In recent years, efforts have been aimed at defining the airway changes associated with COPD. Polymorphonuclear leukocytes play a major role in airway inflammation. New information on the mechanisms of polymorphonuclear leukocyte recruitment and other actions in airway and parenchymal dysfunction has included observations about a role for mononuclear cell-mediated inflammation in COPD patients. Such cells infiltrate the bronchial submucosa in increased numbers in patients with COPD. In addition, neutrophil chemotaxis into the airways is evidence that chemokines and chemokine receptors play a role in the inflammatory response.1–2 Chemotaxis is stimulated by smoking, and yet airway inflammation continues even after smoking cessation. Many molecules induce chemotactic activity for neutrophils, including leukotrienes (LTs). These molecules are now known to comprise the main ingredients of the slow-reacting substance of anaphylaxis, a mediator of hypersensitivity reactions.