Mercury contamination Minamata disease

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. 

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... 

The Japanese diet contains a lot of fish, and the local fishermen and their families would eat more fish than most. The fishermen were catching fish and seafood in the waters of Minamata Bay, waters which proved to be heavily contaminated with methyl mercury. In 1956 the first case of what became known as Minamata disease was reported and then other people started to present themselves to doctors and at hospitals with various symptoms such as muscular incoordination and difficulties in speech. Their pet cats, which were also eating the fish, suffered similar symptoms. 

Dr Hosokawa, director of the Minamata City hospital was conducting his own experiments based on the theory from the university He fed cats waste effluent from the factory that was producing acetaldehyde and was able to produce similar symptoms in them, and he detected other changes by pathological examination at autopsy The company that owned the factory, the Chisso Minamata Chemical Company, was aware of his work and by 1959 knew that it was likely that Minamata disease was caused by the effluent from their factory In i960 methyl mercury was detected in seafood and in 1961 it was detected in sediments derived from the factory. In 1966 the factory installed a water circulation system which removed the mercury pollution. The factory eventually stopped the process in 1968 and in the same year the Japanese government announced its opinion that the disease was due to consumption of methyl mercury in contaminated fish and seafood. 

Harada, M. (1982). Minamata disease organic mercury poisoning caused by ingestion of contaminated fish. In Adverse Effects of Food, Jellife, E.F. and Jellife, D.B. (eds), pp. 135— 148. Plenum Press, New York. 

All forms of mercury are considered to be poisonous. However, it is methylmer-cury (or as the chloride, C HgCl) which is considered to be the most toxic because of its ability to bioaccumulate in fish. The best example of the toxicity of methylmercury occurred in Minamata in Japan in 1955. It was found that methylmercury-contaminated fish consumed by pregnant women resulted in the new-born children having severe brain damage (Minamata disease). As a consequence of these initial findings, methylmercury is routinely monitored for in fish. 

Minamata disease was first discovered in 1956 around Minamata Bay, Japan. A similar epidemic occurred in 1965 along the Agano river, Japan. Minamata disease is methyl mercury poisoning that occurred in humans who ingested fish contaminated with methylmercury discharged in waste water from a chemical plant. Methylmercury is also teratogenic (Ui 1992, Harada 1995, Eto 1997, Schardein 2000 see also Part III, Chapter 17). 

The so-called Minamata disease" is a form of poisoning that developed in the coastal area of Minamata Bay, Japan, in 1956. Industrial waste waters, contaminated primarily with inorganic mercury salts, caused this mass catastrophe. In the water, the mercury was methylated by bacteria to... 

Minamata Disease is defined as neuropathy arising from intake of fish and shellfish containing high concentrations of methylmer-cury. The outbreak is dependent on factors that include mercury concentrations in water, bioconcentration and biomagnification of mercuric compounds by aquatic plants and animals, and continuous daily intake of mercury-contaminated fish in large quantities. Minamata Disease patients have neurological symptoms that include paresthesia, visual field... 

In 1984, tbe clearance rate for mercury in Minamata Bay sediments was estimated at 18.2 years, with 90% clearance via natural processes estimated by the year 2000. This natural cleanup rate was judged unacceptably low and in 1984 dredging was initiated to remove aU sediments containing more than 25.0 mg total mercury/kg. By 1987, 1.5 million m of contaminated sediments had been removed from 2.09 km of Bay areas and used as landfill at an isolated 58-ha site. This site, with an estimated 7.5 tons of mercury, is now the site of Minamata Disease Park, replete with playing fields and a museuna. The landhll was capped with a layer of vinyl plastic sheet, then by volcanic ash, and topped with soil. The mercury at the site will be exposed to physical and microbial activities and subsequently volatilized to... 

Mathews T, Fisher NS (2008) Evaluating the trophic transfer of cadmium, polonium, and methyl-mercury in an estuarine food chain. Environ Toxicol Chem 27 1093-1101 McAlpine D, Araki S (1959) Minamata disease late effects of an unusual neurological disorder caused by contaminated fish. AM A Arch Neurol 1 522-530 McGeer J, Brix KV, Skeaff JM, Deforest DK, Brigham SI, Adams WJ, Green AS (2003) The inverse relationship between bioconcentration factor and exposiure concentration for metals implications for hazard assessment of metals in the aquatic environment. Environ Toxicol Chem 22 1017-1037... 

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