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III. Appropriate and Necessary Finding

In the preamble to the proposed rule1, EPA determined 

that that it is appropriate and necessary to regulate 

emissions of mercury (Hg) and other Hazardous Air 

Pollutants (HAP) from U.S. EGUs, confirming the finding 

made in 2000.

As discussed fully in the preamble to the proposed 

rule, EPA interprets the Clean Air Act (CAA) to require the 

Agency to find it appropriate to regulate U.S. EGUs under

section 112 if the Agency determines that the emissions of 

one or more HAP emitted from U.S. EGUs pose an identified 

or potential hazard to public health or the environment.

The Agency must find it necessary to regulate EGUs under 

section 112 if the imposition of other requirements of the 

CAA would not adequately address the identified or 

potential hazards to public health or the environment.

Moreover, it may be necessary to regulate utilities under 

section 112 for a number of other reasons, including, for 

example, that section 112 standards will assure permanent 

 

1 76 FR 24986
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reductions in EGU HAP emissions, which cannot be assured 

based on other requirements of the CAA. 

In this section, we describe revisions to the 

technical analyses that accompanied the proposed rule and 

the responses to public comments on legal, technical, and 

policy aspects of the finding. We first summarize the 

elements of the appropriate and necessary finding, as 

discussed in the preamble to the proposed rule. We then 

discuss the results of the peer reviews of our nationalscale mercury risk assessment (hereafter referred to as the 

Hg Risk TSD) and non-Hg HAP risk assessment. In this 

discussion, we describe the peer review processes, the 

charges provided to the peer review panels, the findings 

and recommendations from the peer review panels, and EPA’s 

responses to those peer reviews. We also summarize the 

results of revisions to the Hg Risk TSD and the case 

studies of non-Hg HAP inhalation risks and compare these 

results to those reported in the preamble to the proposed 

rule.

In the next subsection, we summarize and respond to 

the major categories of comments on the legal, technical, 

and policy aspects of the appropriate and necessary 
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finding. The first portion of the response to comments 

subsection addresses legal aspects of the appropriate and 

necessary finding. This subsection includes comments on the 

history of Section 112(n)(1)(a), the definition and 

interpretation of the terms “appropriate” and “necessary”, 

regulation of all HAP, consideration of both health and 

environmental effects in making the appropriate finding, 

consideration of costs in making the appropriate finding, 

consideration of CAA requirements in making the necessary 

finding, listing of U.S. EGU under section 112, and the 

2000 finding. 

The second portion of the response to comments 

subsection addresses comments related to the new technical 

analyses confirm that HAP emissions from U.S. EGUs remain a 

hazard to public health. This includes comments on the 

inputs, methods, and assumptions used in Hg Risk TSD, the 

non-Hg inhalation risk case studies, and the assessment of 

excess local deposition due to U.S. EGU Hg emissions. 

Comments on the Hg risk analysis included comments on the 

modeling of Hg emissions (both global and U.S.) and 

deposition, the reference dose (RfD) for methylmercury 

(MeHg), fish tissue Hg concentrations, the assumed linear 
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relationship between changes in Hg deposition and changes 

in fish tissue Hg concentrations, the behavior of 

subsistence fishing populations, and fish consumption 

rates. Comments on the non-Hg inhalation risk case studies 

included comments on non-Hg HAP emissions, modeling 

parameters, estimating nickel (Ni) and chromium (Cr) risk, 

and an alternative risk analysis. Comments on the 

assessment of excess local deposition addressed the 

definition of hotspots, evidence for local Hg deposition 

from U.S. EGU emissions, documentation of methods, and 

limitations of deposition modeling. We also received 

comments related to ecosystem impacts from HAP, focused on 

the adverse impact of acid gases on ecosystems.

Based on our review of the comments and our updated 

analyses in response to the peer reviews, we affirm 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. The revised 

analyses for Hg and non-Hg risk, which fully addresses the 

advice we received from the peer reviews, confirm that 

emissions of both Hg and non-Hg HAP from U.S. EGUs are a 

hazard to public health. These results, along with the 
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other elements of the finding, confirm that it remains 

appropriate and necessary to regulate EGUs under CAA 

section 112 and that such units are properly listed 

pursuant to section 112(c).

A. Summary of EPA’s Finding that it is Appropriate and 

Necessary to Regulate EGUs to Address Public Health and 

Environmental Hazards Resulting from Emissions of Hg and 

Non-Hg Hazardous Air Pollutants (HAP) from EGUs

In the preamble to the proposed rule, we confirmed our 

2000 finding that it is appropriate to regulate emissions 

of Hg) and other HAP from EGUs because emissions of those 

pollutants pose hazards to public health and the 

environment, and EGUs are the largest or among the largest 

contributors of many of those HAP. We also confirmed that 

it is necessary to regulate EGUs under section 112 for a 

variety of reasons, including that hazards to public health 

and the environment posed by HAP emissions from EGUs remain

after imposition of the requirements of the CAA. Our 

confirmation of the 2000 finding was supported in part by 

several new analyses of the hazards to public health posed 

by both Hg and non-Hg HAP.
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In this section, we summarize the finding as reported 

in the preamble to the proposed rule. Specifically, we 

address the Agency’s determination that it is appropriate 

and necessary to regulate coal- and oil-fired EGUs under 

CAA section 112. The extensive analyses summarized in the 

preamble to the proposed rule and documented in several 

Technical Support Documents2,3 confirmed that it remains 

appropriate and necessary today to regulate EGUs under 

section 112. The analyses demonstrated that it is 

appropriate to regulate emissions from coal- and oil-fired 

EGUs under CAA section 112 because: 1) Hg and non-Hg HAP 

continue to pose a hazard to public health, and U.S. EGU 

emissions cause and/or contribute to this hazard; 2) Hg and 

some non-Hg HAP pose a hazard to the environment; 3) U.S. 

EGU emissions are still the largest domestic source of U.S. 

Hg, HCl, and HF emissions, and a significant source of 

other HAP emissions; 4) Hg emissions from individual EGUs 

leads to excess local deposition in areas directly 

 

2 U.S. EPA. 2011a. National-Scale Assessment of Mercury Risk to 

Populations with High Consumption of Self-caught Freshwater Fish In 

Support of the Appropriate and Necessary Finding for Coal- and OilFired Electric Generating Units. Office of Air Quality Planning and 

Standards. November. EPA-452/R-11-009.

3 U.S. EPA. 2011b. Supplement to Non-Hg Case Study Chronic Inhalation 

Risk Assessment for the Utility MACT Appropriate and Necessary 

Analysis. Office of Air Quality Planning and Standards. November.
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surrounding those individual EGUs (not solely the result of 

regionally transported emissions), and would not be 

adequately addressed through reductions in regional levels 

of Hg emissions, requiring controls to be in place at all 

U.S. EGU sources that emit Hg; 5) Hg emissions from EGUs 

affect not only deposition, exposures, and risk today, but 

may contribute to future deposition, exposure and risk due 

to the processes of reemission of Hg that occur given the 

persistent nature of Hg in the environment and that Hg 

will remain part of the global burden of Hg; in fact, the 

delay in issuing Hg regulations under section 112 has 

already resulted in several hundred additional tons of Hg 

being emitted to the environment, and 6) effective controls 

for Hg and non-Hg HAP are available for U.S. EGU sources.

EPA concluded that Hg emissions from U.S. EGUs are a 

public health hazard today due to their contribution to Hg 

deposition that leads to potential MeHg exposures above the 

reference dose (RfD). EPA also concluded that Hg emissions

from U.S. EGUs contribute to environmental concentrations 

of Hg that are harmful to wildlife and can affect 

production of important ecosystem services, including 

recreational hunting, fishing, and wildlife viewing. EPA 
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further concluded that non-Hg HAP emissions from U.S. EGU 

are a public health hazard because they contribute to 

elevated cancer risks. Finally, EPA concluded that HCl and 

HF emissions from U.S. EGUs contribute to acidification in 

sensitive ecosystems and, therefore, pose a risk of adverse 

effects on the environment. 

The analyses demonstrated that it is necessary to 

regulate emissions from coal- and oil-fired EGUs under CAA 

section 112 because 1) Hg emissions from EGUs remaining in 

2016 still pose a hazard to public health and the 

environment in the absence of regulations under Section 112 

that would be required to be implemented at that time, 2) 

U.S. EGU emissions of Hg after imposition of the 

requirements of the CAA were projected to be 29 tons per 

year in 2016, similar to levels of Hg emitted today, 3) 

EGUs are the largest source of Hg in the U.S. and thus 

contribute to the risk associated with exposure to MeHg, 4) 

we cannot be certain that the identified cancer risks 

attributable to EGUs will be addressed through imposition 

of the requirements of the CAA, 5)the environmental hazards 

posed by acidification will not be fully addressed through 

imposition of the CAA, 6) regulation under section 112 is 
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the only way to ensure that HAP emissions reductions that 

have been achieved since 2005 remain permanent, 7) direct 

control of Hg emissions affecting U.S. deposition is only 

possible through regulation of U.S. emissions; we are 

unable to control global emissions directly.

a. Finding that Hg Emissions from U.S. EGUs Continue to 

Pose a Hazard to Public Health and the Environment

In support of the finding that Hg emissions from U.S. 

EGUs are a hazard to public health, EPA assessed the Hgrelated risk to populations with high consumption of selfcaught freshwater fish, which is the population most likely 

to experience elevated risk from Hg emissions from U.S. 

EGUs. This Hg Risk TSD incorporated detailed emissions, air 

quality, exposure, and risk modeling, which provided 

estimates of the watersheds in which populations with high 

levels of fish consumption experience the potential for 

risk due to deposition of Hg. The Hg Risk TSD assessed the 

hazard to public health posed by Hg emissions from U.S. 

EGUs focused on comparisons of the RfD to exposures caused 

or contributed to by Hg emissions from U.S. EGUs. In the Hg

risk assessment, almost all (98 percent) of the more than 

2,400 watersheds for which we identified fish tissue data, 
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exceeded the RfD, above which there is the potential for an 

increased risk of adverse effects on human health. U.S. 

EGU-attributable deposition of Hg contributes to a large 

number of those watersheds in which total potential 

exposures to MeHg from all sources exceed the RfD and, 

thus, pose a hazard to public health. We focused on the 

watersheds (where U.S. EGU-attributable deposition alone 

resulted in potential MeHg exposures above the RfD, 

regardless of the additional deposition from other sources 

of Hg deposition, and where U.S. EGU-attributable 

deposition contributed at least 5 percent of the total Hg 

deposition. This approach is likely to understate risk 

because any contribution of Hg to watersheds where 

potential exposures to MeHg exceed the RfD poses a public 

health hazard. Thus, because we found a large percentage of 

modeled watersheds with populations potentially at-risk

even using this approach, we have confidence that emissions 

of Hg from U.S. EGUs are causing a hazard to public health, 

as there are additional watersheds where U.S. EGUs

contribute to mercury risk at lower percent benchmarks.

In total, the Hg risk assessment found an estimated 28 

percent of modeled watersheds with populations with
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potentially at-risk from exposure to MeHg based on the 

contribution of U.S. EGUs. This total includes watersheds 

that are potentially at-risk either because U.S. EGUattributable deposition is sufficient to cause potential 

exposures to exceed the RfD even excluding the deposition 

from other U.S. and non-U.S. sources, or because the U.S. 

EGU-attributable deposition contributes greater than 5 

percent of total deposition and total exposure from all 

sources is greater than the RfD.

We found that at the 99th percentile fish consumption 

level for subsistence fishers, 22 percent of sampled 

watersheds where total potential exposures to MeHg exceed 

the RfD received at least 5 percent of Hg deposition from 

U.S. EGUs. Although the most complete estimate of potential 

risk is based on total exposures to Hg, including 

deposition from U.S. EGU sources, U.S. non-EGU sources, and 

global sources, the deposition resulting from Hg emissions

from U.S. EGUs is large enough in some watersheds that 

persons consuming contaminated fish would have exposures 

that exceed the RfD even without additional deposition from 

other sources. Based on these considerations, we found that 

at the 99th percentile fish consumption level for 
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subsistence fishers, in 12 percent of the sampled 

watersheds, U.S. EGUs are responsible for deposition that 

causes the RfD to be exceeded, even excluding consideration 

of the additional deposition from other sources.

In addition, we highlighted in the preamble to the 

proposed rule that the estimate of modeled watersheds with

populations potentially at-risk from U.S. EGU-attributable 

Hg deposition is likely understated because the data on 

fish tissue MeHg concentrations that we were able to 

identify for the Hg risk assessment was limited in some 

regions of the U.S., such as Pennsylvania, with very high 

U.S. EGU attributable Hg deposition. Thus, it is possible 

that watersheds with potentially high MeHg exposures were 

excluded from the Hg Risk TSD. In addition, due to 

limitations in our models and available data, we did not 

estimate risks in near-coastal waters, and some of these 

waters, such as the Chesapeake Bay, could have substantial 

EGU-attributable Hg deposition.

Further, scientific studies have found strong evidence 

of adverse impacts on species of fish-eating birds with 

high bird-watching value, including loons, white ibis, and 

great snowy egrets. Studies have also shown adverse effects 
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on insect-eating birds including many songbirds. Adverse

effects in fish-eating mammals, such as mink and otter, 

include neurological responses (impaired escape and 

avoidance behavior) which can influence survival rates. 

Because EGUs contribute to Hg deposition in the U.S., we 

reasonably concluded that EGUs are contributing to the 

identified adverse environmental effects.

Hg emitted into the atmosphere persists for years, and 

once deposited, can be reemitted into the atmosphere by a 

number of processes, including forest fires and melting of 

snow packs. As a result, Hg emitted today can have impacts 

for many years. In fact, Hg emitted by U.S. EGUs in the 

past, including over the last decade, is still affecting 

concentrations of Hg in fish today. Failing to control Hg 

emissions from U.S. EGU sources will result in long-term 

environmental loadings of Hg, beyond those loadings caused 

by immediate deposition of Hg within the U.S. Although we 

are not able to quantify the impact of U.S. EGU emissions 

on the global pool of Hg, U.S. EGUs contribute to that 

global pool. Controlling Hg emissions from U.S. EGUs helps 

to reduce the potential for environmental hazard from Hg 

now and in the future. 
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In the preamble to the proposed rule, we concluded 

that all of these findings independently support a 

determination that it is appropriate to regulate Hg 

emissions from EGUs.

b. Finding that U.S. EGU Non-Hg HAP Emissions Continue to 

Pose a Hazard to Public Health and the Environment

In addition to the Hg risk assessment, EPA also 

reported in the preamble to the proposed rule the results 

of 16 case studies of inhalation risks of cancer for U.S. 

EGUs for which we had 2007 to 2009 emissions data (based on 

the 2010 ICR) and that we anticipated would have relatively 

higher emissions of non-Hg HAP compared to other U.S. EGUs. 

The results of that analysis showed that of the 16 

facilities modeled, four facilities (three coal-fired 

facilities and one oil-fired facility) have estimated risks 

of greater than one in 1 million4 for the most exposed 

individual. Given Congress’ determination that categories 

of sources which emit HAP resulting in a lifetime cancer 

risk greater than one in 1 million should not be removed 

 

4 A risk level of 1 in a million implies a likelihood that up to one 

person, out of one million equally exposed people would contract cancer 

if exposed continuously (24 hours per day) to the specific 

concentration over 70 years (an assumed lifetime). This would be in 

addition to those cancer cases that would normally occur in an 

unexposed population of one million people.
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from the section 112(c) source category list and should 

continue to be regulated under 112, we concluded that risks 

above that level from U.S. EGUs represent a hazard to 

public health such that it is appropriate to regulate EGUs 

under section 112.

Although our case studies did not identify significant 

chronic non-cancer risks from acid gas emissions from the 

specific EGUs assessed, the Administrator remains concerned 

about the potential for acid gas emissions to add to 

already high atmospheric levels of other chronic 

respiratory toxicants and to environmental loading and 

degradation due to acidification. EGUs emit over half of 

the nationwide emissions of HCl and HF, based on 2010 

emissions estimates. Given that acidification affects many 

sensitive ecosystems across the country, it is appropriate 

to reduce emissions of this magnitude, which may aggravate 

acidification. The Administrator concluded that, in 

addition to the regulation of non-Hg HAP that cause 

elevated cancer risks, it is appropriate to regulate those 

HAP that are not known to cause cancer but are known to 

contribute to chronic non-cancer toxicity and environmental 

degradation, such as the acid gases. 
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These findings independently supported the 

determination that it remains appropriate to regulate HAP 

emissions from EGUs.

c. Finding that Effective Controls are Available to Reduce 

Hg and Non-Hg HAP Emissions

Particle-bound Hg can be effectively removed along 

with other flue gas PM (including non-Hg metal HAP) in 

primary or secondary PM control devices. Electrostatic 

precipitators, fabric filters, and wet flue gas 

desulfurization (FGD) scrubbers are all effectively remove 

Hg; the degree of effectiveness depends on the specific 

characteristics of the EGU and fuel types. Additionally, 

these devices all effectively remove Non-Hg metal HAP. 

Activated carbon injection is the most successfully 

demonstrated Hg-specific control technology. Acid gases are 

readily removed in typical FGD systems due to their 

solubility or their acidity (or both). The availability of 

controls for HAP emissions from EGUs supported the 

appropriate finding because sources will be able to reduce 

their emissions effectively and, thereby, reduce the 

hazards posed by HAP emissions from EGUs.
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d. The Administrator’s Finding that it Remains Necessary to 

Regulate Coal- and Oil-fired EGUs Under CAA Section 112

EPA determined that in 2016, the hazards posed to 

human health and the environment by HAP emissions from EGUs 

will not be addressed; therefore, it is necessary to

regulate EGUs under section 112. In addition, it is 

necessary to regulate EGUs under section 112 because the 

only way to ensure permanent reductions in U.S. EGU 

emissions of HAP and the associated risks to public health 

and the environment is through standards set under section 

112.

The Agency first evaluated whether it is necessary to 

regulate HAP emissions from EGUs “after imposition of the 

requirements of the CAA.” As explained above, we interpret 

that phrase to require the Agency to consider only those

requirements that Congress directly imposed on EGUs through 

the CAA as amended in 1990 and for which EPA could 

reasonably predict HAP emission reductions at the time of 

the Utility Study5. Nonetheless, the Agency recognizes that 

it has discretion to look beyond the Utility Study in 

 

5 U.S. EPA. Study of Hazardous Air Pollutant Emissions from Electric 

Utility Steam Generating Units —Final Report to Congress. EPA–453/R–98–

004a. February 1998.
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determining whether it is necessary to regulate EGUs under 

section 112. Because several years have passed since the

2000 Finding, we conducted an additional, updated analysis, 

examining a broad array of diverse requirements.

Specifically, we analyzed HAP emissions from U.S. EGUs 

remaining in 2016. The baseline for our analysis included 

emission reductions anticipated from the proposed Transport 

Rule (finalized in June 2011 as the Cross-State Air 

Pollution Rule(CSAPR)7); CAA section 112(g); the Acid Rain 

Program; settlements of federal, state, and citizen 

enforcement actions related to criteria pollutant emissions 

from EGUs; and some state rules related to criteria 

pollutant emissions. We included state requirements and 

citizen and state enforcement action settlements associated 

with criteria pollutants because those requirements may 

have a basis under the CAA. However, we did not conduct an 

 

7. Since the time of the analyses conducted in support of the 

appropriate and necessary finding, EPA has updated IPM modeling to 

reflect to the most recently available information, including public 

comments and the final CSAPR (see IPM Documentation for further details 

on these updates, which is available in the docket). Compared to the 

modeling conducted at proposal, these updates are projected to result 

in greater reductions in criteria pollutants, and also to have a 

slightly greater impact on U.S. EGU Hg emissions. The current 

projection in 2016, there will be 27 tons of Hg emitted by U.S. EGU, as 

compared to the 29 tons we modeled for the Hg Risk TSD. We do not 

expect that the 2 tons less of Hg will substantially change the mercury 

risks that we reported in the preamble to the proposed rule, as this 

represents less than a 10 percent reduction in Hg emissions. 
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analysis to determine whether the state requirements are

based on requirements of the CAA. As such, there may be 

instances where we should not have considered certain state 

rules or state and citizen suit enforcement settlements in 

our analysis, because those requirements may be based 

solely in state law and not be required by the CAA as 

contemplated under section 112(n)(1)(A). To the extent that 

these non-federal actions do not result in permanent 

reductions in Hg emissions, their inclusion in the baseline 

Hg emissions estimates for the Hg Risk TSD would

underestimate the risks associated with Hg emissions from 

U.S. EGUs. We did not include in our analysis any stateonly requirements or voluntary actions to reduce HAP 

emissions because there is no Federal backstop for those 

requirements and actions.

Our analysis confirmed that Hg emissions from EGUs 

remaining in 2016 still pose a hazard to public health and 

the environment and, for that reason, it remains necessary 

to regulate EGUs under section 112. Specifically, we 

estimated that U.S. EGU emissions of Hg after imposition of 

the requirements of the CAA will be 29 tons per year in 

2016, the same as the level of Hg that we estimated at the 
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time of proposal would be emitted by U.S. EGUs today. As

stated above, we evaluated the hazards to public health and 

the environment from Hg based on the estimated Hg emissions 

in 2016 and found that a hazard exists. Because a hazard 

remains after imposition of the requirements of the CAA, we 

determined it is necessary to regulate EGUs.

It is necessary to regulate HAP emissions from EGUs, 

even though the hazards from Hg will not be fully resolved 

through regulation under section 112. EPA concluded in the 

preamble to the proposed rule that incremental reductions 

in Hg are important because as exposure above the RfD 

increases, the likelihood and severity of adverse effects 

increases. 

In the preamble to the proposed rule, we also found

that it is necessary to regulate EGUs under section 112 

based on non-Hg HAP emissions because we could not be 

certain that the identified cancer risks attributable to 

EGUs will be addressed through imposition of the 

requirements of the CAA. In addition, the environmental 

hazards posed by acidification would not be fully addressed 

through imposition of the CAA.
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In the preamble to the proposed rule, we also found it 

necessary to regulate EGUs because regulation under section 

112 is the only way to ensure that HAP emissions reductions 

that have been achieved since 2005 remain permanent. Real 

reductions between 2005 and 2010 are attributable to state 

Hg regulations and to the Clean Air Interstate Rule (CAIR) 

and Federal enforcement actions that achieve Hg reductions 

as a co-benefit of controls for PM, NOX, and SO2 emissions. 

However, there are no national, federally-binding 

regulations for Hg. State Hg regulations can potentially 

change or be revoked without EPA approval, and reductions 

that occur as a co-benefit of criteria pollutant 

regulations can also change. Furthermore, companies can 

change their criteria pollutant compliance strategies and 

use methodologies that do not achieve the same level of Hg 

or other HAP co-benefit (e.g., purchasing allowances in a 

trading program instead of using add-on controls).

As with Hg, the most recent data on HCl and HF 

emissions U.S. EGUs show a significant reduction between 

2005 and 2010. These reductions in HCl and HF are the cobenefit of controls installed to meet other CAA 

requirements, including enforcement actions, and to a 
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lesser extent, state regulations. There is no guarantee 

other than regulation under section 112 that these 

significant decreases in HCl and HF emissions will be 

permanent. Although we do not have estimates for the 

remaining HAP emitted from U.S. EGUs, it is likely that 

such emissions have also decreased between 2005 and 2010. 

Thus, the Administrator found it necessary to regulate HAP 

emissions from U.S. EGUs to ensure that HAP emissions 

reductions are permanent.

Finally, direct control of Hg emissions affecting U.S. 

deposition is only possible through regulation of U.S. 

emissions; we are unable to control global emissions 

directly. Although the U.S. is actively involved in 

international efforts to reduce Hg pollution, the ability 

of the U.S. to argue effectively in these negotiations for 

strong international policies to reduce Hg air emissions 

depends in large part on our domestic policies, programs 

and regulations to control Hg.

All of these findings independently supported the 

finding that it is necessary to regulate U.S. EGUs under 

section 112.
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Therefore, given the Agency’s finding that it remains 

appropriate and necessary to regulate coal- and oil-fired 

EGUs under CAA section 112, EPA confirmed in the preamble 

to the proposed rule its decision to include coal- and oilfired EGUs on the list of source categories regulated under 

CAA section 112(c).

B. Peer Review of the Hg Risk TSD Supporting the 

Appropriate and Necessary Finding for Coal and Oil-Fired 

EGUs and EPA Response

In the preamble to the proposed rule, EPA stated that 

“in making the finding that it remains appropriate and 

necessary to regulate EGUs to address public health and 

environmental hazards associated with emissions of Hg and 

Non-Hg HAP from EGUs, EPA determined that the Hg Risk TSD

supporting EPA’s 2011 review of U.S. EGU health impacts 

should be peer-reviewed.”8 We also indicated that due to the 

court-ordered schedule for the final rule, we would conduct 

the peer review as expeditiously as possible after issuance 

of the proposed rule, and that the results of the peer 

review and any EPA response would be published before the 

final rule.

 

8 76 FR 25012
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We have completed the peer review of the Hg Risk TSD, 

which is fully documented in the revised Technical Support 

Document (TSD): National-Scale Assessment of Hg Risk to 

Populations of High Consumption of Self-Caught Fish In 

Support of the Appropriate and Necessary Finding for Coal 

and Oil-Fired Electric Generating Units.

9 The following 

sections describe the peer review process that we followed, 

provide the peer review charge questions presented to the 

peer review panel, summarize the key recommendations from 

the peer review, and summarize our responses to those 

recommendations.

1. Summary of Peer Review Process

Peer review is consistent with EPA’s routine open and 

transparent process to ensure that the Agency’s scientific 

assessments and rulemakings are based on the best science 

available. This regulatory action was supported by the Hg

Risk TSD, which is a highly influential scientific 

assessment. Therefore, EPA conducted a peer review in 

accordance with OMB’s Final Information Quality Bulletin 

 

9 U.S. EPA, 2011a.
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for Peer Review10 as described below. All the materials 

related to the peer review, including the SAB’s final

report, can be found in the docket for this rulemaking.

EPA commissioned the peer review through EPA’s Science 

Advisory Board (SAB), which provides independent advice and 

peer review to EPA's Administrator on the scientific and 

technical aspects of environmental issues. The SAB convened

a 22-member peer review committee. The SAB process for 

selecting the panel began with two Federal Register Notices 

requesting nominations for the Mercury Review Panel11. Based 

on nominations received, a list of potential panel members, 

along with bio-sketches, was posted for public comment on 

the SAB website on April 15, 2011. The members of the 

Mercury Review Panel were announced on May 24, 2011. The 

membership of the panel included representatives of 16 

academic institutions, four state health or environmental 

agencies, one federal agency, and one utility industry 

 

10 Office of Management and Budget (OMB). 2004. Final Information 

Quality Bulletin for Peer Review. December. Available on the Internet 

at http://www.whitehouse.gov/omb/memoranda_fy2005_m05-03. 

11 76 FR 10896 and 76 FR 17649. The first notice requested nominations 

to a Clean Air Scientific Advisory Committee (CASAC) panel. Upon review 

of the scope of the CASAC charter (resulting from a public comment 

received in response to the first notice), the SAB determined that it 

would be more appropriate to form a panel under the SAB, rather than 

CASAC. The second notice announced this change and requested 

nominations for the SAB panel.
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organization12. The panel held a public meeting in Research 

Triangle Park, NC on June 15-17, 2011, which included the 

opportunity for public comment on the Hg Risk TSD and the 

peer review process13. At the June 15-17 public meeting, the 

panel completed a draft peer review report. The minutes of 

that meeting and the draft peer review report were posted 

to the SAB public website within the public comment period 

for the proposed rule. The panel discussed the draft report 

at a public teleconference on July 12, 2011, during which

additional opportunities for public comment were provided14, 

and submitted a revised draft for quality review by the 

Chartered SAB. The Chartered SAB held a public 

teleconference on September 7, 2011 to conduct a quality 

review of the draft report; this teleconference also 

included a final opportunity for public comment15. The SAB

submitted its final report to EPA on September 29, 201116. 

All of the materials discussed at the SAB meetings, 

 

12 The full list of panel members is documented at 

http://yosemite.epa.gov/sab/sabproduct.nsf/0/9F048172004D93BB8525783900

503486/$File/Determination%20memo%20with%20addendum-05.24.11.pdf

13 76 FR 29746

14 76 FR 39102

15 76 FR 50729

16 U.S. Environmental Protection Agency-Science Advisory Board (U.S. 

EPA-SAB). 2011. Peer Review of EPA’s Draft National-Scale Mercury Risk 

Assessment. EPA-SAB-11-017. September. Available on the internet at 

http://yosemite.epa.gov/sab/sabproduct.nsf/BCA23C5B7917F5BF8525791A0072

CCA1/$File/EPA-SAB-11-017-unsigned.pdf. 
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including technical documents, presentations, meeting 

minutes, and draft reports were posted for public access on 

the SAB website and were added to the docket for the final 

rule on October 14, 2011.17

2. Peer Review Charge Questions

EPA asked the SAB to comment on the Hg Risk TSD, 

including the overall design and approach and the use of 

specific models and key assumptions. EPA also asked the SAB 

to comment on the extent to which specific facets of the 

assessment were well characterized in the Hg Risk TSD. The 

specific charge questions are listed below: 

Question 1. Please comment on the scientific 

credibility of the overall design of the mercury risk 

assessment as an approach to characterize human health 

exposure and risk associated with U.S. EGU mercury 

emissions (with a focus on those more highly exposed). 

Question 2. Are there any additional critical health 

endpoint(s) besides IQ loss, which could be quantitatively 

estimated with a reasonable degree of confidence to 

supplement the mercury risk assessment (see section 1.2 of 

the Mercury Risk TSD for an overview of the risk metrics 

 

17 See http://yosemite.epa.gov/sab/sabpeople.nsf/WebCommittees/BOARD
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used in the risk assessment)? 

Question 3. Please comment on the benchmark used for 

identifying a potentially significant public health impact 

in the context of interpreting the IQ loss risk metric 

(i.e., an IQ loss of 1 to 2 points or more representing a 

potential public health hazard). Is there any 

scientifically credible alternate decrement in IQ that 

should be considered as a benchmark to guide interpretation 

of the IQ risk estimates (see section 1.2 of the Mercury 

Risk TSD for additional detail on the benchmark used for 

interpreting the IQ loss estimates)?

Question 4: Please comment on the spatial scale used 

in defining watersheds that formed the basis for risk 

estimates generated for the analysis (i.e., use of 12-digit 

hydrologic unit code classification). To what extent do 

[Hydrologic Unit Code] HUC12 watersheds capture the 

appropriate level of spatial resolution in the relationship 

between changes in mercury deposition and changes in MeHg 

fish tissue levels? (see section 1.3 and Appendix A of the 

Mercury Risk TSD for additional detail on specifying the 

spatial scale of watersheds used in the analysis). 

Question 5: Please comment on the extent to which the 
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fish tissue data used as the basis for the risk assessment 

are appropriate and sufficient given the goals of the 

analysis. Please comment on the extent to which focusing on 

data from the period after 1999 increases confidence that 

the fish tissue data used are more likely to reflect more

contemporaneous patterns of mercury deposition and less 

likely to reflect earlier patterns of mercury deposition. 

Are there any additional sources of fish tissue MeHg data 

that would be appropriate for inclusion in the risk 

assessment? 

Question 6: Given the stated goal of estimating 

potential risks to highly exposed populations, please 

comment on the use of the 75th percentile fish tissue MeHg 

value (reflecting targeting of larger but not the largest 

fish for subsistence consumption) as the basis for 

estimating risk at each watershed. Are there scientifically 

credible alternatives to use of the 75th percentile in 

representing potential population exposures at the 

watershed level? 

Question 7: Please comment on the extent to which 

characterization of consumption rates and the potential 

location for fishing activity for high-end self-caught fish 
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consuming populations modeled in the analysis are supported 

by the available study data cited in the Mercury Risk TSD. 

In addition, please comment on the extent to which 

consumption rates documented in Section 1.3 and in Appendix 

C of the Mercury Risk TSD provide appropriate 

representation of high-end fish consumption by the 

subsistence population scenarios used in modeling exposures 

and risk. Are there additional data on consumption behavior 

in subsistence populations active at inland freshwater 

water bodies within the continental U.S.? 

Question 8: Please comment on the approach used in the 

risk assessment of assuming that a high-end fish consuming 

population could be active at a watershed if the “source 

population” for that fishing population is associated with 

that watershed (e.g. at least 25 individuals of that 

population are present in a U.S. Census tract intersecting 

that watershed). Please identify any additional alternative 

approaches for identifying the potential for population 

exposures in watersheds and the strengths and limitations 

associated with these alternative approaches (additional 

detail on how EPA assessed where specific high-consuming 

fisher populations might be active is provided in section 
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1.3 and Appendix C of the Mercury Risk TSD). 

Question 9: Please comment on the draft risk 

assessment’s characterization of the limitations and 

uncertainty associated with application of the Mercury Maps 

approach (including the assumption of proportionality 

between changes in mercury deposition over watersheds and 

associated changes in fish tissue MeHg levels) in the risk 

assessment. Please comment on how the output of CMAQ

[Community Multiscale Air Quality] modeling has been 

integrated into the analysis to estimate changes in fish 

tissue MeHg levels and in the exposures and risks 

associated with the EGU-related fish tissue MeHg fraction 

(e.g., matching of spatial and temporal resolution between 

CMAQ modeling and HUC12 watersheds). Given the national 

scale of the analysis, are there recommended alternatives 

to the Mercury Maps approach that could have been used to 

link modeled estimates of mercury deposition to monitored 

MeHg fish tissue levels for all the watersheds evaluated? 

(additional detail on the Mercury Maps approach and its 

application in the risk assessment is presented in section 

1.3 and Appendix E of the Mercury Risk TSD). 

Question 10: Please comment on the EPA’s approach of 
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excluding watersheds with significant non-air loadings of 

mercury as a method to reduce uncertainty associated with 

application of the Mercury Maps approach. Are there 

additional criteria that should be considered in including 

or excluding watersheds? 

Question 11: Please comment on the specification of 

the concentration-response function used in modeling IQ 

loss. Please comment on whether EPA, as part of uncertainty 

characterization, should consider alternative 

concentration-response functions in addition to the model 

used in the risk assessment. Please comment on the extent 

to which available data and methods support a quantitative 

treatment of the potential masking effect of fish nutrients 

(e.g. omega-3 fatty acids and selenium) on the adverse 

neurological effects associated with mercury exposure, 

including IQ loss. (detail on the concentration-response 

function used in modeling IQ loss can be found in section 

1.3 of the Mercury Risk TSD). 

Question 12: Please comment on the degree to which key 

sources of uncertainty and variability associated with the 

risk assessment have been identified and the degree to 

which they are sufficiently characterized. 
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Question 13: Please comment on the draft Mercury Risk 

TSD’s discussion of analytical results for each component 

of the analysis. For each of the components below, please 

comment on the extent to which EPA’s observations are 

supported by the analytical results presented and whether 

there is a sufficient characterization of uncertainty, 

variability, and data limitations, taking into account the

models and data used: mercury deposition from U.S. EGUs , 

fish tissue MeHg concentrations, patterns of Hg deposition 

with HG fish tissue data, percentile risk estimates, and 

number and frequency of watersheds with populations 

potentially at risk due to U.S. EGU mercury emissions. 

Question 14: Please comment on the degree to which the 

final summary of key observations in Section 2.8 is 

supported by the analytical results presented. In addition, 

please comment on the degree to which the level of 

confidence and precision in the overall analysis is 

sufficient to support use of the risk characterization 

framework described on page 18.

3. Summary of Peer Review Findings and Recommendations
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The SAB was generally supportive of EPA’s approach.18

The SAB concluded, “[i]n summary, based on its review of 

the draft Technical Support Document and additional 

information provided by EPA representatives during the 

public meetings, the SAB supports the overall design of and 

approach to the risk assessment and finds that it should

provide an objective, reasonable, and credible 

determination of the potential for a public health hazard 

from mercury emitted from U.S. EGUs.”

19 The SAB further 

concluded, “[t]he 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.”20

The SAB report contained many recommendations for 

improving the Hg Risk TSD, which the SAB organized into 

three general themes: (1) improve the clarity of the Hg

Risk TSD regarding methods and presentation of results, (2) 

expand the discussion of sources of variability and 

 

18 U.S. EPA-SAB, 2011.

19 Id.

20 Id.
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uncertainty, and (3) de-emphasize IQ loss as an endpoint. 

In the following section, we provide EPA’s response to 

these recommendations.

4. EPA Responses to Peer Review Recommendations

In response to the peer review, EPA has substantially 

revised the Hg Risk TSD. The revised Hg Risk TSD addresses 

all of the recommendations from the SAB peer review panel 

and includes a detailed list of the specific revisions made 

to the Hg Risk TSD. Revisions in response to the main 

recommendations are summarized below. Italicized statements 

are the SAB’s recommendations, followed by EPA’s response.

 The watershed-focus of the Hg Risk TSD should be 

clearly stated early in the introduction to the 

document. We have stated clearly in the introduction 

to the revised Hg Risk TSD that the focus of the 

analysis is on scenarios of high fish consumption by 

subsistence level fishing populations, assessed at 

watersheds where there is the potential for such

subsistence fishing activity. Specifically, we modeled

risk for a set of subsistence fisher scenarios at 

those watersheds where (a) we have measured fish 

tissue Hg data and (b) it is reasonable to assume that 
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subsistence-level fishing activity could occur. We 

emphasize the point that the analysis is not a 

representative population-weighted assessment of risk. 

Rather, it is based on evaluating these potential 

exposure scenarios.

 Because IQ does not fully capture the range of 

neurodevelopmental effects associated with Hg 

exposure, analysis of this endpoint should be 

deemphasized (and moved to an appendix) and primary 

focus should be placed on the MeHg RfD-based hazard 

quotient metric. We modified the structure of the 

Revised Hg Risk TSD accordingly.

 Clarify the rationale for using an Hazard Quotient

(HQ) at or above 1.5 as the basis for selecting 

potentially impacted watersheds. The SAB fully 

supported using HQ as the risk metric, but we revised 

the discussion in the Hg Risk TSD to clarify why we 

selected 1.5 as the benchmark. Reflecting precedent in 

interpreting HQ estimates, we clarified that exposures 

above the RfD (i.e., an HQ above one) represent a 
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potential public health hazard.

21 We further clarified 

that the HQ is calculated to only one significant 

digit, based on the precision in the underlying RfD 

calculations. As a result, rounding convention 

requires that any values at or above 1.5 be expressed 

as an HQ of 2, while any values below 1.5 (e.g. 1.49)

be rounded to an HQ of 1. Thus, exposures at or above 

1.5 are considered above the RfD and represent a 

potential public health hazard.

 Regarding the fish tissue dataset used in the Hg Risk 

TSD, clarify which species of Hg is reflected in the 

underlying samples and discuss the implications of 

differences across states in sampling protocols in 

introducing bias into the analysis. We clarified that 

in most cases, the fish tissue is measured for total 

Hg. Furthermore, based on the literature22, it is 

reasonable to assume that more than 90 percent of fish 

tissue Hg is MeHg. Therefore, we incorporated an Hg 

 

21 As stated in the preamble to the proposal, based on the current 

literature, exposures above the RfD contribute to risk of adverse 

effects.

22 See the literature summary in Chapter 4 of U.S. EPA. 2000. Guidance 

for Assessing Chemical Contaminant Data for Use in Fish Advisories. 

Office of Science and Technology, Office of Water, Washington, DC. EPA 

823-B-00-007.
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conversion factor23 into our exposure calculations to 

account for the fraction of total Hg that is MeHg in 

fish. We also expanded the discussion of uncertainty 

to address the potential for different sampling 

protocols across states to introduce bias into the Hg 

Risk TSD.

 Additional detail should be provided on the 

characteristics of the fish tissue Hg dataset, 

including its derivation and the distribution of 

specific attributes across the dataset (e.g., number 

of fish tissue samples and number of different 

waterbodies in a watershed, number of species 

reflected across watersheds). We included additional 

figures and tables describing the derivation of the 

watershed-level fish tissue Hg dataset, including the 

filtering steps applied to the original water body 

level data and the additional steps taken to generate 

the watershed-level fish tissue Hg percentile 

estimates. In addition, we included tables summarizing 

 

23 In the March Hg Risk TSD, we assumed that 100 percent of Hg in fish 

was MeHg. We derived the 0.95 conversion factor for the Revised Hg Risk 

TSD to reflect that most studies show that more than 90 percent of 

total Hg in fish is MeHg. See Chapter 4 of U.S. EPA, 2000.
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key attributes of the dataset (e.g., distribution of 

fish tissue sample size and number of species across 

the watershed-level estimates). 

