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Barath, Stefan
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Publications (10 of 17) Show all publications
Langrish, J. P., Watts, S. J., Hunter, A. J., Shah, A. S. V., Bosson, J. A., Unosson, J., . . . Mills, N. L. (2014). Controlled exposures to air pollutants and risk of cardiac arrhythmia. Journal of Environmental Health Perspectives, 122(7), 747-753
Open this publication in new window or tab >>Controlled exposures to air pollutants and risk of cardiac arrhythmia
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2014 (English)In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 122, no 7, p. 747-753Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Epidemiological studies have reported associations between air pollution exposure and increases in cardiovascular morbidity and mortality. Exposure to air pollutants can influence cardiac autonomic tone and reduce heart rate variability, and may increase the risk of cardiac arrhythmias, particularly in susceptible patient groups. OBJECTIVES: We investigated the incidence of cardiac arrhythmias during and after controlled exposure to air pollutants in healthy volunteers and patients with coronary heart disease. METHODS: We analyzed data from 13 double-blind randomized crossover studies including 282 participants (140 healthy volunteers and 142 patients with stable coronary heart disease) from whom continuous electrocardiograms were available. The incidence of cardiac arrhythmias was recorded for each exposure and study population. RESULTS: There were no increases in any cardiac arrhythmia during or after exposure to dilute diesel exhaust, wood smoke, ozone, concentrated ambient particles, engineered carbon nanoparticles, or high ambient levels of air pollution in either healthy volunteers or patients with coronary heart disease. CONCLUSIONS: Acute controlled exposure to air pollutants did not increase the short-term risk of arrhythmia in participants. Research employing these techniques remains crucial in identifying the important pathophysiological pathways involved in the adverse effects of air pollution, and is vital to inform environmental and public health policy decisions.

National Category
Occupational Health and Environmental Health Pharmacology and Toxicology Environmental Sciences
Identifiers
urn:nbn:se:umu:diva-91845 (URN)10.1289/ehp.1307337 (DOI)000338928000026 ()
Available from: 2014-08-27 Created: 2014-08-18 Last updated: 2018-06-07Bibliographically approved
Langrish, J. P., Unosson, J., Bosson, J., Barath, S., Muala, A., Blackwell, S., . . . Mills, N. L. (2013). Altered nitric oxide bioavailability contributes to diesel exhaust inhalation-induced cardiovascular dysfunction in man. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 2(1), e004309
Open this publication in new window or tab >>Altered nitric oxide bioavailability contributes to diesel exhaust inhalation-induced cardiovascular dysfunction in man
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2013 (English)In: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, ISSN 2047-9980, E-ISSN 2047-9980, Vol. 2, no 1, p. e004309-Article in journal (Refereed) Published
Abstract [en]

Background Diesel exhaust inhalation causes cardiovascular dysfunction including impaired vascular reactivity, increased blood pressure, and arterial stiffness. We investigated the role of nitric oxide (NO) bioavailability in mediating these effects.

Methods and Results In 2 randomized double-blind crossover studies, healthy nonsmokers were exposed to diesel exhaust or filtered air. Study 1: Bilateral forearm blood flow was measured during intrabrachial infusions of acetylcholine (ACh; 5 to 20 mu g/min) and sodium nitroprusside (SNP; 2 to 8 mu g/min) in the presence of the NO clamp (NO synthase inhibitor N-G-monomethyl-L-arginine (L-NMMA) 8 mu g/min coinfused with the NO donor SNP at 90 to 540 ng/min to restore basal blood flow). Study 2: Blood pressure, arterial stiffness, and cardiac output were measured during systemic NO synthase inhibition with intravenous L-NMMA (3 mg/kg). Following diesel exhaust inhalation, plasma nitrite concentrations were increased (68 +/- 48 versus 41 +/- 32 nmol/L; P=0.006) despite similar L-NMMA-induced reductions in basal blood flow (-20.6 +/- 14.7% versus -21.1 +/- 14.6%; P=0.559) compared to air. In the presence of the NO clamp, ACh and SNP caused dose-dependent vasodilatation that was not affected by diesel exhaust inhalation (P>0.05 for both). Following exposure to diesel exhaust, L-NMMA caused a greater increase in blood pressure (P=0.048) and central arterial stiffness (P=0.007), but reductions in cardiac output and increases in systemic vascular resistance (P>0.05 for both) were similar to those seen with filtered air.

