Background: Organophosphate (OP) pesticides are widely used in agriculture. Studies suggest that prenatal exposure to low levels of OP pesticides may adversely affect fetal neurodevelopment. Disruption of thyroid function is an important candidate mechanism relating OP pesticides to brain development. While animal studies suggest that OP pesticides exposure affects thyroid function, evidence in human studies remains sparse and inconclusive.

Objective: To investigate the association of repeatedly measured OP pesticides exposure during pregnancy with maternal and new born thyroid function.

Methods: Mother-child pairs of the Generation R Study with repeatedly measured OP pesticides exposure and data on maternal (N=715) or newborn (N=482) thyroid function were included. OP pesticide exposure was assessed at <18, 18–25, and >25 weeks gestation by measuring six urinary dialkylphosphate (DAP) metabolites. Thyroid stimulating hormone (TSH), free thyroxine (FT4), total thyroxine (TT4), and TPO antibodies (TPOAbs) were measured in maternal and cord blood at a median of 12.9 and 40.3 weeks gestation, respectively. Linear regression models, with adjustment for relevant confounders, were used to estimate associations between DAP metabolite concentrations expressed as molar concentrations divided by creatinine levels and thyroid measures.

Results: DAP metabolite concentrations were not associated with maternal or newborn thyroid function. Average DAP concentrations were not associated with maternal TSH, FT4, TT4 or TPOAb concentrations. Similarly, average and gestational age-specific DAP concentrations were not associated with newborn TSH or FT4 concentrations.

Conclusion: Prenatal OP pesticides exposure, as assessed by urinary DAP metabolite concentrations in an urban population, is not associated with maternal or newborn thyroid function. These findings suggest that associations of prenatal OP pesticides exposure with neurodevelopment are not mediated by thyroid function.