CARCINOGENICITY OF BLACK ROCK HARBOR SEDIMENT TO THE EASTERN OYSTER AND TROPHIC TRANSFER OF BLACK ROCK HARBOR CARCINOGENS FROM THE BLUE MUSSEL TO THE WINTER FLOUNDER

The eastern oyster (Crassostrea virginica) developed neoplastic disorders when experimentally exposed both in the laboratory and field to chemically contaminated sediment from Black Rock Harbor (BRH), Bridgeport, Connecticut. Neoplasia was observed in oysters after 30 and 60 days of continuous exposure in a laboratory flow-through system to a 20 mg/L suspension of BRH sediment plus postexposure periods of 0, 30, or 60 days. Composite tumor incidence was 13.6% (49 neoplasms in 40, n = 295) for both exposures. Tumor occurrence was highest in the renal excretory epithelium, followed in order by gill, gonad, gastrointestinal, heart, and embryonic neural tissue. Regression of experimental neoplasia was not observed when the stimulus was discontinued. In field experiments, gill neoplasms developed in oysters deployed in cages for 30 days at BRH and 36 days at a BRH dredge material disposal area in Central Long Island Sound, and kidney and gastrointestinal neoplasms developed in caged oysters deployed 40 days in Quincy Bay, Boston Harbor. Oysters exposed to BRH sediment in the laboratory and in the field accumulated high concentrations of polychlorinated biphenyls (PCBs), polyaromatic hydrocarbons (PAHs), and chlorinated pesticides. Chemical analyses demonstrated high concentrations of PCBs, PAHs, chlorinated pesticides, and heavy metals in BRH sediment. Known genotoxic carcinogens, cocarcinogens, and tumor promoters were present as contaminants. The uptake of parent PAH and PCBs from BRH sediment observed in oysters also occurs in blue mussels (Mytilus edulis). Winter flounder fed BRH-contaminated blue mussels contained xenobiotic chemicals analyzed in mussels. The flounder developed renal and pancreatic neoplasms and hepatotoxic neoplastic precursor lesions, demonstrating trophic transfer of sediment-bound carcinogens up the food chain.