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Abstract
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.
Acknowledgements
We would like to thank our research nurses Annika Johansson and Frida Holmström; Jamshid Pourazar, Ann-Britt Lundström, Neil Johnston, and the Clinical Pharmacology Department, Edinburgh, for their laboratory work; and the Department of Respiratory Medicine and Allergy, Umeå.
Trial Registration: www.ClinicalTrials.gov; NCT00774514.
Declaration of interest
Dr. Langrish is supported by a British Heart Foundation clinical PhD studentship (FS/07/048). Dr. Blomberg is the holder of the Lars Werkö distinguished research fellowship from the Swedish Heart Lung Foundation. The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.