Copper-enriched automotive brake wear particles perturb human alveolar cellular homeostasis.

ABSTRACT:

Background

Airborne 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.

Methods

We 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

SUBMITTER: Parkin JGH 

PROVIDER: S-EPMC11823208 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature