Brain health and pollution
Effects of pollution on the brain
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Through Pollution, Child and Adolescence
The criteria air pollutants particulate matter, nitrogen dioxide, sulfur dioxide, carbon monoxide, ozone, and lead have been identified as harmful to human health by the World Health Organization and the U.S. Environmental Protection Agency (EPA). Many of them are linked to the burning of fossil fuels, through vehicle use, heating and cooking. Indoor and outdoor air pollution can contain particulate matter, dioxins, heavy metals, and endocrine-disrupting chemicals and microplastics that have negative effects on the central nervous system (CNS). Increased exposures to pollutants such as particulate matter and black carbon are associated with increases in cognitive impairment. Pollutants can interfere with neuroplasticity (the brain's ability to grow new neurons, adapt, and reorganize itself) and lead to long-term structural changes. Neurotoxicity is mediated by processes such as oxidative stress, mitochondrial dysfunction, and neuroinflammation. Pollutants such as microplastics may affect the neurophysiology of individuals after the structure of the CNS has mostly stabilized.
In terms of long-term social and economic impacts, air pollution exposure is linked to poorer cognitive development, academic performance and learning capacity in children. In adults, the effects of air pollution are linked to lower incomes, and decreased personal and workplace productivity. Economically, lowered IQ levels (as a measure of cognitive ability) are also related to increased healthcare costs and greater burden on the health system.
As a contributor to disease burden, environmental pollution is potentially preventable. Steps can be taken to minimize exposures to pollutants such as avoiding smoking, minimizing dust, using glass instead of plastics, carefully selecting cleaning products and cosmetics, and exercising away from heavy traffic routes. Control strategies can also be implemented to improve industrial safety and public health.
Pollutants
Pollutants can be inhaled, eaten, drunk, or absorbed through skin, with inhalation of air pollution being a dominant exposure route. Air pollution can result both from natural causes such as sea spray or desert dust and from human activities such as first and second-hand tobacco and cannabis smoke, household air pollution (HAP), and automobile exhaust fumes from fossil fuel combustion. Air pollution is a complex mixture that includes solids, liquids and gases. Air pollution also contains combinations of tiny particles of solid or liquid matter suspended in air, called particulate matter.
Air pollution is consistently associated with neurostructural and neurofunctional changes such as increased inflammation and oxidative stress and altered activity of neurotransmitters, neuromodulators and their metabolites. Exposure to air pollution is also associated with changes to gray matter volume and white matter structure within some brain regions.
Particulate matter
Particulate matter is made up of tiny particles of solid or liquid matter suspended in air, which are referred to in terms of the size of the particles measured (e.g. PM10, PM2.5, PM1, ultrafine particles). PM2.5 contains particulates with a diameter of 2.5 micrometers or less. Small particulates are extremely harmful as they can penetrate deep into the lungs and travel through the bloodstream to the brain. Particulate matter can contain many toxic components, including carbon and heavy metals, with its chemical composition influencing its effects. As of 2022, the World Health Organization reported that 99% of the world’s population lives in places with unhealthy levels of PM2.5 pollution. Increased exposures to pollutants such as particulate matter (PM10, PM2.5, PM1) and black carbon are associated with increases in cognitive impairment and neurodegenerative diseases such as dementia, Alzheimer's disease and Parkinson's disease. Airborne particulate matter is a Group 1 carcinogen. There is no safe level of particulate exposure.
Particulate matter can be both manufactured and naturally occurring. Hot volcanic lava, ocean spray, and wildfire smoke are common natural sources of particulates. Aerosols can be intentionally fabricated to serve a vast range of applications in both medicine and technology. Other particulates are produced as byproducts of specific processes or combustion reactions, such as printer toner and automobile exhaust. Anthropogenic sources of particulate matter include combustion of gas, coal, and other hydrocarbons (fossil fuels); burning of biomass fuels (firewood, charcoal, agricultural crop residues, and animal dung) in kitchens, domestic wood stoves, and outdoors; cigarette and cannabis smoking; human-caused forest fires and agricultural burns; waste disposal; industrial emissions; vehicular traffic and wear to roads, tires, and brakes; air traffic; seaport and maritime transportation; construction, demolition, restoration and concrete processing.
