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Genetic Epidemiology of COPD*

Edwin K. Silverman, MD, PhD
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*From the Channing Laboratory and Pulmonary and Critical Care Division, Department of Medicine, Brigham and Women’s Hospital, Boston, MA.

Correspondence to: Edwin K. Silverman, MD, Channing Laboratory, Pulmonary and Critical Care Division, Department of Medicine, Brigham and Women’s Hospital, 181 Longwood Ave, Boston, MA 02115; e-mail: ed.silverman@channing.harvard.edu



Chest. 2002;121(3_suppl):1S-6S. doi:10.1378/chest.121.3_suppl.1S-a
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Although cigarette smoking is the major environmental risk factor for the development of COPD, there is marked variability in the development of airflow obstruction in response to smoking. A dose-response relationship between FEV1 % predicted and the number of pack-years of cigarette smoking was demonstrated by Burrows and colleagues.1 Heavier smokers were more likely to develop airflow obstruction, which is indicated by reduced FEV1 levels. However, many smokers had pulmonary function values within the normal range. Although the number of pack-years was the smoking-related variable that correlated most closely with FEV1 in the study by Burrows et al,,1 it only accounted for 15% of the variability in FEV1. Mounting evidence suggests that genetic factors likely influence the variable susceptibility to develop COPD. We will briefly review α1-antitrypsin (AAT) deficiency, discuss the case-control genetic association studies that have been performed in patients with COPD, and describe our ongoing research into the genetic determinants of severe, early-onset COPD.

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