2001 Progress Report: Physical and Chemical Characteristics of PM in the LAB (Source Receptor Study)

EPA Grant Number: R827352C014
Subproject: this is subproject number 014 , established and managed by the Center Director under grant R827352
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).

Center: Southern California Particle Center
Center Director: Froines, John R.
Title: Physical and Chemical Characteristics of PM in the LAB (Source Receptor Study)
Investigators: Sioutas, Constantinos , Cho, Arthur K. , Froines, John R. , Harkema, Jack , Hinds, William C. , Kleinman, Michael T. , Miguel, Antonio , Nel, Andre E.
Current Investigators: Sioutas, Constantinos
Institution: University of Southern California , Michigan State University , University of California - Irvine , University of California - Los Angeles
Current Institution: University of Southern California , University of Southern California
EPA Project Officer: Chung, Serena
Project Period: June 1, 1999 through May 31, 2005 (Extended to May 31, 2006)
Project Period Covered by this Report: June 1, 2000 through May 31, 2001
RFA: Airborne Particulate Matter (PM) Centers (1999) RFA Text |  Recipients Lists
Research Category: Air Quality and Air Toxics , Particulate Matter , Air

Objective:

This project includes two components—the Source/Receptor Study and the Freeway Animal Study.

The objective of this research project is to focus on the central hypothesis of the Southern California Particle Center and Supersite (SCPCS), which is that organic constituents associated with particulate matter (PM)—including quinones, other organic compounds (polycyclic aromatic hydrocarbons [PAHs], nitro-PAHs, and aldehydes/ketones), and metals—are capable of generating reactive oxygen species and acting as electrophilic agents. They have a central role in allergic airway disease such as asthma and cardiovascular effects through their ability to generate oxidative stress, inflammation, and immunomodulating effects in the lungs and airways.

By taking measurements at three sites, one source and two receptor sites (the receptor sites are locations in which the PM composition has been modified by atmospheric chemistry), we hope to evaluate: (1) the role of atmospheric chemistry in the toxicity of PM and copollutants; and (2) if airway disease and cardiovascular effects are more severe during periods of high photochemical activity (summer) than in periods of low photochemical activity (winter). A mouse and a rat model are being used. The mouse model will be used to test the hypothesis that ambient particles can act as an adjuvant, and will contribute to the development of allergic and asthmatic responses. The rat model tests hypotheses related to the exacerbation of asthma.

The specific hypotheses for the Source/Receptor Study are that:

  • Atmospheric chemistry is important in the toxicity of particulate matter and co-pollutants, and airway injury and cardiovascular effects will be greater at receptor sites downwind of source sites along the mobile source trajectory in the Los Angeles Basin (LAB).
  • Airway disease and cardiovascular effects will be more severe during periods of high photochemical activity in the summer than in periods of low photochemical activity during the winter.

The specific hypotheses for the Freeway Animal Study are:

  • Mobile source emissions will exacerbate airway inflammation and allergic airway disease and produce cardiopulmonary effects.
  • The magnitude of allergic airway disease and cardiovascular effects from mobile sources are a function of the size distribution of PM.
  • Exposure in proximity to selected freeways with either heavy diesel or gasoline powered vehicles will cause exacerbation of inflammatory airway health effects, and exposure to ultrafine particles at very close proximity to a freeway will result in the most severe effects.

Progress Summary:

Source/Receptor Study

To test the hypotheses for this study, we have installed ultrafine, fine, and coarse particle concentrators and inhalation exposure systems in an existing trailer for animal studies and, after suitable evaluation and testing, use that facility to perform animal studies at a source (University of Southern California main campus in downtown Los Angeles) and two distinctly different receptor sites (Azusa and Upland). Receptor sites are those locations in which the PM composition has been modified by atmospheric chemistry with emphasis on hydroxyl radical and nitrate chemistry.

