Prenatal air pollution exposure, smoking, and uterine vascular resistance

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Abstract

Background:

Prenatal exposure to air pollution and smoking increases the risk of pregnancy complications and adverse birth outcomes, but pathophysiologic mechanisms are still debated. Few studies to date have examined the influence of air pollution on uterine vascular resistance, and no studies have examined the independent impact of these exposures. We aimed to assess the impact of prenatal exposure to traffic-related air pollution and smoking on uterine vascular resistance.

Methods:

Our study included 566 pregnant women recruited between 1993 and 1996 in Los Angeles who completed visits at three gestational ages. Information on smoking was collected, and uterine vascular resistance was measured at each visit by Doppler ultrasound. We calculated three resistance indices: the resistance index, the pulsatility index, and the systolic/diastolic ratio. We estimated exposure to NO2 at the home address of the mother using a land use regression model and to nitrogen oxides using CALINE4 air dispersion modeling. We used generalized linear mixed models to estimate the effects of air pollution and smoking on uterine vascular resistance indices.

Results:

Land use regression–derived NO2 and CALINE4-derived nitrogen oxides exposure increased the risk of high uterine artery resistance in late pregnancy. Smoking during pregnancy also increased the risk of higher uterine resistance and contributed to bilateral notching in mid-pregnancy.

Conclusion:

Our results suggest that uterine vascular resistance is a mechanism underlying the association between smoking and air pollution and adverse birth outcomes.

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