Abstract
Epidemiological studies of air pollution have shown associations between exposure to particles and dementia. The mechanism of this is unclear. As these seem unlikely in terms of the very small dose likely to reach the brain in usual Western urban circumstances, we extend our 1995 hypothetical explanation of the association of air pollution with cardiac deaths as a plausible alternative explanation of its associations with dementia. Since our original proposal, it has become apparent that inflammation may be carried by blood from organ to organ by biologic microparticles derived from cell membranes. These transmit inflammatory messages to endothelial cells throughout the body as part of a general defensive response to assumed bacterial infection; particulate air pollution has recently been shown to be associated with their release into the blood. We propose that episodic release of biologic microparticles from pollution-induced lung inflammation causes secondary inflammation in the blood-brain barrier and cerebral microbleeds, culminating over time in cognitive impairment. Ultimately, by incomplete repair and accumulation of amyloid, this increases the risk of Alzheimer’s disease. Importantly, this mechanism may also explain the relationships of other inflammatory conditions and environmental factors with cognitive decline, and point to new opportunities to understand and prevent dementia.
Highlights
High air pollution episodes associated with fossil fuel combustion have been linked to excess deaths in the exposed population since the 1930s [1]
The excesses were from lung and heart disease and the risk was related mainly to particle concentrations; lung deaths were explicable in terms of lung inflammation, but the more frequent cardiac deaths less
In 1999, following our observation of falls in red blood cell and platelet counts in association with rises in particulate air pollution in healthy elderly people, we extended this hypothesis to propose that the vascular endothelial cell was central to the response to pollution [10]
Summary
High air pollution episodes associated with fossil fuel combustion have been linked to excess deaths in the exposed population since the 1930s [1]. In 1999, following our observation of falls in red blood cell and platelet counts in association with rises in particulate air pollution in healthy elderly people, we extended this hypothesis to propose that the vascular endothelial cell was central to the response to pollution [10]. These early observations had a significant impact, notably on risk assessment of nanotechnologies [11,12]
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