Air pollution has been found to trigger chronic obstructive pulmonary disease (COPD) exacerbations and deaths, but it is unknown whether chronic outdoor air pollution in the U.S. contributes to the development of COPD. One in four patients in the U.S. with COPD has never smoked, yet little is known about the role of exposures other than smoking in COPD pathogenesis. Few studies have been able to measure spirometry repeatedly and examine multiple exposures, including constituents of fine particulate matter, to understand which exposures are most harmful to lung function. The purpose of this project is to identify the acute effects of exposure to ambient pollutants (from traffic, power plants and industrial processes) on lung function in subjects with and without COPD and secondly to determine, using state-of-the art exposure assessment tools, if chronic exposures to air pollution increase risk of developing clinical or subclinical COPD. We will investigate these questions in the more than 7,000 subjects of the Framingham Heart Study's Offspring and Third Generation cohorts, who have been followed from 1995 to the present with repeated spirometry, a quantitative chest CT in a subset of nearly 3,000 subjects, and detailed geocoded exposure assessment data recently developed by our group. We hypothesize that elevations in short-term exposure to air pollutants (fine particulate matter, black carbon, ozone, nitrogen oxides, sulfates and metals) will impair lung function by spirometry and DLCO after adjustment for smoking. We further hypothesize that long-term exposure to fine particulate matter (using a satellite model), black carbon (using a regional tempero-spatial model) and traffic (using distance from residence to major roadway and traffic density around residence) will be associated with (1) increased airflow obstruction on spirometry and (2) increased percentage of low attenuation area (a measure of emphysema) and wall area thickness (a measure of airways disease) measured by quantitative CT. As part of the research training program, the principle investigator will complete a Master of Public Health with a concentration in Quantitative Methods in order to master the needed skills in epidemiology and biostatistics to complete this work. This research project will be performed under the guidance of a well-established investigator in epidemiology and air pollution health effects research and with advice from experts in environmental obstructive lung disease and quantitative CT analysis.

Public Health Relevance

The purpose of this project is to study the acute effects of exposure to multiple ambient pollutants (from traffic, power plants and industrial processes) on lung function in subjects with and without COPD and to determine if chronic exposure to air pollution and traffic contribute to COPD risk. We anticipate that this work will help elucidate COPD pathogenesis, identify environmental risk factors for clinical and subclinical COPD and inform air quality regulations targeting the most harmful particles.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32ES023352-01
Application #
8596211
Study Section
Special Emphasis Panel (ZRG1-F10A-S (20))
Program Officer
Chadwick, Lisa
Project Start
2013-09-01
Project End
2015-06-30
Budget Start
2013-09-01
Budget End
2014-08-31
Support Year
1
Fiscal Year
2013
Total Cost
$63,932
Indirect Cost
Name
Massachusetts General Hospital
Department
Type
DUNS #
073130411
City
Boston
State
MA
Country
United States
Zip Code
02199
Rice, Mary B; Thurston, George D; Balmes, John R et al. (2014) Climate change. A global threat to cardiopulmonary health. Am J Respir Crit Care Med 189:512-9
Rice, Mary B; Rifas-Shiman, Sheryl L; Oken, Emily et al. (2014) Exposure to traffic and early life respiratory infection: A cohort study. Pediatr Pulmonol :
Wilker, Elissa H; Ljungman, Petter L; Rice, Mary B et al. (2014) Relation of long-term exposure to air pollution to brachial artery flow-mediated dilation and reactive hyperemia. Am J Cardiol 113:2057-63
Ljungman, Petter L; Wilker, Elissa H; Rice, Mary B et al. (2014) Short-term exposure to air pollution and digital vascular function. Am J Epidemiol 180:482-9