Published ahead of print on May 13, 2004, doi:10.1164/rccm.200402-244OC
American Journal of Respiratory and Critical Care Medicine Vol 170. pp. 383-387, (2004)
© 2004 American Thoracic Society
Ambient Air Pollution and Oxygen Saturation
Dawn L. DeMeo,
Antonella Zanobetti,
Augusto A. Litonjua,
Brent A. Coull,
Joel Schwartz and
Diane R. Gold
Channing Laboratory, Department of Medicine, and Department of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School; and Exposure, Epidemiology, and Risk Program, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts
Correspondence and requests for reprints should be addressed to Dawn L. DeMeo, M.D., M.P.H., Channing Laboratory, 181 Longwood Avenue, Boston, MA 02115. E-mail: redld{at}channing.harvard.edu
We investigated the association between fine particulate air pollution and oxygen saturation as measured with a peripheral oxygen saturation monitor during a 12-week repeated-measures study of 28 older Boston residents. Oxygen saturation and air pollution particulates with a mean diameter less than or equal to 2.5 µm were measured continuously during a protocol of rest, standing, exercise, postexercise rest, and 20 cycles of slow, paced breathing. In fixed-effect models, mean pollution concentration was associated with reduced oxygen saturation during the baseline rest period (6 hours: mean, 0.173%; 95% confidence interval [CI], 0.345 to 0.001), postexercise (6 hours: mean, 0.173%; 95% CI, 0.332 to 0.014), with a trend toward decrease during postexercise paced breathing (6 hours: mean, 0.142%; 95% CI, 0.292 to 0.007) but not during exercise. Participants taking ß-blockers had a greater pollution-related decrease in oxygen saturation at rest (6 hours: mean, 0.769%; 95% CI, 1.210 to 0.327) (interaction for particulates with a mean diameter less than or equal to 2.5 µm by ß-blocker, p < 0.0005) than did those not taking ß-blockers (p > 0.25). The reduction in oxygen saturation associated with air pollution may result from subtle particulate-related pulmonary vascular and/or inflammatory changes. Further investigation may contribute to our understanding of the mechanisms through which particulates may increase respiratory and cardiac morbidity among vulnerable populations.
Key Words: air pollution epidemiology respiratory physiology
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