Grantee Research Project Results
Final Report: Toxicological Evaluation of Realistic Emission Source Aerosol (TERESA): Investigation of Vehicular Emissions
EPA Grant Number: R832416C005Subproject: this is subproject number 005 , established and managed by the Center Director under grant R832416
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
Center: Health Effects Institute (2015 - 2020)
Center Director: Greenbaum, Daniel S.
Title: Toxicological Evaluation of Realistic Emission Source Aerosol (TERESA): Investigation of Vehicular Emissions
Investigators: Koutrakis, Petros , Godleski, John J.
Institution: Harvard University
EPA Project Officer: Chung, Serena
Project Period: October 1, 2005 through September 30, 2010 (Extended to September 30, 2011)
RFA: Particulate Matter Research Centers (2004) RFA Text | Recipients Lists
Research Category: Human Health , Air
Objective:
Because particulate and gaseous source emissions undergo many transformations once released into the atmosphere, it is likely that secondary and primary pollutants exhibit different toxicities. Because most of the source-specific toxicity studies to date have focused on primary pollutants, there remains a great need to investigate the relative toxicity of source-specific primary and secondary particles. The objective of this project was to probe directly into the toxicity of primary and secondary particles derived from mobile source emissions, using the technologies developed for the TERESA (Toxicological Evaluation of Realistic Emission Source Aerosol) Power Plant study.
The TERESA Power Plant study, funded by the Electric Power Research Institute (EPRI) and the previous and current Harvard EPA PM Centers, was designed to investigate the relative toxicity of primary and secondary particulate emissions from coal-fired power plants, in situ, and to explore the relationship between secondary particle formation processes and particle toxicity. We developed techniques and facilities to sample source emissions, form secondary particles inside a photochemical chamber, remove gases, and expose animals to both primary and secondary particles. The current project adapted the TERESA technologies to investigate the toxicity of primary and secondary particles from vehicular (mobile source) emissions, contained within the ventilation stack of a large roadway tunnel within the northeastern United States.
The specific hypotheses of this project were:
· Exposures to fresh and to photochemically oxidized mobile source emissions induce cardiovascular responses in normal animals;
· Atmospheric photochemical processes enhance the toxicity of gases and particles emitted from motor vehicles; and
· Animal models of susceptible populations (e.g., spontaneously hypertensive or myocardial infarction model rats) have greater biological responses to particles originating from motor vehicles than the corresponding normal animal model.
Summary/Accomplishments (Outputs/Outcomes):
The project featured a field study, conducted at the ventilation building of an urban highway tunnel, to investigate the toxicity of primary and simulated secondary particles from fleet vehicular emissions. The start of the field study was delayed by factors beyond our control, relating to construction at the highway tunnel where the study was conducted. During this delay, we took the opportunity to conduct a pilot-scale laboratory study using the exhaust of a single gasoline vehicle. The pilot lab study findings are included in this report, as are the final results of the power plant TERESA study, which was supported by this Center as well as the previous PM Center.
(1) Pilot Scale Laboratory Study: Laboratory experiments simulating atmospheric aging of gasoline vehicular exhaust were conducted using a single compact automobile and a photochemical chamber. Tailpipe exhaust was diluted with ambient air to achieve carbon monoxide concentrations similar to those observed in the tunnel where the field study would ultimately take place. Diluted exhaust was introduced into the photochemical chamber and irradiated with ultraviolet light. Photochemical reactions in the chamber resulted in nitric oxide depletion, nitrogen dioxide formation, ozone accumulation and secondary organic aerosol (SOA) formation. Stable SOA concentration of approximately 40 μg/m3 were achieved using a chamber residence time of 30 min. This relatively short residence time was used to provide adequate chamber flow output for both particle characterization and animal exposures. SOA mass generated from the car exhaust diluted with ambient air was almost entirely in the ultrafine mode. Chamber performance was improved by using different types of seed aerosol to provide a surface for condensation of semi-volatile reaction products, thus increasing the yield of SOA. For toxicological experiments, Mt. Saint Helens Ash (MSHA), a known non-toxic particle, was used as a seed aerosol.
