Placental DNA hypomethylation in association with particulate air pollution in early life
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BACKGROUND: There is evidence that altered DNA methylation is an important epigenetic mechanism in prenatal programming and that developmental periods are sensitive to environmental stressors. We hypothesized that exposure to fine particles (PM2.5) during pregnancy could influence DNA methylation patterns of the placenta. METHODS: In the ENVIRONAGE birth cohort, levels of 5'-methyl-deoxycytidine (5-mdC) and deoxycytidine (dC) were quantified in placental DNA from 240 newborns. Multiple regression models were used to study placental global DNA methylation and in utero exposure to PM2.5 over various time windows during pregnancy. RESULTS: PM2.5 exposure during pregnancy averaged (25th-75th percentile) 17.4 (15.4-19.3) μg/m3. Placental global DNA methylation was inversely associated with PM2.5 exposures during whole pregnancy and relatively decreased by 2.19% (95% confidence interval [CI]: -3.65, -0.73%, p = 0.004) for each 5 μg/m3 increase in exposure to PM2.5. In a multi-lag model in which all three trimester exposures were fitted as independent variables in the same regression model, only exposure to PM2.5 during trimester 1 was significantly associated with lower global DNA methylation (-2.13% per 5 μg/m3 increase, 95% CI: -3.71, -0.54%, p = 0.009). When we analyzed shorter time windows of exposure within trimester 1, we observed a lower placental DNA methylation at birth during all implantation stages but exposure during the implantation range (6-21d) was strongest associated (-1.08% per 5 μg/m3 increase, 95% CI: -1.80, -0.36%, p = 0.004). CONCLUSIONS: We observed a lower degree of placental global DNA methylation in association with exposure to particulate air pollution in early pregnancy, including the critical stages of implantation. Future studies should elucidate genome-wide and gene-specific methylation patterns in placental tissue that could link particulate exposure during in utero life and early epigenetic modulations.
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Gestational PM2.5 exposure results in altered DNA methylation, including global hypomethylation in placental tissue, as well as gene specific alterations in methylation.
“Studies support gestational PM2.5 exposure results in altered DNA methylation, including global hypomethylation in placental tissue [178], as well as gene specific alterations in methylation.”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [178]
The Results report an inverse association between gestational PM2.5 exposure and global DNA methylation in placental tissue, particularly for first-trimester exposure. The claim’s wording, “results in,” implies causation, whereas the paper reports an association. The gene-specific clause follows the citation and is not assessed as a claim attributed to this source. (LLM, conf=0.86)
Experimental — accuracy not yet measuredExposure to PM2.5 during the first trimester was significantly associated with decreased (2.2%) global DNA methylation in placenta tissue.
“In a cohort study, exposure to PM2.5 during the first trimester was significantly associated with decreased (2.2%) global DNA methylation in placenta tissue [178] and was also significantly correlated with gene expression of S-adenosylmethionine (SAM), a key substrate involved in methyl group transfers [184].”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [178]
The Results section reports a significant association between first-trimester PM2.5 exposure and lower global DNA methylation in placental tissue. The stated 2.2% decrease corresponds to the whole-pregnancy estimate (2.19%), however; the first-trimester estimate was 2.13% per 5 μg/m3 increase in the multi-lag model, or 2.41% in the trimester-specific analysis. (LLM, conf=0.87)
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“2%) global DNA methylation in placenta tissue [178] and was also significantly correlated with gene expression of S-adenosylmethionine (SAM), a key substrate involved in methyl group transfers [184].”
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Prenatal Exposure to Ambient Air Pollution and Epigenetic Aging at Birth in Newborns
Song, A., Feinberg, J. I., Bakulski, K. M., Croen, L., Fallin, M. D., Newschaffer, C. J., Hertz‐Picciotto, I., Schmidt, R. J., Ladd‐Acosta, C., & Volk, H. E. (2022) · Frontiers in Genetics · doi:10.3389/fgene.2022.929416 · Cited by 27 · see citing works
- Authors
- Janssen, B. G., Godderis, L., Pieters, N., Poels, K., Kiciński, M., Cuypers, A., Fierens, F., Penders, J., Plusquin, M., Gyselaers, W., & Nawrot, T. S.
- Affiliations
- Hasselt University (BE)
- KU Leuven (BE)
- Ziekenhuis Oost-Limburg (BE)
- Corresponding author
- Nawrot, Tim S
- ORCID
- Venue
- Particle and Fibre Toxicology
- Published
- 2013-06-07
- Volume
- 10
- Issue
- 1
- Pages
- 22-22
- ISSN
- 1743-8977 (ISSN-L)
- PMC
- PMC3686623
- OpenAlex
- W2143882086
- Cited by
- 222
- References
- 70
- Citations by year
- 2026: 19 · 2025: 7 · 2024: 14 · 2023: 11 · 2022: 25 · 2021: 31 · 2020: 10 · 2019: 22 · 2018: 18 · 2017: 16 · 2016: 19 · 2015: 14 · 2014: 12 · 2013: 3
- FWCI
- 7.17
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Particle and Fibre Toxicology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Document Server@UHasselt (UHasselt) (submittedVersion, cc-by)
- Lirias (submittedVersion)
- Funders
- Fonds Wetenschappelijk Onderzoek
- KU Leuven
- Universiteit Hasselt
- Vlaamse regering
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Keywords
- placental DNA methylation, particulate matter, PM2.5, prenatal air pollution exposure, prenatal programming, epigenetics, implantation, first trimester, placenta, ENVIRONAGE birth cohort, 5-methylcytosine
- MeSH terms
- Adolescent, Adult, Deoxycytidine, Female, Gestational Age, Humans, Infant, Newborn, Placenta, Pregnancy, Pregnancy Trimesters, Biomarkers, Maternal Exposure, DNA Methylation, Inhalation Exposure, Epigenesis, Genetic, Particulate Matter, Young Adult
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