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CFR Citation: 40 CFR Part 63

DOCUMENT ID: [A-99-03, OAR-2003-0028; FRL-7504-9]

NOTICE: Part III

DOCUMENT ACTION: Proposed rule.

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

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.

DOCUMENT 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) (2Butanone) (CAS No. 78933). 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.

SUMMARY: Environmental Protection Agency,

SUPPLEMENTAL 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. A9903, and Electronic Docket No. OAR2003 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 B108, 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) 5661744, and the telephone number for the Air Docket is (202) 5661742.

Electronic Access. An electronic version of the public docket is available through EPA's electronic public docket and comment system, EPA Dockets. You may use EPA Dockets at http://www.epa.gov/edocket/ to submit or view public comments, access the index of the contents of the official public docket, and access those documents in the public docket that are available electronically. Once in the system, select ``search'' and key in the appropriate docket identification number.

Certain types of information will not be placed in the EPA dockets. Information claimed as confidential business information (CBI) and other information whose disclosure is restricted by statute, which is not included in the official public docket, will not be available for public viewing in EPA's electronic public docket. The EPA's policy is that copyrighted material will not be placed in EPA's electronic public docket but will be available only in printed, paper form in the official public docket. Although not all docket materials may be available electronically, you may still access any of the publicly available docket materials through the EPA Docket Center.

For public commenters, it is important to note that EPA's policy is that public comments, whether submitted electronically or in paper, will be made available for public viewing in EPA's electronic public docket as EPA receives them and without change unless the comment contains copyrighted material, CBI, or other information whose disclosure is restricted by statute. When EPA identifies a comment containing copyrighted material, EPA will provide a reference to that material in the version of the comment that is placed in EPA's electronic public docket. The entire printed comment, including the copyrighted material, will be available in the public docket.

Public comments submitted on computer disks that are mailed or delivered to the docket will be transferred to EPA's electronic public docket. Public comments that are mailed or delivered to the docket will be scanned and placed in EPA's electronic public docket. Where practical, physical objects will be photographed, and the photograph will be placed in EPA's electronic public docket along with a brief description written by the docket staff.

Comments. You may submit comments electronically, by mail, by facsimile, or through hand delivery/courier. To ensure proper receipt by EPA, identify the appropriate docket identification number in the subject line on the first page of your comment. Please ensure that your comments are
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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 email 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. A9903, or Electronic Docket Id. No. OAR20030028. The system is an ``anonymous access'' system, which means EPA will not know your identity, email address, or other contact information unless you provide it in the body of your comment.

Comments may be sent by electronic mail (email) to aandr
docket@epa.gov, Attention Docket ID No. A9903, or Electronic Docket ID. No. OAR20030028. In contrast to EPA's electronic public docket, EPA's email system is not an ``anonymous access'' system. If you send an email comment directly to the docket without going through EPA's electronic public docket, EPA's email system automatically captures your email address. Email addresses that are automatically captured by EPA's email 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, (MD6102T), Room B108, 1200 Pennsylvania Avenue, NW., Washington, DC 20460, Attention Docket ID No. OAR20030028.

By Hand Delivery or Courier. Deliver your comments (in duplicate, if possible) to: EPA Docket Center, Room B108, U.S. EPA West, 1301 Constitution Avenue, NW., Washington, DC 20004, Attention Docket ID No. OAR20030028. Such deliveries are only accepted during the Docket Center's normal hours of operation.

By Facsimile. Fax your comments to: (202) 5661741, Docket ID No. OAR20030028.

CBI. Do not submit information that you consider to be CBI through EPA's electronic public docket or by email. Send or deliver information identified as CBI only to the following address: Kelly Rimer, c/o Roberto Morales, OAQPS Document Control Officer (C40402), U.S. EPA, 109 TW Alexander Drive, Research Triangle Park, NC 27709, Attention Docket ID No. OAR20030028. 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) 5415384.

