2005 Progress Report: Cardiovascular Responses to Particulate Exposure

EPA Grant Number: R830838
Title: Cardiovascular Responses to Particulate Exposure
Investigators: Christiani, David , Eisen, Ellen , Magari, Shannon , Schwartz, Joel
Institution: Harvard T.H. Chan School of Public Health
EPA Project Officer: Chung, Serena
Project Period: May 5, 2003 through May 4, 2006 (Extended to May 4, 2009)
Project Period Covered by this Report: May 5, 2005 through May 4, 2006
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

Objective:

The overall objective of this research project is to investigate the role of exposure to ambient airborne particulates in the development of adverse cardiovascular responses, with the primary objective of identifying possible mechanisms of action. These relationships will be investigated in a community cohort living in close proximity to a large Boston bus terminal. Specific objectives include examining cardiovascular changes in healthy individuals and those with predisposing risk factors, such as chronic bronchitis, chronic obstructive pulmonary disease (COPD), and asthma. Serum fibrinogen and C-reactive protein levels also will be investigated in this group.

Progress Summary:

  • Additional laboratory assessment of integrated air samples and blood assays was performed (reflectance, X-ray fluorescence [pending], 8-OHdG).
  • Information on several time-varying possible confounders was abstracted from participant activity diaries and entered for further analysis.
  • Additional descriptive statistics have been generated to characterize the study population.
  • The calibration for the real-time SidePak particle monitor was completed. This line allows real-time data to be directly corrected to account for the difference between the environmental particles encountered in this study and those of Arizona road dust to which the SidePak is factory calibrated.
  • Additional mixed models defining heart rate and heart rate variability, such as the 5-minute standard deviation of the normal-to-normal ratio, were fit to the data set. Models that allow for individual slopes and intercepts, along with a variety of potential confounders and effect modifiers, have been investigated.
  • 8-OHdG results were analyzed to determine impact of increased particulate exposure on oxidative damage. Results showed that, as expected, in healthy individuals (here, those without doctor diagnosis of high blood pressure), oxidative damage increases with increasing exposure to fine particulate matter (PM2.5), measured as 12-hour interval adjusted PM2.5 (rs = 0.33, p = 0.11, +4.7 μg/g [95% CI: -2.1, 11.4] for highest PM2.5 quartile). However, in those with doctor-diagnosed high blood pressure, a negative association was observed (rs = -0.41, p = 0.04, -4.8 μg/g [95% CI: -8.9, -0.7] for highest PM2.5 quartile). This interaction between high blood pressure and fine particulate exposure (in quartiles) was statistically significant (p = 0.02).

Future Activities:

During the next year we plan to advance the data analyses to generate final descriptive statistics and regression models. Mixed models examining individual slopes and intercepts along with traditional categorical and linear control for confounding will be developed utilizing potential time-varying confounder information, in some cases exploring the use of splines to reduce confounding with less risk of model misspecification for these factors. These data will be incorporated into draft manuscripts for submission to peer-reviewed journals.

Journal Articles:

No journal articles submitted with this report: View all 5 publications for this project

Supplemental Keywords:

particulate matter, heart rate variability, C-reactive protein, fibrinogen, 8-OHdG, oxidative damage,, RFA, Scientific Discipline, Health, Air, HUMAN HEALTH, particulate matter, Health Risk Assessment, air toxics, Exposure, Epidemiology, Susceptibility/Sensitive Population/Genetic Susceptibility, Risk Assessments, 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:

Original Abstract
  • 2003 Progress Report
  • 2004
  • 2006 Progress Report
  • 2007 Progress Report
  • Final