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Editorials |

Carbon Monoxide Poisoning, or Carbon Monoxide Protection?

Robert L. Owens, MD; Susie Yim-Yeh, MD; Atul Malhotra, MD, FCCP
Author and Funding Information

Correspondence to: Robert L. Owens, MD, Pulmonary & Critical Care and Sleep Medicine Fellow, Brigham and Women's Hospital, Sleep Disorders Research Program, 221 Longwood Ave, Boston, MA 02115; e-mail: rowens@partners.org

Dr. Owens is a fellow in the Divisions of Pulmonary, Critical Care, and Sleep Medicine, Brigham and Women's Hospital.

Dr. Yim-Yeh is affiliated with the Sleep Disorders Research Program, Brigham and Women's Hospital.

Dr. Malhotra is affiliated with the Divisions of Pulmonary, Critical Care, and Sleep Medicine, Brigham and Women's Hospital, and Harvard Medical School.


Dr. Malhotra is funded by the National Institute of Health (grants P50 HL060292, RO1-HL73146, and AG024837) and the Established Investigator Award from the American Heart Association.

Drs. Owens and Yim-Yeh have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article. Dr. Malhotra has received consulting and/or research grants from Respironics, Itamar Medical, Restore Medical, NMT Medical, Inspiration Medical, Apnex Medical, Sepracor, Cephalon, and Pfizer.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2008;134(5):895-896. doi:10.1378/chest.08-1728
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Carbon monoxide (CO) is a molecule generally presumed to be deleterious when inhaled at high concentrations, but is a marker of oxidative stress and inflammation when endogenously produced. Many reports13 have focused on increased endogenous CO production in pulmonary diseases, including asthma, COPD, acute pneumonia, and ARDS. In this issue of CHEST (see page 904), Kobayashi and colleagues4 add obstructive sleep apnea (OSA) to the list. In documented nonsmokers with OSA and control subjects, CO levels were measured before and after polysomnography. Although CO levels were similar in OSA patients and control subjects prior to sleep, those patients with OSA had elevations in venous CO level after sleep. Moreover, the nocturnal change in CO correlated modestly with the apnea-hypopnea index and duration of hypoxemia during sleep. Treatment with continuous positive airway pressure (CPAP) in some of these patients attenuated the rise in CO, so that treated OSA patients had no difference in CO when compared to control subjects. Linking OSA to cardiovascular morbidity, the authors conclude that “normalization of venous CO levels by CPAP therapy can potentially reduce the risk of disease associated cardiovascular events.”

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