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NYU-EPA PM Center: Health Risks of PM Components
EPA Grant Number: R827351Center: EPA NYU PM Center: Health Risks of PM Components
Center Director: Lippmann, Morton
Title: NYU-EPA PM Center: Health Risks of PM Components
Investigators: Lippmann, Morton , Chen, Lung Chi , Cohen, Beverly S. , Cohen, Mitchell , Gordon, Terry , Heikkmen, Maire M. , Hoffman, Eric , Ito, Kazuhiko , McLennan, G. , Nadas, Arthur , Nadziejko, Christine , Reibman, Joan , Reinhardt, J. , Thurston, George D. , Zelikoff, Judith T.
Current Investigators: Lippmann, Morton , Chen, Lung Chi , Cohen, Beverly S. , Cohen, Mitchell , Gordon, Terry , Hoffman, Eric , Ito, Kazuhiko , Kendall, Michaela , Nadziejko, Christine , Reibman, Joan , Salnikow, Konstantin , Thurston, George D. , Zelikoff, Judith T.
Institution: NYU School of Medicine , University of Iowa
EPA Project Officer: Stacey Katz/Gail Robarge,
Project Period: June 1, 1999 through May 31, 2005 (Extended to May 31, 2006)
Project Amount: $8,076,438
RFA: Airborne Particulate Matter (PM) Centers (1999)
Research Category: Particulate Matter
Description:
Objective:The overall objective of this Center is to develop and conduct a comprehensive research program focused on the identification and characterization of the physical and chemical properties of particulate matter (PM) that adversely impact human health. The focal hypothesis of this PM Center is that specific chemical species within PM and within certain particle size ranges are primarily responsible for PM's mortality, morbidity, and functional effects. Approach:
The NYU School of Medicine (NYUSOM) PM Center will perform innovative research proposed by Center members targeted at critical knowledge gaps on PM exposures and their health effects, and will coordinate such research with other ongoing active research on airborne PM being conducted at NYUSOM. It will also provide for collaboration and coordination with other scientists actively engaged in PM research at other institutions, including NHEERL and NERL at EPA, other EPA and NIEHS-sponsored Academic Center programs, and other academic, governmental and industrial facilities in the U.S. and elsewhere. The Administrative and Service Core units supported by the Center will optimize coordination and efficiency of shared resource utilization.
The Administrative Core, consists of the Program Director (PD) and Co-PD, and the Center Administrator (CA), and is responsible for all aspects of scientific program management. An Internal Management Committee (IMC), consisting of the PD, the Co-PD, CA, the Research Core Directors, and the Coordinator for Core Services, meets monthly to discuss program planning and coordination, allocation of Center resources, overall research progress, adequacy of core services, recruitment of new PM Center investigators, invitations to Visiting Scientists and seminar speakers, and opportunities for additional extramural support for PM research projects. On an annual basis, the IMC reviews and, as appropriate, revises the focus of the PM Center's research agenda and call for applications for research support for new Center-sponsored projects and for post-doctoral research positions and/or clinical fellowships. All applications responsive to the call undergo scientific peer reviews and review by the External Scientific Advisory Committee (ESAC). However, the ultimate decisions for Center priorities and operations rests with the Program Directors. The final decisions on PM Center funding for meritorious first year research proposals were made by the PD and Co-PD after full consideration of all the internal and external peer review comments, program balance, and potentially available funds.
The projects selected were:
PROJECT 1. Assessment of Variations in Human Airway Geometry: Evaluation of Particle Deposition and Dose. B. Cohen;*: E. Hoffman;+ J. Reinhardt,+ G. McLennan,+ N. Harley.* (*NYUSOM, +U. Iowa)
The objectives of this pilot project are to: 1) develop methods for retrieval of morphometric data from three dimensional images of conducting airways obtained by volumetric x-ray Computerized Tomography (CT) to assess airway variability in healthy adults and children and in individuals with compromised lungs; and 2) use the resulting computerized data files to produce hollow airway casts (for PM deposition studies) by stereo lithography (STL). The project joins the extensive imaging expertise at U. Iowa with NYUSOM PM expertise. The ultimate goal is to quantify the effect of airway variability on PM deposition and dose, thus addressing an important issue in PM susceptibility.
Patients will be scanned supine, at 65% Vital Capacity, to acquire 1.5 mm thick sections in a continuous volume (spiral) scanning mode whereby 140 sections are acquired from apex to base. Reconstruction will utilize the smallest allowable field of view relative to an individual patient's thoracic cavity size and a high spatial frequency reconstruction algorithm. The 3-D images will be converted to an STL file. A physical solid model of the airway lumens, and a hollow cast model, for each subject will be created.
This project will develop methods both for the quantification of airway morphometry in human subjects, and for utilizing the data in STL format to produce hollow airway cast models. Since the STL can make an infinite number of accurate replicas, duplicate casts can be made for experimental studies and for distribution to other EPA PM Centers.
PROJECT 2. Exposure Characterization Error. K. Ito (Lead); Co-I: A. Nadas;: G.D. Thurston.
Our objectives are to: 1) quantitatively characterize spatio-temporal error of PM components and gaseous co-pollutants measured at the routine regulatory-based air monitors as a function of site characteristics using the entire U.S. air monitoring network; 2) establish the relationship between the estimated error at a given monitoring site and the effect size/significance in mortality and morbidity models; and 3) evaluate the relative contribution of the error due to site-to-site and person-to-site variability. We will first characterize spatio-temporal variation of PM at metropolitan and regional scales for the entire U.S. between 1985 and 1994 (n 900 sites for PM10; n 40 sites for PM2.5). The site-to-site correlation of temporal variation will be modeled as a function of qualitative (e.g., location setting) and quantitative (e.g., distance to and quantity of emission sources) variables. The second stage of this project will investigate the relationship between the estimated exposure characterization error associated with a given site's data and its effect size/significance in health effects models for MSAs or regions where a large number (10-30 sites) of monitors are available (approximately 20 regions covering over 70 million residents). In addition, as data become available from the ongoing EPA-funded NYUSOM PM personal exposure study in NYC in 1999, we will be able to determine the error associated with person-to-central monitor difference, and to evaluate the relative importance of these two types of errors. The initial analyses for PM10 and PM2.5 will set the stage for the later analyses for PM constituents data that will become available to Center investigators in the next few years. The results will help in the design future population exposure monitoring systems (e.g., location of monitors, sampling frequencies) for epidemiological purposes and compliance monitoring.
