Predators and prey may be simultaneously exposed to environmental toxins, but one may be more susceptible than the other. To study the effects of environmental toxins on food web dynamics, we develop a toxin-dependent predator-prey model that combines both direct and indirect toxic effects on two trophic levels. The direct effects of toxins typically reduce organism abundance by increasing mortality or reducing fecundity. Such direct effects, therefore, alter both bottom-up food availability and top-down predatory ability. However, the indirect effects, when mediated through predator-prey interactions, may lead to counterintuitive effects. This study investigates how the balance of the classical predator-prey dynamics changes as a function of environmental toxin levels. While high toxin concentrations are shown to be harmful to both species, possibly leading to extirpation of both species, intermediate toxin concentrations may affect predators disproportionately through biomagnification, leading to reduced abundance of predators and increased abundance of the prey. This counterintuitive effect significantly increases biomass at the lower trophic level. Environmental toxins may also reduce population variability by preventing populations from fluctuating around a coexistence equilibrium. Finally, environmental toxins may induce bistable dynamics, in which different initial population levels produce different long-term outcomes. Since our toxin-dependent predator-prey model is general, the theory developed here not only provides a sound foundation for population or community effects of toxicity, but also could be used to help develop management strategies to preserve and restore the integrity of contaminated habitats.
Keywords: Bifurcation; Methylmercury; Predator–prey model; Rainbow trout; Toxin.
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