Individual and joint exposure to PM2.5 constituents and incident risk of metabolic syndrome: A national cohort study

Abstract

Cohort evidence linking fine particulate matter (PM2.5) constituents to metabolic syndrome (MetS) was extensively scarce. A nationwide MetS-free cohort of 3658 participants aged 45 and above, followed up from 2011 to 2015, were enrolled from 125 cities across China's mainland. Cox proportional hazards models and quantile-based g-computation were adopted to investigate individual and joint effects of exposure to PM2.5 constituents with MetS and its components. Monte Carlo simulations (n = 1000) were utilized to generate quasi-concentration-response (C-R) curve of joint exposure. A total of 633 MetS events occurred during 14,766.5 person-years follow-up (median 4.1 years). An estimated excess risk of 33 %−51 % in MetS incidence was linked to per interquartile range (IQR) increase in individual exposure to PM2.5 constituents. For an IQR-equivalent increase in joint exposure, we estimated a hazard ratio of 1.45 (95 % confidence internal: 1.23−1.69) for MetS, 1.49 (1.31−1.69) for central obesity, 1.19 (1.06−1.34) for high BP, 1.57 (1.34−1.84) for low HDL-C, 1.31 (1.14−1.51) for high TG, and 1.23 (1.02−1.48) for elevated FBG, respectively. Approximately linear or J-shaped C-R curves were consistently observed in individual and joint associations of PM2.5 constituents with MetS and its components. Joint-exposure analyses provided consistent evidence for the greatest contribution of SO42− in triggering PM2.5-associated risks of overall MetS and its components. Stratified analysis suggested higher PM2.5-related MetS risks among older participants and urban residents. These findings added longitudual population-based evidence for increased incident risks of MetS and its components associated with long-term exposures to PM2.5 constituents in middle-aged and older adults.