Final Report: Toxicological Evaluation of Realistic Emissions of Source Aerosols (TERESA) StudyEPA Grant Number: R827353C013
Subproject: this is subproject number 013 , established and managed by the Center Director under grant R827353
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
Center: EPA Harvard Center for Ambient Particle Health Effects
Center Director: Koutrakis, Petros
Title: Toxicological Evaluation of Realistic Emissions of Source Aerosols (TERESA) Study
Investigators: Koutrakis, Petros , Lawrence, Joy , Ruiz, Pablo , Wolfson, Jack M.
Institution: Harvard University
EPA Project Officer: Chung, Serena
Project Period: June 1, 1999 through May 31, 2005 (Extended to May 31, 2006)
RFA: Airborne Particulate Matter (PM) Centers (1999) RFA Text | Recipients Lists
Research Category: Air Quality and Air Toxics , Particulate Matter , Air
Theme III: Biological Mechanisms/Dosimetry: Theme III focused upon mechanisms of cardiac vulnerability as a result of air pollution exposure. Many of our concentrated ambient particles (CAPs) animal toxicology and human panel studies have linked pulmonary and cardiovascular health outcomes to different particulate matter (PM) components such as trace metals, elemental carbon (EC), sulfates and silicon (Batalha, et al., 2002; Clarke, et al., 2000; Saldiva, et al., 2002). Reanalysis of the Harvard Six Cities study provided strong evidence of increased toxicity associated with combustion-related PM from traffic and power plants compared to soil dust (Laden, et al., 2000).
The objectives of Theme III were to identify the particulate and gaseous air pollutants responsible for increased cardiac vulnerability as an adverse health effect and to define the biological mechanisms that lead to this outcome. As part of this theme, we specifically worked to: (1) identify the physical and chemical properties of particulate matter responsible for the observed adverse health effects; (2) determine whether gaseous co-pollutants exacerbate the effects of particles; (3) investigate the biological mechanisms by which particulate matter produces mortality and acute or chronic morbidity; and (4) examine particle deposition patterns and fate in the respiratory tract. These objectives were addressed in several areas of research that explored the components of air pollution that cause adverse health effects and the biological mechanisms that may lead to fatal outcomes. The projects under this theme built upon the findings from a number of our previous animal studies, which made it possible to explore and define both cardiac and pulmonary responses to inhaled fly ash and concentrated ambient particles (Killingsworth, et al., 1997).
The TERESA study is a large scale project requiring extensive method development. This research was initiated under the Center with additional funding provided by the Electric Power Research Institute and the US Department of Energy. The primary goal of TERESA is to evaluate the comparative toxicity of secondary particles derived from coal-fired power plant emissions and vehicular sources. Three power plants were included in the project to allow assessment of different coals and pollution control configurations. Toxicological tests have been completed for two of the three plants and are currently underway at the third. Future work will include toxicological tests of both primary and secondary vehicle emissions.
Primary emissions were drawn from the power plant stacks into a mobile reaction laboratory, where several atmospheric scenarios were simulated: 1) primary particles only; 2) oxidized emissions; 3) oxidized emissions + secondary organic aerosol (SOA), and; 4) oxidized emissions + ammonia + SOA. The study design included a two-stage toxicological assessment. In Stage I, overall cardiac and pulmonary toxicity was to be determined in normal laboratory rats, followed by a more comprehensive and cardiac-focused Stage II assessment in a compromised rat model. Because no adverse biological effects were observed in Stage I for the first power plant, the Stage II assessment was only conducted at the second plant.
