Neurological and Neurocognitive Impairments in Adults with a History of Prenatal Methylmercury Poisoning: Minamata Disease.

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.

Latent effects of early-life methylmercury exposure on motor function in Drosophila.

The developmental toxicant, methylmercury (MeHg), can elicit motor deficits that last well into adulthood. Recent studies using Drosophila showed that the developing musculature is sensitive to high doses of MeHg, where a larval feeding paradigm resulted in compromised myotendinous junction (MTJ) formation during development, by a mechanism involving the NG2 homologue, kon-tiki (kon). Low-dose exposures to MeHg that do not produce muscle pathology during development, nevertheless result in impaired flight behavior later in adult life. The present study evaluated the potential for relatively low-dose exposure to produce latent adult muscle pathology and motor impairments, as assayed by climbing and flight, as well as to evaluate molecular mechanisms that may contribute to motor deficits. Wildtype larvae were fed 0, 2, 2.5, or 5 µM MeHg laden food until eclosion. The effect of 5 µM MeHg on MTJ-related gene expression during pupal development was assessed via quantitative RT-qPCR analysis. Upon eclosion, adults were transferred to standard food bottles for 4, 11, or 30 days prior to motor testing. Survivorship (%) was determined from a subset of 200 flies per treatment. Average climbing speed (cm/s) was quantified 4-days post-eclosion (PE). Flight ability was assayed 11- or 30-days PE by measuring landing height (cm) of flies dropped into an adhesive-lined vertical column. In parallel, total body mercury was measured to estimate the influence of residual MeHg at the time of motor testing. Muscle morphology was assessed using immuno-fluorescence microscopy. Exposure to 5uM MeHg significantly reduced climbing speed, and flight ability 4 and 11 - days PE, respectively. While age-related flight deficits were seen in each sex, flight deficits due to MeHg persisted to 30-day PE timepoints exclusively in males. Expression of kon was upregulated across the window of pupal development essential to establishing adult MTJ. However, experimentally restricting the induction of comparable levels of kon to muscle during the same periods did not recapitulate the flight deficits, indicating that muscle-specific induction of kon alone is not sufficient to contribute to latent flight impairments. Adult flight muscle morphology of 11-day PE flies treated with 5 µM MeHg was indistinct from controls, implying muscle structure is not grossly perturbed to impair flight. Collectively, the current data suggest that developmental exposure to 5 µM MeHg reduces flight ability in each sex at 11 day-PE and that latent deficits at 30-day PE are male-specific. It remains to be determined whether the developing MTJ of Drosophila is a sensitive target of MeHg, and whether or not kon acts in conjunction with additional MTJ factors to constitute a MeHg target.

Photography's Underappreciated Contributions to Neuropsychiatry: The Photographs of W. Eugene Smith in Minamata, Japan.

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.

Methylmercury Poisoning Induces Cardiac Electrical Remodeling and Increases Arrhythmia Susceptibility and Mortality.

This study aims to investigate the cardiac electrical remodeling associated with intoxication by methylmercury (MeHg). We evaluated the chronic effects of MeHg on in vivo electrocardiograms and on ex vivo action potentials and depolarizing (ICa-L) and repolarizing (Ito) currents. The acute effect of MeHg was evaluated on HEK293 cells expressing human ERG, Kv4.3 and KCNQ1/KCNE1 channels. Chronic MeHg treatment increased QTc and Tpeak-Tend interval duration, prolonged action potential duration and decreased amplitude of Ito and ICa-L. In addition, heterologously expressed IhKv4.3, IhERG or IhKCNQ1/KCNE1 decreased after acute exposure to MeHg at subnanomolar range. The introduction of the in vitro effects of MeHg in a computer model of human ventricular action potentials triggered early afterdepolarizations and arrhythmia. In conclusion, cardiac electrical remodeling induced by MeHg poisoning is related to the reduction of Ito and ICa-L. The acute effect of MeHg on hKv4.3; hERG and hKCNQ1/KCNE1 currents and their transposition to in silico models show an association between MeHg intoxication and acquired Long QT Syndrome in humans. MeHg can exert its high toxicity either after chronic or acute exposure to concentrations as low as picomolar.

