Hooper Helen L, Sibly Richard M, Hutchinson Thomas H, Maund Stephen J
School of Animal and Microbial Sciences, University of Reading, P.O. Box 228, Reading RG6 6AJ, United Kingdom.
Environ Toxicol Chem. 2005 May;24(5):1140-5. doi: 10.1897/04-254r.1.
Results of previous laboratory studies suggest that high population density often buffers the effects of chemical stressors that predominately increase mortality. Mortality stressors act to release more resources for the survivors and, therefore, produce less-than-additive effects. By contrast, growth stressors are expected to have opposite results or more-than-additive effects. We investigated the effects of a growth inhibitor (lufenuron) on larval growth and survival of Chironomus riparius and examined its joint effects with density on population growth rate (PGR). Exposure to 60 microg/kg sediment or greater inhibited larval growth, and exposure to 88 microg/kg or greater often resulted in mortality before reaching emergence. The effects of lufenuron, however, differed with population density. At 88 microg/kg, mortalities and, to a lesser extent, reduced fecundity resulted in a reduction in PGR at low density. Conversely, when populations were initiated at high density, PGR was similar to that of controls, because the few survivors reached maturity sooner and started producing offspring earlier. The effect of density as a growth stressor therefore was stronger than the effect of lufenuron, which had effects similar to those of a mortality stressor and produced less-than-additive effects. Long-term studies under field conditions, however, are needed before less-than-additive effects are considered to be the norm.
