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List of Hazardous Air Pollutants, Petition Process, Lesser Quantity Designations, Source Category List
Note: EPA no longer updates this information, but it may be useful as a reference or resource.
[Federal Register: May 30, 2003 (Volume 68, Number 104)]
[Proposed Rules]
[Page 32605-32621]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr30my03-35]
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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.regulations.gov/. 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 rimer.kelly@epa.gov.
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.regulations.gov/ 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 a-and-r-
docket@epa.gov, 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'' (59 FR 22951, 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]
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