There is evidence for particulate air pollution to raise the risk of age-related diseases via mechanisms such as increased levels of chronic inflammation. While the burden of age-related disease varies widely from region to region, establishing the relative weight of specific contributions is a challenge. Poverty, particulate air pollution, high rates of chronic infection, and other environmental factors thought likely to lead to a greater risk of age-related disease all tend to overlap to some degree.
Thus while there are plausible mechanisms for particulate air pollution to spur chronic inflammation and thus speed the onset of age-related disease, and these mechanisms are well-demonstrated in laboratory animals, one cannot rule out the possibility that it is nonetheless the case that much of the observed differences in life expectancy and incidence of age-related conditions in human populations are primarily a result of worse access to medical resources. Or differences in culture that lead to differing levels of physical activity or differences in diet that add up over time. And so forth.
That said, some of the more recent epidemiological research on this topic uses comparison populations that allow for the elimination of most of the uncertainties. The results strongly suggest that exposure to wood smoke or exposure to coal smoke accelerates cardiovascular disease and reduces life expectancy. It isn’t just cardiovascular disease: all of the more common age-related conditions with a strong inflammatory component are candidates for this sort of effect. That includes forms of dementia, as the two articles here discuss.
Overall, scientists are reporting that people with the highest exposures to pollutants are more likely to get dementia. Some of the risk may lie in chronic deterioration of the cardiovascular and cerebrovascular systems. Alas, researchers are finding that particulate matter can also get into the brain through olfactory nerves or across the blood-brain barrier, whereupon they may affect neurons and glia directly. Diffuse Aβ plaques, hyperphosphorylated tau, and aggregates of α-synuclein have been detected in olfactory bulbs in the brains of young people who lived in Mexico City, where air pollution is high.
With the field heating up, are epidemiologists ready to claim that air pollution increases a person’s risk for dementia? “I think we are comfortably suspicious. The toxicology suggests it is biologically plausible, but there’s a lot of diversity in the exposure and outcome data. Air pollution is similar to other risk factors. There is a signal that may be far from certain but is strong enough to warrant more attention.” Some researchers call air pollution a gerogen. “It accelerates aging, weakens blood vessels in the brain, and promotes amyloid production. The argument that air pollution is a risk factor for dementia is doubly strong because it also accelerates atherosclerosis, which is a risk factor independently of everything else.”
For decades, studies of pulmonary and vascular systems dominated the air-pollution-research landscape. Researchers paid scant attention to the brain, which they considered safely ensconced behind the blood-brain barrier. But the science has begun to change. Evidence has been steadily trickling in that exposure to ambient air pollution, even at levels near the upper limits set by the World Health Organization, can affect the central nervous system. ver the last decade, numerous epidemiological studies have tied pollution to increased risk for cognitive decline and dementia.
Though the data is often equivocal, scientist are asking just how do pollutants damage the brain? Chronic deterioration of the cardiovascular and cerebrovascular systems may be to blame, but researchers are also finding that particulate matter gets into the central nervous system, either through olfactory nerves or across the blood-brain barrier, and then harms neurons and glia directly. Olfactory nerves in the nose carry a variety of cargo into the brain. In the case of pollutants, the research has focused on ultrafine particles (UFPs). At less than 0.1 micrometers in diameter, UFPs are even smaller than PM2.5. The EPA does not regulate them, hence they are not routinely monitored in the U.S. Researchers are setting up their own monitoring equipment to measure levels in ambient air that is pumped into animal facilities. While this research is still coming in, it already indicates these small particles could be particularly harmful. “This has become a topic of great interest, but we need much more data on the olfactory system.”