FISHERY BULLETIN: VOL. 71, NO. 3 



grain. Since 1965 the mercury levels in the 

 feathers of Swedish seed-eating birds have 

 decreased coinciding with the prohibition of 

 alkyl mercury dressings for seed (Johnels and 

 Westermark, 1969). 



It should be noted that the increase of 

 mercury in fish-eating birds in Sweden, based 

 on the examination of museum specimens and 

 those of more recent times, is at variance with 

 the situation noted earlier concerning museum 

 specimens of tunas and swordfish. This seeming 

 contradiction may be due to the fact that these 

 fish species are high-seas animals inhabiting 

 waters which are normally far removed from 

 the concentrated effects of mercury pollution 

 caused by man. Furthermore it has been calcu- 

 lated that if the total amount of mercury pro- 

 cessed by man since 1900 were put into the 

 world's oceans and well mixed, it would increase 

 the average mercury concentration of seawater 

 (approximately 0.1 part per billion) by at most 

 1% (Hammond, 1971). Other investigators 

 (Weiss et al., 1971) have calculated that even if 

 the atmospheric mercury load resulting from 

 man's activities equaled the natural degassing 

 rate (which is very unlikely) it would add an- 

 nually only 15% to the mercury burden of the 

 upper 100 m of the oceans (the mixed layer). 

 With a residence time of mercury in this layer 

 of as much as 5 yr, the mercury content would 

 be increased by a factor of only 0.75. The in- 

 creased mercury content in surface waters, if 

 transmitted through the food web to the large 

 predatory fishes such as tunas and billfishes, 

 would, at most, double the mercury content 

 in these animals. 



Under circumstances whereby large amounts 

 of mercury enter the aquatic environment, 

 freshwater and marine fishes as well as in- 

 vertebrates will accumulate large amounts of 

 organic mercury, mostly in the form of methyl- 

 mercury (Hannerz, 1968). Ingestion of sub- 

 stantial quantities of such contaminated aquatic 

 organisms may lead to toxicological symptoms 

 ranging from temporary or permanent afflic- 

 tions to death. Fortunately, it appears that the 

 contamination caused by industrial discharges 

 and agricultural use of grain treated with 

 mercury compounds, although persistent, tends 

 to become localized. 



MERCURY POISONING AND 

 ITS EFFECTS 



Methylmercury poisoning resulting from in- 

 gestion of contaminated aquatic organisms 

 became evident in 1953 when an epidemic of 

 neurological debility and deaths in people and 

 animals which had eaten fish and other seafood 

 from Minamata Bay in Japan was traced to 

 dumping of large amounts of inorganic mercury 

 into the sea and subsequent microbial methyla- 

 tion of that mercury (Ui, 1971). 



It is of no surprise that health authorities 

 around the world became concerned about the 

 possible presence of mercury contamination 

 in their waters. In 1967, Sweden became alarmed 

 to the extent that it closed about 40 contami- 

 nated freshwater areas to commercial fishing. 

 At the same time Swedish health authorities 

 established a legal limit of 1.0 ppm as the 

 maximum permissible concentration of mercury 

 in the flesh of fish destined for human con- 

 sumption. In 1970, fishes of the Great Lakes 

 region were investigated and found to have 

 high mercury levels. A survey of fishes in 

 various lakes showed a direct correspondence 

 between mercury levels in fishes and their 

 relative proximity to industrial mercury sources. 

 Fish-eating birds from the same areas were 

 collected for study. Some of the species of 

 aquatic birds were found to have levels of 

 mercury much higher than in the fishes, which 

 has been related to their relative position 

 within the food chain. 



When the clinical aspects of mercury poison- 

 ing are considered (Katz and Krenkel, 1972) 

 it becomes more evident why such great con- 

 cern exists in many parts of the world about 

 the occurrence of unduly high amounts of 

 methylmercury in food. All indications are 

 that mercury, in the form of its methyl com- 

 pound, readily crosses the blood-brain barrier. 

 As with most toxic substances, the effect of 

 methylmercury varies from person to person. 

 Symptoms can manifest themselves gradually 

 so that the afflicted individual scarcely notices, 

 or they can manifest themselves rapidly in 

 agitation, convulsions, or even coma. In extreme 

 cases of poisoning, destruction of the central 

 nervous system can be so rapid that serious, 



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