in the preamble to the proposed rule, and commenters' assertions do not
cause us to revisit these issues. The commenter is also incorrect in
suggesting that a change in interpretation is per se invalid and
provided no support for that position. See National Cable &
Telecommunications Ass'n, et al., v. Brand X Internet Services, et al.,
545 U.S. 967, 981 (discussing the deference provided to an Agency
changing interpretations, the Court stated ``change is not
invalidating, since the whole point of Chevron deference is to leave
the discretion provided by ambiguities of a statute with the
implementing Agency.'') (Internal citations and quotations omitted).
    The EPA disagrees with the commenters who raise concerns about the
validity of the 2000 finding because the data on which that finding was
based were more than 10 years old. The EPA made the finding at that
time based on the scientific and technical information available, and
the finding is wholly supported by that information. In addition, even
though not required to do so, the EPA has since conducted new technical
analyses utilizing the best information available in 2010 as several
years have passed since the 2000 finding. These new analyses confirm
that HAP emissions from EGUs continue to pose a hazard to public health
and the environment, even after taking into account emission reductions
that have occurred since 2000 from promulgated rules, settlements, and
consent decrees. See 76 FR 24991.
    Contrary to the commenter's assertion, the EPA did not violate CAA
section 307(d) by not providing a notice and comment opportunity before
making the December 2000 appropriate and necessary finding. One
commenter challenged EPA's 2000 finding and listing on the same
grounds, and the D.C. Circuit dismissed the case because CAA section
112(e)(4) clearly states that listing decisions cannot be challenged
until the Agency issues final emission standards for the listed source
category. See UARG v. EPA, 2001 WL 936363, No. 01-1074 (D.C. Cir. July
26, 2001). The EPA has provided the public an opportunity to comment on
both the 2000 finding and the 2011 analyses that support the
appropriate and necessary determination as part of the proposed rule,
and anyone may challenge the listing in the D.C. Circuit in conjunction
with a challenge to this final rule. The commenters could have also
commented on the CAA section 112(n)(1) (e.g., the Utility Study and the
Mercury Study) studies in 2000 as they were included in the docket, but
EPA is not aware of any comments on those studies. In any case, these
studies were peer reviewed and considered the best information
available at that time. The EPA has fully complied with the rulemaking
requirements of CAA section 307(d).
    The EPA also disagrees with the commenters' characterization of the
New Jersey case. The D.C. Circuit did not say, as one commenter
suggested, that EPA is not able to consider additional information that
is collected after the 2000 finding; instead, the Court stated that EPA
could not revise its appropriate and necessary finding and remove EGUs
from the CAA section 112(c) list without complying with the delisting
provisions of CAA section 112(c)(9). See New Jersey, 517 F.3d at 582-
83. The EPA also disagrees with the commenter's assertion that EPA
disregarded EO 12866 when making the 2000 finding. As stated in the
Federal Register notice, the 2000 finding did not impose regulatory
requirements or costs and was reviewed by the Office of Management and
Budget (OMB) in accordance with the EO.\76\
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    \76\ 65 FR 79831.
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2. New Technical Analyses
a. General Comments on New Technical Analyses
    Comment: Several commenters stated that the new analyses, including
the risk assessments and technology assessments, confirm that it
remains appropriate and necessary to regulate U.S. EGU HAP under CAA
section 112. These commenters stated that the new analyses provide even
more support than the risk and technology information available at the
time the 2000 finding was made, including information on further
developed emissions control technology, proven and cost-effective
control of acid gases using trona and dry sorbent injection, stabilized
natural gas prices that makes fuel switching and switching dispatch to
underutilized combined cycle plants more feasible, more information on
ecosystem impacts from HAP, ``hotspots'' from the deposition of Hg
around EGUs, the potential for re-emission of Hg, updated emissions
data and future projections of HAP emissions, and modern air pollution
modeling tools. One commenter states affordable control technology has
been in use in this sector for 10 to 40 years, and studies on EGU-
attributable Hg hazard has undergone two in-depth EPA reviews, as well
as a review by the NAS. Several commenters claimed that regulating U.S.
EGUs is appropriate and necessary to protect public health based on
information provided in the new technical analyses. These commenters
acknowledged the substantial reductions in HAP from recent regulations
and new studies that confirm serious health risks from HAP exposure.
One commenter stated that new studies show higher risks to fetuses than
previously estimated, increasing the potential for neurodevelopmental
effects in newborns. One commenter noted that EGUs are a major source
of HAP, including HCl, HF, As, antimony, Cr, Ni, and selenium, all of
which adversely affect human health. The commenter stated that because
of these health effects, the EPA has ample evidence to support a
determination

that non-Hg HAP emissions present a risk to human health.
    Other commenters disagreed that the new analyses confirm that it
remains appropriate and necessary to regulate U.S. EGUs. One commenter
claims that EPA tried to use the new technical analyses to provide
retroactive justification for the 2000 finding, which only found
``plausible links'' of health effects and ``potential concerns'' of
health effects of certain metal emissions, dioxins and acid based
aerosols. The commenter also asserted that none of these new analyses
demonstrate that EGU regulation under section 112 is necessary and
appropriate.
    One commenter agreed that EPA may supplement its finding with new
information, analyses and arguments to reaffirm the 2000 finding up
until EPA issues final emissions standards. The commenter noted that
the CAA does not freeze the finding. However, another commenter argued
that EPA does not have the authority to rely on new technical analyses
because the CAA requires EPA to make the finding on the basis of the
Utility Study alone. According to that commenter, the EPA unreasonably
stretched the language of CAA section 112 by considering new technical
analyses.
    Citing a report from Dr. Willie Soon that was submitted to the SAB,
one commenter stated that the new technical analyses supporting the
proposed rule do not conform to the Information Quality Act, which
requires that information relied on by EPA be accurate, reliable,
unbiased, and presented in a complete and unbiased manner.
    Response: The EPA agrees with the commenters that state that the
new technical analyses (e.g., the risk assessments and technology
assessment) confirm the 2000 finding and disagrees with the commenters
that state otherwise. The EPA also agrees with the commenters that the
2000 finding was valid at the time it was made based on the CAA section
112(n)(1) studies and other information available to the Agency at that
time. Furthermore, the EPA agrees with commenters that the final rule
will lead to substantial reductions in HAP emissions from EGUs, that
control of the HAP is estimated to lead to public health and
environmental benefits as discussed in the RIA, that Hg emissions from
U.S. EGUs pose a hazard to public health, and that non-Hg HAP emissions
from EGUs pose a hazard to public health.
    Although these new analyses were not required, the EPA agrees with
the commenters that stated that EPA is authorized to conduct additional
analyses to confirm the 2000 finding. The EPA disagrees with the
commenter's assertion that the Agency is not authorized to consider new
information and at the same time unable to use the information
available in 2000 because, according to the commenter, that information
is ``stale.'' Under this theory, the Agency could not ever make an
appropriate and necessary finding prospectively, thereby excusing the
Agency from its obligations to protect public health and the
environment because it did not diligently act in undertaking its
statutory responsibility to establish CAA section 112(d) standards
within two years of listing EGUs. See CAA section 112(c)(5). This is an
illogical result that finds no basis in the statute. The EPA also
disagrees with the commenter's assertion that EPA may not consider new
analyses conducted after the Utility Study in determining whether it is
appropriate and necessary to regulate EGUs under section 112 for the
reasons set forth in the preamble to the proposed rule.\77\
---------------------------------------------------------------------------