Use of power tools and hand tools for demolition, renovation and construction can produce large amounts of dust particulates. High energy tools (cut-off saws, grinders, wall chasers and grit blasters) can produce lots of dust in a short time. Using power tools to cut, grind, drill or prepare a surface, and sanding taped plaster board joints, can produce high dust levels. The more enclosed a work area, the more dust will collect there. The longer one works, the more dust there will be. Work methods such as dry sweeping raise more dust than vacuuming or wet brushing. Knowing that dust is generated during construction and can cause serious health hazards, some manufacturers market power tools equipped with dust collection systems or integrated water delivery systems. However, there are few industry standards for production of dust from tools. As of Q1 2024, California banned the sale of new gas-powered landscaping and outdoor equipment <25 horsepower.
Pollutants such as particulate matter are theorized to affect the brain via multiple pathways. The small particles found in PM2.5 can reach the brain through different entry routes via the olfactory system, lungs, circulatory system, and digestive system. PM2.5 can enter the nervous system through the nose and olfactory bulb. Inhaled PM2.5 can lead to respiratory inflammation and trigger systematic inflammation. This produces proinflammatory cytokines that can disrupt the blood–brain barrier, enabling pollutants to enter the brain. Once PM2.55 enters the circulatory system, it can be transported to the brain and across the blood–brain barrier. Within the brain, PM2.5 interferes with cellular and molecular mechanisms and can injure neurons. Neuroinflammation involves the activation of microglial cells and the production and release of inflammatory cascade mediators, including reactive oxygen species (ROS), proinflammatory cytokines, and nitric oxide. Elevated levels of ROS can interfere with the body’s ability to detoxify cells and to repair cellular damage, resulting in oxidative stress. This can damage cellular components such as DNA, proteins, and lipids. Responses to oxidative stress can lead to changes in mitochondria or other organelles within the cell, like the endoplasmic reticulum (ER), and trigger cell death. A buildup of misfolded proteins in the brain can lead to cognitive decline and neurodegenerative diseases.
Nitrogen oxides (NOx)
Nitrogen and oxygen combine during combustion to produce nitrogen oxides (NOx) such as nitric oxide (NO) and nitrogen dioxide (NO2). NO2 is generated by fuel burning in vehicles, power plants, and industrial facilities, and is often used as an indicator of the presence of NOx generally and of traffic-related air pollution (TRAP). NO2 concentration tends to be highest in urban areas but nitrogen oxides can also be produced through agriculture. NO2 reacts with other pollutants and can dissipate quickly, varying hour by hour and from one neighborhood to another. When sunlight reacts with NOx and volatile organic compounds (VOCs) this can produce the pollutant ground level ozone (O3).
NO2 can increase oxidative stress and inflammation in the brain, resulting in neuronal damage. Meta-analysis suggests that NO2 is also related to depression, possibly due to an increase in reactive oxygen species, oxidative stress and inflammation. Prolonged exposure can interfere with the generation of new neurons and the brain's ability to adapt, and lead to structural changes. Long-term exposure to NO2 is associated with lower gray and white matter volume and enlargement of ventricles (fluid-filled spaces) in the brain. This has been linked to accelerated biological aging, reduced cognitive abilities, cognitive decline, increased susceptibility to depression, and higher risk of dementia. NO2 may also be linked to Alzheimer's Disease and Parkinson's Disease.
Sulfur dioxide (SO2)
SO2 is a widespread air pollutant, emitted from natural sources such as volcanoes, hot springs, geysers, wildfires, and marine processes, and through human activities such as fossil fuel combustion, manufacturing, and wine preservation. Both acute and chronic exposure to SO2 are known to cause respiratory and cardiovascular illnesses and fatalities. Chronic exposure to SO2 also appears to cause neurological damage, through mechanisms such as oxidative stress, neuroinflammation, and vascular compromise. SO2 exposure can damage synapses and affect the expression of synaptic structural and functional proteins.
