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Final Report: 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 , 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:Introduction
The Particulate Matter Health Effects Research Center (PM Center) at New York University (NYU), supported by Center Grant R827351 from the U.S. Environmental Protection Agency (EPA) from June 1999 through May of 2006, pursued a broad range of research to identify the health effects produced by exposure to particulate matter (PM) in ambient community air and the specific PM components most responsible for producing these effects. It also was engaged in post-doctoral training for future research leaders in air pollution studies, in organizing research Workshops for the PM Centers program, in organizing an in vitro collaborative PM Center effort to compare the toxicities of thoracic coarse, fine, and ultra-fine PM, and played a lead role in the preparation of papers for Environmental Health Perspectives on the overall PM Centers program. The most notable accomplishments of the NYU PM Center were to demonstrate, in Project #11 (R827351C013), that: 1) six months of 5 days/week exposures of a mouse model of atherosclerosis to a northeastern U.S. regional ambient air fine PM, that had an average concentration of 110 μg/m3 for the 6-hour/day exposures, produced acute and chronic changes in cardiac function, an increase in aortic plaque and its invasiveness, genetic marker changes, and a reduction of cells in the substantia nigra region of the brain; and 2) in a follow-up six-month study, exposure to fine particles, at an average concentration of only 85 μg/m3, altered vasomotor tone, induced vascular inflammation, and potentiated atherosclerosis. During this second 6-month study, we were also able to identify a remote point source of nickel that was responsible for significant acute changes in cardiac function. These subchronic studies in mice have thereby enabled us to establish a new level of biological plausibility for the human cohort studies of fine particle associated excess annual mortality, and that it is possible to identify singe causal PM components.
Summary/Accomplishments (Outputs/Outcomes):Exposure Characterization Error, R827351C001, K. Ito
Description and Objective of Research. The main objective of this project was to quantitatively characterize spatio-temporal error of PM and gaseous co-pollutants measured at routine regulatory-based air monitors as a function of site characteristics. The rationale was that the closer association of PM10 with health outcomes than those of criteria air pollutants may have been due, in part, to differential exposure characterization error, i.e., PM10 may have less error. Furthermore, we expected that PM10 might have varying exposure characterization error across U.S. due to varying source types, which may result in heterogeneity of estimated PM10 risk estimates across cities. The prevailing hypothesis was that the PM10 and gaseous co-pollutants data from a single air monitoring station could adequately reflect the population exposure for the entire city. Also, during the course of this project, the new PM2.5 chemical speciation network’s data became available (from ~ 2001), and we examined exposure characterization error across components of PM2.5.
Summary of Findings. In the analyses of monitor-to-monitor correlation for PM10 and gaseous criteria pollutants in 7 North-Central States for the years 1988-1990 (Ito, et al., 2001), O3, PM10, and NO2 had generally higher monitor-to-monitor temporal correlations (r: 0.8-0.6) than CO or SO2 (r<0.5). For the nationwide data (Ito, et al., 2005), the overall average rankings in monitor-to-monitor correlations were, in descending order: O3, NO2, and PM10, (r ~ 0.6 to 0.8) > CO (r < 0.6) > SO2 (r < 0.5). The correlations were modeled as a function of qualitative site characteristics (i.e., land-use, location-setting, and monitoring-objective), and quantitative information (median separation distance, longitude/latitude or regional indicators) for each pollutant using Generalized Additive Models (GAM). Both separation distance and regional variation were important predictors of the correlation. For PM10, the correlation for the monitors along the East Coast was higher by ~0.2 than for western regions. The qualitative monitor characteristics were often significant predictors of the variation in correlation, but their impacts were not substantial in magnitude for most categories. Thus, the apparent regional heterogeneity in PM effect estimates, as well as the differences in the significance of health outcome associations across pollutants may, in part, be explained by the differences in monitor-to-monitor correlations. To examine this issue, we conducted a regression analysis to see if the heterogeneity of PM10 risk estimates across the National Morbidity, Mortality, and Air Pollution Study (NMMAPS) 90 cities were due to PM10 monitor-to-monitor correlation. For the 83 cities that could be matched, the inverse-variance weighted regression of PM10 mortality risk estimates on the median PM10 correlation showed a positive prediction of PM10 mortality risk estimates with a slope of 0.14 (95%CI: [-0.02, 0.30]) per 0.1 increment of PM10 correlation.
Possible exposure characterization error across PM2.5 components were examined using PM2.5 chemical speciation data for 3 locations in New York City (Ito, et al., 2004). Secondary aerosol species (e.g., SO4, NH4, NO3, organic carbon [OC], etc.) tended to show high monitor-to-monitor correlations, whereas the species associated with more local sources (e.g., elemental carbon [EC] as a traffic source marker) showed lower correlations. Source-apportionment was also conducted for each monitor’s data. The estimated source-apportioned PM2.5 mass generally showed the highest monitor-to-monitor correlation for the secondary aerosol factor (r range: 0.72–0.93). The correlation for the more localized traffic-related factor was more variable (r range: 0.26–0.95). The estimated mean PM2.5 mass contributions by source/pollution type across the monitors varied least for the secondary aerosol factor. We extended the analysis to 28 metropolitan statistical areas (MSAs) where multiple monitors generated PM2.5 chemical speciation data for the years 2001-2003. We analyzed a set of key PM2.5 components that were of interest in terms of toxicological effects, source signature, and generally large signal-to-noise ratios: i.e., Ni, V, Pb, Cr, Mn, Fe, Si, As, Se, SO4, NH4, NO3, EC, and OC. Again, the species associated with secondary aerosols (e.g., SO4, NO3) showed high monitor-to-monitor correlation. However, the monitor-to-monitor correlation for other species varied widely across the MSAs, likely reflecting the variation in the levels and major source types across the MSAs.
The monitor-to-monitor correlations are pertinent to the interpretation of results from short-term effects (i.e., time-series and longitudinal) studies. We also examined potential exposure characterization errors pertinent to long-term effects (i.e., cohort and cross-sectional) studies, using the same 28 MSAs. We found that, for the key PM2.5 components, the coefficient of variation (CV) for across-MSA variation was generally far larger than those for within-MSA variations, with only a few exceptions. The result suggests that the quality of spatial resolution of the key PM2.5 components is sufficient and adequate for the analysis of cross-sectional cohort data.
