[Federal Register Volume 68, Number 104 (Friday, May 30, 2003)]
[Proposed Rules]
[Pages 32606-32621]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 03-13428]



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Part III





Environmental Protection Agency





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40 CFR Part 63



List of Hazardous Air Pollutants, Petition Process, Lesser Quantity 
Designations, Source Category List; Proposed Rules

  Federal Register / Vol. 68, No. 104 / Friday, May 30, 2003 / Proposed 
Rules  

[[Page 32606]]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 63

[A-99-03, OAR-2003-0028; FRL-7504-9]
RIN: 2060-AI72


List of Hazardous Air Pollutants, Petition Process, Lesser 
Quantity Designations, Source Category List

AGENCY: Environmental Protection Agency (EPA).

ACTION: Proposed rule.

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SUMMARY: The EPA is proposing to amend the list of hazardous air 
pollutants (HAP) contained in section 112(b)(1) of the Clean Air Act 
(CAA) by removing the compound methyl ethyl ketone (MEK) (2-Butanone) 
(CAS No. 78-93-3). This action is being taken in response to a petition 
submitted by the Ketones Panel of the American Chemistry Council 
(formerly the Chemical Manufacturers Association) on behalf of MEK 
producers and consumers to delete MEK from the HAP list. Petitions to 
remove a substance from the HAP list are permitted under section 
112(b)(3) of the CAA.
    The proposed rule is based on EPA's evaluation of the available 
information concerning the potential hazards and projected exposures to 
MEK. We have made an initial determination that there are adequate data 
on the health and environmental effects of MEK to determine that 
emissions, ambient concentrations, bioaccumulation, or deposition of 
the compound may not reasonably be anticipated to cause adverse human 
health or environmental effects. This action includes a detailed 
rationale for delisting MEK, and we request comment on the proposal.

DATES: Comments. Written comments on the proposed rule must be received 
by August 28, 2003.
    Public Hearing. A public hearing regarding the proposed rule will 
be held if requests to speak are received by the EPA on or before July 
29, 2003. If requested, a public hearing will be held approximately 90 
days after the date of publication of this notice in the Federal 
Register.

ADDRESSES: Comments. Comments may be submitted electronically, by mail, 
or through hand delivery/courier. Electronic comments may be submitted 
on-line at http://www.epa.gov/edocket/. Written comments sent by U.S. 
mail should be submitted (in duplicate if possible) to: Air and 
Radiation Docket and Information Center (Mail Code 6102T), Attention 
Docket Number A-98-44, Room B108, U.S. EPA, 1301 Constitution Avenue, 
NW., Washington, DC 20460. Written comments delivered in person or by 
courier (e.g., FedEx, Airborne, and UPS) should be submitted (in 
duplicate if possible) to: Air and Radiation Docket and Information 
Center (Mail Code 6102T), Attention Docket Number A-98-44, Room B102, 
U.S. EPA, 1301 Constitution Avenue, NW., Washington, DC 20460. The EPA 
requests a separate copy also be sent to the contact person listed 
below (see FOR FURTHER INFORMATION CONTACT).
    Public Hearing. If a public hearing is requested by July 29, 2003, 
the public hearing will be held in our EPA Office of Administration 
Auditorium, Research Triangle Park, NC. Persons interested in 
presenting oral testimony or inquiring as to whether a hearing is to be 
held should contact Ms. Kelly A. Rimer, Risk and Exposure Assessment 
Group, Emission Standards Division (C404-01), U.S. EPA, Research 
Triangle Park, North Carolina 27711, telephone number (919) 541-2962. 
Persons interested in attending the public hearing should also contact 
Ms. Rimer to verify the time, date and location of the hearing.

FOR FURTHER INFORMATION CONTACT: Ms. Kelly A. Rimer, Risk and Exposure 
Assessment Group, Emission Standards Division (C404-01), U.S. EPA, 
Research Triangle Park, NC 27711, telephone number (919) 541-2962, 
electronic mail address [email protected].

SUPPLEMENTARY INFORMATION: 
    Regulated Entities. Entities potentially affected by this action 
are those industrial facilities that manufacture or use MEK. This 
action proposes to amend the list of HAP contained in section 112(b)(1) 
of the CAA by removing the compound MEK. The decision to grant the 
petition and issue a proposed rule to delist MEK removes MEK from 
regulatory consideration under section 112(d) of the CAA.
    Docket. The EPA has established an official public docket for this 
action under Docket ID No. A-99-03, and Electronic Docket No. OAR-2003-
0028. The official public docket is the collection of materials that is 
available for public viewing at the EPA Docket Center (Air Docket), EPA 
West, Room B-108, 1301 Constitution Avenue, NW., Washington, DC 20004. 
The Docket Center is open from 8:30 a.m. to 4:30 p.m., Monday through 
Friday, excluding legal holidays. The telephone number for the Reading 
Room is (202) 566-1744, and the telephone number for the Air Docket is 
(202) 566-1742.
    Electronic Access. An electronic version of the public docket is 
available through EPA's electronic public docket and comment system, 
EPA Dockets. You may use EPA Dockets at http://www.epa.gov/edocket/ to 
submit or view public comments, access the index of the contents of the 
official public docket, and access those documents in the public docket 
that are available electronically. Once in the system, select 
``search'' and key in the appropriate docket identification number.
    Certain types of information will not be placed in the EPA dockets. 
Information claimed as confidential business information (CBI) and 
other information whose disclosure is restricted by statute, which is 
not included in the official public docket, will not be available for 
public viewing in EPA's electronic public docket. The EPA's policy is 
that copyrighted material will not be placed in EPA's electronic public 
docket but will be available only in printed, paper form in the 
official public docket. Although not all docket materials may be 
available electronically, you may still access any of the publicly 
available docket materials through the EPA Docket Center.
    For public commenters, it is important to note that EPA's policy is 
that public comments, whether submitted electronically or in paper, 
will be made available for public viewing in EPA's electronic public 
docket as EPA receives them and without change unless the comment 
contains copyrighted material, CBI, or other information whose 
disclosure is restricted by statute. When EPA identifies a comment 
containing copyrighted material, EPA will provide a reference to that 
material in the version of the comment that is placed in EPA's 
electronic public docket. The entire printed comment, including the 
copyrighted material, will be available in the public docket.
    Public comments submitted on computer disks that are mailed or 
delivered to the docket will be transferred to EPA's electronic public 
docket. Public comments that are mailed or delivered to the docket will 
be scanned and placed in EPA's electronic public docket. Where 
practical, physical objects will be photographed, and the photograph 
will be placed in EPA's electronic public docket along with a brief 
description written by the docket staff.
    Comments. You may submit comments electronically, by mail, by 
facsimile, or through hand delivery/courier. To ensure proper receipt 
by EPA, identify the appropriate docket identification number in the 
subject line on the first page of your comment. Please ensure that your 
comments are

[[Page 32607]]

submitted within the specified comment period. Comments submitted after 
the close of the comment period will be marked ``late.'' The EPA is not 
required to consider these late comments.
    Electronically. If you submit an electronic comment as prescribed 
below, EPA recommends that you include your name, mailing address, and 
an e-mail address or other contact information in the body of your 
comment. Also include this contact information on the outside of any 
disk or CD ROM you submit and in any cover letter accompanying the disk 
or CD ROM. This ensures that you can be identified as the submitter of 
the comment and allows EPA to contact you in case EPA cannot read your 
comment due to technical difficulties or needs further information on 
the substance of your comment. The EPA's policy is that EPA will not 
edit your comment and any identifying or contact information provided 
in the body of a comment will be included as part of the comment that 
is placed in the official public docket and made available in EPA's 
electronic public docket. 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.
    Your use of EPA's electronic public docket to submit comments to 
EPA electronically is EPA's preferred method for receiving comments. Go 
directly to EPA Dockets at http://www.epa.gov/edocket, and follow the 
online instructions for submitting comments. Once in the system, select 
``search'' and key in Docket ID No. A-99-03, or Electronic Docket Id. 
No. OAR-2003-0028. The system is an ``anonymous access'' system, which 
means EPA will not know your identity, e-mail address, or other contact 
information unless you provide it in the body of your comment.
    Comments may be sent by electronic mail (e-mail) to [email protected], Attention Docket ID No. A-99-03, or Electronic Docket 
ID. No. OAR-2003-0028. In contrast to EPA's electronic public docket, 
EPA's e-mail system is not an ``anonymous access'' system. If you send 
an e-mail comment directly to the docket without going through EPA's 
electronic public docket, EPA's e-mail system automatically captures 
your e-mail address. E-mail addresses that are automatically captured 
by EPA's e-mail system are included as part of the comment that is 
placed in the official public docket and made available in EPA's 
electronic public docket.
    You may submit comments on a disk or CD ROM that you mail to the 
mailing address identified in this document. These electronic 
submissions will be accepted in WordPerfect or ASCII file format. Avoid 
the use of special characters and any form of encryption.
    By Mail. Send your comments (in duplicate, if possible) to: EPA 
Docket Center (Air Docket), U.S. EPA West, (MD-6102T), Room B-108, 1200 
Pennsylvania Avenue, NW., Washington, DC 20460, Attention Docket ID No. 
OAR-2003-0028.
    By Hand Delivery or Courier. Deliver your comments (in duplicate, 
if possible) to: EPA Docket Center, Room B-108, U.S. EPA West, 1301 
Constitution Avenue, NW., Washington, DC 20004, Attention Docket ID No. 
OAR-2003-0028. Such deliveries are only accepted during the Docket 
Center's normal hours of operation.
    By Facsimile. Fax your comments to: (202) 566-1741, Docket ID No. 
OAR-2003-0028.
    CBI. Do not submit information that you consider to be CBI through 
EPA's electronic public docket or by e-mail. Send or deliver 
information identified as CBI only to the following address: Kelly 
Rimer, c/o Roberto Morales, OAQPS Document Control Officer (C404-02), 
U.S. EPA, 109 TW Alexander Drive, Research Triangle Park, NC 27709, 
Attention Docket ID No. OAR-2003-0028. You may claim information that 
you submit to EPA as CBI by marking any part or all of that information 
as CBI (if you submit CBI on disk or CD ROM, 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 CBI). Information so marked 
will not be disclosed except in accordance with procedures set forth in 
40 CFR part 2.
    Worldwide Web (WWW). In addition to being available in the docket, 
an electronic copy of today's proposed rule will also be available on 
the WWW through the Technology Transfer Network (TTN). Following the 
Administrator's signature, a copy of the proposed rule will be placed 
on the TTN's policy and guidance page for newly proposed or promulgated 
rules at http://www.epa.gov/ttn/oarpg. The TTN provides information and 
technology exchange in various areas of air pollution control. If more 
information regarding the TTN is needed, call the TTN HELP line at 
(919) 541-5384.

