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, K Audouze, R Slama, J Heindel, P Grandjean, T Kawamoto, K Nohara

Publikation: Bidrag til tidsskriftReviewForskningpeer review

Resumé

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.

OriginalsprogEngelsk
TidsskriftEnvironment International
Vol/bind114
Sider (fra-til)77-86
Antal sider10
ISSN0160-4120
DOI
StatusUdgivet - maj 2018

Fingeraftryk

toxicity
health and disease
endocrine disruptor
methylation
smoking
environmental effect
sperm
RNA
atmospheric pollution
DNA
exposure
long-term effect
effect
health
tissue

Citer dette

Barouki, R., Melén, E., Herceg, Z., Beckers, J., Chen, J., Karagas, M., ... Nohara, K. (2018). Epigenetics as a mechanism linking developmental exposures to long-term toxicity. Environment International, 114, 77-86. https://doi.org/10.1016/j.envint.2018.02.014
Barouki, R ; Melén, E ; Herceg, Z ; Beckers, J ; Chen, J ; Karagas, M ; Puga, A ; Xia, Y ; Chadwick, L ; Yan, W ; Audouze, K ; Slama, R ; Heindel, J ; Grandjean, P ; Kawamoto, T ; Nohara, K. / Epigenetics as a mechanism linking developmental exposures to long-term toxicity. I: Environment International. 2018 ; Bind 114. s. 77-86.
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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.",
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Barouki, R, Melén, E, Herceg, Z, Beckers, J, Chen, J, Karagas, M, Puga, A, Xia, Y, Chadwick, L, Yan, W, Audouze, K, Slama, R, Heindel, J, Grandjean, P, Kawamoto, T & Nohara, K 2018, 'Epigenetics as a mechanism linking developmental exposures to long-term toxicity', Environment International, bind 114, s. 77-86. https://doi.org/10.1016/j.envint.2018.02.014

Epigenetics as a mechanism linking developmental exposures to long-term toxicity. / Barouki, R; Melén, E; Herceg, Z; Beckers, J; Chen, J; Karagas, M; Puga, A; Xia, Y; Chadwick, L; Yan, W; Audouze, K; Slama, R; Heindel, J; Grandjean, P; Kawamoto, T; Nohara, K.

I: Environment International, Bind 114, 05.2018, s. 77-86.

Publikation: Bidrag til tidsskriftReviewForskningpeer review

TY - JOUR

T1 - Epigenetics as a mechanism linking developmental exposures to long-term toxicity

AU - Barouki, R

AU - Melén, E

AU - Herceg, Z

AU - Beckers, J

AU - Chen, J

AU - Karagas, M

AU - Puga, A

AU - Xia, Y

AU - Chadwick, L

AU - Yan, W

AU - Audouze, K

AU - Slama, R

AU - Heindel, J

AU - Grandjean, P

AU - Kawamoto, T

AU - Nohara, K

N1 - Copyright © 2018 Elsevier Ltd. All rights reserved.

PY - 2018/5

Y1 - 2018/5

N2 - 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.

AB - 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.

KW - Developmental vulnerability

KW - Endocrine disrupting compounds

KW - Mechanistic toxicology

KW - Particulate matter

KW - Tobacco smoking

U2 - 10.1016/j.envint.2018.02.014

DO - 10.1016/j.envint.2018.02.014

M3 - Review

VL - 114

SP - 77

EP - 86

JO - Environment International

JF - Environment International

SN - 0160-4120

ER -