Previous Project

DEPS: "Diabetes and the Environment Panel Study in Chapel Hill, North Carolina, USA"

A cooperation project between Helmholtz Zentrum München Institute of Epidemiology II and U.S. Environmental Protection Agency (U.S. EPA, Chapel Hill, North Carolina)

Study objective:
The primary hypothesis of the study is: exposure of subjects with type 2 diabetes to increased ambient air pollutants results in further impairment of endothelial function as measured by changes in flow-mediated dilatation during brachial artery ultrasound.
The secondary hypotheses are: Exposure of these subjects to ambient air pollutants results in altered cardiac autonomic balance and pulmonary and systemic inflammation.

Specific aims:
Determine the association between fine particulate matter (PM2.5) and its components and changes in health effect parameters which provide information about responses by the immune, vascular, cardiac, hematologic and autonomic nervous systems. These include changes in:

  • vascular reactivity as assessed by measures of endothelium-dependent flow-mediated arterial dilatation
  • serum levels of pro-inflammatory proteins, coagulation proteins and acute phase reactants
  • peripheral blood red cell and white cell indices
  • markers of cellular activation as assessed by flow-cytometry
  • heart rate variability, frequency and complexity of ectopic heart beats, T wave measures and measures of repolarization

Moreover, the study aims to evaluate synergistic effects between air temperature and PM2.5, the effects of personally measured and modeled air pollution exposure as well as the effects of PM components.

Study design:
Epidemiological panel study with four repeated measurements per participant.

Study population:
22 non-smoking subjects with type 2 diabetes within a 30 mile radius of air monitoring stations in Chapel-Hill/Durham/Raleigh, North Carolina, USA.

Study area:
Chapel-Hill/Durham/Raleigh area, North Carolina, USA;
Clinical exam site: Environmental Public Health Division (EPHD) of Environmental Protection Agency (EPA) National Health and Environmental Effects Research Laboratory (NHEERL) in Chapel Hill, North Carolina, USA.

Study methods:
Exposure assessment:

  • Daily 24-hour concentrations (midnight – midnight) of official ambient PM2.5 mass network data (particles with aerodynamique diameter < 2.5µm) were obtained from a monitoring station located approximately 44km (27 miles) east of the EPHD.
  • Concentrations of ambient PM2.5 mass (9AM – 9AM) data were measured on the EPHD rooftop approximately 30 meters above ground level.
  •  PM2.5-components: Filter extraction of water-soluble and acid-soluble components and XRF-analysis of filters.
  • Concentrations of subject-specific PM2.5 mass (9AM – 9AM) data were measured by personal PM2.5 monitors.
  • Continuous 2-minute measurements of air temperature, barometric pressure and relative humidity were obtained from the EPAD rooftop.

Health outcome:

Health assessment via clinical examinations including:

  • Interview
  • Diary
  • Brachial artery ultrasound
  • Pulse waveform measures
  • Blood withdrawal
  • 10 minutes-ECG and 24 hour-ECG

Statistical Methods:
Mixed models with random patient intercept

Study period:
November 2004 to December 2005

Current status:
Analyses ongoing;
Field work ended December 2005.

Environmental Protection Agency–EPHD: Robert B. Devlin (PI);
University of North Carolina, School of Medicine, Chapel Hill, North Carolina: Alan Hinderliter (Co-PI) and John Buse (Co-PI).

The study was funded through a U.S. Environmental Protection Agency cooperative agreement CR83346301 with the Center for Environmental Medicine, Asthma and Lung Biology at the University of North Carolina at Chapel Hill. The analysis was performed in cooperation with the Helmholtz Zentrum München - German Research Center for Environmental Health and partly funded by the Rochester Particle Center (grant RD832415). The study was supported in part by a grant (RR00046) from the General Clinical Research Centers program of the Division of Research Resources, National Institutes of Health. Moreover, this study was supported by a grant from the German Federal Ministry of Education and Research (BMBF) to the German Center for Diabetes Research (DZD e.V.). Analysis and paper preparation were funded by a contract between the U.S. EPA and Dr. Alexandra Schneider.

Related publications:

  • Schneider A, Neas L, Herbst MC, Case M, Williams RW, Cascio W, Hinterliter A, Holguin F, Buse JB, Dungan K, Styner M, Peters A, Devlin RB (2008): Endothelial Dysfunction: Associations with Exposure to Ambient Fine Particles in Diabetic Individuals. Environ HealthPerspect, 116(12): 1666-1674

  • Schneider A, Neas LM, Graff DW, Herbst MC, Cascio WE, Schmitt MT, Buse JB, Peters A, Devlin RB (2010): Association of cardiac and vascular changes with ambient PM2.5 in diabetic individuals. Part Fibre Toxicol. 2010 Jun 2;7:14

  • Schneider A, Alexis N, Diaz-Sanchez D, Neas LM, Harder S, Herbst MC, Cascio WE, Peters A, Devlin RB. 2011. Ambient PM2.5-exposure up-regulates the expression of co-stimulatory molecules on monocytes in diabetic individuals. Environ Health Perspect 119(6): 778-783.

  • Lanzinger S, Breitner S, Neas L. Cascio W, Diaz-Sanchez D, Hinderliter A, Peters A, Devlin RB, Schneider A (2014).The impact of decreases in air temperature and increases in ozone on markers of endothelial function in individuals having type-2 diabetes. Environ Res, 134C: 331-338.

  • Breen MS, Long TC, Schultz BD, Williams RW, Richmond-Bryant J, Breen M, Langstaff JE, Devlin RB, Schneider A, Burke JM, Batterman SA, Meng QY (2015). Air Pollution Exposure Model for Individuals (EMI) in Health Studies: Evaluation for Ambient PM2.5 in Central North Carolina. Environ Sci Technol, 49(24): 14184-14194.

Back to overview