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CHRONIC LABORATORY EXPOSURE OF MUMMICHOG, FUNDULUS HETEROCLITUS, TO PAH-CONTAMINATED SEDIMENT AND DIET CAUSES LIVER NEOPLASMS
Citation:
Vogelbein, W. K., D. E. Zwerner, M. A. Unger, AND J W. Fournie. CHRONIC LABORATORY EXPOSURE OF MUMMICHOG, FUNDULUS HETEROCLITUS, TO PAH-CONTAMINATED SEDIMENT AND DIET CAUSES LIVER NEOPLASMS. Presented at American Fisheries Society Fish Health Section 2000 Annual Meeting, Pensacola Beach, FL, 6-8 September 2000.
Description:
The mummichog, Fundulus heteroclitus, is a common estuarine teleost inhabiting tidal marshes of the eastern United States. We previoiusly reported on high prevalences of hepatic and extra-hepatic neoplasms in populations of this species from chemically contaminated environments in Virginia and Maryland, implicating anthropogenic chemical contaminants as the etiological agents of these lesions. Because this widely distributed, non-migratory fish appears to have utility as an indicator of environmental quality, we conducted long-term laboratory exposures to examine the bioavailability and role of sediment and dietary chemical contaminants in the etiology of liver cancer in this species. Lab-reared mummichog were exposed (in an environmentally realistic fashion) for 12 months to creosote-contaminated sediment or sediment and diet amended with eight PAHs identified by the U.S. EPA as suspected carcinogens and priority pollutants. Fish were exposed continuously in a flow-through system and sampled for histopathological evaluation at 3, 9, and 12 months post-initiation. No hepatic proliferative lesions were observed at 3 mo. However, high liver lesion prevalences occurred in later samples. At 9 mo, 23.3% of the fish exposed to creosote-contaminated sediment (GR 1) and 11.8% of the fish exposed to amended sediment and diet (GR 2) exhibited altered hepatocellular foci (AHF) but no hepatic neoplasms (HN). At 12 mo, 40% of the GR 1 fish and 30% of the GR 2 fish exhibited AHF, and 6.2% and 1.1% respectively, exhibited HN. Control animals exhibited no hepatic proliferative lesions. These studies provide some of the first direct experimental evidence that environmental contaminants, in particular the PAHs, play a direct role in the etiology of liver cancer in this wild species. This study was supported by U.S. EPA CR 821731-01-0.