![[logo] US EPA](https://webarchive.library.unt.edu/eot2008/20081106024804im_/http://www.epa.gov/epafiles/images/logo_epaseal.gif){kind=logo}
Final Report: Health Effects
EPA Grant Number: R827355C002Subproject: 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. , Allen, Ryan , Jansen, Karen , Larson, Timothy V. , Lippmann, Morton , Lumley, Thomas , Mar, Therese , Sheppard, Lianne
Institution: University of Washington
EPA Project Officer: Stacey Katz/Gail Robarge,
Project Period: June 1, 1999 through May 31, 2004 (Extended to May 31, 2006)
Project Amount: Refer to main center abstract for funding details.
RFA: Airborne Particulate Matter (PM) Centers (1999)
Research Category: Particulate Matter
Description:
Objective:Our overarching objective is to identify health outcomes that are associated with PM exposures. Our data come from our large 2-3 year panel study, our Year 4 panel study in collaboration with NYU, and Project 2c measurements of fine aerosols in Seattle.
Summary/Accomplishments (Outputs/Outcomes):The objective of the health effects component of the extensive exposure assessment study is to identify health outcomes that are associated with PM exposures. A secondary objective is to investigate associations with PM air pollution in the Pacific Northwest and signs of aggravation of asthma. The health outcomes measured in our panel study were: lung function, exhaled nitric oxide (in children), blood pressure, oxygen saturation of arterial blood, heart rate variability, and blood biomarkers of effect.
With respect to airway inflammation we investigated associations between the fraction concentration of nitric oxide in exhaled breath (FENO) and various measures of PM air pollution. We found that FENO was most strongly associated with PM2.5. An increase in FENO was associated with outdoor, indoor, personal and central site monitors in children with asthma. Using a polynomial distributed lag model, we found that the lag time between exposure and increases in FENO and was 10-12 hours. We also estimated exposure to ambient-generated versus indoor-generated particles and found that the ambient-generated particles were strongly associated with FENO whereas the indoor-generated particles were not. Several studies of asthma status and exposure to air pollution were conducted by the Health Effects group which add more substance to the conclusion that PM2.5 exposure is associated with airway inflammation in children with asthma. We found that symptoms and medication use were associated with PM2.5 and other air pollutants in the Seattle cohort of the Childhood Asthma Management Project. Analysis of the all the children in the eight cities in CAMP revealed an association between NO2 exposure and decrements in lung function. No associations with PM were found, however the PM data set was incomplete for most of the cities.
We also noted associations between various spirometric measures and PM2.5, in children and but not in adults over the age of 65. In addition, no associations between PM and oxygen saturation of arterial blood were observed in the adult subjects. Use of heart rate variability (HRV) as a marker of PM exposure were reported by the epidemiology project (Project 1). No associations were seen between PM2.5 and HRV in subjects over age 65 years enrolled in our panel studies.
With respect to measures of cardiac health, we did observe small changes in heart rate and blood pressure in older adult subjects, but mainly in the healthy subjects in the panel study. Other studies of sudden cardiac death and onset of myocardial infarction were reported earlier in the summary of results for Project 1. No associations between PM exposure and these measures of cardiac effects were observed.
Summaries project by project follow.
1. Use of exhaled nitric oxide as a marker of airway inflammation
Three manuscripts have been published describing the relationships between PM2.5 exposure and airway inflammation in children with asthma. The first paper, “Measurement of offline exhaled nitric oxide in a study of community exposure to air pollution,” (Koenig et al, 2003) established the association between exposure and increases in exhaled nitric oxide (NO).
The second paper, “Exhaled nitric oxide in children with asthma and short term PM exposure in Seattle,” (Mar et al, 2005) evaluated the lag time between exposure and increases in exhaled NO. The objective of this study was to evaluate associations between short-term (hourly) exposures to PM and exhaled nitric oxide concentrations in children with asthma participating in an intensive panel study in Seattle. The exposure data were collected with Tapered Element Oscillation Microbalance (TEOM) PM monitors operated by the local air agency at three sites in the Seattle area. The fractional concentration of exhaled nitric oxide (FENO) is a marker of airway inflammation and is elevated in individuals with asthma. Previously, we have reported that offline measurements of FENO are associated with 24-hour average PM2.5 in a panel of 19 children with asthma in Seattle. In the present study using the same children, we used a polynomial distributed lag (pdl) model to assess the association between hourly lags in PM exposure and FENO levels. Our model controlled for age, ambient NO levels, temperature, relative humidity and use of inhaled corticosteroids (ICS). We found that FENO was associated with hourly averages of PM2.5 up to 10-12 hours after exposure. These data present new information concerning the lag structure between PM exposure and a respiratory health outcome in children with asthma.
A third manuscript was published, “Pulmonary effects of indoor-and outdoor-generated particles in children with asthma,” (Koenig et al, 2005) which ties together data from the exposure assessment project on particle infiltration of ambient generated PM with data from the health effects project on air way inflammation. A summary of these findings follows.
The majority of particulate matter (PM) health effects studies use outdoor (ambient) PM as a surrogate for personal exposure. However, people spend the majority of their time indoors exposed to a combination of indoor-generated particles and ambient particles that have infiltrated. Thus, it is important to investigate the differential health effects of indoor- and ambient-generated particles. We combined our recently adapted recursive model and a predictive model for estimating infiltration efficiency to separate personal exposure to PM2.5 into its indoor- (Eig)and ambient-generated (Eag) components for 19 children with asthma. We then compared Eig and Eag to changes in the fractional concentration of exhaled nitric oxide (FENO), a marker of airway inflammation. Based on the recursive model with a sample size of 8 children, Eag was marginally associated with increases in FENO (5.6 ppb per 10 μg/m3 increase in PM2.5, 95% CI: -0.6 to 11.9, p = 0.08). Eig was not associated with FENO (-0.19 ppb change per 10 μg/m3). Our predictive model allowed us to estimate Eag and Eig for all 19 children. For those combined estimates, only Eag was significantly associated with an increase in FENO (Eag: 5.0 ppb per 10 μg/m3 increase in PM2.5, 95% CI: 0.3 to 9.7, p = 0.04; Eig: 3.3 ppb per 10 μg/m3 increase in PM2.5, 95% CI: -1.1 to 7.7. p = 0.15). Effects were seen only in children who were not using corticosteroid therapy. We conclude that the ambient-generated component of PM2.5 exposure is consistently associated with increases in FENO and the indoor-generated component is less strongly associated with eNO.
2. An analysis of the association between fine particles and blood pressure, heart rate and pulse oximetry in elderly subjects
The objective of this study was to determine the relationship between residence and personal measures of air pollution and cardiorespiratory effects in older subjects. We performed a study that included repeated measures of pulmonary function (arterial oxygen saturation), and cardiac function (heart rate and blood pressure) in a panel of 88 elderly individuals who had concurrent intensive air pollution monitoring. Healthy subjects or those with respiratory disease 65 years of age or older and subjects with heart disease 57 years of age or older were recruited for this study. Each subject participated for 10 consecutive days (session) for up to 2 sessions that required daily exposure PM monitoring and daily collection of health outcomes. We had 1179 person-days of arterial oxygen saturation and heart rate data and 1029 person-days of blood pressure data. Associations between health outcomes and indoor, outdoor and personal measures of PM2.5 or PM10 were evaluated using generalized estimating equations (GEE) with an exchangeable working correlation matrix and robust standard errors. The model included terms for the within subject, within session effect; the within subject, between session effect; and an interaction term for medication usage. The model also controlled for temperature, relative humidity, body mass index, and age. Associations between PM and health measurements were primarily found in healthy subjects. We observed decreases in heart rate associated with indoor and outdoor PM2.5 and PM10 in healthy subjects not taking any medication and small increases in systolic blood pressure associated with indoor PM2.5 and outdoor PM10 among those healthy subjects on medications. Our test of heterogeneity suggests unequal effects of PM among the three groups of subjects. We conclude that small changes in cardiac function were associated with modest concentrations of air pollution. Heterogeneity analysis found differences among the health groups for associations with PM in heart rate but not in blood pressure. The differential effects on heart rate changes among different susceptibility groups of older subjects add new information on the adverse health effects of fine particles.
3. An analysis of the association between respiratory symptoms in subjects with asthma and daily air pollution in Spokane, Washington
The association between respiratory symptoms and ambient levels of particulate matter (PM) air pollution has been the focus of several panel studies. The majority of studies focused only on PM10, were conducted for relatively short periods, reported peak flow data, and involved children with asthma. The goal of our study was to evaluate the effect of particulate matter of various size fractions (PM10, PM2.5, PM1.0 and PM coarse fraction) on respiratory symptoms in both adults and children with asthma monitored over many months. Daily diary data on respiratory symptoms, and medication use were collected. Air pollution data were collected by the local air agency and Washington State University. Data were collected in Spokane, WA, a semi-arid city with diverse sources of particulate matter, including motor vehicles, wood stoves, agricultural burning, resuspended road dust and dust storms. Sixteen adults and nine children living in Spokane participated in the study. The majority of adult subjects participated for over a year and the children were studied for over 8 months. In the children, we found a strong association between cough and PM10, PM2.5, PM coarse fraction and PM1.0 (p<0.05). Sputum production and runny nose were associated with PM10 and coarse fraction. However, no association was found between the presence of any respiratory symptom any PM metric in the adult subjects. These positive associations between various metrics of PM and respiratory symptoms in children, suggest that children are more sensitive than adults to the effects of increased levels of PM air pollution or that the central site monitor was more representative for children who spend more time outdoors than adults. These findings also suggest that both larger and smaller particles can aggravate asthma symptoms.
4. HEPA intervention study:
Exposure to PM2.5 is associated with an increase in fractional exhaled nitric oxide (FENO) levels in subjects with respiratory disease. We hypothesized that a decrease in daily PM2.5 exposure, through intermittent use of an indoor HEPA filter, would be associated with a reduction in daily FENO in elderly subjects with respiratory disease. Older subjects with asthma and/or COPD, monitored in their homes for one month, were given an indoor air cleaner either with or without an enclosed HEPA filter. The initial filter/no filter state was randomly chosen and subsequently alternated every four days. The device fan operated at all times so as to blind the filtration state (on/off) to the subject. PM2.5 was measured using nephelometers. Triplicate measures of offline FENO were sampled three times per day. Within subject associations between FENO and PM2.5 were analyzed using a linear mixed effects model with random intercept, controlling for age, day on study, relative humidity, and temperature. The HEPA filters reduced the indoor levels of PM2.5 by 2.6 μg/m3and the average indoor/outdoor ratio from 0.172 to 0.030 in 3 of the 5 homes. For all subjects, a 10 μg/m3increase in 24 hour average outdoor PM2.5 was associated with a 1.6 ppb increase in FENO (95% CI: 0.51, 2.61). However, there was a suggestion of a weak association between daily FENO and presence or absence of the HEPA filter (p =0.15). We also observed a significant reduction in FENO over the duration of the study (p=0.01) for all subjects, even though there was not a similar decline in outdoor PM2.5. Conclusions: This study did not support the hypothesis that the HEPA filter influenced the association between outdoor PM2.5 and FENO, but did suggest a possible sub-chronic relationship between HEPA filter use and airway inflammation.
5. Association between health effects and PM and black carbon
K Jansen, TV Larson, JQ Koenig, T Mar, C Fields, J Steward, M Lippmann
Exhaled nitric oxide (FENO), spirometry, exhaled breath condensate (EBC), blood pressure, oxygen saturation of the blood (SaO2), and pulse rate were measured in 16 older subjects with asthma or chronic obstructive pulmonary disease (COPD) in Seattle. Data were collected daily for 12 days. PM10 and PM2.5 filter samples were simultaneously collected at a central outdoor site, as well as outside and inside the subject’s home. Personal PM10 filter samples were also collected. All filters were analyzed for mass and light absorbance. Within-subject associations between health outcomes and air pollution metrics were analyzed using a linear mixed effects model with random intercept, controlling for age, ambient relative humidity, and ambient temperature. For the seven subjects with asthma, a 10 μg/m3 increase in 24-hour average outdoor PM10and PM2.5was associated with a 5.9 (95% CI: 2.9, 8.9) and 4.2 ppb (95% CI: 1.3, 7.1) increase in FENO respectively. A 1 μg/m3 increase in outdoor, indoor, and personal light absorbing carbon (LAC) was associated with increases in FENO of 2.3 ppb (95% CI: 1.1, 3.6), 4.0 ppb (95% CI: 2.0, 5.9), and 1.2 ppb (95% CI: 0.2, 2.2), respectively. No significant association was found between PM or LAC measures and changes in lung function, EBC, blood pressure, or SaO2 in these subjects. Results from this study indicate that FENO may be a more sensitive marker of PM exposure than traditional health outcomes and that particle associated light absorbance is useful for examining associations between primary combustion constituents of PM and associated health outcomes. This research conducted in association with researchers from New York University and was partially supported by EPA Cooperative Agreement #C R827164 as well as the EPA NW PM Center.
