support the appropriate and necessary finding. It is the policy of EPA
to use the most current peer reviewed, publicly available data and
methodologies in its risk assessments. However, the EPA noted in the
preamble to the proposed rule that ``data published since 2001 are
generally consistent with those of the earlier studies that were the
basis of the RfD, demonstrating persistent effects in the Faroe Island
cohort, and in some cases associations of effects with lower MeHg
exposure concentrations than in the Faroe Islands. These new studies
provide additional confidence that exposures above the RfD are
contributing to risk of adverse effects, and that reductions in
exposures above the RfD can lead to incremental reductions in risk.''
However, the EPA has not completed a comprehensive review of the new
literature, and as such, it would be premature to draw conclusions
about the overall implications for the RfD.
    The EPA agrees that EPA's RfD is not the same as the levels used by
other federal agencies. In their advice to the EPA on the appropriate
bases for a MeHg RfD, NAS specifically recommended that EPA use neither
the study nor the uncertainty factor employed by the Agency for Toxic
Substances Disease Registry (ATSDR) in the calculation of the minimal
risk level.\216\
---------------------------------------------------------------------------

    \216\ NAS, 2000.
---------------------------------------------------------------------------

    The EPA disagrees that the uncertainty factor is ``unusually
high''. The uncertainty factor used in calculation of EPA's peer-
reviewed RfD is small (10 fold); half of this factor is to account for
measured variability in human pharmacokinetics, which is based on
advice of the NAS \217\ and an independent panel of scientific peer
reviewers convened as part of the IRIS process.\218\
---------------------------------------------------------------------------

    \217\ Id.
    \218\ U.S. EPA, 2001b.
---------------------------------------------------------------------------

    The IRIS makes this statement regarding a threshold for MeHg, ``It
is also important to note that no evidence of a threshold arose for
methylmercury-related neurotoxicity within the range of exposures in
the Faroe Islands study. This lack [of a threshold] is indicated by the
fact that, of the K power models, K = 1 provided a better fit for the
endpoint models than did higher values of K.'' \219\
---------------------------------------------------------------------------

    \219\ U.S. EPA-IRIS, 2001.
---------------------------------------------------------------------------

    The EPA disagrees that it is using the MeHg RfD as an absolute
bright line for health effects in the risk assessment. As stated in the
preamble to this proposed rule, the RfD is an estimate of a daily
exposure to the human population that is likely to be without an
appreciable risk of deleterious effects during a lifetime. The EPA also
stated that no RfD defines an exposure level corresponding to zero
risk. Because mercury is a cumulative neurotoxin, it is important to
distinguish health effects from public health hazard. Within the
context of the appropriate and necessary finding, we interpret a public
health hazard as risk, rather than certain occurrence of health
effects.
    The EPA disagrees that exposure levels in the U.S. are lower than
those in the Faroe Islands study. Exposure to MeHg in the U.S. has been
reported at the same levels as those published in the Faroe
Islands.\220\ One study notes that in the NHANES data (1999 to 2004),
the highest five percent of women's blood Hg exceeded 8.2 microgram per
liter ([micro]g/L) in the Northeast U.S. and 7.2 [micro]g/L in coastal
areas.\221\ Higher levels have been reported among subjects known to
consume fish. For example, one study reported mean blood Hg for adult
women to be 15 [micro]g/L; range for

men and women was 2 to 89.5 [micro]g/L.\222\ Note that some
publications have reported Hg effects in U.S. populations at or below
the current U.S. RfD.223 224 Also, the EPA disagrees with
the commenter stating all ocean fish throughout the world contain about
the same amount of MeHg. Marine fish in commerce differ widely in Hg
concentration by species, and fish within the same species but caught
at different locations have variable amounts of Hg in their
tissues.225 226
---------------------------------------------------------------------------

    \220\ Schober Susan E, Sinks Thomas H, Jones Robert L, Bolger P
Michael, McDowell Margaret, Osterloh John, Garrett E Spencer, Canady
Richard A, Dillon Charles F, Sun Yu, Joseph Catherine B, Mahaffey
Kathryn R. Blood mercury levels in U.S. children and women of
childbearing age, 1999-2000. JAMA. 2003 Apr 2; 289(13): 1667-1674.
    \221\ Mahaffey, K.R., R.P. Clickner and R.A. Jeffries. 2009.
Adult Women's Blood Mercury Concentrations Vary Regionally in the
U.S.: Association with Patterns of Fish Consumption (NHANES 1999-
2004). Environ. Health Perspect., 117: 47-53.
    \222\ Hightower Jane M, Moore Dan. Mercury levels in high-end
consumers of fish. Environ Health Perspect. 2003 Apr; 111(4): 604-
608.
    \223\ Oken, E., Radesky, J.S., Wright, R.O., Bellinger, D.C.,
Amarasiriwardena, C.J., Kleinman, K.P., Hu, H., Gillman, M.W. 2008.
Maternal fish Intake during Pregnancy, Blood Mercury Levels, and
Child Cognition at Age 3 Years in a U.S. Cohort. American Journal of
Epidemiology, 167(10), 1,171-1,181.
    \224\ Lederman, Sally Ann Robert L. Jones, Kathleen L. Caldwell,
Virginia Rauh, Stephen E. Sheets, Deliang Tang, Sheila Viswanathan,
Mark Becker, Janet L. Stein, Richard Y. Wang, and Frederica P.
Perera. 2008. Relation between Cord Blood Mercury Levels and Early
Child Development in a World Trade Center Cohort. Environmental
Health Perspectives 118(8) 1085-1091.
    \225\ Hisamichi Y, Haraguchi K, Endo T. 2010. ``Levels of
mercury and organochlorine compounds and stable isotope ratios in
three tuna species taken from different regions of Japan.'' Environ
Sci Technol 44(15): 5971-8.
    \226\ Sunderland EM. 2007. ``Mercury exposure from domestic and
imported estuarine and marine fish in the U.S. seafood market.''
Environ Health Perspect. 115(2): 235-42. Epub 2006 Nov 20.
---------------------------------------------------------------------------

    The EPA disagrees that there is a statistically discernible
downward trend in the NHANES data on blood Hg. The EPA is unaware that
a formal statistical analysis for temporal trends has been completed
for NHANES data on blood Hg levels for the period 1999 to 2008.
Mahaffeyet al., evaluating NHANES data collected 1999 to 2004 for women
at child-bearing age, could ``not support the conclusion that there was
a general downward trend in blood Hg concentrations over the 6-year
study period.'' \227\ However, the same publication noted that ``there
was a decline in the upper percentiles reflecting the most highly
exposed women'' having blood Hg concentration greater than established
levels of concern. Visual observations of the data show a slight
decrease in Hg blood level concentrations from 1999-2008 at the
geometric mean, but this decrease may not be statistically significant.
The EPA remains concerned that substantial numbers of women of
childbearing age in the U.S. may have blood Hg levels that are
equivalent to exposures at or above the RfD. While mean and 95th
percentiles from recent NHANES data are below the blood Hg
concentration equivalent to the RfD, blood levels for some portions of
the population (high consumers of fish, for example) show exposures
above this level. One study estimated very high blood Hg levels at the
99th percentile for females of child-bearing age.\228\ Other published
studies have shown that various population groups can have high blood
Hg levels.229 230 231 232 233 For example, one study found
that 83 percent of the NHANES Asian population exceeded the RfD-
equivalent blood mercury level.\234\
---------------------------------------------------------------------------

    \227\ Mahaffey, K.R., R.P. Clickner and R.A. Jeffries. 2009.
Adult Women's Blood Mercury Concentrations Vary Regionally in the
U.S.: Association with Patterns of Fish Consumption (NHANES 1999-
2004). Environ. Health Perspect., 117: 47-53.
    \228\ Tran, N.L., L. Barraj, et al., 2004. ``Combining food
frequency and survey data to quantify long-term dietary exposure: a
methyl mercury case study.'' Risk Anal 24(1): 19-30.
    \229\ Id.
    \230\ Miranda, M.L., S. Edwards, et al., 2011. ``Mercury levels
in an urban pregnant population in Durham County, North Carolina.''
Int J Environ Res Public Health 8(3): 698-712.
    \231\ Hightower and Moore, 2003.
    \232\ Hightower, J.M., A. O'Hare, et al., (2006). ``Blood
mercury reporting in NHANES: identifying Asian, Pacific Islander,
Native American, and multiracial groups.'' Environ Health Perspect
114(2): 173-175.
    \233\ McKelvey, W., R.C. Gwynn, et al., 2007. ``A biomonitoring
study of lead, cadmium, and mercury in the blood of New York city
adults.'' Environ Health Perspect 115(10): 1435-1441.
    \234\ Hightoweret al., 2006.
---------------------------------------------------------------------------

    The EPA disagrees with the commenter regarding confounding by PCBs
and lead. Exposure to MeHg in the Faroe Islands was largely from
consumption of pilot whale meat; exposure to PCBs was found in the
portion of the population who also consume whale blubber. Numerous
analyses have shown neurobehavioral effects of PCBs; however, the
effects of MeHg and PCB in the Faroe Islands study are separable.\235\
The EPA also documented the independence of PCB and MeHg effects in the
Faroe Islands population.\236\ The National Institute of Environmental
Health Sciences (NIEHS) concluded that both PCB and Hg had adverse
effects.\237\ The NAS concluded that there was no empirical evidence or
theoretical mechanism to support the opinion that in utero Faroese
exposure to PCBs exacerbated the reported MeHg effect.\238\ A second
set of analyses found that the effect of prenatal PCB exposure was
reduced when the data were sorted into tertiles by cord PCB
concentrations.\239\ These analyses support a conclusion that there are
measurable effects of MeHg exposure in the Faroese children that are
not attributable to PCB toxicity. We also note that there was no report
of lead exposure in the Faroe Islands population.
---------------------------------------------------------------------------

    \235\ NAS, 2000.
    \236\ U.S. EPA, 2001a.
    \237\ National Institute of Environmental Health Sciences
(NIEHS). 1998. Scientific issues relevant to assessment of health
effects from exposure to methylmercury. Workshop organized by
Committee on Environmental and Natural Resources (CENR) Office of
Science and Technology Policy (OSTP), The White House, November 18-
20, 1998, Raleigh, NC.
    \238\ NAS, 2000.
    \239\ Budtz-J[oslash]rgensen, E., N. Keiding, and P. Grandjean.
1999. Benchmark modeling of the Faroese methylmercury data. Final
Report to U.S. EPA.
---------------------------------------------------------------------------

    The EPA disagrees with the commenter's assertion that the
connection between MeHg in fish and observed health effects is not
understood due to evidence from the cited Texas study.\240\ This is an
exposure study rather than a study on measures of neurobehavioral or
any other health endpoint. TCEQ noted that none of the Caddo Lake study
participants had blood Hg levels above the benchmark dose level (BMDL)
of 5.8 [mu]g/L (one of the several used by EPA in the calculation of
the MeHg RfD). The BMDL is not a ``no effect'' level. Rather it is an
effect level for a percentage of the population. The EPA has noted in
correspondence with TCEQ that, as an exposure study, the Caddo Lake
study may be representative of the surrounding population; however, the
sample size is very small. It is not appropriate to extrapolate from
Caddo Lake to larger regional or national populations.
---------------------------------------------------------------------------

    \240\ DSHA, 2005.
---------------------------------------------------------------------------

    The EPA is aware of the possibility of both interactions among
environmental contaminants and cumulative effects of pollutants that
produce the same adverse endpoint. The EPA guidance exists for dealing
with such scenarios.241 242 243 244 The Agency's concern
with the likelihood of human exposure to multiple contaminants is

reflected in the multi-chemical scope of the rulemaking. However, the
EPA focused the technical analyses supporting the proposed regulation
on effects of individual pollutants rather than cumulative effects.
---------------------------------------------------------------------------

    \241\ U.S. EPA. 1986. Guidelines for the Health Risk Assessment
of Chemical Mixtures. U.S. Environmental Protection Agency, Office
of Research and Development, Washington, DC September. EPA/630/R-98/
002. Available at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=2256.
    \242\ U.S. EPA. 1999. Guidance for Performing Aggregate Exposure
and Risk Assessments. U.S. Environmental Protection Agency, Office
of Pesticide Programs, Washington, DC October. Available at http://www.pestlaw.com/x/guide/1999/EPA-19991029A.html.
    \243\ U.S. EPA. 2000a. Supplementary Guidance for Conducting
Health Risk Assessment of Chemical Mixtures. U.S. Environmental
Protection Agency, Risk Assessment Forum, Washington, DC EPA/630/R-
00/002. Available at http://www.epa.gov/ncea/raf/pdfs/chem_mix/chem_mix_08_2001.pdf.
    \244\ U.S. EPA. 2003a. Framework for Cumulative Risk Assessment.
Risk Assessment Forum, U.S. Environmental Protection Agency.
Washington, DC EPA/630/P-02/001F. EPA/600/P-02/001F. Available at
http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54944.
---------------------------------------------------------------------------

    The EPA disagrees with commenters suggesting that the RfD-based HQ
is inappropriate. The SAB ``agreed that EPA's calculation of a hazard
quotient for each watershed included in the assessment is appropriate
as the primary means of expressing risk,'' and that ``because the RfD
from which the HQ is calculated is an integrative metric of
neurodevelopmental effects of methylmercury, it constitutes a
reasonable basis for assessing risk.'' \245\
---------------------------------------------------------------------------