 Determine whether there is additional (more recent) 

fish tissue data for key states including 

Pennsylvania, New Jersey, Kentucky and Illinois where 

U.S. EGUs Hg deposition may be more significant. We 

expanded the fish tissue dataset by incorporating 

additional fish tissue data from the National Listing 

of Fish Advisories (NLFA), which included additional 

data for four states (MI, NJ, PA, and MN). We also 

obtained additional data for Wisconsin. This 

additional data expanded the number of watersheds in 

the analysis from 2,317 to 3,141, an increase of 36 

percent. The additional watersheds improve coverage in

areas with high levels of U.S. EGU-attributable Hg 

deposition, and thus increase our confidence in the 

overall results of the Hg Risk TSD.

 Include additional discussion of the potential that 

the low sampling rates reflected across many of the 

watersheds may low-bias the 75th percentile fish tissue 

Hg estimates used in estimating potential exposures. 
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In addition, include a sensitivity analysis using the 

50th percentile estimates to provide a bound on the 

risk. The SAB expressed support for the use of the 75th

percentile fish tissue Hg value in the Hg Risk TSD, 

while recommending additional discussion of the issue. 

We provided additional description of the fish tissue 

dataset, including distribution of sample sizes and 

fish species across the watersheds, and an improved 

discussion of uncertainty and potential low bias 

resulting from estimation of the 75th percentile fish 

tissue levels. We also included a sensitivity analysis 

that used the 50th percentile watershed-level fish 

tissue Hg level. This sensitivity analysis showed that 

using the 50th percentile estimates resulted in a 

decrease in the number and percentage of modeled

watersheds with populations potentially at-risk from 

U.S. EGU-attributable MeHg exposures, from 29 percent 

in the revised Hg Risk TSD to 26 percent in the 

sensitivity analysis in the revised Hg Risk TSD.

 Expand the discussion of caveats associated with the 

fish consumption rates used in the analysis. The SAB 

was generally supportive of the consumption rates 
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used, while recommending additional discussion of 

caveats. We expanded the discussion of uncertainty 

related to the fish consumption rates to address the 

caveats identified by the SAB. The uncertainty 

discussion now explains 1) that high-end consumption 

rates for South Carolina reflect small sample sizes, 

and therefore may be more uncertain, 2) that the 

consumption surveys underlying the studies are older 

(i.e., mostly based on survey data from the 1990s) and 

behavior may have changed (i.e., consumption rates may 

have changed since the surveys were conducted), and 3) 

that consumption rates used in the Hg Risk TSD are 

annualized rather than seasonal rates and thus 

contribute little to overall uncertainty. None of 

these sources of uncertainty is associated with a 

particular directional bias (e.g., neither 

systematically higher nor lower risk).

 Verify whether the consumption rates are daily values 

expressed as annual averages and whether they are “as 

caught” or “as prepared.” We carefully reviewed the 

studies underlying the fish consumption rates used in 

the Hg Risk TSD and verified that the rates are annual
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averages of the daily consumption rates and that they 

represent as prepared estimates. We also expanded the 

explanation of the exposure calculations to describe 

more completely the exposure factors and equation used 

to generate the average daily MeHg intake estimates 

for the subsistence scenarios. 

 Explain the criteria for exclusion of fish less than 7 

inches in length from analysis. We provided the 

rationale for the 7-inch cutoff for edible fish used

in the Hg Risk TSD. Seven inches represents a minimum 

size limit for a number of key edible freshwater fish 

species established at the state level. For example, 

Pennsylvania establishes 7 inches as the minimum size 

limit for both trout and salmon (other edible fish 

species such as bass, walleye and northern pike have 

higher minimum size limits). The impact of the 7-inch 

cutoff is likely to be quite small, as only 6 percent 

of potential fish samples were excluded due to this 

criterion.

 Identify the number of watersheds excluded from the 

analysis due to the criterion for excluding watersheds 

with less than 25 members of a source population. The 
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SAB was generally supportive of the approach used for 

identifying watersheds with the potential for 

subsistence activity, while recommending additional 

information on the results of applying the approach. 

We added a figure to illustrate the number of 

watersheds with fish tissue Hg data used to model risk 

for each of the subsistence fishing scenarios. For all 

scenarios except the female subsistence fishing 

scenario, the exposure scenarios significantly limited

the number of watersheds. Because the female 

subsistence fishing scenario does not differentiate

with regard to ethnicity or socio-economic 

status(SES), we applied this scenario to all regions 

of the country and to all watersheds with fish tissue 

Hg data. This reflects our assumption that, given the 

generalized nature of the female subsistence fishing

scenario, it is reasonable to assume that it could 

potentially occur at any watershed with fish tissue Hg 

data. The female subsistence fishing scenario included 

in the revised risk assessment is similar to the highconsuming female scenario included in the Hg Risk 
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TSD.24 However, the female subsistence fishing scenario 

is applied to all watersheds, while in the scenario 

for the high-consuming low-income female angler, we 

only evaluated watersheds with a population of at 

least 25 low-income females. The female subsistence

fishing scenario provides greater coverage 

geographically than the high-consuming low-income 

female scenario.

 Enhance the discussion of the assumption of a linear 

relationship between changes in Hg deposition and 

changes in fish tissue Hg at the watershed level, 

including providing citations to more recent studies 

supporting the proportional relationship between 

changes in Hg deposition and changes in MeHg fish 

tissue levels. The SAB supported the assumption of a 

linear relationship between changes in Hg deposition 

and changes in fish tissue Hg at the watershed level, 

while recommending additional supporting language. We 

expanded our discussion of the scientific basis for 

the proportionality assumption and added citations for 

 

24 In the Revised Mercury Risk TSD, this population is also referred to 

as the “typical female subsistence consumer”. 
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the more recent studies supporting the assumption. We 

also expanded the discussion of uncertainties 

associated with this assumption, including 

uncertainties related to the potential for sampled 

fish tissue Hg level to reflect previous Hg 

deposition, and the potential for non-air sources of 

Hg to contribute to sampled fish tissue Hg levels. 

Each of these sources of uncertainty may result in 

potential bias in the estimate of exposure associated 

with current deposition. If the fish tissue Hg levels 

are too high due to either previous Hg deposition or 

non-air sources of Hg, then the absolute level of 

exposure attributed to both total Hg deposition and 

U.S. EGU-attributable Hg deposition will be biased 

high. However, the percent contribution from U.S. EGUs 

will not be affected as it depends entirely on 

deposition. EPA took steps to minimize the potential 

for these biases by 1) only using fish tissue Hg 

samples from after 1999, and 2) screening out 

watersheds that either contained active gold mines or 

had other substantial non-U.S. EGU anthropogenic 

emissions of Hg. The SAB concluded that EPA’s approach 
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to minimizing the potential for these biases to affect 

the results of the Hg Risk TSD is sound. In addition, 

we conducted several sensitivity analyses to gauge the 

impact of excluding watersheds with the potential for 

non-EGU Hg emissions. We found that the estimates of 

the percent of modeled watersheds with populations 

potentially at-risk were largely insensitive to these 

exclusions, suggesting that any potential biases from 

including watersheds with potential non-air Hg 

loadings are likely to be small.

 Additional sources of variability should be discussed 

in terms of the degree to which they are reflected in 

the design of the risk assessment and the impact that 

they might have on risk estimates. These include: 1) 

the geographic patterns of populations of subsistence 

fishers, including how this factor interacts with the 

limited coverage we have for watersheds with our fish 

tissue Hg data, 2)the protocols used by states in 

collecting fish tissue Hg data, 3) body weights for 

subsistence fishing populations and the impact that 

this might have on exposure estimates, and 4) 

preparation and cooking methods which affect the 
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conversion of fish tissue Hg levels (as measured) into 

“as consumed” values. We expanded the discussion of 

sources of variability in the revised Hg Risk TSD to 

more fully address these sources of variability. The 

Hg Risk TSD quantitatively reflected many aspects of 

variability, including spatial and temporal 

variability in Hg emissions, Hg deposition, fish 

tissue Hg levels, and subsistence behavior. We do not 

believe that the aspects of variability assessed 

qualitatively in the Hg Risk TSD such as temporal 

response in fish tissue would substantially change the 

risk results given the stated goal of the analysis.

 Additional sources of uncertainty should be discussed 

in terms of their potential impact on risk estimates. 

These include: 1) emissions inventory used in 

projecting total and U.S. EGU-attributable Hg 

deposition, including the projection of reductions in 

U.S. EGU emissions for the 2016 scenario, 2) air 

quality modeling with CMAQ including the prediction of 

future air quality scenarios, 3) ability of the 

Mercury Maps-based approach for relating Hg deposition 

to MeHg in fish to capture Hg hotspots, 4) the limited 
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coverage that we have with fish tissue Hg data for 

watersheds in the U.S. and implications for the Hg 

Risk TSD, 5) the preparation factor used to estimate 

“as consumed” fish tissue Hg levels, 6) the 

proportionality assumption used to relate changes in 

Hg deposition to changes in fish tissue Hg levels at 

the watershed-level, 7)characterization of the spatial 

location of subsistence fisher populations (including 

the degree to which these provide coverage for highconsuming recreational fishers), and 8) application of 

the RfD to low SES populations and concerns that this 

could low-bias the risk estimates. We expanded the 

discussion of sources of uncertainty presented in the 

revised TSD to address more fully these sources of 

uncertainty and the potential impact on risk 

estimates. Regarding these eight additional sources of 

uncertainty, we have 1) evaluated the uncertainties in 

the emissions and determined that while an important 

source of uncertainty, we are not able to quantify 

emissions uncertainty in the risk analysis, but have 

determined that the emissions inventories and 

emissions models represent the best available methods 
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for predicting Hg emissions in the U.S., 2) evaluated 

the uncertainties in the Hg deposition predictions and 

determined that while an important source of 

uncertainty, we are not able to quantify uncertainty 

in Hg deposition in the Hg Risk TSD, but the CMAQ

model used to estimate deposition is based on peer 

reviewed science and represents the best available 

method for predicting Hg deposition in the U.S., 3) 

evaluated the ability of the Mercury Maps-based 

approach for relating Hg deposition to MeHg in fish to 

capture Hg hotspots and determined that while finer 

resolution deposition modeling might reveal additional 

areas with elevated deposition, the 12 km deposition 

modeling matches well with the watershed size selected 

for the analysis, and thus the use of 12 km deposition 

estimates with the Mercury Maps based approach will 

not be a large source of uncertainty, 4)evaluated the 

limited coverage that we have with fish tissue Hg data 

for watersheds in the U.S. and implications for the Hg 

Risk TSD and based on the SAB’s recommendations, we 

supplemented the coverage of watersheds by obtaining 

additional fish tissue Hg samples for areas heavily 
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impacted by U.S. EGU deposition, thus reducing the 

uncertainty in the analysis 5) evaluated the 

uncertainty in the preparation factor and determined 

that the level of uncertainty is low, and as such 

would have minimal impact on the risk estimates, 6)

evaluated the uncertainty resulting from the 

proportionality assumption used to relate changes in 

Hg deposition to changes in fish tissue Hg levels at 

the watershed-level, and determined, based both on 

quantitative sensitivity analyses and qualitative 

assessments, that this source of uncertainty is not 

likely to greatly influence the results, and is not 

likely to have a specific directional bias, 7) 

evaluated the uncertainty related to characterization 

of the spatial locations of subsistence populations 

and determined that uncertainty could be reduced by 

focusing the risk estimates on female subsistence 

fishing populations, which are assumed to have the 

potential to fish in all watersheds, and 8) evaluated

the potential impact of the uncertainty in application 

of the RfD to low SES populations, and determined that 

due to the method used in calculating the RfD, have 
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confidence that the RfD may coverage for low SES 

populations.

 Expand the sensitivity analyses (over those included 

in the original risk assessment) to address 

uncertainty related to the use of the 75th percentile 

fish tissue Hg value (at each watershed) as the core 

risk estimate. Based on the SAB’s recommendation, we

added a sensitivity analysis using the median fish 

tissue Hg estimate (at the watershed level). This 

sensitivity analysis showed that use of the median 

fish tissue Hg concentration instead of the 75th

percentile resulted in only a small decrease in the 

estimates of risk.

C. Summary of Results of Revised Hg Risk TSD of Risks to 

Populations with High Levels of Self-Caught Fish 

Consumption

Based on the recommendations we received from the SAB, 

we revised the quantitative analysis of risk to subsistence 

fishing populations with high levels of fish consumption. 

Our revision to the quantitative risk results reflects 

three key recommendations from the SAB, including 1) 

addition of 824 watersheds based on additional fish tissue 
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Hg sample data we obtained from states and the National 

Listing of Fish Advisories, 2) application of a 0.95 

adjustment factor to the reported fish tissue Hg 

concentrations to account for the fraction that is MeHg, 

and 3) inclusion of all watersheds with fish samples that 

meet the filtering criteria25 in representing potential 

risks for low income female subsistence fishing 

populations. Based on these revisions, our estimates of the 

number and percent of modeled watersheds with populations 

potentially at-risk from exposure to EGU-attributable MeHg 

changed from those presented in the preamble to the 

proposed rule. For the 99th percentile consumption scenario, 

the number of watersheds with fish tissue Hg samples where 

subsistence fishing populations may be at-risk from 

exposure to EGU-attributable MeHg increased from 672 to 917 

(an increase of 36 percent). For this same scenario, the 

percent of modeled watersheds with populations potentially

at-risk increased from 28 percent to 29 percent. For the 

95th percentile consumption scenario, the percent of modeled 

watersheds with populations potentially at-risk has 

 

25 The watersheds were filtered to exclude watersheds that: (a) were not 

freshwater, (b) did not have fish sampling data since 2000, (c) did not 

have fish larger than 7 inches in length, (d) contained active gold 

mines or (e) had substantial non-air Hg loading.
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increased from 22 percent to 24 percent. The increase in 

the percent of modeled watersheds with populations 

potentially at-risk using the expanded geographic coverage 

of watersheds provides additional confidence that emissions 

of Hg from U.S. EGUs are a hazard to public health.

The additional sensitivity analyses conducted in 

response to the SAB peer review showed that the estimates 

of the percent of modeled watersheds with populations 

potentially at-risk are robust to alternative assumptions 

about both the watersheds included in the analysis and the 

selection of the 50th percentile or 75th percentile fish 

tissue Hg level. Sensitivity analyses excluding entire 

states with the potential for historical loadings of Hg 

from non-air sources26 resulted in an increase in the 

percent of modeled watersheds with populations potentially 

at-risk, from 29 percent to 33 percent. Including only 

watersheds in the top 25th percentile of U.S. EGU deposition 

resulted in an increase in the percent of modeled 

watersheds with populations potentially at-risk, from 29 

 

26 The SAB noted that areas with substantially elevated fish tissue Hg 

levels could also be characterized by lakes and rivers with high 

natural methylation rates, and thus some of the states we excluded for 

this sensitivity analysis might not have fish tissue Hg levels that 

reflect non-U.S. EGU Hg loadings.
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percent to 30 percent. Using the 50th percentile fish tissue 

Hg level resulted in a decrease in the percent of modeled 

watersheds with populations potentially at-risk, from 29 

percent to 26 percent. On balance, these sensitivity 

analyses do not substantially reduce the percent of modeled 

watersheds with populations potentially at-risk, and thus

confirm the finding that Hg emissions from U.S. EGUs are a 

hazard to public health. In fact, given the broader 

coverage of modeled watersheds in the revised analysis, we 

have greater confidence in our finding that U.S. EGU Hg 

emissions result in deposition that causes a hazard to 

public health.

D. Peer Review of the Approach for Estimating Cancer Risks 

Associated with Cr and Ni Emissions in the U.S. EGU Case 

Studies of Cancer and Non-Cancer Inhalation Risks for NonHg HAP and EPA Response

As explained in the preamble to the proposed rule, EPA 

determined to peer review its characterization of the 

chemical speciation for the emissions of Cr and Ni used in 

the non-Hg HAP inhalation risk case studies. The Agency 

determined that the remaining aspects of the non-Hg HAP 

case study risk assessments used methods that were already 
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been subject to adequate peer review. The methodologies 

used to conduct those risk assessments were consistent with 

those used to conduct inhalation risk assessments under

EPA’s Risk and Technology Review (RTR) program. Because the 

RTR assessments are considered to be highly influential 

science assessments, the methodologies used to conduct them 

were subject to a peer review by the SAB in 2009. The SAB 

issued its peer review report in May 2010.27 The report 

endorsed the risk assessment methodologies used in the 

program, and made a number of technical recommendations for 

EPA to consider as the RTR program evolves.

EPA’s case studies identified Cr and Ni emissions as 

the key drivers of the estimated inhalation cancer risks 

for EGUs. Because these results hinged on specific 

scientific interpretations of data used to characterize EGU 

emissions of Cr and Ni, EPA conducted a letter peer review 

of its analysis and interpretation of those data relative 

to the quantification of inhalation risks associated with 

 

27 U.S. Environmental Protection Agency – Science Advisory Board (U.S. 

EPA-SAB). 2010. Review of EPA’s draft entitled, “Risk and Technology 

Review (RTR) Risk Assessment Methodologies: For Review by the EPA’s 

Science Advisory Board with Case Studies – MACT I Petroleum Refining 

Sources and Portland Cement Manufacturing”. EPA-SAB-10-007. May. 

Available on-line at: 

http://yosemite.epa.gov/sab/sabproduct.nsf/4AB3966E263D943A8525771F0066

8381/$File/EPA-SAB-10-007-unsigned.pdf
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Cr and Ni emissions from U.S. EGUs . The following sections 

describe the peer review process, enumerate the peer review 

charge questions presented to the peer review panel, 

summarize the key recommendations from the peer review, and 

summarize our responses to those recommendations.

1. Summary of Peer Review Process

EPA asked three independent, external peer reviewers 

representing government, academic and the private sector to 

review of the methods for developing inhalation cancer risk 

estimates associated with emissions of Cr and Ni compounds 

from coal- and oil-fired EGUs in support of the appropriate 

and necessary finding. The approaches and rationale for the 

technical and scientific considerations used to derive 

inhalation cancer risks were summarized in the draft 

document entitled, “Methods to Develop Inhalation Cancer 

Risk Estimates for Chromium and Nickel Compounds.” The peer 

reviewers received several charge questions (three 

questions on Cr and two questions on Ni, which are provided 

below) on the technical and scientific relevance of the 

approaches used to develop the inhalation unit risk 

estimates. EPA also provided information on Cr speciation 

profiles for different industrial sources, as well as 
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information on the Ni speciation of particulate matter from 

oil-fired power plants.

2. Peer Review Charge Questions

Below we present the charge questions posed to the 

peer reviewers to help guide their review and development 

of recommendations to EPA on key issues relevant to the 

characterization of risks from EGU emissions containing 

either Cr or Ni compounds. 

EPA asked three questions regarding Cr and Cr

compounds:

Question 1: Do EPA’s judgments related to speciated 

chromium emissions adequately take into account the 

available chromium speciation data? 

Question 2: Has EPA selected the species of chromium 

(i.e., hexavalent chromium) that accurately represents the 

toxicity of chromium and chromium compounds? 

Question 3: Are the assumptions used in past analysis 

scientifically defensible, and are there alternatives that 

EPA should consider for future analysis? 

EPA asked two questions regarding Ni and Ni compounds:

Question 1: Do EPA's judgments related to speciated 

nickel emissions adequately take into account available 
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speciation data, including recent industry spectrometry 

studies?

Question 2: Based on the speciation information 

available and on what we know about the health effects of 

nickel and nickel compounds, and taking into account the 

existing Unit Risk Estimates (URE) values (i.e., values 

derived for EPA’s Integrated Risk Information System 

(IRIS), California Environmental Protection Agency (Cal 

EPA) and Texas Commission on Environmental Quality (TCEQ)), 

EPA has provided several approaches28 to derive unit risk 

estimates that may be more scientifically defensible than 

those used in past analyses. Which of the options presented 

would result in more accurate and defensible 

characterization of risks from exposure to nickel and 

nickel compounds? Are there alternative approaches that EPA 

should consider?

3. Summary of Peer Review Findings and Recommendations

Regarding Cr and Cr compounds, all three reviewers 

considered hexavalent Cr as the species likely to be 

driving cancer risks based on solid evidence from the 

 

28 See section 3.3 of U.S. Environmental Protection Agency (U.S. EPA). 

2011c. Methods to Develop Inhalation Cancer Risk Estimates for Chromium 

and Nickel Compounds. Office of Air Quality Planning and Standards.

October.
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health effects database for Cr and Cr compounds. All three 

authors also considered EPA’s use of the average of the 

range of the available speciation data (i.e., 12 percent 

and 18 percent hexavalent Cr contained in coal- and oilfired EGUs, respectively) as a reasonable approach for the 

derivation of default speciation profiles to be used when 

there is no speciation data available. All reviewers agreed 

that there is high uncertainty associated with the 

variability in the speciation data available for Cr (e.g., 

range of approximately 4 to 23 percent hexavalent Cr from 

coal-fired units). One of the reviewers recommended several 

additional studies for EPA’s consideration; EPA considered 

these in finalizing the report. 

Regarding Ni and Ni compounds, the reviewers agreed 

with the views of the international scientific bodies, 

which consider Ni compounds carcinogenic as a group. One

reviewer recommended that EPA review several additional Ni

speciation data that suggests that sulfidic Ni compounds 

(which the reviewer considered as the most potent 

carcinogens within the group of all Ni compounds) are 

present at low levels in emissions from EGUs. In addition, 

this reviewer pointed out that there is a recently proposed 
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model that may explain the differences in carcinogenic 

potential across Ni compounds.

4. EPA Responses to Peer Review Recommendations

We summarize EPA’s basic responses to the peer review 

comments below, first for Cr-related issues, and second for 

Ni-related issues, which are reflected in the revised 

document.

34

a. Cr and Cr compounds:

In agreement with the peer reviewers and based on the 

health effects information available for Cr, EPA assigns

high confidence in the assumption that hexavalent Cr is the 

carcinogenic species driving the risk of Cr-emitting 

facilities. In agreements with the reviews, EPA considers

derivation of default speciation profiles based on the mass 

of hexavalent Cr a reasonable approach. As suggested by one 

of the reviewers, EPA reviewed two potentially relevant 

studies, one of which showed coal combustion emissions 

containing as much as 43 percent hexavalent Cr35, which 

suggests that EPA's quantitative approach could actually

underestimate hexavalent Cr inhalation risks. However, the 

 

34 U.S. EPA, 2011c.

35 Galbreath KC, Zygarlicke CJ. 2004. “Formation and chemical speciation 

of arsenic-, chromium-, and nickel-bearing coal combustion PM2.5,” Fuel 

Process Technol 85:701-726.
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other study reviewed by EPA on speciation of Cr in coal 

combustion showed hexavalent Cr percentage levels close to 

detection limits (i.e., three to five percent of total Cr, 

which was close to limit of detection in this study).36

Thus, the more recent speciation data available is unlikely 

to reduce the uncertainty of the Cr speciation analyses 

used by EPA as the bases for risk characterization 

analysis.

In agreement with the peer reviewers, EPA also 

recognizes that the confidence in the default speciation 

profiles is low because the profiles are based on a limited 

data set with a wide range of percentages of hexavalent Cr

across the different samples. 

b. Ni and Ni compounds:

Based on the views of the major scientific bodies 

mentioned above and the peer reviewers that commented on 

EPA’s approaches to risk characterization of Ni compounds, 

EPA considers all Ni compounds to be carcinogenic as a

group and, contrary to the point of view expressed by 

representatives of oil-fired EGUS, EPA does not consider Ni

 

36 Huggins FE, Najih M, Huffman GP. 1999. “Direct speciation of chromium 

in coal combustion by-products by X-ray absorption fine structure 

spectroscopy,” Fuel Process Technol 78:233-242.
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speciation or Ni solubility to be strong determinants of Ni

carcinogenicity. These scientific bodies also recognize 

that based on the data available, the precise Ni 

compound(s) responsible for the carcinogenic effects in 

humans is not always clear, and that there may be 

differences in the potential toxicity and carcinogenic 

potential across Ni compounds. Nevertheless, studies in 

humans indicate that various mixtures of Ni compounds 

(including Ni sulfate, sulfides and oxides, alone or in 

combination) encountered in the Ni refining industries may 

cause cancer in humans, and there is no reason to expect 

anything different from this for mixtures of nickel 

compounds from other emission sources. One of the reviewers 

suggested we consider views by some authors that believe 

that water soluble Ni, such as Ni sulfate, should not be 

considered a human carcinogen. This view is based primarily 

on a negative Ni sulfate 2-year NTP rodent bioassay (which 

is different from the positive 2-year NTP bioassay for Ni

subsulfide).37,38,39 One review article identifies the 

 

37 Oller A. 2002. “Respiratory carcinogenicity assessment of soluble 

nickel compounds.” Environ Health Perspect. 110:841-844.

38 Heller JG, Thornhill PG, Conard BR. 2009. “New views on the hypothesis 

of respiratory cancer risk from soluble nickel exposure; and 
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discrepancies between the animal and human data (i.e., from 

studies of cancers in workers inhaling certain forms of Ni

versus inhalation studies suggesting different carcinogenic 

potential in rodents with different Ni compounds) and 

states that the epidemiological data available clearly 

support an association between Ni and increased cancer 

risk, although the article acknowledges that the data are 

weakest regarding water soluble Ni. In addition, EPA 

identified a recent review40 that 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. 

Regarding the second charge question on Ni compounds, 

two reviewers suggested using the URE derived by the TCEQ41

for all Ni compounds as a group, rather than the one 

derived by the Integrated Risk Information System (IRIS, 

 

reconsideration of this risk's historical sources in nickel 

refineries.” J Occup Med Toxicol. 4:23.

39 Goodman JE, Prueitt RL, Thakali S, and Oller AR. 2011. “The nickel 

iron bioavailability model of the carcinogenic potential of nickelcontaining substances in the lung.” Crit Rev Toxicol 41:142-174.

40 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.

41 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
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1991)42 specifically for Ni subsulfide. The third reviewer 

did not comment on an alternative approach. Considering 

this, EPA decided to use a health protective approach by 

applying 100 percent of the current IRIS URE for Ni

subsulfide, rather than assuming that 65 percent of the 

total mass of emitted Ni might be Ni subsulfide, as used in 

previous analyses. We used the IRIS URE value because IRIS 

values are preferred given the conceptual consistency with 

EPA risk assessment guidelines and the level of peer review 

that such values receive. We used 100 percent of the IRIS 

value because of the concerns about the potential 

carcinogenicity of all forms of Ni raised by the major 

national and international scientific bodies, and 

recommendations of the peer reviewers. Nevertheless, taking 

into account that there are potential differences in 

toxicity and/or carcinogenic potential across the different 

Ni compounds, and given that two URE values have been 

derived for exposure to mixtures of Ni compounds that are

two to three fold lower than the IRIS URE for Ni

subsulfide, EPA also considers it reasonable to use a value 

 

42 U.S. EPA, 1991. Integrated Risk Information Service (IRIS) assessment 

for nickel subsulfide. Available at: 

http://www.epa.gov/iris/subst/0273.htm.
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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.

Although this report focused primarily on cancer risks 

associated with emissions containing Ni compounds, it is 

important to note that comparative quantitative analyses of 

non-cancer toxicity of Ni compounds indicate that Ni

sulfate is as toxic or more toxic than Ni subsulfide or Ni

oxide which does not support the notion that the solubility 

of Ni compounds is a strong determinant of its toxicity.43,44

E. Summary of Results of Revised U.S. EGU Case Studies of 

Cancer and Non-Cancer Inhalation Risks for Non-Hg HAP 

Based on the results of the peer review and public 

comments on the non-Hg case study chronic inhalation risk 

assessment, we made several changes to the emissions 

estimates, dispersion modeling, and risk characterization 

for the modeled case study facilities. Key changes include 

 

43 Haber LT, Allen BC, Kimmel CA. 1998. “Non-Cancer Risk Assessment for 

Nickel Compounds: Issues Associated with Dose-Response Modeling of 

Inhalation and Oral Exposures.” Toxicol Sci. 43:213-229.

44 National Toxicology Program (NTP). 1996. Technical Report Series No. 

454, Toxicology and carcinogenesis studies of nickel sulfate 

hexahydrate. July. Available online at 

http://ntp.niehs.nih.gov/ntp/htdocs/LT_rpts/tr454.pdf.
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1) changes in emissions, 2) changes in stack parameters for 

some facilities based on new data received during the 

public comment period, 3) use of updated versions of AERMOD 

and its input processors (AERMAP, AERMINUTE, and AERMET),

and 4) use of 100 percent of the current IRIS URE for Ni

subsulfide to calculate Ni-associated inhalation cancer 

risks (rather than assuming that the Ni might be 65 percent 

as potent as Ni subsulfide). 

Based on estimated actual emissions, the highest 

estimated individual lifetime cancer risk from any of the 

sixteen case study facilities was 20 in a million, driven 

by Ni emissions from the one case study facility with oilfired EGUs. Of the facilities with coal-fired EGUs, five 

facilities had maximum individual cancer risks greater than

one in a million (the highest was five in a million), with 

the risk from four due to emissions of hexavalent Cr and 

the risk from one due to emissions of Ni. There were also 

two facilities with coal-fired EGUs that had maximum 

individual cancer risks equal to one in a million. All of 

the facilities had non-cancer Target Organ Specific Hazard 

Index (TOSHI) values less than one, with a maximum TOSHI 
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value of 0.4 (also driven by Ni emissions from the one case 

study facility with oil-fired EGUs).

Since these case studies do not cover all facilities 

in the category, and since our assessment does not include 

the potential for impacts from different EGU facilities to 

overlap one another (i.e., these case studies only look at 

facilities in isolation), the maximum risk estimates from 

the case studies may underestimate true maximum risks for 

the source category.

Based on the fact that six EGUs were estimated to meet 

or exceed the CAA 112(c)(9) criterion of one in a million, 

EGUs cannot be removed from the list of source categories 

to be regulated under CAA 112.

F. Public Comments and Responses to the Appropriate and 

Necessary Finding

1. Legal Aspects of Appropriate and Necessary Finding

a. History of Section 112(n)(1)(A)

Comment: One commenter provided a detailed history of 

EPA’s regulatory actions concerning EGUs and implementation 

of section 112(n)(1)(A). The same commenter implies that 

EPA’s 2000 appropriate and necessary finding and listing of 

EGUs was flawed because the Agency did not comply with CAA 
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section 307(d) rulemaking process. The commenter sought 

review of the 2000 notice in the U.S. Court of Appeals for 

the District of Columbia Circuit, which was dismissed by 

the D.C. Circuit. Utility Air Regulatory Group v. EPA, No. 

01-1074 (D.C. Cir. July 26, 2001). The commenter then 

characterizes at length the 2005 EPA action that revised 

the interpretation of section 112(n)(1)(A) and, which the 

D.C. Circuit concluded illegally removed EGUs from the 

section 112(c) list of sources that must be regulated under 

section 112. See New Jersey v. EPA, 517 F.3d 574 (D.C. Cir. 

2008). The commenter notes that the D.C. Circuit did not 

rule on the legal correctness or the sufficiency of the 

factual record supporting EPA’s 2000 listing decision or on 

the factual correctness of EPA’s later decision to reverse 

its section 112(n)(1)(A) determination. The commenter noted 

further that the D.C. Circuit indicated that the listing 

decision could be challenged when the Agency issued the 

final section 112(d) standards pursuant to section 

112(e)(4). The commenter concluded by asserting that the 

Agency could not ignore the history associated with the 

regulation of EGUs under section 112 and that two earlier 

dockets - Docket ID. No. A-92-55 and Docket ID. No. EPA-HQ-
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OAR-2002-0056 – are also part of this long rulemaking 

effort and must be accounted for in conjunction with Docket 

No. EPA-HQ-OAR-2009-0234 if all pertinent material and 

comments are to be part of the rulemaking record.

Response: The commenter characterizes the regulatory 

history of the rule EPA proposed on May 3, 2011. To the 

extent that characterization is inconsistent with the 

lengthy regulatory history EPA provided in the preamble to 

the May 3, 2011 rule, we disagree. We address several of 

the statements in more detail below.

First, the commenter makes much of the fact that EPA 

did not go through CAA section 307(d) notice and comment 

rulemaking when making the appropriate and necessary 

finding and listing decision in 2000. However, the 

commenter’s complaint is without foundation. The CAA does 

not require section 307(d) rulemaking for listing 

decisions. In fact, section 112(e)(4) specifically provides 

that listing decisions may only be challenged “when the 

Administrator issues emission standards for such . . . 

[listed] category.” Second, the commenter challenged the 

listing decision in the U.S. Court of Appeals for the 

District of Columbia Circuit (Court) and, on July 26, 2001, 
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the Court granted EPA’s motion to dismiss that action based 

on the plain language of section 112(e)(4). EPA clearly 

articulated its basis for listing EGUs in this proposed 

rule, which is consistent with CAA section 307(d), and the 

commenter was provided an ample opportunity to comment.

Third, the commenter asserts that the rulemaking docket for 

this action is incomplete because the Agency did not 

include two earlier dockets - Docket ID. No. A-92-55 and 

Docket ID. No. EPA-HQ-OAR-2002-0056 - for the Section 

112(n) Revision Rule, 70 F.R. 15994 (March 29, 2005), and 

the reconsideration of the Section 112(n) Revision Rule, 71 

F.R. 33388 (June 9, 2006), respectively. The commenter is 

incorrect because EPA incorporated by reference the two 

dockets at issue. See EPA-HQ-OAR-2009-0234-3056. 

Comment: One commenter stated that EPA has assessed 

the public health risks posed by HAP emissions from coaland oil-fired EGUs for the last 40 years. According to the 

commenter, throughout that time, EPA has come to a single 

repeated conclusion that HAP emissions from EGUs pose 

little or no risk to public health. Based on this 

conclusion, EPA has properly chosen not to require EGUs to 

install expensive, new pollution control equipment to 
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control HAP emissions. The commenter asserts that in this 

proposed rule, EPA shifts its opinion on the health impacts 

of EGU HAP emissions 180 degrees and now seeks to impose 

sweeping regulatory requirements on all power plants. 

According to the commenter, EPA’s newfound concern about 

HAP emissions from EGUs is not based on new and different 

assessments of the public health consequences of EGU HAP 

emissions but instead on health benefits from the reduction 

of non-hazardous air pollutants, primarily PM, which the 

Agency is required to regulate under other provisions of 

the CAA. One commenter stated that for decades, EPA set 

primary ambient air quality standards that protect public 

health with an adequate margin of safety, CAA section 

109(b)(1), and set secondary standards that are [sic] 

“requisite to protect the public welfare from any known or 

anticipated adverse effects associated with the presence of 

such air pollutant in the ambient air,” CAA 109(b)(2). The 

commenter notes that even if EPA now views those past PM 

standards as inadequate, EPA has ongoing regulatory 

proceedings in which it can address any perceived health 

concerns. The commenter concludes that regulation of EGU 
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HAP emissions under 112 is an unlawful way to address those 

concerns. 

Response: The commenter is incorrect in its assertion 

that the Agency has consistently concluded that HAP 

emissions from EGUs do not present a hazard to public 

health. In the 2000 Finding, the Agency concluded that HAP 

emissions from coal- and oil-fired EGUs do pose a hazard to 

public health and determined that it was appropriate and 

necessary to regulate such units under section 112 of the 

CAA. As a result of that finding, EPA added coal- and oilfired EGUs to the CAA section 112(c) list of source 

categories for which emission standards are to be 

established pursuant to section 112(d). Further, in support 

of the proposed rule published in the Federal Register on 

May 3, 2011, EPA conducted additional extensive 

quantitative analyses, which confirm that it remains 

appropriate and necessary to regulate EGUs under CAA 

section 112. Among other things, those analyses demonstrate 

that emissions from coal- and oil-fired EGUs continue to 

pose a hazard to public health. The commenter also fails to 

note that EPA found that HAP emissions from EGUs pose a 

hazard to the environment as well.
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The commenter seems confused about the basis for the 

Agency’s appropriate and necessary finding because it 

maintains that EPA made the appropriate and necessary 

finding based on the health co-benefits attributable to PM 

reductions that will be achieved as a result of the 

Agency’s regulation of HAP emissions from EGUs. Nowhere in 

the May 2011 proposal does EPA state that it based the 

appropriate and necessary finding on hazards to public 

health attributable to PM emissions. The commenter’s 

allegation simply lacks foundation. The proposal 

unmistakably focuses on the hazards to public health 

associated with HAP emissions from EGUs.

Comment: One commenter stated that section 112

required EPA to make a risk-based determination in order to 

regulate HAP. According to the commenter, EPA may regulate 

substances “reasonably ... anticipated to result in an 

increase in mortality or increase in serious illness” to a 

level that protects public health with an “ample margin of 

safety.” According to the commenter, EPA has regulated a 

number of HAP emitted from industrial source categories 

other than EGUs. 
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As for EGUs, according to the commenter, EPA found 

that the combustion of fossil fuels produces extremely 

small emissions of a broad variety of substances that are 

present in trace amounts in fuels and that are removed from 

the gas stream by control equipment installed to satisfy 

other CAA requirements. EPA, in past reviews, found that 

these HAP emissions did not pose hazards to public health. 

See 48 Fed. Reg. 15,076, 15,085 (1983) (radionuclides). In 

the case of Hg specifically, EPA found that “coal-fired 

power plants ... do not emit mercury in such quantities that 

they are likely to cause ambient mercury concentration to 

exceed” a level that “will protect public health with an 

ample margin of safety.” 40 Fed. Reg. 48,297-98 (Oct. 

19,1975) (mercury); 52 Fed. Reg. 8724, 8725 (Mar. 19, 1987) 

(reaffirming mercury conclusion).

In the late 1980s, EPA was concerned that its prior 

risk assessments of individual HAP emissions from fossilfuel-fired power plants may not reflect the total risks 

posed by all HAP emitted by those sources. EPA modeled the 

risks posed by all HAP emitted by power plants (very much 

like the analyses the Agency would conduct for the Utility 

Study ten years later). The commenter asserts that the 
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modeling again failed to identify threats to public health 

that warranted regulation under an “ample margin of safety” 

test.

Response: The commenter’s statements concerning the 

pre-1990 CAA are not relevant to the current action. As the 

commenter notes, Congress enacted CAA section 112(n)(1) as 

part of the 1990 amendments to the Act. That provision 

requires, among other things, that the Agency evaluate the 

hazards to public health posed by HAP emissions from 

fossil-fuel fired EGUs. Had Congress concluded, as 

commenter appears to assert, that HAP emissions from EGUs 

did not pose a hazard to public health or the environment, 

it defies reason that Congress would have required EPA to 

conduct the three studies at issue in section 112(n)(1) 

(titled “Electric utility steam generating units”) and 

regulate EGUs under section 112 if the Administrator 

determined in her discretion that it was appropriate and 

necessary to do so. The Agency complied with the statutory 

mandates in section 112(n)(1) in conducting the studies and 

reasonably exercised its discretion in making the 

appropriate and necessary finding. 
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We acknowledge that Congress treated radionuclide 

emissions from EGUs differently. For radionuclides from 

EGUs (and certain other sources), Congress included CAA 

section 112(q)(3), which authorizes but does not require 

the Agency to maintain the regulations of radionuclides in 

effect prior to the 1990 amendments. The fact that Congress 

made an exception for radionuclides and no other HAP from 

EGUs further demonstrates that the HAP-related actions EPA 

took with regard to EGUs prior to the 1990 amendments to 

the CAA were not germane. 

As for the commenter’s statements about Hg emissions 

from EGUs, we find their conclusions wholly inconsistent 

with CAA section 112(n)(1). That provision is titled 

“Electric utility steam generating units,” and it directs 

EPA to conduct two Hg-specific studies. See CAA sections 

112(n)(1)(B) and 112(n)(1)(C). The commenter’s suggestion 

that EPA could or should rely on assessments of Hg from 

EGUs conducted prior to the 1990 amendments is not tenable. 

Finally, one commenter stated that EPA conducted a 

risk assessment of all HAP from EGUs prior to the 1990 

amendments and that the Agency did not identify any HAP 

that failed the “ample margin of safety” test. The 
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commenter did not cite the study or provide any information 

to support the statements so we are unable to respond to 

the alleged study directly; however, the risk assessments

conducted in support of the appropriate and necessary 

finding, as well as the 2000 finding, demonstrate that HAP 

emissions from EGUs pose hazards to public health and the 

environment.

b. Interpretation of “Appropriate” and “Necessary”

Comment: One commenter stated that in the preamble to 

the proposed rule, EPA sets out its “interpretation of the 

critical terms in CAA 112(n)(1),” arguing that this latest 

interpretation is “wholly consistent with the CAA” and with 

the Agency’s earlier “2000 Finding.” See 76 Fed. Reg. 

