Exhaled breath condensate biomarkers in asbestos-related lung disorders

Chow, Sharron; Campbell, Charlotte; Sandrini, Alessandra; Thomas, Paul S.; Johnson, Anthony R.; Yates, Deborah H.

doi:10.1016/j.rmed.2009.04.009

Next »Respiratory Medicine
Volume 103, Issue 8 , Pages 1091-1097, August 2009

Exhaled breath condensate biomarkers in asbestos-related lung disorders

Sharron Chow
- Research and Education Unit, Workers' Compensation (Dust Diseases) Board of New South Wales, Sydney, Australia
- Centre for Infection and Inflammation Research, School of Medical Sciences, University of New South Wales, Sydney, Australia
Charlotte Campbell
- Department of Thoracic Medicine, St Vincent's Hospital, Sydney, Australia
Alessandra Sandrini
- Research and Education Unit, Workers' Compensation (Dust Diseases) Board of New South Wales, Sydney, Australia
- Department of Thoracic Medicine, St Vincent's Hospital, Sydney, Australia
Paul S. Thomas
- Centre for Infection and Inflammation Research, School of Medical Sciences, University of New South Wales, Sydney, Australia
Anthony R. Johnson
- Research and Education Unit, Workers' Compensation (Dust Diseases) Board of New South Wales, Sydney, Australia
Deborah H. Yates
- Research and Education Unit, Workers' Compensation (Dust Diseases) Board of New South Wales, Sydney, Australia
- Department of Thoracic Medicine, St Vincent's Hospital, Sydney, Australia
- Corresponding author: Department of Thoracic Medicine, St Vincent's Hospital, Victoria Street, Darlinghurst, Sydney 2010, Australia. Tel.: +61 2 8382 2330; fax: +61 2 8382 2550.

Received 4 September 2008; accepted 2 April 2009. published online 11 June 2009.

Summary

Objectives

Asbestos induces generation of reactive oxygen and nitrogen species in laboratory studies. Several such species can be measured non-invasively in humans in exhaled breath condensate (EBC) but few have been evaluated. This study aimed to assess oxidative stress and lung inflammation in vivo.

Methods

Eighty six men were studied: sixty subjects with asbestos-related disorders (asbestosis: 18, diffuse pleural thickening (DPT): 16, pleural plaques (PPs): 26) and twenty six age- and gender-matched normal individuals.

Results

Subjects with asbestosis had raised EBC markers of oxidative stress compared with normal controls [8-isoprostane (geometric mean (95% CI) 0.51 (0.17–1.51) vs 0.07 (0.04–0.13) ng/ml, p<0.01); hydrogen peroxide (13.68 (8.63–21.68) vs 5.89 (3.99–8.69) μM, p<0.05), as well as increased EBC total protein (17.27 (10.57–28.23) vs 7.62 (5.13–11.34) μg/ml, p<0.05), and fractional exhaled nitric oxide (mean±SD) (9.67±3.26 vs 7.57±1.89ppb; p<0.05). EBC pH was lower in subjects with asbestosis compared with subjects with DPT (7.26±0.31 vs 7.53±0.24; p<0.05). There were no significant differences in exhaled carbon monoxide, EBC total nitrogen oxides and 3-nitrotyrosine between any of the asbestos-related disorders, or between these and controls.

Conclusion

In asbestos-related disorders, markers of inflammation and oxidative stress are significantly elevated in subjects with asbestosis compared with healthy individuals but not in pleural diseases.

Keywords: Exhaled breath condensate, Asbestos, Exhaled nitric oxide, Oxidative stress