Children’s Health Article

590 VOLUME 113 | NUMBER 5 | May 2005 • Environmental Health Perspectives

Mercury is a ubiquitous environmental toxicant (Goldman et al. 2001). It exists in three

forms, each of which possesses different

bioavailability and toxicity: the metallic element, inorganic salts, and organic compounds

(methyl mercury, ethyl mercury, and phenyl

mercury) (Franzblau 1994). Although volcanoes and other natural sources release some

elemental mercury to the environment, anthropogenic emissions from coal-fired electric

power generation facilities, chloralkali production, waste incineration, and other industrial

activities now account for approximately 70%

of the 5,500 metric tons of mercury that are

released into the earth’s atmosphere each year

[United Nations Environmental Programme

(UNEP) 2002]. Elemental mercury is readily

aerosolized because of its low boiling point, and

once airborne it can travel long distances to

eventually deposit into soil and water. In the

sediments of rivers, lakes, and the ocean, metallic mercury is transformed within microorganisms into methyl mercury (Guimaraes et al.

2000). This methyl mercury biomagnifies in

the marine food chain to reach very high concentrations in predatory fish such as swordfish, tuna, king mackerel, and shark (Dietz

et al. 2000; Gilmour and Riedel 2000;

Mason et al. 1995; Neumann and Ward

1999). Consumption of contaminated fish is

the major route of human exposure to methyl

mercury.

The toxicity of methyl mercury to the

developing brain was first recognized in the

1950s in Minamata, Japan, where consumption of fish with high concentrations of methyl

mercury by pregnant women resulted in at

least 30 cases of cerebral palsy in children;

exposed women were affected minimally if at

all (Harada 1968). A similar episode followed

in 1972 in Iraq when the use of a methyl

mercury fungicide led to poisoning in thousands of people (Bakir et al. 1973); again,

infants and children were most profoundly

affected (Amin-Zaki et al. 1974, 1979). The

vulnerability of the developing brain to

methyl mercury reflects the ability of lipophilic methyl mercury to cross the placenta

and concentrate in the central nervous system

(Campbell et al. 1992). Moreover, the

blood–brain barrier is not fully developed

until after the first year of life, and methyl

mercury can cross this incomplete barrier

(Rodier 1995).

Three recent, large-scale prospective epidemiologic studies have examined children

who experienced methyl mercury exposures

in utero at concentrations relevant to current

U.S. exposure levels. The first of these studies,

a cohort in New Zealand, found a 3-point

decrement in the Wechsler Intelligence ScaleRevised (WISC-R) full-scale IQ among

children born to women with maternal hair

mercury concentrations > 6 μg/g (Kjellstrom

et al. 1986, 1989). A second study in the

Seychelles Islands in the Indian Ocean found

only one adverse association with maternal

hair mercury concentration among 48 neurodevelopmental end points examined (prolonged time to complete a grooved pegboard

test with the nonpreferred hand) (Myers et al.

2003). However, the grooved pegboard test

was one of the few neurobehavioral instruments in the Seychelles study not subject to

the vagaries of translation that can degrade

the validity of culture-bound tests of higher

cognitive function when they are applied in

developing nations (Landrigan and Goldman

2003). A third prospective study in the Faroe

Islands, a component of Denmark inhabited

by a Scandinavian population in the North

Atlantic, has followed a cohort of children

for 14 years and collected data on 17 neurodevelopmental end points, as well as on the

impact of methyl mercury on cardiovascular

function. The Faroes researchers found significant dose-related, adverse associations

between prenatal mercury exposure and performance on a wide range of memory, attention, language, and visual-spatial perception

tests (Grandjean et al. 1997). The significance

of these associations remained evident when

Address correspondence to L. Trasande, Center for

Children’s Health and the Environment, Department

of Community and Preventive Medicine, Mount

Sinai School of Medicine, One Gustave L. Levy Place,

Box 1057, New York, NY 10029 USA. Telephone:

(212) 241-8029. Fax: (212) 996-0407. E-mail:

leo.trasande@mssm.edu

We are grateful for the helpful advice of P.

Grandjean, E. Budtz-Jorgensen, D. Laraque, P. Leigh,

and J. Palfrey as well as to D.P. Rice and W. Max for

their assistance with lifetime earnings estimates.

This research was supported by a grant from the

National Institute of Environmental Health Sciences

through the Superfund Basic Research Program

(PT42ES07384) to Mount Sinai School of

Medicine, and by the Jenifer Altman Foundation,

Physicians for Social Responsibility, and the Rena

Shulsky Foundation.

The authors declare they have no competing

financial interests.

Received 10 November 2004; accepted 28 February

2005.

