Label-free detection of uptake, accumulation, and translocation of diesel exhaust particles in ex vivo perfused human placenta

Abstract

Background Pregnant 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. Results Here, 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. Conclusions Overall, 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.

An Attempt to Detect Ambient Black Carbon in the Human Brain Using Mass Spectrometry Imaging

“…Exogenous black carbon particles have been identified in many human organs such as adult human lung, healthy children urine, and the fetal side of human placenta, − so we were curious to see if it is present in the human brain as well. For reference, we summarized the existing reports about the detection of PM 2.5 species inside human brains.…”

“…Fine particulate matter (PM 2.5 , particles with aerodynamic diameter less than 2.5 μm) pollution seriously threatens human health. − Ultrafine particles (UFPs, particles with aerodynamic diameter less than 0.1 μm) are particularly important, as they may be able to translocate across the respiratory epithelium and other biological barriers to translocate in the human body via the circulatory system. − Black carbon (or soot) is a frequent component of PM 2.5 , which exists ubiquitously in the atmosphere. − It may be able to invade into the human body through the respiratory system or cross other biological barriers due to their nanoscale size and then accumulate in intracorporeal organs. − It has been documented that long-term exposure to black carbon particles may cause a range of health risks, including respiratory diseases, cardiovascular diseases, and neurodevelopmental disorders. − Notably, earlier studies have detected black carbon particles in different human organs, including human lung, healthy children urine, and the fetal side of human placenta. − Regarding the human brain, some human and animal experiments have suggested that the ambient PM 2.5 species may invade the brain, resulting in the upregulation of inflammatory cytokines and disorder of the central nervous system (CNS). ,− However, evidence is still insufficient to unravel the exact exposure pathways of PM 2.5 species entering the human brain and their related toxicological mechanisms.…”

Placental-fetal distribution of carbon particles in a pregnant rabbit model after repeated exposure to diluted diesel engine exhaust

“…Previously, we have identified the presence of ambient air pollution particles in rabbit (i.e., small particles and CP-like particles indicative of diesel exhaust particles) [ 8 ] and human maternal-fetal tissue samples [ 25 , 28 ] with a particular emphasis on the placenta and its role as a protective barrier for the fetus. In this study, we confirm and elaborate on these findings by identifying the translocation of CPs, originating from diesel engine exhaust, to the fetal circulation and organs in a pregnant rabbit model using our detection technique based on the white-light generation of CPs under ultrashort pulsed laser illumination [ 25 , 26 ].…”

Novel electrospun chitosan/PEO membranes for more predictive nanoparticle transport studies at biological barriers

“…59 The CTB layer was omitted since it considerably thins after the first trimester and has been suggested to play a negligible role in substance transfer via the syncytium. 60 Furthermore, we did not include the endothelial cells for this study, since previous work indicated that NPs are often retained in the trophoblast layer [61][62][63] and the barrier capacity of a placental trophoblast monolayer to NPs was equal to the one of a co-culture with trophoblast cells and placental microvascular endothelial cells (HPEC). 32 Among the different trophoblast cell lines that are available, the BeWo b30 clone derived from a human malignant choriocarcinoma was favored, because it best resembles the in vivo STB structure and function.…”