List of Hazardous Air Pollutants, Petition Process, Lesser Quantity Designations, Source Category List, 75047-75059 [05-24200]

Agencies

• ENVIRONMENTAL PROTECTION AGENCY

[Federal Register Volume 70, Number 242 (Monday, December 19, 2005)]
[Rules and Regulations]
[Pages 75047-75059]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 05-24200]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 63

[OAR-2003-0028, FRL-8009-5]
RIN: 2060-AI72


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

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: EPA is amending the list of hazardous air pollutants (HAP) 
contained in section 112 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 of the CAA.
    Based on the available information concerning the potential hazards 
of and projected exposures to MEK, EPA has made a determination 
pursuant to CAA section 112(b)(3)(C) that there are ``adequate data on 
the health and environmental effects [of MEK] to determine that 
emissions, ambient concentrations, bioaccumulation, or deposition of 
the substance may not reasonably be anticipated to cause adverse 
effects to human health or adverse environmental effects.''

EFFECTIVE DATE: December 19, 2005.

[[Page 75048]]


ADDRESSES: EPA has established a docket for this action under Docket ID 
No. OAR-2003-0028 and A-99-03. All documents in the docket are listed 
in the EDOCKET index at https://www.epa.gov/edocket. Although listed in 
the index, some information is not publicly available, i.e., 
confidential business information or other information whose disclosure 
is restricted by statute. Certain other material, such as copyrighted 
material, is not placed on the Internet and will be publicly available 
only in hard copy form. Publicly available docket materials are 
available either electronically in EDOCKET or in hard copy at EPA 
Docket Center (Air Docket), EPA/DC, EPA West, Room B-108, 1301 
Constitution Avenue, NW., Washington, DC 20004. The Public Reading Room 
is open from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding 
legal holidays. The telephone number for the Public Reading Room is 
(202) 566-1744, and the telephone number for the Air Docket is (202) 
566-1742.

FOR FURTHER INFORMATION CONTACT: Mr. Mark Morris, Office of Air Quality 
Planning and Standards, Emission Standards Division, C404-01, 
Environmental Protection Agency, Research Triangle Park, NC 27711; 
telephone number: (919) 541-5416; fax number: 919-541-0840; e-mail 
address: morris.mark@epa.gov.

SUPPLEMENTARY INFORMATION:
    Regulated Entities. Entities potentially affected by this action 
are those industrial facilities that manufacture or use MEK. This 
action amends the HAP list contained in section 112(b)(1) of the CAA by 
removing the compound MEK. The decision to issue a final rule to delist 
MEK removes MEK from regulatory consideration under section 112(d) of 
the CAA.
    Judicial Review. Under section 307(b)(1) of the CAA, judicial 
review is available only by filing a petition for review in the U.S. 
Court of Appeals for the District of Columbia Circuit by 60 days from 
publication in the Federal Register. Under section 307(d)(7)(B) of the 
CAA, only an objection to a rule or procedure raised with reasonable 
specificity during the period for public comment can be raised during 
judicial review. Moreover, under section 307(b)(2) of the CAA, the 
requirements established by the final rule may not be challenged 
separately in any civil or criminal proceeding brought to enforce these 
requirements.
    Outline. The information presented in this preamble is organized as 
follows:

I. Introduction
    A. The Delisting Process
    B. The Present Petition and Rulemaking
II. Completion of Final Inhalation Reference Concentration
III. Acute Effects From Exposure to MEK
IV. Voluntary Children's Chemical Evaluation Program Peer Review
V. Adverse Comments and EPA Responses
VI. Final Rule
    A. Rationale for Action
    B. Effective Date
VII. References
VIII. Statutory and Executive Order Reviews
    A. Executive Order 12866: Regulatory Planning and Review
    B. Paperwork Reduction Act
    C. Regulatory Flexibility Analysis
    D. Unfunded Mandates Reform Act
    E. Executive Order 13132: Federalism
    F. Executive Order 13175: Consultation and Coordination With 
Indian Tribal Governments
    G. Executive Order 13045: Protection of Children From 
Environmental Health & Safety Risks
    H. Executive Order 13211: Actions That Significantly Affect 
Energy Supply, Distribution, or Use
    I. National Technology Transfer and Advancement Act
    J. Congressional Review Act

I. Introduction

A. The Delisting Process

    Section 112 of the CAA contains a mandate for EPA to evaluate and 
control emissions of HAP. Section 112(b)(1) includes an initial HAP 
list that is composed of specific chemical compounds and compound 
classes to be used by EPA to identify source categories for which EPA 
will subsequently promulgate emissions standards.
    CAA section 112(b)(2) requires EPA to make periodic revisions to 
the initial HAP list set forth in CAA 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. * * *
    To assist EPA in making judgments about whether a pollutant causes 
an adverse environmental effect, CAA section 112(a)(7) defines an 
``adverse environmental effect'' as:

* * * any significant and widespread adverse effect, which may 
reasonably be anticipated, to wildlife, aquatic life, or other 
natural resources, including adverse impacts on populations of 
endangered or threatened species or significant degradation of 
environmental quality over broad areas.

    Section 112(b)(3) establishes general requirements for petitioning 
EPA to modify the HAP list by adding or deleting a substance. Although 
the Administrator may add or delete a substance on his own initiative, 
in the case where a party petitions the Agency to add or delete a 
substance, the burden has historically been on the petitioner to 
include sufficient information to support the requested addition or 
deletion under the substantive criteria set forth in CAA section 
112(b)(3)(B) and (C). The Administrator must either grant or deny a 
petition within 18 months of receipt of a complete petition. If the 
Administrator decides to grant a petition, EPA publishes a written 
explanation of the Administrator's decision, along with a proposed rule 
to add or delete the substance. If the Administrator decides to deny 
the petition, EPA publishes a written explanation of the basis for 
denial. A decision to deny a petition is final Agency action subject to 
review in the DC Circuit Court of Appeals under CAA section 307(b).
    To promulgate a final rule deleting a substance from the HAP list, 
CAA 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 or deposition of the substance may 
not reasonably be anticipated to cause any adverse effects to the 
human health or adverse environmental effects.

