Brain health and pollution
Research indicates that living in areas of high pollution has serious long term health effects. Living in these areas during childhood and adolescence can lead to diminished mental capacity and an increased risk of brain damage. People of all ages who live in high pollution areas for extended periods place themselves at increased risk of various neurological disorders. Both air pollution and heavy metal pollution have been implicated as having negative effects on central nervous system functionality. The ability of pollutants to affect the neurophysiology of individuals after the structure of the CNS has become mostly stabilized is an example of negative neuroplasticity.
Air pollution
Air pollution is the impurity of the atmosphere caused by substances like gases, particles and smoke from sources such as vehicles, industries, fires, etc. Air pollution may increase the risk of developmental disorders, neurodegenerative disorders, mental disorders, and suicide. It is associated with neurological conditions including stroke, multiple sclerosis, dementia, Parkinson's disease, Alzheimer's disease, schizophrenia and headaches.Effects in adolescents
A 2008 study compared children and dogs raised in Mexico City with children and dogs raised in Polotitlán, Mexico. Children raised in areas of higher pollution were found to score lower in intelligence, 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.Effects in adults
Effects of physical activity and air pollution on neuroplasticity may counteract. Physical activity is known for its benefits to the cardiovascular system, brain plasticity processes, cognition and mental health. The neurotrophin, brain-derived neurotrophic factor is thought to play a key role in exercise-induced cognitive improvements. Brief bouts of physical activity may increase serum levels of BDNF, but this increase may be offset by increased exposure to traffic-related air pollution.Over longer periods of physical exercise, the cognitive improvements which were demonstrated in rural joggers were found to be absent in urban joggers who were partaking in the same 12-week start-2-run training programme. During exercise, traffic-related air pollution may reduce the beneficial effects of that exercise.
Cognitive performance
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."We found evidence suggesting that fine particulate matter can reduce attention in adults within just hours of exposure. 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. It was also found that prolonged exposure to particulate pollution shortens attention spans in younger populations specifically. In both the long-term and short-term analyses, exposure to harmful particulates caused lower game scores.
Pollutants
Dioxin poisoning
compounds, such as dioxins, are commonly found in pesticides or created as by-products of pesticide manufacture or degradation. These compounds can have a significant impact on the neurobiology of exposed organisms. Some observed effects of exposure to dioxins are altered astroglial intracellular calcium ion, decreased glutathione levels, modified neurotransmitter function in the CNS, and loss of pH maintenance. A study of 350 chemical plant employees exposed to a dioxin precursor for herbicide synthesis between 1965 and 1968 showed that 80 of the employees displayed signs of dioxin poisoning. The study suggested that the effects of dioxins were not limited to initial toxicity. Dioxins, through neuroplastic effects, may cause long-term damage that may not manifest itself for years or even decades.Metal exposure
exposure can result in an increased risk of various neurological diseases. The two most neurotoxic heavy metals are mercury and lead. The impact of the two heavy metals is highly dependent upon the individual due to genetic variations. Mercury and lead are particularly neurotoxic for many reasons: they easily cross cell membranes, have oxidative effects on cells, react with sulfur in the body, and reduce glutathione levels inside cells. Methylmercury, in particular, has an extremely high affinity for sulfhydryl groups. Organomercury is a particularly damaging form of mercury because of its high absorbability Lead also mimics calcium, a very important mineral in the CNS, and this mimicry leads to many adverse effects. Mercury's neuroplastic mechanisms work by affecting protein production. Elevated mercury levels increase glutathione levels by affecting gene expression, and this in turn affects two proteins that are contained in astrocytes and neurons.Lead's ability to imitate calcium allows it to cross the blood–brain barrier. Lead also upregulates glutathione. Blood lead concentrations ≥ 5·0 μg/dL could result in children scoring 3–5 points lower in intelligence tests than those with the concentrations < 5·0 μg/dL. Higher blood lead concentrations are also associated with serious cognitive function losses. "Lead-related IQ losses are associated with increased rates of school failure, behavioural disorders, diminished economic productivity, and global economic losses of almost $1 trillion annually."
