2001 Progress Report: NYU-EPA PM Center: Health Risks of PM Components

EPA Grant Number: R827351
Center: EPA NYU PM Center: Health Risks of PM Components
Center Director: N/A
Title: NYU-EPA PM Center: Health Risks of PM Components
Investigators: Lippmann, Morton
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: New York University School of Medicine
Current Institution: New York University School of Medicine , University of Iowa
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
Project Amount: $8,076,438
RFA: Airborne Particulate Matter (PM) Centers (1999) RFA Text |  Recipients Lists
Research Category: Air Quality and Air Toxics , Particulate Matter , Air

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 the mortality, morbidity, and functional effects of PM.

The New York University School of Medicine (NYUSOM) PM Center performs innovative research proposed by Center members targeted at critical knowledge gaps on PM exposures and their health effects and coordinates such research with other ongoing active research on airborne PM being conducted at NYUSOM. The Center also provides for collaboration and coordination with other scientists actively engaged in PM research at other institutions, including National Health and Environmental Effects Research Laboratory and National Exposure Research Laboratory at the U.S. Environmental Protection Agency (EPA), other EPA and National Institute of Environmental Health Sciences-sponsored Academic Center programs, and other academic, governmental, and industrial facilities in the United States and elsewhere. The Administrative and Service Core units supported by the Center will optimize the coordination and efficiency of shared resource utilization. The Administrative Core, consists of the Program Director (PD), 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, Co-PD, CA, Research Core Directors, and 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 postdoctoral research positions and/or clinical fellowships. All applications responsive to the call undergo scientific peer review and review by the External Scientific Advisory Committee (ESAC). However, the ultimate decisions for Center priorities and operations rest with the PDs. 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.

Progress Summary:

Currently, the Center supports 11 projects. This section provides a brief overview of the objectives for each project; more detail on report progress can be found in each individual 2001 Annual Report Summary.

Exposure Assessment: Exposure Characterization Errors. The objectives of this research project are to: (1) quantitatively characterize spatiotemporal error of PM components and gaseous copollutants measured at 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. This research project tests the prevailing hypothesis that the PM and gaseous copollutants data from a single air monitoring station can adequately reflect the population exposure for the entire city and that resulting risk estimates and their significance are not biased.

Assessment of Variations in Human Airway Geometry: Evaluation of Particle Deposition and Dose. This research project seeks to utilize the accomplishments of our original PM Center project, which provided the tools for utilization and retrieval of morphometric data from three-dimensional images of human conducting airways obtained by volumetric x-ray. The computerized data files are used to produce hollow airway casts by stereolithography. The research project continues the collaboration between the extensive imaging expertise at the University of Iowa with the NYU PM Center particle deposition expertise. The ultimate objective is to quantify the impact of the airway variability on PM deposition and dose. This current project seeks to compare inhaled particle deposition pattern and efficiency in sheep in vivo with the deposition measured in a hollow airway cast prepared from the same animal’s three-dimensional image. We also will explore deposition for a variety of breathing patterns, and when particles are inhaled at different points in the respiratory cycle. A second objective of this proposal is to examine in vivo bolus deposition to validate the hypothesis that regional deposition can be predicted via a mathematical algorithm based on a progressive series of varying depth bolus deposition measurements.

Asthma Susceptibility to PM. The objectives of this research project are to investigate which PM component(s) and PM mechanisms affect asthmatics most strongly and to prospectively follow a cohort of nonsmoker asthmatics and evaluate PM effects on their health status. The ultimate objectives are to: (1) establish technical and operational feasibility for a combined epidemiological/clinical research study; (2) demonstrate associations between specific PM components and commonly occurring asthma exacerbations attributable to air pollution; and (3) develop hypotheses regarding the mechanisms of the PM-health effects association that can be tested via toxicological studies by other researchers in the NYU-EPA PM Research Center (e.g., via controlled exposure studies). Moreover, the results of this research project may be used as preliminary results for the funding of a follow-up study in this already characterized population.

