Grantee Research Project Results
2001 Progress Report: Health Effects of Concentrated Ambient Particles from the Central Valley of California
EPA Grant Number: R827995Title: Health Effects of Concentrated Ambient Particles from the Central Valley of California
Investigators: Pinkerton, Kent E.
Current Investigators: Pinkerton, Kent E. , Smith, Kevin R. , Sioutas, Constantinos
Institution: University of California - Davis
Current Institution: University of California - Davis , University of Southern California
EPA Project Officer: Chung, Serena
Project Period: February 1, 2000 through January 31, 2003 (Extended to July 31, 2003)
Project Period Covered by this Report: February 1, 2001 through January 31, 2002
Project Amount: $633,328
RFA: Airborne Particulate Matter Health Effects (1999) RFA Text | Recipients Lists
Research Category: Particulate Matter , Air , Human Health
Objective:
The overall objective of this project is examine the mechanisms of particulate toxicity in the lungs of rats following short-term (3-day) exposure to concentrated ambient particles of the Fresno area during the fall and winter months when particle size and composition in this region of California are dramatically different. We will examine the effects these particles exerted on epithelial cells of the airways, centriacinar regions, and alveoli. Because epithelial cells are the first cells in the respiratory tract to come into contact with inhaled particles, we hypothesize that damage to these cells can serve as a direct and highly sensitive measure of particle toxicity. We hypothesize that epithelial-particle interactions initiate a cascade of events that underly adverse effects associated with inhaled particles. We hypothesize that particle toxicity begins with DNA damage in epithelial cells, thus accentuating cytotoxic events, leading to cell death. In turn, cell death begins the process of cellular proliferation. Each of these events impact negatively on the ability of the lungs to translocate and clear particles, thus leading to further irritation and injury. We will test each of these hypotheses using novel approaches to examine epithelial cell structure and function throughout the airways and alveoli.
Progress Summary:
Epidemiological studies have shown that airborne particulate matter (PM) with an aerodynamic diameter less than 10 µm (PM10) is associated with an increase in respiratory-related disease. However, there is a general consensus that particles less than 2.5 µm (PM2.5) may elicit the greatest toxic effects. Particulate matter is a complex mixture of organic and inorganic compounds, but the components or properties responsible for its effects on the respiratory system have yet to be determined. During the fall and winter of 2000-2001, healthy adult Sprague-Dawley rats were exposed in Fresno, CA, to filtered air or combined ultrafine and fine fractions of PM enhanced approximately 20-fold over ambient levels in six separate experiments. Exposures were conducted for 4 hours per day for 3 consecutive days. PM was concentrated while preserving chemical composition, size distribution, and surface morphology. PM mass and particle numbers were measured during each exposure. Chemical analysis of the concentrated PM was conducted for each study and included the measurement of elemental and organic carbon, sulfate, nitrate, trace elements, and metal content. The mean mass concentration of particles ranged from 190 to 847 micrograms/m3. PM was enriched primarily with ammonium nitrate, organic and elemental carbon, and metals. Bronchoalveolar lavage (BAL) was performed on each group of rats following exposure. Viability, total cells, numbers, and relative proportions of macrophages, neutrophils and lymphocytes in the BAL were determined. Viability of BAL cells from rats exposed to concentrated PM was significantly decreased during 4 of 6 weeks, compared to rats exposed to filtered air (P < 0.05). Total BAL cells were increased during 1 week of the 6-week study, while macrophages and neutrophils were increased during 1 week and 2 weeks, respectively. The decreased cell viability in PM-exposed rats is indicative of cell membrane damage, possibly because oxidative stress is catalyzed by transition metals or polar organic compounds. Increased neutrophils in PM-exposed rats indicate a mild inflammatory response. These observations suggest that exposure to enhanced concentrations of ambient ultrafine and fine particles in Fresno, CA, is associated with significant cellular effects in the lungs of healthy adult rats.
Future Activities:
Future activities include continuing PM concentrator studies in Fresno, CA, during the fall season, when particle size and composition are significantly different from other seasons. We will continue to improve our understanding of concentrated ambient PM effects on the respiratory tract within anatomically distinct regions from the trachea to the alveolus for better extrapolation of findings to humans. We also will evaluate causal relationships between specific PM components and biological responses and compare outcomes of real-life ambient PM studies in Fresno to those of previous health studies at University of California?Davis using artificial preparations of carbonaceous and ammonium nitrate aerosols.
Journal Articles:
No journal articles submitted with this report: View all 9 publications for this projectSupplemental Keywords:
PM2.5, PM10, particle size, particle, composition, air pollution., RFA, Health, Scientific Discipline, Air, Geographic Area, particulate matter, Toxicology, air toxics, Environmental Chemistry, Health Risk Assessment, State, Risk Assessments, Molecular Biology/Genetics, ambient air quality, particle size, airway epithelial cells, PM 2.5, DNA damage, cytotoxic events, chemical mixtures, lung inflammation, particulate exposure, Acute health effects, inhaled, PM, California (CA), respiratory, ultrafine particles, animal inhalation studyRelevant Websites:
http://www.envtox.ucdavis.edu/cehs/ Exit
http://agcenter.ucdavis.edu/agcenter/ Exit
Progress and Final Reports:
Original AbstractThe 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.