Conditions and disorders
Developmental disorders
Autism
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.Early-life exposure to air pollution may be a risk factor for autism. Children of mothers living near a freeway, and traffic-related pollution, during the third trimester of pregnancy were twice as likely to develop ASD. A distance of 1,014 feet, or a little less than 3.5 football fields, was considered near a freeway. Children with a mutation in a gene called MET, combined with high levels of exposure to air pollution, may have increased risk.
Prenatal and early childhood exposure to heavy metals, like mercury, lead, or arsenic; altered levels of essential metals like zinc or manganese; pesticides; and other contaminants cause concern. A study of twins used baby teeth to determine and compare levels of lead, manganese, and zinc in children with autism to their twin without the condition. Autistic children were low on manganese and zinc, metals essential to life, but had higher levels of lead, a harmful metal during specific developmental time periods studied. Altered zinc-copper cycles, which regulate metal metabolism in the body, are disrupted in ASD cases.
Maternal exposure to insecticides during early pregnancy was associated with higher risk of autism in their children. Contaminants such as Bisphenol A, phthalates, flame retardants, and polychlorinated biphenyls are also being studied.
Neurodegenerative disorders
Accelerated neural aging
is associated with increased rates of neurodegeneration. Inflammation tends to increase naturally with age. By facilitating inflammation, pollutants such as air particulates and heavy metals cause the CNS to age more quickly. Many late-onset diseases are caused by neurodegeneration. Multiple sclerosis, Parkinson's disease, amyotrophic lateral sclerosis, and Alzheimer's disease are all believed to be exacerbated by inflammatory processes, resulting in individuals displaying signs of these diseases at an earlier age than is typically expected.Multiple sclerosis occurs when chronic inflammation leads to the compromise of oligodendrocytes, which in turn leads to the destruction of the myelin sheath. Then axons begin exhibiting signs of damage, which in turn leads to neuron death. Multiple sclerosis has been correlated to living in areas with high particulate matter levels in the air.
According to Lancet, exposure to "environmental pollution with toxins, such as pesticides or chemicals, known to be harmful to Parkinson's disease-related neurons and brain circuits," is associated with Parkinson's disease. 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. Other chemical risk factors include manganese, suspended particles from traffic fumes, and exposure to other heavy metals such as mercury and lead.
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. Tiny particles can bypass the blood-brain barrier and enter the brain as they are breathed in.
A study on the young adult citizens in Metropolitan Mexico City found association between air pollution exposure and olfactory dysfunction and pathology in the olfactory bulb. The young adults demonstrated olfactory bulb endothelial hyperplasia, neuronal accumulation of particles, and immunoreactivity to Aβ or α-synuclein in neurons, glial cells, or blood vessels. There were ultrafine particles deposited in their endothelial cytoplasm and basement membranes of the olfactory bulb.
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. The central role of oxidative stress was highlighted in the neuronal injury caused by PM. Neuroinflammation could further damage the neurons and other cells such as the endothelial cells in the neurovascular unit. The neurovascular unit consists of neurons, astrocytes, vasculature, the vasomotor apparatus, and microglia. Targeting the HMGB1/TLR4/NF-κB pathways or oxidative stress by pharmacological inhibitors or genetic knockdown has demonstrated potential as a therapeutic intervention.
Effects of PM on metabolism should be further studied according to the results in the neurometabolomics analysis as studies not only showed the implication of disturbed glutathione metabolism in the pathogenesis of PM-induced neuronal injury but also demonstrated that PM may affect the fatty acid and energy metabolism in the neurons. Injury in the NVU after exposure to PM would also impair energy metabolism in the affected brain regions. Therefore, the disturbed metabolic homeostasis may also play a crucial pathogenic role in the development of PM-induced neuropathology. Restoring these metabolic disturbances may enhance the resistance of neurons against the stress caused by exposure to PM.