Mediation of metabolic syndrome in the association between long-term exposure to particulate matter and incident cardiovascular disease: Evidence from a population-based cohort in Chengdu.

BACKGROUND: Particulate matter (PM) exposure has been linked with cardiovascular disease (CVD) and metabolic syndrome (MetS), the latter characterized by concurrent multiple metabolic disorders. As a result, the mechanisms assumption from PM to CVD through MetS have emerged, thus requiring further epidemiological evidence. This cohort study aimed to assess whether MetS mediates the associations of PM with CVD risk. METHODS: This study included 14,195 participants from the Chengdu cohort of the China Multi-Ethnic Cohort (CMEC) study in 2018. The primary outcome of incident CVD diagnoses was identified using matched hospital records from the Health Information Center of Sichuan Province. Residence-specific levels of PM with aerodynamic diameters of ≤ 1 µm (PM1), ≤ 2.5 µm (PM2.5), and ≤ 10 µm (PM10) were estimated by spatiotemporal models. Causal mediation analyses were applied to evaluate the indirect effect of MetS. RESULTS: Increased exposure levels to PM were significantly associated with MetS and CVD. Mediation analyses indicated that the associations between PM exposure and CVD were mediated by MetS, with the proportion of multiple mediations being 19.3%, 12.1%, and 13.5% for PM1, PM2.5, and PM10, respectively. Further moderated mediation analyses suggested that male, overweight individuals, alcohol drinkers, and those suffering from indoor air pollution may experience more significant adverse effects from PM exposure on CVD via MetS than others. CONCLUSIONS: Our findings suggest that MetS partially mediates the association between long-term exposure to PM and CVD. These mediation effects appear to be amplified by demographic characteristics and unhealthy lifestyles.

Age at menarche and metabolic dysfunction-associated fatty liver disease: Evidence from a large population-based epidemiological study in Southwest China.

BACKGROUND: The relationship between age at menarche and metabolic dysfunction-associated fatty liver disease remains largely not clear. The objective of this study was to examine the association between age at menarche (AAM) and metabolic dysfunction-associated fatty liver disease (MAFLD) in Chinese women and whether any observed associations were mediated by early adulthood adiposity. METHODS: The cross-sectional study included 46,873 Chinese women, aged 30-79 from baseline data of the China Multi-Ethnic Cohort study. Logistic regression models were used to evaluate the association between AAM and MAFLD. Mediation analysis was adopted to examine whether early adulthood adiposity (around 25 years) mediated the association between AAM and MAFLD. RESULTS: AAM was linearly and inversely associated with the risk of MAFLD (P for nonlinearity =0.743). In a multivariable-adjusted model, the odds ratios and 95% confidence interval (ORs (95% CI)) for MAFLD comparing menarche at <12, 12, 13, 15, 16, 17, ≥18 years to menarche at 14 years were 1.290 (1.082-1.537), 1.172 (1.068-1.285), 1.042 (0.960-1.131), 0.937 (0.861-1.020), 0.911(0.835-0.994), 0.868 (0.786-0.959), and 0.738 (0.670-0.814), respectively (P for trend <0.001). The 6.4% increased MAFLD risk was associated with each preceding year in AAM. The association between AAM and MAFLD was modified by age, ethnicity, and menopause. Early adulthood adiposity partially mediated this association. CONCLUSION: The findings of this study suggest that obesity prevention strategies are needed from young adulthood in women who undergo early menarche to reduce the risk of MAFLD.

Associations and pathways between residential greenness and hyperuricemia among adults in rural and urban China.

BACKGROUND: Residential greenness may decrease the risk for hyperuricemia in rural areas, but the urban-rural disparities in this association and underlying pathways have not been studied. OBJECTIVES: To investigate the associations and potential pathways between residential greenness and hyperuricemia in urban and rural areas. METHODS: The baseline survey of the China Multi-Ethnic Cohort (CMEC) was used. Hyperuricemia was defined as serum uric acid (SUA) > 417 µmol/L for men and >357 µmol/L for women. The satellite-based normalized difference vegetation index (NDVI) and enhanced vegetation index (EVI) were used to capture residential greenness. A propensity score inverse-probability weighting method was used to assess urban-rural differences in the associations between residential greenness and hyperuricemia, with possible mediation effects of physical activity (PA), body mass index (BMI), PM2.5, and NO2 examined by causal mediation analyses. RESULTS: A total of 72,372 participants were included. The increases in the EVI500m and NDVI500m residential greenness were associated with a decreased risk for hyperuricemia and the SUA level in both urban and rural areas. For example, each 0.1-unit increase in EVI500m was associated with a decreased hyperuricemia risk of 7% (OR = 0.93 [0.91, 0.96]) and a decreased SUA level of -1.77 µmol/L [-2.60, -0.93], respectively; such associations were stronger in urban areas for both the risk for hyperuricemia (OR = 0.84 [0.83, 0.86]) and SUA level (-7.18 µmol/L [-7.91, -6.46]). The subgroup analysis showed that the greenness-hyperuricemia/SUA association varied by age, sex, and annual household income. The percentage of the joint mediation effect of PA, BMI, PM2.5, and NO2 on the association between EVI500m and the risk for hyperuricemia was higher in urban (34.92%) than rural areas (15.40%). BMI, PM2.5, and PA showed significantly independently mediation effects for the greenness-hyperuricemia association in both rural and urban areas. CONCLUSIONS: Exposure to residential greenness was associated with a decreased risk for hyperuricemia, partially through the pathways of PA, BMI, PM2.5, and NO2, which varied in urban and rural areas.