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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 PM 2.5 , PM 10 , SO 2 , 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 (PM 2.5 , PM 10 , SO 2 , and CO) exposure, particularly in the first trimester, was associated with reduced fetal size from later pregnancy to birth. An IQR increase in PM 2.5 (β = 0.082, 95% CI : 0.029, 0.135), PM 10 (β = 0.086, 95% CI : 0.036, 0.136), SO 2 (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. • Prenatal air pollutant exposure impaired fetal growth from late pregnancy to birth. • Exposure to air pollutants was associated with higher cord blood cortisol levels. • Air pollutant exposure increased the ratio of cord to maternal blood cortisol levels. • The critical windows of air pollutant exposure were in the first trimester. • Cord blood cortisol mediated the effect of air pollutant exposure on fetal growth. [ABSTRACT FROM AUTHOR]

Mounting evidence has demonstrated that air pollution exposure is associated with the increased prevalence of gestational diabetes mellitus (GDM). However, the long-term exposure effect and the time window of the maximum effect of these air pollutants on GDM and glucose homeostasis during pregnancy are unclear. We conducted this study on 5427 nondiabetic pregnant women who were admitted from three hospitals in Hefei City, China, between 2015 and 2018. The data regarding the average exposure to particulate matter (PM), sulfur dioxide (SO 2), and ozone (O 3) were estimated in a fixed monitoring station in Hefei. We used logistic regression and multiple linear regression to assess the effects of air pollutants on GDM and glucose homeostasis. Of the 5427 participants, 1119 (20.6%) had GDM. We found prepregnancy exposure to air pollutants was associated with the risk of GDM in the single pollutant model [odds and 95% confidence interval (CI) of GDM for an interquartile range (IQR) increase was 1.24 (1.06–1.45) for PM 2.5 , 1.42 (1.26–1.59) for PM 10 , 1.21 (1.10–1.33) for SO 2 and1.19 (1.08–1.31) for O 3. The risk of GDM before pregnancy was higher with long-term exposure to high-concentration pollutants compared with the risk in pregnant women who were not exposed to high-concentration pollutants (χ2 = 41.52, p for trend <0.0001); the ORs and 95% CI values for the exposure times of 1, 2, and 3 months were 1.28 (0.96–1.72), 1.52 (1.06–2.19), and 1.69 (1.11–2.57), respectively. The results showed a positive effect of exposure to higher-concentration air pollutants 1 year before pregnancy on glucose homeostasis during pregnancy. The time windows of the maximum effect of PM 2.5 , PM 10 , SO 2 , and O 3 on GDM were different. The time windows of the maximum effect of PM 2.5 , PM 10 , and SO 2 were 6 months, 5 months, and 1 month before the last menstrual period (LMP) and 3 months after the LMP, respectively. The time windows of the maximum effect of air pollution on glucose homeostasis indicators from the 2-h 75-g oral glucose tolerance test were similar to the abovementioned results. Prepregnancy long-term air pollution exposure was associated with a higher risk of developing GDM by affecting glucose metabolism. The time window of the maximum effect of PM on GDM and glucose metabolism indicators was observed earlier than that of SO 2 and O 3. Image 1 • The GDM risk increased gradually with prolonged exposure time to high-concentration pollutants before pregnancy. • Long-term air pollution exposure before pregnancy was positively associated with glucose levels during pregnancy. • The time window of PM on GDM and glucose indicators was observed earlier than that of SO 2 and O 3. [ABSTRACT FROM AUTHOR]

This study enrolled 3266 pregnant women, to explore the relationship of prenatal phthalate exposure with the risk of preterm birth and gestational age. All participants filled questionnaires and provided with up to three urine samples during three trimesters. Seven phthalate metabolites in urines were measured. The incidences of very preterm, late preterm, early-term, late-term and postterm births were 0.58%, 3.52%, 24.22%, 10.53%, and 0.34%, respectively. Non-linear relationships were shown between phthalate metabolites and gestational age. Except for monomethyl phthalate (OR = 1.65, 95%CI = 1.17–2.34), the average concentrations of phthalate metabolites were associated with a slightly and insignificantly increased risk of overall preterm birth (<37+0 gestational weeks). Through a restricted cubic spline regression, phthalate metabolites were found to be related to the risk of overall preterm birth in a linear manner (p -value >0.05) or a non-linear manner (p -value <0.05). All curves indicated the overall preterm birth risk rose with the increase of phthalate metabolite concentrations. Finally, compared with full-term birth (39+0 to 40+6 gestational weeks), phthalate metabolites were associated with the elevated risks of very preterm, late preterm and postterm births, although some relationships were not statistically significant. In conclusion, these findings suggested non-linear associations between phthalate metabolites and gestational age. Exposure to some phthalate metabolites was associated with increased risks of overall preterm birth and postterm birth. • Rates of very preterm, late preterm, early-term and late-term births were 0.58%, 3.52%, 24.22% and 10.53%, respectively. • Non-linear relationship was observed between certain phthalate metabolites and the odds ratio of overall preterm birth. • Some phthalates were associated with increased risks of very preterm, late preterm and postterm births. • Non-linear curves for associations between phthalates and gestational age were revealed. Capsule: Based on a cohort study with large sample size, the levels of phthalate metabolites in urine at 3 time points during pregnancy were analyzed in relation to gestational age and preterm birth, which aimed to confirm the previous findings in this topic. [ABSTRACT FROM AUTHOR]