Amicus Curiae Brief — Michigan v. Envtl. Prot. Agency, 135 S. Ct. 702 (2014) (No. 14-46)

Nos. 14-46, 14-47, and 1

a

IN THE

Supreme Court of the Anited States

STATE OF MICHIGAN, ET AL.,

PETITIONERS,

Vv.

ENVIRONMENTAL PROTECTION AGENCY, ET AL.,

RESPONDENTS.

On Writs of Certiorari to the United States

Court of Appeals for the District of Columbia Circuit

BRIEF OF AMICI CURIAE

HEALTH SCIENTISTS,

DR. LYNN GOLDMAN ET AL,

IN SUPPORT OF RESPONDENTS

ALAN B. MORRISON

(COUNSEL OF RECORD)

ROBERT L. GLICKSMAN

THE GEORGE WASHINGTON

UNIVERSITY LAW SCHOOL

2000 H STREET NW

Washington, DC 20052

(202) 994-7120

(202) 994 5157 (Fax)

March 4, 2015 abmorrison@law.gwu.edu

TABLE OF CONTENTS

TABLE OF AUTHORIT TES ...cccccccccccsccccsscocccsseee il

INTERESTS OF THE AMICT ................cccsceccres 1

MERCURY EXPOSURE FROM POWER

PLANT EMISSIONS PRESENTS HIGHLY

SIGNIFICANT AND SERIOUS RISKS TO

PAPERS: SUED el Olle siinsssnnaictdninasinoenncnausnanetincineesee 6

METHYLMERCURY FROM COAL FIRED

PES BF ET Oi ncecstenernntinseeinmntassnieninennss 7

METHYLMERCURY EXPOSURES IN THE

Sdn siceescnenbietakeietiiaeniiisaistetiannimiaalianiniicnptneiietdes 18

CAPO POLPEREEIDT cctyinntiiinssciiasindninmniinmeaniinimiiesmiiindand 23

FRPP G ITE scerentinrisncsinnnviiincitiatitevinaiintiniiatiininsion A-1

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TABLE OF AUTHORITIES

Statutes

I Poe OF We ecikcniactenisinatinssieseniphiuminionatiessanihs 2,4

RSA ee eee rey ee Fe 4

RN Wi ia eacceccisaciceaiaongsmnicennatien 2, 3, 4

Section 7412(c).......... iiticnaalisttdentactcdateniensateis 2,3

RN a nlaiesionnemaiods 2.5

RN arcsec ncceecibiussstetiedumpddantnibepemslins 3

I en a naliden 2

RN tI ns wtaasinsiesimianigiinmssemninediniioonniail 3, 4,5

SION FE A iicsisiccecciecsectecencseses 3, 4, 5,6

RN Fi Re oiicinnsnansttcincnisvnntaccenasiensssnned 4

I na eetaaieciiianans 4,5

I I oi rcs cdisnewnescnannsmntinienedavedncs 5

ee ee ee FN iiinccicediscnssienceninainsienienves 3

1]

Other Authorities

13th Report on Carcinogens, National Toxicology

NIN, CIINILIIEG SUID doch iciectis ckscotrecinictinkchienisoscnctibueen 7

77 Fed. Reg. 9310 (2012)...........cececcecesesesesesesescecnees 8

A Probabilistic Characterization of the Health

Benefits of Reducing Methylmercury Intake in

the United States. ES&T (2010);

NP geen SE ee eee 12, 13, 16, 17

Adult Women’s Blood Mercury Concentrations

Vary Regionally in the United States:

Association with Patterns of Fish Consumption

(NHANES 1999-2004), Environ. Health

Perspect. (2009); Mahaffey, K.R., et al. 16, 19, 21

An Assessment of the Cord Blood: Maternal Blood

Methylmercury Ratio: Implications for Risk

Assessment, Environ. Health Perspect (2003);

I I i I dusuiie nia aneniniabioiocliite 16

Arsenic Exposure and Type 2 Diabetes: A

Systematic Review of the Experimental and

Epidemiologic Evidence, Environ. Health

Perspect. (2006); Navas-Acien A.., et al. ............ 7

Blood Mercury Levels in US Children and Women

of Childbearing Age, 1999-2000, J. Am. Med.

Assoc. (2003); Schober, S, et al. ....................... 19

iv

Blood Mercury Levels in Young Children and

Childbearing-aged Women --- United States,

i SS ds > eee 18

Cognitive Deficit in 7-year-old Children with

Prenatal Exposure to Methylmercury,

Neurotoxicol Teratol. (1997);

NII OMI iiccskcticsdinclannscniaveedeisnesscnsensis 12

Developmental Neurotoxicity of Industrial

Chemicals, Lancet (2006); Grandjean P. et al... 7

Estimated Fish Consumption Rates for the U.S.

Population and Selected Subpopulations

(NHANES 2003-2010) Final Report (2014);

ER aa aT MCA SOREY, CES EAD SPRUE Ne EON 21

Evaluation of the Association between Arsenic

and Diabetes: A National Toxicology Program

Workshop Review. Environ. Health Perspect

Se OE Oi 6 OU I as csaventetdentinecsbivedevtues 7

Evaluation of the Cardiovascular Effects of

Methylmercury Exposures: Current Evidence

Supports Development of a Dose-Response

Function for Regulatory Benefits Analysis,

Environ. Health Perspect (2011);

SS OE 2 RR eee eer 12, 15

Evidence on the Human Health Effects of Low-

Level Methylmercury Exposure. Environ.