24,976, 24,986/2 (May 3, 2011). The commenter stated that 

throughout the proposal EPA tries to suggest that it is 

returning to some earlier, “correct” interpretation of CAA 

section 112(n)(1) set forth in its 2000 action. See, e.g., 

76 Fed. Reg. at 24,989/1-2 (“The Agency’s interpretation of 

the term ‘appropriate’... is wholly consistent with the 

Agency’s appropriate finding in 2000”); id. at 24,992/1 

(“Our interpretation of the necessary finding is reasonable 

and consistent with the 2000 Finding”). According to the 
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commenter, EPA did not provide in 2000 any interpretation 

of what it now characterizes as the “critical terms” of 

section 112(n)(1). See, e.g., 70 Fed. Reg. at 15,999 n.13 

(the “2000 finding does not provide an interpretation of 

the phrase ‘after imposition of the requirements of the 

Act”); id. at 16,000/2 (in 2000, EPA “did not provide an 

interpretation of the term ‘appropriate’”); 76 Fed. Reg. at 

24,992/1 (the “Agency did not expressly interpret the term 

necessary in the 2000 Finding”). The commenter believes 

that for that reason alone, it is impossible to credit 

EPA’s assertion that it “appropriately concluded that it 

was appropriate and necessary to regulate hazardous air 

pollutants . . . from EGUs” in 2000, and that it is today 

merely “confirm[ing] that finding and conclud[ing] that it 

remains appropriate and necessary to regulate these 

emissions...”45

Response: The commenter disagrees with certain 

statements in the preamble to the proposed rule that 

provide that the Agency’s interpretation of section 

112(n)(1) is reasonable and consistent with the 2000

Finding. It is difficult to decipher the exact complaint 

 

45 Id. at 24,977/3.
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that the commenter has with EPA’s proposed rule in this 

regard, but the commenter does assert that “the Agency did 

not provide in 2000 any interpretation of what it now 

characterizes as the “critical terms” of CAA 112(n)(1).”

The commenter’s assertion lacks foundation. While the 2000 

finding did not provide detailed interpretations of the 

regulatory terms at issue, it discussed the types of 

considerations relevant to the A and N inquiry. For 

example, it is clear that the Agency was concerned with the 

then current hazards to public health and the environment 

when assessing whether it was appropriate to regulate EGUs 

under section 112.

46 In addition, when evaluating whether it 

was necessary to regulate utilities, the Agency 

specifically noted that “section 112 is the authority 

intended to address” hazards to public health and the 

environment posed by HAP emissions. Id. 

The detailed interpretation set forth in the preamble 

to the proposed rule is consistent with the 2000 Finding, 

but EPA does not assert that the interpretation is in any 

way necessary to support the factual conclusions reached in 

the 2000 finding. Instead, we noted in the preamble to the 

 

46 65 FR 79830.
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proposed rule that our interpretation is consistent with 

the 2000 Finding because in 2005 we interpreted the statute 

in a manner that was not consistent with the 2000 finding. 

If anything, making an interpretation in 2005 that directly 

contradicted a prior factual conclusion was improper. At 

least one commenter who takes issue with the interpretation 

in the preamble to the proposed rule participated in the 

2005 action and it did not complain at that time about the 

Agency establishing an express interpretation that 

obviously was in conflict with a prior Finding. In any 

case, the commenter has provided no legal support for its 

position that the Agency erred in interpreting the statute 

in a manner that is consistent with a prior factual 

finding. 

Comment: Several commenters stated that a finding that 

HAP regulation is “appropriate” for a single HAP does not 

indicate that it is “appropriate” to regulate all HAP. 

According to the commenters the sponsor of the House bill 

that became section 112(n)(1)(A) provides an explanation 

that contradicts EPA’s approach. “Pursuant to section 

112(n), the Administrator may regulate fossil fuel fired 

electric utility steam generating units only if the studies 
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described in section 112(n) clearly establish that 

emissions of any pollutant, or aggregate of pollutants, 

from such units cause a significant risk of serious adverse 

effects on the public health. Thus, . . . he may regulate 

only those units that he determines – after taking into 

account compliance with all provisions of the act and any 

other Federal, State, or local regulation and voluntary 

emission reductions – have been demonstrated to cause a 

significant threat of serious adverse effects on the public 

health.” 136 Cong. Rec. H12,934 (daily ed. Oct. 26, 1990) 

(statement of Rep. Michael Oxley).

The commenters stated that EPA position is premised on 

the assumption that “regulation under section 112” 

necessarily means “regulation under 112(d)” and falsely 

premised on the assumption that source categories listed by 

operation of section 112(n)(1)(A) cannot be regulated 

differently. The commenters conclude that the language of 

section 112(n)(1)(a) reflects Congress’ intent that 

“regulation of HAP from EGUs was not intended to operate 

under section 112(d) but was instead intended to be 

tailored to the findings of the utility study mandated by

section 112(n)(1)(A).” 
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Response: The commenter maintains that the Agency’s 

interpretation of CAA section 112(n)(1) is flawed in many 

respects. The primary support for commenter’s arguments 

against EPA’s interpretation, including in the comment 

above, is legislative history in the form of statements 

from one Congressman, Representative Oxley. The Supreme 

Court has repeatedly stated that the statements of one 

legislator alone should not be given much weight. See Brock 

v. Pierce County, 476 U.S. 253, 263 (1986) (finding that 

“statements by individual legislators should not be given 

controlling effect, but when they are consistent with the 

statutory language and other legislative history, they 

provide evidence of Congress’ intent.”) (emphasis added) 

(citation omitted); Garcia, et. al., v. U.S., 469 U.S. 70, 

78 (1984), citing Zuber v. Allen, 396 U.S. 168, 187 (1969) 

(reiterating its prior findings, the Court indicated that 

isolated statements “are ‘not impressive legislative 

history.’”); Weinberger, et. al., v. Rossi et. al., 456 

U.S. 25, 35 (declining to make a ruling based on “one 

isolated remark by a single Senator”); Consumer Product 

Safety Comm., et. al. v. GTE Sylvania, Inc., et. al., 447 

U.S. 102, 117-118 (1980) (declining to give much weight to 
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isolated remarks of one Representative); Chrysler Corp. v. 

Brown, et. al., 441 U.S. 281, 311 (1979) (finding that 

“[t]he remarks of a single legislator, even the sponsor, 

are not controlling in analyzing legislative history.”); 

Zuber, 396 U.S. at 186 (concluding that “[f]loor debates 

reflect at best the understanding of individual 

Congressmen.”); and U.S. v. O’Brien, 391 U.S. 367, 384 

(1968) (in evaluating the statements of a handful of 

Congressmen, the Court concluded that “[w]hat motivates one 

legislator to make a speech about a statute is not 

necessarily what motivates scores of others to enact 

it...”).47 As these cases show, the Supreme Court does not

 

47 The D.C. Circuit has similarly refused to rely on such limited 

legislative history, as evidenced by NRDC v. EPA in which that Court 

stated:

It is true . . . that we 'may examine the statute's legislative 

history in order to "shed new light on congressional intent, 

notwithstanding statutory language that appears superficially 

clear."'" Consumer Elecs. Ass'n v. FCC, 358 U.S. App. D.C. 180, 

347 F.3d 291, 298 (D.C. Cir. 2003) (quoting NRA of Am., Inc. v. 

Reno, 342 U.S. App. D.C. 231, 216 F.3d 122, 127 (D.C. Cir. 2000)

(quoting Natural Res. Def. Council, Inc. v. Browner, 313 U.S. 

App. D.C. 37, 57 F.3d 1122, 1127 (D.C. Cir. 1995))). But "'the 

bar is high,'" id. (quoting Williams Cos. v. FERC, 358 U.S. App. 

D.C. 109, 345 F.3d 910, 914 (D.C. Cir. 2003)), and "only rarely 

have we relied on legislative history to constrict the otherwise 

broad application of a statute indicated by its text," id. Here, 

EPA cannot clear the high bar relying solely on the isolated 

remarks of a few senators. Cf. Davis County Solid Waste Mgmt. v. 

EPA, 322 U.S. App. D.C. 107, 101 F.3d 1395, 1407 (D.C. Cir. 1996)

(finding contradictory comments of individual [**23] senators 

during section 129 debates "too 'meager [a] record'" to rely on 

"'given the clear statutory language' to the contrary") (quoting 

Engine Mfrs. Ass'n v. EPA, 319 U.S. App. D.C. 12, 88 F.3d 1075, 
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give any weight to the statements of an individual 

legislator, except when the statements are supported by 

other legislative history and the clear intent of the 

statute. The commenters cited no case law that would 

support any reliance on such limited legislative history. 

We could not find, and the commenter has not cited, 

any other legislative history to support Representative 

Oxley’s statement, and the lack of additional support makes 

the statement of little utility or import under the case 

law. In fact, there does not appear to be anything in the 

House, Senate, or Committee Reports that supports Oxley’s 

statement. The lack of support for Oxley’s statement in the 

Committee Report particularly telling since, as the 

commenter notes, the House and Senate bills required 

different approaches to regulating EGUs under section 112, 

with the Senate bill requiring EGUs be regulated prior to 

the Utility Study. In fact, legislative statements from 

 

1091 (D.C. Cir. 1996)). In any event, the remarks that EPA cites, 

when viewed in the context of the express and unambiguous 

provisions in the statute, show only that when the Congress 

wanted to exempt a particular kind of solid waste combustor from 

section 129's coverage--based on the desirability of resource 

recovery or any other interest--it knew how to accomplish this 

through an express statutory exception and in fact did so for 

four specific classes of combustion units. See 42 USC section

7429(g)(1)

489 F.3d 1250, 1259 (D.C. Cir. 2007).
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Senator Durenberger, a supporter of the Senate version, 

demonstrate that others would almost certainly not have 

agreed with Oxley’s interpretation. For example, Senator 

Durenberger stated, “It seems to me inequitable to impose a 

regulatory regime on every industry in America and then 

exempt one category, especially a category like power 

plants which are a significant part of the air toxics 

problem.”

Senator Durenberger discussed the negotiations with 

the Administration and the industry push to avoid 

regulation, including industry arguments for not regulating 

Hg from U.S. EGUs: “[t]he utility industry continued to 

adamantly oppose [regulation under section 112]. First, 

they argued that mercury isn’t much of an environmental 

problem. But as the evidence mounted over the summer and it 

became clear that mercury is a substantial threat to the 

health of our lakes, rivers and estuaries and that power 

plants are among the principal culprits, they changed their 

tactic. Now they are arguing that mercury is a global 

problem so severe that just cleaning up U.S. power plants 

won’t make enough of a difference to be worth it. They’ve 

gone from “we’re not a problem” to “you can’t regulate us 
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until you address the whole global problem.” Recasting an 

issue that way is not new around here. So, it is not a 

surprise. But it does suggest the direction in which this 

debate will be heading in the next few years.”

Senator Durenberger also explained why the House 

version was adopted: “[g]iven that a resolution of the 

difficult issues in the conference were necessary to 

conclude work on this bill, the Senate proposed to recede 

to the House provision which was taken from the original 

administration bill. It provides for a 3-year study of 

utility emissions followed by regulation to the extent that 

the Administrator finds them necessary.”

Senator Durenberger’s statements indicate that it is 

unlikely that he would agree with Oxley’s interpretation of 

section 112(n)(1), a provision that provides the Agency 

with considerable discretion, and nothing indicates that 

others in the Senate (or for that matter anyone else in the 

House) would agree with that interpretation. Given the 

Supreme Court’s views on the use of such limited 

legislative history, EPA reasonably declined to consider 

(or even discuss) the legislative history in the preamble 

to the proposed rule and we believe it would be improper to 
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ascribe Representative Oxley’s statements to the entire 

Congress.

Moreover, Representative Oxley’s statement directly 

conflicts with the statutory text. Representative Oxley 

stated that “[the Administrator may regulate only those 

units that he determines – after taking into account 

compliance with all provisions of the act and any other 

Federal, State, or local regulation and voluntary emission 

reductions - have been demonstrated to cause a significant 

threat of serious adverse effects on the public health.” 

136 Cong. Rec. H12934 (daily ed. Oct. 26, 1990), reprinted 

in 1 1990 Legis. Hist. at 1416-17 (emphasis added). 

However, the Utility Study required under section 

112(n)(1)(A) directs the Agency to consider the hazards to 

public health reasonably anticipated to occur after 

“imposition of the requirements of [the Clean Air Act].” 

EPA was not required to consider state or local regulations 

or voluntary emission reduction programs in the Utility 

Study, and that study is the only condition precedent to 

making the appropriate and necessary finding.49

 

49 In addition, EPA only considered CAA requirements in the Utility 

Study and this was the correct approach because Congress knew how to 
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Our interpretation, not commenters’, should be 

afforded deference because the legislative history the 

commenters rely on is not controlling. In addition, 

commenters often cite Representative Oxley’s statements as 

support for alternative interpretations of section 

112(n)(1). We believe that any arguments that rely such 

limited legislative history are without merit. 

Comment: One commenter stated that EPA does 

acknowledge that, in many significant respects, its new 

interpretation of CAA 112(n)(1) “differs from that set 

forth” in the Agency’s 2005 rulemaking, but argues that its 

change of position is permissible. See 76 Fed. Reg. at 

24,988/1 (“[T]o the extent our interpretation differs from 

that set forth in the 2005 Action, we explain the basis for 

that difference and why the interpretation, as set forth in 

this preamble, is reasonable.”). In support, commenters 

note that EPA cites National Cable & Telecommunication 

Ass’n v. Brand X Internet Services, 545 U.S. 967 (2005). 

The commenters agree that it is true that, in Brand X 

 

require consideration of non-Federal requirements when directing EPA to 

conduct a study or assessment. See CAA section 112(n)(5) (Congress 

required EPA to conduct an assessment of hydrogen sulfide from oil and 

gas extraction activities and provided that the assessment “shall 

include review of existing State and industry control standards, 

techniques and enforcement.”).
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Internet Services, the Supreme Court explained that, if an 

agency “adequately explains the reasons for a reversal of 

policy,” such change is “not invalidating,” since the 

“whole point of Chevron is to leave the discretion provided 

by the ambiguities of a statute with the implementing 

agency.” 545 U.S. at 981 (internal quotations omitted). The 

commenters maintain that all Brand X Internet Services was 

saying is that “[a]gency inconsistency is not a basis for 

declining to analyze the agency’s interpretation under the 

Chevron framework.” Id.

According to the commenter, it is not enough that EPA 

has purported to “explain” why it has abandoned the 

interpretation of CAA 112(n)(1) adopted in 2005. The 

commenter states that under the first step of Chevron, the 

Agency’s latest interpretation must still be consistent 

with congressional intent. See Chevron v. NRDC, 467 U.S. at 

842-43. The commenters state that under the second step of 

Chevron, if there is discretion for EPA to exercise in 

interpreting the “critical terms” of CAA 112(n)(1), the 

Agency must properly define the range of that discretion 

and then act reasonably in exercising that discretion. See 

Chevron, 467 U.S. at 843; see also Village of Barrington, 
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Ill. v. Surface Transportation Bd., No. 09-1002 (D.C. Cir. 

Mar. 15, 2011).The commenters allege that EPA failed to 

properly define and exercise the scope of its discretion.

In each instance, the commenter maintains that the Agency 

has departed from the correct interpretation of CAA 

112(n)(1) that it adopted in 2005, seizing instead upon a 

new approach that is contrary to the plain language of the 

CAA itself, as interpreted after considering the statements 

of Representative Oxley.

Response: The commenter appears to argue that EPA’s 

interpretation of section 112(n)(1) is not consistent with 

the plain language of the statute, implying that the 

statute is clear and must be evaluated under step one of 

Chevron. See Chevron v. NRDC, 467 U.S. 837 842-42 (1984) 

(finding that when the legislative intent is clear no 

additional analysis is required). However, as noted above, 

much of the commenter’s argument that the plain language of 

the statute precludes EPA’s interpretation is based on the 

flawed legislative history discussed above. As explained in 

the preamble to the proposed rule, the statute is subject 

to multiple interpretations, and we provided a reasoned 

basis for all the changes made to the 2005 interpretation. 
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Furthermore, we properly considered the scope of our 

discretion in interpreting the statute as explained in 

detail in the preamble to the proposed rule. We believe the 

interpretation set forth in the preamble to the proposed 

rule is consistent with the Act and, therefore, the Agency 

should be afforded deference pursuant to National Cable & 

Telecommunication Ass’n v. Brand X Internet Services, 545 

U.S. 967 (2005). 

Comment: One commenter asserts that EPA’s ultimate 

motivation for rejecting its prior interpretation of CAA 

112(n)(1) and embracing this flawed new approach is made 

clear from the very outset of the proposal. According to 

the commenter, EPA touts the fact that “one consequence” of 

the MACT rule would be that the “market for electricity in 

the U.S. will be more level” and “no longer skewed in favor 

of the higher polluting units that were exempted from the 

CAA at its inception on Congress’ assumption that their 

useful life was near an end.” See 76 Fed. Reg. at 24,979/2. 

The MACT rule would “require companies to make a decision –

control HAP emissions from virtually uncontrolled sources” 

or else “retire these sometimes 60 year old units and shift 
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their emphasis to more efficient, cleaner modern methods of 

generation, including modern coal-fired generation.” Id.

The commenter stated that this remarkably forthright 

statement establishes that the underlying basis for EPA’s 

proposal to regulate EGUs under CAA 112 is not to address 

any “hazards to public health” that might be attributed to 

the emission by EGUs of HAP listed under CAA section

112(b). Rather, according to commenter, EPA is utilizing 

the regulation of EGUs under CAA 112 as a means to an 

entirely different end: to force the imposition of controls 

that will also have the result of reducing non-HAP 

emissions (primarily PM) or force the shutdown of those 

units for which the cost of such controls would be 

prohibitive. At the same time, according to commenter, EPA 

tacitly acknowledges that it cannot hope to make out a case 

that the regulation of EGU HAP emissions is “appropriate 

and necessary” within the meaning of CAA 112(n)(1). The 

commenter asserts that the only HAP whose health-related 

benefits EPA quantifies is Hg. Elsewhere, the commenter 

stated that EPA contends there are “additional health and 

environmental effects” attributable to HAP other than Hg, 

but admits that it has “not quantified” those risks due 
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supposedly to “insufficient information.” See 76 Fed. Reg. 

at 24,999/2. With respect to Hg the commenter stated that 

the benefits are so questionable and miniscule, some $4 

million to $6 million (given a 3% discount rate), that 

compared to the total social costs of the rule (i.e., 

nearly $11 billion) the rule cannot be justified were EPA 

properly to interpret section 112(n)(1) and undertake the 

sort of regulatory analysis Congress intended. The 

commenter stated that the reason that EPA touts in this 

rulemaking the health benefits EPA attributes to the 

reduction of non-hazardous air pollutants (again, primarily 

PM), the regulation of which is authorized under provisions 

of the CAA apart from CAA 112, is to elide the inconvenient 

truth regarding the truly trivial nature of the benefits 

attributable to HAP regulation itself. The commenter 

concludes that EPA distorts CAA 112(n)(1)(A) “beyond all 

recognition.” 

One commenter stated that EPA is directed by CAA 

112(n)(1)(A) to study the “hazards to public health 

anticipated to occur as a result of emissions” by EGUs of 

“pollutants listed under subsection (b) of this section” –

i.e., HAP and HAP alone. Thereafter, EPA is authorized to 
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regulate EGU HAP emissions if, and only if, they determine 

that “such regulation” of HAP emissions is “appropriate and 

necessary” to address the “hazards to public health” that 

may be attributable to HAP emissions. According to the 

commenter, by contrast, in this rulemaking, EPA has seized 

upon the fact that the control of EGU HAP emissions will 

also control non-HAP (such as PM), and then seeks to

justify the regulation of HAP emissions based almost 

entirely on the health benefits of the reductions in nonHAP emissions that would be coincidentally achieved. The 

commenter believes that this “regulatory sleight-of-hand” 

runs afoul of congressional intent and is unlawful. 

Response: The commenter alleges that the healthrelated benefits to regulating HAP emissions from EGUs are 

“questionable and miniscule,” and that the only real 

benefits stem from non-HAP emissions, such as PM. The 

commenter also implies that regulation of HAP is nothing 

more than a straw man and that the Agency’s ultimate goal 

is to regulate other pollutants, and specifically PM. These 

allegations are wholly without merit. The Agency has 

conducted comprehensive technical analyses that confirm 

that HAP emissions from EGUs pose a hazard to public 
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health. The analyses are discussed at length elsewhere in 

this final rule, and a review of the proposed and final 

rules utterly refutes commenter’s assertion that PM 

reductions form the basis for the appropriate and necessary 

finding. PM benefits are only discussed in the Regulatory 

Impact Analysis accompanying the rule

In addition, the commenter appears to ignore the 

Agency’s findings concerning the hazards to public health 

and the environment posed by HAP emissions simply because 

the Agency is not able to quantify the benefits associated 

with reductions of HAP emissions from EGUs or because the 

benefits that are quantified are small in relation to the 

co-benefits achieved through reductions in non-HAP air 

pollutants. What the commenter omits is the fact that the 

Agency is not required to quantify any benefits under the 

CAA before regulating HAP emissions from EGUs. The statute 

does not require any consideration of costs or benefits and 

the commenter has not shown that such considerations are 

required under section 112. As explained below, EPA does 

not consider costs when determining whether to regulate 

EGUs under section 112.
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Comment: One commenter stated that EPA has ignored the 

language and intent of section 112(n)(1)(A), as 

interpreted based on Representative Oxley’s statements, and 

that the Agency’s interpretation of this provision violates 

step one of Chevron. Under Chevron where the “intent of 

Congress is clear,” that is the “end of the matter,” for 

both the implementing agency and a reviewing court “must 

give effect to the unambiguously expressed intent of 

Congress.” Chevron, 467 U.S. at 842-43. The commenter 

asserts that the legislative history of CAA section 

112(n)(1)(A) “sheds considerable light on Congress’ unique 

approach to regulation of EGUs under CAA §112.” According 

to the commenter, on April 3, 1990, the Senate passed S. 

1630. The Senate bill would have required EPA to list EGUs 

under CAA section 112(c) and to regulate them under the 

MACT provisions of CAA section 112(d). See S. 1630 section 

301, 3 1990 Legis. Hist. at 4407. Thereafter, the House of 

Representatives passed a modified version of S. 1630 on May 

23, 1990. This House version substantially changed the 

provisions of CAA section 112 as they applied to EGUs. See 

1 1990 Legis. Hist. at 572-73 The House version was 

virtually identical to the current CAA section 
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112(n)(1)(A), and was ultimately adopted by the conference 

committee, enacted by Congress and signed into law. 

According to the commenter, Congress expressly rejected the 

“list-under-(c)-and-regulate-under-(d)” approach that S. 

1630 would have applied to EGUs, and which Congress did 

choose to apply to other source categories. The commenter

stated that EPA’s interpretation that the Agency is 

“required to establish emission standards for EGUs 

consistent with the requirements set forth in section 

112(d)” (Id. at 24,993/3) fails to take the legislative 

history into account, and in a footnote, the commenter 

states that the Agency erred by not addressing the 

legislative history as it did in the 2005 action.

Response: For the reasons stated above, we believe 

commenter’s reliance on the single statement of one 

legislator is flawed. In addition, in a footnote the 

commenter stated that EPA recognized “that it had to 

address” the legislative history in its 2005 action, and 

that EPA erred in this case because we did not address the 

legislative history. The commenter cites no case law to 

support its contention that an Agency must “address” 

unpersuasive legislative history. Further, in the 2005 
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action, EPA relegated to a footnote the Oxley statement 

that commenter relies on so heavily even though the 

statement supported the interpretation we provided in that 

rule. We recognized what then commenter fails to recognize 

now, that the Agency cannot argue that the meaning of 

section 112(n)(1)(A) is clear based on the statements of 

one legislator. 

The commenter is incorrect when it asserts that EPA’s 

opinion is of no moment. The Agency tasked with 

implementing an ambiguous statute is given considerable 

deference in interpreting the provision. The commenter’s

assertion that Congress unambiguously defined the factors 

to consider in making the appropriate determination is 

wholly without merit. We explain in the preamble to the 

proposed rule the basis for the Agency’s interpretation, 

and we are not revising that interpretation based on the 

comments received.

c. Consideration of Both Public Health and Environmental 

Effects

Comment: Several commenters stated that EPA misreads 

CAA section 112(n)(1)(B) and (C) to inject environmental 

effects in the CAA section 112(n)(1)(A) determination. 
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According to one commenter the plain language of CAA

section 112(n)(1) establishes that regulation of EGUs is to 

be predicated solely on “hazards to public health” 

attributable to HAP emissions. The legislative history 

providing that EPA “may regulate [EGUs] only if the studies 

described in section 112(n) clearly establish that 

emissions of any pollutant... from such units cause a 

significant risk of serious adverse risk to the public 

health” confirms that plain language. See Oxley Statement 

at 1416-17. The commenter further stated that nothing on 

the face of (n)(1)(A) indicates that Congress intended that 

EPA should (or must) take into account any additional 

information that might be developed through the other 

studies mentioned in subparagraphs (n)(1)(B) and (C) (i.e., 

the Mercury Study50 and the NAS Study51). The commenter also 

identified other provisions of section 112 that 

specifically require consideration of environmental effects 

and states that Congress would have requires such 

consideration in section 112(n)(1) if it had wanted EPA to 

consider environmental effects.

 

50 U.S. EPA. 1997. Mercury Study Report to Congress. EPA–452/R–97–003. 

December.

51 NAS, 2000.
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Response: The commenter again relies on the statements 

of one legislator to attack EPA’s reasoned interpretation 

of an ambiguous statute. To the extent the commenter’s 

arguments rely on this paltry evidence, we need not address 

them as we have explained above. As we stated above, 

section 112(n)(1) is an ambiguous statutory provision; 

thus, EPA’s interpretation, not commenter’s, is entitled to 

considerable deference because it is a reasonable reading 

of the statute. Chevron, 467 U.S. at 843-44. The Agency 

directs attention to section III.A. of the proposed rule 

for responses to commenter’s arguments as we are not 

revising our interpretation.

The commenter appears to maintain that EPA must 

interpret the scope of the appropriate and necessary 

finding in the context of the section 112(n)(1)(A) Utility 

Study, such that only hazards to public health and only EGU 

HAP emissions may be considered. The commenter incorrectly 

conflates the requirements for the Utility Study with the 

requirement to regulate EGUs under section 112 if EPA 

determines it is appropriate and necessary to do so. The 

commenter concedes that the Agency may consider information 

other than that contained in the Utility Study, but only to 
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the extent it relates specifically to hazards to public 

health directly attributable to HAP emissions from EGUs. We 

agree that we may consider additional information other 

than that contained in the Utility Study, as we stated in 

the preamble to the proposed rule, because courts do not 

interpret phrases like “after considering the results of” 

in a manner that precludes the consideration of other 

information. See United States v. United Technologies 

Corp., 985 F.2d 1148, 1158 (2nd Cir. 1993) (“based upon” 

does not mean “solely)52; see also 76 FR 24988. We further 

explained in the preamble to the proposed rule that it was 

reasonable to interpret the scope of the appropriate and 

necessary finding in the context of all three studies 

required under section 112(n)(1) because the provision is 

title “Electric utility steam generating units.”53 The 

commenter has provided little more than unpersuasive 

 

52 Several commenters have taken issue with our citation to United 

States v. United Technologies Corp. because the language at issue in 

that case was “based upon” and the language of section 112(n)(1)(A) is 

“after considering the results of.” We believe that, if anything, 

“based upon” is more prescriptive than “after considering the results 

of” such that the case supports the Agency’s interpretation that 

additional information other than the Utility Study may be considered 

in making the appropriate and necessary finding. 

53 76 FR 24986-87.
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legislative history to support its restrictive

interpretation of our authority. Id. 

The commenter also argues that the statute clearly 

prohibits the Agency from considering adverse environmental 

effects or the cumulative effects of HAP emissions from 

EGUs and other sources based on its claim that the statute 

is clear when one properly considers the legislative 

history. Again, the commenter has provided no support for 

its contention other than the statements of one 

Representative and the improper conflation of the section 

112(n)(1)(A) direction on the conduct of the Utility Study 

and the appropriate and necessary finding. Congress left it 

to the Agency to determine whether it is appropriate and 

necessary to regulate EGUs under section 112 and the 

statute does not limit the Agency to considering only 

hazards to public health and only harms directly 

attributable to EGUs. 

The commenter stated that Congress specifically told 

EPA when it wanted EPA to consider adverse environmental 

effects in section 112 and cites to several provisions of 

the Act that require consideration of adverse environmental 

effects. The commenter ignores section 112(n)(1)(B), which 
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requires consideration of adverse environmental effect, and 

all of the other provisions of section 112 that 

specifically require consideration of environmental effects 

have purposes that are distinguishable from section 

112(n)(1). Furthermore, the lack of a requirement to 

consider environmental effects in section 112(n)(1) does 

not equate to a prohibition on the consideration of 

environmental effects as the commenter concludes. EPA 

maintains that it reasonably concluded that we should 

protect against identified or potential adverse 

environmental effects absent clear direction to the 

contrary. 

Concerning the consideration of the cumulative effect 

of HAP emissions from EGUs and other sources, we provided a 

reasonable interpretation of the statute and noted that our 

interpretation, unlike commenters, does not “ignore the 

manner in which public health and the environment are 

affected by air pollution. An individual that suffers 

adverse health effects as the result of the combined HAP 

emissions from EGUs and other sources is harmed, 
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irrespective of whether HAP emissions from EGUs alone would 

cause the harm.”54

d. Finding for all HAP to be Regulated

Comment: Several commenters stated that for those EGU 

HAP for which the Agency makes no section 112(n)(1)(A) 

determination, their regulation under CAA section 112 is 

not authorized. For example, the commenter maintains that 

the Agency could regulate HAP emissions from EGUs under 

section 112(n). Accordingly, to the extent that EPA reads 

CAA section 112, as construed by National Lime Ass’n, as 

compelling it to regulate all HAP emitted by EGUs, should 

the Agency make an “appropriate and necessary” 

determination under CAA section 112(n)(1)(A) with respect 

to a single HAP (e.g., Hg), EPA stands poised to commit a 

fundamental legal error that will condemn the final rule on 

review. Cf., e.g., PDK Laboratories, Inc., 362 F.3d at 797-

98; Holland v. Nat’l Mining Ass’n, 309 F.3d at 817 (where 

an agency applies a Court of Appeals “interpretation ... 

because it believed that it had no choice” and that it “was 

effectively ‘coerced’ to do so,” then the agency “cannot be 

deemed to have exercised its reasoned judgment”).

 

54 76 FR 24988.
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Response: We do not agree with commenter’s assertion 

that Congress intended EPA to regulate only those EGU HAP 

emissions for which an appropriate and necessary finding is 

made, and commenter has cited no provision of the statute 

that states a contrary position. EPA reasonably concluded 

that we must find it “appropriate” to regulate EGUs under 

section 112 if we determine that a single HAP emitted from 

EGUs poses a hazard to public health or the environment. If 

we also find that regulation is necessary, the Agency is 

authorized to list EGUs pursuant to section 112(c) because 

listing is the logical first step in regulating source 

categories that satisfy the statutory criteria for listing 

under the statutory framework of section 112. See New 

Jersey, 517 F.3d at 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 

section 112(c). National Lime Ass’n v. EPA, 233 F.3d 625, 

633 (D.C. Cir. 2000).55

 

55 76 FR 24989.
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The commenter does not explain its issues with our 

interpretation of how regulation under section 112 works –

i.e. making a determination that a source category should 

be listed under section 112(c), listing the source category 

under section 112(c), regulating the source category under 

section 112(d), and conducting the residual risk review for 

sources subject to MACT standards pursuant to section 

112(f). Instead, it asserts that our decision is flawed 

because the interpretation we provided does not account for 

all the alternatives for regulating EGUs under section 112, 

and that we have not properly exercised our discretion 

leading to a fatal flaw in our rulemaking. The commenter 

has not provided an alternative theory for regulating EGUs 

under section 112, other than to state that EPA could 

regulate under section 112(n)(1), and we have been unable 

to identify one absent clear statutory direction. However, 

even if we were to determine that we could issue standards 

pursuant to section 112(n)(1), or some other alternative, 

we would decline to do so for several reasons. First, 

section 112(n)(1) provides no guidance on how to establish 

standards and any mechanism we devised, absent explicit 

statutory support, would likely receive less deference than 
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a section 112(d) standard issued in the same manner in 

which the Agency issues standards for other listed source 

categories. Second, Congress did provide a mechanism under 

sections 112(d) and (f) for establishing emission standards 

for HAP emissions from stationary sources and it is 

reasonable to use that mechanism to regulate HAP emissions 

from EGUs. Finally, we do not believe that Congress 

intended to treat EGUs differently from other source

categories for purposes of establishing standards once they 

are listed.

56

e. Considering Cost in Finding

Comment: Two commenters stated that a natural reading 

of the term “appropriate” would include the consideration 

of costs. According to the commenters, something may be 

found to be “appropriate” where it is “specially suitable,” 

“fit,” or “proper.” See Webster’s Third New International 

Dictionary at 106 (1993). The term “appropriate” carries 

with it the connotation of something that is “suitable or 

proper in the circumstances.” See New Oxford American 

Dictionary (2d Ed. 2005). Considering the costs associated 

 

56 Congress defined EGUs is section 112(a)(8). That definition defines 

the EGU source category and it includes both major and area sources. 
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with undertaking a particular action is inextricably linked 

with any determination as to whether that action is 

“specially suitable” or “proper in the circumstances.” The 

commenter notes that in 2005 (70 Fed. Reg. 15,994, 16,000 

(Mar. 29, 2005)) EPA used the dictionary definition of 

“appropriate,” as being “especially suitable or compatible” 

and that it would be difficult to fathom how a regulatory 

program could be either “suitable” or “compatible” for a 

given public health objective without consideration of 

cost.

Response: The commenters first take issue with EPA’s 

explanation of why the Agency determined that costs should 

not be considered in making the appropriate determination. 

What commenters do not identify is an express statutory 

requirement that the Agency consider costs in making the 

appropriate determination. Congress treated the regulation 

of HAP emissions differently in the 1990 CAA amendments 

because the Agency was not acting quickly enough to address 

these air pollutants with the potential to adversely affect 

human health and the environment. See New Jersey, 517 F.3d 

at 578. For this reason alone, it is reasonable to make the 

listing decision, including the appropriate determination, 
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without considering costs. Congress could easily have 

required the Agency to consider costs, and, because it did 

not, commenter’s assertion that the Agency’s decision not 

to consider costs does not withstand scrutiny are 

unfounded. 

The commenters next argue that the Agency is compelled 

by the statute to consider costs based on a dictionary 

definition of “appropriate” and the section 112(n)(1)(A) 

direction to consider alternative control strategies for 

regulating HAP emissions in the Utility Study. 

Concerning the definition of “appropriate”, commenters

stated: “Not only is it “reasonable” for EPA to consider 

costs in determining whether it is “appropriate” to 

regulate EGU HAP emissions, a natural reading of the term 

indicates that excluding the consideration of costs would 

be entirely unreasonable. Something may be found to be 

“appropriate” where it is “specially suitable,” “fit,” or 

“proper.” See Webster’s Third New International Dictionary 

at 106 (1993). The term “appropriate” carries with it the 

connotation of something that is “suitable or proper in the 

circumstances.” See New Oxford American Dictionary (2d Ed. 

2005) at 76. Considering the costs associated with 
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undertaking a particular action is inextricably linked with 

any determination as to whether that action is “specially 

suitable” or “proper in the circumstances.”

EPA believes the definition of “appropriate” that the 

commenters provide wholly support our interpretation and 

nothing about the definition compels a consideration of 

costs. It is appropriate to regulate EGUs under section 112 

because EPA has determined that HAP emissions from EGUs 

pose hazards to public health and the environment, and 

section 112 is “specially suitable” for regulating HAP 

emissions, and Congress specifically designated section 112 

as the “proper” authority for regulations HAP emissions 

from stationary sources, including EGUs. Section 112 is 

“suitable [and] proper in the circumstances” because EPA 

has identified a hazard to public health and the 

environment and Congress directed the Agency to regulate 

HAP emissions from EGUs under that provision if we make 

such a finding. Cost does not have to be read into the 

definition of “appropriate” as commenter suggests.

The commenters’ argument that costs must be considered 

based on the section 112(n)(1)(A) requirement to “develop 

and describe alternative control strategies” in the Utility 
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Study is equally flawed. The argument is flawed because 

Congress did not direct the Agency to consider in the 

Utility Study the costs of the controls when evaluating the 

alternative control strategies. In addition, EPA did not 

consider the costs of the alternative controls in the 

Utility Study, as implied by the commenter. In a footnote, 

the commenter attempts to refute EPA’s statement in the 

preamble to the proposed rule that EPA did not consider 

costs in the 2000 Finding by pointing to the only two 

mentions of cost in that notice. However, EPA did not say 

that costs were not mentioned in the 2000 Finding and a 

review of the regulatory finding will show that costs were 

not considered in the regulatory finding. 65 FR 79830 

(December 20, 2000) (“Section III. What is EPA’s Regulatory 

Finding?”).

f. Considering requirements of the CAA in “Necessary”

Comment: Several commenters disagree with EPA’s 

position that it need consider “only those requirements 

that Congress directly imposed on EGUs through the CAA as 

amended in 1990,” for which “EPA could reasonably predict 

HAP emission reductions at the time of the Utility Study.” 

According to the commenters, the statutory language of
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section 112(n)(1) requires that EPA consider the scope and 

effect of EGU HAP emissions after the imposition of all of 

the “requirements” of the CAA, not just the Acid Rain 

program. It would have been easy enough for Congress in 

subparagraph 112(n)(1)(A) to specify “after imposition of 

the requirements of Title IV of this chapter,” but Congress 

did not. The commenters further add that the legislative 

history confirms that Congress meant something much broader 

than that, providing that EPA is authorized to regulate 

EGUs under CAA section 112 only after “taking into account 

compliance with all provisions of the act and any other 

Federal, State, or local regulation and voluntary emission 

reductions.” The commenters stated that the CAA’s 

“requirements” include the submission by states of ozone 

and fine PM attainment demonstrations, as well as SIP 

provisions needed to reach attainment of the NAAQS because 

such provisions could include controls on EGUs to reduce 

SO2 and NOx, which controls could also result in a 

reduction in Hg emissions.

Response: The commenter’s characterization of the 

facts is flawed and its reliance on legislative history 
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that is in direct conflict with the express terms of the 

statute is unfounded. 

On the facts, EPA explained in the preamble to the 

proposed rule its interpretation of the phrase “after 

imposition of the requirements of [the Act]” as it related 

to the conduct of the Utility Study.

57 We reasonably 

concluded that, since Congress only provided three years 

after enactment to conduct the study, the phrase referred 

to requirements that were directly imposed on EGUs through 

the CAA amendments and for which the Agency could 

reasonably predict co-benefit HAP emission reductions. Id. 

EPA did not state that the phrase only applied to the Acid 

Rain program, as commenter asserts and the Utility Study in 

fact discussed other regulations, including the NSPS for 

EGUs and revised NAAQS. With regard to the latter, EPA 

ultimately determined that it could not sufficiently 

quantify the reductions that might be attributable to the 

NAAQS because states are tasked with implementing those 

standards. See Utility Study, pages ES-25, 1-3, 2-32. 

Conversely, commenter’s position is that EPA must consider 

implementation of all the requirements of the CAA, but it 

 

57 76 FR 24990.
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does not indicate how in conducting the Utility Study the 

Agency could have possibly considered co-benefit HAP 

reductions attributable to all future CAA requirements. 

In the preamble to the proposed rule, EPA recognized 

that we could consider requirements beyond those considered 

in the Utility Study, and we did consider a number of 

requirements that far exceed what Congress contemplated 

when enacting section 112(n)(1)(A). 76 FR 24991. We 

maintain that we have reasonably interpreted the 

requirement to consider the hazards to public health and 

the environment reasonably anticipated to occur after 

imposition of the requirements of the Act as explained in 

the preamble to the proposed rule.

58 In addition, as stated 

above, we also believe it would be reasonable to find it 

necessary to regulate HAP emissions from EGUs based on our 

finding that such emissions pose a hazard to public health 

and the environment today. 

With regard to the legislative history, as stated 

above, Representative Oxley’s supposedly authoritative 

statement is not even consistent with the express terms of 

section 112(n)(1)(A) on this issue, and commenter here 

 

58 76 FR 24990.
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relies on that misstatement as support for its attack on 

the Agency’s reasonable interpretation of the statute. 

Specifically, Representative Oxley stated that EPA was to 

take “into account compliance with all the provisions of 

the act and any other Federal, State, or local regulation 

and voluntary emission reductions,” but section 

112(n)(1)(A) directed the Agency to consider only 

“imposition of the requirements of [the CAA].” We need not 

address this argument further. 

Finally, commenter implies that EPA’s position is that 

the Agency will only consider requirements of the Act that 

directly regulate HAP emissions. EPA never stated or 

suggested that interpretation and a fair reading of the 

proposed rule will demonstrate that EPA considered 

requirements that achieve co-benefit HAP emission 

reductions, for example the Transport Rule (known as 

CSAPR).

Comment: One commenter stated that, under CAA section 

112, regulating EGUs is permissible only insofar as it is 

focused, targeted, and predicated on concrete findings by 

the Agency that such regulation is indeed “necessary.” 

According to the commenter, EPA construes CAA section
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112(n)(1)(A) as permitting it to find that it is 

“necessary” to regulate EGUs even where the Agency does not 

actually know whether it is “necessary” to regulate EGUs. 

