FISHERY BULLETIN: VOL. 76. NO. 4 



sues of mussels from polluted areas. The chemical 

 nature of the mutagens was not identified, except 

 that the mussels came from areas with heavy in- 

 dustrial pollution. 



EXPERIMENTALLY INDUCED LESIONS 



There is a vast and almost unmanageable 

 amount of published information about the induc- 

 tion of various lesions in fish by experimental ex- 

 posure to chemical contaminants (see for example 

 Ribelin and Migaki 1975). A "lesion" may be 

 defined generally as "any localized abnormal 

 structural change in the body." Such a definition 

 obviousl)' includes too much, so the term can be 

 reduced to encompass "those cellular and tissue 

 changes, demonstrable histologically, that result 

 from a disease process." Histopathology offish and 

 shellfish is still a developing science, and as such it 

 still draws from human and veterinary (mamma- 

 lian) patholog}' for its concepts and much of its 

 terminology. Histopathology has been a basic tool 

 in human medicine for some time, and a large 

 amount of information is available about cellular 

 responses to toxicants. A similar core of knowl- 

 edge is being developed for fish and shellfish — 

 relating cell and tissue changes to kinds and 

 amounts of contaminants. 



Early experimental exposures of estuarine and 

 marine animals to contaminants usually had the 

 purpose of determining lethal dosages, either from 

 acute or chronic exposures. More recently, atten- 

 tion has been redirected to sublethal toxic 

 effects — expressed in behavioral, physiological, or 

 cytological responses to specific contaminants. An 

 extensive literature exists concerning cell and tis- 

 sue damage resulting from experimental exposure 

 to contaminant chemicals. Generalizations that 

 can be made are almost predictable: 1) increas- 

 ing dosages, beyond a threshold level, produce in- 

 creasingly severe tissue abnormalities; 2) particu- 

 lar contaminants often exert effects on specific 

 target tissues; 3) principal target tissues seem to 

 be gill epithelium, liver (or in the invertebrate, the 

 hepatopancreas), and neurosensory cells; 4) 

 specific lesions cannot usually be described as 

 characteristic of any group or class of chemicals; 

 and 5) effects that may be of chemical origin can be 

 obscured by stress-provoked infections with facul- 

 tative pathogens. Some information about ex- 

 perimental induction of fin erosion and skeletal 

 abnormalities has been included in earlier sec- 

 tions of this paper, but because of the sheer volume 



736 



of published information about other types of ex- 

 perimental lesions, it seems worthwhile to sum- 

 marize some of the observations here. 



Couch (1975) published a recent and excellent 

 review of the histopathological effects of pesticides 

 and related chemicals on the livers of fishes. The 

 liver and fatty tissues of fish from natural waters 

 are known to accumulate a number of chlorinated 

 hydrocarbons (Duke and Wilson 1971), and ex- 

 perimental exposures offish to pesticides result in 

 high concentrations and greatest effects on the 

 liver (Johnson 1968; Eisler and Edmunds 1969; 

 Hansen et al. 1971; Eller 1971). Some of the ob- 

 served liver histopathology includes: 



Chlorinated hydrocarbon pesticides: Focal 

 areas of parenchymal cell vacuolation and de- 

 generation (Eller 1971), inflammation, and 

 loss of glycogen and fat (Lowe 1965). 



Clorinated hydrocarbon herbicides: Increase 

 in connective tissue, massive focal necrosis 

 (Cope et al. 1969), and loss of glycogen (Cope 

 et al. 1970). 



PCB's: Focal degenerative regions, paren- 

 chymal cell vacuolation and pleomorphism 

 (Eller''*), lipid accumulation in hepatic cell 

 vacuoles, and leucocytic infiltration (Couch 

 1975). 



Organophosphates: Edema, hyperemia, vacuo- 

 lation, and necrosis of parenchymal cells (El- 

 ler, see footnote 14). 



Carbamates: Hypertrophy and vacuolation of 

 acinar cells (Couch 1975). 



It should be noted that not all experimental 

 exposures to pesticides, even for prolonged 

 periods, necessarily caused demonstrable tissue 

 pathology, but in many instances additional expo- 

 sure experiments are needed (even though the lit- 

 erature as summarized by Couch (1975) seems 

 voluminous). Couch pointed out that over 900, 

 commercial pesticide formulations are in general 

 use, and of these fewer than 30 have been tested 

 for pathological effects on livers of fishes. 



Pesticides can, of course, affect fish tissues other 

 than liver. A summarization of general his- 

 topathological effects of pesticides on fish was pub- 

 lished by Walsh and Ribelin (1975). Data from 

 their own studies with coho salmon, Oncorhyn- 

 chus kisutch, and lake trout, as well as from other 



'••Eller, L. L. 1970 and 1971. Annual reports. U.S. Bur. 

 Sport Fish. Wildl., Fish Pestic. Lab., Columbia, Mo. 



