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Mercury is a highly toxic metal widely used in human activities worldwide, therefore considered a global public health problem. Many cases of mercury intoxication have occurred in history and represent a huge challenge nowadays. Of particular importance is its methylated form, methylmercury (MeHg). This mercurial species induces damage to several organs in the human body, especially to the central nervous system. Neurological impairments such as executive, memory, motor and visual deficits are associated with MeHg neurotoxicity. Molecular mechanisms involved in MeHg-induced neurotoxicity include excitotoxicity due to glutamatergic imbalance, disturbance in calcium homeostasis and oxidative balance, failure in synaptic support, and inflammatory response. Although neurons are largely affected by MeHg intoxication, they only represent half of the brain cells. Glial cells represent roughly 50 % of the brain cells and are key elements in the functioning of the central nervous system. Particularly, astrocytes and microglia are deeply involved in MeHg-induced neurotoxicity, resulting in distinct neurological outcomes depending on the context. In this review, we discuss the main findings on astroglial and microglial involvement as mediators of neuroprotective and neurotoxic responses to MeHg intoxication. The literature shows that these responses depend on chemical and morphophysiological features, thus, we present some insights for future investigations, considering the particularities of the context, including time and dose of exposure, brain region, and species of study.
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Mercurio , Compuestos de Metilmercurio , Humanos , Compuestos de Metilmercurio/toxicidad , Encéfalo , Oxidación-Reducción , Neuronas , Estrés OxidativoRESUMEN
Human intoxication to mercury is a worldwide health problem. In addition to the type and length of exposure, the genetic background plays an important role in mercury poisoning. However, reviews on the genetic influence in mercury toxicity are scarce and not systematic. Therefore, this review aimed to systematically overview the most recent evidence on the genetic influence (using single nucleotide polymorphisms, SNPs) on human mercury poisoning. Three different databases (PubMed/Medline, Web of Science and Scopus) were searched, and 380 studies were found that were published from 2015 to 2022. After applying inclusion/exclusion criteria, 29 studies were selected and data on characteristics (year, country, profile of participants) and results (mercury biomarkers and quantitation, SNPs, main findings) were extracted and analyzed. The largest number of studies was performed in Brazil, mainly involving traditional populations of the Tapajós River basin. Most studies evaluated the influence of the SNPs related to genes of the glutathione system (GST, GPx, etc.), the ATP-binding cassette transporters and the metallothionein proteins. The recent findings regarding other SNPs, such as those of apolipoprotein E and brain-derived neurotrophic factor genes, are also highlighted. The importance of the exposure level is discussed considering the possible biphasic behavior of the genetic modulation phenomena that could explain some SNP associations. Overall, recommendations are provided for future studies based on the analysis obtained in this scoping review.
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Physical exercise is well known as a non-pharmacological and holistic therapy believed to prevent and mitigate numerous neurological conditions and alleviate ageing-related cognitive decline. To do so, exercise affects the central nervous system (CNS) at different levels. It changes brain physiology and structure, promoting cognitive improvements, which ultimately improves quality of life. Most of these effects are mediated by neurotrophins release, enhanced adult hippocampal neurogenesis, attenuation of neuroinflammation, modulation of cerebral blood flow, and structural reorganisation, besides to promote social interaction with beneficial cognitive outcomes. In this review, we discuss, based on experimental and human research, how exercise impacts the brain structure and function and how these changes contribute to cognitive improvements. Understanding the mechanisms by which exercise affects the brain is essential to understand the brain plasticity following exercise, guiding therapeutic approaches to improve the quality of life, especially in obesity, ageing, neurodegenerative disorders, and following traumatic brain injury.
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Encéfalo , Calidad de Vida , Adulto , Humanos , Sistema Nervioso Central , Ejercicio Físico , CogniciónRESUMEN
The Euterpe genus (mainly Euterpe oleracea Martius, Euterpe precatoria Martius, and Euterpe edulis Martius) has recently gained commercial and scientific notoriety due to the high nutritional value of its fruits, which are rich in polyphenols (phenolic acids and anthocyanins) and have potent antioxidant activity. These characteristics have contributed to the increased number of neuropharmacological evaluations of the three species over the last 10 years, especially açaí of the species Euterpe oleracea Martius. The fruits of the three species exert neuroprotective effects through the modulation of inflammatory and oxidative pathways and other mechanisms, including the inhibition of the mTOR pathway and protection of the blood-brain barrier, all of them intimately involved in several neuropathologies. Thus, a better understanding of the neuropharmacological properties of these three species may open new paths for the development of therapeutic tools aimed at preventing and treating a variety of neurological conditions.
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Euterpe , Antocianinas , Neuroprotección , Antioxidantes/farmacología , Antioxidantes/uso terapéutico , Frutas , Extractos Vegetales/farmacología , Extractos Vegetales/uso terapéuticoRESUMEN
Amazon conservation is essential for the global future. Mercury is currently among the worst global pollutants and most (78.5%) of the South-American emissions are from the Amazon. Current Brazilian legislation on mining activities and trade of gold, and economic interests in soy, beef and large-scale projects such as dams, are key influences in mercury mobilization and emissions in the Amazon with the potential to affect the global environment. However, banning mercury in mining, while desirable, is not an efficient strategy if no other action is taken. The interconnected issues, such as exports (soy, beef and gold) and energy generation, must be addressed together to provide effective protection for human health and the environment. Realistically, to improve mercury emissions in the Amazon, we must stop looking solely at "the single story" (a limited view of reality) of supposedly "artisanal and small-scale gold mining" in the region and understand the complex economic, social, political, and international aspects of this problem. We propose some recommendations for international agencies, governments, communities and the private sector.
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Contaminantes Ambientales , Mercurio , Animales , Bovinos , Humanos , Mercurio/análisis , Contaminantes Ambientales/análisis , Brasil , Minería , OroRESUMEN
This cross-sectional study evaluated the association between human exposure to mercury and cardiovascular risk using lipid profile (including apolipoproteins) and genetic analysis of Amazonian riverine population. Anthropometric data (gender, age, height, weight, blood pressure, and neck and waist circumferences) of the participants were recorded. Total mercury and methylmercury (MeHg) content were quantified in hair by ICP-MS and GC-pyro-AFS system. Polymorphisms rs662799, rs693, rs429358 and rs7412 (of genes of apolipoproteins A-V, B, and E at positions 112 and 158, respectively) were genotyped by real-time PCR. The population presented a dyslipidemia profile significantly correlated with high mercury levels. The apolipoprotein B/apolipoprotein A-I (ApoB/ApoA-I) index was also positively correlated with mercury, supporting a possible causal relationship. Allelic distributions were similar to those described in other populations, suggesting that genetic susceptibility may not have a significant role in the lipid alterations found in this work. This study demonstrated for the first time: i) the relationship between mercury exposure and cardiovascular risk-related apolipoproteins in humans, ii) the ApoB levels and the ApoB/ApoA-I index as the risk factors more strongly associated to the mercury-related dyslipidemia in humans, and iii) the prevalence of high/moderate risk of acute myocardial infarction in the vulnerable and chronically exposed-populations of the Amazon, in addition to the genotypic profile of the three most frequent polymorphisms in apolipoproteins of relevance for cardiovascular risk. This early detection of lipid alterations is essential to prevent the development of cardiovascular diseases (CVD), especially in chronically exposed populations such as those found in the Amazon. Therefore, in addition to provide data for the Minamata Convention implementation, our work is in line with the efforts joined by all members of the World Health Organization committed to reducing premature deaths originating from non-communicable diseases by 25% in 2025, including CVD.
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Enfermedades Cardiovasculares , Dislipidemias , Mercurio , Humanos , Estudios Transversales , Apolipoproteína A-I/genética , Apolipoproteína A-I/análisis , Enfermedades Cardiovasculares/inducido químicamente , Enfermedades Cardiovasculares/epidemiología , Enfermedades Cardiovasculares/genética , Factores de Riesgo , Poblaciones Vulnerables , Mercurio/toxicidad , Mercurio/análisis , Apolipoproteínas B/análisis , Apolipoproteínas/análisis , Factores de Riesgo de Enfermedad Cardiaca , Dislipidemias/inducido químicamente , Dislipidemias/epidemiología , Dislipidemias/genética , Cabello/químicaRESUMEN
The COVID-19 pandemic affected billions of people worldwide, and exposure to toxic metals has emerged as an important risk factor for COVID-19 severity. Mercury is currently ranked as the third toxic substance of global concern for human health, and its emissions to the atmosphere have increased globally. Both COVID-19 and mercury exposure present a high prevalence in similar regions: East and Southeast Asia, South America and Sub-Saharan Africa. Since both factors represent a multiorgan threat, a possible synergism could be exacerbating health injuries. Here, we discuss key aspects in mercury intoxication and SARS-CoV-2 infection, describing the similarities shared in clinical manifestations (especially neurological and cardiovascular outcomes), molecular mechanisms (with a hypothesis in the renin-angiotensin system) and genetic susceptibility (mainly by apolipoprotein E, paraoxonase 1 and glutathione family genes). Literature gaps on epidemiological data are also highlighted, considering the coincident prevalence. Furthermore, based on the most recent evidence, we justify and propose a case study of the vulnerable populations of the Brazilian Amazon. An understanding of the possible adverse synergism between these two factors is crucial and urgent for developing future strategies for reducing disparities between developed and underdeveloped/developing countries and the proper management of their vulnerable populations, particularly considering the long-term sequelae of COVID-19.
