Comment: Multiple commenters expressed dissatisfaction related to EPA's model performance evaluation of CMAQ estimated Hg deposition. The commenters stated 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. The commenters also stated that EPA needs to assess how predicted values of deposition compare to Mercury Deposition Network (MDN) data and how predicted values of ambient speciated Hg concentrations compare to measurement networks like AMNet and SEARCH. In addition, commenters stated that 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 suggested that 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 Hg wet deposition at MDN monitors. Finally, several commenters noted that EPA presented a negative modeled wet deposition total in the air quality modeling TSD, which is physically impossible.
Response: The 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 provided additional model performance evaluation by season to the air quality modeling TSD. In addition, in response to comments, EPA has now included model performance evaluation for total Hg wet deposition for the 36 km modeling domain.
      The EPA disagrees that it did not conduct an assessment comparing CMAQ total Hg wet deposition estimates to MDN data. The air quality modeling TSD clearly shows a comparison of CMAQ estimated total Hg wet deposition with MDN data for the entire length of the modeling period. The characterization of wet and dry deposition processes relating to speciated Hg in global and regional scale photochemical models should be continually evaluated by the academic community and improved when appropriate. The CMAQ wet deposition of Hg 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. The EPA disagrees that an evaluation of ambient speciated Hg against routine monitor networks such as AMNet or SEARCH would be useful for this particular modeling application. The AMNet Hg network did not exist in 2005, which is EPA's baseline model simulation time period, and the SEARCH network started making preliminary measurements of Hg at one or two sites in 2005. In addition, measurement artifacts related to gaseous oxidized Hg are difficult to quantify and make direct comparison to model estimates problematic. Considering the problems associated with TEKRAN measurements of ambient Hg and the sparse nature of routine measurements in the U.S., EPA did not compare ambient Hg against model estimates.
      The EPA disagrees that the model performance presented in the air quality TSD is insufficient. The EPA asserts that the model performance evaluation is generally similar to the level of model performance presented in literature. One commenter presented the results of several Hg modeling studies as providing information that the commenter believes to be relevant for this assessment in terms of model performance metric estimation and the level of model performance evaluation shown for assessments modeling Hg near point sources. For example, one cited study titled "Modeling Mercury in Power Plant Plumes" models near-source Hg chemistry from U.S. EGUs, but provides absolutely no information about model performance evaluation. Another commenter identified two studies as supposedly having Hg modeling results that are applicable to EPA's analysis.[,]
      These studies present similar model performance metrics as EPA and aggregate the metrics across many monitor locations as did EPA; however, these articles calculate long term annual averages of modeled and observed total Hg wet deposition before estimating performance metrics, which presents a more favorable evaluation. The Seigneur et al. paper employs a less stringent approach for matching observations and model estimates of total Hg wet deposition by calculating 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), 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. The EPA finds the performance evaluation presented in the modeling TSD consistent with and 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 Hg wet deposition has been compared with other Hg models.
      The EPA agrees that the commenter accurately restated total wet deposition model performance information provided by EPA in the Air Quality Modeling TSD. To provide context, other Hg modeling studies show a positive bias for annual total Hg wet deposition.[,] An annual Hg 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 Hg modeling applications.
4. Excess Local Deposition from Hg Emissions from U.S. EGUs(Deposition Hotspots)
Comment: One commenter stated that reducing Hg will benefit local environments. The commenter stated that a 2007 study confirmed the presence of Hg "hotspots" downwind from coal-fired power plants and confirmed that coal-fired power plants within the U.S. are the primary source of Hg to the Great Lakes and the Chesapeake Bay. The commenter also stated that the study is consistent with a major Hg deposition study conducted by EPA and the University of Michigan that concluded that approximately 70 percent of Hg wet deposition resulted from local fossil fuel emissions in the region.
      One commenter agreed 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 stated that this excess Hg deposition would substantially increase the health and environmental risks associated with emissions at these sites. The same commenter also stated that EPA applied a conservative methodology to quantify near-source Hg deposition is conservative. The commenter stated that 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 12x12 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 stated that the Hubbard Brook Research Foundation issued a report in 2007 that identified five Hg hotspots, one of which was in the Adirondack Park, along with four suspected hotspots. The commenter stated that this study also provides a good description of the impacts of Hg on the Common Loon, which is a symbol of a healthy Adirondack environment.
      One commenter stated that there is there is no evidence of Hg hotspots due to local deposition associated with coal-fired power plants. According to the commenter, EPA's use of a 50 km radius to calculate hotspots is flawed. The commenter stated that modeling studies show that deposition of Hg 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 stated that EPA does not adequately define hotspots in this proposed rule. Those same commenters cited a previous EPA definition of hotspots as "a waterbody that is a source of consumable fish with MeHg tissue concentrations, attributable solely to utilities, greater than EPA's MeHg water quality criterion of 0.3 mg/kg" (milligrams per kilogram). The same commenters stated that it is unclear why EPA changed from defining a hotspot by fish tissue MeHg concentration to defining a hotspot by depositional excess. Two commenters suggested that a Hg hotspot is a specific location that is characterized by elevated concentrations of Hg exceeding a well-established criterion, such as a reference concentration (RfC) when compared to its surroundings. Those same commenters stated that identifying Hg hotspots should not be constrained to locations where concentrations can be attributed to a single source or sector. One of those two commenters noted 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 three standard deviations above the relevant mean."
	One commenter stated that Hg concentrations are not always highest at sites closest to a major source. The commenter referred to a study by Kolker, et al. (2010) that demonstrated that concentrations of atmospheric reactive gaseous Hg, gaseous elemental Hg, and fine particulate Hg were lower when measured 25 km from a 1,114 MW coal-fired EGU than when measured 100 km away. The commenter stated that these findings contradict the idea, implicit in EPA's hotspot analysis, that reactive gaseous Hg decreases with distance from a large point source.
