Daily variation of particulate air pollution and poor cardiac autonomic control in the elderly

Particulate matter air pollution (PM) has been related to cardiovascular di sease mortality in a number of recent studies. The pathophysiologic mechani sms for this association are under study. Low heart rate variability, a mar ker of poor cardiac autonomic control, is associated with higher risk of my ocardial infarction and sudden cardiac death. To address the possible mecha nisms for PM-cardiovascular disease mortality, we examined the cardiac auto nomic response to daily variations in PM in 26 elderly (mean age 81) indivi duals for 3 consecutive weeks. Several standardized methods were used to me asure 24-hr average PM concentrations prior to the clinical test inside (in door PM2.5) and immediately outside (outdoor PM2.5 and PM2.5-10) of partici pants' residences. Resting, supine, 6-min R wave to R wave (R-R) interval d ata were collected to estimate high frequency (0.15-0.40 Hz) and low freque ncy (0.04-0.15 Hz) powers and standard deviation of normal R-R intervals (S DNN) as cardiac autonomic control indices. Participant-specific lower heart rate variability days were defined as days for which the high-frequency in dices fell below the first tertile of the individual's high-frequency distr ibution over the study period. Indoor PM2.5 > 15 mu g/m(3) was used to defi ne high pollution days. Results show that the odds ratio (95% confidence in terval) of low heart rate variability high frequency for high (vs. not high ) pollution days was 3.08 (1.43, 6.59). The beta-coefficients (standard err or) from mixed models to assess the quantitative relationship between varia tions in indoor PM2.5 and the log-transformed high frequency, low frequency , and SDNN were: -0.029 (0.010), -0.027 (0.009), and -0.004 (0.003), respec tively. This first study of cardiac autonomic control response to daily var iations of PM2.5 indicates that increased levels of PM2.5 are associated wi th lower cardiac autonomic control, suggesting a possible mechanistic link between PM and cardiovascular disease mortality.