1 October 23, 2005 MEMORANDUM TO: Docket No. OAR 2003 0028 FROM: Mark Morris, REAG SUBJECT: Summary of and Response to Public Comments Received on the May 30, 2003 Proposed Rule to Delete Methyl Ethyl Ketone 1.0 Overview The U. S. Environmental Protection Agency ( EPA) is proposing to amend the list of hazardous air pollutants ( HAP) contained in section 112( b) 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 proposal to delist MEK appeared in the Federal Register on May 30, 2003 ( 68 FR 32606). The notice summarized the American Chemistry Council= s petition to delist MEK and EPA's analysis of that petition, and provided a detailed rationale for delisting MEK.

The proposal notice invited comment from interested parties on the proposal to delist MEK. In addition, the notice specifically requested comments on the prospective reference concentration ( RfC) for MEK ( the interim health value EPA developed for the proposal). The notice also solicited comment on the portion of the human health risk characterization based on this RfC, and whether it would be appropriate to delist MEK if the RfC resulting from an updated Integrated Risk Information System ( IRIS) review were different from the prospective RfC.

Comments were received from a number of industry, State, environmental group, and other commenters. These comments are summarized below in Sections 2.0 through 5.0. Section 7.0 presents a table identifying the commenters.

2.0 General Support for and Opposition to the Proposed Delisting 2.1 General Support 2 Many commenters ( 58, 61 65, 69 75, 77, 79 82, 85, 86, 88 90, 92 94, 98, 101, 103, 106 108, 112 114, 115, 119, 124, 126, 127, 131) generally supported the proposed rule to delist MEK from the HAP list as specified in section 112( b) of the CAA. These commenters also believe that the proposed delisting is supported by adequate data.

Several commenters ( 80, 92, 124) noted that delisting MEK would allow switching to MEK from more costly solvents, and would reduce volatile organic compound ( VOC) emissions. One commenter ( 80) stated that if ethyl acetate is replaced with MEK, VOC emissions are reduced by 20 percent; that MEK is not as sensitive to temperature changes as replacement solvents; and that MEK costs less than other solvents currently in use ( e. g., 16 percent less than ethyl acetate). Additionally, two commenters ( 92, 124) stated that should MEK be delisted, some sources would change from major to area, potentially saving them money. Two commenters ( 82, 92) noted that delisting MEK would not change the VOC status of MEK, which subjects it to regulation under New Source Review ( NSR), National Ambient Air Quality Standards ( NAAQS), State Implementation Plans ( SIP), and Reasonably Available Control Technology ( RACT) standards. Another commenter ( 65) suggested that substitutes for MEK currently in use may pose an increased risk to health and environment; therefore, by delisting MEK, the risks would be decreased.

2.2 General Opposition Several commenters ( 57, 59, 60, 76, 83, 87, 91, 97, 99, 102, 104, 120, 128) were generally opposed to the delisting of MEK. Some of these commenters ( 83, 104, 128) maintained that the proposed rule did not take into account the future increases in MEK use. According to one commenter ( 91), MEK was not delisted in 1998 because it contributes to ozone formation. Another commenter ( 120) asserted that the delisting of MEK is not supported by new or compelling scientific evidence.

3.0 Comments Pertaining to the Prospective RfC EPA specifically requested comments regarding the prospective RfC for MEK. The prospective RfC was 9 mg/ m3, while the RfC at the time the proposed rule was published was 1 mg/ m3. The following comments either oppose or support the prospective RfC.

3.1 Opposition Comment: One commenter ( 83) asserted that the RfC of 1 mg/ m3 was set to protect against birth defects and should not be changed. Another commenter ( 120) maintained that the 2003 RfC is based on the same study from 1991 that was used to determine the 1992 RfC. In 2002, EPA reduced the uncertainty after correcting the no observed adverse effect level ( NOAEL) to reflect the lifetime continuous exposure, using the same 1991 data. In 2003, EPA 3 abandoned the NOAEL for a benchmark dose. The commenter expressed the opinion that the benchmark dose and the RfC, which were based on the same study from 1991, do not adequately provide an estimate that is likely to be without appreciable risk of deleterious effects during a lifetime.

Response: The RfC is designed to consider all adverse noncancer effects associated with lifetime exposure to a chemical. The 2003 RfC is based on developmental effects, and is based on the methodologies that were in place at the time of derivation, including ( 1) the methods for the use of inhalation dosimetry to extrapolate from animal to human exposures ( U. S. EPA, 1994) and ( 2) benchmark dose methods ( U. S. EPA, 2000, external review draft). Those methods have been subject to peer review.

Comment: One commenter ( 99) stated that the toxicological database is not complete regarding developmental effects, and that there is inadequate evidence to assess the carcinogenic potential of MEK ( i. e., there are no 2 year animal cancer bioassays).

Response: There are adequate data on developmental effects and on cancer effects to support a decision to delist MEK. The principal study ( Schwetz et al., 1991), a developmental toxicity study in the mouse, is well designed and tests several exposure concentrations over a reasonable range that include maximum tolerated doses for dams and fetuses. Also, animal studies in a second species ( rats) corroborate the effect level for developmental toxicity ( Deacon et al., 1981; Schwetz et al., 1974).

Regarding carcinogenicity, the current IRIS file ( completed in September of 2003) states that the data for MEK are characterized as " inadequate for an assessment of human carcinogenic potential." The " Toxicological Review of Methyl Ethyl Ketone" ( U. S. EPA, 2003)( Toxicological Review of MEK), upon which the IRIS file is based states, " Under EPA's draft revised cancer guidelines ( U. S. EPA, 1999), data are inadequate for an assessment of human carcinogenic potential for MEK because studies of humans chronically exposed to MEK are inconclusive, and MEK has not been tested for carcinogenicity in animals by the oral or inhalation routes." Recent revision of these guidelines does not materially affect this conclusion.

The traditional 2 year animal cancer study has not been conducted for MEK, nor is EPA aware of any organization planning to conduct one. EPA believes one reason no cancer assay has been done is that the results from the majority of the genotoxicity tests ( which are often used as an indicator of the need to pursue a 2 year cancer study) are negative, indicating that MEK is a low priority for further study. In 1997, the Organization for Economic Cooperation and Development ( OECD) reached this conclusion. OECD's report states that " MEK is not genotoxic and is not likely to be carcinogenic." ( OECD, 1997). The report also states that MEK is ". . . currently of low priority for further work." ( OECD, 1997). 4 The general descriptors recommended by EPA's " Guidelines for Carcinogen Risk Assessment" ( U. S. EPA, 1999) for characterizing the weight of evidence with regard to a chemical's potential for human carcinogenicity did not explicitly recognize this situation. The descriptor applied to MEK in the 2003 IRIS assessment ( i. e., " data are inadequate for an assessment of human carcinogenic potential") pertains to cases where ". . . there is a lack of pertinent or useful data." ( U. S. EPA, 1999). While lacking data or studies that would clearly support their placement in other categories ( e. g., the traditional 2 year rodent study), chemicals included within this broad category may, however, have pertinent or useful data which do not indicate any potential for carcinogenicity, consequently providing no support for the performance of the traditional, resource intensive studies.

Accordingly, EPA's Toxicological Review of MEK also states, " the majority of short term genotoxicity testing of MEK has demonstrated no activity, and the Structure Activity Relationship ( SAR) analysis suggests that MEK is unlikely to be carcinogenic." ( U. S. EPA, 2003). One study ( Woo et al., 2002) has given MEK and other unsubstituted mono ketones ( a compound class to which MEK belongs) a low concern rating ( unlikely to be of cancer concern) because these chemicals lack electrophilic activity ( i. e., a structural alert of carcinogenicity) and are generally not associated with carcinogenicity.

There is an absence of positive results in the majority of mutagenicity and genotoxicity tests which are designed to indicate the potential for carcinogenicity. Methyl ethyl ketone has been tested for activity in an extensive spectrum of in vitro and in vivo genotoxicity assays and has shown no evidence of genotoxicity in most conventional assays ( National Toxicology Program, no date; World Health Organization 1992; Zeiger et al., 1992). Methyl ethyl ketone tested negative in bacterial assays ( both the S. typhimurium ( Ames) assay, with and without metabolic activation, and E. coli), the unscheduled deoxyribonucleic acid ( DNA) synthesis assay, the assay for sister chromatid exchange ( SCE) in Chinese hamster ovary ( CHO) cells, the mouse lymphoma assay, the assay for chromosome aberrations in CHO cells, and the micronucleus assay in the mouse and hamster. The only evidence of mutagenicity was mitotic chromosome loss at high concentrations in a study of aneuploidy in yeast S. cerevisiae ( Zimmerman et al., 1985), but the relevance of this finding to humans is questionable. Overall, studies of MEK yield little or no evidence of genotoxicity.

