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A 17-year-old boy was referred after jumping from a ladder onto the ground, crushing a medical thermometer with his right foot. Some days later, he complained of loss of appetite and weakness. A radiograph of the affected foot demonstrated radiopaque densities. Blood and 24-h urine assays for mercury demonstrated toxic levels. Chelation therapy cured the patient dramatically.

Contamination with mercury is a real health issue for humans with physiological consequences. The main objective of the present study was to assess the neurotoxicological effect of inorganic mercury: HgCl 2 . For this, adult mice were exposed prenatally, postnatally, and during the adult period to a low level of the metal, and their behavior and antioxidant status were analyzed. First, we showed that mercury concentrations in brain tissue of treated animals showed significant bioaccumulation, which resulted in behavioral deficits in adult mice. Thus, the treated mice developed an anxiogenic state, as evidenced by open field and elevated plus maze tests. This anxiety-like behavior was accompanied by a decrease in social behavior. Furthermore, an impairment of memory in these treated mice was detected in the object recognition and Y-maze tests. The enzymatic activity of the antioxidant system was assessed in eight brain structures, including the cerebral cortex, olfactory bulb, hippocampus, hypothalamus, mesencephalon, pons, cerebellum, and medulla oblongata. The results show that chronic exposure to HgCl 2 caused alterations in the activity of catalase, thioredoxin reductase, glutathione peroxidase, superoxide dismutase, and glutathione S-transferase, accompanied by peroxidation of membrane lipids, indicating a disturbance in intracellular redox homeostasis with subsequent increased intracellular oxidative stress. These changes in oxidative stress were concomitant with a redistribution of essential heavy metals, i.e., iron, copper, zinc, and magnesium, in the brain as a possible response to homeostatic dysfunction following chronic exposure. The alterations observed in overall oxidative stress could constitute the basis of the anxiety-like state and the neurocognitive disorders observed.

The Brazilian Amazon is known to be a region with high levels of mercury (Hg) in the environment and studies point to an association between high levels of natural mercury in the mother rock and the vast number of clandestine gold mines. Other studies already report the contamination of fish in this region, as well as high levels of Hg in biological material from environmentally exposed populations. On the other hand, this is one of the least developed regions of the planet and it is necessary to understand the vulnerability factors in these populations that may be intoxicated by this element. The purpose of the present study was to investigate the vulnerability factors in communities from Xingu River-Amazon basin probably exposed to Hg. A cross-selection study in two cities localized in Xingu River was conducted, and the sample contained was 268 individuals. sociodemographic questions, lifestyle, diet habits and health conditions were collated. The majority of the sample was female, between 30 and 59 years old, had less than 3 years of educational level and lived in the local of study more than 240 months. There was regular fish consumption (95.9%), principally carnivorous species (80.5%). The visual problem has a highest prevalence (43.3%) between the health problems and about the symptoms of Hg intoxication, memory loss (42.9%), weakness (35.1%), fatigue (34.3%), mood changes (28.7%) and difficulties in concentration (27.2%) was most reported. The female sex, age over 60, educational level below 3 years of study, did not had flush toilet, smoke and least one chronic non-communicable disease represent higher probability to had symptoms of Hg intoxication. Lack of access to health services, low education level and income evidence the susceptibility of this community to diseases and injuries. The vulnerable groups identified in this study should be a priority in public health and environmental health policies.

Introduction: There is increasing evidence that the pathophysiological target of mercury is in fact selenium, rather than the covalent binding of mercury to sulfur in the body's ubiquitous sulfhydryl groups. The role of selenium in mercury poisoning is multifaceted, bidirectional, and central to understanding the target organ toxicity of mercury., Methods: An initial search was performed using Medline/PubMed, Toxline, Google Scholar, and Google for published work on mercury and selenium. These searches yielded 2018 citations. Publications that did not evaluate selenium status or evaluated environmental status (e.g., lake or ocean sediment) were excluded, leaving approximately 500 citations. This initial selection was scrutinized carefully and 117 of the most relevant and representative references were selected for use in this review. Binding of mercury to thiol/sulfhydryl groups: Mercury has a lower affinity for thiol groups and higher affinity for selenium containing groups by several orders of magnitude, allowing for binding in a multifaceted way. The established binding of mercury to thiol moieties appears to primarily involve the transport across membranes, tissue distribution, and enhanced excretion, but does not explain the oxidative stress, calcium dyshomeostasis, or specific organ injury seen with mercury. Effects of mercury on selenium and the role this plays in the pathophysiology of mercury toxicity: Mercury impairs control of intracellular redox homeostasis with subsequent increased intracellular oxidative stress. Recent work has provided convincing evidence that the primary cellular targets are the selenoproteins of the thioredoxin system (thioredoxin reductase 1 and thioredoxin reductase 2) and the glutathione-glutaredoxin system (glutathione peroxidase). Mercury binds to the selenium site on these proteins and permanently inhibits their function, disrupting the intracellular redox environment. A number of other important possible target selenoproteins have been identified, including selenoprotein P, K, and T. Impairment of the thioredoxin and glutaredoxin systems allows for proliferation intracellular reactive oxygen species which leads to glutamate excitosis, calcium dyshomeostasis, mitochondrial injury/loss, lipid peroxidation, impairment of protein repair, and apoptosis. Methylmercury is a more potent inhibitor of the thioredoxin system, partially explaining its increased neurotoxicity. A second important mechanism is due to the high affinity of mercury for selenium and the subsequent depletion of selenium stores needed for insertion into de novo generation of replacement selenoproteins. This mercury-induced selenium deficiency state inhibits regeneration of the selenoproteins to restore the cellular redox environment. The effects of selenium on mercury and the role this plays in biological response to mercury: Early research suggested selenium may provide a protective role in mercury poisoning, and with limitations this is true. The roles selenium plays in this reduction of mercury toxicity partially depends on the form of mercury and may be multifaceted including: 1) facilitating demethylation of organic mercury to inorganic mercury; 2) redistribution of mercury to less sensitive target organs; 3) binding to inorganic mercury and forming an insoluble, stable and inert Hg:Se complex; 4) reduction of mercury absorption from the GI tract; 5) repletion of selenium stores (reverse selenium deficiency); and 6) restoration of target selenoprotein activity and restoring the intracellular redox environment. There is conflicting evidence as to whether selenium increases or hinders mercury elimination, but increased mercury elimination does not appear to be a major role of selenium. Selenium supplementation has been shown to restore selenoprotein function and reduce the toxicity of mercury, with several significant limitations including: the form of mercury (methylmercury toxicity is less responsive to amelioration) and mercury dose., Conclusions: The interaction with selenium is a central feature in mercury toxicity. This interaction is complex depending on a number of features such as the form of mercury, the form of selenium, the organ and dose. The previously suggested "protective effect" of selenium against mercury toxicity may in fact be backwards. The effect of mercury is to produce a selenium deficiency state and a direct inhibition of selenium's role in controlling the intracellular redox environment in organisms. Selenium supplementation, with limitations, may have a beneficial role in restoring adequate selenium status from the deficiency state and mitigating the toxicity of mercury.

