(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.
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Abstract |
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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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Introduction |
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Epidemiological analyses throughout the world have shown that high 24-hour average levels of ambient particulate air pollution are associated with an increase in all-cause, respiratory, and cardiovascular disease mortality1 2 3 4 ; nevertheless, little information is available on the effect of shorter-term exposures. The harmful effects of elevation of ambient concentrations of particulate matter are well documented in multiple studies of hospital admissions and emergency department visits for respiratory diseases.1 4 In addition, increased hospital admissions for cardiovascular diseases have been associated with particulate air pollution in studies of numerous American, Canadian, and European cities.5 6 7 8 9 These results indicate that ambient particulate air pollution is a risk factor not only for respiratory diseases but also for acute cardiovascular events.
Inhaled particles could lead to acute exacerbation of cardiovascular disease through pulmonary inflammation triggering systemic hypercoagulability.10 Increases in plasma viscosity11 and C-reactive protein12 were observed in randomly selected healthy adults after episodes of high particulate air pollution. Increased heart rate,13 14 decreased heart rate variability,15 16 17 and increased risk of implanted cardioverter-defibrillator discharges18 associated with episodes of particulate air pollution indicate an autonomic nervous system response.
The US Environmental Protection Agency has promulgated a new ambient air quality standard for fine particles (particulate matter <2.5 µm aerodynamic diameter, PM2.5).19 This new standard regulates 24-hour and annual average concentrations and does not address transient elevations (minutes to hours) in fine-particle concentration. There are no published data on the risk of myocardial infarction (MI) in human populations after transient exposures to elevated concentrations of ambient fine particles.
We therefore evaluated the effect of short-term exposure to fine-particulate air pollution on the risk of acute MIs, comparing data from the Determinants of Myocardial Infarction Onset Study (Onset Study) with hourly measurements of fine particles in Boston. We used a case-crossover design20 21 to specifically assess the risk of exposure to high levels of PM2.5 and the timing of the impact of this exposure on the onset of MI.
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Methods |
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Study Design
The design of the Onset Study has been described in detail elsewhere.20 21 22 23 In brief, we used a case-crossover study design to assess the change in risk of acute MI during a brief "hazard period" after exposure to potential triggers of MI onset. An important feature of the case-crossover design is that control information for each patient is based on his or her own past exposure experience. Self-matching results in freedom from confounding by risk factors that are stable over time within an individual but often differ between study subjects.
Patient Population
The Onset Study is a multicenter case-crossover study
conducted between 1989 and 1996 in 64 centers throughout the United
States.24 Participants were
interviewed a median of 4 days after their MI. We analyzed data
from 772 Onset Study participants living in the greater Boston area
collected between January 20, 1995, and May 25, 1996. Data were
collected in 6 centers with 
50 cases (455 cases), 6 centers with 25
to 49 cases (209 cases), and 14 centers with <25 cases (108
cases).
Interviewers identified eligible cases by reviewing
coronary care unit admission logs and patients’ charts. For
inclusion in the study, patients were required to meet all of the
following criteria: symptom onset while in the greater Boston area, 1
creatine kinase level above the upper limit of normal for the clinical
laboratory performing the test, positive MB isoenzymes, an identifiable
onset of pain or other symptoms typical of infarction, and the ability
to complete a structured interview. The protocol was approved by the
Institutional Review Board at each participating center, and informed
consent was obtained from each patient.
Detailed chart reviews and patient interviews were conducted by trained research personnel.22 23 Data were collected on standard demographic variables as well as risk factors for coronary artery disease. The interview identified the time, place, and characteristics of MI pain and other symptoms.
Air Pollution Measurements
Daily air pollution measurements were collected at a
Harvard School of Public Health–operated monitoring site in South
Boston starting January 15,
1995.18
PM2.5 and PM10
concentrations were measured continuously with a Tapered Element
Oscillating Microbalance (Rupprecht and Patashnick model 1400A TEOM).
Elemental carbon concentration was determined continuously with an
Aethalometer (Magee Scientific Inc), a light-absorption method to
measure "black carbon." Ozone concentration was measured
with a UV photometer analyzer (TECO model 49, Thermal
Environmental). CO concentration was measured with a continuous
nondispersive infrared analyzer (Bendix model 8501-5CA).
Relative humidity and temperature were measured continuously (Vaisala
model MP113Y). The Massachusetts Department of Environmental Protection
measured concentrations of sulfur dioxide and nitrogen dioxide hourly
in Chelsea, which is 
7.5 km north of the South Boston site. We
calculated 24-hour mean values when 16 valid hourly measurements were
available.
Statistical Analyses
The analysis of case-crossover data is an
application of standard methods for stratified data
analysis.20 21
The stratifying variable is the individual patient, as in a
crossover experiment. For each subject, 1 case period was matched to 3
control periods exactly 24 hours apart. Thus, by matching time of day
for case and control periods, potential confounding by the circadian
pattern of MI onset or diurnal patterns in the air pollution were
controlled.
Conditional logistic regression analyses were used to analyze the data. Exposure to particles and gases were entered into the model as continuous variables. Odds ratios are expressed for a change in air pollution concentrations from the 5th to the 95th percentile for all measurements available. Separate models were constructed to evaluate the impact of hourly and 24-hour average air pollution concentrations on the onset of MI.
We also evaluated the effect of hourly (2-hour average) and daily (24-hour average) exposures jointly in 1 model. Control periods were selected as multiples of 24 hours starting 3 days before the date and time of the onset of the symptoms. In addition, multivariate analyses adjusting for season, day of the week, and meteorological parameters on the same time scales were estimated. The final model included sine and cosine functions with periods of 1 year plus 1/2, 1/3, 1/4, 1/5, and 1/6 of a year. It also included quadratic terms for minimum temperature and relative humidity during the 2-hour and 24-hour period of exposure and an indicator for the day of week. Results are presented as odds ratios (OR) and 95% CI.
The unidirectional case-crossover analyses might be sensitive to trends in the outcome and the exposure.25 26 Therefore, control periods close to the event were chosen to minimize the impact of a potential trend. Particulate air pollution concentrations increased over time (0.4 µg/m3 per 100 days, P=0.0002). Although there was weak evidence of a linear downward trend in the number of cases (-0.05 cases per 100 days, P=0.23), the sampling fraction of cases decreased substantially during 1996. Consequently, a downward bias of the estimates would have been expected. This could be demonstrated by choosing control periods >5 days before the event. The bidirectional design has been shown to give unbiased estimates when full case ascertainment was present.26 Analyses of the present data, however, indicated a bias with the bidirectional design due to incomplete case ascertainment during 1996.
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Results |
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The baseline characteristics of the study population are shown in Table 1
. The distribution of 24-hour average and 1-hour
average concentrations of the particulate and gaseous air pollutants is
presented in
Table 2. PM2.5 and
PM10 were highly correlated, whereas the coarse
fraction of PM10, ie, difference of
PM10 and PM2.5, and the
gaseous pollutants were only moderately correlated with
PM2.5.
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Figures 1 and 2 show results from the conditional logistic
regression models, in which
PM2.5 was entered as a linear continuous
variable. Odds ratios are expressed for an hourly change of 25
µg/m3 in PM2.5
(Figure 1) or a daily change of 20
µg/m3 PM2.5
(Figure 2) corresponding the 5th to 95th percentile intervals
(Table 2
).
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A positive association between the onset of MI and the
concentrations of PM2.5 was observed within the
first 3 hours
(Figure 1) that was statistically significant for the
PM2.5 concentrations 1 hour and 2 hours before
the onset of symptoms of an MI. Exposures before this time period
seemed to have little impact on the risk of acute MI. In addition, a
more delayed response to air pollution was observed when 24-hour
averages of the particles were considered
(Figure 2). A positive association was observed with elevated
concentrations between 24 and 48 hours before the onset of the
symptoms.
A combined analysis considered 2-hour averages
(between 60 and 180 minutes before the onset of symptoms) and 24-hour
averages (between 24 and 48 hours before the onset of the symptoms)
jointly, with pollution levels divided into quintiles
(Table 3). When concentrations of
PM2.5 were elevated immediately before the onset
of symptoms as well as 1 day before the onset of symptoms, the risk of
an MI was increased.
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Table 4 summarizes the association between ambient air
pollution as a continuous measure and the risk of onset of MI. The
estimates of the combined analyses of 2-hour averages and
24-hour averages were larger than the analyses considering the
time periods individually. Statistically significantly elevated risks
of MI were observed for PM2.5. The coarse
fraction of PM10, black carbon, and the gaseous
air pollutants including carbon monoxide, NO2,
SO2, and ozone showed positive associations, but
none were statistically significant.
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A strong seasonal pattern was observed, with increased risks
of MI between May and December. Temperature and humidity immediately
before the onset of symptoms were not associated with the onset of
symptoms, but the 24-hour averages of higher temperatures and lower
humidity 1 day before the onset of symptoms showed an increased risk.
After adjustment for seasonal and meteorological conditions, the
association of PM2.5 with the onset of MI was
sustained
(Table 4).
