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2008 Progress Report: Southern California Particle Center (SCPC)
EPA Grant Number: R832413Center: Southern California Particle Center
Center Director: Froines, John R.
Title: Southern California Particle Center (SCPC)
Investigators: Froines, John R. , Cho, Arthur K. , Delfino, Ralph , Harkema, Jack , Hinds, William C. , Kleinman, Michael T. , Kumigai, Yoshito , Lusis, Aldons , Nel, Andre E. , Neuhausen, Susan , Schauer, James J. , Shafer, M. M. , Sioutas, Constantinos , Staimer, Norbert , Vaziri, Nostratola
Institution: Michigan State University , University of California - Irvine , University of California - Los Angeles , University of Southern California , University of Tsukuba , University of Wisconsin
EPA Project Officer: Stacey Katz/Gail Robarge,
Project Period: October 1, 2005 through September 30, 2010
Project Period Covered by this Report: October 1, 2007 through September 30,2008
Project Amount: $7,999,994
RFA: Particulate Matter Research Centers (2004)
Research Category: Particulate Matter
Description:
Objective:Southern California Particle Center Overview
The overall objective of the Southern California Particle Center (SCPC) is to bring together outstanding scientists to conduct high priority research to elucidate the underlying basis for health effects associated with exposure to ambient particulate matter (PM). The strengths of the investigators in this center and our demonstrated record of progress, the powerful assortment of equipment available and the unique characteristics of the Los Angeles basin airshed are key factors in why Southern California is an important setting for PM research studies. The overall goal of the SCPC is to establish the linkage between PM source emissions, underlying mechanisms and resulting health effects. Fine and ultrafine particles derived from traffic continue to serve as foci for SCPC interdisciplinary studies that include exposure, toxicology, chemical characterization and epidemiology. Health effects research has centered around identifying mechanisms of PM-induced cardiovascular effects and allergic airways disease and the exposure conditions and components that are associated with observed mechanisms.
The LAB has been described as the most polluted airshed in the nation, with complex, persistent and unique PM. Covering approximately 12,000 square miles, the population is projected to reach 19 million by the year 2020, a 1.5 fold increase from 1990 levels. Vehicle miles traveled are increasing at an even greater rate and the LAB continues to exhibit the most severe ozone and PM air quality problems in the U.S. PM is emitted from numerous sources in the basin, including millions of motor vehicles, nearly 300,000 diesel trucks, the nation’s largest marine ports, expanding airports, and tens of thousands of factories.
Major research findings from the initial years of the SCPC have included the following. More recent findings follow:
- The most extensive chemical characterization of PM and intensive monitoring studies in the LAB ever conducted.
- Development of continuous monitors for size-fractionated particle mass and chemical composition, and mobile, size-selective PM concentrators capable of collecting large amounts of ambient samples for toxicological and human studies.
- Characterization of the formation and dynamics of PM near freeways.
- Demonstration of mitochondrial uptake of ultrafine particles and related toxicity.
- Demonstration that pro-oxidative chemicals induce hierarchical oxidative stress effects and development of murine in vivo models for induction of acute airway inflammation.
- Demonstration of in vivo allergic airway responses, neurological and cardiovascular effects in close proximity to a freeway.
- Exposure of healthy and impaired human volunteers to concentrated PM; first CAP exposure studies of human volunteers to coarse and ultrafine particles.
- Demonstration of a linkage between traffic density and human developmental toxicity.
- Demonstration of the relationship between traffic density (at schools and homes) and primary respiratory outcomes.