Egg turning behavior is an important determinant of egg hatchability, but it remains relatively understudied. Here, we examined egg turning rates and egg temperatures in Forster's terns (Sterna forsteri). We used artificial eggs containing a data logger with a 3-D accelerometer, a magnetometer, and a temperature thermistor to monitor parental incubation behavior of 131 tern nests. Overall, adults turned their eggs an average (±SD) of 3.8 ± 0.8 turns h-1, which is nearly two times higher than that of other seabirds. Egg turning rates increased with nest initiation date. We also examined egg turning rates and egg temperatures in relation to egg mercury contamination. Mercury contamination has been shown to be associated with reduced egg hatchability, and we hypothesized that mercury may decrease egg hatchability via altered egg turning behavior by parents. Despite the high variability in egg turning rates among individuals, the rate of egg turning was not related to mercury concentrations in sibling eggs. These findings highlight the need for further study concerning the potential determinants of egg turning behavior.

Mercury intoxication is a serious public health problem and a worldwide concern. The Minamata Convention on Mercury has been signed by 128 countries and endorsed by the World Health Organization with the recommendation of promoting the management of epidemiological information. The Central Nervous System is the main target organ for mercury. Symptoms of intoxication include altered motor coordination, visual and tactile dysfunction and paralysis, caused by neurodegeneration with a key role for oxidative damage. Recently, some studies have demonstrated a correlation between mercury intoxication and isoforms of apolipoprotein E (ApoE). In this review, epidemiological data and hypotheses about the possible molecular mechanisms underlying the association between ApoE and mercury intoxication are assessed. Based on the evidence and the neuropathological changes that the presence of ApoE4 and mercury neurotoxicity have in common, we propose a convergent action of both factors. ApoE4 seems to potentiate the damage caused by mercury. Increased knowledge of this interaction using epidemiological and pre-clinical studies is essential to improve prevention strategies to adequately manage intoxicated patients.

Objectives: The aim of this study was to evaluate the possible roles of endothelin-1 and angiotensin-II in urotensin-II vasoconstriction and in endothelial dysfunction induced by mercury., Background: Urotensin-II, the most potent vasoactive peptide, is entwined with the cardiovascular diseases and has been labelled as a new pathophysiological biomarker., Methods: Rat aortic rings were pre-incubated with sb-710411, bq-123, and captopril. Doses of human urotensin-II with increased concentrations were applied in all groups in the presence or absence of mercury chloride. In another set of the experiment, aortic rings were treated with a single dose of mercury chloride in the presence of each of the above blockers., Results: Angiotensin-II and endothelin-1 mediated the vascular responses to the peptide urotensin-II under conditions of both intact endothelium and endothelial impairments induced by mercury. Urotensin-II, angiotensin-II and endothelin-1 significantly participated in vascular responses to mercury chloride., Conclusion: The novel finding was that urotensin-II is potentiated under the condition of endothelial dysfunction. Endothelin-1 and angiotensin-II pathways could be heavily exploited in modulating endothelial dysfunction impacts and peptide vascular actions (Tab. 1, Fig. 4, Ref. 30).

The article deals with frequency data on polymorphism of candidate genes participating in endothelial dysfunction (EDN1 Lys198Asn, NOS3 T786C, AGT Thrl74Met and AGT Met23SThr) in totality with concentrations of their active substances in individuals exposed to mercury. Findings are changes in levels of nitrogen oxide, endothelin-1, angiotensin II metabolites in examinees including those without cardiovascular diseases. The genetic conditionality is connected with unfavorable genotypes of polymorphic variants - Met235Thr of AGT gene and Lys198Asn of EDNI gene. Changes in levels of biochemical markers of endothelial dysfunction in individuals exposed to mercury indicate serious endothelial function disorders and are not genetically determined processes.

The growth of the influence of anthropogenic factors aimed on the improvement of human life has its side effect, for example, living organisms receive increasing exposure to toxic mercuric compounds. Experimental data show that mercury (Hg) salts are able to induce systemic autoimmunity in rodents. This Hg-induced autoimmune process (HgIA) is characterized by T cell-dependent polyclonal activation of B lymphocytes, increased level of serum immunoglobulin G1 (IgG1) and immunoglobulin E (IgE), production of antinucleolar autoantibodies (ANoA), and immune complex deposition in multiple organs. HgIA in mice is used as a model of human systemic autoimmune disorders. However, the dose of mercuric chloride (HgCl2) usually used in laboratory mice to induce HgIA is above the allowable limit for everyday levels of Hg exposure in humans. So, we decided to determine the lowest dose of HgCl2 that is able to trigger autoimmunity in outbred Carworth Farms Swiss Webster (CFW) mice not genetically prone to HgIA development. The lowest dose (50 µg/kg body weight (b.w.)/week) was chosen to match the World Health Organization provisional weekly tolerable intake of total Hg for humans. We also tested HgCl2 at 500 and 1500 µg/kg b.w./week (6.5- and 2-fold less than usually used for induction of HgIA in mice). We found that even the lowest dose of Hg resulted in a statistically significant increase in serum level of IgG1 after 8 weeks of treatment. HgCl2 in doses 500 and 1500 µg/kg b.w./week resulted in a significant increase in serum level of IgG1 after 4 weeks of treatment, followed by ANoA production. Sera of HgCl2-treated mice stained the regions in which the major autoantigen in HgIA, fibrillarin, was revealed. These results suggest that low doses of Hg are able to induce the main features of HgIA in genetically heterozygous mice, and that humans chronically exposed to low doses of Hg may be at risk of autoimmunity induction regardless of their genetic background., (© The Author(s) 2015.)

This study focuses on investigating the possible protective effect of sodium selenite (Na2SeO3) and/or vitamin E against mercuric chloride (HgCl2)-induced hepatotoxicity in rat. Male rats were given HgCl2 (1 mg/kg body weight (bw)) and HgCl2 plus Na2SeO3 (0.25 mg/kg bw) and/or vitamin E (100 mg/kg bw) daily via gavage for 4 weeks. HgCl2-treated groups had significantly higher white blood cell and thrombocyte counts than the control group. Serum activities of alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, γ-glutamyl-transferase, and lactate dehydrogenase significantly increased and serum levels of total protein, albumin, triglyceride, total cholesterol, and low-density lipoprotein cholesterol significantly decreased in the HgCl2-treated groups compared with control group. Malondialdehyde level significantly increased and superoxide dismutase, catalase, and glutathione peroxidase activities decreased in liver tissue of HgCl2-treated rats. Also, HgCl2 exposure resulted in histopathological changes. Supplementation of Na2SeO3 and/or vitamin E provided partial protection in hematological and biochemical parameters that were altered by HgCl2 As a result, Na2SeO3 and/or vitamin E significantly reduced HgCl2-induced hepatotoxicity, but not protected completely., (© The Author(s) 2015.)