    \245\ U.S. EPA-SAB, 2011.
---------------------------------------------------------------------------

    The SAB also recommended that EPA revise the Hg Risk TSD to include
additional qualitative discussion about uncertainty in the revised Hg
Risk TSD. Specifically, the SAB recommended that EPA revise the Hg Risk
TSD ``to better explain the methods and choices made in the analysis,
and analytical results, and where the uncertainties lie.'' The SAB
noted several uncertainties related to the RfD. The EPA agrees with
this recommendation and included a more complete discussion of these
uncertainties in the revised Hg Risk TSD.
    The EPA disagrees that the IQ metric threshold is questionable. The
SAB concluded that it was reasonable to consider a loss of >1 or >2 IQ
points a public health concern. The SAB stated, ``The Panel agreed that
if IQ loss is retained in the risk assessment despite these
reservations, a loss of one or two points would be an appropriate
benchmark.'' \246\ The SAB further comments in their report: ``The
consensus is that if IQ were to be used, then a loss of 1 or 2 points
as a population average is a credible decrement to use for this risk
assessment. This metric seems to be derived from the lead literature
and was peer reviewed by the Clean Air Scientific Advisory Committee
(U.S. EPA CASAC 2007).\247\ Although its applicability to methylmercury
is questionable, the size of the decrement is justified based on the
extensive analyses available from the literature reviewed by CASAC.''
\248\  As noted in other studies,\249\ \250\ a decrease of 1-2 points
at the mean results in a much larger decrease in those with IQs that
are much lower or higher than the mean.
---------------------------------------------------------------------------

    \246\ U.S. EPA-SAB, 2011.
    \247\ U.S. Environmental Protection Agency--Science Advisory
Board (U.S. EPA-SAB). 2007. Clean Air Scientific Advisory
Committee's (CASAC) Review of the 1st Draft Lead Staff Paper and
Draft Lead Exposure and Risk Assessments. EPA-CASAC-07-003. March.
Available on the internet at http://yosemite.epa.gov/sab/
sabproduct.nsf/989B57DCD436111B852572AC0079DA8A/$File/casac-07-
003.pdf.
    \248\ U.S. EPA-SAB, 2011.
    \249\ Axelrad, D. A.; Bellinger, D. C.; Ryan, L. M.; Woodruff,
T. J. 2007. ``Dose-response relationship of prenatal mercury
exposure and IQ: An integrative analysis of epidemiologic data.''
Environmental Health Perspectives, 115, 609-615.
    \250\ Bellinger DC. 2005. Neurobehavioral Assessments Conducted
in the New Zealand, Faroe Islands, and Seychelles Islands Studies of
Methylmercury Neurotoxicity in Children. Report to the U.S.
Environmental Protection Agency. EPA-HQ-OAR-2002-0056-6045.
---------------------------------------------------------------------------

    Although EPA disagrees that the IQ results are too uncertain to
rely upon, the EPA acknowledges that IQ is not the most sensitive
neurodevelopmental endpoint affected by MeHg exposure, as also noted by
the SAB. The SAB recommended that the IQ analyses be retained but be
de-emphasized in the documentation underlying the final regulation. The
SAB concluded, ``The Panel does not consider it appropriate to use IQ
loss in the risk assessment and recommended that this aspect of the
analysis be de-emphasized, moving it to an appendix where IQ loss is
discussed along with other possible endpoints not included in the
primary assessment. While the Panel agreed that the concentration-
response function for IQ loss used in the risk assessment is
appropriate, and no better alternatives are available, IQ loss is not a
sensitive response to methylmercury and its use likely underestimates
the impact of reducing methylmercury in water bodies.'' \251\ The EPA
is following the SAB's recommendation by deemphasizing the IQ analysis
and placing that analysis in an appendix to the revised Hg Risk TSD.
---------------------------------------------------------------------------

    \251\ U.S. EPA-SAB, 2011.
---------------------------------------------------------------------------

    The SAB, however, supported the use of the IQ dose-response
function calculated by EPA in the Hg Risk TSD. The SAB noted, ``The
function used came from a paper by Axelrad and Bellinger (2007) that
seeks to define a relationship between methylmercury exposure and IQ. A
whitepaper by Bellinger (Bellinger, 2005) \252\ describes the sequence
of steps in relating methylmercury exposure to maternal hair mercury
and then that to IQ. The Mercury Risk TSD furthers notes that IQ has
shown utility in describing the health effects of other neurotoxicants.
These are appropriate bases for examining a potential impact of
reducing methylmercury on IQ, but the SAB does not consider these
compelling reasons for using IQ as a primary driver of the risk
assessment.'' \253\
---------------------------------------------------------------------------

    \252\ Bellinger, 2005.
    \253\ U.S. EPA-SAB, 2011.
---------------------------------------------------------------------------

    The EPA disagrees that the Agency has overstated or failed to
review the scientific literature on cardiovascular effects from MeHg
exposure. As summarized in the preamble to the proposal, the EPA stated
that the NAS study concluded that ``Although the data base is not as
extensive for cardiovascular effects as it is for other end points
(i.e., neurologic effects) the cardiovascular system appears to be a
target for MeHg toxicity in humans and animals.'' \254\ The EPA also
stated that additional cardiovascular studies have been published since
2000. The EPA did not develop a quantitative dose response assessment
for cardiovascular effects associated with MeHg exposures, as there is
no consensus among scientists on the dose-response functions for these
effects, and there is inconsistency among available studies as to the
association between MeHg exposure and various cardiovascular system
effects. In the future, the EPA may update the MeHg RfD and will review
all of the relevant scientific literature available at that time,
including data on all relevant endpoints, and weight of evidence for
likelihood that MeHg produces specific effects in humans.
---------------------------------------------------------------------------

    \254\ 76 FR 25001.
---------------------------------------------------------------------------

    The EPA acknowledges the research regarding the effectiveness of
fish advisories. However, the proposed regulation does not address the
subject of fish advisories, consumer advice on fish or efficacy of such
advice. The EPA rejects the commenter's speculation regarding whether
the estimated IQ impacts for the regulation are real. Adverse effects
of in utero Hg exposure have been reported in populations in the
U.S.255 256 In another study on neurobehavioral effects of
prenatal exposure to MeHg through maternal consumption of seafood,
adverse effects are observed for MeHg even without controlling for fish
consumption.\257\ That study suggests that at normal Japanese dietary
intake of MeHg and fish nutrients, the overall effect is adverse. While
Japanese fish consumption and Hg exposure are both somewhat higher than
the mean U.S. exposure, these levels are still within the distribution
of U.S. consumers.
---------------------------------------------------------------------------

    \255\ Oken et al., 2008.
    \256\ Lederman et al., 2008.
    \257\ Suzuki, K., Nakai, K., Sugawara, T., Nakamura, T., Ohba,
T., Shimada, M., Hosokawa, T., Okamura, K., Sakai, T., Kurokawa, N.,
Murata, K., Satoh, C., and Satoh, H. 2007. ``Neurobehavioral effects
of prenatal exposure to methylmercury and PCBs, and seafood intake:
neonatal behavioral assessment scale results of Tohoku study of
child development.'' Environ Res 110, 699-704.

---------------------------------------------------------------------------

    Moreover, many studies show that beneficial effects of fish on both
cardiovascular and neurodevelopmental health are decreased by
concomitant exposure to MeHg. Several studies describe one or more
aspects of exposure to fish nutrients and
MeHg.258 259 260 261 262 263 264 Recent studies
265 266 267 and analyses indicate the potential for
nutrients in fish (particularly marine fish) to mask some of the
observed adverse effects of MeHg. Because EPA did not adjust for
potential confounding by nutrients in marine fish and mammals, the
benchmark doses used in the RfD derivation may be underestimated.
---------------------------------------------------------------------------

    \258\ Grandjean P, Bjereve K, Wihe P, and Sterewald u. 2001a.
``UBirthweight in a fishing community: significance of essential
fatty acids and marine food contaminants.'' In. J. Epidemiol.
30:1272-1278.
    \259\ Budtz-Jorgensen, E.; Grandjean, P.; Weihe, P. 2007.
``Separation of risks and benefits of 16 seafood intake.''
Environmental Health Perspectives. Vol. 115, 323-327.
    \260\ Choi et al., 2008a.
    \261\ Choi et al., 2008b.
    \262\ Oken et al., 2008.
    \263\ Strain, J.J. et al., 2008. Associations of maternal long
chain polyunsaturated fatty acids, methyl mercury, and infant
development in the Seychelles Child Development Nutrition Study.''
Neurotoxicology. 29(5): 776-782.
    \264\ Suzuki, et al., 2007.
    \265\ Oken et al., 2008.
    \266\ Choi AL, Cordier S, Weihe P, Grandjean P. 2008a.
``Negative confounding in the evaluation of toxicity: the case of
methylmercury in fish and seafood.'' Crit Rev Toxicol.
2008;38(10):877-93.
    \267\ Choi AL, Budtz-J[oslash]rgensen E, J[oslash]rgensen PJ,
Steuerwald U, Debes F, Weihe P, Grandjean P. 2008b. ``Selenium as a
potential protective factor against mercury developmental
neurotoxicity.'' Environ Res. May;107(1):45-52. Epub 2007 Sep 12.
---------------------------------------------------------------------------

    The EPA recognizes the potential for confounding of the effects of
Hg on the developing nervous system by a range of nutrients and
discusses this uncertainty in the revised Hg Risk TSD. Regarding
selenium, the SAB commented that ``one SAB member suggests the use of
blood markers of selenium-dependent enzyme function, noting that
methylmercury irreversibly inhibits selenium-dependent enzymes that are
required to support vital-but-vulnerable metabolic pathways in the
brain and endocrine system. Impaired selenoenzyme activities would be
observed in the blood before they would be observed in brain, but the
effect is also expected to be transitory. The use of these measures is
a minority view among the SAB members.'' \268\ The SAB did not express
a consensus recommendation on adjustments to the risk estimates for
exposure to selenium or other nutrients, noting that ``there is not
enough known about their quantitative impact to support a
recommendation of a re-analysis.'' \269\
---------------------------------------------------------------------------

    \268\ U.S. EPA-SAB, 2011.
    \269\ Id.
---------------------------------------------------------------------------

6. General Comments on Hg Risk Assessment
    Comment: Several commenters generally supported the Hg risk
assessment, but several other commenters generally disagreed with the
Hg risk assessment. One supporter stated that EPA reasonably determined
that Hg emissions pose a public health hazard, correctly requested peer
review of Hg risk analysis and correctly concluded EGU-attributable
MeHg poses a hazard to public health at watersheds when considering all
sources of Hg deposition and U.S. EGUs alone. Two commenters noted that
the contribution of U.S. EGUs to total Hg deposition can significantly
contribute to hundreds of watersheds, and U.S. EGU deposition alone may
endanger sensitive populations near many of these watersheds.
    Several commenters claimed that overly conservative assumptions in
the risk analysis render the results flawed and unreliable, including
using CMAQ to model deposition, Mercury Maps, fish consumption rate and
fish MeHg concentrations, overly stringent RFD, national-scale model,
using poverty as a surrogate for subsistence fishing, assuming a
subsistence fisher resides in most watersheds with fish tissue data,
fishers only eat larger fish with high Hg concentrations, cooking loss
adjustment, unrealistically high fish ingestion rates (a large fish
meal every day), focused on the extremes of the distributions, cast
many assumptions as an underestimate of the effect despite evidence to
the contrary, and created inappropriate metrics for risk that show no
improvement despite significant Hg emissions reductions in the U.S.
    Several commenters cite Tetra Tech's analysis that assessed Hg risk
using different consumption rates, cooking factor, mean fish tissue
concentrations, and EGU-attributable Hg deposition only, which showed
considerably fewer watersheds that exceed an HQ of 1 at 2016 deposition
levels.
    Several commenters claim that this regulation would not
significantly reduce Hg exposure via fish consumption because EGU-
attributable deposition is a small fraction of total deposition. One
commenter stated that EPA's data shows Hg emissions from U.S. EGUs have
little influence on fish Hg concentrations despite a reduction of 41
tons of Hg in the U.S. between 2005 and 2016. One commenter requested
that EPA accurately describe the low health risks posed by utility
hazardous air pollutant emissions. One commenter stated that EPA did
not consider scientific information showing that there is no
straightforward connection between Hg emissions from U.S. EGUs to the
Hg level in fish, which is dependent upon many environmental factors,
such as sunlight and organic matter, pH, water temperature, sulfate,
bacteria, and zooplankton present in the ecosystem. One commenter
stated that there is not any demonstrable evidence that anyone in the
U.S. has suffered adverse health problems as a result of Hg emissions
from coal-fired EGUs. One commenter stated that EPA's findings are
similar to the 2000 findings where EPA found a plausible link between
anthropogenic emissions of Hg from sources in the U.S. and MeHg in
fish, and ``plausible'' is a euphemism for unproven.
    Several commenters had recommendations for the Hg risk analysis.
One commenter stated that more data from Florida should have been
included because Florida is known to have a rich data set on fish Hg
concentrations. One commenter stated that EPA should characterize
general recreational angler fishers instead of subsistence fishers. One
commenter claims that EPA made math errors in the Hg Risk TSD regarding
the deposition in watersheds at specific percentiles. One commenter
questioned EPA's policy metrics used to characterize Hg risk.
    Several commenters stated that the Hg TSD is unclear and lacks
detail, as noted by the SAB. One commenter stated that the SAB is
critical of EPA's efforts, stating that the SAB found it difficult to
evaluate the risk assessment based solely upon Hg Risk TSD and
recommended that EPA transparently explain the methods and
uncertainties. One commenter stated that because of insufficient review
time and the lack of detail in the Hg Risk TSD, they could not assess
key questions, such as the nation-wide representativeness of the fish
tissue data.
    One commenter stated the subset of watersheds considered in the
analysis (i.e., with fish tissue data) have clearly higher U.S. EGU-
attributable deposition than the distribution of all watersheds.
    One commenter stated EPA's reporting of IQ point loss is erroneous
and not relevant to informing policy, and the U.S. EGU contribution to
risk is marginal as evidenced by the null values for the 50th
percentile watershed.
    One commenter notes that U.S. EGU-attributable emissions of Hg have
decreased significantly between 2005