Normal male Sprague-Dawley rats were exposed for 5 hours to either filtered air or one of two different exposure atmospheres: diluted car exhaust (P) + MSHA; or P+MSHA+SOA. During both exposures, primary and secondary gases were removed using a non-selective diffusion denuder (Ruiz, et al., 2007).
A variety of biological outcomes were measured. Breathing pattern was monitored continuously during exposure; in vivo chemiluminescence (IVCL) of the heart and lung were assessed immediately after exposure, and broncho-alveolar lavage (BAL) and complete blood counts (CBC) were performed 24 hours after exposure. For both exposure atmospheres, we observed decreases in breathing rate, tidal and minute volumes, peak and median flows, along with increases in breathing cycle times compared to sham. These results indicate that the animals changed their breathing pattern when exposed to these test atmospheres. Exposure to the photochemically aged exhaust, P+MSHA+SOA, produced significant increases in IVCL of the lung, and also several BAL parameters, including total cells, macrophages and neutrophils. There were no significant differences in CBC parameters. Our data suggest that simulated atmospheric photochemistry, producing SOA in the P+MSHA+SOA exposures, enhanced the toxicity of gasoline vehicle tailpipe emissions.
(2) TERESA Mobile Source Emissions Field Study: Note, sample and data analysis from this study are not yet complete. Findings presented here are to date.
Exposure Generation System. We developed and characterized a generation system that provides stable and reproducible atmospheres, adequate for animal exposures to fresh and aged particles derived from traffic emissions. The three main components of the exposure generation system are the primary emissions sampling system, the photochemical reaction chamber, and the non-selective denuder to remove secondary and unreacted primary gases. These components were designed and built specifically for this study, as the counterparts used for the TERESA Power Plant study were not adequate for the very different characteristics of the fleet vehicular emissions in the tunnel ventilation stack.
Chamber Exposure Atmospheres Developed. Three types of reaction chamber atmospheres were developed for animal exposure studies:
a. P (Primary Particles): The tunnel plenum air sample, dominated by vehicular emissions, was passed through a size selective inlet to remove particles larger than 2.5 μm in aerodynamic diameter. The aerosol then was introduced into the chamber. Lamps were turned off and no O3 was added.
b. P +SOA (Aged Primary plus Secondary Organic Aerosol): The tunnel air sample, containing primary gases and particles, was passed through the size selective inlet to remove particles larger than 2.5 μm in aerodynamic diameter. The aerosol then was diluted with clean air and mixed inside the chamber with sufficient O3 to titrate NO. The lamps were turned on and the emissions were photochemically oxidized to generate a mixture of aged primary particles and secondary aerosol, mostly organic but also containing a small amount of sulfate and nitrate.
c. SOA (Secondary Organic Aerosol): The tunnel air sample was filtered to remove primary particles and the primary gases were introduced into the chamber with sufficient O3 to titrate NO. The lamps were turned on and the primary gas emissions were photochemically oxidized to form secondary aerosol, predominantly organic.
Chamber Performance. Experiments characterizing the atmosphere types generated during this project focused on producing consistent concentrations among the different types of exposures; to do this, it was necessary to generate sufficient amounts of secondary particle mass, with and without primary particles. Initial experiments with undiluted tunnel air containing primary gases and particles, unlike the laboratory experiment with the single gasoline vehicle, produced no change in the baseline/initial NO/NOx ratio and no O3 or SOA formation after several hours of irradiation. This was observed even after adding sufficient O3 to titrate NO. These initial experiments suggested that the primary carbonaceous particles in the tunnel air were serving as a sink for radicals. Thus, it was necessary to dilute the tunnel primary particle mass concentration to levels that would not completely inhibit the formation of O3 and SOA, while still maintaining a large enough concentration of primary particles for the P+SOA exposure.
Another finding of the initial experiments was that, with the chamber operating in dynamic mode with continuous flow, it took 16-20 hours of irradiation to generate a stable concentration of secondary aerosol, in both the SOA and P+SOA atmospheres. For this reason, it was more practical operate the system under continuous flow and irradiation for several days. A benefit of this, since the chamber output was relatively stable over the duration, was that two sets of exposures could be conducted per day, reducing the overall length of the study.