    Outline. This preamble is organized as follows:

I. Background
II. Criteria for Delisting
III. Summary of the Petition
    A. Background
    B. Exposure Assessment
    C. Human Health Effects Assessment
    D. Risk Characterization and Conclusions Regarding Risks to 
Human Health
    E. Ecological Assessment and Conclusions
IV. EPA Analysis of the Petition
    A. Exposure Assessment
    B. Human Health Effects Assessment
    C. Determination of an Appropriate Health Effects Criterion for 
Chronic Noncancer Effects
    D. Human Health Risk Characterization and Conclusions
    E. Ecological Risk Characterization and Conclusions
    F. Transformation Characterization
    G. Public Comments and EPA Responses
    H. Other Issues
    I. Discussion and Conclusion
V. References
VI. Statutory and Executive Order Reviews
    A. Executive Order 12866, Regulatory Planning and Review
    B. Paperwork Reduction Act
    C. Regulatory Flexibility Act (RFA)
    D. Unfunded Mandates Reform Act of 1995
    E. Executive Order 13132, Federalism
    F. Executive Order 13175, Consultation and Coordination with 
Indian Tribal Governments
    G. Executive Order 13045, Protection of Children from 
Environmental Health Risks and Safety Risks
    H. Executive Order 13211, Actions Concerning Regulations that 
Significantly Affect Energy supply, Distribution, or Use
    I. National Technology Transfer and Advancement Act

I. Background

    Section 112 of the CAA contains a mandate for EPA to evaluate and 
control emissions of HAP. Section 112(b)(1) includes a list of 188 
specific chemical compounds and classes of compounds that Congress 
identified as HAP. The EPA must evaluate the emissions of substances on 
the HAP list to identify source categories for which the Agency must 
establish emission standards under section 112(d). We are required to 
periodically review the list of HAP and, where appropriate, revise this 
list by rule. In addition, under section 112(b)(3), any person may 
petition us to modify the list by adding or deleting one or more 
substances. A petitioner seeking to delete a substance must demonstrate 
that there are adequate data on the health and environmental effects of 
the substance to determine that emissions, ambient concentrations, 
bioaccumulation, or deposition of the substance may not reasonably be 
anticipated to cause any adverse effects to human health or the 
environment. A petitioner must provide a detailed evaluation of the 
available data concerning the substance's potential adverse health and 
environmental effects and estimate the potential exposures through 
inhalation or other routes resulting from emissions of the substance.
    On November 27, 1996, the American Chemistry Council's Ketones 
Panel

[[Page 32608]]

submitted a petition to delete MEK (CAS No. 78-93-3) from the HAP list 
in section 112(b)(1), 42 U.S.C., 7412(b)(1). Following the receipt of 
the petition, we conducted a preliminary evaluation to determine 
whether the petition was complete according to Agency criteria. To be 
deemed complete, a petition must consider all available health and 
environmental effects data. A petition must also provide comprehensive 
emissions data, including peak and annual average emissions for each 
source or for a representative selection of sources, and must estimate 
the resulting exposures of people living in the vicinity of the 
sources. In addition, a petition must address the environmental impacts 
associated with emissions to the ambient air and impacts associated 
with the subsequent cross-media transport of those emissions. We 
determined the petition to delete MEK to be complete and published a 
notice of its receipt in the Federal Register on June 23, 1999, at 64 
FR 33453 and requested information to assist us in technically 
reviewing the petition in addition to other comments.
    We received 10 submissions in response to our request for comment 
and information which would aid our technical review of the petition. 
We responded to substantive comments in our technical review of the 
petition.

II. Criteria for Delisting

    Section 112(b)(2) of the CAA requires us to make periodic revisions 
to the initial list of HAP set forth in section 112(b)(1) and outlines 
criteria to be applied in deciding whether to add or delete particular 
substances. Section 112(b)(2) identifies pollutants that should be 
listed as:

* * * pollutants which present, or may present, through inhalation 
or other routes of exposure, a threat of adverse human health 
effects (including, but not limited to, substances which are known 
to be, or may reasonably be anticipated to be, carcinogenic, 
mutagenic, teratogenic, neurotoxic, which cause reproductive 
dysfunction, or which are acutely or chronically toxic) or adverse 
environmental effects whether through ambient concentrations, 
bioaccumulation, deposition, or otherwise * * *.

    Section 112(b)(3) establishes general requirements for petitioning 
the Agency to modify the HAP list by adding or deleting a substance. 
Although the Administrator may add or delete a substance on his or her 
own initiative, the burden is on a petitioner to include sufficient 
information to support the requested addition or deletion under the 
substantive criteria set forth in section 112(b)(3)(B) and (C).
    The Administrator must either grant or deny a petition to delist a 
HAP within 18 months of receipt of a complete petition. If the 
Administrator decides to deny a petition, the Agency publishes a 
written explanation of the basis for denial in the Federal Register. A 
decision to deny a petition is final Agency action subject to review. 
If the Administrator decides to grant a petition, the Agency publishes 
a written explanation of the Administrator's decision, along with a 
proposed rule to add or delete the substance. The proposed rule is open 
to public comment and public hearing, and all additional substantive 
information received is considered prior to the issuance of a final 
rule.
    To delete a substance from the HAP list, section 112(b)(3)(C) 
provides that the Administrator must determine that:

* * * there is adequate data on the health and environmental effects 
of the substance to determine that emissions, ambient 
concentrations, bioaccumulation of deposition of the substance may 
not reasonably be anticipated to cause any adverse effects to the 
human health or adverse environmental effects.

    If the Administrator decides to grant a petition, the Agency 
publishes a written explanation on the Administrator's decision, along 
with a proposed rule to add or delete the substance. The proposed rule 
is open to public comment and public hearing. We evaluate all 
substantive information received during public comment prior to taking 
any final action related to a proposed rule.
    We do not interpret section 112(b)(3)(C) to require absolute 
certainty that a pollutant will not cause adverse effects on human 
health or the environment before it may be deleted from the list. The 
use of the terms ``adequate'' and ``reasonably'' indicate that the 
Agency must weigh the potential uncertainties and likely significance. 
Impact of the uncertainties concerning the risks of adverse health or 
environmental effects may be mitigated if we can determine that 
projected exposures are sufficiently low to provide reasonable 
assurance that such adverse effects will not occur. Similarly, impacts 
of uncertainties due to the magnitude of projected exposures may be 
mitigated if we can determine that the levels which might cause adverse 
health or environmental effects are sufficiently high to provide 
reasonable assurance that exposures will not reach harmful levels. 
However, the burden remains on a petitioner to demonstrate that the 
available data support an affirmative determination that emissions of a 
substance may not be reasonably anticipated to result in adverse 
effects on human health or the environment (that is, EPA will not 
remove a substance from the list of HAP based merely on the inability 
to conclude that emissions of the substance will cause adverse effects 
on human health or the environment). As a part of the requisite 
demonstration, a petitioner must resolve any critical uncertainties 
associated with missing information. We will not grant a petition to 
delete a substance if there are major uncertainties that need to be 
addressed before we would have sufficient information to make the 
requisite determination.

III. Summary of the Petition

A. Background

    The petition to delist MEK is presented in the form of a risk 
assessment that considers multiple routes of exposure and evaluates the 
likelihood and severity of adverse effects to human health and the 
environment arising from exposures to ambient levels of MEK. The 
petition presents a characterization of the sources and releases of 
MEK, estimates exposures, identifies the potential hazard and the dose-
response relationship of MEK, and characterizes the risk from a 
reasonable worst-case lifetime exposure to MEK, and to worst-case 
short-term (24 hour) exposure to MEK. This section of today's proposed 
action presents an overview of the petition to delist MEK, and the 
petitioner's conclusions based on that information. Please consult the 
docket for more detail about the petition or EPA's evaluation of the 
petition.
    The petition to delist MEK presents background information on MEK, 
including chemical and physical properties data and production and use 
data. The petitioner used the 1994 Toxic Release Inventory (TRI) as the 
basis of an emissions inventory intended to quantify annual emissions 
of MEK, to identify and locate emissions sources, and to acquire some 
facility-specific emissions information. The 1994 TRI shows that there 
are over 2,000 sources with reported emissions of MEK. The petition 
states that over 85 percent of these facilities (approximately 1,700) 
emit 25 tons per year (tpy) or less. The petition also states that 
approximately 800 facilities emit between 10 and 200 tpy, and 27 
facilities emit 200 tpy or more. In addition to using the 1994 TRI, the 
petitioner queried a subset of individual sources to obtain site-
specific source, release, and facility information for the purpose of 
conducting more detailed risk assessments.

[[Page 32609]]

B. Exposure Assessment

    The petition's emissions inventory provides the basis for a tiered 
air dispersion modeling analysis as described in ``Tiered Modeling 
Approach for Assessing Risk due to Sources of Hazardous Air 
Pollutants'' (EPA-450/4-92-001). That tiered analysis applies 
successive refinements in model selection and input data to derive 
conservative estimates of the maximum annual average ambient 
concentration of MEK. ``Conservative'' refers to the selection of 
models and modeling parameters that are more likely to overestimate, 
rather than underestimate, the ambient concentrations of a given 
pollutant when data are limited.
    Tier 1 air dispersion modeling requires limited source information 
and provides the most conservative estimate of maximum concentrations 
of the tiers. Tier 2 modeling requires additional source information 
and a simple air dispersion model and results in air concentrations 
that are more realistic than tier 1 estimates, but which are still 
considered to be conservative. In the assessment, the petition used 
EPA's SCREEN3 model for tier 2 analyses. Tier 3 requires extensive data 
from a source and recommends using EPA's most advanced dispersion 
modeling techniques to provide even more realistic, though generally 
still conservative, estimates of maximum concentrations. In the 
assessment, the petitioner used EPA's Industrial Source Complex Short 
Term 3 (ISCST3) model for the tier 3 analysis. Because each successive 
tier provides a less conservative and more realistic estimate of the 
ambient MEK concentration, the petitioner performed tier 3 modeling 
only where the tier 2 modeling predicted maximum annual average ambient 
concentrations of MEK above a designated threshold. Using this 
approach, the petitioner developed a reasonable worst-case exposure 
scenario by estimating the maximum annual average ambient concentration 
expected to result from emissions of MEK from a single facility. The 
petition also accounts for emissions of MEK from several sources 
located within close proximity to each other (often called a cluster of 
sources). The petition does this in order to assess the potential 
impact to a person who may live close to a cluster of MEK-emitting 
facilities.
    The petition reasoned that the majority of risk would come from 
facilities that emit large amounts of MEK. The petitioner identified 
facilities which emitted 200 tpy or more of MEK as large. The 
petitioner contacted each of the 27 large facilities to gather data 
with which to model maximum, off-site ambient concentrations of MEK. 
That analysis also used information from title V permits. The 
petitioner was able to obtain the necessary modeling information for 21 
of the 27 facilities, including the six highest emitters of MEK, and 13 
of the top 15 emitters. The analysis for these facilities applied tier 
2 and tier 3 modeling techniques. The maximum annual average 
concentration estimated from the largest MEK emission source using the 
tier 3 model was approximately 1.2 milligrams per cubic meter (mg/
m\3\). However, that concentration was located at the entrance to an 
adjacent industrial facility where there were no environmental or human 
receptors. The MEK emissions from the other sources modeled in the 
tiered approach were all less than 0.9 mg/m\3\. For the seven 
facilities with the highest predicted fence line concentrations, the 
maximum annual average ambient levels of MEK decreased to below 0.5 mg/
m\3\ within 175 meters from the fence line.
    In addition to modeling sources emitting 200 tpy or more, the 
petition also includes an analysis of sources emitting lesser amounts. 
The petitioner used a tier 2 analysis to model those MEK sources 
(approximately 800 in all) which, based on the inventory, emitted more 
than 10 tpy but less than the 200 tpy. The petitioner divided these 
emission sources into source categories based on their two digit 
Standard Industrial Classification (SIC) codes. For each SIC, the 
petitioner modeled a ``worst case'' prototype plant using conservative 
site configurations (e.g., distance to fence lines), the highest 
reported emissions rate for the individual category, and worst-case 
dispersion meteorology. The maximum predicted annual average ambient 
concentration of MEK from the sources emitting less than 200 tpy of MEK 
was approximately 0.7 mg/m\3\. The remaining MEK emission sources 
included under this approach were determined to have maximum annual 
average ambient concentrations less than 0.6 mg/m\3\.
    The petition includes estimates of 24-hour average concentrations 
in addition to estimates of annual average concentrations. The highest 
24-hour average concentration as predicted by tier 3 modeling was 12.8 
mg/m\3\. That concentration was at the same location where the highest 
annual concentration was predicted to occur. The petition states that 
there are no people or environmental receptors at that location. The 
petition states further that all other modeled 24-hour concentrations 
are below 10 mg/m\3\ and concludes that people would not be exposed to 
24-hour concentrations greater than this value.
    To address the potential impact of MEK sources that are located 
within close proximity to each other, the petitioner identified, from 
the 1994 TRI, every facility in the United States with MEK emissions 
greater than 10 tpy. The petitioner used postal ZIP codes to determine 
areas in which emission sources were situated near one another. Using 
this approach, the petition analyzed 91 facilities. Of these 
facilities, only three ZIP codes contained groups of facilities that 
collectively emitted more than 200 tpy. The petitioner used results 
from the previous tiered analysis to evaluate the potential for these 
facilities to have significant overlapping impacts. Based on the 
analysis, the petition concluded that the combined impacts from 
multiple MEK emission sources situated close to one another will not 
result in maximum annual average ambient MEK concentrations greater 
than 1 mg/m\3\, or in 24-hour concentrations greater than 10 mg/m\3\. 
In most cases, the concentrations will be well below these values.
    The petitioner reviewed available ambient air monitoring studies to 
determine the potential contribution of ambient background MEK to the 
maximum annual average and 24-hour average MEK concentrations. Here, 
background refers to air concentrations of MEK from sources not modeled 
in the analysis (e.g., mobile). The review showed that MEK has been 
monitored in both urban and rural locations. The highest reported MEK 
concentrations occurred in the Houston ship channel where the yearly 
averages from 1987-1995 for seven sites ranged from approximately 
0.0009 to 0.0018 mg/m\3\. The maximum 24-hour average concentration 
also occurred in the Houston ship channel over the same time period 
where the highest reported average was 0.09 mg/m\3\. Based on this 
review, the petitioner concluded that background MEK is not a 
significant contributor to the maximum annual average, or maximum 24-
hour average concentration of MEK.
    The petitioner reviewed MEK's fate in the environment to determine 
the most probable routes of human exposures to ambient MEK. The 
petitioner used physical chemical data taken from the literature and a 
number of EPA databases to conclude that MEK does not persist or 
bioaccumulate in the environment. The petition also states that due to 
its high vapor pressure, MEK discharged onto a terrestrial environment 
is expected to rapidly volatilize to air. Volatilization from

