Association between prenatal exposure to air pollutants and newborn thyroxine (T4) levels

Abstract

BACKGROUND AND AIM: Thyroid hormones play a key role in fetal and child development. Recent studies have linked prenatal exposure to atmospheric contaminants with changes in thyroid hormone levels in newborns, but the data from the few studies that have explored this issue are inconclusive. The present study aims to assess the association of total thyroxine (TT4) levels in newborns with weekly prenatal exposure to PM2.5 and NO2 and to identify sensitivity windows to exposure to air pollution in different developmental stages. METHODS: This prospective cohort study included 463 mother-child pairs from the INMA-Gipuzkoa project with data on PM2.5 and NO2 exposure and TT4 levels at birth. PM2.5 and NO2 levels were measured by high-volume aerosol samplers and passive samplers respectively during the women’s pregnancies. TT4 levels were measured in heel-prick blood samples from infants. Data on maternal and infant covariates were gathered through questionnaires administered in the first and third trimesters of pregnancy and review of clinical records. Potential associations of PM2.5 and NO2 with TT4 levels over the entire pregnancy was assessed by linear regression models and DLMs were used to identify susceptibility windows. RESULTS:PM2.5 exposure during pregnancy was positively associated with infant TT4 level at birth (β [95% CI]= 0.198 [0.091, 0.305]. DLMs identified three different sensitivity windows, one in the periconceptional period with a negative association between PM2.5 exposure and TT4 levels at birth, and a second (weeks 12-17) and a third one (weeks 31-37) with a positive association. In addition, the later the exposure, the stronger the association. In contrast, no association was observed between NO2 exposure and TT4 levels. CONCLUSIONS:The results indicate that prenatal exposure to PM2.5 could lead to a thyroid function impairment in newborns. Further, they suggest that the effect of PM2.5 could be partially mediated by maternal thyroid function. KEYWORDS: Prenatal exposure, PM2.5, NO2, TT4 at birth, sensitivity windows