Abstract：
BACKGROUND: The association between exposure to air pollutants and cardiovascular disease (CVD) trajectory in individuals with circadian syndrome remains inconclusive.
METHODS: The individual exposure levels of air pollutants, including particulate matter (PM) with aerodynamic diameter ≤ 2.5 μm (PM2.5), PM with aerodynamic diameter ≤ 10 μm (PM10), PM2.5 absorbance, PM with aerodynamic diameter between 2.5 μm and 10 μm, nitrogen dioxide (NO2), nitrogen oxides (NOx), and air pollution score (overall air pollutants exposure), were estimated for 48,850 participants with circadian syndrome from the UK Biobank. Multistate regression models were employed to estimate associations between exposure to air pollutants and trajectories from circadian syndrome to CVD/CVD subtypes (including coronary heart disease [CHD], atrial fibrillation [AF], heart failure [HF], and stroke) and death. Mediation roles of CVD/CVD subtypes in the associations between air pollutants and death were evaluated.
RESULTS: After a mean follow-up time over 12 years, 12,570 cases of CVD occurred, including 8192 CHD, 1693 AF, 1085 HF, and 1600 stroke cases. In multistate model, per-interquartile range increment in PM2.5 (hazard ratio: 1.08; 95 % confidence interval: 1.06, 1.10), PM10 (1.04; 1.01, 1.06), PM2.5 absorbance (1.04; 1.02, 1.06), NO2 (1.07; 1.03, 1.11), NOx (1.08; 1.04, 1.12), or air pollution score (1.06; 1.03, 1.08) was associated with trajectory from circadian syndrome to CVD. Significant associations between the above-mentioned air pollutants and trajectories from circadian syndrome and CVD to death were observed. CVD, particularly CHD, significantly mediated the associations of PM2.5, NO2, NOx, and air pollution score with death.
CONCLUSIONS: Long-term exposure to air pollutants during circadian syndrome was associated with subsequent CVD and death. CHD emerged as the most prominent CVD subtype in CVD progression driven by exposure to air pollutants during circadian syndrome. Our study highlights the importance of controlling air pollutants exposure and preventing CHD in people with circadian syndrome.
METHODS: The individual exposure levels of air pollutants, including particulate matter (PM) with aerodynamic diameter ≤ 2.5 μm (PM2.5), PM with aerodynamic diameter ≤ 10 μm (PM10), PM2.5 absorbance, PM with aerodynamic diameter between 2.5 μm and 10 μm, nitrogen dioxide (NO2), nitrogen oxides (NOx), and air pollution score (overall air pollutants exposure), were estimated for 48,850 participants with circadian syndrome from the UK Biobank. Multistate regression models were employed to estimate associations between exposure to air pollutants and trajectories from circadian syndrome to CVD/CVD subtypes (including coronary heart disease [CHD], atrial fibrillation [AF], heart failure [HF], and stroke) and death. Mediation roles of CVD/CVD subtypes in the associations between air pollutants and death were evaluated.
RESULTS: After a mean follow-up time over 12 years, 12,570 cases of CVD occurred, including 8192 CHD, 1693 AF, 1085 HF, and 1600 stroke cases. In multistate model, per-interquartile range increment in PM2.5 (hazard ratio: 1.08; 95 % confidence interval: 1.06, 1.10), PM10 (1.04; 1.01, 1.06), PM2.5 absorbance (1.04; 1.02, 1.06), NO2 (1.07; 1.03, 1.11), NOx (1.08; 1.04, 1.12), or air pollution score (1.06; 1.03, 1.08) was associated with trajectory from circadian syndrome to CVD. Significant associations between the above-mentioned air pollutants and trajectories from circadian syndrome and CVD to death were observed. CVD, particularly CHD, significantly mediated the associations of PM2.5, NO2, NOx, and air pollution score with death.