Mercury Involvement in Neuronal Damage and in Neurodegenerative Diseases.

Neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis are characterized by a chronic and selective process of neuronal cell death. Although the causes of neurodegenerative diseases remain still unknown, it is now a well-established idea that more factors, such as genetic, endogenous, and environmental, are involved. Among environmental causes, the accumulation of mercury, a heavy metal considered a toxic agent, was largely studied as a probable factor involved in neurodegenerative disease course. Mercury exists in three main forms: elemental mercury, inorganic mercury, and organic mercury (methylmercury and ethylmercury). Sources of elemental mercury can be natural (volcanic emission) or anthropogenic (coal-fired electric utilities, waste combustion, hazardous-waste incinerators, and gold extraction). Moreover, mercury is still used as an antiseptic, as a medical preservative, and as a fungicide. Dental amalgam can emit mercury vapor. Mercury vapor, being highly volatile and lipid soluble, can cross the blood-brain barrier and the lipid cell membranes and can be accumulated into the cells in its inorganic forms. Also, methylmercury can pass through blood-brain and placental barriers, causing serious damage in the central nervous system. This review describes the toxic effects of mercury in cell cultures, in animal models, and in patients with neurodegenerative diseases. In vitro experiments showed that mercury exposure was principally involved in oxidative stress and apoptotic processes. Moreover, motor and cognitive impairment and neural loss have been confirmed in various studies performed in animal models. Finally, observational studies on patients with neurodegenerative diseases showed discordant data about a possible mercury involvement.

[Mercury as a Global Pollutant and Mercury Exposure Assessment and Health Effects].

Mercury and its compounds are classified into three main groups: metallic mercury (Hg0), inorganic mercury (Hg2+), and organic mercury (methyl mercury: CH3Hg+, etc.). Metallic mercury is the only metal that is liquid at ambient temperature and normal pressure, which readily forms an amalgam with other metals. Therefore, mercury has long been used for refining various metals, and mercury amalgam has been used for dental treatment. Mercury has also been used in measuring instruments such as thermometers, barometers and blood pressure monitors, as well as electric appliances such as lighting equipment and dry batteries. Large amounts of metallic mercury are still used in other countries as a catalyst in the production of caustic soda by electrolysis. In addition, mercury compounds have been used in various chemicals such as mercurochrome, agricultural chemicals, and mildew-proofing agents. However, the use of mercury has also caused health problems for people. Minamata disease in Japan is a typical example. Also, since mercury is highly volatile, it is discharged as a product of industrial activities or derived from volcanoes, and it has been concluded on the basis of the findings of the United Nations Environment Program (UNEP) that it is circulating globally. Therefore, with the aim of establishing an internationally legally binding treaty for the regulation of mercury use to reduce risk, an intergovernmental negotiating committee was established in 2009. Japan actively contributed to this negotiation owing to its experience with Minamata disease, which led to the Convention on the regulation of mercury use being discharged as the "Minamata Convention on Mercury" and the treaty came into force on August 16, 2017. In this review, we introduce 1) the Global Mercury Assessment by UNEP; 2) mercury kinetics, exposure assessment and toxicity of different chemical forms; 3) large-scale epidemics of methylmercury poisoning; 4) methylmercury exposure assessment and health survey in whale-eating populations; 5) elemental mercury exposure assessment and health survey of mercury mine workers in China.

Effects of Prenatal Methylmercury Exposure: From Minamata Disease to Environmental Health Studies.

