Effects of Inhaled Ultrafine Particles on Asthma

EPA Grant Number: R826785
Title: Effects of Inhaled Ultrafine Particles on Asthma
Investigators:
Institution: Lovelace Respiratory Research Institute
EPA Project Officer: Hunt, Sherri
Project Period: October 1, 1998 through September 30, 2001 (Extended to September 30, 2002)
Project Amount: $545,147
RFA: Health Effects of Particulate Matter and Associated Air Pollutants (1998) RFA Text |  Recipients Lists
Research Category: Health Effects , Air , Particulate Matter

Description:

Epidemiological studies show that hospital admissions for asthma are positively associated with the concentrations of particulate matter (PM) in the air. However, experimental data are limited to support or contradict the possibility that the inhalation of low concentrations of ultrafine PM increases asthma attacks. Immune and inflammatory cells localized to the lungs of asthmatics respond to inhaled allergens with the production and release of cytokines and mediators that play central roles in asthma attacks. Although the inhalation of allergens usually stimulates the release of these cytokines and mediators, exposures to ultrafine particles may also trigger their release in the lungs of allergic individuals. The objective of the studies described in this proposal is to test two hypotheses: inhaled ultrafine particles trigger asthma attacks 1) directly by stimulating the release of allergic-response cytokines in the lungs of asthmatics, or 2) indirectly by decreasing the concentration of inhaled allergen necessary to cause asthma attacks.

Approach:

Mice that produce allergic immune responses in their lungs to inhaled ovalbumin will be exposed to ultrafine (0.03 µm) carbon particles. Three exposure scenarios will examine the effects of short-term increases in the concentration of ultrafine particles as observed in the environment on the induction of asthma. All three exposures will be at set at 50 µg total particulate material (TPM)/m3 for 6 h with an increase in the ultrafine particle concentration to 200 µg TPM/m3 for 1 hr. These scenarios will differ in the time that the particle concentration is increased. The increase to 200 µg TPM/m3 will start at 1 h, 3 h, or 5 h after the start of the 6 h exposure. The effects of each exposure scenario on the release of allergic cytokines in the lungs and the maximum number of inflammatory cells in lung lavage fluid and lung tissues will be evaluated.

Expected Results:

We expect that inhaled ultrafine particles will stimulate the release of allergic mediators in the lung, and that the increased pulmonary inflammation will reduce the level of inhaled antigen necessary to induce allergic immune responses in the lungs that cause asthma.

Improvements in Risk Assessment or Risk Management: Data from the studies described in this proposal are important to 1) estimate the risk of inhaling ultrafine particles on the induction of asthma attacks in susceptible individuals, and 2) identify potential mechanisms responsible for the increased risk of asthma attacks by inhaled PM.

Publications and Presentations:

Publications have been submitted on this project: View all 5 publications for this project

Supplemental Keywords:

particles, health effects, susceptibility, genetic predisposition, RFA, Health, Scientific Discipline, Air, particulate matter, Toxicology, Environmental Chemistry, Allergens/Asthma, Atmospheric Sciences, ambient air quality, asthma, cytokine production, particulates, lungs, fine particles, human health effects, inhalability, cytokines, carbon, pulmonary disease, allergic airway, exposure, carbon black, airway inflammation, chronic health effects, human exposure, lung inflammation, airborne pollutants, inhalation, Acute health effects, allergens, respiratory

Progress and Final Reports:

2000 Progress Report
2001 Progress Report
Final Report