Original Article
Ischemic and Thrombotic Effects of Dilute Diesel-Exhaust Inhalation in Men with Coronary Heart Disease
N Engl J Med 2007; 357:1075-1082September 13, 2007
- Abstract
Background
Exposure to air pollution from traffic is associated with adverse cardiovascular events. The mechanisms for this association are unknown. We conducted a controlled exposure to dilute diesel exhaust in patients with stable coronary heart disease to determine the direct effect of air pollution on myocardial, vascular, and fibrinolytic function.
Methods
In a double-blind, randomized, crossover study, 20 men with prior myocardial infarction were exposed, in two separate sessions, to dilute diesel exhaust (300 μg per cubic meter) or filtered air for 1 hour during periods of rest and moderate exercise in a controlled-exposure facility. During the exposure, myocardial ischemia was quantified by ST-segment analysis using continuous 12-lead electrocardiography. Six hours after exposure, vasomotor and fibrinolytic function were assessed by means of intraarterial agonist infusions.
Results
During both exposure sessions, the heart rate increased with exercise (P<0.001); the increase was similar during exposure to diesel exhaust and exposure to filtered air (P=0.67). Exercise-induced ST-segment depression was present in all patients, but there was a greater increase in the ischemic burden during exposure to diesel exhaust (−22±4 vs. −8±6 millivolt seconds, P<0.001). Exposure to diesel exhaust did not aggravate preexisting vasomotor dysfunction, but it did reduce the acute release of endothelial tissue plasminogen activator (P=0.009; 35% decrease in the area under the curve).
Conclusions
Brief exposure to dilute diesel exhaust promotes myocardial ischemia and inhibits endogenous fibrinolytic capacity in men with stable coronary heart disease. Our findings point to ischemic and thrombotic mechanisms that may explain in part the observation that exposure to combustion-derived air pollution is associated with adverse cardiovascular events. (ClinicalTrials.gov number, NCT00437138.)
Media in This Article
Figure 1
Myocardial Ischemia during 15-Minute Intervals of Exercise-Induced Stress and Exposure to Diesel Exhaust or Filtered Air in the 20 Subjects.Figure 2
Forearm Blood Flow 6 to 8 Hours after Exposures to Diesel Exhaust and Filtered Air.Article Activity
- Article
The World Health Organization (WHO) estimates that air pollution is responsible for 800,000 premature deaths worldwide each year.1 Short-term exposure to air pollution has been associated with increases in cardiovascular morbidity and mortality, with deaths due to ischemia, arrhythmia, and heart failure.2 In a large cohort study from the United States, Miller et al. recently reported that long-term exposure to air pollution increases the risk of death from cardiovascular disease by 76%.3 These associations are strongest for fine particulate air pollutants (particulate matter of less than 2.5 μm in aerodynamic diameter [PM2.5]), of which the combustion-derived nanoparticulate in diesel exhaust is an important component.4 Substantial improvements in air quality have occurred in the developed world over the past 50 years, yet the association between PM2.5 and mortality has no apparent threshold and is evident below current air-quality standards.5
Preclinical models of exposure to particulate air pollution demonstrate accelerated atherosclerotic plaque development6 and increased in vitro7 and in vivo8 platelet aggregation. Epidemiologic and observational clinical studies suggest that exposure to air pollution may worsen symptoms of angina,9 exacerbate exercise-induced myocardial ischemia,10,11 and trigger acute myocardial infarction.12,13 These clinical findings are limited by imprecision in the measurement of pollution exposure, the effect of potential confounding environmental and social factors, and the lack of mechanistic data.14 Controlled exposures to air pollutants can help address these shortcomings by providing a precisely defined exposure in a regulated environment that facilitates investigation with validated biomarkers and surrogate measures of cardiovascular health. Using a carefully characterized exposure system, we have previously shown that exposure to dilute diesel exhaust in healthy volunteers causes lung inflammation,15 depletion of airway antioxidant defenses,16 and impairment of vascular and fibrinolytic function.17
To our knowledge, there have been no controlled exposures in patients with coronary heart disease, an important population that may be particularly susceptible to the adverse cardiovascular effects of air pollution. We assessed the effect of inhalation of dilute diesel exhaust on myocardial, vascular, and fibrinolytic function in a population of patients with stable coronary heart disease.
Methods
Subjects
Twenty men with stable coronary artery disease participated in this study, which was performed with the approval of the local research ethics committee, in accordance with the Declaration of Helsinki, and with the written informed consent of all participants.
All the men had proven coronary heart disease, with a previous myocardial infarction (>6 months before enrollment) treated by primary angioplasty and stenting, and were receiving standard secondary preventive therapy. Men with angina pectoris (Canadian Cardiovascular Society class ≥2), a history of arrhythmia, diabetes mellitus, uncontrolled hypertension, or renal or hepatic failure, as well as those with unstable coronary disease (acute coronary syndrome or symptoms of instability 3 months before enrollment), were excluded. All eligible volunteers were invited to a prestudy screening for exercise stress testing; subjects who were unable to achieve stage 2 of the Bruce protocol or who had marked changes on an electrocardiogram (left bundle-branch block, early ST-segment depression >2 mm) and those in whom hypotension developed were excluded. Current smokers and men with asthma, substantial occupational exposure to air pollution, or an intercurrent illness were also excluded from the study.
Study Design
Using a randomized, double-blind, crossover study design, we evaluated the subjects in two 8 a.m. sessions at least 2 weeks apart. In each session, the subjects were exposed to controlled amounts of dilute diesel exhaust or filtered air. Each subject was exposed for 1 hour in an exposure chamber, as previously described.15 During each exposure, the subjects performed two 15-minute periods of exercise on a bicycle ergometer separated by two 15-minute periods of rest. For each subject, the ergometer workload was calibrated to achieve a ventilation of 15 liters per minute per square meter of body-surface area to ensure a similar exposure on both occasions. The workload was constant for both exposures and was equivalent to stage 2 of the Bruce protocol (range, 110 to 150 watts; 5 to 7 metabolic equivalents). All subjects were fitted with 12-lead Holter electrocardiographic monitors (Medical Lifecard 12 Digital Holter Recorder, Del Mar Reynolds). In accordance with previous exposure studies in healthy volunteers, vascular assessments were made 6 to 8 hours after exposure to diesel exhaust or filtered air.17
Diesel-Exhaust Exposure
The diesel exhaust was generated from an idling Volvo diesel engine (Volvo TD45, 4.5 liters, 4 cylinders, 680 rpm) from low-sulfur gas-oil E10 (Preem), as described previously.15 More than 90% of the exhaust was shunted away, and the remainder diluted with filtered air heated to 20°C (relative humidity approximately 50%) before being fed into a whole-body exposure chamber (3.0 m by 3.0 m by 2.4 m) at a steady-state concentration.
