Abstract
Air pollution, a pervasive environmental issue, has been increasingly linked to adverse mental health outcomes. This review examines the impact of air pollution on mental health, focusing on epidemiological evidence, biological mechanisms, and public health implications. Epidemiological studies demonstrate strong associations between exposure to pollutants like PM2.5 and NO2 and heightened risks of depression, anxiety and neurodevelopmental disorders. Key findings include increased rates of depression and anxiety linked to high pollution levels in urban areas. Biological mechanisms underlying these associations involve systemic inflammation, oxidative stress, neurotransmitter imbalance, and epigenetic changes, all contributing to neuroinflammation and neuronal damage – all plausible explanations for the observed mental health effects of air pollution. Public health implications underscore the necessity for stringent air quality regulations and effective policies to mitigate emissions from transportation, industry, and residential sources. Community and individual interventions, including education and protective measures, are crucial in minimising exposure and its mental health impacts. Continuous research is essential to deepen our understanding of the causal pathways and to inform policy decisions. This review highlights the urgent need for integrated efforts to address air pollution and protect mental health, emphasising the critical role of environmental factors in the broader context of public health.
Introduction
Air pollution refers to the presence of harmful substances in the air we breathe, which can pose serious risks to human health. The World Health Organization estimates that air pollution is responsible for around 800,000 premature deaths annually (Anderson et al., 2012). The most common air pollutants include particulate matter (PM), carbon monoxide (CO), ozone (O₃), nitrogen dioxide (NO₂), sulphur dioxide (SO₂), and volatile organic compounds (VOCs). PM is mostly generated from combustion processes, construction activities, and natural sources like wildfires (Pope et al., 2006). NO₂ and SO₂ primarily come from the burning of fossil fuels in vehicles, power plants, and industrial facilities (Galloway et al., 2008). CO is mainly produced by incomplete combustion in vehicles and residential heating (Raub et al., 2000). VOCs originate from vehicle emissions, industrial processes, and natural vegetation (Atkinson et al., 2000), while ozone forms from chemical reactions between NO₂ and VOCs in sunlight (Monks et al., 2015). Air pollution concentrations vary according to several factors and are highly dependent on geography. For example, NO₂ and PM2.5 tend to be found at higher concentrations in populations with higher socioeconomic status, such as in China, whereas the opposite tends to be true for the US (Wang et al., 2022).
Air pollution is strongly linked to poor health, including respiratory, cardiovascular, and mental health issues. A study in Istanbul, Turkey, found a strong association between respiratory issues and exposure to PM10, PM2.5, and NO₂ (Çapraz, Ö. et al., 2017). Various trials have consistently shown an association between air pollution exposure and cardiovascular health. Populations exposed to higher levels of air pollution have a notably higher number of cardiovascular incidents and a higher mortality rate (Pope et al., 2004). Areas that experience short-term heavy exposure to PM also see increased heart incidents, usually a few days after the pollution spike (Anderson et al., 2012). Recent research has focused on the link between air pollution and mental health, finding that PM2.5 exposure is associated with higher levels of depression, while higher NO₂ exposure is linked to worsening depressive disorders (Buoli, M. et al., 2018). However, the potential impact of air pollution on anxiety is less understood.
Ill mental health can broadly be defined as disturbances in cognition, behaviour, or emotional regulation (WHO, 2022). There are more than 200 diagnosable mental health disorders, all of which exhibit a heterogeneous collection of symptoms. Depression is characterised by persistent sadness, lack of interest or pleasure in previously enjoyable activities, and symptoms such as disturbed sleep, feelings of guilt, or low self-worth (American Psychiatric Association 2013). Depression affected roughly 350 million people globally in 2020 (Santomauro et al., 2021). Anxiety is another common mental health disorder, characterised by feelings of tension, worried thoughts, and physical changes like increased blood pressure (American Psychiatric Association, 2013). An estimated 300 million people globally suffer from anxiety (WHO, 2019).
