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 31232 people aged 18+ from 2006 to 2015 from the Dutch Lifelines cohort study. By linking current and past home addresses to air pollution exposure data from ELAPSE, long-term average exposure (≥ ten years) to PM_2.5 and BC was calculated. Lung function was assessed 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 the direct/indirect associations.

Results Higher exposure to PM_2.5 but not BC was directly related to higher CPT and thus slower cognitive processing speed [18.33 (×10⁻³) SD above the mean (95% CI: 6.84, 29.81)]. 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 1.78% (FEV₁) and 2.62% (FVC), but higher for BC (28.49% and 46.22% respectively).

Discussion Our results emphasize 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 emphasizes the health-relevance of fine particles due to their ability to reach vital organs directly.