 III. Appropriate and Necessary Finding
A. Summary of EPA's Finding that it is Appropriate and Necessary to Regulate EGUs to Address Public Health and Environmental Hazards Resulting from Emissions of Hg and Non-Hg Hazardous Air Pollutants (HAP) from EGUs
	In the preamble to the proposed rule, we confirmed our December 2000 finding that it is appropriate to regulate emissions of Hg and other HAP from EGUs because emissions of those pollutants pose hazards to public health and the environment, and EGUs are the largest or among the largest contributors of many of those HAP. We also confirmed that it is necessary to regulate EGUs under section 112 for a variety of reasons, including that hazards to public health and the environment posed by HAP emissions from EGUs remain after imposition of the requirements of the CAA. Our confirmation of the December 2000 finding was supported in part by several new analyses of the hazards to public health posed by both mercury and non-mercury HAP.
      Congress did not define the phrase "appropriate and necessary" in section 112(n)(1)(A). Rather, Congress expressly delegated to the Agency the authority to interpret and apply those terms. Courts have interpreted the terms "appropriate" and "necessary" in other provisions of the CAA and other statutes, and concluded that those terms convey upon the Agency a wide degree of discretion. We evaluate the terms "appropriate" and "necessary" within the statutory context in which they appear to determine the meaning of the words.
      In this context, we interpret the statute to require the Agency to find it appropriate to regulate EGUs under CAA section 112 if the Agency determines that the emissions of one or more HAP emitted from EGUs pose an identified or potential hazard to public health or the environment at the time the finding is made. The hazard to public health or the environment may be the result of HAP emissions from EGUs alone or the result of HAP emissions from EGUs in conjunction with HAP emissions from other sources. In addition, EPA must find that it is appropriate to regulate EGUs if it determines that any single HAP emitted by utilities poses a hazard to public health or the environment. We further interpret the term "appropriate" to not allow for the consideration of costs in assessing whether HAP emissions from EGUs pose a hazard to public health or the environment. Finally, we may conclude that it is appropriate, in part, to regulate EGUs if we determine that there are controls available to address HAP emissions from EGUs.
      The Agency must find it necessary to regulate EGUs under section 112 if the identified or potential hazards to public health or the environment will not be adequately addressed by the imposition of the requirements of the CAA. Moreover, it may be necessary to regulate utilities under section 112 for a number of other reasons, including, for example, that section 112 standards will assure permanent reductions in EGU HAP emissions, which cannot be assured based on other requirements of the CAA. We maintain that we must find it necessary based on such a finding even if regulation under section 112 will not fully resolve the identified hazard to public health or the environment. We may also find it necessary to regulate EGUs under section 112 to further the policy goal of supporting international efforts to reduce HAP emissions, including Hg.
	In this section, we summarize the finding as reported in the preamble to the proposed rule. Specifically, we address the Agency's determination that it is appropriate and necessary to regulate coal- and oil-fired EGUs under CAA section 112. The extensive analyses summarized in the preamble to the proposed rule and documented in several Technical Support Documents[,] confirmed that it remains appropriate and necessary today to regulate EGUs under section 112. The analyses demonstrated that it is appropriate to regulate emissions from coal- and oil-fired EGUs under CAA section 112 because: 1) Hg and non-Hg HAP continue to pose a hazard to public health, and U.S. EGU emissions cause and/or contribute to this hazard; 2) Hg and some non-Hg HAP pose a hazard to the environment; 3) U.S. EGU emissions are still the largest domestic source of U.S. Hg, HCl, and HF emissions, and a significant source of other HAP emissions; 4) Hg emissions from individual EGUs leads to excess local deposition in areas directly surrounding those individual EGUs (not solely the result of regionally transported emissions), and will not be adequately addressed through reductions in regional levels of Hg emissions, requiring controls to be in place at all U.S. EGU sources that emit Hg; 5) Hg emissions from EGUs affect not only deposition, exposures, and risk today, but may contribute to future deposition, exposure and risk due to the processes of reemission of Hg that occur given the persistent nature of Hg in the environment  -  the delay in issuing Hg regulations under section 112 has already resulted in several hundred additional tons of Hg being emitted to the environment, and that Hg will remain part of the global burden of Hg; and 6) effective controls for Hg and non-Hg HAP are available for U.S. EGU sources.
EPA concluded that Hg emissions from U.S. EGUs are a public health hazard today due to their contribution to Hg deposition that leads to potential MeHg exposures above the RfD. EPA also concluded that U.S. EGU Hg emissions contribute to environmental concentrations of Hg that are harmful to wildlife and can affect production of important ecosystem services, including recreational hunting, and fishing, and wildlife viewing. EPA further concluded that non-Hg HAP emissions from U.S. EGU are a public health hazard because they contribute to elevated cancer risks. Finally, EPA concluded that U.S. EGU's HCl and HF emissions contribute to acidification in sensitive ecosystems and, therefore, pose a risk of adverse effects on the environment. 
      The analyses demonstrated that it is necessary to regulate emissions from coal- and oil-fired EGUs under CAA section 112 because 1) Hg emissions from EGUs remaining in 2016  still pose a hazard to public health and the environment in the absence of regulations under Section 112 that would be required to be implemented at that time, 2) U.S. EGU emissions of Hg after imposition of the requirements of the CAA are projected to be 29 tons per year in 2016, the same as the level of Hg emitted today, 3) EGUs are the largest source of Hg in the U.S. and thus contribute to the risk associated with exposure to MeHg, 4) we cannot be certain that the identified cancer risks attributable to EGUs will be addressed through imposition of the requirements of the CAA, 5)the environmental hazards posed by acidification will not be fully addressed through imposition of the CAA, 6) regulation under section 112 is the only way to ensure that HAP emissions reductions that have been achieved since 2005 remain permanent, 7) direct control of Hg emissions affecting U.S. deposition is only possible through regulation of U.S. emissions; we are unable to control global emissions directly.  
a. Finding that U.S. EGU Hg Emissions Continue to Pose a Hazard to Public Health and the Environment
      In support of the finding that U.S. EGU mercury emissions are a hazard to public health, in the preamble to the proposed rule, EPA reported the results of a national scale assessment of mercury risk to populations with high consumption of self-caught freshwater fish, which is the population most likely to experience elevated risk from U.S. EGU mercury emissions. This assessment was based on detailed emissions, air quality, exposure, and risk modeling, which provided estimates of the watersheds in which populations with high levels of fish consumption experience the potential for risk due to deposition of mercury. The national scale mercury risk assessment ("the mercury risk assessment") of the hazard to public health posed by U.S. EGU Hg emissions focused on comparisons to the RfD of exposures caused or contributed to by U.S. EGU Hg emissions. In the mercury risk assessment, almost all (98 percent) of the more than 2,400 watersheds for which we identified fish tissue data, exceeded the RfD, above which there is the potential for an increased risk of adverse effects on human health. U.S. EGU-attributable deposition of Hg contributes to a large number of those watersheds in which total potential exposures to MeHg from all sources exceed the RfD and, thus, pose a hazard to public health. We focused on the watersheds to which EGUs contributed at least 5 percent of the total Hg deposition and related MeHg exposures at a watershed, or contributed enough Hg deposition to result in potential MeHg exposures above the RfD, regardless of the additional deposition from other sources of Hg deposition. This approach is likely to understate risk because any contribution of Hg to watersheds where potential exposures to MeHg exceed the RfD poses a public health hazard. Thus, because we found a large percentage of watersheds with populations potentially at risk even using this approach, we have confidence that emissions of Hg from U.S. EGUs are causing a hazard to public health, as there are additional watersheds that have contributions at lower percent benchmarks.
      In total, the mercury risk assessment found an estimated 28 percent of sampled watersheds with populations that are potentially at risk from exposure to MeHg based on the contribution of U.S. EGUs. This total includes watersheds that are potentially at risk either because U.S. EGU attributable deposition is sufficient to cause potential exposures to exceed the reference dose even excluding the deposition from other U.S. and non-U.S. sources, or because the U.S. EGU-attributable deposition contributes greater than 5 percent of total deposition and total exposure from all sources is greater than the reference dose. 
      We found that at the 99[th] percentile fish consumption level for subsistence fishers, 22 percent of sampled watersheds where total potential exposures to MeHg exceed the RfD received at least 5 percent of Hg deposition from U.S. EGUs. Although the most complete estimate of potential risk is based on total exposures to Hg, including deposition from U.S. EGU sources, U.S. non-EGU sources, and global sources, the deposition resulting from U.S. EGU Hg emissions is large enough in some watersheds that persons consuming contaminated fish would have exposures that exceed the RfD even excluding consideration of the deposition from other non-U.S. EGU sources. Based on these considerations, we found that at the 99[th] percentile fish consumption level for subsistence fishers, in 12 percent of the sampled watersheds, U.S. EGUs are responsible for deposition that causes the RfD to be exceeded, even excluding consideration of the additional deposition from other sources.
      In addition, we highlighted in the preamble to the proposed rule that the estimate of where populations may be at risk from U.S. EGU-attributable Hg deposition is likely understated because the data on fish tissue MeHg concentrations that we were able to identify for the mercury risk assessment was limited in some regions of the U.S., such as Pennsylvania, with very high U.S. EGU attributable Hg deposition, and it is possible that watersheds with potentially high MeHg exposures were excluded from the risk analysis. In addition, due to limitations in our models and available data, we did not estimate risks in near-coastal waters, and some of these waters, such as the Chesapeake Bay, could have substantial EGU-attributable Hg deposition.
      Further, scientific studies have found strong evidence of adverse impacts on species of fish-eating birds with high bird-watching value, including loons, white ibis, and great snowy egrets. Studies have also shown adverse effects on insect-eating birds including many songbirds. Adverse effects in fish-eating mammals, such as mink and otter, include neurological responses (impaired escape and avoidance behavior) which can influence survival rates. Because EGUs contribute to Hg deposition in the U.S., we reasonably conclude that EGUs are contributing to the identified adverse environmental effects.
      Mercury emitted into the atmosphere persists for years, and once deposited, can be reemitted into the atmosphere by a number of processes, including forest fires and melting of snow packs. As a result, Hg emitted today can have impacts for many years. In fact, Hg emitted by U.S. EGUs in the past, including over the last decade is still affecting concentrations of Hg in fish today. Failing to control Hg emissions from U.S. EGU sources will result in long-term environmental loadings of Hg, beyond those loadings caused by immediate deposition of Hg within the U.S. Although we are not able to quantify the impact of U.S. EGU emissions on the global pool of Hg, U.S. EGUs contribute to that global pool. Controlling Hg emissions from U.S. EGUs helps to reduce the potential for environmental hazard from Hg now and in the future. The findings described above independently support a determination that it is appropriate to regulate HAP emissions from EGUs.
b. Finding that U.S. EGU Non-Hg HAP Emissions Continue to Pose a Hazard to Public Health and the Environment
      In addition to the mercury risk assessment, EPA also reported in the preamble to the proposed rule the results of 16 case studies of inhalation risks of cancer for U.S. EGUs for which we had 2007 to 2009 emissions data (based on the 2010 ICR) and that we anticipated would have relatively higher emissions of non-Hg HAP compared to other U.S. EGUs. The results of that analysis showed that of the 16 facilities modeled (4 facilities, 3 coal-fired facilities and 1 oil-fired facility), have estimated risks of greater than 1 in 1 million for the most exposed individual. Given Congress' determination that categories of sources which emit HAP resulting in a lifetime cancer risk greater than 1 in 1 million should not be removed from the section 112(c) source category list and should continue to be regulated under 112, risks above that level represent a hazard to public health such that it is appropriate to regulate EGUs under section 112.
      Although our case studies did not identify significant chronic non-cancer risks from acid gas emissions from the specific EGUs assessed, the Administrator remains concerned about the potential for acid gas emissions to add to already high atmospheric levels of other chronic respiratory toxicants and to environmental loading and degradation due to acidification. EGUs emit over half of the nationwide emissions of HCl and HF, based on 2010 emissions estimates. In addition, given that acidification affects many sensitive ecosystems across the country, it is appropriate to reduce emissions of this magnitude, which may aggravate acidification. The Administrator concluded that, in addition to the regulation of non-Hg HAP that cause elevated cancer risks, it is appropriate to regulate those HAP that are not known to cause cancer but are known to contribute to chronic non-cancer toxicity and environmental degradation, such as the acid gases. 
      These findings independently supported the determination that it remains appropriate to regulate HAP emissions from EGUs.
c. Finding that Effective Controls are Available to Reduce Hg and Non-Hg HAP Emissions
      Particle-bound Hg can be effectively removed along with other flue gas PM (including non-Hg metal HAP) in primary or secondary PM control devices. Electrostatic precipitators, fabric filters, and wet FGD scrubbers are all effectively remove Hg; the degree of effectiveness depends on the specific characteristics of the EGU and fuel types. Additionally, these devices all effectively remove Non-Hg metal HAP. Activated carbon injection is the most successfully demonstrated Hg-specific control technology. Acid gases are readily removed in typical FGD systems due to their solubility or their acidity (or both). The availability of controls for HAP emissions from EGUs supported the appropriate finding because sources will be able to reduce their emissions effectively and, thereby, reduce the hazards posed by HAP emissions from EGUs.
d. The Administrator's Finding that it Remains Necessary to Regulate Coal- and Oil-fired EGUs Under CAA Section 112
      EPA determined that in 2016, the hazards posed to human health and the environment by HAP emissions from EGUs will not be addressed; therefore, it is necessary to regulate EGUs under section 112. In addition, it is necessary to regulate EGUs under section 112 because the only way to ensure permanent reductions in U.S. EGU emissions of HAP and the associated risks to public health and the environment is through standards set under section 112.
      The Agency first evaluated whether it is necessary to regulate HAP emissions from EGUs "after imposition of the requirements of the CAA." As explained above, we interpret that phrase to require the Agency to consider only those requirements that Congress directly imposed on EGUs through the CAA as amended in 1990 and for which EPA could reasonably predict HAP emission reductions at the time of the Study. Nonetheless, the Agency recognizes that it has discretion to look beyond the Utility Study in determining whether it is necessary to regulate EGUs under section 112. Because several years have passed since the December 2000 Finding, we conducted an additional, updated analysis, examining a broad array of diverse requirements.
      Specifically, we analyzed EGU HAP emissions remaining in 2016. Our analysis included emission reductions anticipated from the proposed Transport Rule (finalized in June 2011 as the Cross State Air Pollution Rule); CAA section 112(g); the ARP; Federal, state, and citizen enforcement actions related to criteria pollutant emissions from EGUs; and some state rules related to criteria pollutant emissions. We included state requirements and citizen and state enforcement action settlements associated with criteria pollutants because those requirements may have a basis under the CAA. However, we did notconduct an analysis to determine whether the state requirements arebased on requirements of the CAA. As such, there may be instances where we should not have considered certain state rules or state and citizen suit enforcement settlements in our analysis, because those requirements are based solely in state law and are not required by the CAA as contemplated under section 112(n)(1)(A).  To the extent that these non-federal actions do not result in permanent reductions in Hg emissions, their inclusion in the baseline Hg emissions estimates for the national scale mercury risk analysis will result in an underestimate of the risks associated with U.S. EGU Hg emissions. We did not include in our analysis any state-only requirements or voluntary actions to reduce HAP emissions because there is no Federal backstop for those requirements and actions.
      Our analysis confirmed that Hg emissions from EGUs remaining in 2016 still pose a hazard to public health and the environment and, for that reason, it remains necessary to regulate EGUs under section 112. Specifically, we estimated that U.S. EGU emissions of Hg after imposition of the requirements of the CAA will be 29 tons per year in 2016, the same as the level of Hg that we estimated at the time of proposal would be emitted by U.S. EGUs today. As we stated above, we evaluated the hazards to public health and the environment from Hg based on the estimated Hg emissions in 2016 and found that a hazard exists. Because a hazard remains after imposition of the requirements of the CAA, we determined it is necessary to regulate EGUs.
      It is necessary to regulate HAP emissions from EGUs, even though the hazards from Hg will not be fully resolved through regulation under section 112. EPA finds that incremental reductions in Hg are important because as exposure above the RfD increases the likelihood and severity of adverse effects increases. 
      EGUs are the largest source of Hg in the U.S. and thus contribute to the risk associated with exposure to MeHg. By reducing Hg emissions from U.S. EGUs, this proposed rule will help to reduce the risk to public health and the environment from Hg exposure.
      We also find that it is necessary to regulate EGUs under section 112 based on non-Hg HAP emissions because we cannot be certain that the identified cancer risks attributable to EGUs will be addressed through imposition of the requirements of the CAA. In addition, the environmental hazards posed by acidification will not be fully addressed through imposition of the CAA.
      We also find it necessary to regulate EGUs because regulation under section 112 is the only way to ensure that HAP emissions reductions that have been achieved since 2005 remain permanent. Real reductions between 2005 and 2010 are attributable to state Hg regulations and to the Clean Air Interstate Rule (CAIR) and Federal enforcement actions that achieve Hg reductions as a co-benefit of controls for PM, NOX, and SO2 emissions. However, there are no national, federally binding regulations for Hg. State Hg regulations can potentially change or be revoked without EPA approval, and reductions that occur as a co-benefit of criteria pollutant regulations can also change. Furthermore, companies can change their criteria pollutant compliance strategies and use methodologies that do not achieve the same level of Hg or other HAP co-benefit (e.g., purchasing allowances in a trading program instead of using add-on controls).
      As with Hg, the most recent data on U.S. EGU HCl and HF emissions show a significant reduction between 2005 and 2010. These reductions in HCl and HF are the co-benefit of controls installed to meet other CAA requirements, including enforcement actions, and to a lesser extent, state regulations. There is no guarantee other than regulation under section 112 that these significant decreases in HCl and HF emissions will be permanent. Although we do not have estimates for the remaining HAP emitted from EGUs, it is likely that such emissions have also decreased between 2005 and 2010. Thus, the Administrator finds it necessary to regulate HAP emissions from EGUs to ensure that HAP emissions reductions are permanent.
      Finally, direct control of Hg emissions affecting U.S. deposition is only possible through regulation of U.S. emissions; we are unable to control global emissions directly. Although the U.S. is actively involved in international efforts to reduce Hg pollution, the ability of the U.S. to argue effectively in these negotiations for strong international policies to reduce Hg air emissions depends in large part on our domestic policies, programs and regulations to control Hg.
      All of these findings independently support the finding, as reported in the preamble to the proposed rule, that it is necessary to regulate U.S. EGUs under section 112.
      Therefore, given the Agency's finding that it remains appropriate and necessary to regulate coal- and oil-fired EGUs under CAA section 112, EPA confirmed in the preamble to the proposed rule its decision to include coal- and oil-fired EGUs on the list of source categories regulated under CAA section 112(c).
B. Peer Review of the National-Scale Mercury Risk Assessment Supporting the Appropriate and Necessary Finding for Coal and Oil-Fired EGUs and EPA Response
	In the preamble to the proposed rule, EPA stated that "in making the finding that it remains appropriate and necessary to regulate EGUs to address public health and environmental hazards associated with emissions of Hg and Non-Hg HAP from EGUs, EPA determined that the National-Scale Mercury Risk Analysis supporting EPA's 2011 review of U.S. EGU health impacts should be peer-reviewed." We also indicated that due to the court-ordered schedule for the final rule, we would conduct the peer review as expeditiously as possible after issuance of the proposed rule, and that the results of the peer review and any EPA response would be published before the final rule.
	We have completed the peer-review of the national scale mercury risk analysis, which is fully documented in the revised Technical Support Document (TSD): National-Scale Assessment of Mercury Risk to Populations of High Consumption of Self-Caught Fish In Support of the Appropriate and Necessary Finding for Coal and Oil-Fired Electric Generating Units. The following sections describe the peer-review process that we followed, provide the peer-review charge questions presented to the peer-review panel, summarize the key recommendations from the peer-review, and summarize our responses to those recommendations.
1. Summary of Peer Review Process
      Peer review is consistent with EPA's routine open and transparent process to ensure that the Agency's scientific assessments and rulemakings are based on the best science available. This regulatory action was supported by the National-Scale Mercury Risk Assessment, which is a highly influential scientific assessment. Therefore, EPA conducted a peer review in accordance with OMB's Final Information Quality Bulletin for Peer Review as described below. The peer review report is located in the docket for today's action. 
      EPA commissioned the peer review through EPA's Science Advisory Board (SAB), which provides independent advice and peer review to EPA's Administrator on the scientific and technical aspects of environmental issues. The SAB formed a 22-member peer-review committee, which included a diverse mix of experts from industry, states and academia. The SAB process for selecting the panel began with two Federal Register Notices requesting nominations for the Mercury Review Panel. Based on nominations received, a list of potential panel members, along with bio-sketches, was posted for public comment on the SAB website on April 15, 2011. The final members of the Mercury Review Panel were announced on May 24, 2011. The membership of the panel included members representing 16 academic institutions, 4 state health or environmental agencies, 1 federal agency, and 1 utility industry organization. The charge to the panel was provided on May 23, 2011. The panel met at a public meeting in Research Triangle Park, NC on June 15-17, 2011, which included the opportunity for public comment on the March Mercury Risk TSD and the peer review process. At the June 15-17 public meeting, the panel completed a draft peer review report. The minutes of that meeting and the draft peer review report were posted to the SAB public website within the public comment period for the proposed rule. The panel discussed the draft report at a public teleconference on July 12, 2011, during which additional opportunities for public comment were provided, and submitted a revised draft for quality review by the Chartered SAB. The Chartered SAB held a public teleconference on September 7, 2011 to conduct a quality review of the draft report; this teleconference also included a final opportunity for public comment. The SAB submitted its final peer-review report to EPA on September 29, 2011. All of the materials discussed at the SAB meetings, including technical documents, presentations, meeting minutes, and draft reports were posted for public access on the SAB website and were added to the docket for the final rule on October 14, 2011. 
2. Peer Review Charge Questions
      EPA asked the SAB to comment on the risk assessment, including the overall design and approach, as well as the use of specific models and key assumptions. EPA also asked the SAB to comment on the extent to which specific facets of the assessment are well characterized in the March Mercury Risk TSD. The specific charge questions are listed below: 
      Question 1. Please comment on the scientific credibility of the overall design of the mercury risk assessment as an approach to characterize human health exposure and risk associated with U.S. EGU mercury emissions (with a focus on those more highly exposed). 
      Question 2. Are there any additional critical health endpoint(s) besides IQ loss, which could be quantitatively estimated with a reasonable degree of confidence to supplement the mercury risk assessment (see section 1.2 of the Mercury Risk TSD for an overview of the risk metrics used in the risk assessment)? 
      Question 3. Please comment on the benchmark used for identifying a potentially significant public health impact in the context of interpreting the IQ loss risk metric (i.e., an IQ loss of 1 to 2 points or more representing a potential public health hazard). Is there any scientifically credible alternate decrement in IQ that should be considered as a benchmark to guide interpretation of the IQ risk estimates (see section 1.2 of the Mercury Risk TSD for additional detail on the benchmark used for interpreting the IQ loss estimates)?
      Question 4: Please comment on the spatial scale used in defining watersheds that formed the basis for risk estimates generated for the analysis (i.e., use of 12-digit hydrologic unit code classification). To what extent do [Hydrologic Unit Code] HUC12 watersheds capture the appropriate level of spatial resolution in the relationship between changes in mercury deposition and changes in MeHg fish tissue levels? (see section 1.3 and Appendix A of the Mercury Risk TSD for additional detail on specifying the spatial scale of watersheds used in the analysis). 
      Question 5: Please comment on the extent to which the fish tissue data used as the basis for the risk assessment are appropriate and sufficient given the goals of the analysis. Please comment on the extent to which focusing on data from the period after 1999 increases confidence that the fish tissue data used are more likely to reflect more contemporaneous patterns of mercury deposition and less likely to reflect earlier patterns of mercury deposition. Are there any additional sources of fish tissue MeHg data that would be appropriate for inclusion in the risk assessment? 
      Question 6: Given the stated goal of estimating potential risks to highly exposed populations, please comment on the use of the 75th percentile fish tissue MeHg value (reflecting targeting of larger but not the largest fish for subsistence consumption) as the basis for estimating risk at each watershed. Are there scientifically credible alternatives to use of the 75th percentile in representing potential population exposures at the watershed level? 
      Question 7: Please comment on the extent to which characterization of consumption rates and the potential location for fishing activity for high-end self-caught fish consuming populations modeled in the analysis are supported by the available study data cited in the Mercury Risk TSD. In addition, please comment on the extent to which consumption rates documented in Section 1.3 and in Appendix C of the Mercury Risk TSD provide appropriate representation of high-end fish consumption by the subsistence population scenarios used in modeling exposures and risk. Are there additional data on consumption behavior in subsistence populations active at inland freshwater water bodies within the continental U.S.? 
      Question 8: Please comment on the approach used in the risk assessment of assuming that a high-end fish consuming population could be active at a watershed if the "source population" for that fishing population is associated with that watershed (e.g. at least 25 individuals of that population are present in a U.S. Census tract intersecting that watershed). Please identify any additional alternative approaches for identifying the potential for population exposures in watersheds and the strengths and limitations associated with these alternative approaches (additional detail on how EPA assessed where specific high-consuming fisher populations might be active is provided in section 1.3 and Appendix C of the Mercury Risk TSD). 
      Question 9: Please comment on the draft risk assessment's characterization of the limitations and uncertainty associated with application of the Mercury Maps approach (including the assumption of proportionality between changes in mercury deposition over watersheds and associated changes in fish tissue MeHg levels) in the risk assessment. Please comment on how the output of CMAQ modeling has been integrated into the analysis to estimate changes in fish tissue MeHg levels and in the exposures and risks associated with the EGU-related fish tissue MeHg fraction (e.g., matching of spatial and temporal resolution between CMAQ modeling and HUC12 watersheds). Given the national scale of the analysis, are there recommended alternatives to the Mercury Maps approach that could have been used to link modeled estimates of mercury deposition to monitored MeHg fish tissue levels for all the watersheds evaluated? (additional detail on the Mercury Maps approach and its application in the risk assessment is presented in section 1.3 and Appendix E of the Mercury Risk TSD). 
      Question 10: Please comment on the EPA's approach of excluding watersheds with significant non-air loadings of mercury as a method to reduce uncertainty associated with application of the Mercury Maps approach. Are there additional criteria that should be considered in including or excluding watersheds? 
      Question 11: Please comment on the specification of the concentration-response function used in modeling IQ loss. Please comment on whether EPA, as part of uncertainty characterization, should consider alternative concentration-response functions in addition to the model used in the risk assessment. Please comment on the extent to which available data and methods support a quantitative treatment of the potential masking effect of fish nutrients (e.g. omega-3 fatty acids and selenium) on the adverse neurological effects associated with mercury exposure, including IQ loss. (detail on the concentration-response function used in modeling IQ loss can be found in section 1.3 of the Mercury Risk TSD). 
      Question 12: Please comment on the degree to which key sources of uncertainty and variability associated with the risk assessment have been identified and the degree to which they are sufficiently characterized. 
      Question 13: Please comment on the draft Mercury Risk TSD's discussion of analytical results for each component of the analysis. For each of the components below, please comment on the extent to which EPA's observations are supported by the analytical results presented and whether there is a sufficient characterization of uncertainty, variability, and data limitations, taking into account the models and data used: mercury deposition from U.S. EGUs , fish tissue methyl mercury concentrations, patterns of Hg deposition with HG fish tissue data, percentile risk estimates, and number and frequency of watersheds with populations potentially at risk due to U.S. EGU mercury emissions. 
      Question 14: Please comment on the degree to which the final summary of key observations in Section 2.8 is supported by the analytical results presented. In addition, please comment on the degree to which the level of confidence and precision in the overall analysis is sufficient to support use of the risk characterization framework described on page 18.
3. Summary of Peer Review Findings and Recommendations
      The SAB peer review panel was generally supportive of EPA's approach. SAB concluded, "In summary, based on its review of the draft Technical Support Document and additional information provided by EPA representatives during the public meetings, the SAB supports the overall design of and approach to the risk assessment and finds that it should provide an objective, reasonable, and credible determination of the potential for a public health hazard from mercury emitted from U.S. EGUs." SAB further concluded, "The SAB regards the design of the risk assessment as suitable for its intended purpose, to inform decision-making regarding an "appropriate and necessary finding" for regulation of hazardous air pollutants from coal and oil-fired EGUs, provided that our recommendations are fully considered in the revision of the assessment." 
      The SAB report contained many recommendations for improving the Mercury Risk TSD, which SAB organized into three general themes: (1) improve clarity of the Mercury Risk TSD regarding methods and presentation of results, (2) expand discussion of sources of variability and uncertainty, and (3) de-emphasize IQ loss as an endpoint. In the following sections, we describe each of the specific recommendations along with EPA's response to these recommendations.
4. EPA Responses to Specific Peer Review Recommendations
      In response to the peer review, EPA has substantially revised the TSD as part of the final rulemaking and has made that revised Mercury Risk TSD available in the rule docket. The revised Mercury Risk TSD addresses all of the recommendations from the SAB peer review panel and includes a detailed list of the specific revisions made to the Mercury Risk TSD. Revisions in response to the main recommendations are summarized below. Italicized statements are the SAB's recommendations, followed by EPA's response.
   * The watershed-focus of the risk assessment should be clearly stated early in the introduction to the document. We have stated clearly in the introduction to the revised Mercury Risk TSD that the focus of the analysis is on scenarios of high fish consumption by subsistence level fishing populations, assessed at watersheds where there is the potential for this type of subsistence fishing activity. Specifically, we are modeling risk for a set of subsistence fisher scenarios at those watersheds where (a) we have measured fish tissue Hg data and (b) it is reasonable to assume that subsistence-level fishing activity could occur. We emphasize the point that the analysis is not a representative population-weighted assessment of risk. Rather, it is based on evaluating these potential exposure scenarios.
   * Because IQ does not fully capture the range of neurodevelopmental effects associated with Hg exposure, analysis of this endpoint should be deemphasized (and moved to an appendix) and primary focus should be placed on the MeHg RfD-based hazard quotient metric. We modified the structure of the Revised Mercury Risk TSD accordingly.
   * Clarify the rationale for using an [Hazard Quotient] HQ at or above 1.5 as the basis for selecting potentially impacted watersheds. We revised this discussion accordingly. Reflecting precedent in interpreting HQ estimates, we clarified that exposures above the RfD (i.e., an HQ above one) to represent a potential public health hazard. We further clarified that the HQ is calculated to only one significant digit, based on the precision in the underlying RfD calculations. As a result, rounding convention requires that any values at or above 1.5 be expressed as an HQ of 2, while any values below 1.5 (e.g. 1.49) will be rounded to an HQ of 1. Thus, exposures at or above 1.5 are considered above the RfD and represent a potential public health hazard.
   * Regarding the fish tissue dataset used in the risk assessment, clarify which species of Hg is reflected in the underlying samples and discuss the implications of differences across states in sampling protocols in introducing bias into the analysis. We clarified that in most cases, the fish tissue is measured for total Hg. Furthermore, based on the literature, it is reasonable to assume that more than 90 percent of fish tissue Hg is methylmercury (MeHg). Therefore, we incorporated a Hg conversion factor into our exposure calculations to account for the fraction of total Hg that is MeHg in fish. We also expanded the discussion of uncertainty to include the potential for different sampling protocols across states to introduce bias into the risk assessment. 
   * Additional detail should be provided on the characteristics of the fish tissue Hg dataset, including its derivation and the distribution of specific attributes across the dataset (e.g., number of fish tissue samples and number of different waterbodies in a watershed, number of species reflected across watersheds). We included additional figures and tables describing the derivation of the watershed-level fish tissue Hg dataset, including the filtering steps applied to the original water body level data and the additional steps to generate the watershed-level fish tissue Hg percentile estimates. In addition, we included tables summarizing the distribution of key attributes within that dataset highlighted by the SAB (e.g., distribution of fish tissue sample size and number of species across the watershed-level estimates). 
   * Determine whether there is additional (more recent) fish tissue data for key states including Pennsylvania, Jew Jersey, Kentucky and Illinois where U.S. EGUs Hg deposition may be more significant. We expanded the fish tissue dataset by incorporating additional fish tissue data from the National Listing of Fish Advisories (NLFA), which included additional data for four states (MI, NJ, PA, and MN). We also obtained additional data for Wisconsin. This additional data expanded the number of watersheds in the analysis from 2,317 to 3,141, an increase of 36 percent. The increase in watersheds provides greater coverage of areas with high levels of U.S. EGU Hg deposition.
   * Include additional discussion of the potential that the low sampling rates reflected across many of the watersheds may low-bias the 75[th] percentile fish tissue Hg estimates used in estimating potential exposures. In addition, the SAB recommended including a sensitivity analysis using the 50[th] percentile estimates to provide a bound on the risk assessment. The SAB expressed support for the use of the 75[th] percentile fish tissue Hg value in the risk assessment, while recommending additional discussion of the issue. We provided additional description of the fish tissue dataset, including distribution of sample sizes and fish species across the watersheds, which includes an improved discussion of uncertainty and potential bias resulting from estimation of the 75[th] percentile fish tissue levels. We also included a sensitivity analysis that used the 50[th] percentile watershed-level fish tissue Hg level. This sensitivity analysis showed that using the 50[th] percentile estimates resulted in a decrease in the number and percentage of  watersheds identified as having populations potentially at risk from U.S. EGU-attributable MeHg exposures, from 29 percent to 26 percent.
   * Expand the discussion of caveats associated with the fish consumption rates used in the analysis. The SAB was generally supportive of the consumption rates used, while recommending additional discussion of caveats. We expanded the discussion of uncertainty related to the fish consumption rates to address the caveats identified by the SAB. The uncertainty discussion now describes 1) how high-end consumption rates for South Carolina reflect small sample sizes, and therefore may be more uncertain, 2) that the consumption surveys underlying the studies are older and behavior may have changed, and 3) that consumption rates used in the risk analysis are annualized rather than seasonal rates and thus contribute little to overall uncertainty. None of these sources of uncertainty are associated with a particular directional bias (e.g., neither systematically higher nor lower risk).
   * Verify whether the consumption rates are daily values expressed as annual averages and whether they are "as caught" or "as prepared." These factors have important implications for the exposure calculations. We carefully reviewed the studies underlying the fish consumption rates used in the risk assessment and verified that the rates are annual-average daily consumption rates and that they represent as prepared estimates. We also expanded the explanation of the exposure calculations to more completely describe the exposure factors and equation used to generate the average daily MeHg intake estimates for the subsistence scenarios. 
   * Explain the criteria for exclusion of fish less than 7 inches in length from analysis. We provided the rationale for the 7-inch cutoff for edible fish used in the risk analysis. Seven inches represents a minimum size limit for a number of key edible freshwater fish species established at the state level. For example, Pennsylvania establishes 7 inches as the minimum size limit for both Trout and Salmon (other edible fish species such as Bass, Walleye and Northern Pike have higher minimum size limits). The impact of the 7-inch cutoff is likely to be quite small, as only 6 percent of potential fish samples were excluded due to this criterion.
   * Identify the number of watersheds excluded from the analysis due to the criterion for excluding watersheds with less than 25 members of a source population. The SAB was generally supportive of the approach used for identifying watersheds with the potential for subsistence activity, while recommending additional information on the results of applying the approach. We added a figure to illustrate the number of watersheds with fish tissue Hg data used to model risk for each of the subsistence fisher scenarios. For all scenarios except the female subsistence scenario, there were significant limitations to the number of watersheds where the exposure scenario was applied. Because this scenario represents female subsistence fishers without differentiation with regard to ethnicity or socio-economic status(SES), we applied this scenario to all regions of the country and to all watersheds with fish tissue Hg data. This reflects our assumption that, given the generalized nature of this subsistence scenario, it is reasonable to assume that it could potentially occur at any watershed with fish tissue Hg data. The female subsistence scenario included in the revised risk assessment is similar to the high consuming female scenario included in the Mercury Risk TSD. However, the female subsistence scenario is applied without consideration for a source population, while in the scenario for the high-consuming low-income female angler, we considered a source population based on poverty. The female subsistence scenario provides greater coverage geographically than the high-consuming low-income female scenario from the March assessment that was only applied to watersheds with fish tissue Hg data and at least 25 members of the source population (individuals living below the poverty line). This also helps to address the concern raised by the SAB that more remote water bodies are fished by subsistence anglers as well, and exclusion of those more remote watersheds could lead to underestimation of the percent of watersheds where Hg exposure from U.S. EGU sources is a risk.