The results from the Source Apportionment Workshop (Thurston, et al., 2005; Hopke, et al., 2006; Ito, et al., 2006; Mar, et al., 2006) also provided information regarding exposure characterization errors for source-apportioned PM2.5. Comparisons of source-apportioned PM2.5 across investigators for PM2.5 chemical speciation data sets from Phoenix, AZ and Washington, DC found that soil-, secondary sulfate-, residual oil combustion-, and salt-associated mass were most unambiguously identified by various methods, whereas vegetative burning and traffic were less consistently identified. Combined with the result suggestive of varying exposure characterization error across PM2.5 species, and U.S. regions, a systematic examination of multi-city time-series health effects analysis will be needed. We compared the mean levels of key PM2.5 chemical species and the published PM10 mortality risk estimates in 60 MSAs in the NMMAPS study, and found that the city-to-city variation of PM10 risk estimates could be better explained by some PM2.5 chemical species (Ni and V) than others (Lippmann, et al., 2006). Thus, the city-to-city variation in PM health risk estimates may be modified by components of PM2.5.
Conclusions. There are differential exposure characterization errors across PM and gaseous pollutants at ambient levels. PM10, PM2.5, O3, and NO2 have moderate to high temporal correlations within cities, compared to CO and SO2. These errors also vary by region and site-specific characteristics. Some of the differences in the observed health effects across pollutants in past health effect studies may be explained by our findings. However, the estimated ecologic level exposure characterization errors did not explain the city-to-city variation in the PM10 mortality risk estimates substantively. Components of PM may play roles in the city-to-city variation of PM health risks. A more comprehensive assessment of the overall exposure characterization error will need to consider personal level exposure error.
References:
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 Analysis and Environmental Epidemiology 2006;16:275-286.
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 inter-method variability in associations between source-apportioned fine particle mass and daily mortality in Washington, DC. Journal of Exposure Analysis and Environmental Epidemiology 2006;16:300-310.
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 and Environmental Epidemiology 2001;11:21-32.
Ito K, Xue N, Thurston GD. Spatial variation of PM2.5 chemical species and source-apportioned mass concentrations in New York City. Atmospheric Environment 2004;38:5269-5282.
Ito K, DeLeon SF, Nadas A, Thurston GD, Lippmann M. Monitor-to-monitor temporal correlation of air pollution in the contiguous U.S. Journal of Exposure Analysis and Environmental Epidemiology 2005;15:172-184.
Mar TF, Ito K, Koenig JQ, Larson TV, Christensen WF, Eatough DJ, Henry RC, Kim E, Laden F, Lall R, Neas L, Hopke PK, Thurston GD. PM source apportionment and health effects. 3. An investigation of inter-method variability in associations between source apportioned fine particle mass and daily mortality in Phoenix, AZ. Journal of Exposure Analysis and Environmental Epidemiology 2006;16:311-320.
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, Paatero P, Hopke PK. The Workshop on the Source Apportionment of PM Health Effects: Inter-Comparison of Results and Implications. Environmental Health Perspectives 2005;113:1768-1774 .
X-ray CT-based Assessment of Variations in Human Airway Geometry: Implications for Evaluation of Particle Deposition and Dose to Different Populations, R827351C002, B.S. Cohen, E.A. Hoffman
Description and Objective of Research. To address the paucity of data regarding PM deposition in the lungs of people with pre-existing pulmonary disease and the normal elderly, subpopulations which may be at special risk, this project investigated the potential for retrieval of morphometric data from three-dimensional images of tracheobronchial airways obtained in vivo by x-ray Computerized Tomography (CT). The study also explored the potential for the use of stereolithography (STL) to produce hollow airway casts of normal and abnormal lung airways for the experimental determination of site-specific deposition and for experimental verification of particle deposition models. The project was a collaboration between the extensive imaging expertise at the University of Iowa and NYU PM Center particle deposition expertise.
A volumetric rendering of the interior surface of a hollow airway cast (used in previous studies at NYU) was generated, producing a surface representation of the airway tree. These three-dimensional images were then converted to a STL file format required for the rapid prototyping of airway casts. Close concordance was seen between the original hollow airway cast and the STL produced replicate. The casting process was subsequently converted to utilize a water soluble material to build supporting structures. Thin multi-slice helical CT scanning allows the acquisition of high-resolution volumetric image data sets of the lung in a breath-hold or at multiple phases within a respiratory cycle. From these scans, hollow airway casts that include 5 or 6 bronchial generations can be created.
Iowa collaborators continued to work on the development of sheep models for the testing of various measures of pulmonary perfusion, regional ventilation, airway structure and distensibility, diaphragm and rib cage mechanics, etc. We fine-tuned our methods of respiratory gating and succeeded in developing methodology that allows us to gate image acquisition very accurately to an inductance plethysmographic (Respitrace) signal, and acquire volumetric images of the lung at multiple points within the respiratory cycle over a period of 30 cycles. Significant advancements in computerized analysis have been made in the areas of lung, lobe and airway segmentation, airway tree matching, and lung feature matching. A set of reproducible feature points are first identified, including airway branching points, for each CT image to establish correspondences across subjects.
We have tried to develop a suitable monodisperse radio-opaque test aerosol. We have x-ray tested common contrast media to determine the smallest layer that can be distinguished from a unit density background, but results to date are not satisfactory.
Summary of Findings. This project developed a computational capacity to create a 3-D computer model of lung airway dimensions from CT scans of an original cast model on which measurements had been made of airway branch diameter, length, and branching angle. We then demonstrated excellent agreement on measurements made from a silastic reproduction as compared with the original to assure accurate reproduction of these metrics. The process was utilized to obtain an image based on CT scanning, and then produce a tracheobronchial cast, from a living person. An aerosol suitable for CT scanning during inhalation in a live individual has not yet been developed.
Conclusions. This project demonstrated for the first time that hollow airway casts can be produced from CT scans of the lungs of living individuals. The technique can be used to accurately replicate the airways of both healthy and diseased individuals, and also children who have undergone CT scanning of the lung. Dr. Hoffmann has a large database of patients of all ages who have undergone CT scanning for medical purposes. It includes individuals who demonstrated no lung disease as well as those with cancer, and various other lung pathologies. The database also includes standard medical data such as age, height and weight, symptoms, diagnosis, and results of related pulmonary testing. This will make it possible to examine deposition in healthy and diseased airways using replicate casts and realistic breathing parameters.
