Abstract
Background: Long-term exposures to airborne particles are linked to cardiovascular events, possibly through accelerated atherosclerosis. Relationships between fine particles and atherosclerosis have been reported but associations for coarse particles (PM10-2.5) have yet to be explored. Such associations plausibly differ due to divergent generating sources, composition, surface chemistry, and deposition. We examined longitudinal associations of PM10-2.5, selected chemical components [copper (Cu), zinc (Zn), phosphorus (P), and silicon (Si)] with three atherosclerosis indicators: carotid intima-media thickness (IMT), coronary artery calcium (CAC), and ankle brachial index (ABI). Methods: Multi-Ethnic Study of Atherosclerosis participants from Chicago, St Paul, and Winston-Salem (N=3,081) were eligible for inclusion. Baseline and follow-up (~ 3yrs) measures of IMT by ultrasound, CAC by computed tomography, and ABI were used. PM10-2.5 levels were estimated for each participant using 5-yr residential histories and spatial prediction models constructed with cohort-specific measures and geographic data. Mixed models were employed for progression of IMT, CAC, and ABI and relative risk regression for incident CAC, all adjusted for demographics, traditional risk factors, and study site. Results: Participants with an average age of 62 yrs at baseline (52% female, 53% white, 9% Chinese, 24% black, 14% Hispanic) showed no associations for PM10-2.5 mass or chemical component with any indicator of atherosclerosis. Effect sizes for IMT progression (µm/yr per IQR) ranged from: -1.2 (95% CI: -11.1, 8.6) for Cu to 1.2 (95% CI: -8.5, 10.8) for P. For CAC progression (Agatston score/yr per IQR), associations ranged from -9.6 (95% CI: -43.6, 24.4) for P to 1.35 (95%CI: -17.3, 20.0) for Si. No associations were observed with incident CAC or ABI progression. Conclusion: We found no evidence of an association for PM10-2.5 mass or selected chemical components with atherosclerosis acceleration.
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