Evidence map›Paper›PMID 34523531›Full record

ArticleEnvironmental pollution (Barking, Essex : 1987)2021

Pregnancy exposure to synthetic phenols and placental DNA methylation - An epigenome-wide association study in male infants from the EDEN cohort.

Paulina Jedynak, Jörg Tost, Antonia M Calafat, Ekaterina Bourova-Flin, Florence Busato, Anne Forhan, Barbara Heude, Milan Jakobi, Sophie Rousseaux, Joel Schwartz and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Environmental pollution (Barking, Essex : 1987), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 6% of its field
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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

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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

14 authors at 5 institutions in 2 countries.

Paulina JedynakUniversity Grenoble Alpes, Inserm, CNRS, Team of Environmental Epidemiology Applied to Development and Respiratory Health, Institute for Advanced Biosciences, Grenoble, France. Electronic address: paulina.jedynak@univ-grenoble-alpes.fr.
Jörg TostLaboratory for Epigenetics and Environment, Centre National de Recherche en Génomique Humaine, CEA - Institut de Biologie François Jacob, University Paris Saclay, Evry, France.
Antonia M CalafatNational Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA, USA.
Ekaterina Bourova-FlinUniversity Grenoble Alpes, Inserm, CNRS, EpiMed Group, Institute for Advanced Biosciences, Grenoble, France.
Florence BusatoLaboratory for Epigenetics and Environment, Centre National de Recherche en Génomique Humaine, CEA - Institut de Biologie François Jacob, University Paris Saclay, Evry, France.
Anne ForhanUniversité de Paris, Centre for Research in Epidemiology and Statistics (CRESS), INSERM, INRAE, F-75004, Paris, France.
Barbara HeudeUniversité de Paris, Centre for Research in Epidemiology and Statistics (CRESS), INSERM, INRAE, F-75004, Paris, France.
Milan JakobiUniversity Grenoble Alpes, Inserm, CNRS, Team of Environmental Epidemiology Applied to Development and Respiratory Health, Institute for Advanced Biosciences, Grenoble, France.
Sophie RousseauxUniversity Grenoble Alpes, Inserm, CNRS, EpiMed Group, Institute for Advanced Biosciences, Grenoble, France.
Joel SchwartzDepartment of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Rémy SlamaUniversity Grenoble Alpes, Inserm, CNRS, Team of Environmental Epidemiology Applied to Development and Respiratory Health, Institute for Advanced Biosciences, Grenoble, France.
Daniel VaimanGenomics, Epigenetics and Physiopathology of Reproduction, Institut Cochin, U1016 Inserm - UMR 8104 CNRS - Paris-Descartes University, Paris, France.
Claire PhilippatUniversity Grenoble Alpes, Inserm, CNRS, Team of Environmental Epidemiology Applied to Development and Respiratory Health, Institute for Advanced Biosciences, Grenoble, France.
Johanna LepeuleUniversity Grenoble Alpes, Inserm, CNRS, Team of Environmental Epidemiology Applied to Development and Respiratory Health, Institute for Advanced Biosciences, Grenoble, France.
Centre National de la Recherche Scientifique · FRCommissariat à l'Énergie Atomique et aux Énergies Alternatives · FRInserm · FRCenters for Disease Control and Prevention · USHarvard University · US

Funding

Intramural CDC HHS CC999999
6 · The paper itself

Abstract

In utero exposure to environmental chemicals, such as synthetic phenols, may alter DNA methylation in different tissues, including placenta - a critical organ for fetal development. We studied associations between prenatal urinary biomarker concentrations of synthetic phenols and placental DNA methylation. Our study involved 202 mother-son pairs from the French EDEN cohort. Nine phenols were measured in spot urine samples collected between 22 and 29 gestational weeks. We performed DNA methylation analysis of the fetal side of placental tissues using the IlluminaHM450 BeadChips. We evaluated methylation changes of individual CpGs in an adjusted epigenome-wide association study (EWAS) and identified differentially methylated regions (DMRs). We performed mediation analysis to test whether placental tissue heterogeneity mediated the association between urinary phenol concentrations and DNA methylation. We identified 46 significant DMRs (≥5 CpGs) associated with triclosan (37 DMRs), 2,4-dichlorophenol (3), benzophenone-3 (3), methyl- (2) and propylparaben (1). All but 2 DMRs were positively associated with phenol concentrations. Out of the 46 identified DMRs, 7 (6 for triclosan) encompassed imprinted genes (APC, FOXG1, GNAS, GNASAS, MIR886, PEG10, SGCE), which represented a significant enrichment. Other identified DMRs encompassed genes encoding proteins responsible for cell signaling, transmembrane transport, cell adhesion, inflammatory, apoptotic and immunological response, genes encoding transcription factors, histones, tumor suppressors, genes involved in tumorigenesis and several cancer risk biomarkers. Mediation analysis suggested that placental cell heterogeneity may partly explain these associations. This is the first study describing the genome-wide modifications of placental DNA methylation associated with pregnancy exposure to synthetic phenols or their precursors. Our results suggest that cell heterogeneity might mediate the effects of triclosan exposure on placental DNA methylation. Additionally, the enrichment of imprinted genes within the DMRs suggests mechanisms by which certain exposures, mainly to triclosan, could affect fetal development.

Indexed as

DNA MethylationEpigenomeFemaleHistonesHumansInfantMalePhenolsPlacentaPregnancyHistonesPhenolsAlu and LINE-1Bisphenol ADNA methylationPlacentaPrenatal exposureTriclosan

Identifiers

PMID34523531
PMCPMC8590835
OpenAlexW3193443227

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.