Meta-analysis and reviews indicate that exposure to SO2 is associated with decreases in global cognitive function, and with increased risk of cognitive decline and cognitive impairment. Cognitive function includes a broad range of skills such as attention, perception, memory, learning, and executive function. Cognitive impairment can include difficulty in thinking, learning, remembering, judgement and decision-making. SO2 is linked to memory impairment in aging. Synaptic alterations are considered an early marker for cognitive decline and are correlated with neurodegenerative processes in Alzheimer's and other neurodegenerative diseases. SO2 has a potential role in the onset of epileptic seizures and in relapses from schizophrenia.
Carbon monoxide (CO)
Carbon monoxide (CO) is most commonly associated with acute carbon monoxide poisoning, in which hemoglobin in the blood bonds to CO instead of oxygen, preventing the body from getting enough oxygen to function. Exposure to CO most commonly occurs as a result of incomplete combustion of carbon-based fuels, from engine exhaust, fires, or gasoline-powered tools.
CO exposure is also associated with permanent brain damage which can occur days and weeks after exposure, and involve long-term neurological and cognitive deficits, PTSD, and depression. Mechanisms involved are not well understood, but may involve reactive oxygen species (ROS), oxidative damage, inflammation, and changes to myelin basic protein (MBP) that trigger immune responses and lead to brain damage. Meta-analysis also suggests that exposure to CO is associated with Parkinson's disease.
Heavy metals
Exposure to heavy metals can result in an increased risk of various neurological diseases. Among the most neurotoxic heavy metals are lead (Pb), mercury (Hg), and cadmium (Cd).
Lead (Pb)
Lead (Pb) has a long history of known toxicity. In Han dynasty (206 BC–220 AD) China, mercury, lead, and arsenic were used as ingredients in immortality elixirs. By the Tang dynasty alchemists in China wrote that their use could be dangerous. In Rome, in the second century B.C.E., Nicander wrote an account describing lead poisoning. The Industrial Revolution led to increased use of lead in manufacturing, smelting, and various trades, including the production and use of paints and enamels. The impact of lead, mercury and other poisons was documented in investigations such as Alice Hamilton's pioneering surveys of industrial illnesses. As of 1925, lead and mercury were included in the first list of compensable occupational diseases compiled by the International Labour Organization (ILO).
Despite the known dangers of lead, tetraethyl or tetramethyl lead was introduced as an additive for gasoline in the 1920s. Its use resulted in world-wide increases in environmental concentrations and toxic effects of inorganic and organic lead compounds, which became ubiquitous as a contaminant in soil, water and air. Although the United States introduced federal policies to remove lead from paint and passenger car gasoline in the 1970s’ and 1980s’, lead continues to be found in older paint and pipes and in soil and household dust. Water can become contaminated from contact with lead in pipes, plumbing fittings, fixtures, solder and flux, and from dishes containing lead. Cookware, foods, toys, jewelry, cosmetics, spices, and folk remedies that pre-date lead regulations or are made in countries where regulations are not applied may still contain dangerous levels of lead. Another major source of lead exposure comes from the improper recycling of lead–acid batteries and electronic waste. Plants grown in contaminated soil may contain lead, which can then enter the human food chain and increase risks to food safety and human health. Lead is most likely to enter the human body by being inhaled, eaten or drunk. Because small children naturally crawl on the ground and put their hands and other objects into their mouths, they are at higher risk for exposure to pollutants from paint, dust, and soil as well as air, food, and water.
