Related Experiment Video
Updated: Aug 14, 2026
Systems Analysis of the Neuroinflammatory and Hemodynamic Response to Traumatic Brain Injury
Published on: May 27, 2022
Association Between PM2.5 Components and Cerebral Hypoperfusion: A Mediation Role of Inflammatory Biomarkers
Xingyan Xu1, Xinyue Lu2, Nan Wang3
1Department of Scientific Research, The Second Affiliated Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China.
Background:
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 PM2.5 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 PM2.5 and its components exposure with cerebral hypoperfusion, and assess mediation by inflammatory indicators.
Methods:
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 PM2.5 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.
Results:
PM2.5 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 PM2.5 and cerebral hypoperfusion, whereas leukocytes (4.30%) and monocytes (2.73%) demonstrated significant mediation effects.
Conclusion:
Prolonged exposure to PM2.5 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.