Public Health and Economic Consequences of Methyl Mercury Toxicity 

to the Developing Brain

Leonardo Trasande,1,2,3,4 Philip J. Landrigan,1,2 and Clyde Schechter5

1Center for Children’s Health and the Environment, Department of Community and Preventive Medicine, and 2Department of Pediatrics,

Mount Sinai School of Medicine, New York, New York, USA; 3Division of General Pediatrics, Children’s Hospital, Boston, Massachusetts,

USA; 4Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA; 5Department of Family Medicine, Albert Einstein

College of Medicine, Bronx, New York, USA

Methyl mercury is a developmental neurotoxicant. Exposure results principally from consumption

by pregnant women of seafood contaminated by mercury from anthropogenic (70%) and natural

(30%) sources. Throughout the 1990s, the U.S. Environmental Protection Agency (EPA) made

steady progress in reducing mercury emissions from anthropogenic sources, especially from power

plants, which account for 41% of anthropogenic emissions. However, the U.S. EPA recently proposed to slow this progress, citing high costs of pollution abatement. To put into perspective the

costs of controlling emissions from American power plants, we have estimated the economic costs

of methyl mercury toxicity attributable to mercury from these plants. We used an environmentally

attributable fraction model and limited our analysis to the neurodevelopmental impacts—specifically loss of intelligence. Using national blood mercury prevalence data from the Centers for

Disease Control and Prevention, we found that between 316,588 and 637,233 children each year

have cord blood mercury levels > 5.8 μg/L, a level associated with loss of IQ. The resulting loss of

intelligence causes diminished economic productivity that persists over the entire lifetime of these

children. This lost productivity is the major cost of methyl mercury toxicity, and it amounts to

$8.7 billion annually (range, $2.2–43.8 billion; all costs are in 2000 US$). Of this total, $1.3 billion (range, $0.1–6.5 billion) each year is attributable to mercury emissions from American power

plants. This significant toll threatens the economic health and security of the United States and

should be considered in the debate on mercury pollution controls. Key words: children’s health,

cognitive development, cord blood, electrical generation facilities, environmentally attributable

fraction, fetal exposure, lost economic productivity, mercury, methyl mercury, power plants.

Environ Health Perspect 113:590–596 (2005). doi:10.1289/ehp.7743 available via http://dx.doi.org/

[Online 28 February 2005]
Environmental Health Perspectives • VOLUME 113 | NUMBER 5 | May 2005 591

blood levels of polychlorinated biphenyls,

which are known developmental neurotoxicants (Jacobson and Jacobson 1996), were

included in the analysis (Budtz-Jorgensen

et al. 2002; Steuerwald et al. 2000). Methyl

mercury exposure was also associated with

decreased sympathetic- and parasympatheticmediated modulation of heart rate variability

(Grandjean et al. 2004) and with persistent

delays in peaks I–III brainstem evoked potentials (Murata et al. 2004).

An assessment of these three prospective

studies by the National Academy of Sciences

(NAS) (National Research Council 2000)

concluded that there is strong evidence for the

fetal neurotoxicity of methyl mercury, even at

low concentrations of exposure. Moreover,

the NAS opined that the most credible of the

three prospective epidemiologic studies was

the Faroe Islands investigation. In recommending a procedure for setting a reference

dose for a methyl mercury standard, the NAS

chose to use a linear model to represent the

relationship between mercury exposure and

neurodevelopmental outcomes, and based this

model on the Faroe Islands data. The NAS

found that the cord blood methyl mercury

concentration was the most sensitive biomarker of exposure in utero and correlated

best with neurobehavioral outcomes. The

NAS was not deterred by the apparently negative findings of the Seychelles Islands study,

which it noted was based on a smaller cohort

than the Faroe Islands investigation and had

only 50% statistical power to detect the effects

observed in the Faroes (National Research

Council 2000).

Since January 2003, the issue of early

life exposure to methyl mercury has become

the topic of intense debate after the U.S.

Environmental Protection Agency (EPA)

announced a proposal to reverse strict controls

on emissions of mercury from coal-fired power

plants. This proposed “Clear Skies Act” would

slow recent progress in controlling mercury

emission rates from electric generation facilities

and would allow these releases to remain as

high as 26 tons/year through 2010 (U.S. EPA

2004a). By contrast, existing protections under

the Clean Air Act will limit mercury emissions

from coal-fired power plants to 5 tons/year by

2008 (U.S. EPA 2004b). The U.S. EPA’s technical analyses in support of “Clear Skies” failed

to incorporate or quantify consideration of the

health impacts resulting from increased mercury emissions (U.S. EPA 2004c). After legislative momentum for this proposal faded, the

U.S. EPA proposed an almost identical Utility

Mercury Reductions Rule, which again failed

to examine impacts on health. The U.S. EPA

issued a final rule on 15 March 2005 (U.S.

EPA 2005).

To assess the costs that may result from

exposure of the developing brain to methyl

mercury, we estimated the economic impact

of anthropogenic methyl mercury exposure in

the 2000 U.S. birth cohort. We calculated the

fraction of this cost that could be attributed to

mercury emitted by American electric power

generation facilities.

Materials and Methods

Environmentally attributable fraction model.

To assess the disease burden and the costs

due to methyl mercury exposure, we used an

environmentally attributable fraction (EAF)

model. The EAF approach was developed by

the Institute of Medicine (IOM) to assess the

“fractional contribution” of the environment

to causation of illness in the United States

(IOM 1981), and it has been used to assess

the costs of environmental and occupational

disease (Fahs et al. 1989; Leigh et al. 1997). It

was used recently to estimate the environmentally attributable costs of lead poisoning,

asthma, pediatric cancer, and neurodevelopmental disabilities in American children

(Landrigan et al. 2002). The EAF is defined

by Smith et al. (1999) as “the percentage of a

particular disease category that would be

eliminated if environmental risk factors were

reduced to their lowest feasible concentrations.” The EAF is a composite value and is

the product of the prevalence of a risk factor

multiplied by the relative risk of disease associated with that risk factor. Its calculation is

useful in developing strategies for resource

allocation and prioritization in public health.