Health Perspect (2012):

po ee eg eres ie 12, 13, 15, 17

Fourth National Report on Human Exposure to

Environmental Chemicals Updated Tables

(BR Eds CII. ic ccensecvncnscvcssctucazasusneaieueenaee 22

Genetic Susceptibility to Methylmercury

Developmental Neurotoxicity Matters, Frontiers

in Genetics, (2013); Julvez, et al.......... ee. 17

Global Methylmercury Exposure from Seafood

Consumption and Risk of Developmental

Neurotoxicity: a Systematic Review, Bull. World

Health Organ. (2014);

Ghecionm, BEC. G6 GB. cvcensdiescssacsutectee eae 19, 21

Hair Mercury Levels in U.S. Children and Women

of Childbearing Age: Reference Range Data

from NHANES 1999-2000, Environmental

Health Perspectives (2004); McDowell et al.... 20

Integrated Risk Information System-

Methylmercury (MeHg) (2001); EPA............... 16

Long Range Transport of Mercury to the Arctic

and across Canada, Atmos. Chem. Phys. 10:13

(3010); Dumiered BD... 66 Ob. ccieiitdiicsincccmee 10

Low Level Methylmercury Exposure Affects

Neuropsychological Function in Adults.

Environ. Health Glob. Access Sci. Source 2, 8

CRS WU, MiIIE. GE GL, ..cccccccccccccccccoccscess 15, 16

Materna! Fish Intake during Pregnancy, Blood

Mercury Levels, and Child Cognition at Age 3

Years in a US Cohort, Am. J. Epidemiol. (2008):

Ne ea msgmiswaosensasese 14

Mercurial but Not Swift: U.S. EPA's Initiative to

Regulate Coal Plant Mercury Emissions

Changes Course Again as its Enters a Third

Decade, 86 Chi.-Kent. L. Rev. 277 (2011);

I ssucprenewvevecwsenscce 22

Mercury Levels in High-End Consumers of Fish,

Environmental Health Perspectives (2002);

EE HII cvccccnacnctessossescoeeveverceses 20

Mercury Study Report to Congress (1997); EPA. . 7

Vil

Recent Trends in hg Emissions, Deposition, and

Biota in the Florida Everglades: A Monitoring

and Modeling Analysis. In: Dynamics of

Mercury Pollution on Regional and Global

Scales: Atmospheric Processes, Human

Exposure around the World, Springer

Publisher, Norwell, MA, (2005);

PI, TET Ge Gi crescents nnsiprercninitwinennants 10

Recognizing and Preventing Overexposure to

Methylmercury from Fish and Seafood

Consumption: Information for Physicians. J.

Toxicol (2011); Silbernagel, S.M. et al............. 15

Relation Between Cord Blood Mercury Levels and

Early Child Development in a World Trade

Center Cohort, Environ. Health Perspect.

(2008), Lederman SA, et all. ...........c0cc..cccosccceess 14

Risk Tradeoffs in Fish Consumption: A Public

Health Perspective, ES&T 46: (2012);

INIT, CF. 2its 0 Gis ceseenerececcinsvctdavncnccntansvetas 14

Summary and Conclusions, Food and Agriculture

Organization of the United Nations & World

Health Organization; 2003; Jomnt FAO/WHO

Expert Committee on Food Additives, In Sixty-

First Meeting; Rome, June 2003...................... 16

Vill

Technical Fact Sheet: Trends in Blood Mercury

Concentrations among Women of Reproductive

po REE eh ee SES i]

Technics! Report: Mercury in the Environment:

Impiications for Pediatricians. Pediatrics

(2001); Goldman, L.R. et al. ....................... 13, 15

Temporal and Spatial Trends in Freshwater Fish

Tissue: Mercury Concentrations Associated

with Mercury Emissions Reductions, ES&T

(2014); Hutcheson M.S., et al....................0..005 10

The Welfare Value of FDA’s Mercury in Fish

Advisory: A Dynamic Reanalysis, J. Health

Econ. 37: (2014); Rhienberger, C.M. et al........ 14

Total and Methyl Mercury in Whole Blood

Measured for the First Time in the U.S.

Population: NHANES 2011-2012, Environ. Res.

(2014); Mortensen M.E. et al. .......................... 22

Toxicological Effects of Methylmercury (National

Academies Press, 2001); National Research

NI concen et oa eee scrsascuecocneacanrammammnen eas 8

Toxicological Profile for Mercury-Potential for

Human Exposure (1999); Agency for Toxic

Substances and Disease Registry. ..................... S)

Trends in Blood Mercury Concentrations and Fish

Consumption Among U.S. Women of

Childbearing Age NHANES, 1999-2010, Final

ns CI inca cicdacdnacndeeroasadtiieiie 18

United Nations Minamata Convention on

SIIEIN <.dacinsd- adtininanbibesisaaineicunispbisieebinnbichideiasaatan 10, 11

Utility Hazardous Air Pollutant Report to

IRE TI sacietininiceateianeinsstndansustnionitesesemsiti 7

INTERESTS OF THE AMICI!

Each of the amici is an expert in

environmental public health. Dr. Lynn Goldman is

the Dean of the Milken Institute School of Public

Health and Professor of Environmental and

Occupational Health at George Washington

University. A pediatrician and an environmental

epidemiologist, she has an MD, a Masters of

Science in Health and Medical Sciences, and a

Masters of Public Health. She has served as the

Assistant Administrator for Toxic Substances at

the Environmental! Protection Agency, a professor

of Environmental Health Sciences at the

Bloomberg School of Public Health, and a Public

Health Medical Administrator with the California

Department of Public Health. The other 15 health

science experts who are amici are listed in the

Addendum to this brief, along with their specific

areas of expertise and their current affiliations.

