RESUMO
El mercurio es un elemento químico metálico que está presente de forma natural en el aire, el agua y los suelos. Asimismo, se utiliza en la minería de oro artesanal y en pequeña escala (MAPE). El problema es que la exposición al mercurio y sus compuestos (incluso a pequeñas cantidades) puede causar graves problemas de salud; puede ser tóxico para los sistemas nervioso e inmunitario, el aparato digestivo, la piel y los pulmones, así como los riñones y la vista. La principal vía de exposición humana al metilmercurio es el consumo de pescado y mariscos contaminados. Este material en forma de rotafolio ha sido elaborado por la Organización Panamericana de la Salud (OPS), inicialmente con el Ministerio de Salud de Perú, y en esta segunda versión, modificada para el contexto de Bolivia, con la colaboración del Ministerio de Salud y Deportes de este último país y profesionales que han contribuido con datos nacionales para tratar el tema. El rotafolio servirá como apoyo en las sesiones de orientación dirigidas a los hombres y mujeres responsables de la salud de los menores, así como del bienestar integral de quienes acuden a los establecimientos de salud, o en las sesiones educativas que se realicen en las comunidades afectadas por la MAPE. Se espera que el material sirva de apoyo para las acciones de prevención a la exposición por mercurio y para el cuidado de la salud en Bolivia, especialmente para las poblaciones en condiciones de vulnerabilidad, como poblaciones indígenas, mujeres, niños y niñas.
Assuntos
Mercúrio , Intoxicação por Mercúrio , Intoxicação do Sistema Nervoso por Mercúrio , BolíviaRESUMO
Methylmercury (MeHg) is a well-known environmental neurotoxicant that causes severe brain disorders such as Minamata disease. Although some patients with Minamata disease develop olfactory dysfunction, the underlying pathomechanism is largely unknown. We examined the effects of MeHg on the olfactory system using a model of MeHg poisoning in which mice were administered 30 ppm MeHg in drinking water for 8 weeks. Mice exposed to MeHg displayed significant mercury accumulation in the olfactory pathway, including the nasal mucosa, olfactory bulb, and olfactory cortex. The olfactory epithelium was partially atrophied, and olfactory sensory neurons were diminished. The olfactory bulb exhibited an increase in apoptotic cells, hypertrophic astrocytes, and amoeboid microglia, mainly in the granular cell layer. Neuronal cell death was observed in the olfactory cortex, particularly in the ventral tenia tecta. Neuronal cell death was also remarkable in higher-order areas such as the orbitofrontal cortex. Correlation analysis showed that neuronal loss in the olfactory cortex was strongly correlated with the plasma mercury concentration. Our results indicate that MeHg is an olfactory toxicant that damages the central regions involved in odor perception. The model described herein is useful for analyzing the mechanisms and treatments of olfactory dysfunction in MeHg-intoxicated patients.
Assuntos
Intoxicação do Sistema Nervoso por Mercúrio , Mercúrio , Compostos de Metilmercúrio , Transtornos do Olfato , Humanos , Camundongos , Animais , Compostos de Metilmercúrio/toxicidade , Microglia/patologia , Transtornos do Olfato/induzido quimicamente , Transtornos do Olfato/complicaçõesAssuntos
Saúde da Criança , Proteção da Criança , Saúde Ambiental , Exposição Ambiental , Mercúrio , Compostos de Mercúrio , Intoxicação do Sistema Nervoso por Mercúrio , Atividades Humanas , Atmosfera , Água , Solo , Pessoal de Saúde , Avaliação de Resultados em Cuidados de Saúde , Materiais de EnsinoRESUMO
We had an opportunity to perform a general autopsy of a case with chronic organic mercury toxicosis in 2017. He had been engaged in synthesizing a variety of organic mercury compounds throughout the four years from 1966 and developed chronic organic mercury poisoning in 1969. Almost forty years on, he still remained to complain of persistent paresthesia at finger tips and tongue, and of narrowed visual field. Neurological examinations clarified a rise of two-point discrimination thresholds, a systemic increase of touch thresholds, constriction of the visual field caused by general visual depression, and sensorineural hearing loss while primary modalities of his somatic, visual, and auditory sensations were preserved. These symptoms and signs are characteristic of human organic mercury poisoning. Furthermore, he had difficulty in processing a lot of visual and auditory information at a time. His two-point discrimination thresholds and systemic elevation of touch thresholds were comparable to those of mild organic mercury poisoning cases. He had slight sensory ataxia, but not cerebellar ataxia. Brain [18F]-2-fluorodeoxyglucose positron emission tomography analysis exhibited marked hypometabolism at bilateral postcentral gyrus, striate cortex, and superior temporal gyrus, but not the cerebellum. Histopathological studies revealed considerable decrease of granular neurons and neuronal networks in bilateral primary somatosensory, visual, and auditory cortices. Those characteristic brain lesions fairly explain increase of thresholds of somatic, visual, and auditory sensations, and degradation of integrating sensory information. It is noted that damages to the peripheral nervous system and the cerebellum were not detected and that his intellectual faculties were preserved.