Methylmercury, the causative agent of Minamata disease, can easily penetrate the brain, and adult-type Minamata disease patients showed neurological symptoms according to the brain regions where the neurons, mainly in the cerebrum and cerebellum, were damaged. In addition, fetuses are exposed to methylmercury via the placenta from maternal fish consumption, and high-level exposure to methylmercury causes damage to the brains of infants. Typical patients with fetal-type Minamata disease (i.e., serious poisoning caused by in utero exposure to methylmercury) were born during the period of severe methylmercury pollution in 1955-1959, although they showed no abnormality during gestation nor at delivery. However, they showed difficulties in head control, sitting, and walking, and showed disturbances in mental development, these symptoms that are similar to those of cerebral palsy, during the growth periods after birth. The impaired development of fetal-type Minamata disease patients was one of the most tragic and characteristic feature of Minamata disease. In this review, we first summarize 1) the effects of prenatal methylmercury exposure in Minamata disease. Then, we introduce the studies that were conducted mainly by Sakamoto et al. as follows: 2) a retrospective study on temporal and regional variations of methylmercury pollution in Minamata area using preserved umbilical cord methylmercury, 3) decline in male sex ratio observed in Minamata area, 4) characteristics of hand tremor and postural sway in fetal-type Minamata disease patients, 5) methylmercury transfer from mothers to infants during gestation and lactation (the role of placenta), 6) extrapolation studies using rat models on the effects of prenatal methylmercury exposure on the human brain, and 7) risks and benefits of fish consumption.

Methylmercury-Induced Neurotoxicity: Focus on Pro-oxidative Events and Related Consequences.

Methylmercury (MeHg) is a highly neurotoxic environmental pollutant. Even though molecular mechanisms mediating MeHg toxicity are not completely understood, several lines of evidence indicate that the neurotoxic effects resultant from MeHg exposure represent a consequence of its pro-oxidative properties. In this regard, MeHg is a soft electrophile that preferentially interacts with (and oxidize) nucleophilic groups (mainly thiols and selenols) from biomolecules, including proteins and low-molecular-weight molecules. Such interaction contributes to the occurrence of oxidative stress and impaired function of several molecules [proteins (receptors, transporters, enzymes, structural proteins), lipids (i.e., membrane constituents and intracellular messengers), and nucleic acids (i.e., DNA)], culminating in neurotoxicity.In this chapter, an initial background on the general aspects regarding the neurotoxicology of MeHg, with a particular focus on its pro-oxidative properties and its interaction with nucleophilic thiol- and selenol-containing molecules, is provided. Even though experimental evidence indicates that symptoms (i.e., motor impairment) resultant from MeHg exposure are linked to its pro-oxidative properties, as well as to their molecular consequences (lipid peroxidation, disruption of glutamate and/or calcium homeostasis, etc.), data concerning the relationship between molecular parameters and behavioral impairment others that those related to the motor function (i.e., visual impairment, cognitive skills, etc.) are scarce. Thus, even though scientific research has provided a significant amount of knowledge concerning the mechanisms mediating MeHg-induced neurotoxicity in the last decades, the whole scenario is far from being completely understood, and further research in this area is well warranted.

The blood of my veins - mercury, Minamata and the soul of Japan.

The methylmercury contamination of Minamata Bay during the WWII postwar period resulted in thousands of Japanese citizens suffering horrific neurological injury. Fear and miscommunication destroyed and changed family and social structure. In addition, the Minamata poisoning caused momentous changes in the civic discourse in Japan and was an instrumental event in the democratization of the country. This manuscript describes the effects that the environmental contamination and human poising had in the transition of Japan from a feudal society to a democratic one.

Finding vulnerable subpopulations in the Seychelles Child Development Study: effect modification with latent groups.