PROJECT 3. Physicochemical Parameters of Combustion Generated Atmospheres as Determinants of PM Toxicity. L.C. Chen (Lead); R.B. Schlesinger, T. Gordon
This study examines the hypothesis that the toxicological effects associated with combustion-generated PM depend upon specific physicochemical characteristics of the particles. In this study, cardiopulmonary effects will be measured in healthy and compromised animals exposed by inhalation to laboratory generated particle atmospheres having precisely defined physicochemical characteristics. A unique furnace system will be used to produce realistic combustion effluent from a mixture of carbon, SO2, and iron to allow determination of specific components that may be responsible for effects, and assessment of whether any effects follow inhalation of any type of particle. The approaches involve telemetric techniques (heart rate, heart rate variability, blood pressure, and respiratory rates) as well as biochemistry (lung lavage and blood coagulation parameters), lung histopathology, and pulmonary function testing to detect adverse effects of PM on the respiratory and cardiovascular systems. Both healthy and compromised (congestive heart failure) animals (F344 male rats) will be used. Congestive heart failure will be induced by left coronary artery ligation. Animals (n=6/group) will be exposed to either filtered air (control) or combinations of pollutants for 3 hr and the biological endpoints will be evaluated at various time points post exposure. All aerosols will be generated in two size ranges, fine (0.3 µm, initially at 150 µg/m3, a value equal to the 24 hr NAAQS for PM10) and ultrafine (0.03 µm, initially at 1.0 x 106 particles/cc). Effects will be compared across the various atmospheres.
The results of this study will allow a determination of whether cardiopulmonary responses to combustion-generated PM are: 1) nonspecific to particle type; or 2) depend upon particle size and/or chemical characteristics of the particles.
PROJECT 4. Effects of Particle-Associated Organic Irritants on the Cardiovascular System. C. Nadziejko; T. Gordon, L.C. Chen.
Our objective is to examine the effects of particle-associated organic irritants on the cardiovascular system, an increasingly important public health issue. The physical and/or chemical properties of PM responsible for these serious health effects are currently unknown. We will use blood pressure, heart rate, heart rate variability, and selected coagulation parameters as endpoints to test the hypothesis that the irritant properties of PM are responsible for cardiovascular effects of PM inhalation of organic irritants affects cardiovascular function, and the acute effects of smoke are reflexively-mediated by stimulation of irritant receptors in the respiratory tract. Little is known about the effects of organic irritants that are absorbed onto particles. These knowledge gaps will be addressed by exposing normal and compromised rats to laboratory generated carbon particles coated with organic irritants that are known to be constituents of PM. The rats will be exposed to carbon particles coated with formaldehyde or acrolein for 3 hrs, and physiological monitoring will be done before, during, and up to 48 hrs after exposure. Air-exposed rats and rats exposed to uncoated carbon particles will serve as controls. Two sizes of particles will be examined, fine (0.3 µm, at 150 µg/m3) and ultrafine (0.03 µm at 1 x 106 particles per cc). Normal rats and rats with congestive heart failure (induced by ligation of the left coronary artery) will be used. Cardiovascular parameters will be measured in conscious animals using implanted transmitters. Blood will be sampled for measurement of coagulation parameters. Respiratory rate will be measured from fluctuations in blood pressure.
It is expected that each of the particle-associated organic irritants examined will cause cardiovascular changes. The results of this project will be directly compared with Dr. Chen's research project which will examine other chemical constituents of PM using the same animal model and many of the same biological endpoints.
PROJECT 5. Role of Particle Size and Solubility of PM-Associated Transition Metals in Exacerbating Infectious Pneumonia. J.T. Zelikoff; M. Cohen; L.C. Chen, R.B. Schlesinger.
These studies will correlate the physicochemical attributes of ambient PM with its in vivo immunotoxicity, so as to identify and characterize the role of particle size (i.e., fine/ultrafine), form (i.e., soluble vs. insoluble), and constitutive transition metals in the exacerbation of an ongoing S. pneumoniae infection. Previous investigations in this laboratory have demonstrated that a single 5-hr inhalation exposure of Streptococcus pneumoniae-infected rats to concentrated ambient PM2.5 from New York City (NYC) air altered both pulmonary and systemic immunity, as well as exacerbated the infection process, in a time-post-exposure-dependent manner. Bacterial clearance will be used to evaluate the role of the various physico-chemical characteristics of PM upon disease exacerbation. Rats will be exposed nose-only for a single 5 hr exposure to atmospheres containing differentially-sized PM fractions (i.e., fine [0.2 -2.5 µm] and ultrafine [< 0.2 µm]). We will subsequently analyze the role of solubility and composition in PM-induced immunotoxicity, focussing upon the size fraction that demonstrated the most dramatic effects upon intrapulmonary bacterial killing. Samples of ambient NYC PM will be size-separated and collected onto Teflon filters using a MOUDI impactor. The PM will be recovered, and the sized particles will be extracted to generate soluble and insoluble metal-bearing subfractions for use in analytical assessments.
