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 Related EVISA Resources Link Database: Uses of mercury compounds Link database: Toxicity of Organic mercury compounds Brief summary: Speciation and Toxicity
Related Information Wikipedia: Minamata disease Wikipedia: Mercury poisoning Wikipedia: Organo mercury Wikipedia: Methylmercury National Institute for Minamata Disease SHiPS Resource Center: The Poisoning of Minamata
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