Conclusions Diesel exhaust inhalation disturbs normal vascular homeostasis with enhanced NO generation unable to compensate for excess consumption. We suggest the adverse cardiovascular effects of air pollution are, in part, mediated through reduced NO bioavailability.

Place, publisher, year, edition, pages
American stroke association, 2013
Keywords
air pollution, endothelial function, nitric oxide, nitric oxide synthase, vascular biology
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:umu:diva-83653 (URN)10.1161/JAHA.112.004309 (DOI)000326336800023 ()
Funder
Swedish Heart Lung Foundation
Available from: 2013-12-03 Created: 2013-12-03 Last updated: 2018-06-08Bibliographically approved
Barath, S., Mills, N. L., Ädelroth, E., Olin, A.-C. & Blomberg, A. (2013). Diesel exhaust but not ozone increases fraction of exhaled nitric oxide in a randomized controlled experimental exposure study of healthy human subjects. Environmental health, 12, 36
Open this publication in new window or tab >>Diesel exhaust but not ozone increases fraction of exhaled nitric oxide in a randomized controlled experimental exposure study of healthy human subjects
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2013 (English)In: Environmental health, ISSN 1476-069X, E-ISSN 1476-069X, Vol. 12, p. 36-Article in journal (Refereed) Published
Abstract [en]

Background: Fraction of exhaled nitric oxide (FENO) is a promising non-invasive index of airway inflammation that may be used to assess respiratory effects of air pollution. We evaluated FENO as a measure of airway inflammation after controlled exposure to diesel exhaust or ozone. Methods: Healthy volunteers were exposed to either diesel exhaust (particle concentration 300 mu g/m(3)) and filtered air for one hour, or ozone (300 ppb) and filtered air for 75 minutes. FENO was measured in duplicate at expiratory flow rates of 10, 50, 100 and 270 mL/s before, 6 and 24 hours after each exposure. Results: Exposure to diesel exhaust increased FENO at 6 hours compared with air at expiratory flow rates of 10 mL/s (p = 0.01) and at 50 mL/s (p = 0.011), but FENO did not differ significantly at higher flow rates. Increases in FENO following diesel exhaust were attenuated at 24 hours. Ozone did not affect FENO at any flow rate or time point. Conclusions: Exposure to diesel exhaust, but not ozone, increased FENO concentrations in healthy subjects. Differences in the induction of airway inflammation may explain divergent responses to diesel exhaust and ozone, with implications for the use of FENO as an index of exposure to air pollution.

Place, publisher, year, edition, pages
BioMed Central, 2013
Keywords
Air pollution, Particulate matter pollution, Airway inflammation
National Category
Respiratory Medicine and Allergy Occupational Health and Environmental Health Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:umu:diva-71312 (URN)10.1186/1476-069X-12-36 (DOI)000318252700001 ()
Funder
Swedish Heart Lung Foundation
Available from: 2013-05-30 Created: 2013-05-26 Last updated: 2018-06-08Bibliographically approved
Barath, S., Langrish, J. P., Lundbäck, M., Bosson, J. A., Goudie, C., Newby, D. E., . . . Blomberg, A. (2013). Short-Term Exposure to Ozone Does Not Impair Vascular Function or Affect Heart Rate Variability in Healthy Young Men. Toxicological Sciences, 135(2), 292-299
Open this publication in new window or tab >>Short-Term Exposure to Ozone Does Not Impair Vascular Function or Affect Heart Rate Variability in Healthy Young Men
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2013 (English)In: Toxicological Sciences, ISSN 1096-6080, E-ISSN 1096-0929, Vol. 135, no 2, p. 292-299Article in journal (Refereed) Published
Abstract [en]

Air pollution exposure is associated with cardiovascular morbidity and mortality, yet the role of individual pollutants remains unclear. In particular, there is uncertainty regarding the acute effect of ozone exposure on cardiovascular disease. In these studies, we aimed to determine the effect of ozone exposure on vascular function, fibrinolysis, and the autonomic regulation of the heart. Thirty-six healthy men were exposed to ozone (300 ppb) and filtered air for 75min on two occasions in randomized double-blind crossover studies. Bilateral forearm blood flow (FBF) was measured using forearm venous occlusion plethysmography before and during intra-arterial infusions of vasodilators 2–4 and 6–8h after each exposure. Heart rhythm and heart rate variability (HRV) were monitored during and 24h after exposure. Compared with filtered air, ozone exposure did not alter heart rate, blood pressure, or resting FBF at either 2 or 6h. There was a dose-dependent increase in FBF with all vasodilators that was similar after both exposures at 2–4h. Ozone exposure did not impair vasomotor or fibrinolytic function at 6–8h but rather increased vasodilatation to acetylcholine (p = .015) and sodium nitroprusside (p = .005). Ozone did not affect measures of HRV during or after the exposure. Our findings do not support a direct rapid effect of ozone on vascular function or cardiac autonomic control although we cannot exclude an effect of chronic exposure or an interaction between ozone and alternative air pollutants that may be responsible for the adverse cardiovascular health effects attributed to ozone.

