Cited by 91Epigenetics and DNA MethylationBirth, Development, and HealthHealth, Environment, Cognitive Aging

Epidemiologic evidence for association between adverse environmental exposures in early life and epigenetic variation: a potential link to disease susceptibility?

Open access
Vaiserman, Alexander·2015·Clinical Epigenetics

Abstract

A growing body of evidence suggests that the risk of development and progression of a variety of human chronic diseases depends on epigenetic modifications triggered by environmental cues during early life sensitive stages. Exposures to environmental factors such as adverse nutritional, psychological, and social conditions, as well as pollutants and substance abuse in early life, have been shown to be important determinants of epigenetic programming of chronic pathological conditions in human populations. Over the past years, it has become increasingly clear due to the epigenome-wide association studies (EWASs) that early life adverse environmental events may trigger widespread and persistent alterations in transcriptional profiling. Several candidate genes have been identified underlying these associations. In this context, DNA methylation is the most intensively studied epigenetic phenomenon. In this review, the clinical and epidemiological evidence for the role of epigenetic factors in mediating the link between early life experiences and long-term health outcomes are summarized.

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  • DNA methylation is recognized as one of the mechanisms linking prenatal PM2.5 exposure and adverse offspring health outcomes.

    “DNA methylation is one of the most widely investigated epigenetic modifications and is recognized as one of the mechanisms linking prenatal PM2.5 exposure and adverse offspring health outcomes [177].”

    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 [177]

    The Review’s Air pollution section (page unavailable) describes DNA methylation as a possible link between prenatal exposure to traffic-related PAHs and childhood asthma. It does not identify PM2.5 as the exposure, so it does not support the claim specifically about prenatal PM2.5. (LLM, conf=0.86)

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Authors
Vaiserman, A.
Affiliations
D. F. Chebotarev State Institute of Gerontology of the National Academy of Medical Sciences of Ukraine (UA)
Corresponding author
Vaiserman, Alexander
Venue
Clinical Epigenetics
Published
2015-09-11
Volume
7
Issue
1
Pages
96-96
ISSN
  • 1868-7075 (ISSN-L)
  • 1868-7083
OpenAlex
W1779621980
Cited by
91
References
84
Citations by year
2026: 3 · 2025: 7 · 2024: 5 · 2023: 5 · 2022: 2 · 2021: 4 · 2020: 7 · 2019: 14 · 2018: 15 · 2017: 21 · 2016: 6 · 2015: 2
FWCI
1.42
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Clinical Epigenetics (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Health, Environment, Cognitive Aging
Keywords
early life exposure, epigenetic variation, DNA methylation, epigenome-wide association study, disease susceptibility, chronic disease, environmental pollutants, substance abuse, candidate genes, gene expression profiling

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