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Friends of MPP Search MercuryPolicy.orgImportant Report! Hot Topic!One of every 20 cans of "white," or albacore, tuna should be recalled as unsafe
for human consumption, according to MPP independent testing (see press
release and testing
report). Mercury exposure can cause severe learning disabilities and
other neurodevelopmental problems in babies and young children. Recent Centers
for Disease Control findings indicate that 8 percent of woman of childbearing
age in the US have unsafe mercury levels, translating into over 300,000 babies
born at risk each year. MPP's testing found that mercury levels in Albacore
"white "canned tuna averaged over 0.5 ppm mercury. Recently obtained test
results from the Food and Drug Administration confirm MPP's findings
and show "white" canned tuna has three times the mercury levels as the "light"
tuna. An earlier MPP report
reveals that FDA's seafood mercury monitoring program severely lacks in thoroughness,
depth and degree.
Model Mercury LegislationSee model dental legislation drafted by the Mercury Policy Project. See model mercury legislation drafted by the Mercury Policy Project that is reflected in most recent state and federal legislation on mercury. Exposure to MercuryWe are exposed to mercury through the food we eat, primarily freshwater and marine fish. 40 states warn residents to restrict their consumption of certain fish due to mercury contamination. According to the U.S. Environmental Protection Agency, about 7 million women and children are eating mercury-contaminated fish at or above the level it considers safe. Learn more about this issue, actions being taken to address the risk of mercury exposure, and advocacy efforts to eliminate human exposure to mercury. Mercury PollutionThe majority of the mercury entering lakes, streams, rivers, and oceans comes from the atmosphere. Eight-five percent of all mercury pollution in the U.S. is released by power plants burning coal and municipal and medical waste incinerators burning mercury tainted trash. Learn more about the sources of mercury, policies in place to curb
releases, and advocacy strategies pushing toward virtual elimination of mercury
releases in 10 years.
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Letter to FDA about better protecting US women and children from exposure to mercuryFebruary 24, 2004 Mark McClellan, M.D., Ph.D. Dear Commissioner McClellan: We are writing to call your attention to three recent scientific reports that, taken together, underline the urgency of the ongoing FDA/EPA effort to update dietary advice regarding methylmercury exposure from fish and seafood consumption. These recent studies make it clear that FDA must be more assertive about guiding consumers to keep their mercury intake from fish and seafood within scientifically defined safe limits. We urge you to instruct the FDA team working on dietary advice regarding mercury in fish to take these concerns more effectively into account. At the National Forum on Contaminants in Fish, held in San Diego late last month, Dr. Kathryn Mahaffey, EPA’s senior researcher on mercury hazards, presented an analysis estimating that roughly one in six babies born in America, or 630,000 infants born each year, has a blood mercury level above the EPA’s safe level (Mahaffey 2004). This figure doubles a previous estimate (Schober et al. 2003) that some 300,000 such at-risk births occur annually. Prenatal mercury exposure has been associated with an increased risk of developmental toxic effects on the brain, including adverse effects on fine motor skills, memory and learning ability. Dr. Mahaffey’s updated estimate is based on recent data from Japan confirming that the fetal blood mercury level (represented by umbilical cord blood sampled at birth) is higher than the maternal blood mercury level. The earlier estimate of 300,000 at-risk infants per year was based on 1999-2000 NHANES data that indicated that 7.8 percent of women of childbearing age had blood mercury levels above EPA’s safe upper limit, 5.8 µg Hg/L. (Elevated blood mercury levels correlated strongly with a diet rich in fish and seafood in the NHANES survey.) The recent Japanese study confirmed that fetal blood contains 1.6 times as much mercury as maternal blood (several earlier studies had found an average ratio of about 1.7.). At that ratio, fetal blood mercury will exceed 5.8 µg/L when the mother’s blood mercury level exceeds 3.5 µg/L. The NHANES data indicate that 15.7 percent of women have blood mercury above 3.5 µg/L. With about 4.1 million births per year in the U.S., this means that about 630,000 infants per year are exposed in utero to excessive mercury levels. This doubled estimate of the population of newborn Americans at risk for mercury-related brain damage would add urgency to the effort to manage dietary mercury intake from fish and seafood, even if there were no new evidence to refine and strengthen our understanding of the nature of the risks involved. However, two papers published in the February issue of the Journal of Pediatrics add to evidence that methylmercury toxicity in the developing brain is not just a theoretical hazard. The two reports (Murata et al., 2004; Grandjean et al., 2004) are the latest from a long-term study following the development of a cohort of children in the Faroe Islands, where the population consumes a diet rich in fish and seafood. The study, begun in 1986, is being conducted by a team of scientists from the Harvard School of Public Health and institutions in Japan, Denmark and the Faroe Islands. At the outset, mercury body burden was measured in pregnant women and in their newborn infants, and the health status