The chamber was monitored continuously for pollutants, with exposures standardized with the use of nitrogen oxide concentrations to deliver a particulate matter concentration of 300 μg per cubic meter (median particle diameter, 54 nm; range, 20 to 120). There was little variation between exposures in the mean (±SE) number of particles (1.26±0.01×106 particles per cubic centimeter) or in the concentrations of nitrogen oxide (4.45±0.02 ppm), nitrogen dioxide (1.01±0.01 ppm), nitric oxide (3.45±0.03 ppm), carbon monoxide (2.9±0.1 ppm), and total hydrocarbon (2.8±0.1 ppm). The predominant polycyclic aromatic hydrocarbons (approximately 90% of the total) were phenanthrene, fluorene, 2-methylfluorene, dibenzothiophene, and different methyl-substituted phenanthrenes. Only a minor fraction of polycyclic aromatic hydrocarbons (3.5%) was associated with particulate matter: 0.04% total particulate matter and 0.06% particulate-matter organic fraction. The concentration of particulate matter of less than 10 μm in aerodynamic diameter (PM10) in the exposure chamber exceeded the WHO air-quality standard of 50 μg per cubic meter by a factor of 6, and the nitrogen dioxide concentration exceeded the WHO standard of 0.105 ppm by a factor of 10.18
Vascular Study
All subjects underwent brachial-artery cannulation with a 27-standard wire-gauge steel needle. After a 30-minute baseline saline infusion, subjects were given infusions of acetylcholine at rates of 5, 10, and 20 μg per minute (endothelium-dependent vasodilator, Clinalfa), bradykinin at rates of 100, 300, and 1000 pmol per minute (endothelium-dependent vasodilator that releases tissue plasminogen activator [t-PA], Clinalfa), and sodium nitroprusside at rates of 2, 4, and 8 μg per minute (endothelium-independent vasodilator, David Bull Laboratories); each infusion was given for 6 minutes. Infusions of the three vasodilators were separated by 20-minute saline infusions and given in a randomized order. Therapy with angiotensin-converting–enzyme inhibitors was withdrawn 7 days before each vascular study, because it augments bradykinin-induced release of endothelial t-PA.19 All other medications were continued throughout the study.
Forearm blood flow was measured in both arms by venous occlusion plethysmography with the use of mercury-in-Silastic strain gauges, as described previously.20 Heart rate and blood pressure in the noninfused arm were monitored at intervals throughout each study while the subject was in the supine position, with the use of a semiautomated, noninvasive oscillometric sphygmomanometer.
Fibrinolytic and Inflammatory Markers
Blood (10 ml) was withdrawn into acidified buffered citrate (Stabilyte tubes, Biopool International) for t-PA assays and into citrate (BD Vacutainer) for plasminogen activator inhibitor type 1 (PAI-1) assays. Plasma t-PA and PAI-1 antigen concentrations were determined by means of enzyme-linked immunosorbent assays (TintElize t-PA, Biopool EIA; Coaliza PAI-1; and Chromogenix AB). Serum C-reactive protein concentrations were measured with an immunonephelometric assay (BN II nephelometer, Dade Behring).
Data Analysis
Electrocardiographic recordings were analyzed with the use of the Medical Pathfinder Digital 700 Series Analysis System (Del Mar Reynolds). ST-segment deviation was calculated by comparing the ST segment during each 15-minute exercise test with the average ST segment for the 15-minute period immediately before the start of the exposure. The ST-segment amplitude was determined at the J point plus 80 msec. The ischemic burden during each exercise test was calculated as the product of the change in ST-segment amplitude and the duration of exercise. Leads II, V2, and V5 were selected a priori for ST-segment analysis to reflect separate regions of myocardium. The maximum ST-segment depression and ischemic burden were determined for these leads individually and as a composite.
Plethysmographic data and net t-PA release were determined as described previously.20,21
Statistical Analysis
Continuous variables are reported as means ±SE. Analysis of variance with repeated measures and a two-tailed Student's t-test were performed as appropriate with the use of GraphPad Prism software. A two-sided P value of less than 0.05 was considered to indicate statistical significance.
Results
Subjects were all middle-aged men with predominantly single-vessel coronary artery disease (Table 1Table 1
Baseline Characteristics of the 20 Subjects with Coronary Heart Disease.). They reported no symptoms of angina and had no major arrhythmias during exposure or in the subsequent 24 hours.Myocardial Ischemia
The heart rate increased with exercise during exposures to diesel exhaust and filtered air (P<0.001 for both comparisons with the baseline rates; P=0.67 for the comparison of rates during exposure to diesel exhaust and during exposure to filtered air) (Table 2Table 2
Effect of Exercise on Heart Rate and ST Segment in the 20 Subjects during Exposures to Filtered Air and Diesel Exhaust.). Myocardial ischemia was detected during exercise in all subjects, with greater maximum ST-segment depression during exposure to diesel exhaust than during exposure to filtered air (Table 2 and Figure 1A and 1BFigure 1Myocardial Ischemia during 15-Minute Intervals of Exercise-Induced Stress and Exposure to Diesel Exhaust or Filtered Air in the 20 Subjects.) (P<0.05). The ischemic burden induced by exercise was greater during exposure to diesel exhaust (Figure 1C).Vasomotor Function
There were no significant differences in resting heart rate, blood pressure, or baseline blood flow in the noninfused forearm between or during the two study visits. Although there was a dose-dependent increase in blood flow with each vasodilator (P<0.001 for all comparisons), neither endothelium-dependent nor endothelium-independent vasodilatation was affected by inhalation of diesel exhaust (Figure 2Figure 2
Forearm Blood Flow 6 to 8 Hours after Exposures to Diesel Exhaust and Filtered Air.). Comparison of these data with the findings in a contemporary reference population of healthy male volunteers (mean age, 53±4 years) showed impaired vasodilatation in response to acetylcholine (P=0.02) but not to sodium nitroprusside (Figure 2).Fibrinolytic and Inflammatory Markers
There were no significant differences in basal plasma concentrations of t-PA (10.5±1.0 and 9.5±1.0 ng per milliliter, respectively) or its endogenous inhibitor, PAI-1 (18.8±3.0 and 17.0±2.0 ng per milliliter, respectively), 6 hours after exposure to either diesel exhaust or filtered air. Likewise, leukocyte, neutrophil, and platelet counts and serum C-reactive protein concentrations were not altered at 6 or 24 hours by exposure to diesel exhaust or filtered air. Bradykinin caused a dose-dependent increase in plasma t-PA concentrations (data not shown) and net t-PA release (Figure 3Figure 3
Release of Tissue Plasminogen Activator (t-PA) Antigen 6 to 8 Hours after Exposures to Diesel Exhaust and Filtered Air in 17 Subjects.) in the infused arm (P<0.001 for both comparisons) that was suppressed after exposure to diesel exhaust (P=0.009; 35% decrease in the area under the curve).Discussion
We have demonstrated that transient exposure to dilute diesel exhaust, at concentrations occurring in urban road traffic, exacerbates exercise-induced myocardial ischemia and impairs endogenous fibrinolytic capacity in men with coronary heart disease. These findings provide a plausible explanation for the epidemiologic observation that exposure to air pollution is associated with adverse cardiovascular events.