and 2016, but claims that this decrease does not appear to affect the
risk results.
    Response: The purpose of the Hg risk assessment is not to assess
the magnitude of risk reduction under the proposed rule, but rather to
estimate the magnitude of absolute risk attributable to U.S. EGUs
currently and following implementation of other applicable CAA
requirements. That said, any potential risk reductions following
implementation of the MACT rule itself would likely reflect a number of
factors besides the national average U.S. EGU deposition value cited by
the commenter. These additional factors include: (a) Spatial gradients
in the magnitude of absolute U.S. EGU-attributable Hg deposition, (b)
spatial gradients in the magnitude of reductions in Hg deposition
linked to the rule, (c) availability of measured fish tissue Hg levels
in the vicinity of U.S. EGUs experiencing larger Hg emission reductions
to support risk modeling, and (d) the potential for subsistence fishing
activity at watersheds in the vicinity of U.S. EGUs experiencing larger
reductions in Hg emissions (also required to support risk modeling). It
is also important to point out that while the national average U.S.
EGU-attributable Hg deposition (for the 2016 scenario--see revised Hg
Risk TSD) is two percent, values range up to 11 percent for the 99th
percentile watershed. This illustrates the substantial spatial
variation in U.S. EGU-attributable Hg deposition, which translates into
spatial variation in the magnitude of U.S. EGU-attributable subsistence
fisher risk.
    The SAB conducted a comprehensive peer review of all of EPA's
assumptions in the Hg Risk TSD, and concluded that ``the SAB supports
the overall design of and approach to the risk assessment and finds
that it should provide an objective, reasonable, and credible
determination of the potential for a public health hazard from Hg
emitted from U.S. EGUs.'' \270\ Furthermore, the SAB concluded, ``The
SAB regards the design of the risk assessment as suitable for its
intended purpose, to inform decision-making regarding an ``appropriate
and necessary finding'' for regulation of hazardous air pollutants from
coal and oil-fired EGUs, provided that our recommendations are fully
considered in the revision of the assessment.'' \271\ Although the SAB
did indicate difficulty in evaluating the risk assessment based solely
on the Hg Risk TSD, the panel obtained additional information from EPA
through the peer review process and determined that ``the SAB supports
the overall design of and approach to the risk assessment and finds
that it should provide an objective, reasonable, and credible
determination of the potential for a public health hazard from mercury
emitted from U.S. EGUs.'' \272\ The primary advice of the SAB panel was
that EPA should ``revise the Technical Support Document to better
explain the methods and choices made in the analysis, and analytical
results, and where the uncertainties lie.'' \273\ The EPA has revised
the Hg Risk TSD as part of the final rulemaking to address the SAB's
recommendations and has made that revised Hg Risk TSD available in the
rule docket.
---------------------------------------------------------------------------

    \270\ U.S. EPA-SAB, 2011.
    \271\ Id.
    \272\ Id.
    \273\ Id.
---------------------------------------------------------------------------

    The SAB concurred with EPA's analytical assumptions and overall
study design for the Hg Risk TSD, including the RfD-based HQ approach,
fish tissue data, 75th percentile size fish, Mercury Maps assumption,
and consumption rates. Based on the SAB peer review, the EPA strongly
disagrees with commenter statements that the results reported in the Hg
Risk TSD are unreliable, overly conservative, extreme, inconsistent
with EPA risk guidelines, or severely overstate risk based on the
stated objectives of the analysis. The EPA has specifically addressed
each of these assumptions in the previous sections of the preamble, and
thus, does not repeat those responses here. Based on the review by the
SAB, the EPA has accurately described the health risks posed by utility
hazardous air pollutant emissions and disagrees with the commenter's
statement that EPA has not provided any demonstrable evidence to show
that adverse health risks exist. The EPA has applied peer reviewed
modeling to estimate the deposition of Hg attributable to U.S. EGUs.
The EPA asserts that these metrics demonstrate a clear hazard to public
health from Hg emissions from U.S. EGUs.
    The EPA thoroughly evaluated the Tetra Tech analysis. The EPA does
not agree that the analysis by Tetra Tech uses assumptions that are
``more reasonable'', and the SAB agreed that all of EPA's assumptions
in the Hg Risk TSD are reasonable and appropriate. The EPA asserts that
Tetra Tech's analysis does not fully cover subsistence fishers likely
to experience elevated U.S. EGU-related Hg exposure. Specifically, the
risk estimate cited in the comment reflects application of a number of
behavioral assumptions that provide significantly less coverage for
higher risk subsistence fishers. Fish consumption surveys cited in the
revised Hg Risk TSD suggest that higher percentile subsistence fishers
eat more than twice the level of fish assumed by Tetra Tech. Tetra
Tech's analysis also used the median fish tissue levels, but it is
reasonable to assume that subsistence fishers would target somewhat
larger fish to maximize the volume of edible meat per unit time spent
fishing. Tetra Tech's analysis also assumed that cooking fish did not
concentrate Hg, but a number of studies discussed in the revised Hg
Risk TSD explicitly provide adjustment factors involving a higher unit
concentration following preparation. Taken together, Tetra Tech's
analysis does not address the stated goal of the risk assessment to
assess the nature and magnitude of risk for those individuals likely to
experience the greatest risk associated with exposure to U.S. EGU-
attributable Hg.
    The EPA disagrees with the commenter's assertion that this rule
will not affect risks associated with Hg exposure. Hg from U.S. EGUs
contributes to the levels of MeHg in fish across the country and
consumption of contaminated fish can lead to increased risk of adverse
health effects. The EPA has shown in the RIA (Chapter 5) that this rule
will reduce Hg levels in fish.
    The EPA acknowledges that U.S. EGUs contribute only a small
fraction of total Hg deposition in the U.S. However, U.S. EGUs remain
the largest emitter of Hg in the U.S., and the revised Hg Risk TSD
shows that U.S. EGU-attributable Hg deposition results in up to 29
percent of modeled watersheds with populations 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. Mercury risk
is increasing for exposures above the RfD, and as a result, any
reductions in Hg exposures in locations where total exposures exceed
the RfD can result in reduced risks. While these reductions in risk may
be small for most populations and locations, in some watersheds and for
some populations, reductions in risk may be greater.
    The SAB also directly addressed the question of the nation-wide
representativeness of the fish tissue MeHg data in the national Hg risk
assessment. The SAB concluded, ``Although the SAB considers the number
of watersheds included in the assessment adequate, some watersheds

in areas with relatively high mercury deposition from U.S. EGUs were
under-sampled due to lack of fish tissue methy[l]mercury data. The SAB
encourages the Agency to contact states with these watersheds to
determine if additional fish tissue methylmercury data are available to
improve coverage of the assessment.'' \274\ In response to the SAB's
recommendations, the EPA obtained additional fish tissue sample data
from several states, particularly Pennsylvania, Wisconsin, Minnesota,
New Jersey, and Michigan. This additional data increased the total
number of watersheds assessed in the analysis by 33 percent nationally.
In Florida, the EPA assessed the Hg-related health risk for 40
watersheds. Because EPA did not find any additional fish tissue data
for watersheds in Florida that could be incorporated into the analysis,
the total number of watersheds in Florida assessed in the revised Hg
Risk TSD remains the same as the Hg Risk TSD at proposal.
---------------------------------------------------------------------------

    \274\ U.S. EPA-SAB, 2011.
---------------------------------------------------------------------------

    The EPA disagrees with the commenter that there were errors in the
Hg Risk TSD. Instead, the commenter has misinterpreted how EPA
calculated the percentiles. The percentile (and mean) values presented
in Table ES-1 for total and U.S. EGU-attributable Hg deposition are not
matched by watershed. In other words, the EPA queried for the
percentiles (and mean) provided for total Hg deposition and presented
those percentiles and then separately estimated the percentiles for
U.S. EGU-attributable Hg. Therefore, the total and U.S. EGU-
attributable values for the 99th percentile do not necessarily occur at
the same watershed. The EPA has provided additional clarification in
the revised Hg Risk TSD.
    The EPA agrees with the commenter that MeHg levels in fish depend
on a complicated set of environmental factors, and EPA acknowledged
this in the revised Hg Risk TSD. Furthermore, the EPA acknowledges that
total Hg fish tissue levels are not correlated with levels of total Hg
deposition when looking across watersheds because this relationship is
highly dependent on the methylation potential at the specific
waterbody, which is affected by pH, sulfate deposition, turbidity, etc.
However, several recent studies 275 276 277 show, and the
SAB agrees, that it is appropriate for EPA to assume that changes in Hg
deposition are linearly associated with changes in fish tissue
concentration. In addition, the EPA agrees that the subset of
watersheds in the risk analysis have somewhat higher U.S. EGU
deposition than the distribution of all watersheds, but EPA disagrees
that oversampling of high deposition watersheds is inappropriate.
---------------------------------------------------------------------------

    \275\ Orihel et al., 2007.
    \276\ Orihel et al., 2008.
    \277\ Harris et al., 2007.
---------------------------------------------------------------------------

    The EPA does not agree that there is no improvement in fish Hg
concentrations between 2005 and 2016, or that there will be no further
improvement from decreasing Hg emissions from U.S. EGUs from the
baseline in 2016. Although total risk from all Hg exposures will remain
elevated in much of the U.S., much of that risk is associated with
global, non-U.S. Hg emissions. U.S. EGUs remain the largest source of
Hg emissions in the U.S., and reductions in those emissions will result
in reduced Hg deposition in many highly impacted watersheds. As shown
in the revised Hg Risk TSD, average U.S. EGU-attributable fish tissue
Hg concentrations is estimated to decrease by 44 percent between 2005
and 2016. Although we did not remodel risk for the 2005 scenario in the
revised Hg Risk TSD, we estimated at proposal that the total percent of
modeled watersheds with populations potentially at-risk from Hg
emissions from U.S. EGUs exceeding either risk metric (i.e., U.S. EGUs
alone or total potential exposures to MeHg exceed the RfD and U.S. EGUs
contribute at least 5 percent) would decline from 62 percent in 2005 to
28 percent in 2016. This projected decline is primarily due to a
combination of additional pollution control technologies installed to
comply with federal regulations, such as CSAPR, and changing fuels,
such as the shift to natural gas.
    The EPA disagrees that IQ loss is erroneous or irrelevant to
informing policy, but EPA has moved that analysis to an appendix in the
revised Hg Risk TSD, per the SAB's recommendation. The EPA disagrees
that the IQ effects at the 50th percentile watershed are useful in
determining that there is not a hazard to public health because EPA's
stated goal of the risk assessment was to focus on populations likely
to experience relatively higher exposures to U.S. EGU-attributable Hg.
    We also disagree with those commenters that point to the SAB's
statements concerning the clarity of the Hg Risk TSD to suggest that
the public did not have an ample opportunity to comment on the Hg risk
assessment. Although it is correct that the SAB said the Hg Risk TSD
was difficult to evaluate until EPA staff explained it at the public
meeting in June 2011, we note that the commenters that assert that this
issue amounts to a violation of CAA section 307(d) notice requirements
made detailed technical comments, including many of the same comments
as the SAB. Furthermore, the EPA provided notice of the peer review in
the preamble to the proposed rule and a number of Federal Register
notices advised the public of the peer review process and all the
meetings were open to the public for comment and participation and the
minutes of those meetings were posted on the SAB Web site. The minutes
for the June 2011 meeting, during which EPA provided clarifying
information, were available well within the public comment period for
the proposed rule. For these reasons, we maintain that the public was
provided an adequate opportunity to comment on the Hg risk assessment.
e. Non-Hg HAP Case Studies
1. Emissions for Non-Hg Case Studies
    Comment: The commenters raised concerns about a wide variety of
aspects of EPA's approach for emissions used for the non-Hg case
studies, including the use of an arithmetic mean for computing emission
factors for representing emissions of untested units, the suggestion of
statistical outliers in the Cr test data, the claim that metals content
of the fuel is an indicator of flawed test data, the statistical
approaches used by EPA to create emission factors, the absence in EPA's
approach of an equation that commenters claim better represents
emissions values, that EPA's approach to estimate Cr(VI) is flawed, and
the lack of coal rank as a delineating factor for emission factor
calculation. The commenters also suggested that EPA should revise stack
parameters used for the case studies based on better available data.
    Response: In response to the comments on the emission factors, the
EPA has undertaken additional analysis to address all commenter
concerns. The EPA disagrees with commenter's criticisms of emission
factors based on arithmetic means, and EPA demonstrates that the use of
an arithmetic mean provides the most representative result. The EPA
analysis has found that the geometric mean approach recommended by the
commenter always under predicts actual emissions by an average of more
than seventy percent. The EPA agrees with commenters' recommendations
to use statistical outlier tests, but has applied tests different from
those suggested by the commenters. As further explained in the response
to comments document in the docket, this approach did not eliminate the
Cr test data from the Cr