and neurological development of the children have been assessed at intervals since birth. The papers published this month report on findings in some 859 children at age 14. While several similar studies (including an ongoing study in the Seychelles islands) have produced evidence on the developmental neurotoxicity of methylmercury in people with a high-fish diet, a National Research Council committee has identified this study of the Faroese population as the best available evidence on the question (NRC 2000). The two latest papers add to that body of recognized high-quality scientific evidence. The first paper, by Murata et al., reports on tests of brain function in the 14-year-old population. Earlier reports by these investigators had evaluated brain function in these children at the age of 7 years and found delays in transmission of brainstem auditory evoked potentials, which increased with higher pre-natal mercury exposure. The current study found that the impairment persisted at age 14, suggesting that the adverse effects of prenatal methylmercury exposure are irreversible. The investigators also measured the mercury levels in the children’s hair at the ages of 7 and 14, which provides an index of post-natal mercury exposure. Some neurotoxic effects correlated with hair (postnatal) mercury levels, i.e., primarily mercury from the children’s own consumption of fish and seafood, as distinct from their association with prenatal mercury exposure. Most (96 percent) of the mothers at childbirth had hair mercury levels above the 1 ppm level defined by the US EPA as the maximum safe hair mercury concentration. But the 14-year-olds in this study had much lower hair mercury levels (the average level in the study population was 0.96 ppm). Their lower hair mercury levels indicate that these children had lower dietary mercury exposure than their mothers had had. Nevertheless, the children’s postnatal mercury exposure was correlated with latency in neural signal transmission in the midbrain, suggesting that postnatal mercury exposure may damage different neural functions than those affected by prenatal exposure. Most notably, even very low mercury exposure was associated with delays in nerve signal transmission. The researchers observed no threshold of mercury exposure below which impairment was not detected. They concluded that some adverse effects on brain function of methylmercury exposure during childhood appear to occur at doses below the current EPA Reference Dose (RfD). While this new finding needs confirmation, it would not be surprising if, like lead, methylmercury posed some risk of adverse toxic effects on the developing brain across the full range of “normal” human exposure. The second paper, by Grandjean et al., examined heart function in the same 14-year-old Faroese children. The investigators measured variability of heart rate, an objective index of heartbeat regulation by the autonomous nervous system. At higher levels of (mainly prenatal) mercury exposure, regulation of heart rate variability was weaker, confirming a finding by the same investigators when they examined the study population at the age of 7 years. Decreased heart rate variability in adulthood is a risk factor for cardiovascular disease and sudden death. Two recent studies have linked methylmercury exposure with increased risk of cardiovascular mortality (Salonen et al. 1995, Guallar et al. 2002). The latest findings from the Faroes investigation suggest a mechanism (neurotoxicity) underlying the cardiovascular risk from mercury exposure. In summary, these recent studies indicate that methylmercury exposure from fish and seafood consumption is very likely an even more serious public health problem in the United States than was previously recognized. EPA’s updated exposure assessment indicates that the population of newborns at risk is twice as large as estimated just a few years ago; and the latest epidemiological evidence strengthens the inference that adverse effects can occur at current levels of methylmercury exposure from seafood consumption in amounts typical of many Americans’ diets. Evidence that post-natal exposure (as well as pre-natal exposure) has effects on the developing brain highlights the need for advice to help parents keep children’s mercury intake within safe limits, and the suggestion that exposure to methylmercury even below the EPA RfD poses some risk of harm makes it imperative that every effort be made to keep consumer exposures below that RfD. Unfortunately, FDA’s current effort to update its dietary advisory on mercury in fish and seafood seems in danger of falling short of addressing these clear needs. We have been actively participating as stakeholders in the FDA/EPA process to develop a new dietary advisory. We believe the effort up to now (as indicated by the latest draft, presented to a focus group in San Diego on January 28, 2004), is on the right track but still far short of the mark. In particular: (1) FDA’s proposed dietary advice could allow, and might even
encourage, many consumers to eat varieties and amounts of fish that would
result in exposure to methylmercury above the RfD. Conceding that this
was true, FDA’s David Acheson said, at the December 10-11 FDA Food
Advisory Committee meeting, that while FDA endorses the EPA RfD, he sees
it as a “useful guideline,” not as an essential exposure
limit. Acheson and other FDA scientists have expressed a lack of concern
that many consumers will exceed the RfD. We believe, considering recent
evidence summarized here, that much more serious concern about exposure
above the RfD is warranted, and that FDA’s advice should be tailored
to guide consumers to keep their mercury intake within the RfD, as much