Objective: The aim of this study was to assess exercise heart rate recovery (HRR) indices in mercury-exposed individuals when evaluating their cardiac autonomic function., Subjects and Methods: Twenty-eight mercury-exposed individuals and 28 healthy controls were enrolled. All the subjects underwent exercise testing and transthoracic echocardiography. The HRR indices were calculated by subtracting the first- (HRR1), second- (HRR2) and third-minute (HRR3) heart rates from the maximal heart rate. The two groups were evaluated in terms of exercise test parameters, especially HRR, and a correlation analysis was performed between blood, 24-hour urine and hair mercury levels and the test parameters., Results: The mercury-exposed and control groups were similar in age (37.2 ± 6.6 vs. 36.9 ± 9.0 years), had an identical gender distribution (16 females and 12 males) and similar left ventricular ejection fractions (65.5 ± 3.1 vs. 65.4 ± 3.1%). The mean HRR1 [25.6 ± 6.5 vs. 30.3 ± 8.2 beats per min (bpm); p = 0.009], HRR2 (43.5 ± 5.3 vs. 47.8 ± 5.5 bpm; p = 0.010) and HRR3 (56.8 ± 5.1 vs. 59.4 ± 6.3 bpm; p = 0.016) values were significantly lower in the mercury-exposed group than in the healthy controls. However, there were no significant correlations between blood, urine and hair mercury levels and exercise test parameters., Conclusions: Mercury-exposed individuals had lower HRR indices than normal subjects. In these individuals, mercury exposure measurements did not show correlations with the exercise test parameters, but age did show a negative correlation with these parameters. Therefore, cardiac autonomic functions might be involved in cases of mercury exposure., (© 2016 S. Karger AG, Basel.)

Mercury poisoning is a rare but fatal toxicologic emergency. Neurologic manifestations involving the central nervous system are seen usually with chronic mercury intoxication. The most commonly seen complaints are headache, tremor, impaired cognitive skills, weakness, muscle atrophy, and paresthesia. Here, we present a male patient who was chronically exposed to elemental mercury and had papilledema and intracranial hypertension without parenchymal lesion in the central nervous system. A 12-year-old male patient was referred to our emergency room because of severe fatigue, generalized muscle pain and weakness, which was present for a month. Physical examination revealed painful extremities, decreased motor strength and the lack of deep tendon reflexes in lower extremities. He had mixed type polyneuropathy in his electromyography. Whole blood and 24-hour urinary mercury concentrations were high. A chelation therapy with succimer (dimercaptosuccinic acid) was started on the fourth day of his admission. On the seventh day of his admission, he developed headache and nausea, and bilateral papilledema and intracranial hypertension were detected on physical examination. Acetazolamide was started and after 1 month of treatment, the fundi examination was normal. The patient stayed in the hospital for 35 days and was then discharged with acetazolamide, vitamin B6, gabapentin, and followed as an outpatient. His clinical findings were relieving day by day. Although headache is the most common symptom in mercury poisoning, the clinician should evaluate the fundus in terms of intracranial hypertension., (© The Author(s) 2014.)

Background: Fish is a rich source of n-3 polyunsaturated fatty acids (PUFAs) but also contains the neurotoxicant methyl mercury (MeHg). PUFAs may modify the relation between prenatal MeHg exposure and child development either directly by enhancing neurodevelopment or indirectly through the inflammatory milieu., Objective: The objective was to investigate the associations of prenatal MeHg exposure and maternal PUFA status with child development at 20 mo of age., Design: The Seychelles Child Development Study Nutrition Cohort 2 is an observational study in the Republic of Seychelles, a high-fish-eating population. Mothers were enrolled during pregnancy and their children evaluated at 20 mo of age by using the Bayley Scales of Infant Development II (BSID-II), the MacArthur Bates Communicative Development Inventories (CDI), and the Infant Behavior Questionnaire-Revised. There were 1265 mother-child pairs with complete data., Results: Prenatal MeHg exposure had no direct associations with neurodevelopmental outcomes. Significant interactions were found between MeHg and PUFAs on the Psychomotor Developmental Index (PDI) of the BSID-II. Increasing MeHg was associated with lower PDI but only in children of mothers with higher n-6/n-3. Among mothers with higher n-3 PUFAs, increasing MeHg was associated with improved PDI. Higher maternal docosahexaenoic acid (DHA) was associated with improved CDI total gestures (language development) but was significantly adversely associated with the Mental Development Index (MDI), both with and without MeHg adjustment. Higher n-6:n-3 ratios were associated with poorer scores on all 3 CDI outcomes., Conclusions: We found no overall adverse association between prenatal MeHg exposure and neurodevelopmental outcomes. However, maternal PUFA status as a putative marker of the inflammatory milieu appeared to modify the associations of prenatal MeHg exposure with the PDI. Increasing DHA status was positively associated with language development yet negatively associated with the MDI. These findings may indicate the existence of an optimal DHA balance with respect to arachidonic acid for different aspects of neurodevelopment., (© 2015 American Society for Nutrition.)

Juxtaposed alongside the ongoing rise in the incidence and prevalence of dementia, is the surge of recent research confirming widespread exposure and bioaccumulation of chemical toxicants. Evidence from sources such as the Centers for Disease Control reveals that most people have accrued varying degrees of assorted toxic pollutants including heavy metals, flame retardants, and pesticide residues within their bodies. It has been well established that many of these toxicants have neurodegenerative as well as neurodevelopmental impact as a result of various pathophysiologic mechanisms including neuronal mitochondrial toxicity and disruption of neurotransmitter regulation. Elimination of stockpiled toxicants from the body may diminish adverse toxicant impact on human biology and allow restoration of normal physiological function. Incorporating a review of medical literature on toxicant exposure and dementia with a case history of a lead-exposed individual diagnosed with dementia, this paper will discuss a much overlooked and potentially widespread cause of declining brain function and dementia.

In connected sample, the authors studied changes in state of peripheral nerves (electroneuromyography) and central afferent conduction tracts (somatosensory evoked potentials) in patients with long-term chronic mercury intoxication. The study helped to reveal negative changes in peripheral and central afferent conduction tracts in the patients with long-term chronic mercury intoxication, more marked in 3 period of the study--demyelination of sensory and motor components of peripheral nerves and longer impulse propagation time in conduction tracts of subcortical and cortical structures of somatosensory brain cortex.

