Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor.
Department of Epidemiology, Boston University School of Public Health, Boston, Massachusetts.
JAMA Intern Med. 2023 Oct 1;183(10):1080-1089. doi: 10.1001/jamainternmed.2023.3300.
Emerging evidence indicates that exposure to fine particulate matter (PM2.5) air pollution may increase dementia risk in older adults. Although this evidence suggests opportunities for intervention, little is known about the relative importance of PM2.5 from different emission sources.
To examine associations of long-term exposure of total and source-specific PM2.5 with incident dementia in older adults.
DESIGN, SETTING, AND PARTICIPANTS: The Environmental Predictors of Cognitive Health and Aging study used biennial survey data from January 1, 1998, to December 31, 2016, for participants in the Health and Retirement Study, which is a nationally representative, population-based cohort study in the US. The present cohort study included all participants older than 50 years who were without dementia at baseline and had available exposure, outcome, and demographic data between 1998 and 2016 (N = 27 857). Analyses were performed from January 31 to May 1, 2022.
The 10-year mean total PM2.5 and PM2.5 from 9 emission sources at participant residences for each month during follow-up using spatiotemporal and chemical transport models.
The main outcome was incident dementia as classified by a validated algorithm incorporating respondent-based cognitive testing and proxy respondent reports. Adjusted hazard ratios (HRs) were estimated for incident dementia per IQR of residential PM2.5 concentrations using time-varying, weighted Cox proportional hazards regression models with adjustment for the individual- and area-level risk factors.
Among 27 857 participants (mean [SD] age, 61 [10] years; 15 747 [56.5%] female), 4105 (15%) developed dementia during a mean (SD) follow-up of 10.2 [5.6] years. Higher concentrations of total PM2.5 were associated with greater rates of incident dementia (HR, 1.08 per IQR; 95% CI, 1.01-1.17). In single pollutant models, PM2.5 from all sources, except dust, were associated with increased rates of dementia, with the strongest associations for agriculture, traffic, coal combustion, and wildfires. After control for PM2.5 from all other sources and copollutants, only PM2.5 from agriculture (HR, 1.13; 95% CI, 1.01-1.27) and wildfires (HR, 1.05; 95% CI, 1.02-1.08) were robustly associated with greater rates of dementia.
In this cohort study, higher residential PM2.5 levels, especially from agriculture and wildfires, were associated with higher rates of incident dementia, providing further evidence supporting PM2.5 reduction as a population-based approach to promote healthy cognitive aging. These findings also indicate that intervening on key emission sources might have value, although more research is needed to confirm these findings.
新出现的证据表明，暴露于细颗粒物（PM2.5）空气污染可能会增加老年人患痴呆症的风险。尽管这一证据为干预提供了机会，但对于来自不同排放源的 PM2.5 的相对重要性知之甚少。
研究长期暴露于总 PM2.5 和特定来源 PM2.5 与老年人发生痴呆症的关联。
设计、地点和参与者：环境预测认知健康和衰老研究使用了 1998 年 1 月 1 日至 2016 年 12 月 31 日期间的每两年一次的调查数据，参与者来自美国的一项具有全国代表性的、基于人群的队列研究——健康与退休研究。本队列研究包括所有年龄在 50 岁以上、基线时无痴呆且在 1998 年至 2016 年期间有可用暴露、结局和人口统计学数据的参与者（N=27857）。分析于 2022 年 1 月 31 日至 5 月 1 日进行。
在随访期间，每月使用时空和化学传输模型计算参与者居住地的 10 年平均总 PM2.5 和来自 9 个排放源的 PM2.5。
主要结局是通过结合基于应答者的认知测试和代理应答者报告的验证算法来确定的痴呆症发病情况。使用时间变化、加权 Cox 比例风险回归模型，根据个体和地区水平的风险因素，对每个 IQR 的住宅 PM2.5 浓度的痴呆症发病风险进行调整后的危害比（HR）估计。
在 27857 名参与者（平均[标准差]年龄 61[10]岁；15747[56.5%]为女性）中，4105 人（15%）在平均（标准差）10.2[5.6]年的随访中发生了痴呆症。总 PM2.5 浓度较高与较高的痴呆症发病风险相关（HR，1.08/ IQR；95%CI，1.01-1.17）。在单污染物模型中，除灰尘外，所有来源的 PM2.5 均与痴呆症发病风险增加相关，其中农业、交通、煤炭燃烧和野火与痴呆症发病风险的相关性最强。在控制所有其他来源的 PM2.5 和共污染物后，只有来自农业的 PM2.5（HR，1.13；95%CI，1.01-1.27）和野火（HR，1.05；95%CI，1.02-1.08）与较高的痴呆症发病风险仍显著相关。
在这项队列研究中，较高的住宅 PM2.5 水平，特别是来自农业和野火的 PM2.5 水平，与较高的痴呆症发病风险相关，进一步提供了支持减少 PM2.5 以促进健康认知衰老的人群为基础的方法的证据。这些发现还表明，干预关键排放源可能具有价值，尽管需要更多的研究来证实这些发现。