Place, publisher, year, edition, pages
Oxford University Press, 2013
Keywords
Air Pollution, blood flow, endothelium, fibrinolysis, oxidative stress, ozone, Luftföroreningar
National Category
Cardiac and Cardiovascular Systems
Research subject
Cardiology; Lung Medicine; biology, Environmental Science
Identifiers
urn:nbn:se:umu:diva-46528 (URN)10.1093/toxsci/kft157 (DOI)000326384200005 ()23872581 (PubMedID)
Funder
Swedish Heart Lung FoundationSwedish Research Council Formas
Note

Manuscript title included in thesis: Ozone exposure does not impair vascular function or affect heart rate variability in healthy subjects

Available from: 2011-09-06 Created: 2011-09-05 Last updated: 2018-06-08Bibliographically approved
Mills, N. L., Finlayson, A. E., Gonzalez, M. C., Törnqvist, H., Barath, S., Vink, E., . . . Newby, D. E. (2011). Diesel exhaust inhalation does not affect heart rhythm or heart rate variability. Heart, 97(7), 544-550
Open this publication in new window or tab >>Diesel exhaust inhalation does not affect heart rhythm or heart rate variability
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2011 (English)In: Heart, ISSN 1355-6037, E-ISSN 1468-201X, Vol. 97, no 7, p. 544-550Article in journal (Refereed) Published
Abstract [en]

Objective Exposure to air pollution is associated with increases in cardiovascular morbidity and mortality. This study was undertaken to determine the effect of diesel exhaust inhalation on heart rhythm and heart rate variability in healthy volunteers and patients with coronary heart disease.

Design and setting Double-blind randomised crossover studies in a university teaching hospital.

Patients 32 healthy non-smoking volunteers and 20 patients with prior myocardial infarction.

Interventions All 52 subjects were exposed for 1 h to dilute diesel exhaust (particle concentration 300 μg/m(3)) or filtered air.

Main outcome measures Heart rhythm and heart rate variability were monitored during and for 24 h after the exposure using continuous ambulatory electrocardiography and assessed using standard time and frequency domain analysis.

Results No significant arrhythmias occurred during or following exposures. Patients with coronary heart disease had reduced autonomic function in comparison to healthy volunteers, with reduced standard deviations of the NN interval (SDNN, p<0.001) and triangular index (p<0.001). Diesel exhaust did not affect heart rate variability compared with filtered air (p>0.05 for all) in healthy volunteers (SDNN 101±6 vs 91±6, triangular index 20±1 vs 21±1) or patients with coronary heart disease (SDNN 47±5 vs 38±4, triangular index 8±1 vs 7±1).

Conclusions Brief exposure to dilute diesel exhaust does not alter heart rhythm or heart rate variability in healthy volunteers or well-treated patients with stable coronary heart disease. Autonomic dysfunction does not appear to be a dominant mechanism that can explain the observed excess in cardiovascular events following exposure to combustion-derived air pollution.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:umu:diva-39684 (URN)10.1136/hrt.2010.199042 (DOI)20962342 (PubMedID)
Available from: 2011-02-03 Created: 2011-02-03 Last updated: 2018-06-08Bibliographically approved
Lucking, A. J., Lundbäck, M., Barath, S. L., Mills, N. L., Sidhu, M. K., Langrish, J. P., . . . Blomberg, A. (2011). Particle traps prevent adverse vascular and prothrombotic effects of diesel engine exhaust inhalation in men. Circulation, 123(16), 1721-1728
Open this publication in new window or tab >>Particle traps prevent adverse vascular and prothrombotic effects of diesel engine exhaust inhalation in men
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2011 (English)In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 123, no 16, p. 1721-1728Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: In controlled human exposure studies, diesel engine exhaust inhalation impairs vascular function and enhances thrombus formation. The aim of the present study was to establish whether an exhaust particle trap could prevent these adverse cardiovascular effects in men.