Assuntos
Intoxicação do Sistema Nervoso por Mercúrio , Intoxicação por Mercúrio , Doenças do Sistema Nervoso , Masculino , Humanos , Intoxicação do Sistema Nervoso por Mercúrio/complicações , Intoxicação do Sistema Nervoso por Mercúrio/diagnóstico por imagem , Encéfalo/patologia , Intoxicação por Mercúrio/complicações , Intoxicação por Mercúrio/diagnóstico , Intoxicação por Mercúrio/patologia , AutopsiaRESUMO
El fotógrafo de Minamata (2020) de Andrew Levitas es una película importante para comprender cómo la contaminación del medio ambiente puede tener una gran influencia en la salud humana. Muestra cómo la contaminación afecta a las comunidades, cómo éstas se resisten a aceptar la responsabilidad de la empresa responsable y cómo la comunidad y los medios de comunicación pueden trabajar juntos para abordar estas cuestiones y tomar medidas para prevenir y tratar estos problemas. En la docencia universitaria de Ciencias de la Salud se constituye en un recurso pedagógico importante para ilustrar y concientizar sobre la problemática toxicológica del metilmercurio en la salud humana y especialmente durante la gestación promoviendo el desarrollo de diversos defectos congénitos. El visionado del film por otro lado estimula el pensamiento crítico, divergente, analítico, reflexivo, emocional y el aprendizaje significativo, al tiempo que permite integrar conocimientos de las asignaturas que cursan y cultura general en una experiencia inmersiva. Asimismo, permite integrar el arte del filme y la fotografía de W. Eugene Smith como una transversal educativa que contribuye al acervo de cultura general del estudiante. (AU)
Minamata by Andrew Levitas is an important film to understand how environmental pollution can have a great influence on human health. It shows how pollution affects communities, how communities are reluctant to accept the responsibility of the responsible company, and how the community and the media can work together to address these issues and take action to prevent and treat these problems. In the university teaching of Health Sciences, it constitutes an important pedagogical resource to illustrate and raise awareness about the toxicological problems of methyl mercury in human health and especially during pregnancy, promoting the development of various congenital defects. Viewing the film, on the other hand, stimulates critical, divergent, analytical, reflective, emotional thinking and significant learning, while allowing the integration of knowledge of the subjects they are studying and general culture in an immersive experience. Likewise, it allows to integrate the art of the film and the photography of W. Eugene Smith as an educational transversal that contributes to the heritage of the student's general culture. (AU)
Assuntos
Humanos , Filmes Cinematográficos , Intoxicação do Sistema Nervoso por Mercúrio , Anormalidades Congênitas , Compostos de Metilmercúrio/toxicidade , PensamentoRESUMO
Minamata disease, which happened during the 1950s and 1960s in Minamata, Japan, is a well-known case of food poisoning caused by methylmercury-contaminated fish. Although many children were born, in the affected areas, with severe neurological signs after birth (known as congenital Minamata disease (CMD)), few studies have explored the possible effects of low-to-moderate methylmercury exposure in utero, probably at lower levels than in CMD patients, in Minamata. We, therefore, recruited 52 participants in 2020: 10 patients with known CMD; 15 moderately exposed residents; and 27 non-exposed controls. The average umbilical cord methylmercury concentrations were 1.67 parts per million (ppm) for CMD patients and 0.77 ppm for moderately exposed participants. After conducting four neuropsychological tests, we compared the functions among the groups. Compared with the non-exposed controls, both the CMD patients and moderately exposed residents had worse scores in the neuropsychological tests, although the score decline was more severe in the CMD patients. For example, even after adjusting for age and sex, the CMD patients and moderately exposed residents had 16.77 (95% CI: 13.46 to 20.08) and 4.11 (95% CI: 1.43 to 6.78) lower scores in the Montreal Cognitive Assessment, respectively, than the non-exposed controls. The present study indicates that residents of Minamata who experienced low-to-moderate prenatal methylmercury exposure also have neurological or neurocognitive impairments.
