Exposure to Traffic and the Onset of Myocardial Infarction
Annette Peters, Ph.D., Stephanie von Klot, M.P.H., Margit Heier, M.D., Ines Trentinaglia, B.S., Allmut Hörmann, M.S., H. Erich Wichmann, M.D., Ph.D., Hannelore Löwel, M.D., for the Cooperative Health Research in the Region of Augsburg Study Group
Background An association between exposure to vehicular trafficin urban areas and the exacerbation of cardiovascular diseasehas been suggested in previous studies. This study was designedto assess whether exposure to traffic can trigger myocardialinfarction.
Methods We conducted a case–crossover study in which casesof myocardial infarction were identified with the use of datafrom the Cooperative Health Research in the Region of AugsburgMyocardial Infarction Registry in Augsburg, in southern Germany,for the period from February 1999 to July 2001. There were 691subjects for whom the date and time of the myocardial infarctionwere known who had survived for at least 24 hours after theevent, completed the registry's standardized interview, andprovided information on factors that may have triggered themyocardial infarction. Data on subjects' activities during thefour days preceding the onset of symptoms were collected withthe use of patient diaries.
Results An association was found between exposure to trafficand the onset of a myocardial infarction within one hour afterward(odds ratio, 2.92; 95 percent confidence interval, 2.22 to 3.83;P<0.001). The time the subjects spent in cars, on publictransportation, or on motorcycles or bicycles was consistentlylinked with an increase in the risk of myocardial infarction.Adjusting for the level of exercise on a bicycle or for gettingup in the morning changed the estimated effect of exposure totraffic only slightly (odds ratio for myocardial infarction,2.73; 95 percent confidence interval, 2.06 to 3.61; P<0.001).The subject's use of a car was the most common source of exposureto traffic; nevertheless, there was also an association betweentime spent on public transportation and the onset of a myocardialinfarction one hour later.
Conclusions Transient exposure to traffic may increase the riskof myocardial infarction in susceptible persons.
Myocardial infarction is one of the main causes of death fromcardiovascular disease. A myocardial infarction has a suddenonset, and factors related to lifestyle have been identifiedas potential triggers of myocardial infarction. These includestrenuous exercise,1,2,3 anger,4 and the use of cocaine5 andmarijuana.6 Recently, environmental factors such as elevatedconcentrations of ambient particulate matter have been addedto the list of triggers.7
Traffic is an important concern in urban areas as a potentialrisk factor for cardiovascular disease.8 In a cohort study,the risk of death from cardiopulmonary causes was twice as highamong persons living close to a major road or highway, afteradjustment for risk factors such as age, sex, and smoking status,than among those living farther from a major road or highway.9In addition, case–control studies have indicated thatthe work environment of professional drivers may contributeto their risk for myocardial infarction.10,11
In this study we assessed the association between the onsetof a nonfatal myocardial infarction and exposure to traffic.The study assessed the effect of exposure on the basis of acomplete case series of survivors of myocardial infarction,with the use of the case–crossover method.12 The caseswere drawn from the complete case series of the CooperativeHealth Research in the Region of Augsburg (KORA) MyocardialInfarction Registry in Augsburg, southern Germany, for a periodof 2.5 years. A study diary was used to collect informationon the four days before the onset of symptoms, including informationon the number of hours spent in traffic.
Methods
Study Subjects
We identified 906 cases of nonfatal myocardial infarction inthe KORA registry, of which 691 were included in our study.Hospitalized survivors of myocardial infarction who are 25 to74 years of age are routinely entered into this registry.13Cases are identified daily at the Central Hospital and oncea week at six hospitals in the city of Augsburg and the twoadjacent rural districts and at four hospitals near the studyarea. The diagnosis of a myocardial infarction was made withuse of the algorithm of the World Health Organization's MultinationalMonitoring of Trends and Determinants in Cardiovascular Disease(MONICA) project. The criteria of the algorithm include chestpain lasting more than 20 minutes that is not relieved by theadministration of nitrates and either Q waves on electrocardiographicexamination that suggest an evolving myocardial infarction,subsequent increases in the level of creatine kinase, aspartateaminotransferase, or lactate dehydrogenase to more than twicethe upper limit of normal, or both.