Citing the D.C. Circuit, EPA suggests that “‘there are many 

situations in which the use of the word ‘necessary,’ in 

context, means something that is done, regardless of 

whether it is indispensible,’” in order to “‘achieve a 

particular end.’” 76 Fed. Reg. at 24,990, quoting Cellular 

Telecommunications v. FCC, 330 F.3d 502, 510 (D.C. Cir. 

2003). The commenter stated that in the “context” of CAA 

section 112(n)(1)(A), as informed by the relevant 

legislative history from Representative Oxley, it is clear 

that regulation of EGU HAP emissions can be considered 

“necessary” only if EPA were to “clearly establish” that 

such regulation was effectively “indispensible” to address 

the identified harm. As EPA concedes that it has made no 

such determination here, its proposal is fatally flawed for 

that reason alone.

Response: The commenter again relies on the 

legislative statements of one Representative and asserts 

that the statements are controlling. It is commenter’s 

legal analysis that is flawed, not EPA’s interpretation of 
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the statute. 76 FR 24990-92 (Section III.A.2.b of the 

proposed rule contains EPA’s interpretation of the term 

“necessary”). The commenter also, in a footnote, implies 

that EPA based the appropriate and necessary finding on 

non-HAP air pollution. The commenter is wrong as explained 

in more detail above.

Further, the commenter appears to argue that EPA’s 

interpretation authorizes the Agency to find it necessary 

to regulate EGUs when we are uncertain it is necessary, but 

that misconstrues our interpretation. EPA reasonably 

interprets the statute to authorize the Agency to find that 

it is necessary to regulate if we are unable to determine 

that imposition of the requirements of the Act will address 

identified hazards to public health and the environment. 

The statute does not prohibit this interpretation and it is 

a legitimate exercise of our discretion to err on the side 

of regulation in the face of uncertainty concerning the 

level of protection necessary to protect public health and 

the environment. This is particularly true in a 

determination such as the necessary finding that is based 

on modeled projections of emissions four years into the 

future. The CAA requires EPA to exercise its discretion in 
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determining whether regulation under section 112 is 

necessary, and the D.C. Circuit has stated that “there are 

many situations in which the use of the word ‘necessary,’ 

in context, means something that is done, regardless of 

whether it is indispensible, to achieve a particular end.” 

See Cellular Telecommunications & Internet Association, et. 

al. v. FCC, 330 F.3d 502, 510 (D.C. Cir. 2003). EPA’s 

interpretation of “necessary” is reasonable in the context 

of section 112(n)(1)(A).

The commenter stated that EPA concedes that the Agency 

has not “clearly established” that regulation of HAP 

emissions under section 112 is “indispensible.” EPA has 

conceded nothing but, more importantly, the supposed 

standard that commenter presents for evaluating whether it 

is necessary to regulate HAP emissions from EGUs is not 

required by the statute. Even the limited legislative 

history on which the commenter incorrectly relies does not 

espouse such a standard. 

The commenter takes issue with EPA’s statement that 

the Agency may find it is necessary to regulate EGUs under 

section 112 if we are “uncertain whether imposition of the 

other requirements of the CAA will sufficiently address the 
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identified hazards.” 76 Fed. Reg. at 24,990. The commenter 

has again misinterpreted the Agency’s position by stating 

that “EPA construes CAA 112(n)(1)(A) as permitting it to 

find that it is “necessary” to regulate EGUs even where the 

Agency does not actually know whether it is “necessary” to 

regulate EGUs.” Instead, EPA maintains that it may be 

necessary to regulate EGUs under section 112 if we identify 

a hazard to public health or the environment that is 

appropriate to regulate today and our projections into the 

future do not clearly establish that the imposition of the 

requirements of the CAA will address the identified hazard 

in the future. Making a prediction about future emission 

reductions from a source category is difficult for

statutory provisions that do not mandate direct control of 

the given source category or pollutants of concern. We 

maintain that erring on the side of caution is appropriate 

when the protection of public health and the environment 

from HAP emissions is not assured based on our modeling of 

future emissions. Furthermore, as we stated in the preamble 

to the proposed rule, we believe it would be reasonable to 

find it appropriate and necessary today based on a 

determination that HAP emissions from EGUs pose a hazard to 
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public health and the environment without considering 

future HAP emission reductions. 76 FR 24991, n.14. We 

maintain this is reasonable because “Congress could not 

have contemplated in 1990 that EPA would have failed in 

2011 to have regulated HAP emissions from EGU’s where 

hazards to public health and the environment remain.” Id. 

The phrase “after imposition of the requirements of [the 

Act]” as contemplated section 112(n)(1)(A) could be read to 

apply only to those requirements clearly and directly 

applicable to EGUs under 1990 CAA amendments, all of which 

have been implemented and still hazards to public health 

and the environment still remain.

Finally, the commenter does not address all of the 

bases on which the necessary finding is made. Specifically, 

EPA found in the preamble to the proposed rule that it was 

necessary to regulate HAP emissions from EGUs because the 

hazards to public health and the environment would not be 

addressed through imposition of the requirements of the 

Act. 

g. Listing EGUs under 112

Comment: One commenter stated that even if EPA were to 

establish under CAA 112(n)(1)(A) that it is “appropriate 
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and necessary” to regulate HAP emissions from EGUs – and 

the Agency has not done so – regulating those emissions in 

the form of a MACT standard established pursuant to CAA 

112(d) is contrary to the plain language of the Act.

According to the commenter, if EPA proceeds to finalize the 

proposal and adopts such a standard, the rule will for this 

reason alone be dead-on-arrival. According to the 

commenter, EPA apparently believes that its only option in 

regulating EGU HAP emissions is establishing a MACT 

standard under CAA 112(d). In the preamble to its proposal, 

the commenter states that EPA contends that, “once the 

appropriate and necessary finding is made,” EGUs are then 

“subject to section 112 in the same manner as other sources 

of HAP emissions” – i.e., by “listing” EGUs under CAA 

112(c) and adopting a MACT standard under CAA 112(d). See 

76 Fed. Reg. at 24,993/2 (emphasis added). The commenter 

further stated that, given that Congress “directed the 

Agency to regulate utilities ‘under this section’ [i.e., 

CAA 112],” EPA continues, it follows that “EGUs should be 

regulated in the same manner as other categories for which 

the statute requires regulation.” Id. (emphasis added). The 

commenter asserts that as EPA sees it, because “Congress 
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did not exempt EGUs from the other requirements of section 

112,” once EGUs were “listed” under CAA 112(c), the Agency 

was “required to establish emission standards for EGUs 

consistent with the requirements set forth in section 

112(d).” Id. at 24,993/3 (emphasis added).

The commenter stated that, in support of this reading 

of the CAA, EPA invokes the decision of the U.S. Court of 

Appeals for the D.C. Circuit in New Jersey v. EPA, 517 F.3d 

574 (D.C. Cir. 2008). The commenter further alleged that, 

according to EPA, the D.C. Circuit has “already held that 

section 112(n)(1) ‘governs how the Administrator decides 

whether to list EGUs.’” See 76 Fed. Reg. at 24,993/2-3, 

quoting 517 F.3d at 583. The commenter stated that EPA 

construes that holding as indicating that, “once listed, 

EGUs are subject to the requirements of section 112” –

including, EPA presumes, CAA 112(d). Id. The commenter 

stated that elsewhere, EPA construes CAA 112(n)(1) (A) as 

“govern[ing] how the Administrator decides whether to list 

EGUs for regulation under section 112,” and quotes the D.C. 

Circuit’s observation in New Jersey that “Section 112(n)(1) 

governs how the Administrator decides whether to list EGUs; 
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it says nothing about delisting EGUs.” See 76 Fed. Reg. at 

24,981/2, quoting 517 F.2d at 582.

The commenter asserts that EPA misinterprets the 

“under this section” language of CAA 112(n)(1); overstates 

the significance of the New Jersey decision; and, as a 

consequence, misapprehends the scope of its own discretion 

to formulate regulatory standards for EGUs under CAA 112. 

In light of these errors, the commenter maintains that EPA 

should withdraw the proposed MACT rule.

One commenter stated that if Congress had intended 

that EPA regulate EGU HAP emissions only through a MACT 

standard, Congress could have – and presumably would have –

directed the Agency to regulate EGU emissions “under CAA 

112(d).” Thus, the commenter maintained that EPA’s 

authority to regulate EGU HAP emissions is not derived from 

any particular subsection of CAA 112. Rather, the commenter 

stated that EPA is authorized to regulate “under this 

section” – i.e., CAA 112 generally – as may be “appropriate 

and necessary.” The commenter stated that there is nothing 

on the face of CAA 112(n)(1)(A) that specifies that 

regulation of EGUs must occur under CAA 112(d). To the 

contrary, according to the commenter, a plain reading of 
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CAA 112(n)(1)(A), as interpreted based on the Oxley 

statement, indicates that establishing a MACT standard for 

EGUs under CAA 112(d) is not what Congress had in mind at 

all.

Response: We do not agree with the commenter. EPA 

interpreted section 112(n)(1)(A) in a manner that gives 

meaning to all the words used in the provision. See NRDC v. 

EPA, 489 F.3d 1364, 1373 (D.C. Cir. 2007) (admonishing EPA 

for an interpretation of CAA section 112(c)(9) that ignored 

certain words and the context in which they were used. The 

Court stated that “EPA’s interpretation would make the 

words redundant and one of them ‘mere surplusage,’ which is 

inconsistent with a court's duty to give meaning to each 

word used by Congress.”) (citing TRW Inc. v. Andrews, 534 

U.S. 19, 31, 122 S. Ct. 441, 151 L. Ed. 2d 339 (2001)). 

Specifically, in the preamble to the proposed rule, we 

stated: “ The statute directs the Agency to regulate EGUs 

under section 112 if the Agency finds such regulation is 

appropriate and necessary. Once the appropriate and 

necessary finding is made, EGUs are subject to section 112 

in the same manner as other sources of HAP emissions. 

Section 112(n)(1)(A) provision provides, in part, that: 
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‘[t]he Administrator shall perform a study of the hazards 

to public health reasonably anticipated to occur as a 

result of emissions by electric utility steam generating 

units of pollutants listed under subsection (b) of this 

section after imposition of the requirements of this 

chapter... The Administrator shall regulate electric 

utility steam generating units under this section, if the 

Administrator finds such regulation is appropriate and 

necessary after considering the results of the study 

required by this subparagraph.’” Emphasis added.

In the first sentence, Congress described the study 

and directed the Agency to evaluate the hazards to public 

health posed by HAP emissions listed under subsection (b) 

(i.e., section 112(b)). The last sentence requires the 

Agency to regulate under this section (i.e., section 112) 

if the Agency finds such regulation is appropriate and 

necessary after considering the results of the study 

required by this subparagraph (i.e., section 112(n)(1)(A)). 

The use of the terms “section”, “subsection”, and 

“subparagraph” demonstrates that Congress was consciously 

distinguishing the various provisions of section 112 in 

directing the conduct of the study and the manner in which 
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the Agency must regulate EGUs if the Agency finds it 

appropriate and necessary to do so. Congress directed the 

Agency to regulate utilities “under this section,” and 

accordingly EGUs should be regulated in the same manner as 

other categories for which the statute requires regulation. 

See 76 FR 24993.

We maintain that our interpretation of the statute 

gives meaning to all the words, and the commenter’s 

interpretation does not give any particular meaning to the 

requirement to “regulate under this section [112]”. The 

commenter is correct that Congress could have in section 

112(n)(1)(A) directed EPA to regulate HAP from EGUs under 

section 112(d) after making the appropriate and necessary 

finding, but the commenter presumes too much when it stated

that Congress would have directed the Agency to regulate 

HAP emissions from EGUs in such a manner if that is what 

Congress wanted. It is equally true that Congress could 

have directed EPA to regulate HAP emissions from EGUs under 

subparagraph 112(n)(1)(A) if that is what it wanted, but it 

did not. As we explained in the section II.A. of the 

proposed rule, section 112 establishes a mechanism to list 

and regulate stationary sources of HAP emissions. 76 FR 
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24,980-81. Regulation under section 112 generally requires 

listing under section 112(c), regulation under section 

112(d), and, for sources subjected to MACT standards, 

residual risk regulations under section 112(f) (as 

necessary to protect human health and the environment with 

an ample margin of safety). It is fully consistent with the 

plain language of section 112(n)(1)(A) to conclude that EPA 

should list EGUs once the prerequisite appropriate and 

necessary finding is made, and listed sources must be 

regulated under section 112(d). See section 112(c)(2). 

Furthermore, the flaws in the commenter’s 

interpretation are highlighted by other section 112 

provisions wherein Congress provided specific direction as 

to the manner of regulation. For example, section 112(m)(6) 

requires the Administrator to determine “whether the other 

provisions of this section [112] are adequate” and also 

indicates that “[a]ny requirements promulgated pursuant to 

this paragraph . . .shall only apply to the coastal waters 

of the States which are subject to [section 328 of the 

CAA].” (emphasis added). In addition, section 112(n)(3) 

provides that when the Agency is “promulgating any standard 

under this section [112] applicable to publicly owned 
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treatment works, the Administrator may provide for control 

measures that include pretreatment of discharges causing 

emissions of hazardous air pollutants and process or 

product substitutions or limitations that may be effective 

in reducing such emissions.” Finally, section 112(n)(5) 

directs the Agency to assess hydrogen sulfide emissions

from oil and gas extraction and “develop and implement a 

control strategy for emissions of hydrogen sulfide to 

protect human health and the environment . . . using 

authorities under [the CAA] including [section 111] of this 

title and this section [112].” (emphasis added). We believe 

these provisions provide ample evidence that Congress knew 

how to alter or caveat regulation under section 112 when 

that was its intent. For these reasons, we believe 

commenter’s argument is without merit.

Comment: Two commenters stated that Section 

112(n)(1)(A) does not specify that regulation of EGUs must 

proceed under section 112(d). An argument could be made, 

therefore, that the CAA accords EPA with the discretion to 

regulate EGUs using strategies other than emission 

standards in section 112(d). Section 112(n)(1)(A) requires 

that EPA “develop and describe” alternative control 
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strategies for emissions which may warrant regulation under 

section 112. According to the commenters if Congress meant 

for EPA to have one sole regulatory option, i.e., 

regulation of EGUs only under section 112(d), then the 

development of alternative control strategies would be 

rendered meaningless because under CAA section 112(d)(3), 

EPA is required to determine the level of control that is 

achieved by the best performing existing units for which it 

has data and then to impose that level of control on all 

existing units. The development of “alternative control 

strategies” has no role to play in this process. One 

commenter does note that the consideration of “alternative” 

controls becomes relevant, if at all, only in those 

circumstances where EPA might seek to establish a “Beyondthe-Floor” MACT standard pursuant to CAA section 112(d)(2).

Response: The commenters are correct that section 

112(n)(1)(A) directed the Agency to develop alternative 

control strategies for regulating HAP emissions from EGUs 

that may warrant regulation in the Utility Study, but the 

commenters’ interpretation of and conclusion based on that 

language are both factually and legally inaccurate. 
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The commenters appear to interpret the word 

“alternative control strategies” to mean something other 

than the traditional control technologies and control 

measures that are used to control HAP emissions from EGUs. 

We do not believe that is a reasonable interpretation of 

the statute, and the Agency did not interpret the statute 

in that manner when it conducted the Utility Study. In 

Chapter 13 of the Utility Study, EPA considered a range of 

control measures that would reduce the different types of 

HAP emitted from EGUs. 

http://www.epa.gov/ttn/atw/combust/utiltox/eurtc1.pdf. EPA 

considered pre-combustion controls such as coal washing, 

fuel switching, and gasification; combustion controls such 

as boiler design; post-combustion controls such as fabric 

filters, scrubbers, and carbon absorption; and alternative 

controls strategies such as demand-side management, energy 

conservation, and use of alternative fuels (e.g. biomass) 

or renewable energy. The options discussed in the Utility 

Study for controlling HAP emissions from EGUs are almost 

universally available to comply with a section 112(d) 

standard. 
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Given the manner in which the Agency conducted the 

Utility Study, EPA obviously interpreted the statutory 

direction as a requirement to set forth the potential 

alternative control options available to EGUs to comply 

with section 112 standards in the event the Agency 

determined regulation was appropriate and necessary. EPA’s 

development and discussion in the Utility Study of 

alternative control strategies for complying with the 

standards would help prepare EGUs to comply with the 

standards if promulgated. Further, our interpretation is 

consistent with the direction in section 112(n)(1)(A) to 

develop the control strategies for HAP “emissions which may 

warrant regulation under this section.” Thus, the statute 

only directed the Agency to develop alternative control 

strategies for the HAP the Agency determined may warrant 

regulation under section 112, and, tellingly, the Agency 

developed alternative control strategies for all different 

types of HAP emitted from U.S. EGUs. The commenters’

interpretation finds no support under the statute and we 

reject it. 

Furthermore, EPA establishes section 112(d) standards 

for stationary sources and it is the responsibility of the 
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sources to comply with the standards using any mechanism 

available, including pre-combustion and post-combustion 

measures. Also, the establishment of a MACT standard under 

section 112(d)(2) and (3) is a two-step process. In the 

first step, the Agency establishes a floor based on the 

performance of the best controlled unit or units. Section 

112(d)(3). In the second step, the Agency must consider 

additional measures that may reduce HAP emissions and adopt 

such measures if reasonable after considering costs and 

non-air quality health and environmental effects. Section 

112(d)(2). Under the second step, the Agency can consider 

any measure that reduces HAP emissions even if no source in 

the category is employing the option under consideration.

So, even under the commenter’s flawed interpretation of 

“alternative control strategies”, the direction in section 

112(n)(1)(A) is not a “pointless exercise” for the 

development of section 112(d) standards.

Comment: One commenter does not agree with EPA’s 

finding that the word “subsection” in the first sentence of 

CAA section 112(n)(1)(A) demonstrates that Congress was 

consciously distinguishing between the various provisions 

of section 112 in directing the conduct of the study and 
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the manner in which the Agency must regulate EGUs,” were 

EPA to “find[] it appropriate and necessary to do so.” See 

76 Fed. Reg. at 24,993/2. According to the commenter, the 

only evident reason that the word “subsection” is used in 

the first sentence of CAA section 112(n)(1)(A) is because 

reference is made to the “pollutants” which the Utility 

Study is to address – i.e., the “pollutants” that are 

emitted by EGUs and which are “listed under subsection (b)” 

of CAA section 112. Similarly, the word “subparagraph” is 

used in the last sentence of CAA section 112(n)(1)(A) to 

identify “the study” which EPA is directed to undertake by 

subparagraph (A) of CAA section 112(n)(1) – i.e., the 

Utility Study. That the last sentence of subparagraph 

(n)(1)(A) also states that EPA “shall regulate electric 

utility steam generating units under this section” does not 

even imply – much less expressly communicate – that 

regulation “under this section” must mean “regulation under 

section 112(d).” The commenter stated that Congress was 

“consciously distinguishing” between the “various 

provisions of section 112” for the sake of clarity in the 

drafting of CAA section 112(n).
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Response: The commenter makes a number of arguments 

that appear to take issue with EPA’s determination that 

EGUs should be regulated under section 112(d) if the Agency 

determines that regulation of HAP emissions from such units 

is appropriate and necessary. The commenter implies that 

EPA erred because alternative mechanisms for regulation of 

EGUs under section 112 might exist. We do not agree.

The commenter’s argument that EPA erred because we did 

not explain why section CAA section 307(d)(1)(C) 

contemplates regulations under section 112(n) is without 

merit. It is correct that the Agency believes EGUs should 

be regulated in the same manner as other sources if the 

appropriate and necessary finding is made because of the 

structure of section 112. Nothing in section 112(n)(1) 

requires or implies that the Agency should or must 

establish standards for EGUs under that provision. 

Furthermore, unlike sections 112(n)(3) and 112(n)(5) that 

commenter cites, section 112(n)(1)(A) does not provide any 

guidance concerning the manner in which EPA is authorized 

or required to regulate sources under section 112. See 

section 112(n)(3) (specifically authorizing identified 

control measures and other requirements for consideration 
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in issuing standards under section 112); see also section 

112(n)(5) (directing the Agency to develop and implement a 

control strategy for emissions of hydrogen sulfide using 

any authority available under the CAA if regulation is 

appropriate). For these reasons, we disagree that any error 

occurred because we did not specifically discuss in this 

proposed rule whether we could or should regulate EGUs 

under section 112(n)(1) instead of section 112(d). The 

Agency validly listed EGUs in 2000 and listed sources must 

be regulated pursuant to section 112(d). 

Even if we agreed that regulation under section 

112(n)(1) was a viable option prior to the listing, we 

would still list and regulate EGUs like other sources 

because section 112(d) provides a statutory framework for 

regulating HAP emissions from sources and section 112(n)(1) 

does not. Even if section 112(n)(1) were available to 

regulate EGUs, there is sufficient uncertainty about the 

legally vulnerability of such an approach to caution 

against employing it. This is particularly true given that 

we have identified hazards to public health and the 

environment from HAP emissions from EGUs that warrant 

regulation.
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The commenter also takes issue with our statement in

the preamble to the proposed rule that the use of the words 

“section”, “subsection”, and “subparagraph” in section 

112(n)(1)(A) “demonstrates that Congress was consciously 

distinguishing the various provisions of section 112 in 

directing the conduct of the study and the manner in which 

the Agency must regulate EGUs.” See 76 Fed. Reg. at 24,993. 

The commenter appears to make much of our use of the word 

“must” in that sentence and also states that our 

interpretation of the significance of the use of the three 

terms in section 112(n)(1)(A) is flawed because Congress 

only used the three terms for purposes of clarity. The 

commenter is wrong on both points. In regard to commenter’s 

concern with the use of the word “must” in the sentence 

quoted above, we note that in the next sentence we stated

that “Congress directed the Agency to regulate utilities 

‘under this section,’ and accordingly EGUs should be 

regulated in the same manner as other categories for which 

the statute requires regulation.” Id. (emphasis added). We

were not foreclosing the possibility of any alternative 

interpretation and our use of the term “must” should not 

detract from the point we were trying to make - a point 
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that undermines commenter’s argument that EPA should not 

regulate EGUs under section 112(d). Specifically, we 

believe that Congress would have directed us to regulate 

EGUs under section 112(n)(1)(A) if that was its intent and, 

absent that mandate, the best reading of the statute is the 

one we provided in the preamble to the proposed rule.

The commenter also stated that EPA relied on section 

112(c)(6) to support a conclusion that EGUs must be 

regulated under section 112(d). The commenter takes EPA’s 

statements out of context. The statement in whole read: 

“Furthermore, the D.C. Circuit Court has already held that 

section 112(n)(1) “governs how the Administrator decides 

whether to list EGUs” and that once listed, EGUs are 

subject to the requirements of section 112. New Jersey, 517 

F.3d at 583. Indeed, the D.C. Circuit Court expressly noted 

that “where Congress wished to exempt EGUs from specific 

requirements of section 112, it said so explicitly,” noting 

that “section 112(c)(6) expressly exempts EGUs from the 

strict deadlines imposed on other sources of certain 

pollutants.” Id. Congress did not exempt EGUs from the 

other requirements of section 112, and once listed, EPA is 

required to establish emission standards for EGUs 
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consistent with the requirements set forth in section 

112(d), as described below.” See 76 Fed. Reg. at 24,993

As can be seen from this passage, EPA did not rely on 

112(c)(6); instead the Court used that provision as an 

example of Congress’ intent regarding regulating EGUs under 

section 112. The commenter cited the last clause of the 

last sentence of the paragraph quoted above without 

including the prefatory clause “once listed,” and, without 

that clause, the statement is not fairly characterized. The 

point EPA was making in that paragraph is that EGUs are a 

listed source category and listed sources must be regulated 

under section 112(d) unless EPA delists the source 

category.

Comment: One commenter stated that EPA overstates the 

significance of the D.C. Circuit’s holding in New Jersey by 

suggesting that the decision mandates EGU regulation under 

CAA section 112(d) because EGUs “remain listed” under CAA 

section 112(c), See New Jersey, 517 F.3d at 582. According 

to the commenter, the court declined to address the 

lawfulness of EPA’s having “listed” EGUs under CAA section 

112(c), leaving that matter to be decided if and when EPA 

adopted standards for EGUs under CAA section 112. Nowhere 
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in the decision did the D.C. Circuit indicate that EPA must 

regulate EGUs under CAA section 112(d).

Response: The commenter’s arguments are circular and 

it is difficult to fully determine exactly what its issue 

is with EPA’s listing; however, it appears that the 

commenter believes that EPA incorrectly relied on the New 

Jersey decision to justify the listing of EGUs. The 

commenter also appears to argue that the Agency has never 

explained why it has the authority to list EGUs at all. We 

disagree.

As stated in the preamble to the proposed rule, 

section 112(n)(1)(A) requires EPA to conduct a study of HAP 

emissions from EGUs and regulate EGUs under section 112 if 

we determine that regulation is appropriate and necessary, 

after considering the results of the study. 76 FR 24981, 

24986, and 24998. The only condition precedent to 

regulating EGUs under section 112 is a finding that such 

regulation is appropriate and necessary (after conducting 

and considering the Utility Study), and once that finding 

is made the Agency has the authority to list EGUs under 

section 112(c) as the first step in the process of 

establishing regulations under section 112. The D.C. 
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Circuit agrees with that interpretation of the statute as 

evidenced by its statement in New Jersey that “section 

112(n)(1)(A) governs how the Administrator decides whether 

to list EGUs for regulation under section 112,” 517 F.3d at 

582, and the Court’s statement directly contradicts the 

commenter’s position. 

EPA did not rely on the New Jersey decision to justify 

the appropriate and necessary finding as the commenter 

suggests. We based the finding in 2000 on the extensive 

information available to the Agency at the time and we 

reaffirmed the Finding in the preamble to the proposed rule 

based on new information. The commenter had ample 

opportunity to comment on the appropriate and necessary 

finding, and it may challenge the basis of the listing 

(i.e. the appropriate and necessary finding) when EPA 

issues the final standards.

Comment: One commenter believes that the D.C. Circuit 

will condemn the final rule as a result of EPA’s 

“misapprehension” that upon making an “appropriate and 

necessary” finding, the Agency is compelled by the CAA to 

adopt a regulatory standard for EGUs under CAA section

112(d). According to the commenter, a regulation will be 
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invalid if the regulation “‘was not based on the [agency’s] 

own judgment’” but “‘rather on the unjustified assumption 

that it was Congress’ judgment that such [a regulation] is 

desirable’ or required.” See Transitional Hospitals Corp. 

v. Shalala, 222 F.3d 1019, 1029 (D.C. Cir. 2000), quoting 

Prill v. NLRB, 755 F.2d 941, 948 (D.C. Cir. 1985). 

Similarly, the D.C. Circuit has held that, where an agency 

wrongly construes a judicial decision as compelling a 

particular statutory interpretation, and thereby unduly 

limits the scope of its own discretion, the agency’s action 

cannot be sustained. See, e.g., Phillips Petroleum Co. v. 

FERC, 792 F.2d 1165, 1171 (D.C. Cir. 1986). Because the 

commenter believes the rule is bound to be rejected, EPA 

should “reconsider the legal interpretations on which it 

purports to base its rule.”

Response: We do not agree that we have improperly 

interpreted the statute as limiting our discretion in the 

manner suggested by the commenter. The commenter makes only 

one specific allegation in this comment and that concerns 

the Agency’s conclusion that it must establish section 

112(d) standards for EGUs in light of the New Jersey

decision. The commenter does not explain why that 
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conclusion is incorrect. As we state above and in the 

preamble to the proposed rule, because EGUs are a section 

112(c) listed source category, the Agency must establish 

section 112(d) standards or delist EGUs pursuant to section 

112(c)(9). See New Jersey, 517 F.3d at 582-83 (holding that 

EGUs remain listed under section 112(c)); see also section 

112(c)(2) (requiring the Agency to “establish emission 

standards under subsection [112] (d)” for listed source 

categories and subcategories); 76 FR 24998-99. We concluded 

in the preamble to the proposed rule that we could not 

delist EGUs because our appropriate and necessary analysis 

showed that EGUs did not satisfy the 112(c)(9)(B)(i) 

delisting criteria. Id. We did not address in the preamble 

to the proposed rule whether EGUs satisfied the 

112(c)(9)(B)(ii) criteria because EGUs failed the first 

prong of the delisting provisions. Id. We reach the same 

conclusion in the final rule and also address the delisting 

petition submitted by this commenter. Because we cannot 

delist EGUs, we must regulate them under section 112(d). 

The commenter has provided no legitimate argument to rebut 

this conclusion.
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Comment: One commenter alleges that EPA impermissibly 

relied on CAA section 112(c)(9) to interpret “hazards to 

public health”, and argues that the “residual risk” 

provisions in CAA section 112(f)(2) are more appropriate 

for the establishment of standards for EGUs. The commenter 

stated that by using 112(c)(9)(B)(i) in defining “hazards 

to public health”, the Agency has seized on the one 

interpretation of the phrase that is surely contrary to 

congressional intent and, thus, falls outside the 

permissible range of its interpretative discretion. The 

“delisting” criteria of CAA section 112(c)(9) are simply 

irrelevant to the decision whether EGU HAP emissions will 

present any “hazards to public health” sufficient to 

warrant regulation of those emissions under CAA section

112.

The commenter also argues that Congress intended that 

EGUs be treated differently from all other “major sources” 

to which “listing” provisions of CAA section 112(c)(9), and 

the standard-setting provisions of CAA section 112(d) 

necessarily and automatically apply. Therefore, EPA’s 

proposal to utilize the criteria of CAA section 112(c)(9) 

to inform its findings under CAA section 112(n)(1)(A) 
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treats EGUs exactly the same as all other major source 

categories, is contrary to congressional intent, and thus 

unlawful. The commenter goes on to state that in exercising 

its discretion to define “hazards to public health” as the 

phrase is used in CAA section 112(n)(1)(A), EPA would be 

better served to consider the “residual health risk” 

provisions of CAA section 112(f)(2). Those provisions 

provide a better analogy to the establishment of standards 

for EGUs under CAA section 112 than do the “de-listing” 

criteria of CAA section 112(c)(9).

The commenter believes the category-specific criteria 

of paragraph (c)(9) are a poor fit for an evaluation of 

“hazards to public health” that should reasonably include 

such factors as the affected population, the 

characteristics of exposure, the nature of the health 

effects, and the uncertainties associated with the data. 

While CAA section 112(n)(1)(A) does not expressly include 

any requirement that EGU emissions be regulated with an 

“ample margin of safety,” that standard is more appropriate 

than the “one-in-a-million” cancer risk standard of CAA 

section 112(c)(9)(B)(i) that EPA proposes to employ. 
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Response: The commenter acknowledged that EPA has 

broad discretion to interpret the phrase “hazard to public 

health” but argues that the one thing we cannot do is use 

the section 112(c)(9)(B) delisting provisions as a

benchmark in making that interpretation. The commenter 

asserted that the use of the delisting standard is clearly 

contrary to Congressional intent but it does not provide 

any substantive rebuttal to our conclusion that the section 

112(c)(9) standards reflects the level of hazard which 

Congress concluded warranted continued regulation. Instead, 

the commenter reverted to its argument that the statute 

treated EGUs differently. EPA views the disparate treatment 

of EGUs in a different light than commenter. We maintain 

that the only difference applies to the manner in which 

EGUs are added to the list of source categories subject to 

regulation. We do not interpret section 112(n)(1)(A) as a 

Congressional license to ignore risks that Congress 

determined warranted regulation for all other source 

categories. Because section 112(c)(9) defines that level of 

risk, it is reasonable to consider it when evaluating 

hazards to public health. 
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The commenter also suggests that the “ample margin of 

safety standard” of section 112(f)(2) is a better fit than 

the one-in-a-million standard set forth in section 

112(c)(9)(B)(1) for evaluating hazards to public health.

The commenter asserts that an evaluation of “hazards to 

public health” should include such factors as the affected 

population, the characteristics of exposure, the nature of 

the health effects, and the uncertainties associated with 

the data. However, EPA did not rely solely on the delisting 

provisions for evaluating hazards to public health as 

commenter suggests. In fact, EPA considered all of the 

factors the commenter suggests in making our finding.

59

Thus, our approach to evaluating hazards to public health 

and the environment based on this comment.

h. 2000 Finding (and 2005 Reversal)

Comment: Several commenters generally support EPA’s 

2000 finding that regulating HAP emissions from EGUs under 

CAA section 112 is “appropriate and necessary.” According 

to the commenters, the 2000 finding was proper under the 

CAA and within EPA’s discretion, well-supported based on 

sound science available to the Agency at the time on the 

 

59 76 FR 24992.
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harm from HAP emitted by EGUs, and no additional 

information makes the finding invalid. Several commenters 

cited the conclusions of the Utility Study60 and Mercury 

Study61, which they assert supported the finding and 

satisfied the only prerequisite for the finding. One 

commenter specifically asserted that the 2000 finding was 

well-supported by the Utility Study’s conclusions that (1) 

there was a link between anthropogenic Hg emissions and 

MeHg found in freshwater fish, (2) Hg emissions from coalfired utilities were expected to worsen by 2010, and (3) 

MeHg in fish presents a threat to public health from fish 

consumption. One commenter noted that the CAA does not 

require a conclusive link between HAP emissions and harm. 

One commenter stated that the CAA grants the Administrator 

discretion in her finding, and that discretionary decision 

should not be overly scrutinized, citing court opinion.62 In 

support of the finding, one commenter stated that it would 

not make sense for Congress to limit HAP emissions from 

 

60 U.S. EPA, 1998.

61 U.S. EPA, 1997.

62 “Where a statute is precautionary in nature, the evidence difficult 

to come by, uncertain, or conflicting because it is on the frontiers of 

scientific knowledge, the regulations designed to protect the public 

health, and the decision that of an expert administrator, [courts] will 

not demand rigorous step-by-step proof of cause and effect.” Ethyl 

Corp. v. EPA, 541 F.2d 1, 28 (Ct. App. D.C. Circ. 1978)
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small businesses such as dry cleaners but to exempt U.S. 

EGUs, which are the largest sources of many HAP emissions. 

One commenter agreed that finding was further supported 

because numerous control options were available to reduce 

HAP emissions. One commenter agreed with the 200 finding 

that the Agency lacked sufficient evidence to conclude that 

non-Hg HAP from EGUs posed no hazard.

The commenters who generally supported the 2000 

finding also commented on specific aspects of the finding. 

Several commenters asserted that while the evidence on Hg

alone supports the finding, the potential harm from non-Hg 

HAP further supported the 2000 finding. Several commenters 

noted that new science continues to support the 2000 

finding. Several commenters also stated that the 

“appropriate” finding was further supported because 

numerous control options were available at the time of the 

finding that would reduce HAP emissions. One commenter 

concurred with EPA that regulating natural gas-fired EGUs

was not appropriate and necessary because the impacts due 

to HAP emissions from such units are negligible based on 

the results of the Utility Study. 
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Several commenters addressed the 2005 reversal of the 

2000 finding. While one commenter stated that the attempted 

2005 reversal of the 2000 finding was properly rejected by 

the U.S. Court of Appeals, another commenter asserted that 

the 2005 action was reasoned and proper and that EPA 

reverted back to the 2000 finding without adequate 

explanation or support. Several commenters cited the 2005 

action as invalidating the 2000 finding, specifically

noting that EPA concluded that “no hazards to public 

health” remained after accounting for emission reductions 

under CAIR. These commenters assert that EPA’s current 

position is illegal because EPA took the exact opposite 

position on the interpretation of the term “necessary” in 

its 2005 reversal, and thus deserves no judicial

deference. One commenter stated that in 2005 EPA recognized 

the potential for excessive regulation created by section 

112 and determined that the 2000 finding lacked foundation. 

Several commenters generally disagreed with the 2000 

finding, with two commenters stating that EPA did not have 

a rational justification for it and another claiming that 

it was fraught with misinformation and overestimating 

assumptions. One commenter claimed that EPA did not explain 
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the terms “appropriate” and “necessary” in the 2000 finding 

and that the emission control analysis was inadequate. Two 

commenters stated that the 2000 finding was based on data 

that was more than 10 years old, which causes serious 

concern regarding the validity of the findings because 

technology, the regulatory environment, and the economic 

climate have evolved. Furthermore, because the Utility 

Report underestimated emissions controls that EGUs would 

install by 2010 and additional controls that would be later 

required by the CSAPR, the basis for EPA‘s 2000 finding has 

changed. Several commenters stated that a “plausible link” 

between anthropogenic Hg and MeHg in fish is not an 

adequate reason for the 2000 finding. Several commenters 

claim that EPA only identified health concerns for Hg (and 

potentially Ni) but not other HAP from coal-fired EGUs in 

the 2000 finding, and thus cannot regulate HAP other than 

Hg because the 2000 finding authorizes only the regulation 

of Hg. One commenter questioned the Hg emissions underlying 

the 2000 finding, specifically the fraction of total 

deposition attributable to U.S. EGUS and the fact that EPA 

projected an increase in U.S. EGU emissions from 1990 to 

2010 though emissions actually declined. 
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Several commenters raised procedural issues related to 

the 2000 finding. Several commenters stated that the 2000 

finding failed to provide public notice and comment. 

According to the commenters, the CAA requires that any 

decision made under section 112(n) must go through public 

notice and comment. The commenters further stated that the 

failure to provide public notice and comment means that 

this MACT is outside EPA’s statutory authority. One 

commenter stated that because the 2000 finding was never

“fully ventilated” in front of the D.C. Circuit, EPA’s 

authority to regulate EGUs under Section 112(d) is directly 

at issue. The commenters claim that specific issues did not 

undergo public notice and comment, including least-cost 

regulatory options, the impact of regulation on electricity 

reliability, and EPA’s interpretation of the requirements 

under section 112(n)(1)(A). One commenter claims that EPA 

attempted to provide after-the-fact support for its 2000 

finding with new legal analysis and new factual 

information, contrary to New Jersey v. EPA that held that

EPA may not revisit its 2000 finding except through 

delisting under Section 112(c)(9). One commenter stated

that EPA’s 2000 Finding should be reviewed when EPA issues 
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the actual NESHAP.

63 One commenter stated that the 2000 

finding ignored Executive Order 12866.

Response: EPA agrees with the commenters that the 2000

finding was reasonable and disagrees with the commenters 

asserting that the 2000 finding was unreasonable or failed 

to follow proper procedural requirements. 

EPA agrees that reviewing courts defer to the reasoned 

scientific and technical decisions of an Agency charged 

with implementing complex statutory provisions such as 

those at issue in this case. As EPA stated in the preamble 

to the proposed rule, EPA maintains that the 2000 finding 

was reasonable and based on well-supported evidence 

available at the time, including the Utility Study, the 

Mercury Study64, and the NAS study65, which all showed the 

known and potential hazards to public health and the 

environment. New technical analyses conducted by EPA 

confirm that it remains appropriate and necessary to 

regulate HAP emissions from EGUs. Furthermore, EPA agrees 

with the commenters on several points raised, specifically 

that EGUs were and remain the largest anthropogenic source 

 

63 See UARG v. EPA, 2001 WL 936363, No. 01-1074 (D.C. Cir. July 26, 

2001).

64 U.S. EPA, 1997.

65 NAS, 2000.
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of several HAP in the U.S., that risk assessments 

supporting the 2000 finding indicated potential concern for 

several non-Hg HAP, and that several available control 

options would effectively reduce HAP emissions from U.S. 

EGUs.

EPA agrees with the commenters that Congress did not 

exempt EGUs from HAP emission limits while simultaneously 

limiting emissions at other sources with less HAP

emissions. Congress simply provided EPA with a separate 

path for listing EGUs by requiring that the Agency evaluate 

HAP emissions from EGUs and determine whether regulation 

under section 112 was appropriate and necessary. Since 

1990, EPA has promulgated regulations requiring the use of 

available control technology and other practices to reduce 

HAP emissions for more than 50 industrial sectors. U.S. 

EGUs are the most significant source of HAP in the country 

that remains unaddressed by Congress’s air toxics program. 

EPA listed EGUs in 2000 because the considerable amount of 

available data supported the conclusion that regulation of 

EGUs under section 112 was appropriate and necessary. That 

finding was valid at the time, and EPA reasonably added 
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EGUs to the section 112(c) list of sources that must be 

regulated under section 112.

EPA acknowledges that we did not expressly define the 

terms appropriate and necessary in the 2000 finding, but 

the finding is instructive in that it shows that EPA 

considered whether HAP emissions from EGUs posed a hazard 

to public health and the environment and whether there were 

control strategies available to reduce HAP emissions from 

EGUs when determining whether it was appropriate to 

regulated EGUs.

66 When concluding it was necessary, the 

Agency stated that imposition of the requirements of the 

Act would not address the identified hazards to public 

health or environment from HAP emissions and that section 

112 was the proper authority to address HAP emissions.67 EPA 

explained in the preamble to the proposed rule its

conclusion that the 2000 finding was fully supported by the 

information available at the time,

68 and EPA stands by the 

conclusions in that notice. Furthermore, EPA provided an 

interpretation of the terms appropriate and necessary that 

is wholly consistent with the 2000 finding. EPA does not 

 

66 65 FR 79830.