However, the finding of low potential for genotoxicity alone is not the sole criterion for an assessment of carcinogenic potential, as non genotoxic mechanisms can also result in carcinogenesis. While developing the final rule, EPA learned that preliminary results of a recent cancer bioassay by the National Toxicology Program suggested that methyl isobutyl ketone ( MIBK) appears to be a weak or marginally active carcinogen in rats and mice, possibly by a nongenotoxic mode of action. Both MEK and MIBK are small molecular weight alkyl ketones, and this similarity raised some questions regarding the possible relevance of the preliminary MIBK results to MEK. To investigate this further, EPA undertook SAR analysis of MIBK and MEK. These two ketones have a key difference in their chemical structure: MIBK is branched, while 5 MEK is linear. EPA's SAR analysis indicates that MIBK's toxicity and possible carcinogenicity are likely due to its branched alkyl structure. Methyl ethyl ketone, like acetone, is linear and lacks this structure. Thus, the analysis concluded that in analogy to acetone and its metabolite isopropanol ( which has shown no evidence of carcinogenicity), MEK and its metabolite ( 2 butanol) are linear and, therefore, have low concern for carcinogenicity potential. A short document describing the analysis, " Acetone, MEK, and MIBK  SAR Analysis on Carcinogenicity/ Toxicity," is included in the docket. Subsequently, EPA conducted an external peer review of this document. All three reviewers found the reasoning to be sound and supported the conclusions of the analysis. These reviews are also included in the docket. Thus, EPA concludes that the available scientific evidence shows a low potential for carcinogenicity in MEK.

Comment: One commenter ( 104) suggested that the uncertainty factors ( UFs) for the prospective RfC were not adequate. The commenter disagreed with the reduction of the interspecies UF and stated that it should have remained at 10 because there are no developmental and reproductive studies available for humans and animals. Another commenter ( 120) suggested that the human equivalent concentration ( HEC) resulted in low confidence because it was based on the same mouse study ( 1991) as the 1992 RfC, and the prospective RfC was not robust enough to warrant decreasing the interspecies UF from 10 to 3. This commenter also asserted that the chronic and reproductive studies are still missing and, therefore, EPA= s proposal of reducing the database UF is not valid. The commenter contended that the lack of current information results in continued low confidence in the database because the data used are from the original studies used to develop the 1992 RfC. The commenter believes that the Dick study did not provide adequate statistical power. Consequently, the commenter believes that the lack of toxicity was not demonstrated, and that the modifying factor should be maintained at 3. The commenter concluded that the Aabsence of data should not conclude an absence of toxicity.@

Response: An interspecies UF of 3 was applied in deriving both the prospective RfC and the 2003 RfC, consistent with EPA guidance for deriving RfCs in effect at the time ( U. S. EPA, 1994). The UF for interspecies extrapolation is not intended to address database deficiencies. A database UF of 10 was used in developing the 2003 RfC to account for the lack of a chronic inhalation toxicity study and multigeneration reproductive toxicity study.

Modifying factors have been used in the past in RfC derivations, where the magnitude of the factor reflected the scientific uncertainties of the study and database that were not explicitly treated with standard uncertainty factors. For the 2003 RfC, the default modifying factor of one was used because EPA concluded that the modifying factor was sufficiently subsumed in the general database UF.

Comment: One commenter ( 104) advocated maintaining the modifying factor of 3 because the commenter contends that toxicity data addresses the potentiation of the toxic effects from co pollutant exposures. 6 Response: The 1992 RfC of 1 mg/ m3 incorporated a modifying factor of 3 to account for the lack of unequivocal data for respiratory tract ( portal of entry) effects suggested by earlier studies with MEK ( Altenkirch et al., 1978). More recent data concerning the portal of entry effects from MEK address the applicability of a modifying factor to this assessment. Dick et al. ( 1984, 1988, 1989, 1992) found no evidence of a statistically significant increase in respiratory tract irritation among humans who were exposed to MEK at 590 mg/ m3 for 4 hours. In addition, Oleru and Onyekwere ( 1992) found no statistically significant pulmonary effects among MEKexposed leather workers ( mean duration of employment was approximately 10 years). While these studies do not directly address the potential for portal of entry effects for MEK in continuous lifetime exposure scenarios as animal studies evaluating histology would, they do address the concerns raised in the 1992 IRIS assessment. Further, as discussed above, EPA contends that the purpose of the modifying factor is sufficiently subsumed in the general database UF, and has discontinued the use of modifying factors.

3.2 Support Comment: One commenter ( 103) asserted that the prospective RfC of 9 mg/ m3 was adequately recorded and justified in the docket to quantify non cancer health risks from MEK, and this commenter supported the delisting of MEK as long as the RfC was not reduced below 1 mg/ m3 in the final rule. Two commenters ( 82, 108) suggested that delisting should be based on the proposed RfC of 15 mg/ m3 rather than the prospective RfC of 9 mg/ m3.

Response: EPA believes that the most appropriate dose response value to use in evaluating whether to delist MEK is the 2003 RfC of 5 mg/ m3.

4.0 Comments Pertaining to the Human Health Risk Characterization EPA specifically requested comments regarding the portion of the human health risk characterization based on the prospective RfC. The following comments either support or oppose the human health risk characterization.

4.1 Support Two commenters ( 73, 82) agreed that available data indicated that MEK has low acute and chronic toxicity. These commenters also stated that:

$ The data are adequate to determine that emissions, ambient concentrations, bioaccumulation, or deposition of MEK may not reasonably be anticipated to cause adverse human or environmental effects.

$ In 1997, the international community concluded that MEK was not toxic at ambient concentrations. 7 $ The Screening Information Assessment Meeting concluded that MEK had no toxicity following acute or repeated exposures.

$ MEK was also not mutagenic, neurotoxic, or a skin sensitizer.

One commenter ( 108) stated that MEK had been investigated through the Screening Information Data Set ( SIDS) process, an international program, and SIDS concluded that:

$ MEK did not appear to present a significant risk of adverse reproductive or developmental effects.

$ MEK had a low toxicity following acute oral, dermal, and inhalation exposure studies although contact with the eyes, skin, or respiratory tract did produce irritation.

$ There were no significant signs of toxicity after repeated inhalation exposure at high concentrations and MEK has not been shown to have any neurotoxic potential.

$ Human volunteers who underwent exposure did not demonstrate any significant effects other than minor irritation and sensory effects at relatively high levels.

$ MEK was not genotoxic and was not likely to be carcinogenic.

$ MEK has not been shown to produce skin sensitization.

One commenter ( 82) asserted that the petitioner= s dispersion modeling resulted in conservative estimates because the 1996 National Toxics Inventory ( NTI) data used for the analysis is recognized as a conservative estimate of speciated emissions, and because the 1996 NTI did not account for reduced MEK use over the last few years. Therefore, the commenter stated, through using the NTI, all the significant MEK emission sources were identified and evaluated. Additionally, the modeled ambient levels ( 1 mg/ m3) at the facility entrance and not residential areas are one tenth of the proposed RfC ( 15 mg/ m3). Also, the petitioner ( 108) determined that actual exposures to MEK would be far less than modeled exposures, as MEK has a lower solvent emission per unit of surface area compared to many non ketone alternatives, and a smaller amount of MEK is needed to perform the same function.