All subjects gave written informed consent for participation;the protocol was approved by the KORA review board. Personswere excluded from the study if they were in poor health (e.g.,if they had a critical illness or were in a moribund condition)and were unable to communicate with the investigators. Interviewstook place on the general ward as soon as possible after theindex event (median, nine days). Data on the sociodemographiccharacteristics, medical history, and smoking status of thesubjects were collected by a trained research nurse as partof the registry's routine interview. After the subject's discharge,clinical data were abstracted from the medical records accordingto a standardized protocol.
The time of onset of the myocardial infarction was defined asthe time of the onset of chest pain that lasted at least 20minutes. In cases of subjects with atypical chest pain (27 subjects)or with other symptoms (17), the time of the severest symptomswas used. Supporting data were retrieved from the patient'smedical record (e.g., a history of symptoms recorded by thephysician in the ambulance or the emergency room). If the dataconflicted, medical reports were considered to be more reliablethan information provided by the patient.
Diary of Activities
The activities of the subjects on the day of the myocardialinfarction and during the four days preceding the symptoms wererecorded by registry nurses in a standardized, interview-baseddiary after completion of the registry's routine interview.Information recorded in the diary included time (hours) spentsleeping, levels of activity during the day, periods spent outdoors,means of transportation, location (according to postal codes)within the study area, the presence or absence of symptoms ofangina pectoris, the occurrence of extreme anger or joy, andany exposure to dust or solvents. Activities occurring within0 and 59 minutes after a particular hour were ascribed to thatparticular hour. The same importance was given to all four dayspreceding the event.
During a pilot phase in which the diary was tested, we interviewed26 patients in the central hospital between October 3 and November13, 1999, and afterward the diary was revised to improve itsclarity, minimize redundancy, and facilitate the statisticalanalysis. Adherence to standardized procedures for the interviewand coding was ensured by careful training of three researchnurses, who had extensive clinical experience with cardiovasculardisease, subsequent routine supervision of the interviews, anda policy of asking the nurses to contact the study investigatorsimmediately in the event of unforeseen problems.
Statistical Analysis
Conditional logistic-regression models were used to assess theassociation between transient exposure to various levels andtypes of traffic and the onset of the myocardial infarction,as proposed by Mittleman and colleagues.14 With the use of descriptiveanalyses, we calculated the frequency of exposure to trafficfor a particular period of time by dividing the number of person-hoursof exposure by the total number of person-hours within thatperiod. For each subject included in the study, one-hour periodsduring the six hours before the onset were selected as the caseperiods. A "control period" of exposure was defined as an exposureto traffic by the same subject 24 to 71 hours before the hourof the onset of the myocardial infarction. Thus, each subjectrepresented a matched set of data for case and control exposures,and different case periods were tested against the set of controlperiods for the same subject. Only subjects for whom there werediscordant sets of data on exposure were included in the analysis— that is, either subjects who were exposed to trafficin the case period but not in a control period, or those whowere not exposed to traffic in the case period but were exposedin a control period.
Results
Patients
Of 906 persons who had a confirmed myocardial infarction andwho survived for at least 24 hours, 215 (23.7 percent) wereunable to provide diary information, information on the hourof the onset of the myocardial infarction, or both (Table 1).The remaining 691 patients with a confirmed myocardial infarction,who were included in the diary study, were predominantly male,and 70 percent of them were 55 years of age or older. For mostof these subjects, this was their first myocardial infarction,and most of them survived to 28 days.
Table 1. Characteristics of Survivors of Myocardial Infarction (MI) Recruited between February 1999 and July 2001, According to Data from the KORA Myocardial Infarction Registry.
Association of Exposure to Traffic and Onset of Myocardial Infarction
Exposure to traffic was more frequent on the day of the onsetof the myocardial infarction (469 person-hours with exposureto traffic out of 8162 person-hours, or 5.7 percent) than duringthe previous three days (for the day before the onset of themyocardial infarction, 756 person-hours of 15,777 person-hours,or 4.8 percent; for the second day before the onset, 670 person-hoursof 14,154 person-hours, or 4.7 percent; and for the third daybefore the onset, 528 person-hours of 11,478 person-hours, or4.6 percent) (Figure 1A and Figure 1B). On the day of the myocardialinfarction, of all the hours the subjects spent in traffic,72 percent were spent in a car, 16 percent on a bicycle, 10percent on public transportation (buses, trolley cars, and trains),and 2 percent on motorcycles. The percentages of hours spentin a vehicle were similar on the four days preceding the dayof the myocardial infarction. One hour before the onset of themyocardial infarction, exposure to traffic was twice as frequentas at any other time (Figure 1C).