The research of the Center is divided into five project areas, all of which build on the findings and methodological advances that resulted from the first six years of SCPC funding. The primary objective of Project 1 is to examine the relationships between PM sources, exposure, and toxicity within the urban atmosphere. This project is an integral part of Projects 2, 3 and 4, by serving as the field operations to collect PM samples for toxicity testing and for providing elevated levels of ambient PM for animal exposure models described in these projects. The primary objective of project 2 is to elucidate the mechanism(s) of PM-induced asthma and atherosclerosis exacerbation in vitro and in vivo. This is accomplished by animal studies in a mobile trailer as well as in vitro studies in representative tissue culture cells. The principal hypothesis is that a major PM injury mechanism is the induction of oxidative stress that promotes respiratory and cardiovascular inflammation as the major pathology feature underlying asthma and atherosclerosis. We propose that oxidative stress is a hierarchical event in which the induction of antioxidant defense pathways in tier 1 is in dynamic equilibrium and defends against the pro-inflammatory (tier 2) pro-apoptotic (tier 3) effects of higher levels of oxidative stress. In Project 3, the catalytic redox and electrophilic properties of ambient PM samples are characterized using cell-free chemical assays. A primary hypothesis is that PM contains constituents capable of inducing cellular stress by redox or other chemical processes, focusing on two general mechanisms, redox and electrophilic reactions.
The overall goal of Project 4 is to advance knowledge on the importance of particle size and composition to the induction of oxidative stress responses in a high-risk population of elderly people with coronary artery disease. Project 5 consists of three subprojects that either directly or indirectly seek to improve our ability to assess health risk of air pollution by chemical and biological assays used by SCPC. The paragraphs that follow provide an overview of SCPC research progress in selected areas during the first three years of the renewed program.
Progress Summary:Project 1: The SCPC is building upon its history of research addressing public exposure to and health effects of mobile source PM, by investigating a variety of mobile source types. Field sampling campaigns during the last three years have been conducted at freeways, tunnels, an airport, a seaport, and in communities affected by combinations of these sources. Roadway studies have been a central feature of the SCPC since 1999. An in-vehicle study conducted during this renewal period concluded that 33-45% of a typical Los Angeles resident’s exposure to UFP may occur while in a vehicle, confirming the high importance to public health of vehicular emissions. Size segregated chemical composition of freeway samples found that UFP collected at a freeway were composed predominantly of organic carbon and had high acidity relative to larger size fractions. During heavy traffic periods, high concentrations of polycyclic aromatic hydrocarbons (PAH) and organic quinones were detected in traffic-derived particles. Emission factors for particulate matter components have been developed for road and tunnel environments.
A set of studies of ambient PM near busy seaports included chemical characterization of size segregated ambient samples and a focused analysis of spatial variability in particle number concentration and size distribution within communities affected by emissions from the Long Beach and Los Angeles ports. The study incorporated both summer and winter measurements, and toxicological analysis was performed on selected samples. Markers for marine vessel emissions were determined. Traffic sources and secondary formation of UFP were major contributors to the PM, and prevailed over ship emissions and oil combustion even in the community near the harbor. Considerable spatial variability in size distribution and particle number was observed over small, neighborhood-scale distances; this has important implications for exposure assessments conducted in the context of epidemiological studies.
A pilot study at the Los Angeles Airport was performed, and will be the basis for a more detailed study that will include toxicological analysis over the next two years. This pilot study, and other data collected by SCPC investigators detected high counts of UFP downwind of the airport. Measurements of black carbon and particulate phase PAH were not substantially different upwind and downwind of airport activities. Toxicological analysis of UFP and accumulation mode particles will be undertaken in a follow-up study to better characterize the potential public health relevance of offsite movement of aircraft particulate matter emissions.
Wildfires and intentional woodburning are important non-mobile sources of particulate matter in some parts of the US especially California. SCPC investigators found that water-soluble organic carbon was increased during a wildfire episode. The redox-generating activity, per unit mass, of the PM collected during this episode was elevated over background Los Angeles PM samples.
