Final Report: St. Louis Bus, Steubenville and Atlanta Studies

EPA Grant Number: R827353C003
Subproject: this is subproject number 003 , 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: St. Louis Bus, Steubenville and Atlanta Studies
Investigators: Gold, Diane R. , Adamkiewicz, Gary , Coull, Brent , Dockery, Douglas W. , Dubowsky, S. , Luttmann-Gibson, Heike , Sarnat, Jeremy , Schwartz, Joel , Stone, Peter , Suh, Helen H. , Wheeler, A. , Zanobetti, Antonella
Institution: Harvard T.H. Chan School of Public Health , Harvard University
EPA Project Officer: Chung, Serena
Project Period: June 1, 1999 through May 31, 2005 (Extended to May 31, 2006)
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:

Theme I: Assessing Particle Exposures for Health Effects Studies: A large data set on personal exposures and indoor and outdoor concentrations was collected for panels of susceptible individuals across the US (Sarnat, et al., 2000; Sarnat, et al., 2001; Sarnat, et al., 2002; Koutrakis, et al., 2005). These investigations suggest that personal exposures to PM2.5 of ambient origin are highly correlated with outdoor concentrations. However, the regression slopes of personal exposures on outdoor concentrations, which are usually less than one, vary substantially depending on house characteristics, season, and city climatic conditions. The strong correlations between personal and ambient concentrations were unique to PM2.5, as personal exposures to O3, SO2 and NO2 were substantially lower than, and weakly correlated with, corresponding outdoor concentrations (Sarnat, et al., 2005).

The primary focus of Theme I was to assess human exposures to particles and gaseous co-pollutants in order to better understand their heath effects. As such, research conducted as part of Theme I contained five main objectives:

  1. to characterize the inter- and intra- variability in personal particulate and gaseous exposures;
  2. to identify factors affecting the relationship between personal exposures and outdoor levels;
  3. to determine the contribution of outdoor and indoor particles to personal particulate exposures;
  4. to quantify the effect of measurement error for fine particles and their co-pollutants (coarse mass and the criteria gases) on risk estimates from epidemiological studies; and
  5. to differentiate the health effects of particles from outdoor and indoor sources.

These objectives were addressed by three inter-related research projects, which made use of our database of personal, indoor, and outdoor particulate and gaseous exposures.

The St. Louis Bus Study
Investigators: H. Suh, G. Adamkiewicz, S. Dubowsky, D. Gold, S. Sarnat

Objective(s) of the Research Project: As part of Theme 1, we conducted a particle exposure and health effects study that specifically focused on the health effects of traffic-related pollutant exposures. This study examined the effects of ambient and traffic related pollution on intermediate cardiovascular and inflammatory health markers, including heart rate variability (HRV), systemic inflammation and pulmonary inflammation. The field study was conducted in St. Louis, MO during Spring 2002. We monitored the cardiovascular health of 44 individuals living in retirement facilities in metropolitan St. Louis, MO as they traveled on field trips aboard a diesel-powered bus. Markers of altered cardiovascular function including heart rate variability, heart rate, inflammatory indicators in the blood, and oxygen saturation of the blood were measured for participants during four separate 24-hr periods as the individuals traveled between the health testing room, a moving shuttle bus, indoor locations within the city, and his or her senior residence facility. Micro-environmental PM2.5, black carbon (BC) and fine particle count (PC0.3-1.0) exposures were assessed continuously for the study participants using two portable monitoring carts that traveled with the study participants throughout the day. The Environmental Protection Agency (EPA)-funded St. Louis Super Site served as the stationary ambient monitoring (SAM) site for measuring ambient concentrations.

Summary of Findings:

Particle Exposures

As shown in Figure 1, personal exposures to PM2.5, BC and PC0.3-1.0 were significantly higher when participants were aboard the diesel-powered shuttle bus as compared to when they were in their residence facilities (p<0.001). Exposures were the most elevated for BC. It can be assumed that elevated exposures during bus trips were attributed to emissions from surrounding vehicles and the shuttle bus, since mean concentrations at the SAM site during the bus and facility periods were comparable.

Figure 1. Hourly Micro-Environmental and Ambient PM[2.5] Concentrations.

