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 particulate exposure. In this study, blood oxygen saturation using pulse oximetry (SpO2) and pulse rate were measured daily on a panel of 90 elderly subjects during the winter of 1995-1996 in Utah Valley. Associations of SpO2 and pulse rate with respirable particulate pollution (particles with an aerodynamic diameter </= a nominal 10 microm [PM10]) were evaluated. SpO2 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) were associated with PM10 on the previous 1 to 5 d. A 100 microg/m3 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 changes and may be part of the pathophysiology linking particles to cardiopulmonary mortality. The observed lag structure is consistent with particulate-induced pulmonary inflammation and cytokine release, but the biological relevance requires further study.