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APPLICATION OF ELASTICITY ANALYSES AND PERTURBATION SIMULATIONS IN DETERMINING STRESSOR IMPACTS ON POPULATION GROWTH RATE AND EXTINCTION RISK
Citation:
RAIMONDO, SANDY, C. L. MCKENNEY, AND M. G. BARRON. APPLICATION OF ELASTICITY ANALYSES AND PERTURBATION SIMULATIONS IN DETERMINING STRESSOR IMPACTS ON POPULATION GROWTH RATE AND EXTINCTION RISK. Presented at SETAC, Baltimore, MD, November 13 - 17, 2005.
Description:
Population structure and life history strategies are determinants of how populations respond to stressor-induced impairments in individual-level responses, but a consistent and holistic analysis has not been reported. Effects on population growth rate were modeled using five theoretical constructs that represented the life history strategies and elasticity patterns (proportional sensitivities) of a broad range of species. Simulations of low to high ranges of simultaneous reductions in survival and reproduction indicated that stressor impacts on population growth rate were dependent population characteristics and the magnitude of the stressor. Perturbation simulations were performed to assess the extinction risk in two species with similar elasticity patterns but different life history strategies: mysid shrimp, Americamysis bahia, and the gypsy moth, Lymantria dispar, K- and r-strategists, respectively. Extinction risk was greater for the Kstrategist which indicated that population level risks were dependent on life history strategies, and toxicity values (e.g., LC50s) should be interpreted relative to population characteristics. Toxicity test data of mysids exposed to 53 toxicant-concentrations (10 toxicants, 5-6 concentrations each) were used to validate the predictability of the simulation method to determine the decline in population growth rate from different combinations of reduced survival and reproduction. The results of the simulation modeling suggest that the ecological risks of stressors on populations will be dependent on the elasticity patterns and life history strategies in addition to the magnitude of effects on organism-level endpoints.