Persistent prenatal exposure to participate matter 2.5 mum in diameter (PM_(2.5)) during pregnancy has been associated with neurodevelopmental disorders in the offspring, and this is associated with epigenetic modifications in the placenta during fetal development.1 The sources of PM_(2.5) include exhaust fumes from local industries, combustion of fossil fuels in vehicles, power plants and road dust.2 Constant prenatal exposure to PM_(2.5) could affect the offspring's phenotypic traits by altering an epigenetic mechanism which influences gene expression. The major epigenetic mechanism disrupted by PM_(2.5) is placental global DNA methylation.2 A first trimester trophoblast cell line exposed to PM2.5 showed chromatin condensation, organelle swelling and signs of lost membrane integrity.3 A positive correlation has been reported between prenatal exposure to PM_(2.5) and autism spectrum disorder in children.4 Prenatal exposure to PM_(2.5) resulted in spatial memory dysfunction and neurodevelopmental impairment in the hippocampus of mice offspring via the induction of neuronal apo-ptosis through activating apoptotic pathways.5 In conclusion, constant maternal exposure to PM_(2.5) during pregnancy may disrupt placental DNA methylation and increase neuronal apoptosis, consequently affecting neurodevelopment in the offspring.
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