THE INFLAMMATORY EFFECTS OF 2 PPM NO2 ON THE AIRWAYS OF HEALTHY-SUBJECTS

Nitrogen dioxide (NO2) is a free radical and a common oxidant in pollu ted air. Here we present data on the time course of inflammation after NO2 exposure, as reflected in bronchial biopsy and airway lavage spec imens. Healthy, nonsmoking subjects were exposed to air or 2 ppm NO2 f or 4 h in random order on separate occasions. Endobronchial biopsies, bronchial washing (BW), and bronchoalveolar lavage (BAL) were done at 1.5 h (n = 15) or 6 h (n = 15) after exposure. In BW, exposure to NO2 induced a 1.5-fold increase in interleukin-8 (IL-8) (p < 0.05) at 1.5 h and a 2.5-fold increase in neutrophils (p < 0.01) at 6 h. In BAL flu id (BALF), small increases were observed in CD45RO(+) lymphocytes, B-c ells, and natural killer (NK) cells only. Immunohistologic examination of bronchial biopsy specimens showed no signs of upregulation of adhe sion molecules, and failed to reveal any significant changes in inflam matory cells at either time point after NO2 exposure. In summary, NO2 induced a neutrophilic inflammation in the airways that was detectable in BW at 6 h after NO2 exposure. The increase in neutrophils could be related to the enhanced IL-8 secretion observed at 1.5 h after exposu re. The absence of adhesion-molecule upregulation or cellular inflamma tion in mucosal biopsy specimens indicates that the major site of infl ammation following exposure to NO2 may be in the smaller airways and n ot in the alveoli.