    \77\ 76 FR 24988.
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    The EPA disagrees with the commenter's implication that EPA
conducted the new analyses because of alleged flaws in the 2000
finding. As explained in detail in the preamble to the proposed rule,
the 2000 finding was wholly valid and reasonable based on the
information available to the Agency at that time, including the Utility
Study. Further, the EPA maintains that had it complied with the
statutory mandate to issue CAA section 112(d) standards within two
years of listing EGUs, the EPA would likely have declined to conduct
new analyses. The EPA conducted new analyses because over 10 years had
passed since the 2000 finding, and EPA wanted to evaluate HAP emissions
from U.S. EGUs based on the most accurate information available, though
the Agency was not required to reevaluate the 2000 finding. In
conducting the new analyses, the EPA used this updated information to
further support the finding.
    The EPA strongly disagrees with the commenter that stated that EPA
failed to conform to the Information Quality Act. The EPA used peer
reviewed information and quality-assured data in all aspects of the
technical analyses used to support the appropriate and necessary
finding supporting this regulation. In addition, the EPA submitted the
Hg Risk TSD to the SAB for peer review, which ``supports the overall
design of and approach to the risk assessment and finds that it should
provide an objective, reasonable, and credible determination of the
potential for a public health hazard from mercury emitted from U.S.
EGUs.'' \78\ The SAB received the comments from Dr. Willie Soon, and
had those comments available for consideration in their deliberations
regarding the Hg risk analysis. The SAB specifically supported elements
of the analysis criticized by Dr. Willie Soon regarding the use of the
EPA RfD as a benchmark for risk and the connection between Hg emissions
from U.S. EGUs and MeHg concentrations in fish. In addition, the risk
assessment methodology for the non-Hg case studies is consistent with
the methodology that EPA uses for assessments performed for Risk and
Technology Review rulemakings, which underwent peer review by the SAB
in 2009. \79\ During the public comment period, the EPA also completed
a letter peer review of the methods used to develop inhalation cancer
risk estimates for Cr and Ni compounds, and those reviews were
generally supportive. See above description of this peer review. For
the final rulemaking, the EPA revised both risk assessments consistent
with recommendations from the peer reviewers. The EPA relies on the
SAB's review of the quality of the information supporting the
analytical results. Accordingly, contrary to the commenters'
assertions, the EPA acted consistently with the Information Quality Act
as well as EPA's and OMB's peer review requirements.
---------------------------------------------------------------------------

    \78\ U.S. EPA-SAB, 2011.
    \79\ U.S. EPA-SAB, 2010.
---------------------------------------------------------------------------

b. Hg Emissions Estimates
1. Hg Emissions From EGUs
    Comment: The commenters addressed the 2005 and 2016 emissions
estimates for Hg and expressed concern that inaccuracies in these
emissions estimates result in overestimates of risks from Hg
deposition. Further, commenters compared EPA's 2010 estimate and 2016
estimate, and stated that it is not possible for 29 tons to be a
correct inventory total for Hg emissions in both years given expected
reductions from CSAPR. In addition, commenters specifically commented
on assumptions included in the Integrated Planning Modeling (IPM),
including a concern that Hg speciation factors used by IPM overestimate
emissions in 2016. Other commenters noted that EGU sources are the
predominant source of U.S. anthropogenic Hg emissions, particularly the
oxidized and particulate forms of Hg that are of primary concern for Hg
deposition.
    Response: The EPA disagrees with commenters' assertions that the
EPA's

emissions estimates overestimate risk. While EPA agrees that the 2005
Hg emissions may be overestimated, such an overestimate in 2005 would
actually lead to an underestimate of risk in 2016 and not an
overestimate of risk, as claimed by the commenter, because the ratio
approach used by EPA to scale fish tissue data would underestimate risk
if 2005 Hg estimates were overestimated. Since the 2005 emissions are
not used as a starting point for 2016 emissions from IPM, any 2005
overestimate does not affect the 2016 emissions levels. The 2016
emissions are computed by IPM based on forecasts of demand, fuel type,
Hg content of the fuel, and the emissions reductions resulting from
each unit's configurations. See IPM Documentation for further
information, which is available in the docket. No commenter has
provided any evidence that the IPM 2016 emissions projection
methodology resulted in an overestimate.
    The EPA acknowledges that the current Hg emissions estimate would
not be the same as the 2016 Hg emissions estimate given that compliance
with CSAPR is anticipated to have some Hg co-benefits. For this reason,
the EPA reflected emission reductions anticipated from CSAPR in the Hg
deposition modeling for 2016 in the Hg Risk TSD. In the final rule, the
EPA revised the estimate of Hg emissions remaining from U.S. EGUs in
2016, which includes additional emission reductions anticipated from
the final CSAPR. The revised estimate shows that U.S. EGUs would emit
27 tons of Hg in 2016. Although EPA does not use the current Hg
emissions estimates in any of the risk calculations, the EPA estimates
that current Hg emissions are 29 tons. Conclusions about the trend
between current emissions and emissions in 2016 are limited by the fact
that different methods were used to compute the two estimates, as fully
explained in the revised Emissions Overview memo in the docket.
    The EPA disagrees with the commenter's assertion that incorrect Hg
emission factors result in incorrect 2016 emissions. The 2016 projected
Hg emissions are not based on emissions factors. The 2016 Hg emissions
are computed by the IPM based on forecasts of demand, fuel type, Hg
content of the fuel, and the emissions reductions resulting from each
unit's configurations. The speciation factors referenced by the
commenter provide a basis for the speciation of total projected Hg
emissions into particulate, divalent gaseous, and elemental species,
and do not impact the total amount of Hg emissions.
    The EPA agrees with commenters who noted that EGU sources are the
predominant source of U.S. anthropogenic Hg emissions, and in
particular the oxidized and particulate forms of Hg that are of primary
concern for Hg deposition.
2. Global Hg Emissions
    Comment: Several commenters stated that predicted Hg deposition
relies heavily on the amount of gaseous elemental Hg used to define the
boundary and initial conditions of a model, e.g., the Hg that enters
the U.S. from outside the U.S. boundaries. The commenters asserted that
this is especially important because Hg emissions from Asia--the region
immediately upwind of North America that affects U.S. Hg deposition
significantly and also affects it the most compared to other regions--
are expected to continue to increase.80 81 82 83 84 85
According to the commenter, this would affect the amount of Hg in the
boundary and initial conditions. The commenters claim that EPA's
modeling did not account for these emission changes, thus leading to an
overestimate of U.S. EGU-attributable deposition in 2016.
---------------------------------------------------------------------------

    \80\ Jaffe D., Prestbo E., Swartzendruber P., Weiss-Penzias P.,
Kato S., Takami A., Hatakeyama S., Kajii Y., 2005. ``Export of
Atmospheric Mercury From Asia,'' Atmospheric Environment, 39, 3029-
3038.
    \81\ Jaffe D., Strode S., 2008. ``Fate and Transport of
Atmospheric Mercury From Asia,'' Environmental Chemistry, 5, 121.
    \82\ Pacyna E.G., Pacyna J.M., Sundseth K., Munthe J., Kindbom
K., Wilson S., Steenhuisen F., Maxson P., 2010. ``Global Emission of
Mercury to the Atmosphere From Anthropogenic Sources in 2005 and
Projections to 2020,'' Atmospheric Environment, 44, 2487-2499.
    \83\ Pirrone N., Cinnirella S., Feng X., Finkelman R.B., Friedli
H.R., Leaner J., Mason R., Mukherjee A.B., Stracher G.B., Streets D.
G., Telmer K., 2010. ``Global Mercury Emissions to the Atmosphere
From Anthropogenic and Natural Sources,'' Atmospheric Chemistry and
Physics, 10, 5951-5964.
    \84\ Streets, D.G., Zhang, Q., Wu, Y., 2009. ``Projections of
Global Mercury Emissions in 2050.'' Environmental Science &
Technology 43, 2983-2988.
    \85\ Weiss-Penzias P., Jaffe D., Swartzendruber P., Dennison
J.B., Chand D., Hafner W., Prestbo E., 2006. ``Observations of Asian
Air Pollution in the Free Troposphere at Mt. Bachelor Observatory in
the Spring of 2004,'' Journal of Geophysical Research, 110, D10304.
---------------------------------------------------------------------------

