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• W2037333119 abstract "SummaryThis review summarizes the nature of ambient air pollutants, which are either gaseous or particulate of various sizes, the latter determining their penetration into the body, the smallest even translocating from the lung into the systemic circulation. It presents the epidemiological evidence linking air pollution to overall mortality, cardiovascular mortality and myocardial infarction, making the distinction between acute and chronic exposure to the pollutants. It reviews mechanistic investigations that have evaluated the links among exposure to pollutants, thrombosis, pulmonary inflammation, arterial vasoconstriction and heart rate variability. It concludes by attempting to integrate current epidemiological and mechanistic observations into a pathophysiological framework that links ambient air pollution to acute myocardial infarction and cardiovascular mortality. This review summarizes the nature of ambient air pollutants, which are either gaseous or particulate of various sizes, the latter determining their penetration into the body, the smallest even translocating from the lung into the systemic circulation. It presents the epidemiological evidence linking air pollution to overall mortality, cardiovascular mortality and myocardial infarction, making the distinction between acute and chronic exposure to the pollutants. It reviews mechanistic investigations that have evaluated the links among exposure to pollutants, thrombosis, pulmonary inflammation, arterial vasoconstriction and heart rate variability. It concludes by attempting to integrate current epidemiological and mechanistic observations into a pathophysiological framework that links ambient air pollution to acute myocardial infarction and cardiovascular mortality. A link between ambient air pollution and cardiovascular disease, in particular myocardial infarction, has been suggested by a number of epidemiological studies and has attracted substantial attention within the cardiological community, as attested by the recent American Heart Association scientific statement on air pollution and cardiovascular disease [1Brook R.D. Franklin B. Cascio W. Hong Y. Howard G. Lipsett M. Luepker R. Mittleman M. Samet J. Smith S.C. Tager I. Air pollution and cardiovascular disease. A statement for healthcare professionals from the expert panel on population and prevention science of the American Heart Association.Circulation. 2004; 109: 2655-71Crossref PubMed Scopus (1823) Google Scholar]. These reports and comments have mainly appeared in epidemiological, cardiological and respiratory journals, and have hardly received attention in thrombosis journals. The purpose of this review is to provide a brief state‐of‐the‐art on this subject, with particular emphasis on the link between ambient air pollution and thrombosis. A distinction can be made between gaseous and particulate matter (PM)pollutants. The polluting gases include nitrogen oxides, carbon monoxide, sulfur dioxide and ozone. To some extent, these gases serve as an indicator of combustion‐related pollution of ambient air. Ozone may have direct deleterious cardiovascular effects (see further), and other gases may enhance the damaging effects of airborne PM. Airborne PM consists of a heterogeneous mixture of solid and liquid particles suspended in air (well reviewed in Ref. 1Brook R.D. Franklin B. Cascio W. Hong Y. Howard G. Lipsett M. Luepker R. Mittleman M. Samet J. Smith S.C. Tager I. Air pollution and cardiovascular disease. A statement for healthcare professionals from the expert panel on population and prevention science of the American Heart Association.Circulation. 