Conclusions and Recommendations
There is little doubt that methylmercury can produce developmental neurotoxicity, but, like all other substances, its toxicity depends on the dose and on the circumstances of exposure. If exposure occurs to doses that are sufficiently high, particularly during pregnancy or early childhood, toxicity may result.
The dose of methylmercury that is required to produce developmental toxicity is still being debated. Studies of children in the Faroe Islands who were exposed to relatively high doses of methylmercury during pregnancy, from breast milk, and in their diets showed signs of developmental neurotoxicity only when they were also exposed to high levels of PCBs from breast milk. Analyses concluding that PCBs did not interfere with study results were performed after only 2 weeks of exposure, so would not have detected the later responses. The doses of PCBs that the children received were about twice as high as the dose that produces developmental neurotoxicity in infant monkeys exposed through breast milk, and nearly 1000 times higher than the dose of PCBs that the EPA considers safe. It appears likely that the neurotoxicity seen in children was due to PCB exposure or to the mixture of PCBs and methylmercury, and not solely to methylmercury. Therefore, it is possible that the current reference dose established by the EPA for methylmercury alone is lower than is needed to provide adequate public health protection. If PCB exposure were taken into account, the acceptable dose of methylmercury would be higher, similar to that found by other organizations based on the Seychelles data.
Recent evidence suggests a potential relationship between high mercury exposure and adverse cardiovascular effects, although many studies have demonstrated the clear cardiovascular benefits of regular fish consumption. The nature and likelihood of a potential relationship between mercury and cardiovascular toxicity should be explored with further research.
There is likely to be little relationship between US power plant emissions and methylmercury levels in ocean fish, which comprise most of the fish that people in the United States eat and are the source of most methylmercury exposure. For freshwater fish caught in the vicinity of coal-fired power plants, available data neither support nor rule out a relationship between fish methylmercury levels and plant emissions; such relationships appear to be site-specific. The evidence suggests that reducing power plant mercury emissions may have little impact on most US exposure to methylmercury but may affect exposure among those who frequently consume freshwater fish caught near coal-fired power plants where coal chemistry, emissions characteristics, atmospheric characteristics, mercury deposition, and water chemistry are consistent with a relationship between mercury emissions and uptake by fish.
The potential relationship between PCB exposure through breast milk and developmental neurotoxicity requires more careful analysis. If that relationship is supported, the EPA's current RfD for methylmercury should be reclassified as an RfD for a mixture of PCBs and methylmercury, and a different RfD for methylmercury should be developed on the basis of data from the Seychelles Islands, where PCB contamination was absent. Limiting methylmercury exposures to an unnecessarily stringent level would be a poor use of societal resources and send inappropriate risk messages that potentially limit the many benefits of fish consumption.
Pregnant women and children should follow the advice of the EPA and FDA and limit their consumption of high-mercury-containing fish while maintaining the health benefits of fish consumption by eating a variety of other fish.
Although it is clear from the EPA's acid rain trading program that market-based, cap-and-trade approaches to limiting air pollutant emissions can be both successful and cost-effective, whether a similar plan for limiting mercury emissions can address the hot spots issue, in which local mercury deposition and methylmercury contamination are attributable to individual power plants, requires more research. Characterization of the nature and likelihood of mercury hot spot formation and the relationship to power plant emissions should be performed. If mercury hot spots prove to be important contributors to risk in some locations, local concentration-based limits on mercury emissions should be explored so that specific plants can be targeted where needed. However, because there appears to be little relationship overall between mercury emissions from coal-fired power plants in much of the United States and methylmercury exposure from eating fish, reductions in US power plant mercury emissions should not be oversold as a universal means of reducing methylmercury risks to pregnant women and children. On the other hand, a suspicion that the public health benefits may be small should not be used to avoid reducing mercury emissions if doing so can be accomplished cost-effectively.
Because most global mercury emissions that result from human activities come from sources outside the United States and because coal-fired power plant emissions of many pollutants are likely to continue to increase globally without intervention, the United States should lead international efforts to develop and implement effective and affordable clean-coal technologies that limit emissions.
The author thanks the following individuals for their valuable reviews and helpful comments: Michael Dourson, James D. Wilson, Jay Lehr, Robert Brent, Floy Lilley, S. Fred Singer, David Seidermann, Charles Santerre, and William Robertson.Funding information
Preparation of this manuscript was supported in part by a grant from the American Council on Science and Health, which had no control over its content.
Gail Charnley, E-mail: email@example.com
© 2006 Medscape
Cite this: Assessing and Managing Methylmercury Risks Associated With Power Plant Mercury Emissions in the United States - Medscape - Mar 09, 2006.