Airborne particulates and brain health: The role of PM2.5 in blood-brain-barrier dysfunction.

Ambient particulate matter (PM), especially fine and ultrafine particles, has emerged as a significant environmental risk factor for neurological disorders, largely through its impact on the blood-brain barrier (BBB) and the neurovascular unit. This review summarizes current evidence on how PM affects BBB integrity, emphasizing the coordinated and cell-specific responses that drive neurovascular dysfunction. Upon systemic or neural translocation, PM induces oxidative stress and inflammation in endothelial cells, disrupting tight junctions (TJs), enhancing permeability, and upregulating adhesion molecules (e.g. ICAM-1 and VCAM-1), which facilitate immune cell infiltration. Pericytes contribute to these processes in a stage-dependent manner, promoting BBB leakage through detachment and inflammation in acute settings while participating in later reparative processes such as angiogenesis and neurogenesis. Astrocytes respond to PM exposure by adopting a reactive phenotype, releasing pro-inflammatory cytokines and reactive oxygen species that exacerbate barrier disruption and impair neurovascular coupling. Microglia act as central mediators of neuroinflammation, releasing cytokines that weaken TJs and perpetuate endothelial dysfunction. These mechanisms are further modulated by particle properties and host-related factors including age, metabolic status, and pre-existing comorbidities. The resulting cascade of BBB impairment and neuroinflammation underscores the multifaceted nature of PM-induced neurotoxicity and identifies potential cellular targets for intervention.

• Publication year

  2026

• Venue

  Journal of Cerebral Blood Flow and Metabolism

• Publication date

  2026-02-08

• Fields of study

  Medicine, Environmental Science

• Identifiers
  DOI 10.1177/0271678X261418925PMID 41656668PMCID PMC12885965
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar

• No claims are published for this paper.

• No concepts are published for this paper.

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