The destructive lung disorders are diseases in which there is desolution and loss of alveolar structures. The primary mechanism responsible for this is an imbalance of proteases and antiproteases toward proteases, particularly neutrophil elastase. Studies of cigarette smokers have demonstrated that they have neutrophils in their lungs, and the major antielastase of the lower respiratory tract, alpha-1 antitrypsin, is functionally impotent. The alveolar macrophages play a major role in the pathogenesis of cigarette smoking induced emphysema by virture of their ability to mediate lung injury and recruit neutrophils. Biochemical, molecular biologic, and morphologic approaches have been used to understand the biosynthesis of elastin in the alveolar structures in order to give insights as to the control of the macromolecule directly responsible for elastic recoil.