Applying cost analyses to drive policy that protects children: mercury as a case study.
Trasande L, Schechter C, Haynes KA, Landrigan PJ. Center for Children’s Health and the Environment, Department of Community and Preventive Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA. leo.trasande@mssm.edu Ann N Y Acad Sci. 2006 Sep;1076:911-23.
Exposure in prenatal life to methylmercury (MeHg) has become the topic of intense debate in the United States after the Environmental Protection Agency (EPA) announced a proposal in 2004 to reverse strict controls on emissions of mercury from coal-fired power plants that had been in effect for the preceding 15 years. This proposal failed to incorporate any consideration of the health impacts on children that would result from increased mercury emissions. We assessed the impact on children’s health of industrial mercury emissions and found that between 316,588 and 637,233 babies are born with mercury-related losses of cognitive function ranging from 0.2 to 5.13 points. We calculated that decreased economic productivity resulting from diminished intelligence over a lifetime results in an aggregate economic cost in each annual birth cohort of $8.7 billion annually (range: $0.7-$13.9 billion, 2000 dollars). $1.3 billion (range: $51 million-$2.0 billion) of this cost is attributable to mercury emitted from American coal-fired power plants. Downward shifts in intellectual quotient (IQ) are also associated with 1566 (range: 115-2675) excess cases of mental retardation (MR defined as IQ < 70) annually. This number accounts for 3.2% (range: 0.2-5.4%) of MR cases in the United States. If the lifetime excess cost of a case of MR (excluding individual productivity losses) is $1,248,648 in 2000 dollars, then the cost of these excess cases of MR is $2.0 billion annually (range: $143 million-$3.3 billion). Preliminary data suggest that more stringent mercury policy options would prevent thousands of cases of MR and billions of dollars over the next 25 years.
Assessing and managing methylmercury risks associated with power plant mercury emissions in the United States.
Charnley G. HealthRisk Strategies, Washington, DC, USA. MedGenMed. 2006 Mar 9;8(1):64.
Until the Clean Air Mercury Rule was signed in March 2005, coal-fired electric utilities were the only remaining, unregulated major source of industrial mercury emissions in the United States. Proponents of coal-burning power plants assert that methylmercury is not a hazard at the current environmental levels, that current technologies for limiting emissions are unreliable, and that reducing mercury emissions from power plants in the United States will have little impact on environmental levels. Opponents of coal-burning plants assert that current methylmercury exposures from fish are damaging to the developing nervous system of infants, children, and the fetus; that current technology can significantly limit emissions; and that reducing emissions will reduce exposure and risk. One concern is that local mercury emissions from power plants may contribute to higher local exposure levels, or “hot spots.” The impact of the Mercury Rule on potential hot spots is uncertain due to the highly site-specific nature of the relationship between plant emissions and local fish methylmercury levels. The impact on the primary source of exposure in the United States, ocean fish, is likely to be negligible due to the contribution of natural sources and industrial sources outside the United States. Another debate centers on the toxic potency of methylmercury, with the scientific basis of the US Environmental Protection Agency’s (EPA’s) recommended exposure limit questioned by some and defended by others. It is likely that the EPA’s exposure limit may be appropriate for combined exposure to methylmercury and polychlorinated biphenyls (PCBs), but may be lower than the available data suggest is necessary to protect children from methylmercury alone. Mercury emissions from power plants are a global problem. Without a global approach to developing and implementing clean coal technologies, limiting US power plant emissions alone will have little impact.
Associations of maternal long-chain polyunsaturated fatty acids, methyl mercury, and infant development in the Seychelles Child Development Nutrition Study.
