2006 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 , University of Southern California
Current 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, 2006 through May 4,2007
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 proposal 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 and asthma. Serum fibrinogen and C-reactive protein levels will also be investigated in this group.

Progress Summary:

  1. X-ray fluorescence assessment of integrated air samples was completed.
  2. Models were fit for heart rate (bpm), including fixed effects for corrected real-time fine particulate and other factors, indicating no significant alteration of heart rate by increasing exposure to fine particulate after inclusion of anticipated confounders.
  3. Additional mixed models defining heart rate variability, as the five-minute SDNN, were fit to the data set. Models that allow for individual slopes and intercepts, along with a variety of potential confounders and effect modifiers were investigated. After additionally controlling for concomitant heart rate (a surrogate measure for activity), a statistically significant association between 5-minute SDNN and fine particulate remained, showing a 28.5 msec decrease in 5-minute SDNN (p=0.030) associated with a 1 mg/m3 increase in fine particulate.
  4. Oxidative damage, as measured by urinary 8-hydroxy-2’-deoxyguanosine (8-OHdG), associated with fine particulate exposure appeared to be modified by the presence of specific chronic health conditions, particularly hypertension. An interquartile range increase in fine particulate (from 0.011 mg/ m3 to 0.031 mg/ m3) was associated with a 4.29 μg/g, 95% CI [0.44, 8.14] decrease in 8-OHdG in subjects with hypertension compared to those without hypertension.

Future Activities:

Preliminary analyses will be finalized. Splines will be explored as a means of controlling confounding by continuous 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
  • 2005 Progress Report
  • 2007 Progress Report
  • Final