as possible. (4) The current draft advisory puts some, but not enough, emphasis on low-mercury fish and seafood choices. FDA is concerned, legitimately, that advice aimed at limiting mercury exposure from fish and seafood should not frighten people unduly about consuming fish, since a general decrease in fish consumption would have other adverse nutritional and public health implications. The solution, however, is to offer clear advice that puts as much emphasis on a “positive list” (fish that contain low levels of mercury, and can be eaten often) as it does on a “negative list” (fish with moderate or high levels of mercury, whose consumption should be limited or avoided altogether). From the draft advisory presented to the focus group in San Diego, FDA seems to have taken aboard that concept, since the latest draft does include a rudimentary positive list. We strongly recommend that this theme be expanded upon in the final advisory, due to be issued in April. For example, including a list of the 10 most popular seafood choices (based on market data) with their methylmercury content would make it clear that there are many appealing low-mercury options. We also urge that additional details on low- and very-low mercury fish be made available on the FDA website and revised on a regular basis as additional data becomes available. In addition to the critical task of updating its dietary advisory, we also urge FDA to keep collecting data on mercury levels in widely consumed varieties of fish and seafood. The current database is inadequate for assessing the distribution of mercury exposure from many species of interest. To accurately determine how many women and children are exposed to unsafe amounts of methylmercury in the fish they eat, data are needed on both amounts of various fish species consumed and the range of values for methylmercury in those fish. We agree with the recommendation, included in the Fiscal 2004 Agriculture Appropriations bill report, strongly urging FDA to restart its monitoring program for mercury in fish. We believe more extensive data on low-mercury fish, i.e., the safest choices, are needed, as well as data on high-mercury fish. Further, we have recently learned that FDA’s test data on mercury in canned tuna are based on composite samples. While compositing samples allows a survey to cover more of the food supply and gives a good indicator of average methlymercury levels to which consumers of different fish (e.g., light vs. albacore tuna) are exposed, compositing also levels out peaks and valleys in the data. Because even short-term peaks in exposure to methylmercury could have adverse effects on the developing brain (if they occurred at a critical point in brain development), it is important that data also be gathered that reveal the full range of methylmercury values that consumers may occasionally encounter. We urge that FDA’s future testing, especially for frequently-consumed items like tuna, look at both values in individual cans and than composite samples. In conclusion, recent scientific evidence has made it even clearer that FDA needs to act assertively to help consumers minimize their mercury exposure from fish and seafood in their diets. We hope you share our belief that dietary advice can be crafted that helps the consumer enjoy the benefits of a diet rich in fish and seafood, while avoiding excessive exposure to methylmercury. We urge you to instruct Dr. Acheson’s team to thoroughly re-work the draft dietary advisory, until the needs borne out by recent scientific evidence have been effectively addressed. And we urge you to expand and refine FDA’s critical testing program to collect the data needed for a more precise risk assessment. Thank you very much for your attention to this matter. Should you or your staff have questions, please call Michael Bender at 802-223-9000. Sincerely, R. David Pittle, Ph.D. Linda Knobeloch, Ph.D. Karen L. Perry, MPA Jennifer Sass, Ph.D. R. Montgomery Fischer Navis Bermudez Zachary Corrigan John M. Stanton David Wallinga, MD
Nizanna Bathersfield Michael T. Bender, MS Ned Groth III, Ph.D. Philip J. Landrigan*, M.D., M.Sc. Bruce P. Lanphear*, MD Steven G. Gilbert*, PhD, DABT Katherine M. Shea*, MD, MPH, FAAP James R Roberts* MD, MPH *Affiliations listed only for identification purposes, and do not constitute endorsement cc Dr. David Acheson, FDA References Cited: Mahaffey, K.R. (2004) Methylmercury: Epidemiology Update. Presentation at the National Forum on Contaminants in Fish, San Diego, January 28, 2004. Schober, S.E., Sinks, T.H., Jones, R.L., Bolger, P.M., McDowell, M., Osterloh, J., et al. (2003) Blood mercury levels in US Children and women of childbearing age, 1999-2000. Journal of the American Medical Association 289(13): 1667-1674. Murata, K., Weihe, P., Budtz-Jørgensen, E., Jørgensen, P.J., and Grandjean, P. (2004) Delayed brainstem auditory evoked potential latencies in 14-year-old children exposed to methylmercury. Journal of Pediatrics 144:177-183. Grandjean, P., Murata, K., Budtz-Jørgensen, E. and Weihe, P. (2004) Cardiac autonomic activity in methylmercury neurotoxicity: 14-year follow-up of a Faroese birth cohort. Journal of Pediatrics 144:169-176. National Research Council (2000) Toxicological Effects of Methylmercury. Washington, DC: National Academy Press. Salonen, J.T. et al. (1995) Intake of mercury from fish, lipid peroxidation, and the risk of myocardial infarction and coronary, cardiovascular and any death in eastern Finnish men. Circulation 91: 645-655. Guallar, E., et al. (2002) Mercury, fish oils and the risk of myocardial
infarction. New England Journal of Medicine 347:1747-1754. |
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