Background

Exposure to fine particulate matter and black carbon is related to cognitive impairment and poor lung function, but less is known about the routes taken by different types of air pollutants to affect cognition.

Objectives

We tested two possible routes of fine particulate matter (PM_2.5) and black carbon (BC) in impairing cognition, and evaluated their importance: a direct route over the olfactory nerve or the blood stream, and an indirect route over the lung.

Methods

We used longitudinal observational data for 49,705 people aged 18+ from 2006 to 2015 from the Dutch Lifelines cohort study. By linking current home addresses to air pollution exposure data from ELAPSE in 2010, long-term average exposure to PM_2.5 and BC was assessed. Lung function was measured by spirometry and Global Initiative (GLI) z-scores of forced expiratory volume in 1s (FEV₁) and forced vital capacity (FVC) were calculated. Cognitive performance was measured by cognitive processing time (CPT) assessed by the Cogstate Brief Battery. Linear structural equation modeling was performed to test direct/indirect associations.

Results

Higher exposure to PM_2.5 but not BC was related to higher CPT and slower cognitive processing speed [Total Effect PM_2.5: FEV₁ model = 8.31 × 10⁻³ (95% CI: 5.71 × 10⁻³, 10.91 × 10⁻³), FVC model = 8.30 × 10⁻³ (95% CI: 5.69 × 10⁻³, 10.90 × 10⁻³)]. The direct association of PM_2.5 constituted more than 97% of the total effect. Mediation by lung function was low for PM_2.5 with a mediated proportion of 1.32% (FEV₁) and 2.05% (FVC), but higher for BC (7.01% and 13.82% respectively).

Discussion

Our results emphasise the importance of the lung acting as a mediator in the relationship between both exposure to PM_2.5 and BC, and cognitive performance. However, higher exposure to PM_2.5 was mainly directly associated with worse cognitive performance, which emphasises the health-relevance of fine particles due to their ability to reach vital organs directly.

中文翻译：

---

长期接触细颗粒物、肺功能和认知能力：一项关于潜在途径的前瞻性荷兰队列研究

背景

接触细颗粒物和黑碳与认知障碍和肺功能不良有关，但对不同类型空气污染物影响认知的途径知之甚少。

目标

我们测试了细颗粒物 (PM _2.5 ) 和黑碳 (BC) 损害认知的两种可能途径，并评估了它们的重要性：通过嗅觉神经或血流的直接途径，以及通过肺的间接途径。

方法

我们使用了 2006 年至 2015 年荷兰生命线队列研究中 49,705 名 18 岁以上人群的纵向观察数据。通过将当前家庭住址与 2010 年来自 ELAPSE 的空气污染暴露数据联系起来，对 PM _2.5和 BC的长期平均暴露进行了评估。通过肺活量测定法测量肺功能，并计算₁秒内用力呼气量 (FEV ₁ ) 的全球倡议 (GLI) z 分数和用力肺活量 (FVC)。认知表现通过 Cogstate Brief Battery 评估的认知处理时间 (CPT) 来衡量。进行线性结构方程建模以测试直接/间接关联。

结果

较高的 PM _2.5暴露而非 BC 与较高的 CPT 和较慢的认知处理速度有关 [总效应 PM _2.5 : FEV ₁模型 = 8.31 × 10 ^-3 (95% CI: 5.71 × 10 ^-3 , 10.91 × 10 ^-3 ) , FVC 模型 = 8.30 × 10 ^-3 (95% CI: 5.69 × 10 ^-3 , 10.90 × 10 ^-3 )]。PM _2.5的直接关联占总影响的 97% 以上。PM _2.5的肺功能介导较低，介导比例为 1.32% (FEV ₁ ) 和 2.05% (FVC)，但 BC 更高（分别为 7.01% 和 13.82%）。

讨论

我们的研究结果强调了肺在暴露于 PM _2.5和 BC 与认知能力之间的关系中作为中介的重要性。然而，更多地接触 PM _2.5主要与较差的认知能力直接相关，这强调了细颗粒物的健康相关性，因为它们能够直接到达重要器官。