The impairment of mucociliary transport by dry air breathing and the restoration of function with subsequent humidification of inspired air were investigated in anesthetized dogs. Tracheal mucous velocity was measured by a cinebronchofiberscopic technique. The breathing of dry air through an uncuffed endotracheal tube produced almost complete cessation of the flow of tracheal mucus after 3 h. Subsequent breathing of air at 38 degrees C with 100% relative humidity restored tracheal mucous velocity to control values by the end of and additional 3 h. Histologic examination of the trachea at the end of the 3-h dry air breathing period revealed focal areas of sloughing of the ciliated epithelium and submucosal inflammation. Although morphometry was not employed, the inflammatory changes appeared to have progressed during 3 h of breathing fully humidified air subsequent to the dry air breathing period. These findings were consistent with previous reports that the inflammatory response to injury of the tracheobronchial mucosa might be delayed and that the mucociliary transport system has a great deal of functional reserve. We found that an artificial heat and moisture exchanger placed on the proximal end of an endotracheal tube partially protects against the suppression of tracheal mucous velocity caused by dry air breathing.