1. Understanding COPD Slideshow
2. COPD (Chronic Obstructive Pulmonary Disease) Quiz
3. Energy Foods for COPD Slideshow Pictures

Medical Author:

George Schiffman, MD, FCCP

George Schiffman, MD, FCCP

Dr. Schiffman received his B.S. degree with High Honors in biology from Hobart College in 1976. He then moved to Chicago where he studied biochemistry at the University of Illinois, Chicago Circle. He attended Rush Medical College where he received his M.D. degree in 1982 and was elected to the Alpha Omega Alpha Medical Honor Society. He completed his Internal Medicine internship and residency at the University of California, Irvine.

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Medical Editor:

Charles Patrick Davis, MD, PhD

Charles Patrick Davis, MD, PhD

Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.

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Cigarette smoking or exposure to tobacco smoke is the primary cause of COPD. While COPD occurs in 15% of cigarette smokers, tobacco use accounts for as much as 90% of the risk for the development of this disease.

Secondhand smoke or environmental tobacco smoke also increase the risk of respiratory infections and can result in a decrease in lung function.

People with COPD experience a more rapid decline in what is called forced expiratory volume, or FEV. FEV is the maximum volume of air that can be exhaled within a specified time period, starting from maximal inhalation. A subscript indicates the time period in seconds. For example, FEV₁ is the maximum volume of air that can be exhaled within 1 second. A decline in FEV causes a person to become short of breath and to have difficulty breathing.

It is not clear if air pollution causes COPD. However, if it does, the effect is small when compared to cigarette smoking.

The use of solid fuels for cooking and heating may cause high levels of indoor air pollution, which may then lead to the development of COPD, especially in underdeveloped countries where cooking with wood or coal is common.

Some patients who develop COPD have airway hyperresponsiveness, a condition in which their airways overreact to airborne irritants, such as secondhand smoke and air pollution.

The role of airway hyperresponsiveness as a risk factor for COPD in people who smoke is unclear. However, according to one hypothesis, patients who have airway hyperreactivity and who smoke are at an increased risk of COPD and an accelerated rate of decreased lung function.

In patients with chronic asthma, inflammation over time can result in permanent remodeling of the airways and result in fixed airway obstruction. It is in this way that chronic asthma becomes COPD. Generally, patients with asthma have normal lung function when they are not having an attack. It is only after years of inadequate control of airway inflammation that they can develop this fixed airway obstruction.

Alpha1-antitrypsin (AAT) is a protein in the body that is produced by the liver and helps protect the lungs from damage. In AAT deficiency, the liver does not produce enough of this protein.

AAT deficiency is an inherited condition, and it is the only known genetic risk factor for COPD. It accounts for less than 1% of all cases of COPD in the United States. Severe AAT deficiency leads to emphysema at an early age; in nonsmokers, the average age of onset of emphysema is 53 years, and in smokers, it is 40 years.

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