Background: This study aimed to assess the effects of low-level prenatal mercury exposure on neonate neurobehavioral development in China., Methods: In total, 418 mother-neonate pairs were included in the study. Maternal urine, hair, and blood samples and cord blood samples were used to document prenatal exposure to mercury. The Neonatal Behavioral Neurological Assessment was used to estimate neurobehavioral development in the neonates at 3 days of age., Results: Total mercury level was significantly higher in cord blood than that in maternal blood. A strong correlation was found between total mercury levels in maternal blood and those in cord blood (r = 0.7431; P < 0.0001). Trend analysis revealed that mothers who consumed more fish had higher blood and cord blood mercury levels (all P < 0.0001). Significant differences were also found between male and female cord blood mercury levels among groups with different fish consumption frequencies (all P < 0.0001). Cord blood mercury level was significantly associated with total Neonatal Behavioral Neurological Assessment scores (β = 0.03; standard error = 0.01; P = 0.0409), passive muscle tone (odds ratio = 1.07; 95% confidence interval = 1.12-1.13; P = 0.0071), and active muscle tone (odds ratio = 1.06; 95% confidence interval = 1.01-1.11; P = 0.0170) scores after adjustment, respectively., Conclusions: Neonatal neurodevelopment was associated with prenatal exposure to mercury. Women with high mercury levels should avoid intake seafood excessively during pregnancy. Long-term effects of exposure to mercury on childhood development need to be further explored., (Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.)

Intentional self-injection of metallic mercury case report is presented. A 22 year old man with a past medical history of ethylene glycol suicidal poisoning was admitted to a Acad. N. Kipshidze Central University Clinic in Tbilisi, four months after deliberate intravenous injection of an unknown quantity of metallic mercury from several thermometers into his antecubital vein. After 2 months of asymptomatic period, the patient began to complain of pain and tremor in limbs, fatigue and skin rash. CT scan of the thorax and the abdomen confirmed multiple small opacities of metallic density in both lungs, liver and right kidney. After the procedure the patient was transferred to the toxicology center in Baku, Azerbaijan for chelation therapy. On arrival no biochemical abnormalities in hepatic or renal function or clinical pulmonary malfunction were detected, despite presence of slight symptoms of erethism, tremor mercuralis, knee joints arthralgia and lower extremities weakness. Chelation therapy with intramuscular injection of Unithiol (DMPS) was started in dose of 20mg/kg/day. After one month of chelation therapy, mercury blood concentration slowly decreased from initially 134 microgram/L to 105 microgram/L. This case report demonstrates mild acute toxicity following intravenous administration of unknown amounts of elemental mercury. Because of chelation therapy can remove approximately 1 mg of mercury per day the patient was recommended further long-term DMPS treatments under the control blood mercury levels. It is concluded that clinical manifestations of intravenous elemental mercury intoxication may be delayed despite significant increase in blood mercury level.

The article presents the results of the dynamic clinical observation for persons suffered from occupational chronic mercury intoxication in the remote post-exposure period of the disease. The estimation of the dynamics of syndrome manifestations of chronic mercury intoxication and co-morbidity are presented. The important role of mercury exposure load as a predictor of deterioration of actual health of the patients in the remote period of intoxication is demonstrated.

Background: Exposure to methylmercury from fish has been associated with increased risk of myocardial infarction (MI) in some studies. At the same time, marine n-3 (omega-3) PUFAs are an inherent constituent of fish and are regarded as beneficial. To our knowledge, no risk-benefit model on the basis of data on methylmercury, PUFA, and MI risk has yet been presented., Objective: The objective of this study was to describe how exposure to both marine n-3 PUFAs and methylmercury relates to MI risk by using data from Finland and Sweden., Design: We used matched case-control sets from Sweden and Finland that were nested in population-based, prospective cohort studies. We included 361 men with MI from Sweden and 211 men with MI from Finland. MI risk was estimated in a logistic regression model with the amount of mercury in hair (hair-Hg) and concentrations of n-3 PUFAs (EPA and DHA) in serum (S-PUFA) as independent variables., Results: The median hair-Hg was 0.57 μg/g in Swedish and 1.32 μg/g in Finnish control subjects, whereas the percentage of S-PUFA was 4.21% and 3.83%, respectively. In combined analysis, hair-Hg was associated with higher (P = 0.005) and S-PUFA with lower (P = 0.011) MI risk. Our model indicated that even a small change in fish consumption (ie, by increasing S-PUFA by 1%) would prevent 7% of MIs, despite a small increase in mercury exposure. However, at a high hair-Hg, the modeled beneficial effect of PUFA on MI risk was counteracted by methylmercury., Conclusions: Exposure to methylmercury was associated with increased risk of MI, and higher S-PUFA concentrations were associated with decreased risk of MI. Thus, MI risk may be reduced by the consumption of fish high in PUFAs and low in methylmercury.

Acute mercury vapor poisoning is a rare but fatal toxicological emergency. People are exposed to mercury in daily life by the way of foods, vaccines, antiseptics, ointments, amalgam or occupation. We present here, the clinical picture and management of four members of the same family who were exposed to elemental mercury. Three of the family members were seen in another hospital with malaise, fever, eritematous rash and pulmonary problems. Their questioning revealed the mercury exposure. Having a suspicion of heavy metal intoxication, blood and urine mercury levels were measured and mercury intoxication was diagnosed. On admission to our hospital, two patients already had chelation therapy. In three of them we found three distinct abnormalities: encephalopathy, nephrotic syndrome and polyneuropathy. The fourth family member had minor symptoms. This family is an example for the inhalation exposure resulting from inappropriate handling of liquid mercury. During the first days, flu like illness ensues. Then, severe pulmonary, neurological, renal, hepatic, hematological and dermatological dysfunctions develop. Blood and urine mercury levels should be tested on suspicion, but it must be kept in mind that blood level is unreliable in predicting the severity of mercury toxicity. The priority in the treatment should be removing the patient from the source of exposure. Then British anti-Lewisite, edetate calcium disodium, penicillamine, Sodium 2,3-dimercaptopropane-1-sulfhonate and 2,3-dimercaptosuccinic acid can be used for binding the mercury. We conclude that since mercury-containing devices are present in daily life, physicians must be able to recognize the clinical manifestations and treatment of mercury poisoning.

