Maternal residential air pollution and placental imprinted gene expression

Abstract

Background Maternal exposure to air pollution is associated with reduced fetal growth, but its relationship with expression of placental imprinted genes (important regulators of fetal growth) has not yet been studied. Objectives To examine relationships between maternal residential air pollution and expression of placental imprinted genes in the Rhode Island Child Health Study (RICHS). Methods Women-infant pairs were enrolled following delivery between 2009 and 2013. We geocoded maternal residential addresses at delivery, estimated daily levels of fine particulate matter (PM2.5; n=355) and black carbon (BC; n=336) using spatial-temporal models, and estimated residential distance to nearest major roadway (n=355). Using linear regression models we investigated the associations between each exposure metric and expression of nine candidate genes previously associated with infant birthweight in RICHS, with secondary analyses of a panel of 108 imprinted genes expressed in the placenta. We also explored effect measure modification by infant sex. Results PM2.5 and BC were associated with altered expression for seven and one candidate genes, respectively, previously linked with birthweight in this cohort. Adjusting for multiple comparisons, we found that PM2.5 and BC were associated with changes in expression of 41 and 12 of 108 placental imprinted genes, respectively. Infant sex modified the association between PM2.5 and expression of CHD7 and between proximity to major roadways and expression of ZDBF2. Conclusions We found that maternal exposure to residential PM2.5 and BC was associated with changes in placental imprinted gene expression, which suggests a plausible line of investigation of how air pollution affects fetal growth and development.

Reactive oxygen species-induced alterations in H19-Igf2 methylation patterns, seminal plasma metabolites, and semen quality

“…The H19-Igf2 locus has been extensively studied over the past years [56][57][58]. These are located on human chromosome 11p15.5 and expression of H19 is associated with silencing of Igf2.…”

Exposures to Air Pollution and Risk of Acute-onset Placental Abruption

“…41 PM 2.5 has also been associated with changes in placental expression of imprinted genes. 42 Given the seemingly similar pathophysiologic mechanisms through which air pollution may be associated with increased risks of cardiovascular disease, and other adverse pregnancy outcomes, it is plausible that these pollutants may trigger hypoxic-ischemic injury to the placenta, 36 leading to an abruption.…”

<p>The etiologic origins for chronic obstructive pulmonary disease</p>

“…Maternal sulfur dioxide (SO 2 ) and PM2.5 exposure were found to be associated with preterm birth and low birth weight, and childhood asthma 133–135. Residential PM2.5 exposure was showed to influence the expression of placental imprinted genes, suggesting a plausible line of investigation of how air pollution affects fetal growth and development 136. Maternal PM10 exposure was reported to increase the risk of congenital anomaly, notably fetal growth and development, and is related to placental DNA methylation, such as the LINE1 and HSD11B2 genes 137.…”