Institute of Occupational, Social and Environmental Medicine, Center for Health and Society, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.
Institute for Medical Informatics, Biometry and Epidemiology, University Hospital, University Duisburg-Essen, Essen, Germany.
Environ Health Perspect. 2020 Oct;128(10):107003. doi: 10.1289/EHP7077. Epub 2020 Oct 5.
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).
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 (), (), and nitrogen dioxide () 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.
While no clear associations were observed in the full study sample (mean age 59.1 () 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 higher exposure to (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%).
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. https://doi.org/10.1289/EHP7077.
由于空气污染对动脉粥样硬化进展的健康影响的流行病学证据不一致，我们使用颈动脉内膜中层厚度（cIMT）、冠状动脉钙化（CAC）和胸主动脉钙化（TAC）来研究几种空气污染物及其对动脉粥样硬化进展的影响。
我们使用德国 Heinz Nixdorf 回顾队列研究的基线（2000-2003 年）和 5 年随访（2006-2008 年）数据，包括 4814 名中年成年人。使用化学输运和土地利用回归（LUR）模型评估基于居住地的长期空气污染暴露，包括空气动力学直径为（）、（）和二氧化氮（）的颗粒物（PM）。cIMT 通过标准化超声图像从侧特异性中位数 IMT 进行量化。CAC 和 TAC 通过计算机断层扫描使用 Agatston 评分进行量化。使用逻辑回归和线性回归模型分析动脉粥样硬化的发展（是/否）和进展（cIMT 的变化和 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。
虽然在整个研究样本中（平均年龄 59.1（）岁；53%为女性）没有观察到明确的关联，但大多数空气污染物与基线动脉粥样硬化负担低或无的参与者的动脉粥样硬化进展呈边缘相关。最一致的是 CAC，例如，（LUR）的更高暴露导致 CAC 进展的估计比值比为 1.19 [95%置信区间（CI）：1.03，1.39]，每年的增长率增加 2%（95%CI：1%，4%）。
我们的研究表明，在基线时没有或只有轻微动脉粥样硬化负担的中年参与者中，亚临床动脉粥样硬化的发展和进展与长期空气污染有关，而总体上没有观察到一致的关联。https://doi.org/10.1289/EHP7077.