[[Page 32610]]

water is also reported to occur at a significant rate, and the petition 
reports MEK to be readily biodegradable in both aerobic and anaerobic 
environments. The petitioner concluded that MEK is not anticipated to 
pose an exposure problem in drinking water, and that inhalation is the 
primary route of exposure for humans living in the vicinity of MEK 
emission sources.
    The petition states that while in the air, MEK decomposes to carbon 
dioxide, carbon monoxide, and water through various reactions. One of 
the intermediaries is a probable carcinogen: acetaldehyde. The 
petitioner maintained that acetaldehyde formed during MEK's 
transformation disappeared approximately 70 times faster than it was 
created. Therefore, the petitioner concluded, the rapid dispersion of 
MEK, coupled with its half-life of about 9 days and the comparatively 
short half-life of acetaldehyde (about 14 hours), resulted in low 
ambient levels of MEK-produced acetaldehyde. The petition states that 
the resulting concentration levels cannot be reasonably anticipated to 
cause adverse human health effects.

C. Human Health Effects Assessment

    The petition presents toxicological data, which are used for hazard 
identification and to determine dose-response relationships, citing the 
EPA's Integrated Risk Information System (IRIS). These data are also 
supplemented by an extensive review of the literature that includes 
articles published after the most recent review of the IRIS database 
for MEK which occurred in 1992.
    The petition concludes that MEK's acute and chronic toxicity are 
low, and that it demonstrates little or no subchronic toxicity. The 
petition also reports that MEK has been shown to be without genotoxic 
activity, but it has not been specifically tested for carcinogenicity. 
However, the petition states that data on MEK's structure, metabolism, 
subchronic health effects, and genotoxic effects indicate that it is 
not likely to have carcinogenic properties.
    The petition states that MEK by itself has little potential to 
produce damage to the nervous system. The petition discusses MEK's 
ability to potentiate the neurotoxic effects of other chemicals when 
both are present at relatively high concentrations and concluded that 
MEK does not pose a neurotoxic hazard to humans under ambient exposure 
scenarios. The petition also states that MEK has not been shown to 
produce birth defects (i.e., teratogenicity) and does not produce 
reproductive effects in subchronic inhalation studies.
    The petition takes the position that MEK's developmental toxicity 
is low, and that developmental toxicity is the basis for the 1992 EPA 
IRIS Reference Concentration (RfC) for MEK of 1.0 mg/m\3\. The RfC is a 
peer-reviewed value defined as an estimate (with uncertainty spanning 
perhaps an order of magnitude) of a daily inhalation exposure to the 
human population (including sensitive subgroups) that is likely to be 
without appreciable risk of deleterious noncancer effects during a life 
time (i.e., 70 years).
    The petition provides a review of EPA's derivation of the IRIS RfC 
for MEK. Based on this review and the application of EPA guidelines 
that were published after the 1992 update of the MEK RfC, the 
petitioner proposed a revised criterion for human health effects. The 
petitioner's proposed revision suggests an increase in the RfC from 1 
mg/m\3\ to 3.3 mg/m\3\. (The details of the petitioner's reassessment 
are contained in the docket.)
    For short-term exposure, the petition adjusts the revised RfC by 
eliminating the uncertainty factor of 10 that is used for extrapolating 
from subchronic to chronic exposure. The resulting short-term human 
health criterion submitted in the petition is 33 mg/m\3\.

D. Risk Characterization and Conclusions Regarding Risks to Human 
Health

    The petitioner characterized human health risks from exposure to 
the predicted ambient MEK concentration levels by comparing the maximum 
estimated annual average concentration to their proposed revised RfC of 
3.3 mg/m\3\. Based on the conservatism built into the model estimates, 
the petitioner concluded that actual maximum annual average ambient 
concentrations of MEK are unlikely to exceed 1 mg/m\3\ for the highest 
emitting source and will be significantly less than 1 mg/m\3\ for all 
other sources. The petitioner concluded that the available evidence 
demonstrates that actual exposures are not likely to approach the 1992 
IRIS RfC of 1 mg/m\3\ and will not exceed the petitioner's revised 
health criterion of 3.3 mg/m\3\. The petition characterized human 
health risks from 24-hour exposures by comparing the estimated 24-hour 
concentrations, 10 mg/m\3\ with a human health benchmark of 33 mg/m\3\, 
and determined that these short-term concentrations will not approach 
their criterion of 33 mg/m\3\. Therefore, the petitioner concluded that 
adverse human health effects arising from ambient exposures to MEK 
emissions cannot be reasonably anticipated to occur.

E. Ecological Assessment and Conclusions

    The petition presents ecological toxicity data for environmental 
effects as the basis for its assessment of the potential ecological 
risks from the release of MEK to the environment. The petition uses 
data from several EPA databases and from the general literature. The 
petition includes no data on the potential for ecological effects to 
occur due to its presence in media other than water. The petitioner 
concluded that the available data indicate that MEK has low acute 
toxicity for aquatic organisms. Although there are no data on chronic 
aquatic toxicity, the petitioner stated that MEK is not expected to be 
chronically toxic to aquatic organisms because of its limited 
persistence in aqueous habitats, which results from its rapid 
volatilization and biodegradation. The petition compares predicted 
maximum ambient annual average concentrations to the identified 
ecotoxicity endpoints. Based on that comparison and information on 
MEK's environmental behavior, the petitioner concluded that MEK cannot 
reasonably be anticipated to cause significant and widespread adverse 
environmental effects.

IV. EPA Analysis of the Petition

    The following section presents EPA's evaluation and analysis of the 
petition to delist MEK. The technical review was conducted by EPA's 
Office of Air and Radiation, with assistance from EPA's Office of 
Research and Development. The supporting review materials are contained 
in the docket.

A. Exposure Assessment

    Methyl Ethyl Ketone is a clear, colorless, stable, low-boiling 
point (79.6 [deg]C), highly volatile (vapor pressure 90.6 torr at 25 
[deg]C), highly flammable (flash point 1 [deg]C, auto ignition 
temperature 515 [deg]C) liquid. It is very soluble in water (240 grams 
per liter at 20 [deg]C), miscible with organic solvents and forms 
azetropes with water and many organic liquids. Methyl ethyl ketone has 
exceptionally high solvent powers for many natural and synthetic 
resins. It is used as a solvent in the surface coatings industry, 
specifically in vinyl lacquers, nitrocellulose lacquers, and acrylics, 
and is used as a chemical intermediate. Methyl ethyl ketone is also 
used in other industries for producing adhesives, magnetic tapes, 
printing inks, degreasing and cleaning fluids, as a dewaxing agent for 
lubricating oils, as an intermediate in the production of antioxidants, 
perfumes, and as a catalyst. Methyl ethyl ketone also occurs

[[Page 32611]]

naturally. It is emitted from various evergreen trees and has been 
identified as a natural component of several foods.
    We concur with the petition that inhalation is the principal route 
of non-occupational exposures to MEK emissions. The absorption of MEK 
through the skin at the estimated ambient levels is likely to be 
insignificant compared to inhalation. In addition, its relatively rapid 
volatilization and rapid biodegradation in water indicates that humans 
are unlikely to be exposed to significant amounts of MEK in drinking 
water.
    To determine the adequacy of the petition's exposure assessment, we 
first evaluated the emissions inventory and the petition's source 
characterization. We then evaluated the dispersion modeling in terms of 
the methods and application of the models.
    To evaluate the emissions inventory, we compared the petition's 
list of MEK emission sources to EPA's 1996 National Toxics Inventory 
(NTI). We determined that the petition correctly identified the largest 
sources of MEK emissions, and that the quantity of emissions for each 
identified source was comparable to the NTI. There was an overall lack 
of agreement, however, between the total count of MEK emission sources 
listed in the NTI and in the petition's inventory. We determined that 
this resulted from a general weakness in the ability of the 
petitioner's approach to identify facilities emitting less than 25 tpy 
of MEK. However, after reviewing both the inventory and the 
petitioner's tiered modeling approach, we determined that these 
discrepancies are not material to the subsequent exposure analysis, and 
agreed that we would consider the characterization of the maximum 
concentrations from the medium and large sources to account for the 
reasonable worst-case exposure scenario. Therefore, we have concluded 
that the petitioner's emissions inventory provides an adequate basis 
for the dispersion modeling and exposure assessment presented in the 
petition.
    To evaluate the petition's characterization of sources (e.g., stack 
heights, plume rise, distance to the nearest fence line and 
meteorology), we considered the petitioner's use of the TRI database 
and acquired a subset of the parameters the petitioner used in the more 
site-specific (tier 3) assessments. We determined that the petitioner 
appropriately used TRI as a basis for characterizing sources. We 
examined the source parameters the petitioner used in the tier 3 
analyses and determined, based on our engineering knowledge of the 
types of sources included in the analyses, that the parameters are 
reasonable.
    Our evaluation of the petition's dispersion modeling approach 
initially focused on the petitioner's use of the EPA models in the 
tiered analyses. We evaluated the petition's modeling approach for both 
annual average concentrations and for 24-hour concentrations. Our 
evaluation verified that the petitioner applied appropriate EPA 
guidelines in the modeling effort, and that the data inputs used in the 
models are appropriately conservative.
    We first evaluated the petition's modeling of long-term averages. 
To develop a more detailed evaluation of the petition's dispersion 
analyses, we acquired from the petitioner electronic copies of the raw 
data inputs and the model runs for seven of the largest emissions 
sources. This represents a subset of the sources which emit over 200 
tpy. The EPA selected these sources for scrutiny from the tier 3 
analysis set which the petitioner modeled using EPA's ISCST3 model. 
Based on a detailed review of the data inputs and the ISCST3 model 
runs, we confirmed that a conservative estimate (i.e., more likely to 
be over predicted than under predicted) of the highest maximum annual 
average concentration of MEK for all the facilities modeled is 
approximately 1.2 mg/m\3\. We agree with the petitioner's assertion 
that this concentration occurred at the entrance to an industrial 
facility adjacent to a relatively large MEK emission source in an 
industrial park. The maximum annual average concentration for the 
remaining emissions sources were all less than 0.9 mg/m\3\.
    We confirmed that for this subset of emission sources, the maximum 
predicted annual concentration of MEK declined below 0.5 mg/m\3\ within 
175 meters of the facility fence lines. Therefore, we concur with the 
petitioner that the predicted concentrations decline rapidly as the 
distance from the emission source increases. That is, within the 
relatively short distance of 175 meters, the maximum annual 
concentrations of MEK are likely to be at least a factor of two lower 
than the maximum predicted ISCST3 values for all sources in this 
subset.
    We evaluated the petitioner's modeling analyses for sources 
emitting less than 200 tpy of MEK. The petitioner used a tier 2 
analysis to predict maximum annual average concentrations for a series 
of worst-case emission scenarios for this subset of sources. After a 
detailed evaluation of the model parameters and input data, we 
determined that the petitioner's analyses of these emission sources 
also followed the appropriate EPA dispersion model guidelines.
    Based on our review, we have concluded that the predicted maximum 
annual average concentration for those sources emitting less than 200 
tpy of MEK is less than 0.7 mg/m\3\. These predicted concentration 
levels are conservative estimates which are also expected to decline 
rapidly as distance from the facility increases.
    During the review, we questioned the petitioner's designation of 
``large emission sources'' as those sources emitting more than 200 tpy 
of MEK. We requested that they conduct a more detailed analysis on 
sources emitting less than 200 tpy. We suggested that the petitioner 
use a minimum emission rate that could theoretically result in an 
exceedance of the petition's own specified health criterion of 3.3 mg/
m\3\. The petitioner would then assess the impact of this new 
``threshold of significance'' on the number and identity of sources in 
the ``large emission sources'' category and, if appropriate, reassess 
the impacts of this change on concentrations of ambient MEK.
    To accomplish this, the petitioner used very conservative 
assumptions of stack height, plume rise, meteorology, and distance to 
fence line to define a worst-case facility. Using this worst-case 
emission scenario coupled with EPA's SCREEN3 model, the petitioner 
demonstrated that sources emitting less than 90 tpy could not 
reasonably be expected to exceed the petition's proposed criterion of 
3.3 mg/m\3\. The petitioner then updated the emissions inventory using 
the 1996 TRI to identify those sources emitting between 90 and 200 tpy 
of MEK.
    The petitioner then revised the ``threshold of significance'' to 
reflect the use of the 1992 IRIS RfC of 1 mg/m\3\ as a decision 
criterion. To derive the new threshold, the petitioner decreased some 
of the conservatism in the tier 1 parameters and remodeled a new worst-
case scenario. The petitioner determined that with this new set of 
assumptions, emissions greater than 145 tpy would be necessary to 
exceed a 1 mg/m\3\ criterion. However, rather than restrict the new 
analysis to only those sources emitting between 145 and 200 tpy, the 
petitioner chose to evaluate the larger range of emission sources. 
Consequently, the revised dispersion modeling analysis focused on those 
sources emitting between 90 and 200 tpy of MEK. The petitioner 
submitted that analysis to EPA as an addendum to the original petition.
    The petitioner's approach in the revised modeling analysis was to 
limit