The general model developed by the IOM and

used in the present analysis is the following:

Costs = disease rate × EAF × population size 

× cost per case

“Cost per case” refers to discounted lifetime expenditures attributable to a particular

disease, including direct costs of health care,

costs of rehabilitation, and lost productivity.

“Disease rate” and “population size” refer,

respectively, to the incidence or prevalence of

a disease and the size of the population at risk.

In applying the EAF model, we first

reviewed the adverse effects of methyl mercury

exposure. We then estimated the costs of those

effects and subsequently applied a further fraction to parse out the cost of anthropogenic

methyl mercury exposure resulting from emissions of American electrical generation facilities.

Toxic effects of methyl mercury exposure.

The NAS found neurodevelopmental effects in

the children of women who had consumed fish

and seafood during pregnancy to be the most

important and best-studied end point for

methyl mercury toxicity. Although the NAS

identified other potentially significant toxicities

resulting from methyl mercury exposure, such

as nephrotoxicity and carcinogenicity, those

effects were less well characterized (National

Research Council 2000). We therefore limited

our analysis to the neurodevelopmental impact

of methyl mercury toxicity.

There is no evidence to date validating the

existence of a threshold blood mercury concentration below which adverse effects on

cognition are not seen. The U.S. EPA has,

however, set a benchmark dose level (BMDL)

for cord blood mercury dose concentration of

58 μg/L. This level that corresponds to the

lower limit of the 95% confidence interval for

the concentration at which there is a doubling

in the Faroes study in the prevalence of test

scores (5–10%) in the clinically subnormal

range for the Boston Naming Test (Rice et al.

2003). It is important to note that this is not

a concentration below which no observed

adverse effects were found. The Faroes and

New Zealand cohorts both support the conclusion that developmental effects become

apparent at levels of approximately 1 ppm

mercury in hair, or 5.8 μg/L in cord blood

(Grandjean et al. 1997; Kjellstrom et al.

1986, 1989). The Faroes study also found

that effects on delayed brainstem auditory

responses occurred at much lower exposure

concentrations (Murata et al. 2004). In its

report, the NAS concluded that the likelihood

of subnormal scores on neurodevelopmental

tests after in utero exposure to methyl mercury increased as cord blood concentrations

increased from levels as low as 5 μg/L to

the BMDL of 58 μg/L (National Research

Council 2000). In light of those findings, we

decided in this analysis to apply a no adverse

effect level of 5.8 μg/L, the lowest level at

which adverse neurodevelopmental effects

were demonstrated in the cohort studies.

Recent data suggest that the cord blood

mercury concentration may on average be 70%

higher than the maternal blood mercury concentration (Stern and Smith 2003), and a

recent analysis suggests that a modification of

the U.S. EPA reference dose for methyl mercury be made to reflect a cord blood:maternal

blood ratio that is > 1 (Stern 2005). If the

developmental effects of mercury exposure do,

in fact, begin at 5.8 μg/L in cord blood, as suggested by the Faroes (Grandjean et al. 1997)

and New Zealand (Kjellstrom et al. 1986,

1989) data and by the NAS report (National

Research Council 2000), then effects would

occur in children born to women of childbearing age with blood mercury concentrations

≥ 3.41 (ratio, 5.8:1.7) μg/L. National population data from the 1999–2000 National

Health and Nutrition Examination Survey

(NHANES) found that 15.7% of American

women of childbearing age have total blood

mercury concentrations ≥ 3.5 μg/L (Mahaffey

et al. 2004).

To compute IQ decrements in infants that

have resulted from these elevated maternal

mercury exposures, we used published data on

Children’s Health | Cost of methyl mercury toxicity to the developing brain

Environmental Health Perspectives • VOLUME 113 | NUMBER 5 | May 2005 591
percentages of women of childbearing age

with mercury concentrations ≥ 3.5, 4.84, 5.8,

7.13, and 15.0 μg/L. We assumed conservatively that all mercury concentrations within

each of the segments of the distribution were

at the lower bound of the range. We assumed

that the probability of giving birth to a child

did not correlate with mercury level in a

woman of childbearing age. In our base case

analysis, we calculated economic costs assuming that children born to women with mercury concentrations 3.5–4.84 μg/L suffer no

loss in cognition, and that successive portions

of the birth cohort experience loss of cognition

associated with cord blood levels of 8.2, 9.9,

12.1, and 25.5 μg/L, respectively.

Recently, the Faroes researchers reviewed

their cohort data and found fetal blood mercury concentrations to be only 30% higher

than maternal blood concentrations (BudtzJorgensen et al. 2004). In light of these findings and to avoid overestimation of the

magnitude of impacts, we chose not to include

children born to mothers with blood mercury

concentrations between 3.5 and 4.84 μg/L in

our base case analysis.

