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 , co - carcinogens , 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.imagesfigure 2.figure 3.figure 4.figure 5.figure 6.figure 7.figure 8.figure 9.figure 10 .