is a neurological disease caused by severe mercury poisoning. Symptoms include ataxia, numbness in the hands and feet, general muscle weakness, loss of peripheral vision, and damage to hearing and speech. In extreme cases, insanity, paralysis, coma, and death follow within weeks of the onset of symptoms. A form of the disease in babies, with microcephaly, extensive cerebral damage, and symptoms similar to those seen in cerebral palsy also occurred.
Minamata disease was first discovered in the city of Minamata, Kumamoto Prefecture, Japan, in 1956. It was caused by the release of methylmercury in the industrial wastewater from a chemical factory owned by the Chisso Corporation, which continued from 1932 to 1968. It has also been suggested that some of the mercury sulfate in the wastewater was also metabolized to methylmercury by bacteria in the sediment. and references therein. This highly toxic chemical bioaccumulated and biomagnified in shellfish and fish in Minamata Bay and the Shiranui Sea, which, when eaten by the local population, resulted in mercury poisoning. The poisoning and resulting deaths of both humans and animals continued for 36 years, while Chisso and the Kumamoto prefectural government did little to prevent the epidemic. The animal effects were severe enough in cats that they came to be named as having "dancing cat fever."
As of March 2001, 2,265 people had been officially recognized as having Minamata diseaseOfficial government figure as of March 2001. See "Minamata Disease: The History and Measures, ch2" and over 10,000 had received financial compensation from Chisso.See "Minamata Disease Archives" , Frequently asked questions, Question 6 By 2004, Chisso had paid $86 million in compensation, and in the same year was ordered to clean up its contamination.Jane Hightower (2008). Diagnosis Mercury: Money, Politics and Poison, Island Press, p. 77. On March 29, 2010, a settlement was reached to compensate as-yet uncertified victims."Agreement reached to settle Minamata suit", Asahi Shimbun news, 31 March 2010, retrieved 1 April 2010
A second outbreak of Minamata disease occurred in Niigata Prefecture in 1965. The original Minamata disease and Niigata Minamata disease are considered two of the Four Big Pollution Diseases of Japan.
1908–1955
In 1908, the Chisso Corporation first opened a chemical factory in Minamata, Kumamoto Prefecture, located on the west coast of the southern island of Kyūshū. Initially producing fertilisers, the factory followed the nationwide expansion of Japan's chemical industry, branching out into production of acetylene, acetaldehyde, acetic acid, vinyl chloride, and octanol, among others. The Minamata factory became the most advanced in all of Japan, both before and after World War II. The waste products resulting from the manufacture of these chemicals were released into Minamata Bay through the factory wastewater. These pollutants had a deleterious environmental impact. Fisheries were damaged in terms of reduced catches; in response, Chisso reached two separate compensation agreements with the fishery cooperative in 1926 and 1943.Harada, p15
The rapid expansion of the Chisso factory spurred on the local economy, and as the company prospered so did Minamata. This fact, combined with the lack of other industry, meant that Chisso had great influence in the city. At one point, over half of the tax revenue of Minamata City authority came from Chisso and its employees, and the company and its subsidiaries were responsible for creating a quarter of all jobs in Minamata.George, pp35-36 The city was even dubbed Chisso's "castle town," in reference to the capital cities of feudal lords who ruled Japan during the Edo period.George, p26
The Chisso factory first started acetaldehyde production in 1932, with 210 tons that year. In 1951, production had jumped to 6,000 tons and eventually peaked at 45,245 tons in 1960.Report of the Social Scientific Study Group on Minamata Disease, In the Hope of Avoiding Repetition of a Tragedy of Minamata Disease , National Institute for Minamata Disease, p. 13. The factory's output historically amounted to between a quarter and a third of Japan's total acetaldehyde production. The chemical reaction used to produce the acetaldehyde employed mercury sulfate as a catalyst. Starting in August 1951, the co-catalyst was changed from manganese dioxide to ferric sulfide.Eto et al. (2010) A side reaction of this catalytic cycle led to the production of a significant amount (about 5% of the outflow) of extremely toxic and persistent methylmercury.For further information on the chemistry of the reaction that lead to the production of methylmercury see "Information on Mercury" by Mercury Technology Services, retrieved around the 24 October 2006 As a result of the catalyst change, this compound was released into Minamata Bay regularly between 1951 and 1968, when this production method was finally discontinued.Gilhooly, Rob, "Mercury rising: Niigata struggles to bury its Minamata ghosts", Japan Times, 13 June 2015
1956–1959
On 21 April 1956, a 5-year-old girl was examined at Chisso's factory hospital in Minamata. The physicians were puzzled by her symptoms: difficulty walking, difficulty speaking, and convulsions. Two days later, her younger sister also began to exhibit the same symptoms and she, too, was hospitalised. The girls' mother informed doctors that her neighbour's daughter was also experiencing similar problems. After a house-to-house investigation, eight further patients were discovered and hospitalised. On 1 May, the hospital director reported an "epidemic of an unknown disease of the central nervous system" to the local public health office, marking the official discovery of Minamata disease.Harada, p10