	One commenter stated 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 stated that during this period, Plant Crist emitted about 230 pounds of Hg annually, about 85 percent of which was reactive gaseous Hg. The commenter cited a study by Landing et al. (2010) that estimated that 22 - 33 percent of wet-deposited Hg at these sites came from coal combustion, including regional and local sources while the remaining 67 to 78 percent came from the global background. The commenter stated that using the same data from these same wet deposition sites, Caffrey et al. (2010) found that Hg 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 stated that Plant Crist installed a wet scrubber and has operated that scrubber continuously since December 2009. The commenter stated that the scrubber reduces total Hg emissions by about 70 percent and reduces emissions of reactive gaseous Hg by about 85 percent. According to the commenter, using Hg to trace metal (As and selenium) ratios in precipitation collected in the same MDN in (post-scrubber) 2010, Krishnamurthy, et al. (2011) reported that Hg deposition due to local and regional sources had changed between -10 to +6 percent at these sites, relative to historic measurements. The commenter stated that these changes were thought to represent upper bound estimates, since the researchers assumed that all Hg, As, and selenium measured in wet deposition was from local and regional coal combustion sources even though measured deposition can also include global emission sources. The commenter stated 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 stated that a study by the Department of Energy (DOE) that collected and analyzed soil and vegetation samples for Hg 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 stated that analysis of long-term trends in Hg emissions from coal-fired EGUs and wet deposition in Florida concluded that statistical analysis does not show evidence of a significant relationship between temporal trends in Hg emissions from coal-fired EGUs in Florida and Hg concentrations in precipitation during 1998 to 2010. According to the commenters, these observational studies are supported by and consistent with evidence that oxidized Hg emitted from coal-fired power plants rapidly converts to elemental Hg, significantly reducing the potential for "local" or nearby deposition.
	Two commenters stated that the Hg 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 stated that by assessing only Hg deposition attributable to EGUs, EPA fails to provide a context for all other sources of Hg deposition. The commenters stated that the Agency does not explain why deposition from the top 10 percent of EGU Hg emitters does not decline, despite substantial reductions in modeled Hg 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 stated that the CMAQ model has limitations when used to predict local deposition and tends to overestimate local deposition. The commenters stated that modeling studies using either a plume model or an Eulerian model predict that 91 to 96 percent of the Hg emitted by an EGU travels beyond 50 km.
Response: The EPA agrees with the commenters that stated that Hg emissions from EGUs deposit locally and regionally and contribute to excess local deposition near U.S. EGUs. The 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.
	The EPA agrees that there is no generally agreed-upon 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 Hg in areas surrounding power plants would be useful in informing the finding. The EPA disagrees with some commenters who misinterpreted the intent of the Hg deposition hotspot analysis. Specifically, the analysis is not of "Hg hotspots" but rather of Hg deposition hotspots, defined as excess local Hg deposition around power plants, as clarified in the new Local Deposition TSD.
      The EPA disagrees that the analysis assumes that deposition of Hg is confined to a 50-km radius around power plants. The purpose of 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 Hg 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. The EPA does not suggest Hg 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, Hg disperses as it transports, so the average EGU contribution can be lower in areas beyond 50km relative to areas within 50km even though Hg emissions from EGUs are depositing into U.S. watersheds.
      The 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. The EPA has clarified the purpose of the excess local deposition analysis in the new TSD. The 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. The 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. The EPA's analysis did not focus on total Hg deposition, because as EPA acknowledges throughout its analysis, global sources of Hg deposition account for a large percentage of total Hg deposition. In addition, including global sources of Hg deposition would obscure to the comparison of local and regional U.S. EGU-attributable Hg deposition. Because of regional deposition from both domestic and global sources of Hg, total Hg deposition at any location is unlikely to be highly correlated with local sources. The EPA's analysis focused on U.S. EGU-attributable Hg deposition and demonstrates that for some plants (especially those with high Hg emissions), there is local deposition of Hg that exceeds the average regional deposition around the plant.
      The EPA's analysis shows heterogeneity in the amount of excess local deposition around plants. The new Local Deposition TSD shows that some plants can have local deposition that is less than the regional average deposition, suggesting that most of the Hg from those plants is transported regionally or that other EGUs in the vicinity of those plants dominate the deposition of Hg near the plants. This does not detract from the overall finding that around some power plants with high levels of Hg emissions that excess local deposition is on average three times the regional EGU-attributable deposition around those plants.
      The EPA disagrees that the Hg 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.
      The EPA disagrees with the commenters that stated that the discussion of local deposition in the Hg Risk TSD did not demonstrate that Hg deposition from the top 10 percent of EGU Hg 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 micrograms per cubic meter (ug/m[3]) to 1.18 ug/m[3]. What does not change is the percent local excess for EGU-attributable Hg deposition. This implies that while Hg 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 50 km from the plant is lower than the contribution to average deposition within 50 km of the plant.
	The EPA disagrees with the commenter regarding the interpretation of the literature related to the spatial extent of deposition of Hg emitted by U.S. EGUs. The 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 assertion that grid-based models typically overestimate local deposition surrounding EGUs. The EPA maintains that the CMAQ photochemical model represents the best science currently available in simulating atmospheric chemistry, transport, and deposition processes.
       The study cited by the commenter to support the notion that 91 to 96 percent of Hg emitted from power plants travels beyond 50 km is based on a photochemical transport model (the TEAM model) that does not employ current state-of-the-science and is not actively developed or updated. Furthermore, 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 Hg from all sources, an assumption that clearly limits the regional impacts from sources. The methodology of this study cited by the commenter is critically flawed in that it presents no results where individual Hg emission sources are removed and the difference between the zero out simulation and baseline model simulations are directly compared. Finally, the modeling study cited by the commenter presents an illustration of gridded total annual Hg deposition from the TEAM model for the eastern U.S. that clearly shows elevated annual total Hg deposition in the vicinity of coal-fired power plants in the Ohio River Valley and northeast Texas.
