Effects of exposure to polycyclic aromatic hydrocarbons and heavy metals on placental trophoblasts and childhood inflammation

Environmental pollution, the introduction of harmful substances into the environment, is one of our most serious public health issues. The pollutants introduced into the natural environment by human activities not only destroy the natural environment but also have adverse effects on human health. Pregnant women and children are more vulnerable than the general population to the health impacts of environmental pollutant exposure. Polycyclic aromatic hydrocarbons (PAHs), and heavy metals, i.e., lead (Pb) and cadmium (Cd), have been found in the human placenta, which also can cross the placenta into the fetus. In addition, exposure to these environmental pollutants can profoundly affect the immune system, especially in children with immature immune systems. To expand our knowledge about the effects of PAHs and heavy metals on the placental trophoblast, in the present thesis, we separately revealed the impacts of environmental pollutants, such as PAHs, Pb, and Cd, on human placental trophoblast cells in vitro and childhood inflammation. In vitro studies have shown that different placental trophoblast cell lines had cell type-dependent responses to benzo[a]pyrene (BaP) and heavy metals Pb/Cd exposure under normoxic, hypoxic, or pro-inflammatory conditions. This implies that BaP and heavy metals exposure may affect trophoblast cells of different origins differently. Additionally, our cross-sectional population studies provided new insights into the relationship between PAH exposure and inflammation in children: platelets and CYP-derived oxylipins play essential regulatory roles in PAH exposure-induced inflammation. Future studies, including animal models, are necessary to verify our findings.