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This review covers the toxicology of mercury and its compounds. Special attention is paid to those forms of mercury of current public health concern. Human exposure to the vapor of metallic mercury dates back to antiquity but continues today in occupational settings and from dental amalgam. Health risks from methylmercury in edible tissues of fish have been the subject of several large epidemiological investigations and continue to be the subject of intense debate. Ethylmercury in the form of a preservative, thimerosal, added to certain vaccines, is the most recent form of mercury that has become a public health concern. The review leads to general discussion of evolutionary aspects of mercury, protective and toxic mechanisms, and ends on a note that mercury is still an \"element of mystery.\"

Chemical found in 60-year-old cat brain reopens debate over Minamata disaster. The city of Minamata, Japan, is dotted with monuments commemorating victims of an industrial mass poisoning decades ago. High in the hills, a small stone memorial honors other deaths—of cats sacrificed in secret to science. Now, after restudying the remains of one of those cats, a team of scientists is arguing, controversially, that the long-standing explanation for the tragedy is wrong. No one questions the root cause of the disaster, which at minimum poisoned more than 2000 people: mercury in a chemical factory's wastewater that was dumped into Minamata Bay and taken up by seafood eaten by fishermen and their families. At first, the chemical form of the mercury, which ultimately killed many of its victims and left many babies with severe neurological disorders, was unknown. But in 1968, the Japanese government blamed methylmercury, a common byproduct of mercury pollution. Many studies supported that conclusion, finding methylmercury spikes in shellfish, bay sludge, and even hundreds of umbilical cords from babies delivered during the time. Yet researchers at the University of Saskatchewan say methylmercury is not the culprit. Instead, the cat remains point to an obscure organic mercury compound that may say little about the broader threat of mercury pollution.

•Mercury poisoning is rare, especially those that occur in acute and intentional way.•Its phamarcokinetics and biodistribution in human body are not yet fully understood.•The toxicity of this metal in the form of its metabolic kinetics is being clarified at a slow pace.•Liver and kidney seem to assume as key organs in the metabolism of the inorganic mercury.•This case represents a relevant experimental support to a more evidence-based understanding. Mercury is a heavy metal with unique physico-chemical properties, and it is well distributed throughout the environment, being present in soil, water and air. This non-essential element is considered by the World Health Organization (WHO) as one of the ten most troublesome chemical to public health. Its toxicity spectrum depends on the chemical form in which it presents: elemental (metallic), organic or inorganic. The known intoxications are mainly occupational (mining, agriculture, incineration) or related to the use of dental amalgams or the consumption of contaminated fish and shellfish. Nowadays, acute exposures to toxic amounts of mercury are increasingly rare, especially those involving inorganic mercury compounds. The rate is even lower if we refer to intentional poisonings. Although there is a growing understanding of the toxicokinetics of mercury, there is still a lack of studies that support the emerging theories about its bioavailability in humans. In this manuscript we describe a rare case of an individual who committed suicide by ingesting mercuric oxide. The aim is to offer a medical contribution to the better understanding of the kinetics of this metal, making a discussion based on published literature and analyzing its distribution, metabolism, internal doses, target and reservoir organs. The whole case – clinical course of the victim and her fatal destiny, the ante- and post-mortem sample concentrations and the necropsy findings – illustrates a situation that meets specific features of acute poisoning by ingestion of inorganic mercury, thus constituting an important support towards a more realistic and a based on evidence understanding of mercury biodistribution in humans.

A ruling by the European Union heralds the demise of those useful clinical instruments, the mercury thermometer and the mercury sphygmomanometer. The new laws have been passed because of worries about mercury poisoning. Yet you can drink metallic mercury and come to no harm. What does it all mean? There are three forms of mercury from a toxicological point of view: inorganic mercury salts; organic mercury compounds; and metallic mercury. Inorganic mercury salts are water soluble, irritate the gut, and cause severe kidney damage. Organic mercury compounds, which are fat soluble, can cross the blood brain barrier and cause neurological damage. Mercury metal poses two dangers. It can be vaporised: the vapour pressure at room temperature is about 100 times the safe amount, so poisoning can occur if mercury metal is spilled into crevices or cracks in the floorboards. Dentists are occasionally poisoned this way. Mercury easily crosses into the brain, and causes tremor, depression, and behavioural disturbances. A second danger from metallic mercury is that it is biotransformed into organic mercury, by bacteria at the bottom of lakes. This can be passed along the food chain and eventually to man. It was this process that led to the Japanese tragedy at Minimata Bay in the late 1950s when over 800 people were poisoned. It is the need to reduce mercury contamination of the environment which should encourage us to cut the usage of metallic mercury. However, much more metallic mercury is spilled as waste by the chemical industry than is dropped on the floor in the clinic.

The German poet Hölderlin, assumed to have suffered from schizophrenia, in fact has been the victim of a combined calomel and cantharidine intoxication administered by his physician Autenrieth. This new theory explains much better his behavioural changes and also his neurological and other concomitant symptoms; it can be tested by analysing a very few of his hairs for the presence of these compounds.

