Using exhaled NO concentrations to adjust inhaled corticosteroid dose maintained asthma control and reduced the dose.
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Breath analysis is an attractive non-invasive procedure for screening workers exposed to solvents. It has been used in numerous laboratory based studies and for field research. Despite the obvious advantages in routine biological monitoring it has failed to become widely accepted as a tool in occupational hygiene. Recent advances in breath sampling and analysis are such that it is likely to become more widely used in the future. In this paper, the past 5 years have been reviewed to try to assess what developments might now contribute to the increased use of breath analysis in biological monitoring; in particular, the development of a selected ion flow tube mass spectrometer for real time direct analysis of trace gases in breath and the more immediately available and less expensive indirect methods involving collection devices with adsorbent tubes is important. The introduction of guidance values for biological monitoring with clear advice on sampling times and the recognition of the importance of quality assurance programmes will help improve confidence in the technique.
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The purpose of the present study was to determine if nitric oxide (NO) is involved in the pathogenesis of thermally induced asthma. To provide data on this issue, 10 normal and 13 asthmatic subjects performed isocapnic hyperventilation with frigid air while the fractional concentration of NO in the expirate air (FENO) was serially monitored with a chemiluminescence analyzer. FEV1 was measured before and after hyperpnea. Prior to and throughout the challenge, the asthmatics had significantly larger values for FENO (baseline FENO normal, 11 +/- 2 ppb; asthma, 16 +/- 1; p = 0.03). Posthyperpnea, the normal subjects had little change in bronchial caliber (deltaFEV1 baseline to 5 min posthyperpnea, -3.5 +/- 1.5%; p = 0.06), whereas the patients with asthma developed significant airway obstruction (deltaFEV1, -27.7 +/- 2.9%; p = 0.0001). During hyperventilation, the volume of NO rose in both groups. The asthmatic subjects, however, generated approximately 55% more NO/min than did the normal control subjects even though their level of ventilation was approximately 66% less. In contrast to the normal subjects, NO production in the asthmatics continued into the recovery period after the challenge stopped and FENO rose temporally as the airflow limitation developed. These results suggest that NO plays an intimate role in the development of airway obstruction that follows hyperpnea.