Proposed model for the pathogenesis of emphysema in patients with Z α₁-antitrypsin deficiency. The plasma deficiency and reduced inhibitory activity of Z α₁-antitrypsin may be exacerbated by the polymerization of α₁-antitrypsin within the lungs. These processes inactivate the inhibitor, thereby further reducing the antiproteinase screen. α₁-Antitrypsin polymers may also act as a proinflammatory stimulus to attract and activate neutrophils, thereby increasing tissue damage.