Alzheimer's disease (AD) is a neurodegenerative disorder that primarily affects older adults. Gradually impaired memory, attention, and cognitive functions, which affect daily living activities, are the major symptoms of AD. Nowadays, researchers believe that the presence of extracellular β-amyloid1–42 (Aβ1–42) plaques and intraneuronal tau aggregations (neurofibrillary tangles (NFTs) is the major cause of AD. However, the exact cause of Alzheimer's is not fully understood, researchers have identified several more risk factors, which include genetics, neuroinflammation, age, lifestyle, and environmental factors.1
Particulate matter, or PM, refers to particles found in the air, including dust, soot, dirt, smoke, and liquid droplets. PM2.5 stands for particles that are 2.5 micrometers or smaller in diameter. Due to its small size, PM2.5 can remain suspended in the air for long periods of time and can be absorbed deep into the bloodstream, inducing cell inflammation, apoptosis, and DNA damage, which can cause various complications in the human body such as cardiovascular system, respiratory system, immune system, etc.1
A recent systematic review and meta-analysis using more than 6.33 million people from 26 countries across the world showed a significant association between PM2.5 exposure and neurological disorders, especially stroke, dementia, Alzheimer's disease, autism spectrum disorder, and Parkinson's disease. Also, a significant influence by mean PM2.5 concentration and the duration of exposure was found, in which long-term PM2.5 exposure (months to years) was associated with increased risks of dementia (1.16, 95% CI 1.07–1.26) and Alzheimer's disease (3.26, 95% 0.84–12.74). The risk was higher in those who identified as white, women compared to men, and age group 80 years and older. Moreover, for every 5 μg/m³ increase in annual PM2.5 concentration, the hazard ratio was 1.13 (95% CI 1.12–1.14) for the first hospital admission of Alzheimer’s disease and related dementias patients.2
The exact mechanism behind this link between PM 2.5 and AD is still part of ongoing research. A proposed hypothesis from the current evidence is that through inhalation fine particles directly enter the blood circulation and cross the blood-brain barrier (BBB), resulting in PM2.5- aggravated cytokine release, neuronal change, then cell apoptosis. Furthermore, it is hypothesized that PM2.5 causes perivascular injury and induces amyloid aggregation and neurofibrillary tangle. Two studies on microglial cells found that acute high-dose PM2.5 exposure decreased cell survival as a result of neuroinflammation and production of reactive oxygen species (ROS). A neuropathology study using brain tissue donors also showed the significant association of traffic-related PM2.5 (based on home address) with the high CERAD score for the 1 and 3-year exposure window, thus contributing to epidemiologic evidence that PM2.5 affects β-amyloid deposition in the brain. Interestingly, compared to a person with or without APOE ε4, researchers found that the association between PM2.5 and neuropathology markers was strong among donors without APOE ε4 alleles.3
While more research is needed to fully understand the relationship between PM2.5 exposure and Alzheimer's disease, reducing exposure to air pollution, including PM2.5, through measures like improving air quality standards, reducing emissions from vehicles and industrial sources, and increasing green spaces in urban areas, may help mitigate the risk. Additionally, individuals who live in countries with high PM2.5 levels can protect themselves from air pollution by avoiding outdoor activities during times of high pollution, using personal mask protection, and indoor air purifiers, and advocating for policies that promote clean air.4
