FISHERY BULLETIN: VOL. 76. NO. 4 



the principal histopathologic findings. Mortality 

 following acute exposures was attributed to renal 

 failure. These results were similar in most re- 

 spects to cadmium-induced pathology in killifish, 

 reported earlier by Gardner and Yevich (1970). 



Experimental cadmium exposures can cause 

 gill lesions in shrimp, as reported in recent papers 

 by Nimmo et al. (1977) and Couch (1977). Expo- 

 sure of pink shrimp to 763 /tg/l of cadmium for 15 

 days resulted in a "black gill" condition charac- 

 terized by necrosis of all cell types in the distal gill 

 filaments, with coincident appearance of black 

 granules in the cytoplasm, and some hemocyte 

 infiltration at the bases of the necrotic filaments. 

 Couch suggested that the black deposits could be a 

 metallic sulfide or even cadmium. He further 

 pointed out that the distal filament tissue has been 

 postulated to have detoxifying, as well as os- 

 moregulatory and respiratory functions, so that 

 cell death could result from cadmium filtration 

 and accumulation as part of a detoxification pro- 

 cess. 



Zinc has been shown to be toxic for fish (see 

 reviews by Skidmore 1964, 1970). Gill tissues can 

 be destroyed in acute exposures, while chronic 

 levels induce stress which may result in mortality 

 and may also produce severe degenerative 

 changes in the liver and kidneys (Crandall and 

 Goodnight 1963). Synergistic activity of zinc with 

 a wide range of environmental variables — other 

 contaminant heavy metals, low dissolved oxygen, 

 and temperature — has been demonstrated for a 

 number of fish species (Doudoroff 1957; Lloyd 

 1960, 1961a, b). Resistance to zinc poisoning var- 

 ies with individuals, with age, with degree of 

 acclimatization, and with species (Jones 1938, 

 1940). 



Histopathological effects of sublethal concen- 

 trations of copper on the winter flounder were de- 

 scribed by Baker ( 1969). At dosages of 1,000-3,200 

 /Lig/1, the kidney hemopoietic tissue became necro- 

 tic; gill epithelium became disoriented; chloride 

 cells increased in number and size; gill lamellar 

 fusions occurred; and fatty metamorphosis of the 

 liver was observed. Experimental concentrations 

 were far above those levels expected in most 

 marine environments (concentrations in polluted 

 waters have been reported to reach 300/Ltg/l by 

 Fujiya (I960)). 



An interesting study of pathology in American 

 lobsters was made following disclosure of severe 

 yellow phosphorus industrial contamination of 

 Placentia Bay, Newfoundland (Aiken and Byard 



738 



1972). Experimental lobsters, exposed to phos- 

 phorus contaminated sediments in aquaria, ex- 

 hibited degenerative changes in antennal glands 

 and in all cell types in the hepatopancreas, as well 

 as massive coagulation of hemolymph. 



Experimental exposure to petroleum compo- 

 nents and residues may also induce histopatholog- 

 ical changes in fish. Hyperplasia of the olfactory 

 sustentacular epithelium and degeneration of the 

 olfactory mucosa of the Atlantic silverside, 

 Menidia menidia, resulted from exposure to crude 

 oil (Gardner 1975). Additionally, degeneration of 

 the ventricular myocardium of the heart and 

 pseudobranch secretory cells was seen. Soluble 

 components of the crude oil also caused epithelial 

 metaplasia, replacing the sensory epithelium of 

 the olfactory organs by poorly defined cell types 

 ( Gardner 1975). Liver damage occurred in fish fed 

 cyclopropenoid fatty acids (Malevski et al. 1974), 

 but Brocksen and Bailey (1973) found no his- 

 topathology in chinook salmon and striped bass 

 exposed to sublethal concentrations of benzene. 



Histopathological effects of petroleum on 

 bivalve molluscs are varied in the extreme. Ef- 

 fects, particularly on gill epithelium, have been 

 observed by Barry et al. (1971), Jeffries (1972), 

 LaRoche (1972), Clark et al. (1974), and Gardner 

 et al. ( 1975). Fries and Tripp ( 1976) found damage 

 to gill epithelium in hard (hard-shell) clams, Mer- 

 cenaria mercenaria, exposed to as little as 1 ppm 

 phenol. Vaughan^'', however, found little his- 

 topathology after chronic exposures of oysters to 

 No. 2 fuel oil. Stainken ( 1975) found that exposure 

 of soft-shell clams to No. 2 fuel oil at winter seawa- 

 ter temperatures (4°C) for 28 days had little his- 

 topathological effect, beyond signs of starvation 

 (glycogen depletion and vacuolization of digestive 

 diverticula cells), and a generalized leucocytosis, 

 even at 100 ppm. No mortalities occurred, and 

 exposure concentrations dropped rapidly, possibly 

 because much of the oil was trapped in mucus as 

 part of the mucociliary feeding mechanism, and 

 ejected from the clam. 



Experimental lesions are instx'uctive in iden- 

 tifying target organs and tissues for particular 

 contaminants, but they have numerous flaws 

 when attempts are made to relate experimental 

 findings to events in the natural (polluted) envi- 

 ronment: 1) dosage levels are often beyond 



'^Vaughn.B.E. (editor). 1973. Effects of oil and chemically 

 dispersed oil on selected marine biota - a laboratory study. Am. 

 Pet. Inst. Publ. 4191. 



