual fourth
maximum 8-hour concentration is greater than the level of the
standard.
(d) Comparisons with the primary O3 standard is
demonstrated by examples 1 and 2 in paragraphs (d)(1) and (d)(2)
respectively as follows:
Example 1.--Ambient Monitoring Site Attaining the Primary O3 Standard
--------------------------------------------------------------------------------------------------------------------------------------------------------
1st Highest 2nd Highest 3rd Highest 4th Highest 5th Highest
Percent valid daily max 8- daily max 8- daily max 8- daily max 8- daily max 8-
Year days hour Conc. hour Conc. hour Conc. hour Conc. hour Conc.
(percent) (ppm) (ppm) (ppm) (ppm) (ppm)
--------------------------------------------------------------------------------------------------------------------------------------------------------
2004.................................................... 100 0.092 0.090 0.085 0.079 0.078
2005.................................................... 96 0.084 0.083 0.075 0.072 0.070
2006.................................................... 98 0.080 0.079 0.073 0.061 0.060
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[[Page 37918]]
Average............................................. 98 .............. .............. .............. 0.070 ..............
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(1) As shown in example 1, the primary standard is met at this
monitoring site because the 3-year average of the annual fourth-
highest daily maximum 8-hour average O3 concentrations
(i.e., 0.0707 ppm, truncated to 0.070 ppm) is less than or equal to
[0.070 to 0.75] ppm. The data completeness requirement is also met
because the average percent of days with valid ambient monitoring
data is greater than 90%, and no single year has less than 75% data
completeness. In Example 1, the individual 8-hour averages used to
determine the annual fourth maximum are truncated to the third
decimal place.
Example 2.--Ambient Monitoring Site Failing To Meet the Primary O3 Standard
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1st Highest 2nd Highest 3rd Highest 4th Highest 5th Highest
Percent valid daily max 8- daily max 8- daily max 8- daily max 8- daily max 8-
Year days hour Conc. hour Conc. hour Conc. hour Conc. hour Conc.
(percent) (ppm) (ppm) (ppm) (ppm) (ppm)
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2004.................................................... 96 0.105 0.103 0.103 0.102 0.102
2005.................................................... 74 0.104 0.103 0.092 0.091 0.088
2006.................................................... 98 0.103 0.101 0.101 0.095 0.094
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Average............................................. 89 .............. .............. .............. 0.096 ..............
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As shown in example 2, the primary standard is not met at this
monitoring site because the 3-year average of the fourth-highest
daily maximum 8-hour average O3 concentrations (i.e.,
0.0960 ppm, truncated to 0.096 ppm) is greater than [0.070 to 0.075]
ppm. Note that the O3 concentration data for 2005 is used
in these computations, even though the data capture is less than
75%, because the average fourth-highest daily maximum 8-hour average
concentration is greater than [0.070 to 0.075] ppm. In Example 2,
the individual 8-hour averages used to determine the annual fourth
maximum are truncated to the third decimal place.
3. Design Values for Primary Ambient Air Quality Standards for Ozone
The air quality design value at a monitoring site is defined as
that concentration that when reduced to the level of the standard
ensures that the site meets the standard. For a concentration-based
standard, the air quality design value is simply the standard-
related test statistic. Thus, for the primary standard, the 3-year
average annual fourth-highest daily maximum 8-hour average
O3 concentration is also the air quality design value for
the site.