Strain JJ, Davidson PW, Bonham MP, Duffy EM, Stokes-Riner A, Thurston SW, Wallace JM, Robson PJ, Shamlaye CF, Georger LA, Sloane-Reeves J, Cernichiari E, Canfield RL, Cox C, Huang LS, Janciuras J, Myers GJ, Clarkson TW. University of Ulster, United Kingdom. Neurotoxicology. 2008 Jun 11. [Epub ahead of print)
Fish consumption during gestation can provide the fetus with long-chain polyunsaturated fatty acids (LCPUFA) and other nutrients essential for growth and development of the brain. However, fish consumption also exposes the fetus to the neurotoxicant, methyl mercury (MeHg). We studied the association between these fetal exposures and early child development in the Seychelles Child Development Nutrition Study (SCDNS). Specifically, we examined a priori models of Omega-3 and Omega-6 LCPUFA measures in maternal serum to test the hypothesis that these LCPUFA families before or after adjusting for prenatal MeHg exposure would reveal associations with child development assessed by the BSID-II at ages 9 and 30 months. There were 229 children with complete outcome and covariate data available for analysis. At 9 months, the PDI was positively associated with total Omega-3 LCPUFA and negatively associated with the ratio of Omega-6/Omega-3 LCPUFA. These associations were stronger in models adjusted for prenatal MeHg exposure. Secondary models suggested that the MeHg effect at 9 months varied by the ratio of Omega-6/Omega-3 LCPUFA. There were no significant associations between LCPUFA measures and the PDI at 30 months. There were significant adverse associations, however, between prenatal MeHg and the 30-month PDI when the LCPUFA measures were included in the regression analysis. The BSID-II mental developmental index (MDI) was not associated with any exposure variable. These data support the potential importance to child development of prenatal availability of Omega-3 LCPUFA present in fish and of LCPUFA in the overall diet. Furthermore, they indicate that the beneficial effects of LCPUFA can obscure the determination of adverse effects of prenatal MeHg exposure in longitudinal observational studies.
Children’s cognitive health: the influence of environmental chemical exposures.
Bellinger DC. Harvard Medical School, USA. Altern Ther Health Med. 2007 Mar-Apr;13(2):S140-4.
The potential exists for developmental exposure of children to myriad chemicals, many of which are known to be neurotoxic. Some, such as the organophosphate pesticides, are specifically designed to attack the central nervous system. Despite the known and suspected risks associated with such exposures, critical aspects of the dose-response relationships are unknown or, at best, poorly characterized for the overwhelming majority of chemicals. Among the major knowledge gaps for most chemicals are the critical window(s) of vulnerability, the threshold or “no observed adverse effect level,” and the host/environmental characteristics that modify individual vulnerability. Investigation of the role of genetic polymorphisms in determining vulnerability has barely begun. In the real-world, children are not exposed to a single chemical at a time but to complex mixtures of chemicals, and we have only a minimal understanding of the way in which exposures might interact with one another. Effective medical/environmental treatments for the adverse effects associated with chemical exposures are largely unknown, rendering primary prevention of exposure the most effective strategy for protecting children.
Do recent data from the Seychelles Islands alter the conclusions of the NRC Report on the toxicological effects of methylmercury?
Stern AH, Jacobson JL, Ryan L, Burke TA. Bureau for Risk Analysis, Division of Science, Research, and Technology, New Jersey Department of Environmental Protection, 401 East State Street, 1st Floor, PO Box 409, Trenton, NJ 08625, USA. Alan.Stern@dep.state.nj.us Environ Health. 2004 Jan 30;3(1):2.
In 2000, the National Research Council (NRC), an arm of the National Academy of Sciences, released a report entitled, “Toxicological Effects of Methylmercury.” The overall conclusion of that report was that, at levels of exposure in some fish- and marine mammal-consuming communities (including those in the Faroe Islands and New Zealand), subtle but significant adverse effects on neuropsychological development were occurring as a result of in utero exposure. Since the release of that report, there has been continuing discussion of the public health relevance of current levels of exposure to Methylmercury. Much of this discussion has been linked to the release of the most recent longitudinal update of the Seychelles Island study. It has recently been posited that these findings supercede those of the NRC committee, and that based on the Seychelles findings, there is little or no risk of adverse neurodevelopmental effects at current levels of exposure. In this commentary, members of the NRC committee address the conclusions from the NRC report in light of the recent Seychelles data. We conclude that no evidence has emerged since the publication of the NRC report that alters the findings of that report.
Is susceptibility to prenatal methylmercury exposure from fish consumption non-homogeneous? Tree-structured analysis for the Seychelles Child Development Study.
