Cardiovascular Responses to Particulate ExposureEPA Grant Number: R830838
Title: Cardiovascular Responses to Particulate Exposure
Investigators: Christiani, David , Coull, Brent , Herrick, Robert , Levy, Jonathan , Magari, Shannon , Schwartz, Joel , Sioutas, Constantinos
Current Investigators: Christiani, David , Eisen, Ellen , Magari, Shannon , Schwartz, Joel
Institution: Harvard T.H. Chan School of Public Health , University of Southern California
Current Institution: Harvard T.H. Chan School of Public Health
EPA Project Officer: Hunt, Sherri
Project Period: May 5, 2003 through May 4, 2006 (Extended to May 4, 2009)
Project Amount: $1,017,689
RFA: Airborne Particulate Matter Health Effects: Cardiovascular Mechanisms (2002) RFA Text | Recipients Lists
Research Category: Air , Health Effects , Particulate Matter
Population-based epidemiologic studies of communities in the United States have revealed a consistent association between ambient particulate air pollution and increases in morbidity and mortality. More recent studies have focused on the cardiovascular complications of ambient air pollution in primarily elderly cohorts using area PM2.5 monitoring. These studies have begun to examine potential biomarkers of effect, such as heart rate variability. However, the community studies reported cardiovascular mortality in response to airborne particles in persons under age 65, and little is known of the potential mechanisms in that population. The objective of this proposal is to use personal measurements of particulates to investigate the role of both PM2.5 and a smaller fraction, PM1.0 in the development of cardiac responses in a relatively young community cohort. We will employ a detailed continuous, real-time exposure-response assessment with repeated measures of biologic and physiologic markers of response. The continuous real-time exposure assessment will allow for insight into physiologic changes associated with particulate exposure, but also will allow the investigators to examine the time course of action of these toxicants. Determination of the time course of action is critical to identify mechanisms of action of particulates on the cardiovascular system.
Specific hypotheses to be tested will include: (1) particulate exposures will result in acute changes in cardiovascular function, as reflected in changes in heart rate, heart-rate variability and blood pressure; (2) particulate exposure will result in increased serum fibrinogen levels, a known risk factor for cardiovascular disease; (3) particulate exposure will result in increases in C-reactive protein, an identified inflammatory marker; and (4) chronic bronchitis, high blood pressure, diabetes, chronic obstructive pulmonary disease and asthma predispose individuals to particulate-induced changes in cardiac function.
The experimental approach will be an epidemiologic study employing a prospective, repeat-measurement design assessing several biological parameters in relation to exposure to PM2.5 and PM1.0 over a minimum of a 48-hour period in a community-based inner-city population living in close proximity to a large Boston bus terminal.
The expected results will clarify the exposure-response relationship and time course of action between particulate exposure and human cardiovascular responses. Clarification of the exposure-response relationships and time course of action will lend valuable insight into the mechanism of action of particulates, and will have important implications for preventive efforts aimed at reducing morbidity and mortality from exposure to particulates.
Publications and Presentations:Publications have been submitted on this project: View all 2 publications for this project
Supplemental Keywords:air pollution, particulate matter., RFA, Health, Scientific Discipline, Air, HUMAN HEALTH, particulate matter, air toxics, Health Risk Assessment, Exposure, Epidemiology, Risk Assessments, Susceptibility/Sensitive Population/Genetic Susceptibility, genetic susceptability, Biology, copollutant exposures, sensitive populations, atmospheric particulate matter, airway epithelial cells, cardiopulmonary responses, fine particles, PM 2.5, inhaled pollutants, acute cardiovascular effects, acute lung injury, stratospheric ozone, morbidity, air pollutants, motor vehicle emissions, automotive emissions, motor vehicle exhaust, air pollution, susceptible subpopulations, cardiac arrest, diesel exhaust, chronic health effects, lung inflammation, oxidant gas, particulate exposure, cardiopulmonary response, heart rate, human exposure, atmospheric aerosols, Acute health effects, inhaled, chronic obstructive pulmonary disease, highrisk groups, human susceptibility, cardiotoxicity, cardiopulmonary, mortality, concentrated particulate matter, air contaminant exposure, air quality, environmental hazard exposures, toxics, airborne urban contaminants, cardiovascular disease, acute exposure
Progress and Final Reports:2003 Progress Report
2005 Progress Report
2006 Progress Report
2007 Progress Report