title: Does total antioxidant capacity modify adverse cardiac responses associated with ambient ultrafine, accumulation mode, and fine particles in patients undergoing cardiac rehabilitation?
abstract: Previous studies suggest that pathways reducing oxidative stress may have a protective effect against adverse cardiac responses associated with ambient PM. However, few studies have directly assessed total antioxidant capacity (TAC) as a potential effect modifier of cardiac responses to increased ambient PM.
  
  
  
  We examined if TAC modifies the association between ambient PM and markers of heart rate variability (HRV), repolarization, systemic inflammation, and systolic blood pressure (SBP) in post-infarction patients.
  
  
  
  We recruited 76 patients with a recent coronary event (myocardial infarction or unstable angina) who participated in a cardiac rehabilitation program from June 2006 to November 2009 in Rochester, New York. Ambient fine particle (PM2.5,≤2.5µm in aerodynamic diameter), accumulation mode particle (AMP, 100-500nm) and ultrafine particle (UFP, 10-100nm) concentrations were measured continuously by fixed-site monitors. Markers of HRV and repolarization were measured by continuous Holter electrocardiogram (ECG) recordings before and during exercise sessions of the rehabilitation program. Blood pressure was measured and venous blood samples were collected before exercise to measure TAC and inflammation markers. We applied linear mixed models to assess changes in markers of HRV, repolarization, systemic inflammation, and SBP associated with increased PM concentrations in the low, medium and high TAC tertile groups, after adjusting for covariates including temperature, calendar time since the beginning of the study, visit number, month of year, and hour of day.
  
  
  
  Based on subject-visits with available TAC, we observed increases in SBP, C-reactive protein, and fibrinogen, and decreases in rMSSD (square root of the mean of the sum of the squared differences between adjacent normal to normal intervals) and SDNN (standard deviation of normal to normal beat intervals) associated with increased PM2.5, AMP and UFP in the previous 6-120h (e.g. change in SBP associated with each interquartile range (IQR) increase in PM2.5 lagged 0-5h was 1.27mmHg [95%CI: 0.09, 2.46mmHg]). However, we did not observe a consistent pattern of effect measure modification by TAC for any combination of pollutant and outcome (e.g. changes in SBP associated with each IQR increase in PM2.5 lagged 0-5h for the low, medium and high TAC tertile groups were 1.93mmHg [95%CI: 0.23, 3.63 mmHg], -0.31 mmHg [95%CI: -2.62, 2.01 mmHg], and 1.29mmHg [95%CI: -0.64, 3.21 mmHg], respectively. P for interaction=0.28).
  
  
  
  In a post-infarction population, total antioxidant capacity does not appear to modify the association between biomarkers of heart rate variability, repolarization, systemic inflammation, and systolic blood pressure and ambient PM concentrations in the previous 6-120h.
authors.affiliation: Division of Epidemiology, Department of Public Health Sciences, University of Rochester Medical Center, Rochester, NY, USA.
authors.forename: Meng
authors.initials: M
authors.lastname: Wang
authors.affiliation: Division of Pulmonary and Critical Care, Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA.
authors.forename: Mark J
authors.initials: MJ
authors.lastname: Utell
authors.affiliation: Institute of Epidemiology II, Helmholtz Zentrum Muenchen - German Research Center for Environmental Health, Neuherberg, Germany.
authors.forename: Alexandra
authors.initials: A
authors.lastname: Schneider
authors.affiliation: Division of Cardiology, Department of Medicine, University of Rochester Medical Center, NY, USA.
authors.forename: Wojciech
authors.initials: W
authors.lastname: Zareba
authors.affiliation: Division of Pulmonary and Critical Care, Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA.
authors.forename: Mark W
authors.initials: MW
authors.lastname: Frampton
authors.affiliation: Department of Biostatistics and Computational Biology, University of Rochester Medical Center, Rochester, NY, USA.
authors.forename: David
authors.initials: D
authors.lastname: Oakes
authors.affiliation: Center for Air Resources Engineering and Science, Clarkson University, Potsdam, NY, USA.
authors.forename: Philip K
authors.initials: PK
authors.lastname: Hopke
authors.affiliation: Department of Biostatistics and Computational Biology, University of Rochester Medical Center, Rochester, NY, USA.
authors.forename: Jelani
authors.initials: J
authors.lastname: Wiltshire
authors.affiliation: Division of Epidemiology, Department of Public Health Sciences, University of Rochester Medical Center, Rochester, NY, USA.
authors.forename: Cathleen
authors.initials: C
authors.lastname: Kane
authors.affiliation: Institute of Epidemiology II, Helmholtz Zentrum Muenchen - German Research Center for Environmental Health, Neuherberg, Germany.
authors.forename: Annette
authors.initials: A
authors.lastname: Peters
authors.affiliation: Institute of Epidemiology II, Helmholtz Zentrum Muenchen - German Research Center for Environmental Health, Neuherberg, Germany.
authors.forename: Susanne
authors.initials: S
authors.lastname: Breitner
authors.affiliation: Division of Pulmonary and Critical Care, Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA.
authors.forename: David
authors.initials: D
authors.lastname: Chalupa
authors.affiliation: Division of Epidemiology, Department of Public Health Sciences, University of Rochester Medical Center, Rochester, NY, USA. Electronic address: david_rich@urmc.rochester.edu.
authors.forename: David Q
authors.initials: DQ
authors.lastname: Rich
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000393:Air Pollutants / Q000633:toxicity*; D000975:Antioxidants / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D000072038:Cardiac Rehabilitation / Q000706:statistics & numerical data; D004781:Environmental Exposure; D005260:Female; D006331:Heart Diseases / Q000139:chemically induced*; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D007249:Inflammation / Q000139:chemically induced; D008297:Male; D008875:Middle Aged; D009518:New York; D018384:Oxidative Stress / Q000187:drug effects; D010316:Particle Size; D052638:Particulate Matter / Q000633:toxicity*; D013997:Time Factors
chemical_list: D000393:Air Pollutants; D000975:Antioxidants; D052638:Particulate Matter
keywords: Heart rate variability; Inflammation; Particulate matter; Repolarization; Total antioxidant capacity