Asthma Susceptibility to PM2.5, R827351C003, G.D. Thurston, J. Reibman
Description and Objective of Research. The objectives of this research project were to investigate which ambient air PM2.5 component(s) and PM mechanisms affect asthmatics most strongly, and to prospectively follow a cohort of non-smoker asthmatics and evaluate PM effects on their health status. The ultimate goals were: to establish technical and operational feasibility for a combined epidemiological/clinical research study; demonstrate associations between specific ambient air PM2.5 components and commonly occurring asthma effect biomarkers attributable to air pollution; and develop hypotheses regarding the mechanisms of the PM2.5 - health effects association that could potentially then be tested via toxicological studies by other researchers in the NYU-EPA PM Research Center (e.g., via controlled exposure studies).
We monitored a panel of 17 subjects with asthma over a three-month period in the summer of 2001 by spirometry (every 2 weeks), AM and PM peak flow measurements (daily), symptom questionnaire (severity scale, albuterol use), and serum samples (every 2 weeks). We also collected PM2.5 and other pollution data continuously over this 3 month period, and analyzed these samples via X-ray fluorescence for subsequent use in a source apportionment of the PM2.5 mass. Our specific goal was to determine whether there is an association between ambient air PM2.5 levels and these defined health outcomes. In particular, we aimed to test the hypothesis that increases in plasma levels of specific chemokines related to asthma (i.e., those involved in eosinophil recruitment and TH2 responses) are associated with elevations in ambient air PM2.5.
Summary of Findings. There was a general positive trend between the same day PM2.5 and blood serum levels of Regulated on Activation, Normal T Expressed and Secreted (RANTES) cytokine, with one regression “hinge point” (i.e., a very low value from one patient on a high PM2.5 day) that weakened the overall positive slope. In subsequent analyses, this observation was removed, and the effect of PM2.5 on RANTES levels was estimated in the mixed-effects models adjusting for potential confounders to the association such as, hot and humid days, day-of-week effects, hours spent in air conditioning, number of puffs of albuterol, and serial correlation between observations for each individual.
In addition to evaluating associations with the Criteria air pollutants, we also conducted source apportionment of the Hunter College PM2.5 samples during 2001 (Lall and Thurston, 2006). The source components PM2.5 contributions estimated for each day were: Residual oil combustion particles, traffic particles, soil particles, transported sulfate particles, and World Trade Center (WTC) disaster particles. Different cytokines had differing associations with the various PM source component contributions, with the WTC particle components being associated across all the biomarker outcomes and cytokines considered here.
Conclusions. Ambient exposure to PM2.5 mass and its components were indicated to affect the biomarker RANTES in subject’s peripheral blood serum. RANTES is thought to play a key role in the development of airway neutrophilic and eosinophilic inflammation in the lung. Although numbers of samples are limited from September, 2001, initial PM2.5 component results also suggest that the very high WTC pollution had short-term inflammatory effects on some of the subjects in this study.
References:
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):S333-S346.
Health Effects of Ambient Air PM in Controlled Human Exposures, R827351C004, T. Gordon, R. Reibman, L.C. Chen
Description and Objective of Research. The original hypothesis of this Project was that concentrated ambient PM will produce acute adverse respiratory and cardiovascular health outcomes in volunteers under controlled exposure conditions. In Year 02, the project was changed and 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. As a follow-up to these in vitro studies, we coordinated a multi-Center collaboration which examined the in vitro and in vivo effects of size-segregated particles collected at geographically diverse sites throughout the U.S.
Summary of Findings
In Vitro Studies with Airway Epithelial Cells. Drs. Reibman, Chen, and Gordon concentrated their efforts on an examination of in vitro responses of human bronchial epithelial cells to size-fractionated ambient PM. Because of the significant association between ambient PM and exacerbation of allergic asthma, we examined the potential for airway epithelial cells (primary culture) to modulate the immune system. Size-fractionated ambient PM was collected with a MOUDI impactor for 2 week intervals throughout the year, and used to treat human bronchial epithelial cells obtained from normal human volunteers. The fraction of particles less than 0.18 μm produced a dose-dependent increase in GM-CSF released from the epithelial cells. GM-CSF is a cytokine that can elicit inflammation in the airways via an effect on eosinophils and can also modulate immune responses via effects on dendritic cells. There was no change in secreted GM-CSF in cells treated with larger size ambient particles or equivalent doses of control particles, thus suggesting that the human epithelial cell response was not due to a general particle effect. Moreover, treatment of epithelial cells with endotoxin had no effect on GM-CSF. Further experiments with inhibitors demonstrated that MAPK pathways are involved in the ambient particle effects on GM-CSF secretion by epithelial cells.
Multi-Site Ambient PM Study (MAPS). The overall objective of the interdisciplinary MAPS study was to pool resources from multiple Centers to collect particles from several different geographical regions, characterize their physical and chemical properties, and make them available to investigators for in vitro and animal toxicology studies. The results of these studies will be used to relate health effects with PM components and ultimately sources. Recent studies suggest that PM derived from different sources may differ in toxicity and that specific PM components may serve as markers for different sources, suggesting an alternative, more efficient way of regulating PM. To directly study this issue, airborne particles in the ultrafine, fine, and coarse thoracic size ranges were collected in eight different locations in the U.S. and Europe. The sites were selected to take advantage of regional differences in PM sources and components. Weekly samples were collected for a period of a month in each location, using a 3 stage particle impactor, developed at Harvard’s EPA Center, which is capable of collecting 15 to 100 mg of material at 3 size fractions during a weekly sampling interval. The particles have been assayed for a number of chemical components in collaboration with U.S. EPA-National Health and Environmental Effects Research Laboratory (NHEERL) and made available to investigators in several different laboratories. Several studies have been completed and results presented so far demonstrate clear particle size and source dependent differences in toxicity. At least four manuscripts (U.S. EPA, University of Rochester, and NYU) are in preparation for submission.
Conclusions. Our in vitro studies have clearly demonstrated that particle toxicity is dependent on the source of particles and the size of particles. These findings are important for consideration by policy makers in setting regulations for airborne particles.
