Brain Smog: How Pollution Damages the Brain

Madilyn Sandy

Illustrations by Katie Hieb

Disclaimer: This article uses descriptors to refer to populations of color that reflect descriptors utilized in cited literature. The journal wishes to recognize that these terms may not be inclusive or representative of all racial or ethnic identities and communities referred to in this article. 

During the summer of 2023, phones across the East Coast lit up with an alarming notification: an air quality warning [1]. The raging wildfires of Quebec, Canada created an eerie, apocalyptic-looking haze as smoke drifted across the continent, polluting everything in its wake. In New York, the Air Quality Index classified the air as ‘very unhealthy,’ indicating that those exposed to the air could experience adverse health effects [1]. Depending on the severity of the pollution, people were strongly encouraged to remain indoors, especially those with weak respiratory systems. Air quality warnings were partially due to high levels of fine particulate matter in the atmosphere, known as PM2.5. PM2.5 can be various substances — dust and soil particles, exhaust smoke, metals, and chemical compounds — and comes from many natural and human-induced sources [2]. Although the effects of PM2.5 on some bodily systems, such as the cardiovascular and respiratory systems, are relatively well-studied, the long-term neurological effects of PM2.5 exposure require further research [3, 4, 5]. Understanding the full impact of PM2.5 also raises environmental justice and health equity concerns: populations of color and those of low-income status are disproportionately exposed to PM2.5 and its negative side effects, as these groups are more likely to live and work in close proximity to PM2.5 sources [6, 7]. 

Holy Smokes! Where Does PM2.5 Come From? 

The origins of PM2.5 are diverse. From natural causes such as wildfire smoke and dust storms to human-induced sources like traffic-related air pollution and fossil fuel combustion, PM2.5 levels are inextricably linked to weather patterns and global energy consumption [2, 8, 9]. Global fossil fuel consumption — the use of finite energy sources including coal, oil, and natural gas — was responsible for 27.3% of global PM2.5 emissions in 2017 [9]. Fossil fuel emissions come from various origins, such as transportation, industrial, and residential sectors [9, 10]. During your morning commute, cars in the long line of traffic expel PM2.5 through gasoline and diesel emissions [10]. Local factories that rely on coal for energy production release PM2.5 through smoke stacks [9]. The majority of American homes expel PM2.5 by using natural gas, propane, and fuel oil for electricity [11]. As all these aforementioned examples illustrate, our reliance on fossil fuels constantly exposes us to PM2.5. Although global PM2.5 concentrations have declined due to many nations’ efforts to implement renewable energy, levels are still on the rise in some industrializing countries [12]. Beyond human-induced sources, climate change causes extreme weather events such as wildfires, dust storms, and tornadoes to become increasingly common and release extra PM2.5 into the atmosphere [13, 14]. Even though climate change impacts everyone, concentrations of PM2.5 are not distributed equally around the world: some areas experience lower levels of the pollutant, while others contain higher levels [15]. For example, living or working in close proximity to oil and gas plants, coal mines, or industrial facilities increases one’s exposure to PM2.5 [6, 7]. People of color and lower-income groups tend to be disproportionately exposed to air pollution because they are systemically segregated to areas with more environmental hazards and threats [6]. Exposure to PM2.5 is linked to various life-threatening conditions that contribute to almost four million global deaths annually [2]. 

PM2.5: A Small But Mighty Intruder

PM2.5 can access the brain through multiple pathways due to its tiny size [3, 16, 17, 18]. As indicated by its name, PM2.5 molecules are 2.5 micrometers or less in diameter — much too small to be seen by the human eye [19]. To put this into perspective, the tip of one strand of human hair is around 60 micrometers, 24 times larger than a PM2.5 molecule [20]. While the human body recognizes PM2.5's bigger and bulkier cousin PM10 as an invader and prevents it from entering, PM2.5's size makes it stealthy enough to enter the body [19]. One of the ways PM2.5 can enter the body and reach the brain is through the nose [21]. PM2.5 inhalation is unavoidable — these particles are everywhere, suspended in the vast network of air that we breathe. Imagine you are walking down a crowded city street, watching cars slowly creep by, trailing plumes of PM2.5 molecules into the surrounding air. You pass by a café and take a deep breath, relishing in the smell of freshly brewed espresso. As you inhale the heavily polluted city air, PM2.5 molecules, along with gasses like nitrogen and oxygen, rush into your nose. From there, these molecules are able to travel directly to your brain through the olfactory nerve, a communication network that bridges the nose and the brain, allowing us to smell [16]. In the nose, a bundle of tiny nerve fibers extends from smell receptors and enters the brain through small openings in the skull, which PM2.5 can sneak through [17].