Methylmercury (MeHg) is an environmental contaminant that is found in many ecosystems. Many studies reported that MeHg toxicity is accompanied by increased lipid peroxidation that may lead to oxidative damage to DNA, RNA, and proteins. Vitamin E is considered as the most effective antioxidant preventing lipid peroxidation. The aim of this study was to evaluate the effects of MeHg exposure during pregnancy on the development of the appendicular skeleton in rat fetuses and whether vitamin E administration could reduce this toxicity. Positively mated adult female Sprague-Dawley rats were used and divided into the following experimental groups: control group, received only deionized water, and four MeHg treated groups received 1 mg of MeHg/kg/d, 2 mg of MeHg/kg/d, 1 mg of MeHg/kg/d plus 150 mg of vitamin E/kg/d, and 2 mg of MeHg/kg/d, plus 150 mg of vitamin E/kg/d starting from Day 0 of gestation. On Day 20 of gestation, the fetuses from the pregnant rats were extracted and the fetal growth parameters were evaluated. Skeletal evaluation of ossification of both fore- and hind-limbs, and coxal bones were undertaken. Results showed that treatment with MeHg caused adverse effects on fetal growth parameters and ossification of the bones. The coadministration of vitamin E with MeHg revealed an improvement in these parameters. These results suggest that vitamin E may ameliorate some aspects of MeHg developmental toxicity. The underlying and human health implications warrant further investigations., (Copyright © 2012 Wiley Periodicals, Inc.)

The heavy metals mercury, lead, and cadmium are toxicants, which are well-known to cross the placenta and to accumulate in fetal tissues. Prenatal exposure to mercury and lead poses a health threat particularly to the developing brain. Fetal exposures to lead and cadmium correlate with reduced birth weight and birth size. The placental passage of cadmium is limited suggesting a partial barrier for this metal. It is very likely that metallothionein is responsible for placental storage of the metals especially of cadmium. It is unclear, however, which proteins are involved in placental uptake and efflux of the metals and where the transporters are located at the placental barrier. Hence, only certain aspects of placental metal toxicokinetics are known so far. The metals have also been shown to adversely affect placental functions. Both metal-specific placental transfer and impairment of placental function can explain the relationships between prenatal metal exposures and adverse effects on intrauterine growth and (neuro)development.

Mercury is added to the biosphere by anthropogenic activities raising the question of whether changes in the human chromatin, induced by mercury, in a parental generation could allow adaptation of their descendants to mercury. We review the history of Andean mining since pre-Hispanic times in Huancavelica, Peru. Despite the persistent degradation of the biosphere today, no overt signs of mercury toxicity could be discerned in present day inhabitants. However, mercury is especially toxic to the autonomic nervous system (ANS). We, therefore, tested ANS function and biologic rhythms, under the control of the ANS, in 5 Huancavelicans and examined the metal content in their hair. Mercury levels varied from none to 1.014 ppm, significantly less than accepted standards. This was confirmed by microfocused synchrotron X-ray fluorescence analysis. Biologic rhythms were abnormal and hair growth rate per year, also under ANS control, was reduced (P < 0.001). Thus, evidence of mercury's toxicity in ANS function was found without other signs of intoxication. Our findings are consistent with the hypothesis of partial transgenerational inheritance of tolerance to mercury in Huancavelica, Peru. This would generally benefit survival in the Anthropocene, the man-made world, we now live in.

Introduction: Mercury and mercury salts, including mercurous chloride and mercurous oxide, are prohibited for use in cosmetic products as skin-lightening agents because of their high toxicity. Yet, the public continue to have access to these products., Methods: Reports of skin-lightening cosmetic products containing mercury and cases of mercury poisoning following the use of such products were identified using Medline (1950 - 28 March 2011) with mercury, mercury compounds, mercury poisoning, cosmetics and skin absorption as the subject headings. These searches identified 118 citations of which 31 were relevant., Toxicokinetics: The rate of dermal absorption increases with the concentration of mercury and prior hydration of the skin. The degree of dermal absorption varies with the skin integrity and lipid solubility of the vehicle in the cosmetic products. Ingestion may occur after topical application around the mouth and hand-to-mouth contact. After absorption, inorganic mercury is distributed widely and elimination occurs primarily through the urine and feces. With long-term exposure, urinary excretion is the major route of elimination. The half-life is approximately 1-2 months., Features: The kidneys are the major site of inorganic mercury deposition; renal damage includes reversible proteinuria, acute tubular necrosis and nephrotic syndrome. Gastrointestinal symptoms include a metallic taste, gingivostomatitis, nausea and hypersalivation. Although penetration of the blood-brain barrier by inorganic mercury is poor, prolonged exposure can result in central nervous system (CNS) accumulation and neurotoxicity. Inorganic mercury poisoning following the use of skin-lightening creams has been reported from Africa, Europe, USA, Mexico, Australia and Hong Kong. Nephrotic syndrome (mainly due to minimal change or membranous nephropathy) and neurotoxicity were the most common presenting features. As mercury-containing cosmetic products can contaminate the home, some close household contacts were also reported to have elevated urine mercury concentrations., Assessment: Prevention from further exposure is the first step. Cream users and their close contacts should be evaluated for evidence of mercury exposure, the presence of target organ damage and the need for chelation treatment. Laboratory evaluation of affected subjects should include a complete blood count, serum electrolytes, liver and renal function tests, urinalysis, urine and blood mercury concentrations. Since blood mercury concentrations tend to return to normal within days of exposure, blood samples are useful primarily in short-term, higher-level exposures. Estimation of the urine mercury concentration is the best marker of exposure to inorganic mercury and indicator of body burden. A 24-hour urine for measurement of mercury excretion is preferred; a spot urine mercury concentration should be corrected for creatinine output., Management: Chelation therapy is indicated in patients with features of mercury poisoning and elevated blood and/or urine mercury concentrations. Unithiol (2,3-dimercapto-1-propanesulfonic acid, DMPS) is the preferred antidote though succimer (dimercaptosuccinic acid, DMSA) has also been employed., Conclusions: The use of mercury in cosmetic products should be strictly prohibited. The public should be warned not to use such products as their use can result in systemic absorption and accumulation of mercury causing renal, gastrointestinal and CNS toxicity.

Objectives: The aim of this study is to investigate the effect of elemental mercury exposure on renal function and antioxidative enzymes activity as a possible mechanism of renal affection among dental staff., Methods: This study was performed on a group of dental staff exposed to elemental mercury (N = 32) and matched control group (N = 37). Urinary and blood level of mercury, albumin α1 microgloblin in urine, glutathione peroxidase and superoxide dismutase blood level were measured for the exposed and control group., Results: Compared to the control group, urinary and blood mercury were significantly higher in the exposed group. Glutathione peroxidase and superoxide dismutase activities in blood were significantly decreased and were negatively correlated with duration of work., Conclusion: Oxidative stress is an important molecular mechanism for renal dysfunction in mercury exposure, manifested by decreased activities of antioxidant enzymes.

Despite clinical experience that spans more than half a century, chelation for toxic heavy metals represents one of the most controversial and misapplied interventions in clinical toxicology. The prompt use of chelating agents to treat acute, life-threatening intoxication is an indication that is largely supported by experimental animal data and limited clinical research. Although chelating agents administered for chronic intoxication may accelerate the excretion of heavy metals, their therapeutic efficacy in terms of decreased morbidity and mortality is largely unestablished. Recent investigations suggest that their use in such settings might be associated with deleterious effects. Careful attention to risk-benefit issues is warranted, particularly in clinical situations in which the etiological role of heavy metals in the patient's illness is in question.