67 Id.

68 65 FR 24994-24996.
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agree with the commenters that a quantification of 

emissions reductions or a specific identification of the 

available controls was necessary to support the 2000 

finding and listing. EPA considered the Utility Study when 

making the finding, and that study clearly articulated the 

various alternative control strategies that EGUs could 

employ to control HAP emissions.69 As to emission 

reductions, EPA cannot estimate the level of HAP emission 

reductions cannot until the Agency proposes a section 

112(d) standard after a source category is listed.

EPA disagrees with commenters that suggest it was not 

“rational” to determine that it was appropriate to regulate 

HAP emissions from EGUs due to the cancer risks identified 

in the Utility Study or the potential concerns associated 

with other HAP emissions from EGUs. Nothing in section 

112(n)(1)(A) suggests that EPA must determine that every 

HAP emitted by EGUs poses a hazard to public health or the 

environment before EPA can find it appropriate to regulate 

EGUs under section 112. In fact, EPA maintains that it must 

find it appropriate and necessary to regulate EGUs under 

section 112 if it determines that any one HAP emitted from 

 

69 See Chapter 13 of the Utility Study (U.S. EPA, 1998). 
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EGUs poses a hazard to public health or the environment 

that will not be addressed through imposition of the 

requirements of the Act. EPA disputes the commenters’

conclusion that the 2000 finding was limited to Hg and Ni

emissions, but, even if it were, EPA reasonably concluded 

that EGUs should be listed pursuant to section 112(c) based 

on the Hg and Ni finding. As stated in the 2000 finding, 

cancer risks from some non-Hg metal HAP (including arsenic, 

chromium, nickel, and cadmium) were not low enough to be to 

eliminate as potential concern.70 Source categories listed 

for regulation under section 112(c) must be regulated under 

section 112(d), and the D.C. Circuit has stated that EPA 

has a “clear statutory obligation to set emission standards 

for each listed HAP”. See Sierra Club v. EPA, 479 F.3d 875, 

883 (D.C. Cir. 2007), quoting National Lime Association v. 

EPA, 233 F.3d 625, 634 (D.C. Cir. 2000). Therefore, even if 

EPA concluded that section 112(n)(1) authorized a different 

approach for regulating HAP emissions from EGUs, with which 

we disagree, the chosen course which is supported by the 

CAA (i.e. listing under section 112(c)) requires the Agency 

 

70 76 FR 79827.
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to regulate under section 112(d) consistent with the 

statute and case law interpreting that provision. 

EPA disagrees that there is any concern regarding the 

validity of the 2000 finding or that the emissions 

information provided in the 2000 finding makes the finding 

“questionable” as stated by some of the commenters. EPA 

maintains that the 2000 finding was sound and fully 

supported by the record available at the time, including 

the future year emissions projections. Therefore, the 

listing of EGUs is valid based on that finding alone. Even 

though Hg emissions have decreased since the 2000 finding 

instead of increasing as projected, the new technical 

analyses confirm that Hg emissions from EGUs pose known and 

potential hazards to public health and the environment. EPA 

also stated in 2000 that uncertainty associated with the 

potential risk from HAP emissions justified regulation of 

HAP emissions from EGUs. This is true because it is well 

established that even small amounts of HAP can cause 

significant harm to human health and the environment. 

EPA agrees with the commenters who assert that the 

2005 action was in error and disagrees with the commenters 

that the 2005 action invalidated the 2000 finding. As fully 
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described in the preamble to the proposal, EPA erred in the 

2005 action by concluding that the 2000 finding lacked 

foundation. The 2005 action improperly conflated the 

“appropriate” and “necessary” analyses by addressing the 

“after imposition of the requirements of the Act” in the 

appropriate finding as well as the necessary finding. EPA 

also indicated that it was not reasonable to interpret the 

necessary prong of the finding as a requirement to scour 

the CAA for alternative authorities to regulate HAP

emissions from stationary sources, including EGUs, when 

Congress provided section 112 for that purpose. EPA asserts 

that the 2000 finding was sound and fully supported by the 

record available at the time for all the reasons stated in 

this final rule and the proposed rule. The 2005 action 

interpreted the statute in a manner wholly inconsistent 

with the 2000 finding and attempted to delist EGUs without 

complying with the mandates of section 112(c)(9)(B). See 

New Jersey, 517 F.3d at 583 (vacating the 2005 “delisting” 

action). In the preamble to the proposed rule, EPA set 

forth a revised interpretation of section 112(n)(1) that is 

consistent with the statute and the 2000 finding. EPA also 

explained in the preamble to the proposed rule why the 2005 
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action was not technically or scientifically sound. EPA 

specifically addressed the errors associated with the 2005 

action in the preamble to the proposed rule, and 

commenters’ assertions do not cause us to revisit these 

issues. The commenter is also incorrect in suggesting that 

a change in interpretation is per se invalid and provided 

no support for that position. See National Cable & 

Telecommunications Ass’n, et. a., v. Brand X Internet 

Services, et. al., 545 U.S. 967, 981 (discussing the 

deference provided to an Agency changing interpretations,

the Court stated “change is not invalidating, since the 

whole point of Chevron deference is to leave the discretion 

provided by ambiguities of a statute with the implementing 

Agency.”) (Internal citations and quotations omitted).

EPA disagrees with the commenters who raise concerns 

about the validity of the 2000 finding because the data on 

which that finding was based were more than 10 years old. 

EPA made the finding at that time based on the scientific 

and technical information available, and the finding is 

wholly supported by that information. In addition, even 

though not required to do so, EPA has since conducted new 

technical analyses utilizing the best information available 
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in 2010 as several years have passed since the 2000

finding. These new analyses confirm that HAP emissions from 

EGUs continue to pose a hazard to public health and the 

environment, even after taking into account emission 

reductions that have occurred since 2000 from promulgated 

rules, settlements, consent decrees, and closures. 

Some commenters are also incorrect regarding their 

assertion of certain procedural requirements associated 

with the 2000 listing. EPA did not violate CAA section 

307(d) by not providing notice and comment opportunity 

before making the appropriate and necessary finding. One 

commenter challenged EPA’s 2000 finding and listing on the 

same grounds, and the D.C. Circuit dismissed the case 

because CAA section 112(e)(4) clearly states that listing 

decisions cannot be challenged until the Agency issues 

final emission standards for the listed source 

category. See UARG v. EPA, 2001 WL 936363, No. 01-1074 

(D.C. Cir. July 26, 2001). EPA has provided the public an 

opportunity to comment on both the 2000 finding and the 

2011 analyses that support the appropriate and necessary 

determination as part of the proposed rule, and anyone may 

challenge the listing in the D.C. Circuit in conjunction 
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with a challenge to this final rule. The commenters could 

have also commented on the section 112(n)(1) (e.g., the 

Utility Study and the Mercury Study)studies in 2000 as they 

were included in the docket, but EPA is not aware of any 

comments on those studies. In any case, these studies were 

peer reviewed and considered the best information available 

at that time. EPA has fully complied with the rulemaking 

requirement of section 307(d). 

EPA also disagrees with commenters’ characterization 

of the New Jersey case. The D.C. Circuit did not say, as 

one commenter suggested, that EPA is not able to consider 

additional information that is collected after the 2000 

finding; instead, the Court stated that EPA could not 

revise its appropriate and necessary finding and remove 

EGUs from the section 112(c) list without complying with 

the delisting provisions of section 112(c)(9). See New 

Jersey, 517 F.3d at 582-83. EPA also disagrees with the 

commenter’s assertion that EPA disregarded Executive Order 

(EO)12866 when making the 2000 finding. As stated in the 

Federal Register notice, the 2000 finding did not impose 
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regulatory requirements or costs and was reviewed by the 

Office of Management and Budget in accordance with the EO.

71

2. New Technical Analyses

a. General comments on new technical analyses

Comment: Several commenters stated that the new 

analyses, including the risk assessments and technology 

assessments, confirm that it remains appropriate and 

necessary to regulate U.S. EGU HAP under Section 112 of the

CAA. These commenters stated that the new analyses provide 

even more support than the risk and technology information 

available at the time the 2000 finding was made, including

information on further developed emissions control 

technology, proven and cost-effective control of acid gases 

using trona and dry sorbent injection, stabilized natural 

gas prices that makes fuel switching and switching dispatch 

to underutilized combined cycle plants more feasible, more 

information on ecosystem impacts from HAP, “hotspots” from 

the deposition of Hg around EGUs, the potential for reemission of Hg, updated emissions data and future 

projections of HAP emissions, and modern air pollution 

modeling tools. One commenter states affordable control 

 

71 65 FR 79831.
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technology has been in use in this sector for 10 to 40 

years, and studies on EGU-attributable Hg hazard has 

undergone two in-depth EPA reviews, as well as a review by

the NAS. Several commenters claimed that regulating U.S. 

EGUs is appropriate and necessary to protect public health 

based on information provided in the new technical 

analyses. These commenters acknowledged the substantial 

reductions in HAP from recent regulations and new studies 

that confirm serious health risks from HAP exposure. One 

commenter stated that new studies show higher risks to 

fetuses than previously estimated, increasing the potential 

for neurodevelopmental effects in newborns. One commenter 

noted that EGUs are a major source of HAP, including HCl, 

HF, arsenic, antimony, Cr, Ni, and selenium, all of which 

adversely affect human health. The commenter stated that 

because of these health effects, EPA has ample evidence to 

support a determination that non-Hg HAP emissions present a 

risk to human health.

Other commenters disagreed that the new analyses

confirm that it remains appropriate and necessary to 

regulate U.S. EGUs. One commenter claims that EPA tried to 

use the new technical analyses to provide retroactive 
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justification for the 2000 finding, which only found 

“plausible links” of health effects and “potential 

concerns” of health effects of certain metal emissions, 

dioxins and acid based aerosols. The commenter also 

asserted that none of these new analyses demonstrate that 

EGU regulation under section 112 is necessary and 

appropriate.

One commenter agreed that EPA may supplement its 

finding with new information, analyses and arguments to 

reaffirm the 2000 finding up until EPA issues final 

emissions standards. The commenter noted that the CAA does 

not freeze the finding. However, another commenter argued

that EPA does not have the authority to rely on new 

technical analyses because the CAA requires EPA to make the 

finding on the basis of the Utility Study alone. According 

to that commenter, EPA unreasonably stretched the language 

of section 112 by considering new technical analyses.

Citing a report from Dr. Willie Soon that was 

submitted to the SAB, one commenter stated that the new 

technical analyses supporting the proposed rule do not 

conform to the Information Quality Act, which requires that 
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information relied on by EPA be accurate, reliable, 

unbiased, and presented in a complete and unbiased manner. 

Response: EPA agrees with the commenters that state 

that the new technical analyses (e.g., the risk assessments

and technology assessment) confirm the 2000 finding and 

disagrees with the commenters that state otherwise. EPA 

also agrees with the commenters that the 2000 finding was 

valid at the time it was made based on the section 

112(n)(1) studies and other information available to the 

Agency at that time. Furthermore, EPA agrees with 

commenters that the final rule will lead to substantial 

reductions in HAP emissions from EGUs, that control of the 

HAP will lead to public health and environmental benefits 

as discussed in the RIA, that Hg emissions from EGUs pose a 

hazard to public health, and that non-Hg HAP emissions from 

EGUs pose a hazard to public health that warrants 

regulation under section 112.

Although these new analyses were not required, EPA 

agrees with the commenters that stated that EPA is 

authorized to conduct additional analyses to confirm the 

2000 finding. EPA disagrees with the commenter’s assertion 

that the Agency is not authorized to consider new 
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information and at the same time unable to use the 

information available in 2000 because, according to the 

commenter, that information because it is “stale.” Under 

this theory, the Agency could not ever make an appropriate 

and necessary finding prospectively, thereby excusing the 

Agency from its obligations to protect public health and 

the environment because it did not diligently act in 

undertaking its statutory responsibility to establish 

section 112(d) standards within two years of listing EGUs. 

See section 112(c)(5). This is an illogical result that 

finds no basis in the statute. EPA also disagrees with the 

commenter's assertion that EPA may not consider new 

analyses conducted after the Utility Study in determining 

whether it is appropriate and necessary to regulate EGUs

under section 112 for the reasons set forth in the preamble 

to the proposed rule.72

EPA disagrees with the commenter’s implication that

EPA conducted the new analyses because of alleged flaws in 

the 2000 finding. As explained in detail in the preamble to

the proposed rule, the 2000 finding was wholly valid and 

reasonable based on the information available to the Agency 

 

72 76 FR 24988.
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at that time, including the Utility Study. Further, EPA 

maintains that had it complied with the statutory mandate 

to issue section 112(d) standards within two years of 

listing EGUs, EPA would likely have declined to conduct new 

analyses. EPA conducted new analyses because over 10 years 

had passed since the 2000 finding, and EPA wanted to 

evaluate HAP emissions from U.S. EGUs based on the most 

accurate information available, though the Agency not 

required to reevaluate the 2000 finding. In conducting the 

new analyses, EPA used this updated information to further

support the finding.

EPA strongly disagrees with the commenter that stated

that EPA failed to conform to the Information Quality Act. 

EPA used peer reviewed information and quality-assured data 

in all aspects of the technical analyses used to support 

the appropriate and necessary finding supporting this 

regulation. In addition, EPA submitted the Hg Risk TSD to 

the SAB, which “supports the overall design of and approach 

to the risk assessment and finds that it should provide an 

objective, reasonable, and credible determination of the 

potential for a public health hazard from mercury emitted 
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from U.S. EGUs.”76 The SAB received the comments from Dr. 

Willie Soon, and had those comments available for 

consideration in their deliberations regarding the Hg risk 

analysis. The SAB specifically supported elements of the 

analysis criticized by Willie Soon regarding the use of EPA 

RfD as a benchmark for risk and the connection between Hg

emissions from U.S. EGUs and MeHg concentrations in fish.

In addition, the risk assessment methodology for the non-Hg 

case studies is consistent with the methodology that EPA 

uses for assessments performed for Risk and Technology 

Review rulemakings, which underwent peer review by the SAB 

in 2009.77 During the public comment period, EPA also 

completed a letter peer review of the methods used to 

develop inhalation cancer risk estimates for Cr and Ni 

compounds, and those reviews were generally supportive. For 

the final rulemaking, EPA revised both risk assessments 

consistent with recommendations from the peer reviewers. 

EPA relies on the SAB’s review of the quality of the 

information supporting the analytical results.

b. Hg Emissions Estimates

 

76 U.S. EPA-SAB, 2011.

77 U.S. EPA-SAB, 2010.
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1. Hg emissions from EGUs

Comment: The commenters addressed the 2005 and 2016 

emissions estimates for Hg and expressed concern that 

inaccuracies in these emissions estimates result in 

overestimates of risks from Hg deposition. Further, 

commenters compared EPA’s 2010 estimate and 2016 estimate, 

and stated that it is not possible for 29 tons to be a 

correct inventory total for Hg emissions in both years 

given expected reductions from CSAPR. In addition, 

commenters specifically commented on assumptions included 

in the Integrated Planning Modeling (IPM), including a 

concern that Hg speciation factors used by IPM overestimate

emissions in 2016. Other commenters noted that EGU sources 

are the predominant source of U.S. anthropogenic Hg

emissions, particularly the oxidized and particulate forms 

of Hg that are of primary concern for Hg deposition.

Response: EPA disagrees with commenters’ assertions 

that emissions estimates overestimate risk. While EPA 

agrees that the 2005 Hg emissions may be overestimated, 

such an overestimate in 2005 would actually lead to an 

underestimate of risk in 2016 and not an overestimate of 

risk, as claimed by the commenter, because the ratio 
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approach used by EPA to scale fish tissue data would 

underestimate risk if 2005 Hg estimates were overestimated. 

Since the 2005 emissions are not used as a starting point 

for 2016 emissions from IPM, any 2005 overestimate does not 

affect the 2016 emissions levels. The 2016 emissions are 

computed by IPM based on forecasts of demand, fuel type, Hg 

content of the fuel, and the emissions reductions resulting 

from each unit’s configurations. See IPM Documentation for 

further information. No commenter has provided any evidence 

that the IPM 2016 emissions projection methodology resulted

in an overestimate.

EPA acknowledges that the current Hg emissions 

estimate should not be the same as the 2016 Hg emissions 

estimate given that compliance with CSAPR is expected to 

lead to some Hg emission reduction co-benefits. For this 

reason, EPA has included those reductions in the futureyear modeling used for the Hg risk analysis. EPA estimates 

that current Hg emissions are 28 tons, replacing the 

estimated 2010 value of 29 tons reported at proposal. EPA 

has also revised the 2016 base estimate to 27 tons. Any

remaining inconsistency in EPA’s revised values is not 

relevant to the Hg national risk analysis since the 2010 
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emissions are not used in any of the risk calculations, 

which depend only on the modeled 2005 and 2016 Hg 

emissions. 

EPA disagrees with the commenter’s assertion that 

incorrect Hg emission factors result in incorrect 2016 

emissions. The 2016 projected Hg emissions are not based on 

emissions factors. The 2016 Hg emissions are computed by 

the Integrated Planning Model (IPM) based on forecasts of 

demand, fuel type, Hg content of the fuel, and the 

emissions reductions resulting from each unit’s 

configurations. The speciation factors referenced by the 

commenter provide a basis for the speciation of total 

projected Hg emissions into particulate, divalent gaseous, 

and elemental species, and do not impact the total amount 

of Hg emissions.

EPA agrees with commenters who noted that EGU sources 

are the predominant source of U.S. anthropogenic Hg

emissions, and in particular the oxidized and particulate 

forms of Hg that are of primary concern for Hg deposition.

2. Global Hg emissions

Comment: Several commenters stated that predicted Hg

deposition relies heavily on the amount of gaseous 
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elemental Hg used to define the boundary and initial 

conditions of a model, e.g. the Hg that enters the U.S. 

from outside the U.S. boundaries. The commenters asserted

that this is especially important because Hg emissions from 

Asia—the region immediately upwind of North America that 

affects U.S. Hg deposition significantly and also affects 

it the most compared to other regions—are expected to 

continue to increase.78,79,80,81,82,83 This would affect the 

amount of Hg in the boundary and initial conditions. The 

commenters claim that EPA‘s modeling did not account for 

these emission changes, thus leading to an overestimate of 

U.S. EGU-attributable deposition in 2016.

 

78 Jaffe D., Prestbo E., Swartzendruber P., Weiss-Penzias P., Kato S., 

Takami A., Hatakeyama S., Kajii Y., 2005. “Export of Atmospheric 

Mercury from Asia,” Atmospheric Environment, 39, 3029–3038.

79 Jaffe D., Strode S., 2008. “Fate and Transport of Atmospheric Mercury 

from Asia,” Environmental Chemistry, 5, 121. 

80 Pacyna E.G., Pacyna J.M., Sundseth K., Munthe J., Kindbom K., Wilson 

S., Steenhuisen F., Maxson P., 2010. ”Global Emission of Mercury to the 

Atmosphere from Anthropogenic Sources in 2005 and Projections to 2020,”

Atmospheric Environment, 44, 2487–2499.

81 Pirrone N., Cinnirella S., Feng X., Finkelman R.B., Friedli H.R., 

Leaner J., Mason R., Mukherjee A.B., Stracher G.B., Streets D. G., 

Telmer K., 2010. “Global Mercury Emissions to the Atmosphere from 

Anthropogenic and Natural Sources,” Atmospheric Chemistry and Physics, 

10, 5951–5964.

82 Streets, D.G., Zhang, Q., Wu, Y., 2009. “Projections of Global 

Mercury Emissions in 2050.” Environmental Science & Technology 43, 

2983-2988.

83 Weiss-Penzias P., Jaffe D., Swartzendruber P., Dennison J.B., Chand 

D., Hafner W., Prestbo E., 2006. “Observations of Asian Air Pollution 

in the Free Troposphere at Mt. Bachelor Observatory in the Spring of 

2004,” Journal of Geophysical Research, 110, D10304.
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Several commenters noted that Hg emissions from U.S. 

EGUs are small when compared to global Hg emissions totals 

and natural sources within the U.S. These commenters used a 

variety of information to support alternative conclusions 

about the necessity to control U.S. EGU emissions to reduce 

Hg risk: global Hg emissions inventories, global and 

regional photochemical modeling research, and observationbased assessments. A commenter stated that EPA has not 

acknowledged the dramatic decline in Hg emissions from U.S. 

EGUs since the late 1990s (approximately 50 percent) to the 

current level or consider the relative magnitude of Hg

emissions from U.S. EGUs compared to other sources, natural 

(such as fires) and human-caused.

Response: EPA disagrees that boundary condition inflow 

needs adjustment. The first 10 days of the modeling 

simulation are not used in the analysis, which is beyond 

the number of days necessary to remove the influence of 

initial conditions on Hg deposition estimates.84 Accurate 

characterization of speciated ambient Hg inflow is 

 

84 Pongprueksa, P., Lin, C.J., Lindberg, S.E., Jang, C., Braverman, T., 

Bullock, O.R., Ho, T.C., Chu, H.W., 2008. “Scientific uncertainties in 

atmospheric mercury models III: Boundary and initial conditions, model 

grid resolution, and Hg(II) reduction mechanism.” Atmospheric 

Environment 42, 1828-1845.
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problematic due to the lack of observation data near the 

boundaries of the large continental-scale modeling domain. 

EPA has determined that the perturbations applied by

Pongprueksa et al. (2008), of 1 ng/m3 are not realistic 

boundaries of global speciated Hg concentrations and do not 

provide directly applicable information about uncertainty 

related to boundary conditions. The boundary inflow for the 

CMAQ Hg modeling used in the Hg deposition modeling are 

based on a global model GEOS-CHEM simulation using a 2000 

based global inventory.85 A recently published comparison of 

global Hg emissions by continent for 2000 and 2006 was 

found that total Hg emissions from Asia (and Oceania) total 

1,306 Mg/yr in 2000 and 1,317 Mg/yr in 2006.87 EPA has 

determined that because the Asian Hg emissions estimated in 

this study are nearly constant between 2005 and 2006, any 

adjustments to the boundary conditions or adjustments to 

modeled Hg deposition would be invalid and inappropriate. 

Recent research has shown that ambient Hg concentrations 

have been decreasing in the northern hemisphere since 

 

85 Selin, N.E., Jacob, D.J., Park, R.J., Yantosca, R.M., Strode, S., 

Jaegle, L., Jaffe, D. 2007. “Chemical cycling and deposition of 

atmospheric mercury: Global constraints from observations.” Journal of 

Geophysical Research-Atmospheres 112.

87 Streets et al., 2009.
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2000.88 Since emissions from Asia have not appreciably 

changed between 2000 and 2006 and ambient Hg concentrations 

have been decreasing, ENVIRON’s analysis contains incorrect 

assumptions and we need not address them further. For these 

reasons and the large uncertainties surrounding projected 

Hg global inventories, EPA concludes that the most 

appropriate technical choice is to keep the Hg boundary 

conditions the same between the 2005 and 2016 simulations.

EPA disagrees with the commenter’s assertion that EPA 

has not acknowledged the dramatic decline in Hg emissions 

for the U.S. EGUs since the late 1990s. EPA analyzed 

historical, current, and future projected Hg emissions from 

the power generation sector, as cited in the preamble to 

the proposed rule. EPA also disagrees with the commenters’ 

assertions that EPA failed to consider the relative 

magnitude of Hg emissions from U.S. EGUs compared to other 

sources. As noted in the Hg Risk TSD, EPA modeled Hg

emissions from U.S. and non-U.S. anthropogenic and natural 

sources to estimate Hg deposition across the country. EPA 

also determined the contribution of Hg emissions from U.S. 

 

88 Slemr, F., Brunke, E.G., Ebinghaus, R., Kuss, J., 2011. “Worldwide 

trend of atmospheric mercury since 1995.” Atmospheric Chemistry and 

Physics 11, 4779-4787.
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EGUs to total Hg deposition in the U.S. by running modeling 

simulations for 2005 and 2016 with Hg emissions from U.S. 

EGUs set to zero. Based on the Hg Risk TSD, EPA finds that 

total Hg deposition from EGUs do significantly impact human 

health.

The commenters suggest that Hg emissions from U.S. 

EGUs represent a limited portion of the total Hg emitted 

worldwide, including anthropogenic and natural sources. 

While EPA acknowledges that Hg emissions from U.S. EGUs are 

a small fraction of the total Hg emitted globally, it views 

the environmental significance of Hg emissions from U.S. 

EGUs and other domestic sources as a more germane 

consideration. Hg is emitted from EGUs in three forms. Each 

form of Hg has specific physical and chemical properties 

that determine how far it travels in the atmosphere before 

depositing to the landscape. While gaseous oxidized Hg and 

particle-bound Hg are generally local/regional Hg

deposition concerns, all forms of Hg may deposit to local 

or regional watersheds. U.S. coal-fired power plants 

account for over half of the U.S. controllable emissions of 

the quickly depositing forms of Hg. Although emissions from 

international Hg sources contribute to Hg deposition in the 
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U.S., the peer reviewed scientific literature shows that Hg

emissions from U.S. EGUs in the U.S. significantly enhance 

Hg deposition and the response of ecosystems in the 

U.S.89,90,91,92

c. Hg Deposition Modeling

1. General Comments on Deposition Modeling

Comment: Several commenters stated that according to 

the ENVIRON report, EPA overestimated U.S. EGU-attributable

Hg deposition by 10 percent on average (and up to 41 

percent in some areas). The commenters claim this 

overestimation is the result of boundary condition 

treatment, the exclusion of U.S. fire emissions,93 and Hg

plume chemistry approach. In addition, one commenter 

referenced the same ENVIRON report and stated that before 

implementation of controls required by the proposed rule, 

 

89 Caffrey et al., 2010.

90 Driscoll, C. T., Han, Y.-J., Chen, C. Y., Evers, D. C., Lambert, K. 

F., Holsen, T. M., et al. (2007). “Mercury Contamination in Forest and 

Freshwater Ecosystems in the Northeastern United States.” BioScience, 

57(1).

91 Keeler, G.J., Landis, M.S., Norris, G.A., Christianson, E.M., Dvonch, 

J.T., 2006. “Sources of mercury wet deposition in Eastern Ohio, USA.” 

Environmental Science & Technology 40, 5874-5881.

92 White, E.M., Keeler, G.J., Landis, M.S., 2009. “Spatial Variability 

of Mercury Wet Deposition in Eastern Ohio: Summertime Meteorological 

Case Study Analysis of Local Source Influences.” Environmental Science 

& Technology 43, 4946-4953.

93 Finley, B.D., Swartzendruber, P.C., Jaffe, D.A., 2009. “Particulate 

mercury emissions in regional wildfire plumes observed at the Mount 

Bachelor Observatory.” Atmospheric Environment 43, 6074-6083.
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areas with relatively high EGU-attributable Hg deposition 

(one-fifth or more of total deposition) in 2016 constitute 

less than 0.25 percent of the continental U.S. area, and 

only three grid cells have EGU contributions exceeding half 

of total deposition. 

Another commenter suggested that current research 

shows that models of Hg atmospheric fate and transport 

overestimate the local and regional impacts of some 

anthropogenic sources, such as U.S. EGUs. Thus, according 

to the commenter, calculated contributions to Hg deposition 

and fish tissue MeHg levels from these sources represent 

upper bounds of actual contributions,

96,97 and EPA should 

present results as estimates of lower and upper bound 

limits.

Response: EPA disagrees with the information presented 

by ENVIRON. The ENVIRON report is based on the 

misapplication of multiple incommensurate modeling studies 

and false premises which include the incorrect notion that 

 

96 Seigneur, C., Lohman, K., Vijayaraghavan, K., Shia, R.L., 2003. 

“Contributions of global and regional sources to mercury deposition in 

New York State.” Environmental Pollution 123, 365-373.

97 Seigneur, C., Vijayaraghavan, K., Lohman, K., Karamchandani, P., 

Scott, C., 2004. “Modeling the atmospheric fate and transport of 

mercury over North America: power plant emission scenarios.” Fuel 

Processing Technology 85, 441-450.
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the boundary conditions are over-estimated and the idea 

that EPA should use in-plume chemistry that has not been 

explicitly characterized and peer reviewed. Reactions that 

may reduce gas phase oxidized Hg in plumes have not been 

explicitly identified in literature. Recent studies in 

central Wisconsin and central California suggest the 

opposite may happen; elemental Hg may be oxidized to Hg(II) 

in plumes.98,99 Better field study measurements and specific 

reaction mechanisms need to be identified before making 

conclusions about potential Hg in-plume chemistry or 

applying surrogate reactions in regulatory modeling. The 

possibility that Hg(0) is oxidized to Hg(II) in plumes 

suggests coal-fired power plant Hg contribution inside the 

U.S. may be underestimated in EPA modeling. 

EPA asserts that the numbers suggested by the 

commenter are inaccurate, as it is not appropriate to 

adjust EPA’s deposition estimates based on previous Hg

modeling done with older Hg chemistry, in-plume reactions 

 

98 Kolker, A., Olson, M.L., Krabbenhoft, D.P., Tate, M.T., Engle, M.A., 

2010. “Patterns of mercury dispersion from local and regional emission 

sources, rural Central Wisconsin, USA.” Atmospheric Chemistry and 

Physics 10, 4467-4476.

99 Rothenberg, S.E., McKee, L., Gilbreath, A., Yee, D., Connor, M., Fu, 

X.W., 2010. “Wet deposition of mercury within the vicinity of a cement 

plant before and during cement plant maintenance.” Atmospheric 

Environment 44, 1255-1262.
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that have not been explicitly identified, and erroneous 

adjustments to Hg boundary inflow. Recent research has 

shown that ambient Hg concentrations have been decreasing 

in the northern hemisphere since 2000.100 EPA declines to 

revise this analysis as commenter suggests for several 

reasons, including available evidence indicates that

emissions from China have not appreciably changed between 

2000 and 2006101 and ambient Hg concentrations have 

decreased, the commenter inappropriately comingled out–ofdate Hg modeling simulations with EPA results, and

ENVIRON’s analysis has not undergone any scientific peer 

review and presents information with incorrect assumptions 

as noted in this response,.

EPA also disagrees with the commenter’s interpretation 

of the applicability of wildfire Hg emissions to this 

assessment. Finley et al. (2009)102 suggests caution when 

using their field data to make assumptions about Hg(p) 

emissions from wildfires; the estimated particulate Hg 

emissions from wildfires is based on one field site with a 

limited sample size, and the assumptions made (such as the 

 

100 Slemr et al., 2011.

101 Streets et al., 2009.

102 Finley et al. 2009.
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observed Hg(p) to carbon monoxide ratios at this location) 

may not be valid on a broader scale.103 Hg emissions from 

wildfires are a re-volatilization of previously deposited 

Hg.

104 Given that electrical generating power plants are 

currently and historically have been a large Hg-emitting 

source, the inclusion of wildfire emissions in a modeling 

assessment would necessarily increase the contribution from 

this emissions sector.

EPA disagrees with the assertion that EPA failed to 

consider the relative magnitude of Hg emissions from U.S. 

EGUs compared to other sources and disagrees with the 

interpretation of EGU deposition presented in the ENVIRON 

report. As noted in the Hg Risk TSD, EPA modeled Hg

emissions from U.S. and non-U.S. anthropogenic and natural 

sources to estimate Hg deposition across the country. EPA 

also determined the contribution of Hg emissions from U.S. 

EGUs to total Hg deposition in the U.S. by running modeling 

simulations for 2005 and 2016 with Hg emissions from U.S. 

EGUs set to zero. Based on the analysis done for this rule 

EPA finds that total Hg deposition from EGUs do 

 

103 Id.

104 Wiedinmyer, C., Friedli, H., 2007. “Mercury emission estimates from 

fires: An initial inventory for the United States.” Environmental 

Science & Technology 41, 8092-8098.
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significantly impact human health. The ENVIRON report 

provides no risk analysis of EGU contribution. 

EPA disagrees that research105,106 presented by the 

commenter shows that U.S. EGU impacts are over-estimated. 

The commenter’s references do not support this statement. 

The references provided by the commenter are based on Hg

modeling that uses models that are no longer applied and 

that are based on out-dated Hg chemistry and deposition 

assumptions. Given the advances in Hg modeling since the 

early 2000s, EPA does not feel an upper and lower bound 

estimate is necessary.

2. Chemical reactions

Comment: Several commenters stated that the CMAQ 

modeling fails to account for the chemical reduction of 

gaseous ionic Hg to elemental Hg that may occur in EGU 

plumes. The commenters noted that EPA did not use the 

Electric Power Research Institute’s (EPRI) Advanced Plumein-Grid Treatment, which includes a surrogate reaction to 

reduce gaseous ionic Hg to elemental Hg inside plumes. 

Multiple commenters claimed that the reduction of reactive 

 

105 Seigneur et al., 2003.

106 Seigneur et al., 2004.
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gaseous Hg to gaseous elemental Hg has been reported in 

power plant plumes and that supporting data include 

atmospheric concentrations of speciated Hg measured 

downwind of power plant stacks at ground-level monitor 

sites and dispersion model predictions.107,108 A detailed 

description of various plume measurement studies is 

provided in EPRI Comments, Section 3.4: Plant Bowen, 

Georgia, Plant Pleasant, Wisconsin, and Plant Crist, 

Florida. One commenter felt the impact of grid resolution 

(12 km sized grid cells) on the CMAQ modeling was not 

appropriately addressed by EPA. Their concerns due to grid 

resolution include the notion that a source‘s emissions 

will be averaged over the entire grid cell. According to 

the commenter, such averaging causes an artificially fast 

dilution that smoothes out areas of high and low 

deposition, which may limit the ability of the model to 

simulate smaller areas of localized high deposition. This 

 

107 Edgerton, E.S., Hartsell, B.E., Jansen, J.J., 2006. “Mercury 

speciation in coal-fired power plant plumes observed at three surface 

sites in the southeastern U.S.” Environmental Science & Technology 40, 

4563-4570.

108 Lohman, K., Seigneur, C., Edgerton, E., Jansen, J., 2006. “Modeling 

mercury in power plant plumes.” Environmental Science & Technology 40, 

3848-3854.
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commenter felt that using the APT would address these 

issues. 

Response: EPA disagrees with the commenters’ claims

that oxidized Hg chemically reduces to elemental mercury 

within the plume. There is no evidence of these chemical 

reactions in the scientific literature. The references 

cited by the commenters are from non-peer reviewed reports 

and conference proceedings. EPA does not consider 

information presented at conferences or industry reports to 

be peer reviewed literature, and consideration of oral 

presentation material would be inappropriate. Further, even 

these cited references do not provide sufficient 

information for incorporating the supposed reactions into 

the modeling (e.g., specific chemical reactions, reaction 

rates, etc.); rather, the cited references only suggest 

that oxidized gas phase Hg could be reduced and postulate a 

possible pathway.

Recent studies in central Wisconsin and central 

California suggest the opposite may happen; elemental Hg

may be oxidized to Hg(II) in plumes.109,110 Better field study 

 

109 Kolker et al., 2010.

110 Rothenberg et al., 2010.
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measurements and specific reaction mechanisms need to be 

identified before making conclusions about potential Hg inplume chemistry or applying surrogate reactions in 

regulatory modeling. Currently, models such as Advanced 

Plume Treatment (APT) use a surrogate reaction for the 

potential reactive gas phase Hg reduction that may or may 

not occur in plumes.

111 Reactions that may reduce gas phase 

oxidized Hg in plumes have not been explicitly identified 

in literature. The application of potentially erroneous inplume chemistry that is a fundamental component of APT 

would be inappropriate. In addition, the APT is not 

available in the most recent version of CMAQ. It would be 

inappropriate for EPA to apply an out of date photochemical 

model with in-plume chemistry that has not been shown to 

exist.

EPA agrees with the commenter that the CMAQ modeling 

with 12 km grid resolution may provide a lower bound 

estimate on EGU contribution as higher impacts using finer 

grid resolution are possible. The commenter’s assertion 

that EGU impacts are likely higher further supports the 

 

111 Vijayaraghavan, K., Seigneur, C., Karamchandani, P., Chen, S.Y., 

2007. “Development and application of a multipollutant model for 

atmospheric mercury deposition.” Journal of Applied Meteorology and 

Climatology 46, 1341-1353.
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final conclusions of the exposure modeling assessment. EPA 

notes that the application of a photochemical model at a 12 

km grid resolution for the entire continental U.S. is more 

robust in terms of grid resolution and scale that anything 

published in literature and represents the most advanced 

modeling platform used for a national Hg deposition 

assessment.

3. Modeled deposition compared to measured deposition

Comment: Multiple commenters expressed dissatisfaction 

related to EPA’s model performance evaluation of CMAQ 

estimated Hg deposition. The commenters stated that EPA 

failed to evaluate the CMAQ model against real-world 

measurements and that EPA fails to provide first-hand 

information on wet and dry deposition processes. The 

commenters also stated that EPA needs to assess how 

predicted values of deposition compare to Mercury 

Deposition Network (MDN) data and how predicted values of 

ambient speciated Hg concentrations compare to measurement 

networks like AMNet and SEARCH. In addition, commenters 

stated that EPA used highly aggregated performance metrics 

comparing model estimates to observations that they felt 

result in a degraded and lenient operational evaluation of 
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the modeling system. A commenter suggested that EPA’s model 

performance provides no confidence for the intended purpose 

of estimating deposition near point sources. One commenter 

simply noted that EPA’s model over-estimated total Hg wet 

deposition at MDN monitors. Finally, several commenters 

noted that EPA presented a negative modeled wet deposition 

total in the air quality modeling TSD, which is physically 

impossible.

Response: The predicted wet deposition in the air 

quality modeling TSD was incorrectly calculated during 

post-processing of model and observation pairs. This error 

only influenced the calculation of model performance 

metrics. The error has been fixed, and the model 

performance metrics in the revised air quality modeling TSD 

have been updated. In response to comments, EPA provided 

additional model performance evaluation by season to the 

air quality modeling TSD. In addition, in response to 

comments, EPA has now included model performance evaluation 

for total Hg wet deposition for the 36 km modeling domain. 

EPA disagrees that it did not conduct an assessment 

comparing CMAQ total Hg wet deposition estimates to MDN 

data. The air quality modeling TSD clearly shows a 
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comparison of CMAQ estimated total Hg wet deposition with 

MDN data for the entire length of the modeling period. The 

characterization of wet and dry deposition processes 

relating to speciated Hg in global and regional scale 

photochemical models should be continually evaluated by the 

academic community and improved when appropriate. CMAQ wet 

deposition of Hg has been and will continue to be 

extensively evaluated against Mercury Deposition Network 

sites.112 There is no dry deposition monitoring network, and 

the CMAQ dry deposition processes will be evaluated when 

measurement data sets become available. EPA disagrees that 

an evaluation of ambient speciated Hg against routine 

monitor networks such as AMNet or SEARCH would be useful 

for this particular modeling application. The AMNet Hg

network did not exist in 2005, which is EPA’s baseline 

model simulation time period, and the SEARCH network 

started making preliminary measurements of Hg at one or two 

sites in 2005. In addition, measurement artifacts related 

to gaseous oxidized Hg are difficult to quantify and make 

 

112 Bullock, O.R., Atkinson, D., Braverman, T., Civerolo, K., Dastoor, 

A., Davignon, D., Ku, J.Y., Lohman, K., Myers, T.C., Park, R.J., 

Seigneur, C., Selin, N.E., Sistla, G., Vijayaraghavan, K., 2009. “An 

analysis of simulated wet deposition of mercury from the North American 

Mercury Model Intercomparison Study.” Journal of Geophysical ResearchAtmospheres 114.
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direct comparison to model estimates problematic.113

Considering the problems associated with TEKRAN 

measurements of ambient Hg and the sparse nature of routine 

measurements in the U.S., EPA did not compare ambient Hg

against model estimates. 

EPA disagrees that the model performance presented in 

the air quality TSD is insufficient. EPA asserts that the 

model performance evaluation is generally similar to the 

level of model performance presented in literature. One 

commenter presented the results of several Hg modeling 

studies as providing information that the commenter 

believes to be relevant for this assessment in terms of 

model performance metric estimation and the level of model 

performance evaluation shown for assessments modeling Hg

near point sources. For example, one cited study titled 

”Modeling Mercury in Power Plant Plumes” models near-source 

Hg chemistry from U.S. EGUs, but provides absolutely no 

information about model performance evaluation.114 Another

 

113 Lyman, S.N., Jaffe, D.A., Gustin, M.S., 2010. “Release of mercury 

halides from KCl denuders in the presence of ozone.” Atmospheric 

Chemistry and Physics 10, 8197-8204.

