Minamata Bay

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). ... 

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. 

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. 

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... 

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

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].)...

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). 

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,... 

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. 

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. 

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. 

Inorganic mercury compounds were discharged into the sea at Minamata Bay in Japan, from where they were taken up by bacteria and converted into methylmercury compounds. These bacteria entered the food chain to be taken up eventually by fish. Since fish are an important source of food in Japan, in a very short time many people died and many more were permanently affected by mercury poisoning. 

The Minamata Bay disaster in 1953 (see Smith and Smith [9]) triggered an enormous amount of work, internationally, on techniques for determining mercury levels. Mercury occurs naturally in the environment in the form of mineral deposits and also anthropogenically from industrial and agricultural wastes. 

A strange disease was reported in the area around Minamata Bay in Japan. Forty-six people died and many more became ill. The illness was due to mercury poisoning from a plastics factory. The Chisso Corporation used mercury as a catalyst in making acetaldehyde. Dimethylmercury becomes concentrated up the food chain and the heavy reliance on food from the sea life in the bay caused the epidemic. Mercury became a source of worry in many U.S. rivers and has been monitored closely since then. Chisso was finally found guilty in 1973, and 300 people had died by 1980. 

In the late 1950s the subtle and serious consequences of methyl mercury exposure became evident in Minamata, Japan. Initially, early signs of uncoordinated movement and numbness around the lips and extremities, followed by constriction in visual fields in fishermen and their families, baffled health experts. Developmental effects were clearly evident in infants who exhibited subtle to severe disabilities. This spectrum of adverse effects was finally related to methyl mercury exposure from consumption of contaminated fish. Minamata Bay was contaminated with mercury and methyl mercury from a factory manufacturing the chemical acetaldehyde. Mercury was used in the manufacturing process, which also resulted in both mercury and methyl mercury being discharged into Minamata Bay. The fish in the bay accu-... 

The first positive step is the remedial action of cleaning up the environment that has already been damaged by the release of chemicals. This includes the restorations following the disastrous accidents of mercury in Minamata Bay, the Flixborough explosion of a vapor cloud, the Bhopal leaking of methyl isocyanate, and the Valdez oil tanker spill. 

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