Health Effects of Ambient Air PM in Controlled Human Exposures. The general hypothesis of this research project was that concentrated ambient PM will produce acute adverse respiratory and cardiovascular health outcomes in volunteers under controlled exposure conditions. In Year 2 of the project, it was stopped, and with agreement from the External Advisory Committee, we examined whether the stimulation of epithelial cells by ambient particles results in the release of cytokines, which can upregulate antigen presentation by dendritic cells.

Physicochemical Parameters of Combustion Generated Atmospheres as Determinants of PM Toxicity. The effect of PM on the cardiovascular system is an increasingly important public health issue. However, the physical and/or chemical properties of PM responsible for these serious health effects currently are unknown. Several inextricably intertwined questions remain. What are the biologically active components of PM? What are the mechanisms by which PM affects the cardiovascular system? What are the sensitive subpopulations? Any hypothesis about a mechanism of cardiovascular effects rests on some assumptions that a certain type of constituent of PM is the culprit, and vice versa.

This research has focused on particle-associated irritants, based in part on the time course of effects reported in recent epidemiological studies. There is consistent evidence from time-series studies that the lag time between elevated levels of PM2.5 and increases in cardiovascular-related hospital admissions and death is very short (i.e., 1 day or less). There is one well-studied physiological mechanism that is consistent with the rapid effects of PM on both cardiovascular pulmonary function, namely the stimulation of irritant receptors in the respiratory tract. Irritant receptor activation involves a bimolecular reaction between a protein receptor in the lung and an agonist, which triggers a rapid increase in intracellular calcium (Ca++), leading to the activation of nerve fibers that send impulses to the central nervous system. Signals from the central nervous system cause the slowing of respiration and changes in blood pressure and heart rate via neural reflex pathways. The stereotypical response to an inhaled irritant is an immediate change in respiratory rate and heart rate, which returns to normal soon after exposure stops.

The objectives of this combined research project were to: (1) examine the time course of effects of concentrated ambient PM (CAPS) on cardiovascular function in sensitive animals to establish the biological plausibility of short lag times between PM exposure and cardiovascular effects; and (2) expose rats (both normal rats and rat models of cardiac disease) to sulfuric acid aerosols, a known irritant found in PM, to determine whether irritant aerosols cause cardiovascular changes consistent with the adverse health effects of PM. Exposure to carbon black particles was used as a nonirritant control.

The Role of PM-Associated Transition Metals in Exacerbating Infectious Pneumonia. The objective of this research project is to determine the role that PM-associated transition metals might play in causing previously observed changes in host immunocompetence. To this end, Streptococcus pneumoniae-infected rats are exposed to artificially generated atmospheres containing soluble forms of individual metals found in immunoreactive NYC PM samples. Similar studies will employ mixtures of the soluble forms of the metals to ascertain whether the immunosuppression in PM-exposed hosts is dependent, at least in part, on any interactions between the metals present. Immunotoxic effects of metal exposure on noninfected animals also are examined in these studies to determine the extent to which the PM-associated metals are capable of producing immunodysfunction in and of themselves.

Immunomodulation by PM: Role of Metal Composition and Pulmonary Phagocyte Iron Status. PM has been shown in epidemiological analyses to induce/exacerbate infectious lung disease and in toxicological studies to alter the manner by which the lung handles bacteria. This research project seeks to validate the hypotheses that: (1) PM modulates lung phagocyte antibacterial function by altering cellular iron (Fe) status; (2) metals (rather than organics, endotoxin, etc.) in PM underlay any change in leukocyte Fe status; and (3) the relative content of Fe in PM governs these mechanisms. By this, in PM with a high relative Fe content, the uptake/slow dissolution of PM-insoluble Fe and an increase in cellular deposition of soluble Fe (due to lacto- [Lf] or transfer-rin [Tf] activity) will lead to Fe overload and decreased antibacterial function. With PM having a low relative Fe content, the presence of relatively greater levels (with respect to Fe) of competitors for intrapulmonary T-/LF-binding (e.g., aluminum [Al], manganese [Mn], and vanadium [V]) will cause an intracellular Fe deficit and reduced antibacterial function due to inhibited transport of endogenous Fe to the phagocytes.