emission factors used for some of the case study emissions.
    The EPA disagrees with commenters' assertions that the metal
content of the coal is a basis for invalidating the test results of
high Cr emissions. The identification of sources whose measured
emissions do not match the commenters' preconceived idea of emissions
behavior is not surprising. There are many possible explanations for
these differences. For example, the inconsistency between the test data
and the coal analysis could be due to any number of reasons including
unrepresentative coal sampling, control device problems, degradation of
the refractory, or sampling contamination. The idea that test data
should be discarded because it does not match initial expectations is
unfounded.
    The EPA disagrees with the commenter recommendations for using an
equation from AP-42, developed in part by the commenters. Based on
analyses of metal emissions measured at the site compared to
statistically predicted estimates, the EPA concluded that measured
emissions test data better predict actual emissions, and emission
factors based on the arithmetic mean are a reasonable method to
estimate emissions when test data are not available. The EPA analysis
of the ICR data has found that the emissions equation recommended by
the commenter is not a good predictor of actual EGU emissions. The EPA
also disagrees with commenters' concerns about the assumption that 12
percent of the Cr will be Cr(VI) for every coal-fired unit, which was
specifically supported by the peer review on the approach for
estimating cancer risks associated with Cr and Ni emissions. The EPA
disagrees with the commenter's assertion that any impact of scrubbers
will impact the case study analyses. In EPA's revised case study
analysis, 6 facilities have risk greater than 1 in a million, and of
these, four facilities have Cr as the risk driver (James River,
Conesville, TVA Gallatin, and Dominion--Chesapeake Bay). For these
facilities, none of the units contributing the bulk of the Cr emissions
have scrubbers according to the data provided to EPA by those
facilities, so scrubber impacts on Cr speciation is not relevant to
EPA's conclusions based on the non-Hg case studies. In any case, the
EPA disagrees with the commenter's conclusions about the impacts of
scrubbers on Cr speciation and provides evidence that impacts of
scrubbers on Cr speciation can have the opposite effect on Cr(VI)
fractions, concluding that EPA's 12 percent assumption is somewhat
conservative.
    The EPA also disagrees that coal rank must be a factor in computing
Cr emission factors for use in the case studies. The EPA's analysis has
demonstrated that coal rank appears to play no role in non-Hg metals
emissions. The EPA's newly revised emissions factor development
procedures can isolate and compare subgroups based on control device
type or coal rank; the ICR data were subjected to these tests and no
statistical significance was found between coal rank groups.
    Finally, the EPA agrees with one commenter's recommendations on
revised stack parameters for the case studies and has included these
revisions in the case study modeling for the final rule.
2. General Comments on Non-Hg Risk Case Study
    Comment: One commenter stated that EPA's case study assessment
reaffirms the need to regulate HAP emitted by both coal and oil-fired
EGUs. The commenter noted that over 40 percent of the case studies
conducted by EPA to quantify health hazards associated with the
inhalation of non-Hg HAP indicated a cancer risk greater than or equal
to the one in a million threshold level required to delist a source
category under CAA section 112.
    One commenter stated that EPA's case study assessment might be
flawed by the use of ``beta'' tests versions of the AERMOD
meteorological preprocessors (AERMINUTE and AERMET). The commenter
obtained from EPA the meteorological data used for EPA's assessment of
the Conesville facility and processed these data with EPA's current
regulatory versions of these preprocessors, which differ from the beta
version. According to the commenter, a comparison of the hourly wind
speed and hourly wind direction data produced by the beta preprocessor
and by current EPA preprocessors revealed numerous and often
substantial disparities.
    One commenter stated that EPA's finding that only three coal-fired
facilities and one oil-fired facility out of roughly 440 coal-fired
facilities and 97 oil-fired facilities in the U.S. indicated risk
greater than one-in-a-million supports a finding that it is
``appropriate'' to regulate those four and not the other 537. Another
commenter stated that EPA found only a ``few'' facilities that have
estimated maximum cancer risks in excess of one in a million, and that
this does not justify regulating all non-Hg HAP for all sources in this
category.
    One commenter stated that EPA's discussion in the preamble to the
proposed rule misleads the reader into believing that non-Hg HAP
emissions from EGUs are associated with serious human health effects.
According to the commenter, the EPA's discussion of the effects
associated with excessive exposure to an individual HAP would lead the
reader to believe that those effects inevitably occur from EGU
emissions because EGU emissions have trace amounts of non-Hg HAP.
    One commenter stated that with the assumptions in the Utility
Study, both in terms of conservative scientific estimates and
overestimated amounts of oil burned by these units, the EPA concluded
that the risks from oil-fired units would result in only one new cancer
case every 5 years. The commenter does not believe that this level of
risk warrants regulation under CAA section 112(n)(1)(A).
    Several commenters stated that even if the additional studies EPA
performed were accurate, they hardly demonstrate that it is necessary
and appropriate to regulate coal-fired EGU HAP under CAA section 112
because three sites nationwide show risks greater than one in a
million, with the highest at eight in a million.
    One commenter stated that the highest cancer risk estimated for
coal-fired EGUs is still within the acceptable range used by EPA in
other programs and is also far less than the background exposure risks
the average person experiences. The background risk of developing
cancer in a lifetime is approximately one in three (0.33). According to
EPA's own data, the predicted added cancer risk of exposure to HAP from
U.S. EGUs would change the background risk from 0.33 to 0.330001. This
level of change is so minimal that it could not be observed in any
health effects study that might be conducted.
    One commenter stated that EPA conducted a health risk assessment on
a limited number of facilities and found a ``few'' facilities that have
estimated maximum cancer risks in excess of one in a million. The
commenter stated that, based on this limited health risk assessment,
the EPA apparently decided that they were justified to regulate all
non-Hg HAP for all sources in this category.
    Several commenters stated that EPA's assumption implies that a
person stays exactly at the center of a census tract for 70 years and
that a unit will operate in exactly the same manner for 70 years is
unrealistic. The commenters suggest that Tier 3 risk assessment is
warranted

or a lifetime exposure adjustment is needed.
    One commenter asserts that because the alleged health benefits are
derived from total exposure, the EPA should explain how its numerical
emission limit units, which would not directly restrict total exposure
if heat inputs increase, redress this health concern. In its preamble,
the EPA simply notes that its emission limit units are consistent with,
and allow for simple comparison to, other regulations.
    One commenter questioned whether acid gas emissions limits for oil-
fired units are ``appropriate'' or ``necessary'' because EPA's new
technical analyses do not indicate a health concern from acid gas
emissions from oil-fired units. According to the commenter, the EPA
identifies Ni as the main HAP of concern from oil-fired units, even
though cancer-related inhalation risks were well below the RfCs and EPA
states that significant uncertainty remains as to whether those
emissions present a health concern.
    Response: The EPA agrees with the commenter that the non-Hg HAP
risk assessment confirms the appropriate and necessary finding.
    The EPA disagrees that EPA's case study assessment is flawed by the
use of beta versions of AERMINUTE and AERMET. The EPA remodeled the
case study facilities using the current versions of AERMINUTE (version
11059), AERMET (version 11059), and AERMOD (version 11103). Although
there were differences in the number of calm and missing winds in the
current AERMINUTE/AERMET output compared to the beta version, the
resulting risks differed by less than two percent, on average. For
Conesville, which had the largest difference in calms between the beta
and current versions of AERMINUTE/AERMET, the risks differed by three
percent. For the final rule, the case study facilities have been
modeled with the current available versions of AERMINUTE, AERMET, and
AERMOD.
    The EPA disagrees with the commenter that having only a few case
study facilities exceeding one in a million risk invalidates the
``appropriate finding''. The 16 facilities EPA selected as case studies
for assessment may not represent the highest-emitting or highest-risk
sources. Although case study facility selection criteria included high
estimated cancer and non-cancer risks using the 2005 NEI data, high
throughput, and minimal emission control, another necessary criterion
was the availability of Information Collection Request (ICR) data for
the EGUs at those facilities (or for similar EGUs at other facilities).
Because the ICR data were collected for the purpose of developing the
MACT standards, the ICR was targeted towards better performing sources
for non-Hg metal HAP, acid gas HAP, and organic HAP, with a smaller set
of random recipients. Therefore, facilities for which ICR data were
available may not represent the highest-emitting sources. The EPA's
assessment of the case study facilities for the proposed rule concluded
that three coal-fired facilities and one oil-fired facility had
estimated lifetime cancer risks greater than one in a million. For the
final rule, revisions were made to the 16 case studies based on
comments received, and the results indicate that 5 coal-fired
facilities and 1 oil-fired facility had estimated lifetime cancer risks
greater than 1 in a million. The EPA maintains that its finding that
more than 30 percent of the case study facilities had a cancer risk
greater than one in a million is sufficient to support the appropriate
finding.
    The EPA disagrees with the commenter's assertion that the health
effects associated with exposures to non-Hg HAP from U.S. EGUs are
mischaracterized in the preamble to the proposed rule. The discussion
of the health effects of non-Hg HAP provided in the preamble includes
general information on the potential health effects associated with a
broad range of exposure concentrations (from low to high levels) of the
various non-Hg HAP (some of which have been determined to be
carcinogenic to humans) based on peer reviewed scientific information
extracted from priority sources such as IRIS, Cal EPA and ATSDR health
effects assessments.
    The EPA disagrees with the commenter's characterization of the
Utility Study. The Utility Study represented the highest-quality
factual record of information available at the time regarding EGU
emissions and risks. Further, the EPA's revised risk assessments of 16
case studies, performed with more recent data and refined scientific
methods, indicate that there are six U.S. EGU facilities that pose
estimated inhalation cancer risks greater than 1 in a million. The EPA
maintains that the findings of the case studies are one element that
independently supports our determination that it remains appropriate
and necessary to regulate EGUs under CAA section 112.
    The EPA does not agree with the commenter who suggested that EPA
should interpret the results of the non-Hg HAP risk analysis in the
context of background cancer risk. As explained in the preamble to the
proposed rule, the EPA reasonably looked to the cancer risk threshold
established under CAA section 112(c)(9)(B)(1) for delisting a source
category as an indicator of the level of cancer risk that was
appropriate to regulate under CAA section 112. The commenters
comparison of the cancer risk from EGUs as compared with the risk of
contracting cancer from unknown sources is not the standard Congress
established for evaluating HAP emission risk and the commenter has
provided no support for its contention that the Agency should evaluate
risk in that manner. The EPA maintains that the analysis was
reasonable.
    The EPA does not agree with the commenter's implication that EPA
must make a facility-specific finding for each HAP for each source and
then only regulate individual EGU facilities for the individual HAP
that identified as causing an identified hazard to public health or the
environment. That approach is not required under CAA section 112(n)(1)
or anywhere under CAA section 112, and it would be virtually impossible
to undertake such an effort. For these reasons, the EPA does not agree
with the commenter and maintains that the appropriate and necessary
finding is reasonably supported by the record and consistent with the
statute for all the reasons set forth in the preamble to the proposed
rule and this final action.
    The EPA disagrees that an exposure adjustment is needed to account
for conditions changing over 70 years because it runs counter to the
long-standing approach that EPA has taken to estimate the maximum
individual risk, or MIR. The MIR is defined by EPA's Benzene NESHAP
regulation of 1989 \278\ and codified by CAA section 112(f) as the
lifetime risk for a person located at the site of maximum exposure 24
hours a day, 365 days a year for 70 years (e.g., census block
centroids). The MIR is the metric associated with the determination of
whether or not a source category may be delisted from regulatory
consideration under CAA section 112(c)(9). The MIR is the risk metric
used to characterize the inhalation cancer risks associated with the
case study facilities. The EPA used the annual average ambient air
concentration of each HAP at each census block centroid as a surrogate
for the lifetime inhalation exposure concentration of all the people
who reside in the census block. The EPA has used this approach to
estimate MIR values in all of its risk assessments to

support risk-based rulemakings under CAA section 112 to date.
---------------------------------------------------------------------------

    \278\ 54 FR 38044.
---------------------------------------------------------------------------

    The EPA disagrees with the commenter's assertion that the numerical
emission limits being promulgated in today's final rule must be
justified on their ability to redress the health concerns that were
identified as the basis for regulating EGUs. The emission limits in
today's rule are technology-based, as prescribed under CAA section 112,
and do not need to be justified based on their ability to protect
public health. Regarding potential health concerns, the EPA has up to 8
years after the promulgation of the technology-based emission limits
for EGUs to determine whether the regulations protect public health
with an ample margin of safety. If the regulations do not, the CAA
directs EPA to promulgate additional more stringent standards (within
the prescribed 8 years) to achieve the appropriate level of public
health protection.
    Furthermore, the EPA reasonably concluded that it was appropriate
and necessary to regulate oil-fired EGUs in 2000, and EPA confirmed
that conclusion was proper with the analysis set forth in the preamble
to the proposed rule. Certain commenters question the determination
based on their views of how the Agency can and should exercise its
discretion. The EPA disagrees with these commenters and stands by the
determination for the reasons set forth in the preamble to the proposed
rule. The EPA also stands by the determination that the maximum cancer
risks posed by emissions of oil-fired EGUs are greater than one in a
million, due primarily to emissions of Ni compounds. Based on our
analysis, we are unable to delist oil-fired EGUs.
3. Ni Risk
    Comment: Several commenters stated that the assumptions regarding
the speciation and carcinogenic potential of Ni compounds used in EPA's
inhalation risk assessment of the case study facilities are overly
conservative and likely to overstate the risks. With respect to Ni
speciation, the commenters stated that there are substantial
uncertainties regarding the species of Ni being emitted and the risk of
such emissions, and that EPA has made ultraconservative assumptions
aimed at overestimating the risk. The commenters stated that assigning
the same carcinogenic potency of Ni subsulfide to other forms of Ni is
overly conservative and inconsistent with the best available evidence.
    Response: The EPA disagrees with the commenters' assertion that it
is impossible to give an accurate assessment of the risks to human
health from Ni emissions from EGUs, and maintains that its assessment
of the potential inhalation risks from EGU emissions of Ni compounds is
scientifically valid, reasonable, and based on the best-available
current scientific understanding. To that end, in July 2011, the EPA
completed an external peer review (using three independent expert
reviewers) of the methods used to evaluate the risks from Ni and Cr
compounds emitted by EGUs.\279\ There were two charge questions
relating to Ni in that review. First, do EPA's judgments related to
speciated Ni emissions adequately take into account available
speciation data, including recent industry spectrometry studies?
Second, based on the speciation information available and what is known
about the health effects of Ni compounds, and taking into account the
existing URE values (i.e., values derived by the Integrated Risk
Information System,\280\ California Department of Health Services,\281\
and the Texas Commission on Environmental Quality \282\), which of the
following approaches to derive unit risk estimates would result in a
more accurate and defensible characterization of risks from exposure to
Ni compounds?
---------------------------------------------------------------------------

