In recent years, population declines related to viral outbreaks in marine mammals have been associated with polluted coastal waters and high tissue concentrations of certain persistent, lipophilic contaminants. Such observations suggest a contributing role of contaminant-induced suppression of cell-mediated immunity leading to decreased host resistance. Here, we assessed the effects of the prototypic polycyclic aromatic hydrocarbon (PAH), benzo [a]pyrene (B[a]P), and two polychlorinated biphenyls (PCBs), CB-156 and CB-80, on the T-cell proliferative response to mitogen in harbor seal peripheral lymphocytes. Despite the variability associated with our samples from free-ranging harbor seals, we observed a clear suppressive effect of B[a]P (10 uM) exposure on T cell mitogenesis. Exposures to 10 uM CB-156 and CB-80, and 1.0 and 0.1 uM B[a]P, did not produce significant depression in lymphoproliferation. Exposure to the model PAH at 10 uM resulted in a 61% (range 34 -97%) average reduction in lymphoproliferation. We were able to rule out a direct cytotoxic effect of B[a]P, indicating that observed effects were due to altered T cell function. Based on our in vitro results, we hypothesize that extensive accumulation of PAH by top-trophic-level marine mammals could alter T cell activation in vivo and impaired cell-mediated immunity against viral pathogens.Keywords: Benzo[a]pyrene; Harbor seal; Immunotoxicity; Lymphoproliferation; PAH; PCB
INTRODUCTIONUnderstanding immune alterations related to environmental contamination has become an important priority in marine mammal research because of the high incidence in recent years of mass mortality events, unexplained population declines, and strandings among marine mammal populations (Dietz et al., 1989; Marine Mammal Commission, 1999;Kennedy et al., 2000). These events have been largely attributed to disease outbreaks caused by established or newly identified members of the genus Morbillivirus (Geraci et al., 1982;Osterhaus and Vedder, 1988;Duignan et al., 1995). Common features of these massive die-offs include highly polluted habitat and high tissue concentrations in affected individuals of persistent, lipophilic contaminants, including those known to have deleterious effects on the immune systems of rodents and humans (Hall et al., 1992;Visser et al., 1993;Reijnders, 1994). Whereas contaminant-induced immune suppression has been suggested as a major contributing factor in marine mammal disease epizootics, causal relationships and potential mechanisms of immunotoxicity have not been established (Olsson et al., 1994; Marine Mammal Commission, 1999;van Loveren et al., 2000).The harbor seal (Phoca vitulina) is an ideal model organism for investigating contaminant-induced immune alterations in marine mammals. Fish-eating seals are longlived, maintain large adipose deposits, and occupy high trophic levels in the marine food chain, thus accumulating relatively high levels of lipophilic contaminants (Boon et al., 1987;Young et al., 1998; Neale, unpublished data). Among marine m...