[[Page 32612]]

the potential for the model to overestimate exposure (compared to the 
original modeling approach), while maintaining adequate levels of 
conservatism in the final estimate. To accomplish that, the petitioner 
quantified the degree of overestimation in the previous modeling 
approaches due to conservative source-receptor configurations and 
adjusted to current model accordingly. That adjustment removed one 
level of conservatism from the estimates and provided a more realistic, 
but still conservative, estimate of the maximum annual average 
concentrations. The adjustment was applied to each of the emission 
sources in the previous analysis for those sources emitting from 90 to 
200 tpy.
    Based on this approach, the petitioner estimated that the maximum 
annual average concentration for the 18 facilities identified which 
emitted between 90 and 200 tpy of MEK would be less than 0.96 mg/m\3\. 
This value occurred at only one emission source; the remaining 17 
facilities in the 90 to 200 tpy range were all less than 0.75 mg/m\3\.
    We conducted a detailed review of the revised analytical approach 
and determined that it was acceptable. To quantify the conservatism of 
the adjusted model outputs, we recommended a site-specific analysis 
using an ISCST3 model (i.e., tier 3) of the source with the highest 
estimated MEK concentration (i.e., 0.96 mg/m\3\) after the adjustment. 
The tier 3 analysis predicted a maximum annual average concentration of 
0.17 mg/m\3\ of MEK from that facility. The tier 3 estimate was then 
compared to the adjusted emissions estimates to determine the extent of 
the conservatism remaining in the adjusted estimates. That comparison 
indicated that the petitioner's adjusted approach overestimated maximum 
annual average concentration for the source by approximately a factor 
of six.
    The petitioner provided the tier 3 analysis and the supporting data 
for our evaluation. After reviewing the model run and the supporting 
documentation in detail, we concluded that the petitioner's approach 
applies appropriate EPA guidelines and adequately characterizes maximum 
MEK concentrations from industrial sources. Therefore, based on that 
information, we have concluded that the maximum annual average MEK 
concentration from facilities emitting between 90 and 200 tpy of MEK 
may not reasonably be anticipated to exceed 0.96 mg/m\3\, and we expect 
it to be much less in most cases.
    We used the petition's information on the identity and location of 
MEK facilities to assess the impacts of sources located in close 
proximity to one another. Using a tier 2 analysis, we independently 
modeled the emissions from nine sources located relatively close to one 
another in two adjacent postal ZIP codes. Our analysis confirmed that 
MEK disperses rapidly as the distance from the emission source 
increases, and that at the point of maximum impact, the maximum annual 
average MEK concentration from multiple sources located close to each 
other may not reasonably be anticipated to exceed 1 mg/m\3\; in fact, 
we expect it to be much less than 1 mg/m\3\.
    To evaluate the potential contribution of the ambient background 
MEK to the maximum annual concentration of MEK, we reviewed the 
literature and various databases, including our Aerometric Information 
Retrieval System (AIRS) monitoring database and the California Air 
Toxics database. The available data show MEK measurements ranging from 
nondetectable to a high of 0.002 mg/m\3\ reported in AIRS. That value 
occurred in the Houston ship channel and represents mean 
concentrations, averaged over 1 year, from seven sites for the years 
1987-1995. In addition, the 2001 AIRS entries show similar maxima 
(e.g., AIRS shows averages 0f 0.002 mg/m\3\ from sites in Providence, 
Rhode Island). Based on that review, we have concluded that background 
concentrations are not likely to have a significant influence on 
maximum annual exposures to MEK.
    Given that the petitioner used the same modeling approach to 
predict 24-hour concentrations as was used to predict annual average 
concentrations, we accept the conclusion that the maximum 24-hour 
average concentration expected would be less than 10 mg/m\3\. However, 
we also wanted to evaluate predicted concentrations which may occur 
over a 1-hour time period. Using air dispersion modeling principles 
described in EPA's SCREEN3 User's Manual and the estimated annual 
average and 24-hour average concentrations presented in the petition, 
we estimated the maximum 1-hour concentration. The predicted annual 
average concentration is approximately 1 mg/m\3\ and the 24-hour 
average is about 10 mg/m\3\. To estimate the 1-hour maximum, we 
multiply the 24-hour average by 2.5. This results in a 1-hour maximum 
of approximately 25 mg/m\3\.
    In terms of ambient air monitoring data, the 2001 AIRS shows that 
the highest 24-hour concentration is 0.03 mg/m\3\, and the highest 3-
hour concentration is 0.06 mg/m\3\. Both of these concentrations were 
monitored in Rhode Island at the same location as the highest annual 
average concentrations for the year 2001. As with the annual average 
monitoring data, these short-term values are sufficiently low so as not 
to contribute significantly to short-term maximum concentrations.
    To summarize, the petitioner developed a tiered modeling analysis 
of MEK emissions using EPA's tiered approach to regulatory models. We 
determined that the petitioner performed all analyses following EPA 
modeling guidelines, and that the results provide conservative 
estimates of ambient levels of MEK from the inventoried sources. The 
modeling study demonstrated that, with the exception of the one 
location (at the entrance to a facility in an industrial park), 
estimated maximum annual average concentrations of MEK were less than 1 
mg/m\3\ for all facilities modeled, and well below 1 mg/m\3\ for most 
of the facilities modeled. For 24-hour and 1-hour averages, we expect 
the concentrations would not exceed 10 and 25 mg/m\3\, respectively. 
Also, based on the location of the maximum annual and 24-hour off-site 
concentration predicted at the highest emitting facility, EPA has 
concluded that no individual could be reasonably anticipated to 
experience chronic or 24-hour exposures at the level of the predicted 
maximum ambient concentrations. Therefore, given the conservatism built 
into the models and petitioner's modeling assumptions, EPA has 
concluded that we may not reasonably anticipate maximum annual 
exposures to MEK to exceed 1 mg/m\3\. In addition, based on the 
evaluation of multiple sources located relatively close together, we 
may not reasonably anticipate that the collective emissions of MEK will 
result in a maximum annual average off-site concentration of MEK 
greater than 1 mg/m\3\, or a 24-hour average greater than 10 mg/m\3\. 
We, by extrapolation, have concluded that 1-hour concentrations from 
multiple sources would not exceed 25 mg/m\3\. Finally, the petitioner's 
use of air concentrations for each emission source to characterize the 
exposed population is an acceptable, conservative approach to exposure 
modeling. That is, an exposure assessment that would estimate exposures 
for actual people living near these emission sources would likely 
result in maximum individual exposures from ambient air that are lower 
than the estimates presented in the petition. Given the likely 
proximity of inhabitable areas and the variability of human activity 
patterns, it is our expectation that actual

[[Page 32613]]

maximum individual exposures would be up to a factor of ten less than 
the maximum exposures presented in the petition. Therefore, in light of 
our review of the petitioner's exposure analysis, we have concluded 
that exposures to annual average ambient concentrations of MEK may not 
reasonably be anticipated to exceed 1 mg/m\3\, and that the maximum 24-
hour exposures may not reasonably be anticipated to exceed 10 mg/m\3\. 
Also, based on our own analysis, we have concluded that maximum 1-hour 
exposures may not reasonably be anticipated to exceed 25 mg/m\3\.

B. Human Health Effects Assessment

    We determined that the petition uses the same toxicological 
database as the 1992 IRIS assessment of MEK to characterize human 
health effects and to identify an appropriate human health criterion 
for the risk characterization for chronic effects. The IRIS is the 
Agency's official repository of consensus human health risk 
information. It was created and is maintained by the Agency to provide 
assistance to Agency decision makers on the potential adverse human 
health effects of particular substances. In addition, we evaluated 
recent studies reported in the published literature.
    Methyl ethyl ketone is classified in the IRIS (1992) as a Group D 
compound. A Group D compound is one that is not classifiable as to 
human carcinogenicity. This classification is based on the absence of 
human carcinogenicity data and inadequate animal data. There are no 
animal cancer bioassays of MEK by either the oral or inhalation route. 
There are structural data on MEK. One study concludes that MEK is 
unlikely to be carcinogenic based on the lack of any structural 
features or alerts indicative of carcinogenic potential as a result of 
mechanism-based structure-activity relationship (SAR) analysis (Woo et 
al., 2002). Further, Woo has given MEK a low concern rating (unlikely 
to be of cancer concern) based on comparison to acetone for which there 
is no evidence of carcinogenicity, and the fact that there is no 
evidence that unsubstituted mono-ketones have been associated with 
carcinogenicity/genotoxicity. There is also no reason to anticipate any 
electrophillic reactivity for unsubstituted mono-ketones mentioned 
above (i.e., no structural alerts).
    Cancer data on humans from which to draw conclusions about 
potential carcinogenic risks to the human population are weak and 
limited. None of the occupational epidemiology studies we examined 
(four studies of three different worker cohorts were available) 
provided clear evidence of increased cancer risk from occupational 
exposure to MEK. These data do provide some suggestion of evidence of 
an increased risk between multiple solvent exposures which included MEK 
and some cancers including bone and prostate cancer. (Alderson and 
Rattan, 1980; Wen et al., 1985; Spirtas et al., 1991; Blair et al. 
1998.)
    One study that has received some attention is a 1987 study 
investigating potential carcinogenic effects in the children of males 
occupationally exposed to MEK (Lowengart et al., 1987). This study 
included 123 matched pairs of children whose fathers reported, by 
questionnaire only, occupational exposure to various compounds 
including MEK, chlorinated solvents, spray paints, dyes and pigments, 
and cutting oils. The study reported a statistically significant 
positive trend for risk of childhood leukemia based on father's 
frequency of use for all of the chemicals mentioned, including MEK. 
Paternal exposure to MEK also appeared elevated, but not statistically 
significantly so, for the period of paternal exposure after birth of 
the child but not during pregnancy or one year before pregnancy. This 
study is considered as an exploratory study, based solely on 
questionnaires with no other exposure information. Factors that could 
be confounding covariates such as exposures to other chemicals and 
personal lifestyle were not taken into account in the statistical 
analysis of this study.
    Methyl ethyl ketone has been tested for activity in an extensive 
spectrum of in vitro and in vivo genotoxicity assays and has shown no 
evidence of genotoxicity in most conventional assays (National 
Toxicology Program, no date; World Health Organization 1992; Zeiger et 
al., 1992). Methyl ethyl ketone tested negative in bacterial assays 
(both the S. typhimurium (Ames) assay, with and without metabolic 
activation, and E. coli), the unscheduled deoxyribonucleic acid (DNA) 
synthesis assay, the assay for sister chromatid exchange (SCE) in 
Chinese hamster ovary (CHO) cells, the mouse lymphoma assay, the assay 
for chromosome aberrations in CHO cells, and the micronucleus assay in 
the mouse and hamster. The only evidence of mutagenicity was mitotic 
chromosome loss at high concentrations in a study of aneuploidy in 
yeast S. cerevisiae; the relevance of this finding to humans is 
questionable. Overall, studies of MEK yield little or no evidence of 
genotoxicity.
    Overall, the epidemiologic evidence is weak from which to draw 
conclusions about the carcinogenic risk in the human population. While 
none of the studies provides clear evidence of an increased cancer 
risk, with the totality of the evidence considered inconclusive, the 
data do provide some suggestion of an increased risk between multiple 
solvent exposures which include MEK and cancer, specifically childhood 
leukemia, bone cancer and prostate cancer. There is, however, an 
absence of positive results in the majority of mutagenicity and 
genotoxicity tests which are designed to indicate the potential for 
carcinogenicity, and there is a lack of structural features or alerts 
indicative of carcinogenic potential in SAR analysis. Based on these 
results we believe that MEK may not reasonably be anticipated to be 
carcinogenic.
    Developmental toxicity was the basis for the IRIS RfC of 1 mg/m\3\ 
which was verified in 1992. The critical study in the derivation of the 
RfC involved Swiss mice that were exposed to 0; 1,174; 2,978; or 8,906 
mg/m\3\ MEK for 7 hours per day during gestation days 6 through 15 
(Schwetz et al., 1991). Neither material nor developmental toxicity was 
observed at the low- or mid-doses. At the highest dose, there was a 
decrease in fetal body weight that was significant only in males. There 
was also a significant trend in the incidence of misaligned sternebrae 
when measured on a fetus but not a litter basis. At the highest dose, 
there was also an increase in relative liver and kidney weight, but the 
toxicological significance of that effect, if any, is reported in the 
IRIS as unknown. The lowest observed adverse effect level (LOAEL) for 
this study was 8,906 mg/m\3\, and the no observed adverse effect level 
(NOAEL) was 2,978 mg/m\3\.
    The available data indicate that MEK is not likely to be a 
reproductive toxicant. There exists no inhalation reproductive toxicity 
study of MEK; however, an oral two-generation reproductive/
developmental toxicity study of 2-butanol, a metabolic precursor to 
MEK, is available and is the basis for the oral reference dose (RfD) 
for MEK (Cox et al., 1975). 2-Butanol is quantitatively converted to 
MEK within the body. In this two-generation study, administration of 2-
butanol to rats in drinking water at concentrations as high as 3 
percent ([tilde]5000 mg kilograms-day) did not affect reproductive 
performance, but did induce developmental effects consistent with the 
results from inhalation developmental toxicity studies in rodents. The 
absence of any pathological lesions in the reproductive organs of rats 
exposed to MEK by inhalation for 90 days to concentrations as high as 
14,865 mg/m3 also provides