To assess the impact on our findings of a

range of various possible ratios between maternal and cord blood mercury concentrations,

we conducted a sensitivity analysis. In this

analysis, we set as a lower bound for our estimate the costs to children with estimated cord

blood concentrations ≥ 5.8 μg/L (assuming a

cord:maternal blood ratio of 1) and assumed

no IQ impact < 4.84 μg/L (assuming a

cord:maternal blood ratio of 1.19). This estimate assumed no loss of cognition to children

born to women with mercury concentration

< 5.8 μg/L and assumed that subsequent portions of the birth cohort experienced cord

blood mercury concentrations of 5.8, 7.13,

and 15 μg/L, respectively. To estimate economic costs in this scenario, we calculated no

costs for children with blood mercury concentrations < 4.84 μg/L. We calculated costs

resulting from an incremental increase in

blood mercury concentration from 4.84 to

5.8 μg/L in the percentage of the population

with blood mercury levels between 5.8 and

7.13 μg/L, and added those costs to the

costs resulting from increases from 4.84 to

7.13 μg/L and 4.84 to 15 μg/L in the percentages of the population with concentrations

between 7.13 and 15 μg/L and > 15 μg/L,

respectively. The result of this calculation is

expressed in our analysis as a lower bound for

the true economic cost of methyl mercury

toxicity to the developing brain.

Impact of methyl mercury exposure on IQ.

The Faroes study found that a doubling of

mercury concentration was associated with

adverse impacts on neurodevelopmental tests

ranging from 5.69–15.93% of a standard deviation (Grandjean et al. 1999). Assuming that

IQ is normally distributed with a standard

deviation of 15 points, a doubling of mercury

concentration would be associated with a

decrement ranging from 0.85 to 2.4 IQ points.

The Faroes researchers used a structural equation analysis to produce estimates of impact of

methyl mercury on verbal and motor function

at 7 years of age and found an association

between a doubling of blood mercury and loss

of 9.74% of a standard deviation on motor

function and of 10.45% of a standard deviation on verbal function (Budtz-Jorgensen et al.

2002). This analysis suggests that a doubling in

mercury concentration produces a decrement

of approximately 10% of a standard deviation,

or 1.5 IQ points. In the New Zealand study

(Kjellstrom et al. 1986, 1989), the average

WISC-R full-scale IQ for the study population

(n = 237) was 93. In the group with maternal

hair mercury > 6 μg/g (~ 4-fold higher than in

the study population, n = 61), the average was

90 (Kjellstrom et al. 1989). This finding

further supports our use of a loss of 1.5 IQ

points for each doubling in our base case analysis. Confounders such as polychlorinated

biphenyls did not cause significant confounding of the data in the Faroe Islands study

(Budtz-Jorgensen et al. 2002; Steuerwald et al.

2000). As a conservative measure, we nonetheless chose to set as outer bounds for the impact

on intelligence of methyl mercury exposure a

range of IQ decrements from 0.85 to 2.4 IQ

points per doubling, as described by the Faroes

researchers (Jorgensen et al. 2004). In applying

the EAF methodology, we assume that the

relationship between cord blood mercury and

IQ is relatively linear over the range of exposures studied (> 5.8 μg/L).

In our sensitivity analysis, we used the

same linear dose–response model that was

selected by the National Research Council in

setting a reference dose for mercury exposure

(National Research Council 2000). The

Faroes researchers found that, for those children whose mothers had hair mercury concentrations < 10 μg/g, a 1-μg/L increase of cord

blood mercury concentration was associated

with adverse impacts on neurodevelopmental

tests ranging from 3.95 to 8.33% of a standard deviation, or 0.59–1.24 IQ points (average = 0.93 IQ points) (Jorgensen et al. 2004).

We also varied the cord:maternal blood mercury ratio from 1 to 1.7 in calculating IQ

impact from the linear model as part of our

sensitivity analysis. As an upper bound to our

cost estimate using the logarithmic model, we

calculated the economic cost assuming that

children born to women with mercury concentrations 3.5–4.84 μg/L suffer no loss in

cognition and that successive portions of the

birth cohort experience losses of cognition of

1.21, 1.84, 2.55, and 5.13 IQ points, respectively. The lower-bound estimate assumed

that children born to women with mercury

concentrations 4.84–5.8 μg/L suffer no loss in

cognition and that successive portions of the

birth cohort experience losses of cognition of

0.22, 0.48, and 1.39 IQ points.

As an upper bound to our cost estimate

using the linear model, we calculated the

economic cost assuming that children born

to women with mercury concentrations

3.5–4.84 μg/L suffer no loss in cognition and

that successive portions of the birth cohort

experience losses of cognition of 3.01, 5.04,

7.84, and 24.43 IQ points, respectively. The

lower-bound estimate assumed that children

born to women with mercury concentrations

4.84–5.8 μg/L suffer no loss in cognition and

that successive portions of the birth cohort

experience losses of cognition of 0.56, 1.35,

and 5.99 IQ points.

Calculation of economic costs of IQ loss.

