MINAMATA DISEASE

Minamata, Japan

May 1, 2006 is the 50 year anniversary of the identification of "Minimata Disease" and its relationship to the ingestion of mercury.

Minamata is a small village located on the Western coast of Kyushu, Japan's southernmost island. The town faces the Shiranui Sea, of which Minamata Bay is a part. Close to Minamata and located on an estuary that flows into Minamata Bay is a petrochemical facility owned and operated since 1907 by the Chisso Corporation. In Japanese, "Chisso" means nitrogen. The Chisso Corporation had been primarily a fertilizer manufacturer but, in 1932, began to manufacture acetaldehyde, used to produce plastics. The process for acetaldehyde manufacture used a mercury catalyst and mercury was a component of the waste stream derived from the process.

After World War II, Chisso Corporation's became essentially the world's only manufacturer of a primary chemical called D.O.P. (diotyl phthalate), a plasticizer and a derivative of acetaldehyde. Chisso expanded rapidly and since Chisso was the main industry close to Minamata, the town's growth period from 1952 to 1960 paralleled Chisso's advancement. But with the expansion of the local petrochemical industry came a price. From 1932 to 1968, the Chisso plant dumped an estimated 25 to 30 tons of mercury compounds into Minamata Bay.

Minamata residents relied on fish and shellfish from Minamata bay as their main source of protein. The mercury waste in the bay entered the food chain and thousands of people whose normal diet included fish developed symptoms of mercury poisoning. The effects of methylmercury ingestion were not well studied at the time and the relationship of the symptoms to diet was not immediately established. The illness became known as the "Minamata Disease", which is now understood to be related to a degeneration of the nervous system caused by ingestion of methylmercury. Symptoms included numbness in limbs and lips, followed by slurred speech, and constricted vision. Some people developed serious brain damage and lapsed into unconsciousness or suffered from involuntary movements. Some victims developed acute dementia and shouted uncontrollably. Children born to mothers that ate fish were deformed and mentally impaired. People also thought the local house cats were going insane as well when they witnessed so called "cat suicides" in which cats seemingly jumped into the ocean and drowned. Ironically, the cat behavior eventually allowed the connection to be made between fish consumption and the disease.

Dr. Hajime Hosokawa, a physician at the Chisso Corporation Hospital, reported in 1956 that the disease affected the central nervous system but the exact cause remained unexplained. Dr. Hosokawa finally linked the fish diet to the disease based on experiments with cats. The connection to waste from the Chisso plant followed, but not immediately. The Chisso Corporation denied accusations of responsibility and maintained their waste discharge practice. Chisso installed equipment designed to control the emissions but the measures were not completely effective. Chisso began to offer `mimai' (consolation payments) to the patients in an effort to resolve the issue.

In 1958, Chisso Corporation moved their waste discharge from Minamata Bay to the Minamata River hoping to diminish the controversy and accusations toward the company. The Minamata River flows past the town Hachimon, and into the Shiranui Sea. The people of this area also began developing the "disease" after a few months. The Kumamoto Prefecture government responded by imposing a ban which allowed fisherman to "catch" fish, but not to "sell" fish from the bay. Since fish were still the main food source, people continued to eat fish at home, but the ban served to release government officials from any responsibility for those who developed the illness. In July 1959, researchers from Kumamoto University finally concluded that methylmercury was the cause of the "Minamata Disease" and that the ultimate source was Chisso. Chisso finally stopped production of acetaldehyde in 1968--when an alternative technology for producing plastics was developed.

On March 20, 1973, Japan's Kumamoto District Court ruled:

"It must be said that a chemical plant, in discharging the waste water out of the plant, incurs an obligation to be highly diligent; to confirm safety through researches and studies regarding the presence of dangerous substances mixed in the waste water as well as their possible effects upon the animal, the plan, and the human body, always availing itself of the highest skill and knowledge; to provide necessary and maximum preventive measures such as immediate suspension of operation if a case should arise where there be some doubts as to safety... in the final analysis...no plant can be permitted to infringe on and run at the sacrifice of the lives and health of the regional residents."

Of Interest to Chemists

Mercury, in many of its chemical forms, can be methylated in sediments by bacteria. Sediment methylation of mercury has been studied extensively. The amount of methylmercury in the fish in Minamata Bay, the toxic agent that caused Minamata Disease, was many times higher than could be accounted for by methylation of mercury in sediment by bacteria. It is now well established that the source of the methylmercury responsible for the Minamata outbreak was a mercuric sulfate catalyst used by Chisso (and others) in the manufacture of acetaldehyde between 1932 and 1968. But how was methylmercury formed in the process? That methylmercury was a major component in the Chisso waste stream and the ingested poison was confirmed by cat feeding experiments using the actual waste from the process (In the experiments, cats were fed methylmercury from the actual waste from the plant, not from fish exposed to the waste). However, the production of methylmercury in the acetaldehyde process itself has never been adequately explained in industrial chemistry.

The important and only recently answered questions are:

* Why did Minamata disease start suddenly and abruptly in 1953 after 20 years of "safe" operation of the acetaldehyde process? The waste from the Chisso process into Minamata Bay had initiated in 1932 and continued to 1968.


* Why was it only Chisso that caused Minamata disease while 7 factories in Japan and 20 factories in the world were producing acetaldehyde utilizing the same process as Chisso's and discharging waste streams into fished water bodies.

Recently Nishimura reported that large amounts of methylmercury compounds were generated in the Chisso Minamata Plant due to a change in a procedural step in the process. The process to make acetaldehyde (CH3CHO) involved contacting acetylene (HCCH) and water in sulfuric acid containing mercuric sulfate at 50 - 100 C. In August 1951, ferric sulfide was substituted for manganese dioxide, which had been used as a promoter for maintaining the activity of mercuric sulfate catalyst. The ferric sulfide allowed a side reaction to occur in which methylmercury was formed. The methylmercury concentrated in the waste stream from the process.

References

Nishimura H (1998). The resolution of the questions of occurrences in Minamata disease. Gendai Kagakku (Chemistry Today) No. 323, 60-66, No. 324, 14-22 (in Japanese).

Nishimura H. and Okamoto T. (2001). Minamata-Byo no Kagaku (The Science of Minamata Disease). Nihon Hyoronsha Co. LTD., Tokyo (in Japanese).

Smith, Eugene. Minamata. New York: Holt, Rinehart, and Winston, 1975.

Ishimure, Michiko. 1990. Paradise in the Sea of Sorrow. English translation by Livet Monnet. Yamaguchi Publishing House (c/o Japan Publications Trading Co., Ltd., Tokyo).