Abstract
Neonicotinoids, a class of insecticides structurally similar to nicotine that target biting and sucking insects, are the most widely used insecticides today, in part due to their supposed low toxicity in other organisms. However, a growing body of research has found that even low doses of neonicotinoids can induce unexpected negative effects on the physiology and survival of a wide range of non-target organisms. Importantly, no work has been done on the commercial formulations of pesticides that include imidacloprid as the active ingredient, but that also contain many other components. The present study examines the sublethal effects of “Tree and Shrub”™ (“T+S”), a commercial insecticide containing the neonicotinoid imidacloprid as its active ingredient, on Caenorhabditis elegans. We discovered that “T+S” significantly stunted the overall growth in wildtype nematodes, an effect that was exacerbated by concurrent exposure to heat stress. “T+S” also negatively impacted fecundity as measured by increased germline apoptosis, a decrease in egg-laying, and fewer viable offspring. Lastly, exposure to “T+S” resulted in degenerative changes in nicotinic cholinergic neurons in wildtype nematodes. As a whole, these findings demonstrate widespread toxic effects of neonicotinoids to critical functions in nematodes.
Highlights
Neonicotinoids, a relatively new class of insecticides, are the most widely used insecticides today [1]
The findings of this study suggest that environmentally relevant concentrations of “Tree and Shrub”TM (T+S)” exert damaging effects on nematodes, impacting their development, locomotion, and egg-laying behavior, as well as meiosis
While it remains possible that some of the effects we observed were a result of the pesticide affecting bacteria, the nematodes’ food source, we believe this is unlikely because the treatment was not lethal to nematodes and they were able to grow, develop to adulthood and reproduce
Summary
Neonicotinoids, a relatively new class of insecticides, are the most widely used insecticides today [1]. There are no comprehensive studies examining the effects of imidacloprid-containing pesticide formulations on non-target organisms in a preparation available for public use This is significant, as like other commercially-available pesticides, safety assessments are limited to their active ingredient(s), ignoring adjuvants and/or the mixture as a whole. As egg-laying defects are coincident with increased germline apoptosis in other studies examining pesticide exposure in worms [22,26], apoptotic nuclei were quantified in the germ lines of live, wild-type adults exposed to “T+S” for 48 hours (Fig 6). Similar to wild-type (N2) animals, there was no change in the number of apoptotic nuclei in the P0 exposed ced-1::GFP worms while a significant increase in germ cell corpses in the F1 germline in response to “T+S” exposure (Fig 6E and 6F, p
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