Methylmercury is a neurotoxin at high exposures, and the developing fetus is particularly susceptible. Because exposure to methylmercury is primarily through fish, concern has been expressed that the consumption of fish by pregnant women could adversely affect their fetuses. The reference dose for methylmercury established by the U.S. Environmental Protection Agency was based on a benchmark analysis of data from a poisoning episode in Iraq in which mothers consumed seed grain treated with methylmercury during pregnancy. However, exposures in this study were short term and at much higher levels than those that result from fish consumption. In contrast, the Agency for Toxic Substances and Disease Registry (ATSDR) based its proposed minimal risk level on a no-observed-adverse-effect level (NOAEL) derived from neurologic testing of children in the Seychelles Islands, where fish is an important dietary staple. Because no adverse effects from mercury were seen in the Seychelles study, the ATSDR considered the mean exposure in the study to be a NOAEL. However, a mean exposure may not be a good indicator of a no-effect exposure level. To provide an alternative basis for deriving an appropriate human exposure level from the Seychelles study, we conducted a benchmark analysis on these data. Our analysis included responses from batteries of neurologic tests applied to children at 6, 19, 29, and 66 months of age. We also analyzed developmental milestones (age first walked and first talked). We explored a number of dose-response models, sets of covariates to include in the models, and definitions of background response. Our analysis also involved modeling responses expressed as both continuous and quantal data. The most reliable analyses were considered to be represented by 144 calculated lower statistical bounds on the benchmark dose (BMDLs; the lower statistical bound on maternal mercury hair level corresponding to an increase of 0.1 in the probability of an adverse response) derived from the modeling of continuous responses. The average value of the BMDL in these 144 analyses was 25 ppm mercury in maternal hair, with a range of 19 to 30 ppm.

A 57-year-old pharmacist was found dead 11 days after his disappearance. At the autopsy, samples of blood, urine, gastric content were obtained. Presence of ethanol, cyanide and mercury were detected in some samples. Cyanide and mercury were identified and quantified using high-performance liquid chromatography with diode array detector (HPLC) in fluorescence mode and ICP with mass selective detector (ICP-MS) respectively. Whole blood concentrations of ethanol was 1.72 g/L. Cyanide and mercury concentrations in whole blood were respectively 0.16 and 3.8 mg/L. Concentrations of cyanide (27 mg/L) and mercury (150 mg/L) in gastric contents prove a massive oral ingestion of mercuric cyanide or mercuric oxycyanide occurred. In this case report, the death was attributed to the combined toxicity of cyanide and mercury.

Mercury toxicity was suspected, and further questionning revealed that the infants had been given a mercurycontaining \"teething powder\" from India once or twice a week over the 4 preceding months. The girls' blood mercury levels were 176 and 209 (normally < 18) pmol/L. Chelation therapy with 2,3dimercaptosuccinic acid was administered through nasogastric tubes. Before admission the twins had regressed developmentally and were unable to feed orally, sit or walk. Over the 8 weeks in hospital they showed some minor neurocognitive improvements, but their longterm prognosis is uncertain. Mercury exists in inorganic and organic forms. Organic mercury has recently received attention because of the accumulation of methylmercury in some predatory fish' and the use of thimerosal as a preservative in some vaccines.2 A type of inorganic mercury known as calomel (\"sweet mercury\") was once commonly used to treat many ailments, including yellow fever, typhus and syphilis.' Until the recognition of their toxicity in the 1940s, calomel-based teething powders caused a scourge of mercury poisoning called \"pink disease\" or acrodynia among infants and children.4

This October, nations will gather in Japan to sign the Minamata convention, a treaty to address the toxic effects of mercury in the environment. The agreement will become binding once ratified by at least 50 nations. The convention is timely and welcome in that it places controls and limitations on products, processes, and industries that increase the level of exposure of people and the environment to mercury, a naturally occurring element. Mercury bioaccumulates in the form of methylmercury, a powerful neurotoxin that can affect wildlife, domestic animals, and humans alike. Symptoms of mercury poisoning can range from numbness in the hands and feet and muscle weakness in mild cases, to insanity and death.

Clinical manifestations of methylmercury (MeHg) intoxication include cerebellar ataxia, concentric constriction of visual fields, and sensory and auditory disturbances. The symptoms depend on the site of MeHg damage, such as the cerebellum and occipital lobes. However, the underlying mechanism of MeHg-induced tissue vulnerability remains to be elucidated. In the present study, we used a rat model of subacute MeHg intoxication to investigate possible MeHg-induced blood-brain barrier (BBB) damage. The model was established by exposing the rats to 20-ppm MeHg for up to 4 weeks; the rats exhibited severe cerebellar pathological changes, although there were no significant differences in mercury content among the different brain regions. BBB damage in the cerebellum after MeHg exposure was confirmed based on extravasation of endogenous immunoglobulin G (IgG) and decreased expression of rat endothelial cell antigen-1. Furthermore, expression of vascular endothelial growth factor (VEGF), a potent angiogenic growth factor, increased markedly in the cerebellum and mildly in the occipital lobe following MeHg exposure. VEGF expression was detected mainly in astrocytes of the BBB. Intravenous administration of anti-VEGF neutralizing antibody mildly reduced the rate of hind-limb crossing signs observed in MeHg-exposed rats. In conclusion, we demonstrated for the first time that MeHg induces BBB damage via upregulation of VEGF expression at the BBB in vivo. Further studies are required in order to determine whether treatment targeted at VEGF can ameliorate MeHg-induced toxicity.