Brain health and pollution

Last updated

Particulate exposure and increased risk of neurodegeneration Particulates exposure and increased risk of neurodegeneration.jpg
Particulate exposure and increased risk of neurodegeneration

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 (CNS) 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.

Contents

Air pollution

Potential particle pathways as of 2018. Potential particle pathway.png
Potential particle pathways as of 2018.
A scanning electron microscope image of bundles of multiwalled carbon nanotube piercing an alveolar epithelial cell. Carbon nanotubes penetrating lung cell.tif
A scanning electron microscope image of bundles of multiwalled carbon nanotube piercing an alveolar epithelial cell.

Air pollution may increase the risk of developmental disorders (e.g., autism), [3] [4] [5] [6] neurodegenerative disorders, [7] [8] mental disorders, [9] [10] [11] and suicide. [9] [11] [12] It is associated with neurological conditions including stroke, multiple sclerosis, dementia, Parkinson disease, [13] Alzheimer's disease, [1] schizophrenia [14] and headaches. [13]

Effects in adolescents

A 2008 study compared children and dogs raised in Mexico City (a location known for high pollution levels) with children and dogs raised in Polotitlán, Mexico (a city whose pollution levels meet the current US National Ambient Air Quality Standards). [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. [16]

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 neurotrophine, brain-derived neurotrophic factor (BDNF) 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. [17] 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. [18] During exercise, traffic-related air pollution may reduce the beneficial effects of that exercise. [19]

Cognitive performance

Burning of downed vegetation, or "slash". Daily open burning, Tai Po, Hong Kong.png
Burning of downed vegetation, or "slash".

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. [20]

"We found evidence suggesting that fine particulate matter (PM2.5) 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. [20] 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. [20]

Sources of pollution

An angle grinder is used to cut steel chain

Airborne particulate matter is a Group 1 carcinogen. [21] Particulates are the most harmful form (other than ultra-fines) of air pollution [22] as they can penetrate deep into the lungs and brain from blood streams, causing health problems such as heart disease, lung disease, and premature death. [23] There is no safe level of particulates. [24] Ultrafine particles are both manufactured and naturally occurring. Hot volcanic lava, ocean spray, and smoke are common natural UFPs sources. UFPs can be intentionally fabricated as fine particles to serve a vast range of applications in both medicine and technology. Other UFPs are byproducts, like emissions, from specific processes, combustion reactions, or equipment such as printer toner and automobile exhaust. [25] [26] Anthropogenic sources of UFPs include combustion of gas, coal or hydrocarbons,  biomass burning  (i.e. agricultural burning, forest fires and waste disposal), vehicular traffic and industrial emissions, tire wear and tear from car brakes, air traffic, seaport, maritime transportation, construction, demolition, restoration and concrete processing, domestic wood stoves, outdoor burning, kitchen, and cigarette smoke. [27]

While hand-held power tools are very helpful (e.g., in renovation and construction), they also produce large amounts of vibrations [28] and particulates (particulate matter), including ultrafine particles, [29] from both fuel combustion and the mechanical tasks. Not only power tools, hand tools also generate UFPs. [30]

Many construction tasks create dust. High dust levels are caused by one of more the following:

Examples of high dust level tasks include:

Currently there seems to be no or little regulations on the size and amount of dust emitted by power tools. Some industry standards do exist, [32] [33] though it appears that they are not widely known or used globally. Knowing that dust is generated throughout the construction process and can cause serious health hazards, [34] manufacturers are now marketing power tools that are equipped with dust collection system (e.g. HEPA vacuum cleaner) or integrated water delivery system which extract the dust after emission. [35] [36] However, the use of such products is still not common in most places. As Q1 2024 petrol powered tools are banned in California. [37]

Pollutants

Dioxin poisoning

Organohalogen 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 (Ca2+), decreased glutathione levels, modified neurotransmitter function in the CNS, and loss of pH maintenance. [38] 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. [39] 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. [39]

Metal exposure

Heavy metal 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 (leading to disturbances in the many functions that rely upon sulfhydryl groups), and reduce glutathione levels inside cells. Methylmercury, in particular, has an extremely high affinity for sulfhydryl groups. [40] Organomercury is a particularly damaging form of mercury because of its high absorbability [41] Lead also mimics calcium, a very important mineral in the CNS, and this mimicry leads to many adverse effects. [42] 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 (MT1 and MT2) that are contained in astrocytes and neurons. [43]

Lead's ability to imitate calcium allows it to cross the blood–brain barrier. Lead also upregulates glutathione. [44] 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." [45]

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. [46] There have been reports of autism outbreaks occurring in specific locations. [47]

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. [48] 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. [48]

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. [48] 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. [48] 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. [48]

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. [48]

Neurodegenerative disorders

Accelerated neural aging

Neuroinflammation is associated with increased rates of neurodegeneration. [49] 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 (ALS), 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. [49]

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. [50]

According to Lancet (2021), exposure to "environmental pollution with toxins, such as pesticides (eg, paraquat) or chemicals (eg, trichloroethylene), known to be harmful to Parkinson's disease-related neurons and brain circuits," is associated with Parkinson's disease. [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. [55] Tiny particles (e.g., engineered nanoparticles and combustion nanoparticle emissions, also called nanomaterials, including those containing manganese) can bypass the blood-brain barrier (the body's filtering system) and enter the brain as they are breathed in. [56] [57] [58]