114 Lohman et al., 2006.
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commenter identified two studies as supposedly having Hg

modeling results that are applicable to EPA’s analysis.115,116

These studies present similar model performance 

metrics as EPA and aggregate the metrics across many 

monitor locations as did EPA; however, these articles 

calculate long term annual averages of modeled and observed 

total Hg wet deposition before estimating performance 

metrics, which presents a more favorable evaluation. The 

Seigneur et al. paper117 employs a less stringent approach 

for matching observations and model estimates of total Hg

wet deposition by calculating annual averages of both 

before comparison to make model performance seem optically 

better. It is common practice to pair modeled estimates and 

observations in space and time (weekly in this case),

estimate performance metrics, then average all the metrics 

together. The latter is the approach taken by U.S. EPA and 

should have been taken by the studies presented by the 

commenter. EPA finds the performance evaluation presented 

 

115 Seigneur, C., Lohman, K., Vijayaraghavan, K., Jansen, J., Levin, L., 

2006. “Modeling atmospheric mercury deposition in the vicinity of power 

plants.” Journal of the Air & Waste Management Association 56, 743-751.

116 Vijayaraghavan, K., Karamchandani, P., Seigneur, C., Balmori, R., 

Chen, S.-Y., 2008. “Plume-in-grid modeling of atmospheric mercury.” 

Journal of Geophysical Research-Atmospheres 113.

117 Seigneur et al., 2006.
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in the modeling TSD consistent with and far beyond what is 

presented in published articles119 deemed relevant by the 

commenter. In addition to the evaluation presented by EPA 

in the air quality modeling TSD, CMAQ model performance for 

total Hg wet deposition has been compared with other Hg

models.120

EPA agrees that the commenter accurately restated

total wet deposition model performance information provided 

by EPA in the Air Quality Modeling TSD. To provide context, 

other Hg modeling studies show a positive bias for annual 

total Hg wet deposition.121,122 An annual Hg modeling 

application done by ENVIRON123 and the Atmospheric and 

Environmental Research for Lake Michigan Air Directors 

Consortium show seasonal average normalized bias between 70 

and 158 percent and seasonal average normalized error 

between 72 and 503 percent.124 These results indicate a very 

 

119 Lohman, K., Seigneur, C., Edgerton, E., Jansen, J., 2006. Modeling 

mercury in power plant plumes. Environmental Science & Technology 40, 

3848-3854.

120 Bullock et al., 2009.

121 Id.

122 Vijayaraghavan et al., 2007.

123 Yarwood, G, Lau, S., Jia, Y., Karamchandani, P., Vijayaraghavan, K. 

2003. Final Report: Modeling Atmospheric Mercury Chemistry and 

Deposition with CAMx for a 2002 Annual Simulation. Prepared for 

Wisconsin Department of Natural Resources. 

http://www.gypsymoth.wi.gov/air/toxics/mercury/hg_X97579601_appB.pdf

124 Yarwood et al., 2003.
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large over-estimation tendency. The model performance shown 

by EPA is consistent with other long-term Hg modeling 

applications.

4. Excess Local Deposition from Hg Emissions from U.S. 

EGUs(Deposition Hotspots)

Comment: One commenter stated that reducing Hg will 

benefit local environments. The commenter stated that a 

2007 study confirmed the presence of Hg “hotspots” downwind 

from coal-fired power plants and confirmed that coal-fired 

power plants within the U.S. are the primary source of Hg

to the Great Lakes and the Chesapeake Bay.125 The commenter 

also stated that the study is consistent with a major Hg

deposition study conducted by EPA and the University of 

Michigan that concluded that approximately 70 percent of Hg

wet deposition resulted from local fossil fuel emissions in 

the region.126

One commenter agreed with the Agency’s assessment of 

potential for deposition “hotspots” that shows that Hg 

deposition near EGUs can be three times as large as the 

 

125 Evers, David C. et al. 2007. “Biological Mercury Hotspots in the 

Northeastern United States and Southeastern Canada,” Bioscience. Vol. 

57 No. 1. p. 29.

126 Cohen, et al. 2004. “Modeling the Atmospheric Transport and 

Deposition of Mercury to the Great Lakes,” Environmental Research 95, 

(247-265).
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regional average. The commenter stated that this excess Hg 

deposition would substantially increase the health and 

environmental risks associated with emissions at these 

sites. The same commenter also stated that EPA applied a 

conservative methodology to quantify near-source Hg 

deposition is conservative. The commenter stated that

maximum excess local Hg deposition may be significantly 

underestimated by averaging high deposition sites downwind 

of an EGU in the direction of prevailing winds with lower 

excess deposition at locations close to but frequently 

upwind of the facility. The same commenter suggests that 

had EPA used CMAQ and individual 12x12 km2 grid cells to 

quantify local deposition, the model could increase the 

excess Hg deposition at these locations significantly and 

place them at even greater risk of adverse health and 

environmental effects of HAP from U.S. EGUs. 

One commenter stated that the Hubbard Brook Research 

Foundation issued a report in 2007 that identified five Hg

hotspots, one of which was in the Adirondack Park, along 

with four suspected hotspots.127 The commenter stated that 

 

127 Driscoll, C.T., D. Evers, K.F. Lambert, N. Kamman, T. Holsen, Y-J. 

Han, C. Chen, W. Goodale, T. Butler, T. Clair, and R. Munson. Mercury 
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this study also provides a good description of the impacts 

of Hg on the Common Loon, which is a symbol of a healthy 

Adirondack environment.

One commenter stated that there is there is no 

evidence of Hg hotspots due to local deposition associated 

with coal-fired power plants. According to the commenter,

EPA‘s use of a 50 km radius to calculate hotspots is 

flawed. The commenter stated that modeling studies show 

that deposition of Hg emitted from power plants is not 

confined to a 50-km radius around the plants and that most 

emissions from power plants travel beyond 50 km.128

Several commenters stated that EPA does not adequately 

define hotspots in this proposed rule. Those same 

commenters cited a previous EPA definition of hotspots as 

“a waterbody that is a source of consumable fish with MeHg

tissue concentrations, attributable solely to utilities, 

greater than EPA‘s MeHg water quality criterion of 0.3 

mg/kg” (milligrams per kilogram)129. The same commenters 

 

Matters: Linking Mercury Science with Public Policy inthe Northeastern 

United States. 2007. Hubbard Brook Research Foundation. Science Links 

Publication. Vol. 1, no. 3.

128 Seigneur et al., 2006.

129 U.S. EPA, 2005. 40 CFR Part 63 [OAR–2002–0056; FRL–7887–7] RIN 2060–

AM96. Revision of December 2000 Regulatory Finding on the Emissions of 

Hazardous Air Pollutants From Electric Utility Steam Generating Units 
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stated that it is unclear why EPA changed from defining a 

hotspot by fish tissue MeHg concentration to defining a 

hotspot by depositional excess. Two commenters suggested

that a Hg hotspot is a specific location that is 

characterized by elevated concentrations of Hg exceeding a 

well-established criterion, such as a reference 

concentration (RfC) when compared to its surroundings. 

Those same commenters stated that identifying Hg hotspots 

should not be constrained to locations where concentrations 

can be attributed to a single source or sector130. One of 

those two commenters noted that others have defined 

“hotspots as a spatially large region in which 

environmental concentrations far exceed expected values, 

with such values (i.e. concentrations) being 2 to three

standard deviations above the relevant mean”.131

One commenter stated that Hg concentrations are not 

always highest at sites closest to a major source. The 

commenter referred to a study by Kolker, et al. (2010)132

 

and the Removal of Coal- and Oil-Fired Electric Utility Steam 

Generating Units From the Section 112(c). Final rule, March 29.

130 Evers et al., 2007.

131 Sullivan T., 2005. “The Impacts of Mercury Emissions from coal-fired 

Power Plants on Local Deposition and Human Health Risk.” Presented at 

the Pennsylvania Mercury Rule Workgroup Meeting, October 28.

132 Kolker, et al., 2010.
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that demonstrated that concentrations of atmospheric 

reactive gaseous Hg, gaseous elemental Hg, and fine 

particulate Hg were lower when measured 25 km from a 1114 

MW coal-fired EGU than when measured 100 km away. The 

commenter stated that these findings contradict the idea, 

implicit in EPA‘s hotspot analysis, that reactive gaseous 

Hg decreases with distance from a large point source.

One commenter stated that wet deposition measurements 

were taken between November 2004 through December 2007 at 

three sites located downwind from the coal-fired power 

plant Crist in Pensacola, FL. The commenter stated that 

during this period, Plant Crist emitted about 230 pounds of 

Hg annually, about 85 percent of which was reactive gaseous 

Hg.

133 The commenter cited a study by Landing et al. 

(2010)134 that estimated that 22–33 percent of wet-deposited 

Hg at these sites came from coal combustion, including 

regional and local sources while the remaining 67–78 

percent came from the global background. The commenter 

 

133 EPRI, 2010. Atmospheric Deposition of Mercury, Trace Metals and Major 

Ions to a Watershed Around a Coal-Fired Power Plant. Palo Alto, CA: 

1021566.

134 Landing W.M., Caffrey J.M., Nolek S. D., Gosnell K. J., and Parker W. 

C., 2010 “Atmospheric Wet Deposition of Mercury and Other Trace 

Elements in Pensacola, Florida,” Atmospheric Chemistry and Physics, 10, 

4867–4877.
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stated that using the same data from these same wet 

deposition sites, Caffrey et al. (2010)135 found that Hg

deposition and concentrations did not differ in a 

statistically significant manner among these three sites 

and that the concentrations values were similar to those 

from Mercury Deposition Network (MDN) sites that are more 

than 50 km away from Plant Crist located along the Northern 

Gulf of Mexico coast. 

Another commenter stated that Plant Crist installed a 

wet scrubber and has operated that scrubber continuously 

since December 2009. The commenter stated that the scrubber 

reduces total Hg emissions by about 70 percent and reduces 

emissions of reactive gaseous Hg by about 85 percent. 

According to the commenter, using Hg to trace metal 

(arsenic and selenium) ratios in precipitation collected in 

the same MDN in (post-scrubber) 2010, Krishnamurthy, et al. 

(2011)136 reported that Hg deposition due to local and 

 

135 Caffrey, J.M., Landing, W.M., Nolek, S.D., Gosnell, K.J., Bagui, 

S.S., Bagui, S.C., 2010. “Atmospheric deposition of mercury and major 

ions to the Pensacola (Florida) watershed: spatial, seasonal, and 

inter-annual variability.” Atmospheric Chemistry and Physics 10, 5425-

5434.

136 Krishnamurthy N., Landing W.M, Caffrey J.M., 2011. “Rainfall 

Deposition of Mercury and Other Trace Elements to the Northern Gulf of 

Mexico.” Presented at the 10th International Conference on Mercury as a 

Global Pollutant, Halifax, Nova Scotia, Canada, July 27.
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regional sources had changed between -10 to +6 percent at 

these sites, relative to historic measurements. The 

commenter stated that these changes were thought to 

represent upper bound estimates, since the researchers 

assumed that all Hg, arsenic, and selenium measured in wet 

deposition was from local and regional coal combustion 

sources even though measured deposition can also include

global emission sources. The commenter stated that, taken 

collectively, these findings show that increased local 

deposition, possibly due to EGUs, and deposition changes 

due to changes in EGU emissions, are small and within the 

range of natural variability.

Two commenters stated that a study by the Department 

of Energy (DOE) that collected and analyzed soil and 

vegetation samples for Hg near three U.S. coal-fired power 

plants – one in North Dakota, one in Illinois, and one in 

Texas – found no strong evidence of “hotspots” around these 

three plants. 

Two commenters stated that analysis of long-term 

trends in Hg emissions from coal-fired EGUs and wet 

deposition in Florida concluded that statistical analysis 

does not show evidence of a significant relationship 
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between temporal trends in Hg emissions from coal-fired 

EGUs in Florida and Hg concentrations in precipitation 

during 1998-2010. According to the commenters, these 

observational studies are supported by and consistent with 

evidence that oxidized Hg emitted from coal-fired power 

plants rapidly converts to elemental Hg, significantly 

reducing the potential for “local” or nearby deposition.

Two commenters stated that the Hg Risk TSD presents no 

information, summary statistics, and/or actual calculations 

showing how excess deposition within 50 km of an EGU source 

is obtained. The commenters stated that by assessing only 

Hg deposition attributable to EGUs, EPA fails to provide a 

context for all other sources of Hg deposition. The 

commenters stated that the Agency does not explain why 

deposition from the top 10 percent of EGU Hg emitters does 

not decline, despite substantial reductions in modeled Hg

emissions from those sources between 2005 and 2016. 

According to the commenters this implies that the top 10 

percent EGUs may have approximately as much of a regional 

effect as a local effect. 

Two commenters stated that the CMAQ model has 

limitations when used to predict local deposition and tends 
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to overestimate local deposition. The commenters stated

that modeling studies using either a plume model or an 

Eulerian model predict that 91 to 96 percent of the Hg

emitted by an EGU travels beyond 50 km.137

Response: EPA agrees with the commenters that stated 

that Hg emissions from EGUs deposit locally and regionally 

and contribute to excess local deposition near U.S. EGUs. 

EPA acknowledges additional studies

138 cited by those 

commenters that corroborate EPA’s conclusions. However, EPA 

disagrees with those commenters’ characterization of the 

methodology used to calculate the potential for excess 

local deposition. In response, EPA has clarified the 

methodology in the new TSD entitled “Technical Support 

Document: Potential for Excess Local Deposition of U.S. EGU 

Attributable Mercury in Areas near U.S. EGUs”, which is 

available in the docket.

EPA agrees that there is no generally agreed-upon

definition of “hotspot”. As discussed in the preamble and 

TSD, for the purposes of the appropriate and necessary 

finding, EPA determined that information on the potential 

 

137 Edgerton et al., 2006.

138 Driscoll et al., 2007.
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for excess deposition of Hg in areas surrounding power 

plants would be useful in informing the finding. EPA 

disagrees with some commenters who misinterpreted the 

intent of the Hg deposition hotspot analysis. Specifically, 

the analysis is not of “Hg hotspots” but rather of Hg

deposition hotspots, defined as excess local Hg deposition 

around power plants, as clarified in the new Local 

Deposition TSD. 

EPA disagrees that the analysis assumes that 

deposition of Hg is confined to a 50-km radius around power 

plants. The purpose of EPA analysis was to evaluate whether 

there existed “excess deposition of Hg in nearby locations 

within 50 km of EGUs that might result in Hg deposition 

‘hotspots’.” As explained further in the new TSD, EPA 

calculated the average EGU-attributable deposition (based 

on CMAQ modeling of Hg deposition) in the area 500 km 

around each plant and the average EGU-attributable 

deposition in the area 50 km around each plant. The 

difference between those two values is the excess local 

deposition around the plant. EPA does not suggest Hg

emissions from power plants stop at 50 km from the source. 

Some portion of EGU emissions deposit before 50 km, and 
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some portion travels beyond 50 km. In addition, Hg

disperses as it transports, so the average EGU contribution 

can be lower in areas beyond 50km relative to areas within 

50km even though Hg emissions from EGUs are depositing into 

U.S. watersheds.

EPA disagrees with some commenters’ interpretation of 

the analysis as being focused on local deposition from all 

sources. In fact, the focus was on excess local deposition, 

rather than all local deposition. EPA has clarified the 

purpose of the excess local deposition analysis in the new 

TSD. EPA agrees that all EGUs add to local deposition, 

however, not all EGUs have local deposition that greatly 

exceeds regional deposition, which is the relevant 

question. EPA disagrees that the DOE study referenced by 

the commenters attempted to assess the same analytical 

question as EPA’s analysis. The DOE study focused on 

comparisons of total deposition near and far from power 

plants. EPA’s analysis did not focus on total Hg

deposition, because as EPA acknowledges throughout its 

analysis, global sources of Hg deposition account for a 

large percentage of total Hg deposition. In addition,

including global sources of Hg deposition would obscure to 
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the comparison of local and regional U.S. EGU-attributable

Hg deposition. Because of regional deposition from both 

domestic and global sources of Hg, total Hg deposition at 

any location is unlikely to be highly correlated with local 

sources. EPA’s analysis focused on U.S. EGU-attributable Hg

deposition and demonstrates that for some plants 

(especially those with high Hg emissions), there is local

deposition of Hg that exceeds the average regional 

deposition around the plant. 

EPA’s analysis shows heterogeneity in the amount of 

excess local deposition around plants. The new Local 

Deposition TSD shows that some plants can have local 

deposition that is less than the regional average 

deposition, suggesting that most of the Hg from those 

plants is transported regionally or that other EGUs in the 

vicinity of those plants dominate the deposition of Hg near 

the plants. This does not detract from the overall finding 

that around some power plants with high levels of Hg

emissions that excess local deposition is on average three

times the regional EGU-attributable deposition around those 

plants. 
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EPA disagrees that the Hg Risk TSD did not provide 

sufficient information regarding the excess local 

deposition calculation. Nonetheless, EPA has further 

clarified the methodology in the new Local Deposition TSD, 

including further descriptions of the method used to 

calculate the local and regional deposition around power 

plants along with maps and tables of results.

EPA disagrees with the commenters that stated that the 

discussion of local deposition in the Hg Risk TSD did not 

demonstrate that Hg deposition from the top 10 percent of 

EGU Hg emitters declines. Table 1 of the new Local 

Deposition TSD clearly shows that mean local deposition 

(within 50km of a plant) for the top 10 percent of emitters 

declines from 4.89 μg/m3 to 1.18 μg/m3. What does not 

change is the percent local excess for EGU-attributable Hg

deposition. This implies that while Hg deposition from EGUs 

is declining, there is still an excess contribution to 

local deposition relative to regional deposition; e.g.,

because of dispersion, the contribution to average 

deposition outside 50km from the plant is lower than the 

contribution to average deposition within 50km of the 

plant.
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EPA disagrees with the commenter regarding the

interpretation of the literature related to the spatial 

extent of deposition of Hg emitted by U.S. EGUs. EPA also 

disagrees that the CMAQ model has limitations for this 

application or overestimates local deposition. The 

commenter does not provide any credible support for the 

assertion that grid-based models typically overestimate 

local deposition surrounding EGUs. EPA maintains that the 

CMAQ photochemical model represents the best science 

currently available in simulating atmospheric chemistry, 

transport, and deposition processes. 

The study139 cited by the commenter to support the 

notion that 91 to 96 percent of Hg emitted from power 

plants travels beyond 50 km is based on a photochemical 

transport model (the TEAM model) that does not employ 

current state-of-the-science and is not actively developed 

or updated. Furthermore, the modeling is based on grid 

cells that are 20 km in size, which limits generalizability 

to EPA modeling performed at 12 km grid resolution using a 

state of the science photochemical grid model. The cited 

modeling study ignores dry deposition of elemental Hg from 

 

139 Seigneur et al., 2006.
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all sources, an assumption that clearly limits the regional 

impacts from sources140. The methodology of this study cited 

by the commenter is critically flawed in that it presents 

no results where individual Hg emission sources are removed 

and the difference between the zero out simulation and 

baseline model simulations are directly compared. Finally, 

the modeling study cited by the commenter presents an 

illustration of gridded total annual Hg deposition from the 

TEAM model for the eastern U.S. that clearly shows elevated 

annual total Hg deposition in the vicinity of coal-fired 

power plants in the Ohio River Valley and northeast Texas.

The information141 provided by a commenter is not 

relevant to the analysis of excess local deposition from 

EGUs, as it is based on ground level measurements of wet 

deposition alone. Changes to wet deposition over a fairly 

short time frame such as a year (the part of the study 

where the coal-fired power plant (Crist) emitting Hg

installed controls) are not expected to provide a 

meaningful information about the effectiveness of control 

technology. Wet deposition is highly variable from year to 

 

140 Id.

141 EPRI, 2010.
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year and is subject to varying meteorological wind patterns 

from year to year. A more appropriate observation based 

assessment would be to evaluate both wet and dry 

deposition.

d. Hg Risk TSD

1. Assumption of Linear Proportionality in Relationship

between Changes in Hg Deposition and Changes in Fish Tissue 

Hg Concentrations (Mercury Maps)

Comment: Several commenters criticized EPA’s 

assumption that changes in deposition resulting from U.S. 

EGU emissions of Hg will result in proportional changes in 

fish tissue Hg concentrations at the watershed level, as 

supported by the Mercury Maps modeling exercise. According 

to one commenter, the Mercury Maps (MMaps) model has 

limited capability to adequately determine bioaccumulation 

in fish. The same commenter stated that the Mercury Cycling 

Model (MCM) developed by EPRI is a more rigorous model that 

was developed expressly to evaluate the relationship 

between changes in atmospheric Hg deposition to waterbodies 

and changes in fish tissue MeHg levels.

Several commenters stated that the Mercury Maps model 

has many deficiencies. Those commenters stated that Mercury 
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Maps is a static model unable account for the dynamics of 

ecosystems that affect Hg bioaccumulation in fish, cannot 

consider non-air Hg inputs to watersheds, and assumes 

reductions in airborne Hg lead to proportional reductions 

in fish MeHg concentrations. Another commenter claimed that

data that demonstrate a steady-state linear reduction in 

fish tissue MeHg in response to a reduction in atmospheric 

Hg deposition within watersheds do not exist and provided

several references that they claimed show non-linear 

responses to changes in Hg deposition142,143. 

The same commenter disagreed with EPA’s interpretation 

of Figure 2-17 in the March TSD and stated that a U.S. 

Geological Survey national waterway study144 showed that 

 

142 Harris., R. C., John W. M. Rudd, Marc Amyot, Christopher L. Babiarz, 

Ken G. Beaty, Paul J. Blanchfield, R. A. Bodaly, Brian A. Branfireun, 

Cynthia C. Gilmour, Jennifer A. Graydon, Andrew Heyes, Holger 

Hintelmann, James P. Hurley, Carol A. Kelly, David P. Krabbenhoft, 

Steve E. Lindberg, Robert P. Mason, Michael J. Paterson, Cheryl L. 

Podemski, Art Robinson, Ken A. Sandilands, George R. Southworth, 

Vincent L. St. Louis, and Michael T. TateRudd, J. W. M., Amyot M., et 

al., Whole-Ecosystem study Shows Rapid Fish-Mercury Response to Changes 

in Mercury Deposition. Proceedings of the National Academy of Sciences 

Early Edition, PNAS 2007 104 (42) pp. 16586-16591; (published ahead of 

print September 27, 2007).

143 Orihel D.M., Paterson M.J., Blanchfield P.J., Bodaly R.A., Gilmour 

C.C., Hintelmann H., 2007. “Temporal Changes in the Distribution, 

Methylation, and Bioaccumulation of Newly Deposited Mercury in an 

Aquatic Ecosystem,” Environmental Pollution, 154, 77–88. 

144 Scudder B.C., Chasar L.C., Wentz D.A., Bauch N.J., Brigham M.E., 

Moran P.W., Krabbenhoft D.P., 2009. Mercury in fish, bed sediment, and 

water from streams across the United States, 1998–2005: U.S. Geological 

Survey Scientific Investigations Report 2009–5109, 74 p.
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sheet flow and drainage, not deposition, dominated input to 

the waterbodies it surveyed. The commenter stated that 

sheet flow and drainage could contain Hg and thus

complicate the relationship that EPA asserts is linear and 

direct. Another commenter cited Figure 2-17 in the Hg Risk

TSD as showing that there is no well-defined relationship 

between Hg deposition and MeHg concentrations in fish 

tissue on a national basis. 

Several commenters provided comments related to the 

assumption that fish tissue Hg levels used in the analysis 

represent a steady-state. One commenter stated that given 

the demonstrated lag time in response to deposition change, 

it is logical to conclude that a lag time needs to be 

incorporated in MMaps to adjust the estimation of how much 

fish tissue MeHg levels decrease in response to decreases 

in Hg deposition attributable to U.S. EGUs. According to 

the same commenter, the METAALICUS study shows that there 

is a lag time (and a non-proportional response) after 3–4 

years. The same commenter noted that there are numerous 

factors that influence lag time including (1) watershed 
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characteristics145, (2) the fact that watersheds may act as 

legacy sources releasing Hg when disturbed146, (3) the 

magnitude of emission reductions and subsequent changes in 

atmospheric deposition need to be weighed against the 

amount of Hg already in an ecosystem147, (4) the distance of 

an ecosystem from Hg sources148, and (5) the fact that Hg

deposited to aquatic ecosystems becomes less available for 

uptake by biota over time149. Another commenter stated that 

additional Mercury Maps assumptions do not allow for 

considerations of lag in response to changes in: (1) 

deposition, (2) legacy sources of Hg such as mining, (3) 

historical Hg deposition, (4) natural Hg levels in fish,

(5) ecosystem dynamics over time, or (6) the relative 

 

145 Grigal D.F., 2002. “Inputs and Outputs of Mercury from Terrestrial 

Watersheds: A Review,” Environmental Review, 10, 1–39. 

146 Yang H., Rose N.L., Battarbee R.W., Boyle J.F., 2002. “Mercury and 

Lead Budgets for Lochnagar, a Scottish Mountain Lake and Its 

Catchment,” Environmental Science & Technology, 36, 1383–1388.

147 Krabbenhoft D.P., Engstrom D., Gilmour C., Harris R., Hurley J., 

Mason R., 2007. Monitoring and Evaluating Trends in Sediment and Water 

Indicators. In Harris R., Krabbenhoft D., Mason R., Murray M.W., Reash 

R., Saltman T. (Eds.), Ecosystem Responses to Mercury Contamination: 

Indicators of Change. New York: Society of Environmental Toxicology and 

Chemistry (SETAC) North America Workshop on Mercury Monitoring and 

Assessment, CRC, pp. 47–87.

148 Lindberg S. et al. 2007. “A synthesis of progress and uncertainties 

in attributing the sources of mercury in deposition.” Ambio 36(1): 19-

32.

149 Orihel D.M., Paterson M.J., Blanchfield P.J., Bodaly R.A., Hintelmann 

H., 2008. “Experimental Evidence of a Linear Relationship between 

Inorganic Mercury Loading and Methylmercury Accumulation by Aquatic 

Biota,” Environmental Science & Technology, 41, 4952–4958.
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source contributions over time. Another commenter stated 

that lag times need to be included in the modeling and be 

able to vary from watershed to watershed and sometimes even 

from waterbody to waterbody within a watershed. Several 

commenters stated that the emission rates of Hg due to U.S. 

sources have been decreasing for more than a decade, while 

emissions due to sources outside the U.S. have been 

increasing. For this reason, the commenter asserted that 

the system is not at steady-state, a basic premise of the 

model. Another commenter stated that while the time lag for 

deposition to reach a waterbody is mentioned in the Hg Risk 

TSD, there is no discussion of the fact that a portion of 

the deposition is unlikely to reach the water at all. 

One commenter believes EPA incorrectly implied that 

its EGU risk estimates using Mercury Maps are 

underestimated because they do not account for legacy EGUattributable deposition, which EPA assumes to be higher. 

One commenter stated that while EPA properly screened 

out watersheds with significant current non-air sources of 

Hg, EPA did not adequately screened out watersheds with 

significant Hg contributions from non-air sources, 

specifically watersheds with historic Hg or gold mining or 
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other industrial Hg discharges. The same commenter stated 

that EPA’s study was not geographically balanced and was 

dominated by rivers in the coastal region of the southeast 

that has numerous wetlands, which are favorable locations 

for methylation and have conditions are not typical of much 

of the rest of the U.S.

Response: EPA disagrees with the commenters who 

challenged the assumption of a linear proportional 

relationship between changes in U.S. EGU deposition and 

fish tissue Hg levels. EPA specifically asked the SAB to 

evaluate EPA's assumption of linear proportionality in the 

relationship between Hg deposition and fish tissue MeHg

concentrations, supported by the Mercury Maps analysis. The 

SAB peer review committee provided the following overall 

response, which generally supports EPA’s approach:

“The SAB agrees with the Mercury Maps approach 

used in the analysis and has cited additional work 

that supports a linear relationship between mercury 

loading and accumulation in aquatic biota. These 

studies suggest that mercury deposited directly to 

aquatic ecosystems can become quickly available to 

biota and accumulated in fish, and reductions in 

atmospheric mercury deposition should lead to 

decreases in methylmercury concentrations in biota. 

The SAB notes other modeling tools are available to 

link deposition to fish concentrations, but does not 

consider them to be superior for this analysis or 

recommend their use. The integration of Community 
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Multiscale Air Quality Modeling System (CMAQ) 

deposition modeling to produce estimates of changes in 

fish tissue concentrations is considered to be sound. 

Although the SAB is generally satisfied with the 

presentation of uncertainties and limitations 

associated with the application of the Mercury Maps 

approach in qualitative terms, it recommends that the 

document include quantitative estimates of uncertainty 

available in the existing literature.”150

The SAB peer review committee specifically addressed 

the Mercury Cycling Model suggested by the commenter and 

had the following response:

“The SAB agrees with the application of Mercury 

Maps in this assessment. There are other modeling 

tools capable of making a national scale assessment, 

such as the Regional Mercury Cycling Model (R-MCM). 

However, the R-MCM is more data intensive and the 

results produced by the two model approaches should be 

equivalent.

“The R-MCM, a steady-state version of the timedependent Dynamic Mercury Cycling Model, has been 

publicly available to and used by the EPA (Region 4, 

Athens, Environmental Research Laboratory) for a 

number of years. R-MCM requires more detail on water 

chemistry, methylation potential, etc., and yields 

more information as well. Substantial data support the 

Mercury Maps and the R-MCM steady-state results, so 

that the results of the sensitivity analysis and the 

outcomes from using the alternative models would be 

equivalent between the two modeling approaches. Though 

running an alternative model framework may provide 

additional reassurance that the Mercury Maps “base 

case” approach is a valid one, it is unlikely that 

substantial additional insight would be gained with 

the alternative model framework.”151

 

150 U.S. EPA-SAB, 2011.

151 U.S. EPA-SAB, 2011.
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In addition, the SAB stated, “Since the Mercury Maps 

approach was developed, several recent publications have 

supported the finding of a linear relationship between 

mercury loading and accumulation in aquatic biota.152,153,154

These studies suggested that mercury deposited directly to 

aquatic ecosystems can become quickly available to biota 

and accumulated in fish, and that reductions in atmospheric 

mercury deposition should lead to decreases in 

methylmercury concentrations in biota. These results 

substantiate EPA’s assumption that proportionality between 

air deposition changes and fish tissue methylmercury level 

changes is sufficiently robust for its application in this 

risk assessment.”155

Based on the responses of the SAB peer review 

committee, EPA’s use of the linear proportionality 

assumption, supported by the Mercury Maps analysis, is 

well-supported.

EPA also disagrees with commenters’ interpretation of 

Figure 2-17. As stated in the Hg Risk TSD, while this 

 

152 Orihel et al., 2007. 

153 Orihel et al., 2008.

154 Harris et al., 2007. 

155 U.S. EPA-SAB, 2011. 
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figure is useful to demonstrate the lack of correlation 

across watersheds between total deposition of Hg and MeHg 

concentrations in fish tissue, it is not indicative of the 

likely correlation between changes in Hg deposition at a 

given watershed and changes in MeHg concentrations in fish 

tissue from that watershed. The SAB agreed with this 

interpretation, noting the importance of Figure 2-17 

demonstrating that “spatial variability of deposition rates 

is only one major driver of spatial variability of fish 

methylmercury and that variability of ecosystem factors 

that control methylation potential (especially wetlands, 

aqueous organic carbon, pH, and sulfate) also play a key 

role.”156

In response to recommendations from the SAB, EPA

expanded the discussion of uncertainties associated with 

the linearity assumption, including uncertainties related 

to the potential for sampled fish tissue Hg level to 

reflect previous Hg deposition and the potential for nonair sources of Hg to contribute to sampled fish tissue Hg 

levels. Each of these sources of uncertainty may result in 

potential bias in the estimate of exposure associated with 

 

156 U.S. EPA-SAB, 2011. 
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current deposition. EPA took steps to minimize the 

potential for these biases by 1) only using fish tissue Hg 

samples from after 1999, and 2) screening out watersheds 

that either contained active gold mines or had other 

substantial non-U.S. EGU anthropogenic emissions of Hg. The 

SAB commented that EPA’s approach to minimizing the 

potential for these biases to affect the results of the 

risk analysis appears to be sound and that additional 

criteria that could be applied are unlikely to 

substantially change the results. As a result, EPA 

disagrees with the commenter that EPA’s screening process 

is inadequate. In addition, we conducted several 

sensitivity analyses to gauge the impact of excluding 

watersheds with the potential for non-EGU Hg emissions, and 

found that the results were robust to these exclusions.

In response to specific comments regarding the use of 

the Mercury Maps model, EPA clarifies that the Hg Risk TSD

did not directly use the Mercury Maps model. Instead, EPA 

applied an assumption of linear proportionality between 

changes in Hg deposition and changes in MeHg concentrations 

in fish that is supported by the Mercury Maps modeling. By 

assuming steady-state conditions in apportioning fish 
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tissue Hg levels and risk, EPA does not attempt to project 

lag times. Recent research cited by the SAB157,158,159

identifies relatively rapid response of fish tissue Hg to 

changes in Hg loading, which suggests that fish tissue Hg 

levels could react more quickly to reductions in Hg 

deposition than previously thought. This finding reduces 

concern that fish tissue Hg levels could be linked to older 

patterns of Hg deposition and strengthens the approach used 

in the Revised Hg Risk TSD. 

2. Characterization of Subsistence Fishing Populations and 

Exposure Scenario

Comment: Several commenters stated that EPA provides 

no clear definition of subsistence, near subsistence, or 

high-end fish consumption, instead assuming that poverty is 

a direct indication of subsistence fishing and high-end 

fish consumption. One commenter stated no documentation 

exists to supports these assumptions. Another commenter 

stated that EPA’s definitions of subsistence fishers in the 

Hg Risk TSD are not consistent with earlier EPA documents

and are used inconsistently throughout the Hg Risk TSD. 

 

157 Orihel et al., 2007.

158 Orihel et al., 2008.

159 Harris et al., 2007.
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Several commenters stated that while subsistence fishing 

can be associated with poverty, poverty does not indicate 

subsistence fishing. One commenter stated that by including 

watersheds with as few as 25 members of individuals living 

in poverty, EPA overstates risks.

One commenter stated that it is unclear what 

literature the Agency says “generally supports the 

plausibility of high-end subsistence-like fishing ... to some 

extent across the watersheds” and stated that if other 

studies exist, EPA should provide the values for 

comparison. 

One commenter stated that EPA combined two parameters 

with differing scales to establish the geographic unit used 

in the Hg Risk TSD risk assessment. HUC watersheds are 

based on average about 35 square miles in size, while U.S. 

census tracts used to identify watersheds relevant for 

subpopulations of interest—cover a few tenths to hundreds 

of square miles. Several commenters stated that it is 

unclear how the analysis handled differences in geographic 

resolution between watersheds and census tracts were.

One commenter stated that procedure for assigning 

census tracts could bias exposure outcomes. For example,
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the commenter stated that a single influential census tract 

in a watershed could drive risk, even if the watershed had 

only a minimal number of fish samples. The commenter stated

that this possibility is a concern in urban areas, which 

account for the majority of census tracts, because these 

census tracts are more likely to be included in a risk 

analysis because they have more than 25 people living in 

poverty. The commenter stated that these census tracts may 

drive the extremes of the distribution without regard to 

the actual number of high-level, self-caught fish consumers 

within their boundaries. The commenter stated that they 

could not assess the potential bias and noted that EPA did 

not test the bias by sensitivity analyses.

Several commenters stated that EPA was not clear 

whether the poverty criteria were applied in all scenarios 

or just for the high-end female fish consumer scenario. One 

commenter stated that EPA should apply the minimum 25 

source population criteria only to populations of women of 

childbearing age. One commenter stated that EPA assumption 

would result in any densely populated urban census tract 

with a single fish tissue sample being assigned to a 

modeled watershed with populations potentially at-risk, 
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regardless of the actual degree of recreational or 

subsistence fishing taking place there.

Response: EPA agrees with the comments that 

subsistence fish consumption was not clearly defined, and 

we have provided a clearer definition in the revised Hg

Risk TSD, however, this clarification does not result in 

any changes to the quantitative analysis. In the Revised Hg

Risk TSD, EPA clarifies that “subsistence fishers” are 

defined as individuals who rely on noncommercial fish as a 

major source of protein (U.S. EPA, 2000).160 This definition 

is reflected in the range of fish consumption rates used in 

estimating risk. The likely presence of this type of 

subsistence fish consumer is supported by available peer

reviewed literature (see Table 1-5 of the Revised Hg Risk 

TSD). These studies clearly show that a subset of surveyed 

fishers consumes self-caught fish at the rates that were 

cited in the Hg Risk TSD. The SAB peer review concluded 

that the consumption rates and locations for fishing 

activity are supported by the data presented in the Hg Risk 

 

160 U.S. EPA, U.S. Environmental Protection Agency. 2000. Guidance for 

Assessing Chemical Contaminant Data for Use in Fish Advisories, Volume 

3: Overview of Risk Management. Office of Science and Technology, 

Office of Water, U.S. Environmental Protection Agency, Washington, DC. 

EPA 823-B-00-007.
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TSD, and are generally reasonable and appropriate given the

available data.161

EPA notes that there is some confusion in the comments 

related to the size of the watersheds modeled. Several 

commenters stated that HUC watersheds are 35 km on a side. 

The commenters appear to be referring to HUC8 

classifications. HUCs are defined for varying spatial 

resolutions. The geographic unit used as the basis for 

generating risk estimates is HUC12, which are watersheds

about 10 km on a side, which is comparable with the size of 

the 12 km2 grid cells in CMAQ, which are 12km2. EPA has also 

clarified that the specific unit of analysis for this 

assessment is at the watershed, not enumerated 

subpopulations. 

EPA only used the U.S. Census tracts to determine 

whether there are populations in the vicinity of a given 

watershed, which could increase the potential for a 

category of subsistence fishers to be active at that 

watershed. In the Revised Hg Risk TSD, EPA modified the 

female subsistence scenario to apply equally to all 

watersheds with fish tissue Hg data based on the likelihood 

 

161 U.S. EPA-SAB, 2011.
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that these populations have the potential to fish at most 

watersheds. Thus, concerns regarding the use of census data 

to select watersheds with the potential for subsistence 

fishing no longer apply to this scenario. However, for the 

remaining subsistence scenarios, EPA continues to use U.S. 

Census tract-level data to evaluate the presence of a 

“source population” in the vicinity of the watershed being 

modeled for risk. In this context, EPA uses the U.S. Census 

data assess whether a SES-differentiated group similar to 

the particular type of subsistence fisher being modeled 

(e.g., poor Hispanics) are located in the vicinity of the 

watershed. If a source population is nearby, then this 

increases the potential that subsistence fishing activity 

could occur for that population scenario.

EPA continues to model risk for white and black 

subsistence fishers active in the southeast and for 

Hispanics assessed nationally. In this case, EPA links 

poverty with subsistence fishing, as EPA only modeled

locations with poor source populations. However, in 

modeling these three populations, EPA asserts that the 

presence of a poor source population indicates the 

potential for subsistence fishing activity, rather the 
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presence of such activity. The linkage between poverty and 

higher rates of subsistence fish consumption is supported 

by the Burger et al. study,162 which identified 

substantially higher consumption rates for poor individuals 

(see Table 5 of the study). EPA acknowledges that 

subsistence fishing activity by specific subpopulations 

might only be present across a subset of the watersheds EPA 

modeled for risk. However, given the stated goal of the 

analysis to determine the percent of watersheds where the 

potential exists for exposures to U.S. EGU-attributable Hg 

to represent a public health hazard, identifying a set of 

watersheds with the potential for the type of high fish 

consumption that leads to high Hg exposure is appropriate. 

EPA notes that relatively few watersheds (less than 4 

percent) have fish tissue Hg data, thus can be included in 

the risk assessment. Consequently, while there is the 

potential for including some watersheds in the analysis

that may not have currently active subsistence fishing 

activity, there is also the very real possibility that EPA 

excluded other watersheds from the analysis where this type 

 

162 Burger, J., 2002. “Daily Consumption of Wild Fish and Game: Exposures 

of High End Recreationists," International Journal of Environmental 

Research and Public Health, 12 (4), 343–54.
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of subsistence fishing activity occurs due to a lack of 

fish tissue Hg data.

EPA agrees with the comment that it is likely that 

exposure to total MeHg through commercial fish consumption 

represents a more significant risk for the general 

population than consumption of freshwater fish obtained 

through self-caught fishing activity. However, subsistence 

fishers active at inland freshwater watersheds are likely 

to experience the highest levels of individual risk as a 

result of exposure to U.S. EGU-attributable Hg. Therefore, 

EPA focuses on this group of subsistence fishers in the 

risk assessment and did not evaluate exposure for the 

general population related to Hg exposure through seafood.

3. Cooking Loss Adjustment Factor

Comment: Several commenters stated that EPA did not 

justify the selection of a cooking loss factor of 1.5 that, 

according to one commenter, increases estimated intake by 

50 percent, thus increasing the daily MeHg intake rate by a 

constant factor of 33 percent and also increasing any 

resulting (HQ) risk estimate by a similar factor. Several 

commenters stated that the source of EPA’s selected loss 
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factor163 reported a range of cooking losses from 1.1 to 6. 