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
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submitted a petition to delete MEK (CAS No. 78933) 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 crossmedia 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 worstcase lifetime exposure to MEK, and to worstcase shortterm (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 facilityspecific 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.
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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'' (EPA450/492001). 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 worstcase 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 MEKemitting 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, offsite 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 worstcase 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 24hour average concentrations in addition to estimates of annual average concentrations. The highest 24hour 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 24hour concentrations are below 10 mg/m\3\ and concludes that people would not be exposed to 24hour 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 24hour 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 24hour 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 19871995 for seven sites ranged from approximately 0.0009 to 0.0018 mg/m\3\. The maximum 24hour 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 halflife of about 9 days and the comparatively short halflife of acetaldehyde (about 14 hours), resulted in low ambient levels of MEKproduced 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 doseresponse 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 peerreviewed 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 shortterm 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 shortterm 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 24hour exposures by comparing the estimated 24hour concentrations, 10 mg/m\3\ with a human health benchmark of 33 mg/m\3\, and determined that these shortterm 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, lowboiling 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 nonoccupational 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 worstcase 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 sitespecific (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 24hour 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 longterm 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 worstcase 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 worstcase facility. Using this worstcase 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
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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 sourcereceptor 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 sitespecific 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 19871995. 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 24hour concentrations as was used to predict annual average concentrations, we accept the conclusion that the maximum 24hour average concentration expected would be less than 10 mg/m\3\. However, we also wanted to evaluate predicted concentrations which may occur over a 1hour time period. Using air dispersion modeling principles described in EPA's SCREEN3 User's Manual and the estimated annual average and 24hour average concentrations presented in the petition, we estimated the maximum 1hour concentration. The predicted annual average concentration is approximately 1 mg/m\3\ and the 24hour average is about 10 mg/m\3\. To estimate the 1hour maximum, we multiply the 24hour average by 2.5. This results in a 1hour maximum of approximately 25 mg/m\3\.

In terms of ambient air monitoring data, the 2001 AIRS shows that the highest 24hour 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 shortterm values are sufficiently low so as not to contribute significantly to shortterm 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 24hour and 1hour 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 24hour offsite concentration predicted at the highest emitting facility, EPA has concluded that no individual could be reasonably anticipated to experience chronic or 24hour 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 offsite concentration of MEK greater than 1 mg/m\3\, or a 24hour average greater than 10 mg/m\3\. We, by extrapolation, have concluded that 1hour 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
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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 1hour 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 mechanismbased structureactivity 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 monoketones have been associated with carcinogenicity/genotoxicity. There is also no reason to anticipate any electrophillic reactivity for unsubstituted monoketones 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 middoses. 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 twogeneration reproductive/
developmental toxicity study of 2butanol, a metabolic precursor to MEK, is available and is the basis for the oral reference dose (RfD) for MEK (Cox et al., 1975). 2Butanol is quantitatively converted to MEK within the body. In this twogeneration study, administration of 2 butanol to rats in drinking water at concentrations as high as 3 percent ([tilde]5000 mg kilogramsday) 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
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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 treatmentrelated 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 nhexane at 60 ppm. This point should be considered when evaluating mixtures of solvents, especially those containing MEK and the solvents listed above, especially nhexane. 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 lowlevels we are concerned with in this assessment (i.e., much less than 590 mg/m³).

The petition presents a shortterm 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 shortterm human health effects criterion, however, currently there is no EPA human health criterion for shortterm exposures available for us to use in an analysis.

There are 1999 California Environmental Protection Agency (CalEPA) shortterm health criteria (CalEPA 1999). The CalEPA published three levels of acute reference exposure levels (REL) to protect against mild adverse effects (associated with a 1hour exposure), severe effects (associated with a 7hour exposure), and life threatening effects (associated with a 1hour 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 portalofentry 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.

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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 doseresponse 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 me

FOR FURTHER INFORMATION CONTACT Ms. Kelly A. Rimer, Risk and Exposure Assessment Group, Emission Standards Division (C40401), U.S. EPA, Research Triangle Park, NC 27711, telephone number (919) 5412962, electronic mail address rimer.kelly@epa.gov.