Physicochemical Parameters of Combustion Generated Atmospheres as Determinants of PM Toxicity, R827351C005, L.C. Chen
Description and Objective of Research. Combustion generated particles often make up a significant portion of ambient PM in many regions. This study examines the hypothesis that the toxicological effects associated with combustion-generated PM depend upon specific physicochemical characteristics of the particles. PM effluents from high temperature processes, such as fossil fuel combustion and pyrometallurgical systems, consist of inorganic materials having a wide size range and chemical composition, including H2SO4 and unreacted SO2. Such effluents have been shown to be toxicologically active. Freshly formed acidic fly ash atmospheres (containing SO2 and ultrafine particles with transition metals on their surface) produce decrements in lung function (Amdur, et al., 1986; Chen, et al., 1990). Furthermore, sulfuric acid as a coating on particle surfaces has been shown to be 10 fold more potent in producing pulmonary effects than are pure acid droplets of the same H+ concentration (Amdur and Chen, 1989). Epidemiological data have indicated increased daily mortality to be associated with particulate air pollution indices, and a significant contribution from SO2 could not be ruled out (HEI, 1995). Since SO2, by itself, has low toxicity, it is reasonable to speculate that a synergistic interaction between SO2 and particles may have been responsible for these observed effects (Amdur and Chen, 1989; Amdur, et al., 1986).
Several human panel studies in the U.S. and the MONICA study in Europe (Gold, et al., 1998; Pope, et al., 1998; Shy, et al., 1998; Peters, et al., 1998), as well as animal studies (Watkinson, et al., 1998; Lovett, et al., 1998; Nadziejko, et al., 1997) have suggested an association between PM and changes in host homeostasis. In this study, cardiopulmonary effects are measured in healthy and compromised animals exposed by inhalation to laboratory-generated particle atmospheres having precisely defined physicochemical characteristics.
This study examined the hypothesis that the toxicological effects associated with combustion-generated PM depend upon specific physicochemical characteristics of the particles and determined the influence of physicochemical parameters of combustion generated PM on the time course, dose response, and persistence of particle-induced cardiopulmonary effects.
Summary of Findings. This project was closely integrated with Project 4 (R827351C006; Nadziejko, PI) in the measurement of cardiopulmonary effects upon exposures to various PM atmospheres. The accomplishments of Project 4 are separately reported by Dr. Nadziejko.
We have developed two furnace systems to produce realistic combustion effluents, and have successfully produced a mixture of carbon, SO2, and metal (iron or copper). This allows determination of specific components, especially metals, which may be responsible for adverse health effects, and an assessment of whether any effects could be nonspecific, i.e., they follow inhalation of any type of particle. For the work described herein, the electronics for temperature regulations of both furnace systems were updated. To produce Fe (or Cu), and S coated carbon particles, sucrose solutions containing varying concentrations of Fe(NO3)3 (or Cu(NO3)2) were produced by a nebulizer and burned in the furnace system previously used to produce coal fly ash. The mass median diameters (MMD, determined by a Mercer impactor) of particles produced by a Collison nebulizer (before combustion) using 10 sucrose solutions (each containing 1117 ppm Fe) were 0.9 μm. When a 10% sucrose solution containing 1117 ppm Fe (or Cu) was burned in the furnace at 750°C in the presence of 1 ppm SO2, ultrafine particles with a median diameter of 32 ± 1.3 nm (34.0 ± 7.4 nm for Cu) and sg of 1.55 were produced. Number concentrations as high as 1.9 x 107 particles/cc were achieved. XRF was used to measure the concentrations of iron, copper, and sulfur in these particles. At this combustion condition, the particles produced from this furnace contained 35.1% and 3.6% by mass of iron and sulfur, respectively (30.6% copper and 6.9% sulfur when copper was used). It appeared that copper is almost twice as efficient (6.9% vs. 3.6%) in converting sulfur dioxide gas to particle-associated sulfur.
Sprague Dawley rats were exposed to furnace gas or 450 μg/m3 of these particles for 3 hours and their lungs were lavaged 24 hr post exposure. A lead oxide diffusion denuder was used to remove SO2 from the exposure atmospheres. None of the exposure atmospheres produce changes in LDH levels in the lavage fluid. However, those aerosols containing a mixture of iron, SO2, and carbon produced a 6.8 fold increase over the furnace gas control for the total number of cells in the lavage, whereas particles containing copper, SO2, and carbon did not produce any change in this parameter. The results are shown in Table 1.
Table 1. Effects of Ultrafine Particles in Rats
Exposure Atmospheres |
Total Cell Counts (106) |
LDH (BB unit) |
Furnace Gas |
0.70 ± 0.14 |
95.5 ± 10.2 |
SO2 + carbon |
1.52 ± 0.31 |
78.7 ± 6.3 |
Copper + SO2 + carbon |
1.52 ± 0.23 |
80.0 ± 13.5 |
Iron + SO2 + carbon |
4.77 ± 0.41* |
113.7 ± 28.2 |
Values were mean ± SE, (n=4 to 7 per exposure group).
* significantly different than furnace gas control (p < 0.0001).
Conclusions. Sulfur dioxide absorbed/adsorbed on iron particles was capable of inducing lung inflammation that was not seen with sulfur dioxide alone or adsorbed on other types of particles.
References:
Amdur MO, Chen LC. Furnace generated acid aerosols: speciation and pulmonary effects. Environmental Health Perspectives 1989;79:147-150.
Amdur MO, Sarofim AF, Neville M, Quann RJ, McCarthy JF, Elliot JF, Lam HF, Rogers AE, Conner MW. Coal combustion aerosols and SO2: An interdisciplinary analysis. Environmental Science & Technology 1986;20:138-145.
Chen LC, Lam HF, Kim EJ, Guty J, Amdur M.O. Pulmonary effects of ultrafine coal fly ash inhaled by guinea pigs. Journal of Toxicology and Environmental Health 1990;29:169-184.
Gold DR, Litonjua A, Schwartz J, Verrier M, Milstein R, Larson A, Lovett E, Verrier R. Cardiovascular vulnerability to particulate air pollution. American Journal of Respiratory and Critical Care Medicine 1998;157:A261.
Lovett EG, Verrier RL, Catalano P, Sioutas C, Murthy GGK, Wolfson JM, Ferguson ST, Koutrakis P, Reinisch U, Killingsworth CR, Coull B, Godleski JJ. Heart rate variability (HRV) analysis suggests altered autonomic influence in canines exposed to concentrated ambient air particles (CAPs). American Journal of Respiratory and Critical Care Medicine 1998;157:A260.
Nadziejko C, Chen LC, Zelikoff JT, Gordon T. Hematological and cardiovascular effects of acute exposure to ambient particulate matter. American Journal of Respiratory and Critical Care Medicine 155:A247 (1997).