A study on the young adult citizens in Metropolitan Mexico City (MMC) found association between air pollution exposure and olfactory dysfunction and pathology in the olfactory bulb. [1] The young adults demonstrated olfactory bulb endothelial hyperplasia, neuronal accumulation of particles, and immunoreactivity to Aβ and/or α-synuclein in neurons, glial cells and/or blood vessels. There were ultrafine particles deposited in their endothelial cytoplasm and basement membranes of the olfactory bulb. [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] 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 (NVU). [1] The neurovascular unit consists of neurons, astrocytes, vasculature (endothelial and vascular mural cells), the vasomotor apparatus (smooth muscle cells and pericytes), and microglia. [59] Targeting the HMGB1/TLR4/NF-κB pathways or oxidative stress by pharmacological inhibitors or genetic knockdown has demonstrated potential as an therapeutic intervention. [1]

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. [1] Injury in the NVU after exposure to PM would also impair energy metabolism in the affected brain regions. [1] Therefore, the disturbed metabolic homeostasis may also play a crucial pathogenic role in the development of PM-induced neuropathology. [1] Restoring these metabolic disturbances may enhance the resistance of neurons against the stress caused by exposure to PM. [1]

Cognitive decline and dementia

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). [60] There is a "well-recognized link between PM2.5 and vascular injury and the role of vascular injury in dementia". [61] Air pollution in the cerebrovascular system may result in “stroke, vascular dementia, or other types of dementia". [62] The risk of dementia, including Alzheimer's disease and vascular dementia, may be increased by long-term exposure to PM2.5. [63]

Interest in the possible effects of air pollutants on the brain began in about 2002 when Calderon-Garciduenas and colleagues reported that dogs exposed to air pollution in Mexico City showed neuropathological changes of the type associated with Alzheimer's disease. 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. [64]

Magnetite nanoparticles have been found in the brain with a morphology that suggests an exogenous origin. Similar ferrous nanoparticles were found in air collected at traffic roadsides in the UK. These nanoparticles may be able to reach the brain via the olfactory nerves and olfactory bulb, or via the circumventricular organs where the blood-brain barrier is more permeable. 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. [64]

In addition to the possible direct effects from nanoparticles reaching the brain, there are indirect mechanisms by which pollutants could potentially lead to brain injury. These include damage to the vasculature, leading to cerebral ischaemia or extravasation of neurotoxic proteins such as fibrinogen. Brain injury could also be secondary to systemic inflammatory responses to air pollution. [64]

Calderon-Garciduenas et al. reviewed their work in children and youngsters in Mexico City and reported neuropathological changes in children and young adults similar to those in Alzheimer's disease. 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. They also found deposits of amyloid-β42, α-synuclein, hyperphosphorylated tau, and evidence of oxidative stress, neuronal damage and death. Children in Mexico City (with high levels of air pollution) also had low serum BDNF concentrations. [64]

Studies of white matter volume found associations between exposure to air pollution and reduced white matter volume. [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. It mainly affects older people and gets worse over time. Health and lifestyle factors such as high blood pressure and smoking are known to increase the risk of developing dementia. [65]

The Committee on the Medical Effects of Air Pollutants (COMEAP) in UK have reviewed nearly 70 studies in human populations (epidemiological studies) and think it is likely that air pollution can contribute to a decline in mental ability and dementia in older people. It is known that air pollution, particularly small particle pollution, can affect the heart and the circulatory system, including circulation to the brain. These effects are linked to vascular dementia (a form of dementia), which is caused by damage to the blood vessels in the brain. [65] Therefore, it is likely that air pollution contributes to mental decline and dementia caused by effects on the blood vessels. Air pollution might also stimulate the immune cells in the brain, which can then damage nerve cells. [65]

In 2022, COMEAP has concluded that the evidence is suggestive of an association between ambient air pollutants and an acceleration of the decline in cognitive function often associated with ageing, and with the risk of developing dementia. [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. Some of these have been demonstrated in experimental studies. There is a strong case for the effects of air pollutants on the cardiovascular system having a secondary effect on the brain. COMEAP has already concluded that long-term exposure to air pollutants damages the cardiovascular system (COMEAP 2006, 2018). It is likely that such effects have an effect on the blood supply to the brain. That such an effect might well lead to damage to the brain seems likely. 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]

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. The 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. [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. Study of the literature has suggested that particles which enter the brain are cleared from the brain only slowly, if at all. This is clearly a point in favour of the suggestion that particulate material which does enter the brain might produce detrimental effects. [65] Animal and in vitro studies of ultrafine particulate material, diesel engine exhaust or ozone have all shown effects on the brain or brain cells. The 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. A number of common pollutants may affect brain function. [65]

COMEAP concluded that:

  • The 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. [65]
  • There 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. There is likely to be a causal association between particulate air pollution and effects on cognitive function in older people. [65]
  • As of 2022, direct quantification of cognitive decline or dementia associated with air pollution would be subject to unknown uncertainty. [65]
  • It may be possible to develop an indirect method of quantification of cognitive effects secondary to the effects of particulate pollution on cardiovascular disease. [65]

Mental disorders

Schizophrenia

Exposure to air pollution may be associated with elevated risk of schizophrenia. [14]

Others

Epilepsy

Multiple air pollutants are probably associated with the risk of epilepsy, [66] e.g., carbon monoxide, ozone, sulfur dioxide, nitrogen dioxide, large particulate matter, and fine particulate matter. It was hypothesized that air pollutants increase epilepsy risk by increasing inflammatory mediators, and by providing a source of oxidative stress, eventually altering the blood–brain barrier's function and cause brain inflammation. Brain inflammation is known to be a risk factor for epilepsy; thus, the sequence of events provides a plausible mechanism by which pollution may increase epilepsy risk in individuals who are genetically vulnerable to the disease. [66] [ medical citation needed ]

