From: The role of cigarette smoke-induced epigenetic alterations in inflammation
Sample size | Population | Tissue for DNA methylation analysis | Smoking status | Main result | References | Year |
---|---|---|---|---|---|---|
596 | Chinese population | Whole blood | Current smoke | 318 CpG sites were differentially methylated due to cigarette smoking. | Zhu et al. [15] | 2016 |
745 | European women | Whole blood | Current smoke | 461 CpG sites were aberrant methylated due to cigarette smoking. Of them, 448 CpG sites were hypomethylated | Guida et al. [16] | 2015 |
 |  |  | Former smoke | The methylation of 751 CpG sites were changed the recoded smoking status. Of them, 602 CpG sites reverted back to that of never smokers from up to 35 years after smoking cessation. 149 CpG sites remained differentially methylated > 35 years after smoking |  |  |
123 | Arab population | Whole blood | Current smoke | Aberrant methylation was detected due to tobacco smoking. The exact number of CpG sites was not mentioned | Zaghlool et al. [17] | 2015 |
111 | African American women | Peripheral blood mononuclear cells | Current smoke | 910 loci were found to be differentially methylated in smokers | Dogan et al. [18] | 2014 |
192 | South Asian and European men | Whole blood | Current smoke | 29 CpG sites at 18 unique loci were differential methylated in smokers | Elliott et al. [19] | 2014 |
180 | Italian population | Peripheral white blood cells | Current smoke/former smoke | 17 and 19 loci in the breast cancer and colon cancer were differentially methylated between smokers, former smokers and never smokers. In former smokers, methylation levels at AHRR, 2q37 and 6p21 loci returned to the levels of nonsmokers with increasing time from cessation and those who had smoked more intensively had methylation levels that were closer to that of current smokers | Shenker et al. [20] | 2013 |
1793 | Augsburg population | Whole blood | Current smoke/FORMER smoke | 972 CpG sites were differentially methylated after smoking. Of which, 187 CpG sites were differentially methylated in current smokers. | Zeilinger et al. [21] | 2013 |
98 | African Americans | Lymphocyte cells | Current smoke | Aberrant methylation was detected due to tobacco smoking. The authors listed 30 most significant methylated CpG sites without mentioning the exact number of methylated CpG sites | Philibert et al. [22] | 2013 |
972 | African Americans | Peripheral leukocytes | Current smoke | 15 autosomal DNAm sites were significantly associated with current smoking using a Bonferroni corrected p value of 0.05. 89 DNAm sites associated with current smoking with FDR q value less than 0.05 | Sun et al. [23] | 2013 |
20 | Hispanic newborns | CD4+ cells from cord blood | In utero exposure to maternal tobacco smoke | 10,381 CpG sites were differentially methylated by tobacco smoking. Of them, 557 differentially methylated regions were overrepresented in important regulatory regions, including enhancers | Howe et al. [24] | 2019 |
1062Â | Norwegian newborns | Cord blood | In utero exposure to maternal tobacco smoke | Differential DNA methylation of 26 CpG sites mapped to 10 genes were found in newborns born to smoking mothers compared to nonsmoking mothers | Joubert et al. [25] | 2012 |
1042 | Norwegian newborns | Cord blood | In utero exposure to maternal tobacco smoke | Maternal smoking affected DNA methylation of 26 CpG sites that mapped to 10 genes in newborn cord blood if the mother smokes past 18 weeks in pregnancy, whereas significant effects on methylation were not observed for mothers that quit before 18 gestational weeks | Joubert et al. [26] | 2014 |