	The information provided by a commenter is not relevant to the analysis of excess local deposition from EGUs, as it is based on ground level measurements of wet deposition alone. 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 Hg installed controls) are not expected to provide meaningful information about the effectiveness of control technology. Wet deposition is highly variable from year to year and is subject 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. Hg Risk TSD
1. Assumption of Linear Proportionality in Relationship between Changes in Hg Deposition and Changes in Fish Tissue Hg Concentrations (Mercury Maps)
Comment: Several commenters criticized 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 stated 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 Hg deposition to waterbodies and changes in fish tissue MeHg levels.
      Several commenters stated that the Mercury Maps model has many deficiencies. Those commenters stated that Mercury Maps is a static model unable account for the dynamics of ecosystems that affect Hg bioaccumulation in fish, cannot consider non-air Hg inputs to watersheds, and assumes reductions in airborne Hg lead to proportional reductions in fish MeHg concentrations. Another commenter claimed that data that demonstrate a steady-state linear reduction in fish tissue MeHg in response to a reduction in atmospheric Hg deposition within watersheds do not exist and provided several references that they claimed show non-linear responses to changes in Hg deposition.[,]
      The same commenter disagreed with EPA's interpretation of Figure 2-17 in the March TSD and stated 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 stated that sheet flow and drainage could contain Hg and thus complicate the relationship that EPA asserts is linear and direct. Another commenter cited Figure 2-17 in the Hg Risk TSD as showing that there is no well-defined relationship between Hg 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 MeHg levels decrease in response to decreases in Hg deposition attributable to U.S. EGUs. According to the same commenter, the METAALICUS study shows that there is a lag time (and a non-proportional response) after 3 - 4 years. The same commenter noted that there are numerous factors that influence lag time including (1) watershed characteristics, (2) the fact that watersheds may act as legacy sources releasing Hg when disturbed, (3) the magnitude of emission reductions and subsequent changes in atmospheric deposition need to be weighed against the amount of Hg already in an ecosystem, (4) the distance of an ecosystem from Hg sources, and (5) the fact that Hg deposited to aquatic ecosystems becomes less available for uptake by biota over time. Another commenter stated that additional Mercury Maps assumptions do not allow for considerations of lag in response to changes in: (1) deposition, (2) legacy sources of Hg such as mining, (3) historical Hg deposition, (4) natural Hg levels in fish, (5) ecosystem dynamics over time, or (6) the relative source contributions over time. Another commenter stated that lag times 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 Hg 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. For this reason, the commenter asserted that the system is not at steady-state, a basic premise of the model. Another commenter stated that while the time lag for deposition to reach a waterbody is mentioned in the Hg Risk TSD, there is no discussion of the fact that a portion of the deposition is unlikely to reach the water at all.
      One commenter believes EPA incorrectly implied 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 stated that while EPA properly screened out watersheds with significant current non-air sources of Hg, EPA did not adequately screened out watersheds with significant Hg contributions from non-air sources, specifically watersheds with historic Hg 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 have conditions are not typical of much of the rest of the U.S.
Response: The EPA disagrees with the commenters who challenged the assumption of a linear proportional relationship between changes in U.S. EGU deposition and fish tissue Hg levels. The EPA specifically asked the SAB to evaluate EPA's assumption of linear proportionality in the relationship between Hg deposition and fish tissue MeHg 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 stated, "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.
      The EPA also disagrees with commenters' interpretation of Figure 2-17. As stated in the Hg Risk TSD, while this figure is useful to demonstrate the lack of correlation across watersheds between total deposition of Hg and MeHg concentrations in fish tissue, it is not indicative of the likely correlation between changes in Hg deposition at a given watershed and changes in MeHg concentrations in fish tissue from that watershed. The SAB 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, EPA 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. The 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 emissions of Hg. 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-EGU Hg emissions, 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 Hg Risk TSD did not directly use the Mercury Maps model. Instead, EPA applied an assumption of linear proportionality between changes in Hg 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 Hg Risk TSD.
2. Characterization of Subsistence Fishing Populations and Exposure Scenario
Comment: Several commenters stated that 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 stated no documentation exists to supports these assumptions. Another commenter stated that EPA's definitions of subsistence fishers in the Hg Risk TSD are not consistent with earlier EPA documents and are used inconsistently throughout the Hg Risk TSD. Several commenters stated that while subsistence fishing can be associated with poverty, poverty does not indicate subsistence fishing. One commenter stated that by including watersheds with as few as 25 members of individuals living in poverty, EPA overstates risks.
      One commenter stated 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 stated that if other studies exist, EPA should provide the values for comparison.
      One commenter stated that EPA combined two parameters with differing scales to establish the geographic unit used in the Hg Risk TSD risk assessment. The 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 the analysis handled differences in geographic resolution between watersheds and census tracts were.
	One commenter stated that procedure for assigning census tracts could bias exposure outcomes. For example, the commenter stated that 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 stated 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 stated 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 EPA did not test the bias by sensitivity analyses.
	Several commenters stated 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 stated that EPA should apply the minimum 25 source population criteria only to populations of women of childbearing age. One commenter stated that EPA assumption would result in any densely populated urban census tract with a single fish tissue sample being assigned to a modeled watershed with populations potentially at-risk, regardless of the actual degree of recreational or subsistence fishing taking place there.
Response: The EPA agrees with the comments that subsistence fish consumption was not clearly defined, and we have provided a clearer definition in the revised Hg Risk TSD, however, this clarification does not result in any changes to the quantitative analysis. In the Revised Hg 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 Hg Risk TSD). These studies clearly show that a subset of surveyed fishers consumes self-caught fish at the rates that were cited in the Hg Risk TSD. The SAB peer review concluded that the consumption rates and locations for fishing activity are supported by the data presented in the Hg Risk TSD, and are generally reasonable and appropriate given the available data.
	The 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. The HUCs are defined for varying spatial resolutions. The geographic unit used as the basis for generating risk estimates is HUC12, which are watersheds about 10 km on a side, which is comparable with the size of the 12 km[2] grid cells in CMAQ, which are 12km[2]. The EPA has also clarified that the specific unit of analysis for this assessment is at the watershed, not enumerated subpopulations.
