Does prenatal pollution exposure impact a newborn’s thyroid function?
Environmental pollutants are known to be associated with altered thyroid function in newborns. Infants also may be adversely affected by air pollution from particulate matter (PM)—and one of the keys may be a critical window of exposure during pregnancy, according to new research.
Published in JAMA Network Open, the findings are from a cohort study supported by the National Institutes of Health based on data from the Children’s Health Study. The authors looked at the association of prenatal exposure to ambient and traffic-related air pollutants and newborn thyroid functionand prenatal exposures.
The 2050 participants were recruited from schools in 13 southern California communities in 2002 to 2003 when they were aged 5 to 7 years. Pregnancy and birth data were from 1994 to 1997. All of the children could be linked to their newborn blood spot and complete monthly exposure measures were available for them for at least one air pollutant across their mother’s pregnancy.
The investigators used inverse distance-squared weighting of central monitoring data and the California Line Source Dispersion model (CALINE4), respectively, to determine prenatal monthly averages for ambient and traffic-related (freeway, nonfreeway, and total nitrogen oxides) air pollution exposures. (CALINE4 predicts air pollutant concentrations near roadways.) Retrospective data from the participants’ newborn heel-stick blood spot total thyroxine (TT4) measures were provided retrospectively by the California Department of Public Health.
Of the newborns, half were male and more than half were Hispanic white (50.5% and 58.6%, respectively); 66 (3.2%) were black and 144 (7.0%) were from other racial/ethnic groups. Variables assessed by the investigators included maternal and paternal tobacco use during pregnancy, maternal education, newborn sex, and total household income.
The mean (SD) newborn TT4 measure was 16.2 (4.3) µg/dL. A 2-SD increase in prenatal exposure to pollutants that were ambient and small (diameter < 2.5 µm) or larger (diameter < 10 µm) was associated with 1.2-µg/dL and 1.5- µg/dL higher TT4 measures, respectively in covariate-adjusted linear regression models. Other pollutants were not consistently associated with newborn TT4.
Distributed lag models showed that exposure to the smaller ambient pollutants during months 3 to 7 of pregnancy and to the larger particles during months 1 to 8 of pregnancy were associated with significantly higher newborn TT4 concentrations (P< .05). The strongest association between the smallest ambient pollutants and thyroid function was seen during month 5 of pregnancy versus month 1 for the association between the larger air pollutants and TT4. No significant interactions were observed between any of the pollutants and maternal smoking, newborn sex, birth weight, gestational age at birth, or season of birth.
The authors said theirs was only the second study to look at associations between ambient PM air pollution exposure and newborn thyroid function. They theorize that midpregnancy may be a particularly vulnerable time for the interaction because that is when the fetus starts producing its own supply of T4. They noted that only TT4 measures were available for most of the participants and that no information was available on maternal thyroid function. Strengths of the study included the capture of a wide range of multiple air pollutant exposures in southern California and the large sample size.