The Seychelles Child Development Study is a research project with the objective of examining associations between prenatal exposure to low doses of methylmercury from maternal fish consumption and children's developmental outcomes. Whether methylmercury has neurotoxic effects at low doses remains unclear and recommendations for pregnant women and children to reduce fish intake may prevent a substantial number of people from receiving sufficient nutrients that are abundant in fish. The primary findings of the Seychelles Child Development Study are inconsistent with adverse associations between methylmercury from fish consumption and neurodevelopmental outcomes. However, whether there are subpopulations of children who are particularly sensitive to this diet is an open question. Secondary analysis from this study found significant interactions between prenatal methylmercury levels and both caregiver IQ and income on 19-month IQ. These results are sensitive to the categories chosen for these covariates and are difficult to interpret collectively. In this paper, we estimate effect modification of the association between prenatal methylmercury exposure and 19-month IQ using a general formulation of mixture regression. Our mixture regression model creates a latent categorical group membership variable which interacts with methylmercury in predicting the outcome. We also fit the same outcome model when in addition the latent variable is assumed to be a parametric function of three distinct socioeconomic measures. Bayesian methods allow group membership and the regression coefficients to be estimated simultaneously and our approach yields a principled choice of the number of distinct subpopulations. The results show three groups with different response patterns between prenatal methylmercury exposure and 19-month IQ in this population.

Elevated mercury bound to serum proteins in methylmercury poisoned rats after selenium treatment.

Methylmercury is a toxic pollutant and is generated by microbial methylation of elemental or inorganic mercury in the environment. Previous study found decreased hepatic MDA levels and urinary mercury levels in methylmercury poisoned rats after sodium selenite treatment. This study further found increased mercury levels in serum samples from methylmercury poisoned rats after selenium treatment. By using size exclusion chromatography coupled to inductively coupled plasma mass spectrometry, three Hg- binding protein fractions and two Se-binding protein fractions were identified with the molecular weight of approximately 21, 40, and 75 kDa and of 40 and 75 kDa, respectively. Elevated mercury level in the 75 kDa protein fraction was found binding with both Hg and Se, which may explain the decreased urinary Hg excretion in MeHg poisoned rats after Se treatment. MALDI-TOF-MS analysis of the serum found that the 75 kDa protein fractions were albumin binding with both Hg and Se and the 21 kDa fraction was Hg- binding metallothionein.

Heavy metal chelator TPEN attenuates fura-2 fluorescence changes induced by cadmium, mercury and methylmercury.

Stimulation with heavy metals is known to induce calcium (Ca(2+)) mobilization in many cell types. Interference with the measurement of intracellular Ca(2+) concentration by the heavy metals in cells loaded with Ca(2+) indicator fura-2 is an ongoing problem. In this study, we analyzed the effect of heavy metals on the fura-2 fluorescence ratio in human SH-SY5Y neuroblastoma cells by using TPEN, a specific cell-permeable heavy metal chelator. Manganese chloride (30-300 µM) did not cause significant changes in the fura-2 fluorescence ratio. A high concentration (300 µM) of lead acetate induced a slight elevation in the fura-2 fluorescence ratio. In contrast, stimulation with cadmium chloride, mercury chloride or MeHg (3-30 µM) elicited an apparent elevation of the fura-2 fluorescence ratio in a dose-dependent manner. In cells stimulated with 10 or 30 µM cadmium chloride, the addition of TPEN decreased the elevated fura-2 fluorescence ratio to basal levels. In cells stimulated with mercury or MeHg, the addition of TPEN significantly decreased the elevation of the fura-2 fluorescence ratio induced by lower concentrations (10 µM) of mercury or MeHg, but not by higher concentrations (30 µM). Pretreatment with Ca(2+) channel blockers, such as verapamil, 2-APB or lanthanum chloride, resulted in different effects on the fura-2 fluorescence ratio. Our study provides a characterization of the effects of several heavy metals on the mobilization of divalent cations and the toxicity of heavy metals to neuronal cells.

Epidemiological studies of neurological signs and symptoms and blood pressure in populations near the industrial methylmercury contamination at Minamata, Japan.

Severe methylmercury exposure occurred in Minamata, Japan. Only a limited number of epidemiological studies related to that exposure have been carried out. The evidence that methylmercury is cardiotoxic is very limited, and these studies provide only minimal support for that hypothesis. We therefore analyzed the data both from an investigation in Minamata and neighboring communities in 1971 and an investigation in 1974 in another area simultaneously. We included a total of 3,751 participants. We examined the association of residential area with neurological signs or blood pressure using logistic regression or multiple linear regression models, adjusting for sex and age. We found that the prevalence of neurological signs and symptoms was elevated in the Minamata area (high-exposure), followed by the Goshonoura area (medium-exposure). Moreover, blood pressure was elevated in residents of the Minamata area.