      The EPA only used the U.S. Census tracts 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 Hg Risk TSD, EPA modified the female subsistence scenario to apply 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 no longer apply to 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, EPA uses the U.S. Census data 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.
      The 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, as EPA only modeled locations with poor source populations. However, in modeling these three populations, EPA asserts that the presence of a poor source population indicates 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). The 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 to determine 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. The EPA notes that relatively few watersheds (less than 4 percent) have fish tissue Hg data, thus can be included in the risk assessment. Consequently, while there is the potential for including some watersheds in the analysis 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.
      The 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-attributable Hg. Therefore, EPA focuses on this group of subsistence fishers in the risk assessment and did not evaluate exposure for the general population related to Hg exposure through seafood.
3. Cooking Loss Adjustment Factor
Comment: Several commenters stated that 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 MeHg intake rate by a constant factor of 33 percent and also increasing any resulting (HQ) risk estimate by a similar factor. Several commenters stated that the source of 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 suggested that EPA's 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: The EPA disagrees with the commenters that the selection of the cooking loss factor of 1.5 is not justified by the literature. The 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. The 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 disagrees that these studies considered collectively contradict the cooking loss factor in the analysis. Specifically, the first study may have included measurement of non-fish components added to dishes (e.g., onions, heavy breading etc.), which could dilute the post-cooking Hg measurements and give the appearance of a cooking loss even as actual fish tissue Hg levels could have increased. In the second study, the fish species are saltwater and not freshwater, and the authors note that the reduction of water and fat could increase in the Hg concentration without changing absolute content. The third study focused on measurement of bioaccessible Hg in raw and cooked fish. However, available information currently allows us to specify the risk model in terms of total Hg intake, not bioaccessible Hg, thus, this article is potentially informative for guiding future research and methods development, not the current risk assessment. The fourth study found a modest but statistically insignificant increase in Hg levels for most of the cooking methods assessed, which is directionally consistent with EPA's cooking loss adjustment. The fifth study only addressed the issue qualitatively, thus cannot be used for the cooking loss factor. 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.
	The 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 stated 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[,] queried 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 stated 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 stated 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 95[th] percentile fish consumption value. The same commenter stated that EPA applied the 99th percentile to a "small survey of 149 South Carolina female anglers" to calculate an ingestion rate of 373 grams per day (g/day). The commenter stated that if the 95th percentile is used 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 stated that EPA based its fish consumption rates used in the risk analysis on a limited number of studies and that those studies are poorly documented.
	Another commenter stated that 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. The commenter also noted 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 on risk is the fish consumption rate. That same commenter stated that using 99[th] percentile ingestion rate dramatically increases HQ and IQ loss compared to the 50th percentile ingestion rate . The commenter stated that when an estimate of the 95th percentile ingestion rate of the 15 to 44 year old female population is considered, the HQ is a tenth of the value computed with the 99[th] percentile high-end female fisher.
	One commenter stated 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 stated 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 indicated that 60 percent of the watersheds with fish Hg data from rivers have risks calculated based upon a sample size of one or two fish. The commenter stated that it is not reasonable to base a significant policy and regulation decision on watersheds where 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 stated that EPA provided no rationale for its decision to choose the highest of the 75th percentile for fish Hg 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 inflated the risk estimates by assuming consumption of only fish greater than 7 inches and choosing the largest of the 75[th] percentile of fish Hg levels from these larger fish (i.e., larger than 7 inches) for rivers and lakes. That same commenter suggested using the median of all size fish, not just those over 7 inches.
	One commenter stated 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: The EPA acknowledges that the focus of the Hg Risk TSD is characterizing risk for the groups likely to experience the greatest U.S. EGU-attributable Hg risk, which are 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 considered 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 clarified this focus in the introduction to the Revised Hg Risk TSD and 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. The focus on the most highly-exposed individuals is consistent with the appropriate and necessary finding and the treatment of other HAP under CAA section 112.
      The EPA agrees that the fish consumption rate is an important factor in calculating risk from exposure to MeHg in fish. The 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 Hg 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 represents 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 do not have to be eaten all at one meal. The higher consumption rates (i.e., greater than 250 g/day) are supported by all three studies used in the risk assessment, and therefore, there is support across studies near the upper bound of likely consumption rates in this range. The EPA acknowledges uncertainty associated with estimating high-end percentile values in these studies due to relatively low sample sizes for some population groups. However, even if a few individuals reported these high self-caught fish consumption rates, making it difficult to characterize the population percentiles they represent, the values still suggest that these levels of high fish consumption exist among surveyed individuals. To determine 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, EPA acknowledges that 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 Hg Risk TSD.
      The 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. The 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 concluded that the consumption rates and locations for fishing activity are supported by the data presented in the Hg Risk TSD, and are generally reasonable and appropriate given the available data.
	The EPA agrees that the Hg Risk TSD would be improved by clarifying that the literature review focused on identifying studies that characterize subsistence fish consumption for groups active at freshwater locations within the U.S., and EPA has revised the Hg Risk TSD accordingly. In the Hg Risk TSD, EPA summarized 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 moved the summary table to the main body in the Revised Hg 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 Hg Risk TSD, EPA acknowledged the smaller sample sizes for some of the subsistence fisher groups, and in several cases EPA did not use the 99th percentile consumption rates because the sample sizes were too low to support this level of resolution.
      The 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 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. The 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.
      The EPA generally agrees with the comment that some fraction of subsistence fishers likely consume fish without consideration for size (given dietary necessity), however, EPA considers it reasonable to assume that a subset of subsistence fishers could target larger fish on order to maximize the potential consumption per unit of fishing effort. The EPA uses this subset of subsistence fishers targeting larger fish, which is represented by the 75[th] percentile fish tissue value, in the risk assessment. In addition, including the female subsistence fishing population in the analysis also provides coverage for high-end recreational anglers who target larger freshwater fish. The SAB commented that: "Using the 75[th] 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 Hg Risk TSD. This sensitivity analysis showed that using the median estimates had only a small impact on the number and percent of modeled watersheds with populations potentially at-risk from U.S. EGU-attributable MeHg exposures. Regarding the 7-inch criteria, for the Revised Hg 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).
