Most obstructive lung diseases are associated with smoking including pulmonary emphysema (PE) (1). Smoking affects pathogenesis of pulmonary emphysema by exaggerating destruction of alveolar septa (1).
The septa is linked to alpha1-antitrypsin (a1-AT), which is a plasma constitutent that antagonizes action of serine elastase (1). The enzyme degrades elastic tissue in walls of alveoli and is releaseed in the lungs in response to injury by minor infection or inhaled irritant (1). The smoke blocks action of a1-AT causing damage that draws phagocytes to the lungs and their excess release of serine elastase to degrade elastic tissue in walls (1).
PE is the condition that occurs when this disordered process destroys so much septa that the lungs'airways enlarge abnormally beyond terminal bronchioles (1). As septa continues to be distroyed, airways merge to form even larger sacs (1). A bulla is formed when air spaces enlarge to diameters above 1 cm (1). Without the septa, there is less surface area for gas exchange and less connective tissue that drive recoil of the lungs for inhalation (1). The less surface area is worsened by obstructive effects that occur as alveolar walls are destroyed, which can cause airways to collapse (1). Thus, not only is sucking air in more difficult, but breathing out is tough too (1).
1) Nowak TJ, Handford AG. Pathophysiology: Concepts and Applications for Health Professionals. New York: McGraw-Hill, 2004, p318-320.