ArticleParticle and fibre toxicology2025
Copper-enriched automotive brake wear particles perturb human alveolar cellular homeostasis.
Article in Particle and fibre toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Pulmonary toxicity of brake wear particles: effects of composition and surface reactivity.Particle and fibre toxicology · 2026Article
- Synergistically Reinforced Copper-Free Friction Materials with Agricultural Wastes and Carbon Fibers: Evaluation of Tribological Performance.Materials (Basel, Switzerland) · 2026Article
- Physicochemical and Toxicological Characterization of Airborne Brake Wear Particles Reveals Oxidative Stress-Mediated DNA Damage.Environmental science & technology · 2026Article
- Knowledge, Perceptions, and Practices of Traffic Police Officers Towards Air Pollution in Addis Ababa, Ethiopia: An Exploratory Study.International journal of environmental research and public health · 2025Article
Corrections and comments
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Authors and funding
20 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAirborne fine particulate matter with diameter < 2.5 μm (PM2.5), can reach the alveolar regions of the lungs, and is associated with over 4 million premature deaths per year worldwide. However, the source-specific consequences of PM2.5 exposure remain poorly understood. A major, but unregulated source is car brake wear, which exhaust emission reduction measures have not diminished.
methodsWe used an interdisciplinary approach to investigate the consequences of brake-wear PM2.5 exposure upon lung alveolar cellular homeostasis using diesel exhaust PM as a comparator. This involved RNA-Seq to analyse global transcriptomic changes, metabolic analyses to investigate glycolytic reprogramming, mass spectrometry to determine PM composition, and reporter assays to provide mechanistic insight into differential effects.
resultsWe identified brake-wear PM from copper-enriched non-asbestos organic, and ceramic brake pads as inducing the greatest oxidative stress, inflammation, and pseudohypoxic HIF activation (a pathway implicated in diseases associated with air pollution exposure, including cancer, and pulmonary fibrosis), as well as perturbation of metabolism, and metal homeostasis compared with brake wear PM from low- or semi-metallic pads, and also, importantly, diesel exhaust PM. Compositional and metal chelator analyses identified that differential effects were driven by copper.
conclusionsWe demonstrate here that brake-wear PM may perturb cellular homeostasis more than diesel exhaust PM. Our findings demonstrate the potential differences in effects, not only for non-exhaust vs exhaust PM, but also amongst different sources of non-exhaust PM. This has implications for our understanding of the potential health effects of road vehicle-associated PM. More broadly, our findings illustrate the importance of PM composition on potential health effects, highlighting the need for targeted legislation to protect public health.
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