ABSTRACT
Airflow obstruction is the functional consequence of pathological changes induced by cigarette smoking in peripheral airways and lung parenchyma. These include both inflammatory and structural changes, mainly airway remodeling and parenchymal destruction (which characterizes emphysema). Airway remodeling and inflammation will contribute to airflow obstruction by promoting airway narrowing and lumen occlusion, while parenchymal destruction will contribute to airflow obstruction by reducing the elastic recoil of the lung as well as by destroying alveolar attachments and thereby reducing the elastic load applied to the airways (1,2). Whether airflow obstruction is always caused by emphysema or whether a disease of the conducting airways without emphysema could also cause airflow obstruction is still uncertain. Furthermore, it has been reported that smokers may develop emphysema even in the presence of normal lung function (3,4). These facts highlight the complexity of Chronic Obstructive Pulmonary Disease (COPD) and particularly of the relationship among airway pathology, emphysema, and airflow obstruction.