To investigate the epidemic, the city government and various medical practitioners formed the Strange Disease Countermeasures Committee at the end of May 1956. Owing to the localised nature of the disease, it was initially suspected to be contagious; patients were isolated and their homes disinfected as a precaution. Although contagion was later disproved, this initial response contributed to the stigmatisation and discrimination experienced by Minamata survivors from the local community. During its investigations, the Committee uncovered surprising anecdotal evidence of the strange behaviour of cats and other wildlife in the areas surrounding patients' homes. Reports of cats convulsing, going mad and dying started around 1950. Locals called it the "cat dancing disease" in reference to the cats' erratic movements. Crows had fallen from the sky, seaweed no longer grew on the seabed, and fish floated dead on the surface of the sea. As the extent of the outbreak was understood, the committee invited researchers from Kumamoto University (or Kumadai) to help in the research effort.Nicol, C.W., "Minamata: a saga of suffering and hope", Japan Times, 7 October 2012, p. 10
The Kumamoto University Research Group was formed on 24 August 1956. Researchers from the School of Medicine began visiting Minamata regularly and admitted patients to the university hospital for extensive examination. A more complete picture of the symptoms exhibited by patients was gradually uncovered. The disease struck without any prior warning, with patients complaining of a loss of sensation and numbness in their hands and feet. They became unable to grasp small objects or fasten buttons. They could not run or walk without stumbling, their voices changed in pitch, and many patients complained of difficulties seeing, hearing, and swallowing. In general, these symptoms worsened and were followed by severe convulsions, coma, and eventually death. By October 1956, forty patients had been discovered, fourteen of whom had died - an alarming case fatality rate of 35%.Harada, pp23-24
Finding the cause
Researchers from Kumadai also began to focus on the cause of the strange disease. They found that the victims, often members of the same family, were clustered in fishing hamlets along the shore of Minamata Bay. The staple food of victims was invariably fish and shellfish from Minamata Bay. The cats in these areas, who often ate scraps from the family table, showed symptoms similar to humans. This led the researchers to believe that the outbreak was caused by some kind of food poisoning, with contaminated fish and shellfish being the prime suspects.
On 4 November, the research group announced its initial findings: "Minamata disease is rather considered to be poisoning by a heavy metal, presumably it enters the human body mainly through fish and shellfish."Harada, pp26-27
Identification of mercury Methylmercury, an organic mercury compound released in factory wastewater and the cause of Minamata disease
As soon as the investigation identified a heavy metal as the causal substance, the wastewater from the Chisso factory was immediately suspected as the origin. The company's own tests revealed that its wastewater contained many heavy metals in concentrations sufficiently high enough to bring about serious environmental degradation, including lead, mercury, manganese, arsenic, thallium, and copper, plus the chalcogen selenium. Identifying which particular poison was responsible for the disease proved to be extremely difficult and time-consuming. During 1957 and 1958, many different theories were proposed by different researchers. At first, manganese was thought to be the causal substance due to the high concentrations found in fish and the organs of the deceased. Thallium, selenium, and a multiple contaminant theory were also proposed. In March 1958, visiting British neurologist Douglas McAlpine suggested that Minamata symptoms resembled those of organic mercury poisoning, which shifted the focus of the investigation to mercury.
In February 1959, researchers tested the waters of Minamata Bay for mercury. The results were shocking - high quantities of mercury were detected in fish, shellfish, and sludge from the bay. The highest concentrations centred around the Chisso factory wastewater canal in Hyakken Harbour, decreasing as it went out to sea, clearly identifying the plant as the source of contamination. At the mouth of the wastewater canal, a figure of 2 kg of mercury per ton of sediment was measured, a level so high that it would be economically viable to mine (Chisso later set up a subsidiary to reclaim and sell the mercury recovered from the sludge).Harada, p50 Subsequent testing of the bay's marine life revealed that the industrial sludge contained high concentrations of methylmercury, which had bioaccumulated up the local food chain.
Hair samples were taken from the residents of Minamata and tested for mercury. In residents affected by the disease, the highest mercury level recorded was 705 parts per million (ppm), indicating very heavy exposure, and in asymptomatic Minamata residents, the highest level was 191 ppm. This compared to an average level of 4 ppm for people living outside the Minamata area.
On 12 November 1959, the Ministry of Health and Welfare's Minamata Food Poisoning Subcommittee published its results:
1959