Grantee Research Project Results
Cardiovascular Responses to Particulate Air Pollution
EPA Grant Number: R827994Title: Cardiovascular Responses to Particulate Air Pollution
Investigators: Liao, Duanping , Chinchilli, Vernon M. , Shy, Carl , Heiss, Gerardo
Current Investigators: Liao, Duanping , Whitsel, Eric , Heiss, Gerardo , Lin, Hung-Mo , Duan, Yinkang
Institution: Pennsylvania State University , University of North Carolina at Chapel Hill
Current Institution: Pennsylvania State University
EPA Project Officer: Chung, Serena
Project Period: (Extended to April 30, 2004)
Project Amount: $607,630
RFA: Airborne Particulate Matter Health Effects (1999) RFA Text | Recipients Lists
Research Category: Particulate Matter , Air Quality and Air Toxics , Air , Human Health
Description:
The primary objective of this study is to systematically study the adverse effects and the injury mechanisms of the criteria pollutants on cardiovascular health. The specific objectives and related testing hypotheses are listed below:
Criteria pollutants and clinical manifestations of cardiovascular
effects:
Whether the exposures to each individual air pollutant prior to
the clinical examination are associated with higher frequency of arrhythmia?
Whether the associations are independent of other gaseous copollutants? Whether
the PM-arrhythmia association is synergistically modified by the exposure to
other gaseous copollutants? Whether previous history of cardiovascular disease
modifies the above relationships? Whether the air pollution and arrhythmia
association differs by age, sex, social economic status, and ethnicity?
Criteria pollutants and the development of individually validated
cardiovascular diseases (CVD):
Whether the incident rates of validated
cardiovascular events (sudden cardiac death, myocardium infarction [MI],
coronary heart disease [CHD], and stroke) are associated with high levels of
each individual air pollutant? Whether the associations are independent of other
gaseous copollutants? Whether the PM-cardiac events association is
synergistically modified by the exposure to other gaseous copollutants? Whether
previous history of cardiovascular disease modifies the above relationships?
Whether the above associations differ by age, sex, social economic status, and
ethnicity?
Criteria pollutants and cardiac autonomic control - potential
physiological mechanism 1:
Whether the exposures to each individual
ambient air pollutant prior to the clinical examination are associated with poor
cardiac autonomic control, assessed by heart rate variability? Whether the
associations are independent of other gaseous copollutants? Whether the PM-poor
cardiac autonomic control association is synergistically modified by the
exposure to other gaseous copollutants? Whether previous history of
cardiovascular disease modifies the above relationships? Whether the above
associations differ by age, sex, social economic status, and ethnicity?
Criteria pollutants and cardiovascular reactivity - potential
physiological mechanism 2:
Whether the exposures to each individual
ambient air pollutant prior to the clinical examination are associated with
higher cardiovascular reactivity, assessed by postural changes of blood pressure
and heart rate? Whether the associations are independent of other gaseous
copollutants? Whether the PM-cardiac reactivity association is synergistically
modified by the exposure to other gaseous copollutants? Whether previous history
of cardiovascular disease modifies the above relationships? Whether the air
pollution and higher cardiovascular reactivity association differs by age, sex,
social economic status, and ethnicity?
Criteria pollutants and inflammatory /hemostatic markers - potential
physiological mechanism 3:
Whether the exposures to each individual
ambient air pollutant prior to the clinical examination are associated with
higher levels of inflammation / hemostatic factors? Whether the associations are
independent of other gaseous copollutants? Whether the
PM-inflammation/hemostatic factors associations are synergistically modified by
the exposure to other gaseous copollutants? Whether previous history of
cardiovascular disease modifies the above relationships? Whether the air
pollution and higher levels of inflammation/hemostatic factors association
differs by age, sex, social economic status, and ethnicity?
Approach:
This study will be conducted as an ancillary study to the Atherosclerosis Risk in Communities (ARIC) study. The ARIC study, sponsored by the National Heart, Lung and Lung Institute (NHLBI), is an ongoing, bi-racial population-based cohort study of cardiovascular and pulmonary diseases in 15,792 men and women randomly selected from the residents of four U.S. communities. The baseline examination of this cohort was conducted in 1987-1989, followed by yearly contacts and re-examinations every three years. All initial ARIC cohort participants will be eligible for this study. We will assess major exposures at the communities where the study participants were residing over the entire study period (1987-1998). We will abstract ambient air pollution data from the AIRS database, and to create the exposure data for each study participant according to their randomly assigned exam date and community of residences. These exposure data will be combined with the cardiovascular health data already collected by the ARIC investigators. We will perform our analyses to contrast the mean levels or the proportion of cardiovascular responses (the dependent variables) across the levels of air pollution exposures. Since each of the ARIC cohort examinations lasted for three years, with a total of four such examinations, we will have enough variations in the exposure levels to perform cohort examination specific analysis, as well as combining all four cohort examinations adjusting for repeated measures of the dependent variables. All statistical associations between the air pollution exposures and cardiovascular responses will be adjusted for weather factors and other established cardiovascular risk factors, using multivariable regression methods.
The primary pollutant is particulate matter (PM10 and TSP), followed by O3, SO2, CO, and NO2.
The primary cardiovascular health outcomes include:
The occurrence of arrhythmia from regular 2-minute ECG.
Markers of inflammation/blood coagulation including Fibrinogen, Factor VII, Factor VIII activity, von Willebrand factor, Protein C antigen, aPTT (activated partial thromboplastin time), AT-III (antithrombin III), and White Blood Cell (WBC).
Expected Results:
This study will add to our knowledge of the independent and joint effects cardiovascular effects of criteria pollutants. We will be able to, for the first time, systematically evaluate the potential injury mechanisms via which air pollution relates to adverse cardiovascular health outcomes.
Publications and Presentations:
Publications have been submitted on this project: View all 14 publications for this projectJournal Articles:
Journal Articles have been submitted on this project: View all 3 journal articles for this projectSupplemental Keywords:
Human health, US Population, Sex and ethnic groups, Susceptibility, Epidemiology, Analytical, Surveys., RFA, Scientific Discipline, Health, Air, particulate matter, Environmental Chemistry, Health Risk Assessment, Epidemiology, Risk Assessments, Biochemistry, Atmospheric Sciences, Biology, ambient aerosol, copollutant exposures, particulates, air toxics, cardiopulmonary responses, human health effects, cardiovascular vulnerability, heart rate variability, air pollution, chronic health effects, particulate exposure, ethnicity, Acute health effects, blood pressure, PM, cardiotoxicity, myocardium infarction, cardiac arrhythmiasProgress and Final Reports:
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.