Evidence map›Paper›PMID 31530287›Full record

ReviewClinical epigenetics2019

Air pollution-induced placental alterations: an interplay of oxidative stress, epigenetics, and the aging phenotype?

N D Saenen, D S Martens, K Y Neven, R Alfano, H Bové, B G Janssen, H A Roels, M Plusquin, K Vrijens, T S Nawrot

Abstract readReview
In one paragraph

Review in Clinical epigenetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

98 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Uterine Vulnerability to Environmental PMInternational journal of molecular sciences · 2026
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Late-Onset Preeclampsia is characterised by Accelerated Placental Aging.bioRxiv : the preprint server for biology · 2025
    Article
  20. Article

38 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

N D SaenenCentre for Environmental Sciences, Hasselt University, Hasselt, Belgium.
D S MartensCentre for Environmental Sciences, Hasselt University, Hasselt, Belgium.
K Y NevenCentre for Environmental Sciences, Hasselt University, Hasselt, Belgium.
R AlfanoCentre for Environmental Sciences, Hasselt University, Hasselt, Belgium.
H BovéCentre for Environmental Sciences, Hasselt University, Hasselt, Belgium.
B G JanssenCentre for Environmental Sciences, Hasselt University, Hasselt, Belgium.
H A RoelsCentre for Environmental Sciences, Hasselt University, Hasselt, Belgium.
M PlusquinCentre for Environmental Sciences, Hasselt University, Hasselt, Belgium.
K VrijensCentre for Environmental Sciences, Hasselt University, Hasselt, Belgium.
T S NawrotCentre for Environmental Sciences, Hasselt University, Hasselt, Belgium. tim.nawrot@uhasselt.be.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

According to the "Developmental Origins of Health and Disease" (DOHaD) concept, the early-life environment is a critical period for fetal programming. Given the epidemiological evidence that air pollution exposure during pregnancy adversely affects newborn outcomes such as birth weight and preterm birth, there is a need to pay attention to underlying modes of action to better understand not only these air pollution-induced early health effects but also its later-life consequences. In this review, we give an overview of air pollution-induced placental molecular alterations observed in the ENVIRONAGE birth cohort and evaluate the existing evidence. In general, we showed that prenatal exposure to air pollution is associated with nitrosative stress and epigenetic alterations in the placenta. Adversely affected CpG targets were involved in cellular processes including DNA repair, circadian rhythm, and energy metabolism. For miRNA expression, specific air pollution exposure windows were associated with altered miR-20a, miR-21, miR-146a, and miR-222 expression. Early-life aging markers including telomere length and mitochondrial DNA content are associated with air pollution exposure during pregnancy. Previously, we proposed the air pollution-induced telomere-mitochondrial aging hypothesis with a direct link between telomeres and mitochondria. Here, we extend this view with a potential co-interaction of different biological mechanisms on the level of placental oxidative stress, epigenetics, aging, and energy metabolism. Investigating the placenta is an opportunity for future research as it may help to understand the fundamental biology underpinning the DOHaD concept through the interactions between the underlying modes of action, prenatal environment, and disease risk in later life. To prevent lasting consequences from early-life exposures of air pollution, policy makers should get a basic understanding of biomolecular consequences and transgenerational risks.

Indexed as

AgingAir PollutionDNA MethylationEpigenesis, GeneticFemaleHumansMicroRNAsOxidative StressPhenotypePlacentaPregnancyMicroRNAsAgingAir pollutionDOHaDEpigeneticsOxidative stressPlacentaTelomeres

Identifiers

PMID31530287
PMCPMC6749657

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.