Despite their differing symptoms, depression and anxiety are highly comorbid, with research suggesting that 50-60% of people with depression will also experience anxiety symptoms and vice versa (Kessler et al., 2003). Depression and anxiety are commonly treated with pharmacotherapy, talking therapies, or both (Cuijpers et al., 2020). Despite growing awareness and acceptance, barriers to treatment persist, including not only social stigma but long wait times, poor availability, lack of self-reporting, poor medication adherence, lack of treatment efficacy, and failure to adhere to long-term treatment (Clement et al., 2015; Olfson et al., 2006; Rush et al., 2006; Wang et al., 2007). Furthermore, rates of depression and anxiety are predicted to increase by 30% by 2030 (Charlson et al., 2016), highlighting the urgent need for public health interventions.
Epidemiological research has increasingly found a significant link between air pollution and mental health issues, particularly depression and anxiety. Both longitudinal and cross-sectional studies have found that exposure to air pollutants, especially PM2.5, can increase the risk of these conditions (Power et al., 2015). Traffic-related air pollution is prevalent in modern societies, making it a major public health concern. Despite abundant cross-sectional data, there is a lack of both longitudinal epidemiological data and randomised controlled trials that explore causal mechanisms (Braithwaite et al., 2019).
Preliminary research has identified several potential pathways through which air pollutants may impact mental health. One key mechanism involves inflammation and oxidative stress (Lodovici and Bigagli, 2011). Air pollutants can induce systemic inflammation and oxidative stress, leading to the release of inflammatory cytokines and oxidative molecules that can cross the blood-brain barrier (Buoli et al., 2018). Once in the brain, these molecules can trigger neuroinflammation and neuronal damage, contributing to mental health disorders (Buoli et al., 2018).
Other potential mechanisms involve alterations in neurotransmitter systems (Cory-Slechta et al., 2024). Air pollution has been linked to disruptions in neurotransmitter systems, including dopamine and serotonin, which play crucial roles in mood regulation and cognitive function (Baixauli, 2017). Epigenetic changes are another potential mechanism through which air pollution may impact mental health (Shukla et al., 2019). Epigenetics involve modifications to gene expression that do not alter the DNA sequence but can have lasting effects on cellular function and development (Portela and Esteller, 2010). Air pollution may cause epigenetic modifications, such as DNA methylation and histone modifications, that alter the expression of genes involved in neurodevelopment and stress responses.
The link between air pollution and mental health is profoundly impacting public health. Effective policy and regulation are essential to mitigate the mental health burden associated with air pollution. Governments should implement stricter air quality standards based on the latest scientific evidence to protect public health. Reducing allowable levels of PM2.5, NO₂, and other pollutants may help decrease the prevalence of mental health disorders. Policies promoting reduced emissions from transportation, industrial sources, and residential heating can significantly improve air quality.
Incentivising the adoption of cleaner technologies and renewable energy sources can also lower pollution levels. Successful examples include the introduction of various clean air zones, such as London’s Ultra Low Emission Zone (ULEZ), which resulted in a 46% reduction in traffic-related NO₂ (Greater London Authority, 2021). Community and individual interventions are equally important. Public health initiatives should focus on raising awareness about the mental health risks of air pollution and promoting protective measures, such as air purifiers, and reducing outdoor activities during high pollution periods.
Continued research is crucial to further elucidate the relationship between air pollution and mental health. Longitudinal studies and advanced analytical methods can provide more robust evidence, guiding public health interventions and policy decisions. Research priorities should include longitudinal cohort studies to establish causal relationships between air pollution exposure and mental health outcomes. These studies should include diverse populations to assess the differential impacts of pollution on various demographic groups. Mechanistic studies exploring the biological pathways linking air pollution to mental health are essential for developing targeted interventions.