Assuntos
Doenças Transmitidas por Alimentos , Intoxicação do Sistema Nervoso por Mercúrio , Compostos de Metilmercúrio , Animais , Japão , Intoxicação do Sistema Nervoso por Mercúrio/complicações , Compostos de Metilmercúrio/intoxicação , Exame Neurológico , HumanosRESUMO
Mercuric chloride (HgCl2), a heavy metal compound, causes neurotoxicity of animals and humans. Selenium (Se) antagonizes heavy metal-induced organ damage with the properties of anti-oxidation and anti-inflammation. Nevertheless, the molecular mechanism underlying the protective effects of sodium selenite (Na2SeO3) against HgCl2-induced neurotoxicity remains obscure. Therefore, the present study aimed to explore the protective mechanism of Na2SeO3 on HgCl2-induced brain damage in chickens. Morphological observations showed that Na2SeO3 alleviated HgCl2-induced brain tissues damage. The results also showed that Na2SeO3 decreased the protein expression of S100 calcium binding protein B (S100B), and increased the levels of nerve growth factors (NGF), doublecortin domain containing 2 (DCDC2), as well as neurotransmitter to reverse HgCl2-induced brain dysfunction. Further, Na2SeO3 attenuated HgCl2-induced oxidative stress by decreasing the level of malondialdehyde (MDA) and increasing the activities of total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), and total antioxidant capacity (T-AOC). Mechanistically, Na2SeO3 activated the brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase receptor type B (TrKB)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway and suppressed the nuclear factor kappa B (NF-κB) signaling pathway to inhibit apoptosis and inflammation caused by HgCl2 exposure. In summary, Na2SeO3 ameliorated HgCl2-induced brain injury via inhibiting apoptosis and inflammation through activating BDNF/TrKB/PI3K/AKT and suppressing NF-κB pathways.
Assuntos
Encefalopatias/tratamento farmacológico , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Cloreto de Mercúrio/toxicidade , Intoxicação do Sistema Nervoso por Mercúrio/tratamento farmacológico , Fármacos Neuroprotetores/uso terapêutico , Selenito de Sódio/uso terapêutico , Animais , Anti-Inflamatórios/uso terapêutico , Apoptose/efeitos dos fármacos , Encefalopatias/induzido quimicamente , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Galinhas , Inflamação/tratamento farmacológico , Masculino , NF-kappa B/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Receptor trkB/metabolismoRESUMO
Methylmercury (MeHg), the causal substrate in Minamata disease, can lead to severe and chronic neurological disorders. The main symptom of Minamata disease is sensory impairment in the four extremities; however, the sensitivity of individual sensory modalities to MeHg has not been investigated extensively. In the present study, we performed stimulus-response behavioral experiments in MeHg-exposed rats to compare the sensitivities to pain, heat, cold, and mechanical sensations. MeHg (6.7 mg/kg/day) was orally administered to 9-week-old Wistar rats for 5 days and discontinued for 2 days, then administered daily for another 5 days. The four behavioral experiments were performed daily on each rat from the beginning of MeHg treatment for 68 days. The pain sensation decreased significantly from day 11 onwards, but recovered to control levels on day 48. Other sensory modalities were not affected by MeHg exposure. These findings suggest that the pain sensation is the sensory modality most susceptive to MeHg toxicity and that this sensitivity is reversible following discontinuation of the exposure.
