In 1956. cats in the Minamata bay walked around in circles, had convulsions , stumbled around, and seemed to commit suicide by jumping into the Minamata bay of Japan. This finding gave an early break in a series of patients with peculiar clinical features. What both the cats and the people had in common was that both ate the local fish. In 1956, a 5 year old girl developed what looked like encephalitis. 8 days later, her sister also developed similar illness. Altogether 54 patients were found to be suffering from Minmata disease. There were many similarities among these patients. Each one had eaten either fish or shell fish. Nearly all lived along the Minamata bay and were occupied in the fishing industry. Epidemiologists suspected the local fish as the cause but could not say why. To prove their theory, they brought cats from 100 miles away and fed them with the local fish. Same disease followed almost conclusively proving that eating the local fish was the cause.
To understand "why" we have to go back in time . In 1906, a small factory was established in Minamata by the Chisso corporation - a carbide plant for the production of Acetylene. Fertilizer production was also added in 1920. In 1951, the plant began manufacturing acetaldehyde for the used in plastics which involved mercury oxide as the catalyst. Inorganic mercury used was methylated in an acetylene reaction tank forming methyl mercury which was highly toxic. This had to be recycled. As the recycling was expensive, the company started to dump the waste directly into the bay. Locals and the fishermen complained. The silence of the fishermen's onion was bought by paying the fisherman's union to keep quiet. More than 100 tonnes of mercury was deposited in the bay contaminating the water and the marine life within. Only in 1940, mercury as the toxin was seriously considered after a similar poisoning from a seed company in Britain.
The epidemiological research proved that the disease is not infectious or contagious. They said that dumping of the mercury waste was the cause and asked for a ban on fishing. Due to inaction, none of the recommendations were followed and many more persons also became ill. In 1968, another similar outbreak was seen in another town of Japan - Niigata due to water contamination at Agano River. . The public became proactive and saw to it that the Chisso company halted the manufacture of acetaldehyde.
Minamata disease had 2 major victims - the patients who consumed contaminated fish usually in large quantities and their offspring. Clinical features included ataxia, incoordination, Paresthesias, constriction of visual fields, tremors, dysarthria. Autopsy revealed neuronal damage involving the cerebral cortex and the cerebellum. A variety of Congenital Minamata disease was seen with cerebral palsy like features at birth due to intrauterine exposure to toxic mercury. Mental retardation, limb defects, cerebellar ataxia, dysarthria, chorea microcephaly, hypersalivation were seen. The features developed 6 months after the birth reflecting the sensitivity of the developing nervous system. to the industrial toxins.
This episode taught us an expensive lesson - there are no shortcuts to waste disposal. Buying silence does not stop the effects of industrial pollution. This reflects the collective greed of the manufacturers, trade unionists and the society. More than 2 billion were paid as compensation which negated all the concealed illegal savings!
To understand "why" we have to go back in time . In 1906, a small factory was established in Minamata by the Chisso corporation - a carbide plant for the production of Acetylene. Fertilizer production was also added in 1920. In 1951, the plant began manufacturing acetaldehyde for the used in plastics which involved mercury oxide as the catalyst. Inorganic mercury used was methylated in an acetylene reaction tank forming methyl mercury which was highly toxic. This had to be recycled. As the recycling was expensive, the company started to dump the waste directly into the bay. Locals and the fishermen complained. The silence of the fishermen's onion was bought by paying the fisherman's union to keep quiet. More than 100 tonnes of mercury was deposited in the bay contaminating the water and the marine life within. Only in 1940, mercury as the toxin was seriously considered after a similar poisoning from a seed company in Britain.
The epidemiological research proved that the disease is not infectious or contagious. They said that dumping of the mercury waste was the cause and asked for a ban on fishing. Due to inaction, none of the recommendations were followed and many more persons also became ill. In 1968, another similar outbreak was seen in another town of Japan - Niigata due to water contamination at Agano River. . The public became proactive and saw to it that the Chisso company halted the manufacture of acetaldehyde.
Minamata disease had 2 major victims - the patients who consumed contaminated fish usually in large quantities and their offspring. Clinical features included ataxia, incoordination, Paresthesias, constriction of visual fields, tremors, dysarthria. Autopsy revealed neuronal damage involving the cerebral cortex and the cerebellum. A variety of Congenital Minamata disease was seen with cerebral palsy like features at birth due to intrauterine exposure to toxic mercury. Mental retardation, limb defects, cerebellar ataxia, dysarthria, chorea microcephaly, hypersalivation were seen. The features developed 6 months after the birth reflecting the sensitivity of the developing nervous system. to the industrial toxins.
This episode taught us an expensive lesson - there are no shortcuts to waste disposal. Buying silence does not stop the effects of industrial pollution. This reflects the collective greed of the manufacturers, trade unionists and the society. More than 2 billion were paid as compensation which negated all the concealed illegal savings!
Strict regulation is required so that industry disposes of its waste in the correct manner without causing harm to the environment.
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