   * Enhance the discussion of the assumption of a linear relationship between changes in Hg deposition and changes in fish tissue Hg at the watershed level, including providing citations to more recent studies supporting the proportional relationship between changes in Hg deposition and changes in MeHg fish tissue levels. The SAB supported the assumption of a linear relationship between changes in Hg deposition and changes in fish tissue Hg at the watershed level, while recommending additional supporting language. We expanded our discussion of the scientific basis for the proportionality assumption and added citations for the more recent studies supporting the assumption. We also expanded the discussion of uncertainties associated with this assumption, including uncertainties related to the potential for sampled fish tissue Hg level to reflect previous Hg deposition, and the potential for non-air sources of Hg to contribute to sampled fish tissue Hg levels. Each of these sources of uncertainty may result in potential bias in the estimate of exposure associated with current deposition. If the fish tissue Hg levels are too high due to either previous Hg deposition or non-air sources of Hg, then the absolute level of exposure attributed to both total Hg deposition and U.S. EGU-attributable Hg deposition will be biased high. However, the percent contribution from U.S. EGUs will not be affected as it depends entirely on deposition. EPA took steps to minimize the potential for these biases by 1) only using fish tissue Hg samples from after 1999, and 2) screening out watersheds that either contained active gold mines or had other substantial non-U.S. EGU anthropogenic releases of mercury. The SAB commented that EPA's approach to minimizing the potential for these biases to affect the results of the risk analysis appears to be sound. In addition, we conducted several sensitivity analyses to gauge the impact of excluding watersheds with the potential for non-U.S. EGU Hg releases, and we found that the results were largely insensitive to these exclusions.
   * Additional sources of variability should be discussed in terms of the degree to which they are reflected in the design of the risk assessment and the impact that they might have on risk estimates. These include: 1) the geographic patterns of populations of subsistence fishers, including how this factor interacts with the limited coverage we have for watersheds with our fish tissue Hg data, 2)the protocols used by states in collecting fish tissue Hg data, 3) body weights for subsistence fishing populations and the impact that this might have on exposure estimates, and 4) preparation and cooking methods which affect the conversion of fish tissue Hg levels (as measured) into "as consumed" values. We expanded the discussion of sources of variability in the revised TSD to more fully address these sources of variability as recommended. 
   * Additional sources of uncertainty should be discussed in terms of their potential impact on risk estimates. These include: 1) emissions inventory used in projecting total and U.S. EGU-attributable Hg deposition, including the projection of reductions in U.S. EGU emissions for the 2016 scenario, 2) air quality modeling with CMAQ including the prediction of future air quality scenarios, 3) ability of the Mercury Maps-based approach for relating Hg deposition to MeHg in fish to capture Hg hotspots, 4) the limited coverage that we have with fish tissue Hg data for watersheds in the U.S. and implications for the risk assessment, 5) the preparation factor used to estimate "as consumed" fish tissue Hg levels, 6) the proportionality assumption used to relate changes in Hg deposition to changes in fish tissue Hg levels at the watershed-level, 7)characterization of the spatial location of subsistence fisher populations (including degree to which these provide coverage for high-consuming recreational fishers), and 8) application of the RfD to low SES populations and concerns that this could low-bias the risk estimates. We expanded the discussion of sources of uncertainty presented in the revised TSD to more fully address these sources of uncertainty and the potential impact on risk estimates. Regarding these eight additional sources of uncertainty, we have 1) evaluated  the uncertainty in the preparation factor and determined that the level of uncertainty is low, and as such would have minimal impact on the risk estimates, 2) focused the risk estimates on female subsistence fishing populations, which are assumed to have the potential to fish in all watersheds, reducing uncertainties about the coverage of the risk estimates for other populations, 3) continued to include the sensitivity analyses designed to test whether removing watersheds that would potentially violate the proportionality assumption would significantly affect the results (they do not), 4) supplemented the coverage of watersheds by obtaining additional fish tissue Hg samples for areas heavily impacted by U.S. EGU deposition.  We have also assessed the potential impact of the uncertainty in application of the RfD to low SES populations, and have determined that due to the method used in calculating the RfD (which includes an uncertainty factor to capture pharmacokinetic variability across the population), concerns that the RfD may not provide coverage for low SES populations is reduced.  Uncertainty in emissions and air quality modeling is an important source of uncertainty which is not quantified in the risk analysis, however, the models of emissions and air quality are based on peer-reviewed science, and represent the best available method for predicting mercury deposition in the U.S.
   * Expand the sensitivity analyses (over those included in the original risk assessment) to address uncertainty related to the use of the 75th percentile fish tissue Hg value (at each watershed) as the core risk estimate. We added a sensitivity analysis using the median fish tissue Hg estimate (at the watershed level). This sensitivity analysis showed that use of the median fish tissue Hg concentration instead of the 75[th] percentile resulted in only a small change in the estimates of risk.
C.	Summary of Results of Revised National Scale Assessment of Risks to Populations with High Levels of Self-Caught Fish Consumption
      Based on the recommendations we received from the SAB, we revised the quantitative analysis of risk to subsistence fishing populations with high levels of fish consumption. Our revision to the quantitative risk results reflects three key recommendations from the SAB, including 1) addition of 824 watersheds based on additional fish tissue Hg sample data we obtained from states and the National Listing of Fish Advisories, 2) application of a 0.95 adjustment factor to the reported fish tissue Hg concentrations to account for the fraction that is MeHg, and 3) inclusion of all watersheds with fish samples that meet the filtering criteria in representing potential risks for low income female subsistence fishing populations. Based on these changes, our estimates of the number and percent of watersheds where populations may be at risk from exposure to EGU-attributable MeHg changed from those presented in the preamble to the proposed rule. For the 99[th] percentile consumption scenario, the number of watersheds with fish tissue Hg samples where subsistence fishing populations may be at risk from exposure to EGU-attributable MeHg increased from 672 to 917 (an increase of 36 percent). For this same scenario, the percent of watersheds where subsistence fishing populations may be at risk increased from 28 percent to 29 percent. For the 95[th] percentile consumption scenario, the percent of watersheds where subsistence fishing populations may be at risk has increased from 22 percent to 24 percent. The increase in the percent of watersheds at risk using the expanded geographic coverage of watersheds provides additional confidence that emissions of Hg from U.S. EGUs are a hazard to public health.
      The additional sensitivity analyses conducted as a result of the SAB peer review showed that the estimates of the percent of watersheds where subsistence fishing populations may be at risk are robust to alternative assumptions about both the watersheds included in the analysis and the selection of the 50[th] percentile or 75[th] percentile fish tissue Hg level. Sensitivity analyses excluding entire states with the potential for historical loadings of Hg from non-air sources resulted in an increase in the percent of watersheds with populations at risk, from 29 percent to 33 percent. Including only watersheds in the top 25[th] percentile of U.S. EGU deposition resulted in an increase in the percent of watersheds with populations at risk, from 29 percent to 30 percent. Using the 50[th] percentile fish tissue Hg level resulted in a decrease in the percent of watersheds with populations at risk, from 29 percent to 26 percent. None of these sensitivity analyses result in reductions in the percent of watersheds with populations at risk that would challenge the finding that Hg emissions from U.S. EGUs are a hazard to public health.
D. Peer Review of the Approach for Estimating Cancer Risks Associated with Chromium and Nickel Emissions in the U.S. EGU Case Studies of Cancer and Non-Cancer Inhalation Risks for Non-Hg HAP and EPA Response
      In the preamble to the proposed rule, EPA determined that the characterization of the chemical speciation for the emissions of Cr and Ni used in the non-Hg HAP inhalation risk case studies should be peer-reviewed. The Agency determined that the remaining aspects of the non-Hg HAP case study risk assessments used methods that have already been subject to adequate peer-review. The methodologies used to conduct those risk assessments are consistent with those used to conduct inhalation risk assessments under the EPA's Risk and Technology Review (RTR) program. Because the RTR assessments are considered to be highly influential science assessments, the methodologies used to conduct them were subject to a peer review by EPA's Science Advisory Board (SAB) in 2009. The SAB issued its peer review report in May 2010. The report generally endorsed the risk assessment methodologies used in the program.
      The EPA's case studies identified chromium and nickel emissions as the key drivers of the estimated inhalation cancer risks for EGUs. Because these results hinged on specific scientific interpretations of data used to characterize EGU emissions of chromium and nickel, EPA conducted a letter peer review of its analysis and interpretation of those data relative to the inhalation risks associated with EGU HAP emissions. The following sections describe the peer-review process that we followed, enumerate the peer-review charge questions presented to the peer-review panel, summarize the key recommendations from the peer-review, and summarize our responses to those recommendations.
1. Summary of Peer Review Process
      EPA asked three independent, external peer reviewers representing government, academic and the private sector to review of the methods for developing inhalation cancer risk estimates associated with emissions of chromium and nickel compounds from coal- and oil-fired EGUs in support of the appropriate and necessary finding. The approaches and rationale for the technical and scientific considerations used to derive inhalation cancer risks were summarized in the draft document entitled, "Methods to Develop Inhalation Cancer Risk Estimates for Chromium and Nickel Compounds." The peer reviewers were given approximately a month to respond to a series of charge questions on the technical and scientific relevance of the approaches used to develop the inhalation unit risk estimates. These estimates were based on the speciation data available from selected source categories and on the available unit risk estimates (UREs) reflecting the dose that corresponds to a specific level of cancer risk. EPA also provided information on chromium speciation profiles for different industrial sources, as well as information on the nickel speciation of particulate matter from oil-fired power plants to the peer reviewers.
2. Peer Review Charge Questions
      Below we present the charge questions posed to the peer reviewers to help guide their review and development of recommendations to the EPA on key issues relevant to the characterization of risks from EGU emissions containing either chromium or nickel compounds. 
      EPA asked three questions regarding chromium and chromium compounds:
      Question 1: Do EPA's judgments related to speciated chromium emissions adequately take into account the available chromium speciation data? 
      Question 2: Has the EPA selected the species of chromium (i.e., hexavalent chromium) that accurately represents the toxicity of chromium and chromium compounds? 
      Question 3: Are the assumptions used in past analysis scientifically defensible, and are there alternatives that the EPA should consider for future analysis? 
      EPA asked two questions regarding nickel and nickel compounds:
      Question 1: Do EPA's judgments related to speciated nickel emissions adequately take into account available speciation data, including recent industry spectrometry studies?
      Question 2: Based on the speciation information available and on what we know about the health effects of nickel and nickel compounds, and taking into account the existing Unit Risk Estimates (URE) values (i.e., values derived for EPA's Integrated Risk Information System (IRIS), California Environmental Protection Agency (Cal EPA) and Texas Commission on Environmental Quality (TCEQ)), the EPA has provided several approaches to derive unit risk estimates that may be more scientifically defensible than those used in past analyses. Which of the options presented would result in more accurate and defensible characterization of risks from exposure to nickel and nickel compounds? Are there alternative approaches that the EPA should consider?
3. Summary of Peer Review Findings and Recommendations
      Regarding chromium and chromium compounds, all three reviewers considered hexavalent chromium as the species likely to be driving cancer risks based on solid evidence from the health effects database for chromium and chromium compounds. All three authors also considered EPA's use of the average of the range of the available speciation data (i.e., 12 percent and 18 percent hexavalent chromium contained in coal- and oil-fired EGUs, respectively) as a reasonable approach for the derivation of default speciation profiles to be used when there is no speciation data available. All reviewers agreed that there is high uncertainty associated with the variability in the speciation data available for chromium (e.g., range of approximately 4 to 23 percent chromium hexavalent from coal-fired units). One of the reviewers recommended several additional studies for EPA's consideration. 
      Regarding nickel and nickel compounds, two of the reviewers agreed with the views of the international scientific bodies, which consider nickel compounds carcinogenic as a group. Nickel and nickel compounds have been classified as human carcinogens by national and international scientific bodies including the International Agency for Research on Cancer , the World Health Organization, and the European Union's Scientific Committee on Health and Environmental Risks. In their 12[th] Report of the Carcinogens, the National Toxicology Program(NTP) has classified nickel compounds as known to be human carcinogens based on sufficient evidence of carcinogenicity from studies in humans showing associations between exposure to nickel compounds and cancer, and supporting animal and mechanistic data. More specifically, this classification is based on consistent findings of increased risk of cancer in exposed workers, and supporting evidence from experimental animals that shows that exposure to an assortment of nickel compounds by multiple routes causes malignant tumors at various organ sites and in multiple species. The 12th Report of the Carcinogens states that the "combined results of epidemiological studies, mechanistic studies, and carcinogenesis studies in rodents support the concept that nickel compounds generate nickel ions in target cells at sites critical for carcinogenesis, thus allowing consideration and evaluation of these compounds as a single group". The third reviewer recommended that the EPA review several manuscripts on nickel speciation profiles showing that sulfidic nickel compounds (which the reviewer considered as the most potent carcinogens within the group of all nickel compounds) are present at low levels in emissions from EGUs. In addition, this reviewer pointed out that some authors believe that water soluble nickel, such as nickel sulfate, should not be considered a human carcinogen.
4. EPA Responses to Peer Review Recommendations
      After considering the comments of all the peer reviewers, EPA revised the document as appropriate to create the final version of "Methods to Develop Inhalation Cancer Risk Estimates for Chromium and Nickel Compounds". We summarize EPA's basic responses to the peer review comments below, first for chromium-related issues, and second for nickel-related issues.
a. Chromium and chromium compounds:
      The EPA concluded that based on the health effects information available for chromium there is high confidence in the assumption that hexavalent chromium is the carcinogenic species driving the risk of chromium-emitting facilities and thus considered the derivation of default speciation profiles based on the mass of hexavalent chromium contained in the emissions from chromium-emitting facilities is a reasonable approach. As suggested by one of the reviewers, the EPA reviewed two potentially relevant studies, one of which showed coal combustion emissions containing as much as 43 percent hexavalent chromium, which suggests that EPA's quantitative approach could, in fact, underestimate hexavalent chromium inhalation risks. However, the other study reviewed by the EPA on speciation of chromium in coal combustion showed hexavalent chromium percentage levels close to detection limits (i.e., 3 to 5 percent of total chromium, which was close to limit of detection in this study). Thus, the more recent speciation data available is unlikely to reduce the uncertainty of the chromium speciation analyses used by EPA as the bases for risk characterization analysis.
      In agreement with the peer reviewers, the EPA also recognizes that the confidence in the default speciation profiles is low because the profiles are based on a limited data set with a wide range of percentages of hexavalent chromium across the different samples. 
b. Nickel and nickel compounds:
      Based on the views of the major scientific bodies mentioned above and expert peer reviewers that commented on EPA's approaches to risk characterization of nickel compounds, the EPA considers all nickel compounds to be carcinogenic as a group and does not consider nickel speciation or nickel solubility to be strong determinants of nickel carcinogenicity. One of the reviewers suggested we consider different views by some authors that believe that water soluble nickel, such as nickel sulfate, should not be considered a human carcinogen This notion is based primarily on a negative nickel sulfate 2-year NTP rodent bioassay (which is different than the positive 2-year NTP bioassay for nickel subsulfide).[,][,] One review article identifies the discrepancies between the animal and human data (i.e., from studies of cancers in workers inhaling certain forms of nickel versus inhalation studies suggesting different carcinogenic potential in rodents with different nickel compounds) and states that the epidemiological data available clearly supports an association between nickel and increased cancer risk, although the article acknowledges that the data are weakest regarding water soluble nickel. In addition, the EPA identified a recent review that highlights the robustness and consistency of the epidemiological evidence across several decades showing associations between exposure to nickel and nickel compounds (including nickel sulfate) and cancer. 
      Regarding the second charge question on nickel compounds, two reviewers suggested using the URE derived by the TCEQ for all nickel compounds as a group, rather than the one derived by the Integrated Information System (IRIS, 1991) specifically for nickel subsulfide. The third reviewer did not comment on an alternative approach. The EPA decided to continue using 100 percent of the current IRIS URE for nickel subsulfide (rather than assuming that 65 percent of the total mass of emitted nickel might be of nickel subsulfide, as used in previous analyses) because IRIS values are at the top of our hierarchy with respect to the dose-response information used in EPA's risk characterizations, and because of the concerns about the potential carcinogenicity of all forms of nickel raised by the major national and international scientific bodies. Nevertheless, taking into account that there are potential differences in toxicity and/or carcinogenic potential across the different nickel compounds, and given that two URE values have been derived for exposure to mixtures of nickel compounds that are 2 to 3 fold lower than the IRIS URE for nickel subsulfide, the EPA also considers it reasonable to use a value that is 50 percent of the IRIS URE for nickel subsulfide for providing an estimate of the lower end of a plausible range of cancer potency values for different mixtures of nickel compounds.
      Although this report focused primarily on cancer risks associated with emissions containing nickel compounds, it is important to note that comparative quantitative analyses of non-cancer toxicity of nickel compounds indicate that nickel sulfate is as toxic or more toxic than nickel subsulfide or nickel oxide which does not support the notion that the solubility of nickel compounds is a strong determinant of its toxicity.[,] 
E. Summary of Results of Revised U.S. EGU Case Studies of Cancer and Non-Cancer Inhalation Risks for Non-Hg HAP 
      Based on the results of the peer review and public comments on the non-Hg case study chronic inhalation risk assessment, we made several changes to the emissions estimates, dispersion modeling, and risk characterization for the modeled case study facilities. Key changes include 1) changes in emissions, 2) changes in stack parameters for some facilities based on new data received during the public comment period, 3) updated versions of AERMOD and its input processors (AERMAP, AERMINUTE, and AERMET) were used, and 4) 100 percent of the current IRIS URE for nickel subsulfide was used to calculate nickel-associated inhalation cancer risks (rather than assuming that the nickel might be 65 percent as potent as nickel subsulfide). 
      Based on estimated actual emissions, the highest estimated individual lifetime cancer risk from any of the sixteen case study facilities was 20 in a million, driven by nickel emissions from the one case study facility with oil-fired EGUs. Of the facilities with coal-fired EGUs, five facilities had  maximum individual cancer risks greater than 1 in a million (the highest was five in a million), four were driven by emissions of hexavalent chromium and one was driven by emissions of nickel. There were also two facilities with coal-fired EGUs that had maximum individual cancer risks equal to 1 in a million. All of the facilities had non-cancer Target Organ Specific Hazard Index (TOSHI) values less than one, with a maximum TOSHI value of 0.4 (also driven by nickel emissions from the one case study facility with oil-fired EGUs).
      Since these case studies do not cover all facilities in the category, and since our assessment does not include the potential for impacts from different EGU facilities to overlap one another (i.e., these case studies only look at facilities in isolation), the maximum risk estimates from the case studies may underestimate true maximum risks for the source category.
F. Public Comments and Responses to the Appropriate and Necessary Finding
1. Legal Aspects of Appropriate and Necessary Finding
a. History of Section 112(n)(1)(A)
      Comment: One commenter provided a detailed history of EPA's regulatory actions concerning EGUs and implementation of section 112(n)(1)(A). The same commenter implies that the EPA's December 2000 appropriate and necessary finding and listing of EGUs was flawed because the Agency did not comply with CAA section 307(d) rulemaking process. The commenter sought review of the December 2000 notice in the U.S. Court of Appeals for the District of Columbia Circuit, which was dismissed by the D.C. Circuit. Utility Air Regulatory Group v. EPA, No. 01-1074 (D.C. Cir. July 26, 2001). The commenter then characterizes at length the 2005 EPA action that revised the interpretation of section 112(n)(1)(A) and illegally removed EGUs from the section 112(c) list of sources that must be regulated under section 112. See New Jersey v. EPA, 517 F.3d 574 (D.C. Cir. 2008). The commenter notes that the D.C. Circuit did not rule on the legal correctness or the sufficiency of the factual record supporting EPA's December 2000 listing decision or on the factual correctness of EPA's later decision to reverse its 112(n)(1)(A) determination. The commenter noted further that the D.C. Circuit indicated that the listing decision could be challenged when the Agency issued the final section 112(d) standards pursuant to section 112(e)(4). The commenter concluded by asserting that the Agency could not ignore the history associated with the regulation of EGUs under section 112 and that two earlier dockets - Docket ID. No. A-92-55 and Docket ID. No. EPA-HQ-OAR-2002-0056  -  are also part of this long rulemaking effort and must be accounted for in conjunction with Docket No. EPA-HQ-OAR-2009-0234 if all pertinent material and comments are to be part of the rulemaking record.
      Response: The commenter characterizes the regulatory history of the rule EPA proposed on May 3, 2011. To the extent that characterization is inconsistent with the lengthy regulatory history EPA provided in the preamble to the May 3, 2011 rule, we disagree. We address several of the statements in more detail below.
	The commenter makes much of the fact that EPA did not go through CAA section 307(d) notice and comment rulemaking when making the appropriate and necessary finding and listing decision in December 2000. However, the commenter's complaint is without foundation. The CAA does not require 307(d) rulemaking for listing decisions. In fact, section 112(e)(4) specifically provides that listing decisions may only be challenged "when the Administrator issues emission standards for such . . . [listed] category." The commenter challenged the listing decision in the U.S. Court of Appeals for the District of Columbia Circuit (Court) and, on July 26, 2001, the Court granted EPA's motion to dismiss that action based on the plain language of section 112(e)(4). EPA clearly articulated its basis for listing EGUs in this proposed rule, which is consistent with CAA section 307(d), and the commenter was provided an ample opportunity to comment. 
	Finally, the commenter asserts that the rulemaking docket for this action is incomplete because the Agency did not include two earlier dockets - Docket ID. No. A-92-55 and Docket ID. No. EPA-HQ-OAR-2002-0056 - for the Section 112(n) Revision Rule, 70 F.R. 15994 (March 29, 2005), and the reconsideration of the Section 112(n) Revision Rule, 71 F.R. 33388 (June 9, 2006), respectively. Commenter is incorrect because EPA incorporated by reference the two dockets at issue. See EPA-HQ-OAR-2009 -0234-3056. 
      Comment: One commenter states that the EPA has assessed the public health risks posed by HAP emissions from coal- and oil-fired EGUs for the last 40 years. According to the commenter throughout that time, EPA has come to a single repeated conclusion the HAP emissions from EGUs pose little or no risk to public health. Based on this conclusion, EPA has properly chosen not to require EGUs to install expensive, new pollution control equipment to control HAP emissions. The commenter asserts that in this proposed rule, the EPA shifts its opinion on the health impacts of EGU HAP emissions 180 degrees and now seeks to impose sweeping regulatory requirements on all power plants. Again, according to the commenter the EPA's newfound concern about HAP emissions from EGUs is not based on new and different assessments of the public health consequences of EGU HAP emissions but instead on health benefits from the reduction of non-hazardous air pollutants, primarily PM, that the Agency is required to regulate under other provisions of the CAA. One commenter states that for decades the EPA set primary ambient air quality standards that protect public health with an adequate margin of safety, CAA 109(b)(1), and set secondary standards that are [sic] "requisite to protect the public health from any known or anticipated adverse effects associated with the presence of such air pollutant in the ambient air," CAA 109(b)(2). The commenter notes that even if EPA now views those past PM standards as inadequate, the EPA has ongoing regulatory proceedings in which it can address any perceived health concerns. The commenter concludes that regulation of EGU HAP emissions under 112 is an unlawful way to address those concerns. 
      Response: The commenter is incorrect in its assertion that the Agency has consistently concluded that HAP emissions from EGUs do not present a hazard to public health. In the December 2000 Finding, the Agency concluded that HAP emissions from coal- and oil-fired EGUs do pose a hazard to public health and determined that it was appropriate and necessary to regulate such units under section 112 of the CAA. As a result of that finding, EPA added coal- and oil-fired EGUs to the CAA section 112(c) list of source categories for which emission standards are to be established pursuant to section 112(d). Further, in support of the proposed rule published in the Federal Register on May 3, 2011, EPA conducted additional extensive quantitative analyses, which confirm that it remains appropriate and necessary to regulate EGUs under CAA section 112. Among other things, those analyses demonstrate that emissions from coal- and oil-fired EGUs continue to pose a hazard to public health. The commenter also fails to note that EPA found that HAP emissions from EGUs pose a hazard to the environment as well.
      The commenter seems confused about the basis for the Agency's appropriate and necessary finding because it maintains that EPA made the appropriate and necessary finding based on the health co-benefits attributable to PM reductions that will be achieved as a result of the Agency's regulation of HAP emissions from EGUs. Nowhere in the May 2011 proposal does EPA state that it based the appropriate and necessary finding on hazards to public health attributable to PM emissions. The commenter's allegation simply lacks foundation. The proposal unmistakably focuses on the hazards to public health associated with HAP emissions from EGUs.
	Comment: One commenter states that section 112, added to the CAA in 1970, required the EPA to make a risk-based determination in order to regulate substances as HAPs. The EPA may regulate substances "reasonably ... anticipated to result in an increase in mortality or increase in serious illness," to a level that protects public health with an "ample margin of safety." CAA 112(a)(1). Under this provision, EPA regulated a number of HAPs emitted from industrial source categories other than EGUs. See 40 C.F.R. Part 63.
      As for EGUs, according to the commenter, the EPA found that the combustion of fossil fuels produces extremely small releases of a broad variety of substances that are present in trace amounts in fuels and that are removed from the gas stream by control equipment installed to satisfy other CAA requirements. The EPA, in past reviews, found that these HAP releases did not pose hazards to public health. See 48 Fed. Reg. 15,076, 15,085 (1983) (radionuclides). In the case of mercury specifically, EPA found that "coal-fired power plants ... do not emit mercury in such quantities that they are likely to cause ambient mercury concentration to exceed" a level that "will protect public health with an ample margin of safety." 40 Fed. Reg. 48,297-98 (Oct. 19,1975) (mercury); 52 Fed. Reg. 8724, 8725 (Mar. 19, 1987) (reaffirming mercury conclusion).
      In the late 1980s, the EPA was concerned that its prior risk assessments of individual HAP emissions from fossil-fuel-fired power plants may not reflect the total risks posed by all HAPs emitted by those sources. The EPA modeled the risks posed by all HAPs emitted by power plants (very much like the analyses the Agency would conduct for the Utility Study ten years later). The commenter asserts that the modeling again failed to identify threats to public health that warranted regulation under an "ample margin of safety" test.
	Response: The commenter's statements concerning the pre-1990 CAA are not relevant to the current action. As the commenter notes, Congress enacted CAA section 112(n)(1) as part of the 1990 amendments to the Act. That provision requires, among other things, that the Agency evaluate the hazards to public health posed by HAP emissions from fossil-fuel fired EGUs. Had Congress concluded as commenter appears to assert that HAP emissions from EGUs did not pose a hazard to public health or the environment, it defies reason that Congress would have required EPA to conduct the three studies at issue in section 112(n)(1) (titled "Electric utility steam generating units") and regulate EGUs under section 112 if the Administrator determined in her discretion that it was appropriate and necessary to do so. The Agency complied with the statutory mandates in section 112(n)(1) in conducting the studies and reasonably exercised its discretion in making the appropriate and necessary finding. 
      We acknowledge, however, that Congress treated radionuclide emissions from EGUs differently. For radionuclides from EGUs (and certain other sources), Congress included CAA section 112(q)(3), which authorizes but does not require the Agency to maintain the regulations of radionuclides in effect prior to the 1990 amendments. The fact that Congress made an exception for radionuclides and no other HAP from EGUs further demonstrates that the HAP-related actions EPA took with regard to EGUs prior to the 1990 amendments to the CAA were not germane. 
      As for the commenter's statements about mercury emissions from EGUs, we find their conclusions wholly inconsistent with CAA section 112(n)(1). That provision is titled "Electric utility steam generating units," and it directs EPA to conduct two mercury specific studies. See CAA sections 112(n)(1)(B) and 112(n)(1)(C). Commenter's suggestion that EPA could or should rely on assessments of mercury from EGUs conducted prior to the 1990 amendments is not tenable. 
      Finally, one commenter states that EPA conducted a risk assessment of all HAP from EGUs prior to the 1990 amendments and that the Agency did not identify any HAP that failed the "ample margin of safety" test. The commenter does not cite the study or provide any information to support the statements so we are unable to respond to the alleged study directly; however, the risk assessment conducted in support of the proposed rule did identify hazards to public health and the environment. 
b. Interpretation of "Appropriate" and "Necessary"
      Comment: One commenter states that in the preamble to the proposed rule, the EPA sets out its "interpretation of the critical terms in CAA 112(n)(1)," arguing that this latest interpretation is "wholly consistent with the CAA" and with the Agency's earlier "December 2000 Finding." See 76 Fed. Reg. 24,976, 24,986/2 (May 3, 2011). The commenter states that throughout the proposal the EPA tries to suggest that it is returning to some earlier, "correct" interpretation of CAA section 112(n)(1) set forth in its December 2000 action. See, e.g., 76 Fed. Reg. at 24,989/1-2 ("The Agency's interpretation of the term `appropriate'... is wholly consistent with the Agency's appropriate finding in December 2000"); id. at 24,992/1 ("Our interpretation of the necessary finding is reasonable and consistent with the December 2000 Finding"). According to the commenter, the EPA did not provide in December 2000 any interpretation of what it now characterizes as the "critical terms" of section 112(n)(1). See, e.g., 70 Fed. Reg. at 15,999 n.13 (the "December 2000 finding does not provide an interpretation of the phrase `after imposition of the requirements of the Act"); id. at 16,000/2 (in December 2000, EPA "did not provide an interpretation of the term `appropriate'"); 76 Fed. Reg. at 24,992/1 (the "Agency did not expressly interpret the term necessary in the December 2000 Finding"). The commenter believes that for that reason alone, it is impossible to credit EPA's assertion that it "appropriately concluded that it was appropriate and necessary to regulate hazardous air pollutants . . . from EGUs" in December 2000, and that it is today merely "confirm[ing] that finding and conclud[ing] that it remains appropriate and necessary to regulate these emissions..." 
	Response: The commenter disagrees with certain statements in the proposed rule that provide that the Agency's interpretation of section 112(n)(1) is reasonable and consistent with the December 2000 Finding. It is difficult to decipher the exact complaint that the commenter has with EPA's proposed rule in this regard, but the commenter does assert that "the Agency did not provide in December 2000 any interpretation of what it now characterizes as the "critical terms" of CAA 112(n)(1)." Commenter's assertion lacks foundation. While the 2000 finding did not provide detailed interpretations of the regulatory terms at issue, it discussed the types of considerations relevant to the A and N inquiry. For example, it is clear that the Agency was concerned with the then current hazards to public health and the environment when assessing whether it was appropriate to regulate EGUs under section 112. 65 FR 79830. In addition, when evaluating whether it was necessary to regulate utilities, the Agency specifically noted that "section 112 is the authority intended to address" hazards to public health and the environment posed by HAP emissions. Id. The detailed interpretation set forth in the proposed rule is consistent with the 2000 Finding, but EPA does not assert that the interpretation is in any way necessary to support the factual conclusions reached in that notice. Instead, we noted in the proposed rule that our interpretation is consistent with the 2000 Finding because in 2005 we interpreted the statute in a manner that was not consistent with the 2000 finding. If anything, making an interpretation that directly contradicted a prior factual conclusion was improper. At least one commenter that takes issue with the interpretation in the proposed rule participated in the 2005 action and it did not complain at that time about the Agency establishing an express interpretation that obviously was in conflict with a prior Finding. We are confused by the inconsistent approach to evaluating EPA actions. In any case, the commenter has provided no legal support for its position that the Agency erred in interpreting the statute in a manner that is consistent with a prior factual finding. 
      Comment: Several commenters state that a finding that HAP regulation is "appropriate" for a single HAP does not indicate that it is "appropriate" to regulate all HAPs. According to the commenters the sponsor of the House bill that became § 112(n)(1)(A) provides an explanation that contradicts EPA's approach. "Pursuant to section 112(n), the Administrator may regulate fossil fuel fired electric utility steam generating units only if the studies described in section 112(n) clearly establish that emissions of any pollutant, or aggregate of pollutants, from such units cause a significant risk of serious adverse effects on the public health. Thus, . . . he may regulate only those units that he determines  -  after taking into account compliance with all provisions of the act and any other Federal, State, or local regulation and voluntary emission reductions  -  have been demonstrated to cause a significant threat of serious adverse effects on the public health." 136 Cong. Rec. H12,934 (daily ed. Oct. 26, 1990) (statement of Rep. Michael Oxley).
      The commenters state that the EPA position is premised on the assumption that "regulation under section 112" necessarily means "regulation under 112(d)" and falsely premised on the assumption that source categories listed by operation of § 112(n)(1)(A) cannot be regulated differently. The language of § 112(n)(1)(a) reflects Congress' intent that "regulation of HAPs from EGUs was not intended to operate under § 112(d) but was instead intended to be tailored to the findings of the utility study mandated by §112(n)(1)(A)." 
      Response: The commenter maintains that the Agency's interpretation of CAA section 112(n)(1) is flawed in many respects. The primary support for commenter's arguments against EPA's interpretation, including in the comment above, is legislative history in the form of statements from one Congressman, Representative Oxley. In the May 3, 2011, proposed rule, EPA did not give much consideration to, and in fact did not even mention, the legislative history cited by the commenter because the Supreme Court has repeatedly stated that the statements of one Congressperson alone should not be given much weight. See Brock v. Pierce County, 476 U.S. 253, 263 (1986) (finding that "statements by individual legislators should not be given controlling effect, but when they are consistent with the statutory language and other legislative history, they provide evidence of Congress' intent.") (emphasis added) (citation omitted); Garcia, et. al., v. U.S., 469 U.S. 70, 78 (1984), citing Zuber v. Allen, 396 U.S. 168, 187 (1969) (reiterating its prior findings the Court indicated that isolated statements "are `not impressive legislative history.'"); Weinberger, et. al., v. Rossi et. al., 456 U.S. 25, 35 (declining to make a ruling based on "one isolated remark by a single Senator"); Consumer Product Safety Comm., et. al. v. GTE Sylvania, Inc., et. al., 447 U.S. 102, 117-118 (1980) (declining to give much weight to isolated remarks of one Representative); Chrysler Corp. v. Brown, et. al., 441 U.S. 281, 311 (1979) (finding that "[t]he remarks of a single legislator, even the sponsor, are not controlling in analyzing legislative history."); Zuber, 396 U.S. at 186 (concluding that "[f]loor debates reflect at best the understanding of individual Congressmen."); and U.S. v. O'Brien, 391 U.S. 367, 384 (1968) (in evaluating the statements of a handful of Congressmen, the Court concluded that "[w]hat motivates one legislator to make a speech about a statute is not necessarily what motivates scores of others to enact it..."). As these cases show, the Supreme Court does not give any weight to the statements of an individual Congressperson, except when the statements are supported by other legislative history and the clear intent of the statute. The Commenter has cited no case law that would support any reliance on such limited legislative history. 
	We could not find, and the commenter has not cited, any other legislative history to support Representative Oxley's statement, and the lack of additional support makes the statement of little utility or import under the case law we reviewed. In fact, there does not appear to be anything in the House, Senate, or Committee Reports that supports Oxley's statement. We find the lack of support for the Oxley's statement in the Committee Report particularly telling since, as the commenter notes, the House and Senate bills required different approaches to regulating EGUs under section 112, with the Senate bill requiring EGUs be regulated prior to the Utility Study. In fact, legislative statements from Senator Durenberger, a supporter of the Senate version, demonstrate that others would almost certainly not have agreed with Oxley's interpretation. For example, Senator Durenberger stated: "It seems to me inequitable to impose a regulatory regime on every industry in America and then exempt one category, especially a category like power plants which are a significant part of the air toxics problem."
      Senator Durenberger discussed the negotiations with the Administration and the industry push to avoid regulation, including industry arguments for not regulating mercury from EGUs: "[t]he utility industry continued to adamantly oppose [regulation under section 112]. First, they argued that mercury isn't much of an environmental problem. But as the evidence mounted over the summer and it became clear that mercury is a substantial threat to the health of our lakes, rivers and estuaries and that power plants are among the principal culprits, they changed their tactic. Now they are arguing that mercury is a global problem so severe that just cleaning up U.S. power plants won't make enough of a difference to be worth it. They've gone from "we're not a problem" to "you can't regulate us until you address the whole global problem." Recasting an issue that way is not new around here. So, it is not a surprise. But it does suggest the direction in which this debate will be heading in the next few years."
