Skip to content Skip to footer

What is the cause of Minamata Disease?

Minamata disease also known as (aka) Chisso-Minamata disease is a neurological disease which is the result of serve mercury intoxication. Historically, it was first discovered in Minamata city in Kumamoto prefecture, which is located in the southwestern Kyushu island (next to Nagasaki prefecture), Japan in 1956 [1].

As of March 2001, 2,265 victims had been officially recognized as having Minamata disease (1,784 of whom had died) and over 10,000 had received financial compensation from Chisso Corporation [2,3]. By 2004, Chisso had paid $86 million in compensation. In the same year, it was ordered to clean up its contamination [4]. On March 29, 2010, a settlement was reached to compensate as-yet uncertified victims [5]. A second outbreak of Minamata disease occurred in Niigata Prefecture in 1965. The original Minamata disease and Niigata Minamata disease are considered as two of the four big diseases related to the pollution  in Japan.

Japan suffered the consequence of environmental pollution problems during the industrial revolution. Minamata disease is one of the consequence of environmental pollutions due to the mercury poisoning (the release of methylmercury in the industrial wastewater from the Chisso Corporation, a chemical factory, which operated  from 1932 to 1968). 

How it happened?

The industrial wastewater from the Chisso Corporation contaminated with methylmercury bioaccumulated and biomagnified in shellfish and fish which, when widely consumed by the local people, in Minamata Bay and the Shiranui Sea, resulted in mercury poisoning.

The very first known cases

On April 21, 1956, a five-year-old girl was hospitalized at the Chisso Corporation’s factory hospital in Minamata, Kumamoto, where the physicians discovered the symptoms such as difficulty walking, difficulty speaking, and convulsions. Two days later, her younger sister also began to exhibit the same symptoms as she was also hospitalized. The mother informed the doctors that her neighbor’s daughter also have similar symptoms. Eight further patients were discovered the same symptoms after the house-to-house investigation. On May 1, the hospital director reported to the local public health office the discovery of an “epidemic of an unknown disease of the central nervous system”, marking the official discovery of Minamata disease. In order to investigate the epidemic, in May 1956, the city government and various medical practitioners formed the Strange Disease Countermeasures Committee. The investigation discovered the localized nature of the disease as well as the evidence of the strange behaviors in the wildlife in the surrounding areas of the patients. Numerous cases of animals’ strange behavioral patterns such as the erratic movements of the cats local known as “cat dancing disease” and death had been reported during the investigation. 

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:

“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.”


[1] Hamdy MK, Noyes OR. (1975). “Formation of Methyl Mercury by Bacteria” (PDF)Appl. Microbiol30 (3): 424–432. doi:10.1128/AEM.30.3.424-432.1975. PMC 187198. PMID 1180551. and references therein.
[2] Official government figure as of March 2001. See “Minamata Disease: The History and Measures, ch2”
[3] “Minamata Disease Archives” Archived 2016-03-03 at the Wayback Machine, Frequently asked questions, Question 6
[4] Jane Hightower (2008). Diagnosis Mercury: Money, Politics and Poison, Island Press, p. 77.
[5] “Agreement reached to settle Minamata suit”, Asahi Shimbunnews, 31 March 2010, retrieved 1 April 2010

Mercury Free Society Networks © 2020. All Rights Reserved.