rss
Occup Environ Med 69:587-591 doi:10.1136/oemed-2011-100126
  • Environment
  • Original article

Lack of effect of nitrogen dioxide exposure on heart rate variability in patients with stable coronary heart disease and impaired left ventricular systolic function

  1. Jon G Ayres5
  1. 1Department of Environmental and Occupational Medicine, University of Aberdeen, Aberdeen, UK
  2. 2Department of Cardiology, Aberdeen Royal Infirmary, Aberdeen, UK
  3. 3Cardiovascular Division, The George Institute for Global Health, Sydney, Australia
  4. 4Wildlife Conservation Research Unit, The Recanati-Kaplan Centre, Department of Zoology, Oxford University, Oxford, UK
  5. 5Institute of Occupational & Environmental Medicine, University of Birmingham, Birmingham, UK
  1. Correspondence to Professor Jon G Ayres, Institute of Occupational & Environmental Medicine, University of Birmingham, Birmingham B15 2TT, UK; j.g.ayres{at}bham.ac.uk
  • Accepted 3 May 2012
  • Published Online First 12 June 2012

Abstract

Objectives Epidemiological studies of air pollution on cardiovascular health show associations of cardiac mortality and admissions with exposure to nitrogen dioxide (NO2) at low concentrations. These associations could be causal or NO2 could be acting as a surrogate measure for another air pollutant, most likely ultrafine particles. No studies of cardiac susceptibility to acute exposure to NO2 have been undertaken.

Methods Randomised controlled exposures to NO2 (400 ppb for 1 h) and air in subjects with coronary heart disease and impaired left ventricular systolic function not taking β adrenoceptor blocking drugs.

Results There were no significant changes in heart rate, blood pressure, leucocyte coping capacity or any heart rate variability measure following NO2 exposure compared with air.

Conclusion These findings suggest that NO2 does not affect heart rate variability at these concentrations (which are high for urban background levels) and in the absence of other pollutants. While a synergistic effect has not been ruled out, these data lend support to the idea that the epidemiological data associating cardiac outcomes with NO2 are more likely due to an associated pollutant rather than NO2 itself.

Footnotes

  • Funding This project was supported by a grant from the Colt Foundation.

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval Ethical approval was provided by the Grampian NHS Regional Ethics Committee.

  • Provenance and peer review Not commissioned; externally peer reviewed.