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Original Research: COPD |

Sex Differences in Emphysema and Airway Disease in Smokers

Pat G. Camp, PhD, PT; Harvey O. Coxson, PhD; Robert D. Levy, MD; Sreekumar G. Pillai, PhD; Wayne Anderson, PhD; Jørgen Vestbo, MD; Susan M. Kennedy, PhD; Edwin K. Silverman, MD, PhD; David A. Lomas, MD, PhD; Peter D. Paré, MD
Author and Funding Information

Affiliations: From the James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research (Drs. Camp, Coxson, and Paré), St. Paul's Hospital, the School of Environmental Health (Dr. Kennedy), the Respiratory Division (Dr. Levy), and the Department of Radiology (Dr. Coxson), University of British Columbia, Vancouver, BC, Canada; Genetics Research (Drs. Pillai and Anderson), GlaxoSmithKline, Research Triangle Park, NC; the School of Translational Medicine (Dr. Vestbo), University of Manchester, UK; the Department of Cardiology and Respiratory Medicine (Dr. Vestbo), Hvidovre University Hospital, Hvidovre, Denmark; the Channing Laboratory and Pulmonary and Critical Care Division (Dr. Silverman), Brigham and Women's Hospital, Harvard Medical School, Boston, MA; and the Department of Medicine (Dr. Lomas), University of Cambridge, Cambridge, UK.

Correspondence to: Pat G. Camp, PhD, PT, James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, University of British Columbia, Providence Heart and Lung Institute, St Paul's Hospital, 1081 Burrard St, Vancouver, BC, Canada V6Z1Y6; e-mail: pgcamp@interchange.ubc.ca


Funding/Support: The International COPD Genetics Network, the study from which these data originated, was funded by GlaxoSmithKline. When this study was conducted, Dr. Camp was funded by a Canadian Institute of Health Research (CIHR) Fellowship, a Canadian Respiratory Health Professional Fellowship, and a trainee award from Interdisciplinary Capacity Enhancement-Bridging Excellence in Respiratory disease and Gender Studies (ICEBERGS), a CIHR-funded research team. She is currently funded with a postdoctoral fellowship award from the Michael Smith Foundation for Health Research-Provincial Health Services Authority-Child and Family Research Institute Research Trainee Award. Dr. Coxson is a Canadian Institutes of Health Research/British Columbia Lung Association New Investigator. Dr. Paré is a MSFHR Distinguished Scholar and the Jacob Churg Distinguished Researcher.

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


© 2009 American College of Chest Physicians


Chest. 2009;136(6):1480-1488. doi:10.1378/chest.09-0676
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Background:  The authors of previous reports have suggested that women are more susceptible to cigarette smoke and to an airway-predominant COPD phenotype rather than an emphysema-predominant COPD phenotype. The purpose of this study was to test for sex differences in COPD phenotypes by using high-resolution CT (HRCT) scanning in male and female smokers with and without COPD.

Methods:  All subjects completed spirometry and answered an epidemiologic respiratory questionnaire. Inspiratory HRCT scans were obtained on 688 smokers enrolled in a family-based study of COPD. Emphysema was assessed by using a density mask with a cutoff of −950 Hounsfield units to calculate the low-attenuation area percentage (LAA%) and by the fractal value D, which is the slope of a power law analysis defining the relationship between the number and size of the emphysematous lesions. Airway wall thickness was assessed by calculating the square root of the airway wall area (SQRTWA) and the percentage of the total airway area taken by the airway wall (WA%) relative to the internal perimeter.

Results:  Women had a similar FEV1 (women, 65.5% ± 31.9% predicted; men, 62.1% ± 30.4% predicted; p = 0.16) but fewer pack-years of cigarette smoking (women, 37.8 ± 19.7 pack-years; men, 47.8 ± 27.4 pack-years; p < 0.0001). Men had a greater LAA% (24% ± 12% vs 20% ± 11%, respectively; p < 0.0001) and larger emphysematous spaces than women, and these differences persisted after adjusting for covariates (weight, pack-years of smoking, current smoking status, center of enrollment, and FEV1 percent predicted; p = 0.0006). Women had a smaller SQRTWA and WA% after adjusting for covariates (p < 0.0001).

Conclusion:  Male smokers have more emphysema than female smokers, but female smokers do not show increased wall thickness compared with men.

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