In cooperation with the Los Angeles and Seattle Centers, daily PM2.5 samples were collected over a 3-month period. These sites were selected as (along with NYC) having distinct patterns of proportionality of Fe to Al, Mn, and V in their PM. All samples were analyzed by x-ray fluorescence to determine relative and absolute contents of the four metals.

To determine if the presence of Al, Mn, and V might impact on iron homeostasis in phagocytes, in vitro studies using a rat lung macrophage cell line (i.e., NR8383) examined the impact of the competitors on cell iron response protein activation and/or ferritin synthesis. Although varying doses of each metal are used, relative amounts of each are reflective of those when intact PM is utilized. Analyses of these endpoints allow a determination as to whether the cells convert to states of Fe deficit or excess when Mn, Al, and V are present. The use of the "metals only" versus intact PM allows assessment as to whether (in)organic agents in PM might augment or inhibit the responses. Lastly, these studies permit extrapolation of minimal effective doses (MED) of PM for use in in vivo studies.

In in vivo studies (performed for each set of regional samples), PM (using pooled fragments from multiple filters to achieve MED) is instilled into the lungs of adult F344 rats. After 1, 3, 6, and 24 hrs, pulmonary alveolar macrophages (PAM) are recovered by lavage and analyzed to determine any time-related change (as well as type of change) in Fe status. Lavage fluid is assayed for total, apo-, and holo-Fe Tf and Lf. To assess if PM-related changes in PAM Fe status give rise to modified antibacterial function, ex vivo analyses of uptake/intracellular killing of Listeria monocytogenes by PAM (isolated from PM-exposed hosts at time of maximal change in Fe status) are conducted.

Center Service Core. The responsibilities of the NYU EPA PM Center Service Core are to advance the objectives of the three projects underway: (1) XRF Instrument Validation and Optimization, (2) Ion Chromatography, and (3) Mobile Air Monitoring.

Lung Hypoxia as a Potential Mechanism of PM-Induced Health Effects. Several epidemiologic studies have demonstrated a link between exposure to ambient PM and adverse respiratory effects. Based on radiologic studies of the lungs of children residing in urban regions where PM levels are often well above acceptable levels, there is evidence that chronic exposure to PM has led to respiratory tract damage in these otherwise clinically healthy individuals. Other studies of nonsmokers suggest a link between long-term exposure to PM and the increased development of obstructive airway disease. Some investigators have suggested that these changes arising from chronic exposure to PM are due to the repeated induction of inflammatory events in the lungs. Furthermore, the ongoing PM exposures potentiate a cycle of overproduction of proinflammatory cytokines and agents involved in lung tissue repair or fibrosis. Pulmonary hypertension could be another pathologic change in the PM-exposed lungs. This disease may arise from the increased production of potent vasoconstrictor endothelin that will restrict lung blood flow and lead to a state of hypoxia. The objective of this research project is to examine whether exposure to PM results in the activation of a hypoxia-inducible signaling pathway. A determination as to whether or not PM (in this case, as PM2.5) exposure can induce hypoxic changes in vitro in lung cells would permit subsequent follow-up investigations in the mouse lung to be performed. This might help to delineate the mechanisms by which the above-noted changes in lung structure of PM-exposed children and adults might have evolved.

Another objective of this research project was to test the hypothesis that PM2.5 exposure induces hypoxic events, pulmonary hypertension, and proinflammatory and apoptotic responses in lung cells. To do this, we studied the expression of hypoxia-inducible and proinflammatory proteins (VEGF, Cap43, endothelin, IL-1ß, and PAI-1), and the induction of c-Jun, the activation SAPK/JNK kinase and AP-1 transcription factor in rat and human bronchoepithelial and endothelial cells in vitro. The same parameters will be studied in rat lungs exposed to PM2.5 in vivo.

