Minamata Bay Mercury Poisoning Begins to Claim Victims

Date April, 1956

Minamata Bay became a worldwide symbol of industrial pollution when mercury dumped into the bay poisoned the aquatic food chain, killing or debilitating many of the area’s residents.

Also known as Minamata Disease

Locale Minamata Bay, Kyūshū, Japan

Key Figures

• Hajime Hosokawa (1901-1970), Japanese head of Chisso’s Minamata factory hospital
• Tadao Takeuchi (b. 1915), Japanese researcher at Kumamoto University
• Makio Uchida (fl. mid-twentieth century), Japanese researcher at Kumamoto University

Summary of Event

Minamata Bay is a part of the Shiranui Sea, which forms the western boundary of Japan’s southernmost island, Kyūshū. The area is characterized by clusters of homes organized into small villages that are in proximity to the downtown center of Minamata. Throughout its history, this region has been predominantly an agricultural and fishing area. To stimulate the local economy, the Chisso Corporation, a carbide and fertilizer company, was encouraged to build a factory in Minamata in 1907. In 1932, the Chisso Corporation expanded into petrochemicals and began the production of acetaldehyde, a material used for making plastics, at the Minamata factory. By 1950, acetaldehyde production had increased dramatically.

In the early 1950’s, dead fish and seaweed were seen floating on the surface of the bay, while shellfish populations declined. Birds were observed flying in bizarre patterns, while cats developed a disorder known as the “dancing disease,” characterized by a staggering gait and spinning in circles. The mortality rate was so great that by 1957 many areas of Minamata were devoid of cats.

In April, 1956, the first known human victim of an ailment subsequently named “Minamata Disease,” a five-year-old girl, was admitted to the Chisso factory hospital. She exhibited brain damage symptoms, such as disjointed speech, an inability to walk, and delirium. Within a few weeks, this child’s younger sister and three members of a neighbor family developed similar symptoms. On May 1, 1956, Dr. Hajime Hosokawa, head of the Chisso hospital, officially reported the outbreak to the Public Health Department. Although symptoms indicated that the ailment was a disorder of the central nervous system, its cause and identity eluded health officials, who feared a contagious epidemic. Upon investigation, thirty additional cases of the disease were identified, and it became apparent that many of the victims had shown symptoms of illness as early as 1953. Most of those afflicted were residents of Minamata’s fishing villages whose diets were rich in fish and shellfish. The similarities between the symptoms of Minamata Disease and the dancing disease of the cats were noted.

A Minamata Disease Research Group—formed at the Kumamoto University Medical School in August, 1956, to study the disease—reported on October 4, 1956, that the ailment was not an infectious disease but rather some form of heavy-metal poisoning caused by eating marine products from Minamata Bay. Chisso, being the only major industry in the area, was suspected as the source of the contamination. Although a number of metals including manganese, thallium, and selenium which were present in the tissue of the victims were also found in the plant’s wastewater, none of these toxins experimentally produced the symptoms of dancing disease in cats.

When Chisso briefly moved its effluent dumping site from the bay to the Minamata River delta across town in 1958, residents living in this area began to develop symptoms of Minamata Disease. This was another indicator of Chisso’s culpability. Although the state government imposed a ban on the selling of fish from the bay in 1958, catching and consuming the fish was not prohibited, and the number of victims continued to increase.

In September, 1958, Professor Tadao Takeuchi of Kumamoto University recognized the similarities between Minamata Disease and a case of mercury poisoning that had affected workers at an English methyl mercury production factory in 1940. Ingestion of methyl mercury by cats produced the same symptoms as eating the fish of Minamata Bay. In a 1959 environmental survey, extraordinarily high concentrations of mercury were found in the bay. Concentrations were highest near Chisso’s drainage channels and decreased with distance. High mercury concentrations were found in the tissues of the bay’s fish, and cats who were fed this fish accumulated more than one hundred times the amount of mercury in their tissues as cats not eating the fish. Autopsies of victims showed high concentrations of mercury in their brains, which provided evidence for a methyl mercury toxin, since inorganic mercury does not readily cross the blood-brain barrier. In September, 1960, Makio Uchida of Kumamoto University successfully extracted a methyl mercury compound from shellfish of Minamata Bay, proving mercury to be the causal agent of Minamata Disease.