Project 2: SCPC’s interdisciplinary research program on the mechanisms by which particulate matter contributes to cardiovascular morbidity and mortality involves toxicological studies in animal and in vitro model systems and an epidemiological study of oxidative stress biomarkers that is supported by extensive PM characterization to provide a variety of exposure metrics for analysis. Ambient fine and ultrafine particles at a near-freeway location were shown to promote atherosclerotic changes and increase systemic oxidative stress markers in a mouse model. These effects were more associated with ultrafine particles (UFP) than fine particles. In vitro studies of human microvascular endothelial cells are in progress to identify alterations in gene expression involved in the responses to cellular stress that may underlie the PM-induced atherogenesis that was observed in mice, and chemical reactivity studies seek to understand the biomolecular processes at work. Chemical composition of PM may explain the observed health effects
The SCPC is engaged in research on the mechanisms of allergic airways responses, pursuing the hypothesis that oxidative stress plays an important role. In a mouse model for the study of adjuvant effects of particles in promoting allergic sensitization UFP, given by instillation, promoted proinflammatory effects in the lung, epithelial changes and inflammatory cell influx. Immune system responses were skewed toward allergic response in UFP exposed animals. In addition, nasal mucosa changes were observed, providing a possible explanation for associations between PM and allergic rhinitis. The findings are being pursued by performing mechanistic studies in dendritic cells in vitro that characterize the specific pathological processes associated with exposure that may explain how these cells alter immune system responses associated with PM exposure.
The pathophysiological changes that result in PM-associated adverse health effects, such as oxidative stress and gene expression alterations, are being investigated in our epidemiological and animal toxicology studies. We are using genome wide association screening to elucidate gene clusters that can be used for bioassay development that reflect the impact of ambient fine versus UFP exposure in murine lung tissue. We are currently using lungs collected during atherosclerosis studies with the apoE knockout mice and are the process of analyzing promising gene clusters that reflect the pro-the inflammatory effect of different particle sizes.
Project 3: To understand at a fundamental biochemical level how exposure to particulate matter can produce these changes, and to identify the components and sources that are responsible, the chemical reactivity properties of PM samples require investigation. To date, we have developed three assay procedures that can be applied to PM samples to assess their chemical reactivity and potential toxicity as predicted by the considerations above. The assays can detect the ability to generate redox active species, including organics and metals, and measure covalent modification of target proteins. The assays have been applied to different samples collected at sites in the Los Angeles basin. These assays have been used to characterize PM samples from a variety of sources and conditions of collection as part of project 1. Additionally, we have examined a set of diesel exhaust particles with these procedures and have found that the redox activity is associated with the particle fraction in an aqueous suspension and the electrophiles were soluble in the aqueous phase. In a second study of ambient air samples from Riverside, CA, we found that the redox activity was associated with particles and the electrophiles were mostly in the vapor phase which raises important issues about the role of vapor phase co-pollutants. These studies were enabled by sample collection as an element of Project 5. Reductive acetylation studies suggest that quinones or quinone-like compounds may be responsible for the redox and electrophilic activities that partition into the organic and aqueous extracts. These experiments provide a conceptual link between studies of the chemical composition of PM and studies of biological outcomes by attempting to identify the biologically active components of samples.
Project 4: A panel study of elderly individuals with coronary artery disease aims to identify exposure characteristics including particle size and composition that are associated with circulating biomarkers of oxidative stress. The study has found positive associations between a number of measures of particle composition/source and biomarkers of stress responses. Overall, the pattern of results suggests that exposure to primary emissions of UFP and organic carbon in this population may lead to sustained increased systemic inflammation, platelet activation and decreased antioxidant enzymes in erythrocytes. Interindividual variability in responses in the SCPC study was high; possible factors under investigation include statin use and genetic variability at the glutathione S-transferase M1 locus.
In conclusion, the SCPC has been especially successful in collecting and characterizing PM from a wide range of sources; this has been a central theme of the Center. In addition, we have begun to link airborne PM and vapor phase characteristics with toxicological investigations to further identify the underlying mechanisms of action of PM. This represents a unique approach to PM research and the development of assays to conduct such studies has represented a major contribution. We have demonstrated that both fine and ultrafine PM is capable of generating significant atherosclerotic lesions in susceptible mice. The Panel study being conducted by Dr. Delfino represents an innovative approach requiring small numbers of participants and has enabled development of linkages between toxicologic parameters and health considerations. Overall, the Center has been dramatically successful in meeting the objectives set out in our two original applications. We have been successful in leveraging the U.S. EPA funds to obtain extensive funding from other sources, and our publications record is extraordinary. These results demonstrate the overall contributions of our Center.