INTRODUCTION AND SUMMARY OF

ARGUMENT

The issue before this Court is whether the

respondent Environmental Protection Agency

(EPA) properly decided to regulate emissions of

hazardous air pollutants from power plants

without considering the costs imposed by such

regulation at the initial listing stage. This brief

‘| This brief is filed based on the blanket consents of all parties

on file with the Court. No counsel for a party authored this

brief in whole or in part. and no one other than the George

Washington University, the amici, or their counsel

contributed money that was intended to fund the preparation

or submission of this brief.

will focus on the acute and chronic dangers to

public health caused by the exposure of mercury

emissions from power plants, which are among the

principal pollutants under the EPA regulation at

issue in this case. EPA and other amici will

demonstrate more fully the legal basis for EPA’s

decision, but to put the specific arguments

regarding mercury exposure in perspective, this

brief will first outline the legal framework that

EPA properly followed here.?

The provisions of the 1990 amendments to

the Clean Air Act that addressed hazardous air

pollutants, 42 U.S.C. § 7412, significantly changed

the regulation of those pollutants. In subsection

7412(b), Congress listed more than 180 substances

which EPA was required to treat as hazardous air

pollutants and to regulate accordingly. Subsection

7412(c) requires EPA to issue regulations,

pursuant to the standard-setting criteria of

subsection 7412(d), for all industrial sources of

hazardous air pollutants on the list. Paragraph (3)

of subsection 7412(d) requires that the reduction in

emissions for existing sources “shall not be less

stringent, and may be more stringent than - (A) the

average emission limitation achieved by the best

performing 12 percent of the existing sources

[subject to certain qualifications not relevant here]

with the lowest achievable emission rate

applicable to the [relevant] source category

”

2 For a useful pre-2011 history of EPA’s efforts to regulate

mercury and other power plant emissions, see Keith Harley,

Mercurial but Not Swift: U.S. EPA's Initiative to Regulate

Coai Plant Mercury Emissions Changes Course Again as its

Enters a Third Decade, 86 Chi.-Kent. L. Rev. 277 (2011).

There is no requirement that <I“. consider cost in

determining this minimum stringency “floor” for

power plants because, almost by definition, if “the

best performing 12 percent” of such sources is

already complying, the cost must be reasonable.

However, if EPA wishes to impose more stringent

emission reduction requirements than those being

achieved by the best performing sources in a

category, then subsection 7412(d)(2) does require it

to consider costs.

Subsection 7412(c) does not contain an

express exception for power plants, whose

emissions of other pollutants, including sulfur

dioxide and oxides of nitrogen, are subject to

regulation under the acid rain control provisions of

the 1990 Clean Air Act amendments, 42 U.S.C. §§

7651-765lo. However, subsection 7412(n) has

special provisions relating to power plants.

referred to there as “electric utility steam

generating units.” Subparagraph (1)(A) required

EPA to produce a study within three years from the

date of enactment of the 1990 amendments “of the

hazards to public health reasonably anticipated to

occur” as a result of their emissions of the

hazardous air pollutants listed under subsection

(b) which includes mercury compounds. The study

was to be sent to Congress, and it was to include

“alternative control strategies for emissions which

may warrant regulation under this section.”

Thereafter, 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.” Of significance to this case, there

is no mention of costs anywhere in section 7412 in

the directions for the study or in the mandate to

regulate based on the study’s findings.

Other provisions of subsection 7412(n) re-

enforce EPA's position that the decision to regulate

emissions from power plants of hazardous air

pollutants listed under subsection 7412(b) was to

be made without regard to costs. Subparagraph

(1)(B) mandates a separate study to be done by

EPA regarding mercury emissions from power

plants (but without a mandate to regulate), for

which it was given four years. Three aspects of that

study are significant: the study was to include not

only power plants, but also “municipal waste

combustion units, and other sources, including

area sources,” the latter term being defined in

subsection 7412(a)(2). Second, Congress required

that this study cover not only health effects, but

also environmental! effects. Third, and in contrast

to subparagraph (1)(A), subsection (1)(B) required

EPA to consider the “technologies which are

available to control such emissions, and the costs of

such technologies.” (Emphasis added.) The

significance of the addition of environmental

effects and the necessity for considering cost in the

broader study under subparagraph (B), but not the

study on which the regulation at issue is based

under subparagraph (A), is underscored by

subparagraph (C). That provision directs the

National Institute of Environmental Health

Sciences to conduct a study to determine the

threshold level of mercury exposure below which

human adverse health effects are not expected to

occur. That study. which was also required to

include a threshold for mercury concentrations

from the tissue of fish consumed by humans, covers

human health effects only and, like the study

under subparagraph (A), makes no mention of

costs.

Similarly, subparagraph 7412(n)(2)(A)

mandates a study of coke oven emissions, this one

within six years. It was to be done by EPA and the

Department of Energy “to assess coke oven

production emission control technologies and to

assist in the development and commercialization of

technically practicable and economically viable

control technologies which have the potential to

significantly reduce emissions of hazardous air

pollutants from coke oven production facilities.”

There is no mandate to regulate if certain findings

are made, but rather under subparagraph (C), the

study is to make “recommendations to the

Administrator identifying practicable and

economically viable control technologies for coke

oven production facilities to reduce residual risks

remaining after implementation of the standard

under subsection (d) of this section.” These

recommendations must include “economically

viable” solutions for coke ovens, in contrast to the

exclusion of all specific references to costs under

subsection 7412(n)(1)(A) for hazardous. air

pollutant emissions from power plants. Therefore.

the specific inclusions of costs in other parts of

subsection 7412(n) remove all doubt that Congress

intended that EPA’s decision whether to regulate

emissions of hazardous air pollutants, including

mercury emissions, from power plants on the basis

of the results of the study mandated by subsection

7412(n)(1)(A), should be made without regard to

the costs that such basic regulation might impose.

