Linking Particulate Matter Exposure and Neurological Disorders: Evidence from Epidemiology, Biomarkers and Mechanistic Studies

Jan 2, 2026Neurotoxicology

How Air Pollution Particles May Be Connected to Brain Disorders: Evidence from Population Studies, Biological Signs, and Mechanisms

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Abstract

Exposure to particulate matter (PM) is associated with neurological disorders, as evidenced by the integration of 129 research articles from 2002 to 2025.

Particulate matter includes fine (PM₂.₅), coarse (PM₁₀), and ultrafine particles (UFPM), which may contribute to conditions like Alzheimer's and Parkinson's diseases.
Mechanisms of PM-induced neurotoxicity involve oxidative stress, neuroinflammation, mitochondrial dysfunction, and disruption of the blood-brain barrier.
Structural and functional damage may occur in critical brain regions such as the hippocampus and prefrontal cortex due to exposure.
PM₂.₅ can carry neurotoxic metals and organic toxicants, potentially increasing its harmful effects on the nervous system.
Vulnerable populations, particularly children and older adults, may face heightened risks, yet they are underrepresented in existing studies.
Geographic disparities exist in the representation of populations affected by PM, especially in low- and middle-income countries with high PM exposure.

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Exposure to particulate matter (PM) including fine (PM₂.₅), coarse (PM₁₀), and ultrafine particles (UFPM) has emerged as a critical environmental determinant of neurological disorders, including Alzheimer's and Parkinson's diseases, neurodevelopmental impairments, and cognitive decline. This review integrates evidence from 129 research articles (2002-2025) to elucidate the mechanistic, biomarker-based, and public health dimensions of PM-induced neurotoxicity. Mechanistic pathways include oxidative stress, neuroinflammation, mitochondrial dysfunction, and blood-brain barrier disruption, with documented structural and functional damage in brain regions such as the hippocampus and prefrontal cortex. PM₂.₅ serves as a carrier of neurotoxic metals (e.g., lead, cadmium, vanadium) and understudied organic toxicants (e.g., PAHs, pesticides), amplifying its pathogenic potential. Exposure occurs through the olfactory route, systemic circulation, and gut-brain axis, highlighting multiple entry points into the central nervous system. Biomarkers such as Aβ₄₂, phosphorylated tau (p-tau), and α-synuclein are elevated in experimental models, but require greater validation in human PM-exposed populations. Children and older adults represent the most vulnerable groups due to developmental sensitivity and cumulative neuroinflammatory burden, yet remain underrepresented in cohort studies. Geographic disparities further limit generalizability, with low- and middle-income countries underrepresented despite experiencing the highest PM burdens. Future research must advance longitudinal, cohort and life-course studies, multi-omics biomarker discovery, and real-world mixture toxicology to identify intervention targets. These findings call for urgent integration of air pollution control into public health strategies targeting neurological diseases, emphasizing prevention through regulation, early detection, and equity-focused research frameworks.

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Linking Particulate Matter Exposure and Neurological Disorders: Evidence from Epidemiology, Biomarkers and Mechanistic Studies

Abstract

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