Abstract
There is increasingly concern that PM2.5 constituents play a significant role in PM2.5-related cardiovascular outcomes. However, little is known about the associations between specific constituents of PM2.5 and risk for cardiovascular health. To evaluate the exposure to specific chemicals of PM2.5 from various sources and their cardiac effects, a longitudinal investigation was conducted with four repeated measurements of elderly participants’ HRV and PM2.5 species in urban Beijing. Multiple chemicals in PM2.5 (metals, ions and PAHs) were characterized for PM2.5 source apportionment and personalized exposure assessment. Five sources were finally identified with specific chemicals as the indicators: oil combustion (1.1%, V & PAHs), secondary particle (11.3%, SO42− & NO3−), vehicle emission (1.2%, Pd), construction dust (28.7%, Mg & Ca), and coal combustion (57.7%, Se & As). As observed, each IQR increase in exposure to oil combustion (V), vehicle emission (Pd), and coal combustion (Se) significantly decreased rMSSD by 13.1% (95% CI: −25.3%, −1.0%), 27.4% (95% CI: −42.9%, −7.6%) and 24.7% (95% CI: −39.2%, −6.9%), respectively, while those of PM2.5 mass with decreases of rMSSD by 11.1% (95% CI: −19.6%, −1.9%) at lag 0. Elevated exposures to specific sources/constituents of PM2.5 disrupt cardiac autonomic function in elderly and have more adverse effects than PM2.5 mass. In the stratified analysis, medication and gender modify the associations of specific chemicals from variable sources with HRV. The findings of this study provide evidence on the roles of influential constituents of ambient air PM2.5 and their sources in terms of their adverse cardiovascular health effects.
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