Figure 1. Hourly Micro-Environmental and BC Concentrations.

Figure 1. Hourly Micro-Environmental and Ambient PM2.5 and BC Concentrations. Microenvironmental PM2.5 (left) and BC (right) exposures were measured as participants traveled on a field trip via two bus rides and spent time in their residence facility. Micro-environmental exposures are shown in black; ambient concentrations are shown in grey. Exposures and concentrations were averaged by hour.

Heart Rate Variability

Exposure to airborne particles may increase cardiac risk by altering autonomic balance. As these risks may be particularly great for traffic-related particles, we examined associations between particles and heart rate variability for 44 subjects who participated in four repeated trips aboard a diesel bus. Twenty-four hour electrocardiograms were correlated with continuous particle concentrations using generalized additive models controlled for subject, weekday, time, apparent temperature, trip type, activity, medications, and autoregressive terms. Associations were assessed for short and medium-term mean concentrations.

Heart rate variability was significantly and negatively associated with fine particulate matter. Significant positive associations were demonstrated with heart rate and the low to high frequency power ratio. Associations were strongest with 24-hour mean concentrations although strong and significant short-term associations also were found during bus periods, independent of daily exposures. Overall, associations were largest for high frequency power with 16 (95% confidence interval [CI]: -17, –15), 19 (95% CI: -22, –17), and 14 (95% CI: -16, –13) percent decreases per inter-quartile changes in the 24-hour PM2.5 (4.6 μg/m3), black carbon (458 ng/m3), and fine particle count (39 pt/cm3) concentrations, respectively. Eleven percent (95% CI: -13.6, –7.8) decreases in high frequency power were predicted per inter-quartile change in the 5-minute PM2.5 (10 μg/m3) aboard the bus. This investigation indicates that fine particles are negatively associated with heart rate variability, with an overall trend towards reduced parasympathetic tone. While daily associations were evident for all particles, short-term associations were predominantly limited to bus periods and possibly fresh traffic-related particles. These findings were published in Epidemiology (Adar, et al., 2007b).

Systemic Inflammation

Inflammation may represent a pathway through which airborne particles lead to increased cardiac risk. Therefore, we investigated associations between ambient particles and acute systemic inflammation among repeated measures of 44 seniors and examined susceptibility by conditions linked to chronic inflammation. Mixed models were used to identify associations between fine particle concentrations (PM2.5) averaged over 1 to 7 days and measures of C-reactive protein (CRP), interleukin-6 (IL-6), and white blood cell counts (WBC). Effect modification was investigated for diabetes, obesity, hypertension, and elevated mean inflammatory markers.

Positive associations were consistently found between ambient PM2.5 and WBC across all participants, with an 11% (95% CI: 0.19 to 22%) increase per 10 μg/m3 increase in PM2.5 averaged over the previous week. PM2.5 and CRP also exhibited positive associations among all individuals for averaging periods longer than 1 day with the strongest associations for persons with diabetes, obesity, and hypertension. For example, a 10 μg/m3 increase in the 5 day mean PM2.5 was associated with a 24% increase in CRP (95% CI: -8.8 to 67%) for all individuals and a 170% (95% CI: 36 to 420%) increase for persons with diabetes, obesity, and hypertension. Persons with diabetes, obesity, and hypertension also exhibited positive associations between PM2.5 and IL-6. Individuals with elevated mean inflammatory markers exhibited enhanced responsiveness for CRP, IL-6, and WBC. This investigation demonstrates that air pollution is positively associated with acute systemic inflammation and indicates enhanced sensitivity for individuals with diabetes, obesity, hypertension, and elevated mean inflammatory markers. These findings were published in Environmental Health Perspectives (Dubowsky, et al., 2006).

Pulmonary Inflammation

Airborne particles have been linked to pulmonary oxidative stress and inflammation. As these effects may be particularly great for traffic-related particles, we examined associations between particle exposures and exhaled nitric oxide (eNO), a marker of pulmonary inflammation. Samples of eNO collected before and after the trips were correlated with micro-environmental and ambient particle concentrations using mixed models controlled for subject, day, trip, vitamins, collection device, mold, pollen, room air nitric oxide, apparent temperature, and time to analysis. While ambient concentrations were collected at a fixed location, continuous group-level personal samples characterized micro-environmental exposures throughout facility and trip periods. Findings from this analysis have been published in Environmental Health Perspectives (Adar, et al., 2007a).

