Final Report: Asthma Susceptibility to PM2.5EPA Grant Number: R827351C003
Subproject: this is subproject number 003 , established and managed by the Center Director under grant R827351
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
Center: EPA NYU PM Center: Health Risks of PM Components
Center Director: N/A
Title: Asthma Susceptibility to PM2.5
Investigators: Thurston, George D. , Reibman, Joan
Institution: New York University School of Medicine
EPA Project Officer: Chung, Serena
Project Period: June 1, 1999 through May 31, 2005 (Extended to May 31, 2006)
RFA: Airborne Particulate Matter (PM) Centers (1999) RFA Text | Recipients Lists
Research Category: Air Quality and Air Toxics , Particulate Matter , Air
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 New York University (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.
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.
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.
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.
Journal Articles on this Report : 2 Displayed | Download in RIS Format
|Other subproject views:||All 4 publications||2 publications in selected types||All 2 journal articles|
|Other center views:||All 111 publications||100 publications in selected types||All 88 journal articles|
||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.||
||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.||
Supplemental Keywords:asthma, particulate matter, ozone, lung function, cytokines, RANTES,, RFA, Health, PHYSICAL ASPECTS, Scientific Discipline, Air, ENVIRONMENTAL MANAGEMENT, HUMAN HEALTH, particulate matter, Environmental Chemistry, Health Risk Assessment, Risk Assessments, Susceptibility/Sensitive Population/Genetic Susceptibility, Allergens/Asthma, Health Effects, Physical Processes, Environmental Monitoring, genetic susceptability, Atmosphere, Risk Assessment, ambient air quality, atmospheric particulate matter, particulates, asthma, asthma triggers, sensitive populations, air toxics, atmospheric particles, chemical characteristics, toxicology, ambient air monitoring, health risks, airborne particulate matter, ozone, asthma indices, environmental risks, exposure, second hand smoke, airway disease, airway inflammation, air pollution, aerosol composition, atmospheric aerosol particles, human exposure, airborne pollutants, inhalation, ozone monitoring, human susceptibility, allergic response, tobacco smoke, exposure assessment
Progress and Final Reports:Original Abstract
Main Center Abstract and Reports:R827351 EPA NYU PM Center: Health Risks of PM Components
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