Grantee Research Project Results
Inhalation of Particulate Matter Alters the Allergic Airway Response to Inhaled Allergen
EPA Grant Number: R825702C005Subproject: 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: Denver Children’s Environmental Health Center - Environmental Determinants of Airway Disease in Children
Center Director: Schwartz, David A.
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
Objective:
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:
Health, RFA, Air, Scientific Discipline, Health Risk Assessment, Risk Assessments, particulate matter, mobile sources, Environmental Chemistry, Epidemiology, Allergens/Asthma, Biochemistry, vehicle emissions, vehicular exhaust, diesel exhaust, inhalability, inhaled, cytokines, airway inflammation, emissions, pulmonary disease, carbon, diesel, human exposure, lung inflammation, motor vehicle emissions, respiratory, immune response, environmental health effects, lung, particulate exposure, pulmonary, engines, motor vehicles, allergens, particulates, exposure, PM, allergic response, airborne pollutants, air pollution, human health effects, human health risk, automobiles, automotive exhaust, diesel exhaust particles, air toxics, carbon blackProgress and Final Reports:
Main Center Abstract and Reports:
R825702 Denver Children’s Environmental Health Center - Environmental Determinants of Airway Disease in Children 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
The perspectives, information and conclusions conveyed in research project abstracts, progress reports, final reports, journal abstracts and journal publications convey the viewpoints of the principal investigator and may not represent the views and policies of ORD and EPA. Conclusions drawn by the principal investigators have not been reviewed by the Agency.