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COVID-19 , Mercurio , Humanos , Brasil , Exposición a Riesgos Ambientales , Oro , Mercurio/efectos adversos , Mercurio/análisis , Mercurio/toxicidad , Pandemias , SARS-CoV-2RESUMEN
Environmental pollution is a global threat and represents a strong risk factor for human health. It is estimated that pollution causes about 9 million premature deaths every year. Pollutants that can cross the blood-brain barrier and reach the central nervous system are of special concern, because of their potential to cause neurological and development disorders. Arsenic, lead and mercury are usually ranked as the top three in priority lists of regulatory agencies. Against xenobiotics, astrocytes are recognised as the first line of defence in the CNS, being involved in virtually all brain functions, contributing to homeostasis maintenance. Here, we discuss the current knowledge on the astroglial involvement in the neurotoxicity induced by these pollutants. Beginning by the main toxicokinetic characteristics, this review also highlights the several astrocytic mechanisms affected by these pollutants, involving redox system, neurotransmitter and glucose metabolism, and cytokine production/release, among others. Understanding how these alterations lead to neurological disturbances (including impaired memory, deficits in executive functions, and motor and visual disfunctions), by revisiting the current knowledge is essential for future research and development of therapies and prevention strategies.
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Arsénico , Contaminantes Ambientales , Mercurio , Síndromes de Neurotoxicidad , Humanos , Arsénico/toxicidad , Astrocitos/metabolismo , Contaminantes Ambientales/toxicidad , Contaminantes Ambientales/metabolismo , Mercurio/toxicidad , Síndromes de Neurotoxicidad/metabolismoRESUMEN
BACKGROUND: Despite widespread searches, there are currently no validated biofluid markers for the detection of subclinical neuroinflammation in multiple sclerosis (MS). The dynamic nature of human metabolism in response to changes in homeostasis, as measured by metabolomics, may allow early identification of clinically silent neuroinflammation. Using the delayed-type hypersensitivity (DTH) MS rat model, we investigated the serum and cerebrospinal fluid (CSF) metabolomics profiles and neurofilament-light chain (NfL) levels, as a putative marker of neuroaxonal damage, arising from focal, clinically silent neuroinflammatory brain lesions and their discriminatory abilities to distinguish DTH animals from controls. METHODS: 1H nuclear magnetic resonance (NMR) spectroscopy metabolomics and NfL measurements were performed on serum and CSF at days 12, 28 and 60 after DTH lesion initiation. Supervised multivariate analyses were used to determine metabolomics differences between DTH animals and controls. Immunohistochemistry was used to assess the extent of neuroinflammation and tissue damage. RESULTS: Serum and CSF metabolomics perturbations were detectable in DTH animals (vs. controls) at all time points, with the greatest change occurring at the earliest time point (day 12) when the neuroinflammatory response was most intense (mean predictive accuracy [SD]-serum: 80.6 [10.7]%, p < 0.0001; CSF: 69.3 [13.5]%, p < 0.0001). The top discriminatory metabolites at day 12 (serum: allantoin, cytidine; CSF: glutamine, glucose) were all reduced in DTH animals compared to controls, and correlated with histological markers of neuroinflammation, particularly astrogliosis (Pearson coefficient, r-allantoin: r = - 0.562, p = 0.004; glutamine: r = - 0.528, p = 0.008). Serum and CSF NfL levels did not distinguish DTH animals from controls at day 12, rather, significant differences were observed at day 28 (mean [SEM]-serum: 38.5 [4.8] vs. 17.4 [2.6] pg/mL, p = 0.002; CSF: 1312.0 [379.1] vs. 475.8 [74.7] pg/mL, p = 0.027). Neither serum nor CSF NfL levels correlated with markers of neuroinflammation; serum NfL did, however, correlate strongly with axonal loss (r = 0.641, p = 0.001), but CSF NfL did not (p = 0.137). CONCLUSIONS: While NfL levels were elevated later in the pathogenesis of the DTH lesion, serum and CSF metabolomics were able to detect early, clinically silent neuroinflammation and are likely to present sensitive biomarkers for the assessment of subclinical disease activity in patients.
