Toxic responses that are meaningful at the organismic/population/community levels are only beginning to be evaluated in HR taxa. For example, despite their exposure to and bioaccumulation of cancer-causing toxicants, high prevalence of liver neoplasms, and a truncated age structure, laboratory studies have yet to be conducted in which the role of specific contaminants such as PCBs in inducing tumors is investigated in Atlantic tom-cod. Early life-stage toxicities are very sensitive and population-relevant outcomes in fish from exposures to PCDD/Fs and coplanar PCBs. The likelihood of these compounds in eliciting these early life-stage effects in HR fish is only beginning to be explored. Similarly, fish are highly sensitive to EDCs, yet only recently have studies been initiated to evaluate these responses in fish exposed to HR contaminants.
One conclusion from the studies conducted to date is the unexpectedly small number of gross toxicities observed in HR populations despite their exposure to, and bioaccumulation of, high levels of contaminants. In part, this results from the ability of chronically exposed populations to acquire resistance to toxicants through genetic adaptation, physiological acclimation, or a combination of both. The development of resistance may be common in fish populations from highly impacted ecosystems such as the HR. Although evolutionary change is typically viewed as a lengthy process, selection pressure in highly polluted environments may be so intense such that change occurs more rapidly than originally thought possible. This has been empirically demonstrated in oligochaete worms which under controlled laboratory conditions acquired resistance in only a very few generations and perhaps in PCB-exposed kil-lifish. What are the life history characteristics that allow some species to acquire resistance and others not? In rodent models, mechanisms have been elucidated that may provide physiologically-based tolerance of PCDD/Fs and PCBs and the applicability of this and other potential mechanisms of acclimation of natural populations should be explored.
While resistance may provide short-term benefits to populations in the face of insult from individual or single classes of toxicants, they probably do not come without associated costs. These may include enhanced sensitivities to other stressors or decreased physiological performance in the absence of toxicants in remediated environments. Also, the presence of resistant populations increases the likelihood of transfer of contaminants to higher trophic levels in food chains. Furthermore, the widespread occurrence of resistance in challenged populations may compromise the use of biomarker approaches, in that false negative responses may be observed. Mechanistic studies on the bases of resistance may provide insights into their attendant costs and likely persistence in remediated environments and molecular tools are under development in aquatic taxa to address this question.
Another problem in evaluating the toxicity of individual or classes of contaminants to HR populations is their exposure to complex mixtures of chemicals in combination with physical stressors. Even in well-defined rodent model systems, there is much uncertainty regarding the toxic effects of mixtures of chemicals and the mechanistic bases of their actions. Preliminary results with fish suggest that the toxic effects of exposure of adults and young life stages to mixtures of metals and PCBs or PAHs may be profound. Even within individual classes of xenobiotics, such as PCBs, interactive effects among different forms of a single toxicant class may be other than additive and significantly affect toxicity.
Another problem in assessing the toxicity of individual or classes of contaminants is that the extent of interindividual, interpopulation, and interspecific variation in response to environmental exposure is large, making statistical interpretation of results from these studies difficult. For example, should highly sensitive or more tolerant species be used as sentinels? The use of feral animals in laboratory studies introduces difficulties not encountered in typical toxicological experiments.
For the future, investigations are needed which combine field observations of adverse effects at the organismic level that may be detrimental to population/community viability with controlled laboratory studies in which similar alterations are induced in the same species with environmentally realistic levels of model contaminants. Furthermore, studies in which the mechanistic bases of these toxicities are identified may in the future allowfor the application of relatively simple molecular assays in environmental risk assessment. But, successful adoption of this strategy requires long-term commitments on the part of the investigator and funding agencies.
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