Toxicity and mutagenicity of low-metallic automotive brake pad materials

Malachová, Kateřina; Kukutschová, Jana; Rybková, Zuzana; Sezimová, Hana; Plachá, Daniela; Čabanová, Kristína; Filip, Peter

doi:10.1016/j.ecoenv.2016.05.003

Cited by 37 publications

(19 citation statements)

References 28 publications

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“…In the present study, cells were exposed only once to particles, thus more so reflecting an acute exposure scenario. However, according to the authors’ knowledge, only limited amount of the studies using the collected brake wear particles have been performed in a laboratory environment; therefore, it was difficult to estimate the most suitable concentration range for the present study (Kazimirova et al 2016; Kukutschová et al 2009; Malachova et al 2016). …”

Section: Discussionmentioning

confidence: 95%

Biological response of an in vitro human 3D lung cell model exposed to brake wear debris varies based on brake pad formulation

et al. 2018

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Wear particles from automotive friction brake pads of various sizes, morphology, and chemical composition are significant contributors towards particulate matter. Knowledge concerning the potential adverse effects following inhalation exposure to brake wear debris is limited. Our aim was, therefore, to generate brake wear particles released from commercial low-metallic and non-asbestos organic automotive brake pads used in mid-size passenger cars by a full-scale brake dynamometer with an environmental chamber simulating urban driving and to deduce their potential hazard in vitro. The collected fractions were analysed using scanning electron microscopy via energy-dispersive X-ray spectroscopy (SEM–EDS) and Raman microspectroscopy. The biological impact of the samples was investigated using a human 3D multicellular model consisting of human epithelial cells (A549) and human primary immune cells (macrophages and dendritic cells) mimicking the human epithelial tissue barrier. The viability, morphology, oxidative stress, and (pro-)inflammatory response of the cells were assessed following 24 h exposure to ~ 12, ~ 24, and ~ 48 µg/cm2 of non-airborne samples and to ~ 3.7 µg/cm2 of different brake wear size fractions (2–4, 1–2, and 0.25–1 µm) applying a pseudo-air–liquid interface approach. Brake wear debris with low-metallic formula does not induce any adverse biological effects to the in vitro lung multicellular model. Brake wear particles from non-asbestos organic formulated pads, however, induced increased (pro-)inflammatory mediator release from the same in vitro system. The latter finding can be attributed to the different particle compositions, specifically the presence of anatase.Electronic supplementary materialThe online version of this article (10.1007/s00204-018-2218-8) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 95%

Biological response of an in vitro human 3D lung cell model exposed to brake wear debris varies based on brake pad formulation

et al. 2018

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“…Particulate matters (PMs) [1] Air pollution causes 7 million deaths worldwide every year. Ambient air pollution mostly arising from anthropogenic activities [2,3], e.g., using vehicles, combustion of fossil fuels, and power generation, is the cause of 4.2 million deaths due to acute and chronic effects on human health [4].…”

Section: Environmental Emissionsmentioning

confidence: 99%

Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences

Hajirasouliha¹,

Zabiegaj²

2021

Environmental Emissions

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Human health has been affected adversely by air pollution as a serious environmental challenge. Ambient (outdoor) air pollution mainly resulted from human activities (e.g., fuel combustion, heat generation, industrial facilities) causes 4.2 million deaths every year. Moreover, each year, 3.8 million people die from indoor air pollution which means household exposure to smoke from fuels and dirty cook stoves. They are the risks of stroke, heart attack, lung disease, or cancer that resulted from air pollution which assaults our brain, heart, and lungs using its invisible weapons named particulate matter (PM). These inhalable particles are of a nanoscale or microscale size. Upon inhalation, the air with its components enters the human body through the respiratory system. The lungs are the responsible organs for gas exchange with blood. Inhaled particles, such as silica, organic compounds, and metallic dusts, have toxic effects on our pulmonary system. For example, the accumulation of nanoparticles in the kidneys, liver, spleen, and central nervous system through the penetration of the epithelial barriers in the lungs has been observed. The purpose of this chapter is to describe the toxic effects of air particles on the different organs in the human body and to introduce some of the adverse effects of air pollution on human health.

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“…The authors reported a correlation between various components (iron, copper, and manganese) and markers for inflammation at sub-lethal concentrations and differences in oxidative stress based on the composition. Recent research on brake wear debris showed that brake wear particles could contain components with toxic and mutagenic properties (Kazimirova et al 2016;Malachova et al 2016). However, comprehensive studies examining the direct link to brake wear particles and adverse health effects are still scarce.…”

Section: Introductionmentioning

confidence: 99%

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

Gerlofs-Nijland

Bokkers

Sachse³

et al. 2019

Inhalation Toxicology

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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.

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Toxicity and mutagenicity of low-metallic automotive brake pad materials

Cited by 37 publications

References 28 publications

Biological response of an in vitro human 3D lung cell model exposed to brake wear debris varies based on brake pad formulation

Biological response of an in vitro human 3D lung cell model exposed to brake wear debris varies based on brake pad formulation

Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences

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

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