Abstract
Prenatal air pollutant exposure has been linked to impaired fetal growth. However, its special vulnerability windows and biological mechanisms remain unclear. A prospective birth cohort study including 7419 mother-newborn pairs was conducted from 2015 to 2020 to determine critical exposure windows and examine whether cortisol mediates the relationship between air pollutant exposure and fetal growth. Air pollutant data for PM2.5, PM10, SO2, and CO were obtained from the Hefei City Ecology and Environment Bureau. Data on fetal ultrasound measurements and birth size were collected. Maternal and cord blood samples were used for measuring cortisol. Prenatal air pollutant (PM2.5, PM10, SO2, and CO) exposure, particularly in the first trimester, was associated with reduced fetal size from later pregnancy to birth. An IQR increase in PM2.5 (β = 0.082, 95%CI: 0.029, 0.135), PM10 (β = 0.086, 95%CI: 0.036, 0.136), SO2 (β = 0.086, 95%CI: 0.028, 0.144), and CO (β = 0.063, 95%CI: 0.017, 0.109) exposure in the first trimester was associated with higher cord blood cortisol levels. Significant relationships were observed between air pollutant exposure in the first trimester and increased ratio of cord to maternal blood cortisol levels. Exposure to high levels of cord blood cortisol significantly reduced the Z scores of birth weight (β = −0.17, 95%CI: −0.23, −0.10), length (β = −0.09, 95%CI: −0.16, −0.03), and head circumference (β = −0.33, 95%CI: −0.42, −0.25). Mediation analysis showed that the association of air pollutant exposure in the first trimester with neonatal parameters mediated by cord blood cortisol was 20.62%. These results indicated that air pollutant exposure during pregnancy could reduce fetal growth by the increased fetal cortisol levels due to placental barrier impairment, with the critical window of exposure occurring in the first trimester.
Published Version
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