Researchers have shed new light on the way in which air pollution can cause cognitive decline.
Fine particulate matter, known as PM2.5, is a complex mixture of many chemicals that can be inhaled deep into the lungs. While PM2.5 exposure has long been linked to tissue damage and inflammation in the lung, its role in cognitive decline is only now gaining attention.
In a recent population-based study, researchers from the universities of Rostock, Bonn and Luxembourg have uncovered a potential link: systemic inflammation, driven by an increase in monocytes – a type of white blood cells – may be a key mediator in how PM2.5 exposure contributes to cognitive impairment.
PM2.5 are fine airborne particles small enough to enter the lungs and even the bloodstream, posing significant health risks.
Long-term exposure has been linked to neurodegenerative diseases like Alzheimer’s and Parkinson’s, resulting in air pollution being listed as one of the modifiable risk factors in the recent report of the Lancet commission on dementia prevention, intervention and care. However, the mechanisms through which PM2.5 affects cognitive function remain poorly understood.
While most studies on cognitive decline focus on elderly people, there is growing evidence that chronic low-level exposure to PM2.5 may also affect younger adults.
Investigating these effects across a broader demographic may reveal how early and mid-life exposure contributes to long-term cognitive outcomes. To explore this, the researchers analysed data from over 66,000 participants in the Dutch Lifelines cohort.
Combining adult participants’ blood analysis and cognitive testing over a period of 10 years (2006 – 2015) with air polution data at their home address from the ELAPSE project, they uncovered new insights into the mechanisms underlying the effect of PM2.5 exposure on brain health.
The researchers found that PM2.5 exposure correlates with a decline in cognitive processing time (CPT), a measure of how quickly the brain can respond to stimuli. Interestingly, an increase in white blood cell count, particularly monocytes, the largest subtype involved in immune responses, mediated a significant part of this effect.
Dr Benjamin Aretz, research scientist at the University Hospital Bonn and first author of the study, said: “Systemic inflammation may act as a key intermediary, linking PM2.5 exposure to impaired cognitive function.
This is the first large-scale study to directly tie changes in the number of white blood cells to the cognitive effects of fine particulate matter.
While PM2.5 can directly affect the brain by crossing the blood-brain barrier and triggering local inflammation, this study highlights the broader systemic inflammation upon exposure.
Researcher Prof. Gabriele Doblhammer said: “We hypothesise that the number of white blood cells rise in response to pollutants. Inflammation was already shown to play an important role in the development of neurodegenerative diseases. Hence, the inflammation we see in response to air polution may disrupt immune functions in the brain, thereby indirectly impairing cognitive health.”
Senior author Prof. Michael Heneka concluded: “Given the strong correlation between air pollution and cognitive deficits, further studies are essential to pinpoint which pollutants and cellular mechanisms mediate this effect.”
Such markers could inform future public health policies aimed at mitigating the brain health risks posed by long-term PM2.5exposure.