[[Page 32614]]

some indication that MEK is not likely to be a reproductive toxicant.
    The IRIS assessment of MEK states that at present, there is no 
convincing experimental evidence that MEK is neurotoxic ``* * * other 
than possibly inducing CNS (central nervous system) depression at high 
exposure levels.'' The IRIS documentation shows that no peripheral 
neurohistopathological changes were reported in rats exposed 
continuously to 3,320 mg/m3 MEK for up to 5 months (Saida et 
al., 1976). No treatment-related central or peripheral 
neurohistopathology was observed in rats exposed for 90 days (6 hours/
day, 5 days/week) at concentrations of MEK as high as 14,865 mg/
m3, even among animals specifically prepared and examined 
for neurohistopathology (Cavender et al., 1983). Also, ten of ten rats 
exposed to MEK at 17,700 mg/m3 and higher for 8 hours/day, 7 
days/week, died in the 7th week of exposure without neurological 
symptoms or histopathology (Altenkirch et al., 1978).
    Methyl ethyl ketone has been shown to potentiate neurotoxicity of 
other solvents in experiments with laboratory animals when both MEK and 
the other solvent are present in high concentrations. The EPA addressed 
the issue of interactions such as this in the text of the prospective 
RfC. We described several studies with human volunteers (see Dick et 
al., 1992, and references therein) that have MEK exposure groups (at 
100 parts per million (ppm) coexposed to relatively low levels, also 
around 100 ppm) of several other solvents including acetone, methyl 
isobutyl ketone and toluene. At least for the brief exposure periods in 
those studies (around 4 hrs), the authors observed no evidence of 
neurotoxic interactions. However, a recent review (Noraberg and Arlien-
Soborg, 2000) reports evidence of possible interactions even at 
occupational concentrations below the threshold limit values (TLV) (200 
ppm, 590 mg/m3) in solvent mixtures containing MEK at 200-
300 ppm and n-hexane at 60 ppm. This point should be considered when 
evaluating mixtures of solvents, especially those containing MEK and 
the solvents listed above, especially n-hexane. However, the lower 
limits of MEK exposure that may result in potentiation with other 
solvents have not been well established, and the potential of MEK in 
this regard remains a concern, although a minor one. Such concerns are 
especially diminished at the low-levels we are concerned with in this 
assessment (i.e., much less than 590 mg/m3).
    The petition presents a short-term criterion of 33 mg/
m3, which is an adjustment of their RfC of 3.3 mg/
m3. The petitioner calculated this value by simply 
eliminating the uncertainty factor of ten that is used for 
extrapolating from subchronic to chronic exposure in the RfC. We do not 
agree that this is an appropriate method of arriving at an short-term 
human health effects criterion, however, currently there is no EPA 
human health criterion for short-term exposures available for us to use 
in an analysis.
    There are 1999 California Environmental Protection Agency (CalEPA) 
short-term health criteria (CalEPA 1999). The CalEPA published three 
levels of acute reference exposure levels (REL) to protect against mild 
adverse effects (associated with a 1-hour exposure), severe effects 
(associated with a 7-hour exposure), and life threatening effects 
(associated with a 1-hour exposure). The REL for mild effects is 13 mg/
m3, for severe effects it is 32 mg/m3, and for 
life threatening effects it is 1,385 mg/m3. For the purposes 
of our analysis and decision, we focused on the mild REL, to be health 
protective. The CalEPA acute REL to protect against mild effects is 
based on the study of Nakaaki (1974). However, we consider the results 
with MEK from the studies of Dick et al. (1984, 1988, 1989, 1992) to be 
more scientifically defensible for the purposes of our analysis. 
Compared to the Nakaaki study, the Dick et al. studies tested more 
subjects (20+ per study versus four), used control groups extensively, 
better controlled the exposures (constant in the Dick et al. studies 
versus increasing concentrations in Nakaaki), analyzed a greater number 
of endpoints, and apparently longer duration exposures. Collectively, 
the volunteer studies of Dick et al. indicate that exposures to MEK of 
up to 200 ppm (590 mg/m3) and up to 4 hours would be an 
acceptable nonadverse effect concentration in the general population 
for both subjective effects (such as objectionable odor or irritancy) 
and for neurobehavioral effects. We would expect the same nonadverse 
effect concentrations to be relevant for children, as there is no 
reason to consider children as a sensitive subgroup for such a highly 
subjective, nonadverse effect as mild irritancy.

C. Determination of an Appropriate Health Effects Criterion for Chronic 
Noncancer Effects

    For risk assessments which estimate chronic noncancer effects from 
inhalation exposures, the IRIS inhalation RfC is the primary 
quantitative consensus value used by the Agency.
    The RfC for MEK of 1 mg/m3 was placed on IRIS in 1992. 
It was derived from the Schwetz et al. (1991) developmental toxicology 
study by dividing the NOAEL (2,978 mg/m3) by a series of 
uncertainty factors (UF). The UF for the determination of the MEK RfC 
was 3,000. This overall uncertainty factor reflects uncertainties in 
interspecies extrapolation (UF=10), sensitive individuals (UF=10), and 
an incomplete database, including a lack of chronic and reproductive 
toxicity studies (UF=10). In addition, a modifying factor (MF=3) was 
used to account for the absence of unequivocal data for portal-of-entry 
effects. This resulted in a combined UF and MF of 3,000.
    It is Agency policy that the IRIS represents a starting point for 
risk assessments, however, it is not given conclusive weight in the 
context of rulemaking. If an outside party questions information 
presented in the IRIS, we will consider all credible and relevant 
information before us in the course of making our decision.
    Accordingly, the petitioner reviewed the IRIS RfC in light of 
guidelines published by EPA in 1994, which addressed and updated 
methods for calculating RfC. Applying these guidelines to the same 
critical IRIS developmental study used to derive the IRIS RfC, which 
used the older methodology, the petitioner proposed a revised health 
criterion based on a reduction of the MEK uncertainty factor for 
interspecies extrapolation. This involved a reduction of the 
interspecies UF of 10 to a default value of 3. The reduction in the 
interspecies UF is consistent with the guidelines and is warranted if 
standard default dosimetric adjustments are incorporated in the 
original study. As a result, the petitioner proposed a revised RfC 
value of 3.3 mg/m3 (which we view as being equivalent to 3 
mg/m3 since EPA generally expresses the RfC as a whole 
number).
    The EPA's Office of Research and Development (ORD) reviewed the 
petitioner's proposed revision to determine whether such an alternative 
RfC was appropriate. That review indicated that the method that the 
petitioner applied to derive the criterion was consistent with both EPA 
policy and guidance. However, ordinarily, it is Agency policy that 
revisions in the IRIS are performed such that the entire database is 
simultaneously reevaluated for all effects and for all routes of 
exposure. This is done for both administrative efficiency and to ensure 
that we evaluate the breadth of available science.

[[Page 32615]]

    Subsequently, EPA announced in the Federal Register (67 FR 1212, 
January 9, 2002) that it would undertake a formal IRIS review of MEK. 
The announcement recognized that in the decade since the initial IRIS 
assessment of MEK, substantive alterations in the Agency's methods for 
dose-response assessments have occurred. The estimated completion date 
for the assessment, including peer review and external peer review is 
September 2003. We will consider the results of that review prior to 
taking any final action related to the proposed rule.
    In the meanwhile, to support statutory requirements and assist in 
the determination of the technical merits of the petition to delist 
MEK, EPA's ORD initiated a parallel undertaking to derive an interim 
health effects threshold for MEK inhalation exposure that incorporates 
consideration of current data and current EPA science policy. This 
process has resulted in the derivation of a prospective RfC of 9 mg/
m3. The analysis underlying the development of this 
prospective RfC can be found in ``A Prospective Reference Concentration 
for MEK (78-93-3)'' which is in the docket for today's proposed action.
    We consider this prospective RfC to be the most complete and 
current dose-response information on MEK and, therefore, have 
determined that it is the appropriate chronic noncancer health effects 
criterion for EPA to use in today's proposal to remove MEK from the HAP 
list. In our final evaluation about the potential for MEK to cause 
noncancer health effects, we will rely on the final RfC and other 
information resulting from the completed IRIS assessment. Thus, we will 
not take final action on today's proposed rule until such information 
becomes available. In today's action, we request comment generally on 
our prospective RfC and on the portion of our human health risk 
characterization based on this RfC. Also, because we recognize that 
there is some possibility that the RfC may change, we solicit comment 
on whether it would be appropriate for the Agency to delist MEK if the 
final RfC is different from the prospective RfC; for example, if it is 
finalized at 3 mg/m3, the level suggested by industry in its 
petition, or if it remains unchanged from the 1992 RfC of 1 mg/
m3.
    The prospective RfC is based on the same critical study as the 1992 
IRIS. Consistent with recent Agency recommendations for developing RfD 
and RfC, the assessment incorporates a duration adjustment to the 
critical study's NOAEL. This approach adjusted the discontinuous 
inhalation exposure (7 hours per day) in the critical study to a 
continuous (24 hours per day) duration. This procedure is premised on a 
simple concentration x time relationship, and it had the effect of 
reducing the adjusted NOAEL to 863 mg/m3 from the value of 
2,978 mg/m3 used in developing the 1992 RfC.
    Using the adjusted NOAEL, the assessment derives a human equivalent 
concentration (HEC) for MEK. The HEC represents an external air 
concentration estimated to achieve the same blood levels in humans and 
animals. Based on the available blood-to-air coefficient data for MEK 
in animals and humans, EPA applied the default factor of one for this 
derivation which resulted in a NOAELHEC of 863 mg/
m3. As with the standard IRIS assessment, EPA applied 
uncertainty factors to the NOAELHEC to account for 
recognized areas of uncertainty in extrapolating the data to the 
appropriate human scenario. The EPA concluded that the 1992 IRIS 
interspecies uncertainty (UF=10) and the modifying factor (MF=3) should 
be revised. However, we concluded that the intraspecies uncertainty 
(UF=10) should remain unchanged.
    The EPA applied the Agency's 1994 RfC methodology to the 
prospective RfC which results in an interspecies uncertainty factor of 
three. The prospective RfC also eliminates the previous modifying 
factor (MF=3) included in the 1992 IRIS to account for the absence of 
unequivocal data for portal-of-entry (respiratory tract) effects. This 
revision was, in part, due to additional information in a 1992 National 
Institute for Occupational Safety and Health (NIOSH) study in which 24 
volunteers exposed to 590 mg/m3 of MEK for 4 hours reported 
no net complaints of even minor irritation. The consequence of that 
study was a decrease in the uncertainty around irritant type of portal-
of-entry effects in humans.
    The prospective RfC also addresses the 1992 IRIS database 
uncertainty factor (UF=10). The assessment states that the problematic 
situation that existed in 1992 persists; namely, the difficulty of 
establishing a health-based guideline for a lifetime chronic exposure 
without any toxicity studies involving lifetime chronic exposures. The 
existing long-term repeated exposure experiments have certain flaws 
that affect their use in developing an inhalation RfC. However, the 
assessment concludes that EPA can use information from existing 
studies, as well as ancillary information from new sources, to reduce 
the concerns in the database. The assessment concludes that the 
analysis, coupled with the totality of the other available information, 
has the overall effect of reducing uncertainty in the database such 
that it is appropriate to apply a partial database uncertainty factor 
of three, rather than a full database uncertainty factor of ten, in 
developing the prospective RfC.
    This reduction, taken with the reduction in interspecies UF and the 
elimination of the modifying factor, reduced the composite uncertainty 
from 3,000 to 100. Therefore, EPA concludes that the prospective RfC is 
9 mg/m3.

