2003 Progress Report: Health EffectsEPA Grant Number: R827355C002
Subproject: this is subproject number 002 , established and managed by the Center Director under grant R827355
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
Center: Airborne PM - Northwest Research Center for Particulate Air Pollution and Health
Center Director: Koenig, Jane Q.
Title: Health Effects
Investigators: Koenig, Jane Q. , Jansen, Karen , Larson, Timothy V. , Mar, Therese , Shepherd, Kristine
Current Investigators: Koenig, Jane Q. , Allen, Ryan , Jansen, Karen , Larson, Timothy V. , Lippmann, Morton , Lumley, Thomas , Mar, Therese , Sheppard, Lianne (Elizabeth) A.
Institution: University of Washington
EPA Project Officer: Chung, Serena
Project Period: June 1, 1999 through May 31, 2004 (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) RFA Text | Recipients Lists
Research Category: Air Quality and Air Toxics , Particulate Matter , Air
The objective of this research project is to identify health outcomes that are associated with particulate matter (PM) exposures. Our studies primarily are restricted to the Greater Seattle airshed.
Seven accomplishments can be cited: (1) completion of the analyses of the health outcomes in the panel studies and submission of a manuscript detailing the relationship between blood pressure (BP), heart rate, and air pollution; (2) use of the recursive model for estimated particles of indoor and outdoor origin in an analysis of associations with increased exhaled nitric oxide (eNO); (3) an analysis of short-term lags (hourly) and increased eNO using a polynomial distributed lag model; (4) an analysis of associations between PM2.5 and black carbon and eNO in adult subjects with respiratory disease; (5) receipt of a small grant to study cross-boundary air pollution in Vancouver, British Columbia (BC), and the Greater Seattle area and a comparison of both woodsmoke and traffic pollution in cases of bronchiolitis; (6) an analysis of associations between lung function and exposure in wildland firefighters; and (7) an intervention study using a high efficiency particulate air (HEPA) filter to reduce exposure to PM2.5 in adult subjects with respiratory disease.
The results of these studies are as follows:
- A panel of 85 elderly individuals who had concurrent intensive air pollution monitoring associations between health outcomes and indoor, outdoor, and personal measures of PM2.5 or PM 10 were evaluated using a mixed-effects model with random intercepts. Considering subjects not on medication, we saw small increases in BP in compromised subjects and consistent decrements in pulse rate in healthy subjects. Based on a 10 μg/m3 increase, we found a 1-4 mm Hg increase in systolic BP and a 1-3 mm Hg increase in systolic BP in subjects with heart disease associated with PM2.5 or PM 10. Subjects with chronic obstructive pulmonary disease (COPD) showed associations between decreases in systolic BP and either PM2.5 or PM 10. Pulse rate decreased 1.3 beats per minute (bpm) when all subjects not on medications were considered together associated with increases in indoor PM 10. When analyzed by health status, small decrements (1.5-3.4 bpm) in heart rate in the healthy subjects were associated with all PM metrics. We conclude that small changes in cardiac function were associated with modest concentrations of air pollution.
- Our Center recently described a technique for separating personal exposure to PM into its indoor- and outdoor-generated components using hourly light scattering data and a recursive modeling technique (Allen, et al., 2003). We used this technique to derive indoor versus outdoor (ambient) exposures in a study of 19 children with asthma and pulmonary endpoints of eNO and lung function. Using a recursive model in eight children, we found that outdoor-generated particles were more strongly associated with eNO changes (6.8 ppb increase, confidence interval [CI] 0.6-12.9) and that neither category of estimated particles was associated consistently with lung function. The association between the indoor-measured PM2.5 and changes in eNO in those same eight children was 4.1 ppb, CI -0.9-9.1. We conclude that when personal exposure is partitioned into indoor- versus outdoor-generated particles, only PM that was generated outdoors was associated with health outcomes.
- We conducted an analysis of short-term lags (hourly) and associations between eNO and PM2.5 in children with asthma using a polynomial distributed lag model. We found that 1-hour PM2.5 averages up to 7 hours prior to the eNO measurement were associated with increases in eNO. These data were presented at the 2004 Annual American Thoracic Society Meeting (Mar, et al., 2004).
- Another ongoing analysis uses our Year 4 panel study data from a collaborative study with Mort Lippmann at New York University. Intensive PM monitoring and health outcomes were taken in a group of 16 adults with respiratory disease. Our first analysis found that eNO in the senior subjects was associated with both PM2.5 and black carbon. Light-absorbing carbon (black carbon), a measure shown to represent black carbon from motor vehicles and wood stoves in Seattle, was measured with an integrated plate reader. These data were presented at the 2004 Annual American Thoracic Society Meeting (Jansen, et al., 2004). We plan further analyses using black carbon to identify sources of PM.
- In December, we were awarded funds from Health Canada through the British Columbia Centre for Disease Control and Prevention Society Branch to conduct a cross-boundary study of PM exposure and bronchiolitis in Seattle and Vancouver. We are in the process of getting approval from our Institutional Review Board to obtain the case data and are developing a protocol to use traffic, population, home characteristics, and agency monitors to estimate PM from traffic and wood-burning sources.
- We investigated the short-term effects of exposures to PM3.5, acrolein, formaldehyde, and carbon monoxide on lung function in a group of firefighters performing prescribed burns. Spirometric measurements were made on 65 firefighters at the beginning, midpoint, and at the end of their work shifts , and exposure was measured over the entire day. We examined the association between cross-shift lung function decrement and smoke exposure. A 1,000 μg/m3 increase in PM3.5 was associated with a -0.030 L change in the cross-shift forced expiratory volume (FEV)1 (95 % CI [-0.087, 0.026]). Acrolein, formaldehyde, and carbon monoxide exposure also were not significantly associated with changes in FEV1, forced vital capacity, or forced expiratory flow (FEF)25-75. We conclude that although firefighters’ lung function significantly decreased from preshift to postshift, firefighters exposed to greater concentrations of respiratory irritants did not experience greater lung function decrements. We could not establish a significant link to any of the individual toxic components of smoke that we measured.