There is no safe level of lead exposure. Lead affects multiple systems and causes neurological, motor, and behavioral deficits. Lead is easily absorbed through the respiratory tract and the duodenum and can cross the blood–brain barrier. More than 90 % is stored in bones and teeth, where it can remain for decades. Lead also accumulates in the liver, spleen, muscles, brain, kidneys, and lungs and is distributed in soft tissues. Mechanisms by which it affects the brain include oxidative stress, inflammation, calcium mimicry, and altered neurotransmission. Lead imitates ions such as calcium, taking its place in proteins and enzymes. This dysregulates cell processes involved in signaling pathways, ion transportation, enzyme regulation, and cell death. Acute lead exposure can cause decreases in synaptic proteins, synaptic dysfunction, changes to the cytoskeleton, and neuronal death. Acute nervous system effects can include convulsions, coma, and death.
Exposure to lead can also lead to intellectual impairment affecting memory, executive function, attention, and learning. Blood lead concentrations ≥ 5·0 μg/dL may result in children scoring 3–5 points lower in intelligence tests than those with concentrations < 5·0 μg/dL. Chronic lead exposure has been linked to lower brain volume and cognitive impairment. Lead exposure is also linked to psychological disorders including depression, anxiety, bipolar disorder, and schizophrenia, and increases in behaviors such as school failure, juvenile delinquency and adult arrests. Lead may also play a role in Alzheimer’s Disease. The impact on economic productivity has been estimated in terms of global economic losses of almost $1 trillion annually.
Mercury (Hg)
Environmental mercury occurs naturally but also is released into the environment through human activities such as industrial processing, mining, incineration of hazardous waste, and combustion of fossil fuels. Mercury accumulates in aquatic food chains and in the human body, and is able to cross both the blood–brain barrier and the placenta. Mercury exists in multiple forms: elemental mercury (Hg0), inorganic mercury salts (Hg1+ and Hg2+), and organomercury compounds such as methylmercury (MeHg). MeHg most easily crosses cell membranes and is therefore most neurotoxic. Mercury exposure can occur through inhalation, ingestion, or skin contact. Humans are most likely to be exposed domestically, due to eating fish or other foods contaminated by environmental pollution, or, less commonly, through medical or occupational exposures.
The effects of acute high-dose mercury poisoning vary depending on the type, route, amount, and duration of exposure. Chronic exposure to low-doses of mercury can cause serious and irreversible neurological damage in adults and interfere with fetal neurodevelopment. MeHg interferes with synaptic transmission and neuronal signaling, changes cell structures, increases inflammation and oxidative stress, and causes cell death. Because it can cross the blood-brain barrier and accumulate in the brain, mercury can continue to cause effects long after exposure ceases. Mercury poisoning can cause a wide range of symptoms involving multiple systems, including cognitive deficits, mood disorders, motor dysfunction, and death.
Cadmium (Cd)
Cadmium is a heavy metal that has been used in manufacturing of pigments, alloys, plastic stabilizers, nickel-cadmium (Ni-Cd) rechargeable batteries, solar cells, and as a protective coating for iron and steel. Cadmium can remain in contaminated water and soil for long periods, and be absorbed by plants to enter the food chain. The primary exposure route for humans is dietary intake followed less commonly by smoking or occupational exposure. The most frequently contaminated foods and drinks tend to be cereals, vegetables, seafood and chocolate.
Cadmium is highly toxic. Prolonged, low-dose cadmium exposure can significantly affect the nervous system. Cadmium mimics both zinc and calcium. It can travel across the blood-brain barrier (BBB) and accumulate in the central nervous system, where it disrupts mitochondrial respiration, increases the production of reactive oxygen species, and disrupts normal neurotransmission. Cadmium can damage the blood–brain barrier and alter glycogen metabolism. These mechanisms can result in nervous system damage and increased risk of neurological and neurodegenerative disorders.
