Evidence map›Paper›PMID 29499450›Full record

ReviewEnvironment international2018

Epigenetics as a mechanism linking developmental exposures to long-term toxicity.

R Barouki, E Melén, Z Herceg, J Beckers, J Chen, M Karagas, A Puga, Y Xia, L Chadwick, W Yan and 6 more

Abstract readReview
In one paragraph

Review in Environment international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 5 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

86 citing papers in PubMed, 5 syntheses or guidelines pooled it.

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26 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

16 authors.

R BaroukiINSERM UMR-S 1124, Université Paris Descartes, Paris, France; Service de Biochimie Métabolomique et Protéomique, Hôpital Necker Enfants Malades, AP-HP, Paris, France. Electronic address: robert.barouki@parisdescartes.fr.
E MelénInstitute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; Sachs' Children and Youth Hospital, and Centre for Occupational and Environmental Medicine, Stockholm County Council, Sweden.
Z HercegEpigenetics Group, International Agency for Research on Cancer (IARC), 150 Cours Albert Thomas, F-69008 Lyon, France.
J BeckersInstitute of Experimental Genetics, Helmholtz Zentrum München GmbH, 85764 Neuherberg, Germany; Technische Universität München, Experimental Genetics, 85354 Freising, Germany; German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany.
J ChenDepartment of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
M KaragasDepartment of Epidemiology, Children's Environmental Health and Disease Prevention Research Center at Dartmouth, Hanover, NH, USA.
A PugaDepartment of Environmental Health, College of Medicine, University of Cincinnati, Cincinnati, OH, United States.
Y XiaDepartment of Environmental Health, College of Medicine, University of Cincinnati, Cincinnati, OH, United States.
L ChadwickNIEHS, Research Triangle Park, NC, USA.
W YanDepartment of Physiology and Cell Biology, University of Nevada, Reno School of Medicine, 1664 North Virginia Street, Reno, NV 89557, USA MS575; Department of Biology, University of Nevada, Reno, 1664 North Virginia Street, Reno, NV 89557, USA.
K AudouzeINSERM UMR-S973, Molécules Thérapeutiques in silico, University of Paris Diderot, Paris, France.
R SlamaInstitute for Advanced Biosciences, INSERM U1209, CNRS UMR 5309, University Grenoble Alpes, Grenoble, France.
J HeindelProgram in Endocrine Disruption Strategies, Commonweal, Bolinas, CA, USA.
P GrandjeanDepartment of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Department of Environmental Medicine, University of Southern Denmark, Odense, Denmark.
T KawamotoDepartment of Environmental Health, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.
K NoharaCenter for Health and Environmental Risk Research, National Institute for Environmental Studies, Tsukuba 305-8506, Japan.

Funding

The Mount Sinai Transdisciplinary Center on Early Environmental ExposuresP30ES023515 · NIEHS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Manish Arora · 2014 to 2026
$21.3M
Sources, Transport, Exposure & Effects of PFAS (STEEP) Center - RENEWALP42ES027706 · NIEHS · UNIVERSITY OF RHODE ISLAND · PI Elsie Mareca Sunderland · 2017 to 2026
$18.9M
Single Cell Molecular ExpressionP30GM110767 · NIGMS · UNIVERSITY OF NEVADA RENO · PI SANDERS, KENTON M · 2014 to 2018
$5.4M
Messenger RNA Fate Control in SpermatogenesisR01HD085506 · NICHD · UNIVERSITY OF NEVADA RENO · PI SANDERS, KENTON M · 2015 to 2019
$1.5M
Are sperm-borne small RNAs important?R21HD071736 · NICHD · UNIVERSITY OF NEVADA RENO · PI YAN, WEI · 2012 to 2013
$380k
NICHD NIH HHS R01 HD085506NICHD NIH HHS R21 HD071736NIEHS NIH HHS P30 ES023515NIEHS NIH HHS P42 ES027706NIGMS NIH HHS P30 GM110767World Health Organization 001
6 · The paper itself

Abstract

A variety of experimental and epidemiological studies lend support to the Developmental Origin of Health and Disease (DOHaD) concept. Yet, the actual mechanisms accounting for mid- and long-term effects of early-life exposures remain unclear. Epigenetic alterations such as changes in DNA methylation, histone modifications and the expression of certain RNAs have been suggested as possible mediators of long-term health effects of environmental stressors. This report captures discussions and conclusions debated during the last Prenatal Programming and Toxicity meeting held in Japan. Its first aim is to propose a number of criteria that are critical to support the primary contribution of epigenetics in DOHaD and intergenerational transmission of environmental stressors effects. The main criteria are the full characterization of the stressors, the actual window of exposure, the target tissue and function, the specificity of the epigenetic changes and the biological plausibility of the linkage between those changes and health outcomes. The second aim is to discuss long-term effects of a number of stressors such as smoking, air pollution and endocrine disruptors in order to identify the arguments supporting the involvement of an epigenetic mechanism. Based on the developed criteria, missing evidence and suggestions for future research will be identified. The third aim is to critically analyze the evidence supporting the involvement of epigenetic mechanisms in intergenerational and transgenerational effects of environmental exposure and to particularly discuss the role of placenta and sperm. While the article is not a systematic review and is not meant to be exhaustive, it critically assesses the contribution of epigenetics in the long-term effects of environmental exposures as well as provides insight for future research.

Indexed as

Environmental ExposureDNA MethylationEnvironmental PollutantsEpigenesis, GeneticFemaleHumansMalePregnancyEnvironmental PollutantsDevelopmental vulnerabilityEndocrine disrupting compoundsMechanistic toxicologyParticulate matterTobacco smoking

Identifiers

PMID29499450
PMCPMC5899930

What OpenQuestion holds

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Registered trials

None linked

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.