    EPA will grant a petition to delete a substance and publish a 
proposed rule to delete that substance if it makes an initial 
determination that this criterion has been met. After affording an 
opportunity for comment and for a hearing, EPA will make a final 
determination whether the criterion has been met.
    EPA does 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 EPA must 
weigh the potential uncertainties and their likely significance. 
Uncertainties concerning the risk of adverse health or environmental 
effects may be mitigated if EPA can determine that projected exposures 
are sufficiently low to provide reasonable assurance that such adverse 
effects will not occur. Similarly, uncertainties concerning the 
magnitude

[[Page 75049]]

of projected exposure may be mitigated if EPA can determine that the 
levels that 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 resolve any critical uncertainties associated with missing 
information. EPA will not grant a petition to delete a substance if 
there are major uncertainties that need to be addressed before EPA 
would have sufficient information to make the requisite determination.

B. The Petition and Rulemaking

    On November 27, 1996, the American Chemistry Council's Ketones 
Panel submitted a petition to delete MEK (CAS No. 78-93-3) from the HAP 
list in CAA section 112(b)(1). Following the receipt of the petition, 
EPA conducted a preliminary evaluation to determine whether the 
petition was complete according to EPA criteria (58 FR 45081). 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.
    EPA published a notice of receipt of a complete petition to delist 
MEK in the Federal Register on June 23, 1999 (64 FR 33453), and 
requested information to assist us in technically reviewing the 
petition in addition to other comments. In response to the request for 
comment, EPA received ten submissions that included information to aid 
in the technical review of the petition.
    Based on a comprehensive review of the data provided in the 
petition and from other sources, EPA made an initial determination that 
the statutory criterion for deletion of MEK from the HAP list had been 
met. EPA, therefore, granted the petition by the American Chemistry 
Council's Ketones Panel and issued a proposed rule to delist MEK on May 
30, 2003 (68 FR 32608). EPA responded to substantive comments on the 
notice of receipt of a complete petition in the preamble to the 
proposed rule. The delay between receiving a complete petition and 
publishing the proposal to delist was due, in part, to the time it took 
to reevaluate and update the human health toxicity value for MEK.
    EPA received a total of 57 comments on the proposed rule and 
responds to the substantive comments below. There was no request for a 
public hearing.

II. Completion of the 2003 Inhalation Reference Concentration

    In the preamble to the proposed rule, EPA stated that it would not 
make the final decision whether to delist MEK until it considered the 
inhalation reference concentration (RfC) resulting from an updated 
Integrated Risk Information System (IRIS) review. This review was 
completed in 2003. The MEK 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 an appreciable risk of 
deleterious effects during a lifetime.
    The 2003 RfC was not yet finalized when EPA received the petition. 
However, to support statutory requirements and assist in the 
determination of the technical merits of the petition to delist MEK, 
EPA's Office of Research and Development derived an interim health 
effects threshold for MEK inhalation exposure that considered current 
data and current EPA science policy. That process resulted in the 
derivation of a prospective RfC of 9 milligrams per cubic meter (mg/
m3). The analysis underlying the development of the 
prospective RfC can be found in ``A Prospective Reference Concentration 
for MEK (78-93-3),'' which is in the docket. In the preamble to the 
proposed rule, EPA stated that while it would base its initial 
determination to delist MEK on the prospective RfC, it would rely on 
the RfC and other information resulting from the completed IRIS 
assessment in making its determination whether to delist MEK.
    The 2003 RfC was published in IRIS on September 26, 2003. Where the 
prospective RfC was 9 mg/m3, the 2003 RfC is slightly lower 
at 5 mg/m3 because of a difference in dose-response 
methodology and interpretation of remaining uncertainties. To evaluate 
the potential impact of the 2003 RfC on the decision to delist, EPA 
recalculated the inhalation hazard quotient (HQ) using the 2003 RfC and 
the estimate of maximum exposure cited in the proposed rule. Whereas 
the HQ calculated in the proposed rule was 0.1, the new HQ is 0.2, or 
20 percent of the RfC. EPA still finds the recalculated HQ to be below 
a level of concern. Thus, the 2003 RfC did not change the scientific 
basis of EPA's determination that emissions, ambient concentrations, 
bioaccumulation, or deposition of MEK may not reasonably be anticipated 
to cause adverse human health or environmental effects.

III. Acute Effects From Exposure to MEK

    In the preamble to the proposed rule, EPA addressed acute exposure 
from MEK using the Dick et al. (1992) study (Dick study), which 
assessed neurotoxic effects. EPA concluded that the Dick study 
indicated that exposures to MEK of up to 200 parts per million (ppm) 
(590 mg/m3) for up to 4 hours would be an appropriate no-
adverse-effect concentration for the general population for both 
subjective effects (such as objectionable odor or irritancy) and for 
neurobehavioral effects.
    EPA used the Dick study to examine the potential effects of short-
term exposure to MEK because no short-term human health values have 
been finalized for MEK. The Dick study is the best study in the MEK 
database with which to assess short-term effects of MEK exposure.
    During public comment, EPA did not receive any negative comment on 
our interpretation of the Dick study. EPA did, however, receive a 
request to address the potential for developmental effects as a result 
of short-term exposure because the RfC that EPA used to assess long-
term exposure to MEK was based on a developmental endpoint.
    EPA agrees that this is appropriate to do since the Agency, thus 
far, has not finalized an acute reference exposure methodology. EPA is 
in the process of developing this methodology and sought the Science 
Advisory Board's (SAB) review of the draft methodology in 1998 (The SAB 
report is available at: https://www.epa.gov/sab/pdf/ehc9905.pdf). Thus, 
EPA considered several types of analysis. One type of analysis EPA 
considered was a general approach consistent with that used for the 
chronic RfC and based on the developmental study that was the basis for 
the RfC.
    The quantitative aspect of EPA's RfC methodology is a two-step 
approach that distinguishes analysis of the dose-response data from 
inferences made about lower doses. The first step is an analysis of 
dose and response in the range of observation of the experimental and/
or epidemiologic studies. The modeling or statistical significance 
testing yields a point of departure (POD) from the range of 
observation. The second step is extrapolation to lower doses. Thus, the 
RfC is derived from the POD (in terms of human equivalent

