Abstract

Imidacloprid (IM) has emerged as a contaminant of concern in several areas within the United States due to its frequent detections in aquatic ecosystems and pseudo-persistence, posing potential risks to non-target species. Here we summarize our work evaluating the sublethal toxicity of IM to in fathead minnow larvae following chronic exposure beginning just after fertilization. Our in silico analysis and in vivo bioassays suggest that IM has a low binding affinity for the vertebrate nAChR, as expected. However, chronic exposure to ≥ 0.16 µg IM/L reduced survival by 10%, and exposure to ≥ 18 µg IM/L reduced survival by approximately 20-40%. Surviving fish exposed to ≥ 0.16 µg IM/L showed reduced growth, altered embryonic motor activity, and hatched prematurely. Further, a significant proportion of fish exposed to ≥ 0.16 µg IM/L were slower to respond to vibrational stimuli and slower to swim away, indicating a potential for chronic exposure to IM to impair the ability of larvae to escape predation. The adverse health effects observed here indicate that chronic exposure to environmentally-relevant concentrations of IM may elicit sublethal responses that culminate in a significant increase in mortality during early life stages, ultimately translating to reduced recruitment in wild fish populations.

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