Final Report: Air Pollutants: Cardiovascular Effects and MechanismsEPA Grant Number: R831918
Title: 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 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 , Health Effects , Air
Objective:To resolve the underlying mechanism(s) mediating the airborne particulate matter exposure induced reduced heart rate variability in an animal model using environmentally relevant “real world” particulate pollutants.
Summary/Accomplishments (Outputs/Outcomes):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 in 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 particulates would further decrease HRV and increase arrhythmia occurrences evoked by an acute (2 hr) stress, 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/wk for 2 wks) in the Sacramento-Davis area. Heart rate, HRV, premature ventricular contractions, and A-V blocks were measured in freely moving mice before, during and after the acute stress at the end of each week of exposure. Under these background exposure conditions there were no changes in the lung and systemic inflammation profile or baseline HRV measures; however the CAP group displayed greater deficits in HRV with repeated stresses. The acute restraint stress in the first week triggered dramatic falls in HRV measures in the time domain to the same degree in both the CAP and FA-exposed animals. However, following the second week of exposures, the FA (control) animals adapted to the acute stress, experiencing a much smaller decrease in HRV compared to their response to the stress in the first week, while the CAP-exposed group experienced similar reductions in HRV in the second week (p<0.05) as well as an increased arrhythmia occurrence.
Conclusions:The data suggest that background exposures to airborne particulates may increase cardiovascular consequences by attenuating the adaptive response to acute stresses in the absence of apparent inflammation.
Journal Articles on this Report : 2 Displayed | Download in RIS Format
|Other project views:||All 13 publications||2 publications in selected types||All 2 journal articles|
||Chen C-Y, Chow D, Chiamvimonvat N, Glatter KA, Li N, He Y, Pinkerton KE, Bonham AC. Short-term secondhand smoke exposure decreases heart rate variability and increases arrhythmia susceptibility in mice. American Journal of Physiology-Heart and Circulatory Physiology 2008;295(2):H632-H639.||
||Pham H, Bonham AC, Pinkerton KE, Chen CY. Central neuroplasticity and decreased heart rate variability after particulate matter exposure in mice. Environmental Health Perspectives 2009;117(9):1448-1453.||