Economics

Dementia

Dementia is a pressing public health challenge. Its prevalence is strongly age-related: doubling every 5–6 years over the age of 65 years. The number of people living with dementia worldwide is estimated at 50 million and expected to reach 152 million by 2050. Its current economic cost worldwide is US$818 billion/year (as of 2015) and it will rise in proportion to the numbers affected (WHO, 2019). [64]

Mitigations

For point-source pollution: Do not produce the pollutants. If produced, remove at source as soon as possible. If not removed at source, use barriers. If barriers do not work well or not installed properly (i.e., pollutants escaped), neighbours need filtration, sealing, and/or proper ventilation / pollutant dilution, etc. for their premises. Large scale air cleaning system may also help as a passive measure. Clean-up programmes may be needed to prevent further secondary contamination or pollution.

At individual level, exposure reduction of air pollutants maybe achieved by better choice of places that one stays, prevention of cross-contamination or secondary contamination (between persons and/or their personal belongings/environment), better personal hygiene, use of face masks and air purifiers, etc.

Education

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]

Diet

Autism

NIEHS-funded studies have found taking prenatal vitamins may help lower autism risk. Taking vitamins and supplements might provide protective effects for those exposed to certain environmental contaminants during pregnancy. [48] Women were less likely to have a child with autism if they took a daily prenatal vitamin during the three months before and first month of pregnancy, compared to women not taking vitamins. This finding was more evident in women and children with genetic variants that made them more susceptible to developing autism. [48]

Folic acid is a source of the protective effects of prenatal vitamins. Women who took the daily recommended dosage during the first month of pregnancy had a reduced risk of having a child with autism. [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. [48]

Pregnant mothers who used multivitamins, with or without additional iron or folic acid, were less likely to have a child with autism and intellectual disability. [48] Maternal prenatal vitamin intake during the first month of pregnancy may also reduce ASD recurrence in siblings of children with ASD in high-risk families. [48]

Indoor air quality improvement

Air-purifiers with air flow generated by bladeless fan. Some models can act as heaters or humidifiers and may feature oscillation and adjustment of air flow angle. Fans by Dyson 1 2018-06-02.jpg
Air-purifiers with air flow generated by bladeless fan. Some models can act as heaters or humidifiers and may feature oscillation and adjustment of air flow angle.

Large scale cleaning system

First generation SALSCS (Solar-assisted Large Scale Cleaning System), Xi'an First generation SALSCS, Xi'an.jpg
First generation SALSCS (Solar-assisted Large Scale Cleaning System), Xi'an

Incentives

Regulation

Urban planning

Clean-up campaign

Control measures

Life style adjustment

See also

Pollutants

Sources

Others

Related Research Articles

<span class="mw-page-title-main">Smoke</span> Mass of airborne particulates and gases

Smoke is a suspension of airborne particulates and gases emitted when a material undergoes combustion or pyrolysis, together with the quantity of air that is entrained or otherwise mixed into the mass. It is commonly an unwanted by-product of fires, but may also be used for pest control (fumigation), communication, defensive and offensive capabilities in the military, cooking, or smoking. It is used in rituals where incense, sage, or resin is burned to produce a smell for spiritual or magical purposes. It can also be a flavoring agent and preservative.

<span class="mw-page-title-main">Dementia</span> Long-term brain disorders causing impaired memory, thinking and behavior

Dementia is a syndrome associated with many neurodegenerative diseases, characterized by a general decline in cognitive abilities that affects a person's ability to perform everyday activities. This typically involves problems with memory, thinking, behavior, and motor control. Aside from memory impairment and a disruption in thought patterns, the most common symptoms of dementia include emotional problems, difficulties with language, and decreased motivation. The symptoms may be described as occurring in a continuum over several stages. Dementia ultimately has a significant effect on the individual, their caregivers, and their social relationships in general. A diagnosis of dementia requires the observation of a change from a person's usual mental functioning and a greater cognitive decline than might be caused by the normal aging process.

<span class="mw-page-title-main">Indoor air quality</span> Air quality within and around buildings and structures

Indoor air quality (IAQ) is the air quality within buildings and structures. Poor indoor air quality due to indoor air pollution is known to affect the health, comfort, and well-being of building occupants. It has also been linked to sick building syndrome, respiratory issues, reduced productivity, and impaired learning in schools. Common pollutants of indoor air include: secondhand tobacco smoke, air pollutants from indoor combustion, radon, molds and other allergens, carbon monoxide, volatile organic compounds, legionella and other bacteria, asbestos fibers, carbon dioxide, ozone and particulates.

<span class="mw-page-title-main">Diesel exhaust</span> Gaseous exhaust produced by a diesel engine

Diesel exhaust is the exhaust gas produced by a diesel engine, plus any contained particulates. Its composition may vary with the fuel type, rate of consumption or speed of engine operation, and whether the engine is in an on-road vehicle, farm vehicle, locomotive, marine vessel, or stationary generator or other application.

<span class="mw-page-title-main">Memantine</span> Medication used to treat Alzheimers disease

Memantine, sold under the brand name Namenda among others, is a medication used to slow the progression of moderate-to-severe Alzheimer's disease. It is taken by mouth.

