BACKGROUND: The evaluation of exhaled breath profiles by electronic nose (eNose) is considered as a promising non-invasive diagnostic tool, and the discrimination of breathprints between patients with COPD and asthma has been reported. The aim of this study was to assess, whether exhaled breath profile analysis can detect the inflammatory airway response induced by ozone inhalation. METHODS: In a randomized double-blind, cross-over study 14 healthy ozone-responsive subjects were exposed to 250 ppb ozone and filtered room air for 3h with intermittent exercise. Blood biomarkers, exhaled NO, exhaled CO, and breathprints (Cyranose 320(®)) were assessed prior and at 3 time points up to 24h post exposure. Induced sputum was collected at baseline and 3h post exposure. Multivariate analysis of eNose data was performed using transformed and normalized datasets. RESULTS: Significantly increased numbers of sputum and blood neutrophils were observed after ozone, whereas the eNose signals showed no differences between exposures and no correlation with neutrophilic airway inflammation. However, independent of ozone exposure, sensor data correlated with serum SP-D levels and to a smaller extent with blood neutrophil numbers. CONCLUSIONS:Exhaled breath profiles as measured by the Cyranose 320(®) did not reflect airway responses to ozone. This suggests that exhaled volatiles did not change with ozone challenges or that the changes were below the detection limits. Conversely, the correlation of eNose signals with blood neutrophils and serum SP-D, i.e. markers of systemic inflammation and lung permeability, suggested that the Cyranose 320(®) can detect volatile organic compounds of systemic origin.
RCT Entities:
BACKGROUND: The evaluation of exhaled breath profiles by electronic nose (eNose) is considered as a promising non-invasive diagnostic tool, and the discrimination of breathprints between patients with COPD and asthma has been reported. The aim of this study was to assess, whether exhaled breath profile analysis can detect the inflammatory airway response induced by ozone inhalation. METHODS: In a randomized double-blind, cross-over study 14 healthy ozone-responsive subjects were exposed to 250 ppb ozone and filtered room air for 3h with intermittent exercise. Blood biomarkers, exhaled NO, exhaled CO, and breathprints (Cyranose 320(®)) were assessed prior and at 3 time points up to 24h post exposure. Induced sputum was collected at baseline and 3h post exposure. Multivariate analysis of eNose data was performed using transformed and normalized datasets. RESULTS: Significantly increased numbers of sputum and blood neutrophils were observed after ozone, whereas the eNose signals showed no differences between exposures and no correlation with neutrophilic airway inflammation. However, independent of ozone exposure, sensor data correlated with serum SP-D levels and to a smaller extent with blood neutrophil numbers. CONCLUSIONS: Exhaled breath profiles as measured by the Cyranose 320(®) did not reflect airway responses to ozone. This suggests that exhaled volatiles did not change with ozone challenges or that the changes were below the detection limits. Conversely, the correlation of eNose signals with blood neutrophils and serum SP-D, i.e. markers of systemic inflammation and lung permeability, suggested that the Cyranose 320(®) can detect volatile organic compounds of systemic origin.
Authors: Olaf Holz; H Biller; M Mueller; K Kane; M Rosano; J Hanrahan; D L Hava; J M Hohlfeld Journal: BMC Pharmacol Toxicol Date: 2015-08-12 Impact factor: 2.483