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Original Research: COPD |

Persistent Airway Inflammation and Emphysema Progression on CT Scan in Ex-Smokers Observed for 4 Years

Marina Miller, MD, PhD; Jae Youn Cho, MD, PhD; Alexa Pham, BS; Paul J. Friedman, MD; Joe Ramsdell, MD, FCCP; David H. Broide, MBChB
Author and Funding Information

From the Department of Medicine (Drs Miller, Cho, Ramsdell, and Broide, and Ms Pham), and Department of Radiology (Dr Friedman), University of California, San Diego, CA.

Correspondence to: David Broide, MBChB, University of California San Diego, Biomedical Sciences Bldg, Room 5090, 9500 Gilman Dr, La Jolla, CA 92093-0635; e-mail: dbroide@ucsd.edu


Funding/Support: This work was supported by the National Institutes of Health [Grants HL72342, and GCRC MO1RR000827].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;139(6):1380-1387. doi:10.1378/chest.10-0705
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Background:  Tobacco smoking is a principal cause of COPD-emphysema (COPD-E). Whether discontinuing smoking for at least 4 years halts airway inflammation and progression of COPD-E in prior smokers is unknown. In this study we investigated whether discontinuing smoking for approximately 4 years in ex-smokers with GOLD (Global Initiative for Chronic Lung Disease) stage IIb (moderately severe) COPD-E stopped airway inflammation (ie, sputum biomarkers) and halted the progression of COPD-E on chest CT scan.

Methods:  Ten ex-smokers with COPD-E who had quit smoking underwent chest CT scans to document the extent of COPD-E, assessment of lung function (FEV1 and diffusing capacity of lung for carbon monoxide), sputum induction for biomarkers of inflammation (measured by enzyme-linked immunosorbent assay), and blood cotinine levels at baseline and approximately 4 years later. Normal healthy subjects (n = 7) and normal current smokers with no CT scan evidence of COPD-E (n = 8) served as sputum biomarker comparison groups.

Results:  After approximately 4 years of not smoking (documented by cotinine levels), ex-smokers with COPD-E had persistent increased levels of mediators of inflammation in sputum (myeloperoxidase, leukotriene B4, IL-8, monocyte chemoattractant protein-1, matrix metalloprotease-9), which was associated with significant progression of COPD-E on chest CT scan.

Conclusions:  Cessation of tobacco smoking in heavy smokers with moderately severe COPD-E is associated with evidence of persistent airway inflammation and progression of COPD-E on CT scan 4 years later. Discontinuing smoking may slow the rate of progression of moderate severity COPD-E, but it does not prevent persistent airway inflammation and significant progression of COPD-E on CT scan.

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