Huang LS, Myers GJ, Davidson PW, Cox C, Xiao F, Thurston SW, Cernichiari E, Shamlaye CF, Sloane-Reeves J, Georger L, Clarkson TW. Department of Biostatistics and Computational Biology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA. Lhuang@bst.rochester.edu Neurotoxicology. 2007 Nov;28(6):1237-44. Epub 2007 Aug 25.
Studies of the association between prenatal methylmercury exposure from maternal fish consumption during pregnancy and neurodevelopmental test scores in the Seychelles Child Development Study have found no consistent pattern of associations through age 9 years. The analyses for the most recent 9-year data examined the population effects of prenatal exposure, but did not address the possibility of non-homogeneous susceptibility. This paper presents a regression tree approach: covariate effects are treated non-linearly and non-additively and non-homogeneous effects of prenatal methylmercury exposure are permitted among the covariate clusters identified by the regression tree. The approach allows us to address whether children in the lower or higher ends of the developmental spectrum differ in susceptibility to subtle exposure effects. Of 21 endpoints available at age 9 years, we chose the Weschler Full Scale IQ and its associated covariates to construct the regression tree. The prenatal mercury effect in each of the nine resulting clusters was assessed linearly and non-homogeneously. In addition we reanalyzed five other 9-year endpoints that in the linear analysis had a two-tailed p-value <0.2 for the effect of prenatal exposure. In this analysis, motor proficiency and activity level improved significantly with increasing MeHg for 53% of the children who had an average home environment. Motor proficiency significantly decreased with increasing prenatal MeHg exposure in 7% of the children whose home environment was below average. The regression tree results support previous analyses of outcomes in this cohort. However, this analysis raises the intriguing possibility that an effect may be non-homogeneous among children with different backgrounds and IQ levels.
Maternal fish intake during pregnancy, blood mercury levels, and child cognition at age 3 years in a US cohort.
Oken E, Radesky JS, Wright RO, Bellinger DC, Amarasiriwardena CJ, Kleinman KP, Hu H, Gillman MW. Department of Ambulatory Care and Prevention, Harvard Medical School and Harvard Pilgrim Health Care, Boston, MA 02215, USA. emily_oken@harvardpilgrim.org Am J Epidemiol. 2008 May 15;167(10):1171-81. Comment in: Am J Epidemiol. 2008 Jul 15;168(2):236.
The balance of contaminant risk and nutritional benefit from maternal prenatal fish consumption for child cognitive development is not known. Using data from a prospective cohort study of 341 mother-child pairs in Massachusetts enrolled in 1999-2002, the authors studied associations of maternal second-trimester fish intake and erythrocyte mercury levels with children’s scores on the Peabody Picture Vocabulary Test (PPVT) and Wide Range Assessment of Visual Motor Abilities (WRAVMA) at age 3 years. Mean maternal total fish intake was 1.5 (standard deviation, 1.4) servings/week, and 40 (12%) mothers consumed >2 servings/week. Mean maternal mercury level was 3.8 (standard deviation, 3.8) ng/g. After adjustment using multivariable linear regression, higher fish intake was associated with better child cognitive test performance, and higher mercury levels with poorer test scores. Associations strengthened with inclusion of both fish and mercury: effect estimates for fish intake of >2 servings/week versus never were 2.2 (95% confidence interval (CI): -2.6, 7.0) for the PPVT and 6.4 (95% CI: 2.0, 10.8) for the WRAVMA; for mercury in the top decile, they were -4.5 (95% CI: -8.5, -0.4) for the PPVT and -4.6 (95% CI: -8.3, -0.9) for the WRAVMA. Fish consumption of < or =2 servings/week was not associated with a benefit. Dietary recommendations for pregnant women should incorporate the nutritional benefits as well as the risks of fish intake.
Mental retardation and prenatal methylmercury toxicity.
Trasande L, Schechter CB, Haynes KA, Landrigan PJ. Department of Community and Preventive Medicine, Center for Children’s Health and the Environment, Mt. Sinai School of Medicine, One Gustave K. Levy Place, Box 1043, New York, NY 10029, USA. leo.trasande@mssm.edu Am J Ind Med. 2006 Mar;49(3):153-8.