To determine the role that PM-associated transition metal solubility and concentration might play in bringing about the observed changes in host immunocompetence, infected rats will be exposed to artificially-generated atmospheres containing soluble/insoluble forms of the individual metals found at the highest concentrations in the immunoreactive fraction. Similar studies will then employ mixtures of soluble/insoluble forms of more than one metal, so as to ascertain whether the observed immunosuppression in PM-exposed hosts is dependent, in part, upon any synergistic/additive interactions among the transition metals present.
The results should provide necessary information as to characteristics of PM responsible for the observed effects upon host immunocompetence, and help to clarify the role that size plays in host pulmonary immunmodulation.
PROJECT 6. A Prospective Study of Asthma Susceptibility to PM: Epidemiologic Investigations of Key PM Components and Biomarkers of Effects. G.D. Thurston; J. Reibman.
The objective of this research is to exploit available data from a comprehensive ongoing PM characterization field study to investigate by which component(s) of PM are asthmatics most strongly affected, and by what mechanism(s)? We will study a cohort of 30 inner city adult patients with moderate to severe asthma from the Bellevue Hospital Primary Care Asthma Clinic (BHPCAC), directed by Dr. Reibman. Individual daily determinations of asthma symptoms, lung function, medication usage, and activities, as well as biological marker levels (in nasal lavage and serum) will be obtained on days following PM episodes. Daily PM measurements collected at a nearby central monitoring site are being augmented by much more extensive PM component characterization data to be collected at this site as part of an intensive PM air monitoring-hospital visit study continuing into 2000, including PM10, PM2.5, H+, sulfate, elemental and organic carbon, trace elements, and pollens and spore counts. Further, Dr. Lippmann will be conducting daily ultrafine particle counts at this site as part of a separately funded EPA personal sampling project.
The study cohort will be followed by prospective monitoring of their health, and by an evaluation of the effects of ambient elevations of PM on subject health status (i.e., daily diary records of peak flow, symptoms, medication use during study periods). We will also evaluate baselines (during a low PM exposure period) of health, spirometry, and serum and nasal lavage levels of proinflammatory mediators (IL-6, IL-8), as well as of Th1 and Th2 induced cells (interferon-gamma and IL-4, respectively) that are thought to mediate asthma response. Alterations in biomarker levels will be determined on several days for each subject on days following PM days exceeding the historical 80th %ile of PM10, as procured from continuous TEOM measurements of PM10 mass from the nearby air monitoring site.
Time-series analyses will be applied to evaluate the associations between asthma health and the various PM air pollution components during this study, in order to evaluate the extent to which each participant acutely responds to PM. Individual-level personal and biological data will be obtained that will allow for the control of age, sex, race, activities, etc. Statistical comparisons of these results across the various PM components (e.g., fine vs. coarse mass, elemental concentrations, ultrafine aerosol measurements) will allow an evaluation of their relative associations with adverse health effects in asthmatics.
PROJECT 7. Co-Exposure of Human Subjects to Concentrated Ambient PM and Gaseous Pollutants. T. Gordon; J. Fine; L.C. Chen and J. Reibman.
Our objective is to determine whether co-exposure to ozone influences the acute cardiopulmonary effects from controlled exposures to particulate matter (PM) in human volunteers. Co-exposure of human subjects to PM and O3 is likely to produce changes in pulmonary function and inflammation that are greater than that from exposure to PM or O3 alone.
A pilot study, funded by the Health Effects Institute, is currently underway, examining the adverse effects of exposure to concentrated ambient PM alone in normal and asthmatic subjects. The experiments proposed here will build on these studies by enabling the controlled testing of exposure to concentrated ambient PM with and without O3 in normal and asthmatic subjects. Normal subjects (n = 12, ages 18 to 45) will be exposed for 2 hours by face mask to filtered air, 150 µg/m3 concentrated ambient PM alone, 0.12 ppm O3 alone, or 150 µg/m3 concentrated ambient PM and 0.12 ppm O3 together. Biochemical and cellular parameters in sputum, coagulability indices in blood, electrocardiogram and heart rate/heart rate variability changes, and pulmonary function will be measured up to 18 hours after each exposure. Careful chemical characterization of the exposure atmospheres will insure that day-to-day variability in PM composition will be considered in the interpretation of results. Asthmatic subjects (n = 12) will be exposed to test atmospheres as described above. The same endpoints will be examined in addition to studying the TH2 cytokine profile and eosinophil-derived products in recovered sputum. Strict inclusion/exclusion criteria for study participants will ensure that the variability of asthmatics is kept to a minimum, and that medication usage is controlled during the study.
It is anticipated that concentrated ambient PM alone will not produce statistically significant adverse effects in healthy individuals. This project, however, will address the potential synergism that may occur between concentrated ambient PM and O3. The study of human subjects with pre-existing cardiac or pulmonary disease will be an important focus. It is expected that our experiments will demonstrate that asthmatics are made more susceptible to the adverse effects of PM by co-exposure to O3, suggesting that the health effects of very low concentrations PM on this sensitive sub-population should be considered in the setting of PM air quality standards.
Expected Results:The research projects conducted with PM Center support will each contribute significantly to a clearer definition, or resolution, of a critical scientific issue in PM-associated health effects and, thereby provide decision makers with information needed to narrow current uncertainties about the nature and/or extent of these effects. The PM Center will also stimulate and facilitate an increased and more productive range and depth of interdisciplinary and inter-institutional research on PM exposures, their health effects, and their societal impacts, both among the NYUSOM Center members and with colleagues at other PM Centers. The PM Center's Service Core for Data Management that will be a resource for both PM Center members and, through the Information Access and Dissemination Core, for other scientists and the public. The PM Center will also establish and maintain a web-site covering all PM Center publications and activities.