      The EPA disagrees with the comment that it is not reasonable to use watersheds where only a single fish sample is available. Although it is generally preferred to have multiple samples, the SAB noted that 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 suggested that EPA conduct additional analyses of the fish tissue MeHg data, which EPA has done and included in the Revised Hg Risk TSD. The Revised Hg 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 MeHg and Hg Health Effects Studies
Comment: Several commenters stated that EPA's RfD is based on sound science, which was supported by the findings of the NAS Study, and that EPA appropriately applied the RfD in the Hg risk assessment. The commenters also stated that recent studies find clear associations between maternal blood Hg levels and delayed child development and cardiovascular effects, as well as potential for effects due to exposure to pollutant mixtures including lead.
      However, many commenters expressed concerns regarding EPA's use of the MeHg RfD as a benchmark for health risk. Several commenters raised concerns claiming that EPA has not incorporated the best available Hg toxicological data into the RfD, which results in a flawed analysis and an overestimate of the impact of Hg emissions on human health.
      Several commenters stated that, when deriving the RfD, 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) there is potential for confounding by polychlorinated biphenyls (PCBs) and lead, (3) population exposure to MeHg was 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 Americans do; (2) the amount of MeHg in the U.S. population is much lower than the Seychelles islanders; and (3) all ocean fish contain about the same amount of MeHg, so MeHg intake per fish meal is similar between Americans and Seychelles Islanders. However, another commenter stated that industry arguments against using the Faroe Islands study fail 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 the RfD-based HQ metric and the IQ metric. Another commenter stated that the RfD assumes a threshold dose below which an appreciable risk of adverse effects is unlikely, and NAS did not evaluate whether MeHg exposure data were better fit by a linear or non-linear model or by a threshold or non-threshold model.
      Several commenters stated that EPA's MeHg RfD is more conservative than "safe" levels determined by other federal agencies and claim that EPA assigned unusually high uncertainty factors. Several commenters stated that EPA's use of the 1999 National Health and Nutrition Examination Survey (NHANES) blood Hg levels show a downward trend since 1999, and the levels have been below the RfD since 2001.
      One commenter stated that a study by Texas Department of State Health Services (DSHS, 2004) determined that among subsistence fishers who eat fish from Caddo Lake with elevated MeHg, women of child-bearing years did not have blood Hg levels greater than the RfD. Thus, according to the commenter, the connection between MeHg 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, which EPA did not taken into account.
      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 RfD methodology is a screening tool for deciding when risks clearly do not exist.
      Several commenters recommended adding qualitative discussions to the Hg Risk TSD regarding several aspects of  uncertainty, including uncertainty in the RfD, uncertainty in extrapolating a dose-response relationship between MeHg exposure and change in IQ, uncertainty in extrapolating the dose-response relationship from marine fish and marine mammals to freshwater fish, and uncertainty due to potential confounding by PCBs in marine species.
      Several commenters raised concerns regarding the relationship between MeHg exposure and IQ loss. Two commenters stated that changes in IQ are not a well-defined health consequence of MeHg exposure. One commenter stated that the SAB had reservations about EPA's use of IQ loss. Two commenters questioned whether IQ impacts would even occur because in Japan and Korea, where the maternal blood Hg levels are higher than in the U.S., there is no evidence of adverse effects. 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 variation in IQ measures and the intra-individual variation in IQ are higher than the threshold.
      Several commenters question the relationship between cardiovascular effects and MeHg exposure. Two commenters cited studies examining the relationship between MeHg exposure and cardiovascular effects,[,][,][,][,][,] but concluded that it seems premature to use these studies to establish a dose-response relationship.
      Several commenters assert that the risks from eating seafood are low relative to the benefits, that fish advisories can limit the beneficial aspects of fish consumption, and that fish advisories are often unsuccessful in changing behavior.[,] One commenter noted the important protective role of dietary selenium against MeHg toxicity because the binding affinity of Hg to Se is much higher than binding to sulfur.
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. The 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. The EPA did not choose to base the MeHg RfD solely on results from the Seychelles Islands, 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 and disagrees that the information underlying the RfD is "poorly explained". The EPA has provided detailed documentation for the choices underlying calculation of the RfD.[,][,] To correct a misunderstanding by the commenter, the data underlying the Faroe Islands study have been previously published in the peer reviewed literature.
      The EPA disagrees that it did not incorporate the latest Hg 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.
	The EPA agrees that EPA's RfD is not the same as the levels used by other federal agencies. 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 Agency for Toxic Substances Disease Registry (ATSDR) in the calculation of the minimal risk level.
	The 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, which is based on advice of the NAS and an independent panel of scientific peer reviewers convened as part of the IRIS process.
      The 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."
      The 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. The EPA also stated that no RfD defines an exposure level corresponding to zero risk.
      The EPA disagrees that exposure levels in the U.S. are lower than those 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. One study notes that in the NHANES data (1999 to 2004), the highest five percent of women's blood Hg exceeded 8.2 microgram per liter (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, one study reported mean blood Hg for adult women to be 15 ug/L; range for men and women was 2 to 89.5 ug/L. Note that some publications have reported Hg effects in U.S. populations near the current U.S. RfD.[,]  Also, EPA disagrees with the commenter stating all ocean fish throughout the world contain about the same amount of MeHg. Marine fish in commerce differ widely in Hg concentration by species, and fish within the same species but caught at different locations have variable amounts of Hg in their tissues.[,]
      The EPA disagrees that there is a statistically discernible downward trend in the NHANES data on blood Hg. The EPA is unaware that a formal statistical analysis for temporal trends has been completed for NHANES data on blood Hg 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 Hg 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 exposed women" having blood Hg concentration greater than established levels of concern. Visual observations of the data show a slight decrease in Hg blood level concentrations from 1999-2008 at the geometric mean, but this decrease may not be statistically significant. The EPA remains concerned that substantial numbers of women of childbearing age in the U.S. may have blood Hg levels that are equivalent to exposures at or above the RfD. While mean and 95[th] percentiles from recent NHANES data are below the blood Hg concentration equivalent to the RfD, blood levels for some portions of the population (high consumers of fish, for example) show exposures above the this level. One study estimated very high blood Hg levels at the 99[th] percentile for females of child-bearing age. Other published studies have shown that various population groups can have high blood Hg levels.[,][,][,][,] For example, one study found that 83 percent of the NHANES Asian population exceeded the RfD-equivalent blood mercury level.
