Brain health and pollution
People of all ages who live in high pollution areas for extended periods place themselves at increased risk of various neurological disorders.
[15] Children raised in areas of higher pollution were found to score lower in intelligence (i.e., on IQ tests), and showed signs of lesions in MRI scanning of the brain.
In contrast, children from the low pollution area scored as expected on IQ tests and showed no significant sign of the risk of brain lesions.
Concerning traffic-related air pollution, children of mothers exposed to higher levels during the first trimester of pregnancy were at increased risk of allergic sensitization at one year age.
[19] Analyzing 2017 and 2018 data from Lost in Migration, a phone game that test players' ability to keep their focus, researchers found effects of wildfire smoke and pollution particulates on brain performance.
This is a very quick turnaround between exposure and decreased cognitive performance and may have implications when thinking about time-sensitive public health communication during extreme air pollution events like wildfires," Cleland, a predoctoral ORISE fellow at EPA, explained.
Some observed effects of exposure to dioxins are altered astroglial intracellular calcium ion (Ca2+), decreased glutathione levels, modified neurotransmitter function in the CNS, and loss of pH maintenance.
"[45] Heavy metal exposure, when combined with certain genetic predispositions, can place individuals at increased risk for developing autism.
Many examples of CNS pathophysiology, such as oxidative stress, neuroinflammation, and mitochondrial dysfunction, could be by-products of environmental stressors such as pollution, as found in a 2010 study.
Children with a mutation in a gene called MET, combined with high levels of exposure to air pollution, may have increased risk.
[51] Multi-decade studies have identified an increased likelihood of Parkinson's in association with agricultural work, pesticide exposure, and rural habitation.
Chlorinated solvents, used in commercial and industrial application like dry cleaning and degreasing, are associated with increased PD risk, particularly trichloroethylene.
[52][53] Other chemical risk factors include manganese, suspended particles from traffic fumes, and exposure to other heavy metals such as mercury and lead.
[53][54] In the case of Alzheimer's disease, inflammatory processes lead to neuron death by inhibiting growth at axons and activating astrocytes that produce proteoglycans.
This product can only be deposited in the hippocampus and cortex, indicating that this may be the reason these two areas show the highest levels of degeneration in Alzheimer's disease.
[1] Studies consistently suggested a strong link between chronic exposure to PM, especially PM2.5 and UFPM, with the onset of dementia and AD, as well as neurodegenerative-like pathology and cognitive deficits.
[1] Exposure to air pollution was positively associated with an increased risk of stroke hospital admission (PM2.5, PM10, SO2, NO2, CO, and O3), incidence (PM2.5, SO2, and NO2), and mortality (PM2.5, PM10, SO2, and NO2).
This work was an extension of studies undertaken in the 1990s on the effects of Mexico City air pollution on the olfactory epithelium of humans and dogs.
Later, interest in possible effects on the brain has been strengthened by epidemiological studies, which suggest that exposure to air pollutants is associated with a decline of cognitive function and the development of dementia.
In addition, the blood-brain barrier could be made less impermeable by systemic inflammation for which exposure to air pollutants is a known risk factor.
The blood-brain barrier is also more permeable in the very young and old, making these two life stages opportunities for the entry of nanoparticles into the brain, and potential elicitation of neurological damage.
There was increased neuro-inflammation and vascular damage: upregulated mRNA cyclooxygenase-2, interleukin-1β and CD14, and clusters of mononuclear cells around blood vessels and activated microglia in the frontal and temporal cortex, subiculum and brain stem.
[64] Evidence suggests that long-term exposure to air pollutants is associated with cognitive decline and with the risk of development of dementia.
[64] There is epidemiological evidence suggestive of a causal association between exposure to a range of air pollutants and a number of effects on the nervous system including the acceleration of cognitive decline and the induction of dementia.
[64] Dementia is an umbrella term for a range of conditions that affect how the brain works, reducing the ability to remember, think and reason.
[65] There are a number of plausible biological mechanisms by which air pollutants could cause effects on the brain leading to accelerated cognitive decline and dementia.
Therefore it is regarded that the association between exposure to air pollutants and effects on cognitive decline and dementia as likely to be causal with respect to this mechanism.
[65] What is much less clear is whether exposure to ambient concentrations of particulate material results in sufficient translocation to produce damage to the brain.
Priority areas in “Education and Awareness included: (8) making this unrecognised public health issue known; (9) developing educational products; (10) attaching air pollution and brain health to existing strategies and campaigns; and (11) providing publicly available monitoring, assessment and screening tools...”[67] NIEHS-funded studies have found taking prenatal vitamins may help lower autism risk.
[48] Folic acid intake during early pregnancy may reduce the risk of having a child with autism for those women with high exposure to air pollution, and pesticides.