6. Managed Campfire study
Jane Koenig, PhD, Karen Jansen, MS, Eva Dale, MS, Russell Dills, PhD, Chris Simpson, PhD
Measurements of nitric oxide in exhaled breath (FENO) and breath condensate were collected from 10 subjects participating in a managed camp fire exposure study (See Biomarker Core description). No associations between fine PM and FENO were seen. Breath condensate samples were not analyzed.
7. Ambient air pollution and asthma exacerbations in children: An eight-city analysis
Schildcrout JS, Sheppard L, Lumley T, Slaughter JC, Koenig JQ, Shapiro GG
The researchers investigated the relation between ambient concentrations of five of the Environmental Protection Agency’s criteria pollutants and asthma exacerbations (daily symptoms and use of rescue inhalers) among 990 children in eight North American cities during the 22-month pre-randomization phase (November 1993-September 1995) of the Childhood Asthma Management Program. Short-term effects of carbon monoxide, nitrogen dioxide, particulate matter less than 10 μm in aerodynamic diameter (PM10 ), sulfur dioxide, and warm-season ozone were examined in both one-pollutant and two-pollutant models, using lags of up to 2 days. Lags in carbon monoxide and nitrogen dioxide were positively associated with both measures of asthma exacerbation, and the 3-day moving sum of sulfur dioxide levels was marginally related to asthma symptoms. PM10 and ozone were unrelated to exacerbations. The strongest effects tended to be seen with 2-day lags, where a 1-parts-per-million change in carbon monoxide and a 20-parts-per-billion change in nitrogen dioxide were associated with symptom odds ratios of 1.08 (95% confidence interval (CI): 1.02, 1.15) and 1.09 (95% CI: 1.03, 1.15) respectively, and with rate ratios for rescue inhaler use of 1.06 (95% CI: 1.01, 1.10) and 1.05 (95% CI:1.01, 1.09), respectively. The researchers believe that the observed carbon monoxide and nitrogen dioxide associations can probably be attributed to mobile-source emissions, though more research is required.
8. Seasonal associations between particle size and total carbon and emergency department visits for asthma in Seattle
Mar TF, Koenig JQ, Schreuder AB, Lumley T, Larson TV, Covert DS
To date only a few US studies have investigated the association between air pollution and asthma emergency department (ED) visits. These studies have been confined to looking only at the effect of PM10 or PM2.5 mass metrics, rather than PM constituents or other particle size ranges. In this study we investigated the association between asthma ED visits for children and PM2.5, the number concentration of ultrafine particles, and total fine particle carbon. The particles were sampled at a central monitoring site in Seattle, WA. Asthma ED visits for children less than 18 years who resided in one of 8 zip code regions near the monitoring site, 9 zip codes in the adjacent concentric circle, and all Seattle zip codes were used for this analysis. The Poisson regression model included an indicator variable for day of week, a continuous variable for relative humidity, and smooth functions for time trends and temperature. The major source of total fine particle carbon in Seattle in the winter is wood burning. Therefore, to further examine this association, we limited our analysis to the winter heating season – October through March. We found only small associations between the ultrafine particle number concentration and daily ED visits. However, asthma ED visits were associated with an interquartile range (IQR) increase in PM2.5 with a RR of 1.17 ( 95% CI: 1.04, 1.33]), and an IQR increase in total fine particulate carbon with a RR of 1.11 {95% CI: 0.99, 1.25) at 3 days lag.
9. Personal exposure measured by the indoor/outdoor sulfur ratio and changes in airway inflammation in children with asthma
Allen RW, Mar TF, Koenig JQ, Larson TV
Particulate matter (PM) exposure consists of exposure to ambient-generated PM (Eag) and non-ambient PM (Ena),i.e. particles from indoor sources and personal activities. Preliminary evidence suggests that these exposure categories have unequal toxicities. We estimated the associations between these PM2.5 exposure categories and respiratory health among 19 children with asthma in Seattle. Home outdoor and personal PM2.5 (Et) concentrations were measured using Harvard Impactors and Harvard PEMs, respectively. Filters were analyzed by X-ray fluorescence for sulfur, which was used to partition Et into Eag and Ena. Health outcomes included exhaled nitric oxide (eNO) and indicators of lung function: mid-expiratory flow (MEF), peak expiratory flow (PEF), forced expiratory volume in the first second (FEV1), and forced vital capacity (FVC). Significant associations were found only among children not using inhaled corticosteroids (N = 11). A 10 μg/m3 increase in Et was associated with a 4.6 ppb increase in eNO (95% CI: 1.1 to 8.1). After estimating the exposure components, Eag was significantly associated with increased eNO (9.4 ppb per 10 μg/m3, 95% CI: 0.9 to 17.8), but Ena was not (1.9 ppb per 10 μg/m3, 95% CI: -4.8 to 8.7). Eag was marginally associated with decreased PEF (-24.9 L/min per 10 μg/m3, 95% CI: -52.3 to 2.6) and MEF (-15.8 L/min per 10 μg/m3, 95% CI: -31.9 to 0.4), whereas Et and Ena were not associated with lung function changes. These results suggest that in Seattle the ambient-generated component of PM2.5 exposure may be more irritating per unit mass than the non-ambient component.
