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

Abstract

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 mm 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.

Influence of wood species on toxicity of log-wood stove combustion aerosols: a parallel animal and air-liquid interface cell exposure study on spruce and pine smoke

“…It is possible that single-cell suspensions of lung homogenates showed lower viability in general due to the preparation process. Moreover, the deposited PM dose in the lungs was lower than in other studies [60,61], indicating that further studies require more or longer exposures to achieve higher responses from mouse experiments ( Table 3). To summarize, our aim was not to cause cell death per se but to investigate health-related effects at an exposure level high enough to trigger other cellular responses during similar short acute exposures in vitro and in vivo.…”

Brake dust exposure exacerbates inflammation and transiently compromises phagocytosis in macrophages

“…Here, BAD obtained from low and semi-metallic brake pad PM (composed primarily of Fe, the major component of our BAD sample) demonstrated similar potencies to DEP while NAO brake pad PM (rich in Cu, Ti, Al and Ba) caused considerably stronger inflammatory responses than DEP. 21 It must be considered however, that additional particle components could have contributed to the pro-inflammatory response to the particles. While TNF-a concentrations were elevated at the 4 mg ml À1 dose for the diesel samples, a considerably greater dose of metallic BAD (25 mg ml À1 ) was required to cause significant increases in TNF-a secretion ( Fig.…”

“…BAD produced from non-asbestos organic (NAO) brake pads was found to be the most potent of all particles tested: a result that the authors attribute to its high copper content. 21 Other studies have attributed toxicological endpoints to BAD and general abrasion-related particles by examining the toxicity of roadside PM, with and without the use of metal chelators to try and isolate the metal-dependent signature. Using this approach, the metal content of roadside PM in samples collected throughout Europe was shown to be related to the capacity of RAW264.7 monocyte-derived macrophages (MDM) to release arachidonic acid metabolites.…”

Combination of green tea catechins, polysaccharides, and flavonols against urban fine dust particle-induced bronchial damage mediated by modulation of inflammation factors and airway cilia

“…Inhaled FDPs can interact with the epithelial cells lining the airway and with lung cells. Since FDPs are known to cause toxicity in various individual cell types [43,44], we attempted to identify the cellular toxicity and oxidative stress levels in airway and lung cells exposed to FDPs. We evaluated cell survival rates and intracellular ROS levels under FDP treatment to examine the cellular damage induced by FDPs.…”

“…FDP-stimulated airway cells act as components of multicellular immune responses and trigger cellular signaling pathways. Because improper and excessive immune reactions can result in serious infections, malignancies, and autoimmune conditions, proper regulation of the effects of air pollution on the immune system is important [44,58]. The proin ammatory cytokine milieu in the airway that develops after inhalation of FDPs disrupts immune modulation.…”