Asthmatic patients show increased concentrations of nitric oxide (NO) in exhaled air (FENO). The diffusing capacity of NO in the airways (DawNO), the NO concentrations in the alveoli and the airway wall, and the maximal airway NO diffusion rate have previously been estimated noninvasively by measuring FENO at different exhalation flow rates in adults. We investigated these variables in 15 asthmatic schoolchildren (8 -18 y) and 15 agematched control subjects, with focus on their relation to exhaled NO at the recommended exhalation flow rate of 0.05 L/s (FENO 0.05 ), age, and volume of the respiratory anatomic dead space. NO was measured on-line by chemiluminescence according to the European Respiratory Society's guidelines, and the NO plateau values at three different exhalation flow rates (11, 99, and 382 mL/s) were incorporated in a two-compartment model for NO diffusion. The NO concentration in the airway wall (p Ͻ 0.001), DawNO (p Ͻ 0.01), and the maximal airway NO diffusion rate (p Ͻ 0.001) were all higher in the asthmatic children than in control children. In contrast, there was no difference in the NO concentration in the alveoli (p ϭ 0.13) between the groups. A positive correlation was seen between the volume of the respiratory anatomic dead space and FENO 0.05 (r ϭ 0.68, p Ͻ 0.01), the maximal airway NO diffusion rate (r ϭ 0.71, p Ͻ 0.01), and DawNO (r ϭ 0.56, p Ͻ 0.01) in control children, but not in asthmatic children. FENO 0.05 correlated better with DawNO in asthmatic children (r ϭ 0.65, p Ͻ 0.01) and with the NO concentration in the airway wall in control subjects (r Ͻ 0.77, p Ͻ 0.001) than vice versa. We conclude that FENO 0.05 increases with increasing volume of the respiratory anatomic dead space in healthy children, suggesting that normal values for FENO 0.05 should be related to age or body weight in this age group. Furthermore, the elevated FENO 0.05 seen in asthmatic children is related to an increase in both DawNO and NO concentration in the airway wall. Because DawNO correlates with the volume of the respiratory anatomic dead space in control subjects and FENO 0.05 correlates with DawNO in asthmatic children, we suggest that DawNO partly reflects the total NO-producing surface area and that a larger part of the bronchial tree produces NO in asthmatic children than in control children. NO can be measured in exhaled air, and high levels of NO are believed to reflect allergic inflammation in the airways of asthmatic patients (1-3). Correlations between exhaled NO and other markers of airway inflammation such as eosinophils in sputum and blood (4 -6), bronchial hyperresponsiveness (7), and bronchial eosinophilia (5, 8) have been demonstrated. In the lower airways, NO is thought to be produced by iNOS in Received July 8, 2002; accepted December 3, 2002