LAUSR

Background: Evidence on the toxicity of hydroxylated metabolites of polychlorinated biphenyls (OH‐PCBs) for thyroid hormones (TH) is limited, and the underlying mechanism remains unknown. Objectives: We aimed to investigate the effects of environmental prenatal exposure to OH‐PCBs and maternal and neonatal TH levels, taking the maternal‐fetal TH transfer into account. Methods: In this prospective birth cohort (the “Hokkaido study”) we included 222 mother‐neonate pairs. We measured five OH‐PCB isomers in maternal serum samples either during pregnancy or within 5 days of delivery. Thyroid stimulating hormone (TSH) and free thyroxine (FT4) levels were obtained from maternal blood samples at an early gestational stage (median; 11.1 weeks) and from heel prick samples of neonates between 4 and 7 days after birth. Multiple linear regression analysis and structural equation modeling (SEM) were performed to investigate the associations between maternal OH‐PCB and maternal and neonatal TH levels. Results: Median concentration of ∑OH‐PCBs was 25.37 pg/g wet weight. The predominant isomer was 4‐OH‐CB187, followed by 4‐OH‐CB146+3‐OH‐CB153. In the fully adjusted linear regression analysis, maternal ∑OH‐PCBs was positively associated with maternal FT4, and 4‐OH‐CB187 was positively associated with both maternal and neonatal FT4 levels. Maternal OH‐PCBs showed no significant association with TSH among mothers and neonates. Path analysis indicated the indirect pathway from 4‐OH‐CB187 exposure to increased neonatal FT4, via maternal THs and neonatal TSH. Conclusions: These findings suggest that maternal exposure to OH‐PCBs during pregnancy may increase both maternal and neonatal FT4 levels. Neonatal FT4 is presumed to be increased by prenatal 4‐OH‐CB187 indirectly, and this process may be mediated by maternal THs and neonatal TSH. HighlightsWe examined the effect of OH‐PCBs on maternal and neonatal thyroid hormones (THs).Maternal OH‐PCB exposure were positively associated with both maternal and neonatal FT4.Maternal OH‐PCB exposure were not associated with maternal or neonatal TSH.Path analysis suggests the indirect effect of OH‐PCB exposure on neonatal FT4 via maternal THs and neonatal TSH.