Figure 1. The Onset of 691 Nonfatal Myocardial Infarctions (MI) in Relation to Exposure to Traffic, According to the Amount of Time Spent in Traffic, February 1999 to July 2001, in the Region of Augsburg, Germany.
Panel A shows the distribution of times of onset of the myocardial infarctions over the day of the event, Panel B the time subjects spent in traffic on the day of the event and during the three days before it, and Panel C the time spent in traffic during the 72 hours preceding the onset of the myocardial infarction. The percentages are the proportions of subjects with exposure during the hour in question. Data are from the KORA Myocardial Infarction Registry.
Exposure to traffic was associated with an increase by a factorof 2.60 to 3.94 in the risk of the onset of a myocardial infarctionwithin one hour (Table 2). Such exposure was not rare; for example,of the 625 subjects who reported exposure to traffic in thehours before the onset of the myocardial infarction, 75 whowere exposed to traffic one hour before the onset and 375 forwhom there were discordant matched sets of exposure were includedin the analysis (Table 2). The odds ratio for exposure to trafficone hour before a myocardial infarction was 2.73 (95 percentconfidence interval, 2.06 to 3.61) after adjustment for severeexertion, being outside, and getting up in the morning. Theodds ratio associated with severe exertion was 6.38 (95 percentconfidence interval, 3.89 to 10.46); for being outside, 2.21(95 percent confidence interval, 1.61 to 3.03); and for gettingup in the morning, 1.69 (95 percent confidence interval, 1.24to 2.30). The odds ratio associated with travel by bicycle was1.83 (95 percent confidence interval, 0.93 to 3.61) after adjustmentfor severe exertion, being outside, and getting up in the morning.
Table 2. Odds Ratios for the Onset of Myocardial Infarction (MI) after Time Spent in Traffic, According to the Means of Transportation.
Sensitivity Analyses
We used sensitivity analyses to assess whether the results dependedon the selection of the control period, and we compared theresults of the different analyses (Table 2) with the resultsof the final model (Table 3, model A). The estimate was slightlylarger in the sensitivity analysis (Table 3, models B and C)than in the main analysis. Slightly smaller estimates were observedwhen only one control exposure 24 hours before the onset wasincluded in the analysis (Table 3, model D). The equivalentof model D was the analysis of discordant pairs with the useof McNemar's test. The odds ratio of 2.86 was derived by dividing60 cases (of exposure to traffic during the case period butnot during the control period) by 21 cases (of exposure to trafficduring the control period but not during the case period) (P<0.001).The estimated odds ratios were slightly larger if the case–crossoveranalyses made use of three control periods that were matchedwith the case period for time of day (Table 3, models E andF).
Table 3. Sensitivity Analyses of the Effect of Different Control-Selection Strategies on the Association of Exposure to Traffic and the Onset of a Myocardial Infarction (MI).
The patients' differential recall of their activities beforethe onset of the myocardial infarction was a major concern.Information on exposure to traffic for the period from 0 (theonset of myocardial infarction) to –23 hours was availablefor 99 percent of the subjects, for –24 to –47 hoursfor 94 percent, for –48 to –71 hours for 82 percent,and for –72 to –95 hours for 38 percent. To assessthe potential for recall bias within the data, we conductedanalyses within the nonrisk periods defined a priori. We selectedcase periods and control periods from the 24 to 96 hours beforeonset (Table 3, models G through J). No association was observedbetween exposure to traffic and the onset of the myocardialinfarction when case periods 25 hours before onset and controlperiods 49 hours before onset were considered (model G). A nonsignificantelevation in risk (P=0.13) was observed for the case periodof 49 hours before onset and the control period of 73 hoursbefore onset (model H), indicating that recall of activitiesmay be biased 72 to 95 hours before the onset of a myocardialinfarction. Models I and J indicate that with the period consideredin the main analyses, no evidence of differential recall wasfound during control periods.
Subgroup Analyses
Exposure to traffic appeared to be associated with larger risksamong women than among men and among patients 60 years of ageor older than among those younger than 60 (Table 4). Effectestimates were larger for subjects with diabetes and those whowere unemployed, but only employment status significantly modifiedthe association between the risk of a myocardial infarctionand exposure to traffic. The frequency of exposure to trafficdiffered according to the time of day (morning, 8.3 percent;afternoon, 7.1 percent; and night, 0.9 percent; P<0.001)and according to day of the week (Monday, 6.0 percent; Tuesday,5.8 percent; Wednesday, 5.7 percent; Thursday, 4.7 percent;Friday, 5.7 percent; Saturday, 4.4 percent; and Sunday, 2.9percent; P<0.001). Only the time of day showed an effectmodification of borderline significance (Table 4).
