Abstract

Tyre wear particles (TWPs) produced due to friction between tyres and road surface, and release of complex organic and inorganic material into the environment, may have adverse effects on the lung. The respiratory health effects of TWPs are unknown. The aim was to assess the bioreactivity of TWPs (collected into water in real-time; RT) on human lung alveolar epithelium using novel human alveolar epithelial type 1-like (AT1L) and type 2-like (AT2L) cell lines.

A custom-made apparatus was used to collect RT generated samples; RT1, directly behind and above the tyre (peak diameters, 100nm and 750nm; DLS) and RT2, side-on and lower (peak diameters, 365 and 5590nm; DLS), during 2h driving a car. AT1L and AT2L were exposed to 50-250µg/ml of each sample for 24 h.  Neither sample affected AT1L cell viability, metabolism or cytotoxicity. In contrast, the metabolic activity (MTT) of AT2L increased by 1.2-1.3-fold (p<0.01) with increasing concentrations of TWP. Although AT1L mediator release was significantly increased following RT1 exposure - CXCL-8 (2.2-fold; p<0.01) and IL-6 (5-fold; p<0.0001) - RT2 had no effect.  The release of IL6 and CXCL-8 by AT2L was substantially induced after RT1 (up to approx. 10- and 4-fold, p<0.0001) and RT2 (up to approx. 4- and 2-fold, p<0.0001), respectively.

These results indicate AT2L cells were more sensitive to TWP than AT1L cells. Relatively pure, smaller TWP collected directly behind the tyre were remarkably more bioreactive than the larger, mixed TWP/brake/road wear particles collected nearer the road surface. These data suggest that inhalation of respirable airborne TWP may have undesirable effects in the deep lung.