    Several commenters noted that Hg emissions from U.S. EGUs are small
when compared to global Hg emissions totals and natural sources within
the U.S. These commenters used a variety of information to support
alternative conclusions about the necessity to control U.S. EGU
emissions to reduce Hg risk: global Hg emissions inventories, global
and regional photochemical modeling research, and observation-based
assessments. A commenter stated that EPA has not acknowledged the
dramatic decline in Hg emissions from U.S. EGUs since the late 1990s
(approximately 50 percent) to the current level or consider the
relative magnitude of Hg emissions from U.S. EGUs compared to other
sources, natural (such as fires) and human-caused.
    Response: The EPA disagrees that boundary and initial conditions
used in modeling Hg deposition need adjustment for several reasons.
First, the EPA does not use the first 10 days of the modeling
simulation in the analysis, which is more than sufficient to remove the
influence of initial conditions on Hg deposition estimates.\86\ Second,
it is difficult to accurately characterize the speciation of Hg that
flows into the U.S. from other countries due to the lack of data near
the boundaries of the modeling domain. Third, the boundary inflow for
the CMAQ Hg modeling used in the Hg deposition modeling are based on a
global model GEOS-CHEM simulation using a 2000 based global
inventory.\87\ A recently published comparison of global Hg emissions
by continent for 2000 and 2006 found that total Hg emissions from Asia
(and Oceania) total 1,306 Mg/yr in 2000 and 1,317 Mg/yr in 2006.\88\
The EPA has determined that because the Asian Hg emissions estimated in
this study are nearly constant between 2005 and 2006, any adjustments
to the boundary conditions or adjustments to modeled Hg deposition
would be invalid and inappropriate. Recent research has shown that
ambient Hg concentrations have been decreasing in the northern
hemisphere since 2000.\89\ Because emissions from Asia have not
appreciably changed between 2000 and 2006 and ambient Hg concentrations
have been decreasing, ENVIRON's analysis contains incorrect assumptions
and we need not address them further. For these reasons and the large
uncertainties surrounding projected Hg

global inventories, the EPA concludes that the most appropriate
technical choice is to keep the Hg boundary conditions the same between
the 2005 and 2016 simulations.
---------------------------------------------------------------------------

    \86\ Pongprueksa, P., Lin, C.J., Lindberg, SE., Jang, C.,
Braverman, T., Bullock, O.R., Ho, T.C., Chu, H.W., 2008.
``Scientific Uncertainties in Atmospheric Mercury Models III:
Boundary and Initial Conditions, Model Grid Resolution, and Hg (II)
Reduction Mechanism.'' Atmospheric Environment 42, 1828-1845.
    \87\ Selin, NE., Jacob, D.J., Park, R.J., Yantosca, R.M.,
Strode, S., Jaegle, L., Jaffe, D. 2007. ``Chemical Cycling and
Deposition of Atmospheric Mercury: Global Constraints From
Observations.'' Journal of Geophysical Research-Atmospheres 112.
    \88\ Streets et al., 2009.
    \89\ Slemr, F., Brunke, E.G., Ebinghaus, R., Kuss, J., 2011.
``Worldwide Trend of Atmospheric Mercury Since 1995.'' Atmospheric
Chemistry and Physics 11, 4779-4787.
---------------------------------------------------------------------------

    The EPA also disagrees with the commenters' assertion that EPA has
not acknowledged the decline in Hg emissions for the U.S. EGUs since
the late 1990s. The EPA analyzed historical, current, and future
projected Hg emissions from the power generation sector, as cited in
the preamble to the proposed rule. The EPA also disagrees with the
commenters' assertions that EPA failed to consider the relative
magnitude of Hg emissions from U.S. EGUs compared to other sources. As
noted in the Hg Risk TSD, the EPA modeled Hg emissions from U.S. and
non-U.S. anthropogenic and natural sources to estimate Hg deposition
across the country. The EPA also determined the contribution of Hg
emissions from U.S. EGUs to total Hg deposition in the U.S. by running
modeling simulations for 2005 and 2016 with Hg emissions from U.S. EGUs
set to zero. Based on the Hg Risk TSD, Hg emissions from U.S. EGUs pose
a hazard to public health based on the total of 29 percent of modeled
watersheds potentially at-risk. Our analyses show that of the 29
percent of watersheds with population at-risk, in 10 percent of those
watersheds U.S. EGU deposition alone leads to potential exposures that
exceed the MeHg RfD, and in 24 percent of those watersheds, total
potential exposures to MeHg exceed the RfD and U.S. EGUs contribute at
least 5 percent to Hg deposition.
    The commenters suggest that Hg emissions from U.S. EGUs represent a
limited portion of the total Hg emitted worldwide, including
anthropogenic and natural sources. While EPA acknowledges that Hg
emissions from U.S. EGUs are a small fraction of the total Hg emitted
globally, it views the environmental significance of Hg emissions from
U.S. EGUs and other domestic sources as a more germane consideration.
Mercury is emitted from EGUs in three forms. Each form of Hg has
specific physical and chemical properties that determine how far it
travels in the atmosphere before depositing to the landscape. Although
gaseous oxidized Hg and particle-bound Hg are generally local/regional
Hg deposition concerns, all forms of Hg may deposit to local or
regional watersheds. U.S. coal-fired power plants account for over half
of the U.S. controllable emissions of the quickly depositing forms of
Hg. Although emissions from international Hg sources contribute to Hg
deposition in the U.S., the peer reviewed scientific literature shows
that Hg emissions from U.S. EGUs in the U.S. significantly enhance Hg
deposition and the response of ecosystems in the U.S.
90 91 92 93
---------------------------------------------------------------------------

    \90\ Caffrey et al., 2010.
    \91\ Driscoll, C. T., Han, Y.-J., Chen, C. Y., Evers, D. C.,
Lambert, K. F., Holsen, T. M., et al., (2007). ``Mercury
Contamination in Forest and Freshwater Ecosystems in the
Northeastern United States.'' BioScience, 57(1).
    \92\ Keeler, G.J., Landis, M.S., Norris, G.A., Christianson,
E.M., Dvonch, J.T., 2006. ``Sources of Mercury Wet Deposition in
Eastern Ohio, USA.'' Environmental Science & Technology 40, 5874-
5881.
    \93\ White, E.M., Keeler, G.J., Landis, M.S., 2009. ``Spatial
Variability of Mercury Wet Deposition in Eastern Ohio: Summertime
Meteorological Case Study Analysis of Local Source Influences.''
Environmental Science & Technology 43, 4946-4953.
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c. Hg Deposition Modeling
1. General Comments on Deposition Modeling
    Comment: Several commenters stated that according to the ENVIRON
report, the EPA overestimated U.S. EGU-attributable Hg deposition by 10
percent on average (and up to 41 percent in some areas). The commenters
claim this overestimation is the result of boundary condition
treatment, the exclusion of U.S. fire emissions,\94\ and Hg plume
chemistry approach. In addition, one commenter referenced the same
ENVIRON report and stated that before implementation of controls
required by the proposed rule, areas with relatively high EGU-
attributable Hg deposition (one-fifth or more of total deposition) in
2016 constitute less than 0.25 percent of the continental U.S. area,
and only three grid cells have EGU contributions exceeding half of
total deposition.
---------------------------------------------------------------------------

    \94\ Finley, B.D., Swartzendruber, P.C., Jaffe, D.A., 2009.
``Particulate Mercury Emissions in Regional Wildfire Plumes Observed
at the Mount Bachelor Observatory.'' Atmospheric Environment 43,
6074-6083.
---------------------------------------------------------------------------

    Another commenter suggested that current research shows that models
of Hg atmospheric fate and transport overestimate the local and
regional impacts of some anthropogenic sources, such as U.S. EGUs.
Thus, according to the commenter, calculated contributions to Hg
deposition and fish tissue MeHg levels from these sources represent
upper bounds of actual contributions,\95\ \96\ and EPA should present
results as estimates of lower and upper bound limits.
---------------------------------------------------------------------------

    \95\ Seigneur, C., Lohman, K., Vijayaraghavan, K., Shia, R.L.,
2003. ``Contributions of global and regional sources to mercury
deposition in New York State.'' Environmental Pollution 123, 365-
373.
    \96\ Seigneur, C., Vijayaraghavan, K., Lohman, K.,
Karamchandani, P., Scott, C., 2004. ``Modeling the atmospheric fate
and transport of mercury over North America: power plant emission
scenarios.'' Fuel Processing Technology 85, 441-450.
---------------------------------------------------------------------------

    Response: The EPA disagrees with the information presented by
ENVIRON. The ENVIRON report is based on the misapplication of multiple
incommensurate modeling studies and false premises which include the
incorrect notion that the boundary conditions are over-estimated and
the idea that EPA should use in-plume chemistry that has not been
explicitly characterized and peer reviewed. Reactions that may reduce
gas phase oxidized Hg in plumes have not been explicitly identified in
literature. Recent studies in central Wisconsin and central California
suggest the opposite may happen; elemental Hg may be oxidized to Hg(II)
in plumes.\97\ \98\ Better field study measurements and specific
reaction mechanisms need to be identified before making conclusions
about potential Hg in-plume chemistry or applying surrogate reactions
in regulatory modeling. The possibility that Hg(0) is oxidized to
Hg(II) in plumes suggests coal-fired power plant Hg contribution inside
the U.S. may be underestimated in EPA modeling.
---------------------------------------------------------------------------

    \97\ Kolker, A., Olson, M.L., Krabbenhoft, D.P., Tate, M.T.,
Engle, M.A., 2010. ``Patterns of mercury dispersion from local and
regional emission sources, rural Central Wisconsin, USA.''
Atmospheric Chemistry and Physics 10, 4467-4476.
    \98\ Rothenberg, SE., McKee, L., Gilbreath, A., Yee, D., Connor,
M., Fu, X.W., 2010. ``Wet deposition of mercury within the vicinity
of a cement plant before and during cement plant maintenance.''
Atmospheric Environment 44, 1255-1262.
---------------------------------------------------------------------------

    The EPA asserts that the numbers suggested by the commenter are
inaccurate, as it is not appropriate to adjust EPA's deposition
estimates based on previous Hg modeling done with older Hg chemistry,
in-plume reactions that have not been explicitly identified, and
erroneous adjustments to Hg boundary inflow. Recent research has shown
that ambient Hg concentrations have been decreasing in the northern
hemisphere since 2000.\99\ The EPA declines to revise this analysis as
commenter suggests for several reasons, including available evidence
indicates that emissions from China have not appreciably changed
between 2000 and 2006 \100\ and ambient Hg concentrations have
decreased, the commenter inappropriately comingled out-of-date Hg
modeling simulations with EPA results, and ENVIRON's analysis has not
undergone any scientific peer review and presents information with
incorrect assumptions as noted in this response.
---------------------------------------------------------------------------

    \99\ Slemr et al., 2011.
    \100\ Streets et al., 2009.
---------------------------------------------------------------------------

    The EPA also disagrees with the commenter's interpretation of the
applicability of wildfire Hg emissions to

this assessment. Finley et al., (2009) \101\ suggests caution when
using their field data to make assumptions about Hg(p) emissions from
wildfires; the estimated particulate Hg emissions from wildfires is
based on one field site with a limited sample size, and the assumptions
made (such as the observed Hg(p) to carbon monoxide ratios at this
location) may not be valid on a broader scale.\102\ Mercury emissions
from wildfires are a re-volatilization of previously deposited Hg.\103\
Given that electrical generating power plants are currently and
historically have been among the largest Hg-emitting sources, the
inclusion of wildfire emissions in a modeling assessment would
necessarily increase the contribution from this emissions sector.
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    \101\ Finley et al., 2009.
    \102\ Id.
    \103\ Wiedinmyer, C., Friedli, H., 2007. ``Mercury emission
estimates from fires: An initial inventory for the United States.''
Environmental Science & Technology 41, 8092-8098.
    \104\ Seigneur et al., 2003.
    \105\ Seigneur et al., 2004.
---------------------------------------------------------------------------

    The EPA disagrees with the assertion that EPA failed to consider
the relative magnitude of Hg emissions from U.S. EGUs compared to other
sources and disagrees with the interpretation of EGU deposition
presented in the ENVIRON report. As noted in the Hg Risk TSD, the EPA
modeled Hg emissions from U.S. and non-U.S. anthropogenic and natural
sources to estimate Hg deposition across the country. The EPA also
determined the contribution of Hg emissions from U.S. EGUs to total Hg
deposition in the U.S. by running modeling simulations for 2005 and
2016 with Hg emissions from U.S. EGUs set to zero. Hg emissions from
U.S. EGUs pose a hazard to public health based on the total of 29
percent of modeled watersheds potentially at-risk. Our analyses show
that of the 29 percent of watersheds with population at-risk, in 10
percent of those watersheds U.S. EGU deposition alone leads to
potential exposures that exceed the MeHg RfD, and in 24 percent of
those watersheds, total potential exposures to MeHg exceed the RfD and
U.S. EGUs contribute at least 5 percent to Hg deposition. The ENVIRON
report provides no risk analysis of EGU contribution.
    The EPA disagrees that research 104 105 presented by the
commenter shows that U.S. EGU impacts are over-estimated. The
commenter's references do not support this statement. The references
provided by the commenter are based on Hg modeling that uses models
that are no longer applied and that are based on out-dated Hg chemistry
and deposition assumptions. Given the advances in Hg modeling since the
early 2000s, the EPA does not believe an upper and lower bound estimate
is necessary.
2. Chemical Reactions
    Comment: Several commenters stated that the CMAQ modeling fails to
account for the chemical reduction of gaseous ionic Hg to elemental Hg
that may occur in EGU plumes. The commenters noted that EPA did not use
the Electric Power Research Institute's (EPRI) Advanced Plume-in-Grid
Treatment, which includes a surrogate reaction to reduce gaseous ionic
Hg to elemental Hg inside plumes. Multiple commenters claimed that the
reduction of reactive gaseous Hg to gaseous elemental Hg has been
reported in power plant plumes and that supporting data include
atmospheric concentrations of speciated Hg measured downwind of power
plant stacks at ground-level monitor sites and dispersion model
predictions.106 107 A detailed description of various plume
measurement studies is provided in EPRI Comments, Section 3.4: Plant
Bowen, Georgia, Plant Pleasant, Wisconsin, and Plant Crist, Florida.
One commenter believed the impact of grid resolution (12 km sized grid
cells) on the CMAQ modeling was not appropriately addressed by EPA.
Their concerns due to grid resolution include the notion that a
source's emissions will be averaged over the entire grid cell.
According to the commenter, such averaging causes an artificially fast
dilution that smoothes out areas of high and low deposition, which may
limit the ability of the model to simulate smaller areas of localized
high deposition. This commenter believed that using the APT would
address these issues.
---------------------------------------------------------------------------

    \106\ Edgerton, E.S., Hartsell, B.E., Jansen, J.J., 2006.
``Mercury speciation in coal-fired power plant plumes observed at
three surface sites in the southeastern U.S.'' Environmental Science
& Technology 40, 4563-4570.
    \107\ Lohman, K., Seigneur, C., Edgerton, E., Jansen, J., 2006.
``Modeling mercury in power plant plumes.'' Environmental Science &
Technology 40, 3848-3854.
---------------------------------------------------------------------------

    Response: The EPA disagrees with the commenters' claims that
oxidized Hg chemically reduces to elemental mercury within the plume.
There is no evidence of these chemical reactions in the scientific
literature. The references cited by the commenters are from non-peer
reviewed reports and conference proceedings. The EPA does not consider
information presented at conferences or industry reports to be peer
reviewed literature, and consideration of oral presentation material
would be inappropriate. Further, even these cited references do not
provide sufficient information for incorporating the supposed reactions
into the modeling (e.g., specific chemical reactions, reaction rates,
etc.); rather, the cited references only suggest that oxidized gas
phase Hg could be reduced and postulate a possible pathway.
    Recent studies in central Wisconsin and central California suggest
the opposite may happen; elemental Hg may be oxidized to Hg(II) in
plumes.108 109 Better field study measurements and specific
reaction mechanisms need to be identified before making conclusions
about potential Hg in-plume chemistry or applying surrogate reactions
in regulatory modeling. Currently, models such as Advanced Plume
Treatment (APT) use a surrogate reaction for the potential reactive gas
phase Hg reduction that may or may not occur in plumes.\110\ Reactions
that may reduce gas phase oxidized Hg in plumes have not been
explicitly identified in literature. The application of potentially
erroneous in-plume chemistry that is a fundamental component of APT
would be inappropriate. In addition, the APT is not available in the
most recent version of CMAQ. It would be inappropriate for EPA to apply
an out of date photochemical model with in-plume chemistry that has not
been shown to exist.
---------------------------------------------------------------------------