PM Surface Chemistry and Interactions with Bronchoalveolar Lining Fluid (BALF) From Chronic Obstructive Pulmonary Disease (COPD) and Normal Individuals. This research project examines the surface chemistry of PM2.5 collected from concentrated diesel exhaust, at roadside, urban background and rural background locations. In this research project, x-ray photon spectroscopy and time-of-flight secondary ion mass spectrometry are used to determine the surface chemistry. Scanning electron microscopy is used to characterize the particles morphologically. The effects of PM surface chemistry and morphology on determining the interactions with human COPD and normal lavage samples (and components of normal human lavage) are being quantified, using the same techniques. In addition, enzyme-linked immunosorbent assays for specific proteins and a surfactant quantification method will be used to determine lavage component concentrations before and after the introduction of PM.

Subchronic PM2.5 Exposure Study at the NYU PM Center. The NYU PM Center is now conducting the first ever subchronic animal inhalation study using concentrated air particles (CAPs) to provide supplementary and complementary data analogous to that developed in the human cohort studies in cities with varying levels of fine PM. The studies began in 2002, with daily 6-hour exposures to CAPs for 5 days/week over a 6-month period. This study tests the hypothesis that subchronic exposure of normal and compromised mice to CAPs will cause cumulative adverse effects on the respiratory and cardiovascular system.

The objectives of this research project are to: (1) determine the effects of subchronic CAPs exposure on pulmonary histopathology and lavage fluid biomarkers of lung inflammation and lung injury, and (2) determine whether subchronic CAPs exposure accelerates the development of atherosclerotic carciovascular disease (apoE-/-LdLr-/-mice).

Future Activities:

We will continue to develop and conduct a comprehensive research program focused on the identification and characterization of the physical and chemical properties of PM that adversely impart human health.


