Abstract
Background: While common resolutions that people make for healthy lives, such as quitting smoking, are frequently linked to the improvement in lung functioning, little is known about their long-term benefits on smokers.
Methods: To examine whether quit-smoking status and genetic susceptibility of FAM13A (family with sequence similarity 13, member A) gene decrease lung impairment, we conducted a prospective cohort study of a total of 2,921 male participants (659 continuous smokers, 1,758 ex-smokers and 504 non-smokers at a 16-year follow-up time) who have normal lung function and are free of COPD at baseline. Smoking status and pulmonary function test were determined by biennial examination. The association between smoking status and pulmonary function were investigated by generalized linear model to obtain the least squares (LS) mean with age, height, area and pulmonary function values at baseline as covariates.
Results: In comparison to continuous smokers, people who quit-smoking for more than 15 years had a significantly slower decline in the FEV1/FVC (LS mean (standard error (SE)), -0.52%/yr (0.02) in continuous smokers, -0.39%/yr (0.02) in quit-smokers (<15 years) and -0.36%/yr (0.01) in quit-smokers (≥15 years); p for trend <0.001). For rs3756050 variant, quit-smokers who had homozygous non-risk allele showed a significantly lower decline of the FEV1/FVC ratio (-0.32%/yr), as compared to continuous smokers who had homozygous risk allele and heterozygous groups (-0.54%/yr; p <0.001).
Conclusions: Our results suggest that smoking cessation favorably work in lung function decline, especially for those who have a protective susceptible gene.
Footnotes
Cite this article as: European Respiratory Journal 2018 52: Suppl. 62, OA1932.
This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).
- Copyright ©the authors 2018