Concentrations of particulate matter can regularly reach levels of 300 μg per cubic meter in heavy traffic, in occupational settings, and in the world's largest cities.22 A major proportion of this mass is attributable to combustion-derived nanoparticles from traffic, ranging from 20% at remote monitoring sites23 to 70% in a road tunnel.24 Exposure to 300 μg of particulate matter per cubic meter for 1 hour increases a person's average exposure over a 24-hour period by only 12 μg per cubic meter. Changes of this magnitude occur on a daily basis, even in the least polluted cities, and are associated with increases in the rate of death from cardiorespiratory disorders.25 Our model is therefore highly relevant, in terms of both the composition and the magnitude of exposure, to the assessment of short-term health effects in men.
Given potential safety concerns, we recruited patients who had stable and symptomatically well-controlled coronary heart disease, with good exercise tolerance on formal stress testing. The study participants were closely monitored throughout the exposure and reported no adverse effects. Despite similar changes in the heart rate during exposure to diesel exhaust and to filtered air, we documented asymptomatic myocardial ischemia that was increased by a factor of up to three after inhalation of diesel exhaust. This reproducible effect was present despite extensive use of maintenance beta-blocker therapy in patients without limiting angina. Thus, we have established that inhalation of diesel exhaust has an immediate, proischemic effect, and we believe this provides an important mechanism for the observed increase in myocardial infarction in the hour after exposure to traffic.13
Small areas of denudation and thrombus deposition are common findings on the surface of atheromatous plaques and are usually subclinical. Rosenberg and Aird have postulated that vascular-bed–specific defects in hemostasis exist and that propagation of coronary thrombosis is critically dependent on the local fibrinolytic balance.26 The magnitude and rapidity of t-PA release from the vascular endothelium regulate the generation of plasmin and thus determine the efficacy of endogenous fibrinolysis.
We have previously reported impaired t-PA release in healthy volunteers 6 hours after inhalation of diesel exhaust, although this effect was not seen 2 hours after exposure.17 We have now confirmed similar reductions in acute t-PA release 6 hours after inhalation of diesel exhaust in patients with coronary heart disease. This delayed effect on endogenous fibrinolysis cannot explain our findings of immediate myocardial ischemia but is consistent with the observations of Peters and colleagues, who reported a second peak in the incidence of myocardial infarction 5 to 6 hours after exposure to traffic.13 Preclinical thrombotic models also lend support to our findings. Nemmar and colleagues reported that in a hamster model, instillation of diesel-exhaust particulate into the lungs increases venous and arterial thrombus formation at sites of vascular injury.27 Taken together, these findings indicate an important thrombotic effect of diesel-exhaust inhalation that may promote coronary thrombosis.
Although we found important adverse effects of diesel exhaust on vascular fibrinolytic function, we did not detect an effect on vasomotor function. However, vasomotor function was assessed 6 hours after exposure and 5 hours after we documented an increase in the ischemic burden. We have previously demonstrated that exposure to diesel exhaust impairs vasomotor function in healthy volunteers.17 This effect was most marked at 2 hours but was still present 6 hours after exposure. Therefore, we cannot exclude the possibility of a detrimental vasomotor effect in patients at an earlier point in time.
Patients with coronary heart disease are known to have impaired endothelial function,28 and we confirm the presence of endothelial dysfunction in our patients. This may have hindered our ability to demonstrate a further impairment of vascular function after exposure to diesel exhaust. In addition, we performed our assessments while the subjects were taking medications that are known to influence endothelial vasomotor function.29 Furthermore, Brook and colleagues reported that air pollution does not have an effect on endothelium-dependent vasodilatation.30
We have identified two distinct and potentially synergistic adverse cardiovascular effects of air pollution in patients with coronary heart disease. These effects may contribute to the increased incidence of myocardial infarction after exposure to traffic. However, the precise mechanisms by which diesel-exhaust inhalation induces these ischemic and thrombotic effects have not been established in our study and will need to be determined in future work.
Our findings are consistent with epidemiologic studies showing associations between ambient particulate air pollution and increased myocardial ischemia during formal exercise testing.10,11 Myocardial ischemia occurs as a consequence of reduced myocardial oxygen supply, increased demand, or both. We hypothesize that oxidative stress and microvascular dysfunction in the resistance vessels of the myocardium may, in part, explain the adverse ischemic effects of exposure to dilute diesel exhaust. In vitro studies, animal models, and studies of exposures in humans have clearly established the oxidant and proinflammatory nature of combustion-derived particulate matter.31 Indeed, the pattern of vascular dysfunction in our previous studies suggested that oxidative stress and reduced nitric oxide availability may play a role in mediating the adverse vascular effects of diesel-exhaust inhalation.17
Diesel exhaust is a complex mixture of gases and particles, and from our findings, we cannot rule out a nonparticulate cause of the adverse cardiovascular effects. However, on the basis of epidemiologic studies,32 particulate matter is thought to be responsible for the majority of the adverse health effects of air pollution.33 This view is supported by the recent observations of Miller and colleagues, who found that cardiovascular outcomes were strongly associated with long-term exposure to particulate matter but not with gaseous pollutants.3 Ambient nitrogen dioxide can be considered a surrogate for pollution from traffic, but it has little adverse effect in controlled-chamber studies, even at the exposure levels in our study.34 We therefore suggest that the cardiovascular effects described here are mediated primarily by the particulates in diesel exhaust and not by its other components. This argues for the use of diesel-exhaust particle traps to limit the adverse health effects of traffic emissions. However, the causative role of particulates must first be definitively established, and the efficacy of particle traps confirmed.
Brief exposure to dilute diesel exhaust increases myocardial ischemia and impairs endogenous fibrinolytic capacity in men with stable coronary heart disease. Our findings suggest mechanisms for the observation that exposure to combustion-derived air pollution is associated with adverse cardiovascular events, including acute myocardial infarction. Environmental health policy interventions targeting reductions in urban air pollution should be considered in order to decrease the risk of adverse cardiovascular events.
Supported by a Michael Davies Research Fellowship from the British Cardiovascular Society (to Dr. Mills) and by grants from the British Heart Foundation (program grant RG/05/003); the Swedish Heart Lung Foundation; the Swedish Research Council for Environment, Agricultural Sciences, and Spatial Planning; the Swedish National Air Pollution Program; the Swedish Emission Research Program; the Heart and Lung Associations in Sollefteå and Örnsköldsvik; the County Council of Västerbotten; and the Colt Foundation (to Dr. Donaldson).
No potential conflict of interest relevant to this article was reported.
Drs. Mills and Törnqvist contributed equally to this article.
We thank Christopher Ludlam, Pamela Dawson, William MacNee, Joan Henderson, Chris Llewellyn, Frida Holmström, Annika Johansson, Margot Johansson, Veronica Sjögren, Maj-Cari Ledin, Jamshid Pourazar, and the staff in the Department of Respiratory Medicine and Allergy, Umeå, and the Wellcome Trust Clinical Research Facility, Edinburgh, for their assistance; and Peter Bloomfield, for his critical appraisal and review of the manuscript.
Source Information
From the Centre for Cardiovascular Science (N.L.M., E.V., S.D.R., N.A.B., D.E.N.) and ELEGI Colt Laboratory, Center for Inflammation Research (K.D.) — both at Edinburgh University, Edinburgh; and the Department of Respiratory Medicine and Allergy (H.T., T.S., A.B.) and the Department of Medicine (M.C.G., S.S.), Umeå University, Umeå, Sweden.
Address reprint requests to Dr. Mills at the Centre for Cardiovascular Science, University of Edinburgh, Chancellor's Bldg., Edinburgh EH16 4SB, United Kingdom, or at nick.mills@ed.ac.uk.
- References
References
1
The world health report 2002 — reducing risks, promoting healthy life. Geneva: World Health Organization. (Accessed August 17, 2007, at http://www.who.int/whr/2002/en/.)
2
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
CrossRef | Web of Science | Medline3
Miller KA ,Siscovick DS ,Sheppard L , et al. Long-term exposure to air pollution and incidence of cardiovascular events in women. N Engl J Med 2007;356:447-458
Full Text | Web of Science | Medline4
Laden F ,Neas LM ,Dockery DW ,Schwartz J . Association of fine particulate matter from different sources with daily mortality in six U.S. cities. Environ Health Perspect 2000;108:941-947
CrossRef | Web of Science | Medline5
Ware JH . Particulate air pollution and mortality -- clearing the air. N Engl J Med 2000;343:1798-1799
Full Text | Web of Science | Medline6
Sun Q ,Wang A ,Jin X , et al. Long-term air pollution exposure and acceleration of atherosclerosis and vascular inflammation in an animal model. JAMA 2005;294:3003-3010
CrossRef | Web of Science | Medline7
Radomski A ,Jurasz P ,Alonso-Escolano D , et al. Nanoparticle-induced platelet aggregation and vascular thrombosis. Br J Pharmacol 2005;146:882-893
CrossRef | Web of Science | Medline8
Nemmar A ,Hoylaerts MF ,Hoet PH ,Nemery B . Possible mechanisms of the cardiovascular effects of inhaled particles: systemic translocation and prothrombotic effects. Toxicol Lett 2004;149:243-253
CrossRef | Web of Science | Medline9
von Klot S ,Peters A ,Aalto P , et al. Ambient air pollution is associated with increased risk of hospital cardiac readmissions of myocardial infarction survivors in five European cities. Circulation 2005;112:3073-3079[Erratum, Circulation 2006;113:e71.]
CrossRef | Web of Science | Medline10
Pekkanen J ,Peters A ,Hoek G , et al. Particulate air pollution and risk of ST-segment depression during repeated submaximal exercise tests among subjects with coronary heart disease: the Exposure and Risk Assessment for Fine and Ultrafine Particles in Ambient Air (ULTRA) study. Circulation 2002;106:933-938
CrossRef | Web of Science | Medline11
Gold DR ,Litonjua AA ,Zanobetti A , et al. Air pollution and ST-segment depression in elderly subjects. Environ Health Perspect 2005;113:883-887
CrossRef | Web of Science | Medline12
Peters A ,Dockery DW ,Muller JE ,Mittleman MA . Increased particulate air pollution and the triggering of myocardial infarction. Circulation 2001;103:2810-2815
Web of Science | Medline13
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
Full Text | Web of Science | Medline14
Stone PH . Triggering myocardial infarction. N Engl J Med 2004;351:1716-1718
Full Text | Web of Science | Medline15
Salvi S ,Blomberg A ,Rudell B , et al. Acute inflammatory responses in the airways and peripheral blood after short-term exposure to diesel exhaust in healthy human volunteers. Am J Respir Crit Care Med 1999;159:702-709
Web of Science | Medline16
Behndig AF ,Mudway IS ,Brown JL , et al. Airway antioxidant and inflammatory responses to diesel exhaust exposure in healthy humans. Eur Respir J 2006;27:359-365
CrossRef | Web of Science | Medline17
Mills NL ,Tornqvist H ,Robinson SD , et al. Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis. Circulation 2005;112:3930-3936
CrossRef | Web of Science | Medline18
Air quality guidelines for Europe. 2nd ed. No. 91. Copenhagen: World Health Organization Regional Office for Europe, 2000:173-98.
19
Witherow FN ,Dawson P ,Ludlam CA ,Fox KA ,Newby DE . Marked bradykinin-induced tissue plasminogen activator release in patients with heart failure maintained on chronic ACE inhibitor therapy. J Am Coll Cardiol 2002;40:961-966
CrossRef | Web of Science | Medline20
Newby DE ,Wright RA ,Labinjoh C , et al. Endothelial dysfunction, impaired endogenous fibrinolysis, and cigarette smoking: a mechanism for arterial thrombosis and myocardial infarction. Circulation 1999;99:1411-1415
Web of Science | Medline21
Newby DE ,Wright RA ,Ludlam CA ,Fox KA ,Boon NA ,Webb DJ . An in vivo model for the assessment of acute fibrinolytic capacity of the endothelium. Thromb Haemost 1997;78:1242-1248
Web of Science | Medline22
Urban air pollution in megacities of the world: a report from the United Nations Environment Programme and the World Health Organization. Report no. 36. London: Blackwell, 1992.
23
Lanki T ,de Hartog JJ ,Heinrich J , et al. Can we identify sources of fine particles responsible for exercise-induced ischemia on days with elevated air pollution? The ULTRA study. Environ Health Perspect 2006;114:655-660
CrossRef | Web of Science | Medline24
Geller MD ,Sardar SB ,Phuleria H ,Fine PM ,Sioutas C . Measurements of particle number and mass concentrations and size distributions in a tunnel environment. Environ Sci Technol 2005;39:8653-8663
CrossRef | Web of Science | Medline25
Samet JM ,Dominici F ,Curriero FC ,Coursac I ,Zeger SL . Fine particulate air pollution and mortality in 20 U.S. cities, 1987-1994. N Engl J Med 2000;343:1742-1749
Full Text | Web of Science | Medline26
Rosenberg RD ,Aird WC . Vascular-bed-specific hemostasis and hypercoagulable states. N Engl J Med 1999;340:1555-1564
Full Text | Web of Science | Medline27
Nemmar A ,Hoet PH ,Dinsdale D ,Vermylen J ,Hoylaerts MF ,Nemery B . Diesel exhaust particles in lung acutely enhance experimental peripheral thrombosis. Circulation 2003;107:1202-1208
CrossRef | Web of Science | Medline28
Zeiher AM ,Drexler H ,Wollschlager H ,Just H . Modulation of coronary vasomotor tone in humans: progressive endothelial dysfunction with different early stages of coronary atherosclerosis. Circulation 1991;83:391-401
Web of Science | Medline29
Treasure CB ,Klein JL ,Weintraub WS , et al. Beneficial effects of cholesterol-lowering therapy on the coronary endothelium in patients with coronary artery disease. N Engl J Med 1995;332:481-487
Full Text | Web of Science | Medline30
Brook RD ,Brook JR ,Urch B ,Vincent R ,Rajagopalan S ,Silverman F . Inhalation of fine particulate air pollution and ozone causes acute arterial vasoconstriction in healthy adults. Circulation 2002;105:1534-1536
CrossRef | Web of Science | Medline31
Donaldson K ,Stone V ,Borm PJ , et al. Oxidative stress and calcium signalling in the adverse effects of environmental particles (PM10). Free Radic Biol Med 2003;34:1369-1382
CrossRef | Web of Science | Medline32
Brunekreef B ,Holgate ST . Air pollution and health. Lancet 2002;360:1233-1242
CrossRef | Web of Science | Medline33
Schwartz J . What are people dying of on high air-pollution days? Environ Res 1994;64:26-35
CrossRef | Web of Science | Medline34
Blomberg A ,Krishna M ,Bocchino V , et al. The inflammatory effects of 2 ppm NO2 on the airways of healthy subjects. Am J Respir Crit Care Med 1997;156:418-424[Erratum, Am J Respir Crit Care Med 1997;156:2028.]
Web of Science | Medline
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Richard E Peltier, Kevin R Cromar, Yingjun Ma, Zhi-Hua (Tina) Fan, Morton Lippmann. (2011) Spatial and seasonal distribution of aerosol chemical components in New York City: (2) Road dust and other tracers of traffic-generated air pollution. Journal of Exposure Science and Environmental Epidemiology 21:5, 484-494
CrossRef14
M. Franchini, P. M. Mannucci. (2011) Thrombogenicity and cardiovascular effects of ambient air pollution. Blood 118:9, 2405-2412
CrossRef15
Alberto Ayala, Michael Brauer, Joe L. Mauderly, Jonathan M. Samet. (2011) Air pollutants and sources associated with health effects. Air Quality, Atmosphere & Health
CrossRef16
Nicole A.H. Janssen, Gerard Hoek, Milena Simic-Lawson, Paul Fischer, Leendert van Bree, Harry ten Brink, Menno Keuken, Richard W. Atkinson, H. Ross Anderson, Bert Brunekreef, Flemming R. Cassee. (2011) Black Carbon as an Additional Indicator of the Adverse Health Effects of Airborne Particles Compared with PM10 and PM2.5. Environmental Health Perspectives 119:12, 1691-1699
CrossRef17
Regina Rückerl, Alexandra Schneider, Susanne Breitner, Josef Cyrys, Annette Peters. (2011) Health effects of particulate air pollution: A review of epidemiological evidence. Inhalation Toxicology 23:10, 555-592
CrossRef18
Marie S. O’Neill, Carrie V. Breton, Robert B. Devlin, Mark J. Utell. (2011) Air pollution and health: emerging information on susceptible populations. Air Quality, Atmosphere & Health
CrossRef19
Jing Wang, David Y H Pui. (2011) Characterization, Exposure Measurement and Control for Nanoscale Particles in Workplaces and on the Road. Journal of Physics: Conference Series 304, 012008
CrossRef20
Abderrahim Nemmar, Shaheen Zia, Deepa Subramaniyan, Mohamed A. Fahim, Badreldin H. Ali. (2011) Exacerbation of thrombotic events by diesel exhaust particle in mouse model of hypertension. Toxicology 285:1-2, 39-45
CrossRef21
Paulo Sérgio Chiarelli, Luiz Alberto Amador Pereira, Paulo Hilário do Nascimento Saldiva, Celso Ferreira Filho, Maria Lúcia Bueno Garcia, Alfésio Luís Ferreira Braga, Lourdes Conceição Martins. (2011) The association between air pollution and blood pressure in traffic controllers in Santo André, São Paulo, Brazil. Environmental Research 111:5, 650-655
CrossRef22
Jon C. Volkwein, Andrew D. Maynard, Martin Harper. 2011. Workplace Aerosol Measurement. , 571-590.
CrossRef23
John McCracken, Kirk R. Smith, Peter Stone, Anaité Díaz, Byron Arana, Joel Schwartz. (2011) Intervention to Lower Household Wood Smoke Exposure in Guatemala Reduces ST-Segment Depression on Electrocardiograms. Environmental Health Perspectives 119:11, 1562-1568
CrossRef24
Moniek Zuurbier, Gerard Hoek, Marieke Oldenwening, Kees Meliefste, Esmeralda Krop, Peter van den Hazel, Bert Brunekreef. (2011) In-Traffic Air Pollution Exposure and CC16, Blood Coagulation, and Inflammation Markers in Healthy Adults. Environmental Health Perspectives 119:10, 1384-1389
CrossRef25
Åsa Gustafsson, Elsa Lindstedt, Linda Svensson Elfsmark, Anders Bucht. (2011) Lung exposure of titanium dioxide nanoparticles induces innate immune activation and long-lasting lymphocyte response in the Dark Agouti rat. Journal of Immunotoxicology 8:2, 111-121
CrossRef26
Keith T. Kuwata, Brianna J. Kujala, Zachary W. Morrow, Elena Tonc. (2011) Quantum chemical and RRKM/master equation studies of cyclopropene ozonolysis. Computational and Theoretical Chemistry 965:2-3, 305-312
CrossRef27
A. K. Farraj, M. S. Hazari, W. E. Cascio. (2011) The Utility of the Small Rodent Electrocardiogram in Toxicology. Toxicological Sciences 121:1, 11-30
CrossRef28
Jacob D. McDonald, Matthew J. Campen, Kevin S. Harrod, JeanClare Seagrave, Steven K. Seilkop, Joe L. Mauderly. (2011) Engine-Operating Load Influences Diesel Exhaust Composition and Cardiopulmonary and Immune Responses. Environmental Health Perspectives 119:8, 1136-1141
CrossRef29
Yuan-Yuan Guo, Jun Zhang, Yi-Fan Zheng, Jun Yang, Xin-Qiang Zhu. (2011) Cytotoxic and genotoxic effects of multi-wall carbon nanotubes on human umbilical vein endothelial cells in vitro. Mutation Research/Genetic Toxicology and Environmental Mutagenesis 721:2, 184-191
CrossRef30
Peter Møller, Lone Mikkelsen, Lise Kristine Vesterdal, Janne Kjærsgaard Folkmann, Lykke Forchhammer, Martin Roursgaard, Pernille Høgh Danielsen, Steffen Loft. (2011) Hazard identification of particulate matter on vasomotor dysfunction and progression of atherosclerosis. Critical Reviews in Toxicology 41:4, 339-368
CrossRef31
Mehdi S. Hazari, Najwa Haykal-Coates, Darrell W. Winsett, Q. Todd Krantz, Charly King, Daniel L. Costa, Aimen K. Farraj. (2011) TRPA1 and Sympathetic Activation Contribute to Increased Risk of Triggered Cardiac Arrhythmias in Hypertensive Rats Exposed to Diesel Exhaust. Environmental Health Perspectives 119:7, 951-957
CrossRef32
Boris Z. Simkhovich, Michael T. Kleinman, Paul Willet, Glenn Gookin, Karina Salazar, Andrew Keebaugh, Robert A. Kloner. (2011) Chronically inhaled ambient particles cause cardiac inflammation in normal, diseased, and elderly rat hearts. Air Quality, Atmosphere & Health 4:1, 27-36
CrossRef33
Carlo R. Bartoli, John J. Godleski, Richard L. Verrier. (2011) Mechanisms mediating adverse effects of air pollution on cardiovascular hemodynamic function and vulnerability to cardiac arrhythmias. Air Quality, Atmosphere & Health 4:1, 53-63
CrossRef34
Nicholas Birger, Timothy Gould, James Stewart, Mark R. Miller, Timothy Larson, Chris Carlsten. (2011) The Air Pollution Exposure Laboratory (APEL) for controlled human exposure to diesel exhaust and other inhalants: characterization and comparison to existing facilities. Inhalation Toxicology 23:4, 219-225
CrossRef35
Annette Peters. (2011) Ambient Particulate Matter and the Risk for Cardiovascular Disease. Progress in Cardiovascular Diseases 53:5, 327-333
CrossRef36
Nicholas L. Mills, Mark R. Miller. 2011. Particles and the Vascular Endothelium. , 379-402.