Journal Articles: 89 Displayed | Download in RIS Format

Other center views: All 112 publications 101 publications in selected types All 89 journal articles
Type Citation Sub Project Document Sources
Journal Article Chen LC, Thurston G. World Trade Center cough. Lancet 2002;360(Suppl 1):S37-S38. R827351 (2001)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article 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 2001;109(Suppl 3):419-425. R827351 (2003)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article Cohen BS, Heikkinen MSA, 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)
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  • Journal Article Cohen MD, Sisco M, Baker K, Chen L-C, Schlesinger RB. Effect of inhaled chromium on pulmonary A1AT. Inhalation Toxicology 2002;14(7):765-771. R827351 (2001)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article Duvall RM, Norris GA, Dailey LA, Burke JM, Mcgee JK, Gilmour MI, Gordon T, Devlin RB. Source apportionment of particulate matter in the U.S. and associations with lung inflammatory markers. Inhalation Toxicology 2008;20(7):671-683. R827351 (Final)
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  • Journal Article Fanning EW, Froines JR, Utell MJ, Lippmann M, Oberdorster G, Frampton M, Godleski J, Larson TV. Particulate Matter (PM) Research Centers (1999-2005) and the role of interdisciplinary center-based research. Environmental Health Perspectives 2009;117(2):167-174. R827351 (Final)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article Gillespie P, Tajuba J, Lippmann M, Chen LC, Veronesi B. Particulate matter neurotoxicity in culture is size-dependent. NeuroToxicology 2013;36:112-117. R827351 (Final)
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  • Journal Article 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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  • Journal Article Gordon T, Reibman J. Cardiovascular toxicity of inhaled ambient particulate matter. Toxicological Sciences 2000;56(1):2-4. R827351 (Final)
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  • Journal Article 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)
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  • Journal Article Gwynn RC, Thurston GD. The burden of air pollution: impacts among racial minorities. Environmental Health Perspectives 2001;109(Suppl 4):501-506. R827351 (2001)
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  • Journal Article 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)
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  • Journal Article Hopke PK, Ito K, Mar T, Christiansen 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)
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  • Journal Article Hwang J-S, 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)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article Ito K, Christensen 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)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article 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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  • Journal Article Lall R, Ito K, Thurston GD. Distributed lag analyses of daily hospital admissions and source-apportioned fine particle air pollution. Environmental Health Perspectives 2011;119(4):455-460. R827351 (Final)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article 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-JS, 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)
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  • Journal Article Lippmann M. Winter air pollution and respiratory function. Occupational and Environmental Medicine 2003;60(2):81. R827351 (2003)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article Lippmann M, Cassee FR, Costa DL, Costantini M, van Erp AM, Gordon T. International workshop on the design and analysis of experimental studies using PM concentrator technologies, Boston, May 5, 2004. Inhalation Toxicology 2005;17(14):839-850. R827351 (Final)
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  • Journal Article 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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  • Journal Article 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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  • Journal Article 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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  • Journal Article Lippmann M. Semi-continuous speciation analyses for ambient air particulate matter: an urgent need for health effects studies. Journal of Exposure Science and Environmental Epidemiology 2009;19(3):235-247. R827351 (Final)
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  • Journal Article Lippmann M. Toxicological and epidemiological studies of cardiovascular effects of ambient air fine particulate matter (PM2.5 ) and its chemical components: coherence and public health implications. Critical Reviews in Toxicology 2014;44(4):299-347. R827351 (Final)
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  • Journal Article 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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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article Maciejczyk P, Zhong M, Lippmann M, Chen LC. Oxidant generation capacity of source-apportioned PM2.5. Inhalation Toxicology 2010;22(Suppl 2):29-36. R827351 (Final)
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  • Journal Article 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)
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    R832415 (2010)
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  • Journal Article 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)
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  • Journal Article Mehta M, Chen LC, Gordon T, Rom W, Tang MS. Particulate matter inhibits DNA repair and enhances mutagenesis. Mutation Research-Genetic Toxicology and Environmental Mutagenesis 2008;657(2):116-121. R827351 (Final)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article Nadziejko C, Fang K, Narciso S, Zhong M, Su WC, Gordon T, Nadas A, Chen LC. Effect of particulate and gaseous pollutants on spontaneous arrhythmias in aged rats. Inhalation Toxicology 2004;16(6-7):373-380. R827351 (2003)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article 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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  • Journal Article 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)
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  • Journal Article 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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  • Journal Article 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)
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  • Journal Article Peltier RE, Hsu SI, Lall R, Lippmann M. Residual oil combustion: a major source of airborne nickel in New York City. Journal of Exposure Science and Environmental Epidemiology 2008;19(6):603-612. R827351 (Final)
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  • Journal Article Pope III 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. JAMA-Journal of the American Medical Association 2002;287(9):1132-1141. R827351 (2001)
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  • Journal Article Pope III 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)
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  • Journal Article 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:Current Issues 2006;69(10):935-951. R827351 (Final)
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  • Journal Article 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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  • Journal Article 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)
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    R827351C004 (2002)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article 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)
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    R827351C010 (2003)
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  • Journal Article Sama P, Long TC, Hester S, Tajuba J, Parker J, Chen LC, Veronesi B. The cellular and genomic response of an immortalized microglia cell line (BV2) to concentrated ambient particulate matter. Inhalation Toxicology 2007;19(13):1079-1087. R827351 (Final)
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  • Journal Article 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)
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  • Journal Article Spira-Cohen A, Chen LC, Kendall M, Sheesley R, Thurston GD. Personal exposures to traffic-related particle pollution among children with asthma in the South Bronx, NY. Journal of Exposure Science & Environmental Epidemiology 2010;20(5):446-456. R827351 (Final)
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  • Journal Article Spira-Cohen A, Chen LC, Kendall M, Lall R, Thurston GD. Personal exposures to traffic-related air pollution and acute respiratory health among Bronx schoolchildren with asthma. Environmental Health Perspectives 2011;119(4):559-565. R827351 (Final)
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  • Journal Article Sun Q, Wang A, Jin X, Natanzon A, Duquaine D, Brook RD, Aquinaldo 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. JAMA-Journal of the American Medical Association 2005;294(23):3003-3010. R827351 (Final)
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  • Journal Article Sun Q, Yue P, Kirk RI, Wang A, Moatti D, Jin X, Lu B, Schecter AD, Lippmann M, Gordon T, Chen LC, Rajagopalan S. Ambient air particulate matter exposure and tissue factor expression in atherosclerosis. Inhalation Toxicology 2008;20(2):127-137. R827351 (Final)
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  • Journal Article Sun Q, Yue P, Ying Z, Cardounel AJ, Brook RD, Devlin R, Hwang J-S, Zweier JL, Chen LC, Rajagopalan S. Air pollution exposure potentiates hypertension through reactive oxygen species-mediated activation of Rho/ROCK. Arteriosclerosis Thrombosis and Vascular Biology 2008;28(10):1760-1766. R827351 (Final)
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  • Journal Article 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)
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  • Journal Article Thurston GD, Bates DV. Air pollution as an underappreciated cause of asthma symptoms. JAMA-Journal of the American Medical Association 2003;290(14):1915-1917 (editorial). R827351 (2003)
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  • Journal Article 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, Stolzel M, Suh H, Hopke PK. Workgroup report: Workshop on source apportionment of particulate matter health effects—intercomparison of results and implications. Environmental Health Perspectives 2005;113(12):1768-1774. R827351 (Final)
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  • Journal Article Trasande L, Thurston GD. The role of air pollution in asthma and other pediatric morbidities. Journal of Allergy and Clinical Immunology 2005;115(4):689-699. R827351 (Final)
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  • Journal Article 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)
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  • Journal Article 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)
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  • Journal Article Yiin L-M, 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)
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  • Journal Article 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)
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  • Journal Article Zelikoff JT, Schermerhorn KR, Fang K, 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)
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  • Journal Article Zelikoff JT, Chen LC, Cohen MD, Fang K, 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)
  • Abstract from PubMed
  • Full-text: Berkeley-Full Text PDF
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  • Abstract: Taylor and Francis-Abstract
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  • Supplemental Keywords:

