Brake dust exposure exacerbates inflammation and transiently compromises phagocytosis in macrophages.


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Article
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Authors
Schuster, Linda 
Marbach, Helene 
Forsthuber, Theresa 
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.

Description
Keywords
Air Pollutants, Dust, Humans, Inflammation, Interleukin-10, Interleukin-8, Macrophages, Particle Size, Phagocytosis, Staphylococcus aureus, U937 Cells
Journal Title
Metallomics
Conference Name
Journal ISSN
1756-5901
1756-591X
Volume Title
12
Publisher
Oxford University Press (OUP)
Rights
All rights reserved
Sponsorship
MRC