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Longevity briefs provides a short summary of novel research in biology, medicine, or biotechnology that caught the attention of our researchers in Oxford, due to its potential to improve our health, wellbeing, and longevity.
The problem:
There is currently no medical treatment that can slow down the ageing process, but it appears to be the case that some people age at a more rapid pace than others. Some people start developing age-related frailty and debilitating age-related diseases in their early 60s, while others live into their 80s and 90s relatively free of disease, and show signs of biological function that is comparable to someone decades younger than them. There is a large genetic component to this, but we know that environmental factors can also influence some aspects of ageing.
Research suggests that modifying your environment is unlikely to allow you to live to an exceptional age if you don’t also have the right genes. However, it is currently the only way we may be able to put some form of break on the fundamental biology of ageing, thereby extending healthspan (the number of years lived in good health, free of age-related disease). It isn’t easy to scientifically determine which environmental factors have the largest impact on the rate of ageing, or even whether a given factor can truly be said to ‘accelerate ageing’. Usually, the best that scientists can do is to study how an environmental factor correlates with biological processes that are thought to be important in ageing. In this study, researchers investigate the relationship between air pollution, estimates of accelerated ageing, and dementia.
The discovery:
Researchers analysed data from the UK Biobank, a large anonymised health database from the UK. The analysis included 488,348 participants between the ages of 40 and 70 who were free of dementia at the start of the study and who were followed up for a median of 13.5 years (half of participants were followed for 13.5 years or longer). Using participants’ residential addresses, they then estimated their long-term exposure to five common air pollutants:
Researchers then used two different algorithms that incorporate various physical parameters and blood biomarkers (such as white blood cell count and blood sugar levels) in order to estimate ‘biological age’ by comparing these markers to what is expected based on a population average. For example, if these biomarkers were equivalent to those of the average 50 year-old, then they would be deemed to have a biological age of 50, even if their chronological age was actually 45. This person would then be considered to have an ‘age acceleration’ of 5 years.
The researchers found that higher levels of pollution were generally associated with modest but statistically significant increases in age acceleration. For example, the third of participants with the highest NOx exposure had between 0.1 and 0.39 years more biological age acceleration than the third of participants with the lowest exposure.

Researchers also investigated whether there was a relationship between pollution, dementia and brain structure changes based on MRI data (magnetic resonance imaging). They found that there was a dose-dependent relationship between increased pollutant exposure, reduced white and grey matter brain volume, and increased risk of dementia. The risk of dementia was highest with NO2 exposure, with a 20% increased risk for the third of participants with the highest exposure when compared to the third with the lowest exposure, followed by NOx and PM2.5 (14% increased risk in both cases). Furthermore, researchers found that biological age acceleration predicted brain structure changes and dementia risk. For both algorithms, the 25% of people with the highest biological age acceleration had a 41-45% increased risk of dementia compared to the 25% with the least biological age acceleration.
The implications:
Taken together, these findings suggest that pollution may be accelerating some fundamental changes associated with the ageing process, which in turn accelerates loss of brain volume and development of dementia. For example, continuous exposure to pollutants could result in chronic activation of the immune system, leading to higher levels of inflammation which are known to contribute to brain ageing and dementia. Limiting time spent in highly polluted zones, using air purifiers and other such precautions might therefore plausibly delay ageing and reduce the risk of neurodegenerative disease.
Since this was an observational study, it can’t prove that pollution caused dementia or biological age acceleration. People who live in more polluted areas may be less healthy for other reasons, such as being from a disadvantaged socioeconomic background. While researchers attempted to control for confounding factors like this, such controls aren’t perfect. It’s also important to reiterate that the algorithms used in this study don’t measure true biological age – they just provide an approximation based on certain biomarkers. So we can’t definitively say that pollution is associated with accelerated ageing – simply that it is associated with biological changes typically observed in old age.
Accelerated biological aging and brain structural alterations linking air pollution to dementia risk: a prospective cohort study https://doi.org/10.1016/j.jnha.2026.100836
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