Secondary Aerosol Formation and Characterization. The set of conditions that produced comparable, stable, and reproducible mass concentrations for each of the exposure atmospheres were: P, 100% unfiltered tunnel air; SOA, 100% filtered tunnel air plus O3 (and irradiation); P+SOA, 30% unfiltered tunnel air, 70% clean air plus O3 (and irradiation). Because the concentrations of NO and PM in the tunnel varied due to traffic patterns and tunnel ventilation rates, enough O3 was added to titrate the NO and leave a small excess of O3 concentration prior to the start of irradiation.
A set of experiments was performed to assess (1) the role of O3 and ∙NO3 in formation of secondary PM, and (2) the contribution of NH4NO3 and SO42- (as (NH4)2SO4, NH4HSO4 or H2SO4) to the secondary PM in each of the chamber atmospheres. In these experiments, PM samples were collected downstream of the chamber during three stages of an experiment: before starting addition of O3; after addition of O3 but before starting irradiation; and after irradiation. The results of these experiments are included below in Table 1.
Table 1. PM Composition in chamber atmospheres, subset of experiments (concentrations in µg/m3).
|
Species or Diagnostic Ratio
|
EXPOSURE ATMOSPHERE TYPE
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|||||||||||||||||||||||||||||
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Aged Primary + Secondary (P+SOA)
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Secondary Aerosol Only (SOA)
|
Primary (P)
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||||||||||||||||||||||||||||
|
Baseline
|
Plus O3
|
Lights
|
Baseline
|
Plus O3
|
Lights
|
no O3 or light
|
||||||||||||||||||||||||
|
PM
|
6.50
|
5.10
|
22.60
|
0.40
|
1.69
|
50.27
|
47.00
|
|||||||||||||||||||||||
|
EC
|
1.68
|
1.00
|
1.20
|
0.00*
|
0.00*
|
0.00*
|
12.26
|
|||||||||||||||||||||||
|
OC
|
1.57
|
3.62
|
8.82
|
2.91
|
3.90
|
22.85
|
10.87
|
|||||||||||||||||||||||
|
OC1
|
0.04
|
0.05
|
0.06
|
0.02
|
0.12
|
0.25
|
0.23
|
|||||||||||||||||||||||
|
OC2
|
0.79
|
1.73
|
2.59
|
1.45
|
1.79
|
6.88
|
5.30
|
|||||||||||||||||||||||
|
OC3
|
0.62
|
1.30
|
3.35
|
0.85
|
1.16
|
8.54
|
4.29
|
|||||||||||||||||||||||
|
OC4
|
0.16
|
0.37
|
1.16
|
0.23
|
0.32
|
2.49
|
1.23
|
|||||||||||||||||||||||
|
Pyrol C
|
0.00
|
0.16
|
1.66
|
0.36
|
0.51
|
4.69
|
0.19
|
|||||||||||||||||||||||
|
NO3-
|
0.33
|
1.18
|
2.73
|
0.10
|
1.08
|
3.84
|
0.52
|
|||||||||||||||||||||||
|
SO42-
|
0.50
|
0.41
|
4.00
|
0.11
|
0.16
|
7.15
|
2.59
|
|||||||||||||||||||||||
|
EC/PM
|
0.26
|
0.20
|
0.05
|
0.00
|
0.00
|
0.00
|
0.26
|
|||||||||||||||||||||||
|
OC/EC
|
0.93
|
3.62
|
7.35
|
*
|
*
|
*
|
0.89
|
|||||||||||||||||||||||
|
OC1/OC
|
0.03
|
Conclusions (to date). We developed and utilized an exposure system that forms stable and reproducible amounts of SOA from photochemically oxidized primary gas-phase precursors in traffic emissions found in an urban highway tunnel in the northeastern United States, at concentrations that are adequate for inhalation toxicity studies. Our methods allowed us to generate and characterize reproducible exposure atmospheres of: a) primary particles; b) aged primary particles plus secondary particles, and; c) secondary particles only.
In this study, it is clear that the formation of secondary aerosol is influenced significantly by reaction with ∙OH, because secondary aerosol formation for PM, OC, SO42- and NO3- are substantially increased by irradiation and not by the presence of only O3 and ∙NO3. Overall, the P+SOA particles are comparable in terms of the relative composition of major species to those reported in studies of ambient particle matter, especially for northeastern U.S. sites.