2004; 109: 2655-71Crossref PubMed Scopus (1823) Google Scholar). Primary particles, such as diesel soot, are emitted directly into the atmosphere, whereas secondary particles are created through physicochemical transformation of gases, such as the formation of sulfate from sulfur dioxide. The main source of airborne PM is the combustion of fuel, including coal; other sources include forest fires. Some of the more common constituents are elemental and organic carbon, nitrates, sulfates, a variety of metals, and even bacterial endotoxins. Because of the heterogeneous nature of airborne PM, it has mainly been defined on the basis of size distribution. PM10 stands for PM with a median aerodynamic diameter less than 10 μm (the size of an average cell). PM10 can readily penetrate and deposit in the tracheobronchial tree. PM2.5 stands for PM with a median aerodynamic diameter less than 2.5 μm (the size of an average bacterium). This size fraction can reach the small airways and alveoli. Ultrafine particles (UFP) have a diameter less than 100 nm (0.1 μm), the size of a virus. These particles demonstrate very high deposition in human alveoli [2Daigle C.C. Chalupa D.C. Gibb F.R. Morrow P.E. Oberdörster G. Utell M.J. Frampton M.W. Ultrafine particle deposition in humans during rest and exercise.Inhal Toxicol. 2003; 15: 539-52Crossref PubMed Scopus (384) Google Scholar]; the total number of deposited particles also is four‐ to five‐fold higher during exercise than at rest, because of increase both in deposition fraction and in ventilation. Ultrafine particles account for a major portion of the actual number of particles within airborne PM and have a high surface area‐to‐mass ratio, which could lead to enhanced biological toxicity [3Oberdörster G. Pulmonary effects of inhaled ultrafine particles.Int Arch Occup Environ Health. 2000; 74: 1-8Crossref Scopus (1125) Google Scholar]. Ultrafine particles may even be able to pass directly into the blood stream [4Nemmar A. Vanbilloen H. Hoylaerts M.F. Hoet P.H. Verbruggen A. Nemery B. Passage of intratracheally instilled ultrafine particles from the lung into the systemic circulation in hamster.Am J Respir Crit Care Med. 2001; 164: 1665-8Crossref PubMed Scopus (526) Google Scholar, 5Nemmar A. Hoet P.H. Vanquickenborne B. Dinsdale D. Thomeer M. Hoylaerts M.F. Vanbilloen H. Mortelmans L. Nemery B. Passage of inhaled particles into the blood circulation in humans.Circulation. 2002; 105: 411-4Crossref PubMed Scopus (1282) Google Scholar, 6Oberdorster G. Sharp Z. Atudorei V. Elder A. Gelein R. Lunts A. Kreyling W. Cox C. Extrapulmonary translocation of ultrafine carbon particles following whole‐body inhalation exposure of rats.J Toxicol Environ Health A. 2002; 65: 1531-43Crossref PubMed Scopus (846) Google Scholar]. Outdoor UFPs readily enter a house [7LaRosa L.E. Buckley T.J. Wallace L.A. Real‐time indoor and outdoor measurements of black carbon in an occupied house: an examination of sources.J Air Waste Manag Assoc. 2002; 52: 41-9Crossref PubMed Scopus (66) Google Scholar]. It is useful to distinguish between short‐term exposure to high levels of airborne PM and more chronic exposure. There is convincing evidence of a relation between overall and cardiovascular mortality and the degree of air pollution on the previous day. Samet et al. [8Samet J.M. Dominici F. Curriero F.C. Coursac I. Zeger S.L. Fine particulate air pollution and mortality in 20 US cities, 1987–1994.N Engl J Med. 2000; 343: 1742-9Crossref PubMed Scopus (2019) Google Scholar] assessed the effects of five major outdoor air pollutants on daily mortality rates in 20 of the largest cities in the USA from 1987 to 1994. The pollutants were PM10, ozone, carbon monoxide, sulfur dioxide and nitrogen dioxide. They found consistent evidence that the level of PM10 is associated with the rate of death from all causes and from cardiovascular and respiratory illnesses. Daily variations of PM10 were positively associated with daily variations in mortality [9Dominici F. McDermott A. Zeger S.L. Samet J.M. National maps of the effects of particulate matter on mortality: exploring geographical variation.Environ Health Perspect. 2003; 111: 39-44Crossref PubMed Scopus (120) Google Scholar]. There was weaker evidence that increases in ozone levels increased the relative rates of death during the summer, when ozone levels are highest, but not during the winter. Levels of the other pollutants were not significantly related to the mortality rate [8Samet J.M. Dominici F. Curriero F.C. Coursac I. Zeger S.L. Fine particulate air pollution and mortality in 20 US cities, 1987–1994.N Engl J Med. 2000; 343: 1742-9Crossref PubMed Scopus (2019) Google Scholar]. A recent study from South‐West France has indicated that current‐day and 1‐day‐lag ozone measurements are significantly related to the occurrence of myocardial infarction [10Ruidavets J.