258 EISLER 



Several years later, the mercury levels in sediments near the plant 

 outfall were about 2010 mg/kg w^et weight; this decreased sharply 

 with distance from the plant. Sediments in the bay contained 

 between 0.4 and 3.4 mg Hg/kg wet weight. Concentrations of 

 mercury in fish, shellfish, and other food decreased with increasing 

 distance from the point of effluence and appeared to reflect 

 sediment mercury levels. Late in 1953, a severe neurological disorder 

 was recognized among inhabitants of the Minamata Bay region. By 

 1956, the outbreak had reached epidemic proportions; 111 cases of 

 poisoning were found by the end of 1960; and 41 deaths were 

 reported as of August 1965. The poisoning was caused by eating fish 

 and shellfish from Minamata Bay and the neighboring sea, except for 

 19 congenital cases in children bom of mothers who had eaten the 

 same diet. In addition to humans, cats and water fowl living near the 

 bay succumbed to the disease. Experimental cats and rats fed fish 

 and shellfish collected from the bay developed the same symptoms as 

 animals spontaneously affected. Symptoms included cerebellar 

 ataxia, constriction of visual fields, dysarthria, and, in congenital 

 cases, disturbance of physical and mental development. Pathological 

 findings included regressive changes in the cerebellum and the 

 cerebral cortexes. The clinico-pathological features resembled alkyl 

 mercury poisoning. Abnormal mercury content (i.e., > 30.0 mg 

 Hg/kg wet weight) was measured in fish, shellfish, and muds from the 

 bay and in organs of necropsied humans and cats that had 

 succumbed to the disease. Years after the waste-discharge situation 

 was corrected, fish and shellfish still contained levels of mercury 

 hazardous to human health. Mercury levels in Minamata fish and 

 shellfish were significantly higher than levels shown in Table 2 for 

 teleosts and molluscs; note also that the high levels shown for 

 mammals in Table 2 are from liver. 



Potential Health Hazards 



The dangerous mercury level in human blood is about 2000 ng/g; 

 the normal background level in about 80% of people without 

 occupational exposure to mercury is < 5 ng/g (Saha, 1972). Since 

 methyl mercury has a biological half-life of 70 to 200 days in man 

 (Lofroth, 1970), it is not unexpected that mutagenic and teratogenic 

 effects of mercury have been reported at levels well below those 

 associated with acute poisoning (Kazan tzis, 1971; Keckes and 

 Miettinen, 1972). 



The findings of elevated blood mercury levels, increased human 

 chromosome breakage, and easy passage of mercury through 

 placental membranes among people who regularly eat fish containing 