Neurological and neurocognitive functions from intrauterine methylmercury exposure.

In the 1950s, large-scale food poisoning caused by methylmercury was identified in Minamata, Japan. Although severe intrauterine exposure cases (ie, congenital Minamata disease patients) are well known, possible impacts of methylmercury exposure in utero among residents, which is likely at lower levels than in congenital Minamata disease patients, are rarely explored. In 2014, the authors examined neurological and neurocognitive functions among 18 exposed participants in Minamata, focusing on fine motor, visuospatial construction, and executive functions. More than half of the participants had some fine motor and coordination difficulties. In addition, several participants had lower performance for neurocognitive function tests (the Rey-Osterrieth Complex Figure test and Keio version of the Wisconsin card sorting test). These deficits imply diffuse brain damage. This study suggests possible neurological and neurocognitive impacts of prenatal exposure to methylmercury among exposed residents of Minamata.

Selenium Health Benefit Values: Updated Criteria for Mercury Risk Assessments.

Selenium (Se)-dependent enzymes (selenoenzymes) protect brain tissues against oxidative damage and perform other vital functions, but their synthesis requires a steady supply of Se. High methylmercury (CH3Hg) exposures can severely diminish Se transport across the placenta and irreversibly inhibit fetal brain selenoenzymes. However, supplemental dietary Se preserves their activities and thus prevents pathological consequences. The modified Se health benefit value (HBVSe) is a risk assessment criterion based on the molar concentrations of CH3Hg and Se present in a fish or seafood. It was developed to reflect the contrasting effects of maternal CH3Hg and Se intakes on fetal brain selenoenzyme activities. However, the original equation was prone to divide-by-zero-type errors whereby the calculated values increased exponentially in samples with low CH3Hg contents. The equation was refined to provide an improved index to better reflect the risks of CH3Hg exposures and the benefits provided by dietary Se. The HBVSe provides a biochemically based perspective that confirms and supports the FDA/EPA advice for pregnant and breast-feeding women regarding seafoods that should be avoided vs. those that are beneficial to consume. Since Se can be highly variable between watersheds, further evaluation of freshwater fish is needed to identify locations where fish with negative HBVSe may arise and be consumed by vulnerable subpopulation groups.

Mercury in Hazel Bolete Leccinum griseum and soil substratum: Distribution, bioconcentration and dietary exposure.

This study aimed to examine the accumulation and distribution of total mercury (Hg) in fruiting bodies of edible wild-grown mushroom Hazel Bolete Leccinum griseum (Quél.) Singer, collected from six spatially distantly distributed places across Poland and to assess the probable dietary intake of the element by consumers. Mercury content of fungal and soil samples were determined by cold-vapour atomic absorption spectroscopy (CV-AAS) with a direct sample thermal decomposition coupled with gold wool trap of Hg and its further desorption and quantitative measurement at the wavelength of 296 nm. The median values of Hg content in caps of L. griseum collected from less-contaminated places (< 0.10 mg Hg kg(-1) dry matter in upper 0-10 cm layer of soil substratum) were from 0.23 mg kg(-1) dm to 0.43 mg kg(-1) dm. And for more contaminated topsoil (0.15 mg Hg kg(-1) dry matter), the median in caps was about 1.5 mg kg(-1) dry matter. The mushroom L. griseum has potential to accumulate Hg in fruiting bodies, while quantities of this element noted in consignments of this species originating from the forests with typical background values of Hg in topsoil are low. In the light of the published value of PTWI for Hg consumption of fruiting bodies of L. griseus emerged in forests of Poland is without health risk for consumers. Information on total mercury and methylmercury in Fungi of the genus Leccinum is also described briefly.

