Inhalation of Particulate Matter Alters the Allergic Airway Response to Inhaled AllergenEPA Grant Number: R825702C005
Subproject: this is subproject number 005 , established and managed by the Center Director under grant R825702
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
Center: Environmental Lung Disease Center (National Jewish Medical and Research Center)
Center Director: Mason, Robert J.
Title: Inhalation of Particulate Matter Alters the Allergic Airway Response to Inhaled Allergen
Investigators: Gelfand, Erwin , Borish, Larry
Current Investigators: Gelfand, Erwin
Institution: National Jewish Medical and Research Center
EPA Project Officer: Chung, Serena
Project Period: February 16, 1998 through February 28, 2003 (Extended to February 28, 2004)
RFA: Environmental Lung Disease Center (National Jewish Medical and Research Center) (1998) RFA Text | Recipients Lists
Research Category: Targeted Research
Because inhaled diesel particles are deposited in the lung, there is increasing concern that emissions from diesel engines contribute to the exacerbation of lung disease. Among these diseases, asthma is of particular concern. There is much speculation but with little experimental data, suggesting that diesel exhaust particles (DEP) may exacerbate allergic airway disease. Since small, relatively insoluble DEP (or it's surrogate carbon black, CB) can be deposited in the lung and transported to lung-associated lymph nodes, it is possible that inhaled DEP can act as an adjuvant, altering immune responses to inhaled allergen in sensitized hosts. Since such studies are virtually impossible to carry out in humans, animal models can be very informative. We have extensively characterized an animal model of allergen-driven airway hyperresponsiveness. Using this model we propose to directly study the effects on inhaled DEP or CB on allergic responses in the lung as well as effects on airway responsiveness. We will determine the consequences of particle exposure on antibody levels, cytokine production, cellular composition of inflammatory reactions and monitor airway responsiveness to inhaled methacholine in response to particle exposure alone or in combination with allergen sensitization and challenge. These studies will define for the first time whether diesel exhaust particle exposure aggravates or potentially protects against allergic airway disease.
Supplemental Keywords:RFA, Health, Scientific Discipline, Air, particulate matter, Environmental Chemistry, Health Risk Assessment, Epidemiology, Risk Assessments, mobile sources, Allergens/Asthma, Biochemistry, particulates, motor vehicles, air toxics, human health effects, inhalability, lung, vehicle emissions, cytokines, carbon, motor vehicle emissions, engines, exposure, pulmonary disease, air pollution, automobiles, automotive exhaust, carbon black, diesel exhaust, emissions, airway inflammation, environmental health effects, airborne pollutants, human exposure, inhalation, lung inflammation, pulmonary, particulate exposure, diesel, inhaled, PM, vehicular exhaust, diesel exhaust particles, allergens, allergic response, human health risk, immune response
Progress and Final Reports:
Main Center Abstract and Reports:R825702 Environmental Lung Disease Center (National Jewish Medical and Research Center)
Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R825702C001 SP-A and SP-D in Environmental Lung Disease
R825702C003 Adaptation to Nitrogen Dioxide: Role of Altered Glycolytic Pathway Enzyme Expression and NF-κB-Dependent Cellular Defenses Against Apoptosis
R825702C005 Inhalation of Particulate Matter Alters the Allergic Airway Response to Inhaled Allergen
R825702C006 Particle-Induced Lung Inflammation and Extracellular EC-SOD
R825702C007 Indoor-Outdoor Relationships of Airborne Particle Count and Endotoxin Concentrations
R825702C008 The Role of Mitochondrial DNA Mutations in Oxidant-Mediated Lung Injury
R825702C009 Immunopathogenesis of Hypersensitivity Pneumonitis in the Mouse
R825702C010 Activation of Natural T Lymphocytes by Diesel Exhaust Particulates Leads to Their Production of Interleukin-4 and TH2 Lymphocyte Differentiation to Allergen
R825702C011 Latex Antigen Levels During Powdered and Powderless Glove Use
R825702C012 Adjuvant Effects of Ozone in a Model of Allergen-Induced Airway Inflammation and Hyperresponsiveness
R825702C013 Acute Exposure to Particulate Air Pollution in Childhood Asthma
R825702C014 Mechanisms of Ozone Toxicity to the Lung