2002 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 , Kaufman, Joel D. , Larson, Timothy V. , Mar, Therese , Sullivan, Jeff , Trenga, Carol
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, 2002 through May 31, 2003
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 main objectives of the health effects component of the extensive exposure assessment study are to: (1) identify health outcomes that are associated with particulate matter (PM) exposures; (2) investigate associations with PM air pollution in the Pacific Northwest and signs of aggravation of asthma; and (3) concentrate on the use of source apportionment data in health outcome studies. The specific objective of the health effects component for Year 4 of the project was to continue to examine associations between exposure assessment variables and health outcomes in the panel subjects. We have findings relating to exhaled nitric oxide and lung function in children with asthma, as well as blood pressure-pulse rate, oxygen saturation, lung function, heart rate variability, and blood outcomes in elderly subjects with and without respiratory or cardiovascular disease.
Airway Inflammation in Children With Asthma
We estimated airway inflammation using a new, noninvasive assessment tool, exhaled nitric oxide (eNO). Exhaled NO was collected daily in children with asthma during the 10-day exposure assessment/health effects sessions during Year 2 of the project. Nineteen subjects aged 6-13 participated; 10 were not on inhaled corticosteroid (ICS) therapy, and 9 were on ICS. We found that a 10 µg/m3 increase in PM2.5 relative to the session average for that subject was associated with an increase in eNO in all subjects at lag day zero. The effect was 4.3 (confidence interval [CI] 2.5-7.8) ppb with the outdoor monitor, 4.2 ppb with the indoor monitor, 4.5 ppb with the personal monitor, and 3.8 ppb with the central monitors. The interaction term for medication category (ICS users versus ICS nonusers) was significant in all analyses. These findings suggest that eNO is an effective, noninvasive method for estimating lung inflammation in epidemiological studies of health effects of air pollution. A summary of these results has been submitted for publication. Preliminary analyses from data collected during Year 3 of the project's panel sessions from adult subjects with either respiratory or cardiac disease indicate that increases in eNO were associated with increases in exposure to PM2.5 in the older subjects with respiratory disease.
Lung Function in Children With Asthma
Coached spirometry measurements were obtained from the same pediatric subjects in the late afternoon at each daily home visit during the 10-day monitoring session using MicroDL portable spirometers. We applied mixed-effects random intercept regression models to test for a within-subject effect of same-day PM2.5 exposure (main effect) on forced expiratory volume in 1 second (FEV1), peak expiratory flow (PEF), and mid-expiratory flow (MEF). Medication use was examined as a modifier of the PM2.5 effect. Among subjects who were not prescribed anti-inflammatory medications (inhaled corticosteroids or leukotriene inhibitors; n = 5), indoor PM2.5 was consistently associated with decrements (per 10 µg/m3 increase in PM2.5 relative to the session average for each subject) in FEV1 (-75.5 mL, 95 percent CI: -142.9, -8.2), PEF (-11.9 L/min, 95 percent CI: -24.3, 0.4), and MEF (-13.7 L/min, 95 percent CI: -21.7, -5.8). A manuscript based on these results is in preparation.
Lung function also was studied in adult subjects in our panels. Associations between changes in FEV1 and PM2.5 measurements were evaluated using the same mixed-effects random intercept regression model to test for a within-subject effect of PM2.5 exposure on FEV1. Subjects were stratified by health status: healthy (n = 11), chronic obstructive pulmonary disease (COPD) (n = 17), and cardiac disease (n = 16). The overall mean age was 77.2 years (range 57.0-92.0 years). No significant association between 0 through 2 day lag PM2.5 exposure and coached FEV1 was observed among subjects with COPD (145 person days) or cardiac (164 person days) in models adjusted for temperature, relative humidity, age, gender, height, and weight. In subjects without reported COPD or cardiac disease, we observed a decrement in FEV1 of 215 mL for a 10 µg/m3 increase in local outdoor PM2.5 exposure (95 percent CI: [-410, -20]; 92 person days). This was a surprising result, and it warrants further research.
Blood Pressure-Pulse Rate and Oxygen Saturation in Adult Subjects With and Without Respiratory or Cardiac Disease
These endpoints in adult subjects have been analyzed for associations with various PM metrics. We found small associations between health and PM for these endpoints. We see increases in both systolic and diastolic blood pressure in cardiac subjects with both PM2.5 and PM10. Subjects with COPD showed a decrease in blood pressure associated with PM2.5. There were no blood pressure changes in healthy subjects. However, in both healthy subjects and those with COPD, we saw consistent decreases in heart rate associated with PM2.5 and PM10. A manuscript in final draft form is being reviewed by co-authors. Blood pressure effects may be due to alterations in autonomic nervous system function.
Heart rate variability and blood markers of cardiac disease results have been presented in previous progress reports.
In the next year, we will: (1) continue analyses of panel subjects using modeled exposures and short-term (1 hour, 2 hours, etc.) lag times; (2) complete the pilot study of potential gene-environment interactions in panel subjects; (3) continue use of exhaled nitric oxide to understand the relationship between fine particles and asthma aggravation in Seattle; (4) use source apportionment data in health outcome studies; (5) continue analyses of associations between PM and health in the New York University subcontract study; and (6) evaluate the use of breath condensate as a measure of air pollution-induced health effects.
Journal Articles on this Report : 2 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, Jansen K, Mar TF, Lumley T, Kaufman J, Trenga CA, Sullivan J, Liu L-JS, Shapiro GG, Larson TV. Measurement of offline exhaled nitric oxide in a study of community exposure to air pollution. Environmental Health Perspectives 2003;111(13):1625-1629.||
||Wallace LA, Mitchell H, O'Connor GT, Neas L, Lippmann M, Kattan M, Koenig J, Stout JW, Vaughn BJ, Wallace D, Walter M, Adams K, Liu L-JS. Particle concentrations in inner-city homes of children with asthma:the effect of smoking, cooking, and outdoor pollution. Environmental Health Perspectives 2003;111(9):1265-1272.||
Supplemental Keywords:air pollution, health effects, exposure assessment, particulate matter, PM, Pacific Northwest, asthma, nitric oxide, exhaled nitric oxide, lung function, children's health, blood pressure, pulse rate, oxygen saturation, heart rate, heart rate variability, respiratory disease, cardiovascular disease, elderly, children, inhaled corticosteroid therapy, airway inflammation, monitor, PM2.5, fine particulates, spirometry measurements, FEV1, peak expiratory flow, PEF, mid-expiratory flow (MEF), leukotriene inhibitors, chronic obstructive pulmonary disease, COPD, cardiac disease, blood markers., 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