Chisso insisted that, since the acetaldehyde production process utilized an inorganic mercury catalyst rather than methyl mercury, it was not the contamination source and refused to allow any further sampling of factory wastes. In October, 1959, members of the Fisherman’s Union, concerned about the loss of their livelihood, insisted that Chisso clean up the bay and pay indemnities. Aided by government intimidation, Chisso coerced the fishermen into settling for a meager indemnity and no promise of a cleanup. For public relations, a “cyclator” was installed to treat the wastewater. This device did little to diminish the mercury contamination and was often bypassed in the waste disposal process. In 1962, methyl mercury chloride was found in a sample of sludge produced by the factory’s acetaldehyde process, proving that methylation of the inorganic mercury catalyst occurred during the acetaldehyde production process.

By the end of 1962, 121 cases of Minamata Disease had been officially verified and 46 deaths had occurred. A high incidence of a congenital neurological ailment also occurred among children born in the Minamata area. At first, these infants who had not eaten any marine products from the bay were diagnosed as having cerebral palsy. A statistical examination showed that if the affliction was indeed cerebral palsy, its rate was 5.9 percent of all regional births as compared to a national rate of 0.2 to 0.3 percent. Research showed that methyl mercury had passed through the placenta from mother to fetus, resulting in methyl mercury poisoning. This ailment was formally diagnosed as congenital (fetal) Minamata Disease in 1962. More than forty cases of the congenital disease had been reported by 1974.

Significance

Global industrialization has been accompanied by environmental pollution. The industrialization of Japan began around 1868 and peaked in the aftermath of World War II. The first well-documented case of industrial pollution occurred in 1878, when copper and arsenic runoff from the Ashio Copper Mine contaminated the Watarase River. Since the copper produced was largely exported to Europe, this mining operation was an important source of foreign currency that helped fuel Japan’s modernization. The government considered this operation to be of strategic national importance and, thus, afforded it special privileges, allowing the environmental effects of the Ashio Mine to persist into the post-World War II era.

The period following World War II was one of rapid industrial and economic growth for Japan, with emphasis on strengthening the national economy regardless of the expense to regional economies. Villages dependent on the traditional primary industries of agriculture and fishing were particularly affected. Rapid industrial growth coupled with governmental indifference resulted in four major pollution disasters, of which Minamata Bay was the first and most notorious. These incidents gravely injured a multitude of Japanese citizens and ravaged the environment.

Concern with environmental issues has passed through a number of stages in Japan. First, widespread public ignorance of environmental problems was coupled with an apathetic government reluctant to interfere with the rapid economic growth of the postwar period. Minamata Disease appeared in 1956, the cause was discovered in 1960, and the source was proven in 1962, but the government did not officially place responsibility on Chisso until 1968. The dumping of the pollutant did not cease until 1968, when the acetaldehyde factory became technologically obsolete and was closed for economic reasons.

The Minamata Bay disaster had little immediate effect on alleviating industrial pollution. In May, 1965, another incidence of methyl mercury poisoning occurred in Niigata Prefecture. The source of the mercury, which accumulated in freshwater fish, was an upstream acetaldehyde factory. The Niigata victims referred to their ailment as Niigata-Minamata Disease rather than by the generic name methyl mercury poisoning, to remind the Japanese people of the needless horror of Minamata and to make the point that this outbreak was not a local problem, but rather an industrial pollution problem that could happen anywhere. At the time of the Niigata incident, Japan had a total of fourteen acetaldehyde plants utilizing mercury, and even this second health disaster did not motivate the government to ban the dumping of toxic industrial effluents into environmental waters. As a result, two additional water pollution disasters involving the dumping of toxic metal wastes occurred in 1968 and 1972.

The Japanese government was not the only government guilty of ignoring industrial pollution for economic gain. In 1970, methyl mercury contamination was found in the English-Wabigoon River of Canada. The river’s fish were found to contain about thirty times the mercury level deemed acceptable at that time. Although the source of the contamination was found to be the Dryden Paper Company’s chloralkali plant, prosecution was not forthcoming because news of contamination would adversely affect the area’s lucrative tourist-based fishing economy.