Alternatively, PM2.5 molecules may travel through the nose to the lungs, thereby entering the bloodstream and making their way up to the brain. PM2.5 can penetrate the blood-brain barrier (BBB), a tight-knit system of cells that prevents unwanted molecules from passing into and throughout the brain [3]. Prolonged exposure of the brain to high concentrations of PM2.5 can weaken the security system of the BBB by chemically disrupting tight junctions, or proteins that are integral in keeping this tightly-knit structure sealed [3, 18]. PM2.5 is able to breach the BBB by compromising this tight seal, much like widening a gap in a fence. In addition to inhalation, PM2.5 can enter the blood via digestion before it reaches the brain [22].

Neuroinflammation: The Double Agent of the Brain

Regardless of the path it takes through the body, contact with PM2.5 initiates an immune response that can ultimately damage the brain [22, 23]. The brain needs a controlled chemical environment to function properly, which requires specific levels of oxygen and acidity, amongst other conditions [24]. However, the brain’s chemical balance is easily disrupted by invaders like bacteria or foreign molecules [25]. When PM2.5 enters, it is recognized as an invader, resulting in an immune response that fights to maintain the brain’s chemical stability [25]. The PM2.5-provoked immune response and subsequent neuroinflammation is an essential protective mechanism of the brain that can become detrimental if it continues chronically [26, 27]. One mechanism of neuroinflammation is the activation of microglia — cells that function as the ‘immune’ system of the brain — which scan the environment for pathogens and activate in response to potential dangers. While microglia activation can be beneficial in the short-term by protecting the brain from damage, long-term activation of microglia can be harmful [28]. Prolonged neuroinflammation is also correlated with heightened levels of certain immune signaling molecules that can initiate cell death and extend inflammation [27, 29]. In addition, the BBB becomes more penetrable after PM2.5 enters the brain, which allows for greater movement of immune cells into the brain from other parts of the body and subsequent neuron damage and death [30]. Due to these immune responses, individuals continuously exposed to PM2.5 throughout their lifetime may experience chronic neuroinflammation and, consequently, its adverse effects [27]. Communities of color and low-income populations who are pushed into residential areas with greater pollution levels are at higher risk for continuous PM2.5 exposure and the resulting neurological consequences associated with chronic neuroinflammation [6, 7].

Death by a Thousand Particles 

The neuroinflammatory response caused by PM2.5 exposure physiologically alters the brain and is associated with the progressive loss of neurons, a process called neurodegeneration [31]. Upon entering the brain, PM2.5 is recognized as a foreign particle by the brain’s immune cells, which respond by producing proteins that induce neuroinflammation [3, 32, 33]. In this case, neuroinflammation is meant to mitigate damage and get rid of foreign invaders like infectious bacteria [34]. However, the brain's immune system is unable to directly expel foreign molecules like PM2.5. As a result, immune cells release more inflammatory molecules in an attempt to neutralize the threat of PM2.5, which perpetuates a state of chronic inflammation [3, 33]. This PM2.5-mediated neuroinflammatory state may contribute to increased rates of neuron death, cognitive impairments, and abnormal accumulations of a type of protein in the brain called tau [3, 33]. Abnormal tau protein accumulation is associated with neurodegenerative diseases like Alzheimer’s and Parkinson’s; therefore, it is possible that the tau accumulation following PM2.5 exposure could be implicated in these diseases [3, 35]. However, further research is needed to solidify this connection [3]. 

