Traffic and Myocardial Infarction
http://www.100md.com
《新英格兰医药杂志》
To the Editor: We were pleased to see the article by Peters and colleagues (Oct. 21 issue)1 on exposure to traffic and the onset of myocardial infarction. The work they report is part of a larger study funded by the Health Effects Institute that also includes an analysis of air-pollution data.2 However, we do not agree with Stone's conclusions, in the accompanying Perspective article,3 that the findings reported by Peters et al. "provide compelling epidemiologic evidence that particulate air pollution from traffic may trigger the abrupt onset of acute myocardial infarction." Our interpretation is consistent with Peters and colleagues' more tentative conclusions. In the complete data set,2 ambient air-pollution levels just before the myocardial infarctions are not associated with an increased risk of myocardial infarction, although, as the authors note, the exposures of people in traffic are probably higher than those recorded by ambient monitors.
Although there is broader evidence suggesting links between air pollution and health effects,4 the role of air pollution in triggering myocardial infarction is unresolved. Confirming and extending Peters and colleagues' work will be key to ascertaining the full range of risk factors and providing the best guidance on effective public health interventions.
Daniel C. Tosteson, M.D.
Harvard Medical School
Boston, MA 02115
Daniel S. Greenbaum, M.C.P.
Health Effects Institute
Boston, MA 02129
The Health Effects Institute is an independent, nonprofit institute funded equally by the U.S. Environmental Protection Agency and the motor vehicle industry.
References
Peters A, von Klot S, Heier M, et al. Exposure to traffic and the onset of myocardial infarction. N Engl J Med 2004;351:1721-1730.
Peters A, von Klot S, Heier M, et al. Particulate air pollution, personal activities, and the onset of nonfatal myocardial infarction in a case–crossover study: research report 124. Boston: Health Effects Institute (in press).
Stone PH. Triggering myocardial infarction. N Engl J Med 2004;351:1716-1718.
Brook RD, Franklin B, Cascio W, 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 2004;109:2655-2671.
To the Editor: The intriguing correlation between recent exposure to traffic and the onset of acute myocardial infarction found by Peters et al. is cause for concern, given the role of interhospital transfer in the management of the acute coronary syndrome. Transfer from a local hospital capable of providing thrombolytic therapy alone to a center capable of performing percutaneous coronary intervention is a practice that is gaining currency.1 If the increased transit time to these referral centers exposes patients with ongoing plaque rupture to particulate air pollution, the resultant inflammatory and thrombogenic microenvironment may further injure the at-risk coronary circulation. When considering protocols of interhospital transfer, one must therefore balance the known benefits of percutaneous coronary intervention with our evolving understanding of the risks of exposure to traffic.
Benjamin Lebwohl, M.D.
Columbia University Medical Center
New York, NY 10032
bl114@columbia.edu
References
Jacobs AK. Primary angioplasty for acute myocardial infarction -- is it worth the wait? N Engl J Med 2003;349:798-800.
Dr. Stone replies: Dr. Tosteson and Mr. Greenbaum suggest that the interpretation of Peters and colleagues' analyses should be tentative, in contrast to my statement. However, my assignment was to put their results in the context of other information and thus to form a larger sense of the significance of the study. The observations of Peters et al. are based on data related to exposure to traffic and the onset of myocardial infarction; air-pollution measurements were not included. The evidence that air pollution may be responsible for the onset of myocardial infarction is compelling because of the observation that the risk of myocardial infarction was increased regardless of the means of transportation: car, public transportation, or bicycle or motorcycle. I interpreted these results in the context of supportive, short-term epidemiologic data,1 such as those from the Determinants of Myocardial Infarction Onset Study,2 which showed that the risk of the onset of myocardial infarction increased during the two-hour period of exposure to elevated concentrations of air-pollution particles. Mechanistic studies both in humans and in animals provide a plausible explanation for the relationship between transient changes in air pollution and sudden triggering of myocardial infarction.1
In their letter, Dr. Tosteson and Mr. Greenbaum mention new data suggesting that air-pollution levels just before the myocardial infarctions in the study by Peters et al. were not associated with an increased risk of myocardial infarction. As they note, however, air pollution assessed at a central monitoring site may not be a good surrogate for personal exposure in traffic. I agree that it will be critical to confirm and extend Peters and colleagues' work so that public health policies can be based on the most objective data.
In response to Dr. Lebwohl's comments: it should be emphasized that although the relative risk of the onset of acute myocardial infarction increased after exposure to traffic, the absolute risk was low. For patients with acute myocardial infarction there may be minor risks associated with exposure to traffic during transport, but these risks are outweighed by the documented benefit of mechanical reperfusion in appropriately selected and transported patients.3
Peter H. Stone, M.D.
