Abstract

The Developmental Origins of Health and Disease (DOHaD) concept postulates that in utero exposures influence fetal programming and health in later life. Throughout pregnancy, the placenta plays a central role in fetal programming; it regulates the in utero environment and acts as a gatekeeper for nutrient and waste exchange between the mother and the fetus. Maternal exposure to air pollution, including heavy metals, can reach the placenta, where they alter DNA methylation patterns, leading to changes in placental function and fetal reprogramming. This review explores the current knowledge on placental DNA methylation changes associated with prenatal air pollution (including heavy metals) exposure and highlights its effects on fetal development and disease susceptibility. Prenatal exposure to air pollution and heavy metals was associated with altered placental DNA methylation at the global and promoter regions of genes involved in biological processes such as energy metabolism, circadian rhythm, DNA repair, inflammation, cell differentiation, and organ development. The altered placental methylation of these genes was, in some studies, associated with adverse birth outcomes such as low birth weight, small for gestational age, and decreased head circumference. Moreover, few studies indicate that DNA methylation changes in the placenta were sex-specific, and infants born with altered placental DNA methylation patterns were predisposed to developing neurobehavioral abnormalities, cancer, and atopic dermatitis. These findings highlight the importance of more effective and stricter environmental and public health policies to reduce air pollution and protect human health.

Highlights

  • Discipline of Occupational and Environmental Health, School of Nursing and Public Health, College of Academic Editor: Giovanni Amabile

  • The placenta plays a central role in fetal programming, and we suggest that altered placental physiology and function, possibly through epigenetic modifications such as DNA methylation, can provide a mechanism linking prenatal air pollution exposure with pregnancy complications, fetal growth abnormalities, altered newborn phenotypes, and an increased risk of developing certain diseases during the lifespan

  • This review explores the current knowledge on placental DNA methylation changes associated with prenatal air pollution exposure and highlights its effects on fetal development and disease susceptibility

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Summary

Introduction with regard to jurisdictional claims in

Air pollution is an environmental problem that threatens human health and is a major cause of mortality worldwide. Due to their small size, are inhaled into the lungs, and the smallest particles infiltrate into the bloodstream reaching the placenta and fetus [4,5,6] Such in utero exposures can affect fetal development, cause adverse birth outcomes, and increase the risk of developing certain diseases in later life, as postulated by the Developmental Origins of Health and Disease (DOHaD) concept [7,8,9,10]. The placenta transfers nutrients from the mother to the fetus and regulates gas and waste exchanges [27] In this way, the placenta plays a central role in fetal programming, and we suggest that altered placental physiology and function, possibly through epigenetic modifications such as DNA methylation, can provide a mechanism linking prenatal air pollution exposure with pregnancy complications, fetal growth abnormalities, altered newborn phenotypes, and an increased risk of developing certain diseases during the lifespan. This review explores the current knowledge on placental DNA methylation changes associated with prenatal air pollution (including heavy metals) exposure and highlights its effects on fetal development and disease susceptibility

Transfer of Air Pollution Particles across the Human Placenta
Findings
Prenatal Air Pollution Exposure and Placental Candidate Gene Methylation
Prenatal Heavy Metal Exposure and Placental DNA Methylation
Conclusions
The effects of prenatal air pollution exposure on placentalDNA

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