Minamata disease and

Miyakawa T, Murayama E, Sumiyoshi S, et al. 1976. Late changes in human sural nerves in Minamata disease and in nerves of rats with experimental organic mercury poisoning. Acta Neuropath (Berlin) 35 131-138. 

Takizawa Y (2000) Unterstandig minamata disease and strategies to prevent further environmental contamination by methylmercurry. Wat Sci Technol 42, 139-146. 

Mean mercury concentrations in organs of Minamata Disease victims dying between 1973 and 1985 remained elevated over those of residents not afflicted with Minamata Disease and dying between 1973 and 1991. Minamata Disease victims always had mean total mercury (methylmercury) concentrations, in mg/kg FW, >1.51 (().05) in kidney, >0.48 (0.035) in liver, >0.10 (0.016) in brain cerebmm, and 0.05 (0.026) in brain cerebellum. 

By 1989, about 2000 individuals in the Minamata area have been officially certified to have Minamata Disease and eligible for financial compensation. Histopathologi-cal changes in brain were clearly linked to organomercury insult in Minamata Disease victims and the distribution of lesions in the nervous system was characteristic, especially in the cerebral cortices and the cerebellum. Pathological studies of 112 Minamata Disease victims also showed elevated frequencies of sepsis and malignant neoplasms of the thyroid gland when compared to 112 sex-age matched pair control deaths between 1970 and 1983 from various causes (senile dementia of Alzheimer s type, Parkinson s disease of idiopathic type, amyotrophic lateral sclerosis) in western parts of Japan. 

In 1993, more than 2000 patients have been officially designated with Minamata Disease, and 59 had congenital Minamata Disease in Kumamoto Prefecture. Pathological findings of fetal Minamata Disease indicated that... 

It has been stated [11] that about 400 tonnes of mercury lie at the bottom of Minamata Bay near the point of discharge of mercury wastes and although further dumping was finally stopped in 1968, this cannot prevent the future possibility of conversion of inorganic to methyl mercury and its accumulation in fish. By 1973, sixty-five people had died from Minamata disease and many more had been crippled, blinded or otherwise affected. It is now known from experimental work with rabbits, that alkyl mercury can readily pass through the placental barrier in mammals [60] (p. 84) and this is borne out by the fact that a number of children were bom with symptoms of methyl mercury toxicity to women at Minamata who were not evidently themselves affected. 

Fujiki, M. 1963. Studies on the course that the causative agent of Minamata disease was formed, especially on the accumulation of the mercury compound in the fish and shellfish of Minamata Bay. Jour. Kumamoto Med. Soc. 37 494-521. 

Fujiki, N. 1980. The pollution of Minamata Bay by mercury and Minamata disease. Pages 493-500 in R.A. Baker (ed.). Contaminants and Sediments, Vol. 2. Ann Arbor Science Publ., Ann Arbor, MI. 

Irukayama, K. 1967. The pollution of Minamata Bay and Minamata disease. Pages 153-180 in J.P. Maroto and F. Josa (eds.). Advances in Water Pollution Research, Vol. 3. Proc. Third Int. Conf., Munich. 

Most cases of mercury poisoning led to handicap, chronic disease, or death. The most frequent symptoms include numbness of limbs, lips and tongue, speech abnormalities, limb function disorders, visual acuity disorders, deafness, and muscular atrophy. Insomnia, hyperactivity, and coma have also been reported. Methylmercury penetrates the blood-brain barrier and causes central nervous system injuries. Mercury also has a teratogenic effect, leading to congenital abnormalities or congenital Minamata disease. 

Harada, M. and (1995). Minamata disease Methylmercury poisoning in Japan caused by environmental pollution, Crit. Rev. Toxicol., 25, 1-25. 

An epidemic of intoxication from ingestion of fish contaminated with methyl mercury occurred in the Minamata district in Japan, and, as a result, methyl mercury intoxication is often referred to as Minamata disease." Infants born to mothers with exposure to large amounts of methyl mercury had microen-cephaly, mental retardation, and cerebral palsy with convulsions. In an incidence in Iraq, ingestion of wheat products contaminated with methyl mercury fungicide by pregnant women caused similar symptoms of neurological damage and mental retardation. The fetus is... 

Mercury. In Japan in the 1950s and 1060s, wastes from a chemical and plastics plant containing mercury were discharged into Minamata Bay. The mercury was converted to the readily absorbed methylmercury by bacteria in the aquatic sediments. Consumption of fish and shellfish by the local population resulted in numerous cases of mercury poisoning, or Minamata disease. By 1970, at least... 

A common example of neurobehavioral teratogenic effects caused by polluted food is the Minamata disease. In a number of areas in Japan methylmercury from industrial waste accumulated in fish which was one of the main sources of the food of the local population. Another case of poisoning with methylmercury occurred in Iraq, where people consumed grain seed treated with a methylmercury fungicide. Women with only minimal poisoning symptoms gave birth to children that showed many neurological and behavioral abnormalities, such as mental retardation, coordination deficits and seizures (refs. 12, 13). 

Between 1956 and 1960 severe accidents related to Me-Hg, the health consequences of which were afterwards grouped under the name of Minamata disease, occurred in Japan following long-term consumption of contaminated fish and fish products. A large amount of Hg-polluted effluents (from 200 to 600 tons) reached Minamata Bay, Japan, where they accumulated not only in the bottom sediment, but also in fish and shellfish. The consumption of such foods resulted in a mass outbreak of Me-Hg poisoning [9]. 

A case of Minamata disease caused by the methyl mercury discharged by a chemical factory in Japan provides us with bitter lessons. Inappropriate treatments of toxic chemical substances for the duration of 1932 to 1968 resulted in creating and torturing more than 14,000 victims with a neurological syndrome by severe mercury poisoning. It has been fifty years since the disease was official discovered in 1956. The case is not yet fully solved and lawsuits and claims for compensations continue even to this day. 

Uchini, M., Hirano, T., Satoh, H., Nakagawa, M. and Wakamiya, J. (2005) The severity of Minamata disease declined in 25 years Temporal profile of the neurological findings analyzed by multiple logistic regression model. Tohoku J. Exp. Med. 205, 53-63. 

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