BACKGROUND: Methylmercury (MeHg) is a developmental neurotoxicant; exposure results principally from consumption of seafood contaminated by mercury (Hg). In this analysis, the burden of mental retardation (MR) associated with methylmercury exposure in the 2000 U.S. birth cohort is estimated, and the portion of this burden attributable to mercury (Hg) emissions from coal-fired power plants is identified.
METHODS: The aggregate loss in cognition associated with MeHg exposure in the 2000 U.S. birth cohort was estimated using two previously published dose-response models that relate increases in cord blood Hg concentrations with decrements in IQ. MeHg exposure was assumed not to be correlated with native cognitive ability. Previously published estimates were used to estimate economic costs of MR caused by MeHg. RESULTS: Downward shifts in IQ resulting from prenatal exposure to MeHg of anthropogenic origin are associated with 1,566 excess cases of MR annually (range: 376-14,293). This represents 3.2% of MR cases in the US (range: 0.8%-29.2%). The MR costs associated with decreases in IQ in these children amount to $2.0 billion/year (range: $0.5-17.9 billion). Hg from American power plants accounts for 231 of the excess MR cases/year (range: 28-2,109), or 0.5% (range: 0.06%-4.3%) of all MR. These cases cost $289 million (range: $35 million-2.6 billion).
CONCLUSIONS: Toxic injury to the fetal brain caused by Hg emitted from coal-fired power plants exacts a significant human and economic toll on American children.
Mercury exposure and child development outcomes.
Davidson PW, Myers GJ, Weiss B. Strong Center for Developmental Disabilities, Golisano Children’s Hospital at Strong, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA. phil_davidson@urmc.rochester.edu Pediatrics. 2004 Apr;113(4 Suppl):1023-9.
Mercury is ubiquitous in the global environment, ensuring universal exposure. Some forms of mercury are especially neurotoxic, including clinical signs at high doses. However, typical human exposures occur at low to moderate doses. Only limited data about neurotoxicity at low doses are available, and scientists differ in their interpretation. Dose-response data on neurodevelopment are particularly limited. Despite or perhaps because of the lack of sufficient or consistent scientific data, public concern about a link between mercury exposure and developmental disabilities has been rising. After reviewing the data, the US Environmental Protection Agency proposed a reference dose (an estimate of a daily dose that is likely to be without a risk of adverse effects over a lifetime) for methyl mercury that is substantially lower than previous guidelines from the World Health Organization, the US Agency for Toxic Substances and Disease Registry, and the US Food and Drug Administration. Some questions have been raised about the Environmental Protection Agency’s guidelines, but the issue remains unresolved. Meanwhile, consumer groups have raised questions about the potential link between mercury exposure and autism spectrum disorders as well as other adverse neurodevelopmental outcomes. This hypothesis has prompted some parents to seek regulatory, legal, or medical remedies in the absence of firm evidence. This article reviews what is known about mercury neurotoxicity and neurodevelopmental risk. Our intent is to focus the debate about mercury on 1) additional research that should be sought and 2) defining the principal issues that public policy makers face.
Methylmercury and neurodevelopment: longitudinal analysis of the Seychelles child development cohort.
Davidson PW, Myers GJ, Cox C, Wilding GE, Shamlaye CF, Huang LS, Cernichiari E, Sloane-Reeves J, Palumbo D, Clarkson TW. The Department of Pediatrics, University of Rochester School of Medicine and Dentistry, Rochester, New York, 14642, USA. phil_davidson@urmc.rochester.edu Neurotoxicol Teratol. 2006 Sep-Oct;28(5):529-35. Epub 2006 Jun 29.
BACKGROUND: The Seychelles Child Development Study (SCDS) has been longitudinally following a cohort of over 700 children enrolled in 1989. Their mothers consumed a diet high in fish during pregnancy. Repeated examination of the SCDS cohort at six different ages through age 11 years has shown no pattern of adverse effects. Some early appearing beneficial associations between both prenatal and postnatal hair MeHg and several child development endpoints were noted. We hypothesized these might be related to micronutrients in the fish, but they were not found when the children reached middle school age. These findings suggest that the associations observed between MeHg and developmental outcomes may vary with developmental stage.
METHOD: We examined the main cohort of the SCDS to determine if this might be true using a longitudinal multiple regression analysis design that focused on those endpoints that were repeatedly measured at different ages. The primary endpoint analyzed was global cognition, involving a measure of developmental quotient or IQ. Secondary analyses included other domains such as Reading and Mathematics scholastic achievement, social behavior, and memory. Analyses involved two different approaches, one including incorporation of a passage of time variable, the other including a difference of scores across time points.
RESULTS: No significant associations were found between prenatal MeHg exposure and any of the repeatedly measured endpoints.
CONCLUSIONS: These results suggest that even when individual subject variance is controlled there was no consistent pattern of associations between child development outcomes and prenatal exposures to MeHg from maternal consumption of a diet high in fish. The Seychellois diet contains about 10 times more ocean fish than is typically consumed by US citizens. Our primary focus on IQ should further inform growing scientific interest in the analysis of the risks and benefits of fish consumption on overall cognitive ability.
Methylmercury toxicity and functional programming.
Grandjean P. Department of Environmental Health, Harvard School of Public Health, Landmark Center, 3-110E, 401 Park Drive, Boston, MA 02215, USA. pgrandjean@health.sdu.dk Reprod Toxicol. 2007 Apr-May;23(3):414-20. Epub 2007 Mar 12. Comment in: Reprod Toxicol. 2008 Jan;25(1):133; author reply 134.
PURPOSE: Adverse health effects of developmental toxicants may induce abnormal functional programming that leads to lasting functional deficits. This notion is considered from epidemiological evidence using developmental methylmercury neurotoxicity as an example.
MOST IMPORTANT FINDINGS: Accumulating evidence indicates that adverse effects may occur even at low-level methylmercury exposures from seafood and freshwater fish. Neurobehavioral outcomes are usually non-specific, and imprecise exposure assessment results in a bias toward the null. Essential nutrients may promote the development of certain brain functions, thereby causing confounding bias. The functional deficits caused by prenatal methylmercury exposure appear to be permanent, and their extent may depend on the joint effect of toxicants and nutrients.
PRINCIPAL CONCLUSIONS: The lasting functional changes caused by neurodevelopmental methylmercury toxicity fit into the pattern of functional programming, with effects opposite to those linked to beneficial stimuli.
Neurodevelopmental effects of maternal nutritional status and exposure to methylmercury from eating fish during pregnancy.
Davidson PW, Strain JJ, Myers GJ, Thurston SW, Bonham MP, Shamlaye CF, Stokes-Riner A, Wallace JM, Robson PJ, Duffy EM, Georger LA, Sloane-Reeves J, Cernichiari E, Canfield RL, Cox C, Huang LS, Janciuras J, Clarkson TW. University of Rochester, Rochester, NY, USA. Neurotoxicology. 2008 Jun 11. [Epub ahead of print]
Fish contain nutrients that promote optimal brain growth and development but also contain methylmercury (MeHg) that can have toxic effects. The present study tested the hypothesis that the intake of selected nutrients in fish or measures of maternal nutritional status may represent important confounders when estimating the effects of prenatal methylmercury exposure on child development. The study took place in the Republic of Seychelles, an Indian Ocean archipelago where fish consumption is high. A longitudinal cohort study design was used. A total of 300 mothers were enrolled early in pregnancy. Nutrients considered to be important for brain development were measured during pregnancy along with prenatal MeHg exposure. The children were evaluated periodically to age 30 months. There were 229 children with complete outcome and covariate data for analysis. The primary endpoint was the Bayley Scales of Infant Development-II (BSID-II), administered at 9 and 30 months of age. Combinations of four secondary measures of infant cognition and memory were also given at 5, 9 and 25 months. Cohort mothers consumed an average of 537g of fish (nine meals containing fish) per week. The average prenatal MeHg exposure was 5.9ppm in maternal hair. The primary analysis examined the associations between MeHg, maternal nutritional measures and children’s scores on the BSID-II and showed an adverse association between MeHg and the mean Psychomotor Developmental Index (PDI) score at 30 months. Secondary analyses of the association between the PDI and only MeHg alone or nutritional factors alone showed only a borderline significant association between MeHg and the PDI at 30 months and no associations with nutritional factors. One experimental measure at 5 months of age was positively associated with iodine status, but not prenatal MeHg exposure. These findings suggest a possible confounding role of maternal nutrition in studies examining associations between prenatal MeHg exposures and developmental outcomes in children.
