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The prevalence, morbidity, and mortality of chronic obstructive pulmonary disease (COPD) are directly linked to cigarette smoking and air pollution.1 COPD cases are expected to continue to increase, due to the continued exposure to risk factors (cigarette smoke and air pollution) and individuals living longer.1 According to the 2007 United States National Health Interview Survey, approximately 11 million Americans over the age of 18 years have COPD.2 It is projected that worldwide, COPD will become the third leading cause of death by the year 2020.1
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COPD is a preventable chronic disease of the airways that is characterized by gradual, progressive loss of lung function. It is characterized by airflow limitation that is not fully reversible.1 The airflow limitation is associated with an abnormal inflammatory response of the lung to noxious particles or gases.1 Emphysema and chronic bronchitis are often present in COPD, but patients must also have abnormal spirometry to be formally diagnosed with COPD. Emphysema is an abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis. Chronic bronchitis is inflammation of the bronchioles with mucus hypersecretion and chronic productive cough when all other causes of cough have been ruled out.
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The most common risk factor for COPD is cigarette smoking, however, not all smokers develop COPD, which suggests a possible genetic factor or predisposition.3 A rare genetic disorder called alpha 1 antitrypsin (AAT) deficiency is a risk factor for COPD.4 This hereditary deficiency is a recessive trait most commonly seen in individuals of Northern European descent.5 Patients with AAT deficiency develop COPD at an early age (20-50 years). Patients presenting with COPD at an early age or a strong family history should be screened for this disorder.4 Inhalation exposure risk factors include occupational dusts and chemicals (chemical agents and fumes), indoor air pollution (wood, animal dung, crop residues, and coal burned in open fires), and outdoor air pollution.6-9 Another potential risk factor is impaired lung growth during gestation, birth, and childhood. A positive association has been found between birth weight and forced expiratory volume in 1 second (FEV1) in adulthood.10 Oxidative stress, or a depletion of antioxidants in the lungs plays a role in the development of COPD and can initiate lung inflammation and injury.11 Respiratory infections, both viral and bacterial, may contribute to the pathogenesis of COPD and are considered a risk factor.12
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COPD is caused by amplification of the normal inflammatory response to chronic irritants such as cigarette smoke. Inflammatory mediators increased in COPD patients include neutrophils, macrophages, and lymphocytes. Oxidative stress generated by oxidants released by cigarette smoke and other inhaled substances and a reduction in endogenous antioxidants also contribute to lung inflammation. An imbalance between the proteases that break down connective tissue in the lung and the antiproteases that protect against this is also seen ...