Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA, USA.
Department of Biostatistics, University of Washington, Seattle, WA, USA.
J Alzheimers Dis. 2019;71(3):1015-1025. doi: 10.3233/JAD-190563.
Cerebrovascular diseases play an important role in dementia. Air pollution is associated with cardiovascular disease, with growing links to neurodegeneration. Prior studies demonstrate associations between fine particulate matter (PM2.5) and biomarkers of endothelial injury in the blood; however, no studies have evaluated these biomarkers in cerebrospinal fluid (CSF).
We evaluate associations between short-term and long-term PM2.5 exposure with CSF vascular cell adhesion molecule-1 (VCAM-1) and e-selectin in cognitively normal and mild cognitive impairment (MCI)/Alzheimer's disease (AD) individuals.
We collected CSF from 133 community volunteers at VA Puget Sound between 2001-2012. We assigned short-term PM2.5 from central monitors and long-term PM2.5 based on annual average exposure predictions linked to participant addresses. We performed analyses stratified by cognitive status and adjusted for key covariates with tiered models. Our primary exposure windows for the short-term and long-term analyses were 7-day and 1-year averages, respectively.
Among cognitively normal individuals, a 5 μg/m3 increase in 7-day and 1-year average PM2.5 was associated with elevated VCAM-1 (7-day: 35.4 (9.7, 61.1) ng/ml; 1-year: 51.8 (6.5, 97.1) ng/ml). A 5 μg/m3 increase in 1-year average PM2.5, but not 7-day average, was associated with elevated e-selectin (53.3 (11.0, 95.5) pg/ml). We found no consistent associations among MCI/AD individuals.
We report associations between short-term and long term PM2.5 and CSF biomarkers of vascular damage in cognitively normal adults. These results are aligned with prior research linking PM2.5 to vascular damage in other biofluids as well as emerging evidence of the role of PM2.5 in neurodegeneration.
脑血管疾病在痴呆症中起着重要作用。空气污染与心血管疾病有关,与神经退行性变的联系也越来越多。先前的研究表明,细颗粒物(PM2.5)与血液内皮损伤的生物标志物之间存在关联;然而,尚无研究评估这些生物标志物在脑脊液(CSF)中的水平。
我们评估了短期和长期 PM2.5 暴露与认知正常和轻度认知障碍(MCI)/阿尔茨海默病(AD)个体 CSF 血管细胞黏附分子-1(VCAM-1)和 E-选择素之间的关系。
我们于 2001-2012 年间从 VA Puget Sound 社区志愿者中收集 CSF。我们根据与参与者地址相关的年度平均暴露预测值,为中央监测器分配短期 PM2.5,为长期 PM2.5 分配。我们根据认知状态对分析进行分层,并使用分层模型调整关键协变量。我们的短期和长期分析的主要暴露窗口分别为 7 天和 1 年平均。
在认知正常的个体中,PM2.5 浓度每增加 5 μg/m3,与 VCAM-1 水平升高相关(7 天:35.4(9.7,61.1)ng/ml;1 年:51.8(6.5,97.1)ng/ml)。PM2.5 浓度每增加 5 μg/m3,与 E-选择素水平升高相关(1 年:53.3(11.0,95.5)pg/ml),但这种相关性仅见于长期暴露,而与短期暴露无关。我们在 MCI/AD 个体中未发现一致的关联。
我们报告了短期和长期 PM2.5 与认知正常成年人 CSF 血管损伤生物标志物之间的关联。这些结果与先前将 PM2.5 与其他生物流体中的血管损伤联系起来的研究以及 PM2.5 在神经退行性变中的作用的新证据相一致。