Minamata Bay mercury poisoning

THE EVENT: Contamination of the local food chain in Japan’s Minamata Bay by industrial waste containing mercury

DATES: 1950’s-1960’s

The environmental health tragedy caused by the disposal of industrial waste in Minamata Bay represents one of the first identified cases of a clear cause-and-effect relationship between toxic chemical discharge and severe harm to humans and their environment.

The city of Minamata is located on the southwest coast of Kyūshū, the southernmost of Japan’s four main islands, in Kumamoto prefecture. During the 1950’s, a local chemical plant owned by Chisso Corporation was engaged in the production of acetaldehyde and vinyl chloride. One of the chemicals used as a in the production processes was mercury oxide (HgO). The industrial from the plant, including mercury, was discharged into Minamata Bay. At the time, such waste disposal was an acceptable practice, and the amount of increased during the early 1950s. It was generally understood that mercury, a like lead, cadmium, and arsenic, could be injurious to the health of persons who mishandled, ingested, or inhaled it, but because mercury is dense and quite insoluble in water, it was presumed that it would quickly into the sediment at the bottom of the bay, where it would be slowly buried and disappear.

By 1953, unusual medical symptoms began to appear in area residents; most of the symptoms were neurological, such as tremors and impairment of senses. In 1956, the first case of a distinct medical condition was reported. By 1959, the cause of the affliction had been identified and the effects established: The first patients had acute or near-acute levels of mercury poisoning, a condition that became known as Minamata disease.

The residents of the area had not realized that the dense mercury (Hg) on the bay bottom was being acted on by microorganisms such as and and was being converted into methylmercury and dimethyl mercury. Methylmercury, the more injurious and toxic of the two substances, is much less dense than mercury itself and is more soluble. In the bay environment, it worked its way to the upper sediment, was taken up in the by bottom-dwelling shellfish and fish, and was then consumed by the local people, for whom seafood was a dietary staple. Mercury can also be taken up by fish-eating birds and mammals. Heavy metals tend to accumulate in the bodies of organisms that ingest them, as in the edible flesh of fish. They concentrate up the food chain, as one species retains and accumulates the from its regular diet.

In natural environmental cycling and processes, elements such as mercury are weathered out of rock to soil and enter the hydrosphere (lakes, rivers, groundwater, and oceans). They might become more concentrated, but decay eventually returns them to the soil or water. This cycling can be disrupted when industrial or other human activities introduce anomalously large amounts of the element into the cycle that cannot be accommodated by natural means. Whether an element is toxic to humans or others is a function of concentration; some elements are essential in small amounts but become toxic in large concentrations.

Mercury occurs as a trace element in average crustal rock at a level of 0.1 parts per million (ppm); in seawater, it is typically under 0.05 parts per billion. At Minamata Bay, mercury levels in fish and shellfish were measured up to 50 ppm (25 ppm represents a factor of 500,000 over normal seawater). For comparison, the U.S. Food and Drug Administration (FDA) prohibits fish with more than 1 ppm of mercury from being commercially marketed. Residents diagnosed with Minamata disease had mercury levels of 20 to 100 ppm in their livers and kidneys and 3 to 25 ppm in their brains. Minamata Bay sediment levels of mercury were as high as 7,000 ppm.

The medical effects of consuming mercury include progressive damage to the central nervous system and birth defects from prenatal exposure. Symptoms include shakiness (tremors), blurred vision, impaired speech, numbness in limbs, loss of memory and intelligence, nervousness, and, in extreme cases, death. By the time symptoms are apparent, the damage is irreversible. Of the first 34 people diagnosed with Minamata disease, 20 died within six months. By 1960, 43 people had died and 116 were permanently affected. About one-third of the infants born in the area were affected by symptoms. By the mid-2000s, 2,265 people had been officially diagnosed with the disease, and an estimated 900 had died. Several thousand more claimed to have the disease but had not been officially diagnosed by the examining board set up by the Japanese government.

The developing environmental health problem of the 1950’s at Minamata Bay, however inadvertently it may have started, became a broader and more persistent tragedy because of the lack of corporate or governmental response. Chisso Corporation denied responsibility for the problem, arguing that the dumping of was an accepted practice and was legal at the time. Some have speculated that the company may have suspected the cause of the growing problem but concealed it. The national government declined to act on the matter. At the time, there was little governmental consciousness of environmental quality issues, and intervention might have harmed the chemical industry and slowed Japan’s post-World War II industrialization and economic recovery. A similar problem occurred at Niigata in west-central Japan in the 1960’s, when mercury waste was dumped into the Agano River. The national government thus did not intervene in the Minamata situation until 1968, and the dumping of mercury into the bay was not stopped until 1971, twelve years after the problem became known.

The National Institute for Minamata Disease was set up in 1978 to assist with medical studies, conduct research, and follow the progress of victims over time. The Japanese government provides medical care for diagnosed victims, along with financial compensation. Active victims’ movements and support groups have used the court system to pursue responsibility and liability.

It is estimated that the total discharge of mercury from the Chisso plant was between 70 and 150 tons. Major efforts were implemented to clean up the site and restore the local so that it would once again be fit for sea life and human use. From 1977 to 1990 the mercury-contaminated was dredged from 58 hectares (143 acres) of the bay in a project funded by the national and prefectural governments and Chisso Corporation. In 1974 a huge net was placed to isolate 380 hectares (939 acres) of the bay area to prevent fish from swimming in or out. In 1997, Minamata Bay was declared to be free of mercury contamination, and the net was removed.

In 2013, the United Nations Environment Programme adopted the Minamata Convention on Mercury, an environmental protocol that aimed to prevent mercury pollution and mercury poisoning. The United States was one of more than 140 nations to sign the agreement.

Bibliography

D’Itri, Frank M. “Mercury Contamination—What We Have Learned Since Minamata.” Environmental Monitoring and Assessment 19, nos. 1-3 (1991): 165-182.

Eisler, Ronald. Mercury Hazards to Living Organisms. Boca Raton, Fla.: CRC Press, 2006.

George, Timothy S. Minamata: Pollution and the Struggle for Democracy in Postwar Japan. Cambridge, Mass.: Harvard University Asia Center, 2001.

"Minamata Convention on Mercury." Environmental Protection Agency, 13 Dec. 2023, www.epa.gov/international-cooperation/minamata-convention-mercury. Accessed 19 July 2024.

Montgomery, Carla W. “Water Pollution.” In Environmental Geology. 11th ed. New York: McGraw-Hill, 2019, pp. 411–442.