To estimate the costs associated with the

cognitive and behavioral consequences of

mercury exposure, we relied on an economic

forecasting model developed by Schwartz

et al. (1985), and we applied this model to

NHANES data on prevalence of mercury

exposure in women of childbearing age

(Schober et al. 2003; Schwartz et al. 1985). In

this model, lead concentrations are assumed

on the basis of work by Salkever (1995) to

produce a dose-related decrement in IQ score.

Those decrements in IQ are, in turn, associated with lower wages and diminished lifetime earning power. Salkever used three

regression techniques to derive direct and

indirect relationships among IQ, schooling,

probability of workforce participation, and

earnings. He estimated a percentage in lost

earnings per IQ point from the percent loss of

earnings for each microgram per deciliter

increase in blood lead level. Salkever found a

0.473 point decrement in lost lifetime earnings for each microgram per deciliter increase

among men and a 0.806 point decrement for

each microgram per deciliter increase among

women (Salkever 1995). Using Schwartz’s

(1994) estimate that 0.245 IQ points are lost

for each microgram per deciliter increase in

blood lead, Salkever (1995) estimated a percentage loss in lifetime earnings per IQ point

among men (1.931%) and women (3.225%).

We assume that this relationship remains linear across the population range of IQ.

Assuming an annual growth in productivity of 1% and applying a 3% real discount

rate, the present value of lifetime expected

earnings is $1,032,002 for a boy born in

2000 and $763,468 for a girl born in the

same year (Max et al. 2002). The costs of

the diminution in this earning power were

calculated for the 2000 American birth

cohort, using available data on the number of

male and female births in 2000 [Centers

for Disease Control and Prevention (CDC)

2002a]. We diminished our cost estimate by

Children’s Health | Trasande et al.

592 VOLUME 113 | NUMBER 5 | May 2005 • Environmental Health Perspectives
Environmental Health Perspectives • VOLUME 113 | NUMBER 5 | May 2005 593

0.69%, the infant mortality rate in 2000, to

account for those children for whom methyl

mercury exposure is unlikely to result in

diminished economic productivity (CDC

2002b).

American sources of mercury emission.

Mercury emissions result from anthropogenic

as well as from natural sources, and we limited

our analysis to methyl mercury derived from

anthropogenic sources. The UNEP recently

estimated that anthropogenic uses account for

70% of the 5,500 tons of mercury released

into the earth’s atmosphere worldwide (UNEP

2002). Therefore, to limit our analysis to

anthropogenic mercury, we applied a 70%

factor to convert the cost of lost economic productivity resulting from methyl mercury exposure to the cost attributable to anthropogenic

methyl mercury exposure.

We next parsed out the proportion of

anthropogenic methyl mercury in fish that

arises from American sources and then isolated

the subset of that proportion that is emitted

by coal-fired electrical generating plants. In

1995, the most recent year for which federal

data on the relative deposition of mercury

from American and other global sources are

available, 158 tons of mercury were emitted to

the atmosphere by American anthropogenic

sources. Fifty-two (33%) of those 158 tons

were deposited in the lower 48 states, whereas

the remaining two-thirds were added to the

global reservoir (U.S. EPA 2004d). Also in

1995, an additional 35 tons of mercury from

the global reservoir were deposited in the

United States. Therefore, a total of 87 total

tons of mercury were deposited in the United

States in that year, of which 60% (52 of 87)

were attributable to American anthropogenic

sources (U.S. EPA 1996, 1997). This mercury

would have been available to bioaccumulate in

the marine and aquatic food chains and to

enter American freshwater and saltwater fish.

Further complicating our calculations is

the fact that not all of the fish sold in America

is from American sources. Of the 10.4 billion

pounds of edible fish supplied in the United

States in 2002, 4.4 billion (42%) are imported

from sources outside of the United States

(National Marine Fisheries Service 2002).

Because U.S. emissions account for 3% of

global emissions (UNEP 2002; U.S. EPA

1996), we calculate that the mercury content

of imported fish is 2% of American anthropogenic origin: 158 tons of American emissions – 52 tons of American mercury deposited

on American soil = 106 tons of American

mercury available to contaminate imported

fish; 5,500 tons emitted globally – 87 tons

deposited on American soil = 5,413 tons of

mercury from all sources to contaminate

imported fish; 106 tons of mercury available/

5,413 tons of mercury from all sources = 0.02,

or 2% of mercury in imported fish of

American origin. In the remaining 58% of fish

consumed in the United States, we assume that

60% of the mercury content comes from

American anthropogenic sources (U.S. EPA

1996, 1997). We therefore applied a 36% factor (the weighted average of American sources

of mercury content in fish, or 0.6 × 0.58 +

0.02 × 0.42) to specify the economic costs of

anthropogenic methyl mercury exposure

attributable to American sources.

Modeling supported by the Electric Power

Resource Institute (EPRI) estimates that 70%

of the mercury deposited in the United States

comes from foreign sources (Seigneur et al.