Cognitive disorders (CDs), also known as neurocognitive disorders (NCDs), are a category of mental health disorders that primarily affect cognitive abilities including learning, memory, perception, and problem-solving. Neurocognitive disorders include delirium, mild neurocognitive disorders, and major neurocognitive disorder. They are defined by deficits in cognitive ability that are acquired, typically represent decline, and may have an underlying brain pathology. The DSM-5 defines six key domains of cognitive function: executive function, learning and memory, perceptual-motor function, language, complex attention, and social cognition.

Environmental toxicants and fetal development is the impact of different toxic substances from the environment on the development of the fetus. This article deals with potential adverse effects of environmental toxicants on the prenatal development of both the embryo or fetus, as well as pregnancy complications. The human embryo or fetus is relatively susceptible to impact from adverse conditions within the mother's environment. Substandard fetal conditions often cause various degrees of developmental delays, both physical and mental, for the growing baby. Although some variables do occur as a result of genetic conditions pertaining to the father, a great many are directly brought about from environmental toxins that the mother is exposed to.

<span class="mw-page-title-main">Low birth weight</span> Birth weight of an infant of 2,499 g (5 lb 8.1 oz) or less

Low birth weight (LBW) is defined by the World Health Organization as a birth weight of an infant of 2,499 g or less, regardless of gestational age. Infants born with LBW have added health risks which require close management, often in a neonatal intensive care unit (NICU). They are also at increased risk for long-term health conditions which require follow-up over time.

Memory disorders are the result of damage to neuroanatomical structures that hinders the storage, retention and recollection of memories. Memory disorders can be progressive, including Alzheimer's disease, or they can be immediate including disorders resulting from head injury.

Cognitive impairment is an inclusive term to describe any characteristic that acts as a barrier to the cognition process or different areas of cognition. Cognition, also known as cognitive function, refers to the mental processes of how a person gains knowledge, uses existing knowledge, and understands things that are happening around them using their thoughts and senses. Cognitive impairment can be in different domains or aspects of a person's cognitive function including memory, attention span, planning, reasoning, decision-making, language, executive functioning, and visuospatial functioning. The term cognitive impairment covers many different diseases and conditions and may also be symptom or manifestation of a different underlying condition. Examples include impairments in overall intelligence, specific and restricted impairments in cognitive abilities, neuropsychological impairments, or it may describe drug-induced impairment in cognition and memory. Cognitive impairments may be short-term, progressive, or permanent.

<span class="mw-page-title-main">Air pollution</span> Presence of dangerous substances in the atmosphere

Air pollution is the contamination of air due to the presence of substances called pollutants in the atmosphere that are harmful to the health of humans and other living beings, or cause damage to the climate or to materials. It is also the contamination of the indoor or outdoor environment either by chemical, physical, or biological agents that alters the natural features of the atmosphere. There are many different types of air pollutants, such as gases, particulates and biological molecules. Air pollution can cause diseases, allergies, and even death to humans; it can also cause harm to other living organisms such as animals and crops, and may damage the natural environment or built environment. Air pollution can be caused by both human activities and natural phenomena.

The prevention of dementia involves reducing the number of risk factors for the development of dementia, and is a global health priority needing a global response. Initiatives include the establishment of the International Research Network on Dementia Prevention (IRNDP) which aims to link researchers in this field globally, and the establishment of the Global Dementia Observatory a web-based data knowledge and exchange platform, which will collate and disseminate key dementia data from members states. Although there is no cure for dementia, it is well established that modifiable risk factors influence both the likelihood of developing dementia and the age at which it is developed. Dementia can be prevented by reducing the risk factors for vascular disease such as diabetes, high blood pressure, obesity, smoking, physical inactivity and depression. A study concluded that more than a third of dementia cases are theoretically preventable. Among older adults both an unfavorable lifestyle and high genetic risk are independently associated with higher dementia risk. A favorable lifestyle is associated with a lower dementia risk, regardless of genetic risk. In 2020, a study identified 12 modifiable lifestyle factors, and the early treatment of acquired hearing loss was estimated as the most significant of these factors, potentially preventing up to 9% of dementia cases.

Ultrafine particles (UFPs) are particulate matter of nanoscale size (less than 0.1 μm or 100 nm in diameter). Regulations do not exist for this size class of ambient air pollution particles, which are far smaller than the regulated PM10 and PM2.5 particle classes and are believed to have several more aggressive health implications than those classes of larger particulates. Although they remain largely unregulated, the World Health Organization has published good practice statements regarding measuring UFPs.

Air pollution is the introduction of chemicals, particulate matter, or biological materials into the atmosphere that cause harm or discomfort to humans or other living organisms, or damage ecosystems. Health problems attributed to air pollution include premature death, cancer, organ failure, infections, behavioral changes, and other diseases. These health effects are not equally distributed across the U.S. population; there are demographic disparities by race, ethnicity, socioeconomic status, and education. Air pollution can derive from natural sources, such as wildfires and volcanoes, or from anthropogenic sources. Anthropogenic air pollution has affected the United States since the beginning of the Industrial Revolution.

<span class="mw-page-title-main">Alzheimer's disease</span> Progressive neurodegenerative disease

Alzheimer's disease (AD) is a neurodegenerative disease that usually starts slowly and progressively worsens, and is the cause of 60–70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include problems with language, disorientation, mood swings, loss of motivation, self-neglect, and behavioral issues. As a person's condition declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the average life expectancy following diagnosis is three to twelve years.