Apart from the neuroinflammatory response, exposure to PM2.5 is also associated with decreased volume in a type of brain tissue called gray matter, which, when deteriorated, is correlated with neurological deficits [36]. Gray matter is primarily composed of cell bodies of neurons, and plays a key role in processes such as the integration of information, memory, emotions, and cognition [37]. A disruption in these vital processes is catastrophic, exacerbating cognitive decline [8, 38]. PM2.5 exposure is associated with decreased gray matter volume in the prefrontal cortex, an area correlated with higher-level cognitive functions such as working memory and long-term memory retrieval [36]. A further decrease in gray matter due to PM2.5 exposure is also observed in the cerebellum, which results in a loss in coordination and balance, and in the basal ganglia, which can cause an interruption of coordination and motor control [8, 38, 39, 40]. Some PM2.5 particles, such as heavy metals from fuel combustion and industrial processes, damage the basal ganglia by degrading the connections between neurons [38, 39]. Although a loss of gray matter is detrimental for all, children are particularly vulnerable to adverse neurological consequences of PM2.5 exposure since their brains are still developing [39]. PM2.5 activates the brain’s primary means of protecting itself, impacting key neurological structures and impairing a broad array of cognitive processes [8, 38, 39]. 

Thinking Beyond the Skull

While the molecular implications of cell death are frightening, their significance is only fully grasped when contextualized by the overlying social risk factors that dictate who is affected by PM2.5 [6]. The risk of high PM2.5 exposure may vary significantly between different communities, demonstrating systemic socioeconomic and racial inequalities [6, 7]. Those of a lower socioeconomic status are more likely to live and work near hazardous sites, such as coal plants, oil refineries, trash incinerators, and natural gas facilities [41]. Additionally, in urban settings, lower-income residents are more likely to live and work farther away from grassy areas, trees, and parks, all of which mitigate PM2.5 pollution through the absorption and decomposition of the particles [42, 43]. Even though people may be aware of the negative health concerns associated with air pollution, many people subject to environmental threats cannot afford to relocate due to financial constraints, among other logistical factors [44]. In the United States, racial minorities are also more likely to be exposed to sites that emit PM2.5, due to gentrification [45]. Black and Hispanic populations in the U.S. are more likely to be pushed into living in industrial areas with less exposure to green spaces [43, 46, 47]. In the United States, on average, Black populations are exposed to 21% more PM2.5 than the overall population [7]. Comparatively, Hispanic populations are exposed to 12% higher PM2.5 concentrations compared to the national average. White populations, on the other hand, face a 7% lower than average exposure to PM2.5, demonstrating clear health inequities [7].

Air pollution is a persistent problem that poses health risks and potential neurological issues, distributed unequally as certain regions of the globe have higher levels of PM2.5 than others [5, 6, 31]. According to the World Health Organization’s guidelines, the annual mean concentration of PM2.5 should not exceed five micrograms in a cubic meter of air [48]. Unfortunately, 95% of countries surpass this threshold [49]. For example, the United States is among the countries with the lowest average PM2.5 concentrations but still has an average of 7.7 micrograms per cubic meter of pollutant [50]. However, PM2.5 exposure varies significantly within the U.S. and is often less concentrated in rural areas [51]. In 2015, China had an average PM2.5 concentration of 50.0 micrograms per cubic meter of pollutant, and in 2019, India had an average PM2.5 concentration of 91.7 micrograms per cubic meter of pollutant [52, 53]. Notably, higher-income countries, including the United States, tend to have lower levels of PM2.5 exposure [41]. This trend is in part because many lower-income countries rely on industries that burn a lot of fossil fuels to increase economic development [54]. PM2.5 pollution is a potent global threat; therefore, lowering its emission rates is imperative to improving public health, especially for vulnerable populations. Emerging research on PM2.5 demonstrates profound negative neurological consequences resulting from exposure [36, 39]. Given the uncertainty surrounding the long term effects of air pollution on cognitive function, it is crucial to continue reducing PM2.5 in the atmosphere and studying its broad effects to support human and ecological health. 

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