Assuntos
Hipestesia/etiologia , Hipestesia/fisiopatologia , Intoxicação do Sistema Nervoso por Mercúrio/etiologia , Intoxicação do Sistema Nervoso por Mercúrio/fisiopatologia , Compostos de Metilmercúrio/toxicidade , Dor/fisiopatologia , Animais , Masculino , Compostos de Metilmercúrio/administração & dosagem , Ratos WistarRESUMO
We recently found that tumor necrosis factor-α (TNF-α) may be involved in neuronal cell death induced by methylmercury in the mouse brain. Here, we examined the cells involved in the induction of TNF-α expression by methylmercury in the mouse brain by in situ hybridization. TNF-α-expressing cells were found throughout the brain and were identified as microglia by immunostaining for ionized calcium binding adaptor molecule 1 (Iba1). Methylmercury induced TNF-α expression in mouse primary microglia and mouse microglial cell line BV2. Knockdown of apoptosis signal-regulating kinase 1 (ASK1), an inflammatory cytokine up-regulator that is responsible for reactive oxygen species (ROS), decreased methylmercury-induced TNF-α expression through decreased phosphorylation of p38 MAP kinase in BV2 cells. Suppression of methylmercury-induced reactive oxygen species (ROS) by antioxidant treatment largely abolished the induction of TNF-α expression and phosphorylation of p38 by methylmercury in BV2 cells. Finally, in mouse brain slices, the TNF-α antagonist (WP9QY) inhibited neuronal cell death induced by methylmercury, as did the p38 inhibitor SB203580 and liposomal clodronate (a microglia-depleting agent). These results indicate that methylmercury induces mitochondrial ROS that are involved in activation of the ASK1/p38 pathway in microglia and that this is associated with induction of TNF-α expression and neuronal cell death.
Assuntos
Encéfalo/patologia , Intoxicação do Sistema Nervoso por Mercúrio/patologia , Microglia/efeitos dos fármacos , Neurônios/efeitos dos fármacos , Animais , Apoptose/efeitos dos fármacos , Encéfalo/citologia , Linhagem Celular , Ácido Clodrônico/farmacologia , Modelos Animais de Doenças , Poluentes Ambientais/administração & dosagem , Poluentes Ambientais/toxicidade , Técnicas de Silenciamento de Genes , Humanos , Imidazóis/farmacologia , MAP Quinase Quinase Quinase 5/genética , MAP Quinase Quinase Quinase 5/metabolismo , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Sistema de Sinalização das MAP Quinases/genética , Masculino , Intoxicação do Sistema Nervoso por Mercúrio/etiologia , Compostos de Metilmercúrio/administração & dosagem , Compostos de Metilmercúrio/toxicidade , Camundongos , Microglia/patologia , Mitocôndrias/efeitos dos fármacos , Mitocôndrias/metabolismo , Neurônios/patologia , Peptídeos Cíclicos/farmacologia , Fosforilação/efeitos dos fármacos , Cultura Primária de Células , Piridinas/farmacologia , Fator de Necrose Tumoral alfa/antagonistas & inibidores , Fator de Necrose Tumoral alfa/metabolismo , Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismoRESUMO
Exposure to mercury, lead and polychlorinated biphenyls (PCBs) have been associated with emotional dysregulation, but their neuronal correlates have yet to be examined. Inuit from Nunavik (Northern Quebec, Canada) face internalizing problems and are among the most exposed individuals to these environmental contaminants in the world. The aim of this study was to examine the link between pre- and postnatal exposure to these contaminants and brain fear-circuitry in Inuit adolescents. Facial expression stimuli were presented to participants (mean age = 18.3 years) in a magnetic resonance imaging (MRI) scanner. Fear conditioning and extinction tasks included neutral faces as the conditioned threat and safety cues and a fearful face paired with a shrieking scream as the unconditioned stimulus. Functional MRI data were gathered at the conditioning phase (n = 71) and at the extinction phase (n = 62). Mercury, lead and PCB 153 concentrations were measured in blood samples at birth (cord blood) and at the time of the adolescent testing to estimate pre- and postnatal exposure, respectively. For each time point, exposures were categorized in tertiles (low, moderate and high exposed groups). Mixed analyses of variance were conducted for each contaminant of interest controlling for sex, age, socioeconomic status, drug/alcohol use, food insecurity and contaminant co-exposure. Results revealed greater differential activation during the conditioning phase in the right orbitofrontal cortex in participants with moderate and high concentrations of cord blood PCB 153 compared to those in the low exposure group. During the extinction phase, the high prenatal mercury exposed group showed a lower differential activation in the right and left anterior cingulate cortex compared to those in the low-exposed group; whereas there was a higher differential activation in right dorsolateral prefrontal cortex in the high postnatal lead exposed group compared to the moderate- and low-exposed groups. Our study is the first to show alterations in the prefrontal brain areas in fear conditioning and extinction tasks in relation to environmental contaminant exposures. The observed brain correlates may advance our understanding of the emotional problems associated with environmental chemical toxicity.