METHODS AND RESULTS: Nineteen healthy volunteers (mean age, 25±3 years) were exposed to filtered air and diesel exhaust in the presence or absence of a particle trap for 1 hour in a randomized, double-blind, 3-way crossover trial. Bilateral forearm blood flow and plasma fibrinolytic factors were assessed with venous occlusion plethysmography and blood sampling during intra-arterial infusion of acetylcholine, bradykinin, sodium nitroprusside, and verapamil. Ex vivo thrombus formation was determined with the use of the Badimon chamber. Compared with filtered air, diesel exhaust inhalation was associated with reduced vasodilatation and increased ex vivo thrombus formation under both low- and high-shear conditions. The particle trap markedly reduced diesel exhaust particulate number (from 150 000 to 300 000/cm(3) to 30 to 300/cm(3); P<0.001) and mass (320±10 to 7.2±2.0 μg/m(3); P<0.001), and was associated with increased vasodilatation, reduced thrombus formation, and an increase in tissue-type plasminogen activator release.

CONCLUSIONS: Exhaust particle traps are a highly efficient method of reducing particle emissions from diesel engines. With a range of surrogate measures, the use of a particle trap prevents several adverse cardiovascular effects of exhaust inhalation in men. Given these beneficial effects on biomarkers of cardiovascular health, the widespread use of particle traps on diesel-powered vehicles may have substantial public health benefits and reduce the burden of cardiovascular disease.

Keywords
air pollution, endothelium, thrombosis
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:umu:diva-51109 (URN)10.1161/CIRCULATIONAHA.110.987263 (DOI)21482966 (PubMedID)
Available from: 2012-01-10 Created: 2012-01-10 Last updated: 2018-06-08Bibliographically approved
Barath, S. (2011). Respiratory and cardiovascular effects of exposure to oxidative air pollutants. (Doctoral dissertation). Umeå: Umeå Universitet
Open this publication in new window or tab >>Respiratory and cardiovascular effects of exposure to oxidative air pollutants
2011 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Background: The negative effects of air pollution on morbidity and mortality have been known since the mid 20th century. The two most well known examples are the Meuse Valley disaster in the 1930’ies and the London black fog in December 1952. Whilst there are numerous epidemiological studies, in which associations between morbidity and mortality and high levels of pollutants have been reported, the underlying mechanisms are not clear. Two of the main air pollutants are particulate matter (PM) mostly emanating from diesel exhaust (DE), and ozone, both of which are highly oxidative. Exposure to DE has resulted in adverse effects both in the respiratory tract and in the cardiovascular system. High ozone levels have also been shown to be associated with increased admissions to hospital for respiratory as well as cardiovascular conditions.

The main aim of this thesis was to investigate the respiratory and cardiovascular effects of a combination of exposures to ozone and DE. DE generated during the urban part of the standardized European Transient Cycle (ETC) was compared to DE generated by an idling engine. It was also evaluated whether an acute exposure to ozone would have any effects on the cardiovascular system as assessed by venous occlusion forearm plethysmography and heart rate variability (HRV). In addition, fraction of exhaled nitric oxide (FENO) was evaluated as a potential marker for acute exposure to ozone or DE.

Methods: Four double-blind randomized cross-over exposure studies were conducted to investigate the effects of ozone and DE on both the respiratory tract and the vascular function in healthy volunteers. All of the exposures were performed in purposely built “walk-in” chambers with strictly controlled exposures. In the first study, the volunteers were exposed to DE (300µg/m3) generated by an idling engine or to air, for one hour in the morning and to ozone (200 ppb) for two hours in the afternoon. A bronchoscopy with bronchial wash (BW) and bronchoalveolar lavage (BAL) was performed 24 hours after the initial exposure. In study II and III, an assessment of vascular function using venous occlusion forearm plethysmography was performed after an exposure to DE (250 µg/m3) generated under transient running conditions, compared to air exposure (study II) and ozone and air exposure (study III). HRV was assessed under a 24 hour period starting before each exposure (study III). In study IV, FENO measurements were conducted after DE and ozone exposures to investigate whether the previously established airway inflammation would be detectable by this non-invasive method.

Results: DE exposure enhanced the established ozone-induced airway inflammation in terms of a pronounced neutrophilia in BW. DE generated under transient running conditions, impaired vascular function in healthy volunteers, whereas exposure to ozone did not. HRV were not altered by exposure to ozone. Exposure to DE caused a significant increase in FENO at the 10  (FENO10) and 50 (FENO50) mL/s flow rates at 6 hours post-exposure, but ozone exposure did not affect FENO at any flow rate or time point.