      The EPA disagrees with the commenter regarding confounding by PCBs and lead. 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. Numerous analyses have shown neurobehavioral effects of PCBs; however, the effects of MeHg and PCB in the Faroe Islands study are separable. The EPA also documented the independence of PCB and MeHg effects in the Faroe Islands population. The NIEHS concluded that both PCB and Hg had adverse effects.  The 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 MeHg 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 MeHg exposure in the Faroese children that are not attributable to PCB toxicity. We also note that there was no report of lead exposure in the Faroe Islands population.
      The EPA disagrees with the commenter's assertion that the connection between MeHg 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 Hg 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. The 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.
      The EPA is aware of the possibility of both interactions among environmental contaminants and cumulative effects of pollutants that produce the same adverse endpoint. The 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.
      The EPA disagrees with commenters suggesting that the RfD-based HQ is inappropriate. The 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."
      The EPA agrees that additional qualitative discussion about uncertainty would improve the Revised Hg Risk TSD. The SAB also recommended that EPA revise the Hg Risk TSD "to better explain the methods and choices made in the analysis, and analytical results, and where the uncertainties lie." The SAB noted several uncertainties related to the RfD, and EPA is preparing a revised TSD that will address the SAB's recommendations, including a more complete discussion of uncertainties including the RfD.
      The 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 SAB stated, "The Panel agreed that if IQ loss is retained in the risk assessment despite these reservations, a loss of one or two 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). Although 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 in those with IQs that are much lower or higher than the mean.
      Although EPA disagrees that the IQ results are too uncertain to rely upon, EPA acknowledges that IQ is not the most sensitive neurodevelopmental endpoint affected by MeHg exposure, as also noted by the SAB. The SAB recommended that the IQ analyses be retained but be de-emphasized in the documentation underlying the final regulation. The SAB concluded, "The Panel does not consider it appropriate to use 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." The EPA is following up the SAB's recommendation by deemphasizing the IQ analysis and placing that analysis in an appendix to the revised TSD.
      The SAB, however, supported the use of the IQ dose-response function calculated by EPA in the Hg Risk TSD. The SAB noted, "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."
      The 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." The EPA also stated that additional cardiovascular studies have been published since 2000. The 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.
      The 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. The EPA rejects the commenter's speculation regarding whether the estimated IQ impacts for the regulation are real. Adverse effects of in utero Hg exposure have been reported in populations in the U.S.[,] In another study on neurobehavioral effects of prenatal exposure to MeHg 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 Hg 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.[,][,][,][,][,] Recent studies[,][,] and analyses indicate the potential for nutrients in fish (particularly marine fish) to mask some of the observed adverse effects of MeHg. Because EPA did not adjust for potential confounding by nutrients in marine fish and mammals, the benchmark doses used in the RfD derivation may be underestimated.
      The EPA recognizes the potential for confounding of the effects of Hg on the developing nervous system by a range of nutrients and discusses this uncertainty in the Revised Hg Risk TSD. Regarding selenium, the 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 Hg Risk Assessment
Comment: Several commenters generally supported the Hg risk assessment, but several other commenters generally disagreed with the Hg risk assessment. One supporter stated that EPA reasonably determined that Hg emissions pose a public health hazard, correctly requested peer review of Hg 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 MeHg 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 Hg 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 Hg emissions reductions in the U.S.
      Several commenters cite Tetra Tech's analysis that assessed Hg risk using different consumption rates, cooking factor, mean fish tissue concentrations, and EGU-attributable Hg 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 Hg exposure via fish consumption because EGU-attributable deposition is a small fraction of total deposition. One commenter stated that EPA's data shows Hg emissions from U.S. EGUs have little influence on fish Hg 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 stated that EPA did not consider scientific information showing that there is no straightforward connection between Hg emissions from U.S. EGUs to the Hg 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 stated that there is not any demonstrable evidence that anyone in the U.S. has suffered adverse health problems as a result of Hg emissions from coal-fired EGUs. One commenter stated that EPA's findings are similar to the 2000 findings where EPA found a plausible link between anthropogenic emissions 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 Hg 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 Hg concentrations. One commenter stated that EPA should characterize general recreational angler fishers instead of subsistence fishers. One commenter claims that EPA made math errors in the Hg Risk TSD regarding the deposition in watersheds at specific percentiles. One commenter questioned EPA's policy metrics used to characterize Hg risk.
      Several commenters stated that the Hg TSD is unclear and lacks detail, as noted by the SAB. One commenter stated that the SAB is critical of EPA's efforts, stating that the SAB found it difficult to evaluate the risk assessment based solely upon Hg Risk TSD and recommended that EPA transparently explain the methods and uncertainties. One commenter stated that because of insufficient review time and the lack of detail in the Hg Risk TSD, they could not assess key questions, such as the nation-wide representativeness of the fish tissue data.
      One commenter stated 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 stated 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 Hg have decreased significantly between 2005 and 2016, but claims that this decrease does not appear to affect the risk results.
      One commenter questions why EPA has departed from the CAA section 112(n) risk comparison to the 1 in 1 million to use the RfD for Hg.
Response: The purpose of the Hg 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 CAA 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 Hg deposition (for the 2016 scenario  -  see Revised Hg Risk TSD) is two 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 Hg 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 Hg emitted from U.S. EGUs." Furthermore, the 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." Although 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." The EPA has revised the Hg 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.
