Association Between PM_2.5 Components and Cerebral Hypoperfusion: A Mediation Role of Inflammatory Biomarkers.

Authors

Xingyan Xu, Xinyue Lu, Nan Wang, Liuyan Zheng, Jianhui Guo, Tongjin Xu, Yiming Guo, Hao Li, Yi Yang, Le Yang

Published in

European journal of neurology. Volume 33. Issue 8. Pages e70716.

Abstract

Cerebral hypoperfusion, an acute manifestation of intracranial arterial stenosis (ICAS), is particularly concerning among older East Asian adults given its high prevalence. Systemic inflammation triggered by PM_2.5 exposure has been linked to cerebrovascular diseases, yet evidence on its specific components of hypoperfusion in this vulnerable group remains limited. We explore associations between PM_2.5 and its components exposure with cerebral hypoperfusion, and assess mediation by inflammatory indicators.
We analyzed 967 patients with symptomatic ICAS at the First Affiliated Hospital of Soochow University. Hypoperfusion was evaluated using multimodal CT imaging and quantified with MIStar software. Three-year exposure to PM_2.5 and its components was estimated using the TAP database. Associations were evaluated using generalized additive models and restricted cubic spline regression, while weighted quantile sum regression assessed mixture effects. Mediation analysis quantified inflammatory markers' roles in these relationships.
PM_2.5 was significantly association with cerebral hypoperfusion (OR = 4.344, 95% CI: 3.323-5.734), with black carbon (BC) showing the strongest association (OR = 4.396, 95% CI: 3.327-5.869), followed by sulfate (SO₄ ^2-) (OR = 4.359), organic matter (OM) (OR = 4.278), nitrate (NO₃ ^-) (OR = 3.552), and ammonium (NH₄ ⁺) (OR = 3.313). OM (44.2%) and BC (42.2%) contributed 86% of the total mixture effect. Neutrophils mediated 5.37% of the total effect between PM_2.5 and cerebral hypoperfusion, whereas leukocytes (4.30%) and monocytes (2.73%) demonstrated significant mediation effects.
Prolonged exposure to PM_2.5 and its components, particularly OM and BC, was associated with increased cerebral hypoperfusion risk, partially mediated by inflammatory responses. These findings highlight the need for component-targeted air quality policies to reduce cerebrovascular risk in vulnerable populations.

PMID:
42593216
Bibliographic data and abstract were imported from PubMed on 13 Aug 2026.

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