Allergen inhalation in the laboratory can lead to an early (0 to 2 hours) and late (3 to 12 hours) asthmatic response and an increase in airway hyperresponsiveness to a variety of bronchoconstrictor mediators. Also, environmental allergen exposure increases airway responsiveness, symptoms of asthma, and the amount of treatment needed to control symptoms. Allergen inhalation causes an acute inflammatory response with an influx of predominantly neutrophils and/or eosinophils into the airway in both animal preparations and sensitized human subjects. The development of airway hyperresponsiveness is most likely a consequence of the inflammatory response. The mediators involved in initiating the inflammatory response or airway hyperresponsiveness have not yet been clearly identified. However, potent chemotactic factors, such as leukotriene B4 and platelet-activating factor can initiate both airway inflammation and airway hyperresponsiveness. In addition, in some animal preparations, cyclooxygenase products of arachidonate metabolism, possibly thromboxane, play a central role in the pathogenesis of airway hyperresponsiveness after inhalation of inflammatory stimuli such as allergen.