Causes And Risk Factors
Smoking is a primary risk factor for COPD, accounting for up to 75% of all COPD cases globally. Genetics, occupational exposures to gases & fumes, and exposure to biofuel account for the remaining cases (Salvi 2009; ICSI 2011). People exposed to more than one risk factor can develop COPD earlier, or have more severe symptoms and exacerbations (GOLD 2011).
More than half of all long-term smokers will develop COPD (Mannino 2007; IOM 2011). Moreover, life-long cigarette smokers have a significantly higher rate of decline in lung function, are more likely to develop COPD with age, and more frequently die of COPD compared to non-smokers (Rennard 2006; Kohansal 2009).
Secondhand smoke is an independent risk factor for COPD (Eisner 2010; Jordan 2011). Evidence shows that COPD risk doubled among never-smokers exposed to secondhand tobacco smoke for more than 20 hours/week (Jordan 2011).
Occupational exposure is another risk factor in the development of COPD. Studies show that toxic gases in the workplace, such as chemical dust and fumes in factories, can increase the risk of COPD (Mannino 2007; Salvi 2009) and severe exacerbations of COPD (Rodriguez 2008).
Globally, and especially in low- to middle-income countries, another important risk factor for COPD may be exposure to air pollutants such as solid or biomass fuels (e.g., coal, straw, animal dung, and wood) (Mannino 2007; Salvi 2009). Of these fuels, wood smoke, followed by mixed biomass smoke, is the most notable COPD risk factor (Kurmi 2010).
Asthma (Bronchial Hyperresponsiveness)
Childhood asthma is a risk factor for the development of COPD later in life, and asthma in the elderly shares many similarities with COPD (e.g., shortness of breath, wheezing, coughing, decline in lung function and treatment options) (Eisner 2010; Mannino 2011; GOLD 2011). Also, airway obstruction becomes more severe with long-term asthma. Therefore, it is necessary for doctors to distinguish the two conditions in order to properly diagnose and manage them (Tzortzaki 2011).
Clinically distinguishing asthma and COPD is typically straightforward among middle-age and younger people. However, in the elderly, especially those who smoke, differentiating between the two conditions can be difficult using standard clinical lung function assessments. More comprehensive diagnostic testing, including allergy testing, CT scanning of the lungs, and advanced biomarker analyses that characterize COPD vs. asthma based upon the profile of inflammatory mediators in the blood, allow modern clinicians to confidently categorize most patients (Tzortzaki 2011, Hanania 2011).
Treatment response can also aid in the differentiation of the two conditions. For example, asthma is typically significantly reversible using bronchodilators, while COPD is only minimally reversible (Tzortzaki 2011).
Alpha-1-antitrypsin deficiency is a rare (up to 3% of COPD patients), inherited cause of COPD, occurring primarily in individuals of northern European descent. This genetic defect causes the body to produce a decreased amount of the protein alpha-1-antitrypsin, which normally prevents neutrophil elastase from damaging the alveoli. Emphysema typically develops by early middle age in people with severe alpha-1-antitrypsin deficiency, especially in those who smoke (Merck Manual 2008; American Lung Assc. 2011; Fregonese 2008; Ferri 2012).