‐.B. Cournot M. Cassadou S. Giroux M. Meybeck M. Ferrières J. Ozone air pollution is associated with acute myocardial infarction.Circulation. 2005; 111: 563-9Crossref PubMed Scopus (185) Google Scholar]. This study did not include PM measurements. The APHEA2 (Air Pollution and Health: A European Approach 2) project found a positive relation between the daily number of total deaths or cardiovascular deaths and the daily PM10 concentrations, based on the findings in 29 European cities [11Katsouyanni K. Touloumi G. Samoli E. Gryparis A. Le Tertre A. Monopolis Y. Rossi G. Zmirou D. Ballester F. Boumghar A. Anderson H.R. Wojtyniak B. Paldy A. Braunstein R. Pekkanen J. Schindler C. Schwartz J. Confounding and effect modification in the short‐term effects of ambient particles on total mortality: results from 29 European cities within the APHEA2 project.Epidemiology. 2001; 12: 521-31Crossref PubMed Scopus (785) Google Scholar, 12Zanobetti A. Schwartz J. Samoli E. Gryparis A. Touloumi G. Peacock J. Anderson R.H. Le Tertre A. Bobros J. Celko M. Goren A. Forsberg B. Michelozzi P. Rabczenko D. Hoyos S.P. Wichmann H.E. Katsouyanni K. The temporal pattern of respiratory and heart disease mortality in response to air pollution.Environ Health Perspect. 2003; 111: 1188-93Crossref PubMed Scopus (236) Google Scholar]. APHEA‐2 also studied the effects of PM10 exposure on deaths upto 40 days after the exposure; the authors concluded that the effect of air pollution persists for more than 1 month after exposure [12Zanobetti A. Schwartz J. Samoli E. Gryparis A. Touloumi G. Peacock J. Anderson R.H. Le Tertre A. Bobros J. Celko M. Goren A. Forsberg B. Michelozzi P. Rabczenko D. Hoyos S.P. Wichmann H.E. Katsouyanni K. The temporal pattern of respiratory and heart disease mortality in response to air pollution.Environ Health Perspect. 2003; 111: 1188-93Crossref PubMed Scopus (236) Google Scholar]. In the APHEA2 study, cardiovascular deaths were increased by 0.69% (95% CI 0.31%–1.08%) for each 10 μg m−3 increase in PM10. Of interest is that certain populations appear to be at greater risk: the elderly [11Katsouyanni K. Touloumi G. Samoli E. Gryparis A. Le Tertre A. Monopolis Y. Rossi G. Zmirou D. Ballester F. Boumghar A. Anderson H.R. Wojtyniak B. Paldy A. Braunstein R. Pekkanen J. Schindler C. Schwartz J. Confounding and effect modification in the short‐term effects of ambient particles on total mortality: results from 29 European cities within the APHEA2 project.Epidemiology. 2001; 12: 521-31Crossref PubMed Scopus (785) Google Scholar, 13Goldberg M.S. Burnett R.T. Bailar JC, I.I.I. Tamblyn R. Ernst P. Flegel K. Brook J. Bonvalot Y. Singh R. Valois M.F. Vincent R. Identification of persons with cardiorespiratory conditions who are at risk of dying from the acute effects of ambient air particles.Environ Health Perspect. 2001; 109: 487-94PubMed Google Scholar], those with pre‐existing chronic lung disease, coronary heart disease or heart failure [13Goldberg M.S. Burnett R.T. Bailar JC, I.I.I. Tamblyn R. Ernst P. Flegel K. Brook J. Bonvalot Y. Singh R. Valois M.F. Vincent R. Identification of persons with cardiorespiratory conditions who are at risk of dying from the acute effects of ambient air particles.Environ Health Perspect. 2001; 109: 487-94PubMed Google Scholar], or patients with diabetes [14Zanobetti A. Schwartz J. Cardiovascular damage by airborne particles: are diabetics more susceptible.Epidemiology. 2002; 13: 588-92Crossref PubMed Scopus (180) Google Scholar]. Whereas the previous studies describe total and cardiovascular mortality in general, a number of studies have focused specifically on myocardial infarction. Peters et al. [15Peters A. Dockery D.W. Muller J.E. Mittleman M.A. Increased particulate air pollution and the triggering of myocardial infarction.Circulation. 