[[Page 75050]]

exposure) for the critical effect by consistent application of 
uncertainty factors (UFs). The UFs are applied to account for 
recognized uncertainties in the extrapolations from the experimental 
data conditions to an estimate appropriate to the assumed human 
scenario (U.S. EPA, 1994).
    The POD from the developmental study is a 24-hour human equivalent 
exposure concentration of 1,517 mg/m3. In the derivation of 
the chronic RfC, this POD was divided by a cumulative UF of 300. The 
cumulative factor comprised three UFs, accounting for uncertainties in 
interspecies (3) and intraspecies (10) extrapolation, as well as 
uncertainty in the database with regard to chronic exposures (10). In 
calculating an acute reference value, the latter would not be relevant, 
resulting in a cumulative UF of 30. Thus, one analysis of the short-
term exposure potential might result in a short-term (24 hour) 
reference value of 50 mg/m3 by dividing 1,517 mg/
m3 by a cumulative UF of 30. The petitioner's maximum 
modeled 24-hour average MEK concentration in air of 10 mg/m3 is lower 
than this potential short-term reference value by a factor of 5.
    An alternate approach is that routinely employed by EPA's Office of 
Prevention, Pesticides and Toxic Substances (OPPTS), which involves 
consideration of the margin of exposure (MOE) between the POD and the 
estimated exposure concentration of interest (67 FR 60886). For 
decision-making purposes, the OPPTS MOE level of concern is the value 
derived from multiplicative factors representing key outstanding areas 
of uncertainty with regard to the chemical's toxicity. Given the 
available data for MEK, which includes an animal study on developmental 
toxicity, the predominant outstanding areas of uncertainty with regard 
to short-term toxicity are the potential for interspecies and 
intraspecies differences in susceptibility. Assigning them each the 
traditional default value of 10 yields a MOE of 100.\1\ Therefore, in 
evaluating the potential for adverse human health effects to occur from 
acute exposures to MEK from inhalation, EPA considers adverse effects 
to be unlikely if the MOE is at least 100.
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    \1\ Note that the value of 10 that EPA assigned here for 
interspecies variability is greater than the value of 3 that EPA 
assigned in developing the RfC for MEK. This adds another layer of 
conservatism to our evaluation of the potential for MEK to cause 
acute effects.
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    Using the petition's maximum modeled 24-hour average MEK 
concentration in air of 10 mg/m3, and the 24-hour human 
equivalent exposure concentration at the POD from the study used to 
develop the RfC of 1,517 mg/m3, EPA calculates a margin of 
exposure of 152. Therefore, based on either of the two approaches 
outlined above, the predicted 24-hour exposures to MEK may not 
reasonably be anticipated to pose appreciable risk of adverse 
developmental health effects. This conclusion, when added to the 
previous conclusions described in the preamble to the proposed rule, 
further supports our determination that emissions of MEK may not 
reasonably be anticipated to cause adverse health or environmental 
effects.
    Since proposal, EPA's OPPTS has proposed several Acute Exposure 
Guideline Levels (AEGLs) for MEK. The AEGLs represent threshold 
exposure limits for the general public for various degrees of severity 
of toxic effects, and are applicable to emergency exposure periods 
ranging from 10 minutes to 8 hours. It is believed that the recommended 
exposure levels are applicable to the general population including 
infants and children, and other individuals who may be susceptible.
    The AEGL value for the lowest severity level, the AEGL-1, is the 
airborne concentration of a substance above which it is predicted that 
the general population, including susceptible individuals, could 
experience notable discomfort, irritation, or certain asymptomatic 
nonsensory effects. However, the effects are not disabling and are 
transient and reversible upon cessation of exposure. With increasing 
airborne concentrations above each AEGL, there is a progressive 
increase in the likelihood of occurrence and the severity of effects 
described for each corresponding AEGL. Although the AEGL values 
represent threshold levels for the general public, including 
susceptible subpopulations, such as infants, children, the elderly, 
persons with asthma, and those with other illnesses, it is recognized 
that individuals, subject to unique or idiosyncratic responses, could 
experience the effects described at concentrations below the 
corresponding AEGL.
    The interim AEGL-1 value for MEK is 200 ppm (for all exposure 
periods up to 8 hours). This is the same concentration as the no-
adverse-effect concentration for the general population derived from 
the Dick Study, which provides further support for the use of the Dick 
study for assessing short-term exposures.

IV. Voluntary Children's Chemical Evaluation Program Peer Review

    In the preamble to the proposed rule, EPA stated that it would not 
make the final decision whether to delist MEK until it considered the 
results of the peer consultation of the industry's tier 1 submission 
for MEK under the 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 the VCCEP, EPA has asked 
industries that manufacture or import certain chemicals to sponsor 
these chemicals to develop assessments regarding the potential health 
effects, exposures, and risks of those chemicals to children (see 
https://www.epa.gov/chemrtk/vccep/index.htm).
    EPA received the industry's submission under the VCCEP on December 
1, 2003. The peer consultation meeting for MEK was held on February 19, 
2004. On April 19, 2004, EPA received the report of the peer 
consultation. Peer consultation panel members concluded that the MEK 
database and submission were adequate, and the key areas of hazard, 
exposure, and risk were sufficient to characterize risks to children 
for the purposes of the VCCEP. None of the panelists thought that 
further data or analyses were needed to characterize MEK's risks to 
children for the purposes of the VCCEP. Subsequent to completion of the 
final meeting report, EPA requested additional MEK exposure information 
from the industry sponsors. This information was provided to EPA on 
January 12, 2005 (see https://www.tera.org/peer/vccep/MEK/
MEKwelcome.html).
    The only substantive issue raised by the peer consultation that is 
relevant to the final rule pertains to acute exposures to MEK. To 
characterize potential impacts from short-term exposures to MEK, the 
VCCEP submission took much the same approach that EPA took in the 
proposed rule. That is, they estimated maximum short-term exposures and 
compared them to a short-term health value that was based on 
irritation. Like the public commenter, the VCCEP peer consultation 
panel requested that the sponsor compare the short-term exposures to a 
developmental endpoint because the RfC was based on a developmental 
endpoint.
    The sponsors proposed one of the approaches EPA considered above, 
the approach based on the RfC. The sponsors proposed to begin with the 
2003 RfC of 5 mg/m\3\, then remove the 10-fold database uncertainty 
factor. This results in a 24-hour value of 50 mg/m\3\. The reason given 
for the removal of the

[[Page 75051]]

uncertainty factor is that it was applied to the RfC to account for the 
lack of chronic studies. Since considering chronic studies is not 
relevant to the development of a short-term health value, there is no 
need for the 10-fold database uncertainty factor. EPA agrees with the 
approach submitted to the VCCEP and, as described above, EPA considered 
this approach as well as other methods.