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Esclerosis Múltiple , Alantoína , Animales , Biomarcadores , Citidina , Modelos Animales de Enfermedad , Glucosa , Glutamina , Humanos , Filamentos Intermedios , Esclerosis Múltiple/líquido cefalorraquídeo , Proteínas de Neurofilamentos , RatasRESUMEN
Pollution is harmful to human physical health and wellbeing. What is less well established is the relationship between adolescent mental health - a growing public health concern - and pollution. In response, we systematically reviewed studies documenting associations between pollution and mental health in adolescents. We searched Africa Wide, Medline, PsycArticles, PsycInfo, PubMed, CINAHL, ERIC, SciELO, Scopus, and Web of Science Core Collection for studies published up to 10 April 2020 that investigated exposure to any pollutant and symptoms of anxiety; depression; disruptive, impulse-control, and conduct disorders; neurodevelopmental disorders; psychosis; or substance abuse in 10-24-year-olds (i.e., adolescents as per expanded and more inclusive definition of adolescence). This identified 2291 records and we assessed 128 papers for inclusion. We used a narrative synthesis to coalesce the studies' findings. This review is registered on PROSPERO, CRD42020176664. Seventeen studies from Asia, Europe, the Middle East, and North America were included. Air and water pollution exposure was associated with elevated symptoms of depression, generalised anxiety, psychosis, and/or disruptive, impulse control and conduct disorder. Exposure to lead and solvents was associated with neurodevelopmental impairments. Most studies neglected factors that could have supported the mental health resilience of adolescents exposed to pollution. Notwithstanding the limited quality of most reviewed studies, results suggest that pollution exposure is a risk to adolescent mental health. High-quality research is urgently required, including the factors and processes that protect the mental health of pollution-exposed adolescents. Studies with adolescents living in low- and lower middle-income countries and the southern hemisphere must be prioritized.
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Trastorno de la Conducta , Trastornos Relacionados con Sustancias , Adolescente , Ansiedad/epidemiología , Trastornos de Ansiedad , Humanos , Salud MentalRESUMEN
Microglial cells are the scions of foetal macrophages which invade the neural tube early during embryogenesis. The nervous tissue environment instigates the phenotypic metamorphosis of foetal macrophages into idiosyncratic surveilling microglia, which are generally characterised by a small cell body and highly ramified motile processes that constantly scan the nervous tissue for signs of changes in homeostasis and allow microglia to perform crucial homeostatic functions. The surveilling microglial phenotype is evolutionarily conserved from early invertebrates to humans. Despite this evolutionary conservation, microglia show substantial heterogeneity in their gene and protein expression, as well as morphological appearance. These differences are age, region and context specific and reflect a high degree of plasticity underlying the life-long adaptation of microglia, supporting the exceptional adaptive capacity of the central nervous system. Microgliocytes are essential elements of cellular network formation and refinement in the developing nervous tissue. Several distinct patrolling modes of microglial processes contribute to the formation, modification, and pruning of synapses; to the support and protection of neurones through microglial-somatic junctions; and to the control of neuronal and axonal excitability by specific microglia-axonal contacts. In pathology, microglia undergo proliferation and reactive remodelling known as microgliosis, which is context dependent, yet represents an evolutionarily conserved defence response. Microgliosis results in the emergence of multiple disease and context-specific reactive states; in addition, neuropathology is associated with the appearance of specific protective or recovery microglial forms. In summary, the plasticity of microglia supports the development and functional activity of healthy nervous tissue and provides highly sophisticated defences against disease.
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Microglía , Neuronas , Sistema Nervioso Central , Microglía/metabolismo , Neuronas/fisiologíaRESUMEN
Human exposure to methylmercury (MeHg) is currently high in regions such as the Amazon. Understanding the molecular changes associated with MeHg-induced neurotoxicity and the crosstalk with the periphery is essential to support early diagnoses. This work aimed to evaluate cellular and molecular changes associated with behavioral alterations in MeHg acute exposure and the possible changes in extracellular vesicles (EVs) number and S100ß content. Adults male Wistar rats were orally treated with 5 mg/kg for four days. Behavioral performance, molecular and histological changes in the cerebellum, and plasma EVs were assessed. MeHg-intoxicated animals performed significantly worse in behavioral tests. MeHg increased the number of GFAP+ cells and GFAP and S100ß mRNA expression in the cerebellum but no change in NeuN+ or IBA-1+ cells number was detected. The number of exosomes isolated from plasma were decreased by the metal. S100B mRNA was detected in circulating plasma EVs cargo in MeHg exposure. Though preliminary, our results suggest astrocytic reactivity is displaying a protective role once there was no neuronal death. Interestingly, the reduction in exosomes number could be a new mechanism associated with MeHg-induced neurotoxicity and plasma EVs could represent a source of future biomarkers in MeHg intoxication.