2001; 103: 2810-5Crossref PubMed Scopus (1216) Google Scholar] found that the risk of myocardial infarction onset increased in association with elevated concentrations of fine particles (PM2.5) both in the previous 2‐h period and the day before the onset. More recently, an association has been reported between participation in traffic and the onset of a myocardial infarction within 1 h afterward (odds ratio 2.92; 95% CI 2.22–3.83; P < 0.001) [16Peters A. von Klot S. Heier M. Trentinaglia I. Hormann A. Wichmann H.E. Lowel H. Exposure to traffic and the onset of myocardial infarction.N Engl J Med. 2004; 351: 1721-30Crossref PubMed Scopus (771) Google Scholar]. An initial landmark report was that of the Harvard Six Cities study [17Dockery D.W. Pope CA, I.I.I. Xu X. Spengler J.D. Ware J.H. Fay M.E. Ferris BG, J.r. Speizer F.E. An association between air pollution and mortality in six US cities.N Engl J Med. 1993; 329: 1753-9Crossref PubMed Scopus (6420) Google Scholar]. In a cohort of 8111 adults with 14–16 years of follow‐up, the adjusted overall mortality rate for the most polluted city vs. the least polluted city was 1.26 (95% CI 1.08–1.47). Cardiovascular deaths accounted for the largest single category of the increased mortality. Among air pollutants, elevation of PM2.5 was most strongly associated with disease. The interesting study of Hoek et al. [18Hoek G. Brunekreef B. Goldbohm S. Fischer P. van den Brandt P.A. Association between mortality and indicators of traffic‐related air pollution in The Netherlands: a cohort study.Lancet. 2002; 360: 1203-9Abstract Full Text Full Text PDF PubMed Scopus (1232) Google Scholar] followed up 5000 adults for 8 years in The Netherlands. In this cohort, living near a major road was strongly associated with cardiopulmonary mortality (relative risk 1.95, 95% CI 1.09–3.52). Pope et al. [19Pope CA, I.I.I. Burnett R.T. Thurston G.D. Thun M.J. Calle E.E. Krewski D. Godleski J.J. Cardiovascular mortality and long‐term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.Circulation. 2004; 109: 71-7Crossref PubMed Scopus (2111) Google Scholar] linked mortality statistics for a 16‐year period to chronic exposure to multiple air pollutants in approximately 500 000 adults who resided in all 50 states of USA. Each 10 μg m−3 increase in annual PM2.5 mean concentration, based on a number of different averaging periods, linearly enhanced cardiovascular mortality (relative risk per 10 μg m−3 PM2.5 rise 1.12, 95% CI 1.08–1.15). The single largest increase in risk was for ischemic heart disease (relative risk 1.18 95% CI 1.14–1.23). In addition, the risk for arrhythmia, heart failure, or cardiac arrest mortality was also increased (RR 1.13, 95% CI, 1.05–1.21). Künzli et al. [20Künzli N. Jerrett M. Mack W.J. Beckerman B. LaBree L. Gilliland F. Thomas D. Peters J. Hodis H.N. Ambient air pollution and atherosclerosis in Los Angeles.Environ Health Perspect. 2005; 113: 201-6Crossref PubMed Scopus (634) Google Scholar] studied the association between long‐term exposure to PM2.5 and carotid intima‐media thickness in subjects living in different areas of Los Angeles. Subjects living in the areas with highest annual mean concentrations of ambient PM2.5 had an increased intima‐media thickness, providing initial epidemiological evidence of an association between atherosclerosis and ambient air pollution. Whereas hundreds of epidemiological papers have addressed the relation between ambient air pollution and health, mechanistic studies are distinctly fewer. This may in part be related to methodological issues. One way of study is the exposure of humans to concentrated air particles or ozone for limited time periods; another is the inhalation of pollutants or their instillation into the trachea of animals. With regard to cardiovascular disease, the endpoints studied have mainly been inflammation and arrhythmia; investigations of the thrombogenic effects of airborne PM have only recently started. We shall first discuss the latter studies and thereafter the relation between air pollutants and inflammation, arterial vasoconstriction and heart rate variability. Nemmar et al. [4Nemmar A. Vanbilloen H. Hoylaerts M.F. Hoet P.H. Verbruggen A. Nemery B. Passage of intratracheally instilled ultrafine particles from the lung into the systemic circulation in hamster.Am J Respir Crit Care Med. 2001; 164: 1665-8Crossref PubMed Scopus (526) Google Scholar] have initiated a number of investigations on the thrombus enhancing effects of particles instilled into the trachea of hamsters. The thrombosis model they use is based on limited endothelial damage caused by singlet oxygen induced within the lumen by injection of Rose Bengal and brief exposure of the vessel segment to green light; thrombus formation is continuously monitored by