<span class="mw-page-title-main">Particulates</span> Microscopic solid or liquid matter suspended in the Earths atmosphere

Particulates or atmospheric particulate matter are microscopic particles of solid or liquid matter suspended in the air. The term aerosol refers to the particulate/air mixture, as opposed to the particulate matter alone, though it is sometimes defined as a subset of aerosol terminology. Sources of particulate matter can be natural or anthropogenic. They have impacts on climate and precipitation that adversely affect human health, in ways additional to direct inhalation.

The health of a mother directly affects the fetus during pregnancy. High levels of vehicle pollution where pregnant women reside can have adverse health effects on fetuses.

The neuroscience of aging is the study of the changes in the nervous system that occur with ageing. Aging is associated with many changes in the central nervous system, such as mild atrophy of the cortex that is considered non-pathological. Aging is also associated with many neurological and neurodegenerative disease such as amyotrophic lateral sclerosis, dementia, mild cognitive impairment, Parkinson's disease, and Creutzfeldt–Jakob disease.

Committee on the Medical Effects of Air Pollutants (COMEAP) is a group of scientific experts who provide independent and authoritative advice to the UK government on the health effects of air pollution. Its core members are typically senior academics or professionals drawn from fields such as atmospheric chemistry, environmental health, epidemiology, and toxicology; a single lay member helps to ensure the committee's technical work is accessible to the public.

Particulate pollution is pollution of an environment that consists of particles suspended in some medium. There are three primary forms: atmospheric particulate matter, marine debris, and space debris. Some particles are released directly from a specific source, while others form in chemical reactions in the atmosphere. Particulate pollution can be derived from either natural sources or anthropogenic processes.

