Pulmonary alveolar macrophages (PAM) obtained by bronchoalveolar lavage in 13 normal individuals, 17 lung cancer patients and 10 patients with chronic obstructive pulmonary disease (COPD) were incubated in vitro for 24 hours. Every specimen was divided into two portions and lipopolysaccharides were used to stimulate PAMs to produce interleukin-1 (1L-1) in one. The levels of 1L-1 in normal subjects were 5547.65 +/- 2420.42 cpm/10(6) cells (stimulated) and 718.46 +/- 472.25 (unstimulated), which were higher than the 2733.20 +/- 1611.17 (stimulated, P less than 0.01) and 327.57 +/- 226.86 (unstimulated, P less than 0.05) in lung cancer patients, but lower than that of 8716.26 +/- 2977.66 (stimulated, P less than 0.05) in COPD patients. The enhanced 1L-1 activity in COPD patients might contributed to the active inflammatory process and tissue destruction of COPD. Our findings that 1L-1 activity in patients with bronchogenic carcinoma was decreased may reflect the local immune deficiency in malignant disease. The release of 1L-1 by PAMs stimulated by smoking was suggested to be associated with the development of COPD, but its role in immune response has to be determined.