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Air Pollution and Progression of Atherosclerosis in Different Vessel Beds—Results from a Prospective Cohort Study in the Ruhr Area, Germany

机译:不同血管床中动脉粥样硬化的空气污染和进展 - 德国Ruhr地区的前瞻性队列研究结果

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Objectives: Due to inconsistent epidemiological evidence on health effects of air pollution on progression of atherosclerosis, we investigated several air pollutants and their effects on progression of atherosclerosis, using carotid intima media thickness (cIMT), coronary calcification (CAC), and thoracic aortic calcification (TAC). Methods: We used baseline (2000–2003) and 5-y follow-up (2006–2008) data from the German Heinz Nixdorf Recall cohort study, including 4,814 middle-aged adults. Residence-based long-term air pollution exposure, including particulate matter (PM) with aerodynamic diameter ≤ 2.5 μ m ( PM 2.5 ), ( PM 10 ), and nitrogen dioxide ( NO 2 ) was assessed using chemistry transport and land use regression (LUR) models. cIMT was quantified as side-specific median IMT assessed from standardized ultrasound images. CAC and TAC were quantified by computed tomography using the Agatston score. Development (yes/no) and progression of atherosclerosis (change in cIMT and annual growth rate for CAC/TAC) were analyzed with logistic and linear regression models, adjusting for age, sex, lifestyle variables, socioeconomic status, and traffic noise. Results: While no clear associations were observed in the full study sample (mean age 59.1 ( ± 7.6 ) y; 53% female), most air pollutants were marginally associated with progression of atherosclerosis in participants with no or low baseline atherosclerotic burden. Most consistently for CAC, e.g., a 1.5 μ g / m 3 higher exposure to PM 2.5 (LUR) yielded an estimated odds ratio of 1.19 [95% confidence interval (CI): 1.03, 1.39] for progression of CAC and an increased annual growth rate of 2% (95% CI: 1%, 4%). Conclusion: Our study suggests that development and progression of subclinical atherosclerosis is associated with long-term air pollution in middle-aged participants with no or minor atherosclerotic burden at baseline, while overall no consistent associations are observed.
机译:目标:由于流行病学对动脉粥样硬化进展的空气污染的健康影响不一致,我们研究了几种空气污染物及其对动脉粥样硬化的进展的影响,使用颈动脉内膜介质厚度(CIMT),冠状动脉钙化(CAC)和胸主动脉钙化(TAC)。方法:我们使用德国海因斯尼克斯夫召回队列研究的基线(2000-2003)和5-Y后续(2006-2008)数据,包括4,814名中年成年人。使用化学运输和土地利用回归评估基于空气动力学直径≤2.5μm(PM 2.5)和二氧化氮(NO 2)的颗粒状物质(PM),包括颗粒状物质(PM),(PM 10)和氮二氧化碳(NO 2)( lur)模型。将CIMT量化为从标准化超声图像评估的侧面特异性中值IMT。 CAC和TAC通过使用Agatston评分的计算机断层扫描量化。通过物流和线性回归模型分析了动脉粥样硬化的发展(是/否)和动脉粥样硬化的进展(CAC / TAC的年增长率和CAC / TAC的年增长率),调整年龄,性别,生活方式变量,社会经济地位和交通噪音。结果:虽然在完整的研究样本中未观察到明确的关联(平均59.1(±7.6)y; 53%的雌性),大多数空气污染物与参与者在没有或低基线动脉粥样硬化负担的参与者中的动脉粥样硬化的进展略微相关。对于CAC,最始终如一的CAC,低于PM 2.5(LUR)的12.5μg/ m 3的暴露率估计的差异为1.19 [95%置信区间(CI):1.03,1.39]的CAC和增加的年度增长率为2%(95%CI:1%,4%)。结论:我们的研究表明,亚临床动脉粥样硬化的发展和进展与中年参与者的长期空气污染有关,在基线上没有或较小的动脉粥样硬化负担,而总体而言则没有观察到一致的联合。

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