(Circulation. 2001;103:2810.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Increased Particulate Air Pollution and the Triggering of Myocardial Infarction
From the Department of Environmental Health (A.P., D.W.D.) and Department of Epidemiology (M.A.M.), Harvard School of Public Health; the Division of Cardiology, Massachusetts General Hospital, Harvard Medical School (J.E.M.); and the Institute for Prevention of Cardiovascular Disease, Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School (M.A.M.), Boston, Mass; and the Institute of Epidemiology, GSF-National Research Center for Environment and Health, Neuherberg, Germany (A.P.).
Correspondence to Annette Peters, PhD, GSF-National Research Center for Environment and Health, PO Box 1129, 85758 Neuherberg, Germany.
Background—Elevated concentrations of ambient particulate air pollution have been associated with increased hospital admissions for cardiovascular disease. Whether high concentrations of ambient particles can trigger the onset of acute myocardial infarction (MI), however, remains unknown.
Methods and Results—We interviewed 772 patients with MI in the greater Boston area between January 1995 and May 1996 as part of the Determinants of Myocardial Infarction Onset Study. Hourly concentrations of particle mass <2.5 µm (PM2.5), carbon black, and gaseous air pollutants were measured. A case-crossover approach was used to analyze the data for evidence of triggering. The risk of MI onset increased in association with elevated concentrations of fine particles in the previous 2-hour period. In addition, a delayed response associated with 24-hour average exposure 1 day before the onset of symptoms was observed. Multivariate analyses considering both time windows jointly revealed an estimated odds ratio of 1.48 associated with an increase of 25 µg/m3 PM2.5 during a 2-hour period before the onset and an odds ratio of 1.69 for an increase of 20 µg/m3 PM2.5 in the 24-hour period 1 day before the onset (95% CIs 1.09, 2.02 and 1.13, 2.34, respectively).
Conclusions—The present study suggests that elevated concentrations of fine particles in the air may transiently elevate the risk of MIs within a few hours and 1 day after exposure. Further studies in other locations are needed to clarify the importance of this potentially preventable trigger of MI.
Key Words: myocardial infarction • air pollution • heart disease • epidemiology
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 J.E. Sharman, J.R. Cockcroft, and J.S. Coombes Cardiovascular implications of exposure to traffic air pollution during exercise QJM, October 1, 2004; 97(10): 637 - 643. [Abstract] [Full Text] [PDF]
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A. Nemmar, P. H.M. Hoet, J. Vermylen, B. Nemery, and M. F. Hoylaerts Pharmacological Stabilization of Mast Cells Abrogates Late Thrombotic Events Induced by Diesel Exhaust Particles in Hamsters Circulation, September 21, 2004; 110(12): 1670 - 1677. [Abstract] [Full Text] [PDF]
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G. A. Wellenius, J. R. F. Batalha, E. A. Diaz, J. Lawrence, B. A. Coull, T. Katz, R. L. Verrier, and J. J. Godleski Cardiac Effects of Carbon Monoxide and Ambient Particles in a Rat Model of Myocardial Infarction Toxicol. Sci., August 1, 2004; 80(2): 367 - 376. [Abstract] [Full Text] [PDF]
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Y. Goto, J. C. Hogg, C.-H. Shih, H. Ishii, R. Vincent, and S. F. van Eeden Exposure to ambient particles accelerates monocyte release from bone marrow in atherosclerotic rabbits Am J Physiol Lung Cell Mol Physiol, July 1, 2004; 287(1): L79 - L85. [Abstract] [Full Text] [PDF]
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R. D. Brook, B. Franklin, W. Cascio, Y. Hong, G. Howard, M. Lipsett, R. Luepker, M. Mittleman, J. Samet, S. C. Smith Jr, et al. 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, June 1, 2004; 109(21): 2655 - 2671. [Abstract] [Full Text] [PDF]