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Discussion |
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Elevated concentrations of fine particles (PM2.5) were associated with a transient risk of acute MI onset. High 24-hour average concentrations of fine particles were also associated with an elevated risk of MI with a 24-hour delay. The elevated risks during 2 separate time periods appear to be independent of each other. In addition, even changes from low to moderate ambient concentrations were associated with an increased risk of MI, although PM2.5 concentrations were below the new standards.23 Particles >2.5 µm, which consist primarily of resuspended crustal material, showed a substantially smaller association than particles <2.5 µm. Other pollutants, such as black carbon, carbon monoxide, nitrogen dioxide, and sulfur dioxide, showed positive associations, but none of them achieved statistical significance in the single-pollutant multivariate analyses.
These results are consistent with time-series analyses on hospital admissions for cardiac diseases.5 6 7 8 9 Hospital admission data collected for administrative purposes were positively associated with 24-hour average particle mass concentrations collected for regulatory compliance monitoring. The effect of ambient particles on hospital admissions was reported to vary between an immediate response on the same day5 6 7 9 and a 1-day lagged response.8
There are several biological effects of ambient particles that may lead to cardiac events. First, particles deposited in the alveoli lead to activation of cytokine production by alveolar macrophages27 and epithelial cells28 and to recruitment of inflammatory cells.29 Second, increases in plasma viscosity11 and C-reactive protein12 have been observed in randomly selected healthy adults in association with episodes of high particulate air pollution. Third, acceleration of heart rates and diminished heart rate variability in association with air pollution have been documented in elderly persons13 15 16 17 and in a random population sample.14 One study reported that heart rate variability started to decrease within hours of exposure.17 Controlled-exposure experiments in dogs exposed to concentrated ambient particles indicated changes in the ECG within an hour of the onset of exposure.30 Fourth, ambient concentrations of PM2.5 have been associated with ventricular fibrillation and an increased number of therapeutic interventions in patients with implanted cardioverter-defibrillators.18
A proposed mechanism for triggering of MI is that onset occurs when a vulnerable but not necessarily stenotic atherosclerotic plaque disrupts in response to hemodynamic stress; thereafter, hemostatic and vasoconstrictive forces determine whether the resultant thrombus becomes occlusive.31 As reviewed above, particulate air pollution is associated with hemodynamic and hemostatic alterations, which may contribute to MI onset.
Previous studies have shown that physical23 32 and psychological24 stress as well as substances such as cocaine22 can trigger the onset of MI. In this report, we demonstrate that transient exposures to an environmental factor, ie, ambient air pollution, appear to increase the risk of an acute MI.
The available evidence suggests that the mechanisms responsible for the impact of ambient particles on MI may be similar to the mechanisms responsible for triggering by other stressors. If these findings are substantiated, susceptible subgroups could be identified and possible pharmacological interventions could be developed to protect the public from transient exposures to ambient particles, such as that experienced during rush-hour traffic.
Limitations
The case-crossover design controls for chronic risk
factors for MI such as sex, age, and hypertension. Confounding may
occur because of time-varying risk
factors,26 such as time of
day, season, or weather. These potential confounders, however, were
considered in the multivariate
analyses.
Another potential limitation of the study is that only 1 air pollution monitoring site was available. Air pollution measurements throughout the east coast indicate that the elevated concentrations of particulate matter during the summer months are due to regional transport.33 For 11 months, starting in October 1995, concurrent PM2.5 measurements were collected every other day in South Boston and 3 other sites in eastern Massachusetts. There was high concordance between these 24-hour samples, with Pearson correlation between South Boston and downtown Boston (Beacon Hill, 3 km northwest) of 0.86, Lynn (16 km north) of 0.86, and Brockton (27 km south) of 0.81. On a larger scale, a high correlation (0.76) was found between daily concentrations of fine particles measured at sites 200 km apart in Washington and Philadelphia.33 Data on the correlation between hourly concentrations of fine particles at different locations within a metropolitan area are not available.
Conclusions
Knowledge of the induction time between the exposure to
particulate air pollution and adverse health effects is crucial to
understanding the biological mechanisms responsible for these
associations and to setting of standards that reduce the risk for the
population. The present study suggests that elevated concentrations
of fine particles may transiently increase the risk of MI for several
hours as well as for several days after exposure. As a consequence,
24-hour averages might underestimate the association between air
pollution and acute cardiovascular
events.
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Acknowledgments |
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The Determinants of Myocardial Infarction Onset Study was supported by grants from the National Heart, Lung, and Blood Institute (HL-41016) and the American Heart Association (9630115N). Dr Peters was supported in part by HEI Research Agreement 98-1. Dr Dockery was supported in part by Enivornmental Protection Agency grant R827353 and National Institute of Environmental Health Sciences grant ES 00002. The authors acknowledge the access to the air pollution data and advice of Dr Petros Koutrakis, George Allen, and Annie Oh of the Harvard School of Public Health Department of Environmental Health.
Received July 12, 2000; revision received March 19, 2001; accepted March 28, 2001.
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References |
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|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Bascom R, Bromberg PA, Costa DA, et al. Health effects of outdoor air pollution. Am J Respir Crit Care Med. 1996;153:3–50.[Abstract]
2.
Katsouyanni K,
Touloumi G, Spix C, et al. Short term effects of ambient sulphur
dioxide and particulate matter on mortality in 12 European cities:
results from time series data from the APHEA project.
BMJ. 1997;314:1658–1663.
3. Schwartz J. Particulate air pollution and daily mortality: a synthesis. Public Health Rev. 1991;19:39–60.[Medline] [Order article via Infotrieve]
4. Pope CA III, Dockery DW. Epidemiology of particle effects. In: Holgate ST, Samet JM, Koren HS, et al, eds. Air Pollution and Health. San Diego, Calif: Academic Press; 1999:673–705.
5.
Burnett RT, Dales
R, Krewski D, et al. Associations between ambient particulate sulfate
and admissions to Ontario hospitals for cardiac and respiratory
diseases. Am J Epidemiol. 1995;142:15–22.
6.
Schwartz J, Morris
R. Air pollution and hospital admissions for
cardiovascular disease in Detroit, Michigan.
Am J Epidemiol. 1995;142:23–35.
7. Schwartz J. Air pollution and hospital admissions for cardiovascular disease in Tucson. Epidemiology. 1997;8:371–377.[Medline] [Order article via Infotrieve]
8.
Poloniecki JD,
Atkinson RW, Anderson HR. Daily time series for
cardiovascular hospital admissions and previous day’s
air pollution in London, UK. Occup Environ
Med. 1997;54:535–540.
9. Schwartz J. Air pollution and hospital admissions for heart disease in eight US counties. Epidemiology. 1999;10:17–22.[Medline] [Order article via Infotrieve]
10. Seaton A, MacNee W, Donaldson K, et al. Particulate air pollution and acute health effects. Lancet. 1995;345:176–178.[Medline] [Order article via Infotrieve]
11. Peters A, Döring A, Wichmann HE, et al. Increased plasma viscosity during the 1985 air pollution episode: a link to mortality? Lancet. 1997;349:1582–1587.[Medline] [Order article via Infotrieve]
12. Peters A, Fröhlich M, Döring A, et al. Particulate air pollution is associated with an acute phase response in men. Eur Heart J. In press.
13.
Pope CA III,
Dockery DW, Kanner RE, et al. Oxygen saturation, pulse rate, and
particulate air pollution. Am J
Respir Crit Care Med. 1999;159:365–372.
14.
Peters A, Perz S,
Döring A, et al. Increases in heart rate during an air pollution
episode. Am J Epidemiol. 1999;150:1094–1098.
15. Liao D, Creason J, Shy CM, et al. Daily variation of particulate air pollution and poor cardiac autonomic control in the elderly. Environ Health Perspect. 1999;107:521–525.[Medline] [Order article via Infotrieve]
16. Pope CA III, Verrier RL, Lovett EG, et al. Heart rate variability associated with particulate air pollution. Am Heart J. 1999;138:890–899.[Medline] [Order article via Infotrieve]
17.
Gold DR, Litonjua
A, Schwartz J, et al. The relationship between particulate pollution
and heart rate variability.
Circulation. 2000;101:1267–1273.
18. Peters A, Verrier RL, Schwartz J, et al. Air pollution and incidences of cardiac arrhythmia. Epidemiology. 2000;11:11–17.[Medline] [Order article via Infotrieve]
19. EPA. National Ambient Air Quality Standards for Particulate Matter. Washington DC: Environmental Protection Agency; 1997.
20.
Maclure M. The
case-crossover design: a method for studying transient effects on the
risk of acute events. Am J
Epidemiol. 1991;133:144–153.
21.
Mittleman MA,
Maclure M, Robins JM. Control sampling strategies for case-crossover
studies: an assessment of relative efficiency.
Am J Epidemiol. 1995;142:91–98.
22.
Mittleman MA,
Maclure M, Tofler GH, et al. Triggering of acute myocardial infarction
by heavy physical exertion: protection against triggering by regular
exertion. Determinants of Myocardial Infarction Onset Study
Investigators. N Engl J
Med. 1993;329:1677–1683.
23.
Mittleman MA,
Maclure M, Sherwood JB, et al. Triggering of acute myocardial
infarction onset by episodes of anger. Determinants of Myocardial
Infarction Onset Study Investigators.
Circulation. 1995;92:1720–1725.
24.
Mittleman MA,
Mintzer D, Maclure M, et al. Triggering of myocardial infarction by
cocaine. Circulation. 1999;99:2737–2741.
25. Navidi W. Bidirectional case-crossover designs for exposures with time trends. Biometrics. 1998;54:596–605.[Medline] [Order article via Infotrieve]
26. Bateson TF, Schwartz J. Control for seasonal variation and time trend in case crossover studies of acute effects of environmental exposures. Epidemiology. 1999;10:539–544.[Medline] [Order article via Infotrieve]
27. Crystal RG. Alveolar macrophages. In: Crystal RG, West JB, eds. The Lung. New York, NY: Raven Press, Ltd; 1991:527–535.
28. Finkelstein JN, Johnston CJ, Barrett T, et al. Particulate-cell interactions and pulmonary cytokine expression. Environ Health Perspect. 1997;105(suppl 5):1179–1182.
29. Driscoll KE, Carter JM, Hassenbein DG, et al. Cytokines and particle-induced inflammatory cell recruitment. Environ Health Perspect. 1997;105(suppl 5):1159–1164.
30. Godleski JJ, Verrier RL, Koutrakis P, et al. Mechanisms of morbidity und mortality from exposure to ambient air particles. Res Rep Health Eff Inst. 2000;91:5–88.
31. Muller JE, Abela GS, Nesto RW, et al. Triggers, acute risk factors and vulnerable plaques: the lexicon of a new frontier. J Am Coll Cardiol. 1994;23:809–813.[Abstract]
32.
Willich SN, Lewis
M, Lowel H, et al. Physical exertion as a trigger of acute myocardial
infarction: Triggers and Mechanisms of Myocardial Infarction Study
Group. N Engl J Med. 1993;329:1684–1690.
33. Spengler JD, Koutrakis P, Dockery DW, et al. Health effects of acid aerosols on North American children: air pollution exposures. Environ Health Perspect. 1996;104:492–499. [Medline] [Order article via Infotrieve]
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 H. Hwang, R. A. Kloner, M. T. Kleinman, and B. Z. Simkhovich Direct and Acute Cardiotoxic Effects of Ultrafine Air Pollutants in Spontaneously Hypertensive Rats and Wistar--Kyoto Rats Journal of Cardiovascular Pharmacology and Therapeutics, September 1, 2008; 13(3): 189 - 198. [Abstract] [PDF]
|
|
|
|
 |
|
 B. Z. Simkhovich, M. T. Kleinman, and R. A. Kloner Air Pollution and Cardiovascular Injury: Epidemiology, Toxicology, and Mechanisms J. Am. Coll. Cardiol., August 26, 2008; 52(9): 719 - 726. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. G. Tankersley, H. C. Champion, E. Takimoto, K. Gabrielson, D. Bedja, V. Misra, H. El-Haddad, R. Rabold, and W. Mitzner Exposure to inhaled particulate matter impairs cardiac function in senescent mice Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2008; 295(1): R252 - R263. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. V. Diez Roux, A. H. Auchincloss, T. G. Franklin, T. Raghunathan, R. G. Barr, J. Kaufman, B. Astor, and J. Keeler Long-term Exposure to Ambient Particulate Matter and Prevalence of Subclinical Atherosclerosis in the Multi-Ethnic Study of Atherosclerosis Am. J. Epidemiol., March 15, 2008; 167(6): 667 - 675. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Araujo, B. Barajas, M. Kleinman, X. Wang, B. J. Bennett, K. W. Gong, M. Navab, J. Harkema, C. Sioutas, A. J. Lusis, et al. Ambient Particulate Pollutants in the Ultrafine Range Promote Early Atherosclerosis and Systemic Oxidative Stress Circ. Res., March 14, 2008; 102(5): 589 - 596. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
U P Santos, M Terra-Filho, C A Lin, L A A Pereira, T C B Vieira, P H N Saldiva, and A L F Braga Cardiac arrhythmia emergency room visits and environmental air pollution in Sao Paulo, Brazil J Epidemiol Community Health, March 1, 2008; 62(3): 267 - 272. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. N. Krivoshto, J. R. Richards, T. E. Albertson, and R. W. Derlet The Toxicity of Diesel Exhaust: Implications for Primary Care J Am Board Fam Med, January 1, 2008; 21(1): 55 - 62. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. L. Baker, A. Gupta, M. L. Clark, B. R. Valenzuela, L. M. Staska, S. J. Harbo, J. T. Pierce, and J. A. Dill Inhalation Toxicity and Lung Toxicokinetics of C60 Fullerene Nanoparticles and Microparticles Toxicol. Sci., January 1, 2008; 101(1): 122 - 131. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. L. Mills, H. Tornqvist, M. C. Gonzalez, E. Vink, S. D. Robinson, S. Soderberg, N. A. Boon, K. Donaldson, T. Sandstrom, A. Blomberg, et al. Ischemic and Thrombotic Effects of Dilute Diesel-Exhaust Inhalation in Men with Coronary Heart Disease N. Engl. J. Med., September 13, 2007; 357(11): 1075 - 1082. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A. Mittleman Air Pollution, Exercise, and Cardiovascular Risk N. Engl. J. Med., September 13, 2007; 357(11): 1147 - 1149. [Full Text] [PDF]
|
|
|
|
 |
|
 H. Tornqvist, N. L. Mills, M. Gonzalez, M. R. Miller, S. D. Robinson, I. L. Megson, W. MacNee, K. Donaldson, S. Soderberg, D. E. Newby, et al. Persistent Endothelial Dysfunction in Humans after Diesel Exhaust Inhalation Am. J. Respir. Crit. Care Med., August 15, 2007; 176(4): 395 - 400. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Peters When a Myocardial Infarction Comes Out of the Not-So-Blue Air Circulation, December 5, 2006; 114(23): 2430 - 2431. [Full Text] [PDF]
|
|
|
|
|
|
C. A. Pope III, J. B. Muhlestein, H. T. May, D. G. Renlund, J. L. Anderson, and B. D. Horne Ischemic Heart Disease Events Triggered by Short-Term Exposure to Fine Particulate Air Pollution Circulation, December 5, 2006; 114(23): 2443 - 2448. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Shimada, N. Kawamura, M. Okajima, T. Kaewamatawong, H. Inoue, and T. Morita Translocation Pathway of the Intratracheally Instilled Ultrafine Particles from the Lung into the Blood Circulation in the Mouse Toxicol Pathol, December 1, 2006; 34(7): 949 - 957. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P Dilaveris, A Synetos, G Giannopoulos, E Gialafos, A Pantazis, and C Stefanadis CLimate Impacts on Myocardial infarction deaths in the Athens TErritory: the CLIMATE study Heart, December 1, 2006; 92(12): 1747 - 1751. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. M. PETERS, D. OTT, and P. T. O'SHAUGHNESSY Comparison of the Grimm 1.108 and 1.109 Portable Aerosol Spectrometer to the TSI 3321 Aerodynamic Particle Sizer for Dry Particles Ann. Hyg., November 1, 2006; 50(8): 843 - 850. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Zanobetti and J. Schwartz Air pollution and emergency admissions in Boston, MA. J Epidemiol Community Health, October 1, 2006; 60(10): 890 - 895. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Maitre, V. Bonneterre, L. Huillard, P. Sabatier, and R. de Gaudemaris Impact of urban atmospheric pollution on coronary disease Eur. Heart J., October 1, 2006; 27(19): 2275 - 2284. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Bhatnagar Environmental Cardiology: Studying Mechanistic Links Between Pollution and Heart Disease Circ. Res., September 29, 2006; 99(7): 692 - 705. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Schwartz Invited Commentary: Ripeness Is All Am. J. Epidemiol., September 1, 2006; 164(5): 434 - 436. [Full Text] [PDF]
|
|
|
|
 |
|
 E. Andre, T. Stoeger, S. Takenaka, M. Bahnweg, B. Ritter, E. Karg, B. Lentner, C. Reinhard, H. Schulz, and M. Wjst Inhalation of ultrafine carbon particles triggers biphasic pro-inflammatory response in the mouse lung Eur. Respir. J., August 1, 2006; 28(2): 275 - 285. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Wiebert, A. Sanchez-Crespo, J. Seitz, R. Falk, K. Philipson, W. G. Kreyling, W. Moller, K. Sommerer, S. Larsson, and M. Svartengren Negligible clearance of ultrafine particles retained in healthy and affected human lungs Eur. Respir. J., August 1, 2006; 28(2): 286 - 290. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z. Li, X. Hyseni, J. D. Carter, J. M. Soukup, L. A. Dailey, and Y.-C. T. Huang Pollutant particles enhanced H2O2 production from NAD(P)H oxidase and mitochondria in human pulmonary artery endothelial cells Am J Physiol Cell Physiol, August 1, 2006; 291(2): C357 - C365. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Cozzi, S. Hazarika, H. W. Stallings III, W. E. Cascio, R. B. Devlin, R. M. Lust, C. J. Wingard, and M. R. Van Scott Ultrafine particulate matter exposure augments ischemia-reperfusion injury in mice Am J Physiol Heart Circ Physiol, August 1, 2006; 291(2): H894 - H903. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G.B. J. Mancini, M. Etminan, B. Zhang, L. E. Levesque, J. M. FitzGerald, and J. M. Brophy Reduction of Morbidity and Mortality by Statins, Angiotensin-Converting Enzyme Inhibitors, and Angiotensin Receptor Blockers in Patients With Chronic Obstructive Pulmonary Disease J. Am. Coll. Cardiol., June 20, 2006; 47(12): 2554 - 2560. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Thomson, P. Kumarathasan, and R. Vincent Pulmonary Expression of PreproET-1 and PreproET-3 mRNAs Is Altered Reciprocally in Rats After Inhalation of Air Pollutants Exp Biol Med, June 1, 2006; 231(6): 979 - 984. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. B. Low, L. Bielory, A. I. Qureshi, V. Dunn, D. F.E. Stuhlmiller, and D. A. Dickey The Relation of Stroke Admissions to Recent Weather, Airborne Allergens, Air Pollution, Seasons, Upper Respiratory Infections, and Asthma Incidence, September 11, 2001, and Day of the Week Stroke, April 1, 2006; 37(4): 951 - 957. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Murakami and M. Ono Myocardial infarction deaths after high level exposure to particulate matter. J Epidemiol Community Health, March 1, 2006; 60(3): 262 - 266. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Ruckerl, A. Ibald-Mulli, W. Koenig, A. Schneider, G. Woelke, J. Cyrys, J. Heinrich, V. Marder, M. Frampton, H. E. Wichmann, et al. Air Pollution and Markers of Inflammation and Coagulation in Patients with Coronary Heart Disease Am. J. Respir. Crit. Care Med., February 15, 2006; 173(4): 432 - 441. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H C Routledge, S Manney, R M Harrison, J G Ayres, and J N Townend Effect of inhaled sulphur dioxide and carbon particles on heart rate variability and markers of inflammation and coagulation in human subjects Heart, February 1, 2006; 92(2): 220 - 227. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. L. Mills, H. Tornqvist, S. D. Robinson, M. Gonzalez, K. Darnley, W. MacNee, N. A. Boon, K. Donaldson, A. Blomberg, T. Sandstrom, et al. Diesel Exhaust Inhalation Causes Vascular Dysfunction and Impaired Endogenous Fibrinolysis Circulation, December 20, 2005; 112(25): 3930 - 3936. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Forastiere, M. Stafoggia, S. Picciotto, T. Bellander, D. D'Ippoliti, T. Lanki, S. von Klot, F. Nyberg, P. Paatero, A. Peters, et al. A Case-Crossover Analysis of Out-of-Hospital Coronary Deaths and Air Pollution in Rome, Italy Am. J. Respir. Crit. Care Med., December 15, 2005; 172(12): 1549 - 1555. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Schwartz, S. K. Park, M. S. O'Neill, P. S. Vokonas, D. Sparrow, S. Weiss, and K. Kelsey Glutathione-S-Transferase M1, Obesity, Statins, and Autonomic Effects of Particles: Gene-by-Drug-by-Environment Interaction Am. J. Respir. Crit. Care Med., December 15, 2005; 172(12): 1529 - 1533. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Maheswaran, R. P. Haining, P. Brindley, J. Law, T. Pearson, P. R. Fryers, S. Wise, and M. J. Campbell Outdoor air pollution, mortality, and hospital admissions from coronary heart disease in Sheffield, UK: a small-area level ecological study Eur. Heart J., December 1, 2005; 26(23): 2543 - 2549. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. A. Wellenius, J. Schwartz, and M. A. Mittleman Air Pollution and Hospital Admissions for Ischemic and Hemorrhagic Stroke Among Medicare Beneficiaries Stroke, December 1, 2005; 36(12): 2549 - 2553. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. von Klot, A. Peters, P. Aalto, T. Bellander, N. Berglind, D. D'Ippoliti, R. Elosua, A. Hormann, M. Kulmala, T. Lanki, et al. Ambient Air Pollution Is Associated With Increased Risk of Hospital Cardiac Readmissions of Myocardial Infarction Survivors in Five European Cities Circulation, November 15, 2005; 112(20): 3073 - 3079. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. Campen, N. S. Babu, G. A. Helms, S. Pett, J. Wernly, R. Mehran, and J. D. McDonald Nonparticulate Components of Diesel Exhaust Promote Constriction in Coronary Arteries from ApoE-/- Mice Toxicol. Sci., November 1, 2005; 88(1): 95 - 102. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. M. Kipen and D. L. Laskin Smaller is not always better: nanotechnology yields nanotoxicology Am J Physiol Lung Cell Mol Physiol, November 1, 2005; 289(5): L696 - L697. [Full Text] [PDF]
|
|
|
|
|
|
E. Thomson, P. Kumarathasan, P. Goegan, R. A. Aubin, and R. Vincent Differential Regulation of the Lung Endothelin System by Urban Particulate Matter and Ozone Toxicol. Sci., November 1, 2005; 88(1): 103 - 113. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A Zeka, A Zanobetti, and J Schwartz Short term effects of particulate matter on cause specific mortality: effects of lags and modification by city characteristics Occup. Environ. Med., October 1, 2005; 62(10): 718 - 725. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R-S Koskela, P Mutanen, J-A Sorsa, and M Klockars Respiratory disease and cardiovascular morbidity Occup. Environ. Med., September 1, 2005; 62(9): 650 - 655. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Kunzli and C. Schindler A call for reporting the relevant exposure term in air pollution case-crossover studies J Epidemiol Community Health, June 1, 2005; 59(6): 527 - 530. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J H Sullivan, A B Schreuder, C A Trenga, S L-J Liu, T V Larson, J Q Koenig, and J D Kaufman Association between short term exposure to fine particulate matter and heart rate variability in older subjects with and without heart disease Thorax, June 1, 2005; 60(6): 462 - 466. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. M Silva, N. Corson, A. Elder, and G. Oberdorster The Rat Ear Vein Model for Investigating In Vivo Thrombogenicity of Ultrafine Particles (UFP) Toxicol. Sci., June 1, 2005; 85(2): 983 - 989. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. H. R. F. Rivero, S. R. C. Soares, G. Lorenzi-Filho, M. Saiki, J. J. Godleski, L. Antonangelo, M. Dolhnikoff, and P. H. N. Saldiva Acute Cardiopulmonary Alterations Induced by Fine Particulate Matter of Sao Paulo, Brazil Toxicol. Sci., June 1, 2005; 85(2): 898 - 905. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Nemmar, B. Nemery, P. H. M. Hoet, N. Van Rooijen, and M. F. Hoylaerts Silica Particles Enhance Peripheral Thrombosis: Key Role of Lung Macrophage-Neutrophil Cross-Talk Am. J. Respir. Crit. Care Med., April 15, 2005; 171(8): 872 - 879. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. F. van Eeden, A. Yeung, K. Quinlam, and J. C. Hogg Systemic Response to Ambient Particulate Matter: Relevance to Chronic Obstructive Pulmonary Disease Proceedings of the ATS, April 1, 2005; 2(1): 61 - 67. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Issever, R. Disci, B. Hapcioglu, S. Vatansever, M. A. Karan, V. Akkaya, and O. Erk The Effect of Air Pollution and Meteorological Parameters in Istanbul on Hospital Admissions for Acute Coronary Syndrome Indoor and Built Environment, April 1, 2005; 14(2): 157 - 164. [Abstract] [PDF]
|
|
|
|
 |
|
 L. D. Frank and P. Engelke Multiple Impacts of the Built Environment on Public Health: Walkable Places and the Exposure to Air Pollution International Regional Science Review, April 1, 2005; 28(2): 193 - 216. [Abstract] [PDF]
|
|
|
|
 |
|
 P. C. Strike and A. Steptoe Behavioral and Emotional Triggers of Acute Coronary Syndromes: A Systematic Review and Critique Psychosom Med, March 1, 2005; 67(2): 179 - 186. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. C. Tosteson, D. S. Greenbaum, B. Lebwohl, and P. H. Stone Traffic and Myocardial Infarction N. Engl. J. Med., February 10, 2005; 352(6): 623 - 624. [Full Text] [PDF]
|
|
|
|
|
|
J.-B. Ruidavets, M. Cournot, S. Cassadou, M. Giroux, M. Meybeck, and J. Ferrieres Ozone Air Pollution Is Associated With Acute Myocardial Infarction Circulation, February 8, 2005; 111(5): 563 - 569. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
U. de Paula Santos, A. L. F. Braga, D. M. A. Giorgi, L. A. A. Pereira, C. J. Grupi, C. A. Lin, M. A. Bussacos, D. M. T. Zanetta, P. H. do Nascimento Saldiva, and M. T. Filho Effects of air pollution on blood pressure and heart rate variability: a panel study of vehicular traffic controllers in the city of Sao Paulo, Brazil Eur. Heart J., January 2, 2005; 26(2): 193 - 200. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Peters, S. von Klot, M. Heier, I. Trentinaglia, A. Hormann, H. E. Wichmann, H. Lowel, and the Cooperative Health Research in the Region of A Exposure to Traffic and the Onset of Myocardial Infarction N. Engl. J. Med., October 21, 2004; 351(17): 1721 - 1730. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
A. Bhatnagar Cardiovascular pathophysiology of environmental pollutants Am J Physiol Heart Circ Physiol, February 1, 2004; 286(2): H479 - H485. [Full Text] [PDF]
|
|
|
|
|
|
R. L. Johnson Jr Relative Effects of Air Pollution on Lungs and Heart Circulation, January 6, 2004; 109(1): 5 - 7. [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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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