Assuntos
Emoções/fisiologia , Exposição Ambiental/efeitos adversos , Poluentes Ambientais/efeitos adversos , Medo/fisiologia , Inuíte/psicologia , Córtex Pré-Frontal/fisiopatologia , Adolescente , Medo/psicologia , Neuroimagem Funcional , Humanos , Intoxicação do Sistema Nervoso por Chumbo na Infância/fisiopatologia , Intoxicação do Sistema Nervoso por Chumbo na Infância/psicologia , Imageamento por Ressonância Magnética , Masculino , Intoxicação do Sistema Nervoso por Mercúrio/fisiopatologia , Intoxicação do Sistema Nervoso por Mercúrio/psicologia , Córtex Pré-Frontal/diagnóstico por imagem , Córtex Pré-Frontal/efeitos dos fármacos , Adulto JovemRESUMO
Human exposure to mercury is a major public health concern, causing neurological outcomes such as motor and visual impairment and learning disabilities. Currently, human exposure in the Amazon is among the highest in the world. A recent systematic review (doi:10.1016/j.jtemb.2018.12.001), however, highlighted the lack of high-quality studies on mercury-associated neurotoxicity. There is, therefore, a need to improve research and much to still learn about how exposure correlates with disease. In this review, we discuss studies evaluating the associations between neurological disturbances and mercury body burden in Amazonian populations, to generate recommendations for future studies. A systematic search was performed during July 2020, in Pubmed/Medline, SCOPUS and SCIELO databases with the terms (mercury*) and (Amazon*). Four inclusion criteria were used: original article (1), with Amazonian populations (2), quantifying exposure (mercury levels) (3), and evaluating neurological outcomes (4). The extracted data included characteristics (as year or origin of authorship) and details of the research (as locations and type of participants or mercury levels and neurological assessments). Thirty-four studies, most concentrated within three main river basins (Tapajós, Tocantins, and Madeira) and related to environmental exposure, were found. Mercury body burden was two to ten times higher than recommended and main neurological findings were cognitive, vision, motor, somatosensory and emotional deficits. Important insights are described that support novel approaches to researching mercury exposure and intoxication, as well as prevention and intervention strategies. As a signatory country to the Minamata Convention, Brazil has the opportunity to play a central role in improving human health and leading the research on mercury intoxication.
Assuntos
Exposição Ambiental/efeitos adversos , Poluentes Ambientais/toxicidade , Intoxicação do Sistema Nervoso por Mercúrio/etiologia , Mercúrio/toxicidade , Rios/química , Carga Corporal (Radioterapia) , Brasil , Exposição Ambiental/análise , Poluentes Ambientais/análise , Feminino , Cabelo/química , Humanos , Masculino , Mercúrio/análise , Intoxicação do Sistema Nervoso por Mercúrio/epidemiologia , Intoxicação do Sistema Nervoso por Mercúrio/metabolismoRESUMO
ß-HgS, differing from environmental mercury pollutants (MeHgCl and HgCl2) in chemical form, is used as traditional medicine in Asian countries for thousands of years. In this study, Neuro-2a cells were exposed to ß-HgS, MeHgCl and HgCl2 (5 µM) for 6-24 h. The cell viability of ß-HgS was higher than MeHgCl with 25.9% and 72.4% in 12 h and 24 h respectively. As the incubation time increased, MeHgCl had obvious damage to cell morphology, decreased the ratio of Bcl-2 and Bak and increased the expressions of TNF-α, IL-6 and IL-1ß significantly. Furthermore, the expressions of IL-1ß and IL-6 in HgCl2 group were increased significantly in 6 h and 24 h. The apoptotic rates in MeHgCl and HgCl2 group were respectively higher than ß-HgS with 32.2% and 7.30% in 24 h. Our findings indicate that ß-HgS is much less neurotoxicity than MeHgCl and HgCl2 in Neuro-2a cells.