Briefly, we found eNO concentrations collected prior to participation in a bus trip to be significantly associated with PM2.5 and PC0.3-1.0 averaged over the previous 24-hrs. For example, an inter-quartile increase in the 24-hr mean ambient PM2.5 of 10 μg/m3 resulted in a 15% (95% CI: 6–26%) increase in eNO using linear models adjusted for day of week, ambient apparent temperature, past nitrate consumption, recent meal, time between sample collection and analysis, study room nitric oxide (NO) concentrations, and a random subject effect. A similar increase for personal PM2.5 (as measured by the portable monitoring carts inside the facility) corresponded to a 20% (95% CI: 1–43%) increase in eNO, while an inter-quartile range (IQR) change in PC0.3-1.0 of about 70 pt/cc resulted in 30% increase in eNO (95% CI: 1–43%). Changes in BC, carbon monoxide (CO), NO, and NO2 were not significantly associated with deviations in eNO at the 95% confidence level.

On the day following the bus trip, we found similar effect estimates for measures of micro-environmental PM2.5 (20%, CI: 6–35%) and PC0.3-1.0 (23%, CI: 8–40%) when identical models were used. While ambient PM2.5 was predictive of eNO when participants were at their living facilities for the previous 24-hr, ambient PM2.5 was not predictive of eNO when the same individuals took part in a field trip that included two hours on the highway. While the gases remained non-predictive of post-trip eNO, BC became a significant predictor of eNO (20%, CI: 2–40%) for samples collected on the days after the bus trips. Data suggest that elevated exposures to traffic-related particles result in increased pulmonary inflammation as measured by eNO. Future findings will refine our analyses of the effects of motor vehicle exposures on eNO and determine whether autonomic effects such as HRV, ST-segment depression, and arrhythmias are also associated with motor vehicle exposures, as this was shown in a previous Center publication (Gold, et al., 2005).

Conclusions

These results suggest that air pollution exposures are associated with systemic inflammation among seniors having at least one symptom of metabolic syndrome, suggesting pollution impacts for a large proportion of the elderly in the U.S. (approximately 33% with obesity and 50% with hypertension). Inflammation associated with air pollution appears to occur acutely, with most effects within the first day of exposure.

This investigation also indicates that fine particles are negatively associated with heart rate variability with an overall trend towards reduced parasympathetic tone. While daily associations were evident for all particles, short-term associations were predominantly limited to traffic-related particles.

Steubenville
Investigators: D. Gold, H. Suh, B. Coull, D. Dockery, H. Luttmann-Gibson, S. Sarnat, J. Schwartz, P. Stone

Objective(s) of the Research Project: We conducted a particle exposure and health effects study in Steubenville, OH (Sarnat, et al., 2006). This field study included weekly measurement of thirty-two non-smoking older adults for 24 weeks during Summer and Fall 2000. Continuous electrocardiogram (ECG) measurements were made for each subject using a standardized 30 minute protocol. A central ambient monitoring station provided daily concentrations of PM2.5, sulfate, elemental carbon (EC), and gases.

Analysis of these results focused on: (1) the potential effects of particulate matter and gases on autonomic nervous system dysfunction and inflammation, potential pathways by which particles affect cardiac rate and rhythm; and (2) the potential effects of these pollutants on the parasympathetic and sympathetic nervous systems. For the first area of research, published by Sarnat, et al. (2006), the two primary health outcomes were supraventricular ectopy (SVE), defined as extra cardiac depolarizations within the atria, and ventricular ectopy (VE) or extra depolarizations in the ventricles. For the second area of research (Luttmann-Gibson, et al., 2006), the effects of the pollutants on various measures of HRV were assessed. These HRV measures included: (1) the standard deviation of normal R-R intervals in the ECG (SDNN); (2) the mean square of differences between adjacent RR intervals in the ECG (r-RMSSD); (3) high frequency (HF) power; and (4) low frequency (LF) power.

In addition, we measured the fraction of exhaled nitric oxide (FENO) in the study subjects’ breath to evaluate the potential association with air pollution levels, as this metric is a non-invasive measure of airway inflammation (Adamkiewicz, et al., 2004).