CrossRef37
Ken Donaldson, David B. Warheit. 2011. From Ambient Ultrafine Particles to Nanotechnology and Nanotoxicology. , 525-543.
CrossRef38
Thomas Sandström, David Newby. 2011. Role of Inflammation in the Atherogenic Effects of Particulate Matter. , 273-285.
CrossRef39
Robert D. Brook, Sanjay Rajagopalan. 2011. Particulate Matter, Hypertension, and the Metabolic Syndrome. , 351-377.
CrossRef40
Qinghua Sun, Xiaohua Xu. 2011. Particles and the Pathogenesis of Atherothrombosis. , 421-437.
CrossRef41
C. McGuinnes, R. Duffin, S. Brown, N. L. Mills, I. L. Megson, W. MacNee, S. Johnston, S. L. Lu, L. Tran, R. Li, X. Wang, D. E. Newby, K. Donaldson. (2011) Surface Derivatization State of Polystyrene Latex Nanoparticles Determines both Their Potency and Their Mechanism of Causing Human Platelet Aggregation In Vitro. Toxicological Sciences 119:2, 359-368
CrossRef42
Ece A Mutlu, Phillip A Engen, Saul Soberanes, Daniela Urich, Christopher B Forsyth, Recep Nigdelioglu, Sergio E Chiarella, Kathryn A Radigan, Angel Gonzalez, Shriram Jakate, Ali Keshavarzian, GR Budinger, Gökhan M Mutlu. (2011) Particulate matter air pollution causes oxidant-mediated increase in gut permeability in mice. Particle and Fibre Toxicology 8:1, 19
CrossRef43
Denis Dieme, Mathilde Cabral, Anthony Verdin, Mamadou Fall, Sylvain Billet, Fabrice Cazier, Guillaume Garçon, Amadou Diouf, Pirouz Shirali. (2011) Caractérisation physico-chimique et effets cytotoxiques de particules atmosphériques PM 2,5 de la ville de Dakar (Sénégal). Annales de Toxicologie Analytique 23:4, 157-167
CrossRef44
Howard M. Kipen, Sampada Gandhi, David Q. Rich, Pamela Ohman-Strickland, Robert Laumbach, Zhi-Hua Fan, Li Chen, Debra L. Laskin, Junfeng Zhang, Kiran Madura. (2010) Acute Decreases in Proteasome Pathway Activity after Inhalation
of Fresh Diesel Exhaust or Secondary Organic Aerosol. Environmental Health Perspectives 119:5, 658-663
CrossRef45
Miriam E. Gerlofs-Nijland, Annike I. Totlandsdal, Evren Kilinç, A. John F. Boere, Paul H.B. Fokkens, Daan L.A.C Leseman, Constantinos Sioutas, Per E. Schwarze, Henri M. Spronk, Patrick W.F. Hadoke, Mark R. Miller, Flemming R. Cassee. (2010) Pulmonary and cardiovascular effects of traffic-related particulate matter: 4-week exposure of rats to roadside and diesel engine exhaust particles. Inhalation Toxicology 22:14, 1162-1173
CrossRef46
Haiyan Tong, Wan-Yun Cheng, James M. Samet, M. Ian Gilmour, Robert B. Devlin. (2010) Differential Cardiopulmonary Effects of Size-Fractionated Ambient Particulate Matter in Mice. Cardiovascular Toxicology 10:4, 259-267
CrossRef47
Wen Qi Gan, Mieke Koehoorn, Hugh W. Davies, Paul A. Demers, Lillian Tamburic, Michael Brauer. (2010) Long-Term Exposure to Traffic-Related Air Pollution and the Risk of Coronary Heart Disease Hospitalization and Mortality. Environmental Health Perspectives 119:4, 501-507
CrossRef48
Daniel A. Gerardi. (2010) Building-Related Illness. Clinical Pulmonary Medicine 17:6, 276-281
CrossRef49
Ralph J. Delfino, Norbert Staimer, Thomas Tjoa, Mohammad Arhami, Andrea Polidori, Daniel L. Gillen, Steven C. George, Martin M. Shafer, James J. Schauer, Constantinos Sioutas. (2010) Associations of Primary and Secondary Organic Aerosols With Airway and Systemic Inflammation in an Elderly Panel Cohort. Epidemiology 21:6, 892-902
CrossRef50
Ralph J. Delfino, Daniel L. Gillen, Thomas Tjoa, Norbert Staimer, Andrea Polidori, Mohammad Arhami, Constantinos Sioutas, John Longhurst. (2010) Electrocardiographic ST-Segment Depression and Exposure to Traffic-Related Aerosols in Elderly Subjects with Coronary Artery Disease. Environmental Health Perspectives 119:2, 196-202
CrossRef51
Jason D. Sacks, Lindsay Wichers Stanek, Thomas J. Luben, Douglas O. Johns, Barbara J. Buckley, James S. Brown, Mary Ross. (2010) Particulate Matter–Induced Health Effects: Who Is Susceptible?. Environmental Health Perspectives 119:4, 446-454
CrossRef52
R. A. Silverman, K. Ito, J. Freese, B. J. Kaufman, D. De Claro, J. Braun, D. J. Prezant. (2010) Association of Ambient Fine Particles With Out-of-Hospital Cardiac Arrests in New York City. American Journal of Epidemiology 172:8, 917-923
CrossRef53
Steven M. Lee, Mark W. Frampton. 2010. Traffic-Related Urban Air Pollution. , 421-443.