That result is not only clear from the statute itself,

but makes eminent sense given the dangers to

human health from exposure to hazardous air

pollutants such as mercury, and through

methylmercury a well-documented neurotoxin that

poisons brain development in the fetus, and to

which humans are exposed in the food supply

through fish.

ARGUMENT

MERCURY EXPOSURE FROM POWER

PLANT EMISSIONS PRESENTS HIGHLY

SIGNIFICANT AND SERIOUS RISKS TO

HUMAN HEALTH.

This brief will focus specifically on the public

health implications of reducing (or failing to

reduce) toxic air pollutants— most significantly

mercury — under the Mercury and Air Toxics

Standards (MATS) for power plants. Mercury is

one among a number of toxic air contaminants that

will be reduced in consequence of this rule; others

include arsenic, beryllium, cadmium, chromium,

cobalt, lead, manganese, nickel and selenium.

Several other pollutants emitted by power plants

(most notably PMe5, SO2z, NOx, HCl and CO2) also

have serious public health impacts. Although this

brief seeks to inform the Court about the

significant public health impacts of mercury — and

consequent benefits from the MATS rule due to

mercury reduction alone, the rule being challenged

also produces other public health benefits by

reducing emissions of toxics that are known human

carcinogens (arsenic, beryllium, cadmium.

chromium and nickel), or of substances reasonably

anticipated to be human carcinogens (cobalt, lead

and selenium), neurotoxicants (arsenic, lead, and

manganese), and possible diabetogenes.*

METHYLMERCURY FROM COAL FIRED

POWER PLANTS

The principal documents regarding the

health effects of exposure to mercury are the EPA’s

Mercury Study Report to Congress (1997) (“EPA

Mercury Study”),4 EPA’s Utility Hazardous Air

Pollutant Report to Congress (1998) (“Hazardous

Pollutant Report”),°> and the National Research

3 Knowledge of the harmful effects of other pollutants besides

mercury has increased since 1990. For example, arsenic

recently has been linked to tvpe 2 diabetes. HHS, 13th

Report on Carcinogens, National Toxicology Program (2013);

Grandjean P. et al., Developmental Neurotoxicity of

Industrial Chemicals, Lancet 368(9553):2167-2178 (2006);

Navas-Acien A., et al. Arsenic Exposure and Type 2 Diabetes:

A Systematic Review of the Experimental and Epidemiologic

Evidence. Environ. Health Perspect. 114:641-648 (2006):

Maull E. A., et al. Evaluation of the Association between

Arsenic and Diabetes: A National Toxicology Program

Workshop Review. Environ. Health Perspect,

http://dx.doi.org/10.1289/ehp.1104579, Online 10 August

2012.

* Available at http://www.epa.gov/mercury/report.html.

5 Available at

http://www.epa.gov/airtoxics/combust/utiltox/utoxpg. html#T

EC.

Council’s Toxicological Effects of Methylmercury

(2001) (NRC Effects of Methylmercury”).6

Together they demonstrate that mercury is a

ubiquitous environmental toxicant and that coal-

burning electric utilities are the largest source

category of anthropogenic mercury emissions,

accounting for one half of emissions in the United

States. See 77 Fed. Reg. 9310 (2012) (column 2).

These reports also show that the evidence that

environmental emissions of mercury have

significant negative impacts on population health

in the U.S. has advanced considerably since the

time of the 1990 Clean Air Act amendments which

mandated EPA’s study.

As explained in these three studies/reports,

mercury is a toxic metal released into the

environment from both natural and industrial

sources. Coal-fired power plants are the largest

remaining anthropogenic source of mercury

emissions in the U.S. As coal burns, its mercury

content is emitted into the air, transported through

the atmosphere and then readily deposited

(particularly with the rain) onto land and into

water bodies including streams, lakes, and oceans.

Human exposure to mercury originating from

power plant emissions is mostly via a form of

organic mercury called methylmercury. In aquatic

ecosystems, bacteria in sediments transform

inorganic mercury from power plant emissions into

methylmercury, which then bioaccumulates in the

aquatic food chain resulting in high mercury

6 National Research Council. Toxicological Effects of

Methylmercury (National Academies Press, 2001).

concentrations in the tissue of higher trophic level

(i.e., predatory) fish consumed by humans.’ Fish

accumulate mercury from their food as they grow,

as they cannot eliminate it. Older and larger fish

have higher mercury content. Thus, human

exposure to mercury from power plants is indirect;

humans are exposed to methylmercury through

consumption of contaminated fish.

Each year, 2,820 pounds of mercury are

discharged into the Nation’s waters. EPA has

concluded that mercury pollution from coal-fired

steam electric plants may be making fish unsafe for

human consumption in 65% of the waters that

receive discharges. Jd., Mercury is far and away

the leading cause for EPA and States to issue more

than 4000 fish-consumption advisories, warning

fishers “do not eat” or “limit consumption” of some

or all fish from over 40% of lake acres and river

miles and most of the continental U.S. coastline.®

Moreover the number of mercury-based advisories

* Agency for Toxic Substances and Disease Registry,

Toxicological Profile for Mercury-Potential for Human

Exposure (1999) at

http://www.atsdr.cdc.gov/toxprofiles/tp.asp7id=115&tid=24.

8 EPA, Technical Fact Sheet: Trends in Blood Mercury

Concentrations among Women of Reproductive Age (2013) at

http://water.epa.gov/scitech/swguidance/fishshellfish/fishadv

isories/upload/Technical-Fact-Sheet-Trends-in-Blood-

Mercury-Concentrations-among-Women-of-Childbearing-

Age.pdf.

® EPA, National Listing of Fish Advisories: Technical Fact

Sheet 2010 (2012).

http://water.epa.gov/scitech/swguidance/fishshellfish/fishadv

isories/technica!l factsheet_2010.cfm.

