Abstract
BackgroundFine particulate matter originating from traffic correlates with increased morbidity and mortality. An important source of traffic particles is brake wear of cars which contributes up to 20% of the total traffic emissions. The aim of this study was to evaluate potential toxicological effects of human epithelial lung cells exposed to freshly generated brake wear particles.ResultsAn exposure box was mounted around a car's braking system. Lung cells cultured at the air-liquid interface were then exposed to particles emitted from two typical braking behaviours („full stop“ and „normal deceleration“). The particle size distribution as well as the brake emission components like metals and carbons was measured on-line, and the particles deposited on grids for transmission electron microscopy were counted. The tight junction arrangement was observed by laser scanning microscopy. Cellular responses were assessed by measurement of lactate dehydrogenase (cytotoxicity), by investigating the production of reactive oxidative species and the release of the pro-inflammatory mediator interleukin-8. The tight junction protein occludin density decreased significantly (p < 0.05) with increasing concentrations of metals on the particles (iron, copper and manganese, which were all strongly correlated with each other). Occludin was also negatively correlated with the intensity of reactive oxidative species. The concentrations of interleukin-8 were significantly correlated with increasing organic carbon concentrations. No correlation was observed between occludin and interleukin-8, nor between reactive oxidative species and interleukin-8.ConclusionThese findings suggest that the metals on brake wear particles damage tight junctions with a mechanism involving oxidative stress. Brake wear particles also increase pro-inflammatory responses. However, this might be due to another mechanism than via oxidative stress.
Highlights
Fine particulate matter originating from traffic correlates with increased morbidity and mortality
The direct combination of lung cell culture exposure to brake wear particles offers a reliable approach to investigate the cellular effects of directly emitted particles
The exposure to brake wear particles causes the formation of reactive oxygen species (ROS) for both braking behaviours
Summary
Fine particulate matter originating from traffic correlates with increased morbidity and mortality. Riediker and colleagues [15] showed that a particle source with a brake wear signature was strongly linked to health effects They found that PM2.5 originating from speed-changing traffic modulates the autonomic control of the heart rhythm, increases the frequency of premature supraventricular beats and elicits pro-inflammatory and pro-thrombotic responses in healthy young men. These health effects might be associated with the levels of the metals which are an important component of brake wear. A considerable fraction of freshly generated brake wear particles is smaller than 100 nanometres [17,18] Such nanoscaled particles are believed to contribute importantly to the health effects caused by inhaled PM [19]. The potential toxicity of each class of combustion-derived nanoparticles has to be evaluated individually
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