CrossRef54
Judith C. Stewart, David C. Chalupa, Robert B. Devlin, Lauren M. Frasier, Li-Shan Huang, Erika L. Little, Steven M. Lee, Richard P. Phipps, Anthony P. Pietropaoli, Mark B. Taubman, Mark J. Utell, Mark W. Frampton. (2010) Vascular Effects of Ultrafine Particles in Persons with Type 2 Diabetes. Environmental Health Perspectives 118:12, 1692-1698
CrossRef55
Luisa V. Giles, Prabjit Barn, Nino Künzli, Isabelle Romieu, Murray A. Mittleman, Stephan van Eeden, Ryan Allen, Chris Carlsten, Dave Stieb, Curtis Noonan, Audrey Smargiassi, Joel D. Kaufman, Shakoor Hajat, Tom Kosatsky, Michael Brauer. (2010) From Good Intentions to Proven Interventions: Effectiveness of Actions to Reduce the Health Impacts of Air Pollution. Environmental Health Perspectives 119:1, 29-36
CrossRef56
David C. Cone, Carin M. Van Gelder, Donald MacMillan. (2010) Fireground Use of an Emergency Escape Respirator. Prehospital Emergency Care 14:4, 433-438
CrossRef57
Chunli Quan, Qinghua Sun, Morton Lippmann, Lung-Chi Chen. (2010) Comparative effects of inhaled diesel exhaust and ambient fine particles on inflammation, atherosclerosis, and vascular dysfunction. Inhalation Toxicology 22:9, 738-753
CrossRef58
Robert J. Laumbach, Howard M. Kipen. (2010) Acute effects of motor vehicle traffic-related air pollution exposures on measures of oxidative stress in human airways. Annals of the New York Academy of Sciences 1203:1, 107-112
CrossRef59
Thomas W. Hesterberg, Christopher M. Long, Charles A. Lapin, Ali K. Hamade, Peter A. Valberg. (2010) Diesel exhaust particulate (DEP) and nanoparticle exposures: What do DEP human clinical studies tell us about potential human health hazards of nanoparticles?. Inhalation Toxicology 22:8, 679-694
CrossRef60
Thomas J. Grahame, Richard B. Schlesinger. (2010) Cardiovascular health and particulate vehicular emissions: a critical evaluation of the evidence. Air Quality, Atmosphere & Health 3:1, 3-27
CrossRef61
A. Seaton, L. Tran, R. Aitken, K. Donaldson. (2010) Nanoparticles, human health hazard and regulation. Journal of The Royal Society Interface 7:Suppl_1, S119-S129
CrossRef62
A. Nemmar, S. Al-Salam, S. Zia, J. Yasin, I. Al Husseni, B. H. Ali. (2010) Diesel Exhaust Particles in the Lung Aggravate Experimental Acute Renal Failure. Toxicological Sciences 113:1, 267-277
CrossRef63
Shepard D. Weiner, LeRoy E. Rabbani. (2010) Secondary prevention strategies for coronary heart disease. Journal of Thrombosis and Thrombolysis 29:1, 8-24
CrossRef64
Mark S Link, Douglas W Dockery. (2010) Air pollution and the triggering of cardiac arrhythmias. Current Opinion in Cardiology 25:1, 16-22
CrossRef65
Kirk R Smith, Michael Jerrett, H Ross Anderson, Richard T Burnett, Vicki Stone, Richard Derwent, Richard W Atkinson, Aaron Cohen, Seth B Shonkoff, Daniel Krewski, C Arden Pope, Michael J Thun, George Thurston. (2009) Public health benefits of strategies to reduce greenhouse-gas emissions: health implications of short-lived greenhouse pollutants. The Lancet 374:9707, 2091-2103
CrossRef66
Rajesh Beniwal, Vijay Kumar Shivgotra. (2009) An Elementary Framework for Judging the Cardiovascular Toxicity of Carbon Soot: Experiences from an Occupational Health Survey of Diamond Industry Workers. Cardiovascular Toxicology 9:4, 194-200
CrossRef67
Boris Z Simkhovich, Michael T Kleinman, Robert A Kloner. (2009) Particulate air pollution and coronary heart disease. Current Opinion in Cardiology 24:6, 604-609
CrossRef68
Jason Allen, Carol A. Trenga, Alon Peretz, Jeffrey H. Sullivan, Christopher C. Carlsten, Joel D. Kaufman. (2009) Effect of diesel exhaust inhalation on antioxidant and oxidative stress responses in adults with metabolic syndrome. Inhalation Toxicology 21:13, 1061-1067
CrossRef69
Robert D. Brook, Sanjay Rajagopalan. (2009) Particulate matter, air pollution, and blood pressure. Journal of the American Society of Hypertension 3:5, 332-350
CrossRef70
A. F. Folino, M. L. Scapellato, C. Canova, P. Maestrelli, G. Bertorelli, L. Simonato, S. Iliceto, M. Lotti. (2009) Individual exposure to particulate matter and the short-term arrhythmic and autonomic profiles in patients with myocardial infarction. European Heart Journal 30:13, 1614-1620
CrossRef71
Luke D. Knibbs, Richard J. de Dear, Lidia Morawska, Kerrie L. Mengersen. (2009) On-road ultrafine particle concentration in the M5 East road tunnel, Sydney, Australia. Atmospheric Environment 43:22-23, 3510-3519
CrossRef72
Giuliano Polichetti, Stefania Cocco, Alessandra Spinali, Valentina Trimarco, Alfredo Nunziata. (2009) Effects of particulate matter (PM10, PM2.5 and PM1) on the cardiovascular system. Toxicology 261:1-2, 1-8
CrossRef73
Ute Latza, Silke Gerdes, Xaver Baur. (2009) Effects of nitrogen dioxide on human health: Systematic review of experimental and epidemiological studies conducted between 2002 and 2006. International Journal of Hygiene and Environmental Health 212:3, 271-287
CrossRef74
Antonella Zanobetti, Joel Schwartz. (2009) The Effect of Fine and Coarse Particulate Air Pollution on Mortality: A National Analysis. Environmental Health Perspectives 117:6, 898-903
CrossRef75
C. Hassing, M. Twickler, B. Brunekreef, F. Cassee, P. Doevendans, J. Kastelein, M. J. Cramer. (2009) Particulate air pollution, coronary heart disease and individual risk assessment: a general overview. European Journal of Cardiovascular Prevention & Rehabilitation 16:1, 10-15
CrossRef76
Zhu-ming Zhang, Eric A. Whitsel, P. Miguel Quibrera, Richard L. Smith, Duanping Liao, Garnet L. Anderson, Ronald J. Prineas. (2009) Ambient Fine Particulate Matter Exposure and Myocardial Ischemia in the Environmental Epidemiology of Arrhythmogenesis in the Women’s Health Initiative (EEAWHI) Study. Environmental Health Perspectives 117:5, 751-756
CrossRef77
Nicholas L Mills, Ken Donaldson, Paddy W Hadoke, Nicholas A Boon, William MacNee, Flemming R Cassee, Thomas Sandström, Anders Blomberg, David E Newby. (2009) Adverse cardiovascular effects of air pollution. Nature Clinical Practice Cardiovascular Medicine 6:1, 36-44
CrossRef78
