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长期暴露于低水平空气污染、遗传易感性与痴呆风险。

Long-term exposure to low-level air pollution, genetic susceptibility and risk of dementia.

机构信息

Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA, USA.

Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA.

出版信息

Int J Epidemiol. 2023 Jun 6;52(3):738-748. doi: 10.1093/ije/dyac146.

Abstract

BACKGROUND

We aimed to assess the association between low-level air pollution and the risk of dementia, and examine the modification effect by genetic susceptibility on the relationship.

METHODS

A total of 164 447 participants who were free of dementia at baseline and aged ≥60 years were included. Annual average concentrations of particulate matter (PM) with diameters of ≤2.5 μm (PM2.5), between 2.5 and 10 μm (PMcoarse), PM2.5 absorbance and nitrogen dioxides (NO2) were evaluated using the Land Use Regression models. Cox proportional hazards regression was used to estimate the association between air pollutants and incident dementia.

RESULTS

The adjusted hazard ratio (HR) of dementia for a 5-μg/m3 increase in NO2 was 1.09 (95% CI, 1.05-1.14); the adjusted HR of dementia for a 1-μg/m3 increase in PM2.5 was 1.10 (1.04-1.17). Such significant associations were present even within concentration ranges well below the present World Health Organization, US and European annual mean limit values. In addition, higher PM2.5 absorbance, a marker closely related to motorized traffic, was associated with higher risk of dementia. We found the risk of dementia associated with a combination of air pollutants (NO2 or PM2.5) and high genetic susceptibility (APOE-ε4 alleles or overall genetic susceptibility) was greater than the addition of the risk associated with each individual factor, indicating significant interactions on an additive scale (all P-interaction < 0.05).

CONCLUSION

Long-term exposure to PM2.5 or NO2, even at relatively low levels, is associated with a higher risk of dementia. Air pollution may additively interact with the genetic susceptibility on dementia risk.

摘要

背景

本研究旨在评估低水平空气污染与痴呆风险之间的关联,并探讨遗传易感性对此关系的修饰作用。

方法

共纳入 164447 名基线时无痴呆且年龄≥60 岁的参与者。采用土地利用回归模型评估直径≤2.5μm(PM2.5)、2.5-10μm(PMcoarse)、PM2.5 吸光度和二氧化氮(NO2)的年平均浓度。使用 Cox 比例风险回归模型估计空气污染物与新发痴呆的关联。

结果

NO2 浓度每增加 5μg/m3,痴呆的调整后危险比(HR)为 1.09(95%CI,1.05-1.14);PM2.5 浓度每增加 1μg/m3,痴呆的调整后 HR 为 1.10(1.04-1.17)。即使在远低于世界卫生组织、美国和欧洲现行年平均限值的浓度范围内,也存在这种显著关联。此外,与机动车交通密切相关的 PM2.5 吸光度较高与痴呆风险增加相关。我们发现,与空气污染物(NO2 或 PM2.5)和高遗传易感性(APOE-ε4 等位基因或整体遗传易感性)的组合相关的痴呆风险大于每个单独因素相关风险的相加,表明在加性尺度上存在显著的交互作用(所有 P 交互<0.05)。

结论

长期暴露于 PM2.5 或 NO2,即使在相对较低的水平,也与痴呆风险增加相关。空气污染可能与痴呆风险的遗传易感性呈加性交互作用。

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