The shared pathoetiological effects of particulate air pollution and the social environment on fetal-placental development

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.

Figures

Figure 1

A conceptual framework of the shared mechanisms of socioeconomic determinants and particulate air pollution exposure contributing to adverse pregnancy outcomes. The physical environment (orange) consisting of particulate air pollution and the social environment (green) consisting of community and individual-level social factors/stressors converge to affect the fetal-placental environment (blue) via oxidative stress and inflammatory mechanisms potentially leading to adverse pregnancy outcomes.

Figure 2

Proposed pathways contributing to adverse pregnancy outcomes. The co-presence of maternal and paternal biological factors can result in protection or increased susceptibility to the interaction with the physical and social environments. Cumulative negative exposures early in pregnancy resulting in excess oxidative stress and inflammation may cause a cascade of events leading to defective deep placentation. Depending on the degree of severity, the reduced transplacental perfusion can result in various pathologies associated with a range of obstetric complications and outcomes [60, 61, 69, 70].

Figure 3

Proposed pathways of particulate air pollution contributing to oxidative stress and inflammation leading to adverse pregnancy outcomes. Exposure to PM and its associated constituents of transition metals, PAHs, and other organic molecules affect the cardiovascular and metabolic systems which are highly active throughout pregnancy. For example, detoxification of PAHs and other organic toxins activate AhR signalling resulting in additional oxidative stress if antioxidant defenses are limited or impaired [55, 79, 98, 108, 109, 199].

Figure 4

Proposed pathways of how the social environment interacts to produce excess systemic and placental oxidative stress and inflammation leading to adverse pregnancy outcomes. The pregnant woman is nested within and influenced by neighbourhood/community-level factors which can exasperate or buffer the individual-level biological and behavioural factors [24, 26, 54, 128, 224, 225].