Air pollution has been linked to neurological disorders, particularly cognitive decline, stroke, and neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). In this review chapter, we examine the growing body of research connecting air pollution to neurological conditions. Emerging evidence suggests that pollutants, including fine particulate matter (PM2.5), nitrogen dioxide (NO2), carbon monoxide (CO), sulfur dioxide (SO2), and ozone (O3) are associated with cognitive impairments and an increased risk of stroke and ischemic stroke. Long-term exposure to PM2.5, in particular, has been linked to higher mortality rates and increased hospital admissions for conditions like AD, non-AD dementia, and PD, with vulnerable populations facing an even greater risk. Additionally, this review chapter explores the potential mechanisms underlying these associations, including direct neurotoxicity, neuroinflammation, oxidative stress, vascular dysfunction, and disruptions to the glymphatic system, which plays an important role in brain waste clearance, essential to maintain brain homeostasis. Thus, air pollution-induced damage to the blood-brain barrier (BBB), endothelial dysfunction, which leads to increased permeability in the brain, and systemic inflammation further contribute to both neurodegeneration and cerebrovascular events. Besides, the effects of air pollution on neurodevelopment in children and its impact on metabolic processes, such as insulin resistance, underscore the urgent need for targeted public health interventions to reduce this association. In conclusion, this review chapter emphasises the critical need for reducing environmental pollutants to mitigate their detrimental effects on brain health. The growing body of evidence linking air pollution to cognitive decline, neurological diseases, and cerebrovascular events highlights the urgent need for comprehensive public health strategies.

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Air Pollution as a Risk Factor of Neurodegenerative Diseases and Stroke: Mechanisms of Action and Implications

  • Juliana C. S. Chaves,
  • Ian W. Peall,
  • Emily R. Vivian,
  • Anthony Robert White

摘要

Air pollution has been linked to neurological disorders, particularly cognitive decline, stroke, and neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). In this review chapter, we examine the growing body of research connecting air pollution to neurological conditions. Emerging evidence suggests that pollutants, including fine particulate matter (PM2.5), nitrogen dioxide (NO2), carbon monoxide (CO), sulfur dioxide (SO2), and ozone (O3) are associated with cognitive impairments and an increased risk of stroke and ischemic stroke. Long-term exposure to PM2.5, in particular, has been linked to higher mortality rates and increased hospital admissions for conditions like AD, non-AD dementia, and PD, with vulnerable populations facing an even greater risk. Additionally, this review chapter explores the potential mechanisms underlying these associations, including direct neurotoxicity, neuroinflammation, oxidative stress, vascular dysfunction, and disruptions to the glymphatic system, which plays an important role in brain waste clearance, essential to maintain brain homeostasis. Thus, air pollution-induced damage to the blood-brain barrier (BBB), endothelial dysfunction, which leads to increased permeability in the brain, and systemic inflammation further contribute to both neurodegeneration and cerebrovascular events. Besides, the effects of air pollution on neurodevelopment in children and its impact on metabolic processes, such as insulin resistance, underscore the urgent need for targeted public health interventions to reduce this association. In conclusion, this review chapter emphasises the critical need for reducing environmental pollutants to mitigate their detrimental effects on brain health. The growing body of evidence linking air pollution to cognitive decline, neurological diseases, and cerebrovascular events highlights the urgent need for comprehensive public health strategies.