Peters A, Perz S, Doring A, Stieber J, Koenig W, Wichmann HE. Increased heart rate during an air pollution episode. Presented at the Fourteenth HEI Annual Conference, Boston, MA, April 5-7, 1998.
Pope CA III, Dockery DW, Kanner RE, Villegas M, Schwartz J. Daily changes in oxygen saturation and pulse rate associated with particulate air pollution and barometric pressure. Presented at the Fourteenth HEI Annual Conference, Boston, MA, April 5-7, 1998.
Shy C, Creason J, Williams R, Liao D, Zweidinger R, Watts R, Devlin R, Hazucha M, Nestor J. Physiological responses of elderly persons to particulate air pollution. Presented at the Fourteenth HEI Annual Conference, Boston, MA, April 5-7, 1998.
Watkinson WP, Campen MJ, Kodavanti UP, Ledbetter AD, Costa DL. Effects of inhaled residual oil fly ash particles on electrocardiographic and thermoregulatory parameters in normal and compromised rats. American Journal of Respiratory and Critical Care Medicine 1998;157:A150.
Effects of Particle-Associated Irritants on the Cardiovascular System, R827351C006, C. Nadziejko
Description and Objective of Research. 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 are currently unknown. The questions are: 1) What are the biologically active components of PM? 2) What are the mechanisms by which PM affects the cardiovascular system? and 3) What are the sensitive subpopulations? These three questions are inextricably intertwined. Any hypothesis about a mechanism of cardiovascular effects rests on some assumptions that a certain type of constituent of PM is the culprit.
This research focused on particle-associated irritants based in part on the time course of effects reported in recent epidemiological studies. There is consistent evidence from times-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. one day or less. There is one well-studied physiological mechanism that is consistent with rapid effects of PM on both cardiovascular and pulmonary function, namely 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 activation of nerve fibers that send impulses to the central nervous system. Signals from the central nervous system then cause 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 project were: 1) to 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) to 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 non-irritant control.
Summary of Findings. We examined the effects of various PM air pollutants on rats with surgically implanted electrocardiogram (ECG) and blood pressure (BP) transmitters to determine whether inhaled PM causes immediate physiological effects. Spontaneously hypertensive rats (SHR) with BP transmitters (which measure BP, heart rate and respiratory rate) were exposed to CAPS for 4 hrs. The SHR were also exposed to fine and ultrafine sulfuric acid aerosols because acid is one of the components of PM that could potentially activate irritant receptors and cause effects during exposure. Young and old (> 20 months) Sprague Dawley (SD) rats with ECG transmitters (which measure heart rate and core temperature) were exposed to fine and ultrafine acid aerosols and to resuspended carbon black. Inhalation of CAPS by the SHR caused a striking decrease in respiratory rate that was apparent soon after the start of exposure, and that stopped when exposure to CAPS ceased. The decrease in respiratory rate was accompanied by a decrease in heart rate. Exposure of the same SHR to fine particle size sulfuric acid aerosol also caused a significant decrease in respiratory rate similar to the effects of CAPS. Ultrafine acid had the opposite effect on respiratory rate in SHR as CAPS. In both old and young SD rats, inhalation of fine acid aerosol caused an immediate increase in temperature (compared to air-exposed rats) that ceased when exposure stopped. Ultrafine acid caused an immediate decrease in heart rate and temperature during exposure in young SD rats and no significant effect on old SD rats. Carbon black inhalation had no significant effect on heart rate or temperature during exposure in either old or young rats. This study showed that inhalation of ambient PM and acid aerosols have immediate effects on cardiopulmonary function during exposure. The pattern of the response to inhaled PM is consistent with activation of irritant receptors in the respiratory tract. Telemetry data from these experiments is being analyzed to determine whether significant cardiovascular effects from PM or acid persist after exposure stops.
Conclusions. Overall, we did more than 50 experiments exposing rats to CAPS, irritant aerosols, particulate matter surrogates and even some irritant gases. Every experiment involved monitoring of cardiovascular functional data in an air-exposed and pollutant-exposed group before exposure, during exposure and for 48-72 hrs exposure. We did extensive exploratory data analysis while experiments were being performed and solved a number of issues related to quantifying telemetric data. However, it was apparent that there was no suitable statistical method for determining whether there was a significant difference between the treated and control groups because the onset and duration of the effects were unknown. Drs. Nadziejko and Chen, in collaboration with Dr. Jing-Shiang Hwang, a visiting scientist (and statistician) in the NYU PM Center, and Dr. Arthur Nadas, a mathematical statistician in the Department of Environmental Medicine, developed a simple but powerful method of analyzing repeated measures data when the time course of the effect is not known a priori. This method, which is called the Fishing License method, has been published and used to analyze all of the telemetry data performed in the PM Center.
Role of PM-Associated Transition Metals in Exacerbating Infectious Pneumoniae in Exposed Rats, R827351C007, J.T. Zelikoff
Description and Objective of Research. Soluble metals selected for study including Zn, Fe, Cu, Ni, and Mn were based upon those immunomodulating metals identified from filters collected during the original New York City (NYC) study. In the first sets of studies, rats were exposed to a single metal at a concentration of 100 μg/m3. A dose substantially higher than that found on the original PM atmosphere was selected so as to eliminate those metals having no effect on bacterial host resistance. Iron, Zn, and Ni proved most biologically active in this capacity. In addition to host resistance, a number of immune parameters important for resistance of the host against infectious bacterial pathogens were also evaluated. These included: pulmonary histology; lung cell numbers and profiles; lavageable lactate dehydrogenase activity; total protein levels and cytokines; macrophage-mediated production of reactive oxygen species; splenic lymphocyte proliferation; and circulating blood cell profiles. Even at this relatively high metal dose, inhalation of either Cu or Mn had little or no effects on these particular immune parameters. Similar to that observed for host resistance, Zn, Fe, and Ni, had the greatest effects on these biological endpoints. Based upon these results, only these three metals were evaluated at more relevant concentrations. In this case, only Fe and Ni altered host resistance at a 10-fold lower concentration (i.e., 10 μg/m3); Fe compromised pulmonary bacterial clearance by about 60, while exposure to 10 μg Ni/m3 actually enhanced clearance by ~30%. Given that PM-associated metals do not exist in isolation, the biological effects of exposure to PM likely depend upon responses to metals in combination, and that exposure to pollutant combinations often results in responses different from those seen following inhalation of individual materials, mixture studies were performed to examine the interactive toxicity of Zn, Ni, and Fe on anti-bacterial defense mechanisms and the “handling” of ongoing pneumococcal infections. At an equimolar metal concentration of 50 μg/m3, rats were exposed simultaneously to Cu plus Ni, Zn plus Ni, or Fe plus Mn. Both Cu and Mn significantly antagonized the pulmonary toxicity of Ni and Fe, respectively. On the other hand, exposure to Zn acted to reverse the “beneficial” effects of Ni alone on pulmonary bacterial clearance; simultaneous exposure of Zn and Ni reduced clearance of Streptococcus by about 30%.
