COPD can be caused by various factors, including lung infections, asthma, air pollution, childhood growth disorders, and genetic factors, although smoking is a predominant risk factor. The main pathological mechanisms in COPD involve small airway disease, emphysema, mucus hypersecretion, and vascular disorders. COPD in non-smokers is characterized by normal FEV1 decline, equal distribution of sex, younger age of onset, fewer comorbidities, milder airflow obstruction, normal diffusing capacity of the lungs for carbon monoxide (DLCO) and radiological features such as more air-trapping and less severe emphysema, compared to COPD in smokers. COPD in non-smokers is still accompanied by a high prevalence of acute exacerbation almost equal to COPD in smokers. Moreover, COPD per se is an independent risk factor for the development of lung cancer, irrespective of smoking status. Considering that COPD coexists with numerous comorbidities, effective management of these comorbidities is essential, and multifaceted efforts are required for the comprehensive treatment of COPD.
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