      Senator Durenberger also explained why the House version was adopted: "[g]iven that a resolution of the difficult issues in the conference were necessary to conclude work on this bill, the Senate proposed to recede to the House provision which was taken from the original administration bill. It provides for a 3-year study of utility emissions followed by regulation to the extent that the Administrator finds them necessary."
      Senator Durenberger's statements indicate that it is unlikely that he would agree with Oxley's interpretation of section 112(n)(1), a provision that is inarguably ambiguous and that clearly provides the Agency with considerable discretion; and nothing indicates that others in the Senate (or for that matter anyone else in the House) would agree with that interpretation. Given this disparity, EPA reasonably declined to discuss the legislative history in the proposed rule and we think it would be unreasonably to ascribe Oxley's statements to the entire Congress. 
	Moreover, Oxley's statement directly conflicts with the statutory text. Oxley states that "[the Administrator may regulate only those units that he determines  -  after taking into account compliance with all provisions of the act and any other Federal, State, or local regulation and voluntary emission reductions - have been demonstrated to cause a significant threat of serious adverse effects on the public health." 136 Cong. Rec. H12934 (daily ed. Oct. 26, 1990), reprinted in 1 1990 Legis. Hist. at 1416-17 (emphasis added). But the Utility Study required under section 112(n)(1)(A) directs the Agency to consider the hazards to public health reasonably anticipated to occur after "imposition of the requirements of [the Clean Air Act]." EPA was not required to consider state or local regulations or voluntary emission reduction programs in the Utility Study, and that study is the only condition precedent to making the appropriate and necessary finding. 
      For all these reasons, we maintain that our interpretation is reasonable and consistent with the statute and, for those reasons, should be afforded deference. In addition, we believe that any arguments against our interpretation that rely on Congressman Oxley's statements are without merit. 
      Comment: One commenter states that the EPA does acknowledge that, in many significant respects, its new interpretation of CAA 112(n)(1) "differs from that set forth" in the Agency's 2005 rulemaking, but argues that its change of position is permissible. See 76 Fed. Reg. at 24,988/1 ("[T]o the extent our interpretation differs from that set forth in the 2005 Action, we explain the basis for that difference and why the interpretation, as set forth in this preamble, is reasonable."). In support, the EPA cites National Cable & Telecommunication Ass'n v. Brand X Internet Services, 545 U.S. 967 (2005). It is true that, in Brand X Internet Services, the Supreme Court explained that, if an agency "adequately explains the reasons for a reversal of policy," such change is "not invalidating," since the "whole point of Chevron is to leave the discretion provided by the ambiguities of a statute with the implementing agency." 545 U.S. at 981 (internal quotations omitted). But all Brand X Internet Services was saying is that "[a]gency inconsistency is not a basis for declining to analyze the agency's interpretation under the Chevron framework." Id.
      According to the commenter it is not enough that EPA has purported to "explain" why it has abandoned the interpretation of CAA 112(n)(1) which it adopted in 2005. Under the first step of Chevron, the Agency's latest interpretation must still be consistent with congressional intent. See Chevron v. NRDC, 467 U.S. at 842-43. Under the second step of Chevron, if there is discretion for EPA to exercise in interpreting the "critical terms" of CAA 112(n)(1), the Agency must properly define the range of that discretion and then act reasonably in exercising that discretion. See Chevron, 467 U.S. at 843; see also Village of Barrington, Ill. v. Surface Transportation Bd., No. 09-1002 (D.C. Cir. Mar. 15, 2011). As discussed below, EPA has failed to do so here. In each instance, the Agency has departed from the correct interpretation of CAA 112(n)(1) that it adopted in 2005, seizing instead upon a new approach that is contrary to the plain language of the CAA itself.
	Response: Commenter here appears to argue that EPA's interpretation of section 112(n)(1) is not consistent with the plain language of the statute, implying that the statute is clear and must be evaluated under step one of Chevron. See Chevron v. NRDC, 467 U.S. 837 842-42 (1984) (finding that when the legislative intent is clear no additional analysis is required). However, much of the commenter's argument against EPA's interpretation is based on the flawed legislative history discussed above. As explained in the preamble to the proposed rule, the statute is subject to multiple interpretations, and we provided a reasoned basis for all the changes made to the 2005 interpretation. Furthermore, we properly considered the scope of our discretion in interpreting the statute. We believe the interpretation set forth in the proposed rule is a more natural and reasonable interpretation of the Act and, therefore, the Agency should be afforded deference pursuant to National Cable & Telecommunication Ass'n v. Brand X Internet Services, 545 U.S. 967 (2005). 
      Comment: One commenter asserts that the EPA's ultimate motivation for rejecting its prior interpretation of CAA 112(n)(1) and embracing this flawed new approach is made clear from the very outset of the proposal. According to the commenter the EPA touts the fact that "one consequence" of the MACT rule would be that the "market for electricity in the U.S. will be more level" and "no longer skewed in favor of the higher polluting units that were exempted from the CAA at its inception on Congress' assumption that their useful life was near an end." See 76 Fed. Reg. at 24,979/2. The MACT rule would "require companies to make a decision  -  control HAP emissions from virtually uncontrolled sources" or else "retire these sometimes 60 year old units and shift their emphasis to more efficient, cleaner modern methods of generation, including modern coal-fired generation." Id.
      The commenter states that this remarkably forthright statement establishes is that the underlying basis for the EPA's proposal to regulate EGUs under CAA 112 is not to address any "hazards to public health" that might be attributed to the emission by EGUs of HAPs listed under CAA § 112(b). Rather, according to commenter, the EPA is utilizing the regulation of EGUs under CAA 112 as a means to an entirely different end: i.e., to force the imposition of controls that will also have the result of reducing non-HAP emissions (primarily PM) or force the shutdown those units for which the cost of such controls would be prohibitive. At the same time, the EPA tacitly acknowledges that it cannot hope to make out a case that the regulation of EGU HAP emissions is "appropriate and necessary" within the meaning of CAA 112(n)(1). The commenter asserts that the only HAP whose health-related benefits the EPA quantifies is mercury. Elsewhere, the commenter states EPA contends that there are "additional health and environmental effects" attributable to HAPs other than mercury, but admits that it has "not quantified" those risks due supposedly to "insufficient information." See 76 Fed. Reg. at 24,999/2. With respect to mercury the commenter states that the benefits are so questionable and miniscule, some $4 million to $6 million (given a 3% discount rate), that compared to the total social costs of the rule (i.e., nearly $11 billion) the rule cannot be justified were EPA properly to interpret CAA 112(n)(1) and undertake the sort of regulatory analysis Congress intended. The commenter states that the reason that the EPA touts in this rulemaking the health benefits the EPA attributes to the reduction of non-hazardous air pollutants (again, primarily PM), the regulation of which is authorized under provisions of the CAA apart from CAA 112, is to elide the inconvenient truth regarding the truly trivial nature of the benefits attributable to HAP regulation itself. The commenter concludes that the EPA distorts CAA 112(n)(1)(A) "beyond all recognition." 
      One commenter states that the EPA is directed by CAA 112(n)(1)(A) to study the "hazards to public health anticipated to occur as a result of emissions" by EGUs of "pollutants listed under subsection (b) of this section"  -  i.e., HAPs and HAPs alone. Thereafter, EPA is authorized to regulate EGU HAP emissions if, and only if, they determine that "such regulation" of HAP emissions is "appropriate and necessary" to address the "hazards to public health" that may be attributable to HAP emissions. According to the commenter, by contrast, in this rulemaking, the EPA has seized upon the fact that the control of EGU HAP emissions will also control non-HAPs (such as PM), and then seeks to justify the regulation of HAP emissions based almost entirely on the health benefits of the reductions in non-HAP emissions that would be coincidentally achieved. The commenter believes that this "regulatory sleight-of-hand" runs afoul of congressional intent and is unlawful. Apart from EPA's fundamentally unlawful attempt to use the CAA 112(n)(1) process to impose controls on EGUs to regulate non-HAP pollutants, a number of other legal errors pervade EPA's proposal. 
 	Response: The commenter alleges that the health-related benefits to regulating HAP emissions from EGUs are "questionable and miniscule," and that the only real benefits stem from non-HAP emissions, such as PM. The commenter also implies that regulation of HAP is nothing more than a straw man and that the Agency's ultimate goal is to regulate other pollutants, and specifically PM. These allegations are wholly without merit. The Agency has conducted comprehensive technical analyses that confirm that HAP emissions from EGUs pose a hazard to public health. The analyses are discussed at length elsewhere in this final rule, and a review of the proposed and final rules utterly refutes commenter's assertion that PM reductions form the basis for the appropriate and necessary finding. PM benefits are only discussed in the Regulatory Impact Analysis accompanying the rule
 	In addition, the commenter appears to ignore the Agency's findings concerning the hazards to public health and the environment posed by HAP emissions simply because the Agency is not able to quantify the benefits associated with reductions of HAP emissions from EGUs or because the benefits that are quantified are small in relation to the co-benefits achieved through reductions in non-HAP air pollutants. What the commenter conveniently omits is the fact that the Agency is not required to quantify any benefits under the CAA before regulating HAP emissions from EGUs. The statute does not require any consideration of costs or benefits and the commenter has not shown that such considerations are required under section 112. As explained below, EPA does not consider costs when determining whether to regulate EGUs under section 112.
      Comment: One commenter states that EPA has ignored the language and intent of CAA §112(n)(1)(A) and its interpretation of this provision violates step one of Chevron. Under Chevron where the "intent of Congress is clear," that is the "end of the matter," for both the implementing agency and a reviewing court "must give effect to the unambiguously expressed intent of Congress." Chevron, 467 U.S. at 842-43. The commenter asserts that the legislative history of CAA §112(n)(1)(A) "sheds considerable light on Congress' unique approach to regulation of EGUs under CAA §112." According to the commenter on April 3, 1990, the Senate passed S. 1630. The Senate bill would have required EPA to list EGUs under CAA §112(c) and to regulate them under the MACT provisions of CAA §112(d). See S. 1630 §301, 3 1990 Legis. Hist. at 4407. Thereafter, the House of Representatives passed a modified version of S. 1630 on May 23, 1990. This House version substantially changed the provisions of CAA §112 as they applied to EGUs. See 1 1990 Legis. Hist. at 572-73 The House version was virtually identical to the current CAA §112(n)(1)(A), and was ultimately adopted by the conference committee, enacted by Congress and signed into law. According to the commenter Congress expressly rejected the "list-under-(c)-and-regulate-under-(d)" approach that S. 1630 would have applied to EGUs, and which Congress did choose to apply to other source categories. Commenter states that EPA's interpretation that the Agency is "required to establish emission standards for EGUs consistent with the requirements set forth in section 112(d)" (Id. at 24,993/3) fails to take the legislative history into account. 
      Response: For the reasons stated above, we believe commenter's reliance on the single statement of one Representative is flawed. In addition, in a footnote commenter states that EPA did recognize a "need to address" the legislative history in its 2005 action. Commenter cites no case law to support this "need to address" unpersuasive legislative history argument. Further, in the 2005 action, EPA relegated to a footnote the Oxley statement that commenter relies on so heavily even though the statement supported the interpretation we provided in that rule. We recognized what the commenter fails to, that the Agency cannot argue that the meaning of section 112(n)(1)(A) is clear based on the statements of one Congressman. 
	Commenter is incorrect when it asserts that EPA's opinion is of no moment. The Agency tasked with implementing an ambiguous statute is given considerable deference in interpreting the provision. Commenter's assertion that Congress unambiguously defined the factors to consider in making the appropriate determination is wholly without merit. We explain in the proposed rule the basis for the Agency's interpretation, and we are not revising that interpretation based on the comments received.
c. Consideration of Both Public Health and Environmental Effects
      Comment: Several commenters state that EPA misreads CAA §112(n)(1)(B) and (C) to inject environmental effects in the CAA§112(n)(1)(A) determination. According to one commenter the plain language of CAA§112(n)(1) establishes that regulation of EGUs is to be predicated solely on "hazards to public health" attributable to HAP emissions. The legislative history providing that the EPA "may regulate [EGUs] only if the studies described in section 112(n) clearly establish that emissions of any pollutant... from such units cause a significant risk of serious adverse risk to the public health" confirms that plain language. See Oxley Statement at 1416-17. The commenter further states that nothing on the face of (n)(1)(A) indicates that Congress intended that EPA should (or must) take into account any additional information that might be developed through the other studies mentioned in subparagraphs (n)(1)(B) and (C) (i.e., the Mercury Study and the NAS Study).
      Response: Commenter again relies on the statements of one Representative to attack EPA's reasoned interpretation of an ambiguous statute. To the extent the commenter's arguments rely on this paltry evidence, and they rely on it to a significant degree, we need not address them as we have explained above. Because we have established that we are interpreting ambiguous statutory provisions, EPA's interpretation, not commenter's, is entitled to considerable deference because it is a reasonable reading of the statute. Chevron, 467 U.S. at 843-44. The Agency directs attention to section III.A. of the proposed rule for responses to commenter's arguments as we are not revising our interpretation.
	Commenter appears to maintain that EPA must interpret the scope of the appropriate and necessary finding in the context of the section 112(n)(1)(A) Utility Study, such that only hazards to public health and only EGU HAP emissions may be considered. The commenter incorrectly conflates the requirements for the Utility Study with the requirement to regulate EGUs under section 112 if EPA determines it is appropriate and necessary to do so. The commenter concedes that the Agency may consider information other than that contained in the Utility Study, but only to the extent it relates specifically to hazards to public health directly attributable to HAP emissions from EGUs. We agree that we may consider additional information other than that contained in the Utility Study, as we stated in the proposed rule, because courts do not interpret phrases like "after considering the results of" in a manner that precludes the consideration of other information. See United States v. United Technologies Corp., 985 F.2d 1148, 1158 (2[nd] Cir. 1993) ("based upon" does not mean "solely); see also 76 FR 24988. We further explained in the proposed rule that it was reasonable to interpret the scope of the appropriate and necessary finding in the context of all three studies required under section 112(n)(1) because the provision is title "Electric utility steam generating units." 76 FR 24986-87. Commenter has provided nothing of significance to support its stunted interpretation of our authority. Id. 
	The commenter also argues that the statute clearly prohibits the Agency from considering adverse environmental effects or the cumulative effects of HAP emissions from EGUs and other sources based on its claim that the statute is clear when one properly considers the legislative history. Again commenter has provided no support for its contention other than the statements of one Representative and the improper conflation of the section 112(n)(1)(A) direction on the conduct of the Utility Study and the appropriate and necessary finding. Congress left it to the Agency to determine whether it is appropriate and necessary to regulate EGUs under section 112 and the statute does not limit the Agency to considering only hazards to public health and only harms directly attributable to EGUs. Commenter does state that Congress specifically told EPA when it wanted EPA to consider adverse environmental effects in section 112 and cites to several provisions of the Act that require consideration of adverse environmental effects. Commenter conveniently ignores section 112(n)(1)(B), which requires consideration of adverse environmental effect, and all of the other provisions have purposes that are distinguishable from section 112(n)(1). Furthermore, EPA rightly concluded that we should protect against identified or potential adverse environmental effects absent clear direction to the contrary. Concerning the consideration of the cumulative effect of HAP emissions from EGUs and other sources, we provided a reasonable interpretation of the statute and noted that our interpretation, unlike commenters, does not "ignore the manner in which public health and the environment are affected by air pollution. An individual that suffers adverse health effects as the result of the combined HAP emissions from EGUs and other sources is harmed, irrespective of whether HAP emissions from EGUs alone would cause the harm." 76 FR 24988. 
d. Finding for all HAPs to be Regulated
      Comment: Several commenters state that for those EGU HAPs for which the Agency makes no Section 112(n)(1)(A) determination, their regulation under CAA §112 is not authorized. Accordingly, to the extent that the EPA reads CAA § 112, as construed by National Lime Ass'n, as compelling it to regulate all HAPs emitted by EGUs, should the Agency make an "appropriate and necessary" determination under CAA § 112(n)(1)(A) with respect to a single HAP (e.g., mercury), the EPA stands poised to commit a fundamental legal error that will condemn the final rule on review. Cf., e.g., PDK Laboratories, Inc., 362 F.3d at 797-98; Holland v. Nat'l Mining Ass'n, 309 F.3d at 817 (where an agency applies a Court of Appeals "interpretation ... because it believed that it had no choice" and that it "was effectively `coerced' to do so," then the agency "cannot be deemed to have exercised its reasoned judgment").
      Response: We do not agree with commenter's assertion that Congress intended EPA to regulate only those EGU HAP emissions for which an appropriate and necessary finding is made, and commenter has cited no provision of the statute that states a contrary position. EPA reasonably concluded that we must find it "appropriate" to regulate EGUs under section 112 if we determine that a single HAP emitted from EGUs poses a hazard to public health or the environment. If we also find that regulation is necessary, the Agency is authorized to list EGUs pursuant to section 112(c) because listing is the logical first step in regulating source categories that satisfy the statutory criteria for listing under the statutory framework of section 112. See New Jersey, 517 F.3d at As we noted in the preamble to the proposed rule, D.C. Circuit precedent requires the Agency to regulate all HAP from major sources of HAP emissions. National Lime Ass'n v. EPA, 233 F.3d 625, 633 (D.C. Cir. 2000). 76 FR 24989.
      Commenter does not explain its issues with our interpretation of how regulation under section 112 works  -  i.e. making a determination that a source category should be listed under section 112(c), listing the source category under section 112(c), regulating the source category under section 112(d), and conducting the residual risk review for sources subject to MACT standards pursuant to section 112(f). Instead it asserts that our decision is flawed because the interpretation we provided does not account for all the alternatives for regulating EGUs under section 112, thus we have not properly exercised our discretion and that is a fatal flaw. But what commenter has not done is provided an alternative theory for regulating EGUs under section 112, other than to blithely state that EPA could regulate under section 112(n)(1), and we have been unable to identify one absent clear statutory direction. However, even if we were to determine that we could issue standards pursuant to section 112(n)(1), or some other alternative, we would decline to do so for several reasons. First, section 112(n)(1) provides no guidance on how to establish standards and any mechanism we devised, absent explicit statutory support, would likely receive less deference than a section 112(d) standard issued in the same manner in which the Agency issues standards for other listed source categories. Second, Congress did provide a mechanism for establishing emission standards for HAP emissions from stationary sources and it is reasonable to use that mechanism to regulate HAP emissions from EGUs. Third, we do not believe that Congress intended to treat EGUs different from other sources, except in the manner in which they are listed. Finally, we believe section 112(d) standards provide the best chance of addressing the hazards to human health and the environment posed by HAP emissions from EGUs. 
e. Considering Cost in Finding
      Comment: Two commenters state that a natural reading of the term "appropriate" would include the consideration of costs. According to the commenters something may be found to be "appropriate" where it is "specially suitable," "fit," or "proper." See Webster's Third New International Dictionary at 106 (1993). The term "appropriate" carries with it the connotation of something that is "suitable or proper in the circumstances." See New Oxford American Dictionary (2d Ed. 2005) Considering the costs associated with undertaking a particular action is inextricably linked with any determination as to whether that action is "specially suitable" or "proper in the circumstances." Commenter notes that in 2005 (70 Fed. Reg. 15,994, 16,000 (Mar. 29, 2005)) the EPA used the dictionary definition of "appropriate," as being "especially suitable or compatible" and that it would be difficult to fathom how a regulatory program could be either "suitable" or "compatible" for a given public health objective without consideration of cost. 
      Response: Commenters first take issue with EPA's explanation of why the Agency determined that costs should not be considered in making the appropriate determination. What commenters do not identify is an express statutory requirement that the Agency consider costs in making the appropriate determination. Congress treated the regulation of HAP emissions differently in the 1990 CAA amendments because the Agency was not acting quickly enough to address these air pollutants with the potential to adversely affect human health and the environment in such small amounts. See New Jersey, 517 F.3d at 578. For this reason alone, it is reasonable to make the listing decision, including the appropriate determination, without considering costs. Congress could easily have required the Agency to consider costs, and, because it did not, commenter's assertion that the Agency's conclusion does not withstand scrutiny are unfounded. 
      Commenters next argues that the Agency is compelled by the statute to consider costs based on a dictionary definition of "appropriate" and the section 112(n)(1)(A) direction to consider alternative control strategies for regulating HAP emissions in the Utility Study. 
      Concerning the definition of "appropriate", Commenters state: "Not only is it "reasonable" for EPA to consider costs in determining whether it is "appropriate" to regulate EGU HAP emissions, a natural reading of the term indicates that excluding the consideration of costs would be entirely unreasonable. Something may be found to be "appropriate" where it is "specially suitable," "fit," or "proper." See Webster's Third New International Dictionary at 106 (1993). The term "appropriate" carries with it the connotation of something that is "suitable or proper in the circumstances." See New Oxford American Dictionary (2d Ed. 2005) at 76. Considering the costs associated with undertaking a particular action is inextricably linked with any determination as to whether that action is "specially suitable" or "proper in the circumstances."
	EPA believes the definition of "appropriate" commenters provide wholly support our interpretation and nothing about the definition compels a consideration of costs. It is appropriate to regulate EGUs under section 112 because EPA has determined that HAP emissions from EGUs pose hazards to public health and the environment and section 112 is "specially suitable" for regulating HAP emissions, and, furthermore, Congress specifically designated section 112 as the "proper" authority for regulations HAP emissions from stationary sources, including EGUs. Section 112 is "suitable [and] proper in the circumstances" because EPA has identified a hazard to public health and the environment and Congress directed the Agency to regulate HAP emissions from EGUs under that provision if we make such a finding. Cost does not have to be read into the definition of "appropriate" as commenter suggests.
      Commenters' argument that costs must be considered based on the section 112(n)(1)(A) requirement to "develop and describe alternative control strategies" in the Utility Study is equally flawed. The argument is flawed because Congress did not direct the Agency to consider in the Utility Study the costs of the controls when evaluating the alternative control strategies. In addition, EPA did not in fact consider the costs of the alternative controls in the Utility Study. In a footnote, commenter attempts to refute EPA's statement in the proposed rule that EPA did not consider costs in the 2000 Finding by pointing to the only two mentions of cost in that notice. But EPA did not say that costs were not mentioned in the 2000 Finding and a review of the regulatory finding will show that costs were not considered in the regulatory finding. 65 FR 79830 (December 20, 2000) ("Section III. What is EPA's Regulatory Finding?").
f. Considering requirements of the CAA in "Necessary"
      Comment: Several commenters disagree with EPA's position that it need consider "only those requirements that Congress directly imposed on EGUs through the CAA as amended in 1990," for which "EPA could reasonably predict HAP emission reductions at the time of the Utility Study." According to the commenters the statutory language of 112(n)(1) requires that EPA consider the scope and effect of EGU HAP emissions after the imposition of all of the "requirements" of the CAA, not just the Acid Rain program. It would have been easy enough for Congress in subparagraph (n)(1)(A) to specify "after imposition of the requirements of Title IV of this chapter," but Congress did not. Commenters further add that the legislative history confirms that Congress meant something much broader than that, providing that EPA is authorized to regulate EGUs under CAA § 112 only after "taking into account compliance with all provisions of the act and any other Federal, State, or local regulation and voluntary emission reductions." The commenters provides that the CAA's "requirements" include the submission by states of ozone and fine PM attainment demonstrations, as well as SIP provisions needed to reach attainment of the NAAQS because such provisions could include controls on EGUs to reduce SO2 and NOx, which controls could also result in a reduction in mercury emissions.
      Response: Commenter's characterization of the facts is flawed and its reliance on legislative history that is in direct conflict with the express terms of the statute is unfounded. 
      On the facts, EPA explained in the proposed rule its interpretation of the phrase "after imposition of the requirements of [the Act]" as it related to the conduct of the Utility Study. 76 FR 24990. We reasonably concluded that since Congress only provided three years after enactment to conduct the study that the phrase referred to requirements that were directly imposed on EGUs through the CAA amendments and for which the Agency could reasonably predict co-benefit HAP emission reductions. Id. EPA did not state that the phrase only applied to the Acid rain program as commenter asserts and the Utility Study in fact discussed other regulations, including the NSPS for EGUs and revised NAAQS. With regard to the latter, EPA ultimately determined that it could not sufficiently quantify the reductions that might be attributable to the NAAQS because states are tasked with implementing those standards. See Utility Study, pages ES-25, 1-3, 2-32. Conversely, commenter's position is that EPA must consider implementation of all the requirements of the CAA, but it does not indicate how in conducting the Utility Study the Agency could have possibly considered co-befit HAP reductions attributable to all future CAA requirements. 
      In the proposed rule, EPA recognized that we could consider requirements beyond those considered in the Utility Study, and we did consider a number of requirements that we maintain far exceed what Congress contemplated when enacting section 112(n)(1)(A). 76 FR 24991. We maintain that we have reasonably interpreted the requirement to consider the hazards to public health and the environment reasonably anticipated to occur after imposition of the requirement of the Act as explained in the proposed rule. 76 FR 24990. In addition, as stated above, we also believe it would be reasonable to find it necessary to regulate HAP emissions from EGUs based on our finding that such emissions pose a hazard to public health and the environment today. 
      With regard to the legislative history, as stated above, Representative Oxley's supposedly authoritative statement is not even consistent with the express terms of section 112(n)(1)(A) on this issue, and commenter here relies on that misstatement as support for its attack on the Agency's reasonable interpretation of the statute. Specifically, Representative Oxley stated that EPA was to take "into account compliance with all the provisions of the act and any other Federal, State, or local regulation and voluntary emission reductions," but section 112(n)(1)(A) directed the Agency to consider only "imposition of the requirements of [the CAA]." We need not address this argument further. (See also Response to Comment 1F above)
	Finally, commenter implies that EPA's position is that the Agency will only consider requirements of the Act that directly regulate HAP emissions. EPA never stated or suggested that interpretation and a fair reading of the proposed rule will demonstrate that EPA considered requirements that achieve co-benefit HAP emission reductions, for example the Transport Rule.
      Comment: One commenter continues stating under CAA §112 regulating EGUs is permissible only insofar as it is focused, targeted, and predicated on concrete findings by the Agency that such regulation is indeed "necessary." According to the commenter the EPA construes CAA § 112(n)(1)(A) as permitting it to find that it is "necessary" to regulate EGUs even where the Agency does not actually know whether it is "necessary" to regulate EGUs. Citing the D.C. Circuit, EPA suggests that "`there are many situations in which the use of the word `necessary,' in context, means something that is done, regardless of whether it is indispensible,'" in order to "`achieve a particular end.'" 76 Fed. Reg. at 24,990, quoting Cellular Telecommunications v. FCC, 330 F.3d 502, 510 (D.C. Cir. 2003). The commenter states that in the "context" of CAA § 112(n)(1)(A), as informed by the relevant legislative history, it is clear that regulation of EGU HAP emissions can be considered "necessary" only if EPA were to "clearly establish" that such regulation was effectively "indispensible" to address the identified harm. As EPA concedes that it has made no such determination here, its proposal is fatally flawed for that reason alone.
      Response: Commenter again relies on the legislative statements of one Representative and asserts that the statements are controlling. It is commenter's legal analysis that is flawed, not EPA's interpretation of the statute. 76 FR 24990-92 (Section III.A.2.b of the proposed rule contains EPA's interpretation of the term "necessary"). Commenter also, in a footnote, implies that EPA based the appropriate and necessary finding on non-HAP air pollution. Commenter is wrong.
      Further, the Commenter appears to argue that EPA's interpretation authorizes the Agency to find it necessary to regulate EGUs when we are uncertain it is necessary, but that misconstrues our interpretation and makes no sense. Instead, EPA reasonably interprets the statute to authorize the Agency to find that it is necessary to regulate if we are unable to determine that imposition of the requirements of the Act will address identified hazards to public health and the environment. The statute does not prohibit this interpretation and it is a legitimate exercise of our discretion to err on the side of regulation in the face of uncertainty concerning the level of protection necessary to protect public health and the environment. Particularly in a determination such as the necessary finding that is based on modeled projections of emissions four years into the future. The CAA requires EPA to exercise its discretion in determining whether regulation under section 112 is necessary, and the D.C. Circuit has stated that "there are many situations in which the use of the word `necessary,' in context, means something that is done, regardless of whether it is indispensible, to achieve a particular end." See Cellular Telecommunications & Internet Association, et. al. v. FCC, 330 F.3d 502, 510 (D.C. Cir. 2003). EPA's interpretation of "necessary" is reasonable in the context of section 112(n)(1)(A)
      Commenter states that EPA concedes that the Agency has not "clearly established" that regulation of HAP emissions under section 112 is "indispensible." EPA has conceded nothing but, more importantly, the supposed standard that commenter presents for evaluating whether it is necessary to regulate HAP emissions from EGUs is not required by the statute and even the limited legislative history on which the commenter incorrectly relies does not espouse such a standard. 
      Commenter takes issue with EPA's statement that the Agency may find it is necessary to regulate EGUs under section 112 if we are "uncertain whether imposition of the other requirements of the CAA will sufficiently address the identified hazards." 76 Fed. Reg. at 24,990. But commenter has again misinterpreted the Agency's position by stating that "EPA construes CAA 112(n)(1)(A) as permitting it to find that it is "necessary" to regulate EGUs even where the Agency does not actually know whether it is "necessary" to regulate EGUs." Instead, EPA maintains that it may be necessary to regulate EGUs under section 112 if we identify a hazard to public health or the environment that is appropriate to regulate today and our projections into the future do not clearly establish that the imposition of the requirements of the CAA will address the identified hazard in the future. Making a prediction about future emission reductions from a source category is difficult when there are no statutory provisions that mandate direct control of the given source category or pollutants of concern. We maintain that erring on the side of caution is appropriate when the protection of public health and the environment are not assured by our modeling of future emissions, and it is troubling that commenter does not. Furthermore, as we stated in the proposed rule, we believe it would be reasonable to find it appropriate and necessary today based on a determination that HAP emissions from EGUs pose a hazard to public health and the environment without considering future HAP emission reductions. 76 FR 24991, n.14. We maintain this is reasonable because "Congress could not have contemplated in 1990 that EPA would have failed in 2011 to have regulated HAP emissions from EGU's where hazards to public health and the environment remain." Id. The phrase "after imposition of the requirements of [the Act]" as contemplated section 112(n)(1)(A) could be read to apply only to those requirements clearly and directly applicable to EGUs under 1990 CAA amendments, all of which have been implemented and still hazards to public health and the environment remain.
	Finally, commenter does not address all of the bases on which the necessary finding is made. Specifically, EPA found in the May 3, 2011 proposed rule that it was necessary to regulate HAP emissions from EGUs because the modeling showed that the hazards to public health [and the environment?] would not be addressed through imposition of the requirements of the Act. 
g. Listing EGUs under 112
      Comment: One commenter states that even if the EPA were to establish under CAA 112(n)(1)(A) that it is "appropriate and necessary" to regulate HAP emissions from EGUs  -  and the Agency has not done so  -  regulating those emissions in the form of a MACT standard established pursuant to CAA 112(d) is contrary to the plain language of the Act. Accordingly if EPA proceeds to finalize the proposal and adopts such a standard, the rule will for this reason alone be dead-on-arrival. According to the commenter the EPA apparently believes that its only option in regulating EGU HAP emissions is establishing a MACT standard under CAA 112(d). In the preamble to its proposal, the EPA contends that, "once the appropriate and necessary finding is made," EGUs are then "subject to section 112 in the same manner as other sources of HAP emissions"  -  i.e., by "listing" EGUs under CAA 112(c) and adopting a MACT standard under CAA 112(d). See 76 Fed. Reg. at 24,993/2 (emphasis added). Given that Congress "directed the Agency to regulate utilities `under this section' [i.e., CAA 112]," The EPA continues, it follows that "EGUs should be regulated in the same manner as other categories for which the statute requires regulation." Id. (emphasis added). As EPA sees it, because "Congress did not exempt EGUs from the other requirements of section 112," once EGUs were "listed" under CAA 112(c), the Agency was "required to establish emission standards for EGUs consistent with the requirements set forth in section 112(d)." Id. at 24,993/3 (emphasis added).
	In support of this reading of the CAA, the EPA invokes the decision of the U.S. Court of Appeals for the D.C. Circuit in New Jersey v. EPA, 517 F.3d 574 (D.C. Cir. 2008). According to EPA, the D.C. Circuit has "already held that section 112(n)(1) `governs how the Administrator decides whether to list EGUs.'" See 76 Fed. Reg. at 24,993/2-3, quoting 517 F.3d at 583. EPA construes that holding as indicating that, "once listed, EGUs are subject to the requirements of section 112"  -  including, EPA presumes, CAA 112(d). Id. (The commenter states that elsewhere, the EPA construes CAA 112(n)(1) (A) as "govern[ing] how the Administrator decides whether to list EGUs for regulation under section 112," and quotes the D.C. Circuit's observation in New Jersey that "Section 112(n)(1) governs how the Administrator decides whether to list EGUs; it says nothing about delisting EGUs." See 76 Fed. Reg. at 24,981/2, quoting 517 F.2d at 582.
      The commenter asserts that the EPA misinterprets the "under this section" language of CAA 112(n)(1); overstates the significance of the New Jersey decision; and, as a consequence, misapprehends the scope of its own discretion to formulate regulatory standards for EGUs under CAA 112. In light of these errors, EPA should withdraw the proposed MACT rule.
      One commenter states that if Congress had intended that EPA regulate EGU HAP emissions only through a MACT standard, Congress could have  -  and presumably would have  -  directed the Agency to regulate EGU emissions "under CAA 112(d)." Congress did not do so. The EPA's authority to regulate EGU HAP emissions is not derived from any particular subsection of CAA 112. Rather, EPA is authorized to regulate "under this section"  -  i.e., CAA 112 generally  -  as may be "appropriate and necessary." There is nothing on the face of CAA 112(n)(1)(A) that specifies that regulation of EGUs must occur under CAA 112(d). To the contrary, a plain reading of CAA 112(n)(1)(A) indicates that establishing a MACT standard for EGUs under CAA 112(d) is not what Congress had in mind at all.
      Response: We do not agree with the commenter. EPA interpreted section 112(n)(1)(A) in a manner that gives meaning to all the words used in the provision. See NRDC v. EPA, 489 F.3d 1364, 1373 (D.C. Cir. 2007) (admonishing EPA for an interpretation of CAA section 112(c)(9) that ignored certain words and the context in which they were used the Court stated that "EPA's interpretation would make the words redundant and one of them `mere surplusage,' which is inconsistent with a court's duty to give meaning to each word used by Congress.") (citing TRW Inc. v. Andrews, 534 U.S. 19, 31, 122 S. Ct. 441, 151 L. Ed. 2d 339 (2001)). Specifically, in the proposed rule, we stated: " The statute directs the Agency to regulate EGUs under section 112 if the Agency finds such regulation is appropriate and necessary. Once the appropriate and necessary finding is made, EGUs are subject to section 112 in the same manner as other sources of HAP emissions. Section 112(n)(1)(A) provision provides, in part, that: `[t]he Administrator shall perform a study of the hazards to public health reasonably anticipated to occur as a result of emissions by electric utility steam generating units of pollutants listed under subsection (b) of this section after imposition of the requirements of this chapter... The Administrator shall regulate electric utility steam generating units under this section, if the Administrator finds such regulation is appropriate and necessary after considering the results of the study required by this subparagraph.'" Emphasis added.
	In the first sentence, Congress described the study and directed the Agency to evaluate the hazards to public health posed by HAP emissions listed under subsection (b) (i.e., section 112(b)). The last sentence requires the Agency to regulate under this section (i.e., section 112) if the Agency finds such regulation is appropriate and necessary after considering the results of the study required by this subparagraph (i.e., section 112(n)(1)(A)). The use of the terms section, subsection, and subparagraph demonstrates that Congress was consciously distinguishing the various provisions of section 112 in directing the conduct of the study and the manner in which the Agency must regulate EGUs if the Agency finds it appropriate and necessary to do so. Congress directed the Agency to regulate utilities "under this section," and accordingly EGUs should be regulated in the same manner as other categories for which the statute requires regulation. See 76 FR 24993.
