Inflammatory processes of the upper airway may alter the responsiveness of the lower airway. For example, bronchial hyperresponsiveness may be seen in patients with allergic rhinitis. This could represent coexistent but unrecognized asthma, but also suggests that IgE-dependent inflammation may occur in the lower airway that can increase bronchial hyperresponsiveness without at the same time precipitating obvious obstruction. Clearly, allergic rhinitis is a risk factor for asthma. A second example of the interaction of upper airway inflammation and bronchial hyperreactivity are reports that viral upper respiratory tract infections may cause otherwise healthy persons to respond abnormally to inhaled histamine or irritants for several months after the infections. These same viruses usually precipitate attacks in patients with asthma, who already have hyperresponsive airways. Both of these examples suggest that inflammatory processes occurring totally or primarily in the upper airway may participate in the pathogenesis of lower respiratory tract hyperresponsiveness and asthma.