A model semi-metallic brake lining was subjected to full scale automotive brake dynamometer tests. The structural properties and surface topography of brake linings were analyzed at different stages of wear testing and correlated to frictional performance. Characteristics of released wear particles were also addressed. A combination of abrasive and adhesive wear with oxidative processes dominated the friction process. Formation of a friction layer adhering to the friction surfaces of pads and discs is the major feature responsible for friction performance. Characteristics of the friction layer depend mostly on surface temperature, normal pressure, and sliding speed. It is a newly formed sintered composite matter consisting of a mixture of wear particulates. Wear rates and friction levels depend on chemistry, structure and hardness of the friction layer covering the surface of a pad or a disc; however, there is no simple Archard-type relationship between wear and measured hardness.Wear debris generated during the dynamometer tests was collected from containers placed under the brake inside dynamometer chamber. The collected debris was compared with ball-milled particles from identical brake lining. It is necessary to combine several analytical methods to characterize wear particles properly. The presence of copper and iron oxides as well as carbonaceous components is typical for all collected debris samples. Chemistry of wear debris resembles chemistry of the friction layer. Composition, mutagenic potency and pulmonary toxicity of wear debris and ball-milled particles were also analyzed. Mutagenic potency of initial friction composite and wear particles was evaluated by two in vitro bacterial microbioassays (SOS Chromotest, Ames test). Obtained results show potency of wear particles for interacting with DNA after metabolic activation, which indicates the presence of indirect mutagens. The pulmonary toxicity test on rats revealed an acute response of the lung tissue to the ball-milled particles. Further research is necessary to address the role of brake wear particles and potential impact of sub-chronic exposure to wear debris.
Markers of oxidative stress and inflammation were analysed in the exhaled breath condensate (EBC) and urine samples of 14 workers (mean age 43 ± 7 years) exposed to iron oxide aerosol for an average of 10 ± 4 years and 14 controls (mean age 39 ± 4 years) by liquid chromatography-electrospray ionization-mass spectrometry/mass spectrometry (LC-ESI-MS/MS) after solid-phase extraction. Aerosol exposure in the workplace was measured by particle size spectrometers, a scanning mobility particle sizer (SMPS) and an aerodynamic particle sizer (APS), and by aerosol concentration monitors, P-TRAK and DustTRAK DRX. Total aerosol concentrations in workplace locations varied greatly in both time and space. The median mass concentration was 0.083 mg m(-3) (IQR 0.063-0.133 mg m(-3)) and the median particle concentration was 66 800 particles cm(-3) (IQR 16,900-86,900 particles cm(-3)). In addition, more than 80% of particles were smaller than 100 nm in diameter. Markers of oxidative stress, malondialdehyde (MDA), 4-hydroxy-trans-hexenale (HHE), 4-hydroxy-trans-nonenale (HNE), 8-isoProstaglandin F2α (8-isoprostane) and aldehydes C6-C12, in addition to markers of nucleic acid oxidation, including 8-hydroxy-2-deoxyguanosine (8-OHdG), 8-hydroxyguanosine (8-OHG), 5-hydroxymethyl uracil (5-OHMeU), and of proteins, such as o-tyrosine (o-Tyr), 3-chlorotyrosine (3-ClTyr), and 3-nitrotyrosine (3-NOTyr) were analysed in EBC and urine by LC-ESI-MS/MS. Almost all markers of lipid, nucleic acid and protein oxidation were elevated in the EBC of workers comparing with control subjects. Elevated markers were MDA, HNE, HHE, C6-C10, 8-isoprostane, 8-OHdG, 8-OHG, 5-OHMeU, 3-ClTyr, 3-NOTyr, o-Tyr (all p < 0.001), and C11 (p < 0.05). Only aldehyde C12 and the pH of samples did not differ between groups. Markers in urine were not elevated. These findings suggest the adverse effects of nano iron oxide aerosol exposure and support the utility of oxidative stress biomarkers in EBC. The analysis of urine oxidative stress biomarkers does not support the presence of systemic oxidative stress in iron oxide pigment production workers.
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