2002 Progress Report: Epidemiologic Study of Particulate Matter and Cardiopulmonary MortalityEPA Grant Number: R827355C001
Subproject: this is subproject number 001 , established and managed by the Center Director under grant R827355
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
Center: Airborne PM - Northwest Research Center for Particulate Air Pollution and Health
Center Director: Koenig, Jane Q.
Title: Epidemiologic Study of Particulate Matter and Cardiopulmonary Mortality
Investigators: Kaufman, Joel D. , Checkoway, Harvey , Karr, Catharine J. , Koenig, Jane Q. , Sheppard, Lianne (Elizabeth) A. , Siscovick, David , Sullivan, Jeff
Current Investigators: Kaufman, Joel D. , Ishikawa, Naomi , Karr, Catharine J. , Miller, Kristine , Schreuder, Astrid , Shepherd, Kristine , Sheppard, Lianne (Elizabeth) A. , Siscovick, David , Sullivan, Jeff
Institution: University of Washington
EPA Project Officer: Chung, Serena
Project Period: June 1, 1999 through May 31, 2004 (Extended to May 31, 2006)
Project Period Covered by this Report: June 1, 2002 through May 31, 2003
Project Amount: Refer to main center abstract for funding details.
RFA: Airborne Particulate Matter (PM) Centers (1999) RFA Text | Recipients Lists
Research Category: Air Quality and Air Toxics , Particulate Matter , Air
The objective of the epidemiology project in Years 1 through 3 was to investigate associations between ambient particulate matter (PM) exposure and cardiopulmonary disease risks. The objective was addressed mainly through the use of case-crossover study designs. In Years 4 through 6 of the project, the objective is expanded to consider myocardial infarction (MI) onset in Seattle, WA, and PM-health outcomes in multicity settings.
The analysis of cardiac arrest and PM exposure in individuals with and without cardiovascular disease in Seattle was published in the March 15, 2003 issue of the American Journal of Epidemiology. We found no significant association between primary cardiac arrest and air pollution. However, we found a significant association in current smokers with pre-existing coronary artery disease, a finding that warrants further investigation.
We have completed analysis of MI onset time in the Myocardial Infarction Triage and Intervention (MITI) study. Our study did not find an association between short-term exposure to PM2.5 and onset of an MI as the Peters study found in Boston, MA. We convened a meeting of investigators involved in both studies in Seattle, WA, in conjunction with the American Thoracic Society meeting, and developed lists of variables that may provide additional information upon further research.
We have initiated a study of hospital admissions in infants in Los Angeles, CA, assessing the relationship with PM exposures on both acute and chronic exposure timeframes. This study will be conducted by Catherine Karr as partial qualifications for her Ph.D. degree.
Work continued under Dr. Kaufman's direction on the analysis of relationships between coronary heart disease events and chronic exposures to air pollution in a large ongoing cohort study, the Women's Health Initiative Observational Study (WHI). This study was described in detail in the last annual report. The specific aims and methods of the WHI analysis, which remain unchanged, are to:
· Determine the association between medium-term exposures to fine particulate air pollution and incident cardiovascular events and total mortality in 50-79 year-old women, using proportional hazards modeling. The effects of other pollutants also will be considered.
· Determine the degree to which subject characteristics (including sedentary lifestyle and prior health conditions) modify the relationship between air pollution and cardiovascular events.
· Develop exposure assignments with the initial information that we obtained on subject locations from the WHI Clinical Coordinating Center; this exposure assignment is ongoing.
We are conducting an analysis of pulmonary exacerbations in the United States Cystic Fibrosis patient population. We found an increased risk for more pulmonary exacerbations associated with PM2.5, and an association between pulmonary function decline and PM2.5. The work was presented at the 2002 North American Cystic Fibrosis Conference, and a manuscript has been submitted for publication.
In Years 5 and 6 of the project, we will complete the first stage of analysis of the WHI cohort data. We will publish the data from the MITI analysis, and consider additional studies in the cystic fibrosis population as a model for a susceptible population. We will execute an analysis of hospitalizations for bronchiolitis in infancy in relation to PM. Finally, we will design work for the development of future cohort studies of PM, and cardiovascular work will continue.
Journal Articles on this Report : 1 Displayed | Download in RIS Format
|Other subproject views:||All 21 publications||14 publications in selected types||All 14 journal articles|
|Other center views:||All 209 publications||113 publications in selected types||All 109 journal articles|
||Sullivan J, Ishikawa N, Sheppard L, Siscovick D, Checkoway H, Kaufman J. Exposure to ambient fine particulate matter and primary cardiac arrest among persons with and without clinically recognized heart disease. American Journal of Epidemiology 2003;157(6):501-509.||
Supplemental Keywords:epidemiology, particulate matter, PM, cardiopulmonary mortality, cardiac, cardiopulmonary disease risks, ambient particulate matter, cardiac arrest, cardiovascular disease, air pollution, health effects, fine particulates, PM2.5, Myocardial Infarction Triage Intervention Study, Boston, Massachusetts, MA, Seattle, Washington, WA, myocardial infarction, Women?s Health Initiative Observational Study, WHI, exposure, lifestyle, pulmonary function, cystic fibrosis, bronchiolitis., RFA, Health, Scientific Discipline, PHYSICAL ASPECTS, Air, Geographic Area, particulate matter, Toxicology, air toxics, Environmental Chemistry, Health Risk Assessment, Epidemiology, State, Northwest, Risk Assessments, Susceptibility/Sensitive Population/Genetic Susceptibility, Allergens/Asthma, Biochemistry, Physical Processes, Children's Health, genetic susceptability, indoor air, Atmospheric Sciences, Incineration/Combustion, ambient air quality, health effects, risk assessment, particulates, biostatistics, asthma, ambient aerosol, sensitive populations, exposure and effects, health risks, air pollutants, morbidity, cardiopulmonary responses, human health effects, acute cardiovascular effects, animal model, airway disease, hazardous air pollutants, biological response, ambient air, exposure, combustion emissions, epidemelogy, air pollution, children, Human Health Risk Assessment, particle exposure, airway inflammation, human exposure, PAHs, atmospheric aerosols, ambient particle health effects, mortality studies, cardiopulmonary response, inhalation, children's vulnerablity, assessment of exposure, airborne pollutants, combustion, hydrocarbons, harmful environmental agents, epidemeology, human susceptibility, biological markers, incineration, mortality, California (CA), allergens, indoor air quality, aerosols, atmospheric chemistry, exposure assessment, environmental hazard exposures, toxics, air quality, particle transport, allergen, cardiovascular disease, human health risk, combustion contaminants
Progress and Final Reports:Original Abstract
Main Center Abstract and Reports:R827355 Airborne PM - Northwest Research Center for Particulate Air Pollution and Health
Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R827355C001 Epidemiologic Study of Particulate Matter and Cardiopulmonary Mortality
R827355C002 Health Effects
R827355C003 Personal PM Exposure Assessment
R827355C004 Characterization of Fine Particulate Matter
R827355C005 Mechanisms of Toxicity of Particulate Matter Using Transgenic Mouse Strains
R827355C006 Toxicology Project -- Controlled Exposure Facility
R827355C007 Health Effects Research Core
R827355C008 Exposure Core
R827355C009 Statistics and Data Core
R827355C010 Biomarker Core
R827355C011 Oxidation Stress Makers