The rationale used for choosing the specific sites in the LAB for the source/receptor study derives from recent data. The data indicate that there are two distinct air trajectories in the LAB that transport air pollutants emitted from the southwestern part of the LAB eastwards. There is a “vehicular emissions” trajectory that is tangential to freeways 10 and 210, which starts approximately in downtown Los Angeles and follows the direction along freeways 10 and 210. Upland is a site adjacent to freeway 10 and is along a trajectory primarily impacted by mobile source emissions. Azusa also is situated along this trajectory, but is intermediate between the sources (in downtown Los Angeles) and the “receptor” site, Upland, which is farther eastwards along this trajectory. In addition to the “vehicle-oriented” trajectory, there is a distinct wind trajectory that is called the “Nitrate-Oriented Trajectory.” This trajectory starts in the Long Beach area, where a significant portion of PM is mostly generated by nonmobile sources such as petroleum refineries, numerous energy generating facilities, and heavy industry emission (although there also is a significant mobile source contribution). This trajectory progresses through areas that are upwind of, within, and downwind of the Chino dairy farms area, a large source of gas-phase ammonia. The main theme of the Southern California Particle Center and Supersite is PM and compounds emitted from mobile sources, therefore conducting studies along the “nitrate-oriented” trajectory, might dilute the focus on our research hypotheses linking health effects to vehicle-emitted pollutants, given the contributions of nonvehicular sources to PM found along that trajectory. Our plan for the next 3 years is to perform health effect studies at each of the three sites along the “vehicle-oriented” trajectory during periods of high and low photochemical intensity, and to coordinate those studies with particle instrumentation unit (PIU) sampling campaigns to maximize the degree of integration of our Center’s efforts.

We have investigated the physicochemical characteristics of ultrafine particles in urban areas both at the source site and the receptor site located in the LAB. From the semicontinuous measurement of size distribution of ambient aerosols as well as time-integrated sampling of particles, the temporal and diurnal trends in the behavior of ultrafine particles were analyzed to better understand the formation mechanisms in different locations of an urban metropolitan area. Results showed that a western site, located in central Los Angeles, is appropriately characterized as a source site with constant primary emissions. In contrast, ultrafine and accumulation modes of PM in a receptor site were found to originate mostly from secondary reactions, which are more pronounced during the warmer months of the year, particularly during the warmer season of the year between April and October.

Freeway Animal Study

The hypotheses have resulted in a series of near-source studies of concentrated fine and ultrafine ambient particles. A compromised (asthma) animal model is being used to study allergic airway disease associated with exposure to concentrated ambient particles (CAPs) at varying distances from freeways as well as an upwind site. The study specifically seeks to determine the relative toxicity of PM in relation to particle size and composition including quinones, PAHs, and metals as the distance from the freeway varies.

We now are able to position mobile fine (F) and ultrafine (UF) concentrators at varying distances from a freeway with heavy diesel traffic to determine if exposure to emissions from the freeway demonstrates an adjuvant effect of CAPs in relation to asthma in animal models, and we are able to develop protocols that vary the concentration of particulate being studied to evaluate dose-response characteristics. The availability of both fine and ultrafine CAPs provides a basis to study the effects of UF particles and F + UF with implications for the role of fine particles as well. The study assesses exposure to traffic-related pollution to further establish a causal link between asthma enhancement and adjuvant effects on asthma and mobile source emissions.