Summary of Findings: Participant specific mean counts of arrhythmia over the protocol varied between 0.1–363 for SVE and 0–350 for VE. The authors observed odds ratios for having SVE over the length of the protocol of 1.42 (95% CI 0.99 to 2.04), 1.70 (95% CI 1.12 to 2.57), and 1.78 (95% CI 0.95 to 3.35) for 10.0 μg/m3, 4.2 μg/m3, and 14.9 ppb increases in five day moving average PM2.5, sulfate and ozone concentrations, respectively. The other pollutants, including elemental carbon, showed no effect on arrhythmia. Participants reporting cardiovascular conditions (for example, previous myocardial infarction (MI) or hypertension) were the most susceptible to pollution induced SVE. The authors found no association of pollution with VE.

In a community with significant industrial sources for air pollution, our study demonstrated an association of particle pollution with increased odds of supraventricular arrhythmia in a cohort of older adults, with findings of 42%, 70%, and 78% increases in odds of SVE associated with IQR increases in five day moving average PM2.5, sulfate and ozone, respectively. Air pollution effects were greatest for participants with a history of clinically significant cardiac disease. Since two pollutant models demonstrated stability in the effects of both particles and ozone, collectively our results may provide evidence of the combined effect of the secondary pollutant mix in Steubenville on cardiac arrhythmia. Specifically, the strong effects found with sulfate are interesting as Steubenville is located in an industrial area of the Ohio River Valley, with little traffic but with a number of coal-fired power plants, which are the major source of SO2, a sulfate precursor. It is important to note that ambient sulfate concentrations were measured with higher overall precision, and further, that ambient sulfate concentrations were better proxies of corresponding personal exposures as compared to EC. Both factors may have resulted in sufficient power to detect associations between arrhythmia and ambient concentrations of sulfate. A previous study conducted in Boston, reporting on patients with implantable cardioverter defibrillators, found that traffic related pollutants, particularly NO2, showed the greatest odds of arrhythmia (Peters, et al., 2000). Our data suggest that pollution in an industrial location may also contribute to the risk of arrhythmia, and they indicate the potential for varying impacts of air pollution by geographical location and source contributions.

The second paper found significant reductions in HRV measures associated with increased PM2.5 and sulfate, but no significant reductions in HRV associated with EC, NO2, SO2 or O3 levels. An IQR increase in sulfate of approximately 5 μg/m3 resulted in decreases of 3.3% for SDNN, 5.6% for r-RMSSD and 10.3% for HF with similar results for PM2.5.

In addition, an increase in the 24 hour average PM2.5 concentration of 17.7 μg/m3 was associated with an increase in FENO of 1.45 ppb (95% CI 0.33 to 2.57) in models adjusted for subject, week of study, day of the week, hour of the day, ambient barometric pressure, temperature, and relative humidity. This represents a change of approximately 15% compared with the mean FENO in the cohort (9.9 ppb). The associations between FENO and PM2.5 were significantly higher in subjects with a doctor’s diagnosis of chronic obstructive pulmonary disease (COPD) (p value for interaction = 0.03).

Conclusions

Our results suggest that increased levels of ambient air pollution, particularly for regional pollutants, including sulfate and ozone, may increase the risk of supraventricular arrhythmia in the elderly. The highest and most significant effects were found for greater than five day moving average concentrations before the health assessment, which may suggest that a long acting mechanism promoted the ectopic beats in our population. Furthermore, the results suggest that individuals with a history of clinically significant cardiac disease may be at particular risk of air pollution health effects. Additional analysis found that increased levels of sulfate and PM2.5 may adversely affect autonomic nervous system function, resulting in significant cardiac effects. Ambient pollution may also lead to airway inflammation as measured by FENO. These subclinical inflammatory changes may be an important step in the pathogenesis of the cardiopulmonary effects induced by exposure to air pollution.