    \279\ U.S. EPA, 2011c.
    \280\ U.S. EPA, 1991.
    \281\ California Department of Health Services (CDHS) 1991.
Health Risk Assessment for Nickel. Air Toxicology and Epidemiology
Section, Berkeley, CA. Available online at http://oehha.ca.gov/air/toxic_contaminants/html/Nickel.htm.
    \282\ Texas Commission on Environmental Quality (TCEQ), 2011.
Development Support Document for nickel and inorganic nickel
compounds. Available online at http://www.tceq.state.tx.us/assets/public/implementation/tox/dsd/final/june11/nickel_&_compounds.pdf.
---------------------------------------------------------------------------

    1. To continue using the same approach as that developed for use in
the 2000 NATA, which consists of using the IRIS URE for nickel
subsulfide and assuming that nickel subsulfide constitutes 65 percent
of the mass emissions of all Ni compounds.
    2. To consider a more health-protective approach, based on the
consistent views of the most authoritative scientific bodies (i.e., NTP
in their 12th ROC, IARC, and other international agencies) that
consider Ni compounds to be carcinogenic as a group.
    3. To make the same assumptions as in option 2, but considering
alternative UREs derived by the CDHS or TCEQ.
    In responding to these peer review questions, two of the reviewers
agreed with the views of the most authoritative scientific bodies,
which consider Ni compounds carcinogenic as a group. These reviewers,
therefore, did not focus on the availability of Ni speciation profile
data. The third reviewer recommended that EPA review several
manuscripts on Ni speciation profiles showing that sulfidic Ni
compounds (which the reviewer considered as the most potent
carcinogens) are present at low levels in emissions from EGUs.
    Nickel and Ni compounds have been classified as human carcinogens
by national and international scientific bodies including the
IARC,\283\ the World Health Organization,\284\ and the European Union's
Scientific Committee on Health and Environmental Risks.\285\ In their
12th Report of the Carcinogens, the NTP has classified Ni compounds as
known to be human carcinogens based on sufficient evidence of
carcinogenicity from studies in humans showing associations between
exposure to Ni compounds and cancer, and supporting animal and
mechanistic data. More specifically, this classification is based on
consistent findings of increased risk of cancer in exposed workers, and
supporting evidence from experimental animals that shows that exposure
to an assortment of Ni compounds by multiple routes causes malignant
tumors at various organ sites and in multiple species. The 12th Report
of the Carcinogens states that the ``combined results of
epidemiological studies, mechanistic studies, and carcinogenesis
studies in rodents support the concept that Ni compounds generate Ni
ions in target cells at sites critical for carcinogenesis, thus
allowing consideration and evaluation of these compounds as a single
group''.\286\ Although the precise Ni compound (or compounds)
responsible for the carcinogenic effects in humans is not always clear,
studies indicate that Ni sulfate and the combinations of Ni sulfides
and oxides encountered in the Ni refining industries cause cancer in
humans. There have been different views on whether or not Ni compounds,
as a group, should be considered as carcinogenic to humans. Some
authors

believe that water soluble Ni, such as Ni sulfate, should not be
considered a human carcinogen, based primarily on a negative Ni sulfate
2-year NTP rodent bioassay (which is different than the positive 2-year
NTP bioassay for Ni subsulfide).287 288 289 Although these
authors agree that the epidemiological data clearly supports an
association between Ni and increased cancer risk, they sustain that the
data are weakest regarding water soluble Ni. A recent review \290\
highlights the robustness and consistency of the epidemiological
evidence across several decades showing associations between exposure
to Ni and Ni compounds (including Ni sulfate) and cancer.
---------------------------------------------------------------------------

    \283\ International Agency for Research on Cancer (IARC), 1990.
IARC monographs on the evaluation of carcinogenic risks to humans.
Chromium, nickel and welding. Vol. 49. Lyons, France: International
Agency for Research on Cancer, World Health Organization Vol.
49:256.
    \284\ International Labour Organization/United Nations
Environment Programme, World Health Organization (WHO), 1991.
Nickel. In Environmental Health Criteria No 108 Geneva.
    \285\ European Commission, Scientific Committee on Health and
Environmental Risks (SCHER), 2006. Opinion on: Reports on Nickel,
Human Health part. SCHER, 11th plenary meeting of 04 May 2006 http://ec.europa.eu/health/ph_risk/committees/04_scher/docs/scher_o_034.pdf.
    \286\ NTP, 2011.
    \287\ Oller A. Respiratory carcinogenicity assessment of soluble
nickel compounds. Environ Health Perspect. 2002, 110:841-844.
    \288\ Heller JG, Thornhill PG, Conard BR. New views on the
hypothesis of respiratory cancer risk from soluble nickel exposure;
and reconsideration of this risk's historical sources in nickel
refineries. J Occup Med Toxicol. 2009, 4:23.
    \289\ Goodman JE, Prueitt RL, Thakali S, and Oller AR. The
nickel iron bioavailability model of the carcinogenic potential of
nickel-containing substances in the lung. Crit Rev Toxicol. 2011,
41:142-174.
    \290\ Grimsrud TK and Andersen A. Evidence of carcinogenicity in
humans of water-soluble nickel salts. J Occup Med Toxicol. 2010.
5:1-7. Available online at http://www.ossup-med.com/content/5/1/7.
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    Based on the views of the major scientific bodies mentioned above,
and those of expert peer reviewers that commented on EPA's approaches
to risk characterization of Ni compounds, the EPA considers all Ni
compounds to be carcinogenic as a group and does not consider Ni
speciation or Ni solubility to be strong determinants of Ni
carcinogenicity. With regards to non-cancer effects, comparative
quantitative analysis across Ni compounds indicates that Ni sulfate is
as toxic or more toxic than Ni subsulfide or Ni
oxide.291 292
---------------------------------------------------------------------------

    \291\ Haber LT, Allen BC, Kimmel CA. Non-Cancer Risk Assessment
for Nickel Compounds: Issues Associated with Dose-Response Modeling
of Inhalation and Oral Exposures. Toxicol Sci. 1998. 43:213-229.
    \292\ NTP, 1996.
---------------------------------------------------------------------------

    Regarding the second charge question, two of the reviewers
suggested using the URE derived by TCEQ for all Ni compounds as a
group, rather than the one derived by IRIS specifically for Ni
subsulfide. The third reviewer did not comment on alternative
approaches. The EPA decided to continue using 100 percent of the
current IRIS URE for Ni subsulfide because IRIS values are at the top
of the hierarchy with respect to the dose response information used in
EPA's risk characterizations, and because of the concerns about the
potential carcinogenicity of all forms of Ni raised by the major
national and international scientific bodies. Nevertheless, taking into
account that there are potential differences in toxicity and/or
carcinogenic potential across the different Ni compounds, and given
that there have been two URE values derived for exposure to mixtures of
Ni compounds that are 2-3 fold lower than the IRIS URE for Ni
subsulfide, the EPA also considers it reasonable to use a value that is
50 percent of the IRIS URE for Ni subsulfide for providing an estimate
of the lower end of a plausible range of cancer potency values for
different mixtures of Ni compounds.
4. Cr Risk
    Comment: One commenter stated there are several problems with EPA's
analysis related to the fact that Cr emissions were evaluated as being
entirely Cr(VI). The commenter stated that not all of the emitted Cr
will remain in the hexavalent form by the time it reaches the target
population, and that some may be converted to the much less toxic (and
noncarcinogenic) trivalent species. The commenter also stated that the
concentration levels considered in the case study assessment are far
below occupational levels. The commenter concluded that EPA's cancer
estimates should, therefore, be looked on with some skepticism. Another
commenter stated that EPA's estimate of 12 percent Cr(VI) from coal-
fired EGUs is unsupported, and that EPA failed to recognize that Cr(VI)
is highly water-soluble and is easily reduced to Cr(III) in the
presence of SO2 in a low pH environment. The resulting
Cr(III) would be expected to precipitate out in a FGD. The commenter
stated that the actual amount of Cr(VI) that would be present in the
emissions from an EGU with a wet scrubber is likely to be far lower
than the 12 percent estimate made by EPA.
    Several commenters questioned the validity of the chronic
inhalation study by EPA because of (1) the use of surrogate speciated
Cr emissions data instead of actual emissions data, (2) the assumption
that units were run 100 percent of the time which is impossible, (3)
dispersion modeling was used that is biased towards over predicting
downwind impacts, and (4) estimated ambient concentrations were
utilized as substitutes for real exposure concentrations for all people
within a census block.
    Response: The EPA disagrees with the commenters' assertion that all
Cr was considered to be hexavalent. As discussed in ``Methods to
Develop Inhalation Cancer Risk Estimates for Chromium and Nickel
Compounds,'' \293\ existing test data for utility and industrial
boilers indicate that Cr(VI) is, on average, 12 percent of total Cr
from coal-fired boilers. This document underwent peer review by three
external reviewers, and all three reviewers considered EPA's use of the
values to be reasonable given the limited data available for Cr
speciation profiling. The EPRI inhalation study for coal-fired boilers
also used the 12 percent value.
---------------------------------------------------------------------------

    \293\ U.S. EPA, 2011c.
---------------------------------------------------------------------------

    The EPA also disagrees that units were assumed to operate 100
percent of the time. The dispersion modeling performed for the case
study facilities used hourly heat input as a temporalization factor for
estimating hourly emissions, and in some cases hourly heat inputs (and
emissions) were zero or very low. The commenter provided no data or
information to support their claim that the dispersion modeling EPA
used is biased towards overestimating downwind impacts.
    The EPA disagrees with the commenters' assertion that ``real
exposure concentrations for all people within a census block'' must be
considered because it runs counter to the long-standing approach that
EPA has taken to estimate the maximum individual risk, or MIR. The MIR
is defined by EPA's Benzene NESHAP regulation of 1989 \294\ and
codified by CAA section 112(f) as the lifetime risk for a person
located at the site of maximum exposure 24 hours a day, 365 days a year
for 70 years (e.g., census block centroids). The MIR is the metric
associated with the determination of whether or not a source category
may be delisted from regulatory consideration under CAA section
112(c)(9). The MIR is the risk metric used to characterize the
inhalation cancer risks associated with the case study facilities. The
EPA used the annual average ambient air concentration of each HAP at
each census block centroid as a surrogate for the lifetime inhalation
exposure concentration of all the people who reside in the census
block. The EPA has used this approach to estimate MIR values in all of
its risk assessments to support risk-based rulemakings under CAA
section 112 to date.
---------------------------------------------------------------------------