To test hypotheses that mobile source particles, especially those in the ultrafine size mode, would increase allergic reactions and exacerbate inflammatory responses in mice with allergic airway disease, we exposed ovalbumin (OVA)-sensitized and unsensitized mice to CAPs. The pattern of observed responses was consistent with the multiphased mechanism for allergic response. The assays selected as markers of cell injury (total protein and beta glucuronidase) and inflammation (numbers of inflammatory cells) suggested even 2 weeks after the exposure, there was ongoing injury and inflammation in the lungs of CAPs exposed mice. The multiphasic dose response mechanism was further elucidated by evaluating a series of doses that bracketed the ranges in which the allergic response, the anti-oxidant response, and the toxic response occurred in our allergic mouse model. We found that exposures to CAPs at high concentrations resulted in reduced ability to respond to an allergen challenge, while exposures at lower concentrations evoked an allergic response (see Figure 1). The mechanism(s) for reduced responses following high concentration exposures is unclear, but could include cytotoxicity to immunologically active cells or perhaps TH1/TH2 shifting. Using intermediate concentrations of CAPs, we have clearly shown a pattern of allergic responses demonstrated by coherent increases in numbers of eosinophils and increased concentrations of OVA-specific IgE and IL-5 following exposures of mice to CAPs at a site 50 m downwind of a heavily trafficked freeway. Currently, we are performing exposures at increasing distances from the freeway.

Figure 1. Responses of Mice Exposed Downwind of Freeway to CAPs and OVA.

Figure 1. Responses of Mice Exposed Downwind of Freeway to CAPs and OVA.

Future Activities:

Source/Receptor Study

The study will use two animal models, both of which have existing allergic airway disease (asthma). The models will be the OVA sensitized Balb/c mice and Brown Norway (BN) rats, and in vitro studies described earlier also will be conducted. In both the in vivo and in vitro studies, mobile particle concentrators will be used to generate PM of known size ranges.

In the proposed project, BN rats with and without allergic airway disease will be concurrently exposed to either concentrated ambient coarse, F + UF, or UF particles taken from the ambient air in three different locations in the LAB over a period of 3 years. In each location, one series of exposures will be conducted during a period of intense photochemical activity, in early October, and another series will be conducted in January, a period when photochemical reactions are less intense. We have selected the BN rat treated with OVA as our animal model of allergic airway disease because this rodent model has been used extensively in the laboratory of Dr. Jack Harkema of Michigan State University, who will be our primary collaborator in this study. It is one of the few animal models that has been used successfully to demonstrate that inhaled pollutants can enhance allergic airway disease. In addition, the rat provides us more pulmonary tissues, compared to the mouse, to analyze using various microscopic, molecular, and biochemical analyses as outlined in our proposal.

The OVA-sensitized mouse and BN rat models will address a number of issues. The mouse model will be used to test the hypothesis that ambient particles can act as an adjuvant and will contribute to the development of allergic and asthmatic responses. The rat model will be used to test hypotheses related to the exacerbation of asthma and symptoms such as airway inflammation. Increased mucus secretion and increased storage of mucoid substances in lung tissue will be evaluated with the rat model. Results to date indicate that we are able to produce inflammatory responses in sensitized animals at the receptor site.

This study is closely related to other investigations performed by the Center because we will characterize PM and vapor co-pollutants to determine the concentrations of quinones, PAHs, nitro-PAHs, and metals. We hypothesize the concentration of quinones and other oxygenated PAHs and nitro-PAHs will increase across the LAB as a result of atmospheric chemistry. We will investigate how degrees of toxicity vary in animal and in vitro studies as a function of size distribution and composition.

Freeway Animal Study

From 2002 to 2004, we will conduct near-source toxicological studies of concentrated F + UF and UF ambient particles. The proposed studies also will include exposure of sensitized mice upwind, downwind, and at various distances from a freeway more heavily impacted by gasoline engine vehicles. We also will collect coarse, F + UF particles for in vitro toxicity studies from sites downwind of a gasoline-impacted freeway (Freeway 405).