- Finally, a graduate student conducted a study of the use of a HEPA filter in reducing indoor PM2.5. In that study of five adults with respiratory disease, we measured daily eNO. The HEPA filter significantly reduced indoor PM, but did not significantly reduce daily eNO. Unfortunately, we were not able to recruit a larger pool of subjects and were not able to find subjects who were not using anti-inflammatory medications. In addition, the PM was lower than average during the winter of 2003-04. However, the study did encourage us to repeat the experiment with a modified design, which would examine the subchronic effect of a HEPA filter on eNO.
We will continue to analyze the panel data to understand further the relationships between PM and health in Year 6 of the project. Exhaled NO was collected at 4:00 p.m. in the children with asthma and at approximately 10:00 a.m. in the adults with respiratory disease. We plan to use that time difference in our distributed lag model to determine possible differences in lag relationships because 10:00 a.m. is closer to the nighttime woodsmoke peaks. We also will use the adult eNO data as a means to replicate our findings related to the relative potency of indoor- versus outdoor-generated particles. Anticipated manuscripts during Year 6 of the project include: (1) short-term exposure and eNO; (2) Year 4 eNO results including black carbon; (3) Year 4 cardiorespiratory results; (4) use of HEPA filters to mitigate PM-induced airway inflammation; and (5) use of a polynomial-distributed lag model to identify sources. The following articles have been submitted for publication:
Journal Articles on this Report : 3 Displayed | Download in RIS Format
|Other subproject views:||All 27 publications||18 publications in selected types||All 18 journal articles|
|Other center views:||All 209 publications||113 publications in selected types||All 109 journal articles|
||Koenig JQ, Mar TF, Allen RW, Jansen K, Lumley T, Sullivan JH, Trenga CA, Larson TV, Liu L-JS. Pulmonary effects of indoor-and outdoor-generated particles in children with asthma. Environmental Health Perspectives 2005;113(4):499-503.||
||Mar TF, Larson TV, Stier RA, Claiborn C, Koenig JQ. An analysis of the association between respiratory symptoms in subjects with asthma and daily air pollution in Spokane, Washington. Inhalation Toxicology 2004;16(13):809-815.||
||Slaughter JC, Lumley T, Sheppard L, Koenig JQ, Shapiro GG. Effects of ambient air pollution on symptom severity and medication use in children with asthma. Annals of Allergy Asthma & Immunology 2003;91(4):346-353.||
Supplemental Keywords:ambient particles, fine particles, combustion, health, exposure, biostatistics, susceptibility, human susceptibility, sensitive populations, air toxics, genetic susceptibility, indoor air, indoor air quality, indoor environment, tropospheric ozone, California, CA, polyaromatic hydrocarbons, PAHs, hydrocarbons, acute cardiovascular effects, aerosols, air pollutants, air pollution, air quality, airborne pollutants, airway disease, airway inflammation, allergen, ambient aerosol, ambient aerosol particles, ambient air, ambient air quality, ambient particle health effects, animal model, assessment of exposure, asthma, atmospheric aerosols, atmospheric chemistry, biological markers, biological response, cardiopulmonary response, cardiovascular disease, children, children’s vulnerability, combustion, combustion contaminants, combustion emissions, epidemiology, exposure, exposure and effects, exposure assessment, harmful environmental agents, hazardous air pollutants, health effects, health risks, human exposure, human health effects, human health risk, incineration, inhalation, lead, morbidity, mortality, mortality studies, particle exposure, particle transport, particulates, particulate matter, risk assessment,, RFA, Health, Scientific Discipline, Air, Geographic Area, Waste, particulate matter, Toxicology, air toxics, Environmental Chemistry, Health Risk Assessment, Epidemiology, State, Northwest, Risk Assessments, Susceptibility/Sensitive Population/Genetic Susceptibility, Biochemistry, genetic susceptability, indoor air, Incineration/Combustion, biostatistics, health effects, asthma, risk assessment, ambient aerosol, particulates, sensitive populations, ambient air quality, health risks, cardiopulmonary responses, human health effects, exposure and effects, air pollutants, morbidity, airway disease, ambient air, exposure, combustion emissions, animal model, Human Health Risk Assessment, children, air pollution, particle exposure, human exposure, cardiopulmonary response, inhalation, atmospheric aerosols, ambient particle health effects, combustion, elderly, human susceptibility, age dependent response, allergens, incineration, indoor air quality, mortality, California (CA), environmental hazard exposures, toxics, air quality, particle transport, cardiovascular disease, human health risk, combustion contaminants, aerosols, atmospheric chemistry
Progress and Final Reports:Original Abstract
Main Center Abstract and Reports:R827355 Airborne PM - Northwest Research Center for Particulate Air Pollution and Health
Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R827355C001 Epidemiologic Study of Particulate Matter and Cardiopulmonary Mortality
R827355C002 Health Effects
R827355C003 Personal PM Exposure Assessment
R827355C004 Characterization of Fine Particulate Matter
R827355C005 Mechanisms of Toxicity of Particulate Matter Using Transgenic Mouse Strains
R827355C006 Toxicology Project -- Controlled Exposure Facility
R827355C007 Health Effects Research Core
R827355C008 Exposure Core
R827355C009 Statistics and Data Core
R827355C010 Biomarker Core
R827355C011 Oxidation Stress Makers