Future Activities:In the remaining two years of funding, the SCPC will make further, detailed comparisons of the vapor phase co-pollutants and particles, in terms of physical, chemical and toxicological properties in relation to source, and will integrate this work with the efforts described above. Work will continue on improving technical methods for PM aerosol characterization and exposure studies. Attention will be given to using assays from Projects 2 and 3 to evaluate dose-response relationships. We will also focus on the temporal characteristics of PM emissions. Assays for chemical reactivity of PM samples are being adapted to high-throughput conditions, to enable application to a wider range of ambient and source-specific samples. Studies that further address the underlying mechanisms will be undertaken with reference to downstream signal transduction pathways for toxicity and the link with health outcomes. The animal studies on allergic airways sensitization will followed up with inhalation exposures to solidify the relevance of the observations to public health outcomes. Epidemiological analyses of oxidative response markers in elderly subjects with cardiovascular disease will continue, linking biomarkers of oxidative stress to aerosol properties. Genetic analysis of study subjects will be integrated into the overall study findings. These studies will have enormous significance for policy considerations. The integrated efforts of the SCPC overall will produce a strong body of literature, at the disposal of policy makers. The SCPC has been highly successful for nine years and has contributed unique findings to the field. We anticipate continuing to expand our interdisciplinary work in the future and provide new insights to the field.
Journal Articles: 47 Displayed | Download in RIS Format
| Other center views: | All 94 publications | 48 publications in selected types | All 47 journal articles |
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Araujo JA, Barajas B, Kleinman M, Wang X, Bennett BJ, Gong KW, Navab M, Harkema J, Sioutas C, Lusis AJ, Nel AE. Ambient particulate pollutants in the ultrafine range promote atherosclerosis and systemic oxidative stress. Circulation Research 2008;102(5):589-596. |
R832413 (2008) R832413C001 (2008) R832413C002 (2007) R832413C002 (2008) |
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Ayres JG, Borm P, Cassee FR, Castranova V, Donaldson K, Ghio A, Harrison RM, Hider R, Kelly F, Kooter IM, Marano F, Maynard RL, Mudway I, Nel A, Sioutas C, Smith S, Baeza-Squiban A, Cho A, Duggan S, Froines J. Evaluating the toxicity of airborne particulate matter and nanoparticles by measuring oxidative stress potential—a workshop report and consensus statement. Inhalation Toxicology 2008;20(1):75-99. |
R832413 (2008) R832413C001 (2007) R832413C001 (2008) R832413C002 (2008) R832413C003 (2008) |
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Biswas S, Ntziachristos L, Moore KF, Sioutas C. Particle volatility in the vicinity of a freeway with heavy-duty diesel traffic. Atmospheric Environment 2007;41(16):3479-3493. |
R832413 (2008) R832413C001 (2006) R832413C001 (2007) R832413C001 (2008) |
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Chan RC-F, Wang M, Li N, Yanagawa Y, Onoe K, Lee JJ, Nel AE. Pro-oxidative diesel exhaust particle chemicals inhibit LPS-induced dendritic cell responses involved in T-helper differentiation. Journal of Allergy and Clinical Immunology 2006;118(2):455-465. |
R832413 (2008) R832413C002 (2007) R832413C002 (2008) R827352 (Final) R827352C002 (Final) |
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Chatila TA, Li N, Garcia-Lloret M, Kim H-J, Nel AE. T-cell effector pathways in allergic diseases: transcriptional mechanisms and therapeutic targets. Journal of Allergy and Clinical Immunology 2008;121(4):812-823. |
R832413 (2007) R832413 (2008) R832413C002 (2007) R832413C002 (2008) |