Finally, in the 1970’s, environmental mercury pollution gained recognition as a global problem. Mercury contamination was found in fish, bird, and human populations in a number of areas throughout the world. Japanese, Swedish, British, and American researchers began to study the behavior of inorganic mercury in natural ecosystems to discover its mode of conversion into the extremely toxic methyl mercury. It was found that microorganisms present in soils and underwater sediments can convert inorganic mercury to methyl mercury. This research indicated the potential environmental devastation that could result from seemingly innocuous wastes. Minute quantities of toxins appeared to enter and become magnified as they passed through the food chain, becoming poisons for humans. Such knowledge made it impossible for governments to continue to ignore the issue of industrial pollution.

In 1951, the Japanese government had rejected recommendations that a water-pollution control law be enacted, fearing that such a law might hinder economic growth. Thus, no legislation was available to aid victims suffering from environmentally caused disorders, and victims had to form groups to bring lawsuits against the polluting companies. Although Japanese law held negligence liable, each victim had to prove not only a causal relationship between the pollution activities and the disease contracted, but also that company negligence was intentional.

Although Chisso had maintained its innocence, insisting that there was no direct scientific proof that Minamata Disease was caused by the factory, in reality, the company had concealed knowledge of its responsibility since October, 1959, when Dr. Hosokawa found that cats developed symptoms of the disease when fed the factory’s acetaldehyde sludge. After this discovery, Chisso’s management quickly began negotiations with the victims, agreeing to payments called mimai (consolation for misfortune, not indemnity), through which the company accepted no responsibility for the victims’ misfortune. In fact, a clause in the contract absolved Chisso from further compensation even if the company was proven guilty at a later date. Only after years of protest and legal action by the victims and their families was Chisso found legally responsible for the pollution. The court ordered Chisso to pay compensation and to clean up the bay.

The aftermath of Minamata Bay was the 1959 enactment of the Water QualityConservation Law , a law meant more for public relations than for environmental protection, since it established effluent standards while providing no penal provisions. Only when environmental pollution became a social and political issue threatening the dominance of the leading political party did the government begin to take meaningful action. In 1967, the Basic Law for Environmental Pollution Control was enacted. The intent of the basic law was the preservation of nature as it contributes to the maintenance of human health and the living environment. In 1970, the Water Pollution Control Law finally provided penalties for effluent standard violators and eliminated the practice of designating bodies of water for pollution control only after they had become seriously contaminated. Finally, in 1974, the Pollution-Related Health Compensation Law was passed, aiding victims of pollution-induced disorders.

Although Japan, like other industrial countries, was slow to employ measures safeguarding the environment from industrial pollution, it became a global leader in pollution curtailment. Ironically, while the pollution of Minamata Bay persisted for such a long period of time because of the desire to pursue economic growth, economic growth became a driving force in Japan’s development of the world’s most advanced pollution control devices. The Japanese came to view global environmental concerns as both a challenge and an opportunity to sell their environmentally sound technologies to the rest of the world.

Bibliography

George, Timothy S. Minamata: Pollution and the Struggle for Democracy in Postwar Japan. Cambridge, Mass.: Harvard University Press, 2001. Study of the long-term grassroots campaign to compensate the victims of Minamata Disease and its relationship to the development of Japanese democracy in the decades after World War II. Bibliographic references and index.

Gross, Neil. “The Green Giant? It May Be Japan.” BusinessWeek (February 24, 1992): 74-75. This article describes some of the pollution control technology devised by Japanese companies.

Ishimure, Michiko. Paradise in the Sea of Sorrow: Our Minamata Disease. Translated by Livia Monnet. Kyoto, Japan: Yamaguchi Publishing House, 1990. A passionate account of the first fifteen years of the disease. Includes victim accounts and excerpts from clinical and government reports.

Nriagu, James O., ed. Aquatic Chemistry. New York: John Wiley & Sons, 1983. This work has several chapters that discuss the fate of mercury in aqueous environments, including how it accumulates in the food chain. Technical.

Schroeder, Henry A. “Mercury as a Cause of National Paranoia.” In The Poisons Around Us. Bloomington: Indiana University Press, 1974. This chapter discusses the element mercury and its toxicity and effect on human health. Written for a general audience.

Smith, W. Eugene, and Aileen M. Smith. Minamata. New York: Holt, Rinehart and Winston, 1975. Describes outbreak of Minamata Disease and its legacy for the citizens of the Minamata area.