Documento de consenso sobre la prevención de la exposición al metilmercurio en España / Consensus document on the prevention of exposure to methylmercury in Spain

Los efectos beneficiosos del consumo de pescado tanto en niños como en adultos han sido bien reconocidos. Sin embargo, la ingesta de metilmercurio principalmente a través del pescado y marisco contaminado puede producir efectos adversos en la salud. El grupo de estudio para la prevención de la exposición al metilmercurio (GEPREM-Hg), constituido por representantes de diferentes sociedades científicas españolas, ha elaborado un documento de consenso donde se recogen en forma de preguntas y respuestas las principales conclusiones, recomendaciones y propuestas planteadas en el grupo. El objetivo del documento es profundizar en el conocimiento de los factores asociados a la exposición almetilmercurio, los posibles efectos sobre la salud en la población española, los métodos de análisis, la interpretación de los resultados, el coste económico y establecer finalmente recomendaciones de consumo de pescados y mariscos. El grupo considera acertadas todas las iniciativas encaminadas a reducir o prohibir el uso del mercurio y la necesidad de conocer los resultados de los análisis de contaminantes que se realizan en los pescados y mariscos que se comercializan en España. Además, opina que se deberían establecer sistemas de biomonitorización para conocer la evolución de la exposicional metilmercurio en niños y adultos y realizar estudios diseñados para conocer los posibles efectos sobre la salud de las concentraciones halladas en la población española, teniendo en cuenta el estilo de vida, los patrones de consumo alimentarios y la dieta mediterránea (AU)

The beneficial effects of fish consumption in both children and adults are well known. However, the intake of methyl mercury, mainly from contaminated fish and shellfish, can have adverse health effects. The study group on the prevention of exposure to methyl mercury (GEPREM-Hg), made up of representatives from different Spanish scientific societies, has prepared a consensus document in a question and answer format, containing the group's main conclusions, recommendations and proposals. The objective of the document is to provide broader knowledge of factors associated with methyl mercury exposure, its possible effects on health among the Spanish population, methods of analysis, interpretation of the results and economic costs, and to then set recommendations for fish and shellfish consumption. The group sees the merit of all initiatives aimed at reducing or prohibiting the use of mercury as well as the need to be aware of the results of contaminant analyses performed on fish and shellfish marketed in Spain. In addition, the group believes that biomonitoring systems should be set up in order to follow the evolution of methyl mercury exposure in children and adults and perform studies designed to learn more about the possible health effects of concentrations found in the Spanish population, taking into account the lifestyle, eating patterns and the Mediterranean diet (AU)

[The effects of methylmercury on health in children and adults; national and international studies]. / Efectos sobre la salud del metilmercurio en niños y adultos; estudios nacionales e internacionales.

The benefit of fish consumption in children and adults is well-known. However, it has been pointed out that excessive methylmercury intake due to consumption of contaminated fish leads to neurological toxicity in children, affecting cognitive function, memory, visual-motor function and language. After the intoxications in Minamata and Iraq, wide-ranging epidemiological studies were carried out in New Zealand, the Faroe Islands and the Seychelles and international recommendations were established for fish consumption in pregnant women and small children. In Spain, the Childhood and Environmental project (INMA, its Spanish acronym) has studied the effects of diet and the environment on fetal and childhood development in different geographic areas of Spain. National and international sudies have demonstrated that mercury concentrations are mainly dependent on fish consumption, although there are variations among countries which can be explained not only by the levels of fish consumption, but also by the type or species of fish that is consumed, as well as other factors. Although the best documented adverse effects of methylmercury are the effects on nervous sytem development in fetuses and newborns, an increasing number of studies indicate that cognitive function, reproduction and, especially, cardiovascular risk in the adult population can also be affected. However, more studies are necessary in order to confirm this and establish the existance of a causal relationship.