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M. Riediker, W. E. Cascio, T. R. Griggs, M. C. Herbst, P. A. Bromberg, L. Neas, R. W. Williams, and R. B. Devlin Particulate Matter Exposure in Cars Is Associated with Cardiovascular Effects in Healthy Young Men Am. J. Respir. Crit. Care Med., April 15, 2004; 169(8): 934 - 940. [Abstract] [Full Text] [PDF]
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A. Khandoga, A. Stampfl, S. Takenaka, H. Schulz, R. Radykewicz, W. Kreyling, and F. Krombach Ultrafine Particles Exert Prothrombotic but Not Inflammatory Effects on the Hepatic Microcirculation in Healthy Mice In Vivo Circulation, March 16, 2004; 109(10): 1320 - 1325. [Abstract] [Full Text] [PDF]
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N. Agopyan, J. Head, S. Yu, and S. A. Simon TRPV1 receptors mediate particulate matter-induced apoptosis Am J Physiol Lung Cell Mol Physiol, March 1, 2004; 286(3): L563 - L572. [Abstract] [Full Text] [PDF]
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A. Bhatnagar Cardiovascular pathophysiology of environmental pollutants Am J Physiol Heart Circ Physiol, February 1, 2004; 286(2): H479 - H485. [Full Text] [PDF]
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R. L. Johnson Jr Relative Effects of Air Pollution on Lungs and Heart Circulation, January 6, 2004; 109(1): 5 - 7. [Full Text] [PDF]
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C. A. Pope III, R. T. Burnett, G. D. Thurston, M. J. Thun, E. E. Calle, D. Krewski, and J. J. Godleski Cardiovascular Mortality and Long-Term Exposure to Particulate Air Pollution: Epidemiological Evidence of General Pathophysiological Pathways of Disease Circulation, January 6, 2004; 109(1): 71 - 77. [Abstract] [Full Text] [PDF]
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H C Routledge, J G Ayres, and J N Townend Why cardiologists should be interested in air pollution Heart, December 1, 2003; 89(12): 1383 - 1388. [Abstract] [Full Text] [PDF]
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A. Nemmar, B. Nemery, P. H. M. Hoet, J. Vermylen, and M. F. Hoylaerts Pulmonary Inflammation and Thrombogenicity Caused by Diesel Particles in Hamsters: Role of Histamine Am. J. Respir. Crit. Care Med., December 1, 2003; 168(11): 1366 - 1372. [Abstract] [Full Text] [PDF]
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J. Sullivan, N. Ishikawa, L. Sheppard, D. Siscovick, H. Checkoway, and J. Kaufman Exposure to Ambient Fine Particulate Matter and Primary Cardiac Arrest among Persons With and Without Clinically Recognized Heart Disease Am. J. Epidemiol., March 15, 2003; 157(6): 501 - 509. [Abstract] [Full Text] [PDF]
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A. Nemmar, P. H.M. Hoet, D. Dinsdale, J. Vermylen, M. F. Hoylaerts, and B. Nemery Diesel Exhaust Particles in Lung Acutely Enhance Experimental Peripheral Thrombosis Circulation, March 4, 2003; 107(8): 1202 - 1208. [Abstract] [Full Text] [PDF]
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P. K. Shah Mechanisms of plaque vulnerability and rupture J. Am. Coll. Cardiol., February 19, 2003; 41(4_Suppl_S): 15S - 22S. [Abstract] [Full Text] [PDF]
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U. P. Kodavanti, C. F. Moyer, A. D. Ledbetter, M. C. Schladweiler, D. L. Costa, R. Hauser, D. C. Christiani, and A. Nyska Inhaled Environmental Combustion Particles Cause Myocardial Injury in the Wistar Kyoto Rat Toxicol. Sci., February 1, 2003; 71(2): 237 - 245. [Abstract] [Full Text] [PDF]
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U. P. Kodavanti, M. C. J. Schladweiler, A. D. Ledbetter, R. Hauser, D. C. Christiani, J. M. Samet, J. McGee, J. H. Richards, and D. L. Costa Pulmonary and Systemic Effects of Zinc-Containing Emission Particles in Three Rat Strains: Multiple Exposure Scenarios Toxicol. Sci., November 1, 2002; 70(1): 73 - 85. [Abstract] [Full Text] [PDF]
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