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Delfino RJ, Staimer N, Tjoa T, Polidori A, Arhami M, Gillen DL, Kleinman MT, Vaziri ND, Longhurst J, Zaldivar F, Sioutas C. Circulating biomarkers of inflammation, antioxidant activity, and platelet activation are associated with primary combustion aerosols in subjects with coronary artery disease. Environmental Health Perspectives 2008;116(7):898-906. |
R832413 (2007) R832413 (2008) R832413C001 (2007) R832413C001 (2008) R832413C004 (2007) R832413C004 (2008) |
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Delfino RJ, Staimer N, Tjoa T, Gillen D, Kleinman MT, Sioutas C, Cooper D. Personal and ambient air pollution exposures and lung function decrements in children with asthma. Environmental Health Perspectives 2008;116(4):550-558. |
R832413 (2007) R832413 (2008) R832413C001 (2007) R832413C001 (2008) |
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Eiguren-Fernandez A, Avol EL, Thurairatnam S, Hakami M, Froines JR, Miguel AH. Seasonal influence on vapor- and particle-phase polycyclic aromatic hydrocarbon concentrations in school communities located in Southern California. Aerosol Science and Technology 2007;41(4):438-446. |
R832413 (2008) R832413C003 (2007) R832413C003 (2008) R827352 (Final) R827352C009 (Final) R827352C013 (Final) |
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Eiguren-Fernandez A, Miguel AH, Lu R, Purvis K, Grant B, Mayo P, Di Stefano E, Cho AK, Froines J. Atmospheric formation of 9,10-phenanthraquinone in the Los Angeles air basin. Atmospheric Environment 2008;42(10):2312-2319. |
R832413 (2007) R832413 (2008) R832413C003 (2007) R832413C003 (2008) R827352 (Final) |
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Fruin S, Westerdahl D, Sax T, Sioutas C, Fine PM. Measurements and predictors of on-road ultrafine particle concentrations and associated pollutants in Los Angeles. Atmospheric Environment 2008;42(2):207-219. |
R832413 (2008) R832413C001 (2007) R832413C001 (2008) |
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Gong Jr. H, Linn WS, Clark KW, Anderson KR, Sioutas C, Alexis NE, Cascio WE, Devlin RB. Exposures of healthy and asthmatic volunteers to concentrated ambient ultrafine particles in Los Angeles. Inhalation Toxicology 2008;20(6):533-545. |
R832413 (2007) R832413 (2008) R832413C001 (2007) R832413C001 (2008) R827352 (Final) |
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Gong KW, Zhao W, Li N, Barajas B, Kleinman M, Sioutas C, Horvath S, Lusis AJ, Nel A, Araujo JA. Air-pollutant chemicals and oxidized lipids exhibit genome-wide synergistic effects on endothelial cells. Genome Biology 2007;8(7):R149. |
R832413 (2008) R832413C001 (2008) R832413C002 (2007) R832413C002 (2008) |
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Hu S, Polidori A, Arhami M, Schafer MM, Schauer JJ, Cho A, Sioutas C. Redox activity and chemical speciation of size fractioned PM in the communities of the Los Angeles-Long Beach Harbor. Atmospheric Chemistry and Physics Discussions 2008;8(3):11643-11672. |
R832413 (2008) R832413C001 (2008) |
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Inoue K-I, Takano H, Ichinose T, Tomura S, Yanagisawa R, Sakurai M, Sumi D, Cho AK, Hiyoshi K, Kumagai Y. Effects of naphthoquinone on airway responsiveness in the presence or absence of antigen in mice. Archives of Toxicology 2007;81(8):575-581. |
R832413 (2007) R832413 (2008) R832413C003 (2007) R832413C003 (2008) |
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Iwamoto N, Sumi D, Ishii T, Uchida K, Cho AK, Froines JR, Kumagai Y. Chemical knockdown of protein-tyrosine phosphatase 1B by 1,2-naphthoquinone through covalent modification causes persistent transactivation of epidermal growth factor receptor. Journal of Biological Chemistry 2007;282(46):33396-33404. |
R832413 (2008) R832413C003 (2007) R832413C003 (2008) |
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Kleinman MT, Sioutas C, Froines JR, Fanning E, Hamade A, Mendez L, Meacher D, Oldham M. Inhalation of concentrated ambient particulate matter near a heavily trafficked road stimulates antigen-induced airway responses in mice. Inhalation Toxicology 2007;19(Suppl 1):117-126. |