Table 4. Subgroup Analyses of the Association of Exposure to Traffic with the Onset of the Myocardial Infarction (MI) within the Next Hour, with Case–Crossover Analyses Restricted to Activities within the Study Area.
Discussion
We observed an association between exposure to traffic whiletraveling in cars, buses, and trolley cars and while ridingon a bicycle or motorcycle and the onset of a myocardial infarctionwithin one hour afterward. Travel in a car was the most commonsource of exposure, but travel by public transportation wasalso associated with the onset of a myocardial infarction withinone hour afterward.
We used a case–crossover design that made possible theassessment of transient risk factors — that is, risk factorsthat may trigger acute events in susceptible patients. Theserisk factors include strenuous exercise,1,2,3 anger,4 and theuse of cocaine5 or marijuana.6 Transient risk factors have onlya short-term effect, whereas chronic risk factors, such as smoking,the presence of dyslipidemia, and a sedentary lifestyle, whichpromote atherosclerosis and prothrombotic conditions and mayresult in an impaired myocardium, have a long-term effect anddetermine vulnerability to acute coronary events.15
By virtue of the case–crossover design, exposure duringthe case periods and the control periods was determined forthe same individual subject. The strategy for selecting thecontrol periods and the potential for recall bias are of primaryconcern in judging the validity of the analyses. We used dataon activities in each hour from the hour of onset of the myocardialinfarction up to 71 hours before onset that were collected bymeans of bedside interviews. We included multiple control periodsand controlled for the time of day in multivariate analyses.The restriction of the comparison to periods at the same timeof day was designed to control for circadian patterns, but ifdaily routines are slightly modified, the restriction mightresult in an underestimation of exposure to traffic during thecontrol periods and might therefore lead to an overestimationof the effect of exposure, as suggested in the sensitivity analyses.The possibility that patients may have better recall of thehours before the onset of the myocardial infarction than ofthe days before the event cannot be excluded. Consequently,an underestimation of exposure to traffic during the controlperiods would have inflated the estimates of the effect of suchexposure as a trigger in individual cases. Sensitivity analysesin which different control-selection strategies were appliedshowed remarkably similar results. Comparison analyses of trafficexposures at nonrisk periods (control periods defined a priori)suggested there was no substantial recall bias with regard tothe periods 24 to 71 hours before the onset of the myocardialinfarction.
In the case–crossover design, conditions that do not varyover time do not induce confounding. Other transient risk factorssuch as strenuous exercise or stress (e.g., anger) might confoundthe associations we observed. However, multivariate analysesinvolving information on other triggers did not produce evidenceof strong within-person confounding. Strenuous activity wasconfirmed as a substantial risk factor for the onset of a myocardialinfarction in this study, as suggested earlier.1,2,3 Ridinga bicycle might be considered strenuous activity; indeed, therisk estimates associated with the use of a bicycle were reducedwhen we controlled for exercise, but there was no change inthe overall effect estimate for exposure to traffic. Studiesthat assessed the role of anger as a trigger for myocardialinfarction identified major life events as potential triggersbut not moderate levels of psychological stress,4 which areinstead related to an elevation in long-term risk.16 The estimatesfor traffic exposure might be confounded by the stress associatedwith getting up in the morning, which is itself a risk factorfor myocardial infarction.2 Getting up in the morning was anindependent risk factor in our study, but it did not confoundthe association between exposure to traffic and the onset ofa myocardial infarction.
The association between exposure to traffic and the onset ofa myocardial infarction was stronger in the subgroup of subjectswho were unemployed than in the subgroup of those who were employed.This finding indicates that the associations we observed werenot due to commuting regularly to work. The subjects in thisstudy used a car for transportation most of the time. We hadno data on whether the individual subject had been driving thecar or on the reasons for driving. Driving in different volumesof traffic might also be a factor to consider. Unfortunately,data on the circumstances of driving could not be collectedreliably in retrospective interviews. However, because the associationwas also observed for persons who used public transportation,it is unlikely that the effect is entirely attributable to thestress linked with driving a car. No evidence for a statisticallysignificant effect modification according to the day of theweek was observed, but the estimated risks were larger for morningand afternoon hours than for night hours, when the density ofthe traffic is low. When only subjects who had no typical oratypical symptoms during the four days before the onset of themyocardial infarction were considered, no difference in theestimates was observed. Therefore, the possible effects of cartrips undertaken to consult a doctor because of an evolvingmyocardial infarction could be ruled out.
