nous carbon monoxide (CO) levels are recognized as a surrogate marker for activity of heme oxygenase-1, which is induced by various factors, including hypoxia and oxidative stress. Few reports have evaluated endogenous CO in patients with obstructive sleep apnea (OSA). Whether OSA more greatly affects exhaled or blood CO is not known. Sixty-nine patients with suspected OSA were prospectively included in this study. Exhaled and blood CO were evaluated at night and morning. Blood and exhaled CO

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... vels were well correlated both at night and morning (r ϭ 0.52, P Ͻ 0.0001 and r ϭ 0.61, P Ͻ 0.0001, respectively). Although exhaled CO levels both at night and morning significantly correlated with total sleep time with arterial oxygen saturation Ͻ 90% ( ϭ 0.41, P ϭ 0.0005 and ϭ 0.27, P ϭ 0.024, respectively), blood CO levels did not correlate with any sleep parameter. Seventeen patients with an apnea and hypopnea index (AHI) Ͻ 15 (control group) were compared with 52 patients with AHI Ն 15 (OSA group). Exhaled CO levels at night in the OSA group were significantly higher than in the control group (3.64 Ϯ 1.2 vs. 2.99 Ϯ 0.70 ppm, P Ͻ 0.05). Exhaled CO levels at night decreased after 3 mo of continuous positive airway pressure (CPAP) therapy in OSA patients (n ϭ 36; P ϭ 0.016) to become nearly the same level as in the control group (P ϭ 0.21). Blood CO levels did not significantly change after CPAP therapy. Exhaled CO was positively related to hypoxia during sleep in OSA patients, but blood CO was not. Exhaled CO might better correlate with oxidative stress associated with OSA than blood CO.