Aquatic mercury pollution : studies of its occurrence and pathologic effects on fish and mink

Abstract

Mercury pollution of water has been documented in Japan and in several Scandinavian countries. No information was available on the status of North American waters with regard to mercury pollution at the time this work was begun.

Muscle tissue from 81 fish from nine locations in the Saskatchewan River contained an average of more than 1.0 ppm of mercury. Fish from two of the sites had much higher concentrations, with individual fish containing up to 11.2 ppm of mercury. These concentrations correspond to values reported for Scandinavian fish collected in areas of industrial pollution.

The acute toxicity of methyl mercury chloride ( MeHgC1 ) for rainbow trout ( Salmo gairdneri) fry and fingerlings was measured. The median tolerance limit ( TLm ) at 24, 48 and 96 hr was 0.084, 0.045 and 0.024 mg/litre as mercury respectively for fry; and 0.125, 0.066 and 0.042 mg/litre as mercury respectively for fingerlings. The TLm (24 hr) for mercuric chloride ( HgC12) for fingerlings was 0.90 mg/litre as mercury. Fingerlings exposed to MeHgC1 concentrated mercury in their tissues much more rapidly than did those exposed to HgC12. The acute toxic action of MeHgCl and HgC12 was exerted on the gills. Mercuric chloride caused severe epithelial necrosis. Poisoning with MeHgCl was characterized by epithelial cell swelling and hyperplasia, a marked increase in the number of epithelial cells in mitosis and terminally, epithelial desquamation.

Rainbow trout fingerlings were fed rations containing 4, 8, 16 and 24 ppm mercury as MeHgCl over a 105 day period. Fish receiving the 16 and 24 ppm rations had significantly higher blood packed cell volumes than controls. Hyperplasia of the gill epithelium was the only morphologic alteration in these fish. Individual fish accumulated up to 30 ppm mercury in muscle, but no mortality which could be attributed to mercury poisoning occurred. The results suggest that trout can tolerate a large body burden of mercury, if this mercury is acquired over a period of time.

Female and juvenile mink ( Mustela vison ) were fed rations containing 50 and 75 per cent of fish containing 0.44 ppm mercury over a 145 day period. There was no evidence of intoxication in these animals. Mercury concentrations in tissue appeared to have reached equilibrium at a level below that associated with toxicity.

Adult mink were fed rations containing 1.1, 1.8, 4.8, 8.3 and 15.0 ppm mercury as MeHgCl over a 93 day period. Histologic evidence of injury was present in all groups. Mink fed rations containing 1.8 to 15.0 ppm mercury developed clinical intoxication within the experimental period. The rapidity of onset of intoxication was directly related to the mercury content of the ration. Mercury concentrations in tissues of mink which died were similar, despite differences in the mercury content of the diets and time to death. The average mercury concentration in the brain of mink which died was 11.9 ppm. The disease produced by MeHgCl was primarily related to neuronal necrosis. Cortical neurons and those in certain subcortical nuclei were most susceptible. In acute intoxication neuronal damage was diffuse throughout the brain. Involvement of granular cells of the cerebellum and peripheral nerve fibres was seen in acutely poisoned animals.