The Association Between Air Pollution and Mental Health
Many studies have identified a strong association between air pollution and its effects on mental health, specifically depression and anxiety. Animal research has provided significant insights into how air pollution affects anxiety and depression-like symptoms. An experimental study involving the chronic exposure of mice to PM2.5, simulating real-world conditions in a coal-combustion area, found that prolonged exposure to PM2.5 significantly increased behaviours typical of anxiety, such as reduced exploration in mazes, and induced depression-like behaviours, such as decreased swimming ability in swim tests (Mokoena et al., 2022). Additional animal studies have shown that mice exposed to concentrated ambient particles (CAPs) exhibit similar anxiety and depression-like behaviours and show signs of neuroinflammation, specifically in the hippocampus, a region involved in emotional regulation (Yuan et al., 2018). This body of evidence from animal research clearly associates increased air pollution with heightened anxiety and depression-like behaviours. However, while these findings provide an important foundation for understanding the potential link in humans, it is crucial to consider that such controlled research has yet to be replicated in human studies and therefore lacks generalisability.
Although limited, human research has shown strong associations between air pollution and increased mental health issues. A longitudinal study surveying over 1.7 million people in Rome, Italy, indicated a strong statistical trend between increased air pollution and a heightened risk of developing significant mental health disorders. The study revealed that for every 1.13 µg/m3 increase in PM2.5, the risk of developing schizophrenia, depression, or anxiety disorders increased by approximately 7%, 14%, and 10%, respectively. The data also showed similar trends for other pollutants, but no significant link was found for bipolar disorder, personality disorders, or substance use disorder (Nobile et al., 2023). The growth of this body of data confirms that exposure to these harmful pollutants may have detrimental effects, particularly as new and different pollutants emerge. The study spanned from 2011 to 2019, providing an eight-year period to observe trends over time. Despite this study providing significant information about the adverse effects of air pollution on mental health conditions, there are notable limitations that prevent the results from fully contributing to the broader understanding. Firstly, there is an absence of biological mechanistic research, and the reliance solely on longitudinal data limits any causal inference. In the future, randomised controlled trials are needed to provide causal links. Although the survey was conducted only in Rome, its results are not necessarily limited; however, factors such as the specific types of air pollutants in Rome, including traffic-related pollutants and chemical waste, may have affected the results. To account for these various sources of air pollution, it is suggested that a broader sampling be conducted. Overall, the study found significant evidence that increased exposure to a variety of air pollutants can escalate the risk of developing schizophrenia, anxiety, and depression.
Anxiety is another prevalent disorder associated with exposure to air pollution, yet it has received less research attention. Anxiety is characterised by excessive worry, fear, and heightened physiological responses, such as increased heart rate and muscle tension (American Psychiatric Association et al., 2013). A cross-sectional study conducted in South London investigated the association between air pollution and mental health outcomes (Newbury et al., 2021). After studying individuals living in areas with high levels of air pollutants for one year, 23% of participants were found to have a primary psychotic disorder diagnosis, and 77% were diagnosed with a primary mood disorder. This highlights how air pollution increases the likelihood of being diagnosed with a significant mental health disorder (Newbury et al., 2021). There was strong evidence suggesting that air pollutants can affect the brain directly through the blood-brain barrier, causing neuroinflammation and oxidative stress, which could plausibly lead to the development of mental health disorders (Newbury et al., 2021). Furthermore, the study’s focus on major pollutants such as particulate matter (PM2.5 and PM10) and nitrogen dioxide (NO2) is particularly relevant, as these pollutants are commonly associated with adverse health effects and are prevalent in urban areas with high levels of air pollution. The study’s examination of the development of mood and psychotic disorders with prolonged exposure to air pollutants provides a nuanced analysis of how air pollution may differentially impact various aspects of mental health, which is crucial for developing targeted public health interventions and encouraging low-emission zones in urban areas (Newbury et al., 2021).
