Does total antioxidant capacity modify adverse cardiac responses associated with ambient ultrafine, accumulation mode, and fine particles in patients undergoing cardiac rehabilitation?
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 am...
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| Published in | Environmental research Vol. 149; pp. 15 - 22 |
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| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier Inc
01.08.2016
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0013-9351 1096-0953 1096-0953 |
| DOI | 10.1016/j.envres.2016.04.031 |
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| 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.
•Ambient PM pollution associated with increased inflammation, blood pressure, & HRV•Total antioxidant capacity does not modify blood pressure responses to ambient PM•Total antioxidant capacity does not modify inflammatory responses to ambient PM•Total antioxidant capacity does not modify HRV responses to ambient PM•Total antioxidant capacity does not modify T-wave complexity responses to ambient PM |
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| AbstractList | Background 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. Objectives 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. Methods 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, less than or equal to 2.5 mu m 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. Results 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). Conclusions 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. 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. 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. •Ambient PM pollution associated with increased inflammation, blood pressure, & HRV•Total antioxidant capacity does not modify blood pressure responses to ambient PM•Total antioxidant capacity does not modify inflammatory responses to ambient PM•Total antioxidant capacity does not modify HRV responses to ambient PM•Total antioxidant capacity does not modify T-wave complexity responses to ambient PM 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. 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.BACKGROUNDPrevious 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.OBJECTIVESWe 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.METHODSWe 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).RESULTSBased 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.CONCLUSIONSIn 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. |
| Author | Schneider, Alexandra Breitner, Susanne Wiltshire, Jelani Zareba, Wojciech Peters, Annette Wang, Meng Utell, Mark J. Hopke, Philip K. Kane, Cathleen Frampton, Mark W. Chalupa, David Oakes, David Rich, David Q. |
| AuthorAffiliation | 2 Division of Pulmonary and Critical Care, Department of Medicine, University of Rochester Medical Center, Rochester, New York, USA 5 Department of Biostatistics and Computational Biology, University of Rochester Medical Center, Rochester, New York, USA 1 Division of Epidemiology, Department of Public Health Sciences, University of Rochester Medical Center, Rochester, New York, USA 4 Division of Cardiology, Department of Medicine, University of Rochester Medical Center, New York, USA 3 Institute of Epidemiology II, Helmholtz Zentrum Muenchen - German Research Center for Environmental Health, Neuherberg, Germany 6 Center for Air Resources Engineering and Science, Clarkson University, Potsdam, NY, USA |
| AuthorAffiliation_xml | – name: 1 Division of Epidemiology, Department of Public Health Sciences, University of Rochester Medical Center, Rochester, New York, USA – name: 5 Department of Biostatistics and Computational Biology, University of Rochester Medical Center, Rochester, New York, USA – name: 3 Institute of Epidemiology II, Helmholtz Zentrum Muenchen - German Research Center for Environmental Health, Neuherberg, Germany – name: 6 Center for Air Resources Engineering and Science, Clarkson University, Potsdam, NY, USA – name: 4 Division of Cardiology, Department of Medicine, University of Rochester Medical Center, New York, USA – name: 2 Division of Pulmonary and Critical Care, Department of Medicine, University of Rochester Medical Center, Rochester, New York, USA |
| Author_xml | – sequence: 1 givenname: Meng surname: Wang fullname: Wang, Meng organization: Division of Epidemiology, Department of Public Health Sciences, University of Rochester Medical Center, Rochester, NY, USA – sequence: 2 givenname: Mark J. surname: Utell fullname: Utell, Mark J. organization: Division of Pulmonary and Critical Care, Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA – sequence: 3 givenname: Alexandra surname: Schneider fullname: Schneider, Alexandra organization: Institute of Epidemiology II, Helmholtz Zentrum Muenchen - German Research Center for Environmental Health, Neuherberg, Germany – sequence: 4 givenname: Wojciech surname: Zareba fullname: Zareba, Wojciech organization: Division of Cardiology, Department of Medicine, University of Rochester Medical Center, NY, USA – sequence: 5 givenname: Mark W. surname: Frampton fullname: Frampton, Mark W. organization: Division of Pulmonary and Critical Care, Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA – sequence: 6 givenname: David surname: Oakes fullname: Oakes, David organization: Department of Biostatistics and Computational Biology, University of Rochester Medical Center, Rochester, NY, USA – sequence: 7 givenname: Philip K. surname: Hopke fullname: Hopke, Philip K. organization: Center for Air Resources Engineering and Science, Clarkson University, Potsdam, NY, USA – sequence: 8 givenname: Jelani surname: Wiltshire fullname: Wiltshire, Jelani organization: Department of Biostatistics and Computational Biology, University of Rochester Medical Center, Rochester, NY, USA – sequence: 9 givenname: Cathleen surname: Kane fullname: Kane, Cathleen organization: Division of Epidemiology, Department of Public Health Sciences, University of Rochester Medical Center, Rochester, NY, USA – sequence: 10 givenname: Annette surname: Peters fullname: Peters, Annette organization: Institute of Epidemiology II, Helmholtz Zentrum Muenchen - German Research Center for Environmental Health, Neuherberg, Germany – sequence: 11 givenname: Susanne surname: Breitner fullname: Breitner, Susanne organization: Institute of Epidemiology II, Helmholtz Zentrum Muenchen - German Research Center for Environmental Health, Neuherberg, Germany – sequence: 12 givenname: David surname: Chalupa fullname: Chalupa, David organization: Division of Pulmonary and Critical Care, Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA – sequence: 13 givenname: David Q. surname: Rich fullname: Rich, David Q. email: david_rich@urmc.rochester.edu organization: Division of Epidemiology, Department of Public Health Sciences, University of Rochester Medical Center, Rochester, NY, USA |
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| Copyright | 2016 Elsevier Inc. Copyright © 2016 Elsevier Inc. All rights reserved. |
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| Snippet | Previous studies suggest that pathways reducing oxidative stress may have a protective effect against adverse cardiac responses associated with ambient PM.... Background Previous studies suggest that pathways reducing oxidative stress may have a protective effect against adverse cardiac responses associated with... |
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| SubjectTerms | adenosine monophosphate Aged Aged, 80 and over Air Pollutants - toxicity antioxidant activity Antioxidants - metabolism biomarkers Blood Pressure - drug effects blood sampling C-reactive protein Cardiac Rehabilitation - statistics & numerical data electrocardiography Environmental Exposure exercise Female fibrinogen Heart Diseases - chemically induced heart rate Heart Rate - drug effects Heart rate variability Humans Inflammation Inflammation - chemically induced Male Middle Aged myocardial infarction New York oxidative stress Oxidative Stress - drug effects Particle Size Particulate matter Particulate Matter - toxicity particulates patients pollutants protective effect Repolarization statistical analysis systolic blood pressure temperature Time Factors Total antioxidant capacity |
| Title | Does total antioxidant capacity modify adverse cardiac responses associated with ambient ultrafine, accumulation mode, and fine particles in patients undergoing cardiac rehabilitation? |
| URI | https://dx.doi.org/10.1016/j.envres.2016.04.031 https://www.ncbi.nlm.nih.gov/pubmed/27174779 https://www.proquest.com/docview/1797250706 https://www.proquest.com/docview/1808694326 https://www.proquest.com/docview/2116937577 https://pubmed.ncbi.nlm.nih.gov/PMC4907837 |
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