V. Adverse Comments and EPA Responses

    Of the 57 written comments EPA received pertaining to the proposed 
delisting of MEK, 42 supported the proposal to delist, 13 opposed the 
proposal to delist and 2 comments neither supported nor opposed the 
proposal. EPA received comments on the development of the RfC used in 
the decision and on the exposure assessment.
    EPA has considered carefully all the comments, focusing in 
particular on comments which suggested potential deficiencies in the 
substantive rationale upon which EPA based its initial determination 
that the criterion in CAA section 112(b)(3)(C) had been met. A summary 
of the comments and EPA responses has been included in the docket. In 
this preamble, EPA will discuss adverse comments received and our 
responses to them.
    The proposed rule invited comment from interested parties on the 
proposal to delist MEK. In addition, EPA specifically requested 
comments on our prospective RfC for MEK (the interim health value EPA 
developed for the proposal). EPA also solicited comment on the portion 
of our human health risk characterization based on this prospective 
RfC. In addition, EPA requested comment on whether it would be 
appropriate to delist MEK if the RfC resulting from an updated IRIS 
review differed from the prospective RfC; for example, EPA requested 
comment on the appropriateness of delisting if the RfC were 3 mg/m\3\, 
the level suggested by industry in its petition, or if it remained 
unchanged from the 1992 RfC of 1 mg/m\3\.
    Comment: One commenter asserted that the 1992 RfC of 1 mg/m\3\ was 
set to protect against birth defects and it should not be changed. 
Another commenter stated that the 2003 RfC (external review draft), 
which was based on the same study from 1991, does not adequately 
provide an estimate ``likely to be without an appreciable risk of 
deleterious effects during a lifetime.''
    Response: The RfC is designed to consider all adverse noncancer 
effects associated with lifetime exposure to a chemical. The 2003 RfC 
is also based on developmental effects, and is based on the 
methodologies that were in place at the time of derivation, including 
(1) the methods for the use of inhalation dosimetry to extrapolate from 
animal to human exposures (U.S. EPA, 1994) and (2) benchmark dose 
methods (U.S. EPA, 2000, external review draft). Those methods have 
been subject to peer review.
    Comment: One commenter asserted that the toxicological database is 
not complete regarding developmental effects, and stated that there is 
inadequate evidence to assess the carcinogenic potential of MEK (i.e., 
there are no 2-year animal cancer bioassays).
    Response: There are adequate data on developmental effects and on 
cancer effects to support a decision to delist MEK. The principal study 
(Schwetz et al., 1991), a developmental toxicity study in the mouse, is 
well-designed and tests several exposure concentrations over a 
reasonable range that include maximum tolerated doses for dams and 
fetuses. Also, animal studies in a second species (rats) corroborate 
the effect level for developmental toxicity (Deacon et al., 1981; 
Schwetz et al., 1974).
    Regarding carcinogenicity, the current IRIS file (completed in 
September of 2003) states that the data for MEK are characterized as 
``inadequate for an assessment of human carcinogenic potential.'' The 
``Toxicological Review of Methyl Ethyl Ketone'' (U.S. EPA, 2003) 
(Toxicological Review of MEK), upon which the IRIS file is based 
states, ``Under EPA's draft revised cancer guidelines (U.S. EPA, 1999), 
data are inadequate for an assessment of human carcinogenic potential 
for MEK because studies of humans chronically exposed to MEK are 
inconclusive, and MEK has not been tested for carcinogenicity in 
animals by the oral or inhalation routes.'' Recent revision of these 
guidelines does not materially affect this conclusion.
    The traditional 2-year animal cancer study has not been conducted 
for MEK, nor is EPA aware of any organization planning to conduct one. 
EPA believes one reason no cancer assay has been done is that the 
results from the majority of the genotoxicity tests (which are often 
used as an indicator of the need to pursue a 2-year cancer study) are 
negative, indicating that MEK is a low priority for further study. In 
1997, the Organization for Economic Cooperation and Development (OECD) 
reached this conclusion. OECD's report states that ``MEK is not 
genotoxic and is not likely to be carcinogenic.'' (OECD, 1997). The 
report also states that MEK is ``* * * currently of low priority for 
further work.'' (OECD, 1997).
    The general descriptors recommended by EPA's ``Guidelines for 
Carcinogen Risk Assessment'' (U.S. EPA, 1999) for characterizing the 
weight of evidence with regard to a chemical's potential for human 
carcinogenicity did not explicitly recognize this situation. The 
descriptor applied to MEK in the 2003 IRIS assessment (i.e., ``data are 
inadequate for an assessment of human carcinogenic potential'') 
pertains to cases where ``* * * there is a lack of pertinent or useful 
data.'' (U.S. EPA, 1999). While lacking data or studies that would 
clearly support their placement in other categories (e.g., the 
traditional 2-year rodent study), chemicals included within this broad 
category may, however, have pertinent or useful data which do not 
indicate any potential for carcinogenicity, consequently providing no 
support for the performance of the traditional, resource-intensive 
studies.
    Accordingly, EPA's Toxicological Review of MEK also states, ``the 
majority of short-term genotoxicity testing of MEK has demonstrated no 
activity, and the Structure Activity Relationship (SAR) analysis 
suggests that MEK is unlikely to be carcinogenic.'' (U.S. EPA, 2003). 
One study (Woo et al., 2002) has given MEK and other unsubstituted 
mono-ketones (a compound class to which MEK belongs) a low concern 
rating (unlikely to be of cancer concern) because these chemicals lack 
electrophilic activity (i.e., a structural alert of carcinogenicity) 
and are generally not associated with carcinogenicity.
    There is an absence of positive results in the majority of 
mutagenicity and genotoxicity tests which are designed to indicate the 
potential for carcinogenicity. 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

[[Page 75052]]