    \294\ 54 FR 3804.
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5. Acid Gas Risk
    Comment: One commenter stated that acid gas emissions from oil-
fired EGUs are not of the magnitude that triggered EPA's decision to
regulate EGUs in general, raising the question of whether reduction (or
even total elimination) of acid gas emissions from oil-fired EGUs could
have any significant effect on EPA's goals of reducing non-cancer

health risk or acidification of sensitive ecosystems in the U.S.
    Several commenters stated that acid gas concentrations estimated in
the case study facility assessment and the Utility Study do not exceed
human health thresholds of concern. Two commenters stated that HCl
emissions are negligible compared to other primary emissions (such as
SO2) that can lead to potential acidification of ecosystems.
    Response: We do not agree with commenter's implication that
Congress intended EPA to regulate only those HAP emissions from U.S.
EGUs for which an appropriate and necessary finding is made, and
commenter has cited no provision of the statute that states a contrary
position. The EPA concluded that we must find it ``appropriate'' to
regulate EGUs under CAA section 112 if we determine that a single HAP
emitted from EGUs poses a hazard to public health or the environment.
If we also find that regulation is necessary, the Agency is authorized
to list EGUs pursuant to CAA section 112(c) because listing is the
logical first step in regulating source categories that satisfy the
statutory criteria for listing under the statutory framework of CAA
section 112. See New Jersey, 517 F.3d at 582 (stating that ``[s]ection
112(n)(1) governs how the Administrator decides whether to list EGUs *
* *''). As we noted in the preamble to the proposed rule, D.C. Circuit
precedent requires the Agency to regulate all HAP from major sources of
HAP emissions once a source category is added to the list of categories
under CAA section 112(c). National Lime Ass'n v. EPA, 233 F.3d 625, 633
(D.C. Cir. 2000). 76 FR 24989. The EPA discusses in the preamble to the
proposed rule and this final action its concerns with HCl and other
acid gas HAP emissions from EGUs and the Agency's approach for
establishing section 112(d) standards for acid gas HAP.
6. EPRI Risk Analysis
    Comment: Two commenters stated that a comprehensive tiered
inhalation risk assessment (the EPRI study) using EPA-prescribed
methods with improved emission factors, fuel data, and confirmed stack
parameters did not identify significant health risks (cancer or non-
cancer) among U.S. coal-fired power plants (as they existed in 2007).
The commenters noted that these results contrast with those presented
by EPA for its non-Hg case studies on 16 (15 coal-fired) power plants.
The commenters stated that several issues appear to underlie these
differences, indicating the need for EPA to reevaluate its assessment
and to undertake more refined (Tier 3) risk assessment for any facility
of concern. Several commenters stated that for non-Hg HAP EPA produced
one study on chronic inhalation risk assessment that identified three
sites with cancer risks greater that one in a million for Cr(VI), which
was authored by EPA staff and not peer reviewed. One commenter stated
that EPA study is based on misinformation and overestimates
assumptions, and that EPA has no data demonstrating health impacts from
EGU emissions of non-Hg HAP, or the benefit from reducing such
emissions. Two commenters stated that no benefits will be derived from
the non-Hg HAP emission reductions associated with the proposed rule
because no non-Hg HAP health risks were proven, and that no showing was
made that EGU non-Hg HAP emission levels reach levels associated with
adverse health effects. Another commenter stated that EPA must complete
a comparable and separate national-scale risk assessment for non-Hg
metals in order to determine appropriateness of proposing emissions
standards for non-Hg metals.
    Response: The commenters are incorrect in the assertion that EPA's
case studies were performed with less rigor than the EPRI analysis. The
EPRI analysis used a tiered approach to risk assessment, beginning with
Tier 1 using EPA's SCREEN3 dispersion model on all 470 coal-fired power
plants in the U.S., and following with Tier 2 with EPA's Human Exposure
Model (which uses the AERMOD dispersion model) for plants with higher
risks from the Tier 1 modeling. Although tiered risk assessment is an
appropriate approach, the Tier 2 modeling could have been more refined.
For example, more meteorological data could have been used and building
downwash could have been considered. The EPRI analysis ostensibly
concluded that the Tier 2 modeling with HEM was conservative, and that
because the modeled risks did not exceed certain thresholds, no further
refinement was necessary. However, such refinements could result in
higher modeled risks than those from the commenter's Tier 2 modeling.
    The EPA's dispersion modeling of the case study facilities was
actually performed with a greater degree of refinement than the EPRI
analysis, and was consistent with EPA's Guideline on Air Quality
Models.\295\
---------------------------------------------------------------------------

    \295\ Appendix W to 40 CFR Part 51.
---------------------------------------------------------------------------

    In contrast to the approach used in the EPRI analysis, the EPA
used:

    (1) 5 years of recent meteorological data from the weather
station nearest to each facility, rather than one year of
meteorological data. This is more representative of long-term (i.e.,
lifetime) exposures and risks.
    (2) Temporally-varying emissions based on continuous emissions
monitoring data, rather than assuming a constant emission rate for
each facility throughout the entire simulation.
    (3) Building downwash, where appropriate.
    (4) The latest version of AERMOD [version 11103].

    The EPA's assessment of the case study facilities for the proposed
rule concluded that three coal-fired facilities and one oil-fired
facility had estimated lifetime cancer risks greater than one in a
million. For the final rule, revisions were made to the case studies
based on comments received, and the results indicate that five coal-
fired facilities and one oil-fired facility had estimated lifetime
cancer risks greater than one in a million.
    Regarding peer review, the risk assessment methodology used by EPA
for the case studies was consistent with the method that EPA uses for
assessments performed for Risk and Technology Review rulemakings, which
underwent peer review by the Science Advisory Board in 2009.\296\ The
SAB issued its peer review report in May 2010. The report generally
endorsed the risk assessment methodologies used in the program. In
addition, in July 2011, the EPA completed a letter peer review of the
methods used to develop inhalation cancer risk estimates for Cr and Ni
compounds.
---------------------------------------------------------------------------

    \296\ U.S. EPA-SAB, 2010.
---------------------------------------------------------------------------

f. Ecosystem Impacts From HAP
    Comment: Two commenters assert that EPA is not justified in
regulating acid gases based on concern about the potential that acid
gases contribute to ecosystem acidification rather than concerns about
hazards to public health. The commenters further claim that HCl's
contribution to ecosystem acidification is de minimis. The commenters
point out that EPA acknowledges uncertainty in quantification of
acidification and EPA relies on recently published research \297\ that
is irrelevant to the question since it is based on research conducted
in the peat bog ecosystem in the United Kingdom. Another commenter
calls attention to several new studies published in a special issue of
the

journal Ecotoxicology devoted to the effects of MeHg on wildlife.
---------------------------------------------------------------------------

    \297\ Evans, Chris D., Don T. Monteith, David Fowler, J. Neil
Cape, and Susan Brayshaw. 2011. ``Hydrochloric Acid: An Overlooked
Driver of Environmental Change.'' Environmental Science & Technology
45 (5), 1887-1894.
---------------------------------------------------------------------------

    Response: Although EPA agrees that quantification of acidification
effects has remaining uncertainty, the science and methodology has
progressed in recent years. Based on recent peer reviewed research
including Evans et al.,\298\ acid gases can significantly contribute to
acidification. The EPA published a comprehensive risk assessment of
acidification effects of nitrogen and sulfur deposition \299\ and a
policy assessment.\300\ Given the extent and importance of the
sensitive ecosystems evaluated in the review of nitrogen and sulfur
deposition any substance that contributes to further acidification must
be considered to be affecting the public welfare. The EPA disagrees
that the peer reviewed study mentioned by commenter by Evans et al.,
(2011) is not relevant to U.S. ecosystems. The paper presents evidence
that show (1) that HCl is highly mobile in the environment,
transferring acidity easily through soils and water, (2) that HCl can
transport longer distances than previously thought (given its presence
in remote ecosystems, and (3) that it can be a larger driver of
acidification than previously thought. The fact that this study took
place in the U.K. is itself irrelevant. The chemical interactions of
HCl in water are the same the world over and sensitive ecosystems exist
in the U.S. as well as in Europe as illustrated in the ecological risk
assessment \301\ for NOX and SOX. Furthermore,
the commenter is factually incorrect that EPA is justifying that it is
appropriate and necessary to regulate HAP emissions from EGUs based on
this one study. The EPA agrees with the commenter that Hg exposure in
wildlife is responsible for various adverse health effects in many
species across the U.S. and recognizes that research is ongoing in this
area. As discussed in the preamble to the proposed rule, the EPA agrees
that there are potential environmental risks from exposures of
ecosystems through Hg and non-Hg HAP deposition. The EPA cited relevant
articles from the special edition of Ecotoxicology \302\ mentioned by
the commenter in the ecosystem effects section on Chapter 5 of the RIA
for this rule, which is available in the docket.
---------------------------------------------------------------------------

    \298\ Id.
    \299\ U.S. Environmental Protection Agency (U.S. EPA). 2009.
Risk and Exposure Assessment for Review of the Secondary National
Ambient Air Quality Standards for Oxides of Nitrogen and Oxides of
Sulfur (Final). EPA-452/R-09-008a. Office of Air Quality Planning
and Standards, Research Triangle Park, NC. September. Available on
the Internet at http://www.epa.gov/ttn/naaqs/standards/no2so2sec/data/NOxSOxREASep2009MainContent.pdf.
    \300\ U.S. Environmental Protection Agency (U.S. EPA). 2011d.
Policy Assessment for the Review of the Secondary National Ambient
Air Quality Standards for Oxides of Nitrogen and Oxides of Sulfur.
EPA-452/R-11-005a. Office of Air Quality Planning and Standards,
Research Triangle Park, NC. February. Available on the Internet at
http://www.epa.gov/ttnnaaqs/standards/no2so2sec/data/20110204pamain.pdf.
    \301\ U.S. EPA, 2009.
    \302\ Ecotoxicology 17:83-91, 2008.
---------------------------------------------------------------------------

G. EPA Affirms the Finding That It Is Appropriate and Necessary to
Regulate EGUs To Address Public Health and Environmental Hazards
Associated With Emissions of Hg and Non-Hg HAP From EGUs

    In response to peer reviews of both the Hg and non-Hg HAP risk
analyses, and taking into account public comments, the EPA conducted
revised analyses of the risks associated with emissions of Hg and non-
Hg HAP from U.S. EGUs. These revised analyses demonstrated that the
risk results reported in the preamble to the proposed rule are robust
to revisions in response to the peer reviews and public comments.
    Specifically, the revised Hg Risk TSD shows that up to 29 percent
of modeled watersheds have populations potentially at-risk from
exposure to Hg from U.S. EGUs.\303\ This 29 percent of watersheds with
populations potentially at-risk includes up to 10 percent of modeled
watersheds where deposition from U.S. EGUs alone leads to potential
exposures that exceed the MeHg RfD, and up to 24 percent of modeled
watersheds where total potential exposures to MeHg exceed the RfD and
U.S. EGUs contribute at least 5 percent to Hg deposition. Each of these
results independently supports our conclusion that U.S. EGUs pose
hazards to public health.
---------------------------------------------------------------------------

    \303\ This corresponds to 28 percent of modeled watersheds with
populations potentially at-risk in the analysis reported in the
preamble to the proposed rule.
---------------------------------------------------------------------------

    In the preamble to the proposed rule and in the 2000 finding, the
EPA explained at length the serious nature of the health effects
associated with Hg exposures, and the persistent nature of Hg in the
environment. Congress specifically recognized the significant impacts
of persistent bioaccumulative pollutants, like Hg, when it enacted
section 112(c)(6), which requires the EPA to subject source categories
listed pursuant to that section to MACT standards. Congress also
required certain studies be conducted under CAA section 112(n)
regarding the health effects of Hg. The EPA interprets CAA section
112(n)(1), with regard to Hg, as intended to protect the public,
including sensitive populations, against exposures to Hg from EGUs that
would exceed the level determined by the EPA to be without appreciable
risk, e.g., exposures that are above the RfD for methylmercury (MeHg),
or would contribute additional risk in areas where Hg exposures exceed
the RfD due to contributions from all sources of Hg. Our recent
technical analyses show that 98 percent of the watersheds for which we
had fish tissue data have total Hg deposition such that potential
exposures exceed the MeHg RfD, above which there is an increased risk
of adverse effects on human health. In these watersheds, any reductions
in exposures to Hg will reduce risk, and thus the incremental
contribution to Hg exposure from any individual source or group of
sources, such as EGUs, may reasonably be anticipated to cause
additional risk.
    As we have explained, in calculating the estimates described above,
the EPA has used peer-reviewed methods, and focused on populations
likely to be at higher risk of exposure to Hg from U.S. EGUs, e.g.,
female subsistence fishing populations consuming at the 99th percentile
fish consumption rate. The EPA did not, however, use the most
conservative assumptions that would lead to upper bound risk estimates.
As discussed above and in the revised Hg Risk TSD, we did not use the
highest fish tissue cooking loss adjustment factor that was reported in
the literature, which, had we done so, would have increased the
estimates of Hg exposure substantially. Thus, we believe our analysis
could understate risk to the most exposed individual, noting that we
have focused on the 99th percentile consumption rate in our estimates.
    Further, we were able to assess potential Hg exposures in only a
small subset of generally representative watersheds in the U.S. because
our analysis was necessarily premised on those water bodies for which
we had fish tissue Hg samples. Specifically, we analyzed 3,141 of the
approximately 88,000 watersheds in the United States. This limited set
of watersheds excludes several of the watersheds with the highest U.S.
EGU attributable deposition, and may also not have included watersheds
with the highest sensitivity to Hg deposition, e.g., the highest
methylation rates (see above). Nevertheless, our analysis of the subset
of watersheds we examined demonstrates that almost one third of the
watersheds are estimated to have Hg deposition attributable to U.S.
EGUs that contributes to potential exposures above the MeHg RfD. The
SAB

