Research
Impaired vascular function after exposure to diesel exhaust generated at urban transient running conditions
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* Corresponding author: Anders Blomberg anders.blomberg@lung.umu.se
1 Department of Public Health and Clinical Medicine, Respiratory Medicine, Umeå University, Umeå, Sweden
2 Division of Respiratory Medicine and Allergy, Department of Medicine, University Hospital, Umeå, Sweden
3 Centre for Cardiovascular Science, Edinburgh University, Edinburgh, UK
4 Department of Public Health and Clinical Medicine, Medicine, Umeå University, Umeå, Sweden
5 Energy Technology and Thermal Process Chemistry, Umeå University, Umeå, Sweden
6 Arrhenius Laboratory, Dept of Analytical Chemistry, Stockholm University, Stockholm, Sweden
7 Division of Nuclear Physics, Department of Physics, Lund University, Lund, Sweden
8 ELEGI Colt Laboratory, Centre for Inflammation Research, Edinburgh University, UK
9 King's College London, MRC-HPA Centre for Environment and Health, School of Biomedical and Health Sciences, London, UK
Particle and Fibre Toxicology 2010, 7:19 doi:10.1186/1743-8977-7-19
Published: 23 July 2010Abstract
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 μg/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.