Comment: One commenter ( 108) concurred with the use of the Cox et al. ( 1975) study as an appropriate basis for the reference dose ( RfD). However, the commenter noted that the IRIS summary for MEK posted in 1993 considered 1,771 mg/ kg/ day from Cox et al. ( 1975) to be a NOAEL, whereas this dose level was considered to be a lowest observed adverse effect level ( LOAEL) in the external review draft of the 2003 RfC based on reduced pup weight observed in the F1A litter, but not in F1B or F2 litters. In addition, the commenter observed that as part of the application of the benchmark dose ( BMD) methodology to this study, EPA selected a 5 percent decrease in mean pup or fetal body weight per litter as the benchmark response ( BMR) because it fell within the range of experimental dose levels. The commenter disagreed with the selection of the BMR because 5 percent is less than one standard deviation from the mean and the effect is not observed at 1,771 mg/ kg/ day in F1B and F2 litters. The commenter suggested using 10 percent instead, which results in an effective dose ( ED10) of 1,756 mg/ kg/ day and a 95 percent lower bound on the ED ( LED10) of 1,314 mg/ kg/ day. 8 Response: In the 2003 IRIS assessment, the summary of the Cox et al. ( 1975) study was revised such that a NOAEL and LOAEL for the study as a whole were identified. Because the body weight reductions compared to control in the low and mid dose groups in F1A pups were not observed in subsequent generations ( i. e., FIB and F2), a NOAEL and LOAEL for the study as a whole of 1 percent ( 1,771 mg/ kg day) and 2 percent ( 3,122 mg/ kg day), respectively, were presented.

One standard deviation as a BMR serves as a recommended point of comparison across assessments, but is generally considered the last choice as the basis for the BMR if there is no other basis for a biologically relevant degree of change in response. In the case of pup body weight data from the Cox et al. ( 1975) study, there is no specific decrement that is generally regarded as indicative of a biologically relevant response. EPA considered the use of one standard deviation as the BMR. Using data from Cox et al. ( 1975), one standard deviation from the control mean resulted in BMDs that corresponded to body weights 9 to 26 percent below the control mean, values generally outside the range of experimental data. Because an aim in BMD modeling is to select a BMD within the range of observation, other measures of the BMR were examined. A 5 percent reduction in fetal/ pup body weight relative to the control was a response rate that fell within the range of experimental dose levels in the Cox et al. ( 1975) study, and consequently was selected as the BMR. In addition, an ED10 and LED10 for each endpoint were estimated as a consistent point of comparison across chemicals, as recommended in the Benchmark Dose Technical Guidance Document ( U. S. EPA, 2000). Justification for the selection of a BMR of 5 percent is provided in the final IRIS assessment for MEK ( Section <IP_ADDRESS> of the Toxicological Review). See the IRIS toxicological review for the complete discussion on this topic: http:// www. epa. gov/ iris/ subst/ 0071. htm.

Comment: One commenter ( 108) stated that the EPA did not explain why a 10 percent extra risk for misaligned sternebrae was relevant or why it should not be considered a constraint on the BMD modeling outcome.

Response: A 10 percent extra risk for misaligned sternebrae was selected as the benchmark response since the model and data are most consistent in this range of the data set. Also, EPA= s Benchmark Dose Technical Guidance Document ( U. S. EPA, 2000) recommends estimation of a 10% BMR for a point of consistent comparison across chemicals. Further, the nested model did not provide a useful estimate of the lower bound for a BMR of 5 percent for this particular data set ( the lower bound on the BMC was estimated as essentially zero).

Comment: One commenter ( 108) contends that the BMD is too restrictive because it is based on misaligned sternebrae studies, and believes that decreased fetal birth weight is a more scientifically sound basis for determining the LOAEL, NOAEL, and RfC. 9 Response: EPA considered the use of both reduced fetal weight and incidence of misaligned sternebrae as the basis for the RfC point of departure, taking into account external peer reviewers= comments and further analysis of the data from Schwetz et al. ( 1991). Points that support the use of fetal weight rather than misaligned sternebrae included the fact that the incidence of misaligned sternebrae was highly nonlinear with dose, and the incidence showed a high degree of variability. The full laboratory report of this developmental toxicity study ( Mast et al., 1989) also reported a positive trend ( not statistically significant) for reduced ossification of the sternebrae, raising the possibility that misaligned sternebrae may reflect a more general growth delay. None of the external peer reviewers, however, offered an opinion that misaligned sternebrae was not a biologically significant endpoint of toxicity. Selection of the critical effect ( i. e., reduced fetal weight or incidence of misaligned sternebrae) was further deliberated during Agency consensus review. In general, the arguments for using fetal weight as the more supportable critical effect were not found to be sufficiently compelling. Thus, the decision was made to use the more health protective endpoint, misaligned sternebrae, as the critical effect.

Comment: One commenter ( 108) stated that EPA did not present adequate scientific justification for applying a duration adjustment to the inhalation developmental toxicity study and, at the very least, the additional conservatism added by the application of this factor should be explicitly recognized. The commenter pointed to the draft Toxicological Review that indicated that MEK was rapidly absorbed, distributed, and metabolized, suggesting that the duration adjustment may be inappropriate.

Response: Duration adjustment of the exposure concentrations in the developmental study of MEK ( Schwetz et al., 1991) was performed consistent with the EPA Risk Assessment Forum RfD/ RfC Technical Panel report, " A Review of the Reference Dose and Reference Concentration Processes" ( U. S. EPA, 2002). The report recommends that procedures for adjusting to continuous exposure based on the product of concentration and time be used as a default for inhalation developmental toxicity studies as it is for other health effects from inhalation exposure. While the recommendation is based on evidence that shows that some agents cause developmental toxicity more as a function of peak concentration, the effects of other agents are related to area under the curve ( AUC). The latter is true even of some developmental toxicants with a short half life. In the absence of data that support peak concentration or AUC as more closely correlated with developmental toxicity, EPA= s 2002 review document recommends duration adjustment as the more health protective default procedure. As noted in the Toxicological Review of MEK, because the data are insufficient to argue convincingly for either peak exposure level or AUC as the most appropriate metric, the more health protective procedure ( duration adjustment) was applied as a policy matter.

Comment: The petitioner commented on EPA's interpretation of the Cavender et al. ( 1983) study. They stated that EPA regarded 5,000 ppm in a 90 day inhalation study as the LOAEL based on reduced weight gain, increased liver weight, and decreased brain weight. The commenter stated that this was inconsistent with the IRIS database where EPA indicated that a 10 change in liver weight may not be conclusively caused by MEK inhalation. The petitioner recommended that 5,000 ppm be the NOAEL.

Response: In the 2003 IRIS assessment, EPA gave further consideration to the biological significance of the findings in the 5,000 ppm animals in the Cavender et al. ( 1983) study, specifically the organ weight findings. Although the decrease in brain weight in female high dose animals is of some concern, EPA agrees that this effect, in the absence of corresponding histopathology and functional abnormalities, cannot be clearly characterized as being of toxicological relevance. In light of these uncertainties, characterization of the effects associated with the 5,000 ppm exposure level as adverse, use of that level as a LOAEL, and the use of middose group ( 2,518 ppm) as a NOAEL were dropped.

4.2 Opposition Comment: Three commenters ( 83, 128, 120) suggested that the actual emissions of MEK may result in environmental concentrations below the RfC, but allowable emissions would not. This means that should the emissions reach allowable limits, then the concentrations of MEK will be above the RfC. One commenter provided an example of a facility that emits 500 tons per year ( tpy) of MEK but is permitted to emit up to 2,200 tpy. The commenter states that a simple screening model run ( most likely similar to the tier 1 or tier 2 analysis submitted by the petitioner) of this facility at the allowable emission rate predicts 24 hour peak concentrations to be about 75 mg/ m3, which is above the maximum predicted 24 hour average concentration of 10 mg/ m3 that EPA cited in the preamble.

Response: The maximum offsite 24 hr MEK concentration for the worst case facility in the petition as predicted by the Industrial Source Complex Short Term 3 ( ISCST3) model was 10 mg/ m3. The maximum annual concentration was 1.2 mg/ m3. This facility emits about 500 tpy MEK. The maximum offsite concentration occurs within a few hundred meters of the facility.

The commenters provided limited information on the facility that has the potential to emit 2,200 tpy. EPA contacted the commenter in order to understand how they estimated the value of 75 mg/ m3. EPA was told that the SCREEN3 model used to estimate this concentration. However, EPA was unable to obtain the modeling runs which would contain important model input data ( e. g., stack heights and distances from stacks to fence lines). From the comment, EPA does know that the maximum offsite concentration for this facility as predicted by the SCREEN3 model was 75 mg/ m3 for a 24 hr average and 1.1 mg/ m3 for an annual average. If this facility were modeled with a more refined dispersion model, such as the ISCST3 model, EPA would expect impacts that are considerably lower than those predicted with the more conservative SCREEN3 model. Most likely, the maximum offsite concentration for the facility would be much closer to 10 mg/ m3 for a 24 hr average near the facility, and well below 1 mg/ m3 for the annual average. EPA would suspect that the facility to which the commenter refers has much better dispersion characteristics than the petitioner= s worst case facility, which had a very low stack and 11 nearby fenceline.

