TOXICOLOGICAL EVALUATION OF REALISTIC EMISSIONS OF SOURCE AEROSOLS (TERESA): APPLICATION TO POWER PLANT-DERIVED PM2.5

Rohr, Annette C. ; Koutrakis, Petros ; Godleski, John

Electric Power Research Institute, Incorporated

关键词: Lungs;    Males;    Organic Compounds;    Blood;    Ph Value;   

DOI  :  10.2172/1039741
RP-ID  :  FC26-03NT41902
RP-ID  :  1039741

美国|英语

来源: UNT Digital Library

【 摘 要 】

Determining the health impacts of different sources and components of fine particulate matter (PM2.5) is an important scientific goal, because PM is a complex mixture of both inorganic and organic constituents that likely differ in their potential to cause adverse health outcomes. The TERESA (Toxicological Evaluation of Realistic Emissions of Source Aerosols) study focused on two PM sources - coal-fired power plants and mobile sources - and sought to investigate the toxicological effects of exposure to realistic emissions from these sources. The DOE-EPRI Cooperative Agreement covered the performance and analysis of field experiments at three power plants. The mobile source component consisted of experiments conducted at a traffic tunnel in Boston; these activities were funded through the Harvard-EPA Particulate Matter Research Center and will be reported separately in the peer-reviewed literature. TERESA attempted to delineate health effects of primary particles, secondary (aged) particles, and mixtures of these with common atmospheric constituents. The study involved withdrawal of emissions directly from power plant stacks, followed by aging and atmospheric transformation of emissions in a mobile laboratory in a manner that simulated downwind power plant plume processing. Secondary organic aerosol (SOA) derived from the biogenic volatile organic compound {alpha}-pinene was added in some experiments, and in others ammonia was added to neutralize strong acidity. Specifically, four scenarios were studied at each plant: primary particles (P); secondary (oxidized) particles (PO); oxidized particles + secondary organic aerosol (SOA) (POS); and oxidized and neutralized particles + SOA (PONS). Extensive exposure characterization was carried out, including gas-phase and particulate species. Male Sprague Dawley rats were exposed for 6 hours to filtered air or different atmospheric mixtures. Toxicological endpoints included (1) breathing pattern; (2) bronchoalveolar lavage (BAL) fluid cytology and biochemistry; (3) blood cytology; (4) in vivo oxidative stress in heart and lung tissue; and (5) heart and lung histopathology. In addition, at one plant, cardiac arrhythmias and heart rate variability (HRV) were evaluated in a rat model of myocardial infarction. Statistical analyses included analyses of variance (ANOVA) to determine differences between exposed and control animals in response to different scenario/plant combinations; univariate analyses to link individual scenario components to responses; and multivariate analyses (Random Forest analyses) to evaluate component effects in a multipollutant setting. Results from the power plant studies indicated some biological responses to some plant/scenario combinations. A number of significant breathing pattern changes were observed; however, significant clinical changes such as specific irritant effects were not readily apparent, and effects tended to be isolated changes in certain respiratory parameters. Some individual exposure scenario components appeared to be more strongly and consistently related to respiratory parameter changes; however, the specific scenario investigated remained a better predictor of response than individual components of that scenario. Bronchoalveolar lavage indicated some changes in cellularity of BAL fluid in response to the POS and PONS scenarios; these responses were considered toxicologically mild in magnitude. No changes in blood cytology were observed at any plant or scenario. Lung oxidative stress was increased with the POS scenario at one plant, and cardiac oxidative stress was increased with the PONS scenario also at one plant, suggesting limited oxidative stress in response to power plant emissions with added atmospheric constituents. There were some mild histological findings in lung tissue in response to the P and PONS scenarios. Finally, the MI model experiments indicated that premature ventricular beat frequency was increased at the plant studied, while no changes in heart rate, HRV, or electrocardiographic intervals were observed. Overall, the TERESA results should be interpreted as indicating toxicologically mild adverse responses to some scenarios. The varied responses among the three plants indicate heterogeneity in emissions. Ongoing studies using the TERESA approach to evaluate the toxicity of traffic-related pollution will yield valuable data for comparative toxicity assessment and will give us a better understanding of the contribution of different sources to the morbidity and mortality associated with exposure to air pollution.