Atlanta
Investigators: D. Gold, H. Suh, J. Schwartz, P. Stone, A. Wheeler, A. Zanobetti

Objective(s) of the Research Project: Associations between concentrations of PM2.5 and HRV have differed by study population. Results from previous studies suggested that compromised autonomic control of the heart may play a role in the acute cardiovascular toxicity of particles but that this role may differ with the underlying health status of the individual. The impact of health status on the relationship between HRV and ambient PM had not been examined directly, with previous panel studies including participants of only one susceptible disease group. To examine this issue more directly, we conducted a study to evaluate associations between ambient PM2.5 and HRV for sensitive individuals (Wheeler, et al., 2006). We then examined whether these associations differed for individuals with preexisting pulmonary disease compared to those with cardiovascular disease.

We examined the effects of ambient pollution on HRV for 18 individuals with COPD and 12 individuals with recent MI living in Atlanta, Georgia. HRV, baseline pulmonary function and medication data were collected for each participant during 7 days in fall 1999 and/or spring 2000. Hourly ambient pollution concentrations were obtained from monitoring sites in Atlanta. The association between ambient pollution and HRV was examined using linear mixed-effect models. The primary time domain HRV measures presented here include: (1) the standard deviation of normal R-R intervals in the ECG (SDNN); and (2) the square root of the mean of the sum of squares of differences between adjacent NN intervals in the ECG (RMSSD).

Summary of Findings: Ambient pollution had opposing effects on HRV in our COPD and MI participants, resulting in no significant effect of ambient pollution on HRV in the entire population for 1-, 4-, or 24-hr moving averages. Findings from our study provide direct evidence of heterogeneity in the autonomic response to ambient pollution that is dependent on the underlying health status of the study population. Changes in HRV were significantly and positively associated with ambient PM2.5 concentrations for individuals with COPD. Although not statistically significant, observed associations were consistently negative for individuals with recent MI. Further support that the HRV response to ambient PM2.5 differs for individuals with MI and COPD was provided by the fact that we found comparable effect estimates, with significant differences between disease groups, using models that included an interaction term between pollution and disease status. Associations with ambient PM2.5 were strongest for the 4-hr moving average and for SDNN an overall measure of HRV, although consistent trends with disease status were observed for other moving averages and other HRV measures. We also observed strong and significant associations with SDNN by disease group with ambient NO2, and to a lesser extent with ambient EC. Because ambient NO2 and EC originate primarily from motor vehicles, our findings suggest that motor vehicle-related pollution may be partly responsible for the observed effects of ambient particles on HRV.

The effect of medication use, respiratory rate, baseline pulmonary function (based on FEV1), air conditioning use, exercise during HRV measurement, body mass index, age, and heart rate on the association between 4-hr ambient pollution and overall SDNN was examined to determine whether these factors was responsible for the differences in response between the disease groups. Of these, medication use and baseline FEV1 were found to be significant effect modifiers for 4-hr PM2.5 and NO2 concentrations, with results comparable for the two pollutants. Similar effect modification by medication use and baseline pulmonary function was also found for EC but with smaller effect sizes.

Conclusions

Findings from our study provide direct evidence of heterogeneity in the autonomic response to ambient pollution that is dependent on the underlying health status of the study population. Changes in HRV were significantly and positively associated with ambient PM2.5 concentrations for individuals with COPD. Although not statistically significant, observed associations were consistently negative for individuals with recent MI.

References:

Adamkiewicz G, Ebelt S, Syring M, Slater J, Speizer FE, Schwartz J, Suh H, Gold DR. Association between air pollution exposure and exhaled nitric oxide in an elderly population. Thorax 2004;59(3):204-209.

Adar SD, Adamkiewicz G, Gold DR, Schwartz J, Coull BA, Suh H. Ambient and microenvironmental particles and exhaled nitric oxide before and after a group bus trip. Environmental Health Perspectives 2007a ;115(4):507-512.

Adar S, Gold DR, Coull BA, Schwartz J, Stone P, Suh HH. Focused exposures to airborne traffic particles and heart rate variability in the elderly. Epidemiology 2007b;18(1):95-103.

Dubowsky SD, Suh H, Schwartz J, Coull BA, Gold DR. Diabetes, obesity, and hypertension may enhance associations between air pollution and markers of systemic inflammation. Environmental Health Perspectives 2006;114(7):992-998.