R832413 (2008) R832413C001 (2007) R832413C001 (2008) R832413C003 (2007) R827352 (Final) |
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Kleinman MT, Araujo JA, Nel A, Sioutas C, Campbell A, Cong PQ, Li H, Bondy SC. Inhaled ultrafine particulate matter affects CNS inflammatory processes and may act via MAP kinase signaling pathways. Toxicology Letters 2008;178(2):127-130. |
R832413 (2007) R832413 (2008) R832413C001 (2007) R832413C001 (2008) |
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Krudysz MA, Froines JR, Fine PM, Sioutas C. Intra-community spatial variation of size-fractionated PM mass, OC, EC, and trace elements in the Long Beach, CA area. Atmospheric Environment 2008;42(21):5374-5389. |
R832413 (2007) R832413 (2008) R832413C001 (2007) R832413C003 (2007) R832157 (2007) |
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Krudysz M, Moore K, Geller M, Sioutas C, Froines J. Intra-community spatial variability of particulate matter size distributions in southern California/Los Angeles. Atmospheric Chemistry and Physics Discussions 2008;8(3):9641-9672. |
R832413 (2007) R832413 (2008) R832413C001 (2007) R832413C001 (2008) R832413C003 (2007) R832413C003 (2008) |
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Li N, Nel AE. The cellular impacts of diesel exhaust particles: beyond inflammation and death. European Respiratory Journal 2006;27(4):667-668. |
R832413 (2008) R832413C002 (2006) R832413C002 (2008) |
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Li N, Xia T, Nel AE. The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles. Free Radical Biology and Medicine 2008;44(9):1689-1699. |
R832413 (2007) R832413 (2008) R832413C002 (2007) R832413C002 (2008) |
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Majestic BJ, Schauer JJ, Shafer MM, Fine PM, Singh M, Sioutas C. Trace metal analysis of atmospheric particulate matter:a comparison of personal and ambient samplers. Journal of Environmental Engineering and Science 2008;7(4):289-298. |
R832413 (2007) R832413 (2008) R832413C001 (2007) R832413C001 (2008) |
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Moore KF, Ning Z, Ntziachristos L, Schauer JJ, Sioutas C. Daily variation in the properties of urban ultrafine aerosol—Part I: Physical characterization and volatility. Atmospheric Environment 2007;41(38):8633-8646. |
R832413 (2008) R832413C001 (2007) R832413C001 (2008) |
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Ning Z, Moore KF, Polidori A, Sioutas C. Field validation of the new miniature Versatile Aerosol Concentration Enrichment System (mVACES). Aerosol Science and Technology 2006;40(12):1098-1110. |
R832413 (2007) R832413 (2008) R832413C001 (2007) R832413C001 (2008) |
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Ning Z, Geller MD, Moore KF, Sheesley R, Schauer JJ, Sioutas C. Daily variation in chemical characteristics of urban ultrafine aerosols and inference of their sources. Environmental Science & Technology 2007;41(17):6000-6006. |
R832413 (2008) R832413C001 (2007) R832413C001 (2008) |
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Ning Z, Polidori A, Schauer JJ, Sioutas C. Emission factors of PM species based on freeway measurements and comparison with tunnel and dynamometer studies. Atmospheric Environment 2008;42(13):3099-3114. |
R832413 (2007) R832413 (2008) R832413C001 (2007) R832413C001 (2008) |
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Ntziachristos L, Froines JR, Cho AK, Sioutas C. Relationship between redox activity and chemical speciation of size-fractionated particulate matter. Particle and Fibre Toxicology 2007;4:5. |
R832413C001 (2008) R832413C003 (2008) |
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Ntziachristos L, Polidori A, Phuleria H, Geller MD, Sioutas C. Application of a diffusion charger for the measurement of particle surface concentration in different environments. Aerosol Science and Technology 2007;41(6):571-580. |