Lead, cadmium, mercury, and arsenic, often referred to as "heavy metals", are toxic for wildlife, experimental animals, and humans. While experimental animal and human occupational studies with high exposure levels generally support an adverse role for these metals in human reproductive outcomes, information on the effects of low, environmentally-realistic exposure levels of these metals on male reproductive outcomes is limited. We review the literature on effects of exposure to low levels of these metals on measures of male fertility (semen quality and reproductive hormone levels) and provide supporting evidence from experimental and occupational studies. Potentially modifying effects of genetic polymorphisms on these associations are discussed. A brief review of the literature on the effects of three trace metals, copper, manganese, and molybdenum, that are required for human health, yet may also cause adverse reproductive effects, follows. Overall, there were few studies examining the effects of exposure to low levels of these metals on male reproductive health. For all metals, there were several well-designed studies with sufficient populations appropriately adjusted for potential confounders and many of these reported harmful effects. However, many studies lacked sufficient numbers of participants to be able to detect differences in outcomes between exposed and non-exposed individuals, did not clearly identify the source and characteristics of the participants, and did not control for other exposures that could alter or contribute to the outcomes. The evidence for the effects of low exposure was strongest for cadmium, lead, and mercury and less certain for arsenic. The potential modifying effects of genetic polymorphisms has not been fully explored. Additional studies on the reproductive effects of these toxic ubiquitous metals on male reproduction are required to expand the knowledge base and to resolve inconsistencies.

In 2003 UNIDO (United Nations Industrial Development Organization) conducted an environmental and health assessment in a small-scale mining area in Tanzania. BGS (British Geological Survey) performed the environmental assessment. The Institute of Forensic Medicine - University of Munich performed the health assessment. The results of the medical, neurological and neuro-psychological examination of 180 participants from the affected area of Rwamagasa and 31 controls were analyzed. Urine, blood and hair samples were analyzed to detect the level of mercury body burden. Mercury concentrations in the bio-monitors urine, blood and hair were statistically significantly higher in the exposed population from Rwamagasa compared to the control group from Katoro. Only amalgam burners showed mercury levels above the toxicological threshold limits. A speciation of mercury in hair indicated that mainly elemental mercury vapor contributed to the high body burden of the artisanal miners. 104 amalgam-burners, the most exposed population group, were examined. 25 of these workers were found to be intoxicated. Small-scale mining is a serious health hazard for amalgam burners. Reduction of the exposure is essential to prevent further damage., (Copyright 2009 Elsevier B.V. All rights reserved.)

Small scale miners use mercury to extract gold from ore in many countries. An environmental and health assessment was performed in Indonesia in two regions, Galangan in Central Kalimantan and Talawaan in Northern Sulawesi. The environmental assessment showed severe mercury contamination of the sediments, and increased mercury levels in local fish. For the health investigation 281 volunteers were recruited and examined by a standardized questionnaire, a neurological examination and neuro-psychological tests. A medical score was used consisting of significant factors of mercury intoxication. Mercury exposed workers showed typical symptoms of mercury intoxication, such as movement disorders (ataxia, tremor, dysdiadochokinesia, etc.). Blood, urine and hair samples were taken from any participant and analyzed for mercury. The mercury concentration in the biomonitors was high, partly extreme high in the working population, increased in the population living in the same habitat and low in the control group. By a standard protocol which includes a combination of threshold values of mercury in the biomonitors and a medical sum score the diagnosis of chronic mercury intoxication was made for highly burdened workers (amalgam smelters) in 55% in Sulawesi and in 62% in Kalimantan. Less exposed mineral processors and the general population in the mining areas were also intoxicated to a high percentage., (Copyright 2009 Elsevier B.V. All rights reserved.)

Examination of chronic mercury intoxication patients in distant (post-contact) period revealed marked vision disorders and inhibited neuro-conductivity--inhibited neuronal structures of retina and optic nerve.

Heat shock proteins and glucose-regulated proteins represent an extraordinary mechanism of defense induced in the kidney by chemicals or drugs and essential to survive. Here we resume our experience on the presence and regulation of stress proteins into acute and chronic nephrotoxic models in rodents and in vitro. In acute renal damage, induced in rats by a single injection of inorganic mercury, stress proteins enhanced in a dose-dependent manner to recover cytoskeleton and mitochondria and maintain nuclear activity. When we pre-treated mercury injected-rats with antioxidant melatonin or with bimoclomol, a stress proteins-coinducer, stress proteins expression was modulated together with tubular recovery. Similar data were obtained in ischemia-reperfusion in rats treated with stannous chloride, that provided cytoprotection stimulating heme oxygenase induction. During nephrotoxicity induced by administration of cyclosporine A at therapeutic dosage for 1-2 months, stress protein overexpression well correlated with oxidative and cell death, but decreased if we counteracted renal damage using antioxidants. In aluminium intoxication through drinking water for 3-6 months, we detected a time-dependent stress response in the rat kidney that was organ specific and different from the liver. In vitro studies on rat tubular proximal cells exposed to heavy metals demonstrated that stress protein expression was related to peculiar mechanisms of action of each metal. In conclusion, experimental studies on the renal chaperones can greatly contribute to understand their role, and agents able to modulate the stress response might be considered promising therapeutic tools to reduce nephrotoxicity.

Case Report: A 36-year-old jewelry producer presented with tremor, slurred speech, lethargy, headache, and incoordination. On examination he had a coarse tremor of the outstretched hands and protruded tongue, slurred speech, "Hatter's shakes" handwriting, impaired heel-toe walking and heel-shin coordination, mild dysdiadochokinesis, and constricted visual fields to confrontation. The patient received four 5-day courses of oral 2,3-dimercapto-1-propanesulfonate (30 mg/kg/day), which was associated with substantial objective clinical improvement and the excretion of 99,406 microg mercury., Conclusion: We recommend that the administration of 2,3-dimercapto-1-propanesulfonate should be considered in symptomatic patients who have been exposed to mercury vapor and who have supporting analytical confirmation of the diagnosis.