      We maintain that our interpretation of the statute gives meaning to all the word, and commenter's interpretation does not give any particular meaning to the requirement to "regulate under this section [112]". Commenter is correct that Congress could have in section 112(n)(1)(A) directed EPA to regulate HAP from EGUs under section 112(d) after making the appropriate and necessary finding, but commenter presumes too much when it states that Congress would have directed the Agency to regulate HAP emissions from EGUs in such a manner if that is what Congress wanted. It is equally true that Congress could have directed EPA to regulate HAP emissions from EGUs under subparagraph 112(n)(1)(A) if that is what it wanted, but it did not. As we explained in the section II.A. of the proposed rule, section 112 establishes a mechanism to list and regulate stationary sources of HAP emissions. 76 FR 24,980-81. Regulation under section 112 generally requires listing under section 112(c), regulation under section 112(d), and, for sources subjected to MACT standards, residual risk regulations under section 112(f) (as necessary to protect human health and the environment with an ample margin of safety). It is not inconsistent with the plain language of section 112(n)(1)(A) to conclude that EPA should list EGUs once the prerequisite appropriate and necessary finding is made, and listed sources must be regulated under section 112(d). See section 112(c)(2). 
      Furthermore, the flaws in commenter's interpretation are highlighted by other section 112 provisions wherein Congress provided specific direction as to the manner of regulation. For example, section 112(m)(6) requires the Administrator to determine "whether the other provisions of this section [112] are adequate" and also indicates that "[a]ny requirements promulgated pursuant to this paragraph . . .shall only apply to the coastal waters of the States which are subject to [section 328 of the CAA]." (emphasis added). In addition, section 112(n)(3) provides that when the Agency is "promulgating any standard under this section [112] applicable to publicly owned treatment works, the Administrator may provide for control measures that include pretreatment of discharges causing emissions of hazardous air pollutants and process or product substitutions or limitations that may be effective in reducing such emissions." Finally, section 112(n)(5) directs the Agency to assess hydrogen sulfide emissions from oil and gas extraction and "develop and implement a control strategy for emissions of hydrogen sulfide to protect human health and the environment . . . using authorities under [the CAA] including [section 111] of this title and this section [112]." (emphasis added). We believe these provisions provide ample evidence that Congress knew how to alter or caveat regulation under section 112 when that was its intent. For these reasons, we believe commenter's argument is without merit.
      Comment: Two commenters state that Section 112(n)(1)(A) does not specify that regulation of EGUs must proceed under section 112(d). An argument could be made, therefore, that the CAA accords EPA with the discretion to regulate EGUs using strategies other than emission standards in section 112(d). Section 112(n)(1)(A) requires that the EPA "develop and describe" alternative control strategies for emissions which may warrant regulation under section 112. According to the commenters if Congress meant for EPA to have one sole regulatory option, i.e., regulation of EGUs only under section 112(d), then the development of alternative control strategies would be rendered meaningless because under CAA § 112(d)(3), EPA is required to determine the level of control that is achieved by the best performing existing units for which it has data and then to impose that level of control on all existing units. The development of "alternative control strategies" has no role to play in this process. One commenter does note that the consideration of "alternative" controls becomes relevant, if at all, only in those circumstances where EPA might seek to establish a "Beyond-the-Floor" MACT standard pursuant to CAA § 112(d)(2).
      Response: The Commenters are correct that section 112(n)(1)(A) directed the Agency to develop alternative control strategies for regulating HAP emissions from EGUs that may warrant regulation in the Utility Study, but the commenters' interpretation of and conclusion based on that language are both factually and legally inaccurate. 
	The commenters appear to interpret the word "alternative control strategies" to mean something other than the traditional control technologies and control measures that are used to control HAP emissions from EGUs. We do not believe that is a realistic or reasonable interpretation of the statute, and the Agency did not interpret the statute in that manner when it conducted the Utility Study. In Chapter 13 of the Utility Study, EPA considered a range of control measures that would reduce the different types of HAP emitted from EGUs. http://www.epa.gov/ttn/atw/combust/utiltox/eurtc1.pdf. EPA considered pre-combustion controls such as coal washing, fuels switching, and gasification; combustion controls such as boiler design; post-combustion controls such as fabric filters, scrubbers, and carbon absorption; and alternative controls strategies such as demand side management, energy conservation, and use of alternative fuels (e.g. biomass) or renewable energy. The options discussed in the Utility Study for controlling HAP emissions from EGUs are almost universally available to comply with a section 112(d) standard. 
	Given the manner in which the Agency conducted the Utility Study, EPA obviously interpreted the statutory direction as a requirement to set forth the control options available to EGUs to comply with section 112 standards in the event the Agency determined regulation was appropriate and necessary. EPA's development and discussion in the Utility Study of alternative control strategies for complying with the standards would help prepare EGUs to comply with the standards if promulgated. Further, our interpretation is consistent with the direction in section 112(n)(1)(A) to develop the control strategies for HAP "emissions which may warrant regulation under this section." Thus, the statute only directed the Agency to develop alternative control strategies for the HAP the Agency determined may warrant regulation under section 112, and, tellingly, the Agency developed alternative control strategies for all manner of HAP emissions. Commenters' interpretation finds no support under the statute and we reject it. 
	Furthermore, EPA establishes section 112(d) standards for stationary sources and it is the responsibility of the sources to comply with the standards using any mechanism available, including pre-combustion and post combustion measures. Also, the establishment of a MACT standard under section 112(d)(2) and (3) is a two-step process. In the first step, the Agency establishes a floor based on the performance of the best controlled unit or units. Section 112(d)(3). In the second step, the Agency must consider additional measures that may reduce HAP emissions and adopt such measures if reasonable after considering costs and non-air quality health and environmental effects. Section 112(d)(2). Under the second step, the Agency can consider any measure that reduces HAP emissions even if no source in the category is employing the option under consideration. So, even under the commenter's flawed interpretation of "alternative control strategies", the direction in section 112(n)(1)(A) is not a "pointless exercise" for the development of section 112(d) standards.
	Comment: One commenter does not agree with EPA's finding that the word "subsection" in the first sentence of CAA §112(n)(1)(A) demonstrates that Congress was consciously distinguishing between the various provisions of section 112 in directing the conduct of the study and the manner in which the Agency must regulate EGUs," were EPA to "find[] it appropriate and necessary to do so." See 76 Fed. Reg. at 24,993/2. According to the commenter the only evident reason that the word "subsection" is used in the first sentence of CAA § 112(n)(1)(A) is because reference is made to the "pollutants" which the Utility Study is to address  -  i.e., the "pollutants" that are emitted by EGUs and which are "listed under subsection (b)" of CAA § 112. Similarly, the word "subparagraph" is used in the last sentence of CAA § 112(n)(1)(A) to identify "the study" which EPA is directed to undertake by subparagraph (A) of CAA § 112(n)(1)  -  i.e., the Utility Study. That the last sentence of subparagraph (n)(1)(A) also states that EPA "shall regulate electric utility steam generating units under this section" does not even imply  -  much less expressly communicate  -  that regulation "under this section" must mean "regulation under section 112(d)." The commenter states that Congress was "consciously distinguishing" between the "various provisions of section 112" for the sake of clarity in the drafting of CAA § 112(n).
      Response: Commenter here makes a number of arguments that appear to take issue with EPA's determination that EGUs should be regulated under section 112(d) if the Agency determines that regulation of HAP emissions from such units is appropriate and necessary. The commenter implies that EPA erred because alternative mechanisms for regulation of EGUs under section 112 might exist. We do not agree.
      Commenter's argument that EPA erred because we did not explain why section CAA section 307(d)(1)(C) contemplates regulations under section 112(n) is without merit. It is correct that the Agency believes EGUs should be regulated in the same manner as other sources if the appropriate and necessary finding is made because of the structure of section 112. Nothing in section 112(n)(1) requires or implies that the Agency should or must establish standards for EGUs under that provision. Furthermore, unlike sections 112(n)(3) and 112(n)(5) that commenter cites, section 112(n)(1)(A) does not provide any guidance concerning the manner in which EPA is authorized or required to regulate sources under section 112. See section 112(n)(3) (specifically authorizing identified control measures and other requirements for consideration in issuing standards under section 112); see also section 112(n)(5) (directing the Agency to develop and implement a control strategy for emissions of hydrogen sulfide using any authority available under the CAA if regulation is appropriate). For these reasons, we disagree that any error occurred because we did not specifically discuss in this proposed rule whether we could or should regulate EGUs under section 112(n)(1) instead of section 112(d). The Agency validly listed EGUs in 2000 and listed sources must be regulated pursuant to section 112(d). 
      Even if we agreed that regulation under section 112(n)(1) was a viable option prior to the listing, we would still list and regulate EGUs like other sources because section 112(d) provides a statutory framework for regulating HAP emissions from sources and section 112(n)(1) does not. Even if section 112(n)(1) were available to regulate EGUs, there is sufficient uncertainty about the legally vulnerability of such an approach to caution against employing it. This is particularly true given that we have identified hazards to public health and the environment from HAP emissions from EGUs that warrant regulation. 
	Commenter also takes issue with our statement in the proposed rule that the use of the words "section", "subsection", and "subparagraph" in section 112(n)(1)(A) "demonstrates that Congress was consciously distinguishing the various provisions of section 112 in directing the conduct of the study and the manner in which the Agency must regulate EGUs." See 76 Fed. Reg. at 24,993. Commenter appears to make much of our use of the word "must" in that sentence and also states that our interpretation of the significance of the use of the three terms in section 112(n)(1)(A) is flawed because Congress only used the three terms for purposes of clarity. The commenter is wrong on both points. In regard to commenter's concern with the use of the word "must" in the sentence quoted above, we note that in the next sentence we state that "Congress directed the Agency to regulate utilities `under this section,' and accordingly EGUs should be regulated in the same manner as other categories for which the statute requires regulation." Id. (emphasis added). Clearly we were not foreclosing the possibility of any alternative interpretation and our use of the term "must" should not detract from the point we were trying to make - a point that undermines commenter's argument that EPA should not regulate EGUs under section 112(d). Specifically, we believe that Congress would have directed us to regulate EGUs under section 112(n)(1)(A) if that was its intent and, absent that mandate, the best reading of the statute is the one we provided in the proposed rule.
      Commenter also states that EPA relied on section 112(c)(6) to support a conclusion that EGUs must be regulated under section 112(d). Commenter takes EPA's statements out of context. The statement in whole read: "Furthermore, the D.C. Circuit Court has already held that section 112(n)(1) "governs how the Administrator decides whether to list EGUs" and that once listed, EGUs are subject to the requirements of section 112. New Jersey, 517 F.3d at 583. Indeed, the D.C. Circuit Court expressly noted that "where Congress wished to exempt EGUs from specific requirements of section 112, it said so explicitly," noting that "section 112(c)(6) expressly exempts EGUs from the strict deadlines imposed on other sources of certain pollutants." Id. Congress did not exempt EGUs from the other requirements of section 112, and once listed, EPA is required to establish emission standards for EGUs consistent with the requirements set forth in section 112(d), as described below." See 76 Fed. Reg. at 24,993
      As can be seen from this passage, EPA did not rely on 112(c)(6), instead the Court used that provision as an example of Congress' intent regarding regulating EGUs under section 112. The commenter cited the last clause of the last sentence of the paragraph quoted above without including the prefatory clause "once listed," and, without that clause, the statement is not fairly characterized. The point EPA was making in that paragraph is that EGUs are a listed source category and listed sources must be regulated under section 112(d) unless EPA delists the source category.
	Comment: One commenter states that EPA overstates the significance of the D.C. Circuit's holding in New Jersey by suggesting that the decision mandates EGU regulation under CAA §112(d) because EGUs "remain listed" under CAA §112(c), See New Jersey, 517 F.3d at 582. According to the commenter the court declined to address the lawfulness of EPA's having "listed" EGUs under CAA §112(c), leaving that matter to be decided if and when EPA adopted standards for EGUs under CAA §112. Nowhere in the decision did the D.C. Circuit indicate that EPA must regulate EGUs under CAA §112(d).
      Response: Commenter's arguments are circular and it is difficult to fully determine exactly what its issue is with EPA's listing; however, it appears that commenter believes that EPA incorrectly relied on the New Jersey decision to justify the listing of EGUs. Commenter also appears to argue that the Agency has never explained why it has the authority to list EGUs at all. We disagree.
      As we stated in the proposed rule, section 112(n)(1)(A) requires EPA to conduct a study of HAP emissions from EGUs and regulate EGUs under section 112 if we determine that regulation is appropriate and necessary, after considering the results of the study. 76 FR 24981, 24986, and 24998. The only condition precedent to regulating EGUs under section 112 is a finding that such regulation is appropriate and necessary (after conducting and considering the Utility Study), and once that finding is made the Agency has the authority to list EGUs under section 112(c) as the first step in the process of establishing regulations under section 112. The D.C. Circuit agrees with that interpretation of the statute as evidenced by its finding in New Jersey that "section 112(n)(1)(A) governs how the Administrator decides whether to list EGUs for regulation under section 112," 517 F.3d at 582, and the Court's finding directly contradicts the commenter's position. 
      EPA did not rely on the New Jersey decision to justify the appropriate and necessary finding as the commenter suggests. We based the finding in 2000 on the extensive information available to the Agency at the time and we reaffirmed the Finding in the proposed rule based on new information. Commenter had ample opportunity to comment on the appropriate and necessary finding, and it may challenge the basis of the listing (i.e. the appropriate and necessary finding) when EPA issues the final standards.
	Comment: One commenter believes that as a result of EPA's "misapprehension" that upon making an "appropriate and necessary" finding, the Agency is compelled by the CAA to adopt a regulatory standard for EGUs under CAA § 112(d) the D.C. Circuit will condemn the final rule. According the commenter a regulation will be invalid if the regulation "`was not based on the [agency's] own judgment'" but "`rather on the unjustified assumption that it was Congress' judgment that such [a regulation] is desirable' or required." See Transitional Hospitals Corp. v. Shalala, 222 F.3d 1019, 1029 (D.C. Cir. 2000), quoting Prill v. NLRB, 755 F.2d 941, 948 (D.C. Cir. 1985). Similarly, the D.C. Circuit has held that, where an agency wrongly construes a judicial decision as compelling a particular statutory interpretation, and thereby unduly limits the scope of its own discretion, the agency's action cannot be sustained. See, e.g., Phillips Petroleum Co. v. FERC, 792 F.2d 1165, 1171 (D.C. Cir. 1986). Because the commenter believes the rule is bound to be rejected, the EPA should "reconsider the legal interpretations on which it purports to base its rule."
      Response: We do not agree that we have improperly interpreted the statute as limiting our discretion in the manner suggested by the commenter. The commenter makes only one specific allegation in this comment and that concerns the Agency's conclusion that it must establish section 112(d) standards for EGUs in light of the New Jersey decision. The commenter does not explain why that conclusion is incorrect, but as we state above and in the proposed rule, because EGUs are a section 112(c) listed source category, the Agency must establish section 112(d) standards or delist EGUs pursuant to section 112(c)(9). See New Jersey, 517 F.3d at 582-83 (holding that EGUs remain listed under section 112(c)); see also section 112(c)(2) (requiring the Agency to "establish emission standards under subsection [112] (d)" for listed source categories and subcategories); 76 FR 24998-99. We concluded in the proposed rule that we could not delist EGUs because our appropriate and necessary analysis showed that EGUs did not satisfy the 112(c)(9)(B)(i) delisting criteria. Id. We did not address in the proposed rule whether EGUs satisfied the 112(c)(9)(B)(ii) criteria because EGUs failed the first prong of the delisting provisions. Id. We reach the same conclusion in the final rule and also address the delisting petition submitted by this commenter. Because we cannot delist EGUs, we must regulate them under section 112(d). Commenter has provided no legitimate argument to rebut this conclusion.
      Comment: One commenter alleges that EPA impermissibly relied on CAA §112(c)(9) to interpret "hazards to public health", and argues that the "residual risk" provisions in CAA § 112(f)(2) are more appropriate for the establishment of standards for EGUs. The commenter states that by using 112(c)(9)(B)(i) in defining "hazards to public health", the Agency has seized on the one interpretation of the phrase that is surely contrary to congressional intent and, thus, falls out the permissible range of its interpretative discretion. The "delisting" criteria of CAA § 112(c)(9) are simply irrelevant to the decision whether EGU HAP emissions will present any "hazards to public health" sufficient to warrant regulation of those emissions under CAA § 112.
      The commenter also argues that Congress intended that EGUs be treated differently from all other "major sources" to which "listing" provisions of CAA § 112(c)(9), and the standard-setting provisions of CAA §112(d) necessarily and automatically apply. Therefore, EPA's proposal to utilize the criteria of CAA § 112(c)(9) to inform its findings under CAA § 112(n)(1)(A) treats EGUs exactly the same as all other major source categories, is contrary to congressional intent, and thus unlawful. The commenter goes on to state that in exercising its discretion to define "hazards to public health" as the phrase is used in CAA § 112(n)(1)(A), EPA would be better served to consider the "residual health risk" provisions of CAA § 112(f)(2). Those provisions provide a better analogy to the establishment of standards for EGUs under CAA § 112 than do the "de-listing" criteria of CAA § 112(c)(9).
      The commenter believes the category-specific criteria of paragraph (c)(9) are a poor fit for an evaluation of "hazards to public health" that should reasonably include such factors as the affected population, the characteristics of exposure, the nature of the health effects, and the uncertainties associated with the data. While CAA § 112(n)(1)(A) does not expressly include any requirement that EGU emissions be regulated with an "ample margin of safety," that standard is more appropriate than the "one-in-a-million" cancer risk standard of CAA § 112(c)(9)(B)(i) that EPA proposes to employ. 
 	Response: Commenter acknowledges that EPA has broad discretion to interpret the phrase "hazard to public health" but that the one thing we cannot do is use the section 112(c)(9)(B) delisting provisions as a guide. Commenter asserts that the use of the delisting standard is clearly contrary to Congressional intent but it does not provide any substantive rebuttal to our conclusion that the section 112(c)(9) standards reflects the level of hazard which Congress concluded warranted continued regulation. Instead, the commenter reverts to its argument that the statute treated EGUs differently. EPA apparently views the disparate treatment of EGUs in a different light than commenter. We maintain that the only difference applies to the manner in which EGUs are added to the list of source categories subject to regulation. We do not interpret section 112(n)(1)(A) as a Congressional license to ignore risks that Congress determined warranted regulation for all other source categories. Because section 112(c)(9) defines that level of risk, it is reasonable to consider it when evaluating hazards to public health. 
      Commenter also suggests that the "ample margin of safety standard" of section 112(f)(2) is a better fit than the one-in-a-million standard set forth in section 112(c)(9)(B)(1) for evaluating hazards to public health. Commenter asserts that an evaluation of "hazards to public health" should include such factors as the affected population, the characteristics of exposure, the nature of the health effects, and the uncertainties associated with the data. But EPA did not rely solely on the delisting provisions for evaluating hazards to public health as commenter suggests. In fact, EPA considered all of the factors the commenter suggests in making our finding. 76 FR 24992. We decline to adjust our approach to evaluating hazards to public health and the environment based on this comment.
h. December 2000 Finding (and 2005 Reversal)
      Comment: Several commenters generally support the EPA's 2000 finding that regulating HAPs emissions from EGUs under CAA section 112 is "appropriate and necessary." According to the commenters, the 2000 finding was proper under the CAA and within EPA's discretion, well-supported based on sound science available to the Agency at the time on the harm from HAPs emitted by EGUs, and no additional information makes the finding invalid. Several commenters cited the conclusions of the Utility Study and Mercury Study, which they assert well-supported the finding and satisfied the only prerequisite for the finding. One commenter specifically asserted that the 2000 finding was well-supported by the Utility Study's conclusions that (1) there was a link between anthropogenic mercury emissions and methylmercury found in freshwater fish, (2) mercury emissions from coal-fired utilities were expected to worsen by 2010, and (3) methylmercury in fish presents a threat to public health from fish consumption. One commenter noted that the CAA does not require a conclusive link between HAP emissions and harm. One commenter stated that the CAA grants the Administrator discretion in her finding, and that discretionary decision should not be overly scrutinized, citing court opinion. 
      The commenters who generally supported the 2000 finding also commented on specific aspects of the finding. Several commenters asserted that while the evidence on mercury alone supports the finding, the potential harm from non-Hg HAP further supported the 2000 finding. Several commenters noted that new science continues to support the 2000 finding. Several commenters also stated that the "appropriate" finding was further supported because numerous control options were available at the time of the finding that would reduce HAP emissions. One commenter concurred with EPA that regulating natural gas-fired EGUs was not appropriate and necessary because the impacts due to HAP emissions from such units are negligible based on the results of the Utility Study. 
      Several commenters addressed the 2005 reversal of the 2000 finding. While one commenter stated that the attempted 2005 reversal of the 2000 finding was properly rejected by the U.S. Court of Appeals, another commenter asserted that the 2005 action was reasoned and proper and that EPA reverted back to the 2000 finding without adequate explanation or support. Several commenters cited EPA in 2005 as invalidating the 2000 finding, specifically that EPA concluded that "no hazards to public health" remained after accounting for emission reductions under CAIR, and that because EPA took the exact opposite position on the interpretation of the term "necessary" in its 2005 reversal, the commenters assert that EPA's current position is illegal and eliminates any deference to the Agency. One commenter stated that in 2005 EPA recognized the potential for excessive regulation created by section 112 and determined that the December 2000 finding lacked foundation. 
      Several commenters generally disagreed with the 2000 finding, with two commenters stating that the EPA did not have a rational justification for it and another claiming that it was fraught with misinformation and overestimating assumptions. One commenter claimed that EPA did not explain the terms "appropriate" and "necessary" in the 2000 finding and that the emission control analysis was inadequate. Two commenters stated that the 2000 finding was based on data that was more than 10 years old, which causes serious concern regarding the validity of the findings because technology, the regulatory environment, and economic climate have evolved. Furthermore, because the Utility Report underestimated emissions controls that EGUs would install by 2010 and additional controls that would be later required by the Cross State Air Pollution Rule (CSAPR), the basis for EPA`s 2000 finding has changed. Several commenters state that a "plausible link" between anthropogenic mercury and methylmercury in fish is not an adequate reason for the 2000 finding. Several commenters claim that EPA only identified health concerns for mercury (and potentially nickel) not other HAPs from coal-fired EGUs in the 2000 finding, and thus cannot regulate HAPs other than mercury because the 2000 finding authorizes only the regulation of mercury. One commenter questioned the mercury emissions underlying the 2000 finding, specifically the fraction of total deposition attributable to U.S. EGUS and the fact that EPA projected an increase in U.S. EGU emissions from 1990 to 2010 though emission actually declined. 
      Several commenters raised procedural issues related to the 2000 finding. Several commenters stated that the 2000 finding failed to provide public notice and comment. According to the commenters, the CAA requires that any decision made under section 112(n) must go through public notice and comment. The commenters further stated that the failure to provide public notice and comment means that this MACT is outside EPA's statutory authority. One commenter stated that because the 2000 finding was never "fully ventilated" in front of the D.C. Circuit, EPA's authority to regulate EGUs under Section 112(d) is directly at issue. Commenters claimed that specific issues did not undergo public notice and comment, specifically least-cost regulatory options, the impact of regulation on electricity reliability, and EPA's interpretation of the requirements under section 112(n)(1)(A). One commenter claimed that EPA attempted to provide after-the-fact support for its 2000 finding with new legal analysis and new factual information, which is contrary to New Jersey v. EPA which held that the EPA may not revisit its 2000 finding except through delisting under Section 112(c)(9). One commenter stated that the EPA's 2000 Finding should be reviewed when EPA issues the actual NESHAP. One commenter stated that the 2000 finding ignored Executive Order 12866.
      Response: EPA agrees with the commenters that the December 2000 finding was reasonable and disagrees with the commenters asserting that the December 2000 finding was unreasonable or failed to follow proper procedural requirements. 
      EPA agrees that reviewing Courts defer to the reasoned scientific and technical decisions of an Agency charged with implementing complex statutory provisions such as those at issue in this case. As EPA stated in the proposed rule, EPA maintains that the December 2000 finding was reasonable based on well-supported evidence available at the time, including the Utility Study, the Mercury Study, and the NAS study, which all showed the known and potential hazards to public health and the environment. New technical analyses conducted by EPA confirm that it remains appropriate and necessary to regulate HAP emissions from EGUs. Furthermore, EPA agrees with the commenters on several points raised, specifically that EGUs were and remain the largest anthropogenic source of several HAP in the U.S., that risk assessments supporting the December 2000 finding indicated potential concern for several non-mercury HAP, and that several available control options would effectively reduce HAP emissions from U.S. EGUs.
      EPA agrees with the commenters that Congress did not exempt EGUs from HAP emission limits while simultaneously limiting emissions at other sources with less HAP emissions. Congress simply provided EPA with a separate path for listing EGUs by requiring that the Agency evaluate HAP emissions from EGUs and determine whether regulation under section 112 was appropriate and necessary. Since 1990, EPA has promulgated regulations requiring the use of available control technology and other practices to reduce HAP emissions for more than 50 industrial sectors. U.S. EGUs are the most significant source of HAP in the country that remains unaddressed by Congress's air toxics program. EPA listed EGUs in 2000 because the considerable amount of available data supported a conclusion that regulation of EGUs under section 112 was appropriate and necessary. That finding was valid at the time and EPA reasonably added EGUs to the section 112(c) list of sources that must be regulated under section 112.
      EPA acknowledges that we did not expressly define the terms appropriate and necessary in the 2000 finding, but the finding is instructive in that it shows that EPA considered whether HAP emissions from EGUs posed a hazard to public health and the environment and whether there were control strategies available to reduce HAP emissions from EGUs when determining whether it was appropriate to regulated EGUs. When concluding it was necessary, the Agency stated that imposition of the requirements of the Act would not address the identified hazards to public health or environment from HAP emissions and that section 112 was the proper authority to address HAP emissions. EPA explained in the proposed rule the conclusion that the 2000 finding was fully supported by the information available at the time and EPA stands by the conclusions in that notice. Furthermore, EPA provided an interpretation of the terms appropriate and necessary that is wholly consistent with the 2000 finding. EPA does not agree with the commenters that a quantification of emissions reductions or a specific identification of the available controls was necessary to support the 2000 finding and listing. EPA considered the Utility Study when making the finding and that study clearly articulated the various alternative control strategies that EGUs could employ to control HAP emissions. As to emission reductions, the level of HAP emission reductions cannot be estimated until the Agency proposes a section 112(d) standard after a source category is listed.
      EPA further disagrees with commenters that suggest that it was not "rational" to determine that it was appropriate to regulate HAP emissions from EGUs due to the cancer risks identified in the Utility Study or the potential concerns associated with other HAP emissions from EGUs. Nothing in section 112(n)(1)(A) suggest that EPA must determine that every HAP emitted by EGUs poses a hazard to public health or the environment before EPA can find it appropriate to regulate EGUs under section 112. In fact, EPA maintains that it must find it appropriate and necessary to regulate EGUs under section 112 if it determines that any one HAP emitted from EGUs poses a hazard to public health or the environment that will not be addressed through imposition of the requirements of the Act. EPA disputes the commenters' conclusion that the 2000 finding was limited to mercury and nickel emissions, but, even if it was, EPA reasonably concluded that EGUs should be listed pursuant to section 112(c) based on the mercury and nickel finding. Source categories listed for regulation under section 112(c) must be regulated under section 112(d), and the D.C. Circuit Court has stated that EPA has a "clear statutory obligation to set emission standards for each listed HAP". See Sierra Club v. EPA, 479 F.3d 875, 883 (D.C. Cir. 2007), quoting National Lime Association v. EPA, 233 F.3d 625, 634 (D.C. Cir. 2000). Therefore, even if EPA concluded that section 112(n)(1) authorized a different approach for regulating HAP emissions from EGUs, which we question, the chosen course (i.e. listing under section 112(c)) requires the Agency to regulate under section 112(d) consistent with the statute and case law interpreting that provision. 
      EPA disagrees that there is any concern regarding the validity of the December 2000 finding or that the emissions information provided in the December 2000 finding makes the finding "questionable" as stated by some of the commenters. EPA maintains that the December 2000 finding was sound and fully supported by the record available at the time, including the future year emissions projections. Therefore, the listing of EGUs is valid based on that finding alone. Even though mercury emissions have decreased since the December 2000 finding instead of increasing as projected, the new technical analyses confirm that mercury emissions from EGUs pose known and potential hazards to public health and the environment. EPA also stated in 2000 that uncertainty associated with the potential risk from HAP emissions justified regulation of HAP emissions from EGUs. This is true because it is well established that even small amounts of HAP can cause significant harm to human health and the environment. 
      EPA agrees with the commenters that assert that the 2005 action was in error and disagrees with the commenters that the 2005 action invalidated the 2000 finding. As fully described in the preamble to the proposal, EPA erred in the 2005 action by concluding that the December 2000 finding lacked foundation. The 2005 action improperly conflated the "appropriate" and "necessary" analyses by addressing the "after imposition of the requirements of the Act" in the appropriate finding as well as the necessary finding. EPA also indicated that it was not reasonable to interpret the necessary prong of the finding as a requirement to scour the CAA for alternative authorities to regulate HAP emissions from stationary sources, including EGUs, when Congress provided section 112 for that purpose. EPA asserts that the December 2000 finding was sound and fully supported by the record available at the time for all the reasons stated in this final rule and the proposed rule. The 2005 action interpreted the statute in a manner wholly inconsistent with the 2000 finding and attempted to delist EGUs without complying with the mandates of section 112(c)(9)(B). See New Jersey, 517 F.3d at 583 (vacating the 2005 "delisting" action). EPA set forth a revised interpretation of section 112(n)(1) that is consistent with the statute and the December 2000 finding and, as explained in the preamble to the proposed rule, the December 2000 finding was sound and fully supported by the record available at the time. EPA also explained in the proposed rule why the 2005 action was not technically or scientifically sound. EPA specifically addressed the errors associated with the 2005 action in the proposed rule and commenter's assertions do not cause us to revisit those finding in the final rule. The commenter is also incorrect in suggesting that a change in interpretation is per se invalid and the commenter has provided no support for that position. See National Cable & Telecommunications Ass'n, et. a., v. Brand X Internet Services, et. al., 545 U.S. 967, 981 (Discussing the deference provided to an Agency changing interpretations the Court stated "change is not invalidating, since the whole point of Chevron deference is to leave the discretion provided by ambiguities of a statute with the implementing Agency.") (Internal citations and quotations omitted). 
      EPA disagrees with the commenters who raise concerns about the validity of the 2000 finding because the data on which that finding was based in more than 10 years old. EPA made the finding at that time based on the scientific and technical information available, and that finding is wholly supported by that information.  In addition, even though EPA was not required to do so, EPA conducted new technical analyses utilizing the best information available since several years have passed since the December 2000 finding. These new analyses confirm that HAP emissions from EGUs continue to pose a hazard to public health and the environment, even after incorporating emission reductions that have occurred since 2000 from promulgated rules, settlements, consent decrees, and closures. 
      Commenters are also incorrect regarding procedural requirements associated with the 2000 listing. EPA did not violate CAA section 307(d) by not providing notice and comment opportunity before making the appropriate and necessary finding. Commenter UARG challenged EPA's 2000 finding and listing on the same grounds and the D.C. Circuit dismissed the case because CAA section 112(e)(4) clearly states that listing decisions cannot be challenged until the Agency issues final emission standards for the listed source category. See UARG v. EPA, 2001 WL 936363, No. 01-1074 (D.C. Cir. July 26, 2001). EPA has provided the public an opportunity to comment on both the 2000 finding and the 2011 analyses that support the appropriate and necessary determination as part of the proposed rule, and anyone may challenge the listing in the D.C. Circuit in conjunction with a challenge to this final rule. Commenters could have also commented on the section 112(n)(1) studies as they were included in the docket, but EPA is not aware of any comments on those studies. In any case, the studies were peer reviewed and considered the best information available at that time. EPA has fully complied with the rulemaking requirement of section 307(d). EPA also disagrees with commenters' characterization of the New Jersey case. The D.C. Circuit did not say as commenter suggests that EPA is not able to consider additional information that is collected after the 2000 finding; instead, the Court stated that EPA could not just revise its appropriate and necessary finding and remove EGUs from the section 112(c) list without complying with the delisting provisions of section 112(c)(9). See New Jersey, 517 F.3d at 582-83. EPA also disagrees with the commenter's assertion that EPA disregarded Executive Order 12866 when making the 2000 finding. The 2000 finding did not impose regulatory requirements or costs, and the finding was reviewed by the Office of Management and Budget in accordance with the EO.
2. New Technical Analyses
a. General comments on new technical analyses
      Comment: Several commenters state that the new analyses confirm that it remains appropriate and necessary to regulate U.S. EGU HAP under Section 112 of the CAA. These commenters state that the new analyses provide even more support than the information available at the time the 2000 finding was made, including further developed emissions control technology, proven and cost-effective control of acid gases using trona and dry sorbent injection, stabilized natural gas prices that makes fuel switching and switching dispatch to underutilized combined cycle plants more feasible, more information on ecosystem impacts from HAPs, "hotspots" from the deposition of mercury around EGUs, the potential for re-emission of mercury, updated emissions data and future projections of HAP emissions, and modern air pollution modeling tools. One commenter states that a uniform federal requirement that levels the playing field is even more of an imperative today than in 2000.
      Several commenters claim that regulating U.S. EGUs is necessary to protect public health based on information provided in the new technical analyses. These commenters acknowledge the substantial reductions in HAPs from this regulation and new studies that confirm serious health risks from HAP exposure. One commenter stated that new studies show higher risks to fetuses than previously estimated, increasing the potential for neurodevelopmental effects in newborns. One commenter notes that EGUs are a major source of HAPs, including HCl, HF, arsenic, antimony, chromium, nickel, and selenium, all of which adversely affect human health. The commenter states that because of these health effects, EPA has ample evidence to support a determination that non-Hg HAP emissions present a risk to human health.
      One commenter believes that industry data support emissions standards at least as stringent as those proposed by EPA, effective and affordable control technology has been in use in this sector for 10 to 40 years, and studies on EGU-related mercury hazard has undergone two in-depth EPA reviews, as well as a review by the National Academy of Sciences. 
      One commenter agrees that EPA may supplement its finding with subsequent information, analyses and arguments to reaffirm that earlier finding until it issues emissions standards. The commenter notes that the CAA does not freeze the finding. However, another commenter argues that EPA does not have the authority to rely on new technical analyses because the CAA requires EPA to make the finding on the basis of the Utility Study alone. According to the commenter, EPA unreasonably stretched the language of section 112 by considering new technical analyses.
      Other commenters disagree that the new analyses confirm that it remains appropriate and necessary to regulate U.S. EGUs. One commenter claims that EPA tried to use the new technical analyses to provide justification for the 2000 finding, which only found "plausible links" of health effects and "potential concerns" of health effects of certain metal emissions, dioxins and acid based aerosols. The commenter asserts that none of these new analyses demonstrate that EGU regulation under section 112 is necessary and appropriate.
      One commenter questions whether acid gas emissions limits for oil-fired units are "appropriate" or "necessary" because EPA's new technical analyses do not indicate a health concern from acid gas emissions from oil-fired units. According to the commenter, EPA identifies nickel as the main HAP of concern from oil-fired units, even though cancer-related inhalation risks were well below the reference concentrations and EPA admits that significant uncertainty remains as to whether those emissions present a health concern. 
      Citing a report from Dr. Willie Soon that was submitted to the SAB Mercury Review Panel, one commenter states that the proposed rule does not conform to the Information Quality Act, which requires that information relied on by the EPA be accurate, reliable, unbiased, and presented in a complete and unbiased manner. 