      The SAB concurred with EPA's analytical assumptions and overall study design for the Hg Risk TSD, including the RfD-based HQ approach, fish tissue data, 75[th] percentile size fish, Mercury Maps assumption, and consumption rates. Based on the SAB peer review, EPA strongly disagrees with commenter statements that the results reported in the Hg TSD are unreliable, overly conservative, extreme, inconsistent with EPA risk guidelines, or severely overstate risk based on the stated objectives of the analysis. The 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. The EPA has applied peer reviewed modeling to estimate the deposition of Hg attributable to U.S. EGUs. The EPA asserts that these metrics demonstrate a clear hazard to public health from Hg emissions from U.S. EGUs.
      The EPA thoroughly evaluated the Tetra Tech analysis. The EPA does not agree that the analysis by Tetra Tech uses assumptions that are "more reasonable", and the SAB agreed that all of EPA's assumptions are reasonable and appropriate. The EPA asserts that the Tetra Tech analysis does not fully cover 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 Hg 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 Hg, but a number of studies discussed in the Revised Hg 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 Hg.
      The EPA disagrees with the commenter's assertion that this rule will not affect risks associated with Hg exposure. Hg from U.S. EGUs contributes to the levels of MeHg in fish across the country and consumption of contaminated fish can lead to increased risk of adverse health effects. The EPA has shown in the RIA (Chapter 5) that this rule will reduce Hg levels in fish.
      The EPA acknowledges that U.S. EGUs contribute only a small fraction of total Hg deposition in the U.S. However, U.S. EGUs remain the largest emitter of Hg 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 Hg exposures exceeding the RfD to have at least 5 percent of total Hg 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 Hg exposures exceeding the RfD due to Hg emissions from U.S. EGUs even before considering Hg exposures due to other sources. Hg risk is increasing for exposures above the RfD, and as a result, any reductions in Hg 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 Hg risk assessment. The SAB 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's 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 Hg-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 Hg Risk TSD remains the same as proposal.
      The EPA disagrees with the commenter that there were errors in the Hg 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. The EPA has provided additional clarification in the Revised Hg Risk TSD.
      The 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 Hg 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 Hg 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.
      The EPA does not agree that there is no improvement in fish Hg concentrations between 2005 and 2016, or that there will be no further improvement from decreasing Hg emissions from U.S. EGUs from the baseline in 2016. Although total risk from all Hg exposures will remain elevated in much of the U.S., much of that risk is associated with global, non-U.S. Hg 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 Hg risk assessment, average EGU-attributable fish tissue Hg concentrations will be decreased by 65 percent. Likewise, the number of modeled watersheds with populations potentially at-risk from Hg emissions from U.S. EGUs will decline from 62 percent in 2005 to 28 percent in 2016. Emissions reductions due to regulation of Hg under CAA section 112 should result in additional reductions in U.S. EGU-attributable fish tissue Hg concentrations and modeled watersheds with populations potentially at-risk.
      The EPA disagrees that IQ loss is erroneous or irrelevant to informing policy, but EPA has moved that analysis to an appendix in the Revised Hg Risk TSD, per the SAB's recommendation. The EPA disagrees that the IQ effects at the 50[th] 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 Hg.
      Regarding the commenter who questioned the alleged change in risk metrics to use the RfD approach, 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 Hg, 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's statements concerning the clarity of the Hg Risk TSD to suggest that the public did not have an ample opportunity to comment on the Hg risk assessment. Although 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 CAA 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 preamble to 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 Hg risk assessment.
e. Non-mercury HAP Case Studies
1. Emissions for non-mercury case studies
Comment: The commenters raised concerns about a wide variety of aspects of EPA's approach for emissions used for the non-mercury 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 Cr 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 Cr(VI) is flawed, and the lack of coal rank as a delineating factor for emission factor calculation. The 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. The 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. The 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 Cr test data from the Cr emission factors used for some of the case study emissions.
      The EPA disagrees with commenters' assertions that the metal content of the coal is a basis for invalidating the test results of high Cr 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.
      The EPA disagrees with the commenter recommendations for using an equation from AP-42, developed in part by the commenters. The 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.
      The EPA also disagrees with commenters concerns about the assumption that 12 percent of the Cr will be Cr(VI) for every coal-fired unit. The 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 Cr 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 Cr emissions have scrubbers according to the data provided to EPA by those facilities, so scrubber impacts on Cr speciation is not relevant to EPA's conclusions based on the non-mercury case studies. In any case, EPA disagrees with the commenter's conclusions about the impacts of scrubbers on Cr speciation and provides evidence that impacts of scrubbers on Cr speciation can have the opposite effect on Cr(VI) fractions, concluding that EPA's 12 percent assumption is somewhat conservative.
      The EPA also disagrees that coal rank must be a factor in computing Cr emission factors for use in the case studies. The EPA's analysis has demonstrated that coal rank appears to play no role in metals emissions. The 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 commenter's 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-mercury Risk Case Study
Comment: One commenter stated that 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-mercury HAP indicated a cancer risk greater than or equal to the one in one million threshold level required to delist a source category under CAA section 112.
      One commenter stated that 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 EPA's assessment of the Conesville facility and processed these data with 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 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-mercury HAP for all sources in this category.
      One commenter stated that EPA's discussion in the preamble to the proposed rule misleads the reader into believing that non-mercury 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-mercury HAP.
      One commenter stated that with the assumptions in the Utility Study, 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 CAA section 112(n)(1)(A).
      Several commenters stated that even if the additional studies EPA performed were accurate, they hardly demonstrate that it is necessary and appropriate to regulate coal-fired EGU HAP under CAA 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 one in three (0.33). According to EPA's own data, the predicted added cancer risk of exposure to HAP 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-mercury HAP 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.
      One commenter questioned 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 Ni as the main HAP of concern from oil-fired units, even though cancer-related inhalation risks were well below the RfCs and EPA states that significant uncertainty remains as to whether those emissions present a health concern.
Response: The EPA agrees with the commenter that the non-mercury HAP risk assessment confirms the appropriate and necessary finding.
