title: Are ambient ultrafine, accumulation mode, and fine particles associated with adverse cardiac responses in patients undergoing cardiac rehabilitation?
abstract: BACKGROUND
  Mechanisms underlying previously reported air pollution and cardiovascular (CV) morbidity associations remain poorly understood.
  
  
  OBJECTIVE
  We examined associations between markers of pathways thought to underlie these air pollution and CV associations and ambient particle concentrations in postinfarction patients.
  
  
  METHODS
  We studied 76 patients, from June 2006 to November 2009, who participated in a 10-week cardiac rehabilitation program following a recent (within 3 months) myocardial infarction or unstable angina. Ambient ultrafine particle (UFP; 10-100 nm), accumulation mode particle (AMP; 100-500 nm), and fine particle concentrations (PM2.5; ≤ 2.5 μm in aerodynamic diameter) were monitored continuously. Continuous Holter electrocardiogram (ECG) recordings were made before and during supervised, graded, twice weekly, exercise sessions. A venous blood sample was collected and blood pressure was measured before sessions.
  
  
  RESULTS
  Using mixed effects models, we observed adverse changes in rMSSD [square root of the mean of the sum of the squared differences between adjacent normal-to-normal (NN) intervals], SDNN (standard deviation of all NN beat intervals), TpTe (time from peak to end of T-wave), heart rate turbulence, systolic and diastolic blood pressures, C-reactive protein, and fibrinogen associated with interquartile range increases in UFP, AMP, and PM2.5 at 1 or more lag times within the previous 5 days. Exposures were not associated with MeanNN, heart-rate-corrected QT interval duration (QTc), deceleration capacity, and white blood cell count was not associated with UFP, AMP, and PM2.5 at any lag time.
  
  
  CONCLUSIONS
  In cardiac rehabilitation patients, particles were associated with subclinical decreases in parasympathetic modulation, prolongation of late repolarization duration, increased blood pressure, and systemic inflammation. It is possible that such changes could increase the risk of CV events in this susceptible population.
authors.affiliation: Department of Community and Preventive Medicine, University of Rochester Medical Center, Rochester, New York 14642, USA. david_rich@urmc.rochester.edu
authors.forename: David Q
authors.initials: DQ
authors.lastname: Rich
authors.forename: Wojciech
authors.initials: W
authors.lastname: Zareba
authors.forename: William
authors.initials: W
authors.lastname: Beckett
authors.forename: Philip K
authors.initials: PK
authors.lastname: Hopke
authors.forename: David
authors.initials: D
authors.lastname: Oakes
authors.forename: Mark W
authors.initials: MW
authors.lastname: Frampton
authors.forename: John
authors.initials: J
authors.lastname: Bisognano
authors.forename: David
authors.initials: D
authors.lastname: Chalupa
authors.forename: Jan
authors.initials: J
authors.lastname: Bausch
authors.forename: Karen
authors.initials: K
authors.lastname: O'Shea
authors.forename: Yungang
authors.initials: Y
authors.lastname: Wang
authors.forename: Mark J
authors.initials: MJ
authors.lastname: Utell
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D005260:Female; D006331:Heart Diseases / Q000534:rehabilitation*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010316:Particle Size