Assuntos
Poluentes Ambientais/toxicidade , Compostos de Mercúrio/toxicidade , Compostos de Metilmercúrio/toxicidade , Animais , Apoptose/efeitos dos fármacos , Caspases/genética , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Regulação da Expressão Gênica/efeitos dos fármacos , Intoxicação do Sistema Nervoso por Mercúrio , CamundongosRESUMO
Mercury is a severe environmental pollutant with neurotoxic effects, especially when exposed for long periods. Although there are several evidences regarding mercury toxicity, little is known about inorganic mercury (IHg) species and cerebellum, one of the main targets of mercury associated with the neurological symptomatology of mercurial poisoning. Besides that, the global proteomic profile assessment is a valuable tool to screen possible biomarkers and elucidate molecular targets of mercury neurotoxicity; however, the literature is still scarce. Thus, this study aimed to investigate the effects of long-term exposure to IHg in adult rats' cerebellum and explore the modulation of the cerebellar proteome associated with biochemical and functional outcomes, providing evidence, in a translational perspective, of new mercury toxicity targets and possible biomarkers. Fifty-four adult rats were exposed to 0.375 mg/kg of HgCl2 or distilled water for 45 days using intragastric gavage. Then, the motor functions were evaluated by rotarod and inclined plane. The cerebellum was collected to quantify mercury levels, to assess the antioxidant activity against peroxyl radicals (ACAPs), the lipid peroxidation (LPO), the proteomic profile, the cell death nature by cytotoxicity and apoptosis, and the Purkinje cells density. The IHg exposure increased mercury levels in the cerebellum, reducing ACAP and increasing LPO. The proteomic approach revealed a total 419 proteins with different statuses of regulation, associated with different biological processes, such as synaptic signaling, energy metabolism and nervous system development, e.g., all these molecular changes are associated with increased cytotoxicity and apoptosis, with a neurodegenerative pattern on Purkinje cells layer and poor motor coordination and balance. In conclusion, all these findings feature a neurodegenerative process triggered by IHg in the cerebellum that culminated into motor functions deficits, which are associated with several molecular features and may be related to the clinical outcomes of people exposed to the toxicant.
Assuntos
Cerebelo/efeitos dos fármacos , Cerebelo/metabolismo , Intoxicação do Sistema Nervoso por Mercúrio/metabolismo , Mercúrio/toxicidade , Doenças Neurodegenerativas/metabolismo , Proteoma/metabolismo , Animais , Antioxidantes/metabolismo , Apoptose/efeitos dos fármacos , Biomarcadores/metabolismo , Metabolismo Energético/efeitos dos fármacos , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Compostos de Metilmercúrio/toxicidade , Córtex Motor/efeitos dos fármacos , Córtex Motor/metabolismo , Peróxidos/metabolismo , Proteômica/métodos , Células de Purkinje/efeitos dos fármacos , Células de Purkinje/metabolismo , Ratos , Ratos Wistar , Transdução de Sinais/efeitos dos fármacosRESUMO
Mercury and methyl mercury are poisonous to human body. In the recent times, exposure to mercury has been anthropogenic in nature. Within the past several decades, many incidences of mercury poisoning have been documented in several countries including Pakistan. Mercury has been ingested where it has been used to preserve crops, through the point and non-point source discharge into the surface water, and consequently entering the food chain. We conducted this scoping review of mercury and its health effects in Pakistan in order to raise the flag to a silent ongoing Minamata disease in the country. We conducted a systematic search of the available literature in Google Scholar, PubMed, and grey literature of unpublished theses and reports of various universities across the country. We found that in the northern Pakistan, suspended sediments were the major pathway of the riverine mercury transport. Sediments of Hunza and Gilgit River were found high in mercury concentrations. Gold mining leads to an increase in mercury concentration in soil and river waters flowing in this region. High concentrations up to 108 ng/L were found in Shimsal River. It is suspected that that high level of mercury transport may be leading to accumulation of mercury in major water bodies and lakes downstream. Occupational exposure to mercury and other heavy metals is common in an unregulated private sector of the country. Goldsmiths burn the amalgamated gold without personal protective measures. Direct exposure to the fumes of mercury leads to respiratory, dermatological, systemic and neurological ailments specific to mercury poisoning. We found good evidence of bioaccumulation of mercury in fish and fish products in Pakistan. The untreated waste water discharge is responsible to not only afflicted the fish but also the birds which feed on this fish. Further, the same untreated waste water from factories and agriculture runoffs affect vegetables grown in it. Studies looking at the biomarkers for mercury in humans have shown increased and even toxic levels of mercury among the most vulnerable populations of the country. Other sources of mercury exposure included mercury in traditional medicines and cigarette products. Though no evidence was found for its presence in drinking water, its existence in the food chain and occupational exposure pose great threat to the humans as well as animals.