Subjects who had had nonfatal myocardial infarctions were recruitedon the basis of the nearly complete records of a myocardial-infarctionregistry.13 Of the cases of myocardial infarction included inthis study, 8 percent were attributable to exposure to traffic.The subgroup analyses indicated that women, persons 60 yearsof age or older, and patients with diabetes are at higher riskfor the onset of a myocardial infarction after exposure to trafficthan are men, persons younger than 60 years of age, and personswithout diabetes. These results suggest that other persons inthe KORA registry who were unable to provide diary informationand who were therefore not included in our study might havebeen more susceptible to the risk of myocardial infarction afterexposure to traffic than the subjects who were included.
A rather crude measure of exposure to traffic was used in thisstudy. Potentially, a combination of different factors, suchas stress, noise, and traffic-related air pollution, may contributeto the observed associations. While persons are driving a car,symptoms of a possible arrhythmia may be common among thosewho are eligible for treatment with an implantable cardiac defibrillator.17Chronic exposure to stress and noise is a well-documented riskfactor for cardiovascular diseases, since such exposure canlead to elevated stress hormone concentrations.18 A recentlypublished study from the Netherlands indicates that among peoplewho live near major roads, the risk of death due to cardiopulmonarydiseases is nearly twice as high as that among those who donot live near major roads.9 An increase in the risk of deathdue to ischemic heart disease has been documented in those whoseoccupations expose them to traffic, such as police officerswho regulate traffic.19 The short-term health effects of airpollution on the cardiovascular system have been studied intensivelyin the past decade. Particulate matter is considered to be ofprimary concern.20,21 Studies of exposure to ambient particleshave indicated that passengers in cars and buses have a greaterexposure than is measured at a distance of 100 m or more fromvehicular traffic.22,23 The concentrations of particulate mattervaried according to the route and the density of the trafficand might resemble concentrations at urban curbsides. For peopletraveling by car or bus, exposure to particulates is about twotimes as high as for cyclists.22,24,25,26 Although high ratesof ventilation increase the amount of particles deposited inthe airways,22,25,26 cyclists may be able to leave congestedsituations (i.e., polluted microenvironments) more quickly thanpeople in cars or buses.22
The disruption of a vulnerable but not necessarily stenoticatherosclerotic plaque in response to hemodynamic stress hasbeen suggested as a mechanism that triggers a myocardial infarction;thereafter, the hemostatic and vasoconstrictive forces determinewhether the resultant thrombus will become occlusive.27 Particulateair pollution has been associated with transient increases inplasma viscosity,28 acute-phase reactants,29,30,31 and endothelialdysfunction,32 as well as with altered autonomic control ofthe heart.33,34,35,36,37 These changes have also been observedin healthy officers of the highway patrol in association withthe concentration of particulate matter in their vehicles38and might be consistent with an increased risk of a myocardialinfarction after a transient elevation in the concentrationsof ambient particles in vulnerable subjects.39
Given our current knowledge, it is impossible to determine therelative contribution of risk factors such as stress and traffic-relatedair pollution. Nevertheless, patients who are at risk for acutecoronary events are likely to profit from recent efforts toimprove the air quality in urban areas with the use of cleanervehicles and improved city planning.
Supported by a research agreement (98-4) with the Health EffectsInstitute, Boston, by the GSF–National Research Centerfor Environment and Health, Neuherberg, Germany, and by a grant(R-827354) from the Environmental Protection Agency (to Drs.Peters and Wichmann).
Source Information
From the Institute of Epidemiology (A.P., S.K., M.H., I.T., H.E.W., H.L.) and the Institute for Health Economics (A.H.), GSF–National Research Center for Environment and Health, Neuherberg; and the Department of Epidemiology, Medical Faculty, Ludwig-Maximilians-Universität, Munich (H.E.W.) — all in Germany.
Address reprint requests to Dr. Peters at the Institute of Epidemiology, GSF–National Research Center for Environment and Health, Ingolstädter Landstr. 1, 87564 Neuherberg, Germany, or at peters{at}gsf.de.
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