Minamata Disease

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Minamata disease

The town of Minamata, near the southern tip of Japan's Kyushu Island, gave its name to one of the most notorious examples of environmental contamination known. Minamata disease is really alkylmercury poisoning , caused by eating food such as fish or grain contaminated with mercury or its derivatives. At Minamata people were poisoned when they ate large quantities of methylmercury-contaminated fish. Often the victims were the poorest members of society, who could not afford to stop eating the cheap fish known to be affected by effluent discharged from the local chemical company. The first victims were reported in 1956; before that, cats were seen moving strangely, sometimes flinging themselves into the sea, and birds were observed flying awkwardly or even falling out of the sky.

The Chisso Company, a leading chemical manufacturer, produced acetaldehyde by passing acetylene gas across an inorganic mercury catalyst, leaving methylmercury as a by-product. The company was a major local employer and the only significant major source of industrial waste discharged into Minamata Bay. There, methylmercury in the water biomagnified to high levels in fish and shellfish consumed by the local inhabitants. Methylmercury concentrates in specific regions of the central nervous system and readily crosses the blood/brain barrier as well as the placental barrier. It is a human teratogen which causes brain damage during prenatal exposures, resulting in congenital or fetal Minamata disease. The compound has a half-life of about 70 days in the human body, and the damage is generally irreversible. Although company officials knew that similar symptoms could be induced in cats by feeding them fish taken from the bay, Chisso was not blamed by the Japanese government
for the disaster until 1968. Despite the evidence, it was difficult to be certified as a Minamata disease victim. Those affected were not compensated until after another epidemic occurred at Niigata, Japan, in 1965. That one was caused by methylmercury waste discharged from the Showa Denko Corporation Kanose factory into the Agano River. The company also manufactured acetaldehyde using the same process as Chisso.

Nearly four decades after Minamata disease was identified, the full range of its neurological symptoms is still not known, nor have the total number of sufferers been determined. While some children were born with contorted bodies and severe retardation, in milder cases the victims may be moderately retarded or exhibit only sensory disturbances. Even as the symptoms advance in adult patients, it is often difficult to determine whether they are the result of long-term poisoning, delayed effects of residual methylmercury, aging, or other complications. Therefore, even thirty years later, as of December 31, 1992, only 2,945 individuals were officially certified as Minamata Disease victims and 1,343 of them had died. Another 13,761 had been denied certification and the fate of 2,430 was still pending.

Lawsuits dragged on for more than twenty-five years, and victims seeking compensation tried confrontation tactics like an encampment that lasted a year and a half in front of Chisso's main headquarters in Tokyo. Reclamation of the environment has been even slower. The Chisso Company installed waste treatment equipment in 1966 and stopped making acetaldehyde in 1968. By then 400600 tons of mercury and 60,000 tons of sludge had been dumped into the shallow Minamata Bay. Mercury levels in fish remained elevated. Dredging scheduled to begin in 1975 did not get underway until 1982. Since then, mercury levels in ten species of fish have dropped; but as of March 1993, they were still two or three times higher than what the government deems acceptable. Consequently, fishermen have lost their livelihood and health and gained a social stigma. The Chisso company's fortunes also declined and were further strained by lawsuits that mandated restitution.

See also Agricultural chemicals; Biomagnification; Birth defects; Environmental law; Food chain/web; Heavy metals and heavy metal poisoning; Marine pollution; Methylmercury seed dressings; Water pollution; Xenobiotic

[Frank M. D'Itri ]



Harada, M. "Methyl Mercury Poisoning Due to Environmental Contamination (Minamata Disease)." In Toxicity of Heavy Metals in the Environment, Part 1, edited by F. W. Oehme. New York: Marcel Dekker, 1978.

Ui, J. "Minamata Disease." In Industrial Pollution in Japan. Tokyo, Japan: United Nations University Press, 1992.


D'Itri, F. M. "Mercury ContaminationWhat We Have Learned Since Minamata." Environmental Monitoring and Assessment 19 (1991): 165182.

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"Minamata disease" is the term used to describe the poisoning that occurred among residents of Minamata, Japan due to the ingestion of methyl-mercury-containing seafood. From the 1920s through the 1960s, the Chisso Company used mercury as a catalyst in the production of acetaldehyde, a chemical intermediate with numerous uses including plastics and perfume production. The Chisso Company dumped waste methylmercury from the acetaldehyde production into Minamata Bay. The methylmercury bioaccumulated within the food chain, from plankton and other microorganisms up to fish and shellfish. This posed a significant health hazard to residents of the area who obtained much of their protein from Minamata Bay seafood.

In the early 1950s, Minamata Bay residents began to exhibit symptoms of neurological illness, such as uncontrollable trembling, loss of motor control, and partial paralysis. Children also began to be born with Minamata disease, exhibiting symptoms similar to cerebral palsy (impaired neurological development and seizures). By the late 1950s, scientists from Japan's Kumamoto University strongly suspected that methylmercury was the cause of Minamata disease.

Methylmercury concentrates in neural tissues, which explains why neurotoxicity was the major adverse effect observed in Minamata Bay. Offspring of Minamata Bay residents afflicted with Minamata disease also exhibited neurotoxicity because methylmercury can be transferred across the placenta. Between 1953 and 1960, 628 cases of illness were documented, including 78 deaths. Total cases of morbidity and mortality caused by Minamata disease from the 1950s to the year 2000 are thought to range in the thousands but the exact number is not known.

Margaret H. Whitaker

Bruce A. Fowler

(see also: Food-Borne Diseases; Mercury )


Tsubaki, T., and Irukayama, K. (1977). Minimata Disease. Methylmercury Poisoning in Minamata and Niigata, Japan. Amsterdam: Elsevier Scientific Publishers.

Ui, J. (1992). Industrial Pollution in Japan. Tokyo: United Nations University Press. Available at http://www.unu.edu/unupress/unupbooks.

World Health Organization (1990). Methyl Mercury. Environmental Health Criteria 101. Geneva: Author.

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Minamata disease Poisoning by organic mercury compounds, named after Minamata Bay in Japan, where fish contained high levels of organic mercury compounds after waste water from mercury processing was passed into the estuary (between 1953–6).