Grantee Research Project Results
2007 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, 2006 through July 31, 2007
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 or concentrated air particles (6 hrs/day, 5 d/week for 2 wk) in three seasons. 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. For fall season, the average ambient particle concentration for fall was 7.6 μg/m3. 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 ambient particle concentration for first week of winter season was 23.7 7.6 μg/m3. There was a trend for a greater reduction in restraint-induced reduced HRV in the mice exposed to CAP. The data suggest that background exposures to airborne particles may increase cardiovascular consequences by attenuating the adaptive response to acute stressors.
Future Activities:
1) with exposures in spring season, 2) exposing aged mice, 3) analyzing the HRV, particle concentration and composition, stress test results and 3) extend the existing aims 4 and 5 to look at ambient air pollutant-induced changes in the neuromodulators in the nucleus ambiguous and receptor subtypes in the cardiac vagal neurons with immunofluorescence technique. The findings from this extended aim will yield more mechanistic details in exposure-induced changes in synaptic transmission and hence, reduced heart rate variability.
Journal Articles:
No journal articles submitted with this report: View all 13 publications for this projectSupplemental Keywords:
air pollutants, heart rate variability, electrophysiology,, RFA, Scientific Discipline, Health, Air, Toxicology, particulate matter, Health Risk Assessment, Environmental Chemistry, Risk Assessments, Biochemistry, ambient aerosol, lung injury, acute cardiovascular effects, long term exposure, lung disease, airway disease, airborne particulate matter, cardiovascular vulnerability, ambient particle health effectsProgress 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.