Diesel exhaust inhalation does not affect heart rhythm or heart rate variability

作者：Mills Nicholas L^*; Finlayson Alexander E; Gonzalez Manuel C; Tornqvist Hakan; Barath Stefan; Vink Elen; Goudie Colin; Langrish Jeremy P; Soderberg Stefan; Boon Nicholas A; Fox Keith A A; Donaldson Ken; Sandstrom Thomas; Blomberg Anders; Newby David E

来源：Heart, 2011, 97(7): 544-550.

DOI：10.1136/hrt.2010.199042

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 mu g/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 10166 vs 9166, 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.

• 出版日期2011-4