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Introduction
An estimated 40% of the world’s population relies on solid biomass fuels (wood, charcoal, crop residues) for cooking or heating (Bonjour et al. 2013). The smoke generated from the combustion of these fuels is a complex mixture of gases and fine particles including many known harmful pollutants, such as carbon monoxide (CO), suspended fine particulate matter (≤ 2.5 μm; PM2.5), nitrogen oxide, and polycyclic aromatic hydrocarbons. Household air pollution from biomass burning is now acknowledged as a major contributor to the global disease burden (Lim et al. 2012).
During pregnancy, exposure to biomass cooking smoke has been linked with a reduction in birth weight, an increase in stillbirth, and a rise in preterm births in a number of epidemiologic investigations (Amegah et al. 2014). Despite a growing evidence base of reproductive harm from household air pollution, methodological shortcomings remain, including challenges in exposure assessment and the potential for uncontrolled confounding. Pathological examination of placentas from pregnant women exposed to biomass cook smoke may identify lesions that are known to be associated with adverse pregnancy outcomes. Furthermore, specific lesions may shed light on the underlying pathophysiology and suggest targets for amelioration of risk. For these reasons, we aimed to characterize placental pathology associated with household air pollution among women cooking with biomass fuels in an African population.
We hypothesized that the placenta would demonstrate inflammatory lesions in the setting of high household air pollutant exposure, and specifically when levels of PM2.5 exposure are high. Cardiopulmonary researchers have demonstrated both that inhaled ultrafine particles can enter the circulation and that systemic measures of inflammation increase following exposure to air pollution (Donaldson et al. 2005; Scapellato and Lotti 2007). We posited that damage to the placenta may occur directly from exposure to circulating particles or secondary to systemic inflammation, either of which may result in any of the well-defined histologic placental chronic inflammatory lesions-chronic villitis (Figure 1), chronic chorioamnionitis, or intervillositis. Second, we hypothesized that biomass smoke exposed placentas would demonstrate hypoxic lesions, particularly as CO levels increase. CO impairs placental oxygen transport by increasing levels of carboxyhemoglobin, thereby displacing oxygen from hemoglobin and reducing its availability to the fetus (Soothill et al. 1996). The placental response in the setting of hypoxia is an increase in the...