      Response: EPA agrees with the commenters that state that the new technical analyses (e.g., the Mercury Risk Assessment and the Non-Hg Case Study Chronic Inhalation Risk Assessment) confirm the 2000 finding and disagree with the commenters that state otherwise. EPA also agrees with the commenters that the 2000 finding was valid at the time it was made based on the section 112(n)(1) studies and other information available to the Agency at that time. Furthermore, EPA agrees with commenters that the final rule will lead to substantial reductions in HAP emissions from EGUs, that control of the HAP will lead to public health and environmental benefits as discussed in the RIA, that mercury emissions from EGUs pose a hazard to public health, and that non-mercury HAP emissions from EGUs pose a hazard to public health that warrants regulation under section 112.
      Although these new analyses were not required, EPA agrees with the commenters that stated that EPA is authorized to conduct additional analyses to confirm the December 2000 finding. EPA disagrees with the commenter's assertion that the Agency is not authorized to consider new information and at the same time unable to use the information available in 2000 because according to the commenter that information because it is "stale." Under this theory, the Agency could not ever make an appropriate and necessary finding prospectively, thus the Agency would be excused from its obligations to protect public health and the environment because EPA did not diligently act in undertaking its statutory responsibility to establish section 112(d) standards within two years of listing EGUs. See section 112(c)(5). This is an illogical result that finds no basis in the statute. EPA also disagrees with the commenter's assertion that EPA may only consider the Utility Study in determining whether it is appropriate and necessary to regulate EGUs under section 112 for the reasons set forth in the proposed rule. 
      The Mercury Risk TSD was peer reviewed by EPA's independent Science Advisory Board during the public comment period, and the panel assigned to review the assessment concluded "the design of the risk assessment [w]as suitable for its intended purpose, to inform a decision-making regarding an "appropriate and necessary finding" for regulation of hazardous air pollutants from coal and oil-fired EGUs." The risk assessment methodology for the non-Hg case studies was consistent with the methodology that EPA uses for assessments performed for Risk and Technology Review rulemakings, which underwent peer review by the SAB in 2009. During the public comment period, EPA also completed a letter peer review of the methods used to develop inhalation cancer risk estimates for chromium and nickel compounds, and those reviews were generally supportive. EPA has revised both TSDs documenting the two risk assessments consistent with recommendations from the peer reviewers and in response to some public comments as part of the final rulemaking and has made those revised TSDs available in the rule docket. 
      EPA disagrees with the commenter's implication that EPA conducted the new appropriate and necessary analysis because of alleged flaws in the 2000 finding. As explained in detail in the proposed rule, the 2000 finding was wholly valid and reasonable based on the information available to the Agency at that time, including the Utility Study. Further, EPA maintains that had it complied with the statutory mandate to issue section 112(d) standards within 2 years of listing EGUs EPA would likely have declined to conduct new analyses. EPA conducted new analyses because over 10 years had passed since the December 2000 finding, and EPA wanted to evaluate EGUs on the most accurate information available, even though the Agency maintains that it was not required to reevaluate the 2000 finding. In conducting the new analyses, EPA corrected errors that affected the 2005 analysis finding that it was neither appropriate nor necessary to regulate EGUs under section 112 and used updated information to support the finding.
      Under EPA's interpretation of section 112(n)(1) set forth in the proposed rule, the Agency concludes that it may list EGUs under section 112(c) if it determines that even one HAP emitted from EGUs poses a hazard to public health or the environment that will not be addressed through imposition of the requirements of the CAA. Once the Agency lists EGUs under section 112(c), it must regulate such units under section 112(d) unless the Agency can delist such sources, which EPA's risk analyses demonstrates is not possible. The D.C. Circuit has stated that EPA has a "clear statutory obligation to set emission standards for each listed HAP." See Sierra Club v. EPA, 479 F.3d 875, 883 (D.C. Cir. 2007), quoting National Lime Association v. EPA, 233 F.3d 625, 634 (D.C. Cir. 2000). 
      Concerning the acid gas HAP, EPA disagrees with the notion that each emitted HAP requires its own separate appropriate and necessary finding before the Agency may list and regulate EGUs under section 112. Furthermore, in the inhalation case study assessments, EPA was only able to quantify the portion of the acid gas risks, which might be attributable to hydrogen chloride and hydrogen fluoride emissions. While these estimated risks (which are associated with chronic non-cancer impacts, not cancer) by themselves were not very high, EPA noted that they carry the potential to combine with other respiratory irritants from other nearby sources to create cumulative exposures of concern to nearby residents. EPA also noted the sheer tonnage of hydrogen chloride emitted by all EGUs nationally as a potential concern, and indicated that these emissions had the potential to exacerbate the acidification of the natural environments. Additionally, EPA was not able to get quantitative emission information about the other acid gases (including chlorine and hydrogen cyanide), some of which are more potent respiratory irritants than hydrogen chloride. As a result, EPA continues to be concerned about the potential impacts of acid gas emissions from EGUs.
      Furthermore, EPA reasonably concluded that it was appropriate and necessary to regulate oil-fired EGUs in 2000 and EPA confirmed that conclusion was proper with the analysis set forth in the proposed rule. Commenters appear to take issue with the determination based on its view of how the Agency can and should exercise its discretion. EPA disagrees and stands by the determination for the reasons set forth in the proposed rule. EPA also stands by the determination that the maximum cancer risks posed by emissions of oil-fired EGUs are greater than 1 in a million, owing primarily to emissions of nickel compounds, and based on our analysis we are unable to delist oil-fired EGUs. 
      EPA strongly disagrees with the commenter that state that EPA failed to conform to the Information Quality Act. EPA used peer-reviewed information and quality assured data in all aspects of the technical analyses used to support the appropriate and necessary finding supporting the MATS. In addition, EPA submitted the national-scale mercury risk analysis to the SAB, which "supports the overall design of and approach to the risk assessment and finds that it should provide an objective, reasonable, and credible determination of the potential for a public health hazard from mercury emitted from U.S. EGUs." The SAB received the comments from Dr. Willie Soon, and had those comments available for consideration in their deliberations regarding the mercury risk analysis. The SAB specifically supported elements of the analysis criticized by Willie Soon regarding the use of the EPA RfD as a benchmark for risk and the connection between mercury emissions from U.S. EGUs and mercury concentrations in fish. 
b. Mercury Emissions
1. Mercury emissions from EGUs
      Comment: Commenters addressed the 2005 and 2016 emissions estimates for mercury and expressed concern that inaccuracies in these emissions result in overestimates of risks from mercury deposition. Further, commenters compared EPA's 2010 estimate and 2016 estimate, noting that it is not possible for 29 tons to be a correct inventory total for mercury emissions in both years given expected reductions from the Cross-State rule. In addition, commenters made specific comments on assumptions included in the Integrated Planning Modeling (IPM), including a concern that mercury speciation factors used by IPM are resulting in overestimates of emissions in 2016. Other commenters noted that EGU sources are the predominant source of U.S. anthropogenic mercury emissions, and in particular the oxidized and particulate forms of mercury that are of concern for mercury deposition.
      Response: EPA disagrees with commenters assertions that emissions estimates result in overestimates of risk. While EPA agrees that the 2005 Hg emissions may be an overestimate, such an overestimate in 2005 would lead to an underestimate of risk in 2016 and not an overestimate of risk as claimed by the commenter because the ratio approach used by EPA to scale fish tissue data would underestimate risk if 2005 Hg estimates were overestimated. Since the 2005 emissions are not used as a starting point for 2016 emissions from IPM, any 2005 overestimate does not affect the 2016 emissions levels. The 2016 emissions are computed by IPM based on forecasts of demand, fuel type, Hg content of the fuel, and the emissions reductions resulting from each unit's configurations. See IPM Documentation for further information. No commenter has provided any evidence that the IPM 2016 emissions projection methodology result in an overestimate.
      EPA acknowledges that the current Hg emissions estimate should not be the same as the 2016 Hg emissions estimate given that compliance with CSAPR is expected to lead to some Hg emission reduction co-benefits. For this reason, EPA has included those reductions in the future-year modeling used for the final rule mercury risk analysis. EPA estimates that current mercury emissions are 28 tons, replacing the estimated 2010 value of 29 tons reported at proposal. EPA has also revised the 2016 base estimate to 27 tons. Finally, any remaining inconsistency in EPA's revised values is not relevant to the Hg national risk analysis since the 2010 emissions are not used in any of the risk calculations, which depend only on the modeled 2005 and 2016 Hg emissions. 
      EPA disagrees with the commenter's assertion that incorrect mercury emission factors result in incorrect 2016 emissions. The 2016 projected mercury emissions are not based on emissions factors. The 2016 mercury emissions are computed by the Integrated Planning Model (IPM) based on forecasts of demand, fuel type, Hg content of the fuel, and the emissions reductions resulting from each unit's configurations. The speciation factors referenced by the commenter provide a basis for the speciation of total projected mercury emissions into particulate, divalent gaseous, and elemental species, and do not impact the total amount of mercury emissions.
      EPA agrees with commenters who noted that EGU sources are the predominant source of U.S. anthropogenic mercury emissions, and in particular the oxidized and particulate forms of mercury that are of greater concern for mercury deposition.
2. Global Mercury emissions
      Comment: Several commenters state that predicted mercury deposition relies heavily on the amount of gaseous elemental mercury used to define the boundary and initial conditions of a model, e.g. the mercury that enters the U.S. from outside the U.S. boundaries. Commenters assert that this is especially important because mercury emissions from Asia -- the region immediately upwind of North America that affects U.S. mercury deposition significantly and also affects it the most compared to other regions -- are expected to continue to increase.[,][,][,][,][,] This will have implications for the amount of mercury in the boundary and initial conditions. The commenters feel that these emission changes have not been accounted for in EPA`s model exercise, thus leading to an overestimate of U.S. EGU-attributable deposition in 2016. 
      Multiple commenters note that U.S. EGU mercury emissions are small when compared to global mercury emissions totals and natural sources within the U.S. These commenters use a variety of information to support alternative conclusions about the necessity to control U.S. EGU emissions to reduce mercury risk: global mercury emissions inventories, global and regional photochemical modeling research, and observation based assessments. A commenter states that the EPA has not acknowledged the dramatic decline in mercury emissions from U.S. EGUs since the late 1990s (approximately 50 percent) to the current level and also does not consider the relative magnitude of EGU mercury emissions compared to other sources, natural (such as fires) and human-caused.
      Response: EPA disagrees that boundary condition inflow needs adjustment. The first 10 days of the modeling simulation are not used in the analysis, which is beyond the number of days necessary to remove the influence of initial conditions on mercury deposition estimates. Accurate characterization of speciated ambient mercury inflow is problematic due to the lack of observation data near the boundaries of the large continental-scale modeling domain. EPA has determined that the perturbations applied by Pongprueksa et al (2008), of 1 ng/m3 are not realistic boundaries of global speciated mercury concentrations and do not provide directly applicable information about uncertainty related to boundary conditions. The boundary inflow for the CMAQ mercury modeling used in the mercury deposition modeling are based on a global model GEOS-CHEM simulation using a 2000 based global inventory. A comparison of global mercury emissions by continent for 2000 and 2006 was recently published by Streets et al. (2009). Total mercury emissions from Asia (and Oceania) total 1,306 Mg/yr in 2000 and 1,317 Mg/yr in 2006. EPA has determined that these estimates are consistent and there is no discernable change in mercury emissions from Asia between 2000 and 2006 and any adjustments to the boundary conditions or adjustments to modeled mercury deposition would be invalid and inappropriate. Recent research has shown that ambient mercury concentrations have been decreasing in the northern hemisphere since 2000. Since emissions from Asia have not appreciably changed between 2000 and 2006 and ambient mercury concentrations have been decreasing, ENVIRON's analysis presents information with incorrect assumptions and we need not address them further. For these reasons and the large uncertainties surrounding projected mercury global inventories EPA asserts that the most appropriate technical choice is to keep the mercury boundary conditions the same between the 2005 and 2016 simulations.
      EPA disagrees with the commenter's assertion that EPA has not acknowledged the dramatic decline in mercury emissions for the U.S. EGUs since the late 1990s. EPA analyzed historical, current, and future projected mercury emissions from the power generation sector, as cited in the proposed regulatory preamble. EPA also disagrees with the commenters' assertion that EPA failed to consider the relative magnitude of EGU mercury emissions compared to other sources. As noted in the Mercury Risk TSD, EPA modeled mercury emissions from U.S. and non-U.S. anthropogenic and natural sources to estimate mercury deposition across the country. EPA also determined the contribution of U.S. EGU Hg emissions to total Hg deposition in the U.S. by running modeling simulations for 2005 and 2016 with U.S. EGU Hg emissions set to zero. Based on the analysis done for this rule EPA finds that total mercury deposition from EGUs do significantly impact human health.
      Commenters suggest that U.S. EGU Hg emissions represent a limited portion of the total mercury emitted worldwide, including anthropogenic and natural sources. While EPA acknowledges that U.S. EGU Hg emissions are a small fraction of the total mercury emitted globally, it views the environmental significance of mercury emissions from U.S. EGUs and other domestic sources as a more germane consideration. Mercury is emitted from EGUs in three forms. Each form of mercury has specific physical and chemical properties that determine how far it travels in the atmosphere before depositing to the landscape. While gaseous oxidized mercury and particle bound mercury are generally local/regional mercury deposition concerns, all forms of mercury have the potential to deposit to local or regional watersheds. U.S.  coal-fired power plants account for over half of the U.S. controllable emissions of the quickly depositing forms of mercury. Although emissions from mercury sources outside the U.S. contribute to mercury deposition in the United States, the peer reviewed scientific literature shows that EGU mercury emissions in the U.S. significantly enhance mercury deposition and the response of ecosystems in the U.S.[,][,][,][ ]
c. Mercury Deposition Modeling
1. General Comments on Deposition Modeling
	Comment: Several commenters state that according to the ENVIRON report the EPA overestimated U.S. EGU mercury deposition by 10 percent on average (and up to 41 percent in some areas). The commenters feel this overestimation is the result of boundary condition treatment, the exclusion of U.S. fire emissions, and mercury plume chemistry approach. In addition, one commenter references the same ENVIRON report and states that before implementation of controls required by the proposed rule, areas with relatively high EGU-attributable mercury deposition (one-fifth or more of total deposition) in 2016 constitute less than 0.25 percent of the continental U.S. area and only three grid cells have EGU contributions exceeding half of total deposition. 
      Another commenter suggests that current research shows that models of mercury atmospheric fate and transport overestimate the local and regional impacts of some anthropogenic sources, such as U.S. EGUs. Thus, calculated contributions to mercury deposition and fish tissue methylmercury levels from these sources represent upper bounds of actual contributions[,] and EPA should present results as estimates of lower and upper bound limits.
      Response: EPA disagrees with the information presented by ENVIRON. The work by ENVIRON is based on the misapplication of multiple incommensurate modeling studies and false premises which include the incorrect idea that the boundary conditions are over-estimated and the idea that EPA should use in-plume chemistry that has not been explicitly characterized and peer reviewed. Reactions that may reduce gas phase oxidized mercury in plumes have not been explicitly identified in literature. Recent studies in central Wisconsin and central California suggest the opposite may happen; elemental mercury may be oxidized to Hg(II) in plumes.[,] Better field study measurements and specific reaction mechanisms need to be identified before making conclusions about potential mercury in-plume chemistry or applying surrogate reactions in regulatory modeling. The possibility that Hg(0) is oxidized to Hg(II) in plumes suggests  coal-fired power plant mercury contribution inside the United States may be underestimated in the EPA modeling. 
      EPA asserts that the numbers suggested by the commenter are inaccurate as it is not appropriate to adjust EPA estimated deposition estimates based on previous mercury modeling done with older mercury chemistry, in-plume reactions that have not been explicitly identified, and erroneous adjustments to mercury boundary inflow. Recent research has shown that ambient mercury concentrations have been decreasing in the northern hemisphere since 2000. Since emissions from China have not appreciably changed between 2000 and 2006 and ambient mercury concentrations have been decreasing, inappropriate mixing and matching of older out of date mercury modeling simulations with EPA results has been included, and the fact that ENVIRON's analysis has not undergone any scientific peer review and presents information with incorrect assumptions as noted in this response, we decline to revise our analysis as commenter suggests.
      EPA also disagrees with the commenter's interpretation of the applicability of wildfire mercury emissions to this assessment. Finley et al. (2009) suggests caution when using their field data to make assumptions about Hg(p) emissions from wildfires; the estimated particulate Hg emissions from wildfires is based on one field site with a limited sample size and the assumptions made (such as the observed Hg(p) to carbon monoxide ratios at this location) may not be valid on a broader scale. Mercury emissions from wildfires are a re-volatilization of previously deposited mercury. Given that electrical generating power plants are currently and have historically been a large mercury-emitting source the inclusion of wildfire emissions in a modeling assessment would necessarily increase the contribution from this emissions sector.
      EPA disagrees with the assertion that EPA failed to consider the relative magnitude of U.S. EGU mercury emissions compared to other sources and disagrees with the interpretation of EGU deposition presented in the ENVIRON report. As noted in the Mercury Risk TSD, EPA modeled mercury emissions from U.S. and non-U.S. anthropogenic and natural sources to estimate mercury deposition across the country. EPA also determined the contribution of U.S. EGU Hg emissions to total Hg deposition in the U.S. by running modeling simulations for 2005 and 2016 with U.S. EGU Hg emissions set to zero. Based on the analysis done for this rule EPA finds that total mercury deposition from EGUs do significantly impact human health. The ENVIRON report provides no risk analysis of EGU contribution. 
      EPA disagrees that research[,] presented by the commenter shows that U.S. EGU impacts are over-estimated. The commenter's references do not support this statement. The references provided by the commenter are based on mercury modeling that uses models that are no longer applied and that are based on out-dated mercury chemistry and deposition assumptions. Given the advances in mercury modeling since the early 2000s EPA does not feel an upper and lower bound estimate is necessary.
2. Chemical reactions
      Comment: Several commenters state that the CMAQ modeling fails to account for the chemical reduction of gaseous ionic mercury to elemental mercury that may occur in EGU plumes. The commenters note that the EPA did not use the Electric Power Research Institute's (EPRI) Advanced Plume-in-Grid Treatment, which includes a surrogate reaction to reduce gaseous ionic mercury to elemental mercury inside plumes. Multiple commenters contend that the reduction of reactive gaseous mercury to gaseous elemental mercury has been reported in power plant plumes and supporting data include atmospheric concentrations of speciated mercury measured downwind of power plant stacks at ground level monitor sites and dispersion model predictions.[,] A detailed description of various plume measurement studies is provided in EPRI Comments, Section 3.4: Plant Bowen, Georgia, Plant Pleasant, Wisconsin, and Plant Crist, Florida. One commenter felt the impact of grid resolution (12 km sized grid cells) on the CMAQ modeling was not appropriately addressed by EPA. Their concerns due to grid resolution include the idea that a source`s emissions will be averaged over the entire grid cell and such averaging causes an artificially fast dilution and may result in smoothing out areas of high and low deposition and decrease model ability to simulate smaller areas of localized high deposition. This commenter felt that using the APT would address these issues. 
	Response: EPA disagrees with the commenters' suggestions. Reactions that may reduce gas phase oxidized mercury in plumes have not been explicitly identified in literature. The references cited by the commenters are from non-peer-reviewed reports and conference proceedings. EPA does not consider information presented at conferences or industry reports to be peer reviewed literature and consideration of oral presentation material would be inappropriate. Still, the references supplied by the commenter do not contain any explicit mercury reactions. These references suggest that oxidized gas phase mercury may be reduced and postulate a possible pathway, but never describe the specific chemical reaction mechanism. 
      Recent studies in central Wisconsin and central California suggest the opposite may happen; elemental mercury may be oxidized to Hg(II) in plumes.[,] Better field study measurements and specific reaction mechanisms need to be identified before making conclusions about potential mercury in-plume chemistry or applying surrogate reactions in regulatory modeling. Currently, models such as Advanced Plume Treatment (APT) use a surrogate reaction for the potential reactive gas phase mercury reduction that may or may not occur in plumes. Reactions that may reduce gas phase oxidized mercury in plumes have not been explicitly identified in literature. The application of potentially erroneous in-plume chemistry that is a fundamental component of APT would be inappropriate. In addition, the APT is not available in the most recent version of CMAQ. It would be inappropriate for EPA to apply an out of date photochemical model with in-plume chemistry that has not been shown to exist.
      EPA agrees with the commenter that the CMAQ modeling with 12 km grid resolution may provide a lower bound estimate on EGU contribution as higher impacts using finer grid resolution are possible. The commenter's assertion that EGU impacts are likely higher further supports the final conclusions of the exposure modeling assessment. EPA would like to point out that the application of a photochemical model at 12 km grid resolution for the entire continental United States is more robust in terms of grid resolution and scale that anything published in literature and represents the most advanced modeling platform used for a national mercury deposition assessment.
3. Modeled deposition compared to measured deposition
      Comment: Multiple commenters expressed dissatisfaction related to EPA's model performance evaluation of CMAQ estimated mercury deposition. Commenters state that EPA failed to evaluate the CMAQ model against real-world measurements and that EPA fails to provide first-hand information on wet and dry deposition processes. Commenters also state EPA needs to assess how predicted values of deposition compare to Mercury Deposition Network (MDN) data and how predicted values of ambient speciated mercury concentrations compare to measurement networks like AMNet and SEARCH. In addition, commenters state that the EPA used highly aggregated performance metrics comparing model estimates to observations that they felt result in a degraded and lenient operational evaluation of the modeling system. A commenter suggests EPA's model performance provides no confidence for the intended purpose of estimating deposition near point sources. One commenter simply noted that EPA's model over-estimated total mercury wet deposition at MDN monitors. Finally, several commenters note that EPA presented a negative modeled wet deposition total in the air quality modeling TSD, which is physically impossible.
      Response: The model predicted wet deposition in the air quality modeling TSD was incorrectly calculated during post-processing of model and observation pairs. This error only influenced the calculation of model performance metrics. The error has been fixed and the model performance metrics in the revised air quality modeling TSD have been updated. In response to comments, EPA has provided additional model performance evaluation by season to the air quality modeling TSD. In addition, EPA has now included model performance evaluation for total mercury wet deposition for the 36 km modeling domain at the suggestion of the commenters. 
      EPA disagrees that an assessment comparing CMAQ total mercury wet deposition estimates to MDN data was not done. The air quality modeling TSD clearly shows a comparison of CMAQ estimated total mercury wet deposition with MDN data for the entire length of the modeling period. The characterization of wet and dry deposition processes relating to speciated mercury in global and regional scale photochemical models should be continually evaluated by the academic community and improved when appropriate. CMAQ wet deposition of mercury has been and will continue to be extensively evaluated against Mercury Deposition Network sites. There is no dry deposition monitoring network and the CMAQ dry deposition processes will be evaluated when measurement data sets become available. EPA disagrees an evaluation of ambient speciated mercury against routine monitor networks such as AMNet or SEARCH would be useful for the purposes of this particular modeling application. The AMNet mercury network did not exist in 2005, which matches EPA's baseline model simulation time period. The SEARCH network just started making preliminary measurements of mercury at one or two sites in 2005. In addition, measurement artifacts related to gaseous oxidized mercury are difficult to quantify and make direct comparison to model estimates problematic. Given the problems associated with TEKRAN measurements of ambient mercury and the sparse nature of routine measurements in the United States, ambient mercury was not compared against model estimates. 
      EPA disagrees that the model performance presented in the air quality TSD is insufficient. EPA asserts that the model performance evaluation is generally similar to the level of model performance presented in literature. One commenter presents the results of several mercury modeling studies as providing information they believe to be relevant for this assessment in terms of model performance metric estimation and the level of model performance evaluation shown for assessments modeling mercury near point sources. For example, one cited study titled `Modeling mercury in power plant plumes' models near-source EGU mercury chemistry, but provides absolutely no information about model performance evaluation. A commenter identifies two studies as supposedly having mercury modeling results that are applicable to EPA's analysis.[,]
      These studies present similar model performance metrics as EPA, and also aggregated the metrics across many monitor locations similar to U.S. EPA; however, these articles make long term annual averages of modeled and observed total mercury wet deposition before performance metrics are estimated, which presents a more favorable evaluation. The Seigneur et al. paper employs a less stringent approach for matching observations and model estimates of total mercury wet deposition in that this paper makes annual averages of both before comparison to make model performance seem optically better. It is common practice to pair modeled estimates and observations in space and time (weekly in this case) and estimate performance metrics, then average all the metrics together. The latter is the approach taken by U.S. EPA and should have been taken by the studies presented by the commenter. EPA finds the performance evaluation presented in the modeling TSD consistent with and in the case of one study, far beyond what is presented in published articles deemed relevant by the commenter. In addition to the evaluation presented by EPA in the air quality modeling TSD, CMAQ model performance for total mercury wet deposition has been compared with other mercury models.
      EPA agrees that the commenter accurately restates total wet deposition model performance information provided by EPA in the Air Quality Modeling TSD. To provide context, other mercury modeling studies show a positive bias for annual total mercury wet deposition.[,] An annual mercury modeling application done by ENVIRON and the Atmospheric and Environmental Research for Lake Michigan Air Directors Consortium show seasonal average normalized bias between 70 and 158 percent and seasonal average normalized error between 72 and 503 percent. These results indicate a very large over-estimation tendency. The model performance shown by EPA is consistent with other long-term mercury modeling applications. 
4. Excess Local Deposition from U.S. EGU Hg Emissions (Deposition Hotspots)
      Comment: One commenter states that reducing mercury will benefit local environments. The commenter states that a 2007 study confirmed the presence of mercury "hotspots" downwind from coal-fired power plants, and confirmed that coal-fired power plants within the United States are the primary source of mercury to the Great Lakes and the Chesapeake Bay. The commenter also states that the study is consistent with a major mercury deposition study conducted by EPA and the University of Michigan that concluded that approximately 70 percent of mercury wet deposition resulted from local fossil fuel emissions in the region.
      One commenter agrees with the Agency's assessment of potential for deposition "hotspots" that shows that Hg deposition near EGUs can be three times as large as the regional average. The commenter states that this excess Hg deposition would substantially increase the health and environmental risks associated with emissions at these sites. The same commenter also states that the methodology applied by EPA to quantify near-source Hg deposition is conservative. The commenter states maximum excess local Hg deposition may be significantly underestimated by averaging high deposition sites downwind of an EGU in the direction of prevailing winds with lower excess deposition at locations close to but frequently upwind of the facility. The same commenter suggests that had EPA used CMAQ and individual 144 km[2] grid cells to quantify local deposition the model could increase the excess Hg deposition at these locations significantly and place them at even greater risk of adverse health and environmental effects of HAP from U.S. EGUs. 
      One commenter states that the Hubbard Brook Research Foundation issued a report in 2007 that confirmed five mercury hotspots, one of which was in the Adirondack Park, along with four suspected hotspots. The commenter states that this study also provides a good description of the impacts of mercury on the Common Loon, which is a symbol of a healthy Adirondack environment.
      One commenter states that there is there is no evidence of mercury hotspots due to local deposition associated with coal-fired power plants. According to the commenter EPA`s use of a 50km radius to calculate hotspots is flawed. The commenter states that modeling studies show that deposition of mercury emitted from power plants is not confined to a 50-km radius around the plants and that most emissions from power plants travel beyond 50 km. 
      Several commenters state that the EPA does not adequately define hotspots in this proposed rule. Those same commenters cite a previous EPA definition of hotspots as "a waterbody that is a source of consumable fish with methylmercury tissue concentrations, attributable solely to utilities, greater than the EPA`s methylmercury water quality criterion of 0.3 mg/kg" (milligrams per kilogram). The same commenters state that it is unclear why the EPA changed from defining a hotspot by fish tissue methylmercury concentration to defining a hotspot by depositional excess. Two commenters suggest that a mercury hotspot is a specific location that is characterized by elevated concentrations of mercury exceeding a well-established criterion, such as a reference concentration (RfC) when compared to its surroundings. Those same commenters state that identifying mercury hotspots should not be constrained to locations where concentrations can be attributed to a single source or sector. One of those two commenters notes that others have defined "hotspots as a spatially large region in which environmental concentrations far exceed expected values, with such values (i.e. concentrations) being 2 to 3 standard deviations above the relevant mean".
	One commenter states that mercury concentrations are not always highest at sites closest to a major source. The commenter refers to a study by Kolker, et al. (2010) that demonstrated that concentrations of atmospheric reactive gaseous mercury, gaseous elemental mercury, and fine particulate mercury were lower when measured 25 km from a 1114 MW coal-fired EGU than when measured 100 km away. The commenter states that these findings contradict the idea, implicit in EPA`s hotspot analysis, that reactive gaseous mercury decreases with distance from a large point source. 
	One commenter states that wet deposition measurements were taken between November 2004 through December 2007 at three sites located downwind from the coal-fired power plant Crist in Pensacola, FL. The commenter states that during this period, Plant Crist emitted about 230 pounds of mercury annually, about 85 percent of which was reactive gaseous mercury. The commenter cites a study by Landing et al. (2010) that estimated that 22 - 33 percent of wet-deposited mercury at these sites came from coal combustion, including regional and local sources while the remaining 67 - 78 percent came from the global background. The commenter states that using the same data from these same wet deposition sites, Caffrey et al. (2010) found that mercury deposition and concentrations did not differ in a statistically significant manner among these three sites and that the concentrations values were similar to those from Mercury Deposition Network (MDN) sites that are more than 50 km away from Plant Crist located along the Northern Gulf of Mexico coast. 
      Another commenter states that Plant Crist installed a wet scrubber and has operated that scrubber continuously since December 2009. The commenter states that the scrubber reduces total mercury emissions by about 70 percent, but reduces emissions of reactive gaseous mercury by about 85 percent. According to the commenter, using mercury to trace metal (arsenic and selenium) ratios in precipitation collected in the same MDN in (post-scrubber) 2010, Krishnamurthy, et al. (2011) reported that mercury deposition due to local and regional sources had changed between -10 to +6 percent at these sites, relative to historic measurements. The commenter states that these changes were thought to represent upper bound estimates, since the researchers assumed that all mercury, arsenic, and selenium measured in wet deposition was from local and regional coal combustion sources although this is not the case. The commenter states that, taken collectively, these findings show that increased local deposition, possibly due to EGUs, and deposition changes due to changes in EGU emissions, are small and within the range of natural variability. 
      Two commenters state that a study by the Department of Energy (DOE) that collected and analyzed soil and vegetation samples for mercury near three U.S. coal-fired power plants  -  one in North Dakota, one in Illinois, and one in Texas  -  found no strong evidence of "hotspots" around these three plants. 
      Two commenters state that analysis of long-term trends in coal-fired EGU mercury emissions and wet deposition in Florida concluded that statistical analysis does not show evidence of a significant relationship between temporal trends in coal-fired EGU Hg emissions in Florida and Hg concentrations in precipitation during 1998-2010. According to the commenters these observational studies are supported by and consistent with evidence that oxidized mercury emitted from coal-fired power plants rapidly converts to elemental mercury, significantly reducing the potential for "local" or nearby deposition. 
	Two commenters state that the Mercury Risk TSD presents no information, summary statistics, and/or actual calculations showing how excess deposition within 50 km of an EGU source is obtained. The commenters state that by assessing only mercury deposition attributable to EGUs, EPA fails to provide a context for all other sources of mercury deposition. The commenters state that the Agency does not explain why deposition from the top 10 percent of EGU mercury emitters does not decline, despite substantial reductions in modeled mercury emissions from those sources between 2005 and 2016. According to the commenters this implies that the top 10 percent EGUs may have approximately as much of a regional effect as a local effect. 
	Two commenters state that the CMAQ model has limitations when used to predict local deposition and tends to overestimate local deposition. The commenters state that modeling studies using either a plume model or an Eulerian model predict that 91 to 96 percent of the mercury emitted by an EGU travels beyond 50 km. 
 	Response: EPA agrees with the commenters that stated that mercury emissions from EGUs deposit locally and regionally and contribute to excess local deposition near U.S. EGUs. EPA acknowledges additional studies cited by those commenters that corroborate EPA's conclusions. However, EPA disagrees with those commenters' characterization of the methodology used to calculate the potential for excess local deposition. In response, EPA has clarified the methodology in the new TSD entitled, "Technical Support Document: Potential for Excess Local Deposition of U.S. EGU Attributable Mercury in Areas near U.S. EGUs", which is available in the docket.
	EPA agrees that there is no generally agreed upon absolute definition of "hotspot". As discussed in the preamble and TSD, for the purposes of the appropriate and necessary finding, EPA determined that information on the potential for excess deposition of mercury in areas surrounding power plants would be useful in informing the finding. EPA disagrees with some commenters who misinterpreted the intent of the mercury deposition hotspot analysis. Specifically, the analysis is not of "mercury hotspots" but rather of mercury deposition hotspots, defined as excess local mercury deposition around power plants, as clarified in the new Local Deposition TSD. 
      EPA disagrees that the analysis assumes that deposition of mercury is confined to a 50-km radius around power plants. The purpose of the EPA analysis was to evaluate whether there existed "excess deposition of Hg in nearby locations within 50 km of EGUs that might result in Hg deposition `hotspots'." As explained further in the new TSD, EPA calculated the average EGU-attributable deposition (based on CMAQ modeling of mercury deposition) in the area 500 km around each plant and the average EGU-attributable deposition in the area 50 km around each plant. The difference between those two values is the excess local deposition around the plant. 
      EPA disagrees with some commenters' interpretation of the analysis as being focused on local deposition from all sources. In fact, the focus was on excess local deposition, rather than all local deposition. EPA agrees that all EGUs add to local deposition, however, not all EGUs have local deposition that greatly exceeds regional deposition, which is the relevant question. EPA disagrees that the DOE study referenced by the commenters attempted to assess the same analytical question as EPA's analysis. The DOE study focused on comparisons of total deposition near and far from power plants. EPA's analysis was not of total mercury deposition, because as EPA acknowledges throughout its analysis, global sources of mercury deposition account for a large fraction of total mercury deposition, and including those global sources of deposition would simply be adding noise to the comparison of local and regional U.S. EGU sourced mercury deposition. Because of regional deposition from both domestic and global sources of mercury, total mercury deposition at any location is unlikely to be highly correlated with local sources. However, EPA's analysis focused on U.S. EGU sourced mercury deposition, and demonstrates that for some plants (especially those with high mercury emissions), there is local deposition of mercury that exceeds the average regional deposition around the plant. 
      EPA's analysis shows there is heterogeneity in the amount of excess local deposition around plants, and Figure 1 in the new Local Deposition TSD shows that some plants actually have local deposition that is less than the regional average deposition, suggesting that most of the mercury from those plants is transported regionally, or that other EGUs in the vicinity of those plants dominate the deposition of mercury near the plants. This does not detract from the overall finding that around some power plants with high levels of mercury emissions, there is excess local deposition that is on average 3 times the regional EGU-attributable deposition around those plants. EPA has clarified the purpose of the excess local deposition analysis in the new TSD.
      EPA disagrees that the Mercury Risk TSD did not provide sufficient information regarding the excess local deposition calculation. Nonetheless, EPA has further clarified the methodology in the new Local Deposition TSD, including further descriptions of the method used to calculate the local and regional deposition around power plants along with maps and tables of results.
      EPA disagrees with the commenters that stated that the discussion of local deposition in the Mercury Risk TSD did not demonstrate that mercury deposition from the top 10 percent of EGU mercury emitters declines. Table 1 of the new Local Deposition TSD clearly shows that mean local deposition (within 50km of a plant) for the top 10 percent of emitters declines from 4.89 ug/m3 to 1.18 ug/m3. What does not change is the percent local excess for EGU-attributable mercury deposition. This implies that while mercury deposition from EGUs is declining, there is still an excess contribution to local deposition relative to regional deposition, e.g. because of dispersion, the contribution to average deposition outside 50km from the plant is lower than the contribution to average deposition within 50km of the plant.
	EPA disagrees with commenters with respect to interpretation of the literature related to the spatial extent of deposition of mercury emitted by U.S. EGUs. EPA also disagrees that the CMAQ model has limitations for this application or "overestimates" local deposition. The commenter does not provide any credible support for the idea that grid based models typically overestimate "local" deposition surrounding EGUs. EPA maintains that the CMAQ photochemical model represents the best science currently available in simulating atmospheric chemistry, transport, and deposition processes. EPA does not suggest mercury emissions from power plants stop at 50 km from the source. Some portion of EGU emissions deposit before 50 km, and some portion travels beyond 50 km. In addition, mercury disperses as it transports, so the average EGU contribution can be lower in areas beyond 50km relative to areas within 50km even though mercury emissions from EGUs are depositing into U.S. watersheds.