D. Human Health Risk Characterization and Conclusions

    Methyl ethyl ketone is currently listed in IRIS based on a 1989 
evaluation as ``not classifiable as to human carcinogenicity'' 
according to the 1986 Cancer Guidelines. The IRIS summary identified 
the lack of both animal and human data to assess the carcinogenic 
potential of MEK, and at the current time, animal cancer bioassays with 
MEK by either the oral or inhalation route are still lacking, and there 
are no indications that such studies are either ongoing or planned. 
However, genotoxicity information does not indicate any readily 
apparent genetic mechanism of action for MEK, and the existing 
genotoxicity tests for MEK are essentially negative. In addition, 
structural data on MEK do not support any readily apparent basis for a 
carcinogenic hazard.
    The retrospective cohort studies of worker populations exposed to 
MEK provide no clear evidence of a cancer hazard in these populations. 
Because of various study limitations, these studies are weak and cannot 
support conclusions about the carcinogenic potential of MEK in humans. 
A case-control study examining the association between paternal 
exposures to several solvents including MEK and childhood leukemia is 
exploratory in scope such that we cannot use the results to reliably 
support the existence of any such association. Overall, this 
epidemiologic evidence is inconclusive and weak from which to draw 
conclusions about carcinogenic risks in the human population, although 
there is some suggestion between increased risk for some cancers and 
multiple solvent exposures, which included MEK. However, we consider 
the inconclusive nature of these studies to be offset by more 
conclusive results regarding the low potential of MEK to be 
carcinogenic, including the overall lack of positive results from 
genotoxicity tests and mutagenicity tests, and the lack of any 
indication of carcinogenicity from structure-activity relationships. 
Consequently, we conclude that we may

[[Page 32616]]

not reasonably expect MEK to be carcinogenic.
    In the analysis, we use a hazard quotient (HQ) approach to 
characterize the chronic noncancer risk associated with the exposure to 
MEK. The HQ is the ratio of a level of exposure for a given substance 
over a specific time period to a health criterion or reference level 
for that substance derived from a similar exposure period. We use the 
maximum annual average ambient concentration as the exposure for the 
purposes of the chronic HQ calculation. We use EPA's prospective RfC as 
the chronic health criterion, and we also calculate an HQ using the 
petitioner's RfC. These criteria encompass a 70-year lifetime of 
continuous exposure and address the health effect of concern due to 
chronic inhalation exposures to MEK. In addition, the criteria include 
the margins of safety built into the IRIS RfC and are, therefore, 
protective of sensitive subpopulations.
    Based on our evaluation of the modeling data presented in the 
petition, we judge that maximum ambient annual exposures from 
stationary sources to MEK are not likely to exceed 1 mg/m3. 
Using EPA's prospective RfC of 9 mg/m3, the HQ for the 
maximum annual average ambient exposure to MEK is 0.1. This means that 
a person's maximum exposure would be 10 percent of the RfC.
    We judge that the exposures to MEK of actual persons living in the 
immediate vicinity of an MEK emission source would more typically be at 
least a factor of two to ten less than 1 mg/m3. Therefore, 
replacing the maximum ambient concentration with a more realistic 
exposure scenario yields an HQ less than 0.1. Based on the current 
information, and given the conservative nature of the parameters used 
to estimate the maximum exposure, the protective nature of the 
prospective RfC, and because the petition and subsequent analyses 
characterize the vast majority of MEK exposures from stationary 
sources, we conclude that by applying the prospective RfC of 9 mg/
m3, potential ambient exposures to MEK may not reasonably be 
anticipated to cause adverse human health effects.
    With regard to the potential for short-term exposures to MEK to 
result in adverse health effects, we draw a qualitative conclusion. 
From the petition's modeled 24-hour maximum concentration of 10 mg/
m3, and using the conversion factor from EPA's SCREEN3 model 
User's Guide, we estimate that the maximum 1-hour concentration would 
not exceed 25 mg/m3. From the Dick et al. study, we see that 
exposures to MEK of up to 590 mg/m3 and up to 4 hours did 
not cause adverse effects to human subjects. While we have not 
developed a short-term human heath criterion from that study, we 
consider the gap between the adverse effects level in the Dick et al. 
study and the 24-hour and 1-hour concentrations to be large enough that 
we may not reasonably anticipate adverse effects to occur from these 
exposures. Further, as we state above, we consider the maximum annual 
average concentration estimates to be overestimates of true exposure. 
Given that the 24-hour and 1-hour ambient air concentrations were 
estimated using the same information and methods as the annual average 
concentrations, we consider these short-term concentrations to be 
similarly conservative. This provides us with additional confidence 
that adverse effects from short-term exposures will not occur.
    As discussed previously, we will consider the final RfC that 
results from the IRIS review and substantive public comment as that 
information becomes available. In addition, we expect to receive 
information on MEK from industry's submittal to the Agency's Voluntary 
Children's Chemical Evaluation Program (VCCEP). The VCCEP is intended 
to provide information to enable the public to understand the potential 
health risks to children associated with exposures to certain 
chemicals. Under that program, EPA has asked industries which 
manufacture or import certain chemicals to develop assessments 
regarding the potential health effect, exposures, and risks of those 
chemicals to children. We anticipate industry's submission to the first 
tier of the VCCEP program will be available during 2003, and we will 
consider this information when submitted, along with other information 
and comments we receive, before taking final action on the proposal.
    Given the current data, however, we are confident that in applying 
the prospective RfC of 9 mg/m3 to ambient annual average 
concentrations of 1 mg/m3 or less, we may not reasonably 
anticipate MEK to cause chronic adverse human health effects. Neither 
may we reasonably anticipate adverse effects to occur from short-term 
exposures.

E. Ecological Risk Characterization and Conclusions

    Our review of the petition's ecological risk characterization 
supports the findings that MEK has limited persistence in water, soil, 
and air. We further agree that it has a low octanol/water coefficient, 
a low adsorption coefficient, and a low bioconcentration factor; 
therefore, given the available data, it is not anticipated to persist 
or accumulate in the environment.
    A review of the general literature, including EPA databases, 
indicates that MEK has low environmental toxicity. For example, the 
daphnid 48-hour lethal concentrations for 50 percent of the testing 
sample (LC50) range from 2,200 to 5,091 ppm; the green algae 96-hour 
effective concentration for 50 percent of the population is 1,200 ppm; 
and the fish 96-hour LC50 ranges from 2,300 to 3,200 ppm. The fish 
chronic values range is 220 ppm, the daphnid chronic value is 521 ppm, 
and the algal chronic value is 45 ppm. These concentrations are 
significantly higher than what we would expect to see in the 
environment.
    The petition included no data on the potential for ecological 
effects to occur as a result of exposures to media other than water. 
There are no available data on avian exposure to MEK from the air 
pathway. There are also no available data on air exposure to plants 
from MEK. However, there is a database on laboratory mammals regarding 
air exposures to MEK from which we routinely extrapolate to draw 
conclusions regarding potential health effects to humans. From this 
database, we draw a similar conclusion regarding the potential for 
adverse health effects in mammals that may be exposed to ambient levels 
of MEK as we did for humans.
    Based on our review of all pertinent data supplemented by 
additional environmental modeling, we have concluded that there are 
sufficiently adequate data on environmental effects of MEK to determine 
that ambient concentrations, bioaccumulation, or deposition of MEK may 
not reasonably be anticipated to cause adverse environmental effects.

F. Transformation Characterization

    Methyl Ethyl Ketone is one of several volatile organic compounds 
(VOC) that transform into acetaldehyde and formaldehyde in the ambient 
air. Both acetaldehyde and formaldehyde are HAP and classified as 
probable human carcinogens. Based on a simplified analysis, the 
petitioner concluded that the contribution to ambient concentrations of 
acetaldehyde and formaldehyde from MEK transformation is insignificant. 
This conclusion is largely based on the knowledge that MEK's half-life, 
about 9 days, is comparatively longer than its transformation products, 
acetaldehyde and formaldehyde, whose half-lives are about 14 hours and 
3 hours, respectively. This implies that MEK's

[[Page 32617]]

transformation products disappear much faster than they are formed. Our 
evaluation, summarized below, concurs with the petitioner's conclusion 
that atmospheric transformation of MEK emissions may not reasonably be 
anticipated to cause adverse effects to human health.
    First, we assessed whether there would be elevated ambient 
concentrations near individual sources of MEK. Next, we estimated the 
ambient concentrations of these HAP resulting from transformation of 
MEK from multiple sources in urban areas. We then estimated the 
potential for any of these concentrations to cause adverse human health 
effects. Since the atmospheric chemistry for these pollutants is 
complex and not fully understood, we made conservative assumptions in 
the analysis in order to over- rather than under-estimate the 
concentrations of acetaldehyde and formaldehyde that could result from 
MEK transformation. Please refer to the docket for our complete 
analysis.
    In the first step of the analysis, we applied tier 1 dispersion 
modeling (SCREEN3) to the worst-case facility presented in the 
petition, and assuming a conservative average wind speed of 3 miles per 
hour, we determined that the MEK plume from any given source will 
travel about 650 miles over MEK's 9-day half-life. Even at one tenth 
this duration (i.e., about 21 hours), still assuming a wind speed of 3 
miles per hour, the plume will have traveled about 63 miles. In this 
plume, we estimated the unreacted MEK concentration after 21 hours to 
be approximately 1.6x10-3 mg/m3.
    As it disperses, MEK transforms relatively slowly into acetaldehyde 
and formaldehyde and, in turn, these compounds decompose much more 
quickly into by-products, including carbon dioxide, carbon monoxide, 
and water. We estimated that about 7 percent of the MEK would have 
transformed into acetaldehyde and possibly formaldehyde after 21 hours. 
Accordingly, we estimated that the maximum concentrations of 
acetaldehyde and formaldehyde due to MEK transformation at this point 
(21 hours after being emitted) would be roughly 7x10-5 mg/
m3 and 5x10-5 mg/m3, respectively. For 
acetaldehyde, that translates into a lifetime excess cancer risk of 
1x10-7. For formaldehyde, the lifetime excess cancer risk is 
7x10-7. Calculating noncancer hazard quotients, we see that 
the HQ for acetaldehyde is 0.008. This means that the level of 
acetaldehyde to which people are exposed is 0.8 percent of the RfC. For 
formaldehyde, the HQ is 0.005, which means that the exposure level is 
0.5 percent of the appropriate reference level, the Maximum Risk Level 
(MRL) \1\. Thus, since the cancer risks associated with the 
transformation products are below 1 in 1 million, and the noncancer 
exposures are less than 1 percent of the reference concentrations, we 
may not reasonably anticipate adverse health effects to occur from 
transformation of MEK into acetaldehyde and formaldehyde around MEK 
emissions sources. We note here that risk levels in the upwind part of 
the plume (i.e., the risks from the transformation products close to 
MEK emission sources) must be lower than what we estimated since the 
analysis did not account for degradation of acetaldehyde and 
formaldehyde. Further, we note that typical ambient levels of MEK are 
higher than they are in the plume at this point, indicating that the 
``plume,'' as such, would no longer exist, having already merged 
indistinguishably with the ambient background. This turns our attention 
to the analysis of transformation products in the ambient background.
---------------------------------------------------------------------------

