Animal studies have reported that diesel exhaust particles (DEP), which constitute an important fraction of particulate air pollution, lead to inflammation and/or damage of the airways. To investigate the mechanisms underlying DEP-induced airway disease in humans, we have cultured human bronchial epithelial cells (HBEC) from surgically obtained bronchial explants and investigated the effects of purified DEP on the permeability and ciliary beat frequency (CBF) of HBEC, and on the release of inflammatory mediators from these cells. Exposure to 10-100 microg/ml DEP and a filtered solution of 50 microg/ml DEP significantly increased the electrical resistance of the cultures, reaching a maximum of 200% over baseline after 6 h incubation with 100 microg/ml DEP. In contrast, movement of 14C-labeled bovine serum albumin across cell cultures was not significantly altered by incubation of HBEC with DEP. Exposure to 50 microg/ml DEP, filtered DEP solution, and 100 migrog/ml DEP significantly attenuated the CBF of these cells by 51%, 33%, and 73%, respectively, from baseline after 24 h incubation. Similarly, 50 microg/ml DEP, filtered DEP solution, and 100 microg/ml DEP significantly increased the release of interleukin-8 from 12.9 pg/microg cellular protein to 41.6, 114.9, and 44.3 pg/microg cellular protein, respectively, after 24 h incubation. The release of granulocyte-macrophage colony stimulating factor (GM-CSF) and soluble intercellular adhesion molecule-1 (sICAM-1) was also significantly increased after exposure for 24 h to 50 microg/ml DEP (GM-CSF from 0.033 pg/microg cellular protein to 0.056 pg/mug cellular protein and sICAM-1 from 7.2 pg/microg cellular protein to 12.5 pg/microg cellular protein). These results suggest that exposure of HBEC to DEP may lead to adverse functional changes and release of proinflammatory mediators from these cells, and that these effects may influence the development of airway disease.

Background-Although sputum induction is used as a technique to investigate lower airway inflammation in asthmatic subjects, advantages over spontaneous sputum in patients with chronic obstructive pulmonary disease (COPD) have not been investigated. Methods-Samples of spontaneous sputum and sputum induced with 3% hypertonic saline for 14 minutes were collected from 27 patients with chronic obstructive pulmonary disease (COPD) who usually produced spontaneous sputum. Spirometric indices and oxygen saturation (SaO 2 ) were measured at seven minute intervals. The spontaneous, seven and 14 minute sputum samples were analysed for total and diVerential cell counts, cell viability, and interleukin 8 levels. Results-Analysis of the sputum revealed that median cell viability was higher in the seven minute (62.8%; p = 0.004) and 14 minute (65%; p = 0.001) induced sputum samples than in spontaneous sputum (41.2%). There was no significant diVerence in total and diVerential cell counts or in interleukin 8 levels between spontaneous and induced sputum. During the sputum induction procedure the mean (SD) fall in forced expiratory volume in one second (FEV 1 ) was 0.098 (0.111) l (p < 0.001) and in forced vital capacity (FVC) was 0.247 (0.233) l (p < 0.001). There was a small but significant fall in SaO 2 during sputum induction (p = 0.03). Conclusions-Induced sputum contains a higher proportion of viable cells than spontaneous sputum. There are no significant diVerences between the sputum samples obtained at seven minutes and at 14 minutes of hypertonic saline nebulisation. Sputum induction is safe and well tolerated in patients with COPD. (Thorax 1998;53:953-956)

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