Comment: Three commenters ( 83, 104, 120) stated that EPA failed to meet the CAA deadline ( 18 months) for adding or deleting a substance from the HAP list, instead taking 78 months total. Therefore, the commenters believed the 1994 Toxic Release Inventory ( TRI) data used in the assessment were not appropriate and that current TRI data should have been used. These commenters also contended that the calculations in the petition did not consider potential increases in MEK use once MEK is delisted, and that EPA should base its decision to delist MEK on emission levels and locations expected after delisting.

Response: EPA interprets the CAA to require consideration of current emissions. It is not appropriate to make a decision on what can only be speculative emissions. EPA states in the final rule to delist caprolactam ( 61 FR 30816, June 18, 1996) that AEPA does not interpret Section 112( b)( 3)( C) to require consideration of hypothetical emissions from facilities that might be constructed in the future. The logical consequence of such an expansive construction would be that no substance could ever be delisted, due to the hypothetical possibility of some future facility that has uncontrolled emissions large enough to cause adverse effects. In the event some future facility has uncontrolled caprolactam emissions great enough to change the conclusion of the current EPA risk assessment, EPA can revisit its decision to delist caprolactam at that time." It is not the case, however, that EPA can never take potential increases in emissions into account. For example, such consideration is appropriate where EPA has information regarding specific facilities, such as the information it considered in denying the methanol delisting petition.

Using similar logic in this case, EPA does not interpret CAA section 112 ( b)( 3)( C) to require consideration of hypothetical emissions from facilities that might be constructed in the future, nor projections of increases in emissions from existing facilities.

There are several reasons why EPA does not expect that increases in emissions of MEK will cause health or environmental concerns. With regard to increased emissions themselves, EPA believes that such increases will be limited by good housekeeping practices which are designed to save product. Methyl ethyl ketone is an effective solvent, but one that evaporates readily. Employing techniques to prevent wasting the product also results in decreased emissions.

Due to the health protective nature of the analysis upon which the decision to delist is based, EPA concludes that the potential risks from outdoor exposures to MEK are overestimated. It is unlikely that future emissions increases will result in unacceptable risk. For example, the petitioner based the risk assessment on 1994 TRI total air emissions of MEK, which were 628 tpy for the worst case facility. This facility= s modeled annual average concentration is only 20 percent of the RfC. This facility could increase emissions significantly before the concentration would be above a level of concern. The highest emitting facility in the 2003 TRI emits 638 tpy of MEK, only slightly higher than the 1994 TRI emissions for the worst case facility. 12 In addition, the national trend in MEK emissions is distinctly downward. Comparing the 1994 and 2003 TRI MEK emissions data for the 100 highest emitting facilities indicates that air emissions have decreased by approximately 20 percent during that nine year period.

The risk assessment was based on a maximum off site concentration. The assessment did not consider the amount of time people would be at that location, or other factors that address the amount of exposure faced by actual individuals. Further, this maximum concentration was located at the entrance to a facility in an industrial park. The probability that an individual would live at this location in the future is extremely low.

Given the low hazard presented by the worst case facility, the health protective nature of the analysis, and the overall downward trend of MEK emissions over the last several years, EPA believes that emissions of MEK may not reasonably be anticipated to cause adverse human health effects.

The preamble to the proposed rule discussed the March 30, 1998, Federal Register notice ( 63 FR 15195) in which EPA issued a Denial of Petition entitled " Methyl Ethyl Ketone; Toxic Chemical Release Reporting; Community Right to Know." The denial was in response to a petition from the Ketones Panel of the Chemical Manufacturers Association ( CMA) that requested the deletion of MEK from the list of chemicals reportable under section 313 of the Emergency Planning and Community Right To Know Act of 1986 ( EPCRA) and section 6607 of the Pollution Prevention Act.

The American Chemistry Council filed suit challenging EPA's decision in the United States District Court for the District of Columbia. Subsequently, the court granted summary judgment in favor of EPA ( American Chemistry Council v. Whitman, 309 F. Supp. 2d 111 ( D. D. C. 2004)). On appeal, the Court of Appeals for the District of Columbia Circuit reversed the lower court's decision, vacating the lower court's decision, and directed the district court to issue an order to " direct EPA to delete MEK from the TRI" ( 406 F. 3d 738, 742 ( D. C. Cir. 2005)). The circuit court issued its mandate on June 13, 2005 and, accordingly, on June 30, 2005, EPA issued a final rule ( 70 FR 37698) revising the EPCRA section 313 list of reportable chemicals in 40 CFR 372.65 to delete MEK.

The deletion of MEK from the EPCRA section 313 list eliminates the main source of data EPA uses to track MEK emissions. However, there are other data sources available to estimate MEK emissions, including market research data on MEK production, import, export, and consumption. Consumption of MEK should provide an adequate surrogate for emissions to determine whether significant increases in emissions are occurring. If data indicate that MEK emissions are increasing significantly, EPA has the option to add MEK back on the HAP list.

Comment: One commenter ( 120) suggested that the risk was not adequately identified because the industry was not studied comprehensively enough to determine chronic exposure. 13 Response: In order to determine the risks from emissions of MEK, the petitioner used the 1994 TRI as the basis of an emissions inventory intended to quantify annual emissions of MEK, to identify and locate emissions sources, and to acquire some facility specific emissions information. The 1994 TRI shows that there are over 2,000 sources with reported emissions of MEK. The petition states that over 85 percent of these facilities ( approximately 1,700) emit 25 tpy or less. The petition also states that approximately 800 facilities emit between 10 and 200 tpy, and 27 facilities emit 200 tpy or more. In addition to using the 1994 TRI, the petitioner queried a subset of individual sources to obtain site specific source, release, and facility information for the purpose of conducting more detailed risk assessments. EPA has determined that this approach to establishing reasonable worst case exposures to MEK emissions is an adequate basis upon which to base a decision to delist MEK. EPA states in the preamble to the proposed rule that it does not interpret CAA section 112( b)( 3)( C) to require absolute certainty that a pollutant will not cause adverse effects on human health or the environment before it may be deleted from the list. The use of the terms Aadequate@ and Areasonably@ indicate that EPA must weigh the potential uncertainties and likely significance. In this case, the uncertainty in the predicted exposure levels is biased toward protecting public health. Therefore, EPA concludes that delisting MEK is appropriate.

Comment: Several commenters ( 87, 91, 104, 120) contended that chronic effects of MEK had not been adequately studied or evaluated, and that the delisting was not supported by new or compelling scientific evidence. One commenter ( 87) requested that EPA conduct long term health effects studies. Additionally, two of the commenters ( 87, 104) stated that there were no lifetime chronic studies included, no studies evaluating developmental effects, nor studies concerning reproductive toxicity. These commenters also asserted that there were no multigenerational studies included, and the evaluation of the carcinogenic potential was not adequate.

Response: EPA's RfC methodology ( U. S. EPA, 1994) does not always require a complete database in order to develop an RfC; however, the database must at least meet minimum data requirements. For MEK, A. . . confidence in the database is medium . . .. @ ( U. S. EPA, 2003). AThe subchronic study by Cavender et al. ( 1983) satisfies the minimum inhalation database requirements for derivation of an RfC.@ ( U. S. EPA, 2003).

In the case where there are enough quality data with which to set an RfC, but where the database is less than complete, EPA adds a database uncertainty factor to account for the lack of data. For MEK, that factor is 10. EPA acknowledges the lack of a chronic toxicity bioassay and an inhalation multigeneration reproductive toxicity study ( an oral multigeneration is available), but notes that contrary to the commenters= statements, the developmental toxicity of MEK has been well studied.

The MEK RfC is an estimate ( with uncertainty spanning perhaps an order of magnitude) 14 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 lifetime. Because maximum expected ambient air concentrations are well below the RfC, EPA does not expect adverse noncancer effects to result. In addition, the health protective nature of the assessment described above adds to EPA's confidence that no adverse health effects will occur from ambient exposures to MEK.