R832413 (2008) R832413C001 (2006) R832413C001 (2007) R832413C001 (2008) |
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Ntziachristos L, Ning Z, Geller MD, Sheesley RJ, Schauer JJ, Sioutas C. Fine, ultrafine and nanoparticle trace element compositions near a major freeway with a high heavy-duty diesel fraction. Atmospheric Environment 2007;41(27):5684-5696. |
R832413 (2007) R832413 (2008) R832413C001 (2007) R832413C001 (2008) |
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Ntziachristos L, Ning Z, Geller MD, Sioutas C. Particle concentration and characteristics near a major freeway with heavy-duty diesel traffic. Environmental Science & Technology 2007;41(7):2223-2230. |
R832413 (2008) R832413C001 (2006) R832413C001 (2007) R832413C001 (2008) |
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Ntziachristos L, Froines JR, Cho AK, Sioutas C. Relationship between redox activity and chemical speciation of size-fractionated particulate matter. Particle & Fibre Toxicology 2007;4(June):5. |
R832413 (2008) R832413C001 (2007) |
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Phuleria HC, Sheesley RJ, Schauer JJ, Fine PM, Sioutas C. Roadside measurements of size-segregated particulate organic compounds near gasoline and diesel-dominated freeways in Los Angeles, CA. Atmospheric Environment 2007;41(22):4653-4671. |
R832413 (2008) R832413C001 (2007) R832413C001 (2008) |
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Polidori A, Arhami M, Sioutas C, Delfino RJ, Allen R. Indoor/outdoor relationships, trends, and carbonaceous content of fine particulate matter in retirement homes of the Los Angeles Basin. Journal of the Air & Waste Management Association 2007;57(3):366-379. |
R832413 (2008) R832413C001 (2008) |
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Polidori A, Arhami M, Sioutas C, Delfino RJ,Allen R. Indoor/outdoor relationships, trends, and carbonaceous content of fine particulate matter in retirement homes of the Los Angeles Basin. Journal of the Air & Waste Management Association 2007;57(3):366–379. |
R832413C001 (2007) |
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Polidori A, Hu S, Biswas S, Delfino RJ, Sioutas C. Real-time characterization of particle-bound polycyclic aromatic hydrocarbons in ambient aerosols and from motor-vehicle exhaust. Atmospheric Chemistry and Physics Discussions 2008;8(5):1277-1291. |
R832413 (2007) R832413 (2008) R832413C001 (2007) R832413C001 (2008) |
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Shinyashiki M, Rodriguez CE, Di Stefano EW, Sioutas C, Delfino RJ, Kumagai Y, Froines JR, Cho AK. On the interaction between glyceraldehyde-3-phosphate dehydrogenase and airborne particles: evidence for electrophilic species. Atmospheric Environment 2008;42(3):517-529. |
R832413 (2008) R832413C001 (2008) R832413C003 (2007) R832413C003 (2008) |
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Sillanpaa M, Geller MD, Phuleria HC, Sioutas C. High collection efficiency electrostatic precipitator for in vitro cell exposure to concentrated ambient particulate matter (PM). Journal of Aerosol Science 2008;39(4):335-347. |
R832413 (2007) R832413 (2008) R832413C001 (2007) R832413C001 (2008) |
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Taguchi K, Shimada M, Fujii S, Sumi D, Pan X, Yamano S, Nishiyama T, Hiratsuka A, Yamamoto M, Cho AK, Froines JR, Kumagai Y. Redox cycling of 9,10-phenanthraquinone to cause oxidative stress is terminated through its monoglucuronide conjugation in human pulmonary epithelial A549 cells. Free Radical Biology & Medicine 2008;44(8):1645-1655. |
R832413 (2007) R832413 (2008) R832413C003 (2007) R832413C003 (2008) |
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Westerdahl D, Fruin SA, Fine PL, Sioutas C. The Los Angeles International Airport as a source of ultrafine particles and other pollutants to nearby communities. Atmospheric Environment 2008;42(13):3143–3155. |
R832413C001 (2008) |
