The effect of aspirated hydrochloric acid (HCl) on alveolar macrophage function was investigated in a rabbit model. Lung cells were obtained by bronchoalveolar lavage 4 h after an intratracheal injection of HCl. The intratracheal administration of HCl significantly increased (p < 0.005) the number of neutrophils recovered at lavage. Alveolar marcophage adherence to glass was significantly decreased (p < 0.001) in the HCl-treated animals compared with that of the control animals. Alveolar macrophage phagocytosis was not altered, and there was no effect on macrophage migration through micropore filters. In vitro studies showed that incubation of alveolar macrophages from normal rabbits in cell-free supernatants from HCl-treated rabbit lavage significantly decreased (p < 0.01) alveolar macrophage adherence to glass. In vitro incubation of alveolar macrophages from normal rabbits with rabbit peritoneal neutrophils significantly decreased (p < 0.05) adherence to glass. To investigate the effects of corticosteroid treatment, acid-injured rabbits were given 0.5 mg/kg of dexamethasone intravenously within 5 min. Alveolar macrophages from the steroid-treated animals showed a partial, but significant (p < 0.005), reversal of the acid-induced adherence defect. We concluded that acid aspiration is associated with an influx of neutrophils into the alveolar space, and decreased alveolar macrophage adherence to glass. The adherence defect was related to a factor or factors present in lavage fluid and to the presence of activated neutrophils. Corticosteriod treatment partially reversed the adherence defect.