10

grew steadily from early-1990s through 2010

(latest year of data). Studies of past efforts to

reduce mercury emissions from coal-fired boilers

have shown that when these emissions are

reduced, concentrations in fish immediately

downwind from plants in both Massachusetts and

Florida have reduced; the Florida study used

isotopic labels to trace the mercury to coal burning

plants. !°

While mercury emissions from U.S. power

plants have the highest deposition in areas close to

the plants, they also are of global concern due to

the atmospheric transport. Using isotopic labeling,

mercury in the Arctic has been clearly traced to

coal burning emissions not only from the U.S. and

the rest of North America but also from Asia,

Russia and Europe.!! Mercury is of such global

concern that nations have negotiated, with the U.S.

as the first cosignatory. the United Nations

Minamata Convention on Mercury. The Minamata

Convention “recognizes that mercury is a chemical

of global concern owing to its long-range

atmospheric transport, its persistence in the

‘OHutcheson M.S., et al. Temporal and Spatial Trends in

Freshwater Fish Tissue: Mercury Concentrations Associated

with Mercury Emissions Reductions, ES&T 48:2193-2202

(2014); Atkeson, T. D., et al. Recent Trends in hg Emissions,

Deposition, and Biota in the Florida Everglades: A

Monitoring and Modeling Analysis. In: Dynamics of Mercury

Pollution on Regional and Global Scales: Atmospheric

Processes, Human Exposure around the World, Springer

Publisher, Norwell, MA, 26: 637-656. (2005).

11 Dumford D., et al. Long Range Transport of Mercury to the

Arctic and across Canada, Atmos. Chem. Phys. 10:13; 6-63-

6083 (2010).

1]

environment once anthropogenically introduced,

its ability to bioaccumulate in ecosystems and its

significant negative effects on human health and

the environment” Article 8 of this Convention

includes an agreement among all nations to

“ ..control[] and, where feasible, reduc[e] emissions

of mercury and mercury compounds, often

expressed as ‘total mercury’, to the atmosphere...”

Coal-fired power plants are listed as among the

sources that are to be controlled under this regime.

The Convention was negotiated well after the

adoption of the Clean Air Act, but it demonstrates

that not only Congress and the EPA but also

governments and environmental authorities

globally recognize the serious public health

impacts of human-caused (anthropogenic) mercury

releases generally, and emissions from coal-fired

power plants specifically. Developing countries are

contributing increasingly to global emissions from

coal-fired power plants. If the regulation at issue

in this case were set aside, it could provide cover to

other countries for failing to take action to

implement Article 8. Thus, not only will the

benefits to public health that will result from

reductions in mercury exposures under the MATS

be substantial, but the implications of overturning

this rule may encourage other countries to back

away from this agreement, with — global

consequences which in themselves could increase

methylmercury exposure to the U.S. population.

Both freshwater and ocean species of fish

can contain high levels of mercury. Apex predator

fish species, marine species such as shark, tuna,

and swordfish, and freshwater species such as

12

bass, pickerel and wall-eye, which are at the top of

the food chain, and some marine mammals are of

particular concern for causing high human

exposure levels because they accumulate the

highest levels of mercury. Individuals or

populations who consume large amounts of these

types of foods are more highly exposed and have

been found to be disproportionately affected by

adverse health effects, mainly neurologic outcomes

caused by mercury toxicity.

METHYLMERCURY TOXICITY

Mercury has long been recognized as

neurotoxic (toxic to the nervous system), but only

in recent decades has methylmercury, at levels

found in the ambient environment, been recognized

as a neurodevelopmental toxicant, i.e., toxic to the

developing central nervous system. '? It is also

suspected to be cardiotoxic, ie., toxic to the

cardiovascular system.'° At this time, there is no

12 National Research Council, supra, note 6, pp. 174-202;

Grandjean, P. et al. Cognitive Deficit in 7-year-old Children

with Prenatal Exposure to Methylmercury, Neurotoxicol

Teratol. 19, 417-428 (1997).

'5 Roman, H. A. et al. 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 (2011); Karagas, M. R. et al. Evidence on the Human

Health Effects of Low-Level Methylmercury Exposure.

Environ. Health Perspect. 120, 799-806 (2012); Rice, G. E., et

al. A Probabilistic Characterization of the Health Benefits of

Reducing Methylmercury Intake in the United States. ES&T

44, 5216-5224 (2010); Guallar, E. et al. Mercury, Fish Oils,

13

evidence for a_ threshold below which

neurodevelopmental effects do not occur.'4 Such a

threshold is often referred to as a “reference dose”

or RfD, a health standard that incorporates not

only the evidence for a threshold but also the level

of uncertainty around the threshold. This means

that it is reasonable to believe that any reductions

in exposure that can be achieved will have benefits

across the population. Even at low exposure levels.

methylmercury can lead to reductions in IQ for

developing children.'® These deficits in IQ may not

be clinically apparent in individual children, but on

a population level they have cumulative impacts

with large public health and _ economic

consequences.

Precise quantification of the risks

of methylmercury exposure and the benefits of

exposure reduction have been complicated by

the confounding in the relationship between

dietary methylmercury exposure and DHA, a

beneficial omega three fatty acid found in fish oil. '®

This confounding means that some of the negative

health effects of methylmercury are apparently

offset by the benefits attributable to increased

intake of DHA; it also means that methylmercury

is attenuating the benefits of DHA consumption to

and the Risk of Myocardial Infarction. N. Engl. J. Med. 347,

1747-1754 (2002).

‘4 Karagas, supra, note 13: Rice supra, note 13.