Summary of Findings. Previous investigations in this laboratory demonstrated that a single 5 hr inhalation exposure of Streptococcus pneumoniae-infected male rats to concentrated ambient PM2.5 from NYC air [at concentrations approximating or greater than the promulgated 24 hr National Ambient Air Quality Standard (NAAQS) for PM2.5 (~65 - ~150 vs. 50 μg/m3, respectively)], altered both pulmonary and systemic immunity, as well as exacerbated the infection process, in a time- post-exposure-dependent manner. These NYU-PM Center-supported studies were performed to correlate metal content of ambient PM2.5 with its in vivo immunotoxicity so as to identify and characterize the role of constitutive transition metals for exacerbating ongoing S. pneumoniae infections. The central hypothesis of this particular component was that metals (either individually or in combination) associated with inhaled NYC particulates influenced the severity and/or kinetics of pulmonary bacterial clearance induced by concentrated ambient NYC PM2.5. By exposing rats previously-infected with S. pneumoniae (i.e., 48 hr prior to PM exposure) to PM-associated soluble metals, at doses representative of those within the original intact parental PM atmosphere, metals that influence the ability of PM to alter host resistance against infectious agents could be defined. A single major objective was addressed: to ascertain which transition metals (either individually or in combination) found most active in the previously identified portion of ambient PM play significant roles in exacerbating ongoing pneumococcal-induced pneumonia in PM-exposed hosts.
Soluble metals selected for study included zinc (Zn), iron (Fe), copper (Cu), nickel (Ni), and manganese (Mn), which were based upon those immunomodulating metals identified by XRF analyses and atomic absorption spectroscopy from filters collected during the original NYC study. For the first sets of studies, rats were exposed by inhalation (nose-only) to a single metal at a concentration of 100 μg/m3. A dose substantially higher than that found on the original PM atmosphere was selected so as to eliminate those metals having no effect on bacterial host resistance.
Conclusions. These studies demonstrated that even an acute (5 hr) exposure to PM-associated metals including soluble Fe, Zn, and Ni act to exacerbate an ongoing S. pneumoniae infection in particle-exposed rats. Moreover, these same metals in combination can produce responses different from those seen following inhalation of the individual metals alone. This study has provided necessary information as to the particular PM constituents/metal interactions responsible for the observed effects upon host immunocompetence. Taken together, results of these investigations provide biological plausibility for the role of certain PM-associated transition metals to worsen the outcome of an ongoing pulmonary infection.
Immunomodulation by PM: Role of Metal Composition and Pulmonary Phagocyte Iron Status, R827351C008, M.D. Cohen
Description and Objective of Research. PM2.5 induces/exacerbates infectious lung disease and alters the manner by which lungs handle bacteria. This project sought to validate the hypotheses that: 1) PM2.5 modulates lung phagocyte antibacterial function by altering cellular Fe status; 2) metals (rather than organics, biomatter) in PM2.5 underlay any change in lung leukocyte Fe status; and 3) relative Fe content in PM2.5 governs these effects, i.e, a presence of relatively greater levels (with respect to Fe) of competitor metals for transferrin (Tf) binding (e.g., Al, Mn, or V) brings about reduced antibacterial function due to reduced endogenous Fe transport to the cells. The study objectives were: 1) in cooperation with Los Angeles and Seattle PM Centers, to collect and characterize patterns of proportionality of Al, Mn, and V to Fe in daily PM2.5 samples in each city over a 3-mo period; 2) to determine in vitro if a presence of Al, Mn, and V impacted on Fe homeostasis in a rat lung macrophage cell line (i.e., NR8383) were used; and 3) to examine effects from each city’s PM2.5 on lung macrophage Tf, Fe, and antibacterial function.
Summary of Findings. The results indicated that daily PM2.5 samples in NYC, Los Angeles (LA), and Seattle had disparate metal compositions, with wide variations in absolute and relative Fe, Mn, Al, and V content, and significant differences in the relative ratios of each competitor to Fe. In vitro studies with NR8383 cells sought to characterize if each competitor (at levels that could be encountered in PM2.5) could alter cell Fe homeostasis and ultimately, which competitor was most potent. Using induced iron response protein (IRP) binding to iron response elements as an indicator of shift in cellular Fe balance, it was seen that if cells were treated with Fe3+ alone or with V, Al, or Mn (individually or in combinations) at levels equivalent to those expected in 500 μg of a PM2.5 sample, each competitor caused an Fe deficit. Using increasing molar ratios of competitor to Fe, a determination was made that V had the greatest effect on Fe status and Mn the least. In studies using combinations, the competitors showed that there was a synergistic effect when V and Mn were both present; co-presence of Al with Mn or V had little impact. To see if effects observed with varying ratios of Al, Mn, and V would reflect what might occur with actual PM2.5, cells were treated with Fe alone and with Al, Mn, and V. It was found that IRP activation (compared to that from Fe alone) was greatest in cells treated with the combination of Fe+V+Al+Mn that would be found in NYC. Effects from co-treatments using levels of the metals found in PM2.5 from Seattle or Los Angeles were minimal.
