Monthly Letters to Pulmonary Patients by Thomas L. Petty

Thomas L. Petty, M.D.

Professor of Medicine, 
University of Colorado

Chairman, National Lung Health Education Program (NLHEP)


National Lung Health Education Program
A collaborative project with



HealthOne Center
1850 High Street
Denver, CO 80218
Phone: 303 839 6755
Fax: 303 832 8137

Improved Understanding of COPD

August 1999
Second Wind
Lomita, California

     Dear Friends:

     The 42nd Aspen Lung Conference, held in June, 1999, offered new insights into the mechanisms involved in the development of COPD. These Conferences began in 1958 and were initiated to try to understand the basic nature of emphysema and chronic bronchitis, which today we lump together under the designation of COPD. In the 41-years that have followed, we now recognized that COPD has both susceptibility factors in the patient (host), and inciting environmental factors which trigger inflammatory mechanisms which attack alveoli and small airways. Alveoli contain the elastic fibers that allow the lungs to fill in an orderly fashion and to empty during exhalation. Alveoli also attach to small airways and tether them, thus keeping them open during the expiratory phase of respiration. An attack on alveoli appears to come from enzymes, (elastases), which are released from white cells, when stimulated by tobacco smoke and other irritants. When small airways are attacked they become inflamed and overreact with a degree of bronchospasm, in some ways similar to asthma. Tobacco smoke also creates oxidants which destroy protective material in the lung known as antiproteases, so that destructive enzymes become unopposed and do their damage to small lung units.

     Although COPD clusters in families, the exact genetic defect or defects remain unknown. Certainly these familial risks go beyond the rare but important alpha antitrypsin deficiency state, (AAT).

     How to protect the lung from elastase, oxidative, as well as other damages was considered at the Conference. Antioxidants in food may play a protective role. Drugs known as isoretinines may help restore the alveoli in an experimental model of emphysema. Whether the same will be true in humans is a subject of current study.

     The most effective way to prevent or to forestall COPD is to avoid all tobacco smoke, both active and passive. Eating a diet rich in antioxidant vitamins and protective fish oils is probably wise. Understanding the mechanisms of COPD forms a foundation for new therapies. New drugs are on the horizon which may help reduce or eliminate the damage that today results in COPD, the only major disease amongst the top ten killers that continues to rise. Progress is being made, and the future looks bright.

Your friend,

Thomas Petty, MD

Last update:
23 Feb 2002