      The EPA disagrees that EPA's case study assessment is flawed by the use of beta versions of AERMET and AERMET. The EPA remodeled the case study facilities using the current versions of AERMINUTE (version 11059), AERMET (version 11059), and AERMOD (version 11103). Although 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 having only a few case study facilities exceeding one in a million risk invalidates the "appropriate finding". The 16 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. The 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 5 coal-fired facilities and 1 oil-fired facility had estimated lifetime cancer risks greater than 1 in a million. The EPA maintains that its finding that more than 30 percent of the case study facilities had a cancer risk greater than one in a 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 preamble to the proposed rule.
      The EPA disagrees with the commenter's assertion that the health effects associated with exposures to non-mercury HAP from U.S. EGUs are mischaracterized in the preamble to the proposed rule. The discussion of the health effects of non-mercury 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-mercury 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 Study. The Utility Study 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 1 in a million. The 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 CAA section 112.
      The EPA does not agree with the commenter who suggested that EPA should interpret the results of the non-mercury HAP risk analysis in the context of background cancer risk. As explained in the preamble to the proposed rule, EPA reasonably looked to the cancer risk threshold established under CAA 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 CAA section 112. The 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. The EPA maintains that the analysis was reasonable.
      The 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 CAA section 112(n)(1) or anywhere under CAA 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 preamble to 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 EPA's Benzene NESHAP regulation of 1989 and codified by CAA section 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 CAA section 112(c)(9). The MIR is the risk metric used to characterize the inhalation cancer risks associated with the case study facilities. The 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 CAA section 112 to date.
      The 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 CAA 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 the regulations protect public health with an ample margin of safety. If the regulations do not, the CAA directs EPA to promulgate additional more stringent standards (within the prescribed 8 years) to achieve the appropriate level of public health protection.
      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 preamble to the proposed rule. Certain commenters question the determination based on their views of how the Agency can and should exercise its discretion. The EPA disagrees with these commenters and stands by the determination for the reasons set forth in the preamble to the proposed rule. The EPA also stands by the determination that the maximum cancer risks posed by emissions of oil-fired EGUs are greater than one in a million, due primarily to emissions of Ni compounds. Based on our analysis, we are unable to delist oil-fired EGUs.
3. Ni Risk
Comment: Several commenters stated that the assumptions regarding the speciation and carcinogenic potential of Ni 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 Ni speciation, the commenters stated that there are substantial uncertainties regarding the species of Ni 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 Ni subsulfide to other forms of Ni 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 Ni emissions from EGUs, and maintains that its assessment of the potential inhalation risks from EGU emissions of Ni 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 Ni and Cr compounds emitted by EGUs. There were two charge questions relating to Ni in that review. First, do EPA's judgments related to speciated Ni 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 Ni 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 Ni 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 Ni 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 Ni 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 Ni compounds carcinogenic as a group. These reviewers, therefore, did not focus on the availability of Ni speciation profile data. The third reviewer recommended that EPA review several manuscripts on Ni speciation profiles showing that sulfidic Ni compounds (which the reviewer considered as the most potent carcinogens) are present at low levels in emissions from EGUs.
      Nickel and Ni 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 Ni compounds as known to be human carcinogens based on sufficient evidence of carcinogenicity from studies in humans showing associations between exposure to Ni 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 Ni 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 Ni compounds generate Ni ions in target cells at sites critical for carcinogenesis, thus allowing consideration and evaluation of these compounds as a single group". Although the precise Ni compound (or compounds) responsible for the carcinogenic effects in humans is not always clear, studies indicate that Ni sulfate and the combinations of Ni sulfides and oxides encountered in the Ni refining industries cause cancer in humans. There have been different views on whether or not Ni compounds, as a group, should be considered as carcinogenic to humans. Some authors believe that water soluble Ni, such as Ni sulfate, should not be considered a human carcinogen, based primarily on a negative Ni sulfate 2-year NTP rodent bioassay (which is different than the positive 2-year NTP bioassay for Ni subsulfide).[,][,] Although these authors agree that the epidemiological data clearly supports an association between Ni and increased cancer risk, they sustain that the data are weakest regarding water soluble Ni. A recent review highlights the robustness and consistency of the epidemiological evidence across several decades showing associations between exposure to Ni and Ni compounds (including Ni sulfate) and cancer.
      Based on the views of the major scientific bodies mentioned above, and those of expert peer reviewers that commented on EPA's approaches to risk characterization of Ni compounds, EPA considers all Ni compounds to be carcinogenic as a group and does not consider Ni speciation or Ni solubility to be strong determinants of Ni carcinogenicity. With regards to non-cancer effects, comparative quantitative analysis across Ni compounds indicates that Ni sulfate is as toxic or more toxic than Ni subsulfide or Ni oxide.[,]
      Regarding the second charge question, two of the reviewers suggested using the URE derived by TCEQ for all Ni compounds as a group, rather than the one derived by IRIS specifically for Ni subsulfide. The third reviewer did not comment on alternative approaches. The EPA decided to continue using 100 percent of the current IRIS URE for Ni 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 Ni 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 Ni compounds, and given that there have been two URE values derived for exposure to mixtures of Ni compounds that are 2-3 fold lower than the IRIS URE for Ni subsulfide, EPA also considers it reasonable to use a value that is 50 percent of the IRIS URE for Ni subsulfide for providing an estimate of the lower end of a plausible range of cancer potency values for different mixtures of Ni compounds.
4. Cr Risk
Comment: One commenter stated there are several problems with EPA's analysis related to the fact that Cr emissions were evaluated as being entirely Cr(VI). The commenter stated that not all of the emitted Cr 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 Cr(VI) from coal-fired EGUs is unsupported, and that EPA failed to recognize that Cr(VI) is highly water-soluble and is easily reduced to Cr(III) in the presence of SO2 in a low pH environment. The resulting Cr(III) would be expected to precipitate out in a FGD. The commenter stated that the actual amount of Cr(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.