ENVIRONMENTAL POLLUTION

MINAMATA DISEASE

THEORY

Minamata Disease

Minamata disease, sometimes referred to as Chisso-Minamata disease, is a neurological syndrome

caused by severe mercury poisoning. Symptoms include ataxia (loss of full control of bodily movement),
numbness in the hands and feet, general muscle weakness, narrowing of the field of vision and damage
to hearing and speech. In extreme cases, insanity, paralysis, coma and death follow within weeks of the
onset of symptoms. A congenital form of the disease can also affect fetuses.
Minamata disease was first discovered in Minamata City in Kumamoto prefecture, Japan in 1956. It was
caused by the release of methylmercury in the industrial wastewater (point source pollution) from the
Chisso Corporation's chemical factory, which continued from 1932 to 1968. This highly toxic chemical
bioaccumulated in shellfish and fish in Minamata Bay and the Shiranui Sea, which when eaten by the
local populace resulted in mercury poisoning. While cat, dog, pig and human deaths continued over
more than 30 years, the government and company did little to prevent the pollution.
As of March 2001, 2,265 victims had been officially recognized (1,784 of whom had died) and over
10,000 had received financial compensation from Chisso. By 2004, Chisso Corporation had paid $86
million in compensation, and in the same year was ordered to clean up its contamination. Lawsuits and
claims for compensation continue to this day.

The Beginning

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.
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ENVIRONMENTAL POLLUTION

MINAMATA DISEASE

THEORY

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.

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 Ky?sh?. 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-tohouse 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

ENVIRONMENTAL POLLUTION

MINAMATA DISEASE

THEORY

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."

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.

ENVIRONMENTAL POLLUTION

MINAMATA DISEASE

THEORY

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."