Abstract

Exposure to air pollution may adversely impact placental function through a variety of mechanisms; however, epidemiologic studies have found mixed results. We examined the association between traffic exposure and placental-related obstetric conditions in a retrospective cohort study on Cape Cod, MA, USA. We assessed exposure to traffic using proximity metrics (distance of residence to major roadways and length of major roadways within a buffer around the residence). The outcomes included self-reported ischemic placental disease (the presence of at least one of the following conditions: preeclampsia, placental abruption, small-for-gestational-age), stillbirth, and vaginal bleeding. We used log-binomial regression models to estimate risk ratios (RR) and 95% confidence intervals (CI), adjusting for potential confounders. We found no substantial association between traffic exposure and ischemic placental disease, small-for-gestational-age, preeclampsia, or vaginal bleeding. We found some evidence of an increased risk of stillbirth and placental abruption among women living the closest to major roadways (RRs comparing living <100 m vs. ≥200 m = 1.75 (95% CI: 0.82–3.76) and 1.71 (95% CI: 0.56–5.23), respectively). This study provides some support for the hypothesis that air pollution exposure adversely affects the risk of placental abruption and stillbirth; however, the results were imprecise due to the small number of cases, and may be impacted by non-differential exposure misclassification and selection bias.

Highlights

  • Optimal placental vascularization is important for a healthy pregnancy, as the placenta is responsible for the fetal-maternal exchange of gas and nutrients [1]

  • When we examined the individual components of ischemic placental disease and other obstetrical outcomes that may be related to placental dysfunction, we found some evidence that traffic exposure is associated with an increased risk of placental abruption and stillbirth (Table 5; adjusted risk ratios (RR) for living

  • We were unable to stratify models for preeclampsia, placental abruption, and stillbirth due to small numbers. In this retrospective cohort study, we found no substantial association between traffic exposure and ischemic placental disease overall

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Summary

Introduction

Optimal placental vascularization is important for a healthy pregnancy, as the placenta is responsible for the fetal-maternal exchange of gas and nutrients [1]. Preeclampsia, placental abruption, and intrauterine growth restriction are pregnancy conditions that may share a common pathophysiologic mechanism through placental insufficiency, due to the incomplete trophoblast invasion of the maternal spiral arteries [2]. Placental insufficiency causes uteroplacental underperfusion, chronic hypoxia, and placental ischemia [3,4], and can lead to serious maternal and fetal complications including hemorrhaging, maternal mortality, fetal distress, brain damage, preterm delivery, and stillbirth [2,5,6,7]. Given the common mechanistic origins and epidemiologic patterns of preeclampsia, placental abruption, and intrauterine growth restriction, the term ischemic placental. Public Health 2017, 14, 682; doi:10.3390/ijerph14070682 www.mdpi.com/journal/ijerph

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