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PM2.5 与低暴露环境下的痴呆:嗅觉识别能力和 APOE 的影响。

PM2.5 and Dementia in a Low Exposure Setting: The Influence of Odor Identification Ability and APOE.

机构信息

Department of Psychology, Umeå University, Umeå, Sweden.

Centre for Demographic and Ageing Research (CEDAR), Umeå University, Umeå, Sweden.

出版信息

J Alzheimers Dis. 2023;92(2):679-689. doi: 10.3233/JAD-220469.

Abstract

BACKGROUND

Growing evidence show that long term exposure to air pollution increases the risk of dementia.

OBJECTIVE

The aim of this study was to investigate associations between PM2.5 exposure and dementia in a low exposure area, and to investigate the role of olfaction and the APOE ɛ4 allele in these associations.

METHODS

Data were drawn from the Betula project, a longitudinal study on aging, memory, and dementia in Sweden. Odor identification ability was assessed using the Scandinavian Odor Identification Test (SOIT). Annual mean PM2.5 concentrations were obtained from a dispersion-model and matched at the participants' residential address. Proportional hazard regression was used to calculate hazard ratios.

RESULTS

Of 1,846 participants, 348 developed dementia during the 21-year follow-up period. The average annual mean PM2.5 exposure at baseline was 6.77μg/m3, which is 1.77μg/m3 above the WHO definition of clean air. In a fully adjusted model (adjusted for age, sex, APOE, SOIT, cardiovascular diseases and risk factors, and education) each 1μg/m3 difference in annual mean PM2.5-concentration was associated with a hazard ratio of 1.23 for dementia (95% CI: 1.01-1.50). Analyses stratified by APOE status (ɛ4 carriers versus non-carriers), and odor identification ability (high versus low), showed associations only for ɛ4 carriers, and for low performance on odor identification ability.

CONCLUSION

PM2.5 was associated with an increased risk of dementia in this low pollution setting. The associations between PM2.5 and dementia seemed stronger in APOE carriers and those with below average odor identification ability.

摘要

背景

越来越多的证据表明,长期暴露于空气污染会增加痴呆症的风险。

目的

本研究旨在调查低暴露地区 PM2.5 暴露与痴呆症之间的关联,并探讨嗅觉和 APOEɛ4 等位基因在这些关联中的作用。

方法

数据来自于瑞典一项关于衰老、记忆和痴呆症的纵向研究——白桦树项目。使用斯堪的纳维亚嗅觉识别测试(SOIT)评估嗅觉识别能力。每年的平均 PM2.5 浓度由扩散模型获得,并与参与者的居住地址相匹配。使用比例风险回归计算危险比。

结果

在 1846 名参与者中,348 人在 21 年的随访期间患上了痴呆症。基线时的平均年平均 PM2.5 暴露量为 6.77μg/m3,比世界卫生组织清洁空气定义高出 1.77μg/m3。在完全调整的模型中(调整年龄、性别、APOE、SOIT、心血管疾病和危险因素以及教育),每年平均 PM2.5 浓度每增加 1μg/m3,痴呆症的危险比为 1.23(95%CI:1.01-1.50)。根据 APOE 状态(携带者与非携带者)和嗅觉识别能力(高与低)进行分层分析,仅在 APOE 携带者和嗅觉识别能力较低的人群中显示出关联。

结论

在这种低污染环境中,PM2.5 与痴呆症风险增加相关。PM2.5 与痴呆症之间的关联在 APOE 携带者和嗅觉识别能力低于平均水平的人群中似乎更强。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/734a/10041445/f7a96f537ab8/jad-92-jad220469-g001.jpg

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