Inhalation toxicity profiles of particulate matter: a comparison between brake wear with other sources of emission

Objective: There is substantial evidence that exposure to airborne particulate matter (PM) from road traffic is associated with adverse health outcomes. Although it is often assumed to be caused by vehicle exhaust emissions such as soot, other components may also contribute to detrimental effects. T...

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Bibliographic Details
Published in:	Inhalation toxicology Vol. 31; no. 3; pp. 89 - 98
Main Authors:	Gerlofs-Nijland, M. E., Bokkers, B. G. H., Sachse, H., Reijnders, J. J. E., Gustafsson, M., Boere, A. J. F., Fokkens, P. F. H., Leseman, D. L. A. C., Augsburg, K., Cassee, F. R.
Format:	Journal Article
Language:	English
Published:	England Taylor & Francis 23-02-2019
Subjects:	15 Road: Environment Administration, Inhalation Air Pollutants - toxicity Animals Brake brake wear combustion Farms Female Lung - drug effects Metals - toxicity Mice, Inbred BALB C Motor Vehicles Oxidative Stress - drug effects Particulate matter Particulate Matter - toxicity PM sources Poultry Smoke tire/road wear Toxic potency Toxicity Wear Wood Toxic potency brake wear combustion tire/road wear PM sources
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Summary:	Objective: There is substantial evidence that exposure to airborne particulate matter (PM) from road traffic is associated with adverse health outcomes. Although it is often assumed to be caused by vehicle exhaust emissions such as soot, other components may also contribute to detrimental effects. The toxicity of fine PM (PM2.5; <2.5 µm mass median aerodynamic diameter) released from brake pads was compared to PM from other sources. Materials and methods: PM2.5 of different types of brake pads (low-metallic, semi-metallic, NAO and ECE-NAO hybrid), tires and road pavement, poultry as well as the combustion of diesel fuel and wood (modern and old-fashioned stove technologies) were collected as suspensions in water. These were subsequently aerosolized for inhalation exposures. Female BALB/cOlaHsd mice were exposed for 1.5, 3, or 6 hours by nose-only inhalation up to 9 mg/m 3 . Results: Neither cytotoxicity nor oxidative stress was observed after exposure to any of the re-aerosolized PM2.5 samples. Though, at similar PM mass concentrations the potency to induce inflammatory responses was strongly dependent on the emission source. Exposure to most examined PM2.5 sources provoked inflammation including those derived from the poultry farm, wear emissions of the NAO and ECE-NAO hybrid brake pads as well as diesel and wood combustion, as indicated by neutrophil chemoattractant, KC and MIP-2 and lung neutrophil influx. Discussion and conclusions: Our study revealed considerable variability in the toxic potency of brake wear particles. Understanding of sources that are most harmful to health can provide valuable information for risk management strategies and could help decision-makers to develop more targeted air pollution regulation.
ISSN:	0895-8378 1091-7691 1091-7691
DOI:	10.1080/08958378.2019.1606365