• • Systematic review of 58 studies (2001–2024) confirms significant associations between OP exposure and increased risks of spontaneous abortion, gestational diabetes, preeclampsia, and preterm birth, with effect sizes varying by exposure window and outcome.
• • PON1 genotype polymorphisms modulate OP toxicity: individuals with the QQ192 genotype exhibit lower paraoxonase activity, leading to higher accumulation of toxic oxons and increased susceptibility to adverse pregnancy outcomes.
• • Proposed mechanisms include oxidative stress (elevated 8-OHdG), systemic inflammation (increased CRP), and disruption of placental gene networks, as evidenced by altered expression of genes involved in steroidogenesis and immune regulation.
• • Exposure assessment predominantly relies on urinary dialkyl phosphate metabolites, but variability in timing and metabolite specificity limits comparability; future studies should incorporate repeated measures and PON1 phenotyping to refine risk assessment.
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