Air pollution and in utero programming of poor fetal growth.

TitleAir pollution and in utero programming of poor fetal growth.
Publication TypeJournal Article
Year of Publication2017
AuthorsBurris HH, Baccarelli AA
JournalEpigenomics
Volume9
Issue3
Pagination213-216
Date Published2017 03
ISSN1750-192X
KeywordsAir Pollution, DNA Methylation, Epigenesis, Genetic, Epigenomics, Female, Fetal Development, Fetal Growth Retardation, Humans, Maternal Exposure, Pregnancy, Smoking
Abstract

Poor fetal growth is associated with adverse postnatal health outcomes. In the newborn period, compared with well-grown infants, those small-for-gestational age (typically defined as less than 10th percentile are at higher risk of mortality and morbidities including difficulties with glucose homeostasis and thermoregulatory control. They are also more likely to require neonatal intensive care. Subsequently, small-for-gestational age infants are predisposed to hypertension and neurodevelopmental delays and disabilities. The etiology of poor fetal growth is multifactorial. Maternal conditions such as pre-eclampsia, infections such as cytomegalovirus and toxoplasmosis, maternal malnutrition and exposures to environmental pollutants such as lead, can all lead to infants being born smaller than their genetic potential.

Maternal cigarette smoking in pregnancy represents one of the most preventable causes of poor fetal growth. Air pollution, which contains many of the same compounds found in cigarette smoke including fine particulate matter smaller than five microns in diameter (PM2.5), has been shown to increase the risk of many of the same conditions caused by smoking including lung cancer and cardiovascular disease. Further, air pollution exposure in pregnancy is associated with lower birth weight for gestational age. How air pollution affects fetal growth is incompletely understood, but new insights into how the fetal epigenome responds to cigarette smoke may provide clues as to how air pollution may affect the developing fetus.

DOI10.2217/epi-2017-0008
Alternate JournalEpigenomics
PubMed ID28234022
PubMed Central IDPMC5985501
Grant ListK23 ES022242 / ES / NIEHS NIH HHS / United States
P30 ES009089 / ES / NIEHS NIH HHS / United States