chromosome loss at high concentrations in a study of aneuploidy in 
yeast S. cerevisiae (Zimmerman et al., 1985), but the relevance of this 
finding to humans is questionable. Overall, studies of MEK yield little 
or no evidence of genotoxicity.
    However, the finding of low potential for genotoxicity alone is not 
the sole criterion for an assessment of carcinogenic potential, as non-
genotoxic mechanisms can also result in carcinogenesis. While 
developing the final rule, EPA learned that preliminary results of a 
recent cancer bioassay by the National Toxicology Program suggested 
that methyl isobutyl ketone (MIBK) appears to be a weak or marginally 
active carcinogen in rats and mice, possibly by a nongenotoxic mode of 
action. Both MEK and MIBK are small molecular weight alkyl ketones, and 
this similarity raised some questions regarding the possible relevance 
of the preliminary MIBK results to MEK. To investigate this further, 
EPA undertook SAR analysis of MIBK and MEK. These two ketones have a 
key difference in their chemical structure: MIBK is branched, while MEK 
is linear. EPA's SAR analysis indicates that MIBK's toxicity and 
possible carcinogenicity are likely due to its branched alkyl 
structure. Methyl ethyl ketone, like acetone, is linear and lacks this 
structure. Thus, the analysis concluded that in analogy to acetone and 
its metabolite isopropanol (which has shown no evidence of 
carcinogenicity), MEK and its metabolite (2-butanol) are linear and, 
therefore, have low concern for carcinogenicity potential. A short 
document describing the analysis, ``Acetone, MEK, and MIBK--SAR 
Analysis on Carcinogenicity/Toxicity,'' is included in the docket. 
Subsequently, EPA conducted an external peer review of this document. 
All three reviewers found the reasoning to be sound and supported the 
conclusions of the analysis. These reviews are also included in the 
docket. Thus, EPA concludes that the available scientific evidence 
shows a low potential for carcinogenicity in MEK.
    Comment: One commenter suggested that the UFs for the prospective 
RfC were not adequate. The commenter disagreed with the reduction of 
the interspecies UF and stated that it should have remained at 10 
because there are no developmental and reproductive studies available 
for humans and animals. Another commenter suggested that the human 
equivalent concentration (HEC) resulted in low confidence because it 
was based on the same mouse study (1991) as the 1992 RfC, and the 
prospective RfC was not robust enough to warrant decreasing the 
interspecies UF from 10 to 3. This commenter also asserted that the 
chronic and reproductive studies are still missing and, therefore, 
EPA's proposal of reducing the database UF is not valid. The commenter 
contended that the lack of current information results in continued low 
confidence in the database because the data used are from the original 
studies used to develop the 1992 RfC. The commenter believes that the 
Dick study did not provide adequate statistical power. Consequently, 
the commenter believes that the lack of toxicity was not demonstrated, 
and that the modifying factor should be maintained at 3. The commenter 
concluded that the ``absence of data should not conclude an absence of 
toxicity.''
    Response: An interspecies UF of 3 was applied in deriving both the 
prospective RfC and the 2003 RfC, consistent with EPA guidance for 
deriving RfCs in effect at the time (U.S. EPA, 1994). The UF for 
interspecies extrapolation is not intended to address database 
deficiencies. A database UF of 10 was used in developing the 2003 RfC 
to account for the lack of a chronic inhalation toxicity study and 
multigeneration reproductive toxicity study.
    Modifying factors have been used in the past in RfC derivations, 
where the magnitude of the factor reflected the scientific 
uncertainties of the study and database that were not explicitly 
treated with standard uncertainty factors. For the 2003 RfC, the 
default modifying factor of one was used because EPA concluded that the 
modifying factor was sufficiently subsumed in the general database UF.
    Comment: The petitioner stated that EPA did not present adequate 
scientific justification for applying a duration adjustment to the 
inhalation developmental toxicity study and, at the very least, the 
additional conservatism added by the application of this factor should 
be explicitly recognized. The commenter pointed to the draft 
Toxicological Review that indicated that MEK was rapidly absorbed, 
distributed, and metabolized, suggesting that the duration adjustment 
may be inappropriate.
    Response: Duration adjustment of the exposure concentrations in the 
developmental study of MEK (Schwetz et al., 1991) was performed 
consistent with the EPA Risk Assessment Forum RfD/RfC Technical Panel 
report, ``A Review of the Reference Dose and Reference Concentration 
Processes'' (U.S. EPA, 2002). The report recommends that procedures for 
adjusting to continuous exposure based on the product of concentration 
and time be used as a default for inhalation developmental toxicity 
studies as it is for other health effects from inhalation exposure. 
While the recommendation is based on evidence that shows that some 
agents cause developmental toxicity more as a function of peak 
concentration, the effects of other agents are related to area-under-
the-curve (AUC). The latter is true even of some developmental 
toxicants with a short half-life. In the absence of data that support 
peak concentration or AUC as more closely correlated with developmental 
toxicity, EPA's 2002 review document recommends duration adjustment as 
the more health-protective default procedure. As noted in the 
Toxicological Review of MEK, because the data are insufficient to argue 
convincingly for either peak exposure level or AUC as the most 
appropriate metric, the more health-protective procedure (duration 
adjustment) was applied as a policy matter.
    Comment: The petitioner commented on our interpretation of the 
Cavender et al. (1983) study. They stated that EPA regarded 5,000 ppm 
in a 90-day inhalation study as the Lowest Observed Adverse Effect 
Level (LOAEL) based on reduced weight gain, increased liver weight, and 
decreased brain weight. The commenter stated that this was inconsistent 
with the 1992 IRIS database where EPA indicated that a change in liver 
weight may not be conclusively caused by MEK inhalation. The petitioner 
recommended that 5,000 ppm be the No Observed Adverse Effect Level 
(NOAEL).
    Response: In the 2003 IRIS assessment, EPA gave further 
consideration to the biological significance of the findings in the 
5,000 ppm animals in the Cavender et al. (1983) study, specifically the 
organ weight findings. Although the decrease in brain weight in female 
high-dose animals is of some concern, EPA agrees that this effect, in 
the absence of corresponding histopathology and functional 
abnormalities, cannot be clearly characterized as being of 
toxicological relevance. In light of these uncertainties, 
characterization of the effects associated with the 5,000 ppm exposure 
level as adverse, use of that level as a LOAEL, and the use of mid-dose 
group (2,518 ppm) as a NOAEL were dropped.
    Comment: Three commenters suggested that the actual emissions of 
MEK may result in environmental concentrations below the RfC, but 
allowable emissions would not. This

[[Page 75053]]

