Frequencies of external and grossly visible liver tumors were high in brown bullheads Ictalurus nebulosus from Black River, an industrialized Lake Erie tributary. Skin and liver tumors were lacking in brown bullheads from Buckeye Lake, a reference site, and the incidence of lip tumors was low (<2%). Liver tumors, primarily cholangiocarcinomas, increased significantly (P < 0.05) with age in Black River brown bullheads, occurring in 28–44% of the 4‐year‐old fish collected in 1980–1982. External tumors did not increase consistently with age. Within year classes, the occurrence of grossly observable liver tumors was higher in fall than in spring. Liver tumor incidence was not correlated with sex. Organic contaminants were higher in brown bullheads from the Black River than in those from Buckeye Lake. Polynuclear aromatic hydrocarbons were particularly high, including carcinogens such as benz[a]anthracene and benzo[a]pyrene (B[a]P). Limited electron microscopy of cholangiocarcinomas provided no evidence of virus. Since brown bullhead have the ability to hepatically activate B[a]P, and since B[a]P has been shown to induce cancer in fish, the hypothesis of a chemical etiology for the tumors in the Black River brown bullheads best fits the available data.

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Within the last decade unusually high frequencies of neoplasms have been reported in feral fish populations from a variety of locations. At many of these locations organic carcinogens have been noted as a potential cause. We sought to identify toxic effects including neoplasia in fish exposed to an organic carcinogen, and to quantify these effects through time. We exposed guppies (Poecilia reticulata) to multiple doses of DEN, an organic carcinogen. Fish were then subsampled and examined for liver histopathology at 2-month intervals over 12 months. Necrotic zones, macrophage centers, bile duct proliferations, enlarged lipid deposits, neoplastic foci, cholangiocarcinomas and hepatoblastomas were quantified by frequency of occurrence and the percentage of liver area involved. DEN toxicity resulted in necrotic zones that peaked in frequency at the first sample period (2 months). Lipid deposits increased, then plateaued in guppies, indicating a more chronic toxic effect. Similarly, macrophage centers increased through the sampling period. Bile duct proliferation appeared to be of two types: a reversible toxic response which peaked at 4 months and then declined and a less frequent irreversible proliferation which continued to develop into cholangiocarcinoma. Neoplastic foci of mixed hepatocytes and cholangiocytes increased in livers of exposed guppies from the second month, developing into hepatoblastomas, which occurred in almost 100% of exposed guppies by the twelfth month. The irreversible bile duct proliferations and the neoplastic foci had cellular densities different from corresponding control tissue and similar to cellular densities of cholangiocarcinomas and hepatoblastomas, respectively.