Data from: Environmental estrogens cause predation-induced population decline in a freshwater fish

Understanding population-level effects of environmental stressors on
aquatic biota requires knowledge of the direct adverse effects of
pollutants on individuals and species interactions that relate to survival
and reproduction. Here, we connect behavioral assays with survival trials
and a modeling approach to quantify changes in antipredator escape
performance of a larval freshwater fish following exposure to an
environmental estrogen, and predict changes in population abundance. We
quantified the effects of short-term (21 d) exposure to 17-β estradiol
(E2) on the antipredator escape performance of larval fathead minnows
(Pimephales promelas) and the probability of predation by a natural
predator, the bluegill sunfish (Lepomis macrochirus). Compared with
unexposed minnows, minnows exposed to environmentally relevant
concentrations of E2 that approach total estrogenic activity of
waste-water dominated environments (38 and 103 ng/L) had delayed response
times and slower escape speeds, and were more susceptible to predation.
Incorporating these data into a stage-structured population model
demonstrated that enhanced predation mortality at the larval stage is
sufficient to generate marked population declines. These results indicate
that subtle, sub-lethal shifts in the behavior of individuals due to
human-mediated environmental change can impact species interactions with
measurable population-level effects. Such changes have the potential to
alter higher-order trophic interactions and disrupt aquatic communities.