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Air Pollution, Maternal Hypertensive Disorders, and Preterm Birth.

ABSTRACT: Background:Air pollution has been associated with hypertension and preterm birth. We examined if prenatal exposure to air pollutants was associated with gestational hypertension and if its association with preterm birth was modified by maternal hypertension. Methods:Data were from birth certificates and hospital discharge records of 252,205 women in San Joaquin Valley of California from 2000-2006. Air quality data were assigned from 24-hour averages of nitrogen dioxide (NO2), particulate matter <10?m (PM10) and <2.5?m (PM2.5), and carbon monoxide (CO) for different averaging periods over pregnancy. We estimated odds of preterm birth and multiplicative interaction between each pollutant and hypertensive disorder. Results:Among normotensive women, odds of preterm birth were slightly higher for higher exposure to all pollutants over the entire pregnancy. Patterns were similar among women with a hypertensive disorder. Among 32-36 week births there was effect modification for exposure to NO2 and CO during the first trimester with higher odds among hypertensive women, and PM2.5 and CO during the last six weeks with higher odds among normotensive women. For 28-31 week births, there was effect modification by hypertensive status for PM10 exposure for entire pregnancy, first, and second trimester with hypertensive women consistently having lower odds of preterm birth than normotensive. Conclusion:There was some evidence of effect modification in the direction counter to our hypothesis for exposure to PM10 and early preterm birth, and CO and PM2.5 at the end of pregnancy, but overall, hypertension did not modify the relationship between pollution and preterm birth.

SUBMITTER: Weber KA

PROVIDER: S-EPMC7015251 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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Air Pollution, Maternal Hypertensive Disorders, and Preterm Birth.

Weber Kari A KA Yang Wei W Lurmann Frederick F Hammond S Katharine SK Shaw Gary M GM Padula Amy M AM

Environmental epidemiology (Philadelphia, Pa.) 20191001 5

<h4>Background</h4>Air pollution has been associated with hypertension and preterm birth. We examined if prenatal exposure to air pollutants was associated with gestational hypertension and if its association with preterm birth was modified by maternal hypertension.<h4>Methods</h4>Data were from birth certificates and hospital discharge records of 252,205 women in San Joaquin Valley of California from 2000-2006. Air quality data were assigned from 24-hour averages of nitrogen dioxide (NO<sub>2</ ...[more]

PMID: 32051927

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Project description:Recent study results on the association between maternal exposure to ambient air pollution with preterm birth have been inconsistent. The sensitive window of exposure and influence level of air pollutants varied greatly. We aimed to explore the association between maternal exposure to ambient air pollutants and the risk of preterm birth, and to estimate the sensitive exposure time window. A total of 572,116 mother-newborn pairs, daily concentrations of air pollutants from nearest monitoring stations were used to estimate exposures for each participant during 2015-2020 in Chongqing, China. We applied a generalized additive model and estimated RRs and 95% CIs for preterm birth in each trimester and the entire pregnancy period. In the single-pollutant model, we observed that each 10 μg/m3 increase in PM2.5 had a statistically significant effect on the third trimester and entire pregnancy, with RR = 1.036 (95% CI: 1.021, 1.051) and RR = 1.101 (95% CI: 1.075, 1.128), respectively. Similarly, for each 10 μg/m3 increase in PM10, there were 2.7% (RR = 1.027, 95% CI: 1.016, 1.038) increase for PTB on the third trimester, and 3.8% (RR = 1.038, 95% CI: 1.020, 1.057) increase during the whole pregnancy. We found that for each 10 mg/m3 CO increases, the relative risk of PTB increased on the first trimester (RR = 1.081, 95% CI: 1.007, 1.162), second trimester (RR = 1.116, 95% CI: 1.035, 1.204), third trimester (RR = 1.167, 95% CI: 1.090, 1.250) and whole pregnancy (RR = 1.098, 95% CI: 1.011, 1.192). No statistically significant RR was found for SO2 and NO2 on each trimester of pregnancy. Our study indicates that maternal exposure to high levels of PM2.5 and PM10 during pregnancy may increase the risk for preterm birth, especially for women at the late stage of pregnancy. Statistically increased risks of preterm birth were associated with CO exposure during each trimester and entire pregnancy. Reducing exposure to ambient air pollutants for pregnant women is clearly necessary to improve the health of infants.

Project description:IntroductionPrevious research has observed relationships between higher prenatal exposure to air pollutants and neurodevelopmental and academic outcomes later in childhood. Identifying intermediate outcomes mediating this relationship would inform prevention and intervention efforts. We aimed to investigate if previously observed associations between prenatal exposure to common urban air pollutants, diesel and perchloroethylene, and performance on third grade standardized tests were mediated through increased risk of preterm birth.MethodsData from the 1994-1998 birth cohorts within the New York City Longitudinal Study of Early Development were included in this analysis. Exposure was determined by linking the mother's residence at the time of delivery to the U.S. EPA's 1996 National Air Toxic Assessment of estimated ambient concentrations of diesel and perchloroethylene. Children's third grade standardized math and language tests were used as the markers for academic achievement. Missing data on covariates were imputed, while participants with missing information on gestational age and test scores were excluded. Linear regression models and causal mediation analysis were used to examine potential mediation by preterm birth.ResultsIn total, 187,723 and 196,122 participants were included in language and math analyses, respectively. Children with exposure to the fourth quartile of diesel or perchloroethylene had approximately 0.03 (95%CI: 0.02, 0.04) lower math z-scores when compared to individuals with exposure in the first quartile, although there was no consistent decreasing trend in math z-scores over increasing quartiles of diesel or perchloroethylene. We did not find evidence of mediation by preterm birth or exposure-mediator interaction in our models.ConclusionWe did not find evidence that observed relationships between exposure to common urban air pollutants and test z-scores in childhood were mediated through an increased risk of preterm birth. This suggests other pathways between early exposure to air pollution and neurodevelopment should be investigated with causal mediation approaches.

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Air Pollution, Maternal Hypertensive Disorders, and Preterm Birth.

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Air Pollution, Maternal Hypertensive Disorders, and Preterm Birth.

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