References

  1. 1 2 3 4 5 6 7 8 9 10 11 You R, Ho YS, Chang RC (February 2022). "The pathogenic effects of particulate matter on neurodegeneration: a review". J Biomed Sci (review). 29 (1): 15. doi: 10.1186/s12929-022-00799-x . PMC   8862284 . PMID   35189880. Creative Commons by small.svg  This article incorporates textfrom this source, which is available under the CC BY 4.0 license.
  2. ↑ "Air Pollution and the Brain". California Air Resources Board. 31 Aug 2018. Retrieved 14 Mar 2024.
  3. ↑ Flores-Pajot MC, Ofner M, Do MT, Lavigne E, Villeneuve PJ (November 2016). "Childhood autism spectrum disorders and exposure to nitrogen dioxide, and particulate matter air pollution: A review and meta-analysis". Environ Res. 151: 763–776. doi:10.1016/j.envres.2016.07.030. PMID   27609410.
  4. ↑ Chun H, Leung C, Wen SW, McDonald J, Shin HH (January 2020). "Maternal exposure to air pollution and risk of autism in children: A systematic review and meta-analysis". Environ Pollut. 256: 113307. Bibcode:2020EPoll.25613307C. doi: 10.1016/j.envpol.2019.113307 . PMID   31733973.
  5. ↑ Lam J, Sutton P, Kalkbrenner A, Windham G, Halladay A, et al. (2016). "A Systematic Review and Meta-Analysis of Multiple Airborne Pollutants and Autism Spectrum Disorder". PLOS ONE. 11 (9): e0161851. Bibcode:2016PLoSO..1161851L. doi: 10.1371/journal.pone.0161851 . PMC   5031428 . PMID   27653281.
  6. ↑ Weisskopf MG, Kioumourtzoglou MA, Roberts AL (December 2015). "Air Pollution and Autism Spectrum Disorders: Causal or Confounded?". Curr Environ Health Rep. 2 (4): 430–9. doi:10.1007/s40572-015-0073-9. PMC   4737505 . PMID   26399256.
  7. ↑ Fu P, Yung KK (2020). "Air Pollution and Alzheimer's Disease: A Systematic Review and Meta-Analysis". J Alzheimers Dis. 77 (2): 701–714. doi:10.3233/JAD-200483. PMID   32741830.
  8. ↑ Tsai TL, Lin YT, Hwang BF, Nakayama SF, Tsai CH, et al. (October 2019). "Fine particulate matter is a potential determinant of Alzheimer's disease: A systemic review and meta-analysis". Environ Res. 177: 108638. doi:10.1016/j.envres.2019.108638. PMID   31421449.
  9. 1 2 Braithwaite I, Zhang S, Kirkbride JB, Osborn DP, Hayes JF (December 2019). "Air Pollution (Particulate Matter) Exposure and Associations with Depression, Anxiety, Bipolar, Psychosis and Suicide Risk: A Systematic Review and Meta-Analysis". Environ Health Perspect. 127 (12): 126002. doi:10.1289/EHP4595. PMC   6957283 . PMID   31850801.
  10. ↑ Lu JG (April 2020). "Air pollution: A systematic review of its psychological, economic, and social effects". Current Opinion in Psychology. 32: 52–65. doi:10.1016/j.copsyc.2019.06.024. PMID   31557706. S2CID   199147061.
  11. 1 2 Liu Q, Wang W, Gu X, Deng F, Wang X, et al. (February 2021). "Association between particulate matter air pollution and risk of depression and suicide: a systematic review and meta-analysis". Environ Sci Pollut Res Int. 28 (8): 9029–9049. Bibcode:2021ESPR...28.9029L. doi:10.1007/s11356-021-12357-3. PMID   33481201.
  12. ↑ Symons A (2022-12-15). "Suicide rates rise as air quality worsens, study finds". euronews. Retrieved 2022-12-19.
  13. 1 2 Louis S, Carlson AK, Suresh A, Rim J, Mays M, et al. (March 2023). "Impacts of Climate Change and Air Pollution on Neurologic Health, Disease, and Practice: A Scoping Review". Neurology (Review). 100 (10): 474–483. doi:10.1212/WNL.0000000000201630. PMC   9990849 . PMID   36384657.
  14. 1 2 Song R, Liu L, Wei N, Li X, Liu J, et al. (January 2023). "Short-term exposure to air pollution is an emerging but neglected risk factor for schizophrenia: A systematic review and meta-analysis". Sci Total Environ. 854: 158823. doi:10.1016/j.scitotenv.2022.158823. PMID   36116638.
  15. ↑ Calderon-Garciduenas L, Mora-Tiscareno A, Ontiveros E, Gomez-Garza G, Barragan-Mejia G, et al. (2008). "Air pollution, cognitive deficits and brain abnormalities: A pilot study with children and dogs". Brain and Cognition. 68 (2): 117–127. doi:10.1016/j.bandc.2008.04.008. PMID   18550243. S2CID   7714924.
  16. ↑ Sbihi H, Jones MJ, MacIsaac JL, Brauer M, Allen RW, et al. (2019). "Prenatal exposure to traffic-related air pollution, the gestational epigenetic clock, and risk of early-life allergic sensitization". Journal of Allergy and Clinical Immunology. 144 (6): 1729–1731.e5. doi: 10.1016/j.jaci.2019.07.047 . PMID   31470034. S2CID   201756930.
  17. ↑ Bos I, Jacobs L, Nawrot TS, de Geus B, Int Panis L, et al. (August 2011). "No exercise-induced increase in serum BDNF after cycling near a major traffic road". Neuroscience Letters. 500 (2): 129–132. doi:10.1016/j.neulet.2011.06.019. PMID   21708224. S2CID   411730.
  18. ↑ Bos I, De Boever P, Vanparijs J, Pattyn N, Int Panis L, et al. (2013). "Subclinical effects of aerobic training in urban environment". Medicine and Science in Sports and Exercise. 45 (3): 439–47. doi:10.1249/MSS.0b013e31827767fc. hdl: 1942/14628 . PMID   23073213.
  19. ↑ Bos I, De Boever P, Int Panis L, Meeusen R (2014). "Physical Activity, Air Pollution and the Brain". Sports Medicine (review). 44 (11): 1505–18. doi:10.1007/s40279-014-0222-6. PMID   25119155. S2CID   207493297.
  20. 1 2 3 US EPA (4 May 2023). "Fighting the Haze: Effects of Wildfire Smoke and Particulate Matter on Brain Function" . Retrieved 17 Mar 2024.PD-icon.svg This article incorporates text from this source, which is in the public domain .
  21. ↑ "EHP – Outdoor Particulate Matter Exposure and Lung Cancer: A Systematic Review and Meta-Analysis". ehp.niehs.nih.gov. Archived from the original on 29 May 2016. Retrieved 2016-12-29.
  22. ↑ Wasley A, Heal A, Harvey F, Lainio M (13 June 2019). "Revealed: UK government failing to tackle rise of serious air pollutant". The Guardian.
