File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Association of smoking, lung function and COPD in COVID-19 risk: a two-step Mendelian randomization study

TitleAssociation of smoking, lung function and COPD in COVID-19 risk: a two-step Mendelian randomization study
Authors
KeywordsChronic obstructive pulmonary disease
COVID-19
genetics
lung function
Mendelian randomization
smoking
Issue Date2022
Citation
Addiction, 2022, v. 117, n. 7, p. 2027-2036 How to Cite?
AbstractBackground 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 our knowledge, 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 the inverse variance weighted method, and we included a range of sensitivity analyses to assess the robustness of the findings. Setting: GWAS which included international consortia, FinnGen and UK Biobank. Participants: The sample size ranged from 193 638 to 2 586 691. Measurements: Genetic determinants of life-time smoking index, lung function [e.g. forced expiratory volume in 1 sec (FEV1)], chronic obstructive pulmonary disease (COPD) and different severities of COID-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 life-time smoking index, 95% confidence interval (CI) = 1.11–1.27], hospitalized COVID-19 (OR = 1.67, 95% CI = 1.42–1.97) or severe COVID-19 (OR = 1.48, 95% CI = 1.10–1.98), 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 probably 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.
Persistent Identifierhttp://hdl.handle.net/10722/342645
ISSN
2023 Impact Factor: 5.2
2023 SCImago Journal Rankings: 2.129
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorAu Yeung, Shiu Lun-
dc.contributor.authorLi, Albert Martin-
dc.contributor.authorHe, Baoting-
dc.contributor.authorKwok, Kin On-
dc.contributor.authorSchooling, C. Mary-
dc.date.accessioned2024-04-17T07:05:15Z-
dc.date.available2024-04-17T07:05:15Z-
dc.date.issued2022-
dc.identifier.citationAddiction, 2022, v. 117, n. 7, p. 2027-2036-
dc.identifier.issn0965-2140-
dc.identifier.urihttp://hdl.handle.net/10722/342645-
dc.description.abstractBackground 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 our knowledge, 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 the inverse variance weighted method, and we included a range of sensitivity analyses to assess the robustness of the findings. Setting: GWAS which included international consortia, FinnGen and UK Biobank. Participants: The sample size ranged from 193 638 to 2 586 691. Measurements: Genetic determinants of life-time smoking index, lung function [e.g. forced expiratory volume in 1 sec (FEV1)], chronic obstructive pulmonary disease (COPD) and different severities of COID-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 life-time smoking index, 95% confidence interval (CI) = 1.11–1.27], hospitalized COVID-19 (OR = 1.67, 95% CI = 1.42–1.97) or severe COVID-19 (OR = 1.48, 95% CI = 1.10–1.98), 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 probably 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.-
dc.languageeng-
dc.relation.ispartofAddiction-
dc.subjectChronic obstructive pulmonary disease-
dc.subjectCOVID-19-
dc.subjectgenetics-
dc.subjectlung function-
dc.subjectMendelian randomization-
dc.subjectsmoking-
dc.titleAssociation of smoking, lung function and COPD in COVID-19 risk: a two-step Mendelian randomization study-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/add.15852-
dc.identifier.pmid35220625-
dc.identifier.scopuseid_2-s2.0-85125672637-
dc.identifier.volume117-
dc.identifier.issue7-
dc.identifier.spage2027-
dc.identifier.epage2036-
dc.identifier.eissn1360-0443-
dc.identifier.isiWOS:000765504200001-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats