Background: Allergic rhinitis (AR) and asthma are commonly associated, and similar underlying inflammatory processes link both diseases. AR, even in the absence of asthma, is asso-ciated with increased levels of exhaled nitric oxide (ENO) and hydrogen peroxide (H₂O₂) in exhaled breath condensate, 2 noninvasive markers of lower airway inflammation. Objective: We sought to evaluate the effect of treatment with the nasal steroid triamcinolone acetonide on ENO and exhaled H₂O₂ in subjects with AR. Methods: We allocated 23 subjects in a randomized, double-blind, parallel-controlled fashion to 4-week treatment with triamcinolone acetonide (220 μg/d) or matching placebo. Results: ENO levels were greater in the subgroup with concomitant asthma (16/23 subjects) and decreased significantly with triamcinolone acetonide treatment in this subgroup of patients in comparison with patients receiving placebo. Breath condensate levels of H₂O₂ were higher in patients with AR without asthma than in those with asthma but decreased significantly with triamcinolone acetonide treatment in both subgroups. No changes were observed in bronchial hyperresponsiveness, nasal and asthma symptoms, or peak expiratory flow with active treatment or placebo. Conclusion: We conclude that treatment of AR with triamcinolone acetonide results in decrease of 2 noninvasive markers of lower airway inflammation, ENO and H₂O₂, supporting that upper and lower airway inflammation should be seen as a continuum in subjects with AR with and without asthma. ENO might be a more specific marker of the lower airway inflammation present in asthma. (J Allergy Clin Immunol 2003;111:313-20.)