  23. ↑ US EPA O (26 April 2016). "Health and Environmental Effects of Particulate Matter (PM)". US EPA. Retrieved 5 October 2019.
  24. ↑ Raaschou-Nielsen O, Andersen ZJ, Beelen R, Samoli E, Stafoggia M, et al. (August 2013). "Air pollution and lung cancer incidence in 17 European cohorts: prospective analyses from the European Study of Cohorts for Air Pollution Effects (ESCAPE)". The Lancet Oncology. 14 (9): 813–822. doi:10.1016/S1470-2045(13)70279-1. PMID   23849838.
  25. ↑ B. Collins (3 August 2007). "HP Hits Back in Printer Health Scare Row". PC Pro . Archived from the original on 2007-08-10. Retrieved 2009-05-15.
  26. ↑ M. Benjamin (November 2007). "RT for Decision Makers in Respiratory Care". RT Magazine . Archived from the original on 2008-12-04. Retrieved 2009-05-15.
  27. ↑ Moreno-Ríos AL, Tejeda-Benítez LP, Bustillo-Lecompte CF (2022). "Sources, characteristics, toxicity, and control of ultrafine particles: An overview". Geoscience Frontiers. 13: 101147. Bibcode:2022GeoFr..1301147M. doi:10.1016/j.gsf.2021.101147. hdl: 11323/7995 . S2CID   234159865.
  28. ↑ "NIOSH Power tools database". Archived from the original on 2009-11-12. Retrieved 2009-06-19.
  29. ↑ "Particulate matter emissions from activities of building refurbishment".
  30. ↑ https://www.researchgate.net/publication/327918070_Number_concentrations_and_size_distributions_of_nanoparticles_during_the_use_of_hand_tools_in_refurbishment_activities
  31. ↑ UKOpenGovernmentLicence.svg  This article incorporates text published under the British Open Government Licence : "Frequently asked questions – Dust". HSE GOV.UK. 13 Jun 2023. Retrieved 8 Apr 2024.
  32. ↑ "EN 50632-1".
  33. ↑ "EN 50632-2-5".
  34. ↑ "FAQs - Dust, HSE".
  35. ↑ "Beware of dust - Hilti Canada".
  36. ↑ "Dust control - Hilti Hong Kong".
  37. ↑ Shiffler A (2023-12-18). "California's Green Lawn Care Law: What You Need to Know". Lawn Care Blog | Lawn Love. Retrieved 2024-03-13.
  38. ↑ Mates J, Segura J, Alonso F, Marquez J (2010). "Roles of dioxins and heavy metals in cancer and neurological diseases using ros-mediated mechanisms". Free Radical Biology and Medicine. 49 (9): 1328–1341. doi:10.1016/j.freeradbiomed.2010.07.028. PMID   20696237.
  39. 1 2 Urban P, Pelclova D, Lukas E, Kupka K, Preiss J, et al. (2007). "Neurological and neurophysiological examinations on workers with chronic poisoning by 2,3,7,8-tcdd: follow-up 35 years after exposure". European Journal of Neurology. 14 (2): 213–218. doi: 10.1111/j.1468-1331.2006.01618.x . PMID   17250732. S2CID   29676448.
  40. ↑ Gundacker C, Gencik M, Hengstschlager M (2010). "The relevance of the individual genetic background for the toxicokinetics of two significant neurodevelopmental toxicants: mercury and lead". Mutation Research/Reviews in Mutation Research. 705 (2): 130–140. doi:10.1016/j.mrrev.2010.06.003. PMID   20601101.
  41. ↑ Ng DK, Chan CH, SOO MT, Lee RS (2007). "Low-level chronic mercury exposure in children and adolescents: Meta-analysis". Pediatrics International. 49 (1): 80–87. doi:10.1111/j.1442-200X.2007.02303.x. PMID   17250511. S2CID   24367277.
  42. ↑ Bridges CC, Zalups RK (2005). "Molecular and ionic mimicry and the transport of toxic metals". Toxicol. Appl. Pharmacol. 204 (3): 274–308. doi:10.1016/j.taap.2004.09.007. PMC   2409291 . PMID   15845419.
  43. ↑ Liu J, Lei D, Waalkes MP, Beliles RP, Morgan DL (2003). "Genomic analysis of the rat lung following elemental mercury vapor exposure". Toxicol. Sci. 74 (1): 174–181. doi: 10.1093/toxsci/kfg091 . PMID   12730625.
  44. ↑ Stacchiotti A, Morandini F, Bettoni F, Schena I, Lavazza A, et al. (2009). "Stress proteins and oxidative damage in a renal derived cell line exposed to inorganic mercury and lead". Toxicology. 264 (3): 215–224. doi:10.1016/j.tox.2009.08.014. PMID   19720107.
  45. ↑ Fuller R, Landrigan PJ, Balakrishnan K, Bathan G, Bose-O'Reilly S, et al. (June 2022). "Pollution and health: a progress update". Lancet Planet Health (review). 6 (6): e535–e547. doi: 10.1016/S2542-5196(22)00090-0 . PMID   35594895.
  46. ↑ Herbert MR (2010). "Contributions of the environment and environmentally vulnerable physiology to autism spectrum disorders". Current Opinion in Neurology (review). 23 (2): 103–110. doi:10.1097/wco.0b013e328336a01f. PMID   20087183. S2CID   17280526.
  47. ↑ Baron-Cohen S, Saunders K, Chakrabarti S (1999). "Does autism cluster geographically? A research note". Autism. 3: 39–43. doi:10.1177/1362361399003001004. S2CID   146452563.
  48. 1 2 3 4 5 6 7 8 9 10 11 12 "Autism". National Institute of Environmental Health Sciences. 22 Mar 2024. Retrieved 25 Mar 2024.PD-icon.svg This article incorporates text from this source, which is in the public domain .
  49. 1 2 Campbell A (2004). "Inflammation, Neurodegenerative Diseases, and Environmental Exposures". Annals of the New York Academy of Sciences. 1035 (1): 117–132. Bibcode:2004NYASA1035..117C. doi:10.1196/annals.1332.008. PMID   15681804. S2CID   21762775.
  50. ↑ Oikonen M, Laippala P, Oksaranta O, Lilius EM, Lindgren S, et al. (2003). "Ambient air quality and occurrence of multiple sclerosis relapse". Neuroepidemiology. 22 (1): 95–99. doi:10.1159/000067108. PMID   12566960. S2CID   26392841.
  51. ↑ Bloem BR, Okun MS, Klein C (June 2021). "Parkinson's disease" (PDF). Lancet. 397 (10291): 2284–2303. doi:10.1016/S0140-6736(21)00218-X. PMID   33848468. "…However, this more accurate diagnostic process cannot explain why the age-adjusted prevalence of Parkinson's disease is growing faster than other neurological disorders, including diseases such as multiple sclerosis, which has seen substantial advances in diagnostic approaches. Other factors potentially contributing to this rise include prolonged survival and environmental pollution with toxins, such as pesticides (eg, paraquat) or chemicals (eg, trichloroethylene), known to be harmful to Parkinson's disease-related neurons and brain circuits"
