Emphysema Risk Factors and Causes
The primary risk factor for emphysema is cigarette smoking. More than 90 percent of cases occur in people who smoke or have smoked cigarettes (sometimes called "smokers emphysema"). The risk for emphysema increases with the number of cigarettes a person smokes each day and the longer a person smokes. Exposure to second-hand smoke also increases the risk.
Chemicals in cigarette smoke can cause continuous low-grade inflammation in lung tissue. Inflammatory cells release enzymes (i.e., proteins that change the rate of chemical reactions), which break down substances in alveolar walls that maintain the structure and elasticity of the air sacs (e.g., collagen, elastin).
Damage to the alveolar walls limits the ability of the air sacs to shrink during exhalation and increases the size of the alveoli. Eventually, it disrupts the exchange of oxygen and carbon dioxide in lung tissue and increases the size of the lungs, which makes less room in the chest for them to expand during breathing.
Cigarette smoking also increases the effects of other risk factors, including exposure to air pollution, dust, chemicals, and poisonous gases; chronic respiratory infections (e.g., pneumonia, bronchitis); and asthma. People who live in heavily industrialized (urban) areas and people who are exposed to noxious fumes or dust at work may have a higher risk for developing emphysema.
Alpha–1 antitrypsin (AAT), also called alpha-1 protease inhibitor, is an enzyme (protein) that helps to protect lung tissue and allow the alveoli to function properly. People who have a genetic (hereditary) deficiency of alpha-1 antitrypsin are at increased risk for developing alpha-1 antitrypsin deficiency emphysema or familial emphysema.
In this condition, damage to the structure and elasticity of the air sacs occurs unchecked. It is important that people who have this deficiency never smoke. AAT is manufactured in the liver, and patients who have this deficiency also may experience liver damage (e.g., cirrhosis, hepatitis).