Iodine Status, Fluoride Exposure, and Thyroid Function in Pregnant Women in the United States

Abstract

ObjectivesIodine (I) is an essential nutrient for fetal neurodevelopment through its role in thyroid function. Like I, fluoride (F) is a halogen and urinary F concentration (UFC) has been linked to increased thyroid stimulating hormone (TSH) in non-pregnant adults with I deficiency. We hypothesize that F and I may interact in their role on thyroid function among pregnant women.MethodsPregnant women (n = 966) provided urine between 12- and 20-weeks gestation. UIC was measured by the modified Sandell-Kolthoff reaction and UFC by a F-sensitive electrode. Enzyme-linked immunosorbent assay (ELISA) was used to measure plasma TSH. Associations between 1) UIC and TSH, 2) UFC and TSH, and 3) I status, UFC, and TSH were estimated using generalized linear models with gamma distribution and log link. Potential interactions between I status and UFC in association with TSH was also investigated.ResultsThe cohort UIC (median: 154.2 µg/L, IQR: 92.9,271.7) indicated a population with marginally adequate I status by WHO criteria. Nearly half (n = 464, 48%) were I insufficient (UIC ≤ 150 µg/L). Median UFC (0.832 mg/L, IQR: 0.495, 1.29) was above the benchmark used to determine risk for child cognition (0.2 mg/L) (Grandjean et al., Risk Anal 2021; doi: 10.1111/risa.13767). Higher UIC was associated with increased TSH (β = 0.0003, SE = 0.0001, p = 0.01). UFC was not related to TSH (p = 0.13); however, a significant interaction between UIC and UFC was observed (p = 0.01). When analyzing only I insufficient participants, UFC and TSH were inversely associated (β = 0.1488, p = 0.0004). No association between UFC and TSH was observed for I adequate participants (p = 0.63).ConclusionsChanges in TSH in relation to UIC and UFC were counter to our hypothesis as the relationship between UFC and TSH was inverse and only in I insufficient participants. Future research should explore if TSH is the best indicator of thyroid function in pregnancy and the mechanisms underlying the effects of pre-and postnatal F exposure on child cognition.Funding SourcesThe Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) (R01 HD083292).