Ca. Pope et al., Oxygen saturation, pulse rate, and particulate air pollution - A daily time-series panel study, AM J R CRIT, 159(2), 1999, pp. 365-372
Although epidemiological studies have linked particulate air pollution with
cardiopulmonary mortality, underlying biological mechanisms remain largely
unknown. Unexplored pathophysiological pathways include transient declines
in blood oxygenation and/or changes in cardiac rhythm following particulat
e exposure. In this study, blood oxygen saturation using pulse oximetry (Sp
(o2)) and pulse rate were measured daily on a panel of 90 elderly subjects
during the winter of 1995-1996 in Utah Valley. Associations of Sp(o2) and p
ulse rate with respirable particulate pollution (particles with an aerodyna
mic diameter less than or equal to a nominal 10 mu m [PM10]) were evaluated
. Sp(o2) was not consistently associated with PM10. Pulse rate and the odds
of the pulse rate being elevated by 5 or 10 beats per minute (beats/min) w
ere associated with PM10 on the previous 1 to 5 d. A 100 mu g/m(3) increase
in previous-day PM10 was associated with an average increase of 0.8 beats/
min and 29 and 95% increased odds of the pulse rate being elevated by 5 or
10 beats/min, respectively. Although there was little evidence of pollution
-related hypoxia, alterations in pulse rate could reflect cardiac rhythm ch
anges and may be part of the pathophysiology linking particles to cardiopul
monary mortality. The observed lag structure is consistent with particulate
-induced pulmonary inflammation and cytokine release, but the biological re
levance requires further study.