Comment: One commenter ( 104) asserted that the appropriate averaging time for assessing the potential for adverse developmental effects to occur is the 24 hour average not an annual average. The commenter held that evaluating developmental toxicity on a 24 hour basis is supported by EPA guidelines for evaluating developmental risk. This issue was also raised by the Voluntary Children's Chemical Evaluation Program ( VCCEP) review panel as they considered the information industry submitted on MEK and children= s health.

Response: EPA agrees with the commenter that potential concern for developmental effects from short term exposures should be addressed, and EPA did this. With regard to the use of endpoint specific reference values, EPA= s review of the RfD/ RfC processes recommended against the use of endpoint specific reference values, and instead recommended that durationspecific reference values be derived in consideration of the full range of adverse effects.

Comment: One commenter ( 120) remarked that EPA did not take into account all routes of exposure to MEK and, therefore, did not adequately identify the risk.

Response: MEK is neither bioaccumulative nor persistent. It has a half life of approximately 9 days. The releases of MEK to air are unlikely to result in elevated concentrations in surface water, ground water, or the food supply. Therefore, the route of exposure EPA is concerned with is direct inhalation of MEK released to the ambient air. For this reason, inhalation was the focus of the analysis. The petitioner also assessed the potential for risks due to ingestion of water contaminated with MEK. In both cases, the risks were below a level of concern.

Comment: One commenter ( 99) asserted that the risk assessment did not fully address: ( 1) other solvents released from stationary and area sources of MEK, ( 2) actual ambient concentrations near stationary and area sources ( only modeled concentrations were used), and ( 3) the human health effects within the facilities as opposed to fenceline ambient concentrations.

Response: The maximum annual average air concentration resulting from emissions of MEK is not expected to exceed an HQ of 0.2. This value, which is 20 percent of the RfC, is quite low. EPA believes that there is a large enough margin of exposure to preclude a need to address any other emitted HAP that may affect the same target organ as MEK.

The petitioner did not monitor ambient air around actual MEK emitting facilities. Such an effort would not add to the analysis, or change EPA= s conclusion with regard to delisting. This is 15 because the maximum monitored concentration EPA found in the U. S. was over two orders of magnitude below the maximum modeled concentration, and because the modeling conducted was designed to over estimate ambient concentrations. For example, the model assumed that individuals are continuously exposed to the maximum modeled concentrations of MEK in air for 70 years, and EPA used the maximum annual average concentration as a surrogate for long term exposure. Also, the model used 1994 emission rates which are significantly higher than current emissions. EPA believes that the health protective air dispersion modeling performed as part of the petition and described in detail in the proposed rule resulted in higher concentrations than would monitoring around facilities.

EPA cannot consider the health effects of emissions within facility boundaries. That is the purview of the Occupational Safety and Health Administration.

Comment: One commenter ( 102) recommended that a comparative analysis with the 1998 Office of Pollution Prevention and Toxics ( OPPT) assessment ( located in the docket) be done to fully assess the risks of MEK.

Response: EPA agrees with the comment, and EPA conducted a comparison of the 1998 OPPT assessment and the assessment in the proposal to delist MEK.

The assessment presented in the petition to delist MEK estimated a maximum annual average MEK concentration of 1.2 mg/ m3. It used the ISCST3 model, which is a refined air dispersion model that predicts an annual average by averaging 8,760 hours of actual meteorological data. The ISCST3 model predicted a maximum 24 hour average MEK concentration of 10 mg/ m3.

The 1998 OPPT study estimated maximum 24 hour average concentrations of 100 200 mg/ m3. It used a screening model similar to the SCREEN3 model and predicted 1 hour average concentrations under defined meteorological conditions with the assumption that the receptor is always directly downwind from the source. Such screening model runs typically result in high air concentrations as compared to the ISCST3 model. EPA would expect the difference in concentrations to be as high as a factor of 10. In addition, the OPPT study applied a multiplicative factor to predict typical ( 5), stagnant ( 10), and maximum ( 60) acute impacts. Thus, the difference between the two model results can be attributed to the multiplicative factors and differences between a refined and screening model.

5.0 Miscellaneous Comments Comment: One commenter ( 92) recommended that EPA not wait for the formal IRIS review of MEK or the VCCEP results to make a final decision regarding delisting of MEK, as there was enough evidence to delist MEK without the additional information. Another commenter ( 99) asserted that if the new IRIS RfC is different from the proposed RfC, then the 16 petition should be reconsidered and an additional public comment period should be allowed giving the public an opportunity to comment on EPA = s decision. This commenter also stated that the results of the VCCEP should be concluded before the comments on the delisting are due.

Response: Regarding the first comment, EPA waited to make a final decision to delist MEK until the 2003 IRIS RfC was determined and until the information submitted by industry under the VCCEP was reviewed in case the results of each of these processes altered our decision to remove MEK from the HAP list.

Regarding the second comment, EPA considers an additional comment period unnecessary for a number of reasons. First, EPA explicitly solicited comment on the effect of a difference between the prospective RfC and the RfC resulting from the completed IRIS assessment. EPA specifically requested comments on the decision in light of potential values for the RfC of 9 mg/ m3, 3 mg/ m3 and 1 mg/ m3. The 2003 RfC of 5 mg/ m3 is in the middle of the range upon which EPA solicited comment. Second, while the 2003 RfC is lower than the prospective RfC, the result of this change was only to increase the HQ for the maximum annual average ambient exposure from 0.1 to 0.2 ( 20 percent of the RfC). This HQ is well below a level of concern.

In addition, EPA judges that the exposures to MEK of actual persons living in the immediate vicinity of an MEK emission source would more typically be at least a factor of 2 to 10 less than the predicted maximum ambient concentration presented in the petition of 1 mg/ m3. This is because the concentration of MEK declines very rapidly as the plume disperses, and the analysis showed that people do not live at the point of maximum concentration. Therefore, actual exposed individuals would be subject to MEK concentrations less than 1 mg/ m3. If EPA were to replace the maximum ambient concentration with a more realistic exposure scenario, it would yield an HQ less than 0.2. Based on the current information, and given the conservative nature of the parameters used to estimate the maximum exposure, and because the petition and subsequent analyses characterize the vast majority of MEK exposures from stationary sources, EPA concludes that by applying the RfC of 5 mg/ m3, potential ambient exposures to MEK may not reasonably be anticipated to cause adverse human health effects.

With respect to the results of the VCCEP, EPA found it unnecessary to extend the public comment period until after the review of the industry submitted information was complete. This is because the industry provided no new information to EPA that was not already available. Therefore, there was no new information upon which to solicit comments.

Comment: Several commenters ( 87, 91, 104, 120) noted that the interactions with nhexane and other ketones have not been sufficiently investigated should the MEK emissions increase. These commenters stated that MEK interactions with n hexane have been shown to increase neurotoxicity of n hexane. 17 Response: EPA stated in the preamble to the proposed rule that MEK has been shown to potentiate the neurotoxicity of other solvents in experiments with laboratory animals when both MEK and the other solvent are present in high concentrations. EPA also stated that studies of occupationally exposed populations ( as reviewed by Noraberg and Alien Soborg, 2000) provide some evidence of possible interactions in humans. EPA reviewed the occupational epidemiology literature in more depth during the development of the final RfC for MEK. These findings are summarized in the Toxicological Review for MEK ( http:// www. epa. gov/ iris/ toxreviews/ 0071 tr. pdf, section 4.4.4). Available occupational studies involving multiple chemical exposures do not provide information adequate to clearly establish an interaction between MEK and other neurotoxic solvents in humans. In studies suggesting a potential interaction, neurotoxicity has been observed only in workplace populations exposed to solvent mixtures where reported MEK air concentrations reached levels at or above the Threshold Limit Value ( TLV) ( 200 ppm or 590 mg/ m3). EPA concluded that the concerns for chemical interactions are especially diminished at the low levels seen in this assessment: less than 1 mg/ m3 for chronic exposures, 10 mg/ m3 for 24 hour exposures and 25 mg/ m3 for a 1 hour exposure. These exposures are all well below the reversible effects level of 590 mg/ m3. Therefore, EPA does not expect possible potentiation of n hexane by MEK at the low environmental concentrations that would be associated with industrial releases.

Comment: One commenter ( 91) was concerned that MEK was detected by the National Health and Nutrition Examination Survey in biomonitoring programs.