    \108\ Kolker et al., 2010.
    \109\ Rothenberg et al., 2010.
    \110\ Vijayaraghavan, K., Seigneur, C., Karamchandani, P., Chen,
S.Y., 2007. ``Development and application of a multipollutant model
for atmospheric mercury deposition.'' Journal of Applied Meteorology
and Climatology 46, 1341-1353.
---------------------------------------------------------------------------

    The EPA agrees with the commenter that the CMAQ modeling with 12 km
grid resolution may provide a lower bound estimate on EGU contribution
as higher impacts using finer grid resolution are possible. The
commenter's assertion that EGU impacts are likely higher further
supports the final conclusions of the exposure modeling assessment. The
EPA notes that the application of a photochemical model at a 12 km grid
resolution for the entire continental U.S. is more robust in terms of
grid resolution and scale that anything published in literature and
represents the most advanced modeling platform used for a national Hg
deposition assessment.
3. Modeled Deposition Compared to Measured Deposition
    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 believe 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: EPA agrees with the commenters that the negative estimate
for wet deposition in the Air Quality Modeling TSD was an error. This
error reflected an incorrect calculation in the post-processing of
model and observation pairs that 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. This error did not affect Hg deposition. In response to
comments, the EPA provided additional model performance evaluation by
season to the revised Air Quality Modeling TSD. In addition, in
response to comments, the EPA also included model performance
evaluation for total Hg wet deposition for the 36 km modeling domain in
the revised Air Quality Modeling TSD.
    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 CMAQ wet deposition of Hg has been and will continue to be
extensively evaluated against MDN sites.\111\ There is no dry
deposition monitoring network, which precludes evaluating CMAQ dry
deposition processes. 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.\112\ Considering the problems associated with TEKRAN
measurements of ambient Hg and the sparse nature of routine
measurements in the U.S., the EPA did not compare ambient Hg against
model estimates.
---------------------------------------------------------------------------

    \111\ Bullock, O.R., Atkinson, D., Braverman, T., Civerolo, K.,
Dastoor, A., Davignon, D., Ku, J.Y., Lohman, K., Myers, T.C., Park,
R.J., Seigneur, C., Selin, NE., Sistla, G., Vijayaraghavan, K.,
2009. ``An analysis of simulated wet deposition of mercury from the
North American Mercury Model Intercomparison Study.'' Journal of
Geophysical Research-Atmospheres 114.
    \112\ Lyman, S.N., Jaffe, D.A., Gustin, M.S., 2010. ``Release of
mercury halides from KCl denuders in the presence of ozone.''
Atmospheric Chemistry and Physics 10, 8197-8204.
---------------------------------------------------------------------------

    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.\113\
---------------------------------------------------------------------------

    \113\ Lohman et al., 2006.
---------------------------------------------------------------------------

    Another commenter identified two studies as supposedly having Hg
modeling results that are applicable to EPA's
analysis.114 115 These studies present similar model
performance metrics as EPA. The EPA disagrees that the Agency used
``highly aggregated performance metrics'' that result in degraded and
lenient model evaluation. The studies presented 116 117 as
relevant for point source mercury modeling use an approach to aggregate
the operational performance 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. It is common practice to pair modeled estimates
and observations in space and time (weekly in this case) and estimate
performance metrics, then average all the metrics together. The latter
is the approach taken by the EPA and should have been taken by the
studies presented by the commenter. The EPA used a more stringent
approach to match observations and predictions and aggregation of
operational model performance. The EPA agrees that the commenter
accurately restated total wet deposition model performance information
provided by the EPA in the Air Quality Modeling TSD. To provide
context, other Hg modeling studies show a positive bias for annual
total Hg wet deposition.118 119 An annual Hg modeling
application done by ENVIRON \120\ 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.\121\ These results
indicate a very large over-estimation tendency. The model performance
shown by EPA is consistent with other long-term Hg modeling
applications.
---------------------------------------------------------------------------

    \114\ Seigneur, C., Lohman, K., Vijayaraghavan, K., Jansen, J.,
Levin, L., 2006. ``Modeling atmospheric mercury deposition in the
vicinity of power plants.'' Journal of the Air & Waste Management
Association 56, 743-751.
    \115\ Vijayaraghavan, K., Karamchandani, P., Seigneur, C.,
Balmori, R., Chen, S.-Y., 2008. ``Plume-in-grid modeling of
atmospheric mercury.'' Journal of Geophysical Research-Atmospheres
113.
    \116\ Seigneur, C., Lohman, K., Vijayaraghavan, K., Jansen, J.,
Levin, L., 2006. ``Modeling atmospheric mercury deposition in the
vicinity of power plants.'' Journal of the Air & Waste Management
Association 56, 743-751.
    \117\ Vijayaraghavan, K., Karamchandani, P., Seigneur, C.,
Balmori, R., Chen, S.-Y., 2008. ``Plume-in-grid modeling of
atmospheric mercury.'' Journal of Geophysical Research-Atmospheres
113.
    \118\ Id.
    \119\ Vijayaraghavan et al., 2007.
    \120\ Yarwood, G, Lau, S., Jia, Y., Karamchandani, P.,
Vijayaraghavan, K. 2003. Final Report: Modeling Atmospheric Mercury
Chemistry and Deposition with CAMx for a 2002 Annual Simulation.
Prepared for Wisconsin Department of Natural Resources. http://www.gypsymoth.wi.gov/air/toxics/mercury/hg_X97579601_appB.pdf.
    \121\ Yarwood et al., 2003.
---------------------------------------------------------------------------

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.\122\ The
commenter also stated that the study is consistent with a major Hg
deposition study conducted

by the 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.\123\
---------------------------------------------------------------------------

    \122\ Evers, David C. et al., 2007. ``Biological Mercury
Hotspots in the Northeastern United States and Southeastern
Canada,'' Bioscience. Vol. 57 No. 1. p. 29.
    \123\ Cohen, et al., 2004. ``Modeling the Atmospheric Transport
and Deposition of Mercury to the Great Lakes,'' Environmental
Research 95, (247-265).
---------------------------------------------------------------------------

    One commenter agreed with the Agency's assessment of the 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. 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.\124\
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.
---------------------------------------------------------------------------

    \124\ Driscoll, C.T., D. Evers, K.F. Lambert, N. Kamman, T.
Holsen, Y-J. Han, C. Chen, W. Goodale, T. Butler, T. Clair, and R.
Munson. Mercury Matters: Linking Mercury Science with Public Policy
inthe Northeastern United States. 2007. Hubbard Brook Research
Foundation. Science Links Publication. Vol. 1, no. 3.
---------------------------------------------------------------------------

    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, the 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.\125\
---------------------------------------------------------------------------

    \125\ Seigneur et al., 2006.
---------------------------------------------------------------------------

    Several commenters stated that the 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).\126\ 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.\127\ 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.'' \128\
---------------------------------------------------------------------------

    \126\ U.S. EPA, 2005. 40 CFR Part 63 [OAR-2002-0056; FRL-7887-7]
RIN 2060-AM96. Revision of December 2000 Regulatory Finding on the
Emissions of Hazardous Air Pollutants From Electric Utility Steam
Generating Units and the Removal of Coal- and Oil-Fired Electric
Utility Steam Generating Units From the Section 112(c). Final rule,
March 29.
    \127\ Evers et al., 2007.
    \128\ Sullivan T., 2005. ``The Impacts of Mercury Emissions from
coal-fired Power Plants on Local Deposition and Human Health Risk.''
Presented at the Pennsylvania Mercury Rule Workgroup Meeting,
October 28.
---------------------------------------------------------------------------

    One commenter stated that Hg concentrations are not always highest
at sites closest to a major source. The commenter referred to a study
\129\ 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.
---------------------------------------------------------------------------

    \129\ Kolker, et al., 2010.
---------------------------------------------------------------------------

    One commenter provided information from a non-peer reviewed report
with wet Hg deposition measurements downwind from the coal-fired power
plant Crist in Pensacola, FL. The commenter stated that using the same
data from these same wet deposition sites, one study \130\ found that
Hg wet 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.
---------------------------------------------------------------------------

