title: Ambient fine particulate matter exposure and myocardial ischemia in the Environmental Epidemiology of Arrhythmogenesis in the Women's Health Initiative (EEAWHI) study.
abstract: BACKGROUND
  Ambient particulate matter (PM) air pollution is associated with coronary heart disease, but the pathways underlying the association remain to be elucidated.
  
  
  METHODS
  We studied the association between PM and ischemia among 57,908 Women's Health Initiative clinical trial participants from 1999-2003. We used the Minnesota Code criteria to identify ST-segment and T-wave abnormalities, and estimated T amplitude (microvolt) from resting, standard 12-lead electrocardiogram (ECG). We used U.S. Environmental Protection Agency's monitor data to estimate concentrations of PM < 2.5 microm (PM(2.5)) at geocoded participant addresses over 6 days before the ECGs (lag0 through lag5). We excluded 2,379 women with ECG QRS duration > or = 120 msec.
  
  
  RESULTS
  Overall, 6% of the remaining 55,529 women (52-90 years of age; 83% non-Hispanic white) had ST abnormalities and 16% had T abnormalities. Lead-specific T amplitude was normally distributed (range of means from -14 to 349 microV). PM(2.5) (mean +/- SD) averaged over lag(0-2) was 14 +/- 7 microg/m(3). In logistic and linear regression models adjusted for demographic, clinical, temporal, and climatic factors, a 10-microg/m(3) increase in lag(0-2) PM(2.5) was associated with a 4% [95% confidence interval (CI), -3%, to 10%] increase in the odds of ST abnormality and a 5% (95% CI, 0% to 9%) increase in the odds of T abnormality. We observed corresponding decreases in T amplitude in all exam sites and leads except lead V1, reaching a minimum of -2 microV (95% CI, -5 to 0 microV) in lead V3.
  
  
  CONCLUSIONS
  Short-term PM(2.5) exposure is associated with ECG evidence of myocardial ischemia among postmenopausal women. The principal manifestations include subclinical but potentially arrhythmogenic ST-T abnormalities and decreases in T amplitude.
authors.affiliation: Epidemiologic Cardiology Research Center, Department of Epidemiology and Prevention, Division of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27104, USA. zmzhang@wfubmc.edu
authors.forename: Zhu-Ming
authors.initials: ZM
authors.lastname: Zhang
authors.forename: Eric A
authors.initials: EA
authors.lastname: Whitsel
authors.forename: P Miguel
authors.initials: PM
authors.lastname: Quibrera
authors.forename: Richard L
authors.initials: RL
authors.lastname: Smith
authors.forename: Duanping
authors.initials: D
authors.lastname: Liao
authors.forename: Garnet L
authors.initials: GL
authors.lastname: Anderson
authors.forename: Ronald J
authors.initials: RJ
authors.lastname: Prineas
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000393:Air Pollutants / Q000633:toxicity*; D001145:Arrhythmias, Cardiac / Q000139:chemically induced* / Q000453:epidemiology; D002318:Cardiovascular Diseases / Q000139:chemically induced / Q000453:epidemiology; D002986:Clinical Trials as Topic; D004562:Electrocardiography; D004781:Environmental Exposure; D005260:Female; D006801:Humans; D008875:Middle Aged; D015999:Multivariate Analysis; D017202:Myocardial Ischemia / Q000453:epidemiology / Q000209:etiology*; D052638:Particulate Matter / Q000633:toxicity*
chemical_list: D000393:Air Pollutants; D052638:Particulate Matter