Conclusion: We have tried to mimic real-life exposure to air pollutants. In the first study, an exposure to DE followed by an exposure to ozone in the afternoon resulted in an enhanced airway inflammation, suggesting an additive or synergistic effect, supporting the epidemiological findings of unfavorable effects of the combination of these two air pollutants. DE generated by an engine running at the urban part of the standardized European Transient Cycle impaired two important and complementary aspects of vascular function, the regulation of vascular tone and endogenous fibrinolysis. This has previously been shown with DE generated at idling conditions. This suggests that the mechanisms behind the adverse effects can be found in the properties of the particles and not in the gaseous components. In these studies, exposure to ozone did not impair vascular function in healthy subjects, or cause any alterations in HRV. This suggests that the epidemiological evidence for an increased risk of cardiovascular mortality following acute exposure to ozone might not be totally accurate. Previous controlled exposure studies with ozone have not shown an airway inflammation affecting the endothelium, at least not in the same time-frame as following DE exposure. FENO could possibly be a useful tool for assessing airway inflammation caused by DE, whereas the powerful oxidant ozone did not affect FENO. This suggests that the airway inflammatory effects caused by these two pollutants are regulated via different mechanisms.

Place, publisher, year, edition, pages
Umeå: Umeå Universitet, 2011. p. 45
Series
Umeå University medical dissertations, ISSN 0346-6612 ; 1443
Keywords
Air Pollution, Particulate Matter, Diesel Exhaust, Ozone, Experimental Exposure studies, Luftföroreningar, Partiklar, Disel avgaser, ozon, Experimentella exponerings studier
National Category
Respiratory Medicine and Allergy
Research subject
Lung Medicine; Cardiology; biology, Environmental Science
Identifiers
urn:nbn:se:umu:diva-46533 (URN)978-91-7459-279-5 (ISBN)
Public defence
2011-10-05, Sal B, Målpunkt T9, Norrlands Universitetssjukhus, 901 85 Umeå, 09:00 (English)
Opponent
Supervisors
Available from: 2011-09-09 Created: 2011-09-05 Last updated: 2018-06-08Bibliographically approved
Sehlstedt, M., Dove, R., Boman, C., Pagels, J., Swietlicki, E., Löndahl, J., . . . Blomberg, A. (2010). Antioxidant airway responses following experimental exposure to wood smoke in man. Particle and fibre toxicology, 7, 21
Open this publication in new window or tab >>Antioxidant airway responses following experimental exposure to wood smoke in man
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2010 (English)In: Particle and fibre toxicology, ISSN 1743-8977, Vol. 7, p. 21-Article in journal (Refereed) Published
Abstract [en]

Exposure of healthy subjects to wood smoke, derived from an experimental wood pellet boiler operating under incomplete combustion conditions with PM emissions dominated by organic matter, caused an increase in mucosal symptoms and GSH in the alveolar respiratory tract lining fluids but no acute airway inflammatory responses. We contend that this response reflects a mobilisation of GSH to the air-lung interface, consistent with a protective adaptation to the investigated wood smoke exposure.

Identifiers
urn:nbn:se:umu:diva-39427 (URN)10.1186/1743-8977-7-21 (DOI)000282501800001 ()20727160 (PubMedID)
Available from: 2011-01-27 Created: 2011-01-27 Last updated: 2018-06-08Bibliographically approved
Langrish, J., Lundbäck, M., Barath, S., Söderberg, S., Mills, N. L., Newby, D., . . . Blomberg, A. (2010). Exposure to nitrogen dioxide is not associated with vascular dysfunction in man. Inhalation Toxicology, 22(3), 192-198
Open this publication in new window or tab >>Exposure to nitrogen dioxide is not associated with vascular dysfunction in man
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2010 (English)In: Inhalation Toxicology, ISSN 0895-8378, E-ISSN 1091-7691, Vol. 22, no 3, p. 192-198Article in journal (Refereed) Published
Abstract [en]

Background: Exposure to air pollution is associated with increased cardiorespiratory morbidity and mortality. It is unclear whether these effects are mediated through combustion-derived particulate matter or gaseous components, such as nitrogen dioxide.

Objectives: To investigate the effect of nitrogen dioxide exposure on vascular vasomotor and six fibrinolytic functions.