The cross-sectional nature of the research presents a significant limitation, as it only captures a snapshot in time, making it difficult to draw causal inferences. It remains unclear whether pollution exposure directly causes the observed mental health issues or if other factors are contributing to these outcomes. Longitudinal studies would be more effective in establishing causality, and randomised controlled trials could additionally be used to establish causal factors and investigate potential biological mechanisms of action (Levin, 2006). Several confounders may have influenced the current study. Although the study controls for some factors, such as socioeconomic status and pre-existing health conditions, there may be other unmeasured variables influencing the results. For instance, lifestyle factors like diet, exercise, and social support, which are also linked to mental health, might not be fully accounted for (Szklo & Nieto, 2014).
Additionally, this study may not effectively capture micro-level variations in pollution exposure within a city, such as differences in proximity to traffic, green spaces, or industrial areas, potentially leading to exposure misclassification (Jerrett et al., 2005). If the study relies on self-reported measures of depression and anxiety, there is also a risk of reporting bias, where participants may underreport or overreport symptoms based on personal perceptions, leading to inaccurate associations (Schwarz, 1999). Additionally, the study does not account for long-term or cumulative effects of pollution on mental health, a crucial factor given that issues like depression and anxiety often develop over extended periods (Pearlin et al., 2005). Finally, cultural and social differences between the cities included in the study, such as mental health stigmas, healthcare accessibility, and local environmental policies, may affect the generalisability of the findings (WHO, 2013).
This study highlights a link between urban air pollution and mental health in urban areas; however, the findings of this study should be interpreted with caution due to the limitations of cross-sectional research. Future studies should use a longitudinal approach, allowing for more definitive conclusions regarding the causal relationship between pollution and mental health outcomes. Additionally, a deeper exploration of potential confounding factors and more precise exposure assessments would strengthen the validity of the research. Despite these limitations, the study underscores the importance of addressing air pollution as a significant public health issue, with implications not only for physical but also for mental well-being.
In summary, this research consistently shows the correlation between air pollution and the worsening of mental health disorders, especially anxiety and depression. Both animal studies and longitudinal research in human populations support the hypothesis that prolonged exposure to harmful air pollutants can lead to neuroinflammation and disrupt emotional balance, ultimately contributing to the worsening of these mental health conditions. However, there are still some major limitations, including the difficulty of applying animal research to humans, controlling confounding factors in human studies like income and lifestyle, differences between locations and cultures, and the focus on short-term exposure rather than long-term effects.
Inflammation, Oxidative Stress and the Blood-Brain Barrier
Research has increasingly identified the blood-brain barrier as a key biological mediator of the effects of air pollution on depression and anxiety. The blood-brain barrier (BBB) is a membrane composed of endothelial cells and pericytes. Its primary role is to filter out toxins and harmful particles, preventing them from entering the brain, while also transporting essential nutrients to brain tissue.
Particulate matter smaller than 2.5μm (PM2.5) is of particular concern because it can bypass the blood-brain barrier by entering through the nasal pathway and crossing the alveolar-capillary barrier. Once in the circulatory system, PM2.5 gains direct access to the BBB. This exposure causes oxidative stress and proinflammatory effects, leading to an increased production of proinflammatory cytokines, including tumour necrosis factor-alpha (TNFα), interleukin-6 (IL-6), and interleukin-1beta (IL-1β) (Sierra-Margas et al., 2023). These cytokines, along with other defensive proteins from the immune system, can overwhelm and disrupt the BBB, leading to a loss of BBB integrity and the development of brain lesions, particularly in the prefrontal lobe. Researchers have hypothesised that this disruption may contribute to mental disorders, including depression, anxiety, and schizophrenia.
A study by Suwannasual et al. (2019) showed that mice exposed to motor vehicle exhaust (MVE: 200 PM μg/m^3, 50 PM μg/m^3 from gasoline engines) and diesel engine emissions (DEE: 150 PM μg/m^3) exhibited a significant increase in inflammatory cytokines and damage to tight junction proteins compared to a control group exposed to filtered air. There is however a lack of evidence in human samples leading to a lack of actionable evidence.
