Intraspecific interactions affect outcomes of pulse toxicity at different Daphnia magna population phases

Traditional toxicity tests assess stressor effects on individuals, while protection goals are focused on the population-level and above. Additionally, these tests ignore common ecological factors such as resource levels and population growth phase. The objective of this research was to explore effects of - and interactions between - resource availability and stress response at the individual and population levels using Daphnia magna as a model. We hypothesized that density-dependent changes in resources at various phases of population growth would cause different population responses to the same toxicant stress. Laboratory populations of Daphnia magna were exposed to a 48-h pulse of 20 or 30 μg/l pyraclostrobin in one of four distinct phases of laboratory population cycles: growth, peak, decline, and stable. Population size and recovery were observed throughout the 51-day study. Populations exposed to pyraclostrobin during the growth phase had the least mortality and fastest recovery, while populations in the peak phase had the greatest mortality and slowest recovery. These data suggested that high density and low food at the peak phase resulted in more sensitive daphnids. To further test this hypothesis, a resource-amended acute toxicity study was conducted to quantify the effects of food resource on pyraclostrobin toxicity to Daphnia magna. Three age classes of Daphnia magna (neonate, subadult, adult) were fed low or high food levels and exposed to pyraclostrobin for 48 h. Toxicity was greater, as shown by lower 48 h LC50s, for smaller Daphnia magna age classes and lower food levels comporting results in the population study. Importantly, the acute toxicity studies generally yielded lower effect levels than the population studies suggesting that while the standard acute studies are ecologically unrealistic, they may be protective of toxicity under some circumstances. Collectively, these data point to the importance of population phase and the resource environment in modulating toxicity.