Gold DR, Litonjua AA, Zanobetti A, Coull BA, Schwartz J, MacCallum G, Verrier RL, Nearing BD, Canner MJ, Suh H, Stone PH. Air pollution and ST-segment depression in elderly subjects. Environmental Health Perspectives 2005;113(7):883-887.

Koutrakis P, Suh H, Sarnat J, Brown K, Coull B, Schwartz J. Characterization of particulate and gas exposures of sensitive subpopulations living in Baltimore and Boston. Health Effects Institute, Research Report. Health Effects Institute, Boston, MA, 2005.

Luttman-Gibson H, Suh HH, Coull BA, Dockery DW, Sarnat SE, Schwartz J, Stone PH, Gold DR. Short-term effects of air pollution on heart rate variability in senior adults in Steubenville, OH. Journal of Occupational and Environmental Medicine 2006;48(8):780-788.

Peters A, Liu E, Verrier R, Schwartz J, Gold D, Mittleman M, Baliff J, Oh J, Allen G, Monahan K, Dockery D. Air pollution and incidence of cardiac arrhythmia. Epidemiology 2000;11(1):11-17.

Sarnat JA, Brown KW, Schwartz J, Coull BA, Koutrakis P. Ambient gas concentrations and personal particulate matter exposures: implications for studying the health effects of particles. Epidemiology 2005;16(3):385-395.

Sarnat JA, Koutrakis P, Suh H. Assessing the relationship between personal particulate and gaseous exposures of senior citizens living in Baltimore. Journal of the Air and Waste Management Association 2000;50(7):1184-1198.

Sarnat JA, Long CM, Koutrakis P, Coull BA, Schwartz J, Suh HH. Using sulfur as a tracer of outdoor fine particulate matter. Environmental Science & Technology 2002;36(24):5305-5314.

Sarnat JA, Schwartz J, Catalano P, Suh H. Gaseous pollutants in particulate matter epidemiology: confounders or surrogates? Environmental Health Perspectives 2001;109(10):1053-1061.

Sarnat SE, Suh HH, Coull BA, Schwartz J, Stone PH, Gold DR. Ambient particulate air pollution and cardiac arrhythmia in a panel of older adults in Steubenville, Ohio. Occupational and Environmental Medicine 2006;63(10):700-706.

Wheeler A, Zanobetti A, Gold DR, Schwartz J, Stone P, Suh HH. The relationship between ambient air pollution and heart rate variability (HRV) differs for individuals with heart and pulmonary disease. Environmental Health Perspectives 2006;114(4):560-566.