means that should the emissions reach allowable limits, then the 
concentrations of MEK will be above the RfC. One commenter provided an 
example of a facility that emits 500 tons per year (tpy) of MEK but is 
permitted to emit up to 2,200 tpy. The commenter states that a simple 
screening model run (most likely similar to the tier 1 or tier 2 
analysis submitted by the petitioner) of this facility at the allowable 
emission rate predicts 24-hour peak concentrations to be about 75 mg/
m3, which is above the maximum predicted 24-hour average 
concentration of 10 mg/m3 that EPA cited in the preamble.
    Response: The maximum offsite 24-hr MEK concentration for the 
worst-case facility in the petition as predicted by the Industrial 
Source Complex Short Term 3 (ISCST3) model was 10 mg/m3. The 
maximum annual concentration was 1.2 mg/m3. This facility 
emits about 500 tpy MEK. The maximum offsite concentration occurs 
within a few hundred meters of the facility.
    The commenters provided limited information on the facility that 
has the potential to emit 2,200 tpy. EPA contacted the commenter in 
order to understand how they estimated the value of 75 mg/
m3. EPA was told that the SCREEN3 model was used to estimate 
this concentration. However, EPA was unable to obtain the modeling runs 
which would contain important model input data (e.g., stack heights and 
distances from stacks to fence lines). From the comment, EPA does know 
that the maximum offsite concentration for this facility as predicted 
by the SCREEN3 model was 75 mg/m3 for a 24-hr average and 
1.1 mg/m3 for an annual average. If this facility were 
modeled with a more refined dispersion model, such as the ISCST3 model, 
EPA would expect impacts that are considerably lower than those 
predicted with the more conservative SCREEN3 model. Most likely, the 
maximum offsite concentration for the facility would be much closer to 
10 mg/m3 for a 24-hr average near the facility, and well 
below 1 mg/m3 for the annual average. EPA would suspect that 
the facility to which the commenter refers has much better dispersion 
characteristics than the petitioner's worst-case facility, which had a 
very low stack and nearby fenceline.
    Comment: Three commenters stated that EPA failed to meet the CAA 
deadline (18 months) for adding or deleting a substance from the HAP 
list, instead taking 78 months total. Therefore, the commenters 
believed the 1994 Toxic Release Inventory (TRI) data used in the 
assessment were not appropriate and that current TRI data should have 
been used. These commenters also contended that the calculations in the 
petition did not consider potential increases in MEK use once MEK is 
delisted, and that EPA should base its decision to delist MEK on 
emission levels and locations expected after delisting.
    Response: EPA interprets the CAA to require consideration of 
current emissions. It is not appropriate to make a decision on what can 
only be speculative emissions. EPA states in the final rule to delist 
caprolactam (61 FR 30816, June 18, 1996) that ``EPA does not interpret 
section 112(b)(3)(C) to require consideration of hypothetical emissions 
from facilities that might be constructed in the future. The logical 
consequence of such an expansive construction would be that no 
substance could ever be delisted, due to the hypothetical possibility 
of some future facility that has uncontrolled emissions large enough to 
cause adverse effects. In the event some future facility has 
uncontrolled caprolactam emissions great enough to change the 
conclusion of the current EPA risk assessment, EPA can revisit its 
decision to delist caprolactam at that time.'' It is not the case, 
however, that EPA can never take potential increases in emissions into 
account. For example, such consideration is appropriate where EPA has 
information regarding specific facilities, such as the information it 
considered in denying the methanol delisting petition (66 FR 21929, May 
2, 2001).
    Using similar logic in this case, EPA does not interpret CAA 
section 112 (b)(3)(C) to require consideration of hypothetical 
emissions from facilities that might be constructed in the future, nor 
projections of increases in emissions from existing facilities.
    There are several reasons why EPA does not expect that increases in 
emissions of MEK will cause health or environmental concerns. With 
regard to increased emissions themselves, EPA believes that such 
increases will be limited by good housekeeping practices which are 
designed to save product. Methyl ethyl ketone is an effective solvent, 
but one that evaporates readily. Employing techniques to prevent 
wasting the product also results in decreased emissions.
    Due to the health-protective nature of the analysis upon which the 
decision to delist is based, EPA concludes that the potential risks 
from outdoor exposures to MEK are overestimated. It is unlikely that 
future emissions increases will result in unacceptable risk. For 
example, the petitioner based the risk assessment on 1994 TRI total air 
emissions of MEK, which were 628 tpy for the worst-case facility. This 
facility's modeled annual average concentration is only 20 percent of 
the RfC. This facility could increase emissions significantly before 
the concentration would be above a level of concern. The highest-
emitting facility in the 2003 TRI emits 638 tpy of MEK, only slightly 
higher than the 1994 TRI emissions for the worst-case facility.
    In addition, the national trend in MEK emissions is distinctly 
downward. Comparing the 1994 and 2003 TRI MEK air emissions data for 
the 100 highest-emitting facilities indicates that emissions have 
decreased by approximately 20 percent during that nine year period.
    The risk assessment was based on a maximum off-site concentration. 
The assessment did not consider the amount of time people would be at 
that location, or other factors that address the amount of exposure 
faced by actual individuals. Further, this maximum concentration was 
located at the entrance to a facility in an industrial park. The 
probability that an individual would live at this location in the 
future is extremely low.
    Given the low hazard presented by the worst-case facility, the 
health-protective nature of the analysis, and the overall downward 
trend of MEK emissions over the last several years, EPA believes that 
emissions of MEK may not reasonably be anticipated to cause adverse 
human health effects.
    The preamble to the proposed rule discussed the March 30, 1998, 
Federal Register notice (63 FR 15195) in which EPA issued a Denial of 
Petition entitled ``Methyl Ethyl Ketone; Toxic Chemical Release 
Reporting; Community Right-to-Know.'' The denial was in response to a 
petition from the Ketones Panel of the Chemical Manufacturers 
Association (CMA) that requested the deletion of MEK from the list of 
chemicals reportable under section 313 of the Emergency Planning and 
Community Right-To-Know Act of 1986 (EPCRA) and section 6607 of the 
Pollution Prevention Act.
    The American Chemistry Council (formerly the Chemical Manufacturers 
Association) filed suit challenging EPA's decision in the United States 
District Court for the District of Columbia. Subsequently, the court 
granted summary judgment in favor of EPA (American Chemistry Council v. 
Whitman, 309 F.Supp. 2d 111 (D.D.C. 2004)). On appeal, the Court of 
Appeals for the District of Columbia Circuit reversed the lower court's 
decision, vacating the lower court's decision, and directed the 
district court to issue an order to ``direct EPA to delete MEK from

