Pregnancy exposure to atmospheric pollutants and placental weight: an approach relying on a dispersion model

Abstract

Background: Epidemiologic studies suggest an association between air pollution exposure and foetal growth. The possible underlying biological mechanisms have little been studied in humans, but animal studies suggest an impact of atmospheric pollutants on placental function.

Objectives: Our aim was to investigate the association between exposure to atmospheric pollutants' levels during pregnancy and placental weight, birth weight and the placental to foetal weights ratio (PFR). For comparison purposes, the effects of active smoking on the same measures at birth have also been estimated.

Methods: The study relies on women from Eden mother-child cohort recruited in the middle-sized cities of Poitiers and Nancy (France). Nitrogen dioxide (NO(2)) and particulate matter with diameter <10 μm (PM10) home address levels during pregnancy were assessed using ADMS-Urban dispersion model. We characterized associations of NO(2), PM10 levels and active smoking with placental, birth weights and PFR by distinct linear regression models.

Results: Air pollution levels were higher and had greater variability in Nancy (5th-95th centiles, 19.9-27.9 μg/m(3) for PM10) than in Poitiers (5th-95th centiles, 14.3-17.8 μg/m(3)). Associations differed by study area: in Nancy (355 births), air pollution levels were associated with decreased placental weight and PFR, while in Poitiers (446 births), opposite or null associations were observed. Cigarette smoking was not associated with placental weight while it was associated with a decrease in birth weight and an increase in PFR.

Conclusion: Results regarding air pollution estimated effects were not similar in both study areas and should therefore be taken with caution. The placental weight decrease observed with air pollutants in the more polluted area of Nancy is consistent with a recent epidemiological study. In this area, maternal active smoking and PM10 levels tended to have opposite effects on the PFR, suggesting different mechanisms of action of both pollutants on foetal growth.