Several commenters cite several studies that report no or 

highly variable changes in MeHg levels as a result of 

cooking fish164,165,166,167,168. One commenter suggested that 

EPA’s cooking loss adjustment factor of 1.5 is at the highend of the values supported by the literature. Another 

commenter stated that EPA has used other adjustment factors 

in previous documents, and that the adjustment factor 

should not be fixed across different populations given 

potential differences in cooking practices. Several 

commenters noted that the cooking loss adjustment factor 

should only be applied to estimates of consumption rates 

 

163 Morgan, J.N., M.R. Berry, and R.L. Graves. 1997. “Effects of Commonly 

Used Cooking Practices on Total Mercury Concentration in Fish and Their 

Impact on Exposure Assessments.” Journal of Exposure Analysis and 

Environmental Epidemiology 7(1):119-133.

164 Armbruster G., Gerow K.G., Lisk D.J., 1988. “The Effects of Six 

Methods of Cooking on Residues of Mercury in Striped Bass,” Nutrition 

Reports International, 37, 123–126.

165 Gutenmann, W.H. and Lisk D.J., 1991. “Higher Average Mercury 

Concentration in Fish Fillets after Skinning and Fat Removal,” Journal 

of Food Safety, 11, 99–103. 

166 Farias L.A., Favaro, D.I., Santos J.O., Vasconcellos M.B., et al., 

2010. “Cooking Process Evaluation on Mercury Content in Fish,” Acta 

Amazonia, 40 (4), 741–748.

167 Perelló G., Martí-Cid R., Llobet J.M., Domingo J.L., 2008. “Effects 

of Various Cooking Processes on the Concentrations of Arsenic, Cadmium, 

Mercury, and Lead in Foods,” Journal of Agricultural and Food 

Chemistry, 156 (22), 11262–11269. 

168 Torres-Escribano S., Ruiz A., Barrios L., Vélez D., Montoro R., 2011. 

“Influence of Mercury Bioaccessibility on Exposure Assessment 

Associated with Consumption of Cooked Predatory Fish in Spain,” Journal 

of the Science of Food and Agriculture, 91 (6), 981–6.
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for prepared fish, and that some sources of consumption 

rates are based on raw fish.

Response: EPA disagrees with the commenters that the 

selection of the cooking loss factor of 1.5 is not 

justified by the literature. EPA also disagrees with the 

comment that the cooking loss adjustment factor of 1.5 is 

at the high-end of the range of values in the literature. 

EPA selected the Morgan (1997) study as the basis for the 

food preparation/cooking adjustment factor because it 

focused on the types of freshwater fish species 

representative of what might be consumed by subsistence 

fishing populations (i.e., walleye and lake trout). The 

Morgan (1997) study provides a range of adjustment factor 

for each fish type including 1.1 to 1.5 for walleye and 1.5 

to 2.0 for lake trout. Given these two ranges, EPA 

determined it to be reasonable to take an intermediate 

value between the two ranges (i.e., 1.5), rather than focus 

on either the highest or lowest values. The Morgan (1997) 

study explains that preparation/cooking of fish results in 

an increase in MeHg levels per unit fish because Hg 

concentrates in the muscle, while preparation/cooking tends 

to reduce non-muscle elements (e.g., water, bone, fat). 
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Regarding the alternative studies identified by the 

commenters, EPA disagrees that these studies considered 

collectively contradict the cooking loss factor in the 

analysis. Specifically, the first study170 may have included 

measurement of non-fish components added to dishes (e.g., 

onions, heavy breading etc.), which could dilute the postcooking Hg measurements and give the appearance of a 

cooking loss even as actual fish tissue Hg levels could 

have increased. In the second study,171 the fish species are 

saltwater and not freshwater, and the authors note that the 

reduction of water and fat could increase in the Hg 

concentration without changing absolute content. The third 

study focused on measurement of bioaccessible Hg in raw and 

cooked fish.174 However, available information currently 

allows us to specify the risk model in terms of total Hg

intake, not bioaccessible Hg, thus, this article is 

potentially informative for guiding future research and 

methods development, not the current risk assessment. The 

fourth study176 found a modest but statistically 

insignificant increase in Hg levels for most of the cooking 

 

170 Farias et al., 2002. 

171 Perelló et al., 2008. 

174 Torres-Escribano et al., 2011

176 Armbruster et al., 1988.
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methods assessed, which is directionally consistent with 

EPA’s cooking loss adjustment. The fifth study178 only 

addressed the issue qualitatively, thus cannot be used for 

the cooking loss factor. When considered collectively, EPA 

disagrees that the additional studies identified by the 

commenter contradict the cooking loss factor used in the 

risk assessment and maintains that the Morgan study179

remains the most applicable for characterizing 

cooking/preparation effects on Hg concentrations in fish.

EPA agrees that application of the cooking loss 

adjustment factor is appropriate if the fish consumption

rates are for as cooked or as consumed and not for raw 

fish. Careful review of the three studies used in the risk 

assessment to identify subsistence fisher consumption rates 

suggests that all three represent annual-average daily 

intakes (g/day) of as consumed or as cooked fish. One study 

stated that they used models of portion or meal size 

servings (the size of the serving the respondent regularly 

eats).180 Therefore, EPA interprets the fish consumption 

rates provided in the Burger et al. study as representing 

 

178 Gutenmann et al., 1991.

179 Morgan et al., 1997. 

180 Burger et al., 2002.
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as cooked/prepared and not for raw fish and for that 

reason, application of a preparation/ cooking adjustment 

factor is required. The Shilling et al., (2010) study181

used different sized models of cooked fish filets and 

therefore these consumption rates are also interpreted as 

represented as cooked/prepared and not raw fish. One 

study184,

185 queried survey responders for meal portion or 

serving size and therefore, the consumption rates do 

represent as cooked/prepared. Because all three studies 

provide consumption rates based on as cooked/prepared or as 

consumed, it is appropriate to apply the cooking loss 

adjustment factor in modeling exposure.

4. Fish Consumption Rates and Fish Tissue Hg 

Characterization

Comment: One commenter stated that in the past the 

Agency has recommended various default consumption rates 

(in the general range of 130 to <150 g/day) to provide 

default intakes for subsistence fishers under the Risk 

 

181 Shilling, Fraser, Aubrey White, Lucas Lippert, Mark Lubell (2010). 

Contaminated fish consumption in California’s Central Valley Delta. 

Environmental Research 110, p. 334-344.

184 Dellinger JA. 2004. “Exposure assessment and initial intervention 

regarding fish consumption of tribal members of the Upper Great Lakes 

Region in the United States.” Environ Res 95:325–340.

185 Personal communication, Dr. Dellinger, September 27, 2011
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Assessment Guidance for Superfund (RAGS) or the Fish 

Advisory Guidance.

186,187 The commenter stated that these 

default consumption rates are derived from various studies 

and generally are based on 90th or 99th percentile 

distribution estimates. Another commenter stated that EPA’s 

use of the 99th percentile fish consumption for its risk 

analysis is inconsistent with the Agency’s risk assessment 

guidelines, which recommend evaluating a reasonable maximum 

exposure (“RME”) scenario,188 which equates to about a 95th

percentile fish consumption value. The same commenter 

stated that EPA applied the 99th percentile to a “small 

survey of 149 South Carolina female anglers” to calculate 

an ingestion rate of 373 g/day. The commenter stated that 

if the 95th percentile is used the ingestion rate would be 

173 g/day and if the default ingestion rate for determining 

ambient water standards is used the ingestion rate would be 

142 g/day.

 

186 U.S. EPA. 1991. Risk Assessment Guidance for Superfund (RAGS). Part C 

1991 EPA/9285.7-01C. October.

187 U.S. EPA. 2000. National Guidance: Guidance for Assessing Chemical 

Contaminant Data for Use in Fish Advisories, Volume 2. EPA 823-B-00-

008, November.

188 U.S. EPA. 1989. Risk Assessment Guidance for Superfund (RAGS).

EPA/540/1-89/002. December.
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Several commenters stated that EPA based its fish 

consumption rates used in the risk analysis on a limited 

number of studies and that those studies are poorly 

documented. 

Another commenter stated that EPA should summarize 

available supporting studies by basic study content, 

characteristics, design, size, demographics, dietary recall 

period, and fish intake rates by demographic variables. 

According to the commenter, this summary would support the 

scientific validity of the assessment and better illustrate 

the potential variability and uncertainty involved in 

extrapolating data from small populations to the nationalscale. The commenter also noted that the three studies 

actually used to provide subsistence population estimates, 

which were extrapolated to the national-scale, included a 

limited number of individuals living in diverse and 

localized areas.

One commenter stated that the assumption with the 

greatest impact on risk is the fish consumption rate. That 

same commenter stated that using 99th percentile ingestion 

rate dramatically increases HQ and IQ loss compared to the 

50th percentile ingestion rate . The commenter stated that 
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when an estimate of the 95th percentile ingestion rate of 

the 15-44 year old female population is considered, the HQ 

is a tenth of the value computed with the 99th percentile 

high-end female fisher.

One commenter stated that EPA provides broad summary 

statistics of its fish tissue data in Table 5-2 of the 

Regulatory Impact Analysis (RIA), but the summary does not 

allow an assessment of the representativeness and 

robustness of the underlying data for the risk assessment, 

especially at the tails of the distribution. The commenter 

stated that the table does not include a median statistic 

and does not provide any information on the number of lakes 

and river segments in each watershed. According the 

commenter, an analysis of EPA’s database by the SAB 

indicated that 60 percent of the watersheds with fish Hg

data from rivers have risks calculated based upon a sample 

size of one or two fish. The commenter stated that it is 

not reasonable to base a significant policy and regulation 

decision on watersheds where exposure is based on a single 

fish sample in a single water body within it.

Several commenters criticized EPA’s use of the 75th

percentile fish tissue MeHg level in a watershed. One 
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commenter stated that EPA provided no rationale for its 

decision to choose the highest of the 75th percentile for 

fish Hg levels among rivers and lakes within the HUC. 

Several commenters stated that subsistence fishers are less 

likely to target larger fish relative to recreational 

fishers. Several commenters suggested that EPA include a 

sensitivity analysis using the mean or median fish MeHg 

level in a watershed. One commenter also stated that EPA 

arbitrarily inflated the risk estimates by assuming 

consumption of only fish greater than 7 inches and choosing 

the largest of the 75th percentile of fish Hg levels from 

these larger fish (i.e., larger than 7 inches) for rivers 

and lakes. That same commenter suggested using the median 

of all size fish, not just those over 7 inches. 

One commenter stated that EPA should quantify adverse 

effects from the ingestion of MeHg in seafood in addition 

to ingestion of MeHg from self-caught freshwater fish. 

According to the commenter, recent studies demonstrate that 

were EPA to take into account consumption of seafood, MeHg 

consumption in the U.S. is of even greater concern.

Response: EPA acknowledges that the focus of the Hg 

Risk TSD is characterizing risk for the groups likely to 
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experience the greatest U.S. EGU-attributable Hg risk, 

which are subsistence fishing populations active at inland 

freshwater lakes and rivers. Specifically, within that 

subsistence fishing population, EPA is interested in those 

individuals who are most at-risk, which includes those who 

consume the most fish. For that reason, EPA considered a 

range of high-end fish consumption rates including the 99th

percentile representing the most highly-exposed 

individuals. In responding to the SAB peer review, EPA 

clarified this focus in the introduction to the Revised Hg

Risk TSD and changed the full title to Revised Technical 

Support Document: National-Scale Assessment of Mercury Risk 

to Populations with High Consumption of Self-caught 

Freshwater Fish. The focus on the most highly-exposed 

individuals is consistent with the appropriate and 

necessary finding and the treatment of other HAP under 

Section 112.

EPA agrees that the fish consumption rate is an 

important factor in calculating risk from exposure to MeHg

in fish. EPA acknowledges that the distribution of fish 

consumption rates is positively skewed, which means that at 

higher percentiles (e.g., 90th, 95th and 99th) there is a 
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substantial increase in ingestion rates relative to the 

mean or median. The Revised Hg Risk TSD includes a 

reasonableness check on the amount of fish consumed (as a 

daily value) reflected in the different rates. While the 

99th percentile consumption rates for the subsistence female 

fisher (373 g/day) is substantially higher than the 90th or 

95th percentile values (123 and 173 g/day respectively), the 

99th percentile value translates into a 13-ounce meal. While 

this represents a large serving, it is still reasonable if 

representing an individual who receives all of their meat 

protein from self-caught fishing, and the 13 ounces per day 

do not have to be eaten all at one meal. The higher

consumption rates (i.e., greater than 250 g/day) are 

supported by all three studies used in the risk assessment,

and therefore, there is support across studies near the 

upper bound of likely consumption rates in this range. EPA 

acknowledges uncertainty associated with estimating highend percentile values in these studies due to relatively 

low sample sizes for some population groups. However, even 

if a few individuals reported these high self-caught fish 

consumption rates, making it difficult to characterize the 

population percentiles they represent, the values still 
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suggest that these levels of high fish consumption exist 

among surveyed individuals. To determine whether a public 

health hazard could exist, EPA asserts that it is 

reasonable to include these consumption rates as 

representative of the most at-risk populations. In these 

cases, however, EPA acknowledges that it is important to 

highlight uncertainty associated with characterizing the 

specific population percentile that these ingestion rates 

represent, and EPA has done so in the Revised Hg Risk TSD.

EPA disagrees with the comment that high consumption 

rates are poorly documented. Evidence of these high fish 

consuming populations can be found in surveys189 and 

specialized studies.

190,191,192,193,194 Several studies identified 

 

189 Burger et al., 2002.

190 Burger, J., K. Pflugh, L. Lurig, L. Von Hagen, and S. Von Hagen. 

1999a. “Fishing in Urban New Jersey: Ethnicity Affects Information 

Sources, Perception, and Compliance.” Risk Analysis 19(2): 217-229.

191 Burger, J., Stephens, W. L., Boring, C. S., Kuklinski, M., Gibbons, 

J. W., Gochfeld M. 1999b. “Factors in Exposure Assessment: Ethnic and 

Socioeconomic Differences in Fishing and Soncumption of Fish Caught 

along the Savannah River.” Risk Analysis, Vol. 19, No. 3, p. 427.

192 California Environmental Protection Agency (CalEPA). 1997. Chemicals 

in Fish Report No. 1: Consumption of Fish and Shellfish in California 

and the United States Final Draft Report. Pesticide and Environmental 

Toxicology Section, Office of Environmental Health Hazard Assessment, 

July.

193 Tai, S. 1999. “Environmental Hazards and the Richmond Laotian 

American Community: A Case Study in Environmental Justice.” Asian Law 

Journal 6: 189.

194 Corburn, J. 2002. “Combining community-based research and local 

knowledge to confront asthma and subsistence-fishing hazards in 
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additional fishing populations with subsistence or near 

subsistence consumption rates, including urban fishing 

populations (including low-income populations),195,196,197

Laotian communities,198 and Hispanics. EPA participated in 

1999 in a project investigating exposures of poor, minority 

communities in New York City to a number of contaminants 

including Hg, which found these populations can have very 

high fish consumption rates.199 The SAB concluded that the 

consumption rates and locations for fishing activity are 

supported by the data presented in the Hg Risk TSD, and are 

generally reasonable and appropriate given the available 

data.

200

EPA agrees that the Hg Risk TSD would be improved by 

clarifying that the literature review focused on 

identifying studies that characterize subsistence fish 

consumption for groups active at freshwater locations 

within the U.S., and EPA has revised the Hg Risk TSD 

accordingly. In the Hg Risk TSD, EPA summarized important 

 

Greenpoint/Williamsburg, Brooklyn, New York.” Environmental Health 

Perspectives 110(2).

195 Burger et al., 1999a.

196 Burger et al., 1999b.

197 CalEPA, 1997.

198 Tai, 1999..

199 Corburn, 2002.

200 U.S. EPA-SAB, 2011.
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study attributes for the source studies used to obtain fish 

consumption rates. This information was provided in Table 

C-1 in an appendix. To improve clarity, EPA moved the 

summary table to the main body in the Revised Hg Risk TSD. 

In identifying these studies, EPA focused on surveys for 

subsistence fishers that were applicable at the broader 

regional or national level. In the Hg Risk TSD, EPA 

acknowledged the smaller sample sizes for some of the 

subsistence fisher groups, and in several cases EPA did not 

use the 99th percentile consumption rates because the sample 

sizes were too low to support this level of resolution.

EPA disagrees with the comment that it did not provide 

a rationale for choosing the highest 75th percentile fish 

tissue concentration across lakes and rivers in a 

watershed. However, EPA modified the methodology based on 

evaluation of the number of samples within each watershed 

(responding to a recommendation from the SAB). In the 

revised methodology, EPA computes the 75th percentile value 

at each sampling site within a watershed. EPA then computed 

the average of the site-specific 75th percentile fish tissue 

Hg values within a given watershed. This approach does not 

differentiate between rivers and lakes and reflects an 
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improved treatment of behavior, allowing for fishers to 

choose among multiple fishing sites within a watershed. 

EPA generally agrees with the comment that some 

fraction of subsistence fishers likely consume fish without 

consideration for size (given dietary necessity), however, 

EPA considers it reasonable to assume that a subset of 

subsistence fishers could target larger fish on order to 

maximize the potential consumption per unit of fishing 

effort. EPA uses this subset of subsistence fishers 

targeting larger fish, which is represented by the 75th

percentile fish tissue value, in the risk assessment. In 

addition, including the female subsistence fishing 

population in the analysis also provides coverage for highend recreational anglers who target larger freshwater fish. 

The SAB commented that: “Using the 75th percentile of fish 

tissue values as a reflection of consumption of larger, but 

not the largest, fish among sport and subsistence fishers 

is a reasonable approach and is consistent with published 

and unpublished data on predominant types of fish 

consumed.”201 The SAB suggested that EPA include a 

sensitivity analysis based on use of the median value, and 

 

201 U.S. EPA-SAB, 2011.
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EPA has done so in the Revised Hg Risk TSD. This 

sensitivity analysis showed that using the median estimates 

had only a small impact on the number and percent of 

modeled watersheds with populations potentially at-risk

from U.S. EGU-attributable MeHg exposures. Regarding the 7-

inch criteria, for the Revised Hg Risk TSD, EPA clarified 

that this cutoff represents a minimum size limit for a 

number of key edible freshwater fish species established at 

the State-level. For example, Pennsylvania establishes 7 

inches as the minimum size limit for both trout and salmon 

(other edible fish species such as bass, walleye and 

northern pike have higher minimum size limits).202

EPA disagrees with the comment that it is not 

reasonable to use watersheds where only a single fish 

sample is available. While it is generally preferred to 

have multiple samples, the SAB noted that using a single 

sample is likely to underestimate the 75th percentile fish 

MeHg concentration and is therefore likely to underestimate 

the risk estimates for those watersheds. The SAB suggested 

that EPA conduct additional analyses of the fish tissue 

 

202 Pennsylvania Fish and Boat Commission. 2011. Summary Book: 2011 

Pennsylvania Fishing Laws & Regulations available at: 

http://fishandboat.com/fishpub/summary/inland.html.
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MeHg data, which EPA has done and included in the Revised 

Hg Risk TSD. The Revised Hg Risk TSD includes information 

on the number of watersheds modeled in the risk assessment 

with various fish tissue Hg samples sizes (e.g., 1, 2, 3-5, 

6-10 and >10 measurements).

5. Reference Dose (RfD) for MeHg and Hg Health Effects 

Studies

Comment: Several commenters stated that EPA’s RfD203 is 

based on sound science, which was supported by the findings 

of the NAS Study,

204 and that EPA appropriately applied the

RfD in the Hg risk assessment. The commenters also stated

that recent studies find clear associations between 

maternal blood Hg levels and delayed child development and

cardiovascular effects, as well as potential for effects 

due to exposure to pollutant mixtures including lead. 

However, many commenters expressed concerns regarding 

EPA’s use of the MeHg RfD as a benchmark for health risk. 

Several commenters raised concerns claiming that EPA has 

not incorporated the best available Hg toxicological data 

 

203 U.S. Environmental Protection Agency – Integrated Risk Information 

System (U.S. EPA-IRIS). 2001. Methylmercury (MeHg) (CASRN 22967-92-6). 

Available at http://www.epa.gov/iris/subst/0073.htm

204 NAS, 2000.
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into the RfD, which results in a flawed analysis and an 

overestimate of the impact of Hg emissions on human health.

Several commenters stated that, when deriving the RfD,

EPA relied on the flawed Faroe Islands’ children study and 

ignored the Seychelles Islands study,205 which did not 

confirm any harm on children due to MeHg exposure. 

According to the commenters, application of the Faroe 

Island study is suspect because (1) the raw data from the 

study have never been made available for independent 

analysis and scrutiny, (2) there is potential for 

confounding by polychlorinated biphenyls (PCBs) and lead, 

(3) population exposure to MeHg was through consumption of 

highly contaminated pilot whale meats and blubbers, and (4) 

exposure levels in the U.S. remain lower than those 

observed in the primary study. One commenter also notes 

that (1) Seychelles Islanders consume far more fish than 

Americans do; (2) the amount of MeHg in the U.S. population 

is much lower than the Seychelles islanders; and (3) all 

ocean fish contain about the same amount of MeHg, so MeHg 

intake per fish meal is similar between Americans and 

 

205 Budtz-Jorgensen E, Debes F, Weihe P, Grandjean P. 2005. “Adverse 

Mercury Effects in 7-Year-Old Children Expressed as Loss in “IQ”.” EPAHQ-OAR-2002-0056-6046.
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Seychelles Islanders. However, another commenter stated

that industry arguments against using the Faroe Islands 

study fail to acknowledge that the study results were 

consistent with studies in the Seychelles Islands, New 

Zealand207, and Poland208. 

One commenter criticized EPA for using a linear doseresponse model for the RfD-based HQ metric and the IQ 

metric. Another commenter stated that the RfD assumes a 

threshold dose below which an appreciable risk of adverse 

effects is unlikely, and NAS did not evaluate whether MeHg

exposure data were better fit by a linear or non-linear 

model or by a threshold or non-threshold model. 

Several commenters stated that EPA’s MeHg RfD is more 

conservative than “safe” levels determined by other federal 

agencies and claim that EPA assigned unusually high 

uncertainty factors. Several commenters stated that EPA's 

use of the 1999 National Health and Nutrition Examination 

 

207 Kjellstrom, T; Kennedy, P; Wallis, S; et al. 1986. Physical and 

mental development of children with prenatal exposure to mercury from 

fish. Stage 1: Preliminary test at age 4. Natl Swed Environ Protec Bd, 

Rpt 3080 (Solna, Sweden).

208 Wieslaw Jedrychowski et al. 2006. “Effects of Prenatal Exposure to 

Mercury on Cognitive and Psychomotor Function in One-Year-Old Infants: 

Epidemiologic Cohort Study in Poland,” 16 Annals of Epidemiology 439.
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Survey (NHANES) blood Hg levels show a downward trend since 

1999, and the levels have been below the RfD since 2001. 

One commenter stated that a study by Texas Department 

of State Health Services (DSHS, 2004)210 determined that 

among subsistence fishers who eat fish from Caddo Lake with 

elevated MeHg, women of child-bearing years did not have 

blood Hg levels greater than the RfD. Thus, according to 

the commenter, the connection between MeHg in fish and 

adverse health effects in the U.S. is not fully understood 

and could involve other factors, including the protective 

effects of fatty acids and selenium in fish, which EPA did

not taken into account.

Two commenters claim that EPA uses the RfD as if it 

were an absolute threshold for health risk in the risk 

assessment even though the RfD methodology is a screening 

tool for deciding when risks clearly do not exist. 

Several commenters recommended adding qualitative 

discussions to the Hg Risk TSD regarding several aspects of 

uncertainty, including uncertainty in the RfD, uncertainty 

in extrapolating a dose-response relationship between MeHg

 

210 DSHS. 2005. Health Consultation: Mercury Exposure Investigation Caddo 

Lake Area-Harrison County Texas. Agency for Toxic Substances and 

Disease Registry. 

http://www.tceq.state.tx.us/assets/public/comm_exec/pubs/sfr/085.pdf
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exposure and change in IQ, uncertainty in extrapolating the 

dose-response relationship from marine fish and marine 

mammals to freshwater fish, and uncertainty due to 

potential confounding by PCBs in marine species.

Several commenters raised concerns regarding the 

relationship between MeHg exposure and IQ loss. Two 

commenters stated that changes in IQ are not a well-defined 

health consequence of MeHg exposure. One commenter stated

that the SAB had reservations about EPA’s use of IQ loss.

Two commenters questioned whether IQ impacts would even 

occur because in Japan and Korea, where the maternal blood 

Hg levels are higher than in the U.S., there is no evidence 

of adverse effects. Another commenter cited a study211 that 

found verbal IQ scores for children from mothers with no 

seafood intake were 50 percent more likely to be in the 

lowest quartile. One commenter questions using an IQ risk 

metric threshold of >1 or >2 points because variation in IQ 

measures and the intra-individual variation in IQ are

higher than the threshold. 

 

211 Hibbeln JR, Davis JM, Steer C, Emmett P, Rogers I, Williams C, et al. 

2007. “Maternal seafood consumption in pregnancy and neurodevelopmental 

outcomes in childhood (ALSPAC study): an observational cohort study. “ 

Lancet 369:
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Several commenters question the relationship between 

cardiovascular effects and MeHg exposure. Two commenters

cited studies examining the relationship between MeHg

exposure and cardiovascular effects,212,213,214,215,216,217 but 

concluded that it seems premature to use these studies to 

establish a dose-response relationship. 

Several commenters assert that the risks from eating 

seafood are low relative to the benefits, that fish 

advisories can limit the beneficial aspects of fish 

consumption, and that fish advisories are often 

unsuccessful in changing behavior.

218,219 One commenter noted

the important protective role of dietary selenium against 

 

212 Roman HA, Walsh TL, Coull BA, Dewailly É, Guallar E, Hattis D, et al. 

2011. Evaluation of the Cardiovascular Effects of Methylmercury 

Exposures: Current Evidence Supports Development of a Dose–Response 

Function for Regulatory Benefits Analysis. Environ Health Perspect 

119:607-614.

213 Guallar E, Sanz-Gallardo MI, van't Veer P, et al. 2002. “Mercury, 

fish oils, and the risk of myocardial infarction.” N Engl J 

Med.;347:1747.

214 Virtanen JK, Voutilainen S, Rissanen TH, et al. 2005. “Mercury, fish 

oils, and risk of acute coronary events and cardiovascular disease, 

coronary heart disease, and all-cause mortality in men in eastern 

Finland.” Arterioscler Thromb Vasc Biol. 2005;25:228.

215 Yoshizawa, Rimm, Morris, Spate, Hsieh, Spiegelman, Stampfer, Willett.

“Mercury and the Risk of Coronary Heart Disease in Men,” N Engl J Med

2002; 347:1755-1760.

216 Hallgren CG, Hallmans G, Jansson JH, et al. 2001. Markers of high 

fish intake are associated with decreased risk of a first myocardial 

infarction. Br J Nutr: 86:397.

217 Mozaffarian, Dariush. 2011. “Mercury Exposure and Risk of 

Cardiovascular Disease in Two U.S. Cohorts,” N Engl J Med 364: 1116-

1125.

218 Hibbeln et al. 2007.

219 Mozaffarian, et al., 2011
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MeHg toxicity because the binding affinity of Hg to Se is 

much higher than binding to sulfur.

Response: EPA agrees with the commenter that the MeHg 

RfD is the appropriate health value for determining 

elevated risks from MeHg exposure and disagrees with 

commenters that state otherwise. At this time, U.S. EPA is 

neither reviewing nor revising its 2001 RfD for MeHg. The 

2001 RfD for MeHg is EPA’s current peer reviewed RfD, which 

is the value EPA uses in all its risk assessments. EPA’s 

RfD is based on multiple benchmark doses, and RfDs were 

calculated on various endpoints using the three extant 

large studies of childhood effects of in utero exposure: 

Faroe Islands, New Zealand, and an integrative measure 

including data from Seychelles. EPA did not choose to base 

the MeHg RfD solely on results from the Seychelles Islands, 

as both the NAS220 and an independent scientific review 

panel convened as part of the IRIS process221 advised 

strongly against using results from a study that at the 

time had not shown an association between MeHg exposure and 

adverse effects. Further, EPA disagrees with the commenter 

 

220 NAS, 2000.

221 U.S. EPA. 2001b. Responses to Comments of the Peer Review Panel and 

Public Comments on Methylmercury. Available on the Internet at 

http://www.epa.gov/iris/supdocs/methpr.pdf
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that EPA based the MeHg RfD solely on results from the 

Faroe Islands population and disagrees that the information 

underlying the RfD is “poorly explained”. EPA has provided 

detailed documentation for the choices underlying 

calculation of the RfD.222,223,224 To correct a 

misunderstanding by the commenter, the data underlying the 

Faroe Islands study have been previously published in the 

peer reviewed literature.

EPA disagrees that it did not incorporate the latest 

Hg data to support the appropriate and necessary finding. 

It is the policy of EPA to use the most current peer

reviewed, publicly available data and methodologies in its 

risk assessments. However, EPA noted in the preamble to the 

proposed rule that “data published since 2001 are generally 

consistent with those of the earlier studies that were the 

basis of the RfD, demonstrating persistent effects in the 

Faroe Island cohort, and in some cases associations of 

 

222 U.S. EPA, 2001a. Water Quality Criterion for the Protection of the 

Human Health: MethylmercuryEPA-823-T-01-001, available at 

http://water.epa.gov/scitech/swguidance/standards/criteria/aqlife/pollu

tants/methylmercury/index.cfm

223 U.S. Environmental Protection Agency – Integrated Risk Information 

System (U.S. EPA-IRIS). 2001. Methylmercury (MeHg) (CASRN 22967-92-6). 

Available at http://www.epa.gov/iris/subst/0073.htm

224 Rice D, Schoeny R, Mahaffey K. 2003. “Methods and Rationale for 

Derivation of a Reference Dose for Methylmercury by the U.S. EPA.” Risk 

Analysis 23(1)107-115.
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effects with lower MeHg exposure concentrations than in the 

Faroe Islands. These new studies provide additional 

confidence that exposures above the RfD are contributing to 

risk of adverse effects, and that reductions in exposures 

above the RfD can lead to incremental reductions in risk.” 

However, EPA has not completed a comprehensive review of 

the new literature, and as such, it would be premature to 

draw conclusions about the overall implications for the 

RfD. 

EPA agrees that EPA’s RfD is not the same as the 

levels used by other federal agencies. In their advice to 

the U.S. EPA on the appropriate bases for a MeHg RfD, NAS 

specifically recommended that EPA use neither the study nor 

the uncertainty factor employed by Agency for Toxic 

Substances Disease Registry (ATSDR) in the calculation of 

the minimal risk level.225

EPA disagrees that the uncertainty factor is 

“unusually high”. The uncertainty factor used in 

calculation of the RfD is small (10 fold); half of this 

factor is to account for measured variability in human 

 

225 NAS, 2000.
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pharmacokinetics, which is based on advice of the NAS226 and 

an independent panel of scientific peer reviewers convened 

as part of the IRIS process227.

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.”228

EPA disagrees that it is using the MeHg RfD as an 

absolute bright line for health effects in the risk 

assessment. As stated in the preamble to this proposed 

rule, the RfD is an estimate of a daily exposure to the 

human population that is likely to be without an 

appreciable risk of deleterious effects during a lifetime. 

EPA also stated that no RfD defines an exposure level 

corresponding to zero risk.

EPA disagrees that exposure levels in the U.S. are 

lower than those in the Faroe Islands study. Exposure to 

 

226 Id.

227 U.S. EPA, 2001b.

228 U.S. EPA-IRIS, 2001.
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MeHg in the U.S. has been reported at the same levels as 

those published in the Faroe Islands.231 One study notes

that in the NHANES data (1999-2004), the highest five 

percent of women’s blood Hg exceeded 8.2 μg/L in the 

Northeast U.S. and 7.2 μg/L in coastal areas.

233 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 μg/L; range for men and women was 2 to 

89.5 μg/L.

235 Note that some publications have reported Hg

effects in U.S. populations near the current U.S. RfD.236,237 

Also, EPA disagrees with the commenter stating all ocean 

fish throughout the world contain about the same amount of 

 

231 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.

233 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.

235 Hightower Jane M, Moore Dan. Mercury levels in high-end consumers of 

fish. Environ Health Perspect. 2003 Apr;111(4):604–608. 

236 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.

237 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.
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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.

244,245

EPA disagrees that there is a statistically 

discernible downward trend in the NHANES data on blood Hg.

EPA is unaware that a formal statistical analysis for 

temporal trends has been completed for NHANES data on blood 

Hg levels for the period 1999 to 2008. Mahaffey et al., 

evaluating NHANES data collected 1999 to 2004 for women at 

child-bearing age, could “not support the conclusion that 

there was a general downward trend in blood Hg concentrations over the 6-year study period.”246 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 

 

244 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.

245 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.

246 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.
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slight decrease in Hg blood level concentrations from 1999-

2008 at the geometric mean, but this decrease may not be 

statistically significant. 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 the this level. One study

estimated very high blood Hg levels at the 99th percentile 

for females of child-bearing age.

249Other published studies 

have shown that various population groups can have high 

blood Hg levels.250,251,252,253,254 For example, one study found 

 

249 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.

250 Id.

251 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.

252 Hightower and Moore, 2003.

253 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.

254 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.
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that 83 percent of the NHANES Asian population exceeded the 

RfD-equivalent blood mercury level.

255

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.258

EPA also documented the independence of PCB and MeHg 

effects in the Faroe Islands population.259 NIEHS concluded 

that both PCB and Hg had adverse effects. 260 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.261 A 

second set of analyses found that the effect of prenatal 

PCB exposure was reduced when the data were sorted into 

 

255 Hightower et al., 2006.

258 NAS, 2000.

259 U.S. EPA, 2001a.

260 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.

261 NAS, 2000.
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tertiles by cord PCB concentrations.262 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.

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 

study263. This is an exposure study rather than a study on 

measures of neurobehavioral or any other health endpoint. 

TCEQ noted that none of the Caddo Lake study participants 

had blood Hg levels above the BMDL of 5.8 μg/L (one of the 

several used by EPA in the calculation of the MeHg RfD). 

The BMDL is not a “no effect” level. Rather it is an effect 

level for a percentage of the population. EPA has noted in 

correspondence with TCEQ that, as an exposure study, the 

Caddo Lake study may be representative of the surrounding 

population; however, the sample size is very small. It is 

not appropriate to extrapolate from Caddo Lake to larger 

regional or national populations.

 

262 Budtz-Jørgensen, E., N. Keiding, and P. Grandjean. 1999. Benchmark 

modeling of the Faroese methylmercury data. Final Report to U.S. EPA.

263 DSHA, 2005.
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EPA is aware of the possibility of both interactions 

among environmental contaminants and cumulative effects of 

pollutants that produce the same adverse endpoint. EPA 

guidance exists for dealing with such scenarios.264,265,266,267

The Agency’s concern with the likelihood of human exposure 

to multiple contaminants is reflected in the multi-chemical 

scope of the rulemaking. However, EPA focused the technical 

analyses supporting the proposed regulation on effects of 

individual pollutants rather than cumulative effects. 

EPA disagrees with commenters suggesting that the RfDbased 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 

 

264 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

265 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

266 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

267 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
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neurodevelopmental effects of methylmercury, it constitutes 

a reasonable basis for assessing risk.”268

EPA agrees that additional qualitative discussion 

about uncertainty would improve the Revised Hg Risk TSD. 

The SAB also recommended that EPA revise the Hg Risk TSD 

“to better explain the methods and choices made in the 

analysis, and analytical results, and where the 

uncertainties lie.” The SAB noted several uncertainties 

related to the RfD, and EPA is preparing a revised TSD that 

will address the SAB’s recommendations, including a more 

complete discussion of uncertainties including the RfD.

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.”270 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 

 

268 U.S. EPA-SAB, 2011.

270 U.S. EPA-SAB, 2011.
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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) [

271]. While its 

applicability to methylmercury is questionable, the size of 

the decrement is justified based on the extensive analyses 

available from the literature reviewed by CASAC.”272 As 

noted in other studies,273,274 a decrease of 1-2 points at the 

mean results in a much larger decrease in those with IQs 

that are much lower or higher than the mean. 

Although EPA disagrees that the IQ results are too 

uncertain to rely upon, EPA acknowledges that IQ is not the 

most sensitive neurodevelopmental endpoint affected by MeHg 

exposure, as also noted by the SAB. The SAB recommended 

that the IQ analyses be retained but be de-emphasized in 

 

271 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/989B57DCD436111B852572AC0079

DA8A/$File/casac-07-003.pdf

272 U.S. EPA-SAB, 2011.

273 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.

274 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.
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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.”276 EPA is following up the 

SAB’s recommendation by deemphasizing the IQ analysis and 

placing that analysis in an appendix to the revised TSD. 

The SAB, however, supported the use of the IQ doseresponse 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)[277] describes the sequence of 

 

276 U.S. EPA-SAB, 2011.

277 Bellinger, 2005.
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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.”278

EPA disagrees that EPA has overstated or failed to 

review the scientific literature on cardiovascular effects 

from MeHg exposure. As summarized in the preamble to the 

proposal, EPA stated that the NAS study concluded that 

“Although the data base is not as extensive for 

cardiovascular effects as it is for other end points (i.e., 

neurologic effects) the cardiovascular system appears to be 

a target for MeHg toxicity in humans and animals.”279 EPA 

also stated that additional cardiovascular studies have 

been published since 2000. EPA did not develop a 

quantitative dose response assessment for cardiovascular 

effects associated with MeHg exposures, as there is no 

 

278 U.S. EPA-SAB, 2011.

279 76 FR 25001
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consensus among scientists on the dose-response functions 

for these effects, and there is inconsistency among 

available studies as to the association between MeHg 

exposure and various cardiovascular system effects. In the 

future, EPA may update the MeHg RfD and will review all of 

the relevant scientific literature available at that time, 

including data on all relevant endpoints, and weight of 

evidence for likelihood that MeHg produces specific effects 

in humans.

EPA acknowledges the research regarding the 

effectiveness of fish advisories. However, the proposed 

regulation does not address the subject of fish advisories, 

consumer advice on fish or efficacy of such advice. EPA 

rejects the commenter’s speculation regarding whether the 

estimated IQ impacts for the regulation are real. Adverse 

effects of in utero Hg exposure have been reported in 

populations in the U.S.280,281 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 

 

280 Oken et al., 2008,

281 Lederman et al., 2008.
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consumption.282 That study suggests that at normal Japanese 

dietary intake of MeHg and fish nutrients, the overall 

effect is adverse. While Japanese fish consumption and Hg

exposure are both somewhat higher than the mean U.S. 

exposure, these levels are still within the distribution of 

U.S. consumers. 

Moreover, many studies show that beneficial effects of 

fish on both cardiovascular and neurodevelopmental health 

are decreased by concomitant exposure to MeHg. Several 

studies describe one or more aspects of exposure to fish 

nutrients and MeHg.283,284,285,286287,288,289 Recent studies292,293,294

 

282 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.

283 Grandjean P, Bjereve K, Wihe P, and Sterewald u. 2001a. “Birthweight 

in a fishing community: significance of essential fatty acids and 

marine food contaminants.” In. J. Epidemiol. 30:1272-1278. 

284 Budtz-Jorgensen, E.; Grandjean, P.; Weihe, P. 2007. “Separation of 

risks and benefits of 16 seafood intake.” Environmental Health 

Perspectives. Vol. 115, 323-327.

285 Choi et al., 2008a. 

286 Choi et al., 2008b.

287 Oken et al., 2008.

“

288 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.

289 Suzuki, et al., 2007.

292 Oken et al., 2008.

293 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.
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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. 

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.”295 The 

 

294 Choi AL, Budtz-Jørgensen E, Jørgensen 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.

295 U.S. EPA-SAB, 2011.
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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.”296

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 

 

296 Id.
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and unreliable, including using CMAQ to model deposition, 

MMAPs, fish consumption rate and fish MeHg concentrations, 

overly stringent RFD, national-scale model, using poverty 

as a surrogate for subsistence fishing, assuming a 

subsistence fisher resides in most watersheds with fish 

tissue data, fishers only eat larger fish with high Hg

concentrations, cooking loss adjustment, unrealistically 

high fish ingestion rates (a large fish meal every day), 

focused on the extremes of the distributions, cast many 

assumptions as an underestimate of the effect despite 

evidence to the contrary, and created inappropriate metrics 

for risk that show no improvement despite significant Hg

emissions reductions in the U.S. 

