Abstract
BackgroundPregnant women and developing fetuses comprise a particularly vulnerable population as multiple studies have shown associations between prenatal air pollution exposure and adverse pregnancy outcomes. However, the mechanisms underlying the observed developmental toxicity are mostly unknown, in particular, if pollution particles can cross the human placenta to reach the fetal circulation.ResultsHere, we investigated the accumulation and translocation of diesel exhaust particles (DEPs), as a model particle for combustion-derived pollution, in human perfused placentae using label-free detection by femtosecond pulsed laser illumination. The results do not reveal a significant particle transfer across term placentae within 6 h of perfusion. However, DEPs accumulate in placental tissue, especially in the syncytiotrophoblast layer that mediates a wealth of essential functions to support and maintain a successful pregnancy. Furthermore, DEPs are found in placental macrophages and fetal endothelial cells, showing that some particles can overcome the syncytiotrophoblasts to reach the fetal capillaries. Few particles are also observed inside fetal microvessels.ConclusionsOverall, we show that DEPs accumulate in key cell types of the placental tissue and can cross the human placenta, although in limited amounts. These findings are crucial for risk assessment and protection of pregnant women and highlight the urgent need for further research on the direct and indirect placenta-mediated developmental toxicity of ambient particulates.
Highlights
Pregnant women and developing fetuses comprise a vulnerable population as multiple studies have shown associations between prenatal air pollution exposure and adverse pregnancy outcomes
Observed adverse effects could be caused by three major pathways: (i) the placental translocation of particles provoking direct fetotoxic effects, and/or (ii) the indirect maternal mediated effects caused by the accumulation of particles in maternal tissues causing maternal organ dysfunction or release of inflammatory mediators and soluble signaling factors that can reach the placenta and fetus and possibly induce toxic effects and/or (iii) the indirect placental mediated effects caused by the accumulation of particles in placental tissues disrupting essential barrier and transport functions or inducing the release of secondary mediators that indirectly interfere with fetal development [12, 13]
Transmission electron microscopy (TEM) images of aerosolized Diesel exhaust particle (DEP) show a heterogeneous mixture of particles of different sizes and morphologies see references [29, 30])
Summary
Pregnant women and developing fetuses comprise a vulnerable population as multiple studies have shown associations between prenatal air pollution exposure and adverse pregnancy outcomes. Observed adverse effects could be caused by three major pathways: (i) the placental translocation of particles provoking direct fetotoxic effects, and/or (ii) the indirect maternal mediated effects caused by the accumulation of particles in maternal tissues causing maternal organ dysfunction or release of inflammatory mediators and soluble signaling factors that can reach the placenta and fetus and possibly induce toxic effects and/or (iii) the indirect placental mediated effects caused by the accumulation of particles in placental tissues disrupting essential barrier and transport functions or inducing the release of secondary mediators that indirectly interfere with fetal development [12, 13] In this regard, Bové et al recently detected black carbon (BC) particles, a constituent of combustionderived particulate matter, in the placental tissue of pregnant women in function of ambient exposure levels [14]. There is still an urgent and unmet need to provide human-relevant data on fetal translocation of ambient combustion-related particulates, including quantitative data on transfer rates and elucidate cell typespecific localization of the particles in the native placental tissue
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