       The study cited by the commenter supporting the notion that 91-96 percent of mercury emitted from power plants travels beyond 50 km is based on a photochemical transport model that does not employ current state of the science (TEAM model) and that is not actively developed or updated. The modeling is based on grid cells that are 20 km in size which limits generalizability to EPA modeling performed at 12 km grid resolution using a state of the science photochemical grid model. The cited modeling study ignores dry deposition of elemental mercury from all sources which is an assumption that will clearly limit the regional impacts from sources. This study cited by the commenter is critically flawed in methodology in that no results are presented where single mercury emission sources are removed and the difference between the zero out simulation and baseline model simulations are directly compared. Finally, the cited modeling study presents an illustration of gridded TEAM model total annual Hg deposition for the eastern United States that clearly shows elevated annual total mercury deposition in the vicinity of  coal-fired power plants in the Ohio River Valley and northeast Texas. 
	The information provided by a commenter based on the EPRI, 2010 reference, is not relevant to the analysis of excess local deposition from EGUs alone, as it is based on wet deposition alone. It is not expected that changes to wet deposition over a fairly short time frame such as a year (the part of the study where the  coal-fired power plant (Crist) emitting mercury installed controls) will provide a meaningful evaluation about the effectiveness of control technology since this study is based on ground level measurements of wet precipitation which is highly variable from year to year in addition to varying meteorological wind patterns from year to year. A more appropriate observation based assessment would be to evaluate both wet and dry deposition.	 
d. National-Scale Mercury Risk Analysis
1. Assumption of Linear Proportionality in Relationship between Changes in Hg Deposition and Changes in Fish Tissue Hg Concentrations (Mercury Maps)
      Comment: Several commenters are critical of EPA's assumption that changes in deposition resulting from U.S. EGU emissions of Hg will result in proportional changes in fish tissue Hg concentrations at the watershed level, as supported by the Mercury Maps modeling exercise. According to one commenter, the Mercury Maps (MMaps) model has limited capability to adequately determine bioaccumulation in fish. The same commenter states that the Mercury Cycling Model (MCM) developed by EPRI is a more rigorous model that was developed expressly to evaluate the relationship between changes in atmospheric mercury deposition to waterbodies and changes in fish tissue methylmercury levels.
      Several commenters state that the Mercury Maps model has many deficiencies. Those commenters state that Mercury Maps is a static model unable account for the dynamics of ecosystems that affect mercury bioaccumulation is fish, cannot consider non-air mercury inputs to watersheds, and assumes reductions in airborne mercury lead to proportional reductions in fish mercury concentrations. Another commenter states that data that demonstrate a steady-state linear reduction in fish tissue MeHg in response to a reduction in atmospheric mercury deposition within watersheds do not exist, providing several references they state show non-linear responses to changes in mercury deposition[,]. 
      The same commenter disagrees with EPA's interpretation of Figure 2-17 in the March TSD, and states that a U.S. Geological Survey national waterway study showed that sheet flow and drainage, not deposition, dominated input to the waterbodies it surveyed. The commenter states that sheet flow and drainage could well contain mercury, complicating the relationship that EPA claims is linear and direct. Another commenter cited Figure 2-17 in the Mercury TSD as showing that there is no well-defined relationship between mercury deposition and MeHg concentrations in fish tissue on a national basis. 
      Several commenters provided comments related to the assumption that fish tissue Hg levels used in the analysis represent a steady state. One commenter stated that given the demonstrated lag time in response to deposition change, it is logical to conclude that a lag time needs to be incorporated in MMaps to adjust the estimation of how much fish tissue methylmercury levels decrease in response to decreases in mercury deposition attributable to U.S. EGUs. According to the same commenter, the METAALICUS study show that there is a lag time (and a non-proportional response) after 3 - 4 years. The same commenter notes that there are numerous factors that influence lag time including (1) watershed characteristics, (2) watersheds may act as legacy sources releasing mercury when disturbed, (3) the magnitude of emission reductions and subsequent changes in atmospheric deposition need to be weighed against the amount of mercury already in an ecosystem, (4) the distance of an ecosystem from mercury sources, and (5) mercury deposited to aquatic ecosystems becomes less available for uptake by biota over time. Another commenter stated that there are additional Mercury Maps assumptions that do not allow for considerations of lag in response to changes in: (1) deposition; (2) legacy sources of mercury such as mining; (3) historical mercury deposition; (4) natural mercury levels in fish; (5) ecosystem dynamics over time; or (6) the relative source contributions over time. Another commenter stated that lag times would need to be included in the modeling and be able to vary from watershed to watershed and sometimes even from waterbody to waterbody within a watershed. Several commenters stated that the emission rates of mercury due to U.S. sources have been decreasing for more than a decade, while emissions due to sources outside the U.S. have been increasing. Therefore, the commenter asserts that the system is not at steady-state, a basic premise of the model. Another commenter states that while the time lag for deposition to reach a waterbody is mentioned in the Mercury Risk TSD, there is no discussion of that fact that a portion of the deposition is unlikely to reach the water at all. 
      One commenter believes EPA is incorrect in implying that its EGU risk estimates using Mercury Maps are underestimated because they do not account for legacy EGU-attributable deposition, which EPA assumes to be higher. 
      One commenter states that while EPA properly screened out watersheds with significant current non-air sources of Hg, EPA has not adequately screened out watersheds with significant Hg contributions from non-air sources, specifically, EPA does not screen out watersheds with historic mercury or gold mining or other industrial Hg discharges. The same commenter stated that EPA's study was not geographically balanced, and was dominated by rivers in the coastal region of the southeast that has numerous wetlands, which are favorable locations for methylation, and that the conditions in the southeast are not typical of much of the rest of the U.S.
      Response: EPA disagrees with the commenters asserting that the assumption of a linear proportional relationship between changes in U.S. EGU deposition and fish tissue Hg levels. EPA specifically asked SAB to evaluate EPA's assumption of linear proportionality in the relationship between mercury deposition and fish tissue methylmercury concentrations, supported by the Mercury Maps analysis. The SAB peer review committee provided the following overall response, which generally supports EPA's approach:
      "The SAB agrees with the Mercury Maps approach used in the analysis and has cited additional work that supports a linear relationship between mercury loading and accumulation in aquatic biota. These studies suggest that mercury deposited directly to aquatic ecosystems can become quickly available to biota and accumulated in fish, and reductions in atmospheric mercury deposition should lead to decreases in methylmercury concentrations in biota. The SAB notes other modeling tools are available to link deposition to fish concentrations, but does not consider them to be superior for this analysis or recommend their use. The integration of Community Multiscale Air Quality Modeling System (CMAQ) deposition modeling to produce estimates of changes in fish tissue concentrations is considered to be sound. Although the SAB is generally satisfied with the presentation of uncertainties and limitations associated with the application of the Mercury Maps approach in qualitative terms, it recommends that the document include quantitative estimates of uncertainty available in the existing literature."
      The SAB peer review committee specifically addressed the Mercury Cycling Model suggested by the commenter, and had the following response:
      "The SAB agrees with the application of Mercury Maps in this assessment. There are other modeling tools capable of making a national scale assessment, such as the Regional Mercury Cycling Model (R-MCM). However, the R-MCM is more data intensive and the results produced by the two model approaches should be equivalent.
      "The R-MCM, a steady-state version of the time-dependent Dynamic Mercury Cycling Model, has been publicly available to and used by the EPA (Region 4, Athens, Environmental Research Laboratory) for a number of years. R-MCM requires more detail on water chemistry, methylation potential, etc., and yields more information as well. Substantial data support the Mercury Maps and the R-MCM steady-state results, so that the results of the sensitivity analysis and the outcomes from using the alternative models would be equivalent between the two modeling approaches. Though running an alternative model framework may provide additional reassurance that the Mercury Maps "base case" approach is a valid one, it is unlikely that substantial additional insight would be gained with the alternative model framework."
      
      In addition, the SAB states, "Since the Mercury Maps approach was developed, several recent publications have supported the finding of a linear relationship between mercury loading and accumulation in aquatic biota.[,][,] These studies suggested that mercury deposited directly to aquatic ecosystems can become quickly available to biota and accumulated in fish, and that reductions in atmospheric mercury deposition should lead to decreases in methylmercury concentrations in biota. These results substantiate EPA's assumption that proportionality between air deposition changes and fish tissue methylmercury level changes is sufficiently robust for its application in this risk assessment." 
      Based on the responses of the SAB peer review committee, EPA's use of the linear proportionality assumption, supported by the Mercury Maps analysis, is well-supported.
      EPA also disagrees with commenters' interpretation of Figure 2-17. As stated in the Mercury Risk TSD, while this figure is useful in demonstrating the lack of correlation across watersheds between total deposition of mercury and MeHg concentrations in fish tissue, it is not indicative of the likely correlation between changes in mercury deposition at a given watershed and changes in MeHg concentrations in fish tissue from that watershed. The SAB peer review panel agreed with this interpretation, noting the importance of Figure 2-17 demonstrating that "spatial variability of deposition rates is only one major driver of spatial variability of fish methylmercury and that variability of ecosystem factors that control methylation potential (especially wetlands, aqueous organic carbon, pH, and sulfate) also play a key role." 
      In response to recommendations from the SAB, we expanded the discussion of uncertainties associated with the linearity assumption, including uncertainties related to the potential for sampled fish tissue Hg level to reflect previous Hg deposition, and the potential for non-air sources of Hg to contribute to sampled fish tissue Hg levels. Each of these sources of uncertainty may result in potential bias in the estimate of exposure associated with current deposition. EPA took steps to minimize the potential for these biases by 1) only using fish tissue Hg samples from after 1999, and 2) screening out watersheds that either contained active gold mines or had other substantial non-U.S. EGU anthropogenic releases of mercury. The SAB commented that EPA's approach to minimizing the potential for these biases to affect the results of the risk analysis appears to be sound, and that additional criteria that could be applied are unlikely to substantially change the results. As a result, EPA disagrees with the commenter that EPA's screening process is inadequate. In addition, we conducted several sensitivity analyses to gauge the impact of excluding watersheds with the potential for non-U.S. EGU Hg releases, and found that the results were robust to these exclusions.
      In response to specific comments regarding the use of the Mercury Maps model, EPA clarifies that the national scale mercury risk analysis did not directly use the Mercury Maps model. Instead, EPA is applying an assumption of linear proportionality between changes in mercury deposition and changes in MeHg concentrations in fish that is supported by the Mercury Maps modeling. By assuming steady-state conditions in apportioning fish tissue Hg levels and risk, EPA does not attempt to project lag times. Recent research cited by the SAB[,][,] identifies relatively rapid response of fish tissue Hg to changes in Hg loading, which suggests that fish tissue Hg levels could react more quickly to reductions in Hg deposition than previously thought. This finding reduces concern that fish tissue Hg levels could be linked to older patterns of Hg deposition and strengthens the approach used in the Revised Mercury Risk TSD. 
2. Characterization of Subsistence Fishing Populations and Exposure Scenario
      Comment: Several commenters state that the EPA provides no clear definition of subsistence, near subsistence, or high-end fish consumption, instead assuming that poverty is a direct indication of subsistence fishing and high-end fish consumption. One commenter states that there is no documentation supporting these assumptions. Another commenter states that EPA's definitions of subsistence fishers in the Mercury Risk TSD are not consistent with earlier EPA documents, and are used inconsistently throughout the Mercury Risk TSD. Several commenters state that while subsistence fishing can be associated with poverty, poverty does not indicate subsistence fishing. One commenter states that by including watersheds with as few as 25 members of individuals living in poverty, EPA overstates risks.
      One commenter states that it is unclear what literature the Agency says "generally supports the plausibility of high-end subsistence-like fishing ... to some extent across the watersheds" and states that if other studies exist, then the EPA should provide the values for comparison. 
      One commenter states that the EPA combined two parameters with differing scales to establish the geographic unit used in the Mercury Risk TSD risk assessment. HUC watersheds are based on average about 35 square miles in size, while U.S. census tracts used to identify watersheds relevant for subpopulations of interest -- cover a few tenths to hundreds of square miles. Several commenters stated that it is unclear how differences in geographic resolution between watersheds and census tracts were handled in the analyses.
	One commenter states that procedure for assigning census tracts could bias exposure outcomes. For example, a single influential census tract in a watershed could drive risk, even if the watershed had only a minimal number of fish samples. The commenter states that this possibility is a concern in urban areas, which account for the majority of census tracts, because these census tracts are more likely to be included in a risk analysis because they have more than 25 people living in poverty. The commenter states that these census tracts may drive the extremes of the distribution without regard to the actual number of high-level, self-caught fish consumers within their boundaries. The commenter stated that they could not assess the potential bias and noted that the EPA did not test the bias by sensitivity analyses.
	Several commenters state that EPA was not clear whether the poverty criteria were applied in all scenarios or just for the high-end female fish consumer scenario. One commenter states that EPA should apply the minimum 25 source population criteria only to populations of women of childbearing age. One commenter states that the EPA assumption would result in any densely populated urban census tract with a single fish tissue sample being assigned to a potentially at risk watershed, regardless of the actual degree of recreational or subsistence fishing taking place there.
 	Response: EPA agrees with the comments that subsistence fish consumption was not clearly defined, and we have provided a clearer definition in the revised Mercury Risk TSD, however, this clarification does not result in any changes to the quantitative analysis. In the Revised Mercury Risk TSD, EPA clarifies that "subsistence fishers" are defined as individuals who rely on noncommercial fish as a major source of protein (U.S. EPA, 2000). This definition is reflected in the range of fish consumption rates used in estimating risk. The likely presence of this type of subsistence fish consumer is supported by available peer-reviewed literature (see Table 1-5 of the Revised Mercury Risk TSD). These studies clearly show that a subset of surveyed fishers consumes self-caught fish at the rates that were cited in the Mercury Risk TSD. The SAB peer review concluded that the consumption rates and locations for fishing activity are supported by the data presented in the Mercury Risk TSD, and are generally reasonable and appropriate given the available data.
	EPA notes that there is some confusion in the comments related to the size of the watersheds modeled. Several commenters stated that HUC watersheds are 35 km on a side. The commenters appear to be referring to HUC8 classifications. HUCs are defined for varying spatial resolutions. The geographic unit used as the basis for generating risk estimates is the HUC12 scale, which is about 10 km on a side, which is consistent with the size of the CMAQ grid cells, which are 12km[2]. EPA has also clarified that the specific unit of analysis for this assessment is at the watershed, not enumerated subpopulations. 
      The U.S. Census tracts are only used to determine whether there are populations in the vicinity of a given watershed, which could increase the potential for a category of subsistence fishers to be active at that watershed. In the Revised Mercury Risk TSD, EPA modified the female subsistence scenario to be applied equally to all watersheds with fish tissue Hg data based on the likelihood that these populations have the potential to fish at most watersheds. Thus, concerns regarding the use of census data to select watersheds with the potential for subsistence fishing are no longer applicable for this scenario. However, for the remaining subsistence scenarios, EPA continues to use U.S. Census tract-level data to evaluate the presence of a "source population" in the vicinity of the watershed being modeled for risk. In this context, the U.S. Census data are being used to assess whether a SES-differentiated group similar to the particular type of subsistence fisher being modeled (e.g., poor Hispanics) are located in the vicinity of the watershed. If a source population is nearby, then this increases the potential that subsistence fishing activity could occur for that population scenario.
      EPA continues to model risk for white and black subsistence fishers active in the southeast and for Hispanics assessed nationally. In this case, EPA links poverty with subsistence fishing in that these populations are only modeled for locations with poor source populations. However, in modeling these three populations, EPA asserts that the presence of a poor source population is an indicator of the potential for subsistence fishing activity, rather the presence of such activity. The linkage between poverty and higher rates of subsistence fish consumption is supported by the Burger et al. study, which identified substantially higher consumption rates for poor individuals (see Table 5 of the study). EPA acknowledges that subsistence fishing activity by specific subpopulations might only be present across a subset of the watersheds EPA modeled for risk. However, given the stated goal of the analysis of determining the percent of watersheds where the potential exists for exposures to U.S. EGU-attributable Hg to represent a public health hazard, identifying a set of watersheds with the potential for the type of high fish consumption that leads to high Hg exposure is appropriate. EPA notes that a relatively small fraction (less than 4 percent) of watersheds has fish tissue Hg data, thereby allowing them to be included in the risk assessment. Consequently, while there is the potential for including in the analysis some watersheds that may not have currently active subsistence fishing activity, there is also the very real possibility that EPA excluded other watersheds from the analysis where this type of subsistence fishing activity occurs, due to a lack of fish tissue Hg data.
      EPA agrees with the comment that it is likely that exposure to total MeHg through commercial fish consumption represents a more significant risk for the general population than consumption of freshwater fish obtained through self-caught fishing activity. However, subsistence fishers active at inland freshwater watersheds are likely to experience the highest levels of individual risk as a result of exposure to U.S. EGU-sourced mercury. Therefore, EPA focuses on this group of subsistence fishers in the risk assessment and do not evaluate exposure for the general population related to mercury exposure through seafood.
3. Cooking Loss Adjustment Factor
      Comment: Several commenters state that the EPA did not justify the selection of a cooking loss factor of 1.5 that, according to one commenter, increases estimated intake by 50 percent, thus increasing the daily methylmercury intake rate by a constant factor of 33 percent and also increasing any resulting (HQ) risk estimate by a similar factor. Several commenters state that the source of the EPA's selected loss factor reported a range of cooking losses from 1.1 to 6. Several commenters cite several studies that report no or highly variable changes in MeHg levels as a result of cooking fish[,][,][,][,]. One commenter suggests that the EPA cooking loss adjustment factor of 1.5 is at the high-end of the values supported by the literature. Another commenter stated that EPA has used other adjustment factors in previous documents, and that the adjustment factor should not be fixed across different populations given potential differences in cooking practices. Several commenters noted that the cooking loss adjustment factor should only be applied to estimates of consumption rates for prepared fish, and that some sources of consumption rates are based on raw fish.
      Response: EPA disagrees with the commenters that the selection of the cooking loss factor of 1.5 is not justified by the literature. EPA also disagrees with the comment that the cooking loss adjustment factor of 1.5 is at the high-end of the range of values in the literature. EPA selected the Morgan (1997) study as the basis for the food preparation/cooking adjustment factor because it focused on the types of freshwater fish species representative of what might be consumed by subsistence fishing populations (i.e., walleye and lake trout). The Morgan (1997) study provides a range of adjustment factor for each fish type including 1.1 to 1.5 for walleye and 1.5 to 2.0 for lake trout. Given these two ranges, EPA determined it to be reasonable to take an intermediate value between the two ranges (i.e., 1.5), rather than focus on either the highest or lowest values. The Morgan (1997) study explains that preparation/cooking of fish results in an increase in MeHg levels per unit fish because Hg concentrates in the muscle, while preparation/cooking tends to reduce non-muscle elements (e.g., water, bone, fat). 
      Regarding the alternative studies identified by the commenters, EPA makes the following observations. Regarding the first study, the study suggests that the authors may have included measurement of non-fish components added to dishes (e.g., onions, heavy breading etc.) in measuring Hg concentrations post-cooking. These non-fish elements could dilute the post-cooking Hg measurements giving the appearance of a cooking loss, even while actual fish tissue Hg levels could have increased due to preparation. 
      In the second study, the three fish species considered are saltwater and not freshwater which decreases the relevance of this study compared with another study that focused on freshwater species of the type reflected in the risk modeling. Furthermore, this study notes that the absolute content of Hg in fish does not decrease during cooking and instead, it is the reduction of water and fat that result in an increase in the concentration (but not a change in content), which is conceptually consistent with EPA's cooking loss factor. 
      The third study raises an interesting issue with its focus on measurement of bioaccessible mercury in raw and cooked fish. Their analysis shows that the concentration of bioaccessible mercury appears to significantly decrease in cooked fish compared with raw fish and they suggest that this needs to be factored in when measuring risk. However, in order to factor in (quantitatively) measurements of bioaccessible mercury into the risk assessment, the risk model would have to be parameterized to work with this category of mercury. However, available information currently allows us to specify the risk model in terms of total mercury intake (and not bioaccessible mercury). Specifically, the factor linking mercury intake to hair mercury level (which is then used as the exposure metric to estimate risk) is based on intake of total Hg. Consequently, while this article provides information that is potentially informative for guiding future research and methods development, it does not directly impact the current risk assessment. In addition, in terms of total mercury (not differentiated as bioaccessible), the Torres-Escribano study shows a substantial increase in unit fish concentration following cooking (see Table 1 in the article). 
      The Armbruster et al. study focused on the issue of whether cooking of fish decreased Hg levels, as can be the case with lipophilic chemicals. Their study found instead, a modest, but non-statistically significant increase in Hg levels for most of the cooking methods assessed, which is directionally consistent with the values used in the risk assessment. The Gutenmann et al. study focuses on the relationship between fish size and sex and mercury concentration (specifically for brown trout) and only addresses the issue of mercury concentration in relation to cooking and preparation in a qualitative manner. Specifically, while the article does provide results for skin on versus skin off (noting a non-statistically significant increase in mercury concentration with the latter), it qualitatively discusses the potential of fat removal (which could occur through preparation and cooking) to increase mercury concentration given that mercury is associated with protein elements of the fish. Because the article does not provide substantial empirical data regarding preparation/cooking adjustment, it is of little use in informing the food preparation/cooking adjustment factor used in the risk assessment. 
      When considered collectively, EPA disagrees that the additional studies identified by the commenter contradict the cooking loss factor used in the risk assessment and maintains that the Morgan study remains the most applicable for characterizing cooking/preparation effects on Hg concentrations in fish, given the fisher scenarios assessed in this study.
	EPA agrees that application of the cooking loss adjustment factor is appropriate if the fish consumption rates are for as cooked or as consumed and not for raw fish. Careful review of the three studies used in the risk assessment to identify subsistence fisher consumption rates suggests that all three represent annual-average daily intakes (g/day) of as consumed or as cooked fish. One study states that they used models of portion or meal size servings (the size of the serving the respondent regularly eats). Therefore, EPA interprets the fish consumption rates provided in the Burger et al. study as representing as cooked/prepared and not for raw fish and for that reason, application of a preparation/ cooking adjustment factor is required. The Shilling et al., (2010) study used different sized models of cooked fish filets and therefore these consumption rates are also interpreted as represented as cooked/prepared and not raw fish. One study, based on personal communication with the author, did query survey responders for meal portion or serving size and therefore, the consumption rates do represent as cooked/prepared. Because all three studies provide consumption rates based on as cooked/prepared or as consumed, it is appropriate to apply the cooking loss adjustment factor in modeling exposure.
4. Fish Consumption Rates and Fish Tissue Hg Characterization
      Comment: One commenter stated that in the past the Agency has recommended various default consumption rates (in the general range of 130 to <150 g/day) to provide default intakes for subsistence fishers under the Risk Assessment Guidance for Superfund (RAGS) or the Fish Advisory Guidance.[,] The commenter states that these default consumption rates are derived from various studies and generally are based on 90[th] or 99[th] percentile distribution estimates. Another commenter states that EPA's use of the 99th percentile fish consumption for its risk analysis is inconsistent with the Agency's risk assessment guidelines, which recommend evaluating a reasonable maximum exposure ("RME") scenario, which equates to about a 95th percentile fish consumption value. The same commenter states that EPA applies the 99th percentile to a "small survey of 149 South Carolina female anglers" to calculate an ingestion rate of 373 g/day. The commenter states that if the 95th percentile is use the ingestion rate would be 173 g/day and if the default ingestion rate for determining ambient water standards is used the ingestion rate would be 142 g/day.
      Several commenters state that EPA bases its fish consumption rates used in the risk analysis on a limited number of studies, and that those studies are poorly documented. 
	Another commenter states that the EPA should summarize available supporting studies by basic study content, characteristics, design, size, demographics, dietary recall period, and fish intake rates by demographic variables. According to the commenter this summary would support the scientific validity of the assessment, and better illustrate the potential variability and uncertainty involved in extrapolating data from small populations to the national scale, noting that the three studies actually used to provide subsistence population estimates, which were extrapolated to the national scale, included a limited number of individuals living in diverse and localized areas.
	One commenter stated that the assumption with the greatest impact is the fish consumption rate. That same commenter stated that there is a dramatic effect of increased HQs and loss of IQ depending on the ingestion rate considered going from the 50th percentile ingestion rate to the 99th percentile ingestion rate. The commenter states that when an estimate of the 95th percentile ingestion rate of the 15-44 year old female population is considered, the HQ is a tenth of the value computed with the 99th percentile high-end female fisher.
	One commenter states that EPA provides broad summary statistics of its fish tissue data in Table 5-2 of the Regulatory Impact Analysis (RIA), but the summary does not allow an assessment of the representativeness and robustness of the underlying data for the risk assessment, especially at the tails of the distribution. The commenter states that the table does not include a median statistic and does not provide any information on the number of lakes and river segments in each watershed. According the commenter an analysis of EPA's database by the SAB peer review panel indicated that 60 percent of the watersheds with fish mercury data from rivers have risks calculated based upon a sample size of one or two fish. The commenter states that it is not reasonable to base a significant policy and regulation decision on watersheds whose exposure is based on a single fish sample in a single water body within it.
	Several commenters criticized EPA's use of the 75[th] percentile fish tissue MeHg level in a watershed. One commenter states that EPA provides no rationale for its decision to choose the highest of the 75th percentile for fish mercury levels among rivers and lakes within the HUC. Several commenters stated that subsistence fishers are less likely to target larger fish relative to recreational fishers. Several commenters suggested that EPA include a sensitivity analysis using the mean or median fish MeHg level in a watershed. One commenter also stated that EPA arbitrarily inflates the risk estimates by assuming consumption of only fish greater than 7 inches and choosing the largest of the 75th percentile of fish mercury levels from these larger fish (i.e., larger than 7 inches) for rivers and lakes. That same commenter suggests using the median of all size fish, not just those over 7 inches. 
	One commenter states that EPA should quantify adverse effects from the ingestion of MeHg in seafood in addition to ingestion of MeHg from self-caught freshwater fish. According to the commenter, recent studies demonstrate that were EPA to take into account consumption of seafood, MeHg consumption in the U.S. is of even greater concern.
      Response: EPA acknowledges that the focus of the national scale risk assessment is characterizing risk for the group likely to experience the greatest U.S. EGU-sourced mercury risk, which is subsistence fishing populations active at inland freshwater lakes and rivers. Specifically, within that subsistence fishing population, EPA is interested in those individuals who are most at risk, which includes those who consume the most fish. For that reason, EPA included consideration for a range of high-end fish consumption rates including the 99[th] percentile representing the most highly-exposed individuals. In responding to the SAB peer review, EPA has clarified this focus in the introduction to the Revised Mercury Risk TSD, and have changed the full title to "Revised Technical Support Document: National-Scale Assessment of Mercury Risk to Populations with High Consumption of Self-caught Freshwater Fish." This focus for the risk assessment (including modeling of the 99[th] percentile fish consumption rate by subsistence fishers) reflects consideration for the provisions of the Clean Air Act addressing the appropriate and necessary determination for U.S. EGUs, and is consistent with treatment of other HAP under Section 112 of the CAA, which focuses on maximally exposed individuals. 
      EPA agrees that the fish consumption rate is an important factor in calculating risk from exposure to methylmercury in fish. EPA acknowledges that the distribution of fish consumption rates is positively skewed, which means that at higher percentiles (e.g., 90[th], 95[th] and 99[th]) there is a substantial increase in ingestion rates relative to the mean or median. The Revised Mercury Risk TSD includes a reasonableness check on the amount of fish consumed (as a daily value) reflected in the different rates. While the 99[th] percentile consumption rates for the subsistence female fisher (373 g/day) is substantially higher than the 90[th] or 95[th] percentile values (123 and 173 g/day respectively) the 99th percentile value translates into a 13-ounce meal. While this does represent a large serving, it is still reasonable if representing an individual who receives all of their meat protein from self-caught fishing (and the 13 ounces per day does not have to be eaten all at one meal). The larger rates of consumption (values in the 250+ g/day range) are supported by all three studies used in the risk assessment and therefore, there is support across studies for near bounding consumption rates in this range. EPA acknowledges uncertainty associated with estimation of high-end percentile values in these studies due to relatively low samples sizes for some of the population groups. However, even if a few individuals provided these high self-caught fish consumption rates, making it difficult to characterize the population percentiles they represent, the values still suggest the existence of these levels of high fish consumption among surveyed individuals. In the context of determining whether a public health hazard could exist, EPA asserts that it is reasonable to include these consumption rates as representative of the most at risk populations. In these cases, however, it is important to highlight uncertainty associated with characterizing the specific population percentile that these ingestion rates represent, and EPA has done so in the Revised Mercury Risk TSD.
      EPA disagrees with the comment that high consumption rates are poorly documented. Evidence of these high fish consuming populations can be found in surveys and specialized studies.[,][,][,][,] Several studies identified additional fishing populations with subsistence or near subsistence consumption rates, including urban fishing populations (including low-income populations),[,][,] Laotian communities, and Hispanics. EPA participated in 1999 in a project investigating exposures of poor, minority communities in New York City to a number of contaminants including Hg, which found these populations can have very high fish consumption rates. The SAB peer review concluded that the consumption rates and locations for fishing activity are supported by the data presented in the Mercury Risk TSD, and are generally reasonable and appropriate given the available data.
	EPA agrees that the Mercury Risk TSD would be improved by clarifying that the literature review focused on identifying studies characterizing subsistence fish consumption for groups active at freshwater locations within the U.S., and EPA has revised the Mercury Risk TSD accordingly. In the Mercury Risk TSD, EPA provided a summary of important study attributes for the source studies used to obtain fish consumption rates. This information was provided in Table C-1 in an appendix. To improve clarity, EPA has moved the summary table to the main body in the Revised Mercury Risk TSD. In identifying these studies, EPA focused on surveys for subsistence fishers that were applicable at the broader regional or national level. In the Mercury Risk TSD, EPA acknowledged the lower sample sizes for some of the subsistence fisher groups, and in several cases did not use the 99th percentile consumption rates because the sample sizes were too low to support this level of resolution.
      EPA disagrees with the comment that it did not provide a rationale for choosing the highest 75[th] percentile fish tissue concentration across lakes and rivers in a watershed. However, EPA has modified the methodology based on evaluation of the number of samples within each watershed (responding to a recommendation from the SAB). In the revised methodology, EPA computes the 75[th] percentile value at each sampling site within a watershed. EPA then computed the average of the site-specific 75[th] percentile fish tissue Hg values within a given watershed. This approach does not differentiate between rivers and lakes and reflects an improved treatment of behavior, allowing for fishers to choose among multiple fishing sites within a watershed. 
      EPA generally agrees with the comment that some fraction of subsistence fishers likely consume fish without consideration for size (given dietary necessity), however, it is reasonable to assume that a subset of subsistence fishers could target larger fish to maximize the potential consumption per unit of fishing effort. It is this subset of subsistence fishers targeting larger fish, which is represented by the 75[th] percentile fish tissue value used in the risk assessment. In addition, the female subsistence fishing population that is included in the analysis is also likely to provide coverage for high-end recreational anglers who could target larger freshwater fish. The SAB commented that: "Using the 75th percentile of fish tissue values as a reflection of consumption of larger, but not the largest, fish among sport and subsistence fishers is a reasonable approach and is consistent with published and unpublished data on predominant types of fish consumed." The SAB suggested that EPA include a sensitivity analysis based on use of the median value, and EPA has done so in the Revised Mercury Risk TSD. This sensitivity analysis showed that using the median estimates had only a small impact on the number and percent of watersheds identified as having populations potentially at risk from U.S. EGU-attributable MeHg exposures. Regarding the 7-inch criteria, for the Revised Mercury Risk TSD, EPA clarified that this cutoff represents a minimum size limit for a number of key edible freshwater fish species established at the State-level. For example, Pennsylvania establishes 7 inches as the minimum size limit for both Trout and Salmon (other edible fish species such as Bass, Walleye and Northern Pike have higher minimum size limits). 
      EPA disagrees with the comment that it is not reasonable to use watersheds where only a single fish sample is available. While it is preferred to have multiple samples, if anything, based on the comments of the SAB peer review panel, using a single sample is likely to underestimate the 75[th] percentile fish MeHg concentration and is therefore likely to underestimate the risk estimates for those watersheds. The SAB peer review panel provided EPA with several suggested analyses of the fish tissue MeHg data that have been undertaken and are included in the Revised Mercury Risk TSD. The Revised Mercury Risk TSD includes information on the number of watersheds modeled in the risk assessment with various fish tissue Hg samples sizes (e.g., 1, 2, 3-5, 6-10 and >10 measurements).
5. Reference Dose (RfD) for Methylmercury
      Comment: Several commenters state that the EPA's RfD is based on sound science, which was supported by the findings of the National Academy of Sciences' Study on Mercury, and EPA applied an appropriate RfD in the mercury risk assessment. The commenters also state that recent studies find clear associations between maternal blood Hg levels and delayed child development, cardiovascular effects, and potential effects due to exposure to pollutant mixtures including lead. 
      However, many commenters expressed concerns regarding EPA's use of the Methylmercury RfD as a benchmark for health risk. Several commenters raised concerns claiming that EPA has not incorporated the best available mercury toxicological data into the RfD, which results in a flawed analysis and an overestimate of the impact of mercury emissions on human health.
      Several commenters state that, when deriving the RfD, the EPA relied on the flawed Faroe Islands' children study and ignored the Seychelles Islands study, which did not confirm any harm on children due to MeHg exposure. According to the commenters, application of the Faroe Island study is suspect because (1) the raw data from the study have never been made available for independent analysis and scrutiny, (2) confounding by polychlorinated biphenyls (PCBs) and lead, (3) population exposure to MeHg through consumption of highly contaminated pilot whale meats and blubbers, and (4) exposure levels in the U.S. remain lower than those observed in the primary study. One commenter also notes that (1) Seychelles Islanders consume far more fish than do Americans; (2) the amount of MeHg in the U.S. population is 10 to 20 times below that of the Seychelles islanders; and (3) all ocean fish throughout the world contain about the same amount of MeHg, so per fish meal MeHg intake is similar between Americans and Seychelles Islanders. According to one commenter, EPA's reliance on the statistical analysis performed by the Faroe Island researchers at the request of the NAS failed to address the question of why study failed to observe any significant effects from PCBs. However, another commenter states that industry arguments against using the Faroe Islands study in deriving the RfD due to PCB confounding and the differences in the diets of Faroe Islanders fails to acknowledge that the study results were consistent with studies in the Seychelles Islands, New Zealand, and Poland. 
      One commenter criticized EPA for using a linear dose-response model for both the RfD-based HQ metric and the IQ metric without supporting explanation beyond the interpretation that this is NAS`s preference, and that it was "easier to quantify IQ loss." One commenter states that the RfD assumes a threshold dose below which an appreciable risk of adverse effects is unlikely, NAS did not evaluate whether methylmercury exposure data from the Faroe Islands were better fit by a linear or non-linear model, or by a threshold or non-threshold model. 
      Several commenters state that EPA's mercury RfD is more conservative than "safe" levels determined by the U.S. Food And Drug Administration, the World Health Organization, and the U.S. Agency for Toxic Substances and Disease Registry. Several commenters claim that EPA assigned unusually high uncertainty factors, including accounting for pharmacokinetic variability and toxicodynamic variability. According to the commenter, much of pharmacokinetic variability results from EPA selecting a one-compartment model instead of the Psychologically Based Pharmcokinetic Model (PBPK) model suggested by the NAS (2000). Another commenter questions why EPA added an uncertainty factor to address toxicodynamic variability when such a factor was considered unnecessary in previous RfDs. One commenter states that the EPA noted that research demonstrates that the 10 percent risk level of benchmark dose roughly correlates with the NOAEL ("no observed adverse effects level") in EPA's 1995 RfD. According to the commenter, the EPA departed from this approach and used a 5 percent risk level for the benchmark dose and this results in a benchmark dose that is six times more stringent than the traditional 10 percent risk level benchmark dose (BMD) or NOAEL approach.