Neurotransmitter Imbalances and the HPA Axis
Recently, researchers have been examining the connection between air pollution and the nervous system, most notably the hypothalamic-pituitary-adrenal (HPA) axis, which consists of the hypothalamus, pituitary gland, and adrenal glands. These three organs influence stress by regulating cortisol levels (Cleveland Clinic, 2024). Animal studies support the idea that there is a correlation between inhaled pollutants and neurological disorders; however, it is unclear which fundamental biological structures are responsible for these effects (Block et al., 2012). Exposure to fine particulate matter (PM2.5) with an aerodynamic diameter of less than 2.5 µm in four-week-old male mice increased the incidence of depressive characteristics and impairments in learning and memory (Fonken et al., 2011). PM2.5 can be inhaled into the lungs and absorbed into the bloodstream, bypassing the blood-brain barrier, which then leads to inflammation in certain parts of the body, including the release of pro-inflammatory cytokines in the hippocampus (Miller et al., 2020). A study conducted with rats showed that by performing adrenalectomy (surgery to remove the adrenal glands), the pulmonary and systemic effects caused by ozone exposure decreased (Snow et al., 2018). The effects of ozone on the test rats showed hippocampal neurodegeneration and reduced repair. The role of the adrenal glands in this study highlights the connection between the neuroendocrine system and behaviour.
Human research in this field is limited due to ethical concerns; however, a recent study measured salivary cortisol levels in teenage girls exposed to fine air pollution. The results demonstrated that exposure to PM2.5 caused heightened HPA axis activation in adolescent girls when faced with socially stress-inducing tasks (Miller et al., 2020). The salivary cortisol levels of these girls were measured in response to a socially stressful situation, and it was evident that participants from areas with higher exposure to PM2.5 experienced heightened HPA-axis responsiveness to stress (Miller et al., 2020). Another study found that exposure to PM2.5 in pregnant women intensified symptoms of prenatal depression in the third trimester, suggesting that not only is there a correlation between exposure to fine particulate matter and worsening depression, but that pregnant women are particularly vulnerable (Ahlers and Weiss, 2021). No studies have been conducted on newborns who experienced extreme exposure to PM2.5; therefore, potential prenatal effects remain unknown. In infant primates, exposure to ozone causes neuroplasticity in the nucleus tractus solitarius (NTS) neurons, and it can be hypothesised that PM2.5 would have a similar effect on human infants (Chen et al., 2003).
Researchers hypothesise that air pollutants may exacerbate mental health symptoms due to their ability to disrupt neurotransmitter systems (Tran & Miyake, 2017). Pollutants can interfere with neurotransmitters, causing an imbalance that influences serotonin and dopamine levels (Tran & Miyake, 2017). Serotonin and dopamine are crucial chemicals in the regulation of mood and behaviour (Lahoti, 2023). A deficiency of these signals, particularly serotonin, in the brain can lead to increased symptoms and feelings of depression and anxiety (Eison, 1990). A recent study showed a positive correlation between monthly averages of NO2 in specific areas and incidents of antisocial behaviour (Tomoaki et al., 2024). As air pollution concentration increased in Greece and the Netherlands, so did incidents of murder, terrorism, and suicide (Tomoaki et al., 2024): studies have shown a correlation between depleted serotonin levels and increased aggression (Krakowski, 2003; Duke et al., 2013; Cunha-Bang and Knudsen, 2021). There is additionally a lack of studies researching the connection between serotonin, other neurotransmitters, and air pollution, so more research on this particular matter is needed, despite existing challenges in accurately measuring aggression and serotonin levels.
Epigenetic Changes
Although the genome is relatively stable throughout life, gene expression is significantly variable (Smeeth et al., 2021). This variability is regulated by epigenetic mechanisms, a group of mitotically heritable but reversible molecular changes (Allis and Jenuwein, 2016). Epigenetic changes are increasingly acknowledged as key factors in the aetiology and pathophysiology of mental health disorders (Park et al., 2019) and may result from environmental insults, leaving molecular “scars” (Bai et al., 2024). Animal studies have provided evidence that air pollution is associated with epigenetic changes, including alterations in DNA methylation (DNAm), histone modification, and non-coding RNA (Alfano et al., 2018).
