Background Few previous studies examined the impact of prenatal air pollution exposures on fetal development based on ultrasound measures during pregnancy. Methods In a prospective birth cohort of more than 500 women followed during 1993-1996 in Los Angeles, California, we examined how air pollution impacts fetal growth during pregnancy. Exposure to traffic related air pollution was estimated using CALINE4 air dispersion modeling for nitrogen oxides (NOx) and a land use regression (LUR) model for nitrogen monoxide (NO), nitrogen dioxide (NO2) and NOx. Exposures to carbon monoxide (CO), NO2, ozone (O3) and particles <10 μm in aerodynamic diameter (PM10) were estimated using government monitoring data. We employed a linear mixed effects model to estimate changes in fetal size at approximately 19, 29 and 37 weeks gestation based on ultrasound. Results Exposure to traffic-derived air pollution during 29 to 37 weeks was negatively associated with biparietal diameter at 37 weeks gestation. For each interquartile range (IQR) increase in LUR-based estimates of NO, NO2 and NOx, or freeway CALINE4 NOx we estimated a reduction in biparietal diameter of 0.2-0.3 mm. For women residing within 5 km of a monitoring station, we estimated biparietal diameter reductions of 0.9-1.0 mm per IQR increase in CO and NO2. Effect estimates were robust to adjustment for a number of potential confounders. We did not observe consistent patterns for other growth endpoints we examined. Conclusions Prenatal exposure to traffic-derived pollution was negatively associated with fetal head size measured as biparietal diameter in late pregnancy.

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 (RI), the pulsatility index (PI), and the systolic/diastolic (S/D) ratio. We estimated exposure to NO2 at the home address of the mother using a land use regression (LUR) model and to NOx 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: LUR-derived NO2 and CALINE4-derived NOx 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.