Discover 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 cause of dementia. Image credits: Borri_Studio/Shutterstock.com
In a recent systematic review published in BMC Public Health, researchers examined the relationship between air pollutants and dementia.
The study found that chronic exposure to higher levels of air pollutants, especially PM2.5 (particulate matter with a diameter <2.5 micrometers) and NO2 (nitrogen dioxide), has been associated with adverse cognitive effects and an increased risk of dementia.
Background
Dementia is a debilitating neurological condition that affects millions of people worldwide, with numbers expected to more than double by 2050. The current increase in neurological disorders such as dementia is known to place a significant burden on healthcare systems, especially as the world population ages.
Several factors, including genetics, lifestyle and nutritional aspects, contribute to dementia. Notably, exposure to air pollution has emerged as a significant modifiable risk factor associated with cognitive decline, Alzheimer’s disease, and other forms of dementia.
Studies have shown that even a small increase in pollutants such as PM2.5 can significantly increase the risk of dementia. Preventing exposure to air pollution could potentially help reduce the incidence of cognitive decline and dementia, especially in the older population.
In the current systematic review, researchers examined the types and concentrations of several air pollutants and assessed their impact on the risk of dementia in adults with chronic respiratory exposure.
About the study
The current systematic review examined studies related to various pollutants, including PM10, PM2.5 and NO2ozone (O3), black carbon (BC), polycyclic aromatic hydrocarbons (PAHs), benzene, toluene, ethylbenzene and xylenes (BTEX) and formaldehyde (FA).
A comprehensive search of the Scopus, PubMed, and Web of Science databases was conducted until May 22, 2023, using specific keywords. Studies were excluded because they were duplicates, review articles, focused solely on brain volume, did not specify the type of air pollutant, examined other pollutants, had a high risk of bias, or due to inaccessible full texts.
The review also excluded studies that focused on neurological or biochemical changes without dementia, non-peer-reviewed articles, and non-English language articles.
After screening 14,924 articles, 53 were included in the review. These included six case-control studies, seven cross-sectional studies, and forty cohort studies conducted in 17 countries, the 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 synthesized narratively due to the heterogeneity of the study.
The review focused on the relationship between the type and concentration of air pollutants and dementia, with studies categorized by Alzheimer’s disease 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 instruments were used to diagnose Alzheimer’s disease and 28 for non-Alzheimer’s dementia. Specifically, the most common methods were medical records, Mini-Mental Status Examination (MMSE), and medical imaging techniques to detect structural changes in the brain.
MRI was known for its ability to measure brain atrophy, especially in mesial-temporal structures, often detectable before the manifestation of clinical symptoms, with a sensitivity of more than 85%.
According to the study, chronic exposure to pollutants such as PM2.5 and NO2 increases hospitalization for Alzheimer’s disease and worsens neurocognitive disorders. In particular, air pollution affects episodic memory, hippocampal structure and brain atrophy.
Mechanistically, pollutants can disrupt the blood-brain barrier, cause oxidative stress, and promote amyloid and tau pathology, contributing to cognitive decline.
Evidence suggests that chronic exposure to pollutants such as NO2, PM2.5 and O3 increases the risk of VaD and worsens its progression through mechanisms such as vascular damage and impaired blood-brain barrier function. Studies show that air pollution contributes to neurovascular unit dysfunction, cortical infarcts and chronic cerebral hypoperfusion, leading to cognitive decline.
Despite some conflicting findings, the majority support a link between air pollutants and VaD, highlighting the need for further research into environmental factors in the development of dementia. In addition, there is evidence that an increase in PM2.5 exposure increases the risk of hospitalization for Parkinson’s.
More than 80% of Parkinson’s patients develop dementia, with the prevalence rising to 50% after ten years. Only two studies addressed FTD, one of which found no link between air pollutants and FTD, while another reported that chronic exposure to PM2.5 reduced gray matter in areas associated with FTD. The different results may arise from variations in the number of cases, age categories and study locations.
The review is enhanced by a large sample size, examining both Alzheimer’s and non-Alzheimer’s dementia and considering a wider range of pollutants. However, it faces challenges such as limited access to the full texts of some studies and a lack of research on certain pollutants, especially regarding their effects on FTD.
Conclusion
In conclusion, the study highlights the significant link between chronic exposure to air pollutants and the development and progression of Alzheimer’s disease. The findings highlight the need for further research into the mechanisms contributing to cognitive decline due to air pollution.
Addressing modifiable risk factors, including air quality, can help prevent or delay the onset of neurodegenerative diseases and reduce their burden on individuals and healthcare systems.