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While the effects of ambient pollutants on adverse perinatal outcomes have been studied, most studies have focused on preterm birth, stillbirth, and low birthweight. Few studies have examined the effects of ambient pollutants on prelabor rupture of membranes (PROM). This study was designed to explore the acute effects of ambient pollutants on both term PROM (TPROM) and preterm PROM (PPROM). We enrolled pregnant women receiving antenatal care between October 2013 and December 2019 at the International Peace Maternity and Child Health Hospital (IPMCHH). The effects of ambient pollutants (including PM 2.5 , PM 10 , SO 2 , CO, NO 2 , and 8-h O 3) on TPROM and PPROM were estimated using generalized additive models (GAMs). Exposure-response relationship curves were also evaluated using GAMs after adjustment for confounding factors. Potential lagged effects were examined using various lag models. The data of 100,200 pregnant women who delivered at IPMCHH were analyzed. The fitted spline curves for PPROM were similar to the temporal trends of PM 2.5 , PM 10 , SO 2 , CO and NO 2 but not O 3 , while those for TPROM were different from the temporal trends of all six air pollutants. An increased risk of PPROM was associated with increased concentrations of PM 2.5 , PM 10 , SO 2 and CO on lag days 2 and 3, while no association was found between PPROM and daily concentration of O 3. After adjustment for confounding factors, there was a shift in the exposure-response curves, indicating associations between PPROM and PM 2.5 , PM 10 , SO 2 , and CO on lag days 2–3. Interaction effects of PM 2.5 , PM 10 , SO 2 , and CO were also found to increase the risk of PPROM. In conclusion, acute exposures to six critical air pollutants were not associated with an increased risk of TPROM; however, PM 2.5 , PM 10 , SO 2 , and CO were found to interact, increasing the risk for PPROM on lag days 2 and 3. [Display omitted] • Acute exposure to these air pollutants did not increase the risk of TPROM. • PM 2.5 , PM 10 , SO 2 , and CO interacted with each other to increase the risk of PPROM. • No relationship between O 3 and PROM was observed. • Acute effects of 6 critical air pollutants on PROM were first studied in China. [ABSTRACT FROM AUTHOR]

Despite the longstanding evidence on the effect of air pollutants on preterm birth (PTB), few studies have focused on its subtypes, including spontaneous preterm birth (sPTB) and medically indicated preterm birth (miPTB). Most studies evaluated only the short-term or long-term effects of particulate matter (PM) on PTB. Thus, we designed this study, based on a cohort of 179,385 women, to evaluate both short- and long-term effects of PM with diameters ≤2.5 μm and ≤10 μm (PM 2.5 and PM 10) on PTB, sPTB and miPTB in Shanghai. Generalized additive models (GAMs) were applied to evaluate short-term effects. Lagged effects were identified using different lag structures. Exposure-response correlation curves were plotted using GAMs after adjustment for confounders. ORs and 95% CIs were calculated using logistic regression to estimate the long-term effect after adjustment for confounders. There was 5.67%, 3.70% and 1.98% daily incidence of PTB, sPTB, and miPTB on average. Every 10 μg/m3 increase in PM 2.5 and PM 10 was positively associated with PTB and sPTB at lag 2 day. The exposure-response curves (lag 2 day) indicated a rapid increase in sPTB for PM 2.5 and a linear increase for PM 10 , in PTB for PM 2.5 and PM 10 at concentrations over 100 μg/m3. Regarding long-term exposure, positive associations were found between 10 μg/m3 increases in PM 2.5 and PM 10 in 3rd trimester and greater odds of sPTB (aOR: 1.042, 95% CI: 1.018–1.065, and 1.018, 95% CI:1.002–1.034), and during the 3 months before conception and miPTB (aOR: 1.023, 95% CI: 1.003–1.042, and 1.017, 95% CI: 1.000–1.036). Acute exposure to PM 2.5 and PM 10 at lag 2 day and chronic exposure in 3rd trimester was significantly associated with sPTB, while miPTB was related to chronic exposure during the 3 months before pregnancy. These findings indicate that susceptibility windows of PM exposure can be influenced by different underlying etiologies of PTB. [Display omitted] • Short-term exposure to PM 2.5 and PM 10 at lag 2 day was significantly associated with an increased risk of sPTB. • At lag 2 day, the exposure-response curve was steeper in sPTB for PM 2.5 and linear for PM 10 at concentrations > 100 μg/m3. • Long-term exposure to PM 2.5 and PM 10 in the third trimester during pregnancy adversely affected sPTB. • An increased risk of miPTB was related to long-term exposure to PM 2.5 and PM 10 during the 3 months before pregnancy. [ABSTRACT FROM AUTHOR]