There is a need for government agencies to evaluate the toxic impacts of contaminants on the Hudson River (HR) biota to determine if damage to its populations has occurred and to guide remediation efforts. Surveys have quantified the concentrations of these xenobiotics in HR environmental matrices including water, sediment, and biota. The ability of many of these contaminants to bioaccumulate, and for the lipophilic, poorly or non-metabolizable pollutants, to biomagnify in the upper trophic levels of the Hudson River food chain has been documented. Far fewer studies have evaluated toxic effects of these contaminants on Hudson River populations.
Because of its history as a sink for extraordinarily high levels of contaminants, four locales in the HR Estuary (Foundry Cove, New York, river miles (RM) 0 to RM 197 of the main stem HR, the Passaic River, New Jersey, and Berry's Creek, New Jersey), have been designated as U.S. Federal Superfund sites (Fig. 30.1). For some pollutants and exposed taxa, sediment concentrations and tissue burdens of contaminants were among the highest ever observed worldwide. Contamination of the Newark Bay complex in the lower estuary with dioxins/furans (PCDD/Fs) is extensive because of their release from an industrial facility along the tributary Passaic River, which for decades manufactured phenoxy herbicides and DDT. A 197-mile reach of the HR is designated a Superfund Site, the largest in the country, because up to 1.3 million pounds of PCBs were released from two electrical capacitor manufacturing facilities at RM 195 and RM 197. Sediments in Berry's Creek, New Jersey, which drains into the Hackensack River, contained among the highest mercury (Hg) levels known in freshwater ecosystems nationwide.
Populations in the HR Estuary have been exposed to levels of many contaminants that elicit toxic effects inlaboratory animals. However, intrinsic compensatory mechanisms may ameliorate the toxic effects of many of these contaminants. Exposure to contaminants does not necessarily mean that they bioaccumulate to toxic levels. Decreased
uptake and increased efflux are two possible strategies that have evolved to decrease bioaccumulation of toxicants. Furthermore, bioaccumulation does not always translate into toxicity at the cellular, organismic, or population levels. Genetic adaptations and mechanisms of physiological acclimation exist that may modulate the toxicities of environmental pollutants. Strong selective pressure for genetic variants in the structure or expression of enzymes that metabolize contaminants or repair damaged deoxyribonucleic acid (DNA) may decrease toxicities. Similarly, exposure-induced alterations in the expression of receptor or other signal transduction pathway molecules or the intracellular sequestration of toxicants are physiological mechanisms that may modulate toxicity.
The aim of this chapter is to present and evaluate those studies that investigated the toxic effects of HR-borne organic and metals pollutants on its invertebrate and vertebrate populations. Compared to the numerous studies that have documented tissue burdens of HR contaminants in a variety of taxa, far fewer investigations have addressed the ecological effects of these pollutants.
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