Improvements in Risk Assessment and Risk Management: To support the Improvements in Risk Assessment and Risk Management, the PM program at NYUSOM is focused on high priority research gaps identified in the National Research Council's recommendations of March 31, 1998, and will help to reduce many of the residual uncertainties about the level of protection to public health provided by the 1997 PM NAAQS. Its special focus is on how well the PM NAAQS are targeted on the PM components having the greatest public health impacts.
Journal Articles: 74 Displayed | Download in RIS Format
| Other center views: | All 95 publications | 86 publications in selected types | All 74 journal articles |
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Chen LC, Thurston GD. World Trade Center cough. Lancet 2002;360(Suppl 1):S37-S38. |
R827351 (2001) R827351 (2002) R827351 (Final) |
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Chen LC, Nadziejko C. Effects of subchronic exposures to concentrated ambient particles (CAPs) in mice: V. CAPs exacerbate aortic plaque development in hyperlipidemic mice. Inhalation Toxicology 2005;17(4-5):217-224. |
R827351 (2003) R827351 (Final) R827351C013 (2003) R827351C013 (Final) |
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Chen LC, Hwang JS. Effects of subchronic exposures to concentrated ambient particles (CAPs) in mice: IV. Characterization of acute and chronic effects of ambient air fine particulate matter exposures on heart-rate variability. Inhalation Toxicology 2005;17(4-5):209-216. |
R827351 (Final) R827351C013 (2003) R827351C013 (Final) |
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Cifuentes L, Borja-Aburto VH, Gouveia N, Thurston G, Davis DL. Assessing the health benefits of urban air pollution reductions associated with climate change mitigation (2000-2020): Santiago, Sao Paulo, Mexico City, and New York City. Environmental Health Perspectives Supplements 2001;109(S3):419-425. |
R827351 (2003) R827351 (Final) |
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Cifuentes L, Borja-Aburto VH, Gouveia N, Thurston G, Davis DL. Climate change. Hidden health benefits of greenhouse gas mitigation. Science 2001;293(5533):1257-1259. |
R827351 (2001) R827351 (Final) |
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Cohen BS, Li W, Xiong JQ, Lippmann M. Detecting H+ in ultrafine ambient aerosol using iron nano-film detectors and scanning probe microscopy. Applied Occupational and Environmental Hygiene 2000;15(1):80-89. |
R827351 (2003) R827351 (Final) R824791 (Final) R826688 (2000) R826688 (Final) |
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Cohen BS, Heikkinen M, Hazi Y. Airborne fine and ultrafine particles near the World Trade Center disaster site. Aerosol Science and Technology 2004;38(4):338-348. |
R827351 (2003) R827351 (Final) |
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Cohen MD, Sisco M, Baker K, Bowser D, Chen LC, Schlesinger RB. Effects of inhaled chromium on pulmonary A1AT. Inhalation Toxicology 2002;14(7):765-771. |
R827351 (2001) R827351 (Final) |
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Cohen MD. Pulmonary immunotoxicology of select metals: aluminum, arsenic, cadmium, chromium, copper, manganese, nickel, vanadium, and zinc. Journal of Immunotoxicology 2004;1(1):39-69. |
R827351 (2003) R827351 (Final) R827351C008 (2003) R827351C008 (Final) |
not available |
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Cohen MD, Prophete C, Sisco M, Chen LC, Zelikoff JT, Smee JJ, Holder AA, Crans DC. Pulmonary immunotoxic potentials of metals are governed by select physicochemical properties: chromium agents. Journal of Immunotoxicology 2006;3(2):69-81. |
R827351 (Final) R827351C008 (Final) |
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Cohen MD, Sisco M, Prophete C, Chen LC, Zelikoff JT, Ghio AJ, Stonehuerner JD, Smee JJ, Holder AA, Crans DC. Pulmonary immunotoxic potentials of metals are governed by select physicochemical properties: vanadium agents. Journal of Immunotoxicology 2007;4(1):49-60. |
R827351 (Final) R827351C008 (Final) |
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De Leon SF, Thurston GD, Ito K. Contribution of respiratory disease to nonrespiratory mortality associations with air pollution. American Journal of Respiratory and Critical Care Medicine 2003;167(8):1117-1123. |
R827351 (2002) R827351 (Final) |
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Doherty SP, Prophete C, Maciejczyk P, Salnikow K, Gould T, Larson T, Koenig J, Jaques P, Sioutas C, Zelikoff JT, Lippmann M, Cohen MD. Detection of changes in alveolar macrophage iron status induced by select PM2.5-associated components using iron-response protein binding activity. Inhalation Toxicology 2007;19(6-7):553-562. |
R827351 (Final) R827352 (Final) R827355 (2004) R827355 (Final) |
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Gavett SH, Haykal-Coates N, Highfill JW, Ledbetter AD, Chen LC, Cohen MD, Harkema JR, Wagner JG, Costa DL. World Trade Center fine particulate matter causes respiratory tract hyperresponsiveness in mice. Environmental Health Perspectives 2003;111(7):981-991. |
R827351 (2002) R827351 (Final) |
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Ghio AJ, Cohen MD. Disruption of iron homeostasis as a mechanism of biologic effect by ambient air pollution particles. Inhalation Toxicology 2005;17(13):709-716. |
R827351 (Final) R827351C008 (Final) |
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Gilmour MI, McGee J, Duvall RM, Dailey L, Daniels M, Boykin E, Cho SH, Doerfler D, Gordon T, Devlin RB. Comparative toxicity of size-fractionated airborne particulate matter obtained from different cities in the United States. Inhalation Toxicology 2007;19(Suppl 1):7-16. |
R827351 (Final) |
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Gordon T, Reibman J. Cardiovascular toxicity of inhaled ambient particulate matter. Toxicological Sciences 2000;56(1):2-4. |
R827351 (Final) R827351C004 (2002) R827351C004 (Final) R826244 (1999) R826244 (2000) R826244 (Final) |
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Gunnison A, Chen LC. Effects of subchronic exposures to concentrated ambient particles in mice: VI. Gene expression in heart and lung tissue. Inhalation Toxicology 2005;17(4-5):225-233. |
R827351 (Final) R827351C013 (Final) |
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Gwynn RC, Thurston GD. The burden of air pollution: impacts among racial minorities. Environmental Health Perspectives 2001;109(Suppl 4):501-506. |
R827351 (2001) R827351 (Final) R825264 (Final) |
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Hazi Y, Heikkinen MSA, Cohen BS. Size distribution of acidic sulfate ions in fine ambient particulate matter and assessment of source region effect. Atmospheric Environment 2003;37(38):5403-5413. |
R827351 (2001) R827351 (2003) R827351 (Final) |
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Hopke PK, Ito K, Mar T, Christensen WF, Eatough DJ, Henry RC, Kim E, Laden F, Lall R, Larson TV, Liu H, Neas L, Pinto J, Stolzel M, Suh H, Paatero P, Thurston GD. PM source apportionment and health effects: 1. Intercomparison of source apportionment results. Journal of Exposure Science & Environmental Epidemiology 2006;16(3):275-286. |
R827351 (Final) R827351C001 (Final) |
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Hwang JS, Nadziejko C, Chen LC. Effects of subchronic exposures to concentrated ambient particles (CAPs) in mice: III. Acute and chronic effects of CAPs on heart rate, heart-rate fluctuation, and body temperature. Inhalation Toxicology 2005;17(4-5):199-207. |
R827351 (2003) R827351 (Final) R827351C013 (2003) R827351C013 (Final) |
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Ito K, Thurston GD, Nadas A, Lippmann M. Monitor-to-monitor temporal correlation of air pollution and weather variables in the North-Central U.S. Journal of Exposure Analysis & Environmental Epidemiology 2001;11(1):21-32. |
R827351 (Final) R827351C001 (2000) R827351C001 (2002) R827351C001 (2003) R827351C001 (Final) R825271 (Final) |
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Ito K, Xue N, Thurston G. Spatial variation of PM2.5 chemical species and source-apportioned mass concentrations in New York City. Atmospheric Environment 2004;38(31):5269-5282. |
R827351 (2003) R827351 (Final) R827351C001 (2003) R827351C001 (Final) R827997 (2005) R827997 (Final) |
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Ito K, De Leon SF, Thurston GD, Nadas A, Lippmann M. Monitor-to-monitor temporal correlation of air pollution in the contiguous US. Journal of Exposure Analysis and Environmental Epidemiology 2005;15(2):172-184. |
R827351 (2003) R827351 (Final) R827351C001 (2003) R827351C001 (Final) |
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Ito K, Christiansen WF, Eatough DJ, Henry RC, Kim E, Laden F, Lall R, Larson TV, Neas L, Hopke PK, Thurston GD. PM source apportionment and health effects: 2. An investigation of intermethod variability in associations between source-apportioned fine particle mass and daily mortality in Washington, DC. Journal of Exposure Science & Environmental Epidemiology 2006;16(4):300-310. |
R827351 (Final) R827351C001 (Final) R827353 (Final) R827353C015 (Final) R827354 (Final) R827354C001 (Final) R827355 (Final) R827355C008 (Final) R827997 (Final) |
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Kendall M, Brown L, Trought K. Molecular adsorption at particle surfaces: a PM toxicity mediation mechanism. Inhalation Toxicology 2004;16(Suppl 1):99-105. |
R827351 (2003) R827351 (Final) R827351C011 (2003) R827351C011 (Final) |
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Kendall M, Guntern J, Lockyer NP, Jones FH, Hutton BM, Lippmann M, Tetley TD. Urban PM2.5 surface chemistry and interactions with bronchoalveolar lavage fluid. Inhalation Toxicology 2004;16(Suppl 1):115-128. |
R827351 (2003) R827351 (Final) R827351C011 (2002) R827351C011 (Final) |
not available |
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Lall R, Kendall M, Ito K, Thurston GD. Estimation of historical annual PM2.5 exposures for health effects assessment. Atmospheric Environment 2004;38(31):5217-5226. |
R827351 (2003) R827351 (Final) |
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Lall R, Thurston GD. Identifying and quantifying transported vs. local sources of New York City PM2.5 fine particulate matter air pollution. Atmospheric Environment 2006;40(Suppl 2):333-346. |
R827351 (Final) R827351C003 (Final) |
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Landrigan PJ, Lioy PJ, Thurston G, Berkowitz G, Chen LC, Chillrud SN, Gavett SH, Georgopoulos PG, Geyh AS, Levin S, Perera F, Rappaport SM, Small C, NIEHS World Trade Center Working Group. Health and environmental consequences of the World Trade Center disaster. Environmental Health Perspectives 2004;112(6):731-739. |
R827351 (2003) R827351 (Final) R830827 (2004) R830827 (Final) R831711C002 (2004) R832141 (2005) |
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Lioy PJ, Weisel CP, Millette JR, Eisenreich S, Vallero D, Offenberg J, Buckley B, Turpin B, Zhong M, Cohen MD, Prophete C, Yang I, Stiles R, Chee G, Johnson W, Porcja R, Alimokhtari S, Hale RC, Weschler C, Chen LC. Characterization of the dust/smoke aerosol that settled east of the World Trade Center (WTC) in lower Manhattan after the collapse of the WTC 11 September 2001. Environmental Health Perspectives 2002;110(7):703-714. |
R827351 (2001) R827351 (2002) R827351 (Final) |