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Encéfalo/patología , Cerebelo/patología , Contaminantes Ambientales/toxicidad , Vesículas Extracelulares/patología , Compuestos de Metilmercurio/toxicidad , Síndromes de Neurotoxicidad/patología , Animales , Encéfalo/efectos de los fármacos , Cerebelo/efectos de los fármacos , Vesículas Extracelulares/efectos de los fármacos , Masculino , Síndromes de Neurotoxicidad/etiología , Ratas , Ratas WistarRESUMEN
The metabolic syndrome (MetS) epidemic is a global challenge. Although developing countries (including Brazil, India, and South Africa) present a higher proportion of deaths by cardiovascular diseases than developed countries, most of our knowledge is from these developed countries. Amazonian riverine populations (ARP), as well as other vulnerable populations of the Southern Hemisphere, share low-income and traditional practices, among other features. This large cross-sectional study of ARP (n = 818) shows high prevalence of hypertension (51%) and obesity (23%). MetS was diagnosed in 38% of participants (especially in women and 60-69 years-old individuals) without the influence of ancestry. Only 7-8% of adults had no cardio-metabolic abnormalities related to MetS. Atherogenic dyslipidemia (low HDL-cholesterol) was generally observed, including in individuals without MetS. Still, slight differences were detected between settings with a clear predominance of hypertension in Tucuruí. Hypotheses on possible genetic influence and factors (nutrition transition and environmental pollutants -mercury) are proposed for future studies. Moreover, a roadmap to MetS progression based on the most prevalent components is provided for the development of tailored interventions in the Amazon (initially, individuals would present low HDL-cholesterol levels, later progressing to increased blood pressure characterizing hypertension, and ultimately reaching MetS with obesity). Our alarming results support the need to improve our knowledge on these vulnerable populations.
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Lifestyle is one of the most powerful instruments shaping mankind; the lifestyle includes many aspects of interactions with the environment, from nourishment and education to physical activity and quality of sleep. All these factors taken in complex affect neuroplasticity and define brain performance and cognitive longevity. In particular, physical exercise, exposure to enriched environment and dieting act through complex modifications of microglial cells, which change their phenotype and modulate their functional activity thus translating lifestyle events into remodelling of brain homoeostasis and reshaping neural networks ultimately enhancing neuroprotection and cognitive longevity.
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Encéfalo/fisiología , Estilo de Vida , Microglía/fisiología , Plasticidad Neuronal , HumanosRESUMEN
The Amazon is the largest tropical forest in the world and a source of healthy food, such as fruits and fish. Surprisingly, the Amazonian riverine population present an increased prevalence (as high as 58%) of non-communicable diseases, such as hypertension and insulin resistance, even higher than that described for the urban population of the Amazon. Therefore, this work aimed to analyze the nutritional status and associated risk of the riverine population. Body mass index, waist circumference (WC), waist-to-hip ratio, and neck circumference (NC) were evaluated, and risk analysis was assayed. Furthermore, data about occupation and the prevalence of consumers of the different groups of food were analyzed. All anthropometric parameters revealed high proportions of individuals at risk, WC and NC being the factors that had more high-risk women and men, respectively. Our data confirmed the characteristic profile of the riverine communities with a high number of fish consumers, but also observed different patterns probably associated to a phenomenon of nutrition transition. Based on our data, some nudge interventions that take into account the principles of behavior analysis are discussed and proposed for these populations, aiming to improve the nutritional status and avoid the long-term consequences of the results showed by this work.
