A review of respirable fine particulate matter (PM2.5)-induced brain damage

Abstract

Respirable fine particulate matter (PM2.5) has been one of the most widely publicized indicators of pollution in recent years. Epidemiological studies have established a strong association between PM2.5, lung disease, and cardiovascular disease. Recent studies have shown that PM2.5 is also strongly associated with brain damage, mainly cerebrovascular damage (stroke) and neurological damage to the brain (changes in cognitive function, dementia, psychiatric disorders, etc.). PM2.5 can pass through the lung–gas–blood barrier and the “gut–microbial–brain” axis to cause systemic oxidative stress and inflammation, or directly enter brain tissue via the olfactory nerve, eventually damaging the cerebral blood vessels and brain nerves. It is worth mentioning that there is a time window for PM2.5-induced brain damage to repair itself. However, the exact pathophysiological mechanisms of brain injury and brain repair are not yet fully understood. This article collects and discusses the mechanisms of PM2.5-induced brain injury and self-repair after injury, which may provide new ideas for the prevention and treatment of cerebrovascular and cerebral neurological diseases.

A Photoelectrochemical Sensor for Real-Time Monitoring of Neurochemical Signals in the Brain of Awake Animals

“…These particles ingress the respiratory system via the nasal cavity, where their aggregation triggers oxidative stress and inflammation within the lung. Subsequently, a significant influx of inflammatory mediators traverses the air–blood barrier, precipitating systemic inflammation and consequent brain injury. , Recent studies have linked brain injuries resulting from PM2.5 exposure to conditions such as stroke, brain tumors, cognitive decline, dementia, psychiatric disorders, and an increased risk of neurodegenerative diseases . While extensive epidemiological research has been conducted, current experimental investigations focus on the impact of PM2.5 exposure on brain function through behavioral studies (such as memory and cognitive functions) in laboratory animals, histology examinations, and protein detections .…”

Association between Fine Particulate Matter Exposure and Cerebrospinal Fluid Biomarkers of Alzheimer’s Disease among a Cognitively Healthy Population-Based Cohort

“… can pass through the lung gas–blood barrier or through the gut–brain axis, or it can directly enter brain tissue via the olfactory nerve to promote oxidative stress and inflammation, processes directly related to AD pathogenesis. 6 , 7 Growing evidence also suggests that cerebrovascular damage may contribute to dementia and exposure is associated with biomarkers of endothelial injury in blood and cerebrospinal fluid (CSF), further implicating the adverse effect of on CSF biomarkers. 8 Because is a heterogeneous mixture, different sources of exposure often have varying degrees of toxicity, and most existing studies have focused on ambient exposure, rather than those merely from traffic-related emissions.…”

Neuroprotective aftermath of Monodora myristica and Glycyrrhiza glabra against cassava diet containing vacuum gas oil induced brain injury in Wistar rats

“…One of the main groups of organic compounds in particulate matter (PM) is PAHs. Recent research has demonstrated a high correlation between PM2.5 and brain damage, primarily midbrain cerebrovascular injury (stroke) and neurological damage [11] . Furthermore, PM2.5 may harm mitochondria of brain cells thereby producing ROS in brain cells [11] .…”