It is well known that antioxidants containing sulfhydryl (-SH) groups are protective against the toxic effects of mercury. The current study was designed to elucidate the mechanism(s) of the cytoprotective effects of glutathione (GSH) and N-acetylcysteine (NAC) against the toxicity of inorganic mercury (HgCl(2)) in neuroblastoma cells (N-2A). The obtained results demonstrated the protective effects of these compounds in a dose dependant manner up to 95 and 74% cell viability, respectively as compared to the control of HgCl(2) of 10%. The administration of buthionine sulfoximine (BSO), an inhibitor of GSH synthesis, increased the toxicity of HgCl(2) in a dose dependent manner. Moreover, BSO treatment attenuated the levels of the cellular free -SH concentrations at low concentrations (1-100 microM) of HgCl(2). The data also show that cellular thiol concentrations were augmented in the presence of GSH and NAC and these compounds were cytoprotective against HgCl(2) and this is due to up regulating of GSH synthesis. A reduction in intracellular levels of GSH was observed with treatment of HgCl(2). In addition, the ratio of GSH/GSSG increased from 16:1 to 50:1 from 1 to 10 microM concentration of HgCl(2.) The ratio of GSH/GSSG then decreased from 4:1 to 0.5:1 with the increase of concentration of HgCl(2) between 100 microM and 1 mM due to the collapse of the N-2A cells. It was of interest to note that the synthesis of GSH was stimulated in cells exposed to low concentration of HgCl(2) when extra GSH is available. These data support the idea that the loss of GSH plays a contributing role to the toxic effects of HgCl(2) and that inorganic mercury adversely affects viability, through altering intracellular -SH concentrations. The data further indicate that the availability of GSH to the cells may not be sufficient to provide protection against mercury toxicity and the de novo synthesis of intracellular GSH is required to prevent the damaging effects of mercury.

Mercury is known to be associated with both acute and chronic poisoning. A 36-year-old man intentionally ingested mercuric chloride (HgCl(2)) and died within 24h. Post-mortem CT images showed oral, esophageal and gastric wall hyperdense "staining". On toxicological analysis, the blood concentration of mercury was measured at 25.5mg/L; a figure far higher than reported lethal levels. Autopsy was not performed in order to prevent potential inhalation of mercury vapor by pathology staff.

An infant presented with failure to thrive and developmental regression. Physical examination revealed an irritable child with swollen, erythematous extremities, and elevated blood pressure. Extensive investigations, including a metabolic work-up and neuroimaging, were unrevealing. Exposure to self-purchased medication was initially denied. The physical signs were suggestive of acrodynia. Mercury poisoning was ultimately established by measuring paired blood and urine mercury levels. On further enquiry, it was revealed that the child had been given a Chinese medicinal product for 4 months. He responded well to a chelating agent. Acrodynia is a childhood disease considered to be of historical interest only, but making a diagnosis of mercury poisoning is rewarding because the response to treatment is good. This case highlights the common misconception that alternative medicines are safe and benign.

Mercury, an occupational and environmental contaminant, is a well-recognized health hazard. The thymus is a target for inorganic mercury (Hg2+); thymic function is impaired in Hg2+ intoxication and is partially restored by simultaneous L-arginine supplementation. The nitric oxide (NO)-nitric oxide synthase (NOS) pathway and metallothioneins (MTs) were studied to investigate the role of L-arginine in thymic function restoration after mercury exposure. Mice received a higher and a lower dose of inorganic mercury, with and without L-arginine supplementation. Saline-treated mice were used as controls. Thymus weight and thymulin were measured as indices of thymic function. Mice treated with Hg2+ alone displayed an accumulation of metal in the thymus, reduced NOS activity, a lower plasma nitrite plus nitrate concentration and an increased MTs expression compared with control mice. L-arginine supplementation was associated with lower Hg2+ concentrations in the organ and partial preservation of other measures. Reduced accumulation of Hg2+ in mice dosed with L-arginine was probably related to greater NO production and NO-MTs interactions.

Introduction: Intravenous injection of mercury has seldom been reported, especially in cases of attempted suicide, and is associated with variable clinical outcomes., Case Report: A young woman came to our attention after self-injecting and ingesting mercury drawn from 37 thermometers. The patient suffered lung embolization complicated by adult respiratory distress syndrome (ARDS), toxic dermatitis, anemia, mild hepato-renal impairment, and died after 30 days. Mercury was monitored in biological fluids (blood, plasma, urine, and bronchoalveolar fluid) to study its toxicokinetics and to evaluate dose-effect relationships. Its urinary clearance significantly increased after a chelation challenge test with meso-2,3-dimercaptosuccinic acid (DMSA) (median values of 2.48 and 8.85 before and after the test, respectively, p < 0.05)., Conclusions: Mercury poisoning by intravenous injection is a clinical emergency, potentially leading to death. When injected, the element has a very slow clearance, mainly renal. Our data do not allow any conclusion about the effectiveness of chelation therapy.

An 11-year-old female was seen at our outpatient clinic with a broad variety of symptoms that were due to elemental mercury intoxication. Electromyography and sequential electroencephalography findings obtained at days 2, 36, 88 and 148 are described. The patient was treated with chelation therapy during which she clinically improved considerably. A profound decrease in urinary mercury concentration occurred as well as normalization of the electroencephalogram.

Visual field losses associated with mercury (Hg) exposure have only been assessed in patients exposed to methylmercury. Here we evaluate the automated visual field in 35 ex-workers (30 males; 44.20+/-5.92 years) occupationaly exposed to mercury vapor and 34 controls (21 males; 43.29+/-8.33 years). Visual fields were analyzed with the Humphrey Field Analyzer II (model 750i) using two tests: the standard automated perimetry (SAP, white-on-white) and the short wavelength automated perimetry (SWAP, blue-on-yellow) at 76 locations within a 27 degrees central visual field. Results were analyzed as the mean of the sensitivities measured at the fovea, and at five successive concentric rings, of increasing eccentricity, within the central field. Compared to controls, visual field sensitivities of the experimental group measured using SAP were lower for the fovea as well as for all five eccentricity rings (p<0.05). Sensitivities were significantly lower in the SWAP test (p<0.05) for four of the five extra-foveal eccentricity rings; they were not significant for the fovea (p=0.584) or for the 15 degrees eccentricity ring (p=0.965). These results suggest a widespread reduction of sensitivity in both visual field tests. Previous reports in the literature describe moderate to severe concentric constriction of the visual field in subjects with methylmercury intoxication measured manually with the Goldman perimeter. The present results amplify concerns regarding potential medical risks of exposure to environmental mercury sources by demonstrating significant and widespread reductions of visual sensitivity using the more reliable automated perimetry.