Recent animal studies have highlighted that exposure to air pollution causes abnormalities in the methylation of specific genes, which may contribute to the aetiology of various mental disorders (Bai et al., 2024). A study analysing the effects of air pollution on the DNAm of rats found that exposure to air pollution was associated with changes in methylation, resulting in increased symptoms of depression (Ding et al., 2016). Altering the conformation of chromatin – a substance composed of DNA and histone proteins – within a cell’s nucleus influences gene expression (Deussing and Jakovcevski, 2017; Luger et al., 2012). Studies have shown that gene expression can be positively or negatively regulated by histones, as modifications to the histone landscape can alter chromatin conformation. One chemical modification that affects the structure of histone proteins is acetylation (Peterson and Laniel, 2004). Histone deacetylation, which removes acetyl groups from lysine residues (products of histone acetylation at lysine residues), has been associated with mental disorders such as depression (Park et al., 2021), anxiety (Montagud-Romero et al., 2019), schizophrenia (Hasan et al., 2013), and bipolar disorder (Tseng et al., 2020).
Recent studies have clarified that non-coding RNA plays an important role in the pathogenesis of mental disorders (Liu et al., 2020). Non-coding RNA is involved in neurogenesis, synaptic plasticity, brain-derived neurotrophic factor expression, HPA axis regulation, neurotransmission, neuropeptide expression, neuro-inflammation, and polyamine synthesis, all of which are processes implicated in mental disorders such as depression (Liu et al., 2020). A study analysing the effect of air pollution on long non-coding RNA in rat embryos showed that air pollution significantly affected non-coding RNA, with 554 long non-coding RNAs (216 up-regulated and 338 down-regulated) differentially expressed in air pollution-exposed embryos (Li et al., 2019).
Despite the increasingly promising results from animal trials, there remains a lack of generalisability to humans due to limited epigenetic research associating air pollution with mental health in human studies.
Microbiome Gut-Brain Axis
Recent research suggests that the microbiome gut-brain axis (mGBA) may offer a potential mechanistic route through which air pollution impacts mental health. Composed of trillions of microorganisms residing in the gastrointestinal tract, the mGBA connects peripheral intestinal functions with the central nervous system. This communication occurs through several interconnected pathways, including the vagus nerve, which serves as a direct link, the immune system, which involves cytokine signalling, and the production of neurotransmitters like serotonin, gamma-aminobutyric acid (GABA), and dopamine. These pathways enable the gut and brain to influence each other’s functions, ultimately potentially impacting mood, behaviour, and mental health (Kraimi et al., 2019).
Animal studies have shown that germ-free animals, which lack a microbiome, exhibit altered stress responses and anxiety-like behaviours, suggesting a role for gut microbiota in regulating brain function and behaviour (Cryan et al., 2012). Research has proposed that exposure to air pollution may lead to changes in the gut microbiome, which could send signals via the gut-brain axis, thus impacting mental health. Pollutants such as PM2.5 can disrupt the gut microbiome, leading to neurodegeneration and neuroinflammation through the gut-brain axis (Panda et al., 2023). A study on mice exposed to concentrated ambient particles via inhalation demonstrated modest changes in gut microbiota, with noticeable alterations in microbiota diversity throughout the gastrointestinal tract (Mutlu et al., 2018). Additionally, following a study on Alzheimer’s disease (AD), mice exposed to PM2.5 for eight weeks demonstrated significantly aggravated intestines and brain with elevated proinflammatory cytokine levels (Fu et al., 2020).
These studies collectively suggest that higher PM2.5 concentrations may reduce bacterial richness and diversity in animals, which could have implications for brain health. However, translating these findings to humans remains challenging due to differences in biology and limitations of animal models. The primary limitations of animal research include the potential lack of direct applicability to human physiology and variability in responses between species. While animal studies offer valuable insights, they often face issues of validity and reliability when applied to human contexts. For instance, the dose and type of air pollution exposure in animal models may not perfectly mirror human environmental conditions. Furthermore, methodological differences, such as variations in exposure duration and concentrations, can impact the outcomes and their relevance to human health.