Assuntos
Exposição Ambiental/efeitos adversos , Intoxicação do Sistema Nervoso por Mercúrio/etiologia , Mercúrio/toxicidade , Populações Vulneráveis/estatística & dados numéricos , Monitoramento Ambiental , PaquistãoRESUMO
Developmental methylmercury (MeHg) exposure can have lasting consequences on neural development and motor function across the lifespan. Recent evidence for MeHg targeting of myogenic pathways has drawn attention to the possibility that developing skeletal muscle plays a role in the motor deficits stemming from early life MeHg exposure. In this study we examined a potential role for muscle in influencing MeHg developmental toxicity in offspring of female mice exposed to MeHg via drinking water. Dams had access to 0, 0.5 or 5.0 ppm MeHg chloride in drinking water from two weeks prior to mating through weaning. Blood, brain and muscle tissue was harvested from dams at weaning and pups at postnatal days (PND) 6, 21 and 60 for analysis of total Hg. Muscle tissue sections were examined with histological stains. Behavioral testing of offspring was conducted at PND 60 and included locomotor activity, inverted screen, grip strength and rotarod tests to assess motor function. Total Hg (tHg) levels in dam muscles at weaning were 1.7-3-fold higher than Hg levels in blood or brain. In PND6 male and female pups, muscle and brain tHg levels were 2 to 4-fold higher than blood tHg. Brain tHg levels decreased more rapidly than muscle tHg levels between PND 6 and 21. Premised on modeling of growth dilution, brain tissue demonstrated an elimination of tHg while muscle tissue exhibited a net uptake of tHg between PND 6 and 21. Despite overall elevated Hg levels in developing muscle, no gross morphological or cytological phenotypes were observed in muscle at PND 60. At the higher MeHg dose, grip strength was reduced in both females and males at PND 60, whereas only male specific deficits were observed in locomotor activity and inverted screen tests with marginally significant deficits on rotarod. These findings highlight a potential role for developing skeletal muscle in mediating the neuromuscular insult of early life MeHg exposure.
Assuntos
Intoxicação do Sistema Nervoso por Mercúrio/fisiopatologia , Compostos de Metilmercúrio , Atividade Motora , Músculo Esquelético/crescimento & desenvolvimento , Efeitos Tardios da Exposição Pré-Natal , Fatores Etários , Animais , Carga Corporal (Radioterapia) , Encéfalo/metabolismo , Modelos Animais de Doenças , Feminino , Idade Gestacional , Força da Mão , Locomoção , Masculino , Exposição Materna , Intoxicação do Sistema Nervoso por Mercúrio/etiologia , Intoxicação do Sistema Nervoso por Mercúrio/metabolismo , Compostos de Metilmercúrio/sangue , Camundongos Endogâmicos C57BL , Músculo Esquelético/metabolismo , Gravidez , Teste de Desempenho do Rota-Rod , Fatores SexuaisRESUMO
Photographers and filmmakers have made important contributions to the international mental health community through documentation and social commentary, leveraging the power of visual imagery. To illustrate, this article uses the example of W. Eugene Smith who photographed the catastrophic effects of methylmercury poisoning from industrial pollution in the region around Minamata Bay, Japan. Although many art forms have been comfortably integrated into mainstream psychiatry and neuropsychiatry, photography has been underappreciated and underutilized.