  52. ↑ Dorsey ER, Zafar M, Lettenberger SE, et al. (2023). "Trichloroethylene: An Invisible Cause of Parkinson's Disease?". J Parkinsons Dis. 13 (2): 203–218. doi:10.3233/JPD-225047. PMC   10041423 . PMID   36938742.
  53. 1 2 Simon DK, Tanner CM, Brundin P (2020). "Parkinson Disease Epidemiology, Pathology, Genetics, and Pathophysiology". Clinical Geriatric Medicine. 36 (1): 1–12. doi:10.1016/j.cger.2019.08.002. PMC   6905381 . PMID   31733690. S2CID   201961979.
  54. ↑ Bjorklund G, Stejskal V, Urbina MA, Dadar M, Chirumbolo S, et al. (2018). "Metals and Parkinson's Disease: Mechanisms and Biochemical Processes" (PDF). Curr Med Chem. 25 (19): 2198–2214. doi:10.2174/0929867325666171129124616. PMID   29189118. S2CID   4648656.
  55. ↑ Hoke A, Malemud CJ, Silver J (1994). "Regional differences in reactive gliosis induced by substrate-bound β-amyloid". Exp. Neurol. 130 (1): 56–66. doi:10.1006/exnr.1994.1185. PMID   7821397. S2CID   54293885.
  56. ↑ Calderón-Garcidueñas L, Ayala A (June 2022). "Air Pollution, Ultrafine Particles, and Your Brain: Are Combustion Nanoparticle Emissions and Engineered Nanoparticles Causing Preventable Fatal Neurodegenerative Diseases and Common Neuropsychiatric Outcomes?". Environ Sci Technol (review). 56 (11): 6847–6856. Bibcode:2022EnST...56.6847C. doi: 10.1021/acs.est.1c04706 . PMID   35193357.
  57. ↑ Hersh AM, Alomari S, Tyler BM (April 2022). "Crossing the Blood-Brain Barrier: Advances in Nanoparticle Technology for Drug Delivery in Neuro-Oncology". Section 2.1. Int J Mol Sci (review). 23 (8): 4153. doi: 10.3390/ijms23084153 . PMC   9032478 . PMID   35456971.
  58. ↑ Kim H, Harrison FE, Aschner M, Bowman AB (July 2022). "Exposing the role of metals in neurological disorders: a focus on manganese". Trends Mol Med (review). 28 (7): 555–568. doi:10.1016/j.molmed.2022.04.011. PMC   9233117 . PMID   35610122.
  59. ↑ Iadecola C (September 2017). "The Neurovascular Unit Coming of Age: A Journey through Neurovascular Coupling in Health and Disease". Neuron. 96 (1): 17–42. doi:10.1016/j.neuron.2017.07.030. PMC   5657612 . PMID   28957666.
  60. ↑ Niu Z, Liu F, Yu H, Wu S, Xiang H (January 2021). "Association between exposure to ambient air pollution and hospital admission, incidence, and mortality of stroke: an updated systematic review and meta-analysis of more than 23 million participants". Environ Health Prev Med (systematic review and meta-analysis). 26 (1): 15. Bibcode:2021EHPM...26...15N. doi: 10.1186/s12199-021-00937-1 . PMC   7839211 . PMID   33499804. Creative Commons by small.svg  This article incorporates textfrom this source, which is available under the CC BY 4.0 license.
  61. ↑ Calderón-Garcidueñas L (2021). Alzheimer's Disease and Air Pollution: The Development and Progression of a Fatal Disease from Childhood and the Opportunities for Early Prevention. Advances in Alzheimer's Disease. IOS Press. p. 136. ISBN   978-1-64368-159-7 . Retrieved 8 Apr 2024.
  62. ↑ Butler C, Ibanez A, Parra M, Wang H, Chan K, et al. (2022). Dementia in Low and Middle Income Countries. Frontiers Research Topics. Frontiers Media SA. p. 242. ISBN   978-2-88976-426-6 . Retrieved 8 Apr 2024.
  63. ↑ Cheng S, Jin Y, Dou Y, Zhao Y, Duan Y, et al. (November 2022). "Long-term particulate matter 2.5 exposure and dementia: a systematic review and meta-analysis". Public Health (systematic review and meta-analysis). 212: 33–41. doi:10.1016/j.puhe.2022.08.006. PMID   36201876. in adults aged ≥40 years ... long-term exposure to fine particulate matter was related to an increased risk of dementia. A 10 μg/m3 increase in long-term exposure to PM2.5 was associated with an elevated risk of dementia by 40%, AD by 47% and VaD by 100% when adjusting for nearly all potential confounders
  64. 1 2 3 4 5 6 7 8 Delgado-Saborit JM, Guercio V, Gowers AM, Shaddick G, Fox NC, et al. (February 2021). "A critical review of the epidemiological evidence of effects of air pollution on dementia, cognitive function and cognitive decline in adult population". Sci Total Environ (review). 757: 143734. Bibcode:2021ScTEn.75743734D. doi:10.1016/j.scitotenv.2020.143734. hdl: 10234/192544 . PMID   33340865. Creative Commons by small.svg  This article incorporates textfrom this source, which is available under the CC BY 4.0 license.
  65. 1 2 3 4 5 6 7 8 9 10 11 12 UKOpenGovernmentLicence.svg  This article incorporates text published under the British Open Government Licence : UKHSA. "Cognitive decline, dementia and air pollution: a report by the Committee on the Medical Effects of Air Pollutants (COMEAP)" (PDF). GOV.UK. pp. v–viii. Retrieved 14 Mar 2024. (From https://www.gov.uk/government/publications/air-pollution-cognitive-decline-and-dementia)
  66. 1 2 Cakmak S, Dales RE, Vidal CB (2010). "Air pollution and hospitalization for epilepsy in Chile". Environment International. 36 (6): 501–505. Bibcode:2010EnInt..36..501C. doi:10.1016/j.envint.2010.03.008. PMID   20452673.
  67. ↑ Castellani B, Bartington S, Wistow J, Heckels N, Ellison A, et al. (2022). "Mitigating the impact of air pollution on dementia and brain health: Setting the policy agenda". Environmental Research. 215 (Pt 2). doi:10.1016/j.envres.2022.114362. hdl: 10044/1/99989 . PMID   36130664.

Further reading

This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.