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Lippmann M, Frampton M, Schwartz J, Dockery D, Schlesinger R, Koutrakis P, Froines J, Nel A, Finkelstein J, Godleski J, Kaufman J, Koenig J, Larson T, Luchtel D, Liu L-J S, Oberdorster G, Peters A, Sarnat J, Sioutas C, Suh H, Sullivan J, Utell M, Wichmann E, Zelikoff J. The U.S. Environmental Protection Agency Particulate Matter Health Effects Research Centers Program: a midcourse report of status, progress, and plans. Environmental Health Perspectives 2003;111(8):1074-1092. |
R827351 (2002) R827351 (Final) R827352 (Final) R827352C002 (Final) R827352C014 (Final) R827353 (Final) R827353C006 (Final) R827353C015 (Final) R827354 (Final) R827355 (Final) |
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Lippmann M. Winter air pollution and respiratory function. Occupational and Environmental Medicine 2003;60(2):81. |
R827351 (2003) R827351 (Final) |
not available |
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Lippmann M, Gordon T, Chen LC. Effects of subchronic exposures to concentrated ambient particles (CAPs) in mice: I. Introduction, objectives, and experimental plan. Inhalation Toxicology 2005;17(4-5):177-187. |
R827351 (Final) R827351C013 (2003) R827351C013 (Final) |
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Lippmann M, Gordon T, Chen LC. Effects of subchronic exposures to concentrated ambient particles in mice: IX. Integral assessment and human health implications of subchronic exposures of mice to CAPs. Inhalation Toxicology 2005;17(4-5):255-261. |
R827351 (2003) R827351 (Final) R827351C013 (2003) R827351C013 (Final) |
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Lippmann M, Hwang JS, Maciejczyk P, Chen LC. PM source apportionment for short-term cardiac function changes in ApoE-/- mice. Environmental Health Perspectives 2005;113(11):1575-1579. |
R827351 (Final) R827351C013 (Final) |
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Lippmann M. The search for non-linear exposure-response relationships at ambient levels in environmental epidemiology. Nonlinearity in Biology, Toxicology, and Medicine 2005;3(1):125-144. |
R827351 (Final) |
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Lippmann M, Ito K, Hwang JS, Maciejczyk P, Chen LC. Cardiovascular effects of nickel in ambient air. Environmental Health Perspectives 2006;114(11):1662-1669. |
R827351 (Final) R827351C001 (Final) |
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Maciejczyk PB, Offenberg JH, Clemente J, Blaustein M, Thurston GD, Chen LC. Ambient pollutant concentrations measured by a mobile laboratory in South Bronx, NY. Atmospheric Environment 2004;38(31):5283-5294. |
R827351 (2003) R827351 (Final) |
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Maciejczyk P, Zhong MH, Li Q, Xiong J, Nadziejko C, Chen LC. Effects of subchronic exposures to concentrated ambient particles (CAPs) in mice: II. The design of a CAPs exposure system for biometric telemetry monitoring. Inhalation Toxicology 2005;17(4-5):189-197. |
R827351 (2003) R827351 (Final) R827351C013 (2003) R827351C013 (Final) |
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Maciejczyk P, Chen LC. Effects of subchronic exposures to concentrated ambient particles (CAPs) in mice: VIII. Source-related daily variations in in vitro responses to CAPs. Inhalation Toxicology 2005;17(4-5):243-253. |
R827351 (Final) R827351C013 (2003) R827351C013 (Final) |
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Mar TF, Ito K, Koenig JQ, Larson TV, Eatough DJ, Henry RC, Kim E, Laden F, Lall R, Neas L, Stolzel M, Paatero P, Hopke PK, Thurston GD. PM source apportionment and health effects. 3. Investigation of inter-method variations in associations between estimated source contributions of PM2.5 and daily mortality in Phoenix, AZ. Journal of Exposure Science & Environmental Epidemiology 2006;16(4):311-320. |
R827351 (Final) R827353 (Final) R827353C015 (Final) R827354 (Final) R827354C001 (Final) R827355 (Final) R827355C002 (Final) R827355C008 (Final) |
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McGee JK, Chen LC, Cohen MD, Chee GR, Prophete CM, Haykal-Coates N, Wasson SJ, Conner TL, Costa DL, Gavett SH. Chemical analysis of World Trade Center fine particulate matter for use in toxicologic assessment. Environmental Health Perspectives 2003;111(7):972-980. |
R827351 (2001) R827351 (2002) R827351 (Final) |
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Nadziejko C, Fang K, Nadziejko E, Narciso SP, Zhong M, Chen LC. Immediate effects of particulate air pollutants on heart rate and respiratory rate in hypertensive rats. Cardiovascular Toxicology 2002;2(4):245-252. |
R827351 (2003) R827351 (Final) R827351C005 (2001) R827351C005 (2002) R827351C005 (Final) R827351C006 (2003) R827351C006 (Final) |
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Nadziejko C, Fang K, Chen LC, Gordon T, Nadas A. Quantitative analysis of cardiac data from rats monitored by telemetry: reducing within-and between-animal variability. Cardiovascular Toxicology 2002;2(4):237-244. |
R827351 (2003) R827351 (Final) R827351C005 (2002) R827351C005 (Final) R827351C006 (2003) R827351C006 (Final) |
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Nadziejko C, Fang K, Narciso S, Zhong M, Su W, Gordon T, Nadas A, Chen L. Effect of particulate and gaseous pollutants on spontaneous arrhythmias in aged rats. Inhalation Toxicology 2004;16(6-7):373-380. |
R827351 (2003) R827351 (Final) R827351C005 (Final) R827351C006 (2003) R827351C006 (Final) |
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Nadziejko C, Chen LC, Nadas A, Hwang JS. The ‘Fishing License’ method for analysing the time course of effects in repeated measurements. Statistics in Medicine 2004;23(9):1399-1411. |
R827351 (2003) R827351 (Final) R827351C005 (Final) R827351C006 (2003) R827351C006 (Final) |
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Narciso SP, Nadziejko E, Chen LC, Gordon T, Nadziejko C. Adaptation to stress induced by restraining rats and mice in nose-only inhalation holders. Inhalation Toxicology 2003;15(11):1133-1143. |