Petter Ljungman, Tom Bellander, Alexandra Schneider, Susanne Breitner, Francesco Forastiere, Regina Hampel, Thomas Illig, Benedicte Jacquemin, Klea Katsouyanni, Stephanie von Klot, Wolfgang Koenig, Timo Lanki, Fredrik Nyberg, Juha Pekkanen, Riccardo Pistelli, Christos Pitsavos, M�rten Rosenqvist, Jordi Sunyer, Annette Peters. (2009) Modification of the interleukin-6 response to air pollution by interleukin-6 and fibrinogen polymorphisms. Environmental Health Perspectives
CrossRef79
José A. Barrabés, Juan Sanchís, Pedro L. Sánchez, Alfredo Bardají. (2009) Actualización en cardiopatía isquémica. Revista Española de Cardiología 62, 80-91
CrossRef80
D. Charpin, A. Palot. (2009) Pollution atmosphérique et santé : une relation à actualiser. La Revue de Médecine Interne 30:1, 3-4
CrossRef81
A. J. Lucking, M. Lundback, N. L. Mills, D. Faratian, S. L. Barath, J. Pourazar, F. R. Cassee, K. Donaldson, N. A. Boon, J. J. Badimon, T. Sandstrom, A. Blomberg, D. E. Newby. (2008) Diesel exhaust inhalation increases thrombus formation in man. European Heart Journal 29:24, 3043-3051
CrossRef82
J. P. Langrish, N. L. Mills, D. E. Newby. (2008) Air pollution: the new cardiovascular risk factor. Internal Medicine Journal 38:12, 875-878
CrossRef83
X. Halna du Fretay, B. Gérardin. (2008) Infarctus du sportif. Annales de Cardiologie et d'Angéiologie 57:6, 335-340
CrossRef84
Thomas Sandstrom, Bertil Forsberg. (2008) Desert Dust. Epidemiology 19:6, 808-809
CrossRef85
P. L.S. Ljungman, N. Berglind, C. Holmgren, F. Gadler, N. Edvardsson, G. Pershagen, M. Rosenqvist, B. Sjogren, T. Bellander. (2008) Rapid effects of air pollution on ventricular arrhythmias. European Heart Journal 29:23, 2894-2901
CrossRef86
D. Charpin. (2008) Avant-propos série « Pollution atmosphérique ». Revue des Maladies Respiratoires 25:8, 923-924
CrossRef87
Boris Z. Simkhovich, Michael T. Kleinman, Robert A. Kloner. (2008) Air Pollution and Cardiovascular Injury. Journal of the American College of Cardiology 52:9, 719-726
CrossRef88
David Q. Rich, Ronald S. Freudenberger, Pamela Ohman-Strickland, Yong Cho, Howard M. Kipen. (2008) Right Heart Pressure Increases after Acute Increases in Ambient Particulate Concentration. Environmental Health Perspectives 116:9, 1167-1171
CrossRef89
S. von Klot, M. A. Mittleman, A. Peters. (2008) Physical exertion and triggering of myocardial infarction: reply. European Heart Journal 30:2, 251-252
CrossRef90
David Y.H. Pui, Chaolong Qi, Nick Stanley, Günter Oberdörster, Andrew Maynard. (2008) Recirculating Air Filtration Significantly Reduces Exposure to Airborne Nanoparticles. Environmental Health Perspectives 116:7, 863-866
CrossRef91
Alon Peretz, Jeffrey H. Sullivan, Daniel F. Leotta, Carol A. Trenga, Fiona N. Sands, Jason Allen, Chris Carlsten, Charles W. Wilkinson, Edward A. Gill, Joel D. Kaufman. (2008) Diesel Exhaust Inhalation Elicits Acute Vasoconstriction in Vivo. Environmental Health Perspectives 116:7, 937-942
CrossRef92
Nicholas L. Mills, Simon D. Robinson, Paul H. B. Fokkens, Daan L. A. C. Leseman, Mark R. Miller, David Anderson, Evelyn J. Freney, Mathew R. Heal, Robert J. Donovan, Anders Blomberg, Thomas Sandström, William MacNee, Nicholas A. Boon, Ken Donaldson, David E. Newby, Flemming R. Cassee. (2008) Exposure to Concentrated Ambient Particles Does Not Affect Vascular Function in Patients with Coronary Heart Disease. Environmental Health Perspectives 116:6, 709-715
CrossRef93
Andrew D. Maynard. (2008) Living with nanoparticles. Nano Today 3:1-2, 64
CrossRef94
Paul J.A. Borm, David Berube. (2008) A tale of opportunities, uncertainties, and risks. Nano Today 3:1-2, 56-59
CrossRef95
Carlo R. Bartoli, Gregory A. Wellenius, Brent A. Coull, Ichiro Akiyama, Edgar A. Diaz, Joy Lawrence, Kazunori Okabe, Richard L. Verrier, John J. Godleski. (2008) Concentrated Ambient Particles Alters Myocardial Blood Flow during Acute Ischemia in Conscious Canines. Environmental Health Perspectives
CrossRef96
Roddy R. Gottipolu, J. Grace Wallenborn, Edward D. Karoly, Mette C. Schladweiler, Allen D. Ledbetter, Todd Krantz, William P. Linak, Abraham Nyska, Jo Anne Johnson, Ronald Thomas, Judy E. Richards, Richard H. Jaskot, Urmila P. Kodavanti. (2008) One-Month Diesel Exhaust Inhalation Produces Hypertensive Gene Expression Pattern in Healthy Rats. Environmental Health Perspectives
CrossRef97
Mark R. Miller, Stephen J. Borthwick, Catherine A. Shaw, Steven G. McLean, Daniel McClure, Nicholas L. Mills, Rodger Duffin, Ken Donaldson, Ian L. Megson, Patrick W.F. Hadoke, David E. Newby. (2008) Direct Impairment of Vascular Function by Diesel Exhaust Particulate Through Reduced Bioavailability of Endothelium-Derived Nitric Oxide Induced by Superoxide Free Radicals. Environmental Health Perspectives
CrossRef98
Giuseppe Lippi, Emmanuel J. Favaloro, Massimo Franchini, Gian Cesare Guidi. (2008) Air pollution and coagulation testing: A new source of biological variability?. Thrombosis Research 123:1, 50-54
CrossRef99
Aimen K. Farraj, Najwa Haykal-Coates, Darrell W. Winsett, Mehdi S. Hazari, Alex P. Carll, William H. III Rowan, Allen D. Ledbetter, Wayne E. Cascio, Daniel L. Costa. (2008) Increased Non-conducted P-wave Arrhythmias after a Single Oil Fly Ash Inhalation Exposure in Hypertensive Rats. Environmental Health Perspectives
CrossRef100
(2008) Air pollution promotes ischemia and inhibits fibrinolytic function in patients with CHD. Nature Clinical Practice Cardiovascular Medicine 5:1, 5-5
CrossRef101
Alpa P. Shah, Anthony P. Pietropaoli, Lauren M. Frasier, Donna M. Speers, David C. Chalupa, Joseph M. Delehanty, Li-Shan Huang, Mark J. Utell, Mark W. Frampton. (2007) Effect of Inhaled Carbon Ultrafine Particles on Reactive Hyperemia in Healthy Human Subjects. Environmental Health Perspectives 116:3, 375-380
CrossRef102
Ewen Callaway. (2007) Stay in if you're having a bad air day. news@nature
CrossRef103
Mittleman, Murray A., . (2007) Air Pollution, Exercise, and Cardiovascular Risk. New England Journal of Medicine 357:11, 1147-1149
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