Report: Placental DNA Methylation and Prenatal Air Pollution Exposure

Background

Pregnancy and infancy are particularly susceptible to the negative effects of air pollution, which can lead to poor birth outcomes and developmental issues. Outdoor air pollution has been linked to reduced fetal growth and an increased risk of preterm birth. Additionally, exposure to air pollution during pregnancy has been associated with cardiometabolic, respiratory, and neurodevelopmental problems in children. However, there is limited research on the effects of prenatal air pollution exposure on placental epigenomes, which play a crucial role in infant development. Genome-wide placental DNA methylation studies are rare due to limited sample sizes.

About the Study

In a recent study published in The Lancet Planetary Health, researchers investigated the relationship between prenatal air pollutant exposure concentrations and changes in placental DNA methylation (DNAm). The study analyzed data from three population-based maternal-infant cohorts in France: SEPAGES, EDEN, and PELAGIE. The researchers recruited pregnant women from 2003 to 2006 for the PELAGIE and EDEN studies, and from 2014 to 2017 for the SEPAGES study. The study included 1,539 mother-child couples, excluding non-French-speaking women.

Data Collection and Analysis

During and after pregnancy, medical and lifestyle information was collected through midwives or self-administered questionnaires. The researchers used nitrogen dioxide (NO2), particulate matter of ≤2.5mm diameter (PM2.5), and PM10 as proxies for traffic-related air pollutants. Spatiotemporal models were used to predict the mothers’ exposures during each trimester of pregnancy. The researchers estimated PM2.5 and PM10 levels by combining data from various sources, including aerosol optical depth and meteorological data. NO2 exposure was calculated using a model based on the Chemistry Transport CHIMERE model.

The researchers performed epigenome-level association studies using DNA methylation arrays to identify differentially methylated regions (DMR) with CpG sites. Linear regression modeling was used to analyze the data, controlling for various factors such as maternal age, infant gender, and maternal smoking during pregnancy. The effects of prenatal air pollution on DNAm alterations throughout fetal development were investigated, as well as fetal growth indices such as gestational age, birth length, head circumference, and birth weight. Pathway enrichment analysis was conducted to explore the biological activities of differentially methylated sites.

Results

The study identified four CpGs in 28 regions associated with prenatal air pollution exposure among all study participants. Among female newborns, 150 CpGs across 66 regions were identified, and among male newborns, 469 CpGs across 87 regions were identified. The researchers verified 35% of all accessible CpGs. More than 30% of the detected CpGs were associated with at least one birth outcome, with significant enrichment for immunology, brain development, and metabolic pathways. The strongest associations were observed in the third trimester for female newborns, throughout the entire pregnancy period for all newborns, and in the first trimester for male newborns.

The study also identified differentially methylated genes related to fetal development, including DIRAS3, FOXG1, TXNDC15, OTX1, GET1, GGT6, CCDC62, DAXX, ZNF563, LMF1, ADCK5, and BID. The median exposure levels were 20 μg/m³ of NO2, 18 μg/m³ of PM10, and 12 μg/m³ of PM2.5. Stratifying the data by child sex, the study identified 650 CpG sites, with 92 specific to female newborns, 196 specific to male infants, and 362 consistent across both sexes. NO2 showed the strongest relationship with CpG sites.

Conclusion

The study revealed sexually dimorphic associations between prenatal air pollution exposure and placental DNA methylation alterations. These findings suggest that prenatal air pollution exposure may modify epigenetic pathways, potentially impacting fetal growth and neurodevelopment. Female newborns were found to be particularly vulnerable in the third trimester, while male newborns showed sensitivity to air pollutants during the first trimester and throughout pregnancy. Further research is needed to assess the long-term persistence of these epigenetic alterations.

SDGs, Targets, and Indicators

1. SDG 3: Good Health and Well-being

   • Target 3.9: By 2030, substantially reduce the number of deaths and illnesses from hazardous chemicals and air, water, and soil pollution and contamination.
   • Indicator 3.9.1: Mortality rate attributed to household and ambient air pollution.

2. SDG 11: Sustainable Cities and Communities

   • Target 11.6: By 2030, reduce the adverse per capita environmental impact of cities, including by paying special attention to air quality and municipal and other waste management.
   • Indicator 11.6.2: Annual mean levels of fine particulate matter (e.g., PM2.5 and PM10) in cities (population-weighted).

3. SDG 12: Responsible Consumption and Production

   • Target 12.4: By 2020, achieve the environmentally sound management of chemicals and all wastes throughout their life cycle, in accordance with agreed international frameworks, and significantly reduce their release to air, water, and soil to minimize their adverse impacts on human health and the environment.
   • Indicator 12.4.2: Hazardous waste generated per capita and proportion of hazardous waste treated, disaggregated by treatment type.

The issues highlighted in the article are connected to SDG 3, SDG 11, and SDG 12. These goals address the health impacts of air pollution, the need for sustainable cities with good air quality, and responsible consumption and production to minimize the release of pollutants.

Based on the article’s content, the specific targets that can be identified are:

1. Target 3.9: By 2030, substantially reduce the number of deaths and illnesses from hazardous chemicals and air, water, and soil pollution and contamination.
2. Target 11.6: By 2030, reduce the adverse per capita environmental impact of cities, including by paying special attention to air quality and municipal and other waste management.
3. Target 12.4: By 2020, achieve the environmentally sound management of chemicals and all wastes throughout their life cycle, in accordance with agreed international frameworks, and significantly reduce their release to air, water, and soil to minimize their adverse impacts on human health and the environment.

The article mentions or implies several indicators that can be used to measure progress towards these targets:

• Indicator 3.9.1: Mortality rate attributed to household and ambient air pollution.
• Indicator 11.6.2: Annual mean levels of fine particulate matter (e.g., PM2.5 and PM10) in cities (population-weighted).
• Indicator 12.4.2: Hazardous waste generated per capita and proportion of hazardous waste treated, disaggregated by treatment type.

These indicators can help track the reduction in mortality rates due to air pollution, the improvement in air quality in cities, and the progress in managing hazardous waste.

Table: SDGs, Targets, and Indicators

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Fuente: news-medical.net

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