doi: 10.1161/hc3401.095038
(Circulation. 2001;104:986.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Association of Heart Rate Variability With Occupational and Environmental Exposure to Particulate Air Pollution
From the Department of Environmental Health, Occupational Health (S.R.M, R.H., D.C.C.), Environmental Epidemiology (J.S.), and Environmental Science and Engineering (T.J.S) Programs, Harvard School of Public Health; the Pulmonary and Critical Care Unit (D.C.C.), Department of Medicine, Massachusetts General Hospital, Harvard Medical School; and the Department of Biostatistics (P.L.W.), Harvard School of Public Health, Boston, Mass.
Correspondence to Dr David Christiani, Occupational Health Program, Harvard School of Public Health, 665 Huntington Ave, Bldg 1 Room 1402, Boston, MA 02115. E-mail dchris{at}hohp.harvard.edu
Background— Airborne particulate matter has been linked to excess morbidity and mortality. Recent attention has focused on the effects of particulate exposure on cardiac autonomic control. Inhaled particulates may affect the autonomic nervous system either directly, by eliciting a sympathetic stress response, or indirectly, through inflammatory cytokines produced in the lungs and released into the circulation.
Methods and Results— This longitudinal study examined the association of particulates 
2.5 µm in diameter (PM2.5) with heart rate variability (HRV) in an occupational cohort (N=40). Continuous monitoring of exposure and HR was performed during and away from work. PM2.5 levels were higher than ambient levels typically reported in Boston, 0.167±3.205 mg/m3 (geometric mean±geometric SD). We found a 2.66% decrease (95% CI, -3.75% to -1.58%) in the 5-minute SD of normal RR intervals (SDNN) for every 1 mg/m3 increase in the 4-hour moving PM2.5 average and a 1.02% increase (95% CI, 0.59% to 1.46%) in HR after adjusting for potential confounding factors. The decrease in SDNN became larger as the averaging interval increased.
Conclusions— Workers experienced altered cardiac autonomic control after exposure to occupational and environmental PM2.5. There appears to be either a long-acting (several hours) and a short-acting (several minutes) component to the mechanism of action that may be related to the production of cytokines and the sympathetic stress response, respectively, or a cumulative effect that begins shortly after exposure begins. The clinical significance of these effects in a healthy working population is unclear.
Key Words: air pollution • heart rate • nervous system, autonomic • epidemiology
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