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Westerdahl D, Fruin SA, Fine PL, Sioutas C. The Los Angeles International Airport as a source of ultrafine particles and other pollutants to nearby communities. Atmospheric Environment 2008;42(13):3143-3155. |
R832413 (2007) R832413 (2008) R832413C001 (2007) R831861 (2005) |
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Wold LE, Simkhovich BZ, Kleinman MT, Nordlie MA, Dow JS, Sioutas C, Kloner RA. In vivo and in vitro models to test the hypothesis of particle-induced effects on cardiac function and arrhythmias. Cardiovascular Toxicology 2006;6(1):69-78. |
R832413 (2008) R832413C001 (2007) R827352 (Final) |
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Xia T, Kovochich M, Brant J, Hotze M, Sempf J, Oberley T, Sioutas C, Yeh JI, Wiesner MR, Nel AE. Comparison of the abilities of ambient and manufactured nanoparticles to induce cellular toxicity according to an oxidative stress paradigm. Nano Letters 2006;6(8):1794-1807. |
R832413 (2008) R832413C001 (2007) R832413C001 (2008) R832413C002 (2006) R832413C002 (2008) R827352 (Final) R827352C002 (Final) R827352C014 (Final) |
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Xia T, Kovochich M, Nel A. The role of reactive oxygen species and oxidative stress in mediating particulate matter injury. Clinics in Occupational and Environmental Medicine 2006;5(4):817-836. |
R832413 (2008) R832413C002 (2007) R832413C002 (2008) |
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Xia T, Kovochich M, Nel AE. Impairment of mitochondrial function by particulate matter (PM) and their toxic components: implications for PM-induced cardiovascular and lung disease. Frontiers in Bioscience 2007;12(3):1238-1246. |
R832413 (2008) R832413C002 (2007) R832413C002 (2008) |
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Yacobi NR, Phuleria HC, Demaio L, Liang CH, Peng C-A, Sioutas C, Borok Z, Kim K-J, Crandall ED. Nanoparticle effects on rat alveolar epithelial cell monolayer barrier properties. Toxicology in Vitro 2007;21(8):1373-1381. |
R832413 (2008) R832413C001 (2007) R832413C001 (2008) |
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Zhu Y, Eiguren-Fernandez A, Hinds WC, Miguel AH. In-cabin commuter exposure to ultrafine particles on Los Angeles freeways. Environmental Science & Technology 2007;41(7):2138-2145. |
R832413 (2008) R832413C005 (2007) R832413C005 (2008) R827352 (Final) |
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Zhu Y, Fung DC, Kennedy N, Hinds WC, Eiguren-Fernandez A. Measurements of ultrafine particles and other vehicular pollutants inside a mobile exposure system on Los Angeles freeways. Journal of the Air & Waste Management Association 2008;58(3):424-434. |
R832413 (2007) R832413 (2008) R832413C005 (2007) R832413C005 (2008) |
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Airborne particulate matter, ambient air, sources, Southern California, Los Angeles Basin, exposure assessment, oxidative stress, source-receptor, ultrafine, fine, coarse, organics, quinones,
, Air, Scientific Discipline, Health, RFA, Risk Assessments, Health Risk Assessment, particulate matter, Environmental Chemistry, respiratory impact, cardiovascular disease, cardiovascular vulnerability, chemical characteristics, cardiotoxicity, chemical composition, cardiopulmonary responses, human health risk, oxidative stress, human health effects, toxicology, ambient particle health effects, biological mechanism , airborne particulate matter, human exposure, PM, animal modelProgress and Final Reports:
2006 Progress Report
2007 Progress Report
Original Abstract
Subprojects under this Center:
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R832413C001 Contribution of Primary and Secondary PM Sources to Exposure & Evaluation of Their Relative Toxicity
R832413C002 Project 2: The Role of Oxidative Stress in PM-induced Adverse Health Effects
R832413C003 The Chemical Properties of PM and their Toxicological Implications
R832413C004 Oxidative Stress Responses to PM Exposure in Elderly Individuals With Coronary Heart Disease
R832413C005 Ultrafine Particles on and Near Freeways