Evidence map›Paper›PMID 25996590›Full record

ArticleEpigenetics2015

Placental mitochondrial methylation and exposure to airborne particulate matter in the early life environment: An ENVIRONAGE birth cohort study.

Bram G Janssen, Hyang-Min Byun, Wilfried Gyselaers, Wouter Lefebvre, Andrea A Baccarelli, Tim S Nawrot

Abstract read
In one paragraph

Article in Epigenetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
103citing 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

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

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Maternal PMReproductive toxicology (Elmsford, N.Y.) · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Global research trends on the human exposome: a bibliometric analysis (2005-2024).Environmental science and pollution research international · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
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  18. Review
  19. Article
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43 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

6 authors.

Bram G Janssena Centre for Environmental Sciences; Hasselt University ; Diepenbeek , Belgium.
Hyang-Min Byun
Wilfried Gyselaers
Wouter Lefebvre
Andrea A Baccarelli
Tim S Nawrot

Funding

BPA, Phthalates & Stress: Mechanisms and Interactions for Childhood ObesityR01ES021357 · NIEHS · HARVARD SCHOOL OF PUBLIC HEALTH · PI BACCARELLI, ANDREA, WRIGHT, ROBERT O · 2012 to 2016
$3.3M
Molecular and Epigenetic Mitochondriomics of Air Particles, Lead and CognitionR01ES021733 · NIEHS · HARVARD SCHOOL OF PUBLIC HEALTH · PI BACCARELLI, ANDREA · 2012 to 2015
$2.4M
Platelet Mitochondrial Epigenetics: New CVD Markers of Particle and Metal EffectsR21ES022694 · NIEHS · UNIVERSITY OF NEWCASTLE · PI BYUN, HYANG-MIN · 2014 to 2015
$436k
NIEHS NIH HHS R01 ES021357NIEHS NIH HHS R01ES021357NIEHS NIH HHS R01ES021733NIEHS NIH HHS R21 ES022694NIEHS NIH HHS R21ES022694-01A1
6 · The paper itself

Abstract

Most research to date has focused on epigenetic modifications in the nuclear genome, with little attention devoted to mitochondrial DNA (mtDNA). Placental mtDNA content has been shown to respond to environmental exposures that induce oxidative stress, including airborne particulate matter (PM). Damaged or non-functioning mitochondria are specifically degraded through mitophagy, exemplified by lower mtDNA content, and could be primed by epigenetic modifications in the mtDNA. We studied placental mtDNA methylation in the context of the early life exposome. We investigated placental tissue from 381 mother-newborn pairs that were enrolled in the ENVIRONAGE birth cohort. We determined mtDNA methylation by bisulfite-pyrosequencing in 2 regions, i.e., the D-loop control region and 12S rRNA (MT-RNR1), and measured mtDNA content by qPCR. PM2.5 exposure was calculated for each participant's home address using a dispersion model. An interquartile range (IQR) increment in PM2.5 exposure over the entire pregnancy was positively associated with mtDNA methylation (MT-RNR1: +0.91%, P = 0.01 and D-loop: +0.21%, P = 0.05) and inversely associated with mtDNA content (relative change of -15.60%, P = 0.001) in placental tissue. mtDNA methylation was estimated to mediate 54% [P = 0.01 (MT-RNR1)] and 27% [P = 0.06 (D-loop)] of the inverse association between PM2.5 exposure and mtDNA content. This study provides new insight into the mechanisms of altered mitochondrial function in the early life environment. Epigenetic modifications in the mitochondrial genome, especially in the MT-RNR1 region, substantially mediate the association between PM2.5 exposure during gestation and placental mtDNA content, which could reflect signs of mitophagy and mitochondrial death.

Indexed as

DNA MethylationEnvironmental ExposureEpigenesis, GeneticFemaleGenome, MitochondrialHumansInfant, NewbornMaleMitochondriaOxidative StressParticulate MatterPlacentaPregnancyRNA, RibosomalParticulate MatterRNA, RibosomalRNA, ribosomal, 12S12S rRNA, Mitochondrial ribosomal 12S rRNAair pollutionD-loop, Displacement loopDNA methylationepigeneticsIQR, Interquartile rangemitochondriamitochondrial DNA contentmitochondrial DNA methylationmtDNA, Mitochondrial DNAmtDNMT1, Mitochondrial isoform of nuclear-encoded DNA methyltransferase enzyme 1MT-RNR1, Mitochondrial region RNR1particulate matterplacentaPM, Particulate matter

Identifiers

PMID25996590
PMCPMC4623402

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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.