Exhaled breath condensate (EBC) is assumed to reflect processes in the lungs, yet it is unknown whether oxidative stress markers in EBC are affected by systemic disorders (atherosclerosis, hypertension, diabetes) or whether lung diseases increase markers in plasma and urine. 8-isoprostane, 4-hydroxy-trans-2-nonenale (HNE) and malondialdehyde (MDA) were measured using liquid chromatography-electrospray ionization-mass spectrometry (LC-ESI-MS/MS) in EBC, plasma and urine in 82 patients (45 with asbestosis and hyalinosis, and 37 with silicosis) and in 29 control subjects. 8-isoprostane and HNE in EBC, and HNE in urine were higher in both groups of patients. In addition, 8-isoprostane in plasma and urine, and MDA in urine were higher in asbestos-exposed patients and MDA in plasma in silicotics, with this marker in plasma correlated with the grade of silicosis. In all subjects, 8-isoprostane in EBC correlated with urine (r=0.38, p<0.001) and plasma levels (r=0.28, p=0.003), and HNE and MDA with urine levels (r=0.31, p<0.001; r=0.23, p=0.016, respectively). Most markers positively correlated with lung function impairment, EBC markers negatively with vitamin E supplementation. To conclude: The influence of satisfactorily controlled systemic disorders on markers in EBC in patients with pneumoconioses is not significant. In addition to oxidative stress markers in EBC, lung fibroses may increase oxidative stress markers in plasma and urine.