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Home ›› About Speciation ›› Speciation News

Methylmercury: What have we learned from Minamata Bay?

(16.08.2010)

Experts draw lessons from mistakes that delayed regulation of mercury pollution

Background:
Methylmercury is known as one of the strongest neurotoxins. Actually, the toxicity of organic mercury compounds is known for quite a long time. Organic mercury compounds were already described in the 1800s and fatal cases of methylmercury poisoning were reported as early as in 1865. First reports described a distinct set of symptoms of methylmercury neurotoxicity, including altered sensation in the face and extremities, tunnel vision, deafness, loss of coordination, and impaired speech.

Nearly a century later, against a backdrop of widespread environmental contamination, the clinical picture reappeared, and suspicions of additional harm to human health had developed. Despite early knowledge and a great number of victims (e.g. about 17,000 victims in the single case of Minamata only) international agreement to control mercury pollution was reached only in 2009.

A historical review published in the August issue Environmental Health Perspectives suggests that—as one early commenter observed—the tunnel vision, forgetfulness, and lack of coordination that symptomize methylmercury toxicity can also affect the conduct and interpretation of environmental health research.

The historical review:
Environmental health research into the effects of methylmercury poisoning was held back by legal and political barriers, and by disagreements on how to interpret scientific uncertainty, conclude an international group of scientists in their review about health effects of methylmercury and environmental health research implications.

The repeated delays in taking corrective action, from the first report of methylmercury poisoning in 1865 through to the 2009 international agreement on controlling mercury pollution, should serve as a lesson to environmental health researchers in the future, the authors say.

Methylmercury became commercially important as a crop fungicide around 1914. Worldwide use was accompanied by worker poisonings and several large-scale food poisoning incidents when mercury-treated seed intended for planting was eaten during famines in Iran, Pakistan and Guatemala in the 1960s.

The compound emerged as an industrial pollutant in the early 1950s around Japan’s Minamata Bay, where Chisso Corporation's chemical factory released methylmercury as a sideproduct of acetaldehyde production with their industrial wastewater into the bay during the years from 1932 to 1968. Especially local residents consuming the contaminated seafood were plagued by neurologic symptoms mirroring those reported in 1865. At least 1784 people died in the outbreak but the estimated number of victims is about an order of magnitude higher. When the disease was first reported in 1956, the regional government advised people to avoiding eating fish from the bay. However, the Japanese Ministry of Health and Welfare refused to enact a ban on seafood from the area because the chemical had not been definitively identified as the source of the poisoning.

It was not until 1968 that authorities officially recognised methylmercury as the cause of the poisonings. Several factors made it difficult to identify the toxin. While mercury was early found in Minamata sediments, neurological symptoms of poisoned fishermen did not show the typical signs of inorganic mercury poisoning. Early scientific discoveries about the toxicity of methylmercury, and the symptoms of methylmercury poisoning, had been forgotten or disregarded, the authors say. Initially, the inability to identify mercury species in the environment hampered researchers’ efforts to link the presence of methylmercury with poisoning symptoms. In addition, methylmercury poisoning only manifests weeks or months after exposure has occurred, and early symptoms are difficult to recognise and often confused with other psychological disorders.

“The resistance and lack of cooperation from Chisso were also an important factor [in delaying corrective action],” the researchers claim. The company suppressed and withheld from its own staff research showing that the factory wastewater was the source of methylmercury that caused the poisonings. Well into the 1970s it continued to assert that rotten fish were the cause.

The high levels of mercury exposure found in Minamata Bay have thankfully rarely been matched elsewhere. However, epidemiologic evidence from Minamata, paired with a 1952 report from Sweden, indicated even more severe effects from prenatal and early-life exposures at much lower doses, with symptoms including mental retardation, seizures, and impaired motor development. In the 1960s, advances in analytical technology permitted chemical analysis of mercury species in environmental samples, resulting in the discovery of methylmercury biomagnification in the food chain and identification of environmental methylation of inorganic mercury in waterways. Because of upcoming speciation analysis, now the toxin had a name and methylmercury had become a worldwide problem, not simply a local issue. Although mercury has been thought to be a natural component in the biosphere, compilation of mercury analyses from tissues of Arctic indicator species shows that current-day levels are increased by a factor of about 10 above those present in preindustrial times.

However, the developmental effects of methylmercury, and the dose required to cause them, remained the subject of dispute, say Grandjean and colleagues. “Scientific consensus on prenatal vulnerability was hampered by focusing on uncertainties in the evidence.” Meanwhile, industry representatives and regulatory bodies demanded that uncertainties be resolved before taking action. “The insistence on solid evidence promoted by polluters and regulatory agencies therefore agreed with a desire among researchers to expand scientific activities in this area. However, the wish to obtain more complete proof had the untoward effect of delaying corrective action.”

It took 25 years from the time the first reports of developmental neurotoxicity emerged before the disproportionate effects of methylmercury on children and foetuses were recognised by regulatory agencies — and a further 25 years before this was taken into account in risk assessment. More research is certainly needed, the authors write, but prevention and correction of environmental health problems need not and should not be delayed by a desire for absolute proof.

The cited review

Philippe Grandjean, Hiroshi Satoh, Katsuyuki Murata, Komyo Eto, Adverse Effects of Methylmercury: Environmental Health Research Implications, Environ Health Perspect, 118 (2010) 1137-1145. DOI: 10.1289/ehp.0901757

Related studies

Stephen J. Genuis, Toxicant Exposure and Mental Health—Individual, Social, and Public Health Considerations, J. Forensic Sci., 54/2 (2009) 474–477. DOI: 10.1111/j.1556-4029.2008.00973.x

T.W.Clarkson, L. Magos, The toxicology of mercury and its chemical compounds, Crit. Rev. Toxicol., 36/8 (2006) 609–662. DOI: 10.1080/10408440600845619

Komyo Eto, Akira Yasutake, Atsuhiro Nakano, Hirokatsu Akagi, Hidehiro Tokunaga and Teruyoshi Kojima, Reappraisal of the Historic 1959 Cat Experiment in Minamata by the Chisso Factory, Tohoku J. Exp. Med., 194 (2001) 197-203. DOI: 10.1620/tjem.194.197

P.A. D’Itri, F.M. D’Itri, Mercury contamination: a human tragedy, Environ Manag, 2/1 (1978) 3–16. DOI: 10.1007/BF01866442