1. Anti-elastase function in sputum sol-phase from patients with α 1 -proteinase inhibitor (α 1 PI) deficiency was compared with sol-phase from patients with cigarette smoke-induced bronchitis and emphysema. 2. Both α 1 PI (2 P < 0.01) and anti-leucoprotease (ALP) (2 P < 0.01) concentrations were lower in sol-phase from the α 1 PI-deficient group, although α 2 -macroglobulin (α 2 M) levels were similar. 3. There was no difference in α 1 PI function between the two groups, but the inhibitor was only ≃ 30% active. 4. The absolute neutrophil elastase (NE) inhibitory capacity was similar in both groups (median 185 μg of NE inhibited/ml of sputum, range 80–480, for the α 1 PI-deficient group; median 175, range 80–300, for the bronchitic group). A substantial proportion of NE inhibition in secretions could not be accounted for by the amount of α 1 PI, ALP and α 2 M present (median 74.8%, range 43.2–97.4, for α 1 PI-deficient sol-phase; median 50.0%, range 0–80.8, for bronchitic sol-phase). 5. Gel filtration of sol-phase demonstrated the presence of NE inhibition in the low molecular weight fractions which was markedly sensitive to changes in substrate concentration and ionic strength, in contrast to purified α 1 PI and ALP. 6. Sputum sol-phase from both groups failed to prevent hydrolysis of elastin–fluorescein or succinyltrialanyl- p -nitroanilide by NE completely during prolonged incubation in the presence of an excess of functional inhibitors. This was more apparent in secretions from subjects with α 1 PI deficiency and may explain why such patients have a more rapidly progressive form of emphysema.