Long term effects on respiratory function have been found in air divers and have indicated the development of small-airway disease. These effects have been attributed to oxygen toxicity or to venous gas micro emboli (VGM). The airway obstructions observed in air divers raise fundamental questions about whether these alterations exist after one simulated dive. The aim of this report was to study the oxidative stress induced by brief normobaric hyperoxia (FiO2 = 0.6 for 30 min) by measuring breath-exhaled compounds. Oxidative stress was measured by pentane in the expirate of 7 subjects ventilated with hydrocarbon-free air (HFA) before and after the hyperoxic exposure. NO concentration allowed us to determine the inflammatory response in the airway. Venous blood was drawn before and after the O2 breathing period for measurements of malondialdehyde (MDA). In all seven subjects, pentane elimination rates on 60%O2 do not increase after hyperoxia. NO rates during the HFA and hyperoxic exposures are significantly increased (p < 0.05). MDA concentrations are not changed after the hyperoxic exposure. Pulmonary function parameters obtained 225 minutes after hyperoxia are not changed. These results provide evidence that a dry gas and oxygen breathing (FiO2 = 0.6) for 30 min can raise exhaled NO. Oxidative stress assessed by pentane and MDA does not exist. We conclude that dry gas and the mild, 30 minute hyperoxic exposure, frequently encountered by recreational divers may be responsible for an airway inflammation. The consequences of such chronic exposure remains to be established.