Endocrine-disrupting chemicals
Endocrine-disrupting chemicals (EDCs) are defined by the World Health Organization as substances originating outside the body that interfere with the endocrine system. Examples include bisphenol A (BPA), dichlorodiphenyldichloroethylene (DDE), persistent organic pollutants (POPs), phthalates, polybrominated diphenyl ethers (PBDE) and dioxins. Such chemical compounds can be widely found in pollutants, pesticides, plastics, industrial products, consumer goods, and medicines.
Endocrine-disrupting chemicals can interfere with the nervous system's development and function. Exposure to endocrine-disrupting chemicals has been linked to neurodevelopmental disorders including autism spectrum disorder, attention-deficit hyperactivity disorder, global developmental delay, intellectual disability, and communication disorders.
Dioxins and dioxin-like compounds
Dioxins and dioxin-like compounds are highly persistent organic pollutants that contaminate aquatic and terrestrial systems, accumulate in food chains, and persist in the environment for long periods of time. They are extremely dangerous, even at low concentrations such as one part per billion. They include polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins (PCDFs or dioxins), and polychlorinated dibenzofurans (PCDDs or furans). Human activities contribute to their release through industrial processing and wastes, the production of fungicides, herbicides, and pesticides, pulp and paper production, the burning of fossil fuels and wood, waste incineration, e-waste recycling, industrial accidents, and military use. Dioxins also can be naturally released by wildfires and volcanic activity. Dioxins are most commonly found in pesticides or created as by-products of pesticide manufacture or degradation. Their most toxic form is 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD). Agent Orange, which contains dioxins, was used by the military in South Vietnam and the Korean Demilitarized Zone (DMZ) during the 1960s and 1970s, affecting American, Vietnamese, and Korean soldiers and civilians. Dioxins continue to contaminate soil and sediments and have multiple negative effects on the health of dioxin-exposed populations.
Dioxins interfere with the activities of the AhR signaling pathway, mediated by the aryl hydrocarbon receptor (AhR). AhR is widely distributed in the brain, and its activity differs before and after brain development. In addition to processes in brain development, AhR signaling pathways are involved in processes linked to aging, such as glial cell activation, inflammation, oxidative stress, mitochondrial dysfunction, and cellular senescence. AhR activation may regulate genes involved in synaptic plasticity and neurogenesis in the fully developed brain. Dioxins cause the dysregulation of dioxin-responsive genes in AhR signaling pathways. By interfering with hormones and gene expression, dioxins may increase immunotoxicity, endocrine disruption, and oxidative stress.
Dioxins are linked to widespread and potentially fatal health effects across multiple systems of the body. Prenatal and perinatal exposure to dioxins are associated with neurodevelopmental problems such as decreases in cognition, motor skills, attention, social-emotional skills, learning, and language. Exposure to dioxins at critical developmental periods may increase the risk of autism and other developmental disorders. The effects of dioxins are not limited to initial toxicity. Dioxins, through neuroplastic effects, may cause long-term damage that may not manifest itself for years or even decades. Genetic changes may extend health impacts across generations.
Microplastics
Microplastics (<5 mm) and nanoplastics (<1 μm) have become ubiquitous in the environment, in air, water and soil. Microplastics have been measured in human lung tissue, blood, placenta, breast milk, cerebrospinal fluid and olfactory bulb tissue. Microplastics have negative impacts on human health, including neurological processes. Other pollutants can "stick" to the surface of microplastics, including heavy metals (lead, mercury), endocrine-disrupting chemicals (BPA and phthalates), persistent organic pollutants (PCBs and dioxins) and bacteria. Microplastics can cross the blood–brain barrier and placental barrier, and can transport accumulated pollutants to the central nervous system and the developing fetal brain. Exposure to microplastics has been linked to both structural changes and functional deficits, including impaired cognitive function and changes in how the nervous system functions in later life. Oxidative stress has been identified as a pivotal mechanism between microplastic exposure and systemic toxicity.
