Potential Environmental Health Risk Analysis of Neonicotinoids and a Synergist

The extensive use of neonicotinoid pesticides has led to their widespread presence in the environment, resulting in considerable safety risks to the ecosystem and human health. In this study, we investigated the biotransformation behavior of a cocktail of multiple neonicotinoids and piperonyl butoxide (PBO) synergist in vivo and their potential environmental health risk. It was found that neonicotinoids with a cyano group, such as acetamiprid and thiacloprid, tended to accumulate in liver and spleen tissues, while others with nitro groups (imidacloprid, thiamethoxam, clothianidin, dinotefuran, and nitenpyram) were mostly excreted in urine. In the presence of the synergist PBO, the metabolism of neonicotinoids in vivo changed, mainly through the nitro reduction pathway, while a low abundance of related metabolites was observed in the conventional hydroxylation and demethylation metabolic pathways, due to inhibition of CYP450 enzymes by the synergist. Furthermore, DNA methylation damage in vivo was exacerbated by the induction of hydroxylamine metabolites formed in the intermediate process of neonicotinoid metabolism with the synergistic effect of PBO, which resulted in a higher level of the O-6-methyldeoxyguanosine (O-6-medG) biomarker in the liver. Therefore, during the comprehensive evaluation of pesticide environmental risks, attention should be paid not only to the co-exposure mode under real environmental conditions but also to the potential risks of intermediate metabolism and related intermediate metabolites. This study provides a referential strategy and theoretical support for the health risk assessment of co-exposure of chemicals.

Automated summary

The study found that different types of neonicotinoids have different absorption and metabolism pathways in vivo, which may have different impacts on liver and spleen tissues; additionally, the presence of PBO changes the metabolic pathway of neonicotinoids, increasing the risk of DNA methylation damage.