Because nitric oxide (NO) might affect IRP activation, iNOS levels were also assayed in the cells; analyses of ERK-1 and -2 activation were performed concurrently as these play a role in iNOS formation. Only increasing amounts of Al had significant effects on iNOS expression; treatment with increasing ratios of V and Mn failed to induce iNOS to levels significantly above that of Fe alone. This would suggest that observed effects of V on IRP activity were unadulterated (i.e., no significant increase in NO that could enhance IRP-1 binding activity). Results of the ERK studies indicated that increasing ratios of V and Al both caused significant increases in phosphorylation/activation of ERK-1 (p44), but only V increased ERK-2 (p42) activation. These results indicate that at least two PM-associated metals induce effects on cell Fe homeostasis regulatory mechanisms (i.e., the IRPs—in either a direct or indirect manner) even when there is a level of Fe present that should keep the cell Fe-sufficient. A re-examination of the three city IRP studies in the context of the inhibitor-to-Fe ratios present in their daily samples as well as the NO studies’ findings allowed us to ultimately conclude that it is the relative amount of V to Fe that is most critical in determining if a given PM2.5 sample is likely to modify the Fe status of a lung macrophage. Furthermore, in PM that contains moderate-to-high amounts of Al, while effects on cell Fe status are likely, use of the IRP marker as an indicator of this outcome is not practical due to confounding effects introduced by effects on NO formation induced by Al ions.
Performing the in vivo exposure studies outlined for Aim 3 was ultimately not possible due to the limitations in the total amount of any given day’s sample of PM2.5. Instead, the information expected to be gleaned from those studies was obtained, in part, from a concurrent National Institutes of Health/National Institute of General Medicine Sciences (NIH/NIGMS)-funded study. Rats were exposed 5 hr/d for 5 d to atmospheres containing physico-chemically distinct forms of V (or other PM2.5 metals) and their lung fluids were then analyzed for total Fe content, ferritin and Tf levels. Antibacterial activity in the lungs of exposed cohorts, reflecting the functional status of local macrophages, was also examined. These studies indicated that prior to the start of a lung infection, exposure to pentavalent V—the most common form found in PM—caused significant increases in lavage fluid Fe and ferritin levels, but had less overall effect on total Tf levels. Effects from soluble V were greater than those from an insoluble counterpart. These same result patterns were seen in the ability of the exposed rats to clear a viable bacterial challenge from their lungs, i.e., rats that inhaled soluble V had the most significantly reduced resistance against a pathogen as compared to controls.
These rat study results, taken together with those of the in vitro studies performed here, suggest that soluble V ion-induced alterations in the ability of Tf to bind Fe can lead to increases in the levels of free Fe in the airways and concurrently, less Fe delivery to resident phagocytes. With both more Fe available for sustenance and local immune cells less capable of performing their normal sentinel duties, the survival of most common bacterial pathogens that invade the lungs would then be greatly enhanced. The specific mechanisms hypothesized and then validated in these studies now allow us to better explain the means by which PM2.5—and more importantly, its specific constituents—act to induce or exacerbate infectious lung diseases in exposed populations.
Conclusions.
- Select metals within a given sample of PM2.5 can cause altered cellular Fe homeostasis.
- Effects of PM2.5 with respect to altered macrophage Fe homeostasis—from region to region, or site to site in a given region—are governed by the relative content relationships between Fe and at least three co-constituent metals, e.g., V, Mn, and Al. Of these three, V is the most potent effector on this parameter.
- Analysis of IRP activity can be an effective way to examine effects of a variety of criteria pollutants upon Fe homeostasis in the lungs. But, Investigators need to monitor for effects on NO formation by the pollutants to determine if their measured effects on IRP are being adulterated.
Lung Hypoxia as Potential Mechanisms for PM-Induced Health Effects, R827351C010, M.D. Cohen, K. Salnikow
Description and Objective of Research. At-risk individuals with pre-existing hypertensive disease or atherosclerosis, appear to have overtly negative responses to PM. However, mechanisms underlying these effects and which constituents might be causing these outcomes are unclear. Atherosclerosis has been designated a chronic inflammatory process; it has been accepted that circulating levels of IL-6 may reflect the intensity of occult plaque inflammation and vulnerability to rupture. MCP-1 and IL-8 may also play a crucial role in initiating/promoting atherosclerosis. Hypertensive patients are at particular risk of complications related to endothelial damage or abnormal angiogenesis; these processes are correlatable with plasma levels of vascular endothelial growth factor (VEGF). We hypothesized here that select PM constituents (e.g., Al, V, Ni, Mn) act on lung epithelial cells and macrophages to stimulate release of pro-inflammatory cytokines/chemokines that may have a role in initiation or promotion of atherosclerosis. We further hypothesized that the metals contributed to the above noted deleterious responses in patients with pre-existing hypertensive disease/atherosclerosis by: 1) a priori altering the Fe status of these cells that, in turn, 2) results in increased intracellular accumulation of HIF-1α. Due to the latter, lung epithelial cells and macrophages increase their formation/release of proinflammatory cytokines, i.e., IL-6, IL-8, TNF-α, as well as MCP-1 and VEGF, which are then transported to the heart in relatively high (undiluted) concentrations. To validate our hypotheses, lung macrophage and epithelium cell lines were exposed to varying amounts of Fe alone or in combination with Al, V, Mn, or Ni (at levels relevant to those found in ambient urban PM from NYC) and levels of each of the above-cited cytokines/chemokines were measured by ELISA, Northern, and Western analyses (the latter to increase the degree of detectability of effects from the treatments). These results could then be used as a baseline of effects for later comparison against the actual formation of these proteins in the lungs of rodents exposed to the “parent” NYC PM2.5 samples.
Summary of Findings. The initial studies here examined potential effects of Fe and Ni (alone and in combination) on hypoxic stress induction and IL-8 production in human lung epithelial 1HAEo- cells. Exposure to Ni induced both hypoxic stress and IL-8 production; as similar levels of stress and IL-8 were induced by Fe-chelating desferroxamine (DFX), this suggested that Ni interfered with cell Fe status (much in the manner seen with other PM-associated metals in rat lung macrophages (NR8383 [NR]); Project 8; R827351C008). It is also possible that Ni may have become substituted for Fe in Fe-bearing enzymes/proteins, leading to inhibition of their activity and, subsequently, to activation/induction of HIF-1 transcription factors. To assess if treatment with PM-associated metals led to altered Fe homeostasis that should induce an increased HIF-1α expression that subsequently leads to increases in the presence of MIP-2/IL-8 or VEGF, cultures of 1HAEo- or NR were treated overnight with soluble forms of Ni, V, or Al in combination with a fixed amount of Fe (each at levels that would be present in actual NYC PM2.5). Western analysis of cellular products indicated that increases in the relative amounts of V:Fe caused significant increases in HIF-1α expression (to values similar to those from DFX). Exposure to increasing amounts of Ni also caused increased HIF-1α expression, but less so than with V. Al treatments seemed to have no effect on HIF-1α expression; however, as these exposures caused more cell death and proteolytic damage to materials isolated from viable cells, these measurements may have been biased.