Ozone (O3)
Repeated exposure to low doses of ground-level ozone (O3) has been suggested to produce chronic oxidative stress and the loss of synaptic plasticity, negatively affecting cognitive processes and information processing. Such changes may be related to the progression of neurodegenerative diseases. However, meta-analyses have not provided support for the effects of ozone on the brain. O3 exposure was not associated with increased risk of cognitive impairment in a meta-analysis which found effects for PM2.5, PM10, and SO2. Another meta-analysis found effects on health for SO2, NO2, and CO but not O3.
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Effects across the lifespan
Brain cell development begins during the third gestational week of human pregnancy, with synapses connecting neurons and supporting neural communication by the 23rd gestational week. The brain continues to develop beyond the postpartum period, with some regions of the brain continuing to mature through adolescence into the late twenties. In addition, new brain cells can grow and connections between brain cells can continue to adapt in the adult brain, supporting cognitive processes, learning and memory across the lifespan. The brain is particularly vulnerable during embryonic and fetal development. Conditions affecting development can result in structural, physiological and metabolic changes that have permanent life-long effects, including epigenetic changes that affect how cells function. The blood-brain barrier tends to be more permeable in the very young and the old, increasing the risk of pollutants and toxins entering the brain and causing neurological damage during these life stages.
Exposure to pollutants can alter both the structure and function of the brain. Mechanisms of action common to different types of pollutants include increased generation of reactive oxygen species (ROS), oxidative stress, and inflammation. Oxidative stress and inflammation can cause changes in the function of the blood-brain barrier and the placenta, enabling pollutants to cross them more easily. Pollutants may reach the brain by multiple pathways, directly through the olfactory system, or indirectly via the lungs or gut and bloodstream. In cases of direct neurotoxicity, environmental toxins that have reached the brain may directly damage cells. In cases of systemic inflammation, inflammation elsewhere in the body may trigger the release of cytokines which reach the brain through the circulatory system and activate microglia in the brain's immune system. This may lead to persistent neuroinflammation even if the primary environmental toxin does not enter the brain. Specific pollutants can disrupt a wide variety of processes involving cells, proteins, neurotransmitters, and the endocrine system, causing cellular and genetic damage. Many pollutants, including heavy metals, microplastics, and persistent organic pollutants, can accumulate in the body and brain and cause long-term effects including damage to cells and tissues.
Research has consistently shown that exposure to pollutants can affect fertility, fetal development, health in later life, and the genetics of future generations.
Prenatal, Infancy, Childhood
Prenatal exposure to pollution is associated with an increased risk of negative fetal outcomes, including central nervous system damage and developmental delays. Components of air pollution such as polycyclic aromatic hydrocarbons (PAHs) can negatively affect fetal brain development, with impacts on cognition and behavior.
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.
Adolescence
Exposure to pollution can lead to neurodevelopmental disorders involving brain development, cognitive function, intellectual development, and emotional and behavioral regulation, often becoming apparent during childhood or adolescence (e.g. ADHD, autism).
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). 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.
Adulthood
Pollution is also linked to mental health outcomes that are commonly diagnosed in adolescence or adulthood such as schizophrenia, neuroticism, depression, anxiety, and suicide.
Schizophrenia
Exposure to air pollution may be associated with elevated risk of schizophrenia.
Epilepsy
A 2025 meta-analysis indicates that PM2.5 and NO2 are associated with an increased risk of epilepsy. It is hypothesized that air pollutants increase epilepsy risk by increasing neuroinflammation and oxidative stress and disrupting the blood–brain barrier.
Aging
Pollution is associated with neurological conditions in later life such as migraines and stroke, cognitive impairment, and neurodegenerative disorders such as multiple sclerosis, Alzheimer's disease, Parkinson's disease, and dementia.
Accelerated neural aging
Neuroinflammation 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 (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.
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 (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. 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 (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.