Nutrient and methyl mercury exposure from consuming fish.
Myers GJ, Davidson PW, Strain JJ. Department of Neurology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA. gary_myers@urmc.rochester.edu J Nutr. 2007 Dec;137(12):2805-8.
There is controversy about the risks and benefits of consuming fish. Fish consumption provides nutrients, some of which are essential for brain growth and development. All fish, however, contain methyl mercury (MeHg), a known neurotoxicant. The toxic effect of MeHg seems most damaging during brain development, and thus, prenatal exposure is of greatest concern. At present the level of prenatal exposure associated with risk to a child’s neurodevelopment is not known. Balancing the rewards and possible risks of fish consumption presents a dilemma to consumers and regulatory authorities. We review the nutrients in fish that are important in brain development and the current evidence of risk from MeHg at exposure levels achieved by consuming fish. We then review the findings from a large prospective cohort study of a population that consumes fish daily, the Seychelles Child Development Study. The MeHg content of the fish consumed in the Seychelles is similar to that of ocean fish available in industrialized countries, so they represent a sentinel population for any risk from fish consumption. In the Seychelles, evaluations of the children through 9 y of age show no consistent pattern of adverse associations with prenatal MeHg exposure. Recent studies in the Seychelles have focused on nutrients in fish that might influence a child’s development, including long-chain polyunsaturated fatty acids, iodine, iron, and choline. Preliminary findings from this study suggest that the beneficial influence of nutrients from fish may counter any adverse effects of MeHg on the developing nervous system.
Prenatal methylmercury exposure from ocean fish consumption in the Seychelles child development study.
Myers GJ, Davidson PW, Cox C, Shamlaye CF, Palumbo D, Cernichiari E, Sloane-Reeves J, Wilding GE, Kost J, Huang LS, Clarkson TW. Department of Neurology, National Institute for Child Health and Development, National Institutes of Health, Department of Health and Human Services, Bethesda, USA. gary_myers@urmc.rochester.edu Lancet. 2003 May 17;361(9370):1686-92.
Comment in: Lancet. 2003 Aug 23;362(9384):664-5; author reply 665. Lancet. 2003 May 17;361(9370):1667-8.
INTRODUCTION: Exposure to methylmercury (MeHg) before birth can adversely affect children’s neurodevelopment. The most common form of prenatal exposure is maternal fish consumption, but whether such exposure harms the fetus is unknown. We aimed to identify adverse neurodevelopmental effects in a fish-consuming population.
METHODS: We investigated 779 mother-infant pairs residing in the Republic of Seychelles. Mothers reported consuming fish on average 12 meals per week. Fish in Seychelles contain much the same concentrations of MeHg as commercial ocean fish elsewhere. Prenatal MeHg exposure was determined from maternal hair growing during pregnancy. We assessed neurocognitive, language, memory, motor, perceptual-motor, and behavioural functions in children at age 9 years. The association between prenatal MeHg exposure and the primary endpoints was investigated with multiple linear regression with adjustment for covariates that affect child development.
FINDINGS: Mean prenatal MeHg exposure was 6.9 parts per million (SD 4.5 ppm). Only two endpoints were associated with prenatal MeHg exposure. Increased exposure was associated with decreased performance in the grooved pegboard using the non-dominant hand in males and improved scores in the hyperactivity index of the Conner’s teacher rating scale. Covariates affecting child development were appropriately associated with endpoints.
INTERPRETATION: These data do not support the hypothesis that there is a neurodevelopmental risk from prenatal MeHg exposure resulting solely from ocean fish consumption.
Public health and economic consequences of methyl mercury toxicity to the developing brain.
Trasande L, Landrigan PJ, Schechter C. Center for Children’s Health and the Environment, Department of Community and Preventive Medicine, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA. leo.trasande@mssm.edu Environ Health Perspect. 2005 May;113(5):590-6. Comment in: Environ Health Perspect. 2006 Jul;114(7):A399-400; author reply A400-1.
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 microg/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.