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      Particulate matter beyond mass: recent health evidence on the role of fractions, chemical constituents and sources of emission

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          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 PM 2.5 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.

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          Most cited references85

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          Sources and properties of non-exhaust particulate matter from road traffic: a review.

          While emissions control regulation has led to a substantial reduction in exhaust emissions from road traffic, currently non-exhaust emissions from road vehicles are unabated. These include particles from brake wear, tyre wear, road surface abrasion and resuspension in the wake of passing traffic. Quantification of the magnitude of such emissions is problematic both in the laboratory and the field and the latter depends heavily upon a knowledge of the physical and chemical properties of non-exhaust particles. This review looks at each source in turn, reviewing the available information on the source materials and particles derived from them in laboratory studies. In a final section, some of the key publications dealing with measurements in road tunnels and the roadside environment are reviewed. It is concluded that with the exception of brake dust particles which may be identified from their copper (Cu) and antimony (Sb) content, unequivocal identification of particles from other sources is likely to prove extremely difficult, either because of the lack of suitable tracer elements or compounds, or because of the interactions between sources prior to the emission process. Even in the case of brake dust, problems will arise in distinguishing directly emitted particles from those arising from resuspension of deposited brake dust from the road surface, or that derived from entrainment of polluted roadside soils, either directly or as a component of road surface dust.
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            Ischemic and thrombotic effects of dilute diesel-exhaust inhalation in men with coronary heart disease.

            Exposure to air pollution from traffic is associated with adverse cardiovascular events. The mechanisms for this association are unknown. We conducted a controlled exposure to dilute diesel exhaust in patients with stable coronary heart disease to determine the direct effect of air pollution on myocardial, vascular, and fibrinolytic function. In a double-blind, randomized, crossover study, 20 men with prior myocardial infarction were exposed, in two separate sessions, to dilute diesel exhaust (300 mug per cubic meter) or filtered air for 1 hour during periods of rest and moderate exercise in a controlled-exposure facility. During the exposure, myocardial ischemia was quantified by ST-segment analysis using continuous 12-lead electrocardiography. Six hours after exposure, vasomotor and fibrinolytic function were assessed by means of intraarterial agonist infusions. During both exposure sessions, the heart rate increased with exercise (P<0.001); the increase was similar during exposure to diesel exhaust and exposure to filtered air (P=0.67). Exercise-induced ST-segment depression was present in all patients, but there was a greater increase in the ischemic burden during exposure to diesel exhaust (-22+/-4 vs. -8+/-6 millivolt seconds, P<0.001). Exposure to diesel exhaust did not aggravate preexisting vasomotor dysfunction, but it did reduce the acute release of endothelial tissue plasminogen activator (P=0.009; 35% decrease in the area under the curve). Brief exposure to dilute diesel exhaust promotes myocardial ischemia and inhibits endogenous fibrinolytic capacity in men with stable coronary heart disease. Our findings point to ischemic and thrombotic mechanisms that may explain in part the observation that exposure to combustion-derived air pollution is associated with adverse cardiovascular events. (ClinicalTrials.gov number, NCT00437138 [ClinicalTrials.gov].). Copyright 2007 Massachusetts Medical Society.
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              Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis.

              Although the mechanisms are unknown, it has been suggested that transient exposure to traffic-derived air pollution may be a trigger for acute myocardial infarction. The study aim was to investigate the effects of diesel exhaust inhalation on vascular and endothelial function in humans. In a double-blind, randomized, cross-over study, 30 healthy men were exposed to diluted diesel exhaust (300 microg/m3 particulate concentration) or air for 1 hour during intermittent exercise. Bilateral forearm blood flow and inflammatory factors were measured before and during unilateral intrabrachial bradykinin (100 to 1000 pmol/min), acetylcholine (5 to 20 microg/min), sodium nitroprusside (2 to 8 microg/min), and verapamil (10 to 100 microg/min) infusions 2 and 6 hours after exposure. There were no differences in resting forearm blood flow or inflammatory markers after exposure to diesel exhaust or air. Although there was a dose-dependent increase in blood flow with each vasodilator (P<0.0001 for all), this response was attenuated with bradykinin (P<0.05), acetylcholine (P<0.05), and sodium nitroprusside (P<0.001) infusions 2 hours after exposure to diesel exhaust, which persisted at 6 hours. Bradykinin caused a dose-dependent increase in plasma tissue plasminogen activator (P<0.0001) that was suppressed 6 hours after exposure to diesel (P<0.001; area under the curve decreased by 34%). At levels encountered in an urban environment, inhalation of dilute diesel exhaust impairs 2 important and complementary aspects of vascular function in humans: the regulation of vascular tone and endogenous fibrinolysis. These important findings provide a potential mechanism that links air pollution to the pathogenesis of atherothrombosis and acute myocardial infarction.
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                Author and article information

                Journal
                Inhal Toxicol
                Inhal Toxicol
                IHT
                Inhalation Toxicology
                Informa Healthcare USA, Inc.
                0895-8378
                1091-7691
                December 2013
                4 December 2013
                : 25
                : 14
                : 802-812
                Affiliations
                1Department for Environmental Health, National Institute for Public Health and the Environment BilthovenThe Netherlands
                2Institute for Risk Assessment Studies, Utrecht University UtrechtThe Netherlands
                3WHO European Centre for Environment and Health BonnGermany
                4MRC-PHE Centre for Environment and Health, King’s College LondonUK
                Author notes
                Address for correspondence: F. R. CasseeNational Institute for Public Health and the Environment P.O. Box 1, 3720 BA BilthovenThe Netherlands. Tel: +31 30 274 3804. E-mail: Flemming.cassee@ 123456rivm.nl
                Article
                10.3109/08958378.2013.850127
                3886392
                24304307
                48231f05-ed72-492c-872d-32a2ab372aa5
                © 2013 Informa Healthcare USA, Inc. All rights reserved: reproduction in whole or part not permitted

                This is an open-access article distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the source is credited.

                History
                : 22 July 2013
                : 25 September 2013
                : 26 September 2013
                Categories
                Review Article

                Toxicology
                air pollution – adverse effects,toxicology,particulate matter
                Toxicology
                air pollution – adverse effects, toxicology, particulate matter

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