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      Genome-Wide Analysis of DNA Methylation and Cigarette Smoking in a Chinese Population

      research-article
      Author(s): 1 , 2 , 1 , 2 , 3 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 1 , 2 , 4 , 5 , 5 , 6 , 6 , 7 , 1 , 2 , 1 , 2 , 1 , 2 , 3 , 8 , 9 , 3 , 10 , 1 , 2 , †
      Publication date (Electronic):
      Journal: Environmental Health Perspectives
      Publisher: National Institute of Environmental Health Sciences

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          Abstract

          Background:

          Smoking is a risk factor for many human diseases. DNA methylation has been related to smoking, but genome-wide methylation data for smoking in Chinese populations is limited.

          Objectives:

          We aimed to investigate epigenome-wide methylation in relation to smoking in a Chinese population.

          Methods:

          We measured the methylation levels at > 485,000 CpG sites (CpGs) in DNA from leukocytes using a methylation array and conducted a genome-wide meta-analysis of DNA methylation and smoking in a total of 596 Chinese participants. We further evaluated the associations of smoking-related CpGs with internal polycyclic aromatic hydrocarbon (PAH) biomarkers and their correlations with the expression of corresponding genes.

          Results:

          We identified 318 CpGs whose methylation levels were associated with smoking at a genome-wide significance level (false discovery rate < 0.05), among which 161 CpGs annotated to 123 genes were not associated with smoking in recent studies of Europeans and African Americans. Of these smoking-related CpGs, methylation levels at 80 CpGs showed significant correlations with the expression of corresponding genes (including RUNX3, IL6R, PTAFR, ANKRD11, CEP135 and CDH23), and methylation at 15 CpGs was significantly associated with urinary 2-hydroxynaphthalene, the most representative internal monohydroxy-PAH biomarker for smoking.

          Conclusion:

          We identified DNA methylation markers associated with smoking in a Chinese population, including some markers that were also correlated with gene expression. Exposure to naphthalene, a byproduct of tobacco smoke, may contribute to smoking-related methylation.

          Citation:

          Zhu X, Li J, Deng S, Yu K, Liu X, Deng Q, Sun H, Zhang X, He M, Guo H, Chen W, Yuan J, Zhang B, Kuang D, He X, Bai Y, Han X, Liu B, Li X, Yang L, Jiang H, Zhang Y, Hu J, Cheng L, Luo X, Mei W, Zhou Z, Sun S, Zhang L, Liu C, Guo Y, Zhang Z, Hu FB, Liang L, Wu T. 2016. Genome-wide analysis of DNA methylation and cigarette smoking in Chinese. Environ Health Perspect 124:966–973; http://dx.doi.org/10.1289/ehp.1509834

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          R: a language and environment for statistic computing

          R.D.C. Team, R Development Core Team, RDC Team … (2008)
          Article 0 comments Cited 395 times – based on 0 reviews     Review now
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            Molecular networks as sensors and drivers of common human diseases.

            Eric E. Schadt (2009)
            The molecular biology revolution led to an intense focus on the study of interactions between DNA, RNA and protein biosynthesis in order to develop a more comprehensive understanding of the cell. One consequence of this focus was a reduced attention to whole-system physiology, making it difficult to link molecular biology to clinical medicine. Equipped with the tools emerging from the genomics revolution, we are now in a position to link molecular states to physiological ones through the reverse engineering of molecular networks that sense DNA and environmental perturbations and, as a result, drive variations in physiological states associated with disease.
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              Estimates of global mortality attributable to smoking in 2000.

              Majid Ezzati, Alan Lopez (2003)
              Smoking is a risk factor for several diseases and has been increasing in many developing countries. Our aim was to estimate global and regional mortality in 2000 caused by smoking, including an analysis of uncertainty. Following the methods of Peto and colleagues, we used lung-cancer mortality as an indirect marker for accumulated smoking risk. Never-smoker lung-cancer mortality was estimated based on the household use of coal with poor ventilation. Relative risks were taken from the American Cancer Society Cancer Prevention Study, phase II, and the retrospective proportional mortality analysis of Liu and colleagues in China. Relative risks were corrected for confounding and extrapolation to other regions. We estimated that in 2000, 4.83 (uncertainty range 3.94-5.93) million premature deaths in the world were attributable to smoking; 2.41 (1.80-3.15) million in developing countries and 2.43 (2.13-2.78) million in industrialised countries. 3.84 million of these deaths were in men. The leading causes of death from smoking were cardiovascular diseases (1.69 million deaths), chronic obstructive pulmonary disease (0.97 million deaths), and lung cancer (0.85 million deaths). Smoking was an important cause of global mortality in 2000. In view of the expected demographic and epidemiological transitions and current smoking patterns in the developing world, the health loss due to smoking will grow even larger unless effective interventions and policies that reduce smoking among men and prevent increases among women in developing countries are implemented.
              Article 0 comments Cited 277 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Environ Health Perspect
                Journal ID (iso-abbrev): Environ. Health Perspect
                Journal ID (publisher-id): EHP
                Title: Environmental Health Perspectives
                Publisher: National Institute of Environmental Health Sciences
                ISSN (Print): 0091-6765
                ISSN (Electronic): 1552-9924
                Publication date (Electronic): 12 January 2016
                Publication date (Print): July 2016
                Volume: 124
                Issue: 7
                Pages: 966-973
                Affiliations
                [1 ]Department of Occupational and Environmental Health, and
                [2 ]Ministry of Education Key Lab for Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
                [3 ]Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA
                [4 ]Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
                [5 ]Department of Cardiology, People’s Hospital of Zhuhai, Zhuhai, China
                [6 ]Department of Cardiology, Bao’an Hospital, Shenzhen, China
                [7 ]Department of Cardiology, Wuhan Central Hospital, Wuhan, China
                [8 ]Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA
                [9 ]Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
                [10 ]Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA
                Author notes
                [*]

                These authors contributed equally to this work.

                [† ]Address correspondence to T. Wu, Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Rd., Wuhan 430030, Hubei, China. Telephone: 86-27-83692347. E-mail: wut@ 123456mails.tjmu.edu.cn
                Article
                Publisher ID: ehp.1509834
                DOI: 10.1289/ehp.1509834
                PMC ID: 4937856
                PubMed ID: 26756918
                SO-VID: b032cd3e-019a-405a-80d9-075b8ad0a255
                License:

                Publication of EHP lies in the public domain and is therefore without copyright. All text from EHP may be reprinted freely. Use of materials published in EHP should be acknowledged (for example, “Reproduced with permission from Environmental Health Perspectives”); pertinent reference information should be provided for the article from which the material was reproduced. Articles from EHP, especially the News section, may contain photographs or illustrations copyrighted by other commercial organizations or individuals that may not be used without obtaining prior approval from the holder of the copyright.

                History
                Date received : 17 February 2015
                Date accepted : 22 December 2015
                Categories
                Subject: Research

                ScienceOpen disciplines: Public health
                Data availability:
                ScienceOpen disciplines: Public health

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