Aquatic mercury pollution : studies of its occurrence and pathologic effects on fish and mink
Date
1973
Authors
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Journal ISSN
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Publisher
ORCID
Type
Degree Level
Doctoral
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.
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Citation
Degree
Doctor of Philosophy (Ph.D.)
Department
Veterinary Pathology
Program
Veterinary Pathology