4. Secondary Ambient Air Quality Standard for Ozone
4.1 Data Reporting and Handling Conventions
Computing the daily index value (D.I.). The secondary
O3 standard is a seasonal standard expressed as the sum
of weighted hourly concentrations, cumulated over the 12 hour
daylight period, 8 a.m. to 8 p.m. local standard time (LST), during
the maximum consecutive 3-month period within the O3
monitoring season. Hourly average concentrations for each hour from
8 a.m. to 8 p.m. LST shall be reported in parts per million (ppm) to
the third decimal place, with additional digits to the right being
truncated. The first step in computing the daily index value, D.I.,
for the daylight hours is to apply a sigmoidal weighting function in
the form of Equation 1 in this appendix:
[GRAPHIC] [TIFF OMITTED] TP11JY07.002
to each measurement of hourly average concentration, where
O3 is the average hourly O3 concentration
expressed in ppm. The computed value of the sigmoidally weighted
hourly concentration shall be expressed to three decimal places (the
remaining digits to the right are truncated). An illustration of
computing a daily index value is below:
Example 3.--Daily Index Value Calculation for an Ambient O3 Monitoring
Site
------------------------------------------------------------------------
Weighted
Start hour Concentration concentration
(ppm) (ppm)
------------------------------------------------------------------------
8:00 AM................................. 0.045 0.002
9:00 AM................................. 0.060 0.018
10:00 AM................................ 0.075 0.055
11:00 AM................................ 0.080 0.067
12:00 PM................................ 0.079 0.065
1:00 PM................................. 0.082 0.071
2:00 PM................................. 0.085 0.077
3:00 PM................................. 0.088 0.082
4:00 PM................................. 0.083 0.073
5:00 PM................................. 0.081 0.069
6:00 PM................................. 0.065 0.029
7:00 PM................................. 0.056 0.011
------------------------------------------------------------------------
[[Page 37919]]
Daily index value (D.I.) = 0.002 + 0.018 + 0.055 + 0.067 + 0.065 +
0.071 + 0.077 + 0.082 + 0.073 + 0.069 + 0.029 + 0.011 = 0.619 ppm-
hours
Computing the monthly cumulative index (W126). The daily index
value is computed at each monitoring site for each calendar day in
each month during the O3 monitoring. At an individual
monitoring site, a month is counted as a valid O3
monitoring month if hourly average O3 concentrations are
available for at least 75% of the possible index hours in the month.
For months with less than 75% data completeness, the monthly
cumulative index value shall be adjusted for incomplete sampling by
multiplying the unadjusted W126 cumulative index value by the ratio
of the number of possible daylight hours to the number of hours with
valid ambient hourly concentrations using Equation 2 in this
appendix:
[GRAPHIC] [TIFF OMITTED] TP11JY07.003
Where,
M.I. = the monthly sum of the weighted daylight hours,
D.I. = the daily sum of the weighted daylight hours,
n = the number of days in the calendar month,
v = the number of daylight hours (8:00 a.m.--8:00 p.m. LST) with
valid hourly O3 concentrations.
4.2 Secondary Standard-related Summary Statistic
The standard-related summary statistic is the annual maximum
consecutive 3-month W126 value expressed in ppm-hours. Specifically,
the annual W126 value is computed on a calendar year basis using the
three highest, consecutive monthly W126 values.
4.3 Comparisons with the Secondary Ozone Standard
The secondary ambient O3 air quality standard is met
when the annual maximum W126 value based on a consecutive 3-month
period at an O3 air quality monitoring site is less than
or equal to [7 to 21] ppm-hours. The number of significant figures
in the level of the standard dictates the rounding convention for
comparing the computed W126 value with the level of the standard.
The first decimal place of the computed W126 value is rounded, with
values equal to or greater than of 0.5 rounding up.
Example 4.--Calculation of the Maximum 3-Month W126 Value at an Ambient Air Quality Monitoring Site Failing To Meet the Secondary O3 Standard
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April May June July August September October
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Monthly W126................................................. 4.442 9.124 12.983 16.153 13.555 4.364 1.302
3-Month Total................................................ na na 26.549 38.260 42.691 34.072 19.221
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As shown in example 4, the maximum consecutive 3-month W126
value for this site is 43 ppm-hours. Because 43 ppm-hours is greater
than [7 to 21] ppm-hours, the secondary standard is not met at this
ambient air quality monitoring site.
[FR Doc. E7-12416 Filed 7-10-07; 8:45 am]
BILLING CODE 6560-50-P