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Minamata

One of the earhest and most extensively documented cases of mercury poisoning occurred in the 1950s at Minamata Bay, in southwestern Kyushu, Japan - especially among fishermen and their famihes. Deaths and congenital birth defects in humans were attributed to long-term ingestion of marine fish and [Pg.466]

0 mg/kg FW this decreased sharply with increasing distance from the plant, and sediments in the Bay contained between 0.4 and 3.4 mg Hg/kg FW. Concentrations of mercury in fish, shellfish, and other organisms consumed by the Japanese decreased with increasing distance from the point of effluence and appeared to reflect sediment mercury levels. [Pg.467]


Methanol intoxication can cause blindness due to damage to ganglion cells in the retina. The blindness results from the accumulation of formaldehyde and formic acid, which are metabolites of methanol. Chemical compounds can also damage the visual cortex, for example, visual damage was observed among the victims of organic mercury intoxication in Japan (the fishermen of Minamata Bay). ... [Pg.293]

The Minamata disaster in Japan, when 52 people died in 1952, occurred because fish, which formed the staple diet of the small fishing community, contained abnormally high concentrations of mercury in the form of MeHgSMe. This was found to originate from a local chemical works where Hg salts were used (inefficiently) to catalyse the production of... [Pg.1226]

Kudo, A. and Miyahara, S. (1983). Migration of mercury from Minamata Bay. In Toxic Materials - Methods for Control" (N. E. Armstrong and A. Kudo, eds). The Center for Research in Water Resources, University of Texas at Austin, Austin, TX. [Pg.417]

Another major incident concerning methyl mercury was the severe pollution of Minamata bay in Japan (see Box 8.1). Here fish, fish-eating and scavenging birds, and humans feeding upon fish all died from organomercury poisoning. There may have been localized declines of marine species in this area due to methyl mercury, but there is no clear evidence of this. [Pg.171]

Methylation of both metals and metalloids has been observed for both fungi and bacteria. These metabolites may, however, be toxic to higher biota as a result of their volatility. The Minamata syndrome represents the classic example of the toxicity of forms of methylated Hg to man, even though the formation of Hg(CH3)2 was probably the result of both biotic and abiotic reactions. [Pg.173]

Harada, M., Minamata disease Methylmercury poisoning in Japan caused by environmental pollution,... [Pg.1330]

Methylmercury in the marine environment may originate from industrial discharges or be synthesised by natural methylation processes. Fish do not themselves methylate inorganic mercury [62,64], but can accumulate methyl mercury from sea water [63]. Methylmercury has been detected in sea water only from Minamata Bay, Japan, an area with a history of gross mercury pollution from industrial discharge. It has been found in some sediments but at very low concentrations, mainly from areas of known mercury pollution. It represents usually less than 1% of the total mercury in the sediment, and frequently less than 0.1% [65-67]. Microorganisms within the sediments are considered to be responsible for the methylation [65,68], and it has been suggested that methylmercury may be released by the sediments to the sea water, either in... [Pg.460]

Mercury concentrations in selected biological and nonbiological materials collected from Minamata Bay, Japan, and environs... [Pg.25]

There is a strong relationship between the food of birds from Minamata and the mercury content in feathers the content is highest in fish-eating seabirds and lowest in herbivorous waterfowl (Doi et al. 1984 Table 5.4). This same relationship held in birds collected from China and Korea,... [Pg.356]

Table 5.4 Mercury Concentrations in Selected Biological and Nonbiological Materials Collected From Minamata Bay, Japan and Environs (Concentrations are in mg Hg/kg [ppm] fresh weight [FW], or dry weight [DW].)... Table 5.4 Mercury Concentrations in Selected Biological and Nonbiological Materials Collected From Minamata Bay, Japan and Environs (Concentrations are in mg Hg/kg [ppm] fresh weight [FW], or dry weight [DW].)...
Humans, Homo sapiens, dying of Minamata disease, 1957-89, autopsy results Brain 0.1-21.3 FW 9... [Pg.358]

Tokuyama Bay, Japan, received 6.6 metric tons of mercury wastes between 1952 and 1975 in wastewater from two chloralkali plants, although sediment analysis suggests that as much as 380 tons of mercury were released (Nakanishi et al. 1989). Unlike Minamata Bay, however, there were no human sicknesses reported, and the hair of residents contained 0 to 5 mg Hg/kg FW vs. 15 to 100 mg Hg/kg FW in Minamata residents. In 1970, a maximum concentration of 3.3 mg total Hg/kg FW was reported in tissues of Squilla, a crustacean. In 1973, a health safety limit was set of 0.4 mg total Hg/kg FW in edible fish and shellfish tissues with a maximum of 0.3 mg methyl-mercury/kg FW permitted at least five species of fish had more than 0.4 mg total Hg/kg FW, and fishing was prohibited. Contaminated sediments (>15 mg total Hg/kg) were removed by dredging and reclamation between 1974 and 1977. By 1979, the mercury content of all fish, except one species, was less than 0.4 mg total Hg/kg FW fishing was prohibited. By 1983, all fish and shellfish contained less than 0.4 mg Hg/kg FW and fishing was allowed (Nakanishi et al. 1989). [Pg.358]

In aquatic environments where point sources of industrial contamination have been identified, the elimination of mercury discharges has usually improved environmental quality. Such improvement has been reported for Minamata Bay (Table 5.4) for sediments in Saguenay Fjord, Quebec,... [Pg.358]

Davies, F.C.W. 1991. Minamata disease a 1989 update on the mercury poisoning epidemic in Japan. Environ. Geochem. Health 13 35-38. [Pg.428]

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. [Pg.429]

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. [Pg.429]

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. [Pg.432]

Matida, Y. and H. Kumada. 1969. Distribution of mercury in water, bottom mud and aquatic organisms of Minamata Bay, the River Agano and other water bodies in Japan. Bull. Freshwater Fish. Res. Lab. (Tokyo) 19(2) 73-93. [Pg.435]

Nishimura, H. and M. Kumagai. 1983. Mercury pollution of fishes in Minamata Bay and surrounding water analysis of pathway of mercury. Water Air Soil Pollut. 20 401-411. [Pg.437]


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Congenital minamata disease

Disaster, Minamata

Diseases Minamata disease

Mercury Minamata, Japan

Mercury contamination Minamata disease

Methyl mercury Minamata

Minamata Bay

Minamata Bay (Japan)

Minamata City, Japan

Minamata disease

Minamata disease and

Minamata disease, mercury toxicity

Minamata incident

Minamata, Japan

Minamata, Japan methyl mercury incident

National Institute for Minamata

National Institute for Minamata Disease

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