"Minamata disease is a poisoning disease that affects mainly the central nervous system and is caused by the consumption of large quantities of fish and shellfish living in Minamata Bay and its surroundings, the major causative agent being some sort of organic mercury compound."

The Chisso Corporation first opened a chemical factory in Minamata in 1908. Initially producing fertilizers, 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 Japan, both before and after World War II. The waste products resulting from the manufacture of these chemicals were released into Minamata Bay in the factory wastewater. Inevitably, these pollutants had an environmental impact. Fisheries were damaged in terms of reduced catches and in response Chisso reached two separate compensation agreements with the fishery cooperative in 1926 and 1943. 

The rapid expansion of the Minamata factory spurred on the local economy and as Chisso prospered, so did Minamata. This fact, combined with the lack of other industry, meant that Chisso had great influence in Minamata. 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. Minamata was dubbed Chisso's "castle town", in reference to the capital cities of feudal lords who ruled Japan during the Edo period.

The Chisso Minamata factory first started acetaldehyde production in 1932, producing 210 tons that year. By 1951 production had jumped to 6,000 tons per year: over 50% of Japan's total output. The chemical reaction used to produce the acetaldehyde used mercury sulfate as a catalyst. A side reaction of the catalytic cycle led to the production of a small amount of an organic mercury compound, namely methyl mercury. This highly toxic compound was released into Minamata Bay from the start of production in 1932 until 1968 when this production method was discontinued.

1956–1959

On April 21, 1956, a five year-old girl was examined at the Chisso Corporation's factory hospital in Minamata, Japan, a town on the west coast of the southern island of Kyūshū. 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 was hospitalized. The girls' mother informed doctors that her neighbor's daughter was also experiencing similar problems. After a house-to-house investigation, eight further patients were discovered and hospitalized. On May 1, the hospital director to the local public health office reported the discovery of an "epidemic of an unknown disease of the central nervous system", marking the official discovery of Minamata disease.

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 localized nature of the disease, it was suspected to be contagious and as a precaution patients were isolated and their homes disinfected. Unfortunately, this contributed to the stigmatisation and discrimination experienced by Minamata victims from the local community. During its investigations, the committee uncovered surprising anecdotal evidence of the strange behavior of cats and other wildlife in the areas surrounding patients' homes. From around 1950 onwards, cats had been seen to have convulsions, go mad and die. Locals called it the "cat dancing disease", owing to their erratic movement. Crows had fallen from the sky, seaweed no longer grew on the sea bed 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 to help in the research effort.

The Kumamoto University Research Group was formed on August 24, 1956. Researchers from the School of Medicine began visiting Minamata regularly and admitted patients to the university hospital for detailed examinations. Gradually, a more complete picture of the symptoms exhibited by patients was uncovered. The disease developed 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 deteriorated and were followed by severe convulsions, coma and eventual death. By October 1956, 40 patients had been discovered, 14 of whom had died: a mortality rate of 36.7%.

Finding the Cause

Researchers from Kumamoto University 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 the local area, who tended to eat scraps from the family table, had died with symptoms similar to those now discovered in humans. This led the researchers to believe that the outbreak was caused by some kind of food poisoning, with contaminated fish and shellfish the prime suspects.

On November 4, 1956 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."

Identification of Mercury

As soon as the investigation identified a heavy metal as the causal substance, the wastewater from the Chisso plant was immediately suspected as the origin. The company's own tests revealed that its wastewater contained many heavy metals in concentrations sufficiently high to bring about serious environmental degradation; these metals included lead, mercury, manganese, arsenic, selenium, thallium and copper. 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. Initially, 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 but it was not until March 1958, when visiting British neurologist Douglas McAlpine suggested that Minamata symptoms resembled those of organic mercury poisoning, that the focus of the investigation centered on mercury.

In February 1959, the mercury distribution in Minamata Bay was investigated. The results shocked the researchers involved. Large quantities of mercury were detected in fish, shellfish and sludge from the bay. The highest concentrations centered around the Chisso factory wastewater canal in Hyakken Harbour and decreased going out to sea, clearly identifying the factory 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 high enough to be economically viable to mine. Ironically, Chisso did later set up a subsidiary to reclaim and sell the mercury recovered from the sludge.

Hair samples were taken from the victims of the disease and also from the Minamata population in general. In patients, the maximum mercury level recorded was 705 parts per million (ppm), indicating very heavy exposure.  In non-symptomatic Minamata residents, the level was 191 ppm compared to an average level of 4 ppm for people living outside the Minamata area.

On November 12, 1959 the Ministry of Health and Welfare's Minamata Food Poisoning Subcommittee published its results: