Abstract
Exposure to particulate air pollution and socioeconomic risk factors are shown to be independently associated with adverse pregnancy outcomes; however, their confounding relationship is an epidemiological challenge that requires understanding of their shared etiologic pathways affecting fetal-placental development. The purpose of this paper is to explore the etiological mechanisms associated with exposure to particulate air pollution in contributing to adverse pregnancy outcomes and how these mechanisms intersect with those related to socioeconomic status. Here we review the role of oxidative stress, inflammation and endocrine modification in the pathoetiology of deficient deep placentation and detail how the physical and social environments can act alone and collectively to mediate the established pathology linked to a spectrum of adverse pregnancy outcomes. We review the experimental and epidemiological literature showing that diet/nutrition, smoking, and psychosocial stress share similar pathways with that of particulate air pollution exposure to potentially exasperate the negative effects of either insult alone. Therefore, socially patterned risk factors often treated as nuisance parameters should be explored as potential effect modifiers that may operate at multiple levels of social geography. The degree to which deleterious exposures can be ameliorated or exacerbated via community-level social and environmental characteristics needs further exploration.
Highlights
Over the last decade, chronic exposure to ambient air pollution has become increasingly recognized as an important risk factor underlying adverse pregnancy outcomes (APOs) [1,2,3,4,5,6,7,8,9]
We review the role of the placenta in this context, describing its physiology and obstetrical pathologies followed by a description of particulate air pollution and its toxicokinetics in relation to placentation and how it can lead to APOs
The “Great Obstetrical Syndromes” [60] such as early/recurrent miscarriage, pregnancy induced hypertension and preeclampsia (PIH/PE), fetal growth restriction (FGR), placental abruption, prelabour rupture of the fetal membranes (PROM), and spontaneous preterm labour may share common etiological mechanisms arising from defective deep placentation (DDP) [61, 62]
Summary
Chronic exposure to ambient air pollution has become increasingly recognized as an important risk factor underlying adverse pregnancy outcomes (APOs) [1,2,3,4,5,6,7,8,9]. The first is the popularization of multilevel statistical models and the ability to separate the individual-level effects from those of their encompassing social and physical environments [20,21,22,23,24,25,26]. Synergism was observed between aqueous cigarette tar and other respirable particles (e.g., asbestos fibers, particulate matter, and diesel exhaust) [35]. Recognition of these interactions has been incorporated into several conceptual models and study designs of cumulative risk of chemical and nonchemical exposures [36,37,38,39] with models recently developed to identify these potentially double-exposed populations [40, 41]. Two complimentary reviews of these models have been recently published [42, 43]
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