‘8 Karagas, supra, note 13; Goldman, L. R., et al., Technical

Report: Mercury in the Environment: Implications for

Pediatricians. Pediatrics 108, 197—205 (2001).

16 Rice, supra, note 13.

14

pregnant women who eat contaminated fish. Thus,

fish advisories that control mercury exposure via

limiting the consumption of fish for women of

childbearing age and for children invariably

decrease these populations’ intake of beneficial

DHA and other omega three fatty acids, possibly

harming other adults in the household when fish is

less available in household meals.'?’ Where

possible, it is preferable to reduce mercury

exposure, such as by limiting emissions from power

plants. The most recent scientific studies, which

have simultaneously accounted for

methylmercury’s hazardous effects and _ the

benefits of DHA, have demonstrated that

methylmercury is even more toxic than originally

suspected. '8

Methylmercury is also neurotoxic to adults.

There are now a number of reports of

methylmercury poisoning in adults occurring with

regular consumption of §methylmercury-

contaminated fish. Adults with methylmercury

poisoning have had severe and debilitating

symptoms: paresthesia, ataxia, weakness, vision

and hearing impairment, muscle tremor and

17 Rheinberger, C. M., et al, Risk Tradeoffs in Fish

Consumption: A Public Health Perspective, ES&T 46: 12337-

12346 (2012); Rheinberger, C. M., et al., The Welfare Value of

FDA's Mercury in Fish Advisory: A Dynamic Reanalysis, -/.

Health Econ. 37: 113-122, (2014).

18 Oken E, et al. Maternal Fish Intake during Pregnancy,

Blood Mercury levels, and Child Cognition at Age 3 Years in

a US Cohort, Am. J. Epidemiol. 167, 1171 (2008); Lederman

SA, et al. Relation Between Cord Blood Mercury Levels and

Early Child Development in a World Trade Center Cohort,

Environ. Health Perspect. 116:1085 (2008).

15

spasticity and even coma or death.’ A recent

article reviewed 25 clinical cases of methylmercury

poisoning among adult fish eaters. 2° It reported

variable exposure levels (7 to 125 pg/L of mercury

in blood) in association with toxicity from mercury

in fish. Further, there is no medical treatment for

methylmercury exposure other than to eliminate

consumption of mercury contaminated fish and to

wait until blood levels fall to a lower level. Chronic

lower levels of exposure to methylmercury have

been found to cause neurological impairment in

adults. Asymptomatic adults with methylmercury

levels above the WHO standard established for

children (see below) scored significantly lower on

tests of fine motor speed and neurocognitive tests.!

Cardiovascular effects of methylmercury

exposure have emerged as a concern even at

exposure levels below current levels of concern.?”

Evidence also suggests that mercury exposure is a

risk factor for myocardial infarction and possibly

other cardiovascular effects.25 Rice et al. in 2010

additionally pointed out the importance of

including cardiovascular effects in estimating the

value of health benefits achieved by reducing

19 Goldman, supra, note 15.

20 Silbernagel, S. M. et al. Recognizing and Preventing

Overexposure to Methylmercury from Fish and Seafood

Consumption: Information for Physicians. J. Toxicol. 2011,

1-7 (2011).

22 Yokoo, E. M. et al., Low Level Methylmercury Exposure

Affects Neuropsychological Function in Adults. Environ

Health Glob. Access Sci. Source 2, 8 (2003).

22 Roman, supra, note 13; Karagas, supra, note 13.

23 Roman, supra, note 13.

16

methylmercury exposure, and they concluded that

not including cardiovascular effects in benefit

estimations leads to significant underestimation of

the public health benefits that can be achieved by

reducing mercury emissions.”4

As of 2001, the EPA had identified 0.1 pg

/kg-day as a reference dose (RfD) for

methylmercury; this is an exposure level of 5.8 pg/L

methylmercury in umbilical cord blood, the

guideline recommended by the National Research

Council. 2 Methylmercury crosses the placental

barrier and concentrations found in newborn cord

blood are actually about 1.7 times higher than

maternal blood levels. 2 Therefore, the EPA RfD

is equivalent to 3.5 pg/L methylmercury in

maternal blood. In 2004, based on the same

studies, but different estimates of uncertainty, the

WHO established a weekly limit, or provisional

tolerable weekly intake (PTWI) of 1.6 pg/kg-

week.27

24 Rice, supra, note 13.

25 EPA, Integrated Risk Information System-Methylmercury

(MeHg) (CASRN 22967-92-6) (2001);

http://www.epa.gov/iris/subst/0073.htm.; Mahaffey, K. R., et

al. Adult Women’s Blood Mercury Concentrations Vary

Regionally in the United States: Association with Patterns of

Fish Consumption (NHANES 1999-2004), Environ. Health

Perspect. 117, 47—53 (2009).

26 Stern AH, et al. An Assessment of the Cord Blood:

Maternal! Blood Methylmercury Ratio: Implications for Risk

Assessment, Environ. Health Perspect. 111:1465-70 (2003);

Yokoo, supra, note 21.

27 Joint FAO/WHO Expert Committee on Food Additives. In:

Sixty-first Meeting, Rome, 10-19 June 2003: Summary and

Conclusions, Food and Agriculture Organization of the

17

Since these guidelines were developed, new

evidence has emerged that indicates that there are

people in the population with increased genetic

susceptibility to methylmercury _ toxicity.7®

Moreover, as noted above, the most current

evidence on the health effects of mercury suggests

that no threshold can be identified.29 That

evidence is strongest for the neurodevelopmental

effects. Karagas et al.’s review published in 2012

shows that both neurodevelopmental effects and

cardiovascular effects occur at exposure levels

below the levels recorded in the studies used to set

the EPA reference dose.® Rice et al. assumed a

90% probability of a linear no threshold dose-

response for neurodevelopmental toxicity in their

benefits model because they “find no strong

biological support for this population threshold”.*!

