Background: Persistent organic pollutants are organic chemicals (such as pesticides like Dichloro-diphenyl-dichloroethylene [DDE] and industrial chemicals like polychlorinated biphenyls [PCBs]) that are resistant to degradation in the environment, accumulating in animals and human body, that also possess endocrine disrupting capabilities.

Methods: Plasma concentrations of ten PCBs as well as  DDE, hexachlorobenzene (HCB) and trans-nonachlor plus serum concentrations of thyroid stimulating hormone (TSH), free and total thyroxine (FT4 and TT4), free and total triiodothyronine (FT3 and TT3) and thyroid antibodies were measured in pregnant women in early pregnancy in the Swedish Environmental Longitudinal, Mother and child, Asthma and allergy study, a population-based prospective cohort. Outcomes were absolute concentrations of TSH and thyroid hormones, the FT4/FT3 or TT4/TT3 ratios, the TSH/FT4 ratio as a marker of the negative feedback loop, TT4/FT4 or TT3/FT3 ratios as markers of the binding of thyroid hormones to binding proteins.

Results: In 2,008 included pregnant women, higher exposure to most PCBs as well as HCB was associated with lower concentrations of FT4 (Effect estimates ranging from -0.29 to -0.19 [per 1 log-unit increase in a POP]; all P values <0.04). Moreover, higher exposure to all POPs was associated with lower FT3 concentrations (Effect estimates ranging from -0.18 to -0.07; all P values <0.001) and higher FT4/FT3 ratio and TT4/TT3 ratios (Effect estimates ranging from 1.49 to 3.44; all P values <0.0001). There was no association with TSH/FT4 ratio,  but higher exposure to all POPs except for DDE was associated with higher TT4/FT4 ratio.

Conclusions: We identified evidence that exposure to POPs, in line with evidence from experimental studies, can affect thyroid hormone metabolism in pregnant women. Future studies need to focus on potential underlying mechanisms for this finding, such as increased hepatic metabolism or deiodinase activity.