10. Effects of ambient air pollution on lung growth in childhood asthma
EF McKone, JQ Koenig, T Lumley, GG Shapiro, TS Hallstrand
In the Childhood Asthma Management Program (CAMP), airway remodeling, evidenced by a reduction in post-bronchodilator FEV1 over time, occurred in one fourth of the children irrespective of treatment arm (Covar 2004). Because of the known effects of ambient air pollution on lung growth in children, we investigated the relationship between exposure to ambient air pollution and post-bronchodilator lung function in asthmatic children from the CAMP study over a 5 year period (1994-1999). Clinical variables were abstracted from CAMP and CAMPCS clinical trials, and monthly and annual ambient air pollution levels for CO, NO2, SO2, ozone, PM10 and PM2.5 were obtained from the Environmental Protection Agency. Generalized estimating equations were used to examine the influence of ambient pollution levels on rate of lung growth defined by the change in post-bronchodilator FEV1 over the study period. Nine hundred fourteen of the 1041 participants had clinical information that could be linked to pollution data. There was a significant association between NO2 exposure and rate of change in FEV1 (-0.014L/yr per10ppb change in NO2, p=0.019). There were trends towards association between PM10 and PM2.5 exposure and rate of change in FEV1 (-0.032l/yr per 10mcg change in PM10, p=0.085; -0.031l/yr per 10mcg change in PM2.5, p=0.096). There was no association between lung growth and exposure to CO, SO2, or ozone. These results indicate that exposure to ambient air pollution may lead to airway remodeling in some asthmatic children. Since the severity of asthma is often established in childhood, these finding have important public health implications for the acceptable levels of air pollution exposure in this vulnerable population.
What can we conclude from the past 6 years of research? First we can conclude that ambient PM concentrations in Seattle are associated with asthma aggravation as measured by exhaled nitric oxide (FENO). This is true for children with asthma and now has been replicated in adults with asthma. Also FENO is a very useful, non-invasive tool for studying relationships between exposure and health outcome. We found that ambient-generated PM was more toxic per unit mass than indoor-generated PM in the children with asthma. We also were able to define a lag structure of approximately 10 hour post FENO measurement. We still hope to be able to use XRF and levogluosan data to determine the contribution of wood smoke to this documented asthma aggravation. We determined that there is heterogeneity of effect of air pollution on cardiac outcomes in different susceptibility groups of adult subjects.
Journal Articles on this Report: 14 Displayed | Download in RIS Format
| Other subproject views: | All 27 publications | 18 publications in selected types | All 18 journal articles |
| Other center views: | All 191 publications | 97 publications in selected types | All 94 journal articles |
| Type | Citation | ||
|---|---|---|---|
|
|
Allen RW, Mar T, Koenig J, Liu L-J S, Gould T, Simpson C, Larson T. Changes in lung function and airway inflammation among asthmatic children residing in a woodsmoke-impacted urban area. Inhalation Toxicology 2008;20(4):423-433. |
R827355 (Final) R827355C002 (Final) |
|
|
|
Jansen KL, Larson TV, Koenig JQ, Mar TF, Fields C, Stewart J, Lippmann M. Associations between health effects and particulate matter and black carbon in subjects with respiratory disease. Environmental Health Perspectives 2005;113(12):1741-1746. |
R827355 (Final) R827355C002 (2004) R827355C002 (Final) R827355C008 (Final) |
|
|
|
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;(13)111:1625-1629. |
R827355 (2004) R827355 (Final) R827355C002 (2002) R827355C002 (Final) R827355C003 (Final) R827355C009 (2003) |
|
|
|
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. |
R827355 (2004) R827355 (Final) R827355C002 (2003) R827355C002 (2004) R827355C002 (Final) R827355C003 (2004) R827355C003 (Final) R827355C009 (Final) |
|
|
|