2004). This EPRI analysis also finds that U.S.

sources are responsible for > 60% of mercury

deposition in the Boston–Washington, D.C.

corridor. In one of the model’s selected receptor areas—Pines Lake, New Jersey—80% of

the deposition originated from U.S. sources,

showing that regional deposition can be higher

than the 60% number we use in this analysis

(Seigneur et al. 2004). In our sensitivity analysis, we varied the factor used to convert the

economic cost of anthropogenic methyl mercury exposure to the economic cost attributable

to American sources from 18% (0.3 × 0.58 +

0.02 × 0.42, using EPRI’s modeling) to 36%

(using federal data on mercury deposition)

(Seigneur et al. 2004).

In 1999, the most recent year for which

data on American mercury emissions are available, 48 (41%) of the 117 tons of mercury

emissions from anthropogenic sources in the

United States were emitted by electric power

generation facilities (U.S. EPA 2003a). To calculate the economic cost of methyl mercury

exposure attributable to these facilities, we

applied an additional fraction of 41% in our

analysis.

Results

Base-case analysis. Each year in the United

States, between 316,588 (7.8% of the annual

birth cohort) and 637,233 babies are born

with cord blood mercury levels > 5.8 μg/L.

The lower-bound estimate of 316,588 babies

is based on the very conservative assumption

that maternal and cord blood mercury concentrations are equal. But if the cord blood

mercury concentration is on average 70%

higher than the maternal blood mercury concentration, as suggested by recent research

(Stern and Smith 2003), 637,233 babies, or

15.7% of the birth cohort, experience cord

blood mercury levels > 5.8 μg/L. Fetal blood

mercury levels > 5.8 μg/L are associated with

small but significant loss of IQ. This decrement in IQ appears to be permanent and irreversible, and it adversely affects a significant

portion of the annual birth cohort’s economic

productivity over a lifetime.

Using our base-case assumptions (impact

for women with total mercury > 4.84 μg/L,

cord:maternal mercury ratio = 1.7, IQ impact

= 1.5 points per doubling), we calculated costs

for the 405,881 children who suffer IQ decrements resulting from fetal methyl mercury

exposure. Under these assumptions, 89,293

children suffered a 0.76 decrement in IQ and

another 113,647 experienced a 1.15 IQ point

decrement. The 5% most highly exposed

children in the 2000 birth cohort suffered

subclinical losses in IQ in our model ranging

from 1.60 to 3.21 points. Although this

diminution in intelligence is small in comparison with the loss of cognition that can

result from other genetic and environmental

processes, the loss resulting from methyl mercury exposure produces a significant reduction

in economic productivity over a lifetime. We

estimate the aggregate cost of the loss in IQ

that results from exposure of American children to methyl mercury of anthropogenic origin to be $8.7 billion (all costs in 2000 US$)

annually (Table 1).

Sensitivity analysis. We estimate that the

cost of anthropogenic methyl mercury exposure ranges from $2.2 billion (impact only for

the 316,588 children born to women with

total mercury > 5.8 μg/L, IQ impact = 0.85

points per doubling) to $13.9 billion (impact

for the 405,881 women with total mercury

> 4.84 μg/L, IQ impact = 2.4 points per doubling). Using the linear dose–response model

that was selected by the National Research

Council in recommending a reference dose

for mercury exposure (a model that predicts

an average loss of 0.93 IQ points per 1-μg/L

increase in mercury concentration) (Jorgensen

et al. 2004; National Research Council 2000),

we find that the environmentally attributable

cost of methyl mercury exposure is $32.9 billion, assuming a cord:maternal blood mercury

ratio of 1.7. Employing a linear model and

assuming that the true loss in IQ resulting

from a 1-μg/L increase in blood mercury

ranges from 0.59 to 1.24 points, we find that

the outer bounds of our estimate range from

$7.0 billion (impact only for women with total

mercury > 5.8 μg/L, IQ impact = 0.59 points

per μg/L increase, cord:maternal mercury

ratio = 1) to $43.8 billion (impact for women

with total mercury > 4.84 μg/L, IQ impact =

1.24 points for each microgram per deciliter

increase, cord:maternal mercury ratio = 1.7)

(Table 2).

Sources of costs. After applying the 36%

fraction to restrict our analysis to American

anthropogenic sources, we estimate that the

attributable cost of methyl mercury exposure

to the developing fetus from American

anthropogenic sources is $3.1 billion annually, using the logarithmic model developed

by the Faroes researchers (Grandjean et al.

1999; Jorgensen et al. 2004) and assuming a

1.5-point IQ impact for each doubling of

methyl mercury exposure (Budtz-Jorgensen

Children’s Health | Cost of methyl mercury toxicity to the developing brain

Environmental Health Perspectives • VOLUME 113 | NUMBER 5 | May 2005 593
et al. 2002). Our sensitivity analysis, in which

we also varied the attributable fraction for

American sources from 18% (industry data

sources) to 36% (federal data sources) (Seigneur

et al. 2004; U.S. EPA 1996, 1997), suggests

that the true cost of methyl mercury exposure

from American emissions ranges from $0.4 to

$15.8 billion annually.

To focus specifically on the costs of fetal

exposure to mercury released by American coalfired power plants, we examined the impact of

the 41% of U.S. anthropogenic emissions of

mercury attributable to these facilities. We

estimate that the attributable cost of methyl

mercury exposure from American electric generation facilities to the developing fetus is

$1.3 billion. Applying our sensitivity analysis in

this model, we find that the true cost of methyl

mercury exposure from electric generation facilities to the American birth cohort ranges from

$0.1 to $6.5 billion/year (Figure 1). Again, the

major source of these costs is loss of earnings

over a lifetime.