Analyses of HIF-1α-inducible cyto-/chemokines indicated that Al, Ni, and V each induced VEGF formation in NR cells. Induction levels were all equal-to-greater than that from DFX and the strength of effect was Al ≥ Ni > V. Western analyses of MIP-2 levels were inconclusive due to difficulties in resolving the protein in cell lysates; ELISAs yielded indications that Al had the strongest impact on MIP-2 release. With the 1HAEo- line, ELISAs of supernatants from treated cells suggested that at the higher metal:Fe levels tested, each metal induced IL-8 formation. In contrast, any stimulation of VEGF production appeared to occur with increasing Ni levels only. Critical Western analyses to confirm each noted pattern were impossible due to problems with poor antibody specificities. In their place, mRNA levels of respective HIF-1α-inducible genes were measured to obtain an indication of any induced shift in cyto-/chemokine formation. RT-PCR analyses showed that Al and Ni induced significant levels of VEGF mRNA and that the effect was ratio (i.e., Al:Fe, Ni:Fe)-related; oddly, the effect of V treatment was nominal. Similar results were also noted for IL-6 gene induction. With MCP-1, MIP-2, and TNFα, none of the metals tested had any effect.
The results with the rat macrophage (as compared to the human lung epithelial) line suggest there may be potential species-/cell type-related differences in responses to PM-metal-induced alterations in Fe homeostasis. The data also suggest that the relationship between metal-induced HIF-1α expression and levels of select cyto-/chemokine products may not necessarily be linear. However, this latter finding needs to remain tentative as effects of Al, Ni, and V on several relevant processes in cells need to be refined.
Conclusions.
- Select metals within a given sample of PM2.5 can cause altered cellular Fe homeostasis and this effect appears to be governed by the relative content relationships between Fe and at least three co-constituent metals, e.g., Ni, Al, and V.
- Among these metals (that alter Fe homeostasis), Ni and Al (more so than V) also cause changes in the release of select cytokine/chemokine factors that could impact initiation or promotion of atherosclerosis. This effect also is related to relative content relationships between Fe and these metals.
- The observed effects on the inducible release of these factors seem, for now, to be both species- and cell type-dependent.
Urban PM2.5 Surface Chemistry and Interactions with Bronchoalveolar Lavage Fluid (BALF), R827351C011, M. Kendall
Description and Objective of Research. The objective of this research project was to investigate the surface chemistry of urban fine particles (PM2.5), and to quantify the adsorbed and desorbed species exposed to bronchoalveolar lavage fluid (BALF).
Urban background and roadside PM2.5 samples of different mass concentration and total weight were collected in triplicate in the South Bronx region of New York City. Simultaneously, the concentrations of other atmospheric pollutants (CO, NOx, SO2, O3, EC) were measured, and weather conditions recorded. The collected PM2.5 samples underwent one of three treatments; no treatment, treatment in vitro with BALF, or treatment in a saline solution (control). The surfaces of untreated, saline and BALF treated PM2.5 samples were then analyzed using X-ray photoelectron spectroscopy (XPS) and time-of-flight secondary ion mass spectrometry (ToF-SIMS). These results were then compared with ambient air pollutant concentrations, weather variables, selected BALF characteristics, and results from a previous London study conducted using identical methods.
Summary of Findings. Both surface techniques were useful in detecting surface species and observing changes in surface concentrations. The surface of untreated urban PM2.5 consisted of 79 to 87% carbon and 10 to 16% oxygen with smaller contributions of N, S, Si and P in the samples from both locations. A wide variety of other inorganic (metals, Cl-, NH4+) and organic species (aliphatic and aromatic hydrocarbons) were detected with ToF-SIMS. The surface characteristics of particles from the roadside and background sites were very similar, except for higher (p<0.05) nitrate concentrations at the roadside PM2.5 that were attributable to higher roadside NOx concentrations. Comparable species and quantities were identified in a previous study of London PM2.5, but PM2.5 surface chemistry differed considerably from other sources, particularly in surface concentrations of oxygen and trace species.
After treatment with BALF, the N-C signal detected by XPS analysis increased by an average of 372±203%, indicating significant surface adsorption of protein or other N-containing biomolecules. Lower N-C signals were observed for BALF from smokers. ToF-SIMS data confirmed N adsorption after BALF treatment, and also indicated an adsorption of phospholipid on the PM2.5 surfaces in terms of increased fragment ions characteristic of phospholipid adsorption. The primary phospholipid in BALF is DPPC, although positive identification was not possible. Oxygen content of PM2.5 surfaces was the most significant determinant of both N-C and phospholipid adsorption. The XPS signal of the soluble species NH4+, NO32-, Si and S decreased in both saline and BALF treated samples, showing that these species may be bioavailable in the lung.In particular, surface oxygen concentrations were found to increase with “aged” PM2.5, so that clean air PM2.5 was > NYC and London PM2.5, which was > tobacco smoke PM2.5.
Conclusions. We have shown that PM2.5 surface chemistry can be analyzed and differentiated using two sensitive surface analytical techniques, XPS and ToFSIMS. PM2.5 surfaces in New York City are similar in overall composition to PM2.5 surfaces analyzed in London. Distinct differences in surface chemistry were also found comparing urban PM2.5 from different types of locations. The wide variations in carbon:oxygen ratios detected could be used to distinguish smoke, urban and “clean air” PM2.5. It is proposed that such differences may be an important—and hitherto unconsidered—determinant in the health effects of PM2.5
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) |
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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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subchronic, source apportionment, oxidative stress, PM component, tracheobronchial casts, airway models, human lung, particle deposition, asthma, particulate matter, ozone, lung function, cytokines, RANTES, particle size, allergic asthma, GM-CSF, sulfur dioxide, particle, surface reactions, absorption, adsorption, heart rate variability, cardiac function, immune mechanisms, infection, PM2.5, metals, immune, macrophage, iron, IRP, hypoxia, metals, surface chemistry, exposure, measurement error, mortality, morbidity,
,
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
Relevant Websites:
Long Version of Final Report (PDF) (41 pp, 539 K, About PDF)
http://www.med.nyu.edu/environmental/
http://es.epa.gov/ncer/science/pm/centers.html
Progress and Final Reports:
2001 Progress Report
2002 Progress Report
2003 Progress Report
Original Abstract
Subprojects under this Center:
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
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