Anthropogenic factors have contributed to the precipitous decline of wild Pacific salmon stocks, although the mechanisms and processes at work are largely unknown. Pollution may be one of these factors. Sediments in estuaries are known to act as repositories for contaminants , and estuaries are important habitats for ocean-and river-migrating salmon. We have shown that juvenile salmon Oncorhynchus spp. and their prey bioaccumulate chlorinated hydrocarbons and aromatic hydrocarbons-important classes of toxic xenobiotics. Furthermore, we have shown that exposure to these pollutants can lead to immunosuppression and increased disease susceptibility in juvenile salmon. Whether pollution influences natural disease outbreaks in host populations, including salmon, is currently unknown. It is postulated that the occurrence of disease depends on the interaction of the host, the environment, and the pathogen. Absence of pathogens would reduce the potential for adverse environments to influence disease outbreaks. However, a recent reconnaissance survey of juvenile chinook salmon Oncorhynchus tshawytscha from Oregon coastal rivers revealed that pathogens were an integral component in all systems studied, although the prevalence of the pathogens varied. Furthermore, recent studies of natural fish populations have demonstrated that infectious-disease-induced mortality can significantly reduce the size of the host population. By creating adverse environments (e.g., polluted estuaries) which alter the susceptibility of the host to pathogens that are integral and ubiquitous components of the habitat, pollution increases the probability of disease-related impacts on fish populations.

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Saltwater-adapted juvenile chinook salmon Oncorhynchus tshawytscha exposed to aromatic and chlorinated compounds, representative of contaminants found in urban estuaries in Puget Sound, have a higher susceptibility to vibriosis than do fish exposed only to the solvent vehicle. Susceptibility to vibriosis was assessed by examining the percent cumulative mortality of the salmon after exposure to the bacterial pathogen Vibrio anguillarum. The aromatic and chlorinated compounds examined consisted of a sediment extract from the Hylebos Waterway that was enriched in butadienelike compounds (chlorinated-enriched Hylebos Waterway sediment extract [CHWSE]), a model mixture of polycyclic aromatic hydrocarbons (PAHs), a polychlorinated biphenyl mixture (Aroclor 1254), hexachlorobutadiene (HCBD), and 7,12-dimethylbenz[a]anthracene (DMBA). Two trials were conducted. In trial l, the percent cumulative mortality of juvenile chinook salmon exposed to V. anguillarum after receiving either CHWSE, HCBD, or the model mixture of PAHs ranged from 28% to 31% compared with the 16% observed in the acetone: emulphor control group at 7 d post-bacterial challenge. In trial 2, the net cumulative mortality of juvenile chinook salmon exposed to V. anguillarum after receiving either DMBA or Aroclor 1254 ranged from 46% to 49% compared with the 25% observed in the acetone:emulphor control group at 9 d postchallenge. The differences in mortality between groups of fish in the treated and control groups in both trials were significant at P Յ 0.05. These findings suggest that a higher predisposition to infection and subsequent disease can occur in salmon exposed to chemical contaminants found in urban estuaries of Puget Sound, Washington.