    \1\ There is no EPA RfC for formaldehyde. However, the Agency 
for Toxics Substances and Disease Registry has calculated a 
noncancer health effects level, called a MRL. The MRL for 
formaldehyde is 0.01 mg/m3.
---------------------------------------------------------------------------

    To evaluate the potential of acetaldehyde and formaldehyde to form 
from ambient concentrations of MEK significantly downwind of multiple 
emission sources, we looked at ambient monitoring data to determine the 
typical ambient level of MEK in urban environments. We then estimated 
the maximum concentrations of acetaldehyde and formaldehyde that could 
be transformed from this MEK, using conservative, steady-state 
assumptions. Based on available monitoring information, we determined 
that at the 95th percentile, the ambient concentration of MEK is 
4.3x10-3 mg/m3. Using an estimated degradation 
rate of 14 times greater than MEK for acetaldehyde, we estimated the 
ambient concentrations of acetaldehyde from transformed MEK to be 
1.8x10-4 mg/m3. For formaldehyde, we estimated 
that it degrades at a rate of 72 times faster than MEK and, thus, 
calculated that the ambient concentration due to MEK transformation is 
2x10-5 mg/m3. These very small concentrations do 
not represent significant health threats as they translate into 
lifetime excess cancer risks of 4x10-7 for acetaldehyde and 
3x10-7 for formaldehyde.
    We do not expect adverse noncancer health effects to occur from the 
transformation of MEK. The HQ for acetaldehyde is 0.02 which 
corresponds to an exposure which is 2 percent of the RfC. For 
formaldehyde, the resulting HQ is 2x10-3 which represents an 
exposure of 0.2 percent of the MRL. Therefore, we may not reasonably 
anticipate adverse noncancer effects to occur due to exposures to these 
outdoor ambient concentrations of acetaldehyde or formaldehyde. Based 
on the analysis, we conclude that atmospheric transformation of MEK 
into acetaldehyde and formaldehyde may not reasonably be anticipated to 
cause significant human health risks.

G. Public Comments and EPA Responses

    As part of the notice announcing receipt of a complete petition to 
delist MEK (64 FR 33453, June 23, 1999), we requested interested 
parties to provide us with data or comments. Copies of the public 
comments have been included in the docket for this action and have been 
considered in our review of the petition. Substantive comments are 
discussed below.
    Comment. One commenter expressed concern about the overall 
appropriateness of the IRIS RfC as a decision criterion for determining 
human health effects. The commenter maintained that the IRIS RfC is 
itself uncertain and, therefore, the petitioner's proposed revision is 
without merit. To support this position, data from a single long-term 
toxicity study which included MEK was cited. That study was published 
since the IRIS validation and reports adverse health effects as 
measured by decreased neural condition velocities for a set of workers 
(41 exposed, 63 controls) exposed over a period of 14 +/- 7.5 years to 
levels of MEK ranging from 149 to 342 mg/m3.
    Response. The EPA's National Center for Environmental Assessment 
(NCEA) and National Health and Environmental Effects Research 
Laboratory (NHEERL) reviewed the referenced study as a part of our 
technical review. Their review demonstrated that the study has multiple 
and serious methodological shortcomings that greatly reduce its 
meaningfulness. Very few methodological details were presented in the 
study, making it virtually impossible for EPA reviewers to determine 
what had been done. It is not clear what factors were ``matched'' when 
the control groups were selected or how comparable the groups were on 
factors other than age. In addition, the study did not include 
important factors that are relevant to interpreting the results, 
including such factors as the type of work (e.g., office versus 
physical work); lifestyle factors (e.g., drinking, smoking, etc.); and 
height and weight of the subjects (important for nerve

[[Page 32618]]

conduction). Also, the study did not specify the experimental 
procedures that it applied, including whether the subjects were tested 
at the same location and time as the exposed workers, or whether the 
examiners were aware of the exposure status of the subjects at the time 
of testing. Importantly, the study did not address the control of 
temperature, a critical factor in nerve conduction studies, and the 
reported pattern of nerve conduction results is not entirely consistent 
with the reported peripheral neuropathy.
    Of primary importance in EPA's review was the consideration of the 
extent to which the study's findings are supported by the existing 
scientific literature. In this regard, we conclude that the study cited 
in the comment is inconsistent with a large volume of high quality 
neurotoxicological scientific evidence. In fact, animal models of the 
reported condition are excellent predictors of human neuropathy. MEK 
has been well tested for the reported condition and is convincingly 
negative.
    Comment. The EPA received a comment expressing concern over MEK's 
role in potentiating the effect of other substances. The comment stated 
that given the ``ubiquitous'' ambient concentration of certain 
pollutants and general lack of understanding of the mechanisms of 
potentiation, it would be inappropriate for the Agency to allow an 
increase in ambient concentrations of MEK.
    Response. As described in this preamble, MEK has been shown to 
potentiate neurotoxicity of other solvents in experiments with 
laboratory animals when both are present in high concentrations. The 
lower limits of MEK exposure that may result in potentiation with other 
solvents have not been well established in animals, and the potential 
of MEK in this regard remains a concern, although a minor one.

H. Other Issues

    Since the receipt of the petition, MEK has been measured in the 
blood of the general population as reported from the National Health 
and Nutrition Examination Survey (NHANES) database. The NHANES database 
reports median blood levels of 5.4 parts per billion (ppb) and levels 
at the 95th percentile of 16.9 ppb. The EPA estimates that it would 
take continuous exposures at ambient concentrations near 1 mg/
m3 of MEK to result in the reported median blood level.
    However, based on the available information, EPA believes it is 
reasonable to expect that the reported blood levels did not result from 
an air exposure to MEK at the prospective RfC. Primarily, this is 
because concentrations of MEK found in the immediate vicinity of large 
MEK emissions sources are below the RfC, and as previously stated in 
today's action, typical ambient background concentrations of MEK are 
several orders of magnitude lower than the prospective RfC.
    In addition, although MEK has been shown in animal studies to be 
readily absorbed, it is also rapidly metabolized, mostly in the liver. 
The excretion half-life of MEK is quite short, on the order of minutes 
to hours (Liira et al., 1988), and is nearly quantitatively complete in 
both animals and in humans. The data indicate that internal doses 
following experimental air exposures to MEK consist mostly of 
metabolites that are cleared quickly. Therefore, tissue and blood 
levels of MEK would become minimal shortly after termination of 
experimental air exposures due to kinetics and solubility of MEK. 
Likewise, for those persons exposed to relatively high concentrations 
of MEK, blood levels would fall relatively quickly to pre-exposure 
levels following the termination of exposure.
    Consequently, it is the judgment of scientists from both the 
Centers for Disease Control (CDC), who compiled the NHANES database, 
and EPA that the data are not representative of atmospheric exposure of 
national proportions. These authors also state that blood levels of 
both MEK and acetone are highly variable as a result of their 
physiologic metabolism and do not reflect environmental exposures very 
well (Churchill et al., 2001). Thus, it is more likely that the 
reported MEK in human blood is a by-product of normal human metabolism.
    Another issue we addressed in today's action is that of MEK as an 
ozone precursor. The EPA recognizes that MEK is an ozone precursor, but 
after considering this issue, we determined that it is inappropriate to 
include a substance on the HAP list under CAA section 112(b) due 
entirely to its tendency to form ozone. Section 112(b) provides that no 
air pollutant which is listed under CAA section 108(a), such as ozone, 
may be added to the HAP list. It further provides that a pollutant that 
is a precursor to a pollutant listed under section 108(a), such as MEK, 
may not be included on the HAP list unless it independently meets the 
HAP list criteria. As explained in today's action, we believe that the 
petitioner has demonstrated that MEK does not independently meet the 
criteria for listing as a HAP under section 112 of the CAA.
    The Agency has previously determined that MEK could not be removed 
from the list of pollutants under section 313 of the Emergency Planning 
and Community Right-To-Know Act of 1986 (EPCRA) (63 FR 15195). However, 
the EPCRA list serves a very different purpose than the list of HAP 
under section 112(b) of the CAA. Specifically, the EPCRA--which is 
intended to provide information regarding the emissions of air 
pollutants generally--deals collectively with HAP, VOC, and other air 
and water pollutants under section 313 by providing for the listing of 
any pollutant that may reasonably be anticipated to cause adverse 
effects to human health or the environment. The CAA, on the other hand, 
establishes requirements for reducing the emissions of air pollutants 
and deals separately with HAP (which are to be listed and regulated 
under section 112) and criteria air pollutants (which are to be listed 
under section 108 and regulated under various other sections of the 
CAA). The EPA is required to regulate precursors to criteria air 
pollutants, such as VOC, for their contributions to ambient levels of 
criteria pollutants under statutory provisions that do not apply to 
HAP. This dual structure would lose its significance if EPA were to 
include substances on the HAP list solely as a result of their 
contribution to concentrations of criteria air pollutants.
    The decision to grant the petition and issue a proposed rule to 
delist MEK removes MEK from regulatory consideration under section 
112(d) of the CAA. Section 112 requires the development of maximum 
achievable control technology (MACT) standards to reduce routine 
emissions of listed toxic air pollutants. The proposed rule does not 
affect MEK's status under the CAA as a VOC, and EPA will continue to 
regulate it as such. In ozone nonattainment areas, sources of MEK 
emissions must continue to meet applicable standards identified in 
State implementation plans (SIP).
    In addition, the proposed rule does not impact any MEK reporting 
requirements under the TRI (EPCRA, section 313). Recognizing that MEK 
is one of the largest sources listed in the TRI, the Agency will 
continue to track emissions of MEK. Further, under the CAA, the Agency 
has the option to add MEK back onto the HAP list and will do so should 
a need arise.