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The occurrence of neurotoxicity caused by xenobiotics such as pesticides (dichlorodiphenyltrichloroethane, organophosphates, pyrethroids, etc.) or metals (mercury, lead, aluminum, arsenic, etc.) is a growing concern around the world, particularly in vulnerable populations with difficulties on both detection and symptoms treatment, due to low economic status, remote access, poor infrastructure, and low educational level, among others features. Despite the numerous molecular markers and questionnaires/clinical evaluations, studying neurotoxicity and its effects on cognition in these populations faces problems with samples collection and processing, and information accuracy. Assessing cognitive changes caused by neurotoxicity, especially those that are subtle in the initial stages, is fundamentally challenging. Finding accurate, non-invasive, and low-cost strategies to detect the first signals of brain injury has the potential to support an accelerated development of the research with these populations. Saliva emerges as an ideal pool of biomarkers (with interleukins and neural damage-related proteins, among others) and potential alternative diagnostic fluid to molecularly investigate neurotoxicity. As a source of numerous neurological biomarkers, saliva has several advantages compared to blood, such as easier storage, requires less manipulation, and the procedure is cheaper, safer and well accepted by patients compared with drawing blood. Regarding cognitive dysfunction, neuropsychological batteries represent, with their friendly interface, a feasible and accurate method to evaluate the eventual cognitive deficits associated with neurotoxicity in people from diverse cultural and educational backgrounds. The association of these two tools, saliva and neuropsychological batteries, to cover the molecular and cognitive aspects of neurotoxicity in vulnerable populations, could potentially increase the prevalence of early intervention and successful treatment.
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Contaminantes Ambientales , Biomarcadores , Cognición , Contaminantes Ambientales/toxicidad , Humanos , Saliva , Poblaciones VulnerablesRESUMEN
Intoxication by heavy metals such as methylmercury (MeHg) is recognized as a global health problem, with strong implications in central nervous system pathologies. Most of these neuropathological conditions involve vascular, neurotransmitter recycling, and oxidative balance disruption leading to accelerated decline in fine balance, and learning, memory, and visual processes as main outcomes. Besides neurons, astrocytes are involved in virtually all the brain processes and perform important roles in neurological response following injuries. Due to astrocytes' strategic functions in brain homeostasis, these cells became the subject of several studies on MeHg intoxication. The most heterogenous glial cells, astrocytes, are composed of plenty of receptors and transporters to dialogue with neurons and other cells and to monitor extracellular environment responding tightly through fluctuation of cytosolic ions. The overall toxicity of MeHg might be determined on the basis of the balance between MeHg-mediated injury to neurons and protective responses from astrocytes. Although the role of neurons in MeHg intoxication is relatively well-established, the role of the astrocytes is only beginning to be understood. In this review, we update the information on astroglial modulation of the MeHg-induced neurotoxicity, providing remarks on their protective and deleterious roles and insights for future studies.
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Astrocitos/efectos de los fármacos , Encéfalo/efectos de los fármacos , Compuestos de Metilmercurio/toxicidad , Neuronas/efectos de los fármacos , Síndromes de Neurotoxicidad/patología , Astrocitos/patología , Encéfalo/patología , Humanos , Neuronas/patologíaRESUMEN
BACKGROUND: Whilst there is little uncertainty about the deleterious impact of pollution on human and planetary health, pollution's impact on adolescent mental health is less well understood. This is particularly true for young people in underdeveloped and developing world contexts, about whom research is generally lacking. Furthermore, although adolescent resilience continues to be a research priority, little attention has been paid to adolescent pathways of resilience in the face or aftermath of pollution exposure. The objective of this study will be to examine the associations between pollution and mental health in 10- to 24-year-olds (i.e. adolescents). METHODS: We designed and registered a study protocol for a systematic review of studies which link pollution and mental health in adolescents. We will include observational studies (e.g. cohort, case-control, time series analyses) that assess the associations between exposure to any form of pollution and the mental health of 10- to 24-year-olds. The primary outcome will be symptoms associated with neurodevelopmental disorders; disruptive, impulse-control, and conduct disorders; depressive disorders; anxiety disorders; substance disorders; and schizophrenia. No secondary outcomes will be considered. Literature searches will be conducted in multiple electronic databases (from inception onwards), including PubMed, MEDLINE, SCOPUS, Web of Science, CINAHL, PsycINFO, SciELO, ERIC, and Africa-Wide. Two investigators will independently screen all citations, full-text articles, and abstract data. The methodological quality (or bias) of included studies will be appraised using appropriate tools. We will provide a narrative synthesis of the evidence. DISCUSSION: This systematic review will evaluate the evidence on the associations between pollution and the mental health of 10- to 24-year-olds. Our findings will be of potential interest to multiple audiences (including adolescent patients/clients, their families, caregivers, healthcare professionals, scientists, and policy makers) and could be used to develop prevention and intervention strategies as well as focus future research. Results will be published in a peer-reviewed journal. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42020176664.