Additionally, the Karagas study shows that harms

from mercury exposure can occur even with

infrequent consumption of seafood.52 In other

words, the assumption of a threshold or a “safe”

level, as implied by an RfD or a PTWI, probably

underestimates the impacts of mercury on

population health.

United Nations & World Health Organization; 2003.

Available at: ftp://ftp.fao.org/es/esn/jecfa/jecfa61sc.pdf.

2 Julvez J., et al., Genetic Susceptibility to Methylmercury

Developmental Neurotoxicity Matters, Frontiers in Genetics,

4; 278;1-4 (2013).

2 Kareyas, supra, note 13; Rice, supra, note 13.

*® Karagas, supra, note 13.

31 Rice, supra, note 13 at pp. 5218.

32 Karagas, supra, note 13.

18

METHYLMERCURY EXPOSURES IN THE U.S.

Numerous studies have demonstrated that

the developing brain is most sensitive to

methylmercury’s neurotoxic effects and thus the

focus has been on exposure to women of child

bearing age and young children. In 2004 the CDC

reported that 5.7% of women of childbearing age

had blood mercury levels at or above the EPA

reference dose for newborns in the 1999-2002

NHANES survey.* Blood mercury levels have

been tracked over time and the level reduced

sharply to 3.14% in 2001-2002, and leveled off to

around 2.1% thereafter. These same data show no

downward trend in consumption of fish and

seafood.*4 Thus even with reductions in mercury

from past regulation, as well as advice to consume

fish and seafood with lower mercury levels, a

significant percentage of the population has

mercury exposures that are too high for children

and women of childbearing age.

Because of variable emissions levels in

different regions of the U.S., variable levels of

methylmercury in different water bodies, variable

uptake and bioaccumulation of methylmercury in

different species of fish, and variable fish

33 Centers for Disease Control, Blood Mercury Levels in

Young Children and Childbearing-aged Women --- United

States, 1999—2002, MMWR. 53(4); 1018-1020, November 5,

2004.

34 EPA, Trends in Blood Mercury Concentrations and Fish

Consumption Among U.S. Women of Childbearing Age

NHANES, 1999-2010, Final Report EPA-823-R-13-002.

(2013).

19

consumption by different communities and ethnic

groups, some populations are at greater risk of

methylmercury toxicity than others.*

Mercury concentrations are highest in large

apex predator fish and other large fish. While all

fish consuming members of the population are at

risk, a disproportionate burden of exposure and

neurodevelopmental and cardiovascular health

effects fall on specific subpopulations who consume

more of such fish or who habitually eat fish from

contaminated areas. Sensitive populations in the

U.S. include coastal populations, Asian and Pacific

Islander populations, Native American groups and

populations who consume more fish as an effort to

have a more healthful diet.*6 Health-conscious

people may replace all red meat dishes with fish,

consuming fish at one or more meals per day,

ironically jeopardizing their health. Fish

populations downwind from power plant emissions

globally, accumulate methylmercury because of

long-range transport of mercury in air. However.

higher rates of mercury deposition have been found

in areas very close to power plant emissions. EPA

has focused its benefits assessment on

consumption of fish from such locations among

recreational anglers who frequent these areas

3% Mahaffey, supra, note 25; Sheehan, M. C. et al. Global

Methylmercury Exposure from Seafood Consumption and

Risk of Developmental Neurotoxicity: a Svstematic Review,

Bull. World Health Organ. 92, 254—269F (2014); Schober, S,

et al., Blood Mercury Levels in US Children and Women of

Childbearing Age, 1999-2000, J. Am. Med. Assoc. 289

(13):1667-1674 (2003).

* Sheehan, supra, note 35.

20

because of the availability of data on fishing

licenses and localized fish contamination levels.

There has been less information about the extent

to which contaminated fish from such areas

immediately downwind of power plants are

entering commerce, nor is much known about

exposures experienced by subsistence fishers in

those regions.

Underscoring the importance of

understanding subpopulation vulnerabilities, a

2003 study found that some children in middle to

upper income families in San Francisco had

methylmercury levels 40 times the national

average for that age group because of fish ard

seafood consumption.*? That study assessed hair

mercury from NHANES 1999-2000 data and found

that mercury levels were on average three fold

higher for women and two fold higher for children

who were identified as frequent fish consumers in

a food frequency questionnaire.** A 2009 study

using 1999-2004 NHANES data found that women

who lived in the Northeast and in coastal regions

of the U.S. were more likely than residents of other

regions to have mercury levels exceeding 3.5 pg/g,

the concentration (as noted above) considered to be

an appropriate level of concern because it takes

37 Hightower and Moore, “Mercury Levels in High-End

Consumers of Fish,” Environmental Health Perspectives 111,

(4): 604—8. (2002) doi:10.1289/ehp.5837.

38 McDowell et al., “Hair Mercury Levels in U.S. Children and

Women of Childbearing Age: Reference Range Data from

NHANES 1999-2000,” Environmental Health Perspectives

112; (11): 1165—71, (2004) doi:10.1289/ehp.7046.

21

into account the concentration of methylmercury

across the placenta and more accurately reflects

the amplification of exposure to the fetus.%9

A systematic review conducted for the

WHO/FAO also showed that human

methylmercury levels vary globally depending on

geographical location and fish consumption

habits.4° It found that coastal populations and

Artic populations (including those in Alaska) have

mercury concentrations that were elevated above

other subpopulations and that many have

exposures above the WHO reference level. Coastal

regions of the world have the largest number of at

risk individuals for neurodevelopmental and

cardiovascular effects due to methylmercury

exposure. The WHO report concluded that a large

number of individuals worldwide, including in the

United States, are exposed to mercury at levels

above the WHO recommended level.