Several commenters cite Tetra Tech’s analysis that 

assessed Hg risk using different consumption rates, cooking 

factor, mean fish tissue concentrations, and EGUattributable 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 
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total deposition. One commenter stated that EPA’s data 

shows Hg emissions from U.S. EGUs have little influence on 

fish Hg concentrations despite reduction of 41 tons of Hg 

in U.S. between 2005 and 2016. One commenter requested that 

EPA accurately describe the low health risks posed by 

utility hazardous air pollutant emissions. One commenter 

stated that EPA did not consider scientific information 

showing that there is no straightforward connection between 

Hg emissions from U.S. EGUs to the Hg level in fish, which 

is dependent upon many environmental factors, such as 

sunlight and organic matter, pH, water temperature, 

sulfate, bacteria, and zooplankton present in the 

ecosystem. One commenter stated that there is not any 

demonstrable evidence that anyone in the U.S. has suffered 

adverse health problems as a result of Hg emissions from 

coal-fired EGUs. One commenter stated that EPA’s findings 

are similar to the 2000 findings where EPA found a 

plausible link between anthropogenic emissions of Hg from 

sources in the U.S. and MeHg in fish, and “plausible” is a 

euphemism for unproven.

Several commenters had recommendations for the Hg risk 

analysis. One commenter stated that more data from Florida 
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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. 
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One commenter stated EPA's reporting of IQ point loss 

is erroneous and not relevant to informing policy, and the 

U.S. EGU contribution to risk is marginal as evidenced by 

the null values for the 50th percentile watershed.

One commenter notes that U.S. EGU-attributable 

emissions of Hg have decreased significantly between 2005 

and 2016, but claims that this decrease does not appear to 

affect the risk results. 

One commenter questions why EPA has departed from the 

Clean Air Act (CAA) 112(n) risk comparison to the 1 in 1 

million to use the RfD for Hg.

Response: The purpose of the Hg risk assessment is not 

to assess the magnitude of risk reduction under the 

proposed rule, but rather to estimate the magnitude of 

absolute risk attributable to U.S. EGUs currently and 

following implementation of other applicable Clean Air Act 

requirements. That said, any potential risk reductions 

following implementation of the MACT rule itself would 

likely reflect a number of factors besides the national 

average U.S. EGU deposition value cited by the commenter. 

These additional factors include: (a) spatial gradients in 

the magnitude of absolute U.S. EGU-attributable Hg 
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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. EGUattributable 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 
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U.S. EGUs.”297 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.”

298 While the SAB did 

indicate difficulty in evaluating the risk assessment based 

solely on the Mercury Risk TSD, the panel was able to 

obtain enough additional information through the peer 

review process to make the determination that “the overall 

design of and approach to the risk assessment and finds 

that it should provide an objective, reasonable, and 

credible determination of the potential for a public health 

hazard from mercury emitted from U.S. EGUs.”299 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.”300 EPA has revised the Hg

Risk TSD as part of the final rulemaking to address the 

 

297 U.S. EPA-SAB, 2011.

298 Id.

299 Id.

300 Id.
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SAB’s recommendations and has made that revised TSD 

available in the rule docket. 

The SAB concurred with EPA’s analytical assumptions 

and overall study design for the Hg Risk TSD, including the 

RfD-based HQ approach, fish tissue data, 75th percentile 

size fish, Mercury Maps assumption, and consumption rates. 

Based on the SAB peer review, EPA strongly disagrees with 

commenter statements that the results reported in the Hg

TSD are unreliable, overly conservative, extreme, 

inconsistent with EPA risk guidelines, or severely 

overstate risk based on the stated objectives of the 

analysis. EPA has specifically addressed each of these 

assumptions in the previous sections of the preamble, thus, 

does not repeat those responses here. Based on the review 

by the SAB, EPA has accurately described the health risks 

posed by utility hazardous air pollutant emissions and 

disagrees with the commenter’s statement that EPA has not 

provided any demonstrable evidence to show that adverse 

health risks exist. EPA has applied peer reviewed modeling 

to estimate the deposition of Hg attributable to U.S. EGUs. 

EPA asserts that these metrics demonstrate a clear hazard 

to public health from Hg emissions from U.S. EGUs.
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EPA thoroughly evaluated the Tetra Tech analysis. EPA 

does not agree that the analysis by Tetra Tech uses 

assumptions that are “more reasonable”, and the SAB agreed 

that all of EPA’s assumptions are reasonable and 

appropriate. EPA asserts that the Tetra Tech analysis does 

not fully cover subsistence fishers likely to experience 

elevated U.S. EGU-related Hg exposure. Specifically, the 

risk estimated cited in the comment reflects application of 

a number of behavioral assumption that provide 

significantly less coverage for higher risk subsistence 

fishers. Fish consumption surveys cited in the Revised Hg

Risk TSD suggest that higher percentile subsistence fishers 

eat more than twice the level of fish assumed by Tetra 

Tech. The Tetra Tech analysis also used the median fish 

tissue levels, but it is reasonable to assume that 

subsistence fishers would target somewhat larger fish to 

maximize the volume of edible meat per unit time spent 

fishing. The Tetra Tech assumed that cooking fish did not 

concentrate Hg, but a number of studies discussed in the 

Revised Hg Risk TSD explicitly provide adjustment factors 

involving a higher unit concentration following 

preparation. Taken together, Tetra Tech’s analysis does not 
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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.

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. EPA has 

shown in the RIA (Chapter 5) that this rule will reduce Hg

levels in fish. 

EPA acknowledges that U.S. EGUs contribute only a 

small fraction of total Hg deposition in the U.S. However, 

U.S. EGUs remain the largest emitter of Hg in the U.S., and 

the revised risk analysis shows that U.S. EGU-attributable 

Hg deposition results in up to 29 percent of modeled 

watersheds having the potential for subsistence level 

freshwater fish consumers with total Hg exposures exceeding 

the RfD to have at least 5 percent of total Hg risk 

contributed by U.S. EGUs, and up to 10 percent of modeled 

watersheds having the potential for subsistence level 

freshwater fish consumers to have Hg exposures exceeding 
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the RfD due to Hg emissions from U.S. EGUs even before 

considering Hg exposures due to other sources. Hg risk is 

increasing for exposures above the RfD, and as a result, 

any reductions in Hg exposures in locations where total 

exposures exceed the RfD can result in reduced risks. While 

these reductions in risk may be small for most populations 

and locations, in some watersheds and for some populations, 

reductions in risk may be greater. 

The SAB also directly addressed the question of the 

nation-wide representativeness of the fish tissue MeHg data 

in the national Hg risk assessment. The SAB concluded, 

“Although the SAB considers the number of watersheds 

included in the assessment adequate, some watersheds in 

areas with relatively high mercury deposition from U.S. 

EGUs were under-sampled due to lack of fish tissue 

methy[l]mercury data. The SAB encourages the Agency to 

contact states with these watersheds to determine if 

additional fish tissue methylmercury data are available to 

improve coverage of the assessment.”301 In response to the 

SAB’s recommendations, EPA obtained additional fish tissue 

sample data from several states, particularly Pennsylvania, 

 

301 U.S. EPA-SAB, 2011.
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Wisconsin, Minnesota, New Jersey, and Michigan. This 

additional data increased the total number of watersheds 

assessed in the analysis by 33 percent nationally. In 

Florida, EPA assessed the Hg-related health risk for 40 

watersheds. Because EPA did not find any fish tissue data 

for new watersheds in Florida that could be incorporated 

into the analysis, the total number of watersheds in 

Florida assessed in the Revised Hg Risk TSD remains the 

same as proposal. 

EPA disagrees with the commenter that there were 

errors in the Hg Risk TSD. Instead, the commenter has 

misinterpreted how EPA calculated the percentiles. The 

percentile (and mean) values presented in Table ES-1 for 

total and U.S. EGU-attributable Hg deposition are not 

matched by watershed. In other words, EPA queried for the 

percentiles (and mean) provided for total Hg deposition and 

presented those percentiles and then separately estimated 

the percentiles for U.S. EGU-attributable Hg. Therefore, 

the total and U.S. EGU-attributable values for the 99th

percentile do not necessarily occur at the same watershed. 

EPA has provided additional clarification in the Revised Hg

Risk TSD. 
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EPA agrees with the commenter that MeHg levels in fish 

depend on a complicated set of environmental factors, and 

EPA acknowledged this in the Revised Hg Risk TSD. 

Furthermore, EPA acknowledges that total Hg fish tissue 

levels are not correlated with levels of total Hg 

deposition when looking across watersheds because this 

relationship is highly dependent on the methylation 

potential at the specific waterbody, which is affected by 

pH, sulfate deposition, turbidity, etc. However, several 

recent studies (Orihel et al., 2007, Orihel et al., 2008 

and Harris et al., 2007) show, and the SAB agrees, that it 

is appropriate for EPA to assume that changes in Hg

deposition are linearly associated with changes in fish 

tissue concentration. In addition, EPA agrees that the 

subset of watersheds in the risk analysis have somewhat 

higher U.S. EGU deposition than the distribution of all 

watersheds, but EPA disagrees that oversampling of high 

deposition watersheds is inappropriate. 

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. While total risk 
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from all Hg exposures will remain elevated in much of the 

U.S., much of that risk is associated with global, non-U.S. 

Hg emissions. U.S. EGUs remain the largest source of Hg 

emissions in the U.S., and reductions in those emissions 

will result in reduced Hg deposition in many highly 

impacted watersheds. Based on the Hg risk assessment, 

average EGU-attributable fish tissue Hg concentrations will 

be decreased by 65 percent. Likewise, the number of modeled 

watersheds with populations potentially at-risk from Hg 

emissions from U.S. EGUs will decline from 62 percent in 

2005 to 28 percent in 2016. Emissions reductions due to 

regulation of Hg under section 112 should result in 

additional reductions in U.S. EGU-attributable fish tissue 

Hg concentrations and modeled watersheds with populations

potentially at-risk.

EPA disagrees that IQ loss is erroneous or irrelevant 

to informing policy, but EPA has moved that analysis to an 

appendix in the Revised Hg Risk TSD, per the SAB’s

recommendation. EPA disagrees that the IQ effects at the 

50th percentile watershed are useful in determining that 

there is not a hazard to public health because EPA’s stated 

goal of the risk assessment was to focus on populations 
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likely to experience relatively higher exposures to U.S. 

EGU-attributable Hg. 

Regarding the commenter who questioned the alleged 

change in risk metrics to use the RfD approach, the

commenter is referring to cancer risk (i.e., a 1 in 1 

million probability of developing cancer over a lifetime 

due to a specific chemical exposure). For Hg, EPA focused 

on the potential for neurodevelopmental effects in the 

children born to mothers exposed to MeHg during pregnancy 

through fish consumption. This health endpoint is a noncancer endpoint, and risk in this context is assessed by 

comparing an estimate of daily exposure to MeHg for the 

mother to the MeHg RfD. Values greater than one (i.e., 

exposures that exceed the RfD) are considered to represent 

an exposure that could represent a public health hazard, 

this reflecting the methodology and underlying 

epidemiological data used in deriving the MeHg RfD.

We also disagree with those commenters that point to 

the SAB’s statements concerning the clarity of the Hg Risk 

TSD to suggest that the public did not have an ample 

opportunity to comment on the Hg risk assessment. While it 

is correct that the SAB said the Mercury Risk TSD was 
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difficult to evaluate until EPA staff explained it at the 

public meeting in June 2011, we note that the commenters 

that assert that this issue amounts to a violation of 

section 307(d) notice requirements made detailed technical 

comments, including many of the same comments as the SAB.

Furthermore, EPA provided notice of the peer review in the 

preamble to the proposed rule and a number of Federal 

Register notices advised the public of the peer review 

process and all the meetings were open to the public for 

comment and participation and the minutes of those meetings 

were posted on the SAB website. The minutes for the June 

2011 meeting, during which EPA provided clarifying 

information, were available well within the public comment 

period for the proposed rule. For these reasons, we 

maintain that the public was provided adequate opportunity 

to comment on the Hg risk assessment.

e. Non-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 
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emissions of untested units, the suggestion of statistical 

outliers in the Cr test data, the claim that metals content 

of the fuel is a indicator of flawed test data, the 

statistical approaches used by EPA to create emission 

factors, the absence in EPA’s approach of an equation that 

commenters claim better represents emissions values, that 

EPA’s approach to estimate hexavalent Cr is flawed, and the 

lack of coal rank as a delineating factor for emission 

factor calculation. The commenters also suggested that EPA 

should revise stack parameters used for the case studies 

based on better available data.

Response: In response to the comments on the emission 

factors, EPA has undertaken additional analysis to address 

all commenter concerns. EPA disagrees with commenter’s 

criticisms of emission factors based on arithmetic means, 

and EPA demonstrates that the use of an arithmetic mean 

provides the most representative result. EPA agrees with 

commenters’ recommendations to use statistical outlier 

tests, but has applied tests different from those suggested 

by the commenters. This approach did not eliminate the Cr

test data from the Cr emission factors used for some of the 

case study emissions.
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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.

EPA disagrees with the commenter recommendations for 

using an equation from AP-42, developed in part by the 

commenters. EPA conducted regression analyses between 

metals emissions measured at the site and predicted from 

the equations and demonstrates the poor predictive 

capability of these equations, concluding that emission 

test data is a more accurate predictor of actual emissions, 

and emission factors based on the arithmetic mean when test 

data are not available. 
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EPA also disagrees with commenters concerns about the 

assumption that 12 percent of the Cr will be Cr(VI) for 

every coal-fired unit. EPA disagrees with the commenter’s 

assertion that any impact of scrubbers will impact the case 

study analyses. In EPA’s final case study analysis, 6 

facilities have risk greater than 1 in 1 million, and of 

these, four facilities have 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, 

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.

EPA also disagrees that coal rank must be a factor in 

computing Cr emission factors for use in the case studies. 

EPA’s analysis has demonstrated that coal rank appears to 

play no role in metals emissions. EPA’s newly revised 
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emissions factor development procedures can isolate and 

compare subgroups based on control device type or coal 

rank; the ICR data were subjected to these tests and no 

statistical significance was found between coal rank 

groups.

Finally, EPA agrees with commenter’s recommendations 

on revised stack parameters for the case studies and has 

included these revisions in the case study modeling for the 

final rule.

2. General Comments on Non-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 

one million threshold level required to delist a source

category under section 112 of the Clean Air Act.

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 
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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-ina-million supports a finding that it is “appropriate” to 

regulated those four and not the other 537. Another 

commenter stated that EPA found only a “few” facilities 

that have estimated maximum cancer risks in excess of one 

in a million, and that this does not justify regulating all 

non-Hg 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, EPA’s discussion of the effects associated 
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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, EPA concluded that the risks from oil-fired units 

would result in only one new cancer case every five years.

The commenter does not believe that this level of risk 

warrants regulation under Section 112(n)(1)(A) of the CAA. 

Several commenters 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 Section 112 because three 

sites nationwide show risks greater that one in one 

million, with the highest at eight in one million.

One commenter stated that the highest cancer risk 

estimated for coal-fired EGUs is still within the 

acceptable range used by EPA in other programs and is also 

far less than the background exposure risks the average 

person experiences. The background risk of developing 
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cancer in a lifetime is approximately one in three (0.33). 

According to EPA's own data, the predicted added cancer 

risk of exposure to HAP from U.S. EGUs would change the 

background risk from 0.33 to 0.330001. This level of change 

is so minimal that it could not be observed in any health 

effects study that might be conducted.

One commenter stated that EPA conducted a health risk 

assessment on a limited number of facilities and found a 

“few” facilities that have estimated maximum cancer risks 

in excess of one in a million. The commenter stated that, 

based on this limited health risk assessment, EPA 

apparently decided that they were justified to regulate all 

non-Hg HAP for all sources in this category. 

Several commenters stated that EPA’s assumption that 

implies that a person stays exactly at the center of a 

census tract for 70 years and that a unit will operate in 

exactly the same manner for 70 years is unrealistic. The 

commenters suggest that Tier 3 risk assessment is warranted 

or a lifetime exposure adjustment is needed.

One commenter asserts that because the alleged health 

benefits are derived from total exposure, EPA should 

explain how its numerical emission limit units, which would 
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not directly restrict total exposure if heat inputs 

increase, redress this health concern. In its preamble, EPA 

simply notes that its emission limit units are consistent 

with, and allow for simple comparison to, other 

regulations.

One commenter questioned whether acid gas emissions 

limits for oil-fired units are “appropriate” or “necessary” 

because EPA’s new technical analyses do not indicate a 

health concern from acid gas emissions from oil-fired 

units. According to the commenter, EPA identifies Ni as the 

main HAP of concern from oil-fired units, even though 

cancer-related inhalation risks were well below the 

reference concentrations and EPA states that significant 

uncertainty remains as to whether those emissions present a 

health concern. 

Response: EPA agrees with the commenter that the nonHg HAP risk assessment confirms the appropriate and 

necessary finding.

EPA disagrees that EPA’s case study assessment is 

flawed by the use of beta versions of AERMET and AERMET. 

EPA remodeled the case study facilities using the current 

versions of AERMINUTE (version 11059), AERMET (version 
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11059), and AERMOD (version 11103). While there were 

differences in the number of calm and missing winds in the 

current AERMINUTE/AERMET output compared to the beta 

version, the resulting risks differed by less than two 

percent, on average. For Conesville, which had the largest 

difference in calms between the beta and current versions 

of AERMINUTE/AERMET, the risks differed by three percent. 

For the final rule, the case study facilities have been 

modeled with the current available versions of AERMINUTE, 

AERMET, and AERMOD.

EPA disagrees with the commenter that having only a 

few case study facilities exceeding one in a million risk 

invalidates the “appropriate finding”. The sixteen 

facilities EPA selected as case studies for assessment may 

not represent the highest-emitting or highest-risk sources. 

Although case study facility selection criteria included 

high estimated cancer and non-cancer risks using the 2005 

NEI data, high throughput, and minimal emission control, 

another necessary criterion was the availability of 

Information Collection Request (ICR) data for the EGUs at 

those facilities (or for similar EGUs at other facilities). 

Because the ICR data were collected for the purpose of 
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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. 

EPA’s assessment of the case study facilities for the 

proposed rule concluded that three coal-fired facilities 

and one oil-fired facility had estimated lifetime cancer 

risks greater than one in a million. For the final rule, 

revisions were made to the 16 case studies based on 

comments received, and the results indicate that five coalfired facilities and one oil-fired facility had estimated 

lifetime cancer risks greater than one in a million. EPA 

maintains that its finding that more than 30 percent of the 

case study facilities had a cancer risk greater than one in 

one million is sufficient to support the appropriate 

finding. Furthermore, EPA did not base the appropriate 

finding on just the case study analysis as explained in the 

preamble to the proposed rule.

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 
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proposed rule. The discussion of the health effects of nonHg 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

EPA disagrees with the commenter’s characterization of 

the Utility Study. The Utility Study represented the 

highest-quality factual record of information available at 

the time regarding EGU emissions and risks. Further, EPA’s 

recent risk assessments of 16 EGU case studies, performed 

with more recent data and refined scientific methods, 

indicate that there are still multiple EGU facilities that 

pose estimated inhalation cancer risks greater than one in 

a million. EPA maintains that the findings of the case 

studies are one element that independently supports our 

determination that it remains appropriate and necessary to 

regulate EGUs under section 112.
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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, EPA 

reasonably looked to the cancer risk threshold established 

under section 112(c)(9)(B)(1) for delisting a source 

category as an indicator of the level of cancer risk that 

was appropriate to regulate under section 112. 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. EPA maintains that the 

analysis was reasonable. 

EPA does not agree with the commenter’s implication 

that EPA must make a facility-specific finding for each HAP 

for each source and then only regulate individual EGU 

facilities for the individual HAP that identified as 

causing an identified hazard to public health or the 

environment. That approach is not required under section 

112(n)(1) or anywhere under section 112, and it would be 
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virtually impossible to undertake such an effort. For these 

reasons, EPA does not agree with the commenter and maintain 

that the appropriate and necessary finding is reasonably 

supported by the record and consistent with the statute for 

all the reasons set forth in the preamble to the proposed 

rule and this final action.

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 1989302

and codified by CAA 112(f) as the lifetime risk for a 

person located at the site of maximum exposure 24 hours a 

day, 365 days a year for 70 years (e.g. census block 

centroids). The MIR is the metric associated with the 

determination of whether or not a source category may be 

delisted from regulatory consideration under section 112 

(112(c)(9)). The MIR is the risk metric used to 

characterize the inhalation cancer risks associated with 

the case study facilities. EPA used the annual average 

ambient air concentration of each HAP at each census block 

 

302 54 FR 38044
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centroid as a surrogate for the lifetime inhalation 

exposure concentration of all the people who reside in the 

census block. EPA has used this approach to estimate MIR 

values in all of its risk assessments to support risk-based 

rulemakings under section 112 of the CAA to date.

EPA disagrees with the commenter’s assertion that the 

numerical emission limits being promulgated in today's 

final rule must be justified on their ability to redress 

the health concerns that were identified as the basis for 

regulating EGUs. The emission limits in today's rule are 

technology-based, as prescribed under section 112, and do 

not need to be justified based on their ability to protect 

public health. Regarding potential health concerns, EPA has 

up to 8 years after the promulgation of the technologybased emission limits for EGUs to determine whether the 

regulations protect public health with an ample margin of 

safety. If the regulations do not, the CAA directs EPA to

promulgate additional more stringent standards (within the 

prescribed 8 years) to achieve the appropriate level of 

public health protection.

Furthermore, EPA reasonably concluded that it was 

appropriate and necessary to regulate oil-fired EGUs in 
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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. EPA disagrees with these commenters and stands 

by the determination for the reasons set forth in the 

preamble to the proposed rule. 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 
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assigning the same carcinogenic potency of Ni subsulfide to 

other forms of Ni is overly conservative and inconsistent 

with the best available evidence.

Response: EPA disagrees with the commenters’ assertion 

that it is impossible to give an accurate assessment of the 

risks to human health from Ni emissions from EGUs, and 

maintains that its assessment of the potential inhalation 

risks from EGU emissions of Ni compounds is scientifically 

valid, reasonable, and based on the best-available current 

scientific understanding. To that end, in July 2011, EPA 

completed an external peer review (using three independent 

expert reviewers) of the methods used to evaluate the risks 

from Ni and Cr compounds emitted by EGUs.303 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 

 

303 U.S. EPA, 2011c.
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by the Integrated Risk Information System304, California 

Department of Health Services305, and the Texas Commission 

on Environmental Quality306), which of the following 

approaches to derive unit risk estimates would result in a 

more accurate and defensible characterization of risks from 

exposure to nickel compounds?

1. To continue using the same approach as that developed 

for use in the 2000 NATA, which consists of using the 

IRIS URE for nickel subsulfide and assuming that 

nickel subsulfide constitutes 65 percent of the mass 

emissions of all nickel compounds.

2. To consider a more health-protective approach, based 

on the consistent views of the most authoritative 

scientific bodies (i.e., NTP in their 12th ROC, IARC, 

and other international agencies) that consider nickel 

compounds to be carcinogenic as a group.

 

304 U.S. EPA, 1998. Integrated Risk Information Service (IRIS) assessment 

for hexavalent chromium. Available at:

http://www.epa.gov/ncea/iris/subst/0144.htm.

305 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.

306 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
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3. To make the same assumptions as in option 2, but 

considering alternative UREs derived by the CDHS or 

TCEQ.

In responding to these peer review questions, two of 

the reviewers agreed with the views of the most 

authoritative scientific bodies, which consider nickel 

compounds carcinogenic as a group. These reviewers, 

therefore, did not focus on the availability of 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.

Ni and Ni compounds have been classified as human 

carcinogens by national and international scientific bodies 

including the IARC,307 the World Health Organization308, and 

the European Union’s Scientific Committee on Health and 

 

307 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.

308International Labour Organization/United Nations Environment 

Programme, World Health Organization (WHO), 1991. Nickel. In 

Environmental Health Criteria No 108 Geneva.
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Environmental Risks309. 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 nickel compounds generate nickel ions in 

target cells at sites critical for carcinogenesis, thus 

allowing consideration and evaluation of these compounds as 

a single group”.310 Although the precise Ni compound (or 

compounds) responsible for the carcinogenic effects in 

 

309European 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

310 NTP, 2011.
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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).311,312,313

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 review314 highlights 

the robustness and consistency of the epidemiological 

evidence across several decades showing associations 

 

311 Oller A. Respiratory carcinogenicity assessment of soluble nickel 

compounds. Environ Health Perspect. 2002, 110:841-844.

312 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.

313 Goodman JE, Prueitt RL, Thakali S, and Oller AR. The nickel iron 

bioavailability model of the carcinogenic potential of nickelcontaining substances in the lung. Crit Rev Toxicol . 2011, 41:142-174.

314 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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between exposure to Ni and Ni compounds (including Ni

sulfate) and cancer. 

Based on the views of the major scientific bodies 

mentioned above, and those of expert peer reviewers that 

commented on EPA’s approaches to risk characterization of 

Ni compounds, EPA considers all Ni compounds to be 

carcinogenic as a group and does not consider Ni speciation 

or Ni solubility to be strong determinants of Ni

carcinogenicity. With regards to non-cancer effects, 

comparative quantitative analysis across Ni compounds 

indicates that Ni sulfate is as toxic or more toxic than Ni

subsulfide or Ni oxide.315,316

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. 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 

 

315 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.

316 NTP, 1996.
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used in EPA’s risk characterizations, and because of the 

concerns about the potential carcinogenicity of all forms 

of Ni raised by the major national and international 

scientific bodies. Nevertheless, taking into account that 

there are potential differences in toxicity and/or 

carcinogenic potential across the different Ni compounds, 

and given that there have been two URE values derived for 

exposure to mixtures of Ni compounds that are 2-3 fold 

lower than the IRIS URE for Ni subsulfide, EPA also 

considers it reasonable to use a value that is 50 percent 

of the IRIS URE for Ni subsulfide for providing an estimate 

of the lower end of a plausible range of cancer potency 

values for different mixtures of Ni compounds.

4. Cr Risk

Comment: One commenter stated there are several 

problems with EPA's analysis related to the fact that Cr

emissions were evaluated as being entirely Cr (VI). The 

commenter stated that not all of the emitted Cr will remain 

in the hexavalent form by the time it reaches the target 

population, and that some may be converted to the much less 

toxic (and noncarcinogenic) trivalent species. The 

commenter also stated that the concentration levels 
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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 watersoluble 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.
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Response: 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”317, existing test data for 

utility and industrial boilers indicate that hexavalent Cr

is, on average, twelve 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 

twelve percent value.

EPA also disagrees that units were assumed to operate 

100 percent of the time. The dispersion modeling performed 

for the case study facilities used hourly heat input as a 

temporalization factor for estimating hourly emissions, and 

in some cases hourly heat inputs (and emissions) were zero 

or very low. The commenter provided no data or information 

to support their claim that the dispersion modeling EPA 

used is biased towards overestimating downwind impacts.

 

317 U.S. EPA, 2011c.
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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 318 and codified by 

CAA 112(f) as the lifetime risk for a person located at the 

site of maximum exposure 24 hours a day, 365 days a year 

for 70 years (e.g. census block centroids). The MIR is the 

metric associated with the determination of whether or not 

a source category may be delisted from regulatory 

consideration under section 112 (112(c)(9)). The MIR is the 

risk metric used to characterize the inhalation cancer 

risks associated with the case study facilities. EPA used 

the annual average ambient air concentration of each HAP at 

each census block centroid as a surrogate for the lifetime 

inhalation exposure concentration of all the people who 

reside in the census block. EPA has used this approach to 

estimate MIR values in all of its risk assessments to 

support risk-based rulemakings under section 112 of the CAA 

to date.

 

318 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: As explained in the preamble to the proposed 

rule, EPA is not adopting an emissions standard based on 

its authority under section 112(d)(4) in the final rule. 

EPA first notes that the Agency’s authority under section 

112(d)(4) is discretionary. That provision states that EPA 

”may” consider established health thresholds when setting 

emissions standards under section 112(d). By the use of the 
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term “may,” Congress clearly intended to allow EPA to 

decide not to consider a health threshold even for 

pollutants that have an established threshold. As explained 

in the preamble to the proposed rule, it is appropriate for 

EPA to consider relevant factors when deciding whether to 

exercise its discretion under section 112(d)(4), and the 

language of that provision does not prevent the Agency from 

considering factors not specifically enumerated. To 

interpret the statute as commenters suggest would 

effectively require the Agency to establish section 

112(d)(4) standards whenever there is an established health 

threshold for a HAP. EPA has considered the public comments 

received and is not adopting an emissions standard under 

section 112(d)(4) for the reasons explained below and in 

the preamble to the proposed rule.

First, as explained in the preamble to the proposed 

rule, EPA maintains that the potential cumulative public 

health and environmental effects of acid gas emissions from 

EGUs and other acid gas sources located near EGUs supports 

the Agency’s decision not to exercise its discretion under 

section 112(d)(4). EPA did not receive information 

regarding facility-specific emissions of all the acid gases 
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from EGUs as well as sources that may be co-located with 

EGUs or nearby such sources. Additional data were also not 

provided during the comment period, and the data already in 

hand regarding these emissions are not sufficient to 

support the development of emissions standards for any of 

the EGU subcategories under section 112(d) that take into 

account the health threshold for acid gases, particularly 

given that the Act requires EPA’s consideration of health 

thresholds under section 112(d)(4) to protect public health 

with an ample margin of safety. The commenters’ assertions 

that EPA has sufficient data, even for HCl, are incorrect, 

and it appears that they believe that EPA can establish a 

section 112(d) standard for HCl and ignore the other acid 

gas HAP, a belief that is also incorrect. Second, the 

concerns expressed by EPA in the preamble to the proposed 

rule regarding the potential environmental impacts and the 

cumulative impacts of acid gases on public health were not 

assuaged by the comments received.

As explained in the preamble to the proposed rule, EPA 

also considered the co-benefits of setting a conventional 

MACT standard for HCl. EPA considered the comments received 

on this issue and maintains that the co-benefits are 
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significant and provide an additional basis for the 

Administrator to conclude that it is not appropriate to 

exercise her discretion under section 112(d)(4). EPA 

disagrees with the commenters who stated that it is not 

appropriate to consider non-HAP benefits in deciding 

whether to invoke section 112(d)(4). Although MACT 

standards may directly regulate only HAP and not criteria 

pollutants, Congress did recognize, in the legislative 

history to section 112(d)(4), that MACT standards would 

have the collateral benefit of controlling criteria 

pollutants as well and viewed this as an important benefit 

of the air toxics program.319 EPA consequently does not 

accept the argument that it cannot consider reductions of 

criteria pollutants, for example in determining whether to 

take or not take certain discretionary actions, such as 

whether to adopt a risk-based standard under section 

112(d)(4). There appears to be no valid reason that, where 

EPA has discretion in what type of standard to adopt, EPA 

must ignore controls which further the health and 

environmental outcomes at which section 112(d) of the Act 

is fundamentally aimed because such controls not only 

 

319 See S. Rep. No. 101–228, 101st Cong. 1st sess. at 172.
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reduce HAP emissions but emissions of other air pollutants 

as well.

Thus, the issue being addressed is not whether to 

regulate non-HAP under section 112(d) or whether to 

consider other air quality benefits in setting section 

112(d)(2) standards—neither of which EPA is doing—but 

rather whether to make the discretionary choice to regulate 

certain HAP based on the MACT approach and whether EPA must 

put blinders on and ignore collateral environmental 

benefits when choosing whether or not to exercise that 

discretion. EPA knows of no principle in law or common 

sense that precludes it from doing so.

6. EPRI Risk Analysis

Comment: Two commenters stated that a comprehensive 

tiered inhalation risk assessment (the EPRI study) using 

EPA-prescribed methods with improved emission factors, fuel 

data, and confirmed stack parameters did not identify 

significant health risks (cancer or non-cancer) among U.S. 

coal-fired power plants (as they existed in 2007). The 

commenters noted that these results contrast with those 

presented by EPA for its non-Hg case studies on 16 (15 

coal-fired) power plants. The commenters stated that 
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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 one million for hexavalent Cr, 

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.
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Response: The commenters are incorrect in the 

assertion that EPA’s case studies were performed with less 

rigor than the EPRI analysis. The EPRI analysis used a 

tiered approach to risk assessment, beginning with Tier 1 

using EPA’s SCREEN3 dispersion model on all 470 coal-fired 

power plants in the U.S., and following with Tier 2 with 

EPA’s Human Exposure Model (which uses the AERMOD 

dispersion model) for plants with higher risks from the 

Tier 1 modeling. Although tiered risk assessment is an 

appropriate approach, the Tier 2 modeling could have been 

more refined. For example, more meteorological data could 

have been used and building downwash could have been 

considered. The EPRI analysis ostensibly concluded that the 

Tier 2 modeling with HEM was conservative, and that because 

the modeled risks did not exceed certain thresholds, no 

further refinement was necessary. However, such refinements 

could result in higher modeled risks than those from the 

commenter’s Tier 2 modeling.

EPA’s dispersion modeling of the case study facilities 

was actually performed with a greater degree of refinement 
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than the EPRI analysis, and was consistent with EPA’s 

Guideline on Air Quality Models.320

In contrast to the approach used in the EPRI analysis, 

EPA used:

1) 5 years of recent meteorological data from the 

weather station nearest to each facility, rather 

than 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]

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 

 

320 Appendix W to 40 CFR 51
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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 2009.321 The SAB issued its 

peer review report in May 2010. The report generally 

endorsed the risk assessment methodologies used in the 

program. In addition, in July 2011, EPA completed a letter 

peer review of the methods used to develop inhalation 

cancer risk estimates for Cr and nickel compounds.

f. Ecosystem Impacts from HAPs

Comment: Two commenters assert that EPA is not 

justified in regulating acid gases based on concern about 

the potential that acid gases contribute to ecosystem 

acidification rather than concerns about hazards to public 

health. The commenters further claim that HCl’s 

contribution to ecosystem acidification is de minimis. The 

commenters point out that EPA acknowledges uncertainty in 

quantification of acidification and EPA relies on recently 

 

321 U.S. EPA-SAB, 2010. 
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published research322 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.

Response: While EPA agrees that quantification of 

acidification effects has remaining uncertainty, the 

science and methodology has progressed in recent years. 

Based on recent peer reviewed research including Evans et 

al.323, acid gases can significantly contribute to 

acidification. EPA published a comprehensive risk 

assessment of acidification effects of nitrogen and sulfur 

deposition324 and a policy assessment325. Given the extent 

 

322 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.

323 Id.

324 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/NOxSOxREASep2009

MainContent.pdf>.

325 U.S. Environmental Protection Agency (U.S. EPA). 2011. 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 
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and importance of the sensitive ecosystems evaluated in the 

review of nitrogen and sulfur deposition any substance that 

contributes to further acidification must be considered to 

be affecting the public welfare. EPA disagrees that the 

peer reviewed study mentioned by commenter by Evans et al. 

(2011) is not relevant to U.S. ecosystems. The paper 

presents experimental results that show 1) that HCl is 

highly mobile in the environment, transferring acidity 

easily through soils and water, 2) that HCl can transport 

longer distances than previously thought (given its 

presence in remote ecosystems, and 3) that it can be a 

larger driver of acidification than previously thought. The 

fact that this study took place in the U.K. is itself 

irrelevant. The chemical interactions of HCl in water are 

the same the world over and sensitive ecosystems exist in 

the U.S. as well as in Europe as illustrated in the risk 

assessment for NOx and SOx (U.S. EPA, 2009). Furthermore, 

the commenter is factually incorrect that EPA is justifying 

that it is appropriate and necessary to regulate HAP 

emissions from EGUs based on this one study. EPA agrees 

 

<http://www.epa.gov/ttnnaaqs/standards/no2so2sec/data/20110204pamain.pd

f>.
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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, EPA agrees that there are potential 

environmental risks from exposures of ecosystems through Hg 

and non-Hg HAP deposition. EPA cited relevant articles from 

the special edition of Ecotoxicology326 mentioned by the 

commenter in the ecosystem effects section on Chapter 5 of 

the RIA for this rule, which is available in the docket.

G. EPA Affirms the Finding that it is Appropriate and 

Necessary to Regulate EGUs to Address Public Health and 

Environmental Hazards Associated with Emissions of Hg and 

Non-Hg HAP from EGUs

In response to peer reviews of both the Hg and non-Hg 

HAP risk analyses, and taking into account public comments, 

we conducted revised analyses of the risks associated with 

U.S. EGU emissions of Hg and non-Hg HAP. These revised 

analyses demonstrated that the risk results reported in the 

preamble to the proposed rule are robust to the revisions 

made to the risk analyses. 

 

326 Ecotoxicology 17:83-91, 2008
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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.

327

In the revised Hg Risk TSD, up to 24 percent of modeled 

watersheds have potential total Hg exposure greater than 

the RfD and U.S. EGU-attributable Hg deposition accounts 

for 5 percent or more of total deposition to those 

watersheds. In the revised Hg Risk TSD, U.S. EGUs 

contribute to potential exposure greater than the RfD in 10 

percent of modeled watersheds, even excluding consideration 

of other U.S. and non-U.S. sources of Hg deposition. Given 

that 1) the percent of modeled watersheds with populations 

potentially at-risk increased from 28 to 29 percent in the 

revised risk assessment, 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 are a 

hazard to public health is confirmed by the revised Hg Risk 

TSD.

 

327 This corresponds to 28 percent of modeled watersheds with populations 

potentially at-risk in the analysis reported in the preamble to the 

proposed rule.
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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 oilfired 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 

hexavalent Cr, and one of which was driven by emissions of 

Ni. There were also two facilities with coal-fired EGUs 

with maximum individual cancer risks at one in a million, 

for a total of six facilities that meet or exceed the 

criterion for EGUs to be regulated under section 112. In 

the preamble to the proposed rule, we reported that the 

maximum individual lifetime cancer risk for the one 

facility with oil-fired EGUs was estimated to be 10 in a 

million, and that there were three coal-fired EGU 

facilities with maximum individual cancer risks greater 

than one in a million (the highest was eight in a million), 

and one coal-fired EGU facility with maximum individual 

cancer risks equal to one in a million. Given that 1) the 

lifetime cancer risk for the oil-fired EGU facility has 
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increased from 10 to 20 in a million, 2) the number of 

coal-fired EGU facilities with cancer risks greater than

one in a million has increased from three to five, and 3) 

the highest risk coal-fired facility still has cancer risks 

of five in a million, which is above the one in a million 

benchmark, we conclude that the finding that emissions of 

non-Hg HAP from U.S. EGUs are a hazard to public health is 

confirmed by the revised non-Hg risk inhalation case 

studies.

While we did not do new analyses on these topics, we

also reiterate that 1) Hg emissions from U.S. EGUs are a 

hazard to the environment, contributing to adverse impacts 

on fish-eating birds and mammals, 2) Hg is a persistent 

bioaccumulative environmental contaminant, and as a result, 

failing to control Hg emissions from U.S. EGU sources will 

result in long-term environmental loadings of Hg, above and 

beyond those loadings caused by immediate deposition of Hg 

within the U.S.; controlling Hg emissions from U.S. EGUs 

helps to reduce the potential for environmental hazard from 

Hg now and in the future, and 3) it is appropriate to 

regulate those HAP which are not known to cause cancer but 

are known to contribute to chronic non-cancer toxicity and 
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environmental degradation, such as the acid gases. These 

findings independently support a determination that it is 

appropriate to regulate Hg and non-Hg HAP emissions from 

EGUs. In addition, we have identified effective controls 

available to reduce Hg and Non-Hg HAP emissions.

Our revised analyses still show that in 2016 the 

hazards posed to human health and the environment by HAP 

emissions from EGUs will not be addressed by other sections 

of the CAA; therefore, it is necessary to regulate EGUs 

under section 112. In addition, based on evaluation of the 

regulations required by the CAA, including the recent CSAPR,

it is necessary to regulate EGUs under section 112 because 

the only way to ensure permanent reductions in U.S. EGU 

emissions of HAP and the associated risks to public health 

and the environment is through standards set under section 

112. While CSAPR is projected to achieve some Hg reductions 

due to co-control of Hg provided by controls put in place to 

achieve required reductions in SO2 emissions, the Hg Risk TSD

shows that a substantial percent of modeled watersheds with

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
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of 29 tons in our risk analysis compared to the most recent 

estimate of 27 tons, we do not expect that this small change 

would affect our finding that Hg emissions from U.S. EGUs 

are a hazard to public health. 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 section 112.

We reiterate that it is necessary to regulate HAP 

emissions from EGUs because 1) even though the hazards from 

Hg will not be resolved through regulation under section 

112, incremental reductions in Hg are important because as 

exposure above the RfD increases the likelihood and severity 

of adverse effects increases, 2) we cannot be certain that 

the identified cancer risks attributable to EGUs will be 

addressed through imposition of the requirements of the CAA, 

3) the environmental hazards posed by acidification will not 

be fully addressed through imposition of the CAA, 4) 

regulation under section 112 is the only way to ensure that 
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HAP emissions reductions that have been achieved since 2005 

remain permanent, and 5) direct control of Hg emissions 

affecting U.S. deposition is only possible through 

regulation of U.S. emissions as we are unable to control 

global emissions directly.

All of these findings independently support a finding 

that it is necessary to regulate EGUs under section 112. 

Therefore, the agency affirms its finding that it remains 

appropriate and necessary to regulate coal- and oil-fired 

EGUs under CAA section 112, and the inclusion of coal- and 

oil-fired EGUs on the section 112(c) list of source 

categories regulated under CAA section 112.