Mar TF, Norris GA, Koenig JQ, Larson TV. Associations between air pollution and mortality in Phoenix, 1995-1997. Environmental Health Perspectives 2000;108(4):347-353. |
R827355 (2004) R827355 (Final) R827355C002 (1999) R827355C002 (2001) R827355C002 (Final) |
|
|
|
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. |
R827355 (2004) R827355 (Final) R827355C002 (2003) R827355C002 (2004) R827355C002 (Final) |
|
|
|
Mar TF, Jansen K, Shepherd K, Lumley T, Larson TV, Koenig JQ. Exhaled nitric oxide in children with asthma and short-term PM2.5 exposure in Seattle. Environmental Health Perspectives 2005;113(12):1791-1794. |
R827355 (Final) R827355C002 (2004) R827355C002 (Final) |
|
|
|
Mar TF, Koenig JQ, Jansen K, Sullivan J, Kaufman J, Trenga CA, Siahpush SH, Liu L-JS, Neas L. Fine particulate air pollution and cardiorespiratory effects in the elderly. Epidemiology 2005;16(5):681-687. |
R827355 (Final) R827355C002 (2004) R827355C002 (Final) |
|
|
|
Mar TF, Ito K, Koenig JQ, Larson TV, Eatough DJ, Henry RC, Kim E, Laden F, Lall R, Neas L, Stolzel M, Paatero P, Hopke PK, Thurston GD. PM source apportionment and health effects. 3. Investigation of inter-method variations in associations between estimated source contributions of PM2.5 and daily mortality in Phoenix, AZ. Journal of Exposure Science & Environmental Epidemiology 2006;16(4):311-320. |
R827355 (Final) R827355C002 (Final) R827355C008 (Final) R827351 (Final) R827353 (Final) R827353C015 (Final) R827354 (Final) R827354C001 (Final) |
|
|
|
Schildcrout JS, Sheppard L, Lumley T, Slaughter JC, Koenig JQ, Shapiro GG. Ambient air pollution and asthma exacerbations in children: an eight-city analysis. American Journal of Epidemiology 2006;164(6):505-517. |
R827355 (Final) R827355C002 (Final) |
|
|
|
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. |
R827355 (Final) R827355C002 (2003) R827355C002 (Final) R827355C009 (2002) |
|
|
|
Slaughter JC, Koenig JQ, Reinhardt TE. Association between lung function and exposure to smoke among firefighters at prescribed burns. Journal of Occupational and Environmental Hygiene 2004;1(1):45-49. |
R827355 (Final) R827355C002 (2004) R827355C002 (Final) R827355C009 (2003) |
|
|
|
Trenga CA, Sullivan JH, Schildcrout JS, Shepherd KP, Shapiro GG, Liu L-JS, Kaufman JD, Koenig JQ. Effect of particulate air pollution on lung function in adult and pediatric subjects in a Seattle panel study. Chest 2006;129(6):1614-1622. |
R827355 (Final) R827355C002 (Final) R827355C009 (Final) |
|
|
|
Yu O, Sheppard L, Lumley T, Koenig JQ, Shapiro GG. Effects of ambient air pollution on symptoms of asthma in Seattle-area children enrolled in the CAMP study. Environmental Health Perspectives 2000;108(12):1209-1215. |
R827355 (Final) R827355C002 (2001) R827355C002 (Final) |
|
, Air, Geographic Area, Scientific Discipline, Waste, Health, RFA, Susceptibility/Sensitive Population/Genetic Susceptibility, Toxicology, indoor air, Risk Assessments, genetic susceptability, Northwest, Health Risk Assessment, Incineration/Combustion, Epidemiology, air toxics, Biochemistry, particulate matter, Environmental Chemistry, State, aerosols, combustion contaminants, exposure assessment, incineration, risk assessment, California (CA), exposure and effects, environmental hazard exposures, ambient air quality, cardiovascular disease, elderly, health effects, indoor air quality, inhalation, mortality, allergens, air quality, ambient air, cardiopulmonary response, atmospheric aerosols, cardiopulmonary responses, combustion, human health risk, particle exposure, toxics, air pollutants, biostatistics, human health effects, particulates, sensitive populations, ambient particle health effects, air pollution, airway disease, atmospheric chemistry, children, age dependent response, exposure, human susceptibility, ambient aerosol, asthma, health risks, human exposure, Human Health Risk Assessment, morbidity, animal model, particle transport
Progress and Final Reports:
1999 Progress Report
2000 Progress Report
2001 Progress Report
2002 Progress Report
2003 Progress Report
2004 Progress Report
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