All of the exposures produced respiratory changes compared to filtered air, but more prominent respiratory toxicity was found in animals exposed to P+SOA. Overall, P+SOA>P>SOA for respiratory outcomes. The effect was greater in animals with repeated exposures. Significant breathing pattern changes were associated with the different exposure types. These changes were internally consistent, with patterns that indicate an irritative response to exposure. This response is mediated by local (respiratory effort) and central (respiratory drive) components and is augmented with repeated exposure to fresh and aged vehicular emissions. Four day exposures to P+SOA produced the most significant and complex response in breathing pattern, with decreases in volumes, flows, respiratory drive and respiratory effort. This suggests that photochemical oxidation and formation of secondary particle mass enhanced the toxicity of primary traffic derived particles.
The observed inflammatory responses were mild, but more evident in the aged primary plus SOA exposure. The time of the biological measurement (acute response) indicates that this is most likely an initial phase of response to the exposure.
Both primary and secondary traffic-related aerosols can substantially increase SBP and DBP. Initial increases up to 15 mmHg in diastolic blood pressure were recorded for the P exposure. This is a greater blood pressure change than has previously been reported in the literature in animal or human studies for either similar or substantially higher PM2.5 concentrations. The responses are sustained with repeated primary aerosol exposures, but not with secondary aerosols. Animals exposed to secondary aerosols showed a gradual decrease in the magnitude of response with repeated exposures, and subsequently show compensatory decreases in both SBP and DBP after the 3 week protocol. This unexpected but significant compensatory response suggests a biological protective effect with repeated exposures that cannot be explained by simple autonomic nervous system activation. These results confirm the adverse health effects associated with inhalation of fine particles in previous studies and give insight into a potential biological adaptation to maintain blood pressure in response to repeated and anticipated pollutant exposure. Greater limitation in the BP response in animals exposed to secondary particles requires further investigation to define the interaction of this exposure with blood pressure control mechanisms. No exposure had a significant effect on heart rate.
Conclusions from the TERESA Power Plant study. This work shows that statistically significant, but relatively mild, health effects were produced by inhalation exposure experiments using coal-fired power plant emissions that were photochemically aged in a manner that simulated atmospheric oxidation in a power plant plume. Health effect outcomes included mild but significant changes in: breathing pattern; pulmonary inflammation (e.g., BAL total cell count and macrophages); and oxidative stress in the lung and heart (in vivo chemiluminescence). The observed health effects tended to result from scenarios that had more reactants added and more complex chemical reactions (POS, PONS). Sulfate, which is not associated with serious toxicological effect at moderate exposure levels, was (as expected) a large component of the exposure atmospheres.
One of the difficulties with this study was that the primary particle concentrations were exceedingly low. This meant that the P exposures were conducted at much lower levels than the PO, POS and PONS exposures, which were within the same range and comparable to studies using CAPs. This made it very difficult to assess the comparative toxicity of the primary particles. For this reason, the mobile source TERESA study conducted exposures to the three types of aerosol (P, P+SOA, and SOA) at consistent concentrations.
This project defined both the absolute and relative toxicity of secondary particles formed from coal-fired power plants compared to laboratory studies of ambient particles or CAPs. In general, secondary particles formed from power plant emissions were less toxic than inhaled CAPs, though the most complex scenarios approached (but did not equal) the reported toxicity of inhaled CAPs. The project also modeled and provided insight into the formation of secondary particles formed from the gaseous emissions of the power plants, clearly demonstrating that these transformations could be produced in a field laboratory.
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Supplemental Keywords:RFA, Health, Air, Scientific Discipline, Health Risk Assessment, Risk Assessments, particulate matter, Environmental Chemistry, Toxicology, biological mechanisms, chemical characteristics, autonomic dysfunction, biological mechanism , airborne particulate matter, cardiovascular vulnerability, chemical composition, animal model, oxidative stress, ambient particle health effects, PM, atmospheric particulate matter, automobile exhaust, ambient air quality, concentrated ambient particulates (CAPs), human health effects, traffic related particulate matterProgress and Final Reports:Original AbstractMain Center Abstract and Reports:R832416 Health Effects Institute (2015 - 2020) Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center). The 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. Project Research Results
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