SINDERMANN: POLLUTION-ASSOCIATED DISEASES AND ABNORMALITIES 



published work, led them to the conclusion that 

 tissue changes observed as a result of exposure to 

 an array of common pesticides were largely 

 nonspecific, and therefore of limited diagnostic 

 value. Their attempts to identify specific lesions as 

 characteristic of any group or class of pesticides 

 were described by them as "futile," but the amount 

 of histopathological information presented in the 

 paper is substantial, and their summarization of 

 pathology pi'oduced by exposure to widely used 

 pesticides is instructive. 



DDT: Necrosis of hepatic cells; lymphocytic 

 infiltration of intestinal lamina propria; pos- 

 sible degeneration of kidney tubules. 



Carbaryl (Sevin): Intramuscular hemor- 

 rhages adjacent to vertebral column; atrophy 

 of the lateral line musculature; myxomatous 

 degeneration of fat; vacuoles within the optic 

 tectum of the brain. 



Malathion: Subcutaneous hemorrhages at the 

 bases of pectoral fins. 



Endosulfan (Thiodan): Hyperemia of intestine 

 and brain; adrenal cortical hyperplasia. 



2,4-D: Striking degree of brain hyperemia; 

 hyperemia of intestine. 



Atrazine: Marked edema of all tissues; 

 changes in skin pigmentation. 



It is interesting that Walsh and Ribelin (1975) 

 (unlike Couch 1975) found liver changes in fish 

 exposed to pesticides ". . . minimal and diagnosti- 

 cally unimportant . . . ." They also considered gill 

 epithelial hyperplasia, gill hemorrhages, and 

 lymphocyte reduction in the spleen to be 

 nonspecific responses to stress and/or infection. 

 They further pointed out that rapid autolysis of 

 fish tissues after death rather than direct effects of 

 pesticides might account for some reported his- 

 topathological findings. These are all points of im- 

 portance in evaluating histological findings after 

 exposure to any contaminant. 



There are still other histopathological studies of 

 the effects of pesticides on fish that disclose dam- 

 age to neurosensory tissue. Epithelial necrosis 

 was found in lateral line canals of killifish, F»/?- 

 dulus heteroclitus. that survived 96-h exposures to 

 the chlorinated hydrocarbon methoxychlor at 25 

 mg/1 (Gardner 1975). No damage to the 

 mechanoreceptors was evident, but the radius of 

 the canal lumina was reduced. 



Pesticides can produce tissue pathology in in- 

 vertebrates as well. Oysters exposed chronically to 



3 ppb DDT, Toxaphene, and parathion exhibited 

 variable lesions, including leucocytic infiltration 

 or hyperplasia of the gonadal germinal 

 epithelium, necrosis of digestive tubule epithelium, 

 and edema (Lowe et al. 1971). In another study, 

 chronic exposure of oysters to 5 ppb PCB produced 

 atrophy of digestive epithelium, leucocytic in- 

 filtration, and degeneration of vesicular connec- 

 tive tissue (Lowe et al. 1972). Gill edema and pro- 

 gressive necrosis of filaments in the crustacean 

 Gammarus oceanicus resulted from exposure to 

 sublethal concentrations of PCB (Wildish 1970). 

 Examination of pink shrimp, exposed experimen- 

 tally to PCB's, disclosed a variety of nonspecific 

 tissue changes, especially in the hepatopancreas 

 (Couch et al. 1974). Histological changes included 

 lysis of hepatopancreatic epithelium, nuclear pye- 

 nosis, vacuolization of secretory cells, and a vari- 

 ety of ultrastructural changes in absorptive cells. 



The literature on experimentally induced le- 

 sions in estuarine/marine fish caused by exposure 

 to heavy metals was reviewed recently by Gardner 

 ( 1975) in a paper which also presented significant 

 new information. His general conclusion was that 

 sensory organ systems of some species are vulner- 

 able to copper, mercury, and silver. Short-term 

 exposure of the killifish to sublethal concentra- 

 tions of copper resulted in degeneration of anterior 

 lateral line and olfactory sensory tissues (Gardner 

 and LaRoche 1973). Prolonged exposure to copper 

 (copper chloride) resulted in hyperplasia or necro- 

 sis of sustentacular epithelium of the olfactory 

 organs and necrosis of the epithelial lining of ol- 

 factory pits. Mercury (mercuric chloride) also pro- 

 duced severe degenerative changes in cells of the 

 lateral line canals and olfactory organs of killifish, 

 but without associated necrosis of supporting tis- 

 sues. Exposure to silver produced histopathologi- 

 cal changes very similar to copper. Cadmium 

 (cadmium chloride), however, did not seem to af- 

 fect the sensory tissues discussed above, at least in 

 terms of causing demonstrable tissue changes. 

 Cadmium exposure did result in transient thyroid 

 hyperplasia and altered blood cell ratios in long- 

 term exposures. 



Experimental exposure of the cunner, 

 Tautogolabrus adspersus, to cadmium caused 

 pathological changes in kidney, intestine, 

 hemopoietic tissue, epidermis, and gills (Newman 

 and MacLean 1974). Necrosis of tubular 

 epithelium of the kidney, sloughing of intestinal 

 epithelium, hypertrophy and hyperplasia of gill 

 epithelium, and decrease in mucus secretion were 



737 