      Several commenters state that the EPA's use of the 1999 NHANES data is outdated and National Health and Nutrition Examination Survey (NHANES) blood mercury levels show a downward trend since 1999 and the levels have been below the EPA RfD since 2001. 
      One commenter states that a study by Texas Department of State Health Services (DSHS, 2004) determined that even when subsistence fishers are eating fish from Caddo Lake with elevated methylmercury, women of child-bearing years did not have blood mercury levels greater than the RfD. Thus, according to the commenter, the connection between methylmercury in fish and adverse health effects in the U.S. is not fully understood and could involve other factors, including the protective effects of fatty acids and selenium in fish, in populations that eat large amounts of fish, which were not taken into account in the EPA's assessment. 
      Two commenters claim that EPA uses the RfD as if it were an absolute threshold for health risk in the risk assessment even though the RfC/RfD methodology was developed as a screening tool for deciding when risks clearly do not exist. 
      Several commenters recommend adding qualitative discussion about the uncertainty to the Mercury Risk TSD, including the RfD, extrapolating a dose-response relationship between methylmercury exposure and change in IQ, extrapolating the dose-response relationship from marine fish and marine mammals to freshwater fish, and confounding due to PCBs in marine species.
      Several commenters raised concerns regarding the relationship between methylmercury exposure and IQ loss. Two commenters state that changes in IQ are not a well-defined health consequence of methylmercury exposure. One commenter states that SAB had reservations about EPA's use of IQ loss as a second risk measure. One commenter stated that this rulemaking would have little impact on IQ (e.g., only a fraction of an IQ point gain for the most exposed individuals). Two commenters questioned whether IQ impacts would even occur because in Japan and Korea, where the maternal blood mercury levels are higher than in the U.S., there is no evidence of harm to child development or IQs. Another commenter cited a study that found verbal IQ scores for children from mothers with no seafood intake were 50 percent more likely to be in the lowest quartile. One commenter questions using an IQ risk metric threshold of >1 or >2 points because of variation in IQ measures and the intra-individual variation in IQ is higher than the threshold, and EPA should described the reasoning behind this threshold in the Mercury Risk TSD. One commenter states that none of the IQ studies measured full IQ, and EPA relied on summary data results that introduced some uncertainty in the low-dose linear response.
      Several commenters question the relationship between cardiovascular effects and methylmercury exposure. According to a commenter, EPA cites a workshop report as support for a causal relationship between methylmercury exposure and cardiovascular effects, but other studies report no increased risk for cardiovascular events. One commenter states that the two major studies used by EPA to show cardiovascular effects are flawed in design and the results are simply not applicable to U.S. public health. One commenter cited several studies examining the relationship between methylmercury exposure and cardiovascular effects,[,][,][,][,][,] but concluded that it seems premature to use these studies to establish a dose-response relationship. 
      Several commenters mention that the risks from eating seafood are low relative to the benefits, fish advisories can limit the beneficial aspects of fish consumption, and fish advisories are often unsuccessful.[,] One commenter noted the important role of dietary selenium's protective effects against MeHg toxicity because the binding affinity of Hg to Se is up to a million times higher than for sulfur  -  mercury's second-best binding partner.
      Response: EPA agrees with the commenter that the MeHg RfD is the appropriate health value for determining elevated risks from MeHg exposure and disagrees with commenters that state otherwise. At this time, U.S. EPA is neither reviewing nor revising its 2001 RfD for MeHg. The 2001 RfD for MeHg is EPA's current peer-reviewed RfD, which is the value EPA uses in all its risk assessments. EPA's RfD is based on multiple benchmark doses and RfDs were calculated on various endpoints using the three extant large studies of childhood effects of in utero exposure: Faroe Islands, New Zealand, and an integrative measure including data from Seychelles. EPA did not choose to base its MeHg RfD solely on results from the Seychelles Island, as both the NAS and an independent scientific review panel convened as part of the IRIS process advised strongly against using results from a study that at the time had not shown an association between MeHg exposure and adverse effects. Further, EPA disagrees with the commenter that EPA based the MeHg RfD solely on results from the Faroe Islands population. EPA disagrees that the information underlying the RfD is "poorly explained". EPA has provided detailed documentation for the choices underlying calculation of the RfD.[,][,] To correct the statement by the commenter, the data underlying the Faroe Islands study has been previously published in the peer-reviewed literature.
      EPA disagrees that it did not incorporate the latest mercury data to support the "appropriate and necessary" finding. It is the policy of EPA to use the most current peer-reviewed, publicly available data and methodologies in its risk assessments. However, EPA noted in the preamble to the proposed rule that "data published since 2001 are generally consistent with those of the earlier studies that were the basis of the RfD, demonstrating persistent effects in the Faroe Island cohort, and in some cases associations of effects with lower MeHg exposure concentrations than in the Faroe Islands. These new studies provide additional confidence that exposures above the RfD are contributing to risk of adverse effects, and that reductions in exposures above the RfD can lead to incremental reductions in risk." However, EPA has not completed a comprehensive review of the new literature, and as such, it would be premature to draw conclusions about the overall implications for the RfD. Several of the commenters refer to old calculations based on the science available at the time, which have been superseded by advances in knowledge and best practices used by risk assessors. 
	EPA agrees that EPA's RfD is not the same as the levels used by FDA, WHO, or ATSDR. In their advice to the U.S. EPA on the appropriate bases for a MeHg RfD, NAS specifically recommended that EPA use neither the study nor the uncertainty factor employed by ATSDR in the calculation of their minimal risk level. 
	EPA disagrees that the uncertainty factor is "unusually high". The uncertainty factor used in calculation of the RfD is small (10 fold); half of this factor is to account for measured variability in human pharmacokinetics. This uncertainty factor considered advice of NAS and an independent panel of scientific peer reviewers convened as part of the IRIS process. Both groups of scientists felt at that time that the available PBPK model had not undergone sufficient scientific scrutiny to be used in the derivation of the MeHg RfD. The uncertainty factor was applied to multiple calculated effect levels; that is, statistical lower limits on benchmark doses for a 5 percent response level. These methods, including use of benchmark dose and data-derived uncertainty factors, result in more precise and accurate estimates with decreased uncertainty. 
      It is important to clarify that EPA did not model low dose extrapolation for the RfD; rather, an uncertainty factor of 10 was applied to the chosen points of departure (lower limit on a BMD05 for multiple endpoints). IRIS makes this statement regarding a threshold for MeHg: "It is also important to note that no evidence of a threshold arose for methylmercury-related neurotoxicity within the range of exposures in the Faroe Islands study. This lack [of a threshold] is indicated by the fact that, of the K power models, K = 1 provided a better fit for the endpoint models than did higher values of K." This remains a factual statement. 
      It is the best practice of EPA when the data support it, to use benchmark dose modeling (BMD), rather than a point estimate derived from inspection or a pair-wise comparison. EPA is not obliged to use any particular benchmark response level (BMR) in calculation of the BMD. The choice of the BMR for the MeHg RfD was guided by the advice of the NAS and an independent scientific peer review panel. Scientists conversant in the tests and neurobehavioral endpoints to be modeled found that a 5 percent BMR was most appropriate and congruent with practice in the field. 
      EPA disagrees that it is using the MeHg RfD as an absolute bright line for health effects in the risk assessment. As stated in the preamble to this proposed rule, the RfD is an estimate of a daily exposure to the human population that is likely to be without an appreciable risk of deleterious effects during a lifetime. EPA disagrees that exposure levels in the U.S. are lower than in the Faroe Islands study. Exposure to MeHg in the U.S. has been reported at the same levels as those published in the Faroe Islands. Mahaffey et al. note that in the NHANES data (1999-2004), the highest five percent of women's blood mercury exceeded 8.2 ug/L in the Northeast U.S. and 7.2 ug/L in coastal areas. Higher levels have been reported among subjects known to consume fish. For example, Hightower and Moore (2003) reported mean blood mercury for women aged 27 to 87 in their study to be 15 ug/L; range for men and women was 2 to 89.5 ug/L. Note that some publications have reported mercury effects in U.S. populations near the current U.S. RfD.[,]
      The commenter stating that of MeHg in the U.S. population is 10 to 20 times below that of the Seychelles islanders and all ocean fish throughout the world contain about the same amount of MeHg is in error. McKelvey et al. report that NYC residents have mean blood mercury levels of 2.7 ug/L, and women of childbearing age had a mean of 2.64 ug/L, nearly at the 90[th] percentile in NHANES; ethnic Asians had even higher blood mercury levels. Furthermore, marine fish in commerce differ widely in mercury concentration by species, and fish within the same species but caught at different locations have variable amounts of mercury in their tissues[,]. 
      EPA disagrees that the dose-response relationship between mercury and IQ was developed for marine fish because the dose-response function was actually calculated for exposure to MeHg rather than for fish consumption. Recent studies[,][,] and analyses point to the potential for nutrients in fish (particularly marine fish) to ameliorate some of the observed adverse effects of MeHg when co-exposure occurs. There was no correction for potential confounding by nutrients in marine fish and mammals in calculation of the benchmark doses used in the RfD derivation; these benchmark doses may, thus, be underestimates. 
      EPA disagrees that there is a statistically discernible downward trend in the NHANES data on blood mercury. EPA is unaware that a formal statistical analysis for temporal trends has been completed for NHANES data on blood mercury levels for the period 1999 to 2008. Mahaffey et al., evaluating NHANES data collected 1999 to 2004 for women at child-bearing age, could "not support the conclusion that there was a general downward trend in blood mercury concen - trations over the 6-year study period." However, the same publication noted that "there was a decline in the upper percentiles reflecting the most highly exposure women" having blood mercury concentration greater than established levels of concern. Visual observations of the data show a slight decrease in mercury blood level concentrations from 1999-2008 at the geometric mean. This decrease may not be statistically significant based on overlapping confidence intervals. A decrease in mercury blood level concentrations is also observed at the 95[th] percentile. Except for differences observed between 1999 and 2008, the temporal decrease may not be statistically significant. Conclusions cannot be drawn without further and more formal statistical analysis of the data. EPA remains concerned that substantial numbers of women of childbearing age in the U.S. may have blood mercury levels that are equivalent to exposures at or above the RfD. Mean and 95[th] percentiles from recent NHANES data are below 5.8 ug/L (a blood mercury concentration equivalent to the RfD). However, blood levels for some portions of the population (high consumers of fish, for example) may be indicative of exposures above the RfD. EPA did not find data for NHANES blood distributions above the 95[th] percentile. Modeled data from Tran et al.  provided estimates showing high blood mercury levels at the 99[th] percentile for females of child-bearing age (i.e., 24.41 ug/L at the 99[th] percentile). Mahaffey et al. showed that 2.4 percent of women of child-bearing age had blood mercury values above 5.8 ug/L. Other published studies have shown that various population groups can have high blood mercury levels.[,][,][,][,] For example, one study found that Asian populations had mercury exposures greater than 5.8 ug/L in 83 percent of the Asian population compared to 12 percent for the total survey population. 
      EPA disagrees with the commenter regarding confounding by PCBs and lead because the commenter makes several misstatements. PCB congeners were measured in cord tissue for the first Faroese cohort recruited in 1986 and 1987 and in maternal serum in the cohort recruited in 1994  -  1995.[,] Exposure to MeHg in the Faroe Islands was largely from consumption of pilot whale meat; exposure to PCBs was found in the portion of the population who also consume whale blubber. The lipophilic PCBs are found in the fat compartment of the pilot whales; MeHg, by contrast is bound covalently to protein in the whale meat. Numerous analyses have shown neurobehavioral effects of PCBs; however, the effects of MeHg and PCB in the Faroe Islands study are separable. EPA also documented the independence of PCB and MeHg effects in the Faroe Islands population. NIEHS concluded that both PCB and mercury had adverse effects.  NAS concluded that there was no empirical evidence or theoretical mechanism to support the opinion that in utero Faroese exposure to PCBs exacerbated the reported methylmercury effect. A second set of analyses found that the effect of prenatal PCB exposure was reduced when the data were sorted into tertiles by cord PCB concentrations. These analyses support a conclusion that there are measurable effects of methylmercury exposure in the Faroese children that are not attributable to PCB toxicity. We also note that the Faroe Island population was not exposed to lead.
      EPA disagrees with the commenter's assertion that the connection between methylmercury in fish and observed health effects is not understood due to evidence from the cited Texas study. This is an exposure study rather than a study on measures of neurobehavioral or any other health endpoint. TCEQ noted that none of the Caddo Lake study participants had blood mercury levels above the BMDL of 5.8 ug/L (one of the several used by EPA in the calculation of the MeHg RfD). The BMDL is not a "no effect" level. Rather it is an effect level for a percentage of the population. EPA has noted in correspondence with TCEQ that, as an exposure study, the Caddo Lake study may be representative of the surrounding population; however, the sample size is very small. It is not appropriate to extrapolate from Caddo Lake to larger regional or national populations.
      EPA is aware of the possibility of both interactions among environmental contaminants and cumulative effects of pollutants that produce the same adverse endpoint. EPA guidance exists for dealing with such scenarios.[,][,][,] The Agency's concern with the likelihood of human exposure to multiple contaminants is reflected in the multi-chemical scope of the rulemaking. However, EPA focused the technical analyses supporting the proposed regulation on effects of individual pollutants rather than cumulative effects. 
      Further, SAB "agreed that EPA's calculation of a hazard quotient for each watershed included in the assessment is appropriate as the primary means of expressing risk," and that "because the RfD from which the HQ is calculated is an integrative metric of neurodevelopmental effects of methylmercury, it constitutes a reasonable basis for assessing risk." 
      EPA disagrees that the "appropriate and necessary finding" was based on the IQ analysis in the Mercury TSD. As fully described in the preamble, EPA made its finding in part on the HQ-based risk metrics derived from comparisons of MeHg exposure to the RfD. EPA's Mercury Risk TSD evaluated the potential public health hazard on several high-risk subpopulations, specifically high-consuming subsistence fishers. This assessment was not designed to characterize the full range of risk associated with exposure to Hg emitted from U.S. EGUs. For this rulemaking, EPA did not conduct an analysis of risks and benefits of fish consumption. Rather EPA conducted an analysis of the risks of exposure to mercury and the benefits accruing to consumers of freshwater fish from reduction in mercury emissions from EGUs.
      EPA agrees that additional qualitative discussion about uncertainty would improve the Revised Mercury Risk TSD. The SAB recommended that the IQ analyses be retained but de-emphasized in the documentation underlying the final regulation. In their report they stated the following: "The Panel does not consider it appropriate to use of IQ loss in the risk assessment and recommended that this aspect of the analysis be de-emphasized, moving it to an appendix where IQ loss is discussed along with other possible endpoints not included in the primary assessment. While the Panel agreed that the concentration-response function for IQ loss used in the risk assessment is appropriate, and no better alternatives are available, IQ loss is not a sensitive response to methylmercury and its use likely underestimates the impact of reducing methylmercury in water bodies." EPA is following up on the SAB recommendation by deemphasizing the IQ analysis and placing that analysis in an appendix to the revised TSD. The SAB panel also recommended that EPA revise the Mercury Risk TSD "to better explain the methods and choices made in the analysis, and analytical results, and where the uncertainties lie." The SAB panel noted several uncertainties related to the RfD, and EPA is preparing a revised TSD that will address the SAB recommendations, including a more complete discussion of uncertainties including those related to the RfD.
      EPA disagrees that the IQ metric threshold is "questionable". The SAB concluded that it was reasonable to consider a loss of >1 or >2 IQ points a public health concern. The executive summary of their report says the following: "The Panel agreed that if IQ loss is retained in the risk assessment despite these reservations, a loss of 1 or 2 points would be an appropriate benchmark." The SAB further comments in their report: "The consensus is that if IQ were to be used, then a loss of 1 or 2 points as a population average is a credible decrement to use for this risk assessment. This metric seems to be derived from the lead literature and was peer-reviewed by the Clean Air Scientific Advisory Committee (U.S. EPA CASAC 2007) []. While its applicability to methylmercury is questionable, the size of the decrement is justified based on the extensive analyses available from the literature reviewed by CASAC." As noted in other studies,[,] a decrease of 1-2 points at the mean results in a much larger decrease on those with IQs that are much lower or higher than the mean. 
      Although EPA disagrees that the IQ results too uncertain to rely upon, EPA acknowledges that IQ is not the most sensitive neurodevelopmental endpoint affected by MeHg exposure, as also noted by SAB. The SAB recommended that "the appropriate approach would be to mention the IQ analysis in the body of the TSD and to discuss the uncertainties involved with the use of the analysis, offering the conclusion that it would be a less sensitive endpoint than the Hazard Quotient (HQ), which is based on the current reference dose (RfD) for methylmercury". The SAB, however, supported the use of the IQ dose-response function calculated by EPA in support of the proposed regulation. They note, "The function used came from a paper by Axelrad and Bellinger (2007) that seeks to define a relationship between methylmercury exposure and IQ. A whitepaper by Bellinger (Bellinger, 2005)[] describes the sequence of steps in relating methylmercury exposure to maternal hair mercury and then that to IQ. The Mercury Risk TSD furthers notes that IQ has shown utility in describing the health effects of other neurotoxicants. These are appropriate bases for examining a potential impact of reducing methylmercury on IQ, but the SAB does not consider these compelling reasons for using IQ as a primary driver of the risk assessment."  
      EPA disagrees with the commenter's implication that the MATS rule would not have public health benefits. As shown in the RIA accompanying the rule, the public health benefits are substantial, and the monetized benefits exceed the costs by a substantial margin. 
      EPA disagrees that EPA has overstated or failed to review the scientific literature on cardiovascular effects from MeHg exposure. As summarized in the preamble to the proposal, EPA stated that the NAS study concluded that "Although the data base is not as extensive for cardiovascular effects as it is for other end points (i.e., neurologic effects) the cardiovascular system appears to be a target for MeHg toxicity in humans and animals." EPA also stated that additional cardiovascular studies have been published since 2000. EPA did not develop a quantitative dose response assessment for cardiovascular effects associated with MeHg exposures, as there is no consensus among scientists on the dose-response functions for these effects, and there is inconsistency among available studies as to the association between MeHg exposure and various cardiovascular system effects. In the future, EPA may update the MeHg RfD and will review all of the relevant scientific literature available at that time, including data on all relevant endpoints, and weight of evidence for likelihood that MeHg produces specific effects in humans.
      EPA acknowledges the research regarding the effectiveness of fish advisories. However, the proposed regulation does not address the subject of fish advisories, consumer advice on fish or efficacy of such advice. EPA rejects the commenter's speculation regarding whether the estimated IQ impacts for the regulation are real. Adverse effects of in utero mercury exposure have been reported in populations in the U.S.[,] In another study on neurobehavioral effects of prenatal exposure to methylmercury through maternal consumption of seafood, adverse effects are observed for MeHg even without controlling for fish consumption. That study suggests that at normal Japanese dietary intake of MeHg and fish nutrients, the overall effect is adverse. While Japanese fish consumption and mercury exposure are both somewhat higher than the mean U.S. exposure, these levels are still within the distribution of U.S. consumers. 
Moreover, many studies show that beneficial effects of fish on both cardiovascular and neurodevelopmental health are decreased by concomitant exposure to MeHg. Several studies describe one or more aspects of exposure to fish nutrients and MeHg.[,][,][,][,][,] Note that in the Hibbeln et al. study cited by the commenter, there were self-reported levels of fish consumption, but no measures of mercury exposure; no biomarker data such as blood, hair or urine mercury were reported. Daniels et al. (2004) reporting on the same population noted that no significant increase was seen in umbilical cord mercury (the biomarker used) as seafood consumption increased from one meal per 2 weeks to four or more per week. Consequently, no methylmercury-associated suboptimum performance outcomes would be expected in the ALSPAC population.
      EPA recognizes the potential for confounding of the effects of mercury on the developing nervous system by a range of nutrients (including long-chain poly-unsaturated fatty acids) and we discuss this in the uncertainty characterization section of the Revised Mercury Risk TSD. Regarding selenium, SAB commented that "one SAB member suggests the use of blood markers of selenium-dependent enzyme function, noting that methylmercury irreversibly inhibits selenium-dependent enzymes that are required to support vital-but-vulnerable metabolic pathways in the brain and endocrine system. Impaired selenoenzyme activities would be observed in the blood before they would be observed in brain, but the effect is also expected to be transitory. The use of these measures is a minority view among the SAB members." The SAB did not express a consensus recommendation on adjustments to the risk estimates for exposure to selenium or other nutrients, noting that "there is not enough known about their quantitative impact to support a recommendation of a re-analysis." 
6. General comments on Mercury Risk Assessment
      Comment: Several commenters generally supported the mercury risk assessment, but several other commenters generally disagreed with the mercury risk assessment. One supporter stated that EPA reasonably determined that mercury emissions pose a public health hazard, correctly requested peer-review of mercury risk analysis and correctly concluded EGU-attributable MeHg poses a hazard to public health at watersheds when considering all sources of Hg deposition and U.S. EGUs alone. Two commenters noted that the contribution of U.S. EGUs to total Hg deposition can significantly contribute to hundreds of watersheds, and U.S. EGU deposition alone may endanger sensitive populations near many of these watersheds. 
      Several commenters claimed that overly conservative assumptions in the risk analysis render the results flawed and unreliable, including using CMAQ to model deposition, MMAPs, fish consumption rate and fish methylmercury concentrations, overly stringent RFD, national-scale model, using poverty as a surrogate for subsistence fishing, assuming a subsistence fisher resides in most watersheds with fish tissue data, fishers only eat larger fish with high mercury concentrations, cooking loss adjustment, unrealistically high fish ingestion rates (a large fish meal every day), focused on the extremes of the distributions, cast many assumptions as an underestimate of the effect despite evidence to the contrary, and created inappropriate metrics for risk that show no improvement despite significant mercury emissions reductions in the U.S. 
      Several commenters cite Tetra Tech's analysis that assessed mercury risk using different consumption rates, cooking factor, mean fish tissue concentrations, and EGU-attributable mercury deposition only, which showed considerably fewer watersheds that exceed an HQ of 1 at 2016 deposition levels. 
      Several commenters claim that this regulation would not significantly reduce mercury exposure via fish consumption because EGU-attributable deposition is a small fraction of total deposition. One commenter states that EPA's data shows U.S. EGU mercury emissions have little influence on fish mercury concentrations despite reduction of 41 tons of Hg in U.S. between 2005 and 2016. One commenter requested that EPA accurately describe the low health risks posed by utility hazardous air pollutant emissions. One commenter states that the EPA did not consider scientific information showing that there is no straightforward connection between mercury emissions from EGUs to the mercury level in fish, which is dependent upon many environmental factors, such as sunlight and organic matter, pH, water temperature, sulfate, bacteria, and zooplankton present in the ecosystem. One commenter states that there is not any demonstrable evidence that anyone in the U.S. has suffered adverse health problems as a result of mercury emissions from coal-fired EGUs. One commenter states that EPA's findings are similar to the 2000 findings where the EPA found a plausible link between anthropogenic releases of Hg from sources in the U.S. and MeHg in fish, and "plausible" is a euphemism for unproven.
      Several commenters had recommendations for the mercury risk analysis. One commenter stated that more data from Florida should have been included because Florida is known to have a rich data set on fish mercury concentrations. One commenter states that the EPA should characterize general recreational angler fishers instead of subsistence fishers. One commenter claims that EPA made math errors in the Mercury Risk TSD regarding the deposition in watersheds at specific percentiles. One commenter questioned EPA's policy metrics used to characterize mercury risk. One commenter states that EPA should state that lags occur in the response of aquatic ecosystems to changes in mercury deposition, and that some Hg deposition is unlikely to reach the water at all.
      Several commenters state that the Mercury TSD is unclear and lacks detail, as noted by SAB. One commenter states that the SAB is critical of EPA's efforts, stating that SAB found it difficult to evaluate the risk assessment based solely upon Mercury Risk TSD and recommended that EPA transparently explain the methods and uncertainties. One commenter states that because of insufficient review time and the lack of detail in the TSD, they could not assess key questions, such as the nation-wide representativeness of the fish tissue data. 
      One commenter states the subset of watersheds considered in the analysis (i.e., with fish tissue data) have clearly higher U.S. EGU-attributable deposition than the distribution of all watersheds. 
      One commenter states the EPA's reporting of IQ point loss is erroneous and not relevant to informing policy, and the U.S. EGU contribution to risk is marginal as evidenced by the null values for the 50th percentile watershed. 
      One commenter notes that U.S. EGU-attributable emissions of mercury have decreased significantly between 2005 and 2016, but claims that this decrease does not appear to affect the risk results. 
      One commenter questions why the EPA has departed from the Clean Air Act (CAA) 112(n) risk comparison to the 1 in 1 million to use the RfD for mercury.
	Response: The purpose of the mercury risk assessment is not to assess the magnitude of risk reduction under the proposed rule, but rather to estimate the magnitude of absolute risk attributable to U.S. EGUs currently and following implementation of other applicable Clean Air Act requirements. That said, any potential risk reductions following implementation of the MACT rule itself would likely reflect a number of factors besides the national average U.S. EGU deposition value cited by the commenter. These additional factors include: (a) spatial gradients in the magnitude of absolute U.S. EGU-attributable Hg deposition, (b) spatial gradients in the magnitude of reductions in Hg deposition linked to the rule, (c) availability of measured fish tissue Hg levels in the vicinity of U.S. EGUs experiencing larger Hg emission reductions to support risk modeling, and (d) the potential for subsistence fishing activity at watersheds in the vicinity of U.S. EGUs experiencing larger reductions in Hg emissions (also required to support risk modeling). It is also important to point out that while the national average U.S. EGU-attributable mercury deposition (for the 2016 scenario  -  see Revised Mercury Risk TSD) is 2 percent, values range up to 11 percent for the 99[th] percentile watershed. This illustrates the substantial spatial variation in U.S. EGU-attributable Hg deposition, which translates into spatial variation in the magnitude of U.S. EGU-attributable subsistence fisher risk.
      The SAB conducted a comprehensive peer review of all of EPA's assumptions in the Mercury Risk TSD, and concluded that "the SAB supports the overall design of and approach to the risk assessment and finds that it should provide an objective, reasonable, and credible determination of the potential for a public health hazard from mercury emitted from U.S. EGUs." Furthermore, SAB concluded, "The SAB regards the design of the risk assessment as suitable for its intended purpose, to inform decision-making regarding an "appropriate and necessary finding" for regulation of hazardous air pollutants from coal and oil-fired EGUs, provided that our recommendations are fully considered in the revision of the assessment." While the SAB did indicate difficulty in evaluating the risk assessment based solely on the Mercury Risk TSD, the panel was able to obtain enough additional information through the peer review process to make the determination that "the overall design of and approach to the risk assessment and finds that it should provide an objective, reasonable, and credible determination of the potential for a public health hazard from mercury emitted from U.S. EGUs." The primary advice of the SAB panel was that EPA should "revise the Technical Support Document to better explain the methods and choices made in the analysis, and analytical results, and where the uncertainties lie." EPA has revised the Mercury Risk TSD as part of the final rulemaking to address the SAB's recommendations and has made that revised TSD available in the rule docket. 
      SAB concurred with EPA's analytical assumptions and overall study design for the Mercury Risk TSD, including the RfD-based HQ approach, fish tissue data, 75[th] percentile size fish, MMAPs assumption, and consumption rates. Based on the SAB peer review, EPA strongly disagrees with commenter statements that the results reported in the Mercury TSD are unreliable, overly conservative, extreme, inconsistent with EPA risk guidelines, or severely overstate risk based on the stated objectives of the analysis. EPA has specifically addressed each of these assumptions in the previous sections of the preamble, thus, does not repeat those responses here. Based on the review by the SAB, EPA has accurately described the health risks posed by utility hazardous air pollutant emissions and disagrees with the commenter's statement that EPA has not provided any demonstrable evidence to show that adverse health risks exist. EPA has applied peer reviewed modeling to estimate the deposition of Hg attributable to U.S. EGUs. EPA asserts that these metrics demonstrate a clear hazard to public health from U.S. EGU Hg emissions. 
      EPA thoroughly evaluated the Tetra Tech analysis. EPA does not agree that the analysis by Tetra Tech uses assumptions that are "more reasonable", as the SAB agreed that all of EPA's assumptions are reasonable and appropriate. EPA asserts that the Tetra Tech analysis does not provide coverage for subsistence fishers likely to experience elevated U.S. EGU-related Hg exposure. Specifically, the risk estimated cited in the comment reflects application of a number of behavioral assumption that provide significantly less coverage for higher risk subsistence fishers. Fish consumption surveys cited in the Revised Mercury Risk TSD, suggest that higher percentile subsistence fishers eat more than twice the level of fish assumed by Tetra Tech. The Tetra Tech analysis also used the median fish tissue levels, but it is reasonable to assume that subsistence fishers would target somewhat larger fish to maximize the volume of edible meat per unit time spent fishing. The Tetra Tech assumed that cooking fish did not concentrate mercury, but a number of studies discussed in the Revised Mercury Risk TSD explicitly provide adjustment factors involving a higher unit concentration following preparation. Taken together, Tetra Tech's analysis does not address the stated goal of the risk assessment to assess the nature and magnitude of risk for those individuals likely to experience the greatest risk associated with exposure to U.S. EGU-attributable mercury. 
      EPA disagrees with the commenter's assertion that this rule will not affect risks associated with mercury exposure. Mercury from U.S. EGUs is a contributor to the levels of methylmercury in fish across the country and consumption of contaminated fish can lead to increased risk of adverse health effects. EPA has shown in the RIA Chapter 5 that this rule will reduce mercury levels in fish. 
      EPA acknowledges that U.S. EGUs contribute only a small fraction of total mercury deposition in the U.S. However, U.S. EGUs remain the largest emitter of mercury in the U.S., and the revised risk analysis shows that U.S. EGU-attributable Hg deposition results in up to 29 percent of modeled watersheds having the potential for subsistence level freshwater fish consumers with total mercury exposures exceeding the RfD to have at least 5 percent of total mercury risk contributed by U.S. EGUs, and up to 10 percent of modeled watersheds having the potential for subsistence level freshwater fish consumers to have mercury exposures exceeding the RfD due to mercury emissions from U.S. EGUs even before considering mercury exposures due to other sources. Mercury risk is increasing for exposures above the RfD, and as a result, any reductions in mercury exposures in locations where total exposures exceed the RfD can result in reduced risks. While these reductions in risk may be small for most populations and locations, in some watersheds and for some populations, reductions in risk may be greater. 
      The SAB also directly addressed the question of the nation-wide representativeness of the fish tissue MeHg data in the national mercury risk assessment. The SAB panel concluded, "Although the SAB considers the number of watersheds included in the assessment adequate, some watersheds in areas with relatively high mercury deposition from U.S. EGUs were under-sampled due to lack of fish tissue methy[l]mercury data. The SAB encourages the Agency to contact states with these watersheds to determine if additional fish tissue methylmercury data are available to improve coverage of the assessment." In response to the SAB recommendations, EPA obtained additional fish tissue sample data from several states, particularly Pennsylvania, Wisconsin, Minnesota, New Jersey, and Michigan. This additional data increased the total number of watersheds assessed in the analysis by 33 percent nationally. In Florida, EPA assessed the mercury-related health risk for 40 watersheds. Because EPA did not find any fish tissue data for new watersheds in Florida that could be incorporated into the analysis, the total number of watersheds in Florida assessed in the Revised Mercury Risk TSD remains the same as proposal. 
      EPA disagrees with the commenter that there were errors in the Mercury Risk TSD. Instead, the commenter has misinterpreted how EPA calculated the percentiles. The percentile (and mean) values presented in Table ES-1 for total and U.S. EGU-attributable Hg deposition are not matched by watershed. In other words, EPA queried for the percentiles (and mean) provided for total Hg deposition and presented those percentiles and then separately estimated the percentiles for U.S. EGU-attributable Hg. Therefore, the total and U.S. EGU-attributable values for the 99[th] percentile do not necessarily occur at the same watershed. EPA has provided additional clarification in the Revised Mercury Risk TSD. 
      EPA agrees with the commenter that MeHg levels in fish depend on a complicated set of environmental factors, and EPA acknowledged this in the Revised Mercury Risk TSD. Furthermore, EPA acknowledges that total Hg fish tissue levels are not correlated with levels of total Hg deposition when looking across watersheds because this relationship is highly dependent on the methylation potential at the specific waterbody, which is affected by pH, sulfate deposition, turbidity, etc. However, several recent studies (Orihel et al., 2007, Orihel et al., 2008 and Harris et al., 2007) show, and the SAB agrees, that it is appropriate for EPA to assume that changes in mercury deposition are linearly associated with changes in fish tissue concentration. In addition, EPA agrees that the subset of watersheds in the risk analysis have somewhat higher U.S. EGU deposition than the distribution of all watersheds, but EPA disagrees that oversampling of high deposition watersheds is inappropriate. EPA also acknowledges in the Revised Mercury Risk TSD that MMAPS does not account for a time lag in ecosystem response to reductions in mercury emissions. 
      EPA does not agree that there is no improvement in fish mercury concentrations between 2005 and 2016, or that there will be no further improvement from decreasing U.S. EGU mercury emissions from the baseline in 2016. While total risk from all mercury exposures will remain elevated in much of the U.S., much of that risk is associated with global, non-U.S. mercury emissions. U.S. EGUs remain the largest source of Hg emissions in the U.S., and reductions in those emissions will result in reduced Hg deposition in many highly impacted watersheds. Based on the mercury risk assessment, average EGU-attributable fish tissue Hg concentrations will be decreased by 65 percent. Likewise, the number of watersheds identified as having populations potentially at risk from U.S. EGU Hg emissions will decline from 62 percent in 2005 to 28 percent in 2016. Emissions reductions due to regulation of Hg under section 112 should result in additional reductions in U.S. EGU-attributable fish tissue Hg concentrations and watersheds with populations at risk.
      EPA disagrees that IQ loss is erroneous or irrelevant to informing policy, but EPA has moved that analysis to an appendix in the Revised Mercury Risk TSD, per SAB recommendation. EPA disagrees that the IQ effects at the 50th percentile watershed are useful in determining that there is not a hazard to public health because EPA's stated goal of the risk assessment was to focus on populations likely to experience relatively higher exposures to U.S. EGU-attributable mercury. 
      The commenter is referring to cancer risk (i.e., a 1 in 1 million probability of developing cancer over a lifetime due to a specific chemical exposure). For mercury, EPA focused on the potential for neurodevelopmental effects in the children born to mothers exposed to MeHg during pregnancy through fish consumption. This health endpoint is a non-cancer endpoint, and risk in this context is assessed by comparing an estimate of daily exposure to MeHg for the mother to the MeHg RfD. Values greater than one (i.e., exposures that exceed the RfD) are considered to represent an exposure that could represent a public health hazard, this reflecting the methodology and underlying epidemiological data used in deriving the MeHg RfD.
      We also disagree with those commenters that point to the SAB statements concerning the clarity of the Mercury Risk TSD to suggest that the public did not have an ample opportunity to comment on the mercury risk assessment.  While it is correct that the SAB said the Mercury Risk TSD was difficult to evaluate until EPA staff explained it at the public meeting in June 2011, we note that the commenters that assert that this issue amounts to a violation of section 307(d) notice requirements made detailed technical comments, including many of the same comments as the SAB.   Furthermore, EPA provided notice of the peer review in the proposed rule and a number of Federal Register notices advised the public of the peer review process and all the meetings were open to the public for comment and participation and the minutes of those meetings were posted on the SAB website.  The minutes for the June 2011 meeting, during which EPA provided clarifying information, were available well within the public comment period for the proposed rule.  For these reasons, we maintain that the public was provided adequate opportunity to comment on the mercury risk assessment.
e. Non-Mercury HAP Case Studies
1. Emissions for non-mercury case studies 
      Comment: Commenters raised concerns about a wide variety of aspects of EPA's approach for emissions used for the non-Hg case studies, including the use of an arithmetic mean for computing emission factors for representing emissions of untested units, the suggestion of statistical outliers in the chromium test data, the claim that metals content of the fuel is a indicator of flawed test data, the statistical approaches used by EPA to create emission factors, the absence in EPA's approach of an equation that commenters claim better represents emissions values, that EPA's approach to estimate hexavalent chromium is flawed, and the lack of coal rank as a delineating factor for emission factor calculation. Commenters also suggested that EPA should revise stack parameters used for the case studies based on better available data.
