Grantee Research Project Results
2006 Progress Report: Air Pollutants: Cardiovascular Effects and Mechanisms
EPA Grant Number: R831918Title: Air Pollutants: Cardiovascular Effects and Mechanisms
Investigators: Bonham, Ann
Institution: University of California - Davis
EPA Project Officer: Chung, Serena
Project Period: August 1, 2004 through July 31, 2008 (Extended to July 31, 2009)
Project Period Covered by this Report: August 1, 2005 through July 31, 2006
Project Amount: $1,510,000
RFA: The Role of Air Pollutants in Cardiovascular Disease (2003) RFA Text | Recipients Lists
Research Category: Airborne Particulate Matter Health Effects , Air
Objective:
To resolve the underlying mechanisms(s) mediating the airborne particulate matter exposure induced reduced heart rate variability in an animal model using environmentally relevant “real world” particulate pollutants.
Progress Summary:
Epidemiological, clinical and experimental evidence suggest that exposure to airborne particles is correlated with increased cardiovascular disease-related morbidity and mortality, and that impaired cardiac autonomic function, as indexed by an overall reduced heart rate variability (HRV) may be one underlying cause. We hypothesized that subtle impairments of cardiac autonomic function associated with background exposure to airborne particles may be exaggerated during acute stresses associated with daily living. We tested the hypothesis in a mouse model by determining whether exposures to concentrated real world particles would further decrease the HRV evoked by an acute (2 hr) stressor, restraint stress. C57BL/6 mice were exposed to either filtered air (FA, n=18) or concentrated air particles (CAP, n=18) (6 hrs/day, 5 d/week for 2 wk) in the Sacramento-Davis area. Air particles were concentrated 21-fold (160 μg/m3 total suspended particles). Heart rate and heart rate variability were measured in freely moving mice before, during and after the acute stress at the end of each week of exposure. In the FA group, stress reduced HRV measures in the time domain in the first week but not in the second week. In the CAP group, stress reduced HRV measures in the time domain the first week to the same extent as occurred in the FA group. However, in the second week, CAP exposure further reduced stress-induced HRV measures (p<0.05). The data suggest that background exposures to airborne particles may increase cardiovascular consequences by attenuating the adaptive response to acute stressors.
Future Activities:
The investigator plans to: (1) continue with exposures in summer season; (2) expose aged mice; (3) analyze the HRV, particle concentration and composition, and stress test results; and (4) patch-clamping analysis of identified cardiac vagal neurons.
Journal Articles:
No journal articles submitted with this report: View all 13 publications for this projectSupplemental Keywords:
air pollutants, heart rate variability, electrophysiology,, Health, RFA, Scientific Discipline, Air, Health Risk Assessment, Risk Assessments, particulate matter, Environmental Chemistry, Biochemistry, Toxicology, ambient aerosol, lung disease, long term exposure, airborne particulate matter, cardiovascular vulnerability, ambient particle health effects, acute cardiovascular effects, cardiovascular disease, lung injuryProgress and Final Reports:
Original AbstractThe perspectives, information and conclusions conveyed in research project abstracts, progress reports, final reports, journal abstracts and journal publications convey the viewpoints of the principal investigator and may not represent the views and policies of ORD and EPA. Conclusions drawn by the principal investigators have not been reviewed by the Agency.