暴露于空气污染与英国生物库人群中发生痴呆症的风险。
Exposure to air pollution and risk of incident dementia in the UK Biobank.
机构信息
Department of Epidemiology & Biostatistics, University of Arizona Mel and Enid Zuckerman College of Public Health, Tucson, AZ, USA.
Departments of Psychology and Psychiatry, Neuroscience and Physiological Sciences Graduate Interdisciplinary Programs, BIO5 Institute, and Evelyn F. McKnight Brain Institute, University of Arizona, Tucson, AZ, USA; Arizona Alzheimer's Consortium, Phoenix, AZ, USA.
出版信息
Environ Res. 2022 Jun;209:112895. doi: 10.1016/j.envres.2022.112895. Epub 2022 Feb 8.
BACKGROUND
Air pollution may cause inflammatory and oxidative stress damage to the brain, leading to neurodegenerative disease. The association between air pollution and dementia, and modification by apolipoprotein E genotype 4 (APOE-ε4) has yet to be fully investigated.
OBJECTIVES
To examine associations of air pollution with three types of incident dementias (Alzheimer's disease (AD), frontotemporal dementia (FTD), and vascular dementia (VAD)), and their potential modification by APOE-ε4 genotype.
METHODS
The UK Biobank enrolled >500,000 participants (2006-2010) with ongoing follow-up. We used annual averages of air pollution (PM, PM, PM, PM, NO, NO) for 2010 scaled to interquartile ranges (IQR). We included individuals aged ≥60 years, with no dementia diagnosis prior to January 1, 2010. Time to incident dementia and follow-up time were reported from baseline (January 01, 2010) to last censor event (death, last hospitalization, or loss to follow-up). Cox proportional hazard ratios (HR) and 95% confidence intervals (95% CI) were calculated to estimate the association of air pollutants and incident dementia, and modification of these associations by APOE-ε4.
RESULTS
Our sample included 187,194 individuals (including N = 680 AD, N = 377 VAD, N = 63 FTD) with a mean follow-up of 7.04 years. We observed consistent associations of PM with greater risk of all-cause dementia (HR = 1.17, 95% CI: 1.10, 1.24) and AD (HR = 1.17, 95% CI: 1.06, 1.29). NO was also associated with greater risk of any incident dementia (HR = 1.18, 95% CI: 1.10, 1.25), AD (HR = 1.15, 95% CI: 1.04, 1.28) and VAD (HR = 1.18, 95% CI: 1.03, 1.35). APOE-ε4 did not modify the association between any air pollutants and dementia.
DISCUSSION
PM and NO levels were associated with several types of dementia, and these associations were not modified by APOE-ε4. Findings from the UK Biobank support and extend to other epidemiological evidence for the potential association of air pollutants with detrimental brain health during aging.
背景
空气污染可能导致大脑的炎症和氧化应激损伤，从而导致神经退行性疾病。空气污染与痴呆之间的关联，以及载脂蛋白 E 基因型 4（APOE-ε4）的修饰作用尚未得到充分研究。
目的
检查空气污染与三种类型的新发痴呆（阿尔茨海默病（AD）、额颞叶痴呆（FTD）和血管性痴呆（VAD））之间的关联，以及它们与 APOE-ε4 基因型的潜在修饰作用。
方法
英国生物库招募了>500,000 名参与者（2006-2010 年），并持续进行随访。我们使用 2010 年空气污染（PM、PM、PM、PM、NO、NO）的年平均值，并将其缩放到四分位距（IQR）。我们纳入了年龄≥60 岁、在 2010 年 1 月 1 日之前没有痴呆诊断的个体。从基线（2010 年 1 月 1 日）到最后一次删失事件（死亡、最后一次住院或失访）报告新发痴呆和随访时间。使用 Cox 比例风险比（HR）和 95%置信区间（95%CI）来估计空气污染物与新发痴呆的关联，以及 APOE-ε4 对这些关联的修饰作用。
结果
我们的样本包括 187,194 名参与者（包括 N=680 例 AD、N=377 例 VAD、N=63 例 FTD），平均随访时间为 7.04 年。我们观察到 PM 与全因痴呆（HR=1.17，95%CI：1.10，1.24）和 AD（HR=1.17，95%CI：1.06，1.29）的风险增加呈一致关联。NO 也与任何新发痴呆（HR=1.18，95%CI：1.10，1.25）、AD（HR=1.15，95%CI：1.04，1.28）和 VAD（HR=1.18，95%CI：1.03，1.35）的风险增加呈关联。APOE-ε4 并没有修饰任何空气污染物与痴呆之间的关联。
讨论
PM 和 NO 水平与多种类型的痴呆有关，并且这些关联不受 APOE-ε4 的修饰。英国生物库的研究结果支持并扩展了其他流行病学证据，表明空气污染物与衰老过程中大脑健康受损之间可能存在关联。
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