Abstract
Allergic rhinitis is typically associated with excessive nasal secretions and morphologic changes of the nasal mucosa; however, an impairment of mucociliary transport, the ultimate expression of mucociliary function, has so far not been clearly demonstrated. Tracheal mucociliary transport rates are decreased in patients with allergic asthma, and inhalation challenge with antigen causes a further impairment that appears to be related to the liberation of chemical mediators, notably slow reacting substance of anaphylaxis. Physiologic studies of mucociliary function in the nose similar to those that have been reported for the lower airways will be required to assess the role of mucociliary dysfunction in allergic rhinitis.