Summary findings of a report by the Committee on the Medical Effects of Air Pollutants (COMEAP) (1):
- epidemiological evidence is suggestive of an association between exposure to ambient air pollutants and both the risk of developing dementia and acceleration of cognitive decline. The epidemiological literature is inconsistent as to which pollutant is most associated with these effects
- is evidence that air pollution, particularly particulate air pollution, increases the risk of cardiovascular, including cerebrovascular, disease. These diseases are known to have adverse effects on cognitive function. It is therefore our view that there is likely to be a causal association between particulate air pollution and effects on cognitive function in older people
- evidence base is currently inadequate to allow direct quantification using a meta-analysis of epidemiological studies linking air pollution with cognitive decline or dementia. Direct quantification of cognitive decline or dementia associated with air pollution would therefore be subject to unknown uncertainty
- may be possible to develop an indirect method of quantification of cognitive effects secondary to the effects of particulate pollution on cardiovascular disease. This would require a review of evidence regarding the quantitative link between cardiovascular endpoints and effects on cognition
COMEAP reviewed nearly 70 studies in human populations (epidemiological studies) which looked at possible links between air pollution and a decline in mental ability and dementia in older people
- also considered studies which investigated how air pollution might affect the brain
A number of mechanisms have been suggested by which air pollutants could have direct effects on the brain. These include:
- the translocation of small particles from the lung to the blood stream and thence to the brain
- evidence suggests that a small proportion of very small particles that are inhaled can enter the brain, both from the blood and via the olfactory nerves leading from the nasal passages to the olfactory bulbs
- much less clear whether exposure to ambient concentrations of particulate material results in sufficient translocation to produce damage to the brain
- evidence suggests that particles which enter the brain are cleared from the brain only slowly, if at all
- animal and in vitro studies of ultrafine particulate material, diesel engine exhaust or ozone have all shown effects on the brain or brain cells
- mechanisms involved include the generation and release of free radicals within the brain and the induction of an inflammatory response; these 2 mechanisms seem likely to be linked
- experimental studies generally used exposure to higher than ambient concentrations and were conducted over short time periods, so it is not clear how informative they might be about effects in human populations chronically exposed to lower concentrations
- nonetheless, they indicate that a number of common pollutants may affect brain function (1)
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