Increased amount of nitric oxide in exhaled air of asthmatics

TLDR

Nitric oxide has recently been detected in human exhaled air. The study aimed to determine the origin of exhaled NO in normal airways and whether airway inflammation alters its levels. NO was continuously measured by chemiluminescence during tidal breathing through the nose or mouth with a 1 ppb detection limit, comparing 12 controls to 8 mild atopic asthmatics with occupational rhinitis. Control subjects had up to 30 ppb of NO mainly from nasal airways, whereas mild asthmatics showed a 2–3‑fold increase in oral‑breathing NO, implying lower‑airway inflammation that could be monitored via exhaled NO.

Abstract

The presence of nitric oxide (NO) in the exhaled air of humans has recently been described. We wanted to assess at what level exhaled NO originates in normal airways, and to determine whether airway inflammation induces changes in the levels of exhaled NO. Exhaled NO was continuously measured by chemiluminescence technique during normal tidal breathing through the nose or mouth, with a detection limit of 1 part per billion (ppb). Twelve control subjects were compared to eight patients with mild atopic asthma and rhinitis caused by occupational allergen. In control subjects, the major part of NO in exhaled air (up to 30 ppb) seemed to originate in the nasal airways, with only minor contribution from the lower airways and the oral cavity. However, in mild asthmatics, the level of exhaled NO during oral breathing, indicating the involvement of the lower airways, was increased 2-3 fold. Since increased production of NO in the lower airways may involve activated macrophages or neutrophils, we suggest that exhaled NO may be used to instantly monitor ongoing bronchial inflammation, at least when involving inducible NO synthase.