Journal Articles on this Report : 8 Displayed | Download in RIS Format

Other subproject views: All 8 publications 8 publications in selected types All 8 journal articles
Other center views: All 200 publications 198 publications in selected types All 197 journal articles
Type Citation Sub Project Document Sources
Journal Article Adamkiewicz G, Ebelt S, Syring M, Slater J, Speizer FE, Schwartz J, Suh H, Gold DR. Association between air pollution exposure and exhaled nitric oxide in an elderly population. Thorax 2004;59(3):204-209. R827353 (Final)
R827353C003 (Final)
R826780 (Final)
  • Full-text from PubMed
  • Abstract from PubMed
  • Associated PubMed link
  • Full-text: Thorax-Full Text HTML
    Exit
  • Abstract: Thorax-Abstract
    Exit
  • Other: Thorax-Full Text PDF
    Exit
  • Journal Article Adar SD, Adamkiewicz G, Gold DR, Schwartz J, Coull B A, Suh H. Ambient and microenvironmental particles and exhaled nitric oxide before and after a group bus trip. Environmental Health Perspectives 2007;115(4):507-512. R827353 (Final)
    R827353C003 (Final)
  • Full-text from PubMed
  • Abstract from PubMed
  • Associated PubMed link
  • Journal Article Adar SD, Gold DR, Coull BA, Schwartz J, Stone PH, Suh H. Focused exposures to airborne traffic particles and heart rate variability in the elderly. Epidemiology 2007;18(1):95-103. R827353 (Final)
    R827353C003 (Final)
  • Abstract from PubMed
  • Full-text: Epidemiology-Full Text HTML
    Exit
  • Abstract: Epidemiology-Abstract
    Exit
  • Other: Epidemiology-Full Text PDF
    Exit
  • Journal Article Dubowsky SD, Suh H, Schwartz J, Coull BA, Gold DR. Diabetes, obesity, and hypertension may enhance associations between air pollution and markers of systemic inflammation. Environmental Health Perspectives 2006;114(7):992-998. R827353 (Final)
    R827353C003 (Final)
  • Full-text from PubMed
  • Abstract from PubMed
  • Associated PubMed link
  • Full-text: Harvard-Full Text PDF
    Exit
  • Journal Article Gold DR, Litonjua AA, Zanobetti A, Coull BA, Schwartz J, MacCallum G, Verrier RL, Nearing BD, Canner MJ, Suh H, Stone PH. Air pollution and ST-segment depression in elderly subjects. Environmental Health Perspectives 2005;113(7):883-887. R827353 (Final)
    R827353C003 (Final)
    R826780 (Final)
  • Full-text from PubMed
  • Abstract from PubMed
  • Associated PubMed link
  • Journal Article Luttmann-Gibson H, Suh HH, Coull BA, Dockery DW, Sarnat SE, Schwartz J, Stone PH, Gold DR. Short-term effects of air pollution on heart rate variability in senior adults in Steubenville, Ohio. Journal of Occupational and Environmental Medicine 2006;48(8):780-788. R827353 (Final)
    R827353C003 (Final)
    R826780 (Final)
    R832416 (2008)
  • Abstract from PubMed
  • Full-text: ResearchGate-Abstract and Full Text
    Exit
  • Abstract: JOEM-Abstract
    Exit
  • Other: ResearchGate-Full Text PDF
    Exit
  • Journal Article Sarnat SE, Suh HH, Coull BA, Schwartz J, Stone PH, Gold DR. Ambient particulate air pollution and cardiac arrhythmia in a panel of older adults in Steubenville, Ohio. Occupational and Environmental Medicine 2006;63(10):700-706. R827353 (Final)
    R827353C003 (Final)
    R826780 (Final)
    R832416 (2008)
    R834797 (2016)
  • Full-text from PubMed
  • Abstract from PubMed
  • Associated PubMed link
  • Full-text: BioMed Central-Full Text HTML
    Exit
  • Abstract: OEM-Abstract
    Exit
  • Other: BioMed Central-Full Text PDF
    Exit
  • Journal Article Wheeler A, Zanobetti A, Gold DR, Schwartz J, Stone P, Suh HH. The relationship between ambient air pollution and heart rate variability differs for individuals with heart and pulmonary disease. Environmental Health Perspectives 2006;114(4):560-566. R827353 (Final)
    R827353C003 (Final)
    R832416 (2008)
  • Full-text from PubMed
  • Abstract from PubMed
  • Associated PubMed link
  • Supplemental Keywords:

    RFA, Health, Scientific Discipline, Air, particulate matter, Toxicology, air toxics, Environmental Chemistry, Epidemiology, Risk Assessments, Susceptibility/Sensitive Population/Genetic Susceptibility, indoor air, genetic susceptability, tropospheric ozone, Biology, ambient air quality, health effects, monitoring, risk assessment, sensitive populations, particulates, chemical exposure, interindividual variability, molecular epidemiology, air pollutants, exposure and effects, stratospheric ozone, ambient air monitoring, health risks, cardiopulmonary responses, indoor exposure, human health effects, ambient air, developmental effects, epidemelogy, respiratory disease, exposure, pulmonary disease, ambient measurement methods, ambient monitoring, air pollution, particle exposure, biological mechanism , Human Health Risk Assessment, human exposure, inhalation, pulmonary, ambient particle health effects, cardiopulmonary response, particulate exposure, inhaled, inhalation toxicology, human susceptibility, differentiating outdoor and indoor sources, atmospheric monitoring, cardiopulmonary, human health, indoor air quality, inhaled particles, measurement methods , metals, respiratory, genetic susceptibility, air quality, dosimetry, cardiovascular disease, human health risk

    Relevant Websites:

    http://www.hsph.harvard.edu/epacenter/epa_center_99-05/index.html Exit

    Progress and Final Reports:

    Original Abstract
  • 1999 Progress Report
  • 2000 Progress Report
  • 2001 Progress Report
  • 2002 Progress Report
  • 2003 Progress Report
  • 2004 Progress 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