Public Health and Economic Consequences of Methyl Mercury Toxicity to the Developing Brain

Leonardo Trasande; Philip J. Landrigan; Clyde Schechter


Environ Health Perspect. 2005;113(5):590-596. 

In This Article

Abstract and Introduction

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.

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 Scale-Revised (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 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 parasympathetic-mediated 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.


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