    \130\ Caffrey, J.M., Landing, W.M., Nolek, S.D., Gosnell, K.J.,
Bagui, S.S., Bagui, S.C., 2010. ``Atmospheric deposition of mercury
and major ions to the Pensacola (Florida) watershed: spatial,
seasonal, and inter-annual variability.'' Atmospheric Chemistry and
Physics 10, 5425-5434.
---------------------------------------------------------------------------

    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. The commenter cited a non-peer reviewed conference
presentation \131\ that reported changes in Hg wet deposition relative
to historic measurements. The commenter stated that, taken
collectively, these findings show that increased local total Hg
deposition, possibly due to EGUs, and deposition changes due to changes
in EGU emissions, are small.
---------------------------------------------------------------------------

    \131\ Krishnamurthy N., Landing W.M, Caffrey J.M., 2011.
``Rainfall Deposition of Mercury and Other Trace Elements to the
Northern Gulf of Mexico.'' Presented at the 10th International
Conference on Mercury as a Global Pollutant, Halifax, Nova Scotia,
Canada, July 27.
---------------------------------------------------------------------------

    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.
    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, the
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.\132\
---------------------------------------------------------------------------

    \132\ Edgerton et al., 2006.
---------------------------------------------------------------------------

    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 \133\ cited by those commenters that corroborate EPA's
conclusions. However, the EPA disagrees with those commenters'
characterization of the methodology used to calculate the potential for
excess local deposition. In response, the 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.
---------------------------------------------------------------------------

    \133\ Driscoll et al., 2007.
---------------------------------------------------------------------------

    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, the 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'', which are often defined as high Hg concentration in
fish, but rather of Hg deposition hotspots, defined as excess local Hg
deposition around U.S. EGUs, as clarified in the new Local Deposition
TSD. Because EPA did not identify ``Hg hotspots'' of high Hg
concentrations in fish, the EPA's MeHg water quality criterion of 0.3
mg/kg is irrelevant to EPA's analysis of excess local Hg deposition for
this rule.
    The EPA disagrees that the analysis assumes that deposition of Hg
is confined to a 50-km radius around power plants. The purpose of the
EPA's 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, the 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 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 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, the 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 ([micro]g/m\3\) to 1.18
[micro]g/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 that the information \134\ provided by the
commenter regarding the Crist plant and other coal-fired power plants
in Florida is relevant to EPA's analysis of excess local deposition
from U.S. EGUs because it is based on measurements of wet Hg deposition
without consideration of dry Hg deposition, which can be a significant
component of Hg deposition.
---------------------------------------------------------------------------

    \134\ EPRI, 2010.
---------------------------------------------------------------------------

    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 peer-reviewed
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 \135\ 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.\136\ 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 (where emissions from U.S. EGUs are set
to zero) and the 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.
---------------------------------------------------------------------------

    \135\ Seigneur et al., 2006.
    \136\ Id.
---------------------------------------------------------------------------

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 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 to 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.137 138
---------------------------------------------------------------------------

    \137\ Harris., R.C., John W.M. Rudd, Marc Amyot, Christopher L.
Babiarz, Ken G. Beaty, Paul J. Blanchfield, R.A. Bodaly, Brian A.
Branfireun, Cynthia C. Gilmour, Jennifer A. Graydon, Andrew Heyes,
Holger Hintelmann, James P. Hurley, Carol A. Kelly, David P.
Krabbenhoft, Steve E. Lindberg, Robert P. Mason, Michael J.
Paterson, Cheryl L. Podemski, Art Robinson, Ken A. Sandilands,
George R. Southworth, Vincent L. St. Louis, and Michael T. TateRudd,
J. W.M., Amyot M., et al., Whole-Ecosystem study Shows Rapid Fish-
Mercury Response to Changes in Mercury Deposition. Proceedings of
the National Academy of Sciences Early Edition, PNAS 2007 104 (42)
pp. 16586-16591; (published ahead of print September 27, 2007).
    \138\ Orihel D.M., Paterson M.J., Blanchfield P.J., Bodaly R.A.,
Gilmour C.C., Hintelmann H., 2007. ``Temporal Changes in the
Distribution, Methylation, and Bioaccumulation of Newly Deposited
Mercury in an Aquatic Ecosystem,'' Environmental Pollution, 154, 77-
88.
---------------------------------------------------------------------------

    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 \139\ 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.
---------------------------------------------------------------------------

    \139\ Scudder B.C., Chasar L.C., Wentz D.A., Bauch N.J., Brigham
M.E., Moran P.W., Krabbenhoft D.P., 2009. Mercury in fish, bed
sediment, and water from streams across the United States, 1998-
2005: U.S. Geological Survey Scientific Investigations Report 2009-
5109, 74 p.
---------------------------------------------------------------------------

    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 Mercury Maps 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,\140\ (2) the fact that watersheds may act as
legacy sources releasing Hg when disturbed,\141\ (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,\142\ (4) the distance of an ecosystem from Hg sources,\143\
and (5) the fact that Hg deposited to aquatic ecosystems becomes less
available for uptake by biota over time.\144\ 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.
---------------------------------------------------------------------------

    \140\ Grigal D.F., 2002. ``Inputs and Outputs of Mercury from
Terrestrial Watersheds: A Review,'' Environmental Review, 10, 1-39.
    \141\ Yang H., Rose N.L., Battarbee R.W., Boyle J.F., 2002.
``Mercury and Lead Budgets for Lochnagar, a Scottish Mountain Lake
and Its Catchment,'' Environmental Science & Technology, 36, 1383-
1388.
    \142\ Krabbenhoft D.P., Engstrom D., Gilmour C., Harris R.,
Hurley J., Mason R., 2007. Monitoring and Evaluating Trends in
Sediment and Water Indicators. In Harris R., Krabbenhoft D., Mason
R., Murray M.W., Reash R., Saltman T. (Eds.), Ecosystem Responses to
Mercury Contamination: Indicators of Change. New York: Society of
Environmental Toxicology and Chemistry (SETAC) North America
Workshop on Mercury Monitoring and Assessment, CRC, pp. 47-87.
    \143\ Lindberg S. et al. 2007. ``A synthesis of progress and
uncertainties in attributing the sources of mercury in deposition.''
Ambio 36(1): 19-32.
    \144\ Orihel D.M., Paterson M.J., Blanchfield P.J., Bodaly R.A.,
Hintelmann H., 2008. ``Experimental Evidence of a Linear
Relationship between Inorganic Mercury Loading and Methylmercury
Accumulation by Aquatic Biota,'' Environmental Science & Technology,
41, 4952-4958.
---------------------------------------------------------------------------

    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, the EPA did
not adequately screen 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 that 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.\145\
---------------------------------------------------------------------------

    \145\ U.S. EPA-SAB, 2011.

    The SAB peer review committee specifically addressed the MCM
---------------------------------------------------------------------------
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.\146\
---------------------------------------------------------------------------

    \146\ U.S. EPA-SAB, 2011.