Discussion

The major findings in this analysis are a) that

exposure to methyl mercury emitted to the

atmosphere by American electric generation

facilities causes lifelong loss of intelligence in

hundreds of thousands of American babies

born each year and b) that this loss of intelligence exacts a significant economic cost to

American society, a cost that amounts to at

least hundreds of millions of dollars each year.

Moreover, these costs will recur each year with

each new birth cohort as long as mercury emissions are not controlled. By contrast, the cost

of installing stack filters to control atmospheric

mercury emissions is a one-time expense. The

high costs of in utero exposure to methyl mercury are due principally to the lifelong consequences of irreversible injury to the developing

brain. Similar lifelong neurobehavioral consequences have been observed after exposure of

the developing brain to other environmental

toxicants, including lead (Baghurst et al. 1987;

Bellinger 2004; Dietrich et al. 1987; Opler

et al. 2004; Wasserman et al. 2000), polychlorinated biphenyls (Jacobson and Jacobson

1996), and ethanol (Lupton et al. 2004).

Because the literature has presented a range

of possible consequences for methyl mercury

toxicity, we have provided a range of possible

public health and economic consequences.

This range is meant to inform the choices that

environmental and public health officials make

in protecting vulnerable populations from

methyl mercury exposure. Our range for the

true economic costs of methyl mercury toxicity

to the developing brain omits the cost of exposures to the 231,352 children born to women

in 2000 with blood mercury concentrations

between 3.5 and 4.84 μg/L. If the true cord

blood ratio is 1.7 times the maternal blood

concentration, as described in the most recent

and extensive meta-analysis on the matter

(Stern and Smith 2003), these children are also

born with cord blood mercury concentrations

above the 5.8 μg/L concentration at which

adverse neurodevelopmental impact has been

found. We chose not to include them in our

analysis because other studies have found lower

ratios and because we restricted ourselves in

this analysis to the use of available, published

prevalence data of maternal blood mercury

concentrations. In our sensitivity analysis, we

also selected low cord:maternal blood ratios so

as to describe most accurately the range of values for the true cost of methyl mercury exposure to the developing fetus.

Our analysis also omits the cost of the

cardiovascular impacts of mercury exposure

(Grandjean et al. 2004) or the costs of mercury exposure to children in the first 2 years of

postnatal life, when myelination is still continuing and the blood–brain barrier remains vulnerable to penetration by methyl mercury

(Rodier 1995). We chose not to include these

aspects of methyl mercury toxicity in our

range of estimates at this time because there

do not exist sufficient quantitative data to permit construction of a reliable model.

A limitation on our analysis is that it did

not consider other societal costs beyond

decreased lifetime earnings that may result

from exposure of the developing brain to

methyl mercury. For example, if the value of

a child’s social productivity is approximately

$4–9 million, as suggested by studies of

willingness-to-pay (WTP) estimates of a life

(Viscusi and Aldy 2004), then by the WTP

methodology the true cost of methyl mercury

toxicity may be much higher than our estimate. We also chose not to include other

noncognitive impacts. Lead, for example, has

been associated with criminality and antisocial

behavior (Dietrich et al. 2001; Needleman

et al. 1996, 2002; Nevin 2000; Stretesky and

Lynch 2001). However, because these behaviors have not been described as yet for methyl

mercury, we chose not to include such costs in

our estimate.

Some will argue that our range of costs fails

to incorporate the role of confounding factors

in quantifying the economic consequences of

methyl mercury exposure. It is true that efforts

Children’s Health | Trasande et al.

594 VOLUME 113 | NUMBER 5 | May 2005 • Environmental Health Perspectives

Table 1. Cost of anthropogenic mercury (Hg) exposure using a logarithmic model.

Segment of population (percentile)

Variable 90–92.1 Hg 92.2–94.9 Hg 95–99.3 Hg ≥ 99.4 Hg

Range of maternal total Hg concentration 4.84–5.8 μg/L 5.8–7.13 μg/L 7.13–15.0 μg/L > 15.0 μg/L

Assumed maternal total Hg concentration 4.84 5.8 7.13 15

No effect concentration (maternal total Hg) 3.41 3.41 3.41 3.41

IQ points lost at assumed concentration 0.76 1.15 1.60 3.21

Loss of 1 IQ points = decrease in lifetime earnings

For boys, lifetime earnings (1.931% decrease) $1,032,002

For girls, lifetime earnings (3.225% decrease) $763,468

No. of boys in birth cohort affected 45,693 58,155 91,387 12,462

No. of girls in birth cohort affected 43,601 55,492 87,201 11,891

Lost income $1.1 billion $2.0 billion $4.4 billion $1.2 billion

Total cost = $8.7 billion in each year’s birth cohort

Assumptions: EAF = 70%, main consequence = loss of IQ over lifetime.

Table 2. Sensitivity analysis: cost of anthropogenic methyl mercury exposure.