This longitudinal study addresses the reversibility of color vision losses in subjects who had been occupationally exposed to mercury vapor. Color discrimination was assessed in 20 Hg-exposed patients (mean age = 42.4 +/- 6.5 years; 6 females and 14 males) with exposure to Hg vapor during 10.5 +/- 5.3 years and away from the work place (relative to 2002) for 6.8 +/- 4.2 years. During the Hg exposure or up to one year after ceasing it, mean urinary Hg concentration was 47 +/- 35.4 mug/g creatinine. There was no information on Hg urinary concentration at the time of the first tests, in 2002 (Ventura et al., 2005), but at the time of the follow-up tests, in 2005, this value was 1.4 +/- 1.4 microg/g creatinine for patients compared with 0.5 +/- 0.5 microg/g creatinine for controls (different group from the one in Ventura et al. (2005)). Color vision was monocularly assessed using the Cambridge Colour Test (CCT). Hg-exposed patients had significantly worse color discrimination (p < 0.02) than controls, as evaluated by the size of MacAdam's color discrimination ellipses and color discrimination thresholds along protan, deutan, and tritan confusion axes. There were no significant differences between the results of the study in Ventura et al. (2005) and in the present follow-up measurements, in 2005, except for worsening of the tritan thresholds in the best eye in 2005. Both chromatic systems, blue-yellow and red-green, were affected in the first evaluation (Ventura et al., 2005) and remained impaired in the follow-up testing, in 2005. These findings indicate that following a long-term occupational exposure to Hg vapor, even several years away from the source of intoxication, color vision impairment remains irreversible.

Amazonian gold mining activity results in human exposure to mercury vapor. We evaluated the visual system of two Amazonian gold miners (29 and 37 years old) by recording the transient pattern electroretinogram (tPERG) and transient pattern visual evoked potential (tPVEP). We compared these results with those obtained from a regional group of control subjects. For both tPERG and tPVEP, checkerboards with 0.5 or 2 cycles per degree (cpd) of spatial frequency were presented in a 16 degrees squared area, 100% Michelson contrast, 50cd/m2 mean luminance, and 1 Hz square-wave pattern-reversal presentation. Two averaged waveforms (n=240 sweeps, 1s each) were monocularly obtained for each subject in each condition. Both eyes were monocularly tested only in gold miners. Normative data were calculated using a final pooled waveform with 480 sweeps. The first gold miner, LCS, had normal tPERG responses. The second one, RNP, showed low tPERG (P50 component) amplitudes at 0.5 cpd for both eyes, outside the normative data, and absence of response at 2 cpd for his right eye. Delayed tPVEP responses (P100 component) were found at 2 cpd for LCS but the implicit times were inside the normative data. Subject RNP also showed delayed tPVEP responses (all components), but only the implicit time obtained with his right eye was outside the normative data at 2 cpd. We conclude that mercury exposure levels found in the Amazon gold miners is high enough to damage the visual system and can be assessed by non-invasive electrophysiological techniques.

Objective: To investigate the suitability of measurements of mercury (Hg) concentration as a means of identifying patients with health complaints attributed to dental amalgam., Methods: Hg in erythrocytes, plasma, urine, and saliva was determined in 27 patients complaining about health problems attributed to amalgam, 27 healthy volunteers with amalgam fillings, and 27 healthy amalgam-free volunteers., Results: Concentrations of inorganic mercury in blood and of total mercury in urine and saliva differed significantly between individuals with amalgam fillings and amalgam-free volunteers, but not between symptomatic patients and healthy volunteers with amalgam fillings. Urine Hg levels tended to be better correlated with blood than with saliva data. Levels of organic Hg were equal in all groups., Conclusion: Concentrations of total and inorganic mercury in body fluids do not distinguish between asymptomatic amalgam bearers and those who suffer from a poorly defined syndrome of multiple nonspecific symptoms.

Young adult male Wistar rats were treated, by gavage, with 80 or 320 mg/kg Pb2+ (lead acetate), 0.4 or 1.6 mg/kg Hg2+ (mercuric chloride) or both by combining the lower doses. For combination with alcohol, ethanol was added to the rats' drinking water in 5 v/v %. After 12 weeks of treatment, electrophysiological recording was made from the somatosensory cortex in urethane anaesthesia. Evoked potentials obtained by stimulation of the whiskers were recorded. Both metals, and alcohol alone, increased significantly the latency of the evoked response. Alcohol seemed to abolish the effect of Pb, but not of Hg. Fatigue, calculated form the response amplitude, was increased by Pb and Hg treatment and this effect of Hg was reduced by ethanol. Evoked activity and its dynamic characteristics were sensitive to the complex neurotoxic effect induced in the rats and can provide a basis for developing functional markers.

Background: Although mercury is toxic, few studies have measured exposure in children who handled elemental mercury briefly. In 2004, a student spilled approximately 60 milliliters of mercury at a Nevada school. Within 12 hours, all students were removed from the source of exposure. We conducted an exposure assessment at the school., Methods: We administered questionnaires and obtained urine samples from students. Using two-sample t-tests, we compared urine mercury levels from students who self-reported exposure to mercury levels of other students., Results: Two-hundred students participated, including 55/62 (89%) who were decontaminated. The students' geometric mean urine mercury level was 0.36 microg/L (95% confidence interval 0.32-0.40 microg/L). The student who brought the mercury to school was the only one to have an elevated urine mercury level (11.4 microg/L)., Conclusion: Despite environmental contamination, mercury exposure may have been minimized because of rapid identification of the elemental mercury spill and decontamination.

Humans have had a long and tumultuous relationship with heavy metals. Their ubiquitous nature and our reliance on them for manufacturing have resulted at times in exposures sufficient to cause systemic toxicity. Their easy acquisition and potent toxicity have also made them popular choices for criminal poisonings. This article examines the clinical manifestation and pathophysiology of poisoning from lead, mercury, arsenic, and thallium.

The neurobehavioral changes in wild-type and metallothionein (MT)-null mice after the cessation of long-term, low-level exposure to Hg0 were investigated. MT-null and wild-type females were continuously (24 h/day) exposed to mercury vapor (Hg0) at 0.055 mg/m3 (range: 0.043-0.073 mg/m3), which was similar to the current threshold limit value (TLV), for 29 weeks. The effects on behavior, such as locomotor activity in the open field (OPF), learning ability in the passive avoidance response (PA) and spatial learning ability in the Morris water maze (MM) were examined immediately and 12 weeks after the cessation of exposure. Immediately after the exposure had ceased, total locomotor activity in OPF was decreased in the both strain of mice, although the MT-null mice appeared to show more distinct effect. In the PA test, the exposed animals of both strains showed learning impairment as compared to un-exposed mice. Twelve weeks after the cessation of exposure, the locomotor activity in OPF was elevated in the exposed mice of both strains, while the learning ability in the PA test appeared normal in both strains. Spatial learning ability was not affected at all. Immediately after the exposure had ceased, the brain mercury concentration of the exposed wild-type mice was 1.75 microg/g, twofold of that in the MT-null mice. In 12 weeks, brain mercury levels decreased to approximately 1/20 of those in immediately after the exposure in both of the strains. These results for the first time indicated that long-term, low-level exposure to Hg0 could exert neurobehavioral effects, which were not reversible even after a long exposure-free period. Whereas the effects on learning ability were presumably transient, the effects on spontaneous behavior as evaluated in OPF were persistent. Finally, the MT-null mice seemed more susceptible to Hg0-induced neurotoxicity than the wild-type mice, confirming our previous results.