title: The effect of air pollution on spatial dispersion of myocardial repolarization in healthy human volunteers.
abstract: OBJECTIVE
  We tested the hypothesis that exposure to concentrated ambient particles (CAP) and/or ozone (O(3)) would increase dispersion of ventricular repolarization.
  
  
  BACKGROUND
  Elevated levels of air pollution are associated with cardiac arrhythmias through mechanisms yet to be elucidated.
  
  
  METHODS
  Each of 25 volunteers (18 to 50 years of age) had four 2-h exposures to 150 μg/m(3) CAP; 120 parts per billion O(3); CAP + O(3); and filtered air (FA). Exposure-induced changes (Δ = 5-min epochs at end-start) in spatial dispersion of repolarization were determined from continuous 12-lead electrocardiographic recording.
  
  
  RESULTS
  Spatial dispersion of repolarization assessed by corrected ΔT-wave peak to T-wave end interval increased significantly for CAP + O(3) (0.17 ± 0.03, p < 0.0001) exposure only, remaining significant when factoring FA (CAP + O(3) - FA) as control (0.11 ± 0.04, p = 0.013). The influence on repolarization was further verified by a significant increase in ΔQT dispersion (for CAP + O(3) compared with FA (5.7 ± 1.4, p = 0.0002). When the low-frequency to high-frequency ratio of heart rate variability (a conventional representation of sympathetic-parasympathetic balances) was included as a covariate, the effect estimate was positive for both corrected ΔT-wave peak to T-wave end interval (p = 0.002) and ΔQT dispersion (p = 0.038). When the high-frequency component (parasympathetic heart rate modulation) was included as a covariate with corrected ΔT-wave peak to T-wave end interval, the effect estimate for high frequency was inverse (p = 0.02).
  
  
  CONCLUSIONS
  CAP + O(3) exposure alters dispersion of ventricular repolarization in part by increasing sympathetic and decreasing parasympathetic heart rate modulation. Detection of changes in repolarization parameters, even in this small cohort of healthy individuals, suggests an underappreciated role for air pollutants in urban arrhythmogenesis.
authors.affiliation: Division of Cardiology, Toronto General Hospital, Toronto, Ontario, Canada.
authors.forename: Gopal
authors.initials: G
authors.lastname: Sivagangabalan
authors.forename: Danna
authors.initials: D
authors.lastname: Spears
authors.forename: Stephane
authors.initials: S
authors.lastname: Masse
authors.forename: Bruce
authors.initials: B
authors.lastname: Urch
authors.forename: Robert D
authors.initials: RD
authors.lastname: Brook
authors.forename: Frances
authors.initials: F
authors.lastname: Silverman
authors.forename: Diane R
authors.initials: DR
authors.lastname: Gold
authors.forename: Karl Z
authors.initials: KZ
authors.lastname: Lukic
authors.forename: Mary
authors.initials: M
authors.lastname: Speck
authors.forename: Marjan
authors.initials: M
authors.lastname: Kusha
authors.forename: Talha
authors.initials: T
authors.lastname: Farid
authors.forename: Kwaku
authors.initials: K
authors.lastname: Poku
authors.forename: Evelyn
authors.initials: E
authors.lastname: Shi
authors.forename: John
authors.initials: J
authors.lastname: Floras
authors.forename: Kumaraswamy
authors.initials: K
authors.lastname: Nanthakumar
mesh_terms: D000293:Adolescent; D000328:Adult; D000397:Air Pollution / Q000009:adverse effects*; D001145:Arrhythmias, Cardiac / Q000209:etiology* / Q000503:physiopathology; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006329:Heart Conduction System / Q000187:drug effects* / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects* / Q000502:physiology; D006352:Heart Ventricles / Q000187:drug effects* / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D052638:Particulate Matter / Q000009:adverse effects; D012016:Reference Values; D055815:Young Adult
chemical_list: D052638:Particulate Matter