| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4211024 | Respiratory Medicine | 2009 | 7 Pages |
SummaryObjectivesAsbestos 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.MethodsEighty 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.ResultsSubjects 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 ± 1.89 ppb; 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.ConclusionIn 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.