Los efectos beneficiosos del consumo de pescado tanto en niños como en adultos han sido bien reconocidos. Sin embargo, se ha referido que la ingesta excesiva de metilmercurio procedente del pescado contaminado produce toxicidad neurológica en los niños afectando a la función cognitiva, la memoria, la función visual-motora y al lenguaje. Después de las intoxicaciones de Minamata e Iraq, se realizaron grandes estudios epidemiológicos en Nueva Zelanda, las islas Féroe y las islas Seychelles y se establecieron recomendaciones internacionales sobre el consumo de pescado y marisco en las mujeres embarazadas y niños pequeños. En España, el proyecto Infancia y Medio Ambiente (INMA) ha estudiado los efectos del medio ambiente y de la dieta sobre el desarrollo fetal e infantil en diversas zonas geográficas de España. Los estudios realizados nacionales e internacionales muestran que la concentración de mercurio depende principalmente del consumo de pescado, aunque existe una variabilidad entre los países que podría explicarse no solo por la cantidad de pescado consumida, sino también por el tipo o especies de pescados que se consumen, así como por otro tipo de factores. Aunque los efectos perjudiciales del metilmercurio mejor documentados son los que se producen sobre el desarrollo del sistema nervioso en el feto y en el recién nacido, cada vez hay más estudios que indican que también puede afectar a la función cognitiva, reproducción y especialmente al riesgo cardiovascular en la población adulta. Sin embargo, son necesarios más estudios para confirmarlo y establecer la existencia de una relación causal.

Efectos sobre la salud del metilmercurio en niños y adultos; estudios nacionales e internacionales / The effects of methyl mercury on health in children and adults, national and international studies

Los efectos beneficiosos del consumo de pescado tanto en niños como en adultos han sido bien reconocidos. Sin embargo, se ha referido que la ingesta excesiva de metilmercurio procedente del pescado contaminado produce toxicidad neurológica en los niños afectando a la función cognitiva, la memoria, la función visual-motora y al lenguaje. Después de las intoxicaciones de Minamata e Iraq, se realizaron grandes estudios epidemiológicos en Nueva Zelanda, las islas Féroe y las islas Seychelles y se establecieron recomendaciones internacionales sobre el consumo de pescado y marisco en las mujeres embarazadas y niños pequeños. En España, el proyecto Infancia y Medio Ambiente (INMA) ha estudiado los efectos del medio ambiente y de la dieta sobre el desarrollo fetal e infantil en diversas zonas geográficas de España. Los estudios realizados nacionales e internacionales muestran que la concentración de mercurio depende principalmente del consumo de pescado, aunque existe una variabilidad entre los países que podría explicarse no solo por la cantidad de pescado consumida, sino también por el tipo o especies de pescados que se consumen, así como por otro tipo de factores. Aunque los efectos perjudiciales del metilmercurio mejor documentados son los que se producen sobre el desarrollo del sistema nervioso en el feto y en el recién nacido, cada vez hay más estudios que indican que también puede afectar a la función cognitiva, reproducción y especialmente al riesgo cardiovascular en la población adulta. Sin embargo, son necesarios más estudios para confirmarlo y establecer la existencia de una relación causal (AU)

The benefit of fish consumption in children and adults is well-known. However, it has been pointed out that excessive methylmercury intake due to consumption of contaminated fish leads to neurological toxicity in children, affecting cognitive function, memory, visual-motor function and language. After the intoxications in Minamata and Iraq, wide-ranging epidemiological studies were carried out in New Zealand, the Faroe Islands and the Seychelles andinternational recommendations were established for fish consumption in pregnant women and small children. In Spain, the Childhood and Environmental project (INMA, its Spanish acronym) has studied the effects of diet and the environment on fetal and childhood development in different geographic areas of Spain. National and international sudies have demonstrated that mercury concentrations are mainly dependent on fish consumption, although there are variations among countries which can be explained not only by the levels of fish consumption, but also by the type or species of fish that is consumed, as well as other factors. Although the best documented adverse effects of methylmercury are the effects on nervous sytem development in fetuses and newborns, an increasing number of studies indicate that cognitive function, reproduction and, especially, cardiovascular risk in the adult population can also be affected. However, more studies are necessary in order to confirm this and establish the existance of a causal relationship (AU)