Journal Articles:

No journal articles submitted with this report: View all 66 publications for this subproject

Supplemental Keywords:

airborne particulate matter, aerosol, size distribution, particle concentrator, NRC priorities, mechanism, quinones, allergens, bioaerosols, dosimetry, children’s study, indoor exposure, exposure assessment, ultrafine, fine and coarse particles, regional human exposure model, REHEX, asthma, polycyclic aromatic hydrocarbons, PAHs, clinical human exposures, source-receptor, measurement error, study design, susceptible populations, geo-code, toxicology, epidemiology, regional modeling, source/receptor analysis, Southern California, Los Angeles Basin, LAB, photochemistry, meteorology, trajectory modeling, peroxides, Southern California Particle Center and Supersite, SCPCS, air, geographic area, scientific discipline, health, RFA, susceptibility/sensitive population/genetic susceptibility, biology, risk assessments, genetic susceptibility, health risk assessment, atmospheric sciences, biochemistry, particulate matter, environmental chemistry, mobile sources, state, aerosols, automotive exhaust, epidemiology, exposure assessment, California (CA), environmentally caused disease, engine exhaust, environmental hazard exposures, freeway study, allergen, indoor air, indoor air quality, allergens, particle concentrator, air quality, diesel exhaust, particulate emissions, human health risk, toxics, human health effects, particulates, sensitive populations, toxicology, diesel exhaust particles, environmental triggers, air pollution, airway disease, atmospheric chemistry, children, trajectory modeling, automotive emissions, dosimetry, exposure, inhaled particles, motor vehicle emissions, asthma triggers, PM characteristics, ambient aerosol, asthma, human exposure, particle transport,, RFA, Health, Scientific Discipline, PHYSICAL ASPECTS, Air, Geographic Area, HUMAN HEALTH, particulate matter, Environmental Chemistry, Air Pollutants, State, Risk Assessments, Biochemistry, Health Effects, Physical Processes, ambient aerosol, asthma, children's health, aldehydes, epidemiology, quinones, exposure, allergic airway disease, air pollution, children, PAH, air sampling, aerosol composition, California (CA), allergens, aerosols, atmospheric chemistry, dosimetry

Relevant Websites:

http://www.scpcs.ucla.edu Exit

Progress and Final Reports:

Original Abstract
  • 1999
  • 2000
  • 2002 Progress Report
  • 2003 Progress Report
  • 2004
  • Final Report

  • Main Center Abstract and Reports:

    R827352    Southern California Particle Center

    Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
    R827352C001 The Chemical Toxicology of Particulate Matter
    R827352C002 Pro-inflammatory and the Pro-oxidative Effects of Diesel Exhaust Particulate in Vivo and in Vitro
    R827352C003 Measurement of the “Effective” Surface Area of Ultrafine and Accumulation Mode PM (Pilot Project)
    R827352C004 Effect of Exposure to Freeways with Heavy Diesel Traffic and Gasoline Traffic on Asthma Mouse Model
    R827352C005 Effects of Exposure to Fine and Ultrafine Concentrated Ambient Particles near a Heavily Trafficked Freeway in Geriatric Rats (Pilot Project)
    R827352C006 Relationship Between Ultrafine Particle Size Distribution and Distance From Highways
    R827352C007 Exposure to Vehicular Pollutants and Respiratory Health
    R827352C008 Traffic Density and Human Reproductive Health
    R827352C009 The Role of Quinones, Aldehydes, Polycyclic Aromatic Hydrocarbons, and other Atmospheric Transformation Products on Chronic Health Effects in Children
    R827352C010 Novel Method for Measurement of Acrolein in Aerosols
    R827352C011 Off-Line Sampling of Exhaled Nitric Oxide in Respiratory Health Surveys
    R827352C012 Controlled Human Exposure Studies with Concentrated PM
    R827352C013 Particle Size Distributions of Polycyclic Aromatic Hydrocarbons in the LAB
    R827352C014 Physical and Chemical Characteristics of PM in the LAB (Source Receptor Study)
    R827352C015 Exposure Assessment and Airshed Modeling Applications in Support of SCPC and CHS Projects
    R827352C016 Particle Dosimetry
    R827352C017 Conduct Research and Monitoring That Contributes to a Better Understanding of the Measurement, Sources, Size Distribution, Chemical Composition, Physical State, Spatial and Temporal Variability, and Health Effects of Suspended PM in the Los Angeles Basin (LAB)