[[Page 75054]]

the TRI'' (406 F.3d 738, 742 (DC Cir. 2005)). The circuit court issued 
its mandate on June 13, 2005 and, accordingly, on June 30, 2005, EPA 
issued a final rule (70 FR 37698) revising the EPCRA section 313 list 
of reportable chemicals in 40 CFR 372.65 to delete MEK.
    The deletion of MEK from the EPCRA section 313 list eliminates the 
main source of data EPA uses to track MEK emissions. However, there are 
other data sources available to estimate MEK emissions, including 
market research data on MEK production, import, export, and 
consumption. Consumption of MEK should provide an adequate surrogate 
for emissions to determine whether significant increases in emissions 
are occurring. If data indicate that MEK emissions are increasing 
significantly, EPA has the option to add MEK back on the HAP list.
    Comment: One commenter suggested that the risk was not adequately 
identified because the industry was not studied comprehensively enough 
to determine chronic exposure.
    Response: In order to determine the risks from emissions of MEK, 
the petitioner used the 1994 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 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. EPA has determined that this approach to establishing 
reasonable worst-case exposures to MEK emissions is an adequate basis 
upon which to base a decision to delist MEK. EPA states in the preamble 
to the proposed rule that it does 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 EPA must weigh the potential uncertainties 
and likely significance. In this case, the uncertainty in the predicted 
exposure levels is biased toward protecting public health. Therefore, 
EPA concludes that delisting MEK is appropriate.
    Comment: Several commenters contended that chronic effects of MEK 
had not been adequately studied or evaluated, and that the delisting 
was not supported by new or compelling scientific evidence. One 
commenter requested that EPA conduct long-term health effects studies. 
Additionally, the commenters stated that there were no lifetime-chronic 
studies included, no studies evaluating developmental effects, nor 
studies concerning reproductive toxicity. Moreover, these commenters 
asserted, there were no multigenerational studies included, and the 
evaluation of the carcinogenic potential was not adequate.
    Response: EPA's RfC methodology (U.S. EPA, 1994) does not always 
require a complete database in order to develop an RfC; however, the 
database must at least meet minimum data requirements. For MEK, ``* * * 
confidence in the database is medium * * *.'' (U.S. EPA, 2003). ``The 
subchronic study by Cavender et al. (1983) satisfies the minimum 
inhalation database requirements for derivation of an RfC.'' (U.S. EPA, 
2003).
    In the case where there are enough quality data with which to set 
an RfC, but where the database is less than complete, EPA adds a 
database uncertainty factor to account for the lack of data. For MEK, 
that factor is 10. EPA acknowledges the lack of a chronic toxicity 
bioassay and an inhalation multigeneration reproductive toxicity study 
(an oral multigeneration is available), but notes that contrary to the 
commenters' statements, the developmental toxicity of MEK has been well 
studied.
    As stated above, the RfC is 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 an appreciable risk of deleterious effects during a lifetime. 
Because maximum expected ambient air concentrations are well below the 
RfC, EPA does not expect adverse noncancer effects to result.
    In addition, the health-protective nature of the assessment 
described above adds to our confidence that no adverse health effects 
will occur from ambient exposures to MEK.
    Comment: One commenter asserted that the appropriate averaging time 
for assessing the potential for adverse developmental effects to occur 
is the 24-hour average, not an annual average. The commenter held that 
evaluating developmental toxicity on a 24-hour basis is supported by 
EPA guidelines for evaluating developmental risk. This issue was also 
raised by the VCCEP review panel as they considered the information 
industry submitted on MEK and children's health.
    Response: EPA agrees with the commenter that potential concern for 
developmental effects from short-term exposures should be addressed, 
and EPA did so elsewhere in this preamble. With regard to the use of 
endpoint-specific reference values, EPA's review of the RfD/RfC 
processes recommended against the use of endpoint-specific reference 
values, and instead recommended that duration-specific reference values 
be derived in consideration of the full range of adverse effects.
    Comment: A commenter remarked that EPA did not take into account 
all routes of exposure to MEK and, therefore, did not adequately 
identify the risk.
    Response: MEK is neither bioaccumulative nor persistent. It has a 
half-life of approximately 9 days. The releases of MEK to air are 
unlikely to result in elevated concentrations in surface water, ground 
water, or the food supply. Therefore, the route of exposure EPA is 
concerned with is direct inhalation of MEK released to the ambient air. 
For this reason, inhalation was the focus of the analysis. The 
petitioner also assessed the potential for risks due to ingestion of 
water contaminated with MEK. In both cases, the risks were below a 
level of concern.
    Comment: One commenter asserted that the risk assessment did not 
fully address: (1) Other solvents released from stationary and area 
sources of MEK, (2) actual ambient concentrations near stationary and 
area sources (only modeled concentrations were used), and (3) the human 
health effects within the facilities as opposed to fenceline ambient 
concentrations.
    Response: The maximum annual average air concentration resulting 
from emissions of MEK is not expected to exceed an HQ of 0.2. This 
value, which is 20 percent of the RfC, is quite low. EPA believes that 
there is a large enough margin of exposure to preclude a need to 
address any other emitted HAP that may affect the same target organ as 
MEK.
    The petitioner did not monitor ambient air around actual MEK-
emitting facilities. Such an effort would not add to the analysis, or 
change EPA's conclusion with regard to delisting. This is because the 
maximum monitored concentration EPA found in the U.S. was over two 
orders of magnitude below the maximum modeled concentration, and 
because the modeling conducted was designed to over-estimate ambient 
concentrations. For example, the model

[[Page 75055]]

