2004 Progress Report: Health Effects

EPA 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. , Lippmann, Morton , Larson, Timothy V. , Jansen, Karen , Shepherd, Kristine , Allen, Ryan , Mar, Therese , Lumley, Thomas
Current Investigators: Koenig, Jane Q. , Lippmann, Morton , Sheppard, Lianne (Elizabeth) A. , Larson, Timothy V. , Jansen, Karen , Allen, Ryan , Mar, Therese , Lumley, Thomas
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, 2004 through May 31, 2005
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

Objective:

The objective of this research project is to identify health outcomes that are associated with particulate matter (PM) exposures. Our studies are restricted primarily to the Greater Seattle airshed. Our data come from a large 2-3 year panel study, our Year 4 panel study in collaboration with New York University (NYU), and measurements of fine aerosols in Seattle.

Progress Summary:

Project 2a-1. Pulmonary Effects of Indoor- and Outdoor-Generated Particles in Children With Asthma

The majority of PM health effects studies use outdoor (ambient) PM as a surrogate for personal exposure. People spend the majority of their time, however, 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 associated significantly 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 associated consistently with increases in FeNO and the indoor-generated component is associated less strongly with exhaled nitric oxide (eNO).

Project 2a-2 Exhaled Nitric Oxide in Children With Asthma and Short-Term PM Exposure in Seattle

The objective of this study was to evaluate associations between short-term (hourly) exposures to PM and eNO 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 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.

Project 2a-3. 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 1,179 person-days of arterial oxygen saturation and heart rate data and 1,029 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 found primarily 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.

Project 2a-4. 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 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 PM 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, Washington, a semi-arid city with diverse sources of PM, 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. No association, however, 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.

Project 2a-5. HEPA Intervention Study

Exposure to PM2.5 is associated with an increase in 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 chronic obstructive pulmonary disease (COPD), monitored in their homes for 1 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 4 days. The device fan operated at all times 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 (RH), and temperature. The HEPA filters reduced the indoor levels of PM2.5 by 2.6 mg/m3 and the average indoor/outdoor ratio from 0.172 to 0.030 in three of the five homes. For all subjects, a 10 mg/m3 increase in 24-hour average outdoor PM2.5 was associated with a 1.6 ppb increase in FeNO (95% CI: 0.51, 2.61). There was, however, 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.

Project 2a-6. Association Between Health Effects and PM and Black Carbon

eNO, 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 COPD in Seattle. Data were collected daily for 12 days. PM10 and PM2.5 filter samples were collected simultaneously at a central outdoor site, as well as outside and inside the subject’s home. Personal PM10 filter samples also were 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 RH, 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 eNO respectively. A 1 µg/m3 increase in outdoor, indoor, and personal light absorbing carbon (LAC) was associated with increases in eNO 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 eNO 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.

2a-7. Managed Campfire Study

Measurements of eNO and breath condensate were collected from 10 subjects participating in a managed camp fire exposure study (see the Annual Report for R827355C010). No associations between fine PM and FeNO were seen. Breath condensate samples still need to be analyzed.

Conclusions

We can conclude that ambient PM concentrations in Seattle are associated with asthma aggravation as measured by eNO. This is true for children with asthma and now has been replicated in adults with asthma. Also, eNO is a very useful, noninvasive 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-eNO measurement. We still hope to be able to use XRF and levoglucosan 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.

Future Activities:

The work that will be completed during the final year includes: (1) analyses of interactions with gene variants that are available from buccal cell samples collected from most panel subjects; (2) an analysis of short term lags between eNO data and PM in adult subjects in the Year 4 panel; (3) an analysis of the relationship between eNO and estimated indoor- and ambient-generated PM2.5 in the Year 4 panel study; and 4) completion of a longitudinal study of mortality and air pollution in Seattle from 1968 through 1995.


Journal Articles on this Report : 6 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
Type Citation Sub Project Document Sources
Journal Article 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)
R827353 (Final)
  • Full-text from PubMed
  • Abstract from PubMed
  • Associated PubMed link
  • Full-text: ResearchGate - Abstract & Full Text PDF
    Exit
  • Journal Article 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)
  • Full-text from PubMed
  • Abstract from PubMed
  • Associated PubMed link
  • Full-text: ResearchGate - Abstract & Full Text PDF
    Exit
  • Journal Article 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)
  • Abstract from PubMed
  • Abstract: Taylor and Francis-Abstract
    Exit
  • Journal Article 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)
  • Full-text from PubMed
  • Abstract from PubMed
  • Associated PubMed link
  • Full-text: EHP-Full Text HTML
    Exit
  • Other: EHP-Full Text PDF
    Exit
  • Journal Article Mar TF, Koenig JQ, Jansen K, Sullivan J, Kaufman J, Trenga CA, Siahpush SH, Liu LJ, Neas L. Fine particulate air pollution and cardiorespiratory effects in the elderly. Epidemiology 2005;16(5):681-687. R827355 (Final)
    R827355C002 (2004)
    R827355C002 (Final)
  • Abstract from PubMed
  • Full-text: LWW-Full Text HTML
    Exit
  • Abstract: LWW-Abstract
    Exit
  • Other: LWW-Full Text PDF
    Exit
  • Journal Article 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)
  • Abstract from PubMed
  • Abstract: Taylor and Francis-Abstract
    Exit
  • 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, polycyclic aromatic 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, ambient aerosol, ambient air quality, asthma, biostatistics, health effects, particulates, risk assessment, sensitive populations, air pollutants, cardiopulmonary responses, health risks, human health effects, morbidity, exposure and effects, airway disease, ambient air, exposure, animal model, combustion emissions, air pollution, children, Human Health Risk Assessment, particle exposure, cardiopulmonary response, human exposure, inhalation, atmospheric aerosols, ambient particle health effects, combustion, elderly, human susceptibility, incineration, indoor air quality, mortality, California (CA), allergens, age dependent response, aerosols, air quality, atmospheric chemistry, cardiovascular disease, combustion contaminants, exposure assessment, human health risk, particle transport, toxics

    Relevant Websites:

    http://depts.washington.edu/pmcenter/ Exit

    Progress and Final Reports:

    Original Abstract
  • 1999 Progress Report
  • 2000 Progress Report
  • 2001 Progress Report
  • 2002 Progress Report
  • 2003 Progress Report
  • Final Report

  • 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