背景:虽然流行病学证据将较高水平的细颗粒物(PM2.5)暴露与认知功能下降联系起来,较少研究调查与交通相关空气污染(TRAP)的联系,没有人检查过超细颗粒(UFP,≤100nm)和晚期痴呆发病率。
目的:评估TRAP暴露之间的关联(UFP,黑碳[BC],和二氧化氮[NO2])和晚期痴呆症发病率。
方法:我们在西雅图的成人思想变化(ACT)前瞻性队列研究(从1994年开始)中确定了痴呆症的发病率,并根据广泛的移动监测活动得出的预测模型评估了每个参与者的十年平均TRAP暴露。我们应用Cox比例风险模型,以年龄为时间轴并进一步调整性别,研究TRAP暴露和痴呆发病率。自我报告的种族,日历年,教育,社会经济地位,PM2.5和APOE基因型。我们进行了敏感性分析,我们没有调整PM2.5和其他敏感性,我们调整了多种污染物的二次分析,应用的替代暴露模型(包括总体和特定尺寸的UFP),修改了调整协变量,使用日历年作为时间轴,评估不同的暴露期,痴呆亚型,和其他人。
结果:我们在37,102人年的随访中,在4,283名参与者中发现了1,041例全因痴呆病例。我们没有发现证据表明,随着长期TRAP暴露水平的升高,晚期痴呆发病率的风险更大。UFP每增加2000pt/cm3,全因痴呆的估计风险比为0.98(95%CI:0.92-1.05),每增加100ng/m3BC为0.95(0.89-1.01),和0.96(0.91-1.02),每增加2ppb的NO2。这些发现在敏感性和二次分析中是一致的。
结论:在这项以人群为基础的前瞻性队列研究中,我们没有发现长期TRAP暴露升高的老年痴呆风险更大的证据。
BACKGROUND: While epidemiologic evidence links higher levels of exposure to fine particulate matter (PM2.5) 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.
OBJECTIVE: To evaluate associations between TRAP exposures (UFP, black carbon [BC], and nitrogen dioxide [NO2]) and late-life dementia incidence.
METHODS: 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, PM2.5, and APOE genotype. We ran sensitivity analyses where we did not adjust for PM2.5 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.
RESULTS: 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/cm3 increment in UFP, 0.95 (0.89-1.01) for every 100 ng/m3 increment in BC, and 0.96 (0.91-1.02) for every 2 ppb increment in NO2. These findings were consistent across sensitivity and secondary analyses.
CONCLUSIONS: 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.