Response: EPA acknowledged in the preamble to the proposed rule that MEK has been reported to be found in blood. EPA also stated that the data indicated the source of the MEK is likely a by product of normal human metabolism, and it is reasonable to expect it did not result from an air exposure to MEK at the concentrations seen in the ambient air.

Comment: One commenter ( 99) requested that EPA consider the role of MEK as an ozone precursor in deciding the petition.

Response: EPA stated in the preamble to the proposed rule that it was inappropriate to consider the role of MEK as an ozone precursor because the Adual structure ( differentiating between HAP and criteria pollutants/ precursors) would lose its significance if EPA were to include substances on the HAP list solely as a result of their contribution to concentrations of criteria air pollutants.@ Specifically, the structure of the CAA is best protected by including compounds on the HAP list only where such inclusion is warranted based upon the HAP noncriteria pollutant related effects. This interpretation is supported by the following prohibition related to listing of new HAP contained in CAA section 112( b)( 2): ANo air pollutant which is listed under section 7408( a) of this title [ the criteria pollutant list] may be added to the list under this section, except that the prohibition of this sentence shall not apply to any pollutant which independently meets the listing criteria of this paragraph and is a precursor to a pollutant which is listed under section 7408( a) . . ..@ 18 Comment: One commenter ( 99) stated that decisions to list or delist are governed by the precautionary principle. The commenter stated that, Ain considering whether a petitioner has met the heavy burden of demonstrating that a substance should be removed from the hazardous air pollutant list, the precautionary principle requires that EPA resolve uncertainty in favor of more protection, not less. The recognition of uncertainty in the listing and delisting process does not give EPA to delist a chemical based on incomplete and outdated information as it has proposed to do with MEK.@

Response: EPA does not believe it is appropriate to require that all uncertainty be resolved in favor of not delisting. Such a requirement of absolute certainty is inconsistent with EPA's interpretation of the requirement that to delist a HAP, EPA must determine that there are Aadequate 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 effect to human health or adverse environmental effects.@ As explained in denying the petition to delist methanol, EPA does " not interpret CAA section 112( b)( 3)( C) to require absolute certainty that the pollutant will not cause adverse effects on human health . . . before it may be deleted from the list. The use of the terms > adequate= and > reasonably= indicate that EPA must weigh the potential uncertainties and their likely significance.@ ( See 66 FR 21929  21930, May 2, 2001.) For the reasons explained above, EPA determined that this burden has been met here.

Comment: One commenter ( 87) asserted that EPA has not adequately considered the odor problems associated with MEK. The commenter stated that odors can cause neurological problems such as fatigue, dizziness, headache, and nausea resulting in a diminished quality of life. The commenter also stated that odor thresholds for MEK have been reported in the range of 6 250 mg/ m3, and the estimates presented in the proposed rule for a 1 hour maximum concentration near MEK sources is 25 mg/ m3, which is within the range of the reported odor thresholds. The commenter also suggested that EPA recognize that the risk to sensitive individuals could increase after delisting.

Response: While EPA does not expressly consider odor as a health endpoint, EPA considers the physiological effects of chemical exposures, including the neurological effects that the commenter described. In the proposed rule, EPA stated the following, @ 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 of 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 in animal tissues specifically prepared and examined for neurohistopathology ( Cavender et al., 1983). Also, ten of ten rats exposed to MEK at 17,700 19 mg/ m3 and higher for 8 hours/ day, 7 days/ week, died in the seventh week of exposure without neurological symptoms or histopathology@ ( Altenkirch et al., 1978).

Regarding sensitive individuals, EPA could not identify any specific data that address the potential differences in susceptibility to adverse effects from MEK exposure. In the MEK Toxicological Review in support of the IRIS assessment, EPA did note that AThe potential exists for increased susceptibility to neurotoxicity, hepatotoxicity, and renal toxicity following exposure to MEK in combination with certain other solvents . . ..@ The potentiating effects of MEK on the toxicity of other solvents have only been demonstrated at relatively high exposure concentrations ( 200  1,000 ppm or 590  2950 mg/ m3).

Comment: One commenter ( 65) recommended changing the hazardous waste regulations that apply to MEK as follows: remove MEK as a listed toxicity characteristic in 40 CFR 261.64; remove MEK as a toxic constituent in part 261, appendix VIII; and remove MEK from the F005 listing, but it may be appropriate to add it to F2003 listing.

Response: EPA was petitioned under CAA section 112( b)( 3) to remove MEK from the CAA section 112 HAP list. This is the only action under consideration as part of the final rule.

6.0 References Altenkirch, H., G. Stoltenburg, and H. M. Wagner. ( 1978) Experimental studies on hydrocarbon neuropathies induced by methyl ethyl ketone ( MEK). J Neurol 219: 159 70.

Cavender, F. L., H. W. Casey, H. Salem, et al. ( 1983) A 90 day vapor inhalation toxicity study of methyl ethyl ketone. Fundam Appl Toxicol 3( 4): 264 70.

Cox, G. E., D. E. Bailey, and K. Morgareidge. ( 1975) Toxicity studies in rats with 2 butanol including growth, reproduction and teratologic observations. Food and Drug Research Laboratories, Inc. Waverly, NY. Report No. 91MR R 1673.

Deacon, MM, Pilny, MD, John, JA, et al. ( 1984) Embryo and Fetotoxicity of Inhaled Methyl Ethyl Ketone in Rats. Toxicol Appl Pharmacol 59: 620 22.

Dick, R. B., E. F. Krieg Jr., J. Setzer, B. Taylor. ( 1992) Neurobehavioral effects from acute exposures to methyl isobutyl ketone and methyl ethyl ketone. Fundam Appl Toxicol 19( 3): 453 73.

Lowengart, R. A., J. M. Peters, C. Cicioni, et al. ( 1987) Childhood leukemia and parents' occupational and home exposures. J Natl Canc Inst 79( 1): 39 46.

Noraberg J, Arlien Søborg P. 2000. Neurotoxicology 21( 3): 409 18. 20 OECD. ( 1997) SIDS Screening Information Assessment Report for Methyl Ethyl Ketone. ( SIAM 6 1997)

Saida, K., J. R. Mendell, and H. S. Weiss. ( 1976) Peripheral nerve changes induced by methyl n butyl ketone and potentiation by methyl ethyl ketone. J Neuropath Exp Neurol 35( 3): 205 25.

Schwetz, B. A., Leong, BKJ, Gehring, PJ ( 1974) Embryo and Fetotoxicity of Inhaled Carbon Tetrachloride, 1,1 dicloroethane and Methyl Ethyl Ketone in Rats. Toxicol Appl Pharmacol 28: 452 64.

Schwetz, B. A., T. J. Mast, R. J. Weigel, et al. ( 1991) Developmental toxicity of inhaled methyl ethyl ketone in mice. Fundam Appl Toxicol 16: 742 8.

U. S. EPA. ( 1992) Integrated Risk and Information System. Online at: http:// www. epa. gov/ iris/ subst/ 0071. htm U. S. EPA. ( 1994) Methods for Derivation of Inhalation reference Concentrations and Application of Inhalation Dosimetry. EPA/ 600/ 8 90/ 066F. Online at http:// cfpub2. epa. gov/ ncea/ raf/ recordisplay. cfm? deid= 71993 U. S. EPA. ( 1999) Guidelines for Carcinogen Risk Assessment [ Review Draft]. Risk Assessment Forum. NCEA F 0644 http:// www. epa. gov/ ncea/ raf/ cancer/ htm U. S. EPA. ( 2000) Benchmark Dose Technical Guidance Document [ External Review Draft]. Online at: http:// cfpub2. epa. gov/ ncea/ raf/ recordisplay. cfm? deid= 20871 U. S. EPA. ( 2002) A Review of the Reference Dose and Reference Concentration Processes. EPA/ 630/ P 02/ 002F. Online at: http:// cfpub2. epa. gov/ ncea/ raf/ recordisplay. cfm? deid= 55365 U. S. EPA ( 2003) Toxicological Review of Methyl Ethyl Ketone. EPA 635/ R 03/ 009 Online at: http:// www. epa. gov/ iris Woo, Y T., D. Lai, J. L. McLain, et al. ( 2002) Use of mechanism based structure activity relationships analysis in carcinogenic potential ranking for drinking water disinfection byproducts Environ Health Persp 110 ( Suppl. 1): 75 8.

