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Air pollution and DNA methylation: effects of exposure in humans

Air pollution exposure is estimated to contribute to approximately seven million early deaths every year worldwide and more than 3% of disability-adjusted life years lost. Air pollution has numerous harmful effects on health and contributes to the development and morbidity of cardiovascular disease,...

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Autores principales: Rider, Christopher F., Carlsten, Chris
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6724236/
https://www.ncbi.nlm.nih.gov/pubmed/31481107
http://dx.doi.org/10.1186/s13148-019-0713-2
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author Rider, Christopher F.
Carlsten, Chris
author_facet Rider, Christopher F.
Carlsten, Chris
author_sort Rider, Christopher F.
collection PubMed
description Air pollution exposure is estimated to contribute to approximately seven million early deaths every year worldwide and more than 3% of disability-adjusted life years lost. Air pollution has numerous harmful effects on health and contributes to the development and morbidity of cardiovascular disease, metabolic disorders, and a number of lung pathologies, including asthma and chronic obstructive pulmonary disease (COPD). Emerging data indicate that air pollution exposure modulates the epigenetic mark, DNA methylation (DNAm), and that these changes might in turn influence inflammation, disease development, and exacerbation risk. Several traffic-related air pollution (TRAP) components, including particulate matter (PM), black carbon (BC), ozone (O(3)), nitrogen oxides (NO(x)), and polyaromatic hydrocarbons (PAHs), have been associated with changes in DNAm; typically lowering DNAm after exposure. Effects of air pollution on DNAm have been observed across the human lifespan, but it is not yet clear whether early life developmental sensitivity or the accumulation of exposures have the most significant effects on health. Air pollution exposure-associated DNAm patterns are often correlated with long-term negative respiratory health outcomes, including the development of lung diseases, a focus in this review. Recently, interventions such as exercise and B vitamins have been proposed to reduce the impact of air pollution on DNAm and health. Ultimately, improved knowledge of how exposure-induced change in DNAm impacts health, both acutely and chronically, may enable preventative and remedial strategies to reduce morbidity in polluted environments. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13148-019-0713-2) contains supplementary material, which is available to authorized users.
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spelling pubmed-67242362019-09-10 Air pollution and DNA methylation: effects of exposure in humans Rider, Christopher F. Carlsten, Chris Clin Epigenetics Review Air pollution exposure is estimated to contribute to approximately seven million early deaths every year worldwide and more than 3% of disability-adjusted life years lost. Air pollution has numerous harmful effects on health and contributes to the development and morbidity of cardiovascular disease, metabolic disorders, and a number of lung pathologies, including asthma and chronic obstructive pulmonary disease (COPD). Emerging data indicate that air pollution exposure modulates the epigenetic mark, DNA methylation (DNAm), and that these changes might in turn influence inflammation, disease development, and exacerbation risk. Several traffic-related air pollution (TRAP) components, including particulate matter (PM), black carbon (BC), ozone (O(3)), nitrogen oxides (NO(x)), and polyaromatic hydrocarbons (PAHs), have been associated with changes in DNAm; typically lowering DNAm after exposure. Effects of air pollution on DNAm have been observed across the human lifespan, but it is not yet clear whether early life developmental sensitivity or the accumulation of exposures have the most significant effects on health. Air pollution exposure-associated DNAm patterns are often correlated with long-term negative respiratory health outcomes, including the development of lung diseases, a focus in this review. Recently, interventions such as exercise and B vitamins have been proposed to reduce the impact of air pollution on DNAm and health. Ultimately, improved knowledge of how exposure-induced change in DNAm impacts health, both acutely and chronically, may enable preventative and remedial strategies to reduce morbidity in polluted environments. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13148-019-0713-2) contains supplementary material, which is available to authorized users. BioMed Central 2019-09-03 /pmc/articles/PMC6724236/ /pubmed/31481107 http://dx.doi.org/10.1186/s13148-019-0713-2 Text en © The Author(s). 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Rider, Christopher F.
Carlsten, Chris
Air pollution and DNA methylation: effects of exposure in humans
title Air pollution and DNA methylation: effects of exposure in humans
title_full Air pollution and DNA methylation: effects of exposure in humans
title_fullStr Air pollution and DNA methylation: effects of exposure in humans
title_full_unstemmed Air pollution and DNA methylation: effects of exposure in humans
title_short Air pollution and DNA methylation: effects of exposure in humans
title_sort air pollution and dna methylation: effects of exposure in humans
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6724236/
https://www.ncbi.nlm.nih.gov/pubmed/31481107
http://dx.doi.org/10.1186/s13148-019-0713-2
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