Studies were initiated to determine the etiology of the elevated prevalence ofhepatic tumors and pre-neoplastic lesions in the HR population driven by the hypothesis that the epizootic resulted from exposure to chemical contaminants. Initially, no relationship was found between the prevalence or size of lesions and levels of total PCBs, pesticides, or selected heavy metals (Smith et al., 1979; Dey et al., 1993). Unfortunately, levels of these toxicants were not compared between tomcod from the HR and cleaner rivers.
The prevalence of tumors was compared between tomcod from the HR and the cleaner Sheep-scot River, Maine, that were collected in June as juveniles and reared under controlled laboratory conditions to December (spawning time) of that year (Cormier and Racine, 1990). This study was based on the assumption that early life stages in fish are most sensitive to the carcinogenic effects of contaminants and that critical exposures to cancer-causing contaminants had occurred by June in the environment. In December, tumors and other hepatic lesions were absent in tomcod from both populations and therefore no insights were gained into the etiology of neoplasia. These results were consistent with almost all other attempts to induce tumors under controlled laboratory conditions in fishfromnaturalpopulations that exhibit epizootic episodes of neoplasia and suggested that other approaches were needed to identify the cause of disease.
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