Uncover the growing evidence linking air pollution to cognitive decline and what it means for the future of brain health.
Study: Air pollution: a latent key driving force of dementia. Image Credit: Borri_Studio/Shutterstock.com
In a recent systematic review published in BMC Public Health, researchers investigated the relationship between air pollutants and dementia.
The study found that chronic exposure to higher levels of air pollutants, especially PM2.5 (particulate matter of diameter <2.5 micrometers) and NO2 (nitrogen dioxide), was associated with adverse cognitive effects and an increased risk of dementia.
Background
Dementia is a debilitating neurological condition that affects millions globally, with numbers expected to more than double by 2050. The current rise in neurological disorders like dementia is known to significantly burden healthcare systems, particularly with the world’s population aging.
Various factors, including genetics, lifestyle, and dietary aspects, contribute to dementia. Notably, exposure to air pollution has emerged as a significant modifiable risk factor linked to cognitive decline, Alzheimer's disease, and other forms of dementia.
Studies have shown that even a small increase in pollutants like PM2.5 can significantly raise dementia risks. Preventing exposure to air pollution could potentially help reduce the incidence of cognitive decline and dementia, especially in the older population.
In the present systematic review, researchers examined the types and concentrations of various air pollutants and assessed their impact on the risk of dementia in adults with chronic respiratory exposure.
About the study
The present systematic review examined studies related to various pollutants, including PM10, PM2.5, NO2, ozone (O3), black carbon (BC), polycyclic aromatic hydrocarbons (PAHs), benzene, toluene, ethylbenzene, and xylenes (BTEX), and formaldehyde (FA).
A comprehensive search in Scopus, PubMed, and Web of Science databases was conducted until May 22, 2023, using specific keywords. Studies were excluded for being duplicated articles, review articles, focusing solely on brain volume, not specifying the type of air pollutant, examining other pollutants, having a high risk of bias, or due to inaccessible full texts.
The review also excluded studies focusing on neurological or biochemical changes without dementia, non-peer-reviewed articles, and non-English papers.
After screening 14,924 articles, 53 were included in the review. These included six case-control, seven cross-sectional, and 40 cohort studies conducted in 17 countries, with a majority from the United States, and involving a total of 173,698,774 participants.
The Joanna Briggs Institute (JBI) checklist was used for quality control, and findings were narratively synthesized due to study heterogeneity.
The review focused on the relationship between the type and concentration of air pollutants and dementia, categorizing studies based on Alzheimer's and non-Alzheimer's dementia (vascular dementia [VaD], Parkinson's disease [PD], frontotemporal dementia [FTD], and dementia with Lewy bodies [DLB]).
Results and discussion
A total of 21 tools were employed for diagnosing Alzheimer's dementia and 28 for non-Alzheimer's dementia. Notably, the most prevalent methods included medical records, Mini-Mental Status Examination (MMSE), and medical imaging techniques to detect structural changes in the brain.
MRI was noted for its ability to measure brain atrophy, especially in mesial-temporal structures, often detectable prior to clinical symptom manifestation, with sensitivity exceeding 85%.
As per the study, chronic exposure to pollutants like PM2.5 and NO2 increases hospitalization for Alzheimer’s dementia and exacerbates neurocognitive disorders. Notably, air pollution affects episodic memory, hippocampal structure, and brain atrophy.
Mechanistically, pollutants may disrupt the blood-brain barrier, induce oxidative stress, and promote amyloid and tau pathology, contributing to cognitive decline.
Evidence suggests that chronic exposure to pollutants like NO2, PM2.5, and O3 increases the risk of VaD and exacerbates its progression through mechanisms like vascular damage and disrupted blood-brain barrier function. Studies indicate that air pollution contributes to neurovascular unit dysfunction, cortical infarcts, and chronic cerebral hypoperfusion, leading to cognitive decline.
Despite some contradictory findings, the majority support a link between air pollutants and VaD, highlighting the need for further research on environmental factors in dementia development. Furthermore, evidence suggests that an increase in PM2.5 exposure raises the risk of hospitalization for PD.
Over 80% of PD patients develop dementia, with prevalence rising to 50% after ten years. Only two studies addressed FTD, of which one found no association between air pollutants and FTD, while another reported that chronic PM2.5 exposure reduced gray matter in areas linked to FTD. The differing results may stem from variations in case numbers, age ranges, and study locations.
The review is strengthened by a large sample size, addressing both Alzheimer's and non-Alzheimer's dementia and considering a broader range of pollutants. However, it faces challenges such as limited access to full texts of some studies and a lack of research on certain pollutants, particularly regarding their effects on FTD.
Conclusion
In conclusion, the study highlights the significant association between chronic exposure to air pollutants and the development and progression of Alzheimer's dementia. The findings highlight the need for further research on the mechanisms contributing to air pollution-related cognitive decline.
Addressing modifiable risk factors, including air quality, may help prevent or delay the onset of neurodegenerative disorders and alleviate their burden on individuals and healthcare systems.
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