Abstract
INTRODUCTION
Our understanding of how fine particulate matter (PM2.5) impacts cognitive functioning is limited. Systemic inflammation processes may play a role in mediating this effect.
METHODS
This prospective cohort study used data from 66,254 participants aged 18+ between 2006 and 2015 from the Dutch Lifelines Cohort Study and Biobank. Causal mediation analysis was conducted to examine the impact of ambient PM2.5 exposure on cognitive processing time (CPT), using the change in white blood cell (WBC) count and its subtypes as potential mediators.
RESULTS
Heightened PM2.5 exposure was associated with slower CPT (total effect = 81.76 × 10−3, 95% confidence interval [CI] 59.51 × 10−3–105.31 × 10−3). The effect was partially mediated via increased WBC count (indirect effect [IE] = 0.42 × 10−3, 95% CI 0.07 × 10−3–0.90 × 10−3), particularly driven by an increase in monocytes (IE = 0.73 × 10−3, 95% CI 0.24 × 10−3–1.31 × 10−3).
DISCUSSION
Systemic inflammation processes may partially explain the harmful effects of PM2.5 on cognitive functioning, why lower levels of systemic inflammation may help contain its neurotoxic effects.
Highlights
The pathways leading to the neurotoxic effects of fine particulate matter (PM2.5) are poorly understood.
We analyzed data from over 66,000 participants using causal pathway analysis.
Increased white blood cell (WBC) count mediates the effect of PM2.5 on cognitive functioning.
Monocyte count played a crucial role in this low-pollution setting.
Systemic inflammation may contribute to the neurotoxic effects of PM2.5.
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This post is Copyright: Benjamin Aretz,
Gabriele Doblhammer,
Michael T. Heneka | October 16, 2024