    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.147 148 149 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.'' \150\
---------------------------------------------------------------------------

    \147\ Orihel et al., 2007.
    \148\ Orihel et al., 2008.
    \149\ Harris et al., 2007.
    \150\ U.S. EPA-SAB, 2011.
---------------------------------------------------------------------------

    Based on the responses of the SAB peer review committee, the 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.'' \151\
---------------------------------------------------------------------------

    \151\ U.S. EPA-SAB, 2011.
---------------------------------------------------------------------------

    In response to recommendations from the SAB, the 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, the 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, the EPA clarifies that the Hg Risk TSD did not directly use
the Mercury Maps model. Instead, the 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, the EPA does not attempt to project lag
times. Recent research cited by the SAB 152 153 154
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. While fish tissue may respond rapidly to
changes in Hg loading, this does not change the fact that previously
emitted Hg from U.S. EGUs can be re-emitted and re-deposited, and thus
affect Hg concentration in fish.
---------------------------------------------------------------------------

    \152\ Orihel et al., 2007.
    \153\ Orihel et al., 2008.
    \154\ Orihel et al., 2007.
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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, the 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, the 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 the 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's 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, the EPA clarifies that ``subsistence fishers'' are defined
as individuals who rely on noncommercial fish as a major source of
protein.\155\ 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 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.\156\
---------------------------------------------------------------------------

    \155\ U.S. EPA, U.S. Environmental Protection Agency. 2000.
Guidance for Assessing Chemical Contaminant Data for Use in Fish
Advisories, Volume 3: Overview of Risk Management. Office of Science
and Technology, Office of Water, U.S. Environmental Protection
Agency, Washington, DC EPA 823-B-00-007.
    \156\ U.S. EPA-SAB, 2011.
---------------------------------------------------------------------------

    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 12 km\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, the 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. As described in the revised
Hg Risk TSD, the EPA made this change in response to SAB's concerns
regarding the potential exclusion of watersheds with fewer than 25
individuals and regarding coverage for high-end recreational fish
consumption.\157\ 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, the EPA continues to use U.S. Census tract-level data to
evaluate the presence of a ``source population'' in the vicinity of the
watershed being modeled for risk. In this context, the EPA uses the
U.S. Census data to assess whether a socioeconomic status (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.
---------------------------------------------------------------------------

    \157\ This change led to a very small increase in the number of
watersheds with populations potentially at-risk. In the Hg Risk TSD
accompanying the proposed rule, approximately 4 percent of modeled
watersheds were excluded based on the SES-based filtering criteria.
---------------------------------------------------------------------------

    The EPA continues to model risk for white and black subsistence
fishers active in the southeast and for Hispanics assessed nationally.
In this case, the EPA links poverty with subsistence fishing, as EPA
only modeled locations with poor source populations. However, in
modeling these three populations, the

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,\158\ 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, and, 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, it is likely
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.
---------------------------------------------------------------------------

    \158\ Burger, J., 2002. ``Daily Consumption of Wild Fish and
Game: Exposures of High End Recreationists,'' International Journal
of Environmental Research and Public Health, 12 (4), 343-54.
---------------------------------------------------------------------------

    While 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, exposure
to total MeHg through self-caught fish consumption is the most
significant risk for subsistence fishing populations and high-end
recreational fishers. For the subset of these populations that focus
their fishing activity in freshwater streams and lakes, it is also the
case that they will experience a higher fraction of MeHg exposure
attributable to U.S. EGU Hg emissions. As a result, the EPA focused the
risk assessment on subsistence fishers active at inland freshwater
watersheds because they are likely to experience the highest levels of
individual risk as a result of exposure to U.S. EGU-attributable Hg.
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
\159\ 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.160 161 162 163 164 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.
---------------------------------------------------------------------------

    \159\ Morgan, J.N., M.R. Berry, and R.L. Graves. 1997. ``Effects
of Commonly Used Cooking Practices on Total Mercury Concentration in
Fish and Their Impact on Exposure Assessments.'' Journal of Exposure
Analysis and Environmental Epidemiology 7(1):119-133.
    \160\ Armbruster G., Gerow K.G., Lisk D.J., 1988. ``The Effects
of Six Methods of Cooking on Residues of Mercury in Striped Bass,''
Nutrition Reports International, 37, 123-126.
    \161\ Gutenmann, W.H. and Lisk D.J., 1991. ``Higher Average
Mercury Concentration in Fish Fillets after Skinning and Fat
Removal,'' Journal of Food Safety, 11, 99-103.
    \162\ Farias L.A., Favaro, D.I., Santos J.O., Vasconcellos M.B.,
et al., 2010. ``Cooking Process Evaluation on Mercury Content in
Fish,'' Acta Amazonia, 40 (4), 741-748.
    \163\ Perell[oacute] G., Mart[iacute]-Cid R., Llobet J.M.,
Domingo J.L., 2008. ``Effects of Various Cooking Processes on the
Concentrations of Arsenic, Cadmium, Mercury, and Lead in Foods,''
Journal of Agricultural and Food Chemistry, 156 (22), 11262-11269.
    \164\ Torres-Escribano S., Ruiz A., Barrios L., V[eacute]lez D.,
Montoro R., 2011. ``Influence of Mercury Bioaccessibility on
Exposure Assessment Associated with Consumption of Cooked Predatory
Fish in Spain,'' Journal of the Science of Food and Agriculture, 91
(6), 981-6.
---------------------------------------------------------------------------

    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 study \165\ 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). This study \166\ provides a range of adjustment factors 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, the 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, which is not
the most conservative assumption that the EPA could have made. This
study \167\ also 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).
---------------------------------------------------------------------------

    \165\ Morgan et al., 1997.
    \166\ Id.
    \167\ Id.
---------------------------------------------------------------------------

    Regarding the alternative studies identified by the commenters, the
EPA disagrees that these studies considered collectively contradict the
cooking loss factor in the analysis. Specifically, the first study
\168\ 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,\169\ 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.\170\ 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 \171\ 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 \172\ only addressed the issue qualitatively, thus cannot
be used for the cooking loss factor. When considered collectively, the
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 \173\ remains the most

applicable for characterizing cooking/preparation effects on Hg
concentrations in fish.
---------------------------------------------------------------------------

    \168\ Farias et al., 2002.
    \169\ Perell[oacute] et al., 2008.
    \170\ Torres-Escribano et al., 2011.
    \171\ Armbruster et al., 1988.
    \172\ Gutenmann et al., 1991.
    \173\ Morgan et al., 1997.
---------------------------------------------------------------------------

    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).\174\ Therefore, the EPA
interprets the fish consumption rates provided in this study \175\ as
representing as cooked/prepared and not for raw fish and for that
reason, application of a preparation/cooking adjustment factor is
required. Another study \176\ 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
177 178 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.
---------------------------------------------------------------------------

    \174\ Burger et al., 2002.
    \175\ Id.
    \176\ Shilling, Fraser, Aubrey White, Lucas Lippert, Mark Lubell
(2010). Contaminated fish consumption in California's Central Valley
Delta. Environmental Research 110, p. 334-344.
    \177\ Dellinger JA. 2004. ``Exposure assessment and initial
intervention regarding fish consumption of tribal members of the
Upper Great Lakes Region in the United States.'' Environ Res 95:325-
340.
    \178\ Personal communication, Dr. Dellinger, September 27, 2011.
---------------------------------------------------------------------------

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.179 180 The commenter stated that these
default consumption rates are derived from various studies and
generally are based on 90th or 99th 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,\181 \which equates to about a 95th
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.
---------------------------------------------------------------------------

    \179\ U.S. EPA. 1991. Risk Assessment Guidance for Superfund
(RAGS). Part C 1991 EPA/9285.7-01C. October.
    \180\ U.S. EPA. 2000. National Guidance: Guidance for Assessing
Chemical Contaminant Data for Use in Fish Advisories, Volume 2. EPA
823-B-00-008, November.
    \181\ U.S. EPA. 1989. Risk Assessment Guidance for Superfund
(RAGS). EPA/540/1-89/002. December.
---------------------------------------------------------------------------

