2003 Progress Report: Examining Conditions That Predispose Towards Acute Adverse Effects of Particulate Exposures
EPA Grant Number: R827353C004Subproject: this is subproject number 004 , established and managed by the Center Director under grant R827353
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
Center: EPA Harvard Center for Ambient Particle Health Effects
Center Director: Koutrakis, Petros
Title: Examining Conditions That Predispose Towards Acute Adverse Effects of Particulate Exposures
Investigators: Schwartz, Joel
Current Investigators: Schwartz, Joel , O’Neill, M. , Wellenius, Gregory , Zanobetti, Antonella
Institution: Harvard University
EPA Project Officer: Stacey Katz/Gail Robarge,
Project Period: June 1, 1999 through May 31, 2005 (Extended to May 31, 2006)
Project Period Covered by this Report: June 1, 2003 through May 31, 2004
Project Amount: Refer to main center abstract for funding details.
RFA: Airborne Particulate Matter (PM) Centers (1999)
Research Category: Particulate Matter
Description:
Objective:The objectives of this research project are to: (1) test the hypothesis that patients with preexisting respiratory, cardiovascular, or diabetic conditions have an enhanced mortality response to particle exposures; and (2) assess the effects of gaseous copollutants as alternative predictors of mortality and the degree to which they modify the response to particulate matter (PM).
This is one of 10 projects funded by the Center. The progress for the other nine projects is reported separately (see reports for R827353C001 through R827353C003, and R827353C005 through R827353C011).
Progress Summary:The identification of populations that are especially susceptible to PM health effects can further our understanding of biologic mechanisms of heart and lung disease attributable to PM. Our previous research has shown that individuals with diabetes are at higher risk from exposure to PM. We have published several papers addressing this issue. A recent paper examined effect modification by concurrent diagnosis of diabetes overall and by age group in four U.S. cities and found that individuals with diabetes have twice the risk of a PM10-associated cardiovascular admission compared to those without the disease (Zanobetti and Schwartz, 2002).
To further examine susceptibility by diabetes observed in these population studies, we obtained clinical information to gain insights on potential biological mechanisms. With researchers at the Joslin Diabetes Center and Beth Israel/Deaconess Hospital, we analyzed the relationship between air pollution and both inflammation and vascular reactivity in more than 200 greater Boston residents participating in clinical trials. We used particle data (PM2.5, particle number, black carbon, and sulfate) measured at the Harvard School of Public Health site established by the Center. Both black carbon and sulfate particles appeared to have effects on vascular reactivity and endothelial function, especially among people with diabetes (O'Neill, et al., submitted, 2004a). Additional analyses have shown associations between increased particle levels and blood markers of inflammation, including intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and von Willibrand's factor. Manuscripts describing these results are in preparation.
We have continued to explore factors influencing vulnerability to temperature-related mortality. Data on air pollution compiled for Center research projects have been used to control for confounding. In a study of seven U.S. cities, lower educational attainment, black race, and dying outside a hospital were markers of vulnerability to death on extreme temperature days, controlling for PM10 exposure (O'Neill, et al., 2003b). In a follow-up analysis, we found that air conditioning prevalence explained some of the observed racial disparities in heat-related mortality in four of these cities (O'Neill, et al., in review, 2004). An additional analysis found that air pollution and epidemics were important confounders of temperature and mortality associations and suggested inclusion of PM10, ozone, and epidemic periods in future analyses, which can be used in forecasting health impacts of climate change (O'Neill, et al., submitted, 2004b).
The case-crossover approach also was used to examine the PM10-associated risk of emergency hospitalization for myocardial infarction during 1985-1999 among elderly residents in 21 U.S. cities. The results from this study showed increased risk of hospitalization for myocardial infarction for diabetics. Effect sizes roughly were doubled in persons with chronic obstructive pulmonary disease or concurrent pneumonia compared to those without (Zanobetti, et al., 2004).
During the past year, we examined the association of PM2.5 and changes in blood markers of cardiovascular risk, including lipid profiles and markers of acute systemic inflammation, in the Pravastatin Inflammation C-Reactive Protein (CRP) Evaluation study; a large, national randomized trial on the use of statins to lower such risk factors. In the placebo group, we found associations between PM2.5 and CRP total cholesterol and low-density lipoprotein. For the same outcomes, the associations were not significant in the group taking statins (Zanobetti, et al., 2004).
Future Activities:We will continue to: (1) test the hypothesis that patients with preexisting respiratory, cardiovascular, or diabetic conditions have an enhanced mortality response to particle exposures; and (2) assess the effects of gaseous copollutants as alternative predictors of mortality and the degree to which they modify the response to PM.