      Response: In response to the comments on the emission factors, EPA has undertaken additional analysis to address all commenter concerns. EPA disagrees with commenter's criticisms of emission factors based on arithmetic means, and EPA demonstrates that the use of an arithmetic mean provides the most representative result. EPA agrees with commenters' recommendations to use statistical outlier tests, but has applied tests different from those suggested by the commenters. This approach did not eliminate the chromium test data from the chromium emission factors used for some of the case study emissions.
      EPA disagrees with commenters' assertions that the metal content of the coal is a basis for invalidating the test results of high chromium emissions. The identification of sources whose measured emissions do not match the commenters' preconceived idea of emissions behavior is not surprising. There are many possible explanations for these differences. For example, the inconsistency between the test data and the coal analysis could be due to any number of reasons including unrepresentative coal sampling, control device problems, degradation of the refractory, or sampling contamination. The idea that test data should be discarded because it does not match initial expectations is unfounded.
      EPA disagrees with the commenter recommendations for using an equation from AP-42, developed in part by the commenters. EPA conducted regression analyses between metals emissions measured at the site and predicted from the equations and demonstrates the poor predictive capability of these equations, concluding that emission test data is a more accurate predictor of actual emissions, and emission factors based on the arithmetic mean when test data are not available. 
      EPA also disagrees with commenters concerns about the assumption that 12 percent of the chromium will be Cr+6 for every coal-fired unit. EPA disagrees with the commenter's assertion that any impact of scrubbers will impact the case study analyses. In EPA's final case study analysis, 6 facilities have risk greater than 1 in 1 million, and of these, four facilities have chromium as the risk driver (James River, Conesville, TVA Gallatin, and Dominion  -  Chesapeake Bay). For these facilities, none of the units contributing the bulk of the chromium emissions have scrubbers according to the data provided to EPA by those facilities, so scrubber impacts on chromium speciation is not relevant to EPA's conclusions based on the non-Hg case studies. In any case, EPA disagrees with the commenter's conclusions about the impacts of scrubbers on chromium speciation and provides evidence that impacts of scrubbers on chromium speciation can have the opposite effect on Cr+6 fractions, concluding that EPA's 12 percent assumption is somewhat conservative.
      EPA also disagrees that coal rank must be a factor in computing chromium emission factors for use in the case studies. EPA's analysis has demonstrated that coal rank appears to play no role in metals emissions. EPA's newly revised emissions factor development procedures can isolate and compare subgroups based on control device type or coal rank; the ICR data were subjected to these tests and no statistical significance was found between coal rank groups.
      Finally, EPA agrees with commenters recommendations on revised stack parameters for the case studies and has included these revisions in the case study modeling for the final rule.
2. General Comments on Non-Hg Risk Case Study 
      Comment: One commenter stated that the EPA's case study assessment reaffirms the need to regulate HAP emitted by both coal and oil-fired EGUs. The commenter noted that over 40 percent of the case studies conducted by EPA to quantify health hazards associated with the inhalation of non-Hg HAP indicated a cancer risk greater than or equal to the one in one million threshold level required to delist a source category under section 112 of the Clean Air Act.
      One commenter stated that the EPA's case study assessment might be flawed by the use of "beta" tests versions of the AERMOD meteorological preprocessors (AERMINUTE and AERMET). The commenter obtained from EPA the meteorological data used for the EPA's assessment of the Conesville facility and processed these data with the EPA's current regulatory versions of these preprocessors, which differ from the beta version. According to the commenter, a comparison of the hourly wind speed and hourly wind direction data produced by the beta preprocessor and by current EPA preprocessors revealed numerous and often substantial disparities.
      One commenter stated that the EPA's finding that only three coal-fired facilities and one oil-fired facility out of roughly 440 coal-fired facilities and 97 oil-fired facilities in the U.S. indicated risk greater than one-in-a-million supports a finding that it is "appropriate" to regulated those four and not the other 537. Another commenter stated that EPA found only a "few" facilities that have estimated maximum cancer risks in excess of one in a million, and that this does not justify regulating all non-Hg HAPs for all sources in this category.
      One commenter stated that the EPA's discussion in the proposed rule misleads the reader into believing that non-Hg HAP emissions from EGUs are associated with serious human health effects. According to the commenter, EPA's discussion of the effects associated with excessive exposure to an individual HAP would lead the reader to believe that those effects inevitably occur from EGU emissions because EGU emissions have trace amounts of non-Hg HAPs. 
      One commenter stated that with the assumptions in the Utility RTC, both in terms of conservative scientific estimates and overestimated amounts of oil burned by these units, EPA concluded that the risks from oil-fired units would result in only one new cancer case every five years. The commenter does not believe that this level of risk warrants regulation under Section 112(n)(1)(A) of the CAA. 
      Several commenters state that even if the additional studies EPA performed were accurate, they hardly demonstrate that it is necessary and appropriate to regulate coal-fired EGU HAPs under Section 112 because three sites nationwide show risks greater that one in one million, with the highest at eight in one million.
      One commenter stated that the highest cancer risk estimated for coal-fired EGUs is still within the acceptable range used by EPA in other programs and is also far less than the background exposure risks the average person experiences. The background risk of developing cancer in a lifetime is approximately 1 in 3 (0.33). According to EPA's own data, the predicted added cancer risk of exposure to HAPs from U.S. EGUs would change the background risk from 0.33 to 0.330001. This level of change is so minimal that it could not be observed in any health effects study that might be conducted. 
      One commenter stated that EPA conducted a health risk assessment on a limited number of facilities and found a "few" facilities that have estimated maximum cancer risks in excess of one in a million. The commenter stated that, based on this limited health risk assessment, EPA apparently decided that they were justified to regulate all non-Hg HAPs for all sources in this category. 
      Several commenters stated that EPA's assumption that implies that a person stays exactly at the center of a census tract for 70 years and that a unit will operate in exactly the same manner for 70 years is unrealistic. The commenters suggest that Tier 3 risk assessment is warranted or a lifetime exposure adjustment is needed.
      One commenter asserts that because the alleged health benefits are derived from total exposure, EPA should explain how its numerical emission limit units, which would not directly restrict total exposure if heat inputs increase, redress this health concern. In its preamble, EPA simply notes that its emission limit units are consistent with, and allow for simple comparison to, other regulations.
      Response: EPA agrees with the commenter that the non-Hg HAP risk assessment confirms the appropriate and necessary finding.
      EPA disagrees that EPA's case study assessment is flawed by the use of beta versions of AERMET and AERMET. EPA remodeled the case study facilities using the current versions of AERMINUTE (version 11059), AERMET (version 11059), and AERMOD (version 11103). While there were differences in the number of calm and missing winds in the current AERMINUTE/AERMET output compared to the beta version, the resulting risks differed by less than two percent, on average. For Conesville, which had the largest difference in calms between the beta and current versions of AERMINUTE/AERMET, the risks differed by three percent. For the final rule, the case study facilities have been modeled with the current available versions of AERMINUTE, AERMET, and AERMOD.
      The EPA disagrees with the commenter that only a few case study facilities exceeding 1 in a million risk invalidates the "appropriate finding". The sixteen facilities EPA selected as case studies for assessment may not represent the highest-emitting or highest-risk sources. Although case study facility selection criteria included high estimated cancer and non-cancer risks using the 2005 NEI data, high throughput, and minimal emission control, another necessary criterion was the availability of Information Collection Request (ICR) data for the EGUs at those facilities (or for similar EGUs at other facilities). Because the ICR data were collected for the purpose of developing the MACT standards, the ICR was targeted towards better performing sources for non-mercury metal HAP, acid gas HAP, and organic HAP, with a smaller set of random recipients. Therefore, facilities for which ICR data were available may not represent the highest-emitting sources. EPA's assessment of the case study facilities for the proposed rule concluded that three coal-fired facilities and one oil-fired facility had estimated lifetime cancer risks greater than one in a million. For the final rule, revisions were made to the 16 case studies based on comments received, and the results indicate that five coal-fired facilities and one oil-fired facility had estimated lifetime cancer risks greater than one in a million. EPA maintains that its finding that more than 30 percent of the case study facilities had a cancer risk greater than one in one million is sufficient to support the appropriate finding. Furthermore, EPA did not base the appropriate finding on just the case study analysis as explained in the proposed rule.
      The EPA disagrees with the commenter's assertion that the health effects associated with exposures to non-Hg HAP from U.S. EGUs are mischaracterized in the preamble to the proposed rule. The discussion of the health effects of non-Hg HAP provided in the preamble includes general information on the potential health effects associated with a broad range of exposure concentrations (from low to high levels) of the various non-Hg HAP (some of which have been determined to be carcinogenic to humans) based on peer reviewed scientific information extracted from priority sources such as IRIS, Cal EPA and ATSDR health effects assessments
      The EPA disagrees with the commenter's characterization of the Utility RTC. The Utility RTC represented the highest-quality factual record of information available at the time regarding EGU emissions and risks. Further, EPA's recent risk assessments of 16 EGU case studies, performed with more recent data and refined scientific methods, indicate that there are still multiple EGU facilities that pose estimated inhalation cancer risks greater than one in a million. EPA maintains that the findings of the case studies are one element that independently supports our determination that it remains appropriate and necessary  to regulate EGUs under section 112.
      EPA does not agree with the commenter suggesting that EPA should interpret the results of the non-Hg HAP risk analysis in the context of background cancer risk. As explained in the proposed rule, EPA reasonably looked to the cancer risk threshold established under section 112(c)(9)(B)(1) for delisting a source category as an indicator of the level of cancer risk that was appropriate to regulate under section 112. Commenters comparison of the cancer risk from EGUs as compared with the risk of contracting cancer from unknown sources is not the standard Congress established for evaluating HAP emission risk and the commenter has provided no support for its contention that the Agency should evaluate risk in that manner. EPA maintains that the analysis was reasonable. 
      EPA does not agree with the commenter's implication that EPA must make a facility-specific finding for each HAP for each source and then only regulate individual EGU facilities for the individual HAP that identified as causing an identified hazard to public health or the environment. That approach is not required under section 112(n)(1) or anywhere under section 112, and it would be virtually impossible to undertake such an effort. For these reasons, EPA does not agree with the commenter and maintain that the appropriate and necessary finding is reasonably supported by the record and consistent with the statute for all the reasons set forth in the proposed rule and this final action.
      The EPA disagrees that an exposure adjustment is needed to account for conditions changing over 70 years because it runs counter to the long-standing approach that EPA has taken to estimate the maximum individual risk, or MIR. The MIR is defined by the EPA's Benzene NESHAP regulation of 1989 and codified by CAA 112(f) as the lifetime risk for a person located at the site of maximum exposure 24 hours a day, 365 days a year for 70 years (e.g. census block centroids). The MIR is the metric associated with the determination of whether or not a source category may be delisted from regulatory consideration under section 112 (112(c)(9)). The MIR is the risk metric used to characterize the inhalation cancer risks associated with the case study facilities. EPA used the annual average ambient air concentration of each HAP at each census block centroid as a surrogate for the lifetime inhalation exposure concentration of all the people who reside in the census block. The EPA has used this approach to estimate MIR values in all of its risk assessments to support risk-based rulemakings under section 112 of the CAA to date.
      EPA disagrees with the commenter's assertion that the numerical emission limits being promulgated in today's final rule must be justified on their ability to redress the health concerns that were identified as the basis for regulating EGUs. The emission limits in today's rule are technology-based, as prescribed under section 112, and do not need to be justified based on their ability to protect public health. Regarding potential health concerns, EPA has up to 8 years after the promulgation of the technology-based emission limits for EGUs to determine whether they protect public health with an ample margin of safety. If they do not, EPA will promulgate additional more stringent standards (within the prescribed 8 years) to achieve the appropriate level of public health protection.
The commenter claims that prior studies provide no support for establishing standards for non-mercury HAP metals.
3. Nickel Risk
      Comment: Several commenters stated that the assumptions regarding the speciation and carcinogenic potential of nickel compounds used in EPA's inhalation risk assessment of the case study facilities are overly conservative and likely to overstate the risks. With respect to nickel speciation, the commenters stated that there are substantial uncertainties regarding the species of nickel being emitted and the risk of such emissions, and that EPA has made ultraconservative assumptions aimed at overestimating the risk. The commenters stated that assigning the same carcinogenic potency of nickel subsulfide to other forms of nickel is overly conservative and inconsistent with the best available evidence.
      Response: The EPA disagrees with the commenters' assertion that it is impossible to give an accurate assessment of the risks to human health from nickel emissions from EGUs, and maintains that its assessment of the potential inhalation risks from EGU emissions of nickel compounds is scientifically valid, reasonable, and based on the best-available current scientific understanding. To that end, in July 2011, EPA completed an external peer review (using three independent expert reviewers) of the methods used to evaluate the risks from nickel and chromium compounds emitted by EGUs. There were two charge questions relating to nickel in that review. First, do EPA's judgments related to speciated nickel emissions adequately take into account available speciation data, including recent industry spectrometry studies? Second, based on the speciation information available and what is known about the health effects of nickel compounds, and taking into account the existing URE values (i.e., values derived by the Integrated Risk Information System, California Department of Health Services, and the Texas Commission on Environmental Quality), which of the following approaches to derive unit risk estimates would result in a more accurate and defensible characterization of risks from exposure to nickel compounds?
   1. To continue using the same approach as that developed for use in the 2000 NATA, which consists of using the IRIS URE for nickel subsulfide and assuming that nickel subsulfide constitutes 65 percent of the mass emissions of all nickel compounds. 
   2. To consider a more health-protective approach, based on the consistent views of the most authoritative scientific bodies (i.e., NTP in their 12th ROC, IARC, and other international agencies) that consider nickel compounds to be carcinogenic as a group.
   3. To make the same assumptions as in option 2, but considering alternative UREs derived by the CDHS or TCEQ.
      In responding to these peer review questions, two of the reviewers agreed with the views of the most authoritative scientific bodies, which consider nickel compounds carcinogenic as a group. These reviewers, therefore, did not focus on the availability of nickel speciation profile data. The third reviewer recommended that the EPA review several manuscripts on nickel speciation profiles showing that sulfidic nickel compounds (which the reviewer considered as the most potent carcinogens) are present at low levels in emissions from EGUs. 
      Nickel and nickel compounds have been classified as human carcinogens by national and international scientific bodies including the IARC, the World Health Organization, and the European Union's Scientific Committee on Health and Environmental Risks. In their 12th Report of the Carcinogens, the NTP has classified nickel compounds as known to be human carcinogens based on sufficient evidence of carcinogenicity from studies in humans showing associations between exposure to nickel compounds and cancer, and supporting animal and mechanistic data. More specifically, this classification is based on consistent findings of increased risk of cancer in exposed workers, and supporting evidence from experimental animals that shows that exposure to an assortment of nickel compounds by multiple routes causes malignant tumors at various organ sites and in multiple species. The 12[th] Report of the Carcinogens states that the "combined results of epidemiological studies, mechanistic studies, and carcinogenesis studies in rodents support the concept that nickel compounds generate nickel ions in target cells at sites critical for carcinogenesis, thus allowing consideration and evaluation of these compounds as a single group". Although the precise nickel compound (or compounds) responsible for the carcinogenic effects in humans is not always clear, studies indicate that nickel sulfate and the combinations of nickel sulfides and oxides encountered in the nickel refining industries cause cancer in humans. There have been different views on whether or not nickel compounds, as a group, should be considered as carcinogenic to humans. Some authors believe that water soluble nickel, such as nickel sulfate, should not be considered a human carcinogen, based primarily on a negative nickel sulfate 2-year NTP rodent bioassay (which is different than the positive 2-year NTP bioassay for nickel subsulfide).[,][,] Although these authors agree that the epidemiological data clearly supports an association between nickel and increased cancer risk, they sustain that the data are weakest regarding water soluble nickel. A recent review highlights the robustness and consistency of the epidemiological evidence across several decades showing associations between exposure to nickel and nickel compounds (including nickel sulfate) and cancer. 
      Based on the views of the major scientific bodies mentioned above, and those of expert peer reviewers that commented on EPAs approaches to risk characterization of nickel compounds, the EPA considers all nickel compounds to be carcinogenic as a group and does not consider nickel speciation or nickel solubility to be strong determinants of nickel carcinogenicity. With regards to non-cancer effects, comparative quantitative analysis across nickel compounds indicates that nickel sulfate is as toxic or more toxic than nickel subsulfide or nickel oxide.[,]
      Regarding the second charge question, two of the reviewers suggested using the URE derived by TCEQ for all nickel compounds as a group, rather than the one derived by IRIS specifically for nickel subsulfide. The third reviewer did not comment on alternative approaches. The EPA decided to continue using 100 percent of the current IRIS URE for nickel subsulfide because IRIS values are at the top of the hierarchy with respect to the dose response information used in EPA's risk characterizations, and because of the concerns about the potential carcinogenicity of all forms of nickel raised by the major national and international scientific bodies. Nevertheless, taking into account that there are potential differences in toxicity and/or carcinogenic potential across the different nickel compounds, and given that there have been two URE values derived for exposure to mixtures of nickel compounds that are 2-3 fold lower than the IRIS URE for nickel subsulfide, the EPA also considers it reasonable to use a value that is 50 percent of the IRIS URE for nickel subsulfide for providing an estimate of the lower end of a plausible range of cancer potency values for different mixtures of nickel compounds.
4. Chromium Risk
      Comment: One commenter stated there are several problems with EPA's analysis related to the fact that chromium emissions were evaluated as being entirely chromium (VI). The commenter stated that not all of the emitted chromium will remain in the hexavalent form by the time it reaches the target population, and that some may be converted to the much less toxic (and noncarcinogenic) trivalent species. The commenter also stated that the concentration levels considered in the case study assessment are far below occupational levels. The commenter concluded that EPA's cancer estimates should, therefore, be looked on with some skepticism. Another commenter stated that EPA's estimate of 12 percent chromium (VI) from coal-fired EGUs is unsupported, and that EPA failed to recognize that chromium (VI) is highly water-soluble and is easily reduced to chromium (III) in the presence of S02 in a low pH environment. The resulting chromium (III) would be expected to precipitate out in a FGD. The commenter stated that the actual amount of chromium (VI) that would be present in the emissions from an EGU with a wet scrubber is likely to be far lower than the 12 percent estimate made by EPA.
	Several commenters questioned the validity of the chronic inhalation study by the EPA because of (1) the use of surrogate speciated chromium emissions data instead of actual emissions data, (2) the assumption that units were run 100 percent of the time which is impossible, (3) dispersion modeling was used that is biased towards over predicting downwind impacts, and (4) estimated ambient concentrations were utilized as substitutes for real exposure concentrations for all people within a census block.
      Response: EPA disagrees with the commenters' assertion that all chromium was considered to be hexavalent. As discussed in "Methods to Develop Inhalation Cancer Risk Estimates for Chromium and Nickel Compounds", existing test data for utility and industrial boilers indicate that hexavalent chromium is, on average, twelve percent of total chromium from coal-fired boilers. The methods document underwent peer review by three external reviewers, and all three reviewers considered EPA's use of the values to be reasonable given the limited data available for chromium speciation profiling. The EPRI inhalation study for coal-fired boilers also used the twelve percent value.
EPA also disagrees that units were assumed to operate 100 percent of the time. The dispersion modeling performed for the case study facilities used hourly heat input as a temporalization factor for estimating hourly emissions, and in some cases hourly heat inputs (and emissions) were zero or very low. The commenter provided no data or information to support their claim that the dispersion modeling EPA used is biased towards overestimating downwind impacts.
      EPA disagrees with the commenters' assertion that "real exposure concentrations for all people within a census block" must be considered because it runs counter to the long-standing approach that EPA has taken to estimate the maximum individual risk, or MIR. The MIR is defined by the EPA's Benzene NESHAP regulation of 1989  and codified by CAA 112(f) as the lifetime risk for a person located at the site of maximum exposure 24 hours a day, 365 days a year for 70 years (e.g. census block centroids). The MIR is the metric associated with the determination of whether or not a source category may be delisted from regulatory consideration under section 112 (112(c)(9)). The MIR is the risk metric used to characterize the inhalation cancer risks associated with the case study facilities. EPA used the annual average ambient air concentration of each HAP at each census block centroid as a surrogate for the lifetime inhalation exposure concentration of all the people who reside in the census block. EPA has used this approach to estimate MIR values in all of its risk assessments to support risk-based rulemakings under section 112 of the CAA to date.
5. Acid Gas Risk 
      Comment: One commenter stated that acid gas emissions from oil-fired EGUs are not of the magnitude that triggered EPA's decision to regulate EGUs in general, raising the question of whether reduction (or even total elimination) of acid gas emissions from oil-fired EGUs could have any significant effect on EPA's goals of reducing non-cancer health risk or acidification of sensitive ecosystems in the U.S.
 	Several commenters stated that acid gas concentrations estimated in the case study facility assessment and the Utility RTC do not exceed human health thresholds of concern. Two commenters stated that HCl emissions are negligible compared to other primary emissions (such as SO2) that can lead to potential acidification of ecosystems.
      Response: Consistent with the proposed rule, EPA is not adopting an emissions standard based on its authority under section 112(d)(4) in the final rule. EPA first notes that the Agency's authority under section 112(d)(4) is discretionary. That provision states that EPA "may" consider established health thresholds when setting emissions standards under section 112(d). By the use of the term "may," Congress clearly intended to allow EPA to decide not to consider a health threshold even for pollutants that have an established threshold. As explained in the preamble to the proposed rule, it is appropriate for EPA to consider relevant factors when deciding whether to exercise its discretion under section 112(d)(4), and the language of that provision does not prevent the Agency from considering factors not specifically enumerated. To interpret the statute as commenters suggest, would effectively require the Agency to establish section 112(d)(4) standards whenever there is an established health threshold for a HAP. EPA has considered the public comments received and is not adopting an emissions standard under section 112(d)(4) for the reasons explained below and in the proposed rule.
      First, as explained in the preamble to the proposed rule, EPA maintains that the potential cumulative public health and environmental effects of acid gas emissions from EGUs and other acid gas sources located near EGUs supports the Agency's decision not to exercise its discretion under section 112(d)(4). EPA did not receive information regarding facility-specific emissions of all the acid gases from EGUs as well as sources that may be co-located with EGUs or nearby such sources. Additional data were also not provided during the comment period, and the data already in hand regarding these emissions are not sufficient to support the development of emissions standards for any of the EGU subcategories under section 112(d) that take into account the health threshold for acid gases, particularly given that the Act requires EPA's consideration of health thresholds under section 112(d)(4) to protect public health with an ample margin of safety. Commenters' assertions that EPA has sufficient data, even for HCl, are incorrect, and it appears that they believe that EPA can establish a section 112(d) standard for HCl and ignore the other acid gas HAP, a belief that is also incorrect. Second, the concerns expressed by EPA in the proposal regarding the potential environmental impacts and the cumulative impacts of acid gases on public health were not assuaged by the comments received. 
      As explained in the preamble to the proposed rule, EPA also considered the co-benefits of setting a conventional MACT standard for HCl. EPA considered the comments received on this issue and maintains that the co-benefits are significant and provide an additional basis for the Administrator to conclude that it is not appropriate to exercise her discretion under section 112(d)(4). EPA disagrees with the commenters who stated that it is not appropriate to consider non-HAP benefits in deciding whether to invoke section 112(d)(4). Although MACT standards may directly regulate only HAPs and not criteria pollutants, Congress did recognize, in the legislative history to section 112(d)(4), that MACT standards would have the collateral benefit of controlling criteria pollutants as well and viewed this as an important benefit of the air toxics program. EPA consequently does not accept the argument that it cannot consider reductions of criteria pollutants, for example in determining whether to take or not take certain discretionary actions, such as whether to adopt a risk-based standard under section 112(d)(4). There appears to be no valid reason that, where EPA has discretion in what type of standard to adopt, EPA must ignore controls which further the health and environmental outcomes at which section 112(d) of the Act is fundamentally aimed because such controls not only reduce HAP emissions but emissions of other air pollutants as well.
      Thus, the issue being addressed is not whether to regulate non-HAP under section 112(d) or whether to consider other air quality benefits in setting section 112(d)(2) standards -- neither of which EPA is doing -- but rather whether to make the discretionary choice to regulate certain HAP based on the MACT approach and whether EPA must put blinders on and ignore collateral environmental benefits when choosing whether or not to exercise that discretion. EPA knows of no principle in law or common sense that precludes it from doing so.
6. EPRI Risk Analysis
      Comment: Two commenters stated that a comprehensive tiered inhalation risk assessment (the EPRI study) using EPA-prescribed methods with improved emission factors, fuel data, and confirmed stack parameters did not identify significant health risks (cancer or non-cancer) among U.S. coal-fired power plants (as they existed in 2007). The commenters noted that these results contrast with those presented by EPA for its non-mercury case studies on 16 (15 coal-fired) power plants. The commenters state that several issues appear to underlie these differences, indicating the need for EPA to reevaluate its assessment and to undertake more refined (Tier 3) risk assessment for any facility of concern. Several commenters stated that for non-mercury HAPs the EPA produced one study on chronic inhalation risk assessment that identified three sites with cancer risks greater that one in one million for hexavalent chromium, which was authored by EPA staff and not peer reviewed. One commenter stated that the EPA study is based on misinformation and overestimates assumptions, and that the EPA has no data demonstrating health impacts from EGU emissions of non-mercury HAPs, or the benefit from reducing such emissions. Two commenters stated that no benefits will be derived from the non-mercury HAP emission reductions associated with the proposed rule because no non-mercury HAP health risks were proven, and that no showing was made that EGU non-mercury HAP emission levels reach levels associated with adverse health effects. Another commenter stated that EPA must complete a comparable and separate national scale risk assessment in order to determine appropriateness of proposing emissions standards for non-mercury metals.
      Response: The commenters are incorrect in the assertion that EPA's case studies were performed with less rigor than the EPRI analysis. The EPRI analysis used a tiered approach to risk assessment, beginning with Tier 1 using EPA's SCREEN3 dispersion model on all 470 coal-fired power plants in the U.S., and following with Tier 2 with EPA's Human Exposure Model (which uses the AERMOD dispersion model) for plants with higher risks from the Tier 1 modeling. Although tiered risk assessment is an appropriate approach, the Tier 2 modeling could have been more refined. For example, more meteorological data could have been used and building downwash could have been considered. The EPRI analysis ostensibly concluded that the Tier 2 modeling with HEM was conservative, and that because the modeled risks did not exceed certain thresholds, no further refinement was necessary. However, such refinements could result in higher modeled risks than those from the commenter's Tier 2 modeling.
      EPA's dispersion modeling of the case study facilities was actually performed with a greater degree of refinement than the EPRI analysis, and was consistent with EPA's Guideline on Air Quality Models. 
      In contrast to the approach used in the EPRI analysis, EPA used:
   1) 5 years of recent meteorological data from the weather station nearest to each facility, rather than 1 year of meteorological data. This is more representative of long-term (i.e., lifetime) exposures and risks.
   2) Temporally-varying emissions based on continuous emissions monitoring data, rather than assuming a constant emission rate for each facility throughout the entire simulation.
   3) Building downwash, where appropriate.
   4) The latest version of AERMOD [version 11103]
      EPA's assessment of the case study facilities for the proposed rule concluded that three coal-fired facilities and one oil-fired facility had estimated lifetime cancer risks greater than one in a million. For the final rule, revisions were made to the case studies based on comments received, and the results indicate that five coal-fired facilities and one oil-fired facility had estimated lifetime cancer risks greater than one in a million.
      Regarding peer review, the risk assessment methodology used by EPA for the case studies was consistent with the method that EPA uses for assessments performed for Risk and Technology Review rulemakings, which underwent peer review by the Science Advisory Board in 2009. The SAB issued its peer review report in May 2010. The report generally endorsed the risk assessment methodologies used in the program. In addition, in July 2011, EPA completed a letter peer review of the methods used to develop inhalation cancer risk estimates for chromium and nickel compounds.
f. Ecosystem Impacts from HAPs
      Comment: Two commenters assert that EPA is not justified in regulating acid gases based on concern about the potential that acid gases contribute to ecosystem acidification rather than concerns about hazards to public health. The commenters further claim that HCl's contribution to ecosystem acidification is de minimis. The commenters point out that EPA acknowledges uncertainty in quantification of acidification and EPA relies on recently published research that is irrelevant to the question since it is based on research conducted in the peat bog ecosystem in the United Kingdom. Another commenter calls attention to several new studies published in a special issue of the journal Ecotoxicology devoted to the effects of methylmercury on wildlife.
      Response: While EPA agrees that quantification of acidification effects has remaining uncertainty, the science and methodology has progressed in recent years. Based on recent peer-reviewed research including Evans et al., acid gases can significantly contribute to acidification. EPA published a comprehensive risk assessment of acidification effects of nitrogen and sulfur deposition and a policy assessment. Given the extent and importance of the sensitive ecosystems evaluated in the review of nitrogen and sulfur deposition any substance that contributes to further acidification must be considered to be affecting the public welfare. EPA disagrees that the peer-reviewed study mentioned by commenter by Evans et al. (2011) is not relevant to U.S. ecosystems. The paper presents experimental results that show 1) that HCl is highly mobile in the environment, transferring acidity easily through soils and water, 2) that HCl can transport longer distances than previously thought (given its presence in remote ecosystems, and 3) that it can be a larger driver of acidification than previously thought. The fact that this study took place in the U.K. is itself irrelevant. The chemical interactions of HCl in water are the same the world over and sensitive ecosystems exist in the U.S. as well as in Europe as illustrated in the risk assessment for NOx and SOx (U.S. EPA, 2009). Furthermore, the commenter is factually incorrect that EPA is justifying that it is appropriate and necessary to regulate HAP emissions from EGUs based on this one study. EPA agrees with the commenter that mercury exposure in wildlife is responsible for various adverse health effects in many species across the U.S. and recognizes that research is ongoing in this area. As discussed in the preamble to the proposed rule, EPA agrees that there are potential environmental risks from exposures of ecosystems through Hg and non-Hg HAP deposition. EPA cited relevant articles from the special edition of Ecotoxicology mentioned by the commenter in the ecosystem effects section on Chapter 5 of the RIA for this rule, which is available in the docket.
G. EPA Affirms the Finding that it is Appropriate and Necessary to Regulate EGUs to Address Public Health and Environmental Hazards Associated with Emissions of Hg and Non-Hg HAP from EGUs
      In response to peer reviews of both the Hg and non-Hg HAP risk analyses, and taking into account public comments, we conducted revised analyses of the risks associated with U.S. EGU emissions of Hg and non-Hg HAP. These revised analyses demonstrated that the risk results reported in the preamble to the proposed rule are robust to the revisions made to the risk analyses. 
      Specifically, with regards to the revised national scale assessment of mercury risk to populations with high consumption of self-caught freshwater fish, the revised results show that up to 29 percent of modeled watersheds have populations that are potentially at risk from exposure to Hg resulting from U.S. EGU Hg emissions. Up to 24 percent of modeled watersheds have potential total Hg exposure greater than the RfD and U.S. EGU-attributable Hg deposition accounts for 5 percent or more of total deposition. Up to 10 percent of modeled watersheds have exposure that exceeds the RfD based on U.S. EGU-attributable deposition even excluding consideration of other non-U.S. EGU sources of Hg deposition. In the preamble to the proposed rule, we reported that up to 28 percent of modeled watersheds had populations potentially at risk from exposure to Hg resulting from U.S. EGU emissions. Given that 1) the percent of modeled watersheds has increased from 28 to 29 percent in the revised risk assessment, and 2) the revised analysis includes 36 percent more watersheds covering a much larger part of the U.S., we conclude that the finding that emissions of Hg from U.S. EGUs are a hazard to public health is affirmed by the revised risk analysis.
      With regards to the revised non-Hg inhalation case studies, the highest estimated individual lifetime cancer risk for the one case study facility (out of 16) with oil-fired EGUs is estimated to be 20 in a million, driven by nickel emissions. For the facilities with coal-fired EGUs, there were five (out of 16) with maximum individual cancer risks greater than 1 in a million (the highest was five in a million), four of which were driven by emissions of hexavalent chromium, and one which was driven by emissions of nickel. There were also two facilities with coal-fired EGUs with maximum individual cancer risks at 1 in a million. In the preamble to the proposed rule, we reported that the maximum individual lifetime cancer risk for the one facility with oil-fired EGUs was estimated to be 10 in a million, and that there were three coal-fired EGU facilities with maximum individual cancer risks greater than 1 in a million (the highest was eight in a million), and one coal-fired EGU facility with maximum individual cancer risks equal to 1 in a million. Given that 1) the lifetime cancer risk for the oil-fired EGU facility has increased from 10 to 20 in a million, 2) the number of coal-fired EGU facilities with cancer risks greater than 1 in a million has increased from three to five, and 3) the highest risk coal-fired facility still has cancer risks of five in a million, which is substantially greater than the 1 in a million benchmark, we conclude that the finding that emissions of non-Hg HAP from U.S. EGUs are a hazard to public health is affirmed by the revised risk analysis.
	We have affirmed that emissions of Hg and non-Hg HAP are a hazard to public health. We also reiterate that 1) U.S. EGU Hg emissions are a hazard to the environment, contributing to adverse impacts on fish-eating birds and mammals, 2) Hg is a persistent bioaccumulative environmental contaminant, and as a result, failing to control Hg emissions from U.S. EGU sources will result in long term environmental loadings of Hg, above and beyond those loadings caused by immediate deposition of Hg within the U.S.; controlling Hg emissions from U.S. EGUs helps to reduce the potential for environmental hazard from Hg now and in the future, 3) it is appropriate to regulate those HAP which are not known to cause cancer but are known to contribute to chronic non-cancer toxicity and environmental degradation, such as the acid gases. These findings independently support a determination that it is appropriate to regulate Hg and non-Hg HAP emissions from EGUs. In addition, we have identified effective controls available to reduce Hg and Non-Hg HAP emissions.
      Our revised analyses still show that in 2016 the hazards posed to human health and the environment by HAP emissions from EGUs will not be addressed; therefore, it is necessary to regulate EGUs under section 112. In addition, based on evaluation of the regulations required by the Clean Air Act, including the recent Cross State Air Pollution Rule (CSAPR), it is necessary to regulate EGUs under section 112 because the only way to ensure permanent reductions in U.S. EGU emissions of HAP and the associated risks to public health and the environment is through standards set under section 112. While CSAPR is projected to achieve some Hg reductions due to co-control of mercury provided by controls put in place to achieve required reductions in SO2 emissions, our national scale mercury risk assessment shows that there are still a substantial percent of watershed where populations will remain at risk from U.S. EGU Hg deposition after implementation of CSAPR. While we modeled slightly higher U.S. EGU Hg emissions of 29 tons in our risk analysis compared to the most recent estimate of 27 tons, we do not expect that this small change would affect our finding that U.S. EGU Hg emissions are a hazard to public health. In addition, the actual reductions in mercury that will occur due to application of controls to meet the SO2 emissions requirements of CSAPR may differ from those projected to occur, due to differences in the technologies that individual EGU sources choose to install. The only way to ensure reductions in Hg, including those modeled as resulting from the CSAPR, is to directly regulate Hg emissions under section 112.
      We reiterate that it is necessary to regulate HAP emissions from EGUs because 1) even though the hazards from Hg will not be resolved through regulation under section 112, incremental reductions in Hg are important because as exposure above the RfD increases the likelihood and severity of adverse effects increases, 2) we cannot be certain that the identified cancer risks attributable to EGUs will be addressed through imposition of the requirements of the CAA, 3) the environmental hazards posed by acidification will not be fully addressed through imposition of the CAA, 4) regulation under section 112 is the only way to ensure that HAP emissions reductions that have been achieved since 2005 remain permanent, and 5) direct control of Hg emissions affecting U.S. deposition is only possible through regulation of U.S. emissions as we are unable to control global emissions directly.
      All of these findings independently support a finding that it is necessary to regulate EGUs under section 112. Therefore, the agency affirms its finding that it remains appropriate and necessary to regulate coal- and oil-fired EGUs under CAA section 112, and the inclusion of coal- and oil-fired EGUs on the section 112(c) list of source categories regulated under CAA section 112.
      
       
      