assumed that individuals are continuously exposed to the maximum 
modeled concentrations of MEK in air for 70 years, and EPA used the 
maximum annual average concentration as a surrogate for long-term 
exposure. Also, the model used 1994 emission rates which are 
significantly higher than current emissions for the facility with the 
highest estimated HQ of 0.2. EPA believes that the health-protective 
air dispersion modeling performed as part of the petition and described 
in detail in the proposed rule resulted in higher concentrations than 
would monitoring around facilities.
    EPA cannot consider the health effects of emissions within facility 
boundaries. That is the purview of the Occupational Safety and Health 
Administration.
    Comment: One commenter recommended that a comparative analysis with 
the 1998 Office of Pollution Prevention and Toxics (OPPT) assessment 
(located in the docket) be done to fully assess the risks of MEK.
    Response: EPA agrees with the comment, and EPA conducted a 
comparison of the 1998 OPPT assessment and the assessment in the 
proposal to delist MEK.
    The assessment presented in the petition to delist MEK estimated a 
maximum annual average MEK concentration of 1.2 mg/m3. It 
used the ISCST3 model, which is a refined air dispersion model that 
predicts an annual average by averaging 8,760 hours of real time 
meteorological data. The ISCST3 model predicted a maximum 24-hour 
average MEK concentration of 10 mg/m3.
    The 1998 OPPT study estimated maximum 24-hour average 
concentrations of 100-200 mg/m3. It used a screening model 
similar to the SCREEN3 model and predicted 1-hour average 
concentrations under defined meteorological conditions with the 
assumption that the receptor is always directly downwind from the 
source. Such screening model runs typically result in high air 
concentrations as compared to the ISCST3 model. EPA would expect the 
difference in concentrations to be as high as a factor of 10. In 
addition, the OPPT study applied a multiplicative factor to predict 
typical (5), stagnant (10), and maximum (60) acute impacts. Thus, the 
difference between the two model results can be attributed to the 
multiplicative factors and differences between a refined and screening 
model.
    Comment: One commenter recommended that EPA not wait for the formal 
IRIS review of MEK or the VCCEP results to make a final decision 
regarding delisting of MEK, as there was enough evidence to delist MEK 
without the additional information. Another commenter asserted that if 
the RfC resulting from the completed IRIS assessment is different from 
the prospective RfC, then the petition should be reconsidered and an 
additional public comment period should be allowed giving the public an 
opportunity to comment on EPA's decision. This commenter also stated 
that the results of the VCCEP should be concluded before the comments 
on the delisting are due.
    Response: Regarding the first comment, EPA waited to make a final 
decision to delist MEK until the 2003 IRIS RfC was determined and until 
the information submitted by industry under the VCCEP was reviewed in 
case the results of each of these processes altered our decision to 
remove MEK from the HAP list.
    Regarding the second comment, EPA considers an additional comment 
period unnecessary for a number of reasons. First, EPA explicitly 
solicited comment on the effect of a difference between the prospective 
RfC and the RfC resulting from the completed IRIS assessment. EPA 
specifically requested comments on the decision in light of potential 
values for the RfC of 9 mg/m3, 3 mg/m3 and 1 mg/
m3. The 2003 RfC of 5 mg/m3 is in the middle of 
the range upon which EPA solicited comment. Second, while the 2003 RfC 
is lower than the prospective RfC, the result of this change was only 
to increase the HQ for the maximum annual average ambient exposure from 
0.1 to 0.2 (20 percent of the RfC). This HQ is well below a level of 
concern.
    In addition, EPA judges 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 2 to 10 less than the predicted 
maximum ambient concentration presented in the petition of 1 mg/
m3. This is because the concentration of MEK declines very 
rapidly as the plume disperses, and the analysis showed that people do 
not live at the point of maximum concentration. Therefore, actual 
exposed individuals would be subject to MEK concentrations less than 1 
mg/m3. If EPA were to replace the maximum ambient 
concentration with a more realistic exposure scenario, it would yield 
an HQ less than 0.2. Based on the current information, and given the 
conservative nature of the parameters used to estimate the maximum 
exposure, and because the petition and subsequent analyses characterize 
the vast majority of MEK exposures from stationary sources, EPA 
concludes that by applying the RfC of 5 mg/m3, potential 
ambient exposures to MEK may not reasonably be anticipated to cause 
adverse human health effects.
    With respect to the results of the VCCEP, EPA found it unnecessary 
to extend the public comment period until after the review of the 
industry-submitted information was complete. This is because the 
industry provided no new information to EPA that was not already 
available. Therefore, there was no new information upon which to 
solicit comments.
    Comment: Many commenters noted that the interactions with n-hexane 
and other ketones have not been sufficiently investigated should the 
MEK emissions increase. These commenters stated that MEK interactions 
with n-hexane have been shown to increase neurotoxicity of n-hexane.
    Response: EPA stated in the preamble to the proposed rule that MEK 
has been shown to potentiate the neurotoxicity of other solvents in 
experiments with laboratory animals when both MEK and the other solvent 
are present in high concentrations. EPA also stated that studies of 
occupationally-exposed populations (as reviewed by Noraberg and Alien-
Soborg, 2000) provide some evidence of possible interactions in humans. 
EPA reviewed the occupational epidemiology literature in more depth 
during the development of the 2003 RfC for MEK. These findings are 
summarized in the Toxicological Review for MEK (https://www.epa.gov/
iris/toxreviews/0071-tr.pdf, section 4.4.4). Available occupational 
studies involving multiple chemical exposures do not provide 
information adequate to clearly establish an interaction between MEK 
and other neurotoxic solvents in humans. In studies suggesting a 
potential interaction, neurotoxicity has been observed only in 
workplace populations exposed to solvent mixtures where reported MEK 
air concentrations reached levels at or above the Threshold Limit Value 
(TLV) (200 ppm or 590 mg/m3). EPA concluded that the 
concerns for chemical interactions are especially diminished at the low 
levels seen in this assessment: Less than 1 mg/m3 for 
chronic exposures, 10 mg/m3 for 24-hour exposures and 25 mg/
m3 for a 1-hour exposure. These exposures are all well below 
the reversible effects level of 590 mg/m3. Therefore, EPA 
does not expect possible potentiation of n-hexane by MEK at the low 
environmental concentrations that would be associated with industrial 
releases.
    Comment: One commenter was concerned that MEK was detected by

[[Page 75056]]

the National Health and Nutrition Examination Survey in biomonitoring 
programs.
    Response: EPA acknowledged in the preamble to the proposed rule 
that MEK has been reported to be found in blood. EPA also stated that 
the data indicated the source of the MEK is likely a by-product of 
normal human metabolism, and it is reasonable to expect it did not 
result from an air exposure to MEK at the concentrations seen in the 
ambient air.
    Comment: One commenter requested that EPA consider the role of MEK 
as an ozone precursor in deciding the petition.
    Response: EPA stated in the preamble to the proposed rule that it 
was inappropriate to consider the role of MEK as an ozone precursor 
because the ``dual structure (differentiating between HAP and criteria 
pollutants/precursors) 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.'' 
Specifically, the structure of the CAA is best protected by including 
compounds on the HAP list only where such inclusion is warranted based 
upon the HAP noncriteria pollutant related effects. This interpretation 
is supported by the following prohibition related to listing of new HAP 
contained in CAA section 112(b)(2): ``No air pollutant which is listed 
under section 7408(a) of this title [the criteria pollutant list] may 
be added to the list under this section, except that the prohibition of 
this sentence shall not apply to any pollutant which independently 
meets the listing criteria of this paragraph and is a precursor to a 
pollutant which is listed under section 7408(a) * * *.''
    Comment: One commenter stated that decisions to list or delist are 
governed by the precautionary principle. The commenter stated that, 
``in considering whether a petitioner has met the heavy burden of 
demonstrating that a substance should be removed from the hazardous air 
pollutant list, the precautionary principle requires that EPA resolve 
uncertainty in favor of more protection, not less. The recognition of 
uncertainty in the listing and delisting process does not give EPA 
discretion to delist a chemical based on incomplete and outdated 
information as it has proposed to do with MEK.''
    Response: EPA does not believe it is appropriate to require that 
all uncertainty be resolved in favor of not delisting. Such a 
requirement of absolute certainty is inconsistent with our 
interpretation of the requirement that to delist a HAP, EPA must 
determine that there are ``adequate data on the health and 
environmental ef