Methods: Ten healthy male volunteers were exposed to nitrogen dioxide at 4 ppm or filtered air for 1 h during intermittent exercise in a randomized double-blind crossover study. Bilateral forearm blood flow and fibrinolytic markers were measured before and during unilateral intrabrachial infusion of bradykinin (100–1000 pmol/min), acetylcholine (5–20 μg/min), sodium nitroprusside (2–8 μg/min), and verapamil (10–100 μg/min) 4 h after the exposure. Lung function was determined before and after the exposure, and exhaled nitric oxide at baseline and 1 and 4 h after the exposure.

Results: There were no differences in resting forearm blood flow after either exposure. There was a dose-dependent increase in forearm blood flow with all vasodilators but this was similar after either exposure for all vasodilators (p > .05 for all). Bradykinin caused a dose-dependent increase in plasma tissue-plasminogen activator, but again there was no difference between the exposures. There were no changes in lung function or exhaled nitric oxide following either exposure.

Conclusion: Inhalation of nitrogen dioxide does not impair vascular vasomotor or fibrinolytic function. Nitrogen dioxide does not appear to be a major arbiter of the adverse cardiovascular effects of air pollution.

Place, publisher, year, edition, pages
Informa Healthcare, 2010
Keywords
Air pollution, endothelial function, fibrinolysis, nitrogen dioxide, NO2
National Category
Respiratory Medicine and Allergy
Identifiers
urn:nbn:se:umu:diva-27796 (URN)10.3109/08958370903144105 (DOI)000275067200002 ()
Available from: 2009-11-23 Created: 2009-11-20 Last updated: 2018-06-08Bibliographically approved
Barath, S., Mills, N. L., Lundbäck, M., Törnqvist, H., Lucking, A. J., Langrish, J. P., . . . Blomberg, A. (2010). Impaired vascular function after exposure to diesel exhaust generated at urban transient running conditions. Particle and fibre toxicology, 7(1), 19
Open this publication in new window or tab >>Impaired vascular function after exposure to diesel exhaust generated at urban transient running conditions
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2010 (English)In: Particle and fibre toxicology, ISSN 1743-8977, Vol. 7, no 1, p. 19-Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Traffic emissions including diesel engine exhaust are associated with increased respiratory and cardiovascular morbidity and mortality. Controlled human exposure studies have demonstrated impaired vascular function after inhalation of exhaust generated by a diesel engine under idling conditions.

OBJECTIVES: To assess the vascular and fibrinolytic effects of exposure to diesel exhaust generated during urban-cycle running conditions that mimic ambient 'real-world' exposures.

METHODS: In a randomised double-blind crossover study, eighteen healthy male volunteers were exposed to diesel exhaust (approximately 250 mug/m3) or filtered air for one hour during intermittent exercise. Diesel exhaust was generated during the urban part of the standardized European Transient Cycle. Six hours post-exposure, vascular vasomotor and fibrinolytic function was assessed during venous occlusion plethysmography with intra-arterial agonist infusions.

MEASUREMENTS AND MAIN RESULTS: Forearm blood flow increased in a dose-dependent manner with both endothelial-dependent (acetylcholine and bradykinin) and endothelial-independent (sodium nitroprusside and verapamil) vasodilators. Diesel exhaust exposure attenuated the vasodilatation to acetylcholine (P < 0.001), bradykinin (P < 0.05), sodium nitroprusside (P < 0.05) and verapamil (P < 0.001). In addition, the net release of tissue plasminogen activator during bradykinin infusion was impaired following diesel exhaust exposure (P < 0.05).

CONCLUSION: Exposure to diesel exhaust generated under transient running conditions, as a relevant model of urban air pollution, impairs vasomotor function and endogenous fibrinolysis in a similar way as exposure to diesel exhaust generated at idling. This indicates that adverse vascular effects of diesel exhaust inhalation occur over different running conditions with varying exhaust composition and concentrations as well as physicochemical particle properties. Importantly, exposure to diesel exhaust under ETC conditions was also associated with a novel finding of impaired of calcium channel-dependent vasomotor function. This implies that certain cardiovascular endpoints seem to be related to general diesel exhaust properties, whereas the novel calcium flux-related effect may be associated with exhaust properties more specific for the ETC condition, for example a higher content of diesel soot particles along with their adsorbed organic compounds.

Place, publisher, year, edition, pages
BioMed Central, 2010
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:umu:diva-35381 (URN)10.1186/1743-8977-7-19 (DOI)000282501600001 ()20653945 (PubMedID)
Available from: 2010-08-16 Created: 2010-08-16 Last updated: 2018-06-08Bibliographically approved
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