8-epi-prostaglandin-f2alpha and Asbestosis

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.. 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.. 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) microM, p<0.05), as well as increased EBC total protein (17.27 (10.57-28.23) vs 7.62 (5.13-11.34) microg/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.. 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.

Topics: Aged; Asbestos; Asbestosis; Biomarkers; Dinoprost; Forced Expiratory Volume; Humans; Lung Diseases; Male; Nitric Oxide; Oxidative Stress; Prognosis; Tyrosine

Asbestosis and pleural plaques exhibit unpredictable but progressive development, and there are no markers routinely available to measure their prognosis. Asbestos exposure induces the generation of reactive oxygen species, and 8-isoprostane is involved in experimental asbestos-related lung toxicity. This oxidative stress marker was measured in exhaled breath condensate (EBC) in 92 former asbestos workers with mean age 68.8+/-1.7 yr and mean duration of asbestos exposure 24.1+/-2.0 yr. The control group had 46 subjects with mean age 65.2+/-3.3 yr. The mean level of 8-isoprostane, analyzed by liquid chromatography-electrospray ionization-mass spectrometry, was higher in asbestos-exposed subjects (69.5+/-6.6 pg/ml, p=0.0001) compared with the control group, where the concentration was 47.0+/-7.8 pg/ml. The results presented support the hypothesis that oxidative stress due to asbestos is the main cause of increased 8-isoprostane in EBC. Measurement of 8-isoprostane in EBC is a promising non-invasive means for assessing the activity of asbestos-induced diseases.

Topics: Aged; Aged, 80 and over; Asbestos; Asbestosis; Biomarkers; Breath Tests; Case-Control Studies; Dinoprost; Female; Humans; Male; Middle Aged; Occupational Exposure; Oxidative Stress; Prognosis; Risk Assessment

Inhaled asbestos fibres can cause inflammation and fibrosis in the lungs called asbestosis. However, there are no non-invasive means to assess and follow the severity of the inflammation. Exhaled nitric oxide (NO) measured at multiple exhalation flow rates can be used to assess the alveolar NO concentration and bronchial NO flux, which reflect inflammation in the lung parenchyma and airways, respectively. The aim of the present study was to investigate whether exhaled NO or markers in exhaled breath condensate could be used to assess inflammation in asbestosis.. Exhaled NO and inflammatory markers (leukotriene B(4) and 8-isoprostane) in exhaled breath condensate were measured in 15 non-smoking patients with asbestosis and in 15 healthy controls. Exhaled NO concentrations were measured at four constant exhalation flow rates (50, 100, 200 and 300 ml/s) and alveolar NO concentration and bronchial NO flux were calculated according to the linear model of pulmonary NO dynamics.. The mean (SE) alveolar NO concentration was significantly higher in patients with asbestosis than in controls (3.2 (0.4) vs 2.0 (0.2) ppb, p = 0.008). There was no difference in bronchial NO flux (0.9 (0.1) vs 0.9 (0.1) nl/s, p = 0.93) or NO concentration measured at ATS standard flow rate of 50 ml/s (20.0 (2.0) vs 19.7 (1.8) ppb, p = 0.89). Patients with asbestosis had increased levels of leukotriene B4 (39.5 (6.0) vs 15.4 (2.9) pg/ml, p = 0.002) and 8-isoprostane (33.5 (9.6) vs 11.9 (2.8) pg/ml, p = 0.048) in exhaled breath condensate and raised serum levels of C-reactive protein (2.3 (0.3) vs 1.1 (0.2) mug/ml, p = 0.003), interleukin-6 (3.5 (0.5) vs 1.7 (0.4) pg/ml, p = 0.007) and myeloperoxidase (356 (48) vs 240 (20) ng/ml, p = 0.034) compared with healthy controls.. Patients with asbestosis have an increased alveolar NO concentration and high levels of leukotriene B4 and 8-isoprostane in exhaled breath. Measurement of exhaled NO at multiple exhalation flow rates and analysis of inflammatory markers in exhaled breath condensate are promising non-invasive means for assessing inflammation in patients with asbestosis.

Topics: Aged; Asbestosis; Breath Tests; C-Reactive Protein; Case-Control Studies; Dinoprost; Humans; Interleukin-6; Leukotriene B4; Male; Middle Aged; Nitric Oxide; Peroxidase; Pulmonary Alveoli; Respiratory Function Tests

Topics: Asbestosis; Biomarkers; Dinoprost; Fruit; Humans; Occupational Exposure; Selenium; Vegetables