Libby Tanya E, Ilango Sindana D, Leary Cindy S, Semmens Erin O, Adam Claire E, Fitzpatrick Annette L, Kaufman Joel D, Hajat Anjum
Department of Epidemiology, University of Washington, Seattle, Washington.
Center for Population Health Research, School of Public and Community Health Sciences, University of Montana, Missoula, Montana.
Environ Epidemiol. 2024 Apr 12;8(3):e306. doi: 10.1097/EE9.0000000000000306. eCollection 2024 Jun.
Growing evidence links air pollution exposure to the risk of dementia. We hypothesized that hypertension may partially mediate this effect.
We previously documented an association between air pollution and dementia in the Ginkgo Evaluation of Memory Study, a randomized, placebo-controlled trial of 3069 adults ≥75 years across four US sites who were evaluated for dementia every 6 months from 2000-2008. We utilized a two-stage regression approach for causal mediation analysis to decompose the total effect of air pollution on dementia into its natural direct and indirect effect through prevalent hypertension. Exposure to air pollution in the 10 or 20 years before enrollment was assigned using estimates from fine-scale spatial-temporal models for PM, PM, and NO. We used Poisson regression models for hypertension and Cox proportional hazard models for time-to-incident all-cause dementia, adjusting for confounders.
Participants were free of mild cognitive impairment at baseline (n = 2564 included in analyses); 69% had prevalent hypertension at baseline. During follow-up, 12% developed all-cause dementia (Alzheimer's disease [AD] = 212; vascular dementia with or without AD [VaD/AD mixed] = 97). We did not find an adverse effect of any air pollutant on hypertension. Hypertension was associated with VaD/AD mixed (HR, 1.92 [95% CI = 1.14, 3.24]) but not AD. We did not observe mediation through hypertension for the effect of any pollutant on dementia outcomes.
The lack of mediated effect may be due to other mechanistic pathways and the minimal effect of air pollution on hypertension in this cohort of older adults.
越来越多的证据表明,接触空气污染会增加患痴呆症的风险。我们推测高血压可能部分介导了这种效应。
在银杏记忆评估研究中,我们之前记录了空气污染与痴呆症之间的关联。该研究是一项随机、安慰剂对照试验,在美国四个地点对3069名75岁及以上的成年人进行了研究,从2000年至2008年每6个月对他们进行一次痴呆症评估。我们采用两阶段回归方法进行因果中介分析,将空气污染对痴呆症的总效应分解为通过高血压的自然直接效应和间接效应。使用细粒度时空模型对PM、PM和NO的估计值来确定入组前10年或20年的空气污染暴露情况。我们使用泊松回归模型分析高血压,使用Cox比例风险模型分析全因痴呆症发病时间,并对混杂因素进行了调整。
参与者在基线时无轻度认知障碍(分析纳入n = 2564);69%在基线时患有高血压。在随访期间,12%的人患上了全因痴呆症(阿尔茨海默病[AD] = 212;伴有或不伴有AD的血管性痴呆[VaD/AD混合] = 97)。我们没有发现任何空气污染物对高血压有不良影响。高血压与VaD/AD混合相关(HR,1.92[95%CI = 1.14,3.24]),但与AD无关。我们没有观察到任何污染物对痴呆症结局的影响通过高血压介导。
缺乏介导效应可能是由于其他机制途径以及空气污染对该老年人群高血压的影响极小。