Journal Articles on this Report: 14 Displayed | Download in RIS Format
Other subproject views: | All 34 publications | 34 publications in selected types | All 33 journal articles |
Other center views: | All 149 publications | 149 publications in selected types | All 148 journal articles |
Type | Citation | ||
---|---|---|---|
|
Bateson TF, Schwartz J. Selection bias and confounding in case-crossover analyses of environmental time-series data. Epidemiology 2001;12(6):654-661. |
R827353 (Final) R827353C004 (2002) R827353C004 (2003) R827353C004 (2004) R827353C004 (Final) R827353C005 (2001) R827353C005 (2002) R827353C005 (2003) R827353C005 (Final) |
|
|
Braga ALF, Zanobetti A, Schwartz J. The effect of weather on respiratory and cardiovascular deaths in 12 U.S. cities. Environmental Health Perspectives 2002;110(9):859-863. |
R827353 (Final) R827353C004 (2002) R827353C004 (2003) R827353C004 (Final) |
|
|
Braga ALF, Zanobetti A, Schwartz J. The time course of weather-related deaths. Epidemiology 2001;12(6):662-667. |
R827353 (Final) R827353C004 (2002) R827353C004 (2003) R827353C004 (2004) R827353C004 (Final) |
|
|
O’Neill MS. Air conditioning and heat-related health effects. Applied Environmental Science and Public Health 2003;1(1):9-12. |
R827353 (Final) R827353C004 (2002) R827353C004 (2003) R827353C004 (Final) |
not available |
|
O’Neill MS, Jerrett M, Kawachi I, Levy JI, Cohen AJ, Gouveia N, Wilkinson P, Fletcher T, Cifuentes L, Schwartz J. Health, wealth, and air pollution: advancing theory and methods. Environmental Health Perspectives 2003;111(16):1861-1870. |
R827353 (Final) R827353C004 (2003) R827353C004 (Final) |
|
|
O’Neill MS, Zanobetti A, Schwartz J. Modifiers of the temperature and mortality association in seven US cities. American Journal of Epidemiology 2003;157(12):1074-1082. |
R827353 (Final) R827353C004 (2003) R827353C004 (Final) |
|
|
O’Neill MS, Veves A, Zanobetti A, Sarnat JA, Gold DR, Economides PA, Horton ES, Schwartz J. Diabetes enhances vulnerability to particulate air pollution-associated impairment in vascular reactivity and endothelial function. Circulation 2005;111(22):2913-2920. |
R827353 (Final) R827353C004 (2003) R827353C004 (2004) R827353C004 (Final) |
|
|
O’Neill MS, Hajat S, Zanobetti A, Ramirez-Aguilar M, Schwartz J. Impact of control for air pollution and respiratory epidemics on the estimated associations of temperature and daily mortality. International Journal of Biometeorology 2005;50(2):121-129. |
R827353 (Final) R827353C004 (2003) R827353C004 (2004) R827353C004 (Final) |
|
|
Peters A, Dockery DW, Muller JE, Mittleman MA. Increased particulate air pollution and the triggering of myocardial infarction. Circulation 2001;103(23):2810-2815. |
R827353 (Final) R827353C004 (2002) R827353C004 (2003) R827353C004 (Final) |
|
|
Schwartz J. Assessing confounding, effect modification, and thresholds in the association between ambient particles and daily deaths. Environmental Health Perspectives 2000;108(6):563-568. |
R827353 (Final) R827353C004 (2003) R827353C004 (Final) |
|
|
Zanobetti A, Wand MP, Schwartz J, Ryan LM. Generalized additive distributed lag models: quantifying mortality displacement. Biostatistics 2000;1(3):279-292. |
R827353 (Final) R827353C004 (2000) R827353C004 (2002) R827353C004 (2003) R827353C004 (Final) |
|
|
Zanobetti A, Schwartz J, Samoli E, Gryparis A, Touloumi G, Atkinson R, Le Tertre A , Bobros J, Celko M, Goren A, Forsberg B, Michelozzi P, Rabczenko D, Aranguez Ruiz E, Katsouyanni K. The temporal pattern of mortality responses to air pollution: a multicity assessment of mortality displacement. Epidemiology 2002;13(1):87-93. |
R827353 (Final) R827353C004 (2002) R827353C004 (2003) R827353C004 (Final) |
|
|
Zanobetti A, Schwartz J. Cardiovascular damage by airborne particles: Are diabetics more susceptible? Epidemiology 2002;13(5):588-592. |
R827353 (Final) R827353C004 (2001) R827353C004 (2002) R827353C004 (2003) R827353C004 (Final) R827353C005 (2003) R827353C005 (Final) |
|
|
Zanobetti A, Schwartz J, Samoli E, Gryparis A, Touloumi G, Peacock J, Anderson RH, Le Tertre A , Bobros J, Celko M, Goren A, Forsberg B, Michelozzi P, Rabczenko D, Hoyos SP, Wichmann HE, Katsouyanni K. The temporal pattern of respiratory and heart disease mortality in response to air pollution. Environmental Health Perspectives 2003;111(9):1188-1193. |