R827351 (2001) R827351 (Final) R827351C005 (2002) R827351C005 (Final) R827351C006 (2003) R827351C006 (Final) |
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Ng SP, Dimitroulopoulou C, Grossinho A, Chen LC, Kendall M. PM2.5 exposure assessment of the population in Lower Manhattan area of New York City after the World Trade Center disaster. Atmospheric Environment 2005;39(11):1979-1992. |
R827351 (Final) |
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Offenberg JH, Eisenreich SJ, Chen LC, Cohen MD, Chee G, Prophete C, Weisel C, Lioy PJ. Persistent organic pollutants in the dusts that settled across lower Manhattan after September 11, 2001. Environmental Science & Technology 2003;37(3):502-508. |
R827351 (2001) R827351 (2003) R827351 (Final) |
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Offenberg JH, Eisenreich SJ, Gigliotti CL, Chen LC, Xiong JQ, Quan C, Lou X, Zhong M, Gorczynski J, Yiin L-M, Illacqua V, Lioy PJ. Persistent organic pollutants in dusts that settled indoors in lower Manhattan after September 11, 2001. Journal of Exposure Analysis & Environmental Epidemiology 2004;14(2):164-172. |
R827351 (Final) |
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Payne JP, Kemp SJ, Dewar A, Goldstraw P, Kendall M, Chen LC, Tetley TD. Effects of airborne World Trade Center dust on cytokine release by primary human lung cells in vitro. Journal of Occupational and Environmental Medicine 2004;46(5):420-427. |
R827351 (2003) R827351 (Final) |
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Pope CA, Burnett RT, Thun MJ, Calle EE, Krewski D, Ito K, Thurston GD. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. Journal of the American Medical Association 2002;287(9):1132-1141. |
R827351 (2001) R827351 (Final) |
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Pope CA, Burnett RT, Thurston GD, Thun MJ, Calle EE, Krewski D, Godleski JJ. Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease. Circulation 2004;109(1):71-77. |
R827351 (2003) R827351 (Final) |
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Prophete C, Maciejczyk P, Salnikow K, Gould T, Larson T, Koenig J, Jaques P, Sioutas C, Lippmann M, Cohen M. Effects of select PM-associated metals on alveolar macrophage phosphorylated ERK1 and -2 and iNOS expression during ongoing alteration in iron homeostasis. Journal of Toxicology and Environmental Health, Part A 2006;69(10):935-951. |
R827351 (Final) R827351C008 (Final) R827351C010 (Final) R827352 (Final) R827352C014 (Final) R827355 (Final) R827355C008 (Final) |
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Rajagopalan S, Sun Q, Chen LC. Particulate pollution and endothelial function: deja vu all over again in the air. Circulation 2005;111(22):2869-2871 (editorial). |
R827351 (Final) |
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Reibman J, Hsu Y, Chen LC, Kumar A, Su WC, Choy W, Talbot A, Gordon T. Size fractions of ambient particulate matter induce granulocyte macrophage colony-stimulating factor in human bronchial epithelial cells by mitogen-activated protein kinase pathways. American Journal of Respiratory Cell and Molecular Biology 2002;27(4):455-462. |
R827351 (2003) R827351 (Final) R827351C004 (2002) R827351C004 (Final) |
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Reibman J, Hsu Y, Chen LC, Bleck B, Gordon T. Airway epithelial cells release MIP-3α/CCL20 in response to cytokines and ambient particulate matter. American Journal of Respiratory Cell and Molecular Biology 2003;28(6):648-654. |
R827351 (2003) R827351 (Final) R827351C003 (2003) R827351C003 (Final) R827351C004 (2002) R827351C004 (Final) |
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Restrepo C, Zimmerman R, Thurston G, Clemente J, Gorczynski J, Zhong M, Blaustein M, Chen LC. A comparison of ground-level air quality data with New York State Department of Environmental Conservation monitoring stations data in South Bronx, New York. Atmospheric Environment 2004;38(31):5295-5304. |
R827351 (2003) R827351 (Final) |
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Salnikow K, Davidson T, Zhang Q, Chen LC, Su W, Costa M. The involvement of hypoxia-inducible transcription factor-1-dependent pathway in nickel carcinogenesis. Cancer Research 2003;63(13):3524-3530. |
R827351 (Final) R827351C010 (Final) |
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Salnikow K, Li X, Lippmann M. Effect of nickel and iron co-exposure on human lung cells. Toxicology and Applied Pharmacology 2004;196(2):258-265. |
R827351 (2003) R827351 (Final) R827351C010 (2003) R827351C010 (Final) |
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Schlesinger RB. Properties of ambient PM responsible for human health effects: coherence between epidemiology and toxicology. Inhalation Toxicology 2000;12(Suppl 1):23-25. |
R827351 (2003) R827351 (Final) |
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Sun Q, Wang A, Jin X, Natanzon A, Duquaine D, Brook RD, Aaquinaldo JG, Fayad ZA, Fuster V, Lippmann M, Chen LC, Rajagopalan S. Long-term air pollution exposure and acceleration of atherosclerosis and vascular inflammation in an animal model. Journal of the American Medical Association 2005;294:3003-3010. |
R827351 (Final) R827351C013 (Final) |
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Thurston GD, Chen LC. Risk communication in the aftermath of the World Trade Center disaster. American Journal of Industrial Medicine 2002;42(6):543-544. |
R827351 (2001) R827351 (Final) |
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Thurston GD, Bates DV. Air pollution as an underappreciated cause of asthma symptoms. Journal of the American Medical Association 2003;290(14):1915-1917 (editorial). |
R827351 (2003) R827351 (Final) |
