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Howe CG, Eckel SP, Habre R, et al. Association of Prenatal Exposure to Ambient and Traffic-Related Air Pollution With Newborn Thyroid Function: Findings From the Children’s Health Study. JAMA Netw Open. 2018;1(5):e182172. doi:https://doi.org/10.1001/jamanetworkopen.2018.2172
Are prenatal ambient and traffic-related air pollutant exposures associated with newborn total thyroxine concentrations, and are there critical windows of exposure?
In a cohort study of a subset of 2050 newborns from the Children’s Health Study in southern California, an increase of 2 standard deviations in prenatal exposure to particulate matter in air pollution was associated with higher newborn total thyroxine measures. Months 3 to 7 and 1 to 8 of pregnancy were identified as critical windows of exposure to particulate matter and associated higher thyroxine levels.
The fetal thyroid gland may be susceptible to particulate matter air pollution toxicity, especially during early pregnancy and midpregnancy.
Thyroid hormones are critical for fetal growth and development. Prenatal particulate matter (PM) air pollution exposure has been associated with altered newborn thyroid function, but other air pollutants have not been evaluated, and critical windows of exposure are unknown.
To investigate the association of prenatal exposure to ambient and traffic-related air pollutants with newborn thyroid function and identify critical windows of exposure.
Design, Setting, and Participants
This cohort study used data from 2050 participants in the Children’s Health Study. Statistical analyses were conducted from 2017 to 2018 using pregnancy and birth data from 1994 to 1997 for a subset of participants recruited from schools in 13 southern California communities in 2002 to 2003 when participants were 5 to 7 years of age. Participants were included in statistical analyses if they could be linked to their newborn blood spot and had complete monthly exposure measures for at least 1 air pollutant across pregnancy.
Prenatal monthly averages of ambient (PM diameter <2.5 μm [PM2.5] or <10 μm [PM10], nitrogen dioxide, and ozone) and traffic-related (freeway, nonfreeway, and total nitrogen oxides) air pollutant exposures were determined using inverse distance-squared weighting of central monitoring data and the California Line Source Dispersion model, respectively.
Main Outcomes and Measures
Newborn heel-stick blood spot total thyroxine (TT4) measures were acquired retrospectively from the California Department of Public Health.
Participants included 2050 newborns (50.5% male), with a median (interquartile range) age of 20 (15-29) hours. The majority of newborns were Hispanic white (1202 [58.6%]) or non-Hispanic white (638 [31.1%]). Sixty-six (3.2%) were black and 144 (7.0%) were from other racial/ethnic groups. The mean (SD) newborn TT4 measure was 16.2 (4.3) μg/dL. A 2-SD increase in prenatal PM2.5 (16.3 μg/m3) and PM10 (22.2 μg/m3) was associated with a 1.2-μg/dL (95% CI, 0.5-1.8 μg/dL) and 1.5-μg/dL (95% CI, 0.9-2.1 μg/dL) higher TT4 measure, respectively, in covariate-adjusted linear regression models. Other pollutants were not consistently associated with newborn TT4. Distributed lag models revealed that PM2.5 exposure during months 3 to 7 of pregnancy and PM10 exposure during months 1 to 8 of pregnancy were associated with significantly higher newborn TT4 concentrations (P < .05).
Conclusions and Relevance
Prenatal PM exposure, particularly in early pregnancy and midpregnancy, is associated with higher newborn TT4 concentrations. Future studies should assess the health implications of PM-associated differences in newborn TT4 concentrations.
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