Variable Base-case cost estimate (range)a

Children born to women with Hg > 4.84 μg/L, effect > 3.5 μg/L

Logarithmic model $8.7 billion ($4.9–13.9 billion)

Linear model, cord:maternal Hg ratio = 1.7 $32.9 billion ($20.9–43.8 billion)

Linear model, cord:maternal Hg ratio = 1 $19.3 billion ($12.3–25.8 billion)

Children born to women with > 5.8 μg/L, effect > 4.84 μg/L

Logarithmic model $3.9 billion ($2.2–6.3 billion)

Linear model, cord:maternal Hg ratio = 1.7 $18.7 billion ($11.9–24.9 billion)

Linear model, cord:maternal Hg ratio = 1 $11.0 billion ($7.0–14.6 billion)

Range of estimates

Logarithmic model $2.2–13.9 billion

Linear model $7.0–43.8 billion

Assumptions: EAF = 70%, main consequence = loss of IQ over lifetime.

aBased on range of possible IQ decrement:increase cord blood mercury.

Figure 1. Portions of cost of methyl mercury exposure attributed to sources. Assumptions: 18–36%

attributable to American sources; 41% of American

emissions attributable to American power plants.

Cost of

American

power plant

emissions:

$0.1–6.5 billion

Cost of American

anthropogenic emissions:

$0.4–15.8 billion

Cost of anthropogenic

emissions:

$2.2–43.8 billion
Environmental Health Perspectives • VOLUME 113 | NUMBER 5 | May 2005 595

to delineate the potential synergistic role of

methyl mercury and other chemicals in mediating neurocognitive and other effects are

bedeviled by lack of knowledge about possible

interactions and synergies among chemicals or

between chemicals and other environmental

hazards, even though the environment of a

child includes mixtures of chemical and biologic toxicants. Only a study of the magnitude

of the National Children’s Study will facilitate

simultaneous examination of the effects of

multiple chemical exposures, of interactions

among them, and of interactions among biologic, chemical, behavioral, and social factors

(Trasande and Landrigan 2004). However,

we note that loss of cognition resulting from

methyl mercury exposure in the Faroe Islands

study remained evident when blood levels of

polychlorinated biphenyls, which are known

fetal neurotoxicants (Jacobson and Jacobson

1996), were included in the analysis (BudtzJorgensen et al. 2002; Steuerwald et al. 2000).

We note the U.S. EPA’s recent success in

minimizing mercury emissions from medical

waste (U.S. EPA 2004e) and municipal incinerators (U.S. EPA 2004f, 2004g), actions that

resulted in a decrease in total mercury emissions by at least 80 tons per year from 1990 to

1999 (U.S. EPA 2003b). Although data are

not available on blood mercury concentrations

over the past decade that followed from those

actions, the impact of these reductions is likely

to have been substantial.

Some commentators have used data from

the Seychelles study to argue that methyl mercury is not toxic to the fetus at low concentrations and to suggest that fear of mercury

exposure is needlessly preventing women from

ingesting fish and thus denying them access to

beneficial long-chain polyunsaturated fatty

acids (LCPUFAs), especially docosahexaenoic

acid (DHA). We do not dispute that DHA

and other LCPUFAs are important for optimal development of the fetal visual and nervous systems (Innis 1991). The human fetus

has a limited ability to synthesize DHA’s precursor, α-linolenic acid, and therefore it must be

largely supplied from maternal sources (Carnielli

et al. 1996; Larque et al. 2002; Szitanyi et al.

1999). We also note a report that associated an

average monthly decline in fish consumption of

1.4 servings among Massachusetts women with

a U.S. Food and Drug Administration advisory

on the health risks of mercury (Oken et al.

2003). Nonetheless, the American Heart

Association, a strong advocate for the cardioprotective effects of LCPUFAs, recommends

that children and pregnant and lactating

women avoid potentially contaminated fish

(Kris-Etherton et al. 2002). Fish advisories

should not recommend that consumers abstain

from fish, but they should assist in choosing

the best kinds of fish to eat. Lists of fish that

are safe and unsafe from the perspective of

mercury exposure have been published and

made widely available to consumers (U.S. EPA

2004h).

Early reports of disease and dysfunction of

environmental origin in children have on

repeated occasions failed to produce proactive

response to protect children. The long history

of lead use in the United States provides a

chilling reminder of the consequences of failure

to act on early evidence of harm. It is important that we not repeat this sequence with mercury. Within the last century, as a result of

increased industrial activity, mercury emissions

worldwide have increased 2- to 5-fold, and

anthropogenic emissions now surpass emissions from natural sources (Nriagu 1989).

The data from this analysis reinforce the

results of recent epidemiologic studies and

indicate an urgent need on economic grounds

for regulatory intervention at the federal level

to minimize mercury emissions. Our analysis

captures the cost of methyl mercury exposure

for only 1 year’s birth cohort, but the cost of

mercury exposure will continue to accrue in

each succeeding year if power plants fail to

install flue gas filters (U.S. Department of

Energy 2004) or to implement other technologies to reduce mercury emissions. The

cost savings from reducing mercury exposure

now will provide savings in improved productivity and enhanced national security for

generations to come.

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