Zimmermann, FK, Mayer, VM, Scheel, I, et al. ( 1985) Acetone, methyl ethyl ketone, ethyl acetate, acetonitrile and other polar aprotic solvents are strong inducers of aneuploidy in Saccharomyces cerevisiae. Mutat Res 149( 3): 339 351. 21 7.0 Commenters Commenters on the MEK Delisting Proposal Document Number I Author Company/ Affiliation 0057 Anonymous Unspecified 0058 Pat Foust IPS Corporation 0059 Anonymous Quality/ Environmental Systems Assistant from Minnesota Unspecified sheet metal fabrication, welding, and painting company 0060 J. D. Robinson, Director National Environmental Health & Safety Council ( NEHSC)

0061 Richard Winn, MS CSP Safety Consulting Services 0062 Sandra Berg, President CEO Ellis Paint Company 0063 Scott Davidson, President Johnson Laminating & Coating, Inc.

0064 Donald Kugelberg, Technical Director Johnson Laminating & Coating, Inc.

0065 Benjamin Garth Studebaker, CSP Videojet Technologies, Inc.

0068 Don Dickens, Manager Halton Chemical, Inc.

0069 Edward W. Kifer, Director of R& D Ranbar Electrical Materials 0070 W. Pat Foust, Chief Operating IPS Weldon 22 Document Number I Author Company/ Affiliation Officer 0071 Harold Henderson, President Trail Chemical Corporation 0072 Marc Germain, Eng. Technical Service Supervisor Brenntag Canada Inc.

0073 Jeffrey Julis, Technical Director EMCO Chemical Distributors, Inc.

0074 Thuc Nguyen, Technical Services Manager Univar Canada Ltd.

0075 Naresh Patel, President IPS Corporation 0076 Joseph Lucas, President Inland Technology, Incorporated 0077 Richard Hatfield, Director of Environmental Affairs The Haartz Corporation 0079 Line Cormier, Environmental Coordinator Peinture Can Lak, Inc.

0080 Ram Singhal, Director, Regulatory & Government Relations Flexible Packaging Associations 0081 Deborah Chapin, Kodak Park Environmental Services Eastman Kodak Company 0082 Rich Raiders, Manager, Clean Air Act Programs ATOFINA Chemicals, Inc.

0083 Robert Colby, Chair ALAPCO Air Toxics Committee & Lloyd Eagan, Chair STAPPA/ ALAPCO 23 Document Number I Author Company/ Affiliation STAPPA Air Toxics Committee 0084 Hexcel Corporation Hexcel Corporation 0085 DuPont Performance Coatings DuPont Performance Coatings 0086 Jeremy Tovey, CHMM, HSE Manager Akzo Nobel Coatings, Inc.

0087 Catherine Witherspoon, Executive Officer & Joan Denton, Ph. D., Director California Environmental Protection Agency, State of California 0088 Dwayne Meyer, Director Technical Resources Carboline Company 0089 Laura Schubert, EH& S Technician US Paint Corporation 0090 Marcia Kinter, VP Government Affairs The Graphic Arts Coalition 0091 P. Michael Peck, Director of Solvent Technology Dynamold Solvents, Inc.

0092 Desi Chari, Senior Environmental Manager Rohm and Haas Company 0093 Geoffrey Cullen, Director of Government Relations The Can Manufacturers Institute ( CMI)

0094 John Festa, Ph. D., Senior Scientist American Forests & Paper Association 24 Document Number I Author Company/ Affiliation 0096 Identical to 120 0097 Suzie Brindle, Program Organizer Clean Water Action 0098 James Witkowski, Air Subcommittee Chair South Carolina Chamber of Commerce, Environmental Technical Committee 0099 Vicki Patton, Senior Attorney Environmental Defense 100 Frank Black Cloud Spirit Lake Tribe 101 Larry Metzman Quaker City Chemicals, Inc.

102 Henry Weltman Consultant, Retired Senior Engineering Specialist from General Dynamics/ Fort Worth Division 103 Roy Cobb, Jr., Senior Environmental Counsel Smurfit Stone Container Corporation 104 Northeast States for Coordinated Air Use Management ( NESCAUM) NESCAUM 105 Identical to 104 106 Michael Cudahy, Technical Manager FRY Technology 107 Eric Clark, Government Relations Synthetic Organic Chemical Manufacturers Association ( SOCMA)

108 Courtney Price, VP, Chemstar, The The American Chemistry 25 Document Number I Author Company/ Affiliation American Chemistry Council Council Ketones Panel ( Petitioner)

109 The American Chemistry Council Ketones Panel The American Chemistry Council Ketones Panel ( Petitioner)

110 The American Chemistry Council Ketones Panel The American Chemistry Council Ketones Panel ( Petitioner)

111 Identical to 93 112 R. Scott Thomas, Corporate Director, Environmental Affairs The Sherwin Williams Company 113 Valerie Ughetta, Director of Stationary Sources Alliance of Automobile Manufacturers ( The Alliance)

114 Allen Stegman, Corporate Manger of Environmental Affairs The Valspar Corporation 115 Fred Scholer, Director of R& D Hercules Chemical Company Inc.

116 Identical to 112 117 Identical to 99 118 Identical to 97 119 Phillip Pesola, Executive VP & Hordan Dern, Delta Laboratories, Inc. 26 Document Number I Author Company/ Affiliation Engineering Manager 120 Jennifer Sass, Senior Scientist & Jon Devine, Jr., Senior Attorney Natural Resources Defense Council 121 Linda Greer & John Devine Natural Resources Defense Council 122 Identical to 103 124 Alison Keane & David Darling National Paint & Coatings Association ( NPCA)

126 Daniel Peterson, Jr., VP Operations Koala Corporation 127 Larry Brandenburger, VP R& D Valspar Corporation 128 Joann Held, Chief Bureau of Air Quality Evaluation NJ Dept of Environmental Protection 129 Samuel Wolfe, Assistant Commissioner Environmental Regulation, State of NJ 130 Technology Transfer Network National Air Toxics Assessment Technology Transfer Network National Air Toxics Assessment 131 Andre Hozer, President DURO LAK INC I Document number in rulemaking docket OAR 2003 0028


[Federal Register Volume 85, Number 115 (Monday, June 15, 2020)]
[Notices]
[Pages 36256-36257]
[FR Doc No: 2020-12849]

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DEPARTMENT OF TRANSPORTATION

Federal Aviation Administration

[Docket No. FAA-2019-0781]

Agency Information Collection Activities: Requests for Comments;
Clearance of Renewed Approval of Information Collection: Automatic
Dependent Surveillance Broadcast (ADS-B) Out Performance Requirements
To Support Air Traffic Control (ATC) Service

AGENCY: Federal Aviation Administration (FAA), DOT.

ACTION: Notice and request for comments.

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SUMMARY: In accordance with the Paperwork Reduction Act of 1995, the
FAA invites public comments about our intention to request the Office
of Management and Budget (OMB) approval to renew a previously approved
information collection. On May 28, 2010, the FAA published the final
rule, entitled Automatic Dependent Surveillance Broadcast (ADS-B)
Equipage Mandate To Support Air Traffic Control Service. 75 FR 30160.
As of January 2, 2020, when operating in the airspace designated in 14
CFR 91.225(a), (b) and (d), operators must be equipped with ADS-B Out
avionics that meet the performance requirements of 14 CFR 91.227. ADS-B
supports the aircraft surveillance needs of the FAA by requiring
avionics equipment that meet the performance requirements of 14 CFR
91.227 and continuously transmit aircraft information to be received by
the FAA, via automation, for use in providing air traffic surveillance
services. ADS-B is transforming all segments of aviation (e.g., real-
time precision shared situational awareness, and advanced applications
for pilots and controllers alike).

DATES: Written comments should be submitted by July 15, 2020.

ADDRESSES: Interested persons are invited to submit written comments on
the proposed information collection to the Office of Information and
Regulatory Affairs, Office of Management and Budget. Comments should be
addressed to the attention of the Desk Officer, Department of
Transportation/FAA and sent via email to<EMAIL_ADDRESS>
or faxed to<PHONE_NUMBER>, or mailed to the Office of Information and
Regulatory Affairs, Office of Management and Budget, Docket Library,
Room 10102, 725 17th Street NW, Washington, DC 20503.

