Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA, USA.
Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA, USA.
Environ Int. 2024 Jan;183:108418. doi: 10.1016/j.envint.2024.108418. Epub 2024 Jan 3.
While epidemiologic evidence links higher levels of exposure to fine particulate matter (PM) to decreased cognitive function, fewer studies have investigated links with traffic-related air pollution (TRAP), and none have examined ultrafine particles (UFP, ≤100 nm) and late-life dementia incidence.
To evaluate associations between TRAP exposures (UFP, black carbon [BC], and nitrogen dioxide [NO]) and late-life dementia incidence.
We ascertained dementia incidence in the Seattle-based Adult Changes in Thought (ACT) prospective cohort study (beginning in 1994) and assessed ten-year average TRAP exposures for each participant based on prediction models derived from an extensive mobile monitoring campaign. We applied Cox proportional hazards models to investigate TRAP exposure and dementia incidence using age as the time axis and further adjusting for sex, self-reported race, calendar year, education, socioeconomic status, PM, and APOE genotype. We ran sensitivity analyses where we did not adjust for PM and other sensitivity and secondary analyses where we adjusted for multiple pollutants, applied alternative exposure models (including total and size-specific UFP), modified the adjustment covariates, used calendar year as the time axis, assessed different exposure periods, dementia subtypes, and others.
We identified 1,041 incident all-cause dementia cases in 4,283 participants over 37,102 person-years of follow-up. We did not find evidence of a greater hazard of late-life dementia incidence with elevated levels of long-term TRAP exposures. The estimated hazard ratio of all-cause dementia was 0.98 (95 % CI: 0.92-1.05) for every 2000 pt/cm increment in UFP, 0.95 (0.89-1.01) for every 100 ng/m increment in BC, and 0.96 (0.91-1.02) for every 2 ppb increment in NO. These findings were consistent across sensitivity and secondary analyses.
We did not find evidence of a greater hazard of late-life dementia risk with elevated long-term TRAP exposures in this population-based prospective cohort study.
虽然流行病学证据表明，接触更高水平的细颗粒物（PM）与认知功能下降有关，但较少的研究调查了与交通相关的空气污染（TRAP）之间的联系，也没有研究过超细颗粒（UFP，≤100nm）与老年痴呆症发病率之间的关系。
评估 TRAP 暴露（UFP、黑碳 [BC] 和二氧化氮 [NO]）与老年痴呆症发病之间的关联。
我们在西雅图成人思维变化（ACT）前瞻性队列研究（始于 1994 年）中确定了痴呆症的发病率，并根据从广泛的移动监测活动中得出的预测模型，为每个参与者评估了十年平均的 TRAP 暴露情况。我们应用 Cox 比例风险模型，使用年龄作为时间轴，进一步调整性别、自我报告的种族、日历年份、教育程度、社会经济地位、PM 和 APOE 基因型，研究 TRAP 暴露与痴呆症发病率之间的关系。我们进行了敏感性分析，其中我们没有调整 PM 和其他敏感性分析以及二次分析，调整了多个污染物，应用了替代暴露模型（包括总和特定尺寸的 UFP），修改了调整协变量，使用了日历年份作为时间轴，评估了不同的暴露期、痴呆症亚型等。
在 37102 人年的随访中，我们在 4283 名参与者中发现了 1041 例确诊的全因痴呆病例。我们没有发现长期 TRAP 暴露水平升高与老年痴呆症发病风险增加之间存在更大危险的证据。UFP 每增加 2000pt/cm，全因痴呆的估计危险比为 0.98（95%CI：0.92-1.05），BC 每增加 100ng/m，危险比为 0.95（0.89-1.01），NO 每增加 2ppb，危险比为 0.96（0.91-1.02）。这些发现与敏感性和二次分析一致。
在这项基于人群的前瞻性队列研究中，我们没有发现长期 TRAP 暴露水平升高与老年痴呆症发病风险增加之间存在更大危险的证据。
