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(Circulation. 2001;103:2810.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
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.
BackgroundElevated 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 ResultsWe 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).
ConclusionsThe 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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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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A Le Tertre, S Medina, E Samoli, B Forsberg, P Michelozzi, A Boumghar, J M Vonk, A Bellini, R Atkinson, J G Ayres, et al. Short-term effects of particulate air pollution on cardiovascular diseases in eight European cities J Epidemiol Community Health, October 1, 2002; 56(10): 773 - 779. [Abstract] [Full Text] [PDF] |
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A. Nemmar, M. F. Hoylaerts, P. H. M. Hoet, D. Dinsdale, T. Smith, H. Xu, J. Vermylen, and B. Nemery Ultrafine Particles Affect Experimental Thrombosis in an In Vivo Hamster Model Am. J. Respir. Crit. Care Med., October 1, 2002; 166(7): 998 - 1004. [Abstract] [Full Text] |
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R. L. Verrier, M. A. Mittleman, and P. H. Stone Air Pollution: An Insidious and Pervasive Component of Cardiac Risk Circulation, August 20, 2002; 106(8): 890 - 892. [Full Text] [PDF] |
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W. D. Bennett, A. Nemmar, H. Vanbilloen, M. F. Hoylaerts, P. H. M. Hoet, A. Verbruggen, and B. Nemery Rapid translocation of nanoparticles from the lung to the bloodstream? Am. J. Respir. Crit. Care Med., June 15, 2002; 165(12): 1671 - 1672. [Full Text] [PDF] |
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