Brigham and Women's Hospital
Boston, MA 02115
References
Brook RD, Franklin B, Cascio W, 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 2004;109:2655-2671.
Peters A, Dockery DW, Muller JE, Mittleman MA. Increased particular air pollution and the triggering of myocardial infarction. Circulation 2001;103:2810-2815.
Jacobs AK. Primary angioplasty for acute myocardial infarction -- is it worth the wait? N Engl J Med 2003;349:798-800.
Although there is broader evidence suggesting links between air pollution and health effects,4 the role of air pollution in triggering myocardial infarction is unresolved. Confirming and extending Peters and colleagues' work will be key to ascertaining the full range of risk factors and providing the best guidance on effective public health interventions.
Daniel C. Tosteson, M.D.
Harvard Medical School
Boston, MA 02115
Daniel S. Greenbaum, M.C.P.
Health Effects Institute
Boston, MA 02129
The Health Effects Institute is an independent, nonprofit institute funded equally by the U.S. Environmental Protection Agency and the motor vehicle industry.
References
Peters A, von Klot S, Heier M, et al. Exposure to traffic and the onset of myocardial infarction. N Engl J Med 2004;351:1721-1730.
Peters A, von Klot S, Heier M, et al. Particulate air pollution, personal activities, and the onset of nonfatal myocardial infarction in a case–crossover study: research report 124. Boston: Health Effects Institute (in press).
Stone PH. Triggering myocardial infarction. N Engl J Med 2004;351:1716-1718.
Brook RD, Franklin B, Cascio W, 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 2004;109:2655-2671.
To the Editor: The intriguing correlation between recent exposure to traffic and the onset of acute myocardial infarction found by Peters et al. is cause for concern, given the role of interhospital transfer in the management of the acute coronary syndrome. Transfer from a local hospital capable of providing thrombolytic therapy alone to a center capable of performing percutaneous coronary intervention is a practice that is gaining currency.1 If the increased transit time to these referral centers exposes patients with ongoing plaque rupture to particulate air pollution, the resultant inflammatory and thrombogenic microenvironment may further injure the at-risk coronary circulation. When considering protocols of interhospital transfer, one must therefore balance the known benefits of percutaneous coronary intervention with our evolving understanding of the risks of exposure to traffic.
Benjamin Lebwohl, M.D.
Columbia University Medical Center
New York, NY 10032
bl114@columbia.edu
References
Jacobs AK. Primary angioplasty for acute myocardial infarction -- is it worth the wait? N Engl J Med 2003;349:798-800.
Dr. Stone replies: Dr. Tosteson and Mr. Greenbaum suggest that the interpretation of Peters and colleagues' analyses should be tentative, in contrast to my statement. However, my assignment was to put their results in the context of other information and thus to form a larger sense of the significance of the study. The observations of Peters et al. are based on data related to exposure to traffic and the onset of myocardial infarction; air-pollution measurements were not included. The evidence that air pollution may be responsible for the onset of myocardial infarction is compelling because of the observation that the risk of myocardial infarction was increased regardless of the means of transportation: car, public transportation, or bicycle or motorcycle. I interpreted these results in the context of supportive, short-term epidemiologic data,1 such as those from the Determinants of Myocardial Infarction Onset Study,2 which showed that the risk of the onset of myocardial infarction increased during the two-hour period of exposure to elevated concentrations of air-pollution particles. Mechanistic studies both in humans and in animals provide a plausible explanation for the relationship between transient changes in air pollution and sudden triggering of myocardial infarction.1
In their letter, Dr. Tosteson and Mr. Greenbaum mention new data suggesting that air-pollution levels just before the myocardial infarctions in the study by Peters et al. were not associated with an increased risk of myocardial infarction. As they note, however, air pollution assessed at a central monitoring site may not be a good surrogate for personal exposure in traffic. I agree that it will be critical to confirm and extend Peters and colleagues' work so that public health policies can be based on the most objective data.
In response to Dr. Lebwohl's comments: it should be emphasized that although the relative risk of the onset of acute myocardial infarction increased after exposure to traffic, the absolute risk was low. For patients with acute myocardial infarction there may be minor risks associated with exposure to traffic during transport, but these risks are outweighed by the documented benefit of mechanical reperfusion in appropriately selected and transported patients.3
Peter H. Stone, M.D.
Brigham and Women's Hospital
Boston, MA 02115
References
Brook RD, Franklin B, Cascio W, 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 2004;109:2655-2671.
Peters A, Dockery DW, Muller JE, Mittleman MA. Increased particular air pollution and the triggering of myocardial infarction. Circulation 2001;103:2810-2815.
Jacobs AK. Primary angioplasty for acute myocardial infarction -- is it worth the wait? N Engl J Med 2003;349:798-800.