    thoracic particles, particulate matter, PM10, PM2.5, PM0.1, fine particles, PM components, ultrafine particles, lung dosimetry models, human exposure models, pulmonary responses, cardiovascular responses, immunological responses, criteria air pollutants, concentrated ambient aerosols., RFA, Health, Scientific Discipline, Air, Waste, particulate matter, air toxics, Environmental Chemistry, Health Risk Assessment, Epidemiology, climate change, Air Pollution Effects, Risk Assessments, Allergens/Asthma, Biochemistry, Children's Health, tropospheric ozone, Biology, Incineration/Combustion, Environmental Engineering, Atmosphere, asthma, particulates, ambient air quality, criteria air pollutants, health effects, environmental monitoring, morbidity, airway variablity, compliance monitoring, human health effects, air pollutants, exposure and effects, lung, stratospheric ozone, mercury, airway disease, exposure, combustion emissions, heart rate variability, pulmonary disease, ambient air, lead, airway inflammation, air pollution, children, Human Health Risk Assessment, airborne pollutants, assessment of exposure, childhood respiratory disease, human exposure, complinace monitoring, pulmonary, combustion, epidemeology, atmospheric monitoring, PM, biological markers, incineration, allergens, aerosol, human health, asthma morbidity, allergen, dosimetry, combustion contaminants, aerosols, respiratory, human health risk

    Progress and Final Reports:

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