Cognitive decline
The effects of air pollution and particulate matter on cognitive performance are an active area of research. A 2020 meta-analysis reported increased cognitive impairment with increments of 5 μg/m3 of PM2.5. A 2025 meta-analysis indicates that 1 μg/m3 increases in PM2.5, PM10, PM1 and black carbon are associated with decreased cognitive function. Meta-analysis and reviews also indicate that exposure to PM2.5, PM10, and SO2 are associated with decreases in global cognitive function and with cognitive decline. Epidemiological studies also suggest a link between PM2.5 exposure and cognitive decline. PM2.5 is associated with reduced cognitive function in children, as measured by IQ scores. Improved air quality has been found to have a protective effect on cognitive function.
Dementia
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.
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). There is a "well-recognized link between PM2.5 and vascular injury and the role of vascular injury in dementia". Air pollution in the cerebrovascular system may result in "stroke, vascular dementia, or other types of dementia". The risk of dementia, including Alzheimer's disease and vascular dementia, may be increased by long-term exposure to PM2.5.
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.
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.
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.
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.
Studies of white matter volume found associations between exposure to air pollution and reduced white matter volume. Evidence suggests that long-term exposure to air pollutants is associated with cognitive decline and with the risk of development of dementia. 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.
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. 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.
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. 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.
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 bloodstream 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. 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. 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.
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.
- 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.
- As of 2022, direct quantification of cognitive decline or dementia associated with air pollution would be subject to unknown uncertainty.
- It may be possible to develop an indirect method of quantification of cognitive effects secondary to the effects of particulate pollution on cardiovascular disease.
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).
Mitigations
Environmental pollution is a potentially preventable contributor to disease burden. On an individual level, steps can be taken to minimize exposures to pollutants such as avoiding smoking, minimizing dust, using glass instead of plastics, carefully selecting cleaning products and cosmetics, and avoiding idling vehicles and heavy traffic routes. Exposure to air pollutants may be lessened by staying away from places that have high levels of pollution, avoiding cross-contamination or secondary contamination (between persons and their personal belongings/environment), better personal hygiene, use of face masks and air purifiers, etc.
Control strategies can be implemented to improve industrial safety and public health. Urban planning can keep sources of pollutants away from residents and improve conditions. 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), neighbors need filtration, sealing, 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 local, state and national governmental levels, policies can be established and regulatory and cleanup activities can be taken to minimize population exposures to pollution. Governments can participate in international agreements to reduce air pollution, increase use of renewable energy and clean fuels, and support the use of low- or no-pollution vehicles such as electric cars. The most frequently used policy initiatives are directed at the transportation sector. In countries where air pollution control measures have been enacted, most cases have resulted in positive outcomes.
Personal activities
Recommendations for personal strategies to minimise the effects of air pollution have been developed based on scientific research. To minimize personal exposure to indoor pollution:
- Reduce sources of household air pollution including both first- and second-hand smoke. Avoid tobacco, marijuana, and vaping.
- Use clean fuels for heating and cooking rather than solid fuels, ventilate well, and use nonpolluting cooking stoves if possible.
- Use portable air cleaners to improve ventilation (e.g. Portable air cleaners fitted with HEPA filters).
- Eat a healthy, balanced diet high in fruits and vegetables and low in fats.
- Remove and minimize dust: remove shoes when entering a house and use damp mops rather than dry sweeping when cleaning.
- Use glass instead of plastics and avoid plastic packaging.
- Carefully select cleaning products and cosmetics to avoid harmful ingredients.
To minimize personal exposure to outdoor (ambient) pollution:
- Be aware of local air pollution levels using information from local air quality forecasts and maps.
- Wear close-fitting facemasks (e.g. N95 or KN95) when ambient air pollution levels are high.
- Exercise regularly but mimimise outdoor activity when ambient air pollution levels are high.
- When possible, cycle or walk rather than using motorised fossil-fuel driven vehicles, to obtain the benefit of exercise and to minimize contributions to pollution.
- Choose low-traffic routes and routes with open spaces to minimise near-road air pollution exposure. Minimise travel at peak times, and avoid waiting in areas of high air pollution.
- Share rides and use public transportation.
