A Population Study Correlates Air Pollution with Faster Cognitive Aging
A number of large epidemiological studies provide evidence for long-term exposure to greater levels of air pollution to accelerate the onset and progression of age-related disease. A few of these manage to control for the tendency for wealthier people to avoid living in areas with higher particulate air pollution, and the correlation with worse health remains. Mechanistically, it is thought that particulates provoke greater chronic inflammation via their interaction with lung and other tissues, and this in turn contributes to the cell and tissue dysfunction that leads to age-related disease.
The present study assessed cognitive test performance in English older adults in relation to long-term air pollution exposure at the residential address. The follow-up period of 15 years and the large number of repeated measurements make the present study unique in terms of design and data availability. Increasing exposure to NO2, PM10 and PM2.5 was consistently found to be associated with decreased memory and executive function test performance, whilst ozone showed the opposite effect. The results remained similar in the analysis including residents of London only, for whom exposure to NO2 and PM was higher. As an illustrative example, the decline in memory and executive function scores per interquartile range (IQR) increase in long-term NO2 exposure was found equivalent to ageing by about 1.5 and 4 years respectively.
In order to fully elucidate the potentially adverse cognitive effects of air pollution, further study into the underlying biological pathways and mechanisms through which air pollution may contribute to cognitive decline is required alongside the expanding epidemiological work. Translocation of inhaled particles from the lung to the brain via the bloodstream provides one possible pathway through which particulate matter may affect cognition, as well as inhalation through the nose and transportation to the olfactory bulb via olfactory nerves. Evidence for such pathways is currently limited and further experimental studies are required.