Addiction. 2022 Feb 27. doi: 10.1111/add.15852. Online ahead of print.
ABSTRACT
BACKGROUND AND AIMS: Smoking increases the risk of severe COVID-19, but whether lung function or chronic obstructive pulmonary disease (COPD) mediate the underlying associations is unclear. We conducted the largest Mendelian randomization study, to date, to address these questions.
DESIGN: Mendelian randomization study using summary statistics from genome wide association studies (GWAS), FinnGen, and UK Biobank. The main analysis was inverse variance weighted method, and we included a range of sensitivity analyses to assess robustness of findings.
SETTING: GWAS which included international consortia, FinnGen, and UK Biobank PARTICIPANTS: Sample size ranged from 193,638 to 2,586,691.
MEASUREMENTS: Genetic determinants of lifetime smoking index, lung function (e.g forced expiratory volume in 1 second (FEV1 )), COPD and different severities of COVID-19.
RESULTS: Smoking increased the risk of COVID-19 compared with population controls, for overall COVID-19 (odds ratio (OR) 1.19 per standard deviation (SD) of lifetime smoking index, 95% confidence interval (CI) 1.11 to 1.27), hospitalized COVID-19 (OR 1.67, 95% CI 1.42 to 1.97) or severe COVID-19 (OR 1.48, 95% CI 1.11 to 1.98), with directionally consistent effects from sensitivity analyses. Lung function and COPD liability did not appear to mediate these associations.
CONCLUSION: There is genetic evidence that smoking likely increases the risk of severe COVID-19 and possibly also milder forms of COVID-19. Decreased lung function and increased risk of chronic obstructive pulmonary disease do not seem to mediate the effect of smoking on COVID-19 risk.
PMID:35220625 | DOI:10.1111/add.15852