confirmed that the subset of watersheds we examined is sufficient.
    Considering these points and the information on Hg in the record,
the EPA believes that 10 percent of watersheds with populations at risk
due to U.S. EGU emissions alone is unacceptable, as is 24 percent of
watersheds with populations at risk due to U.S. EGU contributions in
conjunction with total deposition from other sources. Taking into
account the percentage of watersheds at risk, and the potential for
even higher percentages to be at risk using more conservative risk
assumptions and a more complete coverage of high U.S. EGU Hg deposition
watersheds, the EPA concludes that Hg emissions from U.S. EGUs pose a
hazard to public health.
    Given these findings, and considering that (1) the revised risk
analysis showed the percent of modeled watersheds with populations
potentially at-risk increased from 28 to 29 percent, and (2) the
revised analysis includes 36 percent more watersheds, which
significantly expands the coverage in several states, we conclude that
the finding that emissions of Hg from U.S. EGUs pose a hazard to public
health is confirmed by the national-scale revised Hg Risk TSD. As a
result, we conclude that it remains appropriate to regulate Hg
emissions from U.S. EGUs because those Hg emissions pose a hazard to
public health.
    With regards to the revised non-Hg inhalation case studies, the
highest estimated individual lifetime cancer risk for the one case
study facility (out of 16) with oil-fired EGUs is estimated to be 20 in
a million, driven by Ni emissions. For the facilities with coal-fired
EGUs, there were five (out of 16) with maximum individual cancer risks
greater than one in a million (the highest was five in a million), four
of which were driven by emissions of Cr(VI), and one of which was
driven by emissions of Ni. Therefore, a total of six facilities exceed
the criterion for EGUs to be regulated under CAA section 112. There
were also two facilities with coal-fired EGUs with maximum individual
cancer risks at one in a million. In the preamble to the proposed rule,
we reported that the maximum individual lifetime cancer risk for the
one facility with oil-fired EGUs was estimated to be 10 in a million,
and that there were 3 coal-fired EGU facilities with maximum individual
cancer risks greater than 1 in a million (the highest was 8 in a
million), and 1 coal-fired EGU facility with maximum individual cancer
risks equal to 1 in a million. Given that (1) the lifetime cancer risk
for the oil-fired EGU facility has increased from 10 to 20 in a
million, (2) the number of coal-fired EGU facilities with cancer risks
greater than 1 in a million has increased from 3 to 5, and (3) the
highest risk coal-fired facility still has cancer risks of 5 in a
million, which is above the 1 in a million benchmark, we conclude that
the finding that emissions of non-Hg HAP from U.S. EGUs pose a hazard
to public health is confirmed by the revised non-Hg risk inhalation
case studies.
    Moreover, some HAP emissions from U.S. EGUs contribute to adverse
ecosystem effects. While we did not do new analyses on these topics, we
reiterate that (1) Hg emissions from U.S. EGUs pose a hazard to the
environment, contributing to adverse impacts on fish-eating birds and
mammals, (2) Hg is a persistent bioaccumulative environmental
contaminant, and as a result, failing to control Hg emissions from U.S.
EGU sources will result in long-term environmental loadings of Hg,
above and beyond those loadings caused by immediate deposition of Hg
within the U.S.; controlling Hg emissions from U.S. EGUs helps to
reduce the potential for environmental hazard from Hg now and in the
future, and (4) it is appropriate to regulate those HAP which are not
known to cause cancer but are known to contribute to chronic non-cancer
toxicity and environmental degradation, such as the acid gases. In
addition, we have identified effective controls available to reduce Hg
and non-Hg HAP emissions.
    In summary, we confirm the findings that Hg and non-Hg HAP
emissions from U.S. EGUs each pose hazards to public health and that it
remains appropriate to regulate U.S. EGUs under CAA section 112 for
those reasons. We also conclude that it remains appropriate to regulate
EGUs under CAA section 112 because of the magnitude of Hg and non-Hg
emissions and the environmental effects of Hg and some non-Hg
emissions, each of which standing alone, supports the appropriate
finding. The availability of controls to reduce HAP emissions from EGUs
only further supports the appropriate finding.
    Our revised analyses still show that in 2016 after implementation
of other provisions of the CAA, HAP emissions from U.S. EGUs are
reasonably anticipated to pose hazards to public health; therefore, it
is necessary to regulate EGUs under CAA section 112. Moreover, HAP
emissions from U.S. EGUs are expected to continue to contribute to
adverse ecosystem effects. In addition, based on evaluation of the
regulations required by the CAA, including the recent CSAPR, it is
necessary to regulate U.S. EGUs under CAA section 112 because the only
way to ensure permanent reductions in HAP emissions from U.S. EGUs and
the associated risks to public health and the environment is through
standards set under CAA section 112. While CSAPR is projected to
achieve some Hg reductions due to co-control of Hg provided by controls
put in place to achieve required reductions in SO2
emissions, the results of the revised Hg Risk TSD indicate that an
unacceptable percentage of modeled watersheds have populations
potentially at-risk from U.S. EGU-attributable Hg deposition would
remain after implementation of CSAPR. While we modeled slightly higher
Hg emissions from U.S. EGUs (i.e., 29 tons of Hg) in our risk analysis
compared to the most recent estimate of 27 tons, we do not believe this
2 ton difference would substantially change our finding that Hg
emissions from U.S. EGUs pose a hazard to public health or the Hg risks
reported in the preamble to the proposed rule, as this represents less
than a 10 percent reduction in Hg emissions. In addition, the actual
reductions in Hg that will occur due to application of controls to meet
the SO2 emissions requirements of CSAPR may differ from
those projected to occur, due to differences in the technologies that
individual EGU sources choose to install. The only way to ensure
reductions in Hg, including those modeled as resulting from the CSAPR,
is to directly regulate Hg emissions under CAA section 112.
    In summary, we confirm the findings that it is necessary to
regulate HAP emissions from U.S. EGUs because (1) the national-scale Hg
Risk TSD shows that the hazards to public health posed by Hg emissions
from U.S. EGUs will not be addressed through imposition of the CAA, (2)
we cannot be certain that the identified cancer risks attributable to
U.S. EGUs will be addressed through imposition of the requirements of
the CAA, (3) the environmental hazards posed by acidification will not
be fully addressed through imposition of the CAA, (4) regulation under
CAA section 112 is the only way to ensure that all HAP emissions
reductions that have been achieved since 2005 remain permanent, and (5)
direct control of Hg emissions affecting U.S. deposition is only
possible through regulation of U.S. emissions as we are unable to
control global emissions directly. All of these findings independently
support a finding that it is necessary to regulate U.S. EGUs under CAA
section 112.
    Based on these findings, the Agency affirms its finding that it
remains appropriate and necessary to regulate

coal- and oil-fired EGUs under CAA section 112, and maintains that the
inclusion of coal- and oil-fired EGUs on the CAA section 112(c) list of
source categories regulated under CAA section 112 remains valid.

IV. Denial of Delisting Petition

    During the comment period on the proposed rule, UARG submitted a
petition pursuant to CAA section 112(c)(9), asking the Agency to delete
a portion of the EGU source category from the list of source categories
to be regulated under CAA section 112. Specifically, UARG asks that EPA
delist coal-fired EGUs from the CAA section 112(c) source category
list. A copy of UARG's petition has been placed in the docket for
today's rulemaking, along with the analysis conducted by EPRI that UARG
uses to support its petition (hereinafter referred to as UARG's
analysis). In support of its petition, UARG asserts that: (1) No coal-
fired EGU or group of coal-fired EGUs will emit HAP in amounts that
will cause a lifetime cancer risk greater than one in one million; and
(2) no coal-fired EGU or group of coal-fired EGUs will emit non-
carcinogenic HAP in amounts that will exceed a level which is adequate
to protect public health with an ample margin of safety or cause
adverse environmental effects. We disagree with UARG's assertions and
for the reasons set forth below are denying UARG's petition to delist
coal-fired EGUs from the section 112(c) source category list.

A. Requirements of CAA Section 112(c)(9)

    CAA section 112(c)(9)(B) provides that ``[t]he Administrator may
delete any source category'' from the section 112(c) source category
list if the Agency determines that: (i) For HAP that may cause cancer
in humans, ``no source in the category (or group of sources in the case
of area sources) emits such hazardous air pollutants in quantities
which may cause a lifetime risk of cancer greater than one in one
million to the individual in the population who is most exposed to
emissions of such pollutants from the source (or group of sources in
the case of area sources)''; and (ii) for HAP that may result in human
health effects other than cancer or adverse environmental effects, ``a
determination that emissions from no source in the category or
subcategory concerned (or group of sources in the case of area sources)
exceed a level which is adequate to protect public health with an ample
margin of safety and no adverse environmental effect will result from
emissions from any source.''
    The EPA has the discretion to delete a source category under CAA
section 112(c)(9)(B), but only if EPA concludes that the relevant
requirements of CAA section 112(c)(9)(B) have been met. HAP emissions
from EGUs present both cancer risks, which implicate the requirements
of CAA section 112(c)(9)(B)(i), and non-cancer human health effects or
adverse environmental effects, which implicate the requirements of CAA
section 112(c)(9)(B)(ii). As such, UARG bears the burden of
demonstrating that the requirements of both clauses are met.

B. Rationale for Denying UARG's Delisting Petition

    The EPA is denying UARG's petition to delist EGUs from the CAA
section 112(c) source category list. UARG improperly seeks to delist a
portion of a CAA section 112(c) listed source category that emits
carcinogens, which is contrary to the plain language of CAA section
112(c)(9). Even setting aside this fundamental defect, UARG has failed
to meet the requirements of CAA section 112(c)(9)(B).
1. UARG's Attempt to Delist a Portion of a Listed Source Category
Conflicts With D.C. Circuit Precedent
    In December 2000, the EPA listed coal- and oil-fired EGUs as a
single source category. UARG asks the Agency to delist a portion of
that listed source category: Coal-fired EGUs. UARG's request conflicts,
however, with D.C. Circuit precedent, which provides that for
categories, like EGUs, that pose cancer risks, the EPA may not delist a
portion of a source category. NRDC v. U.S. EPA, 489 F.3d 1364 (D.C.
Cir. 2007). Specifically, in NRDC, the D.C. Circuit held that the
Agency's attempt to delist a ``low-risk'' subcategory was ``contrary to
the plain language of the statute,'' and that the statute only
authorized the agency to remove source categories pursuant to section
112(c)(9). Id. at 1373 (``Because EPA's interpretation of Section
112(c)(9) as allowing it to exempt the risk-based subcategory is
contrary to the plain language of the statute, the EPA's interpretation
fails at Chevron step one.'').
    UARG's request is indistinguishable from the situation before the
court in NRDC. UARG does not seek to delist coal- and oil-fired EGUs,
which is the source category that EPA listed, but rather a portion of
that category. UARG also does not dispute that coal-fired EGUs emit
carcinogenic HAP. Because UARG's request to delist is contrary to the
plain language of CAA section 112(c)(9)(B) and NRDC, we are denying the
delisting petition.
2. Even Assuming, for the Sake of Argument, That EPA Could Delist a
Portion of a Source Category, UARG has Failed to Meet the Requirements
of CAA Section 112(c)(9)
    Even assuming, for the sake of argument, that EPA could delist a
portion of a source category that emits carcinogens, which it cannot,
UARG has failed to demonstrate that the requirements for delisting in
CAA section 112(c)(9)(i) and (ii) have been met. UARG contends that it
used EPA's models and approaches, as well as the most recent data. We
have carefully reviewed UARG's analyses, however, and found certain
flaws that we believe bias their risk results low. Specifically, we
identified flaws in emissions estimation. UARG developed estimates for
all EGU facilities using data which pre-date the 2010 ICR emissions
measurement data that EPA obtained to support this rule. UARG also
relied upon an emissions equation developed by EPRI and DOE to develop
its metal emissions estimates. With regard to that approach, the EPA
analysis of the ICR data has found that the regression approach is not
a good predictor of actual EGU emissions. Furthermore, we found fault
with their use of the geometric mean and their outlier analysis for
computing emission factors. The EPA analysis has found that the
geometric mean approach underpredicts actual emissions by an average of
more than seventy percent. This had an especially large impact on the
arsenic, chromium, and nickel emissions estimates. These and other
issues are explained in further detail in the response to comments
document. As a result, we believe the resulting risk estimates in
UARG's analysis are biased low. In addition, we note that there are
dispersion model refinements that are not included in the UARG
analyses, but were included in EPA's analysis. For example, for the
dispersion modeling of the 16 non-Hg case studies, the EPA considered
building downwash and used time-varying emissions, neither of which
were used in UARG's analysis. These factors could also bias the UARG
risk estimates low.
    However, even taking UARG's analysis at face value and accepting,
for arguments' sake, their assumptions and emissions estimates, UARG's
own data supports denial of the petition because UARG itself identifies
a maximum individual cancer risk exceeding 1 in a million, which is the
statutory threshold in CAA section 112(c)(9)(B)(i). Specifically,
UARG's multi-pathway

model plant ingestion risk analysis concluded that adult anglers would
face cancer risks of 4 in a million. For this reason alone, the
petition should be denied.
    UARG dismisses the 4 in a million cancer result, arguing that the
refined model plant multipathway risk assessment that it conducted is
``overly conservative.'' UARG conducted its multi-pathway risk analysis
to evaluate the risks associated with ingesting persistent and
bioaccumulative HAP which are emitted into the atmosphere and
subsequently deposit into the environment and bioaccumulate in animals
which are eventually consumed as food. Instead of conducting this
multipathway analysis for each EGU facility, UARG instead analyzed
multi-pathway risks by evaluating a single model plant. Nothing in the
record indicates, however, that UARG's model plant represents the
worst-case scenario for cancer human health risks from any EGU. Indeed,
although UARG claims in its petition that the site selected for its
case study is ``likely as close to a worst-case scenario as is possible
given the numerous variables associated with ingestion pathway risks''
(UARG petition at 12), the supporting documentation for that case study
specifically acknowledges that its fictional model plant scenario ``is
not intended to represent the risk due to emissions from an actual
plant or the highest level of risk that could be associated with a
coal-fired power plant at any location'' (EPRI at 1). The statute
requires that no source in the category may cause a lifetime cancer
risk greater than one in one million to the most exposed individual,
and UARG has failed to make this showing. UARG has neither modeled
multi-pathway risks for a worst-case model facility, nor evaluated the
multipathway risks associated with each individual EGU facility.
Accordingly, UARG has not made the demonstration required by CAA
section 112(c)(9)(B)(i). But, even focusing on the multi-pathway risk
analysis that UARG did conduct, which admittedly does not represent a
worst-case facility, UARG's analysis still shows cancer risks greater
than one in a million. Accordingly, UARG's petition must be denied.
    Although it is not necessary to reach the requirements of CAA
section 112(c)(9)(B)(ii) that address non-cancer human health risks, we
note that UARG has also failed to show that ``emissions from no source
in the category * * * exceed a level which is adequate to protect
public health with an ample margin of safety.'' Again, even accepting,
for argument's sake, the conclusions in UARG's analysis, UARG only
evaluated the non-cancer inhalation risks associated with each EGU
facility. It did not conduct a similar analysis to assess multipathway
risks for each EGU facility. Instead, it conducted a model plant
analysis and admits that such model plant does not represent the worst-
case scenario for noncancer human health risks from any EGU. Thus, the
analysis fails to fully characterize noncancer multipathway risks for
the source category, and UARG's petition must be denied on this basis
as well.
    Finally, UARG failed to meet its burden of showing that ``no
adverse environmental effect will result from emissions from any
source'' pursuant to CAA section 112(c)(9)(B)(ii). UARG analyzed
environmental effects only in conjunction with its model plant. Because
UARG's model plant does not represent the worst-case scenario for
environmental effects, UARG's analysis falls short and fails to
characterize fully the potential environmental impacts, and UARG's
petition must be denied.
    For all of these reasons, the EPA denies UARG's petition to delist
coal-fired EGUs from the CAA section 112(c) source category list.