CONCLUSIONS: Long-term exposure to air pollutants during circadian syndrome was associated with subsequent CVD and death. CHD emerged as the most prominent CVD subtype in CVD progression driven by exposure to air pollutants during circadian syndrome. Our study highlights the importance of controlling air pollutants exposure and preventing CHD in people with circadian syndrome.
摘要：
背景：在患有昼夜节律综合征的个体中，暴露于空气污染物与心血管疾病（CVD）轨迹之间的关系仍然没有定论。
方法：空气污染物的个体暴露水平，包括空气动力学直径≤2.5μm的颗粒物(PM)(PM2.5)，空气动力学直径≤10μm的PM(PM10),PM2.5吸光度，空气动力学直径在2.5μm和10μm之间的PM，二氧化氮(NO2),氮氧化物(NOx),和空气污染评分(总体空气污染物暴露)，估计有48,850名来自英国生物库的昼夜节律综合征参与者。多状态回归模型用于估计暴露于空气污染物与从昼夜节律综合征到CVD/CVD亚型（包括冠心病[CHD]，心房颤动[AF],心力衰竭[HF]，和中风）和死亡。评估了CVD/CVD亚型在空气污染物与死亡之间的关联中的中介作用。
结果：经过12年的平均随访时间，发生了12570例CVD，包括8192冠心病，1693AF,1085HF,和1600例中风病例。在多态模型中，PM2.5的每四分位数范围增量(危险比：1.08；95%置信区间：1.06，1.10)，PM10(1.04;1.01,1.06),PM2.5吸光度(1.04;1.02,1.06),NO2(1.07;1.03,1.11),NOx(1.08;1.04,1.12),或空气污染评分(1.06;1.03,1.08)与从昼夜节律综合征到CVD的轨迹相关.观察到上述空气污染物与从昼夜节律综合征和CVD到死亡的轨迹之间的显着关联。CVD,尤其是CHD,显著介导了PM2.5、NO2、NOx、空气污染与死亡有关。
结论：昼夜节律综合征期间长期暴露于空气污染物与随后的CVD和死亡相关。CHD是昼夜节律综合征期间暴露于空气污染物驱动的CVD进展中最突出的CVD亚型。我们的研究强调了控制空气污染物暴露和预防昼夜节律综合征患者CHD的重要性。
方法：空气污染物的个体暴露水平，包括空气动力学直径≤2.5μm的颗粒物(PM)(PM2.5)，空气动力学直径≤10μm的PM(PM10),PM2.5吸光度，空气动力学直径在2.5μm和10μm之间的PM，二氧化氮(NO2),氮氧化物(NOx),和空气污染评分(总体空气污染物暴露)，估计有48,850名来自英国生物库的昼夜节律综合征参与者。多状态回归模型用于估计暴露于空气污染物与从昼夜节律综合征到CVD/CVD亚型（包括冠心病[CHD]，心房颤动[AF],心力衰竭[HF]，和中风）和死亡。评估了CVD/CVD亚型在空气污染物与死亡之间的关联中的中介作用。
结果：经过12年的平均随访时间，发生了12570例CVD，包括8192冠心病，1693AF,1085HF,和1600例中风病例。在多态模型中，PM2.5的每四分位数范围增量(危险比：1.08；95%置信区间：1.06，1.10)，PM10(1.04;1.01,1.06),PM2.5吸光度(1.04;1.02,1.06),NO2(1.07;1.03,1.11),NOx(1.08;1.04,1.12),或空气污染评分(1.06;1.03,1.08)与从昼夜节律综合征到CVD的轨迹相关.观察到上述空气污染物与从昼夜节律综合征和CVD到死亡的轨迹之间的显着关联。CVD,尤其是CHD,显著介导了PM2.5、NO2、NOx、空气污染与死亡有关。
结论：昼夜节律综合征期间长期暴露于空气污染物与随后的CVD和死亡相关。CHD是昼夜节律综合征期间暴露于空气污染物驱动的CVD进展中最突出的CVD亚型。我们的研究强调了控制空气污染物暴露和预防昼夜节律综合征患者CHD的重要性。