    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 99th 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 99th 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 to 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 75th 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 75th 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, the EPA is interested in
those individuals who are most at-risk, which includes those who
consume the most fish. For that reason, the EPA considered a range of
high-end fish consumption rates including the 99th percentile
representing the most highly-exposed individuals. In responding to the
SAB peer review, the 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 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., 90th,
95th, and 99th) 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 99th percentile consumption
rates for the subsistence female fisher (373 g/day) is substantially
higher than the 90th or 95th 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, the EPA
asserts that it is reasonable to include these consumption rates as
representative of the most at-risk populations. In these cases,
however, the 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 \182\ and specialized
studies.183 184 185 186 187 Several studies identified
additional fishing populations with subsistence or near subsistence
consumption rates, including urban fishing populations (including low-
income populations),188 189 190 Laotian communities,\191\
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.\192\ 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.\193\
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    \182\ Burger et al., 2002.
    \183\ Burger, J., K. Pflugh, L. Lurig, L. Von Hagen, and S. Von
Hagen. 1999a. ``Fishing in Urban New Jersey: Ethnicity Affects
Information Sources, Perception, and Compliance.'' Risk Analysis
19(2): 217-229.
    \184\ Burger, J., Stephens, W. L., Boring, C. S., Kuklinski, M.,
Gibbons, J. W., Gochfeld M. 1999b. ``Factors in Exposure Assessment:
Ethnic and Socioeconomic Differences in Fishing and Soncumption of
Fish Caught along the Savannah River.'' Risk Analysis, Vol. 19, No.
3, p. 427.
    \185\ California Environmental Protection Agency (CalEPA). 1997.
Chemicals in Fish Report No. 1: Consumption of Fish and Shellfish in
California and the United States Final Draft Report. Pesticide and
Environmental Toxicology Section, Office of Environmental Health
Hazard Assessment, July.
    \186\ Tai, S. 1999. ``Environmental Hazards and the Richmond
Laotian American Community: A Case Study in Environmental Justice.''
Asian Law Journal 6: 189.
    \187\ Corburn, J. 2002. ``Combining community-based research and
local knowledge to confront asthma and subsistence-fishing hazards
in Greenpoint/Williamsburg, Brooklyn, New York.'' Environmental
Health Perspectives 110(2).
    \188\ Burger et al., 1999a.
    \189\ Burger et al., 1999b.
    \190\ CalEPA, 1997.
    \191\ Tai, 1999.
    \192\ Corburn, 2002.
    \193\ U.S. EPA-SAB, 2011.
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    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, the 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, the EPA moved the summary table to the main body in
the revised Hg Risk TSD. In identifying these studies, the EPA focused
on surveys for subsistence fishers that were applicable at the broader
regional or national level. In the Hg Risk TSD, the EPA acknowledged
the smaller sample sizes for some of the subsistence fisher groups, and
in several cases the EPA did not use the 99th percentile consumption
rates because the sample sizes were too low to support this level of
resolution. This decision did not affect EPA's finding of a hazard to
public health, which is based on the results for the female subsistence
fishing population, which has an estimate of the 99th percentile
consumption rate that is supported by an adequate sample size.
    The EPA disagrees with the comment that it did not provide a
rationale for choosing the 75th percentile fish tissue concentration
across lakes and rivers in a watershed. However, the 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, the EPA computes the 75th percentile value at each
sampling site within a watershed. The EPA then computed the average of
the site-specific 75th 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, the EPA considers it reasonable to
assume that a subset of subsistence fishers could target larger fish in
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 75th 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 75th percentile of fish tissue values as a
reflection of consumption of larger, but not the largest, fish among
sport and subsistence fishers is a reasonable approach and is
consistent with published and unpublished data on predominant types of
fish consumed.'' \194\ 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. In the revised Hg Risk TSD, the EPA clarified that the 7-
inch 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).\195\
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    \194\ U.S. EPA-SAB, 2011.
    \195\ Pennsylvania Fish and Boat Commission. 2011. Summary Book:
2011 Pennsylvania Fishing Laws & Regulations available at: http://fishandboat.com/fishpub/summary/inland.html.
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    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 75th 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 \196\ is based on
sound science, which was supported by the findings of the NAS
Study,\197\ 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.
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    \196\ U.S. Environmental Protection Agency--Integrated Risk
Information System (U.S. EPA-IRIS). 2001. Methylmercury (MeHg)
(CASRN 22967-92-6). Available at http://www.epa.gov/iris/subst/0073.htm.
    \197\ NAS, 2000.
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    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, the EPA
relied on the flawed Faroe Islands' children study and ignored the
Seychelles Islands study,\198\ 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,\199\
and Poland.\200\
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    \198\ Budtz-Jorgensen E, Debes F, Weihe P, Grandjean P. 2005.
``Adverse Mercury Effects in 7-Year-Old Children Expressed as Loss
in ``IQ''.'' EPA-HQ-OAR-2002-0056-6046.
    \199\ Kjellstrom, T; Kennedy, P; Wallis, S; et al. 1986.
Physical and mental development of children with prenatal exposure
to mercury from fish. Stage 1: Preliminary test at age 4. Natl Swed
Environ Protec Bd, Rpt 3080 (Solna, Sweden).
    \200\ Wieslaw Jedrychowski et al. 2006. ``Effects of Prenatal
Exposure to Mercury on Cognitive and Psychomotor Function in One-
Year-Old Infants: Epidemiologic Cohort Study in Poland,'' 16 Annals
of Epidemiology 439.
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    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) \201\ 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.
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    \201\ DSHS. 2005. Health Consultation: Mercury Exposure
Investigation Caddo Lake Area-Harrison County Texas. Agency for
Toxic Substances and Disease Registry. http://www.tceq.state.tx.us/assets/public/comm_exec/pubs/sfr/085.pdf.
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    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\202\ 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.
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    \202\ Hibbeln JR, Davis JM, Steer C, Emmett P, Rogers I,
Williams C, et al., 2007. ``Maternal seafood consumption in
pregnancy and neurodevelopmental outcomes in childhood (ALSPAC
study): an observational cohort study. '' Lancet 369:
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    Several commenters question the relationship between cardiovascular
effects and MeHg exposure. Two

commenters cited studies examining the relationship between MeHg
exposure and cardiovascular effects,203 204 205 206 207 208
but concluded that it seems premature to use these studies to establish
a dose-response relationship.
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    \203\ Roman HA, Walsh TL, Coull BA, Dewailly [Eacute], Guallar
E, Hattis D, et al., 2011. Evaluation of the Cardiovascular Effects
of Methylmercury Exposures: Current Evidence Supports Development of
a Dose-Response Function for Regulatory Benefits Analysis. Environ
Health Perspect 119:607-614.
    \204\ Guallar E, Sanz-Gallardo MI, van't Veer P, et al., 2002.
``Mercury, fish oils, and the risk of myocardial infarction.'' N
Engl J Med.;347:1747.
    \205\ Virtanen JK, Voutilainen S, Rissanen TH, et al., 2005.
``Mercury, fish oils, and risk of acute coronary events and
cardiovascular disease, coronary heart disease, and all-cause
mortality in men in eastern Finland.'' Arterioscler Thromb Vasc
Biol. 2005;25:228.
    \206\ Yoshizawa, Rimm, Morris, Spate, Hsieh, Spiegelman,
Stampfer, Willett. ``Mercury and the Risk of Coronary Heart Disease
in Men,'' N Engl J Med 2002; 347:1755-1760.
    \207\ Hallgren CG, Hallmans G, Jansson JH, et al., 2001. Markers
of high fish intake are associated with decreased risk of a first
myocardial infarction. Br J Nutr: 86:397.
    \208\ Mozaffarian, Dariush. 2011. ``Mercury Exposure and Risk of
Cardiovascular Disease in Two U.S. Cohorts,'' N Engl J Med 364:
1116-1125.
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    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.209 210 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.
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    \209\ Hibbeln et al., 2007.
    \210\ Mozaffarian, et al., 2011.
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    Response: The EPA agrees with commenters that state 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, the 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
\211\ and an independent scientific review panel convened as part of
the IRIS process \212\ advised strongly against using results from a
study that at the time had not shown an association between MeHg
exposure and adverse effects. Further, the EPA disagrees with comments
stating 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.213 214 215 To correct a misunderstanding by the
commenter, the data underlying the Faroe Islands study have been
previously published in the peer reviewed literature.
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    \211\ NAS, 2000.
    \212\ U.S. EPA. 2001b. Responses to Comments of the Peer Review
Panel and Public Comments on Methylmercury. Available on the
Internet at http://www.epa.gov/iris/supdocs/methpr.pdf.
    \213\ U.S. EPA, 2001a. Water Quality Criterion for the
Protection of the Human Health: MethylmercuryEPA-823-T-01-001,
available at http://water.epa.gov/scitech/swguidance/standards/criteria/aqlife/pollutants/methylmercury/index.cfm.
    \214\ U.S. EPA-IRIS, 2001.
    \215\ Rice D, Schoeny R, Mahaffey K. 2003. ``Methods and
Rationale for Derivation of a Reference Dose for Methylmercury by
the U.S. EPA.'' Risk Analysis 23(1)107-115.
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    The EPA disagrees that it did not incorporate the latest Hg data to