I. Discussion and Conclusion

    Uncertainty is an inherent part of risk assessment. It arises 
because risk assessment is a complex process, requiring the integration 
of multiple factors. In the analysis, uncertainty arises for the 
following reasons. The

[[Page 32619]]

IRIS dataset used to derive the human health effects decision criterion 
is imperfect and leads to uncertainty in the RfC. This uncertainty is 
primarily due to the lack of long-term MEK toxicity data and is 
compensated for in the application of an uncertainty factor of 100 for 
the prospective RfC. In addition, animal cancer bioassays with MEK by 
either the oral or inhalation route are lacking from the database, and 
there is scientific uncertainty in MEK's ability to potentiate the 
action of other neurotoxins. We also recognize that there is 
uncertainty in the computer models used to predict the fate and 
transport of MEK in the environment. These models are simplifications 
of reality and some variables are excluded.
    For decisions which are based largely on risk assessments, some 
degree of uncertainty is acceptable. Such is the case for this 
delisting decision. We do not interpret CAA section 112(b)(3)(C) to 
require absolute certainty that a pollutant will not cause adverse 
effects on human health or the environment before it may be deleted 
from the list. The use of the terms ``adequate'' and ``reasonably'' 
indicate that the Agency must weigh the potential uncertainties and 
their likely significance. To this end, the assessment applies 
conservative assumptions to bias potential error toward protecting 
human and ecological health. Thus, EPA is confident that even when we 
consider the uncertainties in the petition's initial assessment and in 
the additional analyses, the results are more likely to over-estimate 
rather than under-estimate true exposures and risks.
    Based on our evaluation of the petition and the subsequent 
analyses, we judge that the potential for adverse human health and 
environmental effects to occur from projected exposures is sufficiently 
low to provide reasonable assurance that such adverse effects will not 
occur. For example, the petitioner appropriately applied EPA's model 
guidelines and EPA's tiered dispersion modeling approach which we 
designed to be conservative. Also, EPA suggested that the petitioner 
conduct an additional, more site-specific analysis to verify the 
conservatism of the original analysis. The results of that analysis 
increased our confidence that the petition over-rather than under-
estimates exposure. In addition, the petition did not apply a formal 
exposure assessment to the predicted ambient air concentrations. 
Instead, the petition used the air concentrations alone as a surrogate 
for exposure. Based upon the likely proximity of inhabitable areas and 
knowledge of human activity patterns, we believe that actual exposures 
will be far less than predicted exposures that were derived from the 
dispersion analysis. Further, when modeling clusters of MEK sources, 
the petition showed that concentrations resulting from that scenario 
are not likely to adversely affect health. Finally, available data from 
monitors suggest that ambient concentrations of MEK in urban areas are 
over two orders of magnitude lower than the modeled maximum 
concentrations.
    As described above, EPA's proposed decision to delist MEK is based 
on the results of a risk assessment demonstrating that emissions of MEK 
may not reasonably be anticipated to result in adverse human health or 
environmental effects. In addition to the analyses presented and the 
uncertainties inherent in risk assessment, we have considered other 
information related to MEK in making this decision, namely the 
transformation of MEK into acetaldehyde and formaldehyde and recently 
discovered levels of MEK in human blood. The MEK decomposes in the 
ambient air into two probable human carcinogens (acetaldehyde and 
formaldehyde). However, given that the actual contribution of MEK to 
ambient concentrations of these two pollutants is very small, and that 
they decompose rapidly, we do not anticipate that MEK transformation 
into these two pollutants will be significant enough to have an adverse 
impact on human health. We do not expect that ambient concentrations of 
MEK contribute significantly to the blood level burden due to the small 
ambient concentrations of MEK in ambient air.
    We also considered the fact that MEK is one of the top compounds by 
volume reported in the TRI. Under this proposal, it would no longer be 
regulated as a HAP, but it will continue to be reported in the TRI and 
regulated under EPA's criteria pollutant (ozone) program.
    As discussed previously, we will consider the RfC that results from 
the IRIS review and information combined in industry's submission under 
tier 1 of the VCCEP before taking final action on the proposal. We also 
welcome additional data or information that can further clarify these 
and other issues related to MEK. We will evaluate all substantive 
information received during the comment period prior to taking any 
final action on the proposed rule.

V. References

    References cited in the preamble can be viewed in the docket for 
this proposed rule.

VI. Statutory and Executive Order Reviews

A. Executive Order 12866: Regulatory Planning and Review

    Under Executive Order 12866 (58 FR 51735, October 4, 1993), EPA 
must determine whether the regulatory action is ``significant'' and 
therefore subject to Office of Management and Budget (OMB) review and 
the requirements of the Executive Order. The Executive Order defines 
``significant regulatory action'' as one that is likely to result in a 
rule that may:
    (1) Have an annual effect on the economy of $100 million or more or 
adverse affect in a material way the economy, a sector to the economy, 
productivity, competition, jobs, the environment, public health or 
safety, or state, local or tribal governments or communities;
    (2) Create a serious inconsistency or otherwise interfere with an 
action taken or planned by another agency;
    (3) Materially alter the budgetary impact of entitlements, grants, 
user fees, or loan programs, or the rights and obligation of recipients 
thereof; or
    (4) Raise novel legal or policy issues arising out of legal 
mandates, the President's priorities, or the principles set forth in 
the Executive Order.
    Pursuant to the terms of Executive Order 12866, it has been 
determined that the proposed action does not constitute a ``significant 
regulatory action'' and is, therefore, not subject to OMB review.

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. 
The proposed action will remove MEK from the CAA section 112 (b)(1) HAP 
list and, therefore, eliminate the need for information collection 
under 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

[[Page 32620]]

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 are listed in 40 CFR part 9 and 48 CFR 
chapter 15.

C. Regulatory Flexibility Act (RFA)

    The 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 business, small organizations, and small 
governmental jurisdictions. For the purposes of assessing the impacts 
of today's proposed rule on small entities, small entity is defined as: 
(1) A small business that meets the definitions for small business 
based on the Small Business Association (SBA) size standards which, for 
this proposed action, can include manufacturing (NAICS 3999-03) and air 
transportation (NAICS 4522-98 and 4512-98) operations that employ less 
1,000 people and engineering services (NAICS 8711-98) operations that 
earn less than $20 million annually; (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 impact of today's proposed rule on 
small entities, I certify that this proposed action will not have a 
significant economic impact on a substantial number of small entities. 
In determining whether a rule has significant economic impact on a 
substantial number of small entities, the impact of concern is any 
significant adverse economic impact on small entities, since the 
primary purpose of the regulatory flexibility analysis is to identify 
and address regulatory alternatives ``which minimize any significant 
economic impact of the proposed rule on small entities.'' (5 U.S.C. 603 
and 604). Thus, an agency may certify that a rule will not have a 
significant economic impact on a substantial number of small entities 
if the rule relieves regulatory burden, or otherwise has a positive 
economic effect on all of the small entities subject to the rule. The 
proposed rule will eliminate the burden of additional controls 
necessary to reduce MEK emissions and the associated operating, 
monitoring and reporting requirements. We have, therefore, concluded 
that today's proposed rule will relieve regulatory burden for all 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 1044, 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 adopt 
the least costly, most cost-effective or least burdensome alternative 
that achieves the objectives of the rule. The provisions of section 205 
do not apply when they are inconsistent with applicable law. Moreover, 
section 205 allows EPA to adopt an alternative other than the least 
costly, most cost-effective or least burdensome alternative if the 
Administrator publishes with the final rule an explanation why that 
alternative was not adopted. Before EPA establishes any regulatory 
requirements that may significantly or uniquely affect small 
governments, including tribal governments, it must have developed under 
section 203 of the UMRA a small government agency plan. The plan must 
provide for notifying potentially affected small governments, enabling 
officials of affected small governments to have meaningful and timely 
input in the development of EPA regulatory proposals with significant 
Federal intergovernmental mandates, and informing, educating, and 
advising small governments on compliance with the regulatory 
requirements.
    Today's proposed rule contains no Federal mandates for State, 
local, or tribal governments or the private sector. The proposed rule 
imposes no enforceable duty on any State, local or tribal governments 
or the private sector. In any event, EPA has determined that the 
proposed rule does not contain a Federal mandate that may result in 
expenditures of $100 million or more for State, local, and tribal 
governments, in the aggregate, or the private sector in any 1 year. 
Because the proposed rule removes a compound previously labeled in the 
CAA as a HAP, it actually reduces the burden established under the CAA. 
Thus, today's proposed rule is not subject to the requirements of 
sections 202 and 205 of the UMRA.

E. Executive Order 13132, Federalism

    Executive Order 13132 (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.''
    Under Executive Order 13132, EPA may not issue a regulation that 
has federalism implications, that imposes substantial direct compliance 
costs, and that is not required by statute, unless the Federal 
government provides the funds necessary to pay the direct compliance 
costs incurred by State and local governments, or EPA consults with 
State and local officials early in the process of developing the 
proposed regulation. The EPA also may not issue a regulation that has 
federalism implications and that preempts State law unless the Agency 
consults with State and local officials early in the process of 
developing the proposed regulation.
    Today's proposed rule removes the substance MEK from the list of 
HAP contained under section 112(b)(1) of the CAA. It does not impose 
any additional requirements on the States and does not affect the 
balance of power between the States and the Federal government. Thus, 
the requirements of section 6 of the Executive Order do not apply to 
the proposed rule.

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

[[Page 32621]]

regulatory policies that have tribal implications.'' The proposed rule 
does not have tribal implications, as specified in Executive Order 
13175. A review of the available emission inventory does not indicate 
tribal MEK emissions sources subject to control under the CAA, 
therefore, the proposed rule is not anticipated to have tribal 
implications. In addition, the proposed action will eliminate control 
requirements for MEK and, therefore, reduces control costs and 
reporting requirements for any tribal entity operating a MEK source 
subject to control under the CAA which we might have missed. Thus, 
Executive Order 13175 does not apply to the proposed rule.

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

    Executive Order 13045 (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.
    The EPA interprets Executive Order 13045 as applying only to those 
regulatory actions that are based on health or safety risks, such that 
the analysis required under section 5-501 of the Executive Order has 
the potential to influence the regulation. The proposed rule is not 
subject to Executive Order 13045 because it is not economically 
significant as defined in Executive Order 12866, and because the Agency 
does not have reason to believe the environmental health or safety 
risks addressed by this action present a disproportionate risk to 
children. This determination is based on the fact that the RfC is 
determined to be protective of sensitive sub-populations, including 
children. Also, the single study cited during public comment to 
indicate a potential effect on children has been reviewed during this 
petition process and found to be limited in design and execution. 
Consequently, we determined that the study was of insufficient quality 
to provide information regarding health risks (leukemia) of MEK to 
children. However, as we state above, we anticipate industry's 
submission to the first tier of the VCCEP program will be available 
during 2003, and we will consider this information when submitted. In 
addition, the public is invited to submit or identify peer-reviewed 
studies and data, of which the Agency may not be aware, that assessed 
results of early life exposure to MEK.

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

    Executive Order 13211, ``Actions Concerning Regulations that 
Significantly Affect Energy Supply, Distribution, or Use'' (66 FR 
28355, May 22, 2001), requires EPA to prepare and submit a Statement of 
Energy Effects to the Administrator of the Office of Information and 
Regulatory Affairs, Office of Management and Budget, for certain 
actions identified as ``significant energy actions.'' The proposed rule 
is not a ``significant energy action'' because it is not likely to have 
a significant adverse effect on the supply, distribution, or use of 
energy.

I. National Technology Transfer and Advancement Act

    Section 112(d) of the National Technology Transfer and Advancement 
Act of 1995 (NTTAA), Public Law No. 104-113, section 12(d) 915 U.S.C. 
272 note), directs all Federal agencies to use voluntary consensus 
standards instead of government-unique standards in their regulatory 
activities unless to do so would be inconsistent with applicable law or 
otherwise impractical. Voluntary consensus standards are technical 
standards (e.g., material specifications, test method, sampling and 
analytical procedures, business practices, etc.) that are developed or 
adopted by one or more voluntary consensus standards bodies. Examples 
of organizations generally regarded as voluntary consensus standards 
bodies include the American Society for Testing and Materials (ASTM), 
the National Fire Protection Association (NFPA), and the Society of 
Automotive Engineers (SAE). The NTTAA requires Federal agencies like 
EPA to provide Congress, through OMB, with explanations when an agency 
decides not to use available and applicable voluntary consensus 
standards. The proposed rule does not involve technical standards. 
Therefore, EPA is not considering the use of any voluntary consensus 
standards.

List of Subjects in 40 CFR Part 63

    Environmental protection, Air pollution control, Hazardous 
substances, Reporting and recordkeeping requirements.

    Dated: May 22, 2003.
Christine Todd Whitman,
Administrator.
    For the reasons set out in the preamble, part 63, title 40, chapter 
I of the Code of Federal Regulations is proposed to be amended as 
follows:

PART 63--NATIONAL EMISSION STANDARDS FOR HAZARDOUS AIR POLLUTANTS 
FOR SOURCE CATEGORIES

    1. The authority citation for part 63 continues to read as follows:

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

Subpart C--[Amended]

    2. Subpart C is amended by adding Sec.  63.61 and reserving 
Sec. Sec.  63.62 through 63.69 to read as follows:


Sec.  63.61  Deletion of methyl ethyl ketone from the list of hazardous 
air pollutants.

    The substance methyl ethyl ketone (MEK, 2-Butanone) (CAS Number 
105602) is deleted from the list of hazardous air pollutants 
established by 42 U.S.C. 7412(b)(1).


Sec. Sec.  63.62-63.69  [Reserved]

[FR Doc. 03-13428 Filed 5-29-03; 8:45 am]
BILLING CODE 6560-50-P