The association of α1-antitrypsin deficiency with chronic lung disease has led to extensive research into the pathogenic processes involved. The majority of evidence still indicates that human neutrophil elastase is a significant mediator of bronchial and interstitial lung damage. This destructive process is restricted to the immediate area around the neutrophil and can only be partially blocked by physiologic concentrations of inhibitors. Understanding the process involved has led to the conceptualization of treatment or preventative strategies that depend on the condition being treated.