Epidemiological data suggest that persons with asthma may have greater morbidity as measured by health care utilization after O3 exposure than normal, healthy persons. Animal toxicological data provide evidence that O3 exposure can affect immune function, including enhancement of allergic inflammatory responses in the lungs. Previous controlled human exposure studies have confirmed that O3 exposure can enhance both the early and late bronchoconstrictor responses to inhaled antigen in allergic asthmatic subjects. The effects of O3 exposure on lower airway and late-phase inflammatory responses have not been adequately studied. Recently, data from both controlled human exposure and epidemiological studies have suggested that a common genetic polymorphism in an antioxidant enzyme, glutathione S-transferase m1 (GSTM1), is an important determinant of susceptibility to the respiratory effects of inhaled O3. We designed an experiment to determine whether persons with allergic asthma have increased susceptibility to O3 as a consequence of enhanced airway inflammatory responses to local endobronchial allergen challenge. This experiment was also designed to determine whether the effects of inhaled O3 on the specific airway inflammatory responses to allergen were enhanced in asthmatic individuals with the GSTM1 null genotype. The experiment used a repeated-measures design, each subject completing both O3 and filtered air (FA) exposures within the experiment, with the order of the exposures counter-balanced. Subjects were screened prior to beginning the experimental protocol so that 50% had the GSTM1 null genotype.