Nitric oxide (NO) in exhaled air after experimental ozone exposure in humans

• Published in: Respiratory medicine 2001-06, Vol.95 (6), p.491-495
• Main Authors: OLIN, A.-C., STENFORS, N., TORÉN, K., BLOMBERG, A., HELLEDAY, R., LEDIN, M.-C., LJUNGKVIST, G., EKMAN, A., SANDSTRÖM, T.
• Format: Article
• Language: English
• Subjects: administration & dosage; Adult; analysis; Biological and medical sciences; Biological Markers; Biomarkers; blood; Breath Tests; Chemiluminescent Measurements; Confidence Intervals; Environmental Exposure; exhaled air; Female; Humans; Investigative techniques of respiratory function; Investigative techniques, diagnostic techniques (general aspects); Leukocyte Count; Luminescent Measurements; Lungmedicin och allergi; Male; Medical sciences; metabolism; Neutrophils; Nitric Oxide; Nitric Oxide - analysis; Nitric Oxide - metabolism; nitric oxide, ozone, exhaled air, humans; Oxidative Stress; Oxidative Stress - physiology; Ozone; Ozone - administration & dosage; Ozone - metabolism; Peroxidase; Peroxidase - blood; physiology; Predictive Value of Tests; Respiratory Medicine and Allergy
• ISSN: 0954-6111; 1532-3064; 1532-3064
• DOI: 10.1053/rmed.2001.1076

We hypothesized that ozone, a common air pollutant, potent in producing airway inflammation, would increase the production of exhaled nitric oxide (NO). If so, measurement of exhaled NO could potentially be a valuable tool in population studies of air pollution effects. Eleven healthy non-smoking volunteers were exposed to 0·2 ppm ozone (O3) and filtered air for 2 h on two separate occasions. Exhaled NO and nasal NO were measured before and on five occasions following the exposures. Changes in exhaled and nasal NO after ozone exposure were adjusted for changes after air exposure. There was a slight decrease in exhaled NO (−0·6; −3·1–1·2 ppb) (median and 95% confidence interval) and of nasal NO (−57; −173–75 ppb) directly after the ozone exposure. No significant changes in exhaled or nasal NO were however found 6 or 24 h after the exposure. Within the examined group, an O3exposure level proven to induce an airway inflammation caused no significant changes in exhaled or nasal NO levels. Hence, the current study did not yield support for exhaled NO as a useful marker of ozone-induced oxidative stress and airway inflammation after a single exposure. This contrasts with data for workers exposed to repeated high peaks of ozone. The potential for exhaled NO as a marker of oxidative stress therefore deserves to be further elucidated.