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Thurston GD, Ito K, Mar T, Christensen WF, Eatough DJ, Henry RC, Kim E, Laden F, Lall R, Larson TV, Liu H, Neas L, Pinto J, Stotzel M, Suh H, Hopke PK. Workgroup report: workshop on source apportionment of particulate matter health effects--Inter-Comparison of results and implications. Environmental Health Perspectives 2005;113(12):1768-1774. |
R827351 (Final) R827351C001 (Final) R827353 (Final) R827353C015 (Final) R827354 (Final) R827354C001 (Final) R827355 (Final) R827355C008 (Final) |
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Trasande L, Thurston GD. The role of air pollution in asthma and other pediatric morbidities. The Journal of Allergy and Clinical Immunology 2005;115(4):689-699. |
R827351 (Final) |
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Veronesi B, Makwana O, Pooler M, Chen LC. Effects of subchronic exposure to concentrated ambient particles: VII. Degeneration of dopaminergic neurons in Apo E-/-mice. Inhalation Toxicology 2005;17(4-5):235-241. |
R827351 (Final) R827351C013 (2003) R827351C013 (Final) |
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Wesselkamper SC, Chen LC, Kleeberger SR, Gordon T. Genetic variability in the development of pulmonary tolerance to inhaled pollutants in inbred mice. American Journal of Physiology-Lung Cellular and Molecular Physiology 2001;281(5):L1200-L1209. |
R827351 (2001) R827351 (Final) |
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Yiin LM, Millette JR, Vette A, Ilacqua V, Quan C, Gorczynski J, Kendall M, Chen LC, Weisel CP, Buckley B, Yang I, Lioy PJ. Comparisons of the dust/smoke particulate that settled inside the surrounding buildings and outside on the streets of southern New York City after the collapse of the World Trade Center, September 11, 2001. Journal of the Air & Waste Management Association 2004;54(5):515-528. |
R827351 (2003) R827351 (Final) |
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Zelikoff JT, Schermerhorn KR, Fang KJ, Cohen MD, Schlesinger RB. A role for associated transition metals in the immunotoxicity of inhaled ambient particulate matter. Environmental Health Perspectives 2002;110(Suppl 5):871-875. |
R827351 (Final) R827351C007 (2001) R827351C007 (2002) R827351C007 (Final) |
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Zelikoff JT, Chen LC, Cohen MD, Schlesinger RB. The toxicology of inhaled woodsmoke. Journal of Toxicology and Environmental Health-Part B-Critical Reviews 2002;5(3):269-282. |
R827351 (2001) R827351 (Final) |
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Zelikoff JT, Chen LC, Cohen MD, Fang KJ, Gordon T, Li Y, Nadziejko C, Schlesinger RB. Effects of inhaled ambient particulate matter on pulmonary antimicrobial immune defense. Inhalation Toxicology 2003;15(2):131-150. |
R827351 (Final) R827351C007 (2003) R827351C007 (Final) |
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Thoracic particles (PM10), fine particles (PM2.5), ultrafine particles (PM0.1), lung dosimetry models, human exposure models, pulmonary responses, cardiovascular responses, immunological responses, criteria air pollutants, concentrated ambient aerosols. , Air, Scientific Discipline, Waste, Health, RFA, Biology, Risk Assessments, climate change, Health Risk Assessment, Incineration/Combustion, Epidemiology, Air Pollution Effects, Atmosphere, air toxics, Children's Health, Biochemistry, Environmental Engineering, particulate matter, Environmental Chemistry, Allergens/Asthma, tropospheric ozone, aerosols, combustion contaminants, incineration, exposure and effects, aerosol, allergen, ambient air quality, Global Climate Change, health effects, allergens, compliance monitoring, complinace monitoring, ambient air, lead, assessment of exposure, childhood respiratory disease, combustion, human health risk, epidemeology, air pollutants, environmental monitoring, heart rate variability, human health effects, particulates, respiratory, airway variablity, air pollution, airborne pollutants, airway disease, biological markers, children, criteria air pollutants, lung, mercury, stratospheric ozone, asthma morbidity, dosimetry, exposure, pulmonary, human health, atmospheric monitoring, asthma, human exposure, Human Health Risk Assessment, morbidity, PM, pulmonary disease, airway inflammation
Progress and Final Reports:
2001 Progress Report
2002 Progress Report
2003 Progress Report
Final Report
Subprojects under this Center:
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R827351C001 Exposure Characterization Error
R827351C002 X-ray CT-based Assessment of Variations in Human Airway Geometry: Implications for Evaluation of Particle Deposition and Dose to Different Populations
R827351C003 Asthma Susceptibility to PM2.5
R827351C004 Health Effects of Ambient Air PM in Controlled Human Exposures
R827351C005 Physicochemical Parameters of Combustion Generated Atmospheres as Determinants of PM Toxicity
R827351C006 Effects of Particle-Associated Irritants on the Cardiovascular System
R827351C007 Role of PM-Associated Transition Metals in Exacerbating Infectious Pneumoniae in Exposed Rats
R827351C008 Immunomodulation by PM: Role of Metal Composition and Pulmonary Phagocyte Iron Status
R827351C009 Health Risks of Particulate Matter Components: Center Service Core
R827351C010 Lung Hypoxia as Potential Mechanisms for PM-Induced Health Effects
R827351C011 Urban PM2.5 Surface Chemistry and Interactions with Bronchoalveolar Lavage Fluid (BALF)
R827351C012 Subchronic PM2.5 Exposure Study at the NYU PM Center
R827351C013 Long Term Health Effects of Concentrated Ambient PM2.5
R827351C014 PM Components and NYC Respiratory and Cardiovascular Morbidity
R827351C015 Development of a Real-Time Monitoring System for Acidity and Soluble Components in Airborne Particulate Matter
R827351C016 Automated Real-Time Ambient Fine PM Monitoring System