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Air pollution and COPD: mediation by epigenetics in the Life Lines cohort study.

Grant number: 16/13384-0
Support Opportunities:Scholarships abroad - Research
Effective date (Start): October 01, 2016
Effective date (End): September 30, 2017
Field of knowledge:Health Sciences - Medicine
Principal Investigator:Ana Julia de Faria Coimbra Lichtenfels
Grantee:Ana Julia de Faria Coimbra Lichtenfels
Host Investigator: Marike Boezen
Host Institution: Faculdade de Medicina (FM). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Research place: University Medical Center Groningen (UMCG), Netherlands  

Abstract

Chronic Obstructive Pulmonary Disease (COPD) is characterized by progressive airway obstruction and impaired lung function. Research on its origins has been performed almost exclusively on cigarette smoking, and consequently studies on genetics of COPD have mainly focused on smokers. Although cigarette smoking is considered to be the main risk factor for developing airflow obstruction and COPD, other environmental factors including air pollution may contribute to COPD etiology. Air pollution is a major concern in public health. Short- and long term exposure to air pollution has been consistently associated with a higher risk for respiratory exacerbations and lower lung function, even at levels below the current air quality guidelines. While there is clear evidence about the role of genetics in the development of COPD, inconsistent data of population-based cohort studies suggest that apart from specific genetics variants, gene-environment interactions may also play a role in the development of COPD. Epigenetic mechanisms including DNA methylation are increasingly recognized as an important link between environmental exposures and disease. Air pollution exposure has been associated with differential DNA methylation genome wide as well as in candidate genes underlying inflammatory pathways, detoxification metabolism system and lung cancer, but to date no study has examined whether the association between air pollution and higher risk for COPD is mediated via DNA methylation. The rapid expansion of "omic" technologies, including the epigenome-wide association studies (EWAS) has been useful in assessing DNA methylation at a genome-wide level. Therefore, studying the association between air pollution, DNA methylation, and COPD in the general population-based LifeLines cohort study may provide insights into epigenetic loci associated with COPD.

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
LICHTENFELS, ANA JULIA DE F. C.; VAN DER PLAAT, DIANA A.; DE JONG, KIM; VAN DIEMEN, CLEO C.; POSTMA, DIRKJE S.; NEDELJKOVIC, IVANA; VAN DUIJN, CORNELIA M.; AMIN, NAJAF; LA BASTIDE-VAN GEMERT, SACHA; DE VRIES, MAAIKE; et al. Long-term Air Pollution Exposure, Genome-wide DNA Methylation and Lung Function in the LifeLines Cohort Study. ENVIRONMENTAL HEALTH PERSPECTIVES, v. 126, n. 2, . (16/13384-0)

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