title: Reduction in heart rate variability with traffic and air pollution in patients with coronary artery disease.
abstract: BACKGROUND
  Ambient particulate pollution and traffic have been linked to myocardial infarction and cardiac death risk. Possible mechanisms include autonomic cardiac dysfunction.
  
  
  METHODS
  In a repeated-measures study of 46 patients 43-75 years of age, we investigated associations of central-site ambient particulate pollution, including black carbon (BC) (a marker for regional and local traffic), and report of traffic exposure with changes in half-hourly averaged heart rate variability (HRV), a marker of autonomic function measured by 24-hr Holter electrocardiogram monitoring. Each patient was observed up to four times within 1 year after a percutaneous intervention for myocardial infarction, acute coronary syndrome without infarction, or stable coronary artery disease (4,955 half-hour observations). For each half-hour period, diary data defined whether the patient was home or not home, or in traffic.
  
  
  RESULTS
  A decrease in high frequency (HF; an HRV marker of vagal tone) of 16.4% [95% confidence interval (CI), 20.7 to 11.8%] was associated with an interquartile range of 0.3-microg/m3 increase in prior 5-day averaged ambient BC. Decreases in HF were independently associated both with the previous 2-hr averaged BC (10.4%; 95% CI, 15.4 to 5.2%) and with being in traffic in the previous 2 hr (38.5%; 95% CI, 57.4 to 11.1%). We also observed independent responses for particulate air matter with aerodynamic diameter < or = 2.5 microm and for gases (ozone or nitrogen dioxide).
  
  
  CONCLUSIONS
  After hospitalization for coronary artery disease, both particulate pollution and being in traffic, a marker of stress and pollution, were associated with decreased HRV.
authors.affiliation: Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02215, USA. azanobet@hsph.harvard.edu
authors.forename: Antonella
authors.initials: A
authors.lastname: Zanobetti
authors.forename: Diane R
authors.initials: DR
authors.lastname: Gold
authors.forename: Peter H
authors.initials: PH
authors.lastname: Stone
authors.forename: Helen H
authors.initials: HH
authors.lastname: Suh
authors.forename: Joel
authors.initials: J
authors.lastname: Schwartz
authors.forename: Brent A
authors.initials: BA
authors.lastname: Coull
authors.forename: Frank E
authors.initials: FE
authors.lastname: Speizer
mesh_terms: D000328:Adult; D000368:Aged; D000393:Air Pollutants / Q000633:toxicity*; D001900:Boston; D002244:Carbon / Q000633:toxicity; D003324:Coronary Artery Disease / Q000503:physiopathology*; D015716:Electrocardiography, Ambulatory; D005260:Female; D006339:Heart Rate / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D018986:Motor Vehicles; D009203:Myocardial Infarction / Q000503:physiopathology; D010316:Particle Size; D052638:Particulate Matter / Q000633:toxicity*; D013997:Time Factors
chemical_list: D000393:Air Pollutants; D052638:Particulate Matter; D002244:Carbon