Future research should focus on bridging these gaps by conducting more human studies that integrate biological data with environmental exposures. Randomised controlled trials and longitudinal studies in diverse populations can validate the findings from animal models and help us better understand the microbiome gut-brain axis’s role in the impact of air pollution on mental health. If future research confirms that the gut microbiome plays a significant role in the effects of air pollution on mental health through the gut-brain axis, intervention strategies could be explored. Dietary modifications could potentially be one of the most accessible and impactful approaches. By enriching the diet with prebiotics, probiotics, and specific nutrients that support a healthy gut microbiome, it may be possible to enhance resilience against the negative effects of air pollution. Foods rich in fibre, polyphenols, and omega-3 fatty acids could promote the growth of beneficial gut bacteria, thereby supporting the gut-brain axis (Berding et al., 2021).
Public Health Implications
The negative impacts of air pollution on mental health have become increasingly apparent (Kim et al., 2020). Children are particularly vulnerable to these effects as their brains are undergoing crucial stages of development, and evidence has shown that air pollution can cause structural and functional changes in the brain. Research indicates that an additional standard deviation in the pollution index raises the probability of clinical depression measured ten years after exposure by nearly 1% (Kim et al., 2020). Given the harmful effects and widespread prevalence of air pollution, public health interventions are necessary to mitigate air pollution levels and protect mental health. Specifically, interventions targeting traffic-related air pollution are crucial, as vehicular transport is a significant cause of environmental pollution, accounting for approximately 70% of emissions (Sofia et al., 2020). By reducing vehicular emissions, especially from cars, we can significantly lower pollution levels.
Existing policies like clean air zones have proven effective, particularly in congested urban areas. For example, London’s Ultra-Low Emission Zone (ULEZ) achieved a reduction in NO2 and NOx levels by 19% and 20%, respectively (Decker et al., 2022), while Paris’s Low Emission Zone (LEZ) reduced PM10 levels by 22-44% over five years since its implementation in 2015 (Heydecker et al., 2022). These policies have also led to health benefits, such as a 22.5% reduction in certain health conditions, a 6.5% decrease in anxiety, and an 18% reduction in sick leave (Beshir et al., 2022). Despite some criticism that these policies may inconvenience urban residents by restricting car use, the public health benefits are substantial. Therefore, expanding such policies to all urban cities could reduce pollution levels and, consequently, the incidence of mental and physical health problems caused by pollution.
Researchers are yet to fully understand the impact of air pollution on mental health, emphasising the need for urgent research to explore its effects on depression and anxiety. Future research should focus on several key areas. Longitudinal studies are necessary to monitor the long-term effects of air pollution on mental health, uncover causal relationships, and identify exposure windows (Liu et al., 2021). To gain a comprehensive understanding, studies should include diverse populations across various geographic locations, helping to identify how external environmental factors like pre-existing medical conditions and different pollution levels affect the relationship between air pollution and mental health. Randomised controlled trials (RCTs), which are currently lacking in the literature, could provide more robust evidence by controlling for confounding variables and minimising bias, leading to stronger conclusions about the effects of air pollution on mental health (Gómez et al., 2023).
Community interventions also offer potential strategies for mitigating air pollution exposure. Studies show that raising awareness about the impact of air pollution can encourage positive behaviour change. For instance, a study by Wang and colleagues in 2021 used a network-based training application to educate people on how air pollutants affect mental health and encouraged actions to reduce exposure, such as staying indoors during high pollution periods. This approach successfully reduced symptoms of anxiety and depression among those with major symptoms (Wang, Liu & Zhang, 2021).
