Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet and Stockholm University, Stockholm, Sweden.
Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
JAMA Neurol. 2020 Jul 1;77(7):801-809. doi: 10.1001/jamaneurol.2019.4914.
Emerging yet contrasting evidence associates air pollution with incident dementia, and the potential role of cardiovascular disease (CVD) in this association is unclear.
To investigate the association between long-term exposure to air pollution and dementia and to assess the role of CVD in that association.
DESIGN, SETTING, AND PARTICIPANTS: Data for this cohort study were extracted from the ongoing Swedish National Study on Aging and Care in Kungsholmen (SNAC-K), a longitudinal population-based study with baseline assessments from March 21, 2001, through August 30, 2004. Of the 5111 randomly selected residents in the Kungsholmen district of Stockholm 60 years or older and living at home or in institutions, 521 were not eligible (eg, due to death before the start of the study or no contact information). Among the remaining 4590 individuals, 3363 (73.3%) were assessed. For the current analysis, 2927 participants who did not have dementia at baseline were examined, with follow-up to 2013 (mean [SD] follow-up time, 6.01 [2.56] years). Follow-up was completed February 18, 2013, and data were analyzed from June 26, 2018, through June 20, 2019.
Two major air pollutants (particulate matter ≤2.5 μm [PM2.5] and nitrogen oxide [NOx]) were assessed yearly from 1990, using dispersion models for outdoor levels at residential addresses.
The hazard of dementia was estimated using Cox proportional hazards regression models. The potential of CVD (ie, atrial fibrillation, ischemic heart disease, heart failure, and stroke) to modify and mediate the association between long-term exposure to air pollution and dementia was tested using stratified analyses and generalized structural equation modeling.
At baseline, the mean (SD) age of the 2927 participants was 74.1 (10.7) years, and 1845 (63.0%) were female. Three hundred sixty-four participants with incident dementia were identified. The hazard of dementia increased by as much as 50% per interquartile range difference in mean pollutant levels during the previous 5 years at the residential address (hazard ratio [HR] for difference of 0.88 μg/m3 PM2.5, 1.54 [95% CI, 1.33-1.78]; HR for difference of 8.35 μg/m3 NOx, 1.14 [95% CI, 1.01-1.29]). Heart failure (HR for PM2.5, 1.93 [95% CI, 1.54-2.43]; HR for NOx, 1.43 [95% CI, 1.17-1.75]) and ischemic heart disease (HR for PM2.5, 1.67 [95% CI, 1.32-2.12]; HR for NOx, 1.36 [95% CI, 1.07-1.71]) enhanced the dementia risk, whereas stroke appeared to be the most important intermediate condition, explaining 49.4% of air pollution-related dementia cases.
This study found that long-term exposure to air pollution was associated with a higher risk of dementia. Heart failure and ischemic heart disease appeared to enhance the association between air pollution and dementia, whereas stroke seemed to be an important intermediate condition between the association of air pollution exposure with dementia.
新出现但相互矛盾的证据表明，空气污染与痴呆症的发生有关，而心血管疾病（CVD）在这种关联中的潜在作用尚不清楚。
调查长期暴露于空气污染与痴呆症之间的关联，并评估 CVD 在该关联中的作用。
设计、地点和参与者：本队列研究的数据来自正在进行的瑞典 Kungsholmen 老龄化和护理研究（SNAC-K），这是一项基于人群的纵向研究，基线评估时间为 2001 年 3 月 21 日至 2004 年 8 月 30 日。在斯德哥尔摩 Kungsholmen 区随机选择的 60 岁及以上、居住在家庭或机构中的 5111 名居民中，有 521 人不符合条件（例如，由于在研究开始前死亡或没有联系信息）。在其余的 4590 人中，有 3363 人（73.3%）接受了评估。目前的分析针对基线时没有痴呆症的 2927 名参与者进行，随访至 2013 年（平均[SD]随访时间，6.01[2.56]年）。随访于 2013 年 2 月 18 日完成，数据于 2018 年 6 月 26 日至 2019 年 6 月 20 日进行分析。
使用分散模型评估 1990 年以来每年的两种主要空气污染物（≤2.5 μm 颗粒物[PM2.5]和氮氧化物[NOx]）的室外水平。
使用 Cox 比例风险回归模型估计痴呆的风险。使用分层分析和广义结构方程模型测试 CVD（即心房颤动、缺血性心脏病、心力衰竭和中风）是否能够改变和介导长期暴露于空气污染与痴呆症之间的关联。
在基线时，2927 名参与者的平均（SD）年龄为 74.1（10.7）岁，1845 名（63.0%）为女性。确定了 364 名患有痴呆症的参与者。在居住地，前 5 年污染物水平每增加一个四分位距，痴呆的风险就会增加高达 50%（PM2.5 差值 0.88μg/m3，HR 为 1.54[95%CI，1.33-1.78]；NOx 差值 8.35μg/m3，HR 为 1.14[95%CI，1.01-1.29]）。心力衰竭（PM2.5 的 HR 为 1.93[95%CI，1.54-2.43]；NOx 的 HR 为 1.43[95%CI，1.17-1.75]）和缺血性心脏病（PM2.5 的 HR 为 1.67[95%CI，1.32-2.12]；NOx 的 HR 为 1.36[95%CI，1.07-1.71]）增强了痴呆风险，而中风似乎是最重要的中间条件，解释了与空气污染相关的痴呆病例的 49.4%。
本研究发现，长期暴露于空气污染与痴呆症风险增加有关。心力衰竭和缺血性心脏病似乎增强了空气污染与痴呆症之间的关联，而中风似乎是空气污染与痴呆症之间关联的一个重要中间条件。