Sampling and Exposure Methods
The emissions sampling system is described in detail in a manuscript currently in preparation (Ruiz, et al., 2006a). The design of the emissions sampling system represented a technical challenge, with significant care being taken to minimize particle losses in the system. A continuous sample passes from a pre-stack duct to a mobile chemical laboratory on the ground. Controls are used to adjust temperature and particle concentrations. The air is then passed to the atmospheric reaction simulation system. The atmospheric reaction simulation system is described in detail in a manuscript recently submitted for publication (Ruiz, et al., 2006c). This dual-chamber conceptual model includes ultraviolet light to allow for oxidation of SO2 followed by introduction of ammonia to produce acidic sulfate particles. Excess reactive gases are removed from the first stage reaction mixture (while keeping the secondary particles suspended in air) using denuders. The denuder system is described in detail in Ruiz, et al. (2006b).
In field monitoring, analytical measurement of the exposure atmospheres was extensive, to monitor and document performance of the two reaction chambers and to characterize the exposure atmospheres. For exposure characterization, continuous measurements included PM2.5 mass, particle number, SO2, NOx, O3, temperature, and relative humidity. Integrated measurements included PM2.5 mass, particle sulfate, particle nitrate, particle strong acidity, particle ammonium, particle elements, EC, organic carbon (OC), SO2, nitric acid vapor, nitrous acid vapor, ammonia, ketones, aldehydes and α-pinene.
Animal exposures were performed using both normal and compromised female Sprague-Dawley rats in a separate mobile animal exposure laboratory. In the mobile reaction laboratory, photochemically aged air was diluted with humidity-controlled clean air (ambient air with pollutant gases and particles removed) and transmitted to the exposure laboratory. In the exposure laboratory, air was drawn through individual exposure chambers in parallel. Exposures were six hours in duration and were immediately preceded and followed by a one-hour exposure to humidity adjusted zero air (baseline and recovery periods, respectively). Each scenario included four days of exposures, each with five rats (two for in vivo oxidative stress and three for the other biological endpoints). Pulmonary, cardiac, and systemic effects were evaluated via Bronchoalveolar lavage (BAL), histopathology, pulmonary function, in vivo oxidative stress and blood cytology. At autopsy, total lung volumes were determined, and the lungs were cut horizontally into 2 mm numbered sections. Three sections were randomly selected for processing by paraffin histology techniques. In vivo oxidative stress was measured using organ chemiluminescence.
The results of the data analysis for the first two power plants of the TERESA study is summarized as follows: a) the results from the analysis of the lung and cardiac histology BAL and blood data were negative (no effects found for either plant); b) there was evidence for respiratory breathing pattern effects, which were associated with sulfates and mass at the second plant and when both plants were combined, but not at the first plant alone; c) no chemiluminescence effects were found at the first plant; d) these effects were found for both heart and lung at the second plant; e) the data show tissue specific associations for the CL effects, with OC and mass being important contributors to the responses in the heart, and metals and non-sulfate mass more important to the responses in the lung. Results from the proposed organic carbon-only exposures at power plant 3 will help us to interpret these results. The rats with the myocardial infarction model, had an 87% increase in premature ventricular beats which was statistically significant. Papers describing these results in detail are in preparation.
As the results from the toxicological studies are preliminary, conclusions regarding primary exposure scenarios cannot be provided.
Batalha JRF, Saldiva PHN, Clarke RW, Coull BA, Stearns RC, Lawrence J, Krishna Murthy GG, Koutrakis P, Godleski JJ. Concentrated ambient air particles induce vasoconstriction of small pulmonary arteries in rats. Environmental Health Perspectives 2002;110(12):1191-1197.
Clarke RW, Coull BA, Reinisch U, Catalano P, Killingsworth CR, Koutrakis P, Kavouras I, Krishna Murthy GG, Lawrence J, Lovett EG, Wolfson JM, Verrier RL, Godleski JJ. Inhaled concentrated ambient particles are associated with hematologic and bronchoalveolar lavage changes in canines. Environmental Health Perspectives 2000;108(12):1179-1187.
Killingsworth C, Alessandrini F, Murthy G, Catalano P, Paulauskis J, Godleski J. Inflammation, chemokine expression, and death in monocrotaline-treated rats following fuel oil fly ash inhalation. Inhalation Toxicology 1997;9:541-565.