FOR FURTHER INFORMATION CONTACT: For further questions concerning this
action, contact Ms. Ammyanna Williams, Group Manager (A), Surveillance
and Broadcast Services, AJM-42, Air Traffic Organization, Federal
Aviation Administration, by email at<EMAIL_ADDRESS>or
(202) 267-4128.

SUPPLEMENTARY INFORMATION:
    Public Comments Invited: You are asked to comment on any aspect of
this information collection, including (a) whether the proposed
collection of information is necessary for FAA's performance; (b) the
accuracy of the estimated burden; (c) ways for the FAA to enhance the
quality, utility, and clarity of the information collection; and, (d)
ways that the burden could be minimized without reducing the quality of
the collected information. The agency will summarize and/or include
your comments in the request for OMB's clearance of this information
collection.
    OMB Control Number: 2120-0728.
    Title: Automatic Dependent Surveillance-Broadcast (ADS-B) Out
Performance Requirements to Support Air Traffic Control (ATC) Service.
    Form Numbers: None.
    Type of Review: Renewal of an information collection.
    Background: The Federal Register Notice with a 60-day comment
period soliciting comments on the following collection of information
was published on October 16, 2019. 84 FR 55370. The FAA received two
non-substantive comments from the same individual that simply restated
the docket and OMB Control Number. Neither of these comments required
any action.
    Title 14 CFR part 91 includes requirements for certain avionics
equipment on aircraft operating in specified classes of airspace within
the United States National Airspace System (NAS). As of January 2,
2020, unless otherwise authorized by ATC, all aircraft operating in the
airspace identified in Sec.  91.225 must comply with the ADS-B Out
equipage and performance requirements in Sec. Sec.  91.225 and 91.227.
    Title 14 CFR 91.225(f) requires that each person operating an
aircraft equipped with ADS-B Out must always operate such equipment in
the transmit mode unless certain conditions are met. As such, ADS-B
equipment will continuously transmit aircraft information in ``real
time'' to a dedicated network of FAA ground receivers. There are
currently two types of ADS-B equipment approved for use within the
United States: 1090-megahertz (MHz) Mode S extended squitter (ES) and
978 MHz Universal Access Transceiver (UAT).\1\
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    \1\ Aircraft that only fly below 18,000 feet and only in the
U.S. can opt instead of Mode S ES (1090ES) for a dedicated 978 MHz
UAT. The 978 MHz UAT frequency will allow aircraft owners/operators
to keep an existing Mode C or Mode S transponder.
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    ADS-B Out transmitters broadcast an equipped aircraft's position,
altitude, heading, ground speed, vertical speed, call sign (flight
identification), and International Civil Aviation Organization (ICAO)
24-bit aircraft address to dedicated ADS-B ground stations. As ADS-B
data is automatically broadcasted by each equipped
aircraft,2 3 to ADS-B ground stations, within range, the
collected data is integrated with traditional radar targets and used by
air traffic controllers to support separation assurance and traffic
flow management.
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    \2\ These ADS-B data broadcasts can also be received by other
aircraft, appropriate equipped for ADS-B In, to allow pilots
knowledge of nearby air traffic.
    \3\ General aviation operators who equip with 978 MHz or UAT
receivers can also benefit from having access to a variety of no-
cost flight information services, including near-real time composite
weather radar images, winds, lightning, and terminal weather
forecasts.
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    This network of dedicated ground stations receives and send ADS-B
collected data to FAA automation systems to process and then relay
information to ATC displays. ADS-B collected data is also used for
enhanced safety alerting functions such as a minimum safe altitude
warnings and traffic conflict alerts. Operationally, ADS-B collected
information is continually integrated with radar returns to create a
safer and more efficient NAS. ADS-B collected data is integrated into
automation platforms at 24 FAA en route ATC facilities, which
encompasses 20 continental U.S. En Route Automation Modernization
(ERAM) \4\ sites, and 4 overseas Microprocessor-En Route Automated
Radar Tracking System (MEARTS).\5\

ADS-B collected data is also fused into flight tracker automation at
155 Terminal Radar Approach Control Facilities (TRACONs).\6\
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    \4\ En Route Automation Modernization (ERAM) is used at FAA high
altitude en-route centers. ERAM processes flight and surveillance
data, provides communications and generates display data to air
traffic controllers.
    \5\ Microprocessor-En Route Automated Radar Tracking System
(MEARTS) is an automated radar and radar beacon tracking system
capable of employing both short-range (airport surveillance radar)
and long range (air route surveillance radar) radars. Install at 4
overseas MEARTS facilities to include Anchorage, Honolulu, San Jan
and Guam.
    \6\ Terminal Radar Approach Control Facilities (TRACONs) are
facilities where air traffic controllers use integrated radar, ADS-B
and Wide-Area Multilateration (WAM) data to guide aircraft
approaching and departing airports generally within a 30- to 50-mile
radius up to 10,000 feet, as well as aircraft that may be flying
over that airspace.
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    ADS-B collected data provides (ATC) with a more accurate and
timelier surveillance picture allowing ATC to make more-informed
decisions, quickly and effectively. The use of ADS-B collected data has
enabled more efficient aircraft separation and increased aircraft
capacity in the NAS. In many areas of the NAS, ADS-B collected data
provides better surveillance at lower altitudes and in areas that
previously had limited-to-no radar coverage.
    This collection of ADS-B broadcasted data supports the aircraft
surveillance needs of the FAA. ADS-B Out moves ATC from a radar-based
system to a satellite-derived aircraft location system with
capabilities for reducing lateral and longitudinal separation
standards. Aircraft equipped with ADS-B Out enhance the air traffic
controller's awareness of aircraft in the airspace. Radars used today
can take anywhere from 5 to 12 seconds to update an aircraft's
position. ADS-B equipment provides ATC with updated aircraft
information almost every second. This ``real time'' information
collection enables controllers to quickly and effectively identify and
resolve potentially hazardous situations. Moreover, ADS-B coverage
exists at lower altitudes than some current ATC radars.
    ATC is currently using ADS-B collected data to control air traffic
across the nation. The collection of ADS-B Out broadcasted information
from an aircraft via an automated receiver on the ground is solely done
through electronic means. The ADS-B ground stations are small and
easily maintained and can be placed in areas where radar use is not
possible. New, state-of-the-art computer systems have been deployed to
ATC facilities across the country. These systems, the Standard Terminal
Automation Replacement System (STARS) and the En Route Automation
Modernization (ERAM), are enabling ADS-B capabilities for FAA air
traffic controllers.
    As part of the renewal process, OMB requests an estimate of the
hour burden imposed to the public for the collection of information.
ADS-B equipment is automatic because it periodically transmits position
information with no pilot or operator involvement required. ADS-B data
is collected electronically, without input by a human operator.
Subsequently, a 1-second burden is submitted as a placeholder to allow
entry in OMB's burden inventory.
    Respondents: As of May 1, 2020, FAA network has detected 122,051
\7\ aircraft as having successfully installed ADS-B Out equipment. The
FAA anticipates approximately another 57,000 General Aviation (GA)
aircraft [19,000 as a placeholder] over the next three years, will
eventually be equipping with ADS-B Out equipment and automatically
broadcasting data to be collected and used by ATC to support separation
assurance and traffic flow management.
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    \7\ 6,527 air carrier, 103,140 general aviation (GA), 3,037
International Air Carrier, 6,431 International GA and 2,916 U.S.
Military and U.S. Special Use.
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    Frequency: ADS-B information is collected automatically by a
dedicated network of FAA ground receivers each time an aircraft,
continuously and in almost real-time, transmits its identity and GPS-
derived navigational information. Title 14 CFR 91.225(f) requires that
each person operating an aircraft equipped with ADS-B Out must always
operate such equipment in the transmit mode unless certain conditions
are met.
    Estimated Average Burden per Response: 1 second (placeholder).
    Estimated Total Annual Burden on Respondents: 39 hour
(placeholder).

    Issued in Washington, DC, on June 10, 2020.
James C. Tertocha,
Service Performance and Sustainment Program Manager (AJM-422),
Surveillance and Broadcast Services (SBS), Program Management
Organization, Air Traffic Organization, Federal Aviation
Administration.
[FR Doc. 2020-12849 Filed 6-12-20; 8:45 am]
BILLING CODE 4910-13-P