Abstract
<em>Abstract.</em>—Despite recent successes in eliminating or reducing many point sources of chemical contaminants, sediments in the Hudson River Estuary are still highly contaminated with lipophilic and highly persistent polychlorinated biphenyls (PCBs), polychlorinated dibenzo-<em>p</em>-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polycyclic aromatic hydrocarbons (PAHs). These have been shown to bioaccumulate to high levels in resource species and other key ecological components of the Hudson River food web. Resource managers and stewards must consider the possible toxic effects of these pollutants on the Hudson River biota, including its fish community; however, few studies have directly investigated these effects. A series of toxicological studies on Atlantic tomcod <em>Microgadus tomcod </em>from the Hudson River Estuary have demonstrated profound and broad-based changes in response to local contaminants. Levels of contaminants in the tissues of different life stages of tomcod from the Hudson River Estuary far exceed those in tomcod from other Atlantic Coast estuaries. More importantly, a combination of field and laboratory studies has demonstrated molecular to population level perturbations in tomcod from the Hudson River, all of which are consistent with chemical exposures and many of which appear to be mechanistically linked. These effects include induction of hepatic expression of cytochrome P4501A1 mRNA, high levels of hepatic DNA damage, somatic mutations at an oncogene locus critical to the initiation of chemical carcinogenesis, elevated prevalence of gross and histologically defined hepatic tumors, truncated age structure, and dramatic resistance at the molecular and organismal levels to halogenated aromatic hydrocarbons (HAHs). Resistance, a population level effect, was observed in the toxic responses of tomcod embryos and larvae to 2,3,7,8-tetrachlorodibenzo-<em>p</em>-dioxin (TCDD) and TCDD-like PCBs, but not PAHs. Because young of the year tomcod are a critical node in the Hudson River food chain, their evolved resistance to HAHs and high body burden of these and related contaminants has likely resulted in the trophic transfer of these contaminants to secondary and tertiary consumers of the Hudson River, including important resource species, and an elevated tissue burden of these contaminants in those consumers. In total, these studies are consistent with the hypothesis that exposure to Hudson River-borne contaminants has significantly altered its tomcod population and perhaps evoked broad change in the Hudson River fish community.
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