Rhinitis is inflammation of the nose. Allergic rhinitis occurs when an individual who is allergic to a foreign antigen, and who has antibodies against the antigen (bound to mast cells of the nasal mucosa), inhales the antigen. When antigen and tissue-bound antibody inter-react, mediators are released by the mast cells. These mediators cause dilatation of the blood vessels, leakage of fluid, and swelling of membranes, as well as increased production of mucus. Recent work has led to a clearer understanding of the mechanisms in the nasal passages that control blood vessel constriction and dilatation. Research in recent years has clarified somewhat the mechanism of mucociliary clearance. Propelled by microscopic, hairlike protrusions called cilia, mucus continually cleanses the nasal membranes. Scientists know that many physiologic factors are involved. Methods of measuring changes in nasal airway resistance are being perfected, which means that the way in which foreign antigens affect the nasal passages should soon be better understood. Improved understanding of the allergens responsible for rhinitis is a research priority for the future, and the specific reactive parts of many antigens need to be defined. House dust, for example, is a mixture of poorly characterized components. The molecular identifica- tion of spores, pollen, and animal dander has just begun. Identification techniques must become more chemical-oriented. Which treatment methods cause the number of antigens to decrease? What is the optimal level of environment control? What are the most efficient and effective methods for removing danders, molds, and pollen from the environment? Someday allergy researchers will have to address themselves to these and similar questions. The treatment of allergic rhinitis pharmacologically is in the early stages as well. Medications that compete with the mediator histamine at the histamine receptor sites of the nasal mucosa are known as antihistamines. Decongestants are used systematically and topically to shrink blood vessels and thereby decrease fluid leakage and the swelling of membranes. Although effective only for brief periods, topical agents, if overused, can aggravate the nasal membrane swelling already underway. Each of the six families of antihistamine has a different, fundamental chemical structure. If a drug from one family is ineffective in a particular patient, a drug from another family may be tried and found effective. The best-known side effects of antihistamines are drowsiness, dryness of the mouth, and blurred vision. Sometimes combinations of systemic decongestants and antihistamines are used with good results. Topical corticosteroid sprays are a potent adjunct for more serious cases of rhinitis. They are commonly used for brief periods, however, since some degree of systemic absorption occurs, and adrenal gland suppression, a consequence of corticosteroids usage, is a potential adverse effect. The modification of allergic rhinitis by medication is still of uncertain value. Scientists as yet know little of the relationship of dosage to response for either decongestants or antihistamines. Physicians prescribe the drags at dosage levels that appear to relieve distress without adverse effects, but neither they nor scientists have determined the optimal dosage for a given individual. Finally, the development of tolerance to these drugs and how long topical corticosteroids can be used safely are still a mystery.