Assuntos
Intoxicação do Sistema Nervoso por Mercúrio/história , Neuropsiquiatria/métodos , Fotografação/história , História do Século XX , Humanos , Japão , Compostos de Metilmercúrio/intoxicaçãoAssuntos
Desenvolvimento Infantil , Exposição Dietética/efeitos adversos , Peixes , Contaminação de Alimentos , Intoxicação do Sistema Nervoso por Mercúrio , Compostos de Metilmercúrio/efeitos adversos , Sistema Nervoso/efeitos dos fármacos , Alimentos Marinhos/efeitos adversos , Fatores Etários , Animais , Criança , Fenômenos Fisiológicos da Nutrição Infantil , Humanos , Intoxicação do Sistema Nervoso por Mercúrio/diagnóstico , Intoxicação do Sistema Nervoso por Mercúrio/epidemiologia , Intoxicação do Sistema Nervoso por Mercúrio/fisiopatologia , Sistema Nervoso/crescimento & desenvolvimento , Estado Nutricional , Valor Nutritivo , Medição de Risco , Fatores de Risco , Seicheles/epidemiologiaAssuntos
Desenvolvimento Infantil , Exposição Dietética/efeitos adversos , Peixes , Contaminação de Alimentos , Intoxicação do Sistema Nervoso por Mercúrio , Compostos de Metilmercúrio/efeitos adversos , Sistema Nervoso/efeitos dos fármacos , Alimentos Marinhos/efeitos adversos , Fatores Etários , Animais , Criança , Fenômenos Fisiológicos da Nutrição Infantil , Humanos , Intoxicação do Sistema Nervoso por Mercúrio/diagnóstico , Intoxicação do Sistema Nervoso por Mercúrio/epidemiologia , Intoxicação do Sistema Nervoso por Mercúrio/fisiopatologia , Sistema Nervoso/crescimento & desenvolvimento , Estado Nutricional , Valor Nutritivo , Medição de Risco , Fatores de Risco , Seicheles/epidemiologiaRESUMO
BACKGROUND: Studies with children exposed to methylmercury (MeHg) through fish consumption in the Brazilian Amazon region report that the high levels of hair Hg are associated with significant decreases in intelligence, memory, attention, and visuospatial processing. OBJECTIVE: To investigate the relationship between mercury exposure and neuropsychological functions in riverside communities of the Brazilian Amazon. METHOD: 263 participants aged 6 to 14 years old were assessed, from resettlement regions, near the Madeira river, Rondônia, Brazil. To assess the neuropsychological functions we used the following instruments: intelligence (WASI), working memory (Corsi Block-Tapping Task and Digit Span), verbal fluency (Word Generation - NEPSY II), inhibitory control (Inhibition Errors - NEPSY II), shifting (Trail Making Test) and manual motor dexterity (Grooved PegBoard Test). Socioeconomic status was obtained through household surveys. Total Hg levels were quantified hair samples (Total HgH) collected from the occipital region of the scalp and analyzed by Cold Vapor Atomic Absorption Spectrometry. RESULTS: The group in the upper quartile of Total HgH levels presented lower scores on the tasks that assessed estimated IQ, visuospatial working memory, semantic knowledge and phonological verbal fluency, when compared to the group in the lower quartile level. A regression analysis controlled for age, sex, and maternal education showed that for each increase of 10⯵g/g of Total HgH, there was a decrease around half standard deviation in Verbal IQ, estimated IQ scores, semantic knowledge, phonological verbal fluency and for verbal and visuospatial working memory. CONCLUSIONS: High concentrations of Total Hg in hair were associated with a lower performance in neuropsychological functions tests. The results show that environmental exposure to Hg is associated to children and adolescents' lower neuropsychological performance in the riverine and resettled areas of the Brazilian Amazon region.