Background Chronic bronchitis (CB) is strongly associated with cigarette smoking, but not all smokers develop CB. We aimed to evaluate whether measures of structural airway disease on CT are differentially associated with CB.
Methods In smokers between ages 45 and 80 years, and with Global Initiative for Obstructive Lung Disease stages 0–4, CB was defined by the classic definition. Airway disease on CT was quantified by (i) wall area percent (WA%) of segmental airways; (ii) Pi10, the square root of the wall area of a hypothetical airway with 10 mm internal perimeter; (iii) total airway count (TAC) and (iv) airway fractal dimension (AFD), a measure of the complex branching pattern and remodelling of airways. CB was also assessed at the 5-year follow-up visit.
Measurements and main results Of 8917 participants, 1734 (19.4%) had CB at baseline. Airway measures were significantly worse in those with CB compared with those without CB: WA% 54.5 (8.8) versus 49.8 (8.3); Pi10 2.58 (0.67) versus 2.28 (0.59) mm; TAC 156.7 (81.6) versus 177.8 (91.1); AFD 1.477 (0.091) versus 1.497 (0.092) (all p<0.001). On follow-up of 5517 participants at 5 years, 399 (7.2%) had persistent CB. With adjustment for between-visits changes in smoking status and lung function, greater WA% and Pi10 were associated with significantly associated with persistent CB, adjusted OR per SD change 1.75, 95% CI 1.56 to 1.97; p<0.001 and 1.66, 95% CI 1.42 to 1.86; p<0.001, respectively. Higher AFD and TAC were associated with significantly lower odds of persistent CB, adjusted OR per SD change 0.76, 95% CI 0.67 to 0.86; p<0.001 and 0.69, 95% CI 0.60 to 0.80; p<0.001, respectively.
Conclusions Higher baseline AFD and TAC are associated with a lower risk of persistent CB, irrespective of changes in smoking status, suggesting preserved airway structure can confer a reserve against CB.
- COPD pathology
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Contributors Study concept and design: SPB, SB and VK. Acquisition, analysis or interpretation of data: all authors. Drafting of the manuscript: SPB. Critical revision of the manuscript for important intellectual content: all authors. Statistical analysis: SPB. Study supervision: SPB and VK. SPB had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Funding This work was supported by NHLBI R01 HL151421 (SPB and AN), NHLBI K23HL133438 (SPB), and NIBIB R21EB027891 (SPB). SF is supported by the Department of Veterans Affairs (Award No. 14380). The COPDGene study is supported by NIH Grants U01 HL089897 and U01 HL089856. COPDGene is also supported by the COPD Foundation through contributions made to an Industry Advisory Board comprised of AstraZeneca, Boehringer-Ingelheim, Genentech, GlaxoSmithKline, Novartis, Pfizer, Siemens, and Sunovion.
Competing interests SPB has received consulting fees from GlaxoSmithKline and Sunovion. VK reports personal fees from Gala Therapeutics, ABIM Critical Care Test Writing Committee, AstraZeneca and Boehringer Ingelheim.
Patient consent for publication Not required.
Ethics approval Written informed consent was obtained from all participants prior to enrolment and the study protocol was approved by the institutional review boards of all participating centres.
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement Data are available upon reasonable request. COPDGene data are available to investigators upon request through a study proposal.
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