The COPD CO-factor

Abstract

In the current issue of the European Respiratory Journal , Bathoorn et al. 1 present findings that may open up new avenues of treatment for chronic obstructive pulmonary disease (COPD) and provide fundamental insights into the pathogenesis of the condition. Bathoorn et al. 1 present a pilot study on the effect of inhaled carbon monoxide (CO) on inflammation and methacholine responsiveness in COPD. In their study, 22 ex-smokers with stable COPD (forced expiratory volume in one second (FEV1) >1.2 L, FEV1/forced vital capacity <70% predicted) were administered 100–125 ppm CO, a low concentration, for 2 h a day over 4 days in a randomised, cross-over protocol 1. Maximal blood carboxyhaemoglobin peaked at 4.5%, well within safe levels. Eosinophil counts, but not other cells, followed a downward trend in induced sputum, while methacholine responsiveness was slightly and significantly improved. The study was designed and performed with careful attention to ethics and patient safety. However, it is noteworthy that two of the patients experienced exacerbations of COPD during the CO treatment arm. The effects of CO were weak, but tangible, and not uniformly statistically significant. Yet, in several ways this pilot study is intriguing. Why? Because the paper points to the potential therapeutic utility of inhaled CO, a known respiratory system poison that is abundant in tobacco smoke, the cause of most COPD. In addition to this, endogenously generated CO has been discovered by other authors in exhaled breath and blood in COPD 2, 3, and recent fundamental basic research has revealed that endogenous CO is an important physiological regulatory factor in systems as diverse as smooth muscle and the immune system. Like nitric oxide (NO), CO is emerging as a major, and …