Abstract：
:Cigarette smoke exposure is a major risk factor in chronic obstructive pulmonary disease (COPD) and its interactions with genetic variants could affect lung function. However, few gene-smoking interactions have been reported. In this report, we evaluated the effects of gene-smoking interactions on lung function using Korea Associated Resource (KARE) data with the spirometric variables-forced expiratory volume in 1 s (FEV1). We found that variations in FEV1 were different among smoking status. Thus, we considered a linear mixed model for association analysis under heteroscedasticity according to smoking status. We found a previously identified locus near SOX9 on chromosome 17 to be the most significant based on a joint test of the main and interaction effects of smoking. Smoking interactions were replicated with Gene-Environment of Interaction and phenotype (GENIE), Multi-Ethnic Study of Atherosclerosis-Lung (MESA-Lung), and COPDGene studies. We found that individuals with minor alleles, rs17765644, rs17178251, rs11870732, and rs4793541, tended to have lower FEV1 values, and lung function decreased much faster with age for smokers. There have been very few reports to replicate a common variant gene-smoking interaction, and our results revealed that statistical models for gene-smoking interaction analyses should be carefully selected.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Park B,Koo SM,An J,Lee M,Kang HY,Qiao D,Cho MH,Sung J,Silverman EK,Yang HJ,Won Sdoi
10.1038/s41598-018-27463-5subject
Has Abstractpub_date
2018-06-18 00:00:00pages
9319issue
1issn
2045-2322pii
10.1038/s41598-018-27463-5journal_volume
8pub_type
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