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Mercury is ubiquitous in the environment and therefore every human being, irrespective of age and location, is exposed to one form of mercury or another. The major source of environmental mercury is natural degassing of the earth's crust, but industrial activities can raise exposure to toxic levels directly or through the use or misuse of the liquid metals or synthesized mercurial compounds. The aim of this review is to survey differences in human exposure and in the toxicology of different forms of mercury. It covers not only symptoms and signs observed in poisoned individuals by a clinician but also subclinical effects in population studies, the final evaluation of which is the domain of statisticians.

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.

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.\"

Mercury is a toxic heavy metal which is widely dispersed in nature. Most human exposure results from fish consumption or dental amalgam. Mercury occurs in several chemical forms, with complex pharmacokinetics. Mercury is capable of inducing a wide range of clinical presentations. Diagnosis of mercury toxicity can be challenging but can be obtained with reasonable reliability. Effective therapies for clinical toxicity have been described.

Mercury (Hg) is a toxic heavy metal with extensive applications. In children, mercury exposure often occurs inadvertently through laboratories, thermometers, or fluorescent lamps. Inhalation of elemental mercury can affect the central nervous system and urinary system. Early diagnosis and treatment are crucial to prevent severe complications. A retrospective evaluation was conducted on 82 pediatric cases of mercury poisoning who presented to Bingöl State Hospital on January 15, 2020. Blood and urine mercury levels were measured. Patients with mercury levels > 10 μg/L received intravenous treatment with 2,3-dimercaptopropane sulfonic acid (DMPS) for 5 days. Plasma and urine mercury levels were analyzed before and after treatment. Adverse effects of treatment and follow-up processes were also examined. Of the patients, 43.9% were female, and 56.1% were male, with a mean age of 9.