C. EPA's Technical Analyses for the Appropriate and Necessary Finding
Provide Further Support for the Conclusion That Coal-Fired EGUs Should
Remain a Listed Source Category

    The EPA reasonably concluded in December 2000, based on the
information available to the Agency at that time, that it was
appropriate and necessary to regulate coal- and oil-fired EGUs under
CAA section 112 and added such units to the list of source categories
subject to regulation under CAA section 112(d). As discussed in section
III above, the EPA conducted additional, extensive technical analyses
based on recent data that confirm it remains appropriate and necessary
to regulate HAP from coal- and oil-fired EGUs, because such EGUs
continue to pose hazards to public health. HAP emissions from coal- and
oil-fired EGUs also continue to cause adverse environmental effects.
UARG advances several arguments, challenging the analyses the Agency
completed in support of the proposed rule. We address those arguments
in section III above. The Agency's analyses supporting the appropriate
and necessary finding confirm that EGUs cannot be delisted pursuant to
CAA section 112(c)(9).
    Specifically, as explained further in section III above, the EPA
analyzed non-Hg inhalation risks from 16 EGU facility case studies,
including both coal- and oil-fired EGUs, as part of its technical
analyses supporting the appropriate and necessary finding. That
analysis demonstrates that there are 6 EGU facilities (of the 16 that
we analyzed) with cancer risks exceeding one in one million. These
cancer risk levels exceed the delisting criteria set forth in CAA
section 112(c)(9)(B)(i), and confirm that EGUs must remain a listed
source category. As explained above, some commenters assert that EPA's
analysis of non-Hg inhalation risks from EGUs conducted in support of
the proposal for this rulemaking overstated emissions from, and risks
associated with, EGUs. These commenters argue that the analysis
supporting UARG's petition more appropriately assesses EGU risk. The
EPA disagrees with these comments and addresses these comments in
section III above.
    Significantly, the EPA based its analysis of 16 case study EGUs
directly on the 2010 emissions test data from EGUs obtained through the
ICR. The EPA's 16 case study analysis used emissions data either taken
directly from the 2010 emissions test data, or derived using emissions
factors based on the 2010 data for similar EGU units. The EPA also
included dispersion model refinements in its final case studies, as
noted above. Further, the EPA re-analyzed the 16 case studies that we
conducted for the proposal and revised those analyses consistent with
new non-Hg HAP emissions data and corrected stack parameters provided
by commenters (including UARG) during the comment period on the
proposed rule. The EPA received revised information concerning
emissions tests, stack heights and stack diameters for some of the case
study EGU facilities. The EPA incorporated all of these corrections
into our analysis and then re-analyzed the risks for the 16 case study
facilities. When completed, the EPA determined that the corrections
incorporated into the reanalysis had little effect on the overall
results. In the final rule, the EPA concludes that the maximum
individual inhalation cancer risks for 6 out of the 16 case study EGU
facilities are greater than 1 in a million. These cancer risk levels
confirm that EGUs do not satisfy the delisting criterion of CAA section
112(c)(9)(B)(i) and thus should remain a listed source category.
    The EPA's national-scale Hg Risk TSD supporting the appropriate and
necessary finding also confirm that Hg emissions from coal- and oil-
fired US EGUs are reasonably anticipated to pose a hazard to public
health. As discussed

in section III above, the EPA interprets CAA section 112(n)(1), with
regard to mercury, as intended to protect the public, including
sensitive populations, against exposures to Hg from EGUs that would
exceed the level determined by EPA to be without appreciable risk,
e.g., exposures that are above the RfD for methylmercury (MeHg), or
would contribute additional risk in areas where Hg exposures exceed the
RfD due to contributions from all sources of Hg.
    In order to determine whether EGU Hg emissions pose a hazard to
public health, the EPA conducted a national-scale Hg Risk TSD focused
on populations with high levels of self-caught freshwater fish
consumption. The results of the Hg Risk TSD show that 98 percent of
modeled watersheds have total exposures to MeHg that exceed the MeHg
RfD, above which there is an increased risk of adverse effects on human
health. In these watersheds, any reductions in exposures to Hg will
reduce risk, and thus the incremental contribution to Hg exposure from
any individual source or group of sources, such as EGUs, may reasonably
be anticipated to cause additional risk. The Hg Risk TSD focused on
those watersheds that either exceeded the RfD based on U.S. EGU
attributable deposition alone, without considering other sources of
deposition, or watersheds that exceed the RfD due to total Hg
deposition and to which U.S. EGUs contributed at least 5 percent of the
Hg deposition. The results of that analysis show that up to 29 percent
of the modeled watersheds have populations that are potentially at-risk
from exposure to Hg from U.S. EGUs, including up to 10 percent of
modeled watersheds where deposition from U.S. EGUs alone leads to
potential exposures that exceed the MeHg RfD, and up to 24 percent of
modeled watersheds where total potential exposures to MeHg exceed the
RfD and U.S. EGUs contribute at least 5 percent to Hg deposition. This
approach to assessing national risks from Hg deposition from EGUs was
supported by the independent peer review conducted by the Science
Advisory Board, as discussed fully in section III.
    Finally, as discussed in section III, based on this assessment, the
EPA has confirmed that Hg emitted from U.S. EGUs pose a hazard to
public health and it is appropriate to regulate U.S. EGUs under CAA
section 112. This determination and the confirmatory assessments
support our conclusion that UARG's delisting petition must be denied.
    UARG attempts to dismiss the results of EPA's national-scale Hg
Risk TSD, arguing that EPA cannot consider the risks posed by EGUs in
conjunction with any other risks, including those from other source
categories. Nothing in CAA section 112(c)(9), however, provides that
the Agency cannot consider background or emissions due to other
sources. CAA section 112(c)(9)(B)(ii) provides that ``no source in the
category or subcategory concerned (or group of sources in the case of
area sources) exceed a level which is adequate to protect public health
with an ample margin of safety and no adverse environmental effect will
result from emissions from any source.'' This language could be read to
provide that the Agency consider only the risks associated with the
source category at issue, and ignore how those risks fit with real-
world exposures.\304\ However, the language could also be read to
provide that the Agency consider the cumulative effect of HAP emissions
from the individual sources in the category in conjunction with the HAP
emissions from other sources. The latter is a reasonable
interpretation, especially when considering how the public is exposed
to HAP emissions. Considering the individual sources in a source
category in isolation treats the sources as if they exist in a vacuum,
which does not mirror reality. Such an approach is particularly
problematic for environmentally persistent HAP that bio-accumulate in
the food chain, such as mercury.\305\
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    \304\ The same is true with respect to section 112(c)(9)(B)(i).
    \305\ In a prior rulemaking, EPA stated that the language in
section 112(c)(9)(B)(ii) ``does not direct EPA to extend its
analysis to either emissions from other sources in other categories
or subcategories or to non-attributable background concentrations.''
71 FR 8347 (Feb. 16, 2006). The preamble to that rule repeatedly
states that the ``focus'' of the delisting determination in that
rule was on emissions from sources in the category under review. See
71 FR 8346-47. The preamble went on to compare section 112(c)(9)(B)
to section 112(f)(2)(A) in a way that suggested that EPA can
consider risks presented by sources other than the subject source
category under section 112(f)(2), but not under section 112(c)(9).
We do not believe the language of section 112(c)(9) compels any
different treatment. The section 112(f) analysis occurs after a
source category has already complied with section 112(d) standards,
whereas, potential delistings under section 112(c)(9) may involve
source categories unregulated by section 112. A delisting decision
is significant in that the category that is delisted will no longer
be subject to HAP regulation under the Act. It is difficult to
justify why we would examine risks from other sources under section
112(f), but not under section 112(c)(9), where Congress established
such a specific test for delisting.
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    Here, the record demonstrates that 98 percent of the watersheds EPA
modeled have total exposures to MeHg that exceed the MeHg RfD, above
which there is increased risk of adverse effects on human health,
especially on the developing nervous systems of children during
gestation. EGUs remain one of the largest unregulated sources of Hg
emissions, and those emissions continue to contribute to Hg exposures
and risk. UARG seeks to ignore the fact that exposures above the RfD
exist in almost every watershed we modeled, and instead focuses on the
contribution provided solely by EGUs. The EPA did as UARG asked and
found that up to 10 percent of modeled watersheds where deposition from
U.S. EGUs alone leads to potential exposures that exceed the MeHg RfD.
Thus, even focusing on EGU emissions in a vacuum, which we do not
believe is appropriate or required under CAA section 112(c)(9), we
still found that up to 10 percent of the watersheds exceed the RfD due
to EGU emissions even before taking into account the numerous other
sources of Hg deposition, and we believe this to be an unacceptable
percentage of watersheds above the RfD. Due to the persistent,
bioacccumulative nature of Hg, among other factors, we believe it is
appropriate to consider the combined impact of Hg emissions from EGUs
and other sources of Hg. Thus, we also considered the 24 percent of
modeled watersheds where, even though U.S. EGU emissions alone are not
enough to cause exposures that exceed the RfD, those emissions
contribute at least 5 percent of total exposures to MeHg that exceed
the RfD. The combined total of 29 percent of modeled watersheds where
U.S. EGUs cause or contribute to MeHg exposures above the RfD is
clearly unacceptable and thus the UARG petition to delist must be
denied.
    Thus, the technical analyses the Agency conducted in support of the
appropriate and necessary finding confirm that EGUs should remain a
listed source category.

V. Summary of This Final NESHAP

    This section summarizes the requirements of the final EGU NESHAP.
Section VI below summarizes the significant changes to this final rule
following proposal.

A. What is the source category regulated by this final rule?

    This final rule affects coal- and oil-fired EGUs.

B. What is the affected source?

    An existing affected source under this final rule is the collection
of coal- or oil-fired EGUs in a subcategory within a single contiguous
area and under common control. A new affected source is each coal- or
oil-fired EGU for which construction or reconstruction began after May
3, 2011.

    CAA section 112(a)(8) defines an EGU as: a fossil fuel-fired
combustion unit of more than 25 megawatts that serves a generator
that produces electricity for sale. A unit that cogenerates steam
and electricity and supplies more than one-third of its potential
electric output capacity and more than 25 megawatts electrical
output to any utility power distribution system for sale shall be
considered an electric utility steam generating unit.

    If an EGU burns coal (either as a primary fuel or as a
supplementary fuel) or any combination of coal with another fuel
(except for solid waste as noted below) where the coal accounts for
more than 10.0 percent of the average annual heat input during any 3
consecutive calendar years or for more than 15.0 percent of the annual
heat input during any one calendar year after the applicable compliance
date, the unit is considered to be coal-fired under this final rule.
    If a unit is not a coal-fired unit and burns only oil or burns oil
in combination with a fuel other than coal (except solid waste as noted
below) where the oil accounts for more than 10.0 percent of the average
annual heat input during any 3 consecutive calendar years or for more
than 15.0 percent of the annual heat input during any one calendar year
after the applicable compliance date, the unit is considered to be oil-
fired under this final rule.
    As noted below, the EPA is finalizing in this rule a definition to
determine whether the combustion unit is ``fossil fuel fired'' such
that it is considered an EGU as defined in CAA section 112(a)(8) and,
thus, potentially subject to this final rule. In addition, using the
construct of the definition of ``oil-fired'' from the ARP, we are
finalizing in this rule a requirement that the unit fire coal or oil
(or natural gas), or any combination thereof, for more than 10.0
percent of the average annual heat input during any 3 consecutive
calendar years or for more than 15.0 percent of the annual heat input
during any one calendar year to be considered a ``fossil fuel-fired''
EGU as defined in CAA section 112(a)(8). However, if a new or existing
EGU is not coal- or oil-fired, and the unit burns natural gas
exclusively or burns natural gas in combination with another fuel where
the natural gas constitutes 10 percent or more of the average annual
heat input during any 3 calendar years or 15 percent or more of the
annual heat input during any 1 calendar year, the unit is considered to
be natural gas-fired EGU and not subject to this final rule. As
discussed later, we believe that this definition will address those
situations where an EGU co-fires limited amounts of either coal or oil
with natural gas or other non-fossil fuels (e.g., biomass).
    If an EGU combusts solid waste, standards issued pursuant to CAA
section 129 apply to that EGU, rather than this final rule.

C. What are the pollutants regulated by this final rule?

    For coal-fired EGUs, this final rule regulates HCl as a surrogate