Urban planning initiatives, such as adding more green spaces, have also been shown to reduce stress and improve mental health (Gascon et al., 2017). However, these interventions face economic challenges as they often require substantial financial investment. Although green space programmes can generate income through charges or community events, their economic sustainability varies (Barton & Grant, 2006). Consequently, the mental health benefits associated with green spaces are often unequal: such spaces are more prevalent in wealthier communities, increasing health inequalities (Rigolon, 2016). In general, while these interventions have significantly improved pollution-related mental health issues, their broader implementation must consider local circumstances and address underlying equity issues.
Conclusion
Based on the evidence, it is clear that air pollution significantly impacts mental health, particularly by increasing symptoms of anxiety and depression. Both animal studies and longitudinal research on the long-term effects of air pollutants highlight that prolonged exposure to harmful air pollutants increases the vulnerability to serious mental health conditions. Although there are limitations to the current research – including the gap between animal and human research, the difficulty of controlling confounding factors in human studies, and a focus on short-term rather than long-term exposure – the consistent trends across studies support the hypothesis that increased exposure to air pollutants is associated with a higher risk of mental health disturbances.
Several mechanistic pathways have been suggested. Evidence regarding the blood-brain barrier (BBB) remains inconclusive. While direct evidence of PM2.5’s impact on the human BBB is lacking, animal studies indicate that inhalation of motor vehicle exhaust (MVE) can damage the BBB and impair cognition in rodents. The small size of these particles allows them to bypass various protective systems and enter the brain through the bloodstream. Despite extensive animal research, there is a need for more translation to human studies, and the specific mechanisms remain largely unexplored in randomised controlled trials.
There are reports linking air pollution’s effects on mental health to the central nervous system, primarily relying on rodent models. Fine particulate matter (PM2.5, PM10, NOx) can be inhaled into the lungs, absorbed into the bloodstream, and cause inflammation in the hypothalamic-pituitary-adrenal (HPA) axis. These pollutants may also interfere with neurotransmitter balance, leading to imbalances in dopamine and serotonin and worsening symptoms of anxiety and depression. Future research should continue to explore these connections in humans and investigate other biological mechanisms, such as the neuroendocrine system, that may link air pollution to mental health.
Recent studies have also associated air pollution with various epigenetic changes. Animal trials have shown that exposure to air pollution can cause abnormalities in gene methylation, histone modifications, and changes in the expression of non-coding RNA. These epigenetic alterations are critical in the aetiology and pathophysiology of mental health disorders. However, due to a limitation in human studies, the associations between air pollution and other potential biomarkers remain to be fully understood. New approaches, such as evaluating different extracellular vesicle (EV)-carried non-coding RNA signatures and advancing translational research, could offer promising opportunities to identify new biomarkers.
Moreover, recent studies suggest that air pollution may impact mental health through changes in the gut microbiome. Animal research indicates that pollutants like PM2.5 can disrupt the gut microbiota, leading to neuroinflammation, neurodegeneration, and increased pro-inflammatory cytokine levels, potentially affecting brain function and behaviour. However, the relevance of these findings to humans is uncertain, given the physiological differences between animals and humans. Further research involving human participants is necessary to validate these associations and explore potential interventions to mitigate the negative effects of air pollution on the gut-brain axis.
In conclusion, while the physical health impacts of air pollution – such as increased respiratory issues and lung cancer cases – are well-documented, its effects on mental health, though not yet fully proven, are becoming increasingly evident. To address this, it is crucial to implement and expand effective interventions to reduce pollution levels worldwide. One successful strategy has been the establishment of clean air zones in cities like London and Paris, which have demonstrated significant reductions in pollution levels. Expanding such initiatives globally could further decrease pollution levels. Although these measures may not be universally popular due to their impact on daily life, they are necessary for long-term public health benefits, including reducing hospital admissions. Additionally, raising awareness and educating citizens globally can empower individuals to take proactive steps to reduce pollution. However, these efforts must be complemented by robust government legislation and policy action to achieve meaningful and lasting improvements in air quality and public health.
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