According to the EPA's 2014 report, those

with the highest per capita fish consumption were

either of lower income (subsistence consumers) or

higher income groups and resided either in the

coastal Northeast or on the West Coast.4!

Differences in average intakes are substantial;

consumption rates nearly double between the 50th

and 75% percentile for most groups. Asian

3° Mahaffrey, supra, note 25.

© Sheehan, supra, note 335.

41 EPA, Estimated Fish Consumption Rates for the U-S.

Population and Selected Subpopulations (NHANES 2003-

2010); Final Report EPA-820-R14-002.. pp. 49—92 (2014).

22

populations also have higher exposures. to

methylmercury. According to the CDC, in 2011-

2012 when the general population geometric mean

(GM) methylmercury in blood was 0.5 pg/L, the

mean for Asian Americans was 1.58 pg/L.42 Overall

15.8% of Asian Americans were at or above the

EPA level of concern (based on in utero exposure)

of 5.8 pg /L, compared to 2.8% of non-Hispanic

Whites, 2.15 of Non-Hispanic Blacks and 1.3% of

Hispanics.4°

The United States is the world’s third

largest emitter of mercury behind China and India,

and fossil fuel combustion is the largest source.*4

Moreover, given that much of the harm from

mercury releases occurs locally, the emissions from

sources in the US are more harmful to the US

population than those from China and India.

While there are natural sources of mercury in

water, and therefore in fish, these human-caused

(anthropogenic) emissions are causing health risks

that are additive to natural levels and inputs from

other sources and are therefore increasing health

risks significantly.

42 CDC, Fourth National Report on Human Exposure to

Environmental Chemicals Updated Tables (2014), pp. 189-

194

http://www.cdc.gov/exposurereport/pdf/fourthreport_updated

tables_aug2014.pdf.

43 Mortensen M.E., et al. Total and Methy! Mercury in Whole

Blood Measured for the First Time in the U.S. Population:

NHANES 2011-2012, Environ. Res. 134:257-264 (2014).

44 EPA, ORA Mercury Emissions: The Global Context. (2014)

available at http://www?2.epa.gov/international-

cooperation/mercury-emissions-global-context.

CONCLUSION

When Congress enacted the Clean Air Act

Amendments of 1990, there was ample evidence

that mercury was harmful to human health, but

Congress nevertheless mandated further study

before permitting EPA to regulate mercury

emissions from power plants. That study has been

completed and, along with much other research,

has removed all doubts about the harmful health

(and environmental) effects of mercury and the

large public health benefit of reducing mercury

along with arsenic and other pollutants. Under

those Amendments, that set of findings is all EPA

needed to impose the regulations that it did, and

accordingly the decision of the Court of Appeals

should be affirmed.

Respectfully submitted,

Alan B. Morrison

(Counsel of Record)

Robert L. Glicksman

George Washington University Law School

2000 H Street NW

Washington D.C. 20052

(202 994 7120)

abmormrison@law.gwu.edu

March 4, 2015

A-1

ADDENDUM

ALPHABETICAL LIST OF AMICI

ORGANIZATIONAL AFFILIATIONS

FOR IDENTIFICATION PURPOSES ONLY

Lynn R. Goldman, M.D., M.S., M.P.H

Michael and Lori Milken Dean

Professor, Environmental Health Sciences

Milken Institute School of Public Health

George Washington University

Joanna Burger, PhD

Distinguished Professor of Life Sciences

Rutgers University

Brenda Eskenazi, PhD

Professor, Epidemiology

Chair, Community Health and Development

School of Public Health

University of California Berkeley

Bernard D. Goldstein, MD

Emeritus Professor and Emeritus Dean

Graduate School of Public Health

University of Pittsburgh

Michael Gochfeld, MD, PhD

Clinical Professor (retired) Environmental and

Occupational Medicine

Rutgers Robert Wood Johnson Medical School

A-2

Phillipe Grandjean

Adjunct Professor of Environmental! Health

Harvard T.H. Chan School of Public Health

Harvard University

James K. Hammitt

Professor of Economics and Decision Sciences

Harvard T.H. Chan School of Public Health

Director, Harvard Center for Risk Analysis

Harvard University

Richard J. Jackson, MD, MPH

Professor, Environmental Health Sciences

Fielding School of Public Health

University of California Los Angeles

Philip J. Landrigan, Mv, MSc, FAAP

Dean for Global Health

Ethel H. Wise Professor and Chairman,

Department of Preventive Medicine

Professor of Pediatrics

Director, Children's Environmental Health Center

Icahn School of Medicine at Mount Sinai

Bruce Lanphear, MD, MPH

Professor of Children's Environmental! Health

BC Children's Hospital

Simon Frasier University

Ana Navas-Acien, MD, PhD

Associate Professor, Environmental! Health

Sciences and Epidemiology

Johns Hopkins Bloomberg School of Public Health

A-3

Melissa Perry, ScD, MPH

Professor and Chair, Department of

Environmental and Occupational! Health

Milken Institute School of Public Health

George Washington University

Martin A. Philbert, PhD

Dean and Professor of Toxicology

School of Public Health

University of Michigan

Ellen Silbergeld

Professor, Environmental Health Sciences

Johns Hopkins Bloomberg School of Public Health

Johns Hopkins University

Leo Trasande, MD, MPH

Associate Professor, Pediatrics, Environmental

Medicine, and Population Health

School of Medicine

New York University

Roberta White, PhD

Professor, Neurology, Boston University School of

Medicine

Chair and Professor, Environmental Health,

Boston University School of Public Health

Associate Dean for Research, Boston University

School of Public Health