Abstract
Studies have emphasised the importance of combustion-derived particles in eliciting adverse health effects, especially those produced by diesel vehicles. In contrast, few investigations have explored the potential toxicity of particles derived from tyre and brake wear, despite their significant contributions to total roadside particulate mass. The objective of this study was to compare the relative toxicity of compositionally distinct brake abrasion dust (BAD) and diesel exhaust particles (DEP) in a cellular model that is relevant to human airways. Although BAD contained considerably more metals/metalloids than DEP (as determined by inductively coupled plasma mass spectrometry) similar toxicological profiles were observed in U937 monocyte-derived macrophages following 24 h exposures to 4-25 μg ml-1 doses of either particle type. Responses to the particles were characterised by dose-dependent decreases in mitochondrial depolarisation (p ≤ 0.001), increased secretion of IL-8, IL-10 and TNF-α (p ≤ 0.05 to p ≤ 0.001) and decreased phagocytosis of S. aureus (p ≤ 0.001). This phagocytic deficit recovered, and the inflammatory response resolved when challenged cells were incubated for a further 24 h in particle-free media. These responses were abrogated by metal chelation using desferroxamine. At minimally cytotoxic doses both DEP and BAD perturbed bacterial clearance and promoted inflammatory responses in U937 cells with similar potency. These data emphasise the requirement to consider contributions of abrasion particles to traffic-related clinical health effects.
Highlights
PaperMetallomics produced by fuel combustion and lubricant volatilisation, wear of mechanical components and abrasion of the road surface.[4]To date, diesel exhaust has been the major focus of investigations into traffic-derived particulate toxicity
Unlike tailpipe-derived particles, Brake abrasion dust (BAD) is rich in metals,[4] many of which (e.g. Fe and Cu) can catalyse the formation of reactive oxygen species (ROS) within the oxygen-rich conditions of the respiratory tract lining fluids (RTLFs), challenging the high concentrations of low molecular weight antioxidants, antioxidant enzymes and metal-binding proteins, which exist to protect the epithelial surface from oxidative attack.[16]
The BAD sample employed here has not been studied before so required characterisation prior to use
Summary
Diesel exhaust has been the major focus of investigations into traffic-derived particulate toxicity This focus has been supported by epidemiological studies which demonstrate significant associations between adverse health outcomes/ endpoints and tracers of diesel tailpipe emissions.[5,6] concurrent in vitro and in vivo experimentation has demonstrated the capacity of diesel exhaust particles (DEP) to stimulate xenobiotic and antioxidant defences, redox-sensitive signalling pathways, inflammatory cascades and the activation of airway nerve fibres.[7,8,9,10] In contrast, the toxic potential of non-tailpipe particulates, such as those produced by brake, tyre or clutch wear has received little attention. Within cell-free systems, BAD displays greater capacity to elicit damaging oxidation reactions than DEP.[17]
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