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Air pollution-induced placental epigenetic alterations in early life: a candidate miRNA approach.

ABSTRACT: Particulate matter (PM) exposure during in utero life may entail adverse health outcomes in later-life. Air pollution's adverse effects are known to alter gene expression profiles, which can be regulated by microRNAs (miRNAs). We investigate the potential influence of air pollution exposure in prenatal life on placental miRNA expression. Within the framework of the ENVIRONAGE birth cohort, we measured the expression of six candidate miRNAs in placental tissue from 210 mother-newborn pairs by qRT-PCR. Trimester-specific PM2.5 exposure levels were estimated for each mother's home address using a spatiotemporal model. Multiple regression models were used to study miRNA expression and in utero exposure to PM2.5 over various time windows during pregnancy. The placental expression of miR-21 (-33.7%, 95% CI: -53.2 to -6.2, P = 0.022), miR-146a (-30.9%, 95% CI: -48.0 to -8.1, P = 0.012) and miR-222 (-25.4%, 95% CI: -43.0 to -2.4, P = 0.034) was inversely associated with PM2.5 exposure during the 2nd trimester of pregnancy, while placental expression of miR-20a and miR-21 was positively associated with 1st trimester exposure. Tumor suppressor phosphatase and tensin homolog (PTEN) was identified as a common target of the miRNAs significantly associated with PM exposure. Placental PTEN expression was strongly and positively associated (+59.6% per 5 µg/m³ increment, 95% CI: 26.9 to 100.7, P < 0.0001) with 3rd trimester PM2.5 exposure. Further research is required to establish the role these early miRNA and mRNA expression changes might play in PM-induced health effects. We provide molecular evidence showing that in utero PM2.5 exposure affects miRNAs expression as well as its downstream target PTEN.

SUBMITTER: Tsamou M

PROVIDER: S-EPMC5873362 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Air pollution-induced placental epigenetic alterations in early life: a candidate miRNA approach.

Tsamou Maria M Vrijens Karen K Madhloum Narjes N Lefebvre Wouter W Vanpoucke Charlotte C Nawrot Tim S TS

Epigenetics 20180305 2

Particulate matter (PM) exposure during in utero life may entail adverse health outcomes in later-life. Air pollution's adverse effects are known to alter gene expression profiles, which can be regulated by microRNAs (miRNAs). We investigate the potential influence of air pollution exposure in prenatal life on placental miRNA expression. Within the framework of the ENVIRONAGE birth cohort, we measured the expression of six candidate miRNAs in placental tissue from 210 mother-newborn pairs by qRT ...[more]

PMID: 27104955

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Project description:BACKGROUND:Residential proximity to major roadways, and prenatal exposures to particulate matter <2.5??m (PM2.5) and ozone (O3) are linked to poor fetal outcomes but their relationship with childhood development is unclear. OBJECTIVES:We investigated whether proximity to major roadways, or prenatal and early-life exposures to PM2.5 and O3 increase the risk of early developmental delays. STUDY DESIGN:Prospective cohort. SETTINGS:New York State excluding New York City. PARTICIPANTS:4089 singletons and 1016 twins born between 2008 and 2010. EXPOSURES:Proximity to major roadway was calculated using road network data from the NY Department of Transportation. Concentrations of PM2.5 and O3 estimated by the Environmental Protection Agency Downscaler models were spatiotemporally linked to each child's prenatal and early-life addresses incorporating residential history, and locations of maternal work and day-care. OUTCOMES:Parents reported their children's development at ages 8, 12, 18, 24, 30 and 36 months in five domains using the Ages and Stages Questionnaire. Generalized mixed models estimated the relative risk (RR) and 95% CI for failing any developmental domain per 10 units increase in PM2.5 and O3, and for those living <1000?m away from a major roadway compared to those living further. Models adjusted for potential confounders. RESULTS:Compared to those >1000?m away from a major roadway, those resided 50-100?m [RR: 2.12 (1.00-4.52)] and 100-500?m [RR: 2.07 (1.02-4.22)] away had twice the risk of failing the communication domain. Prenatal exposures to both PM2.5 and ozone during various pregnancy windows had weak but significant associations with failing any developmental domain with effects ranging from 1.6% to 2.7% for a 10??g/m3 increase in PM2.5 and 0.7%-1.7% for a 10?ppb increase in ozone. Average daily postnatal ozone exposure was positively associated with failing the overall screening by 8 months [3.3% (1.1%-5.5%)], 12 months [17.7% (10.4%-25.5%)], and 30 months [7.6%, (1.3%-14.3%)]. Findings were mixed for postnatal PM2.5 exposures. CONCLUSIONS:In this prospective cohort study, proximity to major roadway and prenatal/early-life exposures to PM2.5 and O3 were associated with developmental delays. While awaiting larger studies with personal air pollution assessment, efforts to minimize air pollution exposures during critical developmental windows may be warranted.

Project description:BACKGROUND:Although previous studies have reported negative associations between exposure to air pollution and cognition, studies of the effects of prenatal and postnatal exposures in early childhood have been limited. OBJECTIVES:We sought to assess the role exposure to fine particulate matter ([Formula: see text]) during different prenatal and postnatal windows may play in children's cognitive development at school age. METHODS:Within the Brain Development and Air Pollution Ultrafine Particles in School Children (BREATHE) Project, we estimated residential [Formula: see text] exposures by land use regression for the prenatal period and first seven postnatal years of 2,221 children from Barcelona, Spain. The participants ([Formula: see text]) completed computerized tests assessing working memory, attentiveness, and conflict network during four visits in 2012–2013. We used linear mixed effects and distributed lag models to assess the period of exposure to [Formula: see text] in association with cognitive development. RESULTS:Inverse associations were identified between [Formula: see text] exposure during the fifth and sixth postnatal years and working memory, with boys showing much higher vulnerability. Regarding attention functions, exposure to higher [Formula: see text] levels during the prenatal period and from the fourth postnatal year were associated with a reduction in conflict network performance, though we found no association with attentiveness. The overall estimated cumulative effect of a [Formula: see text] increase in [Formula: see text] resulted in a reduction in the working memory [Formula: see text] score of [Formula: see text] [95% confidence interval (CI): [Formula: see text], [Formula: see text]] points and an increase in the conflict attentional network of 11.31 (95% CI: 6.05, 16.57) milliseconds, indicating a poorer performance. CONCLUSIONS:Early life exposure to [Formula: see text] was associated with a reduction in fundamental cognitive abilities, including working memory and conflict attentional network. https://doi.org/10.1289/EHP3169.

Dataset Information

Air pollution-induced placental epigenetic alterations in early life: a candidate miRNA approach.

Publications

Air pollution-induced placental epigenetic alterations in early life: a candidate miRNA approach.

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