HAMBURG — Fine dust particles are about 20 times smaller than the diameter of a human hair, making them invisible to the naked eye, and yet they are very harmful to human health. These particles, released into the air through vehicle emissions, industrial processes and fires, such as those recently seen in Los Angeles, not only contribute to lung cancer and increase the risk of heart attacks or strokes but may also be linked to dementia.
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Numerous epidemiological studies over the years have examined the correlation between air pollution and cognitive decline by analyzing extensive data sets: Where do individuals live? How polluted is their environment? Do they develop Alzheimer’s or other neurodegenerative diseases? Many such studies have identified a connection between increased exposure to fine dust and cognitive impairment, even dementia.
Quantifying the exact impact of air pollution on dementia risk remains challenging. Genetic predisposition, lifestyle factors such as diet and physical activity, and other variables also play a role. “That is one reason why, after more than a century, we still lack a curative therapy for Alzheimer’s,” says neurologist Michael Heneka from the University of Luxembourg. There are simply too many possible causes.
Installing particulate matter monitors in city centers and enforcing environmental restrictions on vehicles will not prevent dementia cases altogether.
Yet researchers may have uncovered another critical piece of the puzzle explaining how this complex and still poorly understood disease develops. What is known so far is that harmful protein deposits, known as amyloid beta plaques, accumulate between neurons and significantly contribute to dementia.
Harmful proteins
Another factor is tau fibrils, strands of a protein that normally stabilize brain cells and facilitate nutrient supply. In Alzheimer’s, tau undergoes chemical changes, rendering it ineffective. Similarly, amyloid beta forms clumps between neurons, which grow into plaques.
The findings consistently indicated a link between air pollution and amyloid beta plaques.
Research suggests that fine dust may accelerate plaque formation. A 2024 study led by German epidemiologist Anke Hüls from Emory University in Georgia examined over a thousand cognitively healthy adults aged 45 to 75, analyzing the concentration of specific proteins in their cerebrospinal fluid. The researchers then compared this data with the subjects’ residential locations and air pollution levels.
A second study involved autopsies of 224 individuals who had donated their brains for Alzheimer’s research. Again, the scientists sought biomarkers of Alzheimer’s and correlated them with the deceased individuals’ places of residence. The findings consistently indicated a link between air pollution and amyloid beta plaques.
“Despite studying two very different population segments, we reached the same conclusion,” says Hüls. Higher fine dust exposure was associated with increased protein deposits in the brain.
Particles trigger inflammation
The mechanisms through which air pollution contributes to plaque formation remain under investigation, but chronic inflammation appears to play a crucial role. Alzheimer’s has long been linked to heightened inflammatory responses. Individuals with elevated inflammation markers seem more prone to developing dementia, and those already exhibiting symptoms often show increased inflammation levels.
The causal relationship, however, is still unclear. Neurologist Heneka and an international research team recently found new evidence suggesting that preventing brain inflammation could be a promising approach to Alzheimer’s treatment. Possible inflammation triggers include high-sugar, high-fat diets, chronic infections, and exposure to fine dust particles.
Heneka, along with researchers from Rostock and Bonn, analyzed data from over 66,000 Dutch adults, examining inflammation markers in their blood, fine dust exposure in their residential areas, and cognitive function. Their study revealed a significant correlation: Prolonged exposure to fine dust was associated with higher inflammation levels and reduced cognitive performance. This was observed even though the studied regions had relatively low air pollution compared to some Asian countries.
The precise biological mechanisms by which airborne fine dust triggers inflammation remain unclear. Yet the particles can enter the brain in two primary ways. One route is directly via the olfactory nerve, while the other involves inhalation into the lungs, where they enter the bloodstream and cross the blood-brain barrier. Once in the brain, these particles can initiate and exacerbate inflammatory processes.
Heneka proposes a third possible mechanism: once fine dust enters the bloodstream and circulates through the body, it may damage other organs, leading to localized inflammation and impaired function. Both factors (systemic inflammation and organ dysfunction) could contribute to cognitive decline individually or in combination. More research is necessary, beginning with cell cultures, followed by animal models, and ultimately human studies.
Every bit is harmful
Many questions remain unanswered. For instance, it is unclear whether prolonged exposure to moderate pollution is more detrimental than short-term exposure to high levels. Is living in Berlin for 20 years more harmful to cognitive function than spending a week in New Delhi annually?
A methodological challenge for epidemiologists like Hüls is that participants’ addresses are often recorded only sporadically. Yet tracking changes in residence could provide insight into how variations in air pollution exposure influence cognitive function over time.
It is also unclear which substances play the greatest role — after all, not all air pollution is the same. Exhaust fumes, tire wear, and even residues from forest fires contain different substances, such as heavy metals, plastics or soot. In order to reduce the risk in the long term, studies are needed to determine which substances exactly trigger the most harmful reactions in the body.
Millions of people worldwide die every year as a result of high levels of fine dust.
But, like many other researchers, there is one thing Hüls is certain about: “Every bit of air pollution is harmful.” The World Health Organization (WHO) estimates that millions of people worldwide die every year as a result of high levels of fine dust. The number of deaths caused by fine dust cannot be calculated precisely — after all, it is impossible to say with certainty in retrospect whether a heart attack or Alzheimer’s disease was actually caused by the small particles. Plus, how harmful fine dust really is depends on whether you have a pre-existing condition and how much you inhale over what period of time.
According to the WHO, in order to avoid potentially harmful consequences, one should not be exposed to more than five micrograms per cubic meter of fine dust on a permanent basis, and no more than 15 micrograms over a 24-hour period. In Germany, an upper limit of 25 micrograms per cubic meter on an annual average has been applied since 2015 for particles up to 2.5 micrometers in size.
Pollution in Germany has decreased significantly since 2000, but it’s still 9.3 micrograms per cubic meter on an annual average, still well above the WHO recommendations. In Heneka’s Dutch study, participants were exposed to fine dust concentrations up to 22 micrograms per cubic meter, which is below Germany’s legal limit. And yet, they still exhibited cognitive impairments.