- Optimise driving style and vehicle settings: drive with windows closed when in traffic, use car air filtration systems, and avoid engine idling.
Healthy life styles
Healthy lifestyle factors include avoiding smoking (tobacco, marijuana and vaping), not drinking alcohol, engaging in regular physical activity, and eating a healthy diet. These factors promote brain health by reducing inflammation, increasing neuroplasticity, and improving cardiovascular functioning. While air pollution can negatively affect cognitive and executive function, a healthy lifestyle can have beneficial effects and may help to counter the harmful effects of pollutants like particulate matter (PM2.5). For example, one study suggests that an extra 13.6 minutes of moderate-to-vigorous physical activity (MVPA) can help to offset the negative cognitive effects of an increase of 10 μg/m3 of PM2.5.
While exercising is beneficial, care should be taken to avoid exercising in polluted environments. Increased respiratory rates during aerobic exercise may increase the inhalation of harmful particulate matter into the lungs. When particulate matter levels are reported to be high outside, consider exercising inside. Avoid exercising near high-pollution areas such as heavily-trafficked roads.
Exercise such as walking and cycling usually stimulates the production of brain-derived neurotrophic factor (BDNF), a protein that helps the growth of new brain cells. Pollutants from heavy traffic or smog interferer with the production of BDNF.
Diet
Vitamins
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. 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.
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. 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.
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. 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.
Professional activities
Urban planners can make the creation of green spaces, parks, and recreational areas away from roads and traffic a priority. Infrastructure that supports urban physical activity can be an important step towards brain health. Best practices should include situating large sources of pollutants such as major roadways, ports, and rail yards away from residential areas, schools, day care centers, playgrounds, and hospitals. Planning efforts in areas such as Camden, New Jersey, and Los Angeles and Long Beach, California, have resulted in emissions reductions.
Medical organizations such as the UK's Royal College of Physicians and the European Respiratory Society recommend that healthcare professionals be able to advise patients about the effects of air pollution and steps that can be taken to avoid negative effects. This is particularly important for higher-at-risk populations such as pregnant women, children, and older people.
In 2022, academics and other stakeholders in the United Kingdom outlined a policy agenda for brain health, identifying priorities for the policy domains of research and funding, education and awareness, and policy evaluation. Education and awareness recommendations included (1) informing people about the importance of air quality as a public health issue (2) developing educational materials (3) providing publicly available monitoring, assessment and screening tools and (4) connecting air pollution and brain health to existing public health initiatives.
Government policies
Policies enacted by governments tend to be either incentive policies (e.g. free public transportation to minimize use of private cars), supportive policies (e.g. subsidies for use of specific household fuels), or punitive policies (e.g. tolls for cars). In most cases where air pollution control measures have been enacted, outcomes have been positive.
In the United States, ambient air quality management is a joint responsibility of the federal and state governments as outlined in the US Clean Air Act and its amendments. Following these initiatives, concentrations of particulate matter (PM2.5) in the United States fell by about 40% between 2000 and 2016. Since then, the U.S.'s overall air quality has worsened.
As of 2019, scientists identified a group of combustion-related air pollutants including particulate matter (PM2.5), nitrogen dioxide, polycyclic aromatic hydrocarbons (PAHs), and black carbon as critical targets for US air pollution policy. Project TENDR (Targeting Environmental Neurodevelopmental Risks) recommended (1) that the US Environmental Protection Agency (EPA) consider the effects of air pollutants on neurodevelopment when setting standards and making cost-benefit assessments of health outcomes (2) strengthen and enforce federal fuel efficiency standards (3) advance clean energy policies to reduce reliance on fossil fuels (4) focus on reducing emissions of combustion-related pollutants from large sources near residential areas, such as major roadways, ports, and rail yards (5) restrict permitting of new sources of combustion-related air pollutants near residential areas (6) increase air monitoring near locations where children spend time such as schools and playgrounds (7) increase research into mitigation and (8) increase research into health effects of ultrafine particles.