Cardiopulmonary responses of intratracheally instilled tire particles and constituent metal components.
ABSTRACT Tire and brake wear particles contain transition metals, and contribute to near-road PM. We hypothesized that acute cardiopulmonary injury from respirable tire particles (TP) will depend on the amount of soluble metals. Respirable fractions of two types of TP (TP1 and TP2) were analyzed for water and acid-leachable metals using ICP-AES. Both TP types contained a variety of transition metals, including zinc (Zn), copper (Cu), aluminum, and iron. Zn and Cu were detected at high levels in water-soluble fractions (TP2 > TP1). Male Wistar Kyoto rats (12-14 wk) were intratracheally instilled, in the first study, with saline, TP1 or TP2 (5 mg/kg), and in the second study, with soluble Zn, Cu (0.5 micromol/kg), or both. Pulmonary toxicity and cardiac mitochondrial enzymes were analyzed 1 d, 1 wk, or 4 wk later for TP and 4 or 24 h later for metals. Increases in lavage fluid markers of inflammation and injury were observed at d 1 (TP2 > TP1), but these changes reversed by wk 1. No effects on cardiac enzymes were noted with either TP. Exposure of rats to soluble Zn and Cu caused marked pulmonary inflammation and injury but temporal differences were apparent (Cu effects peaked at 4 h and Zn at 24 h). Instillation of Zn, Cu, and Zn + Cu decreased the activity of cardiac aconitase, isocitrate dehydrogenase, succinate dehydrogenase, cytochrome-c-oxidase and superoxide dismutase suggesting mitochondrial oxidative stress. The observed acute pulmonary toxicity of TP could be due to the presence of water soluble Zn and Cu. At high concentrations these metals may induce cardiac oxidative stress.
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ABSTRACT: Road transport emissions are a major contributor to ambient particulate matter concentrations and have been associated with adverse health effects. Therefore, these emissions are targeted through increasingly stringent European emission standards. These policies succeed in reducing exhaust emissions, but do not address "nonexhaust" emissions from brake wear, tire wear, road wear and suspension in air of road dust. Is this a problem? To what extent do nonexhaust emissions contribute to ambient concentrations of PM10 or PM2.5? In the near future, wear emissions may dominate the remaining traffic-related PM10 emissions in Europe, mostly due to the steep decrease in PM exhaust emissions. This underlines the need to determine the relevance of the wear emissions as a contribution to the existing ambient PM concentrations, and the need to assess the health risks related to wear particles, which has not yet received much attention. During a workshop in 2011, available knowledge was reported and evaluated so as to draw conclusions on the relevance of traffic-related wear emissions for air quality policy development. On the basis of available evidence, which is briefly presented in this paper it was concluded that nonexhaust emissions and in particular suspension in air of road dust are major contributors to exceedances at street locations of the PM10 air quality standards in various European cities. Furthermore, wear-related PM emissions that contain high concentrations of metals may (despite their limited contribution to the mass of nonexhaust emissions) cause significant health risks for the population, especially those living near intensely trafficked locations. To quantify the existing health risks, targeted research is required on wear emissions, their dispersion in urban areas, population exposure, and its effects on health. Such information will be crucial for environmental policymakers as an input for discussions on the need to develop control strategies. Implications: Road transport particulate matter (PM) emissions are associated with adverse health effects. Stringent policies succeed in reducing the exhaust PM emissions, but do not address "nonexhaust" emissions from brake wear, tire wear, road wear, and suspension in air of road dust. In the near future the nonexhaust emissions will dominate the road transport PM emissions. Based on the limited available evidence, it is argued that dedicated research is required on nonexhaust emissions and dispersion to urban areas from both an air quality and a public health perspective. The implicated message to regulators and policy makers is that road transport emissions continue to be an issue for health and air quality, despite the encouraging rapid decrease of tailpipe exhaust emissions.Journal of the Air & Waste Management Association (1995) 02/2013; 63(2):136-49. DOI:10.1080/10962247.2012.741055 · 1.17 Impact Factor
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ABSTRACT: Particulate matter (PM) is a complex, heterogeneous mixture that changes in time and space. It encompasses many different chemical components and physical characteristics, many of which have been cited as potential contributors to toxicity. Each component has multiple sources, and each source generates multiple components. Identifying and quantifying the influences of specific components or source-related mixtures on measures of health-related impacts, especially when particles interact with other co-pollutants, therefore represents one of the most challenging areas of environmental health research. Current knowledge does not allow precise quantification or definitive ranking of the health effects of PM emissions from different sources or of individual PM components and indeed, associations may be the result of multiple components acting on different physiological mechanisms. Some results do suggest a degree of differential toxicity, namely more consistent associations with traffic-related PM emissions, fine and ultrafine particles, specific metals and elemental carbon and a range of serious health effects, including increased morbidity and mortality from cardiovascular and respiratory conditions. A carefully targeted programme of contemporary toxicological and epidemiological research, incorporating more refined approaches (e.g. greater speciation data, more refined modelling techniques, accurate exposure assessment and better definition of individual susceptibility) and optimal collaboration amongst multidisciplinary teams, is now needed to advance our understanding of the relative toxicity of particles from various sources, especially the components and reactions products of traffic. This will facilitate targeted abatement policies, more effective pollution control measures and ultimately, a reduction in the burden of disease attributable to ambient PM pollution.Atmospheric Environment 12/2012; 60:504–526. DOI:10.1016/j.atmosenv.2012.06.039 · 3.06 Impact Factor
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ABSTRACT: Abstract Particulate matter (PM) is regulated in various parts of the world based on specific size cut offs, often expressed as 10 or 2.5 µm mass median aerodynamic diameter. This pollutant is deemed one of the most dangerous to health and moreover, problems persist with high ambient concentrations. Continuing pressure to re-evaluate ambient air quality standards stems from research that not only has identified effects at low levels of PM but which also has revealed that reductions in certain components, sources and size fractions may best protect public health. Considerable amount of published information have emerged from toxicological research in recent years. Accumulating evidence has identified additional air quality metrics (e.g. black carbon, secondary organic and inorganic aerosols) that may be valuable in evaluating the health risks of, for example, primary combustion particles from traffic emissions, which are not fully taken into account with PM2.5 mass. Most of the evidence accumulated so far is for an adverse effect on health of carbonaceous material from traffic. Traffic-generated dust, including road, brake and tire wear, also contribute to the adverse effects on health. Exposure durations from a few minutes up to a year have been linked with adverse effects. The new evidence collected supports the scientific conclusions of the World Health Organization Air Quality Guidelines and also provides scientific arguments for taking decisive actions to improve air quality and reduce the global burden of disease associated with air pollution.Inhalation Toxicology 12/2013; 25(14):802-12. DOI:10.3109/08958378.2013.850127 · 2.34 Impact Factor