transillumination. Following the observation that intratracheally instilled UFPs pass from the lung into the systemic circulation in hamsters, Nemmar et al. [21Nemmar A. Hoylaerts M.F. Hoet P.H. Dinsdale D. Smith T. Xu H. Vermylen J. Nemery B. Ultrafine particles affect experimental thrombosis in an in vivo hamster model.Am J Respir Crit Care Med. 2002; 166: 998-1004Crossref PubMed Scopus (286) Google Scholar] investigated how such particles affect thrombus formation. They found that intratracheal instillation of well‐defined positively charged ultrafine (60 nm) polystyrene particles significantly enhanced platelet‐rich thrombus formation at the site of partial de‐endothelialization, 1 h after instillation. On the other hand, 400 nm particles, which would not enter the circulation, did not affect early thrombus formation (in the first hour), despite similar increases in neutrophils, lactate dehydrogenase and histamine in the bronchoalveolar lavage (BAL) fluid [22Nemmar A. Hoylaerts M.F. Hoet P.H. Vermylen J. Nemery B. Size effect of intratracheally instilled particles on pulmonary inflammation and vascular thrombosis.Toxicol Appl Pharmacol. 2003; 186: 38-45Crossref PubMed Scopus (195) Google Scholar]. Unmodified and negatively charged ultrafine polystyrene particles had no effect. In vitro addition of positively charged polystyrene particles to hamster blood also shortened the closure time in the platelet function analyzer (PFA100), thus indicating platelet activation. The authors then switched to instillation of diesel exhaust particles; transmission electron microscopy of the particles showed numerous small aggregates of carbonaceous particles 20–50 nm in diameter; most aggregates were less than 2.5 μm in largest diameter [23Nemmar A. Hoet P.H. Dinsdale D. Vermylen J. Hoylaerts M.F. Nemery B. Diesel exhaust particles in lung acutely enhance experimental peripheral thrombosis.Circulation. 2003; 107: 1202-8Crossref PubMed Scopus (249) Google Scholar]. Others have also found that the primary particles in diesel aggregates range from 10 to 40 nm [24Shi J.P. Mark D. Harrison R.M. Characterization of particles from a current technology heavy‐duty diesel engine.Environ Sci Technol. 2000; 34: 748-55Crossref Scopus (185) Google Scholar]. Xiong and Friedlander [25Xiong C. Friedlander S.K. Morphological properties of atmospheric aerosol aggregates.Proc Natl Acad Sci USA. 2001; 98: 11851-6Crossref PubMed Scopus (140) Google Scholar] reported that the primary particle size of atmospheric aggregates emitted from combustion processes such as diesel engines ranges from 6 to 100 nm. These diesel exhaust particles significantly and dose dependently enhanced arterial or venous thrombus formation recorded during the first hour after instillation [23Nemmar A. Hoet P.H. Dinsdale D. Vermylen J. Hoylaerts M.F. Nemery B. Diesel exhaust particles in lung acutely enhance experimental peripheral thrombosis.Circulation. 2003; 107: 1202-8Crossref PubMed Scopus (249) Google Scholar]. Blood samples taken from the hamsters 30 and 60 min after instillation of the diesel exhaust particles yielded significantly shortened closure times in the PFA100. The platelet count was not modified. PFA100 shortening could also be reproduced by adding diesel exhaust particles to hamster blood in vitro [23Nemmar A. Hoet P.H. Dinsdale D. Vermylen J. Hoylaerts M.F. Nemery B. Diesel exhaust particles in lung acutely enhance experimental peripheral thrombosis.Circulation. 2003; 107: 1202-8Crossref PubMed Scopus (249) Google Scholar]. The data thus suggest that diesel exhaust particles are prothrombotic through particle‐induced platelet activation. The acute instillation of a bolus of particles may be criticized as non‐physiological as opposed to the more gradual exposure by inhalation, but it has the advantage of convenience and more accurate knowledge of the dose administered to the lungs. The following study [26Nemmar A. Nemery B. Hoet P.H. Vermylen J. Hoylaerts M.F. Pulmonary inflammation and thrombogenicity caused by diesel particles in hamsters: role of histamine.Am J Respir Crit Care Med. 2003; 168: 1366-72Crossref PubMed Scopus (121) Google Scholar] investigated the duration of the thrombotic tendency following intratracheal instillation of diesel exhaust particles in the hamster, and the possible role of histamine. Enhanced thrombus formation was observed not only 1 h, but also 6 and 24 h after instillation (Fig. 1). Shortened closure times with the PFA100 were found at all time points. In BAL, neutrophils and histamine levels were also increased at all‐time points. In plasma, histamine was increased at 6 and 24 h (Fig. 2), but not at 1 and 3 h. Pretreatment with a histamine H1‐receptor antagonist (diphenhydramine) abolished the diesel exhaust particle‐induced neutrophil influx in BAL at all time points. However, diphenhydramine pretreatment did not affect thrombosis or platelet activation at 1 h, whereas both were markedly reduced at 6 and 24 h. Therefore, at 1 h, the prothrombotic effects do not appear to result from pulmonary inflammation but presumably from the blood penetration of diesel exhaust particles or associated components. At later time points, however, pulmonary inflammation, plasma histamine activity and thrombotic tendency are linked. Histamine by itself is not a potent platelet agonist, but enhances platelet responses to other agonists [27Mannaioni P.F. Di Bello M.G. Gambassi F. Magnai L. Masini E. Platelet histamine: characterization of the proaggregatory effect of histamine in human platelets.Int Arch Allergy Appl Immunol. 1992; 99: 394-6Crossref Scopus (10) Google Scholar]; it may thus ‘prime’ platelets to show an enhanced response when brought into contact with damaged endothelium (or the agonists immobilized on the PFA100 cartridges). Within the time frame studied, diesel exhaust particles did not raise plasma von Willebrand factor (VWF) levels.Figure 2Histamine levels in BAL fluid and in plasma after exposure to particles. Histamine concentrations at 24 h after intratracheal instillation of vehicle (saline containing 0.1% tween 80 or saline alone) or DEP (50 μg per animal) or silica particles (20 μg per animal) in BAL (a) and plasma (b). Means ± SEM (n = 4–6 in each group). Statistical analysis by unpaired Student's t‐test. Modified from Refs. [26Nemmar A. Nemery B. Hoet P.H. Vermylen J. Hoylaerts M.F. Pulmonary inflammation and thrombogenicity caused by diesel particles in hamsters: role of histamine.Am J Respir Crit Care Med. 2003; 168: 1366-72Crossref PubMed Scopus (121) Google Scholar] and [30Nemmar A. Nemery B. Hoet P.H. Van Rooijen N. Hoylaerts M.F. Silica particles enhance peripheral thrombosis: key role of lung macrophage‐neutrophil cross‐talk.Am J Respir Crit Care Med. 2005; 171: 872-9Crossref PubMed Scopus (65) Google Scholar].View Large Image Figure ViewerDownload Hi-res image Download (PPT) In further experiments, sodium cromoglycate, a mast cell stabilizer, strongly inhibited diesel exhaust particle‐induced airway inflammation, late thrombogenicity and histamine release [28Nemmar A. Hoet P.H. Vermylen J. Nemery B. Hoylaerts M.F. Pharmacological stabilization of mast cells abrogates late thrombotic events induced by diesel exhaust particles in hamsters.Circulation. 2004; 110: 1670-77Crossref PubMed Scopus (116) Google Scholar]. Salvi et al. [29Salvi S. Blomberg A. Rudell B. Kelly F. Sandström T. Holgate S.T. Frew A. Acute inflammatory responses in the airways and peripheral blood after short‐term exposure to diesel exhaust in healthy human volunteers.Am J Respir Crit Care Med. 1999; 159: 702-9Crossref PubMed Scopus (745) Google Scholar] had previously reported an increase in mast cell numbers in the bronchial submucosa and elevated histamine levels in bronchoalveolar fluid 6 h after exposure to diesel exhaust particles in humans. In the provisionally last paper of this series, Nemmar et al. [30Nemmar A. Nemery B. Hoet P.H. Van Rooijen N. Hoylaerts M.F. Silica particles enhance peripheral thrombosis: key role of lung macrophage‐neutrophil cross‐talk.Am J Respir Crit Care Med. 2005; 171: 872-9Crossref PubMed Scopus (65) Google Scholar] studied the relationship between pulmonary inflammation and thrombus development. In this study, they used the established model of sustained pulmonary inflammation induced by silica. Intratracheal instillation of silica particles in the hamster triggered pulmonary inflammation and enhanced thrombus formation on photochemically damaged endothelium at 24 h (Fig. 1). Either the selective depletion of lung macrophages by intratracheal administration of clodronate liposomes or the depletion of circulating monocytes and neutrophils by intraperitoneal injection of cyclophosphamide significantly reduced silica‐induced accumulation of macrophages and neutrophils in BAL fluid and also reduced thrombogenicity, the platelet count being unchanged. Silica‐induced inflammation was accompanied by increased neutrophil elastase levels in BAL fluid, and also in plasma; in this instance, histamine levels were not raised (Fig. 2). Pretreatment of hamsters with clodronate liposomes abolished the rise of neutrophil elastase in BAL fluid and in plasma, indicating pulmonary macrophage–neutrophil cross‐talk resulting in release of neutrophil elastase into the blood circulation. Specific neutrophil elastase inhibition in the lung did not affect lung inflammation, but reduced peripheral thrombogenicity, suggesting that in this instance neutrophil elastase could have a role as platelet ‘primer’, as suggested by previous in vitro investigations [31Kornecki E. Ehrlich Y.H. Egbring R. Gramse M. Seitz R. Eckardt A. Lukasiewicz H. Niewiarowski S. Granulocyte‐platelet interactions and platelet fibrinogen receptor exposure.Am J Physiol. 1988; 255: H651-8PubMed Google Scholar]. Khandoga et al. [32Khandoga A. Stampfl A. Takenaka S. Schulz H. Radykewicz R. Kreyling W. Krombach F. Ultrafine particles exert prothrombotic but not inflammatory effects on the hepatic microcirculation in healthy mice in vivo.Circulation. 2004; 109: 1320-25Crossref PubMed Scopus (120) Google Scholar] have observed that, after intra‐arterial injection of UFP, platelets accumulate in the hepatic microvasculature of healthy mice and are associated with prothrombotic changes. Suwa et al. [33Suwa T. Hogg J.C. Quinlan K.B. Ohgami A. Vincent R. van Eeden S.F. Particulate air pollution induces progression of atherosclerosis.J Am Coll Cardiol. 2002; 39: 935-42Crossref PubMed Scopus (488) Google Scholar] made Watanabe heritable hyperlipidemic rabbits breathe air containing PM10 for 4 weeks. Exposure to PM increased the volume and advanced the phenotype of the coronary atherosclerotic lesions. The papers discussed above summarize the only reports, so far, that have experimentally studied the relationship of pollutants and/or pulmonary inflammation with thrombosis or atherosclerosis. There hardly are papers reporting on activation of blood coagulation or of platelets following exposure to ambient air pollutants. The shortening of PFA100 closure times following instillation of diesel exhaust particles in hamsters, as observed by Nemmar et al. [23Nemmar A. Hoet P.H. Dinsdale D. Vermylen J. Hoylaerts M.F. Nemery B. Diesel exhaust particles in lung acutely enhance experimental peripheral thrombosis.Circulation. 2003; 107: 1202-8Crossref PubMed Scopus (249) Google Scholar, 26Nemmar A. Nemery B. Hoet P.H. Vermylen J. Hoylaerts M.F. Pulmonary inflammation and thrombogenicity caused by diesel particles in hamsters: role of histamine.Am J Respir Crit Care Med. 2003; 168: 1366-72Crossref PubMed Scopus (121) Google Scholar], is interesting, but this parameter has not been used before to detect platelet hyperactivity; instead, the PFA100 was developed to aid in the diagnosis of von Willebrand disease and other platelet function defects by providing prolonged closure times in these disorders. While papers on thrombosis and atherosclerosis are few, many have addressed the inflammatory response to ambient air pollution. Ghio et al. [34Ghio A.J. Kim C. Devlin R.B. Concentrated ambient air particles induce mild pulmonary inflammation in healthy human volunteers.Am J Respir Crit Care Med. 2000; 162: 981-8Crossref PubMed Scopus (435) Google Scholar] exposed healthy volunteers to concentrated ambient particles in a chamber for 2 h. Eighteen hours later, there was an increase in neutrophils in BAL fluid and a rise in plasma fibrinogen. They subsequently confirmed these inhalation findings, using instead bronchial instillation of" @default.
• W2037333119 created "2016-06-24" @default.
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• W2037333119 date "2005-09-01" @default.
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• W2037333119 title "Ambient air pollution and acute myocardial infarction" @default.
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