Laden F, Neas L, Dockery D, Schwartz J. Association of fine particulate matter from different sources with daily mortality in six U.S. cities. Environmental Health Perspectives 2000;108(10):941-947.
Ruiz PA, Lawrence JE, Ferguson ST, Wolfson JM, Koutrakis P. A counter-current parallel-plate membrane denuder for the non-specific removal of trace gases. Environmental Science & Technology 2006b;40:5058-5063.
Saldiva PH, Clarke RW, Coull BA, Stearns RC, Lawrence J, Koutrakis P, Suh H, Tsuda A, Godleski JJ. Acute pulmonary inflammation induced by concentrated ambient air particles is related to particle composition. American Journal of Respiratory and Critical Care Medicine 2002;165(12):1610-1617.
Journal Articles on this Report : 1 Displayed | Download in RIS Format
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||Ruiz PA, Lawrence JE, Ferguson ST, Wolfson JM, Koutrakis P. A counter-current parallel-plate membrane denuder for the non-specific removal of trace gases. Environmental Science & Technology 2006;40(16):5058-5063.||
Supplemental Keywords:RFA, Health, Scientific Discipline, Air, Air Pollution Monitoring, particulate matter, Toxicology, air toxics, Environmental Chemistry, Air Pollution Effects, Risk Assessments, Environmental Monitoring, Children's Health, indoor air, Molecular Biology/Genetics, Biology, Environmental Engineering, ambient air quality, health effects, microbiology, monitoring, particulates, risk assessment, sensitive populations, chemical exposure, air pollutants, cardiopulmonary responses, epidemiology, human health effects, indoor exposure, ambient air monitoring, exposure and effects, ambient air, ambient measurement methods, lead, pulmonary disease, developmental effects, biological response, respiratory disease, air pollution, ambient monitoring, children, Human Health Risk Assessment, particle exposure, biological mechanism , human exposure, inhalation, mobile sources, pulmonary, susceptibility, particulate exposure, assessment of exposure, ambient particle health effects, PM, tropospheric ozone, epidemeology, environmental health hazard, inhalation toxicology, cardiopulmonary, indoor air quality, modeling studies, human health, air quality, cardiovascular disease, dosimetry, human health risk, metals, respiratory, genetic susceptibility
Progress and Final Reports:Original Abstract
Main Center Abstract and Reports:R827353 EPA Harvard Center for Ambient Particle Health Effects
Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R827353C001 Assessing Human Exposures to Particulate and Gaseous Air Pollutants
R827353C002 Quantifying Exposure Error and its Effect on Epidemiological Studies
R827353C003 St. Louis Bus, Steubenville and Atlanta Studies
R827353C004 Examining Conditions That Predispose Towards Acute Adverse Effects of Particulate Exposures
R827353C005 Assessing Life-Shortening Associated with Exposure to Particulate Matter
R827353C006 Investigating Chronic Effects of Exposure to Particulate Matter
R827353C007 Determining the Effects of Particle Characteristics on Respiratory Health of Children
R827353C008 Differentiating the Roles of Particle Size, Particle Composition, and Gaseous Co-Pollutants on Cardiac Ischemia
R827353C009 Assessing Deposition of Ambient Particles in the Lung
R827353C010 Relating Changes in Blood Viscosity, Other Clotting Parameters, Heart Rate, and Heart Rate Variability to Particulate and Criteria Gas Exposures
R827353C011 Studies of Oxidant Mechanisms
R827353C012 Modeling Relationships Between Mobile Source Particle Emissions and Population Exposures
R827353C013 Toxicological Evaluation of Realistic Emissions of Source Aerosols (TERESA) Study
R827353C014 Identifying the Physical and Chemical Properties of Particulate Matter Responsible for the Observed Adverse Health Effects
R827353C015 Research Coordination Core
R827353C016 Analytical and Facilities Core
R827353C017 Technology Development and Transfer Core