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The combine effect of air pollutant mixture on atherosclerotic cardiovascular disease (ASCVD) remain undefined. This study aims to explore the association between long-term exposure of air pollutants and ASCVD, focusing on the mediating role of lipids, blood pressure and BMI. This study was based on the CHCN-BTH cohort study. The annual concentrations of air pollutants and PM 2.5 constituents were sourced from in the Tracking Air Pollution in China (TAP) and ChinaHighAirPollutants (CHAP) datasets from 2014 to 2019. A Cox mixed-effects model was used to investigate the associations between long-term exposure of air pollutants and ASCVD. The combined impact of the air pollutant mixture was assessed using Quantile g-Computation. Stratified, sensitivity, and mediation analyses were conducted. A total of 27,134 participants aged 18–80 were recruited in the present study. We found that each IQR increase of PM 2.5 , PM 1 , NO 2 , O 3 , BC, SO 4 2-, and OM were significantly associated with the incidence of ASCVD, the hazard ratios (HRs) and 95 % confidence interval (CI) were 1.55 (1.35, 1.78), 1.46 (1.27, 1.67), 1.30 (1.21, 1.39), 1.66 (1.41,1.95), 2.14 (1.63, 2.83), 1.65 (1.25, 2.17) and 1.92(1.52, 2.45), respectively. The combined effect of air pollutant mixture on ASCVD was 1.79 (1.46, 2.20), PM 2.5 contributed 83.3 % to this combined effect. Mediation effect models suggested that air pollutants and ASCVD might be mediated through SBP, DBP, HDL-C, LDL-C, hsCRP and BMI (mediation proportion range from 1.3 % to 26.1 %), Notably, HDL-C played mediation roles of 11.3 % (7.0 %, 18.4), 26.1 % (17.7 %, 38.1 %) and 25.4 % (15.4, 47.7 %) in the effects of long-term exposure to PM 2.5, PM 1 and OM on ASCVD, respectively. Long-term, high-level air pollutant exposure was significantly associated with an elevated risk of ASCVD, particularly for PM 2.5. Blood pressure, lipids and BMI, especially HDL-C, may mediate the effects of air pollutants exposure on ASCVD. [Display omitted] • Air pollutant mixture were associated with ASCVD incidence, especially IHD. • The main impact component of air pollutant mixture to ASCVD is PM 2.5. • The effect of OM to ASCVD might be greatest among PM 2.5 constituents. • Blood pressure/lipids might mediate the associations of air pollution and ASCVD. [ABSTRACT FROM AUTHOR]

Despite growing evidence that links long-term air pollution exposure to cardiovascular disease (CVD), the combined effects of air pollutants and particulate matter with an aerodynamic diameter of less than 2.5 μm (PM 2.5) components are still limited. A prospective cohort study was performed based on the Cohort Study on Chronic Disease of the Community Natural Population in the Beijing-Tianjin-Hebei Region (CHCN-BTH) to assess the association of long-term air pollutants with incident CVD and the combined effect of the air pollutants mixture among 26,851 adults. Three-year residential exposure to air pollutants (PM 2.5 , O 3 , PM 10 , PM 1 , NO 2 , SO 2 and CO) and PM 2.5 components [black carbon (BC), NH 4 +, SO 4 2-, NO 3 − and organic matter (OM)] were calculated based on well-validated models. Proportional hazard models were applied to assess the association of air pollutants with incident CVD. Quantile g-Computation was used to examine the combined effect of the pollutant mixture. During the 56,090 person-years follow-up, 629 participants reported incident CVD. Adjusted hazard ratios with 95% confidence intervals (CIs) of CVD per interquartile range increase in O 3 , PM 2.5 , PM 1 , NO 2 , BC, and OM concentrations were 4.52 (95%CI: 2.61, 7.83), 2.39 (95%CI: 1.83, 3.13), 2.37 (95%CI: 1.20, 4.70), 1.36 (95%CI: 1.19, 1.56), 3.84 (95%CI: 2.38, 6.18), and 3.07 (95%CI: 2.01, 4.69), respectively. In multi-pollutant models, the combined effect of air pollutant mixture on incident CVD was 2.37 (95%CI: 2.30, 2.44). PM 2.5 and O 3 contributed 54.3% and 44.5% of the combined effect of the air pollutant mixture, respectively. After using PM 2.5 components instead of PM 2.5 as part of the mixture, OM drove 55.2% of the combined effect. The findings indicated associations of air pollutant mixtures with CVD incidence. PM 2.5 (especially OM) and O 3 might strongly contribute to air pollutant mixtures that lead to incident CVD. [Display omitted] • PM 2.5 , PM 1 , O 3 and NO 2 were positively associated with incident CVD. • BC and OM were PM 2.5 components that were associated with incident CVD. • Air pollutant mixture was positively associated with incident CVD. • OM and O 3 were strong contributors to incident CVD. [ABSTRACT FROM AUTHOR]

Growing evidence links long-term air pollution exposure with renal function. However, little research has been conducted on the combined effects of air pollutant mixture on renal function and multiple mediation effects of metabolic risk factors. This study enrolled 8996 adults without chronic kidney disease (CKD) at baseline from the CHCN-BTH cohort study. Three-year exposure to air pollutants [particulate matter ≤ 2.5 µm (PM 2.5), PM 10 , PM 1 , ozone (O 3), nitrogen dioxide (NO 2), sulfur dioxide (SO 2) and carbon monoxide (CO)] and PM 2.5 components [black carbon (BC), ammonium (NH 4 +), nitrate (NO 3 -), sulfate (SO 4 2-) and organic matter (OM)] were assessed using well-validated machine learning methods. Linear mixed models were applied to investigate the associations between air pollutants and estimated glomerular filtration rate (eGFR). Quantile G-computation was used to assess the combined effects of pollutant mixtures. Causal mediation analysis and Bayesian mediation analysis were employed to estimate the mediation effects of metabolic risk factors. An interquartile range increases in BC (−0.256, 95 %CI: −0.331, −0.180) and OM (−0.603, 95 %CI: −0.810, −0.397) were significantly associated with eGFR decline; while O 3 (1.151, 95 %CI: 0.813, 1.489), PM 10 (0.721, 95 %CI: 0.309, 1.133), NH 4 + (0.990, 95 %CI: 0.638, 1.342), and NO 3 - (0.610, 95 %CI: 0.405, 0.815) were associated with higher eGFR. The combined effect of the PM 2.5 component mixture was found to be associated with lower eGFR (−1.147, 95 % CI: −1.456, −0.839), with OM contributing 72.4 % of the negative effect. Univariate mediation analyses showed that high-density lipoprotein (HDL) mediated 7.1 %, 6.9 %, and 6.1 % effects of O 3 , BC, and OM, respectively. However, these mediation effects were not significant in Bayesian mediation analysis. These findings suggest the effect of the PM 2.5 component mixture on eGFR decline and the strong contribution of OM. Metabolic risk factors may not mediate the effects of air pollutants. Further study is warranted to clarify the potential mechanisms involved. • Long-term ozone exposure demonstrated a protective effect against CKD progression. • PM 2.5 component mixture was linked to an increased risk of CKD progression. • Organic matter was a strong contributor to incident CKD progression. • Metabolic risk factors may not mediate the effects of air pollutants. [ABSTRACT FROM AUTHOR]