R827353 (Final) R827353C004 (2002) R827353C004 (2003) R827353C004 (Final) |
|
exposure, health effects, susceptibility, biology, epidemiology, toxicology, environmental chemistry, monitoring, air pollutants, air pollution, air quality, ambient air, ambient air monitoring, ambient air quality, ambient particle health effects, ambient particles, exposure assessment, biological mechanism, biological response, cardiopulmonary, cardiopulmonary response, cardiovascular disease, chemical exposure, environmental health hazard, exposure and effects, susceptibility, susceptible populations, sensitive populations, health risks, human exposure, human health, human health effects, human health risk, human susceptibility, indoor air quality, indoor exposure, inhalation, inhalation toxicology, inhaled particles, particle exposure, particulate exposure, particulates, pulmonary, pulmonary disease, respiratory, respiratory disease, diabetes, elderly, risk assessment. , Air, Geographic Area, Scientific Discipline, Health, RFA, Susceptibility/Sensitive Population/Genetic Susceptibility, Molecular Biology/Genetics, Toxicology, Biology, Risk Assessments, genetic susceptability, Microbiology, Epidemiology, air toxics, Children's Health, Atmospheric Sciences, Environmental Engineering, Environmental Microbiology, particulate matter, Environmental Chemistry, Environmental Monitoring, State, tropospheric ozone, ambient measurement methods, cardiopulmonary, risk assessment, exposure and effects, ambient air quality, cardiovascular disease, elderly, health effects, indoor air, indoor air quality, inhalation, developmental effects, epidemelogy, lung cancer, respiratory disease, inhalation toxicology, air quality, ambient air, cardiopulmonary response, indoor exposure, molecular epidemiology, assessment of exposure, cardiopulmonary responses, human health risk, interindividual variability, monitoring, susceptibility, genetic susceptibility, particle exposure, epidemeology, air pollutants, human health effects, particulates, respiratory, sensitive populations, biological response, ambient particle health effects, air pollution, ambient monitoring, children, inhaled, lung, stratospheric ozone, Utah (UT), Connecticut (CT), ambient air monitoring, chemical exposure, dosimetry, exposure, inhaled particles, pulmonary, human health, Illinois (IL), atmospheric monitoring, human susceptibility, environmental health hazard, biological mechanism , health risks, human exposure, Human Health Risk Assessment, pulmonary disease, Massachusetts (MA)
Relevant Websites:
https://cfserver.hsph.harvard.edu/cfdocs/eer/epa/
Progress and Final Reports:
1999 Progress Report
2000 Progress Report
2001 Progress Report
2002 Progress Report
Original Abstract
2004 Progress Report
Final Report
Main Center Abstract and Reports:
R827353 EPA Harvard Center for Ambient Particle Health Effects
Subprojects under this Center:
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R827353C001 Assessing Human Exposures to Particulate and Gaseous Air Pollutants
R827353C002 Quantifying Exposure Error and its Effect on Epidemiological
Studies
R827353C003 St. Louis Bus, Steubenville and Atlanta Studies
R827353C004 Examining Conditions That Predispose Towards
Acute Adverse Effects of Particulate Exposures
R827353C005 Assessing Life-Shortening Associated with Exposure to
Particulate Matter
R827353C006 Investigating Chronic Effects of Exposure to Particulate
Matter
R827353C007 Determining the Effects of Particle Characteristics on Respiratory Health of Children
R827353C008 Differentiating the Roles of Particle Size, Particle Composition,
and Gaseous Co-Pollutants on Cardiac Ischemia
R827353C009 Assessing Deposition of Ambient Particles in the Lung
R827353C010 Relating Changes in Blood Viscosity, Other Clotting Parameters,
Heart Rate, and Heart Rate Variability to Particulate and Criteria Gas Exposures
R827353C011 Studies of Oxidant Mechanisms
R827353C012 Modeling Relationships Between Mobile Source Particle Emissions and Population Exposures
R827353C013 Toxicological Evaluation of Realistic Emissions of Source Aerosols (TERESA) Study
R827353C014 Identifying the Physical and Chemical Properties of Particulate Matter Responsible for the Observed Adverse Health Effects
R827353C015 Research Coordination Core
R827353C016 Analytical and Facilities Core
R827353C017 Technology Development and Transfer Core