RESUMEN
Introduction: Considerable use of neonicotinoid insecticides has resulted in their detection in surface waters globally, with imidacloprid (IM) and thiamethoxam (TM) frequently found together. Neonicotinoids are selective agonists for invertebrate nicotinic acetylcholine receptors (nAChR) leading to paralysis and death. While not overtly toxic to vertebrates, growing evidence suggests that chronic exposure to individual neonicotinoids can cause adverse health effects in fish. This work examined whether chronic exposure to binary mixtures of imidacloprid (IM) and thiamethoxam (TM) would be more toxic to fathead minnow (Pimephales promelas) larvae than either insecticide alone. Materials and Methods: Embryos were exposed to a 1:1 mixture of IM and TM (0.2, 2, 20, 200 or 2,000 µg/L of each pesticide) or a 1:5, 1:10, or 1:20 mixture of IM and TM (0.02 µg/L of IM with 0.1, 0.2, or 0.4 µg/L of TM) for a total of 8 days. Survival, developmental toxicity, embryonic motor activity, and startle escape responses were quantified. Results: Survival and growth were reduced, and hatching induced by exposure to a 1:1 mixture containing > 2 µg/L of each insecticide, but not following exposure to mixtures containing environmentally-relevant concentrations. Acute exposure to a 1:1 mixture did not alter embryonic motor activity; however, chronic exposure to these mixtures resulted in a slight but significant decrease in embryonic movements. Only 1:1 mixtures of high concentrations of IM and TM altered the startle escape response by increasing latency of response; however, a significant proportion of fish exposed to 1:1 mixtures had altered latency and burst speed. Taken together, these behavioral indicators of nAChR activation suggest that in mixtures, neonicotinoids could interfere with nAChR signaling despite their low affinity for the nAChR. Conclusion: Our findings suggest that toxicity of binary mixtures of IM and TM is primarily driven by IM, and that mixtures of IM with TM do not appear to cause significant additive toxicity when compared with our previous studies evaluating each neonicotinoid alone. Given the limited toxicological data available for mixtures of neonicotinoid insecticides in fish, further study is required to better understand the ecological risks these insecticides may pose to aquatic ecosystems.
RESUMEN
Imidacloprid (IM) has emerged as a contaminant of concern in several areas within the United States due to its frequent detection in aquatic ecosystems and its pseudo-persistence, which pose potential risks to nontarget species. We evaluated the sublethal toxicity of IM to 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 nicotinate acetylcholine receptor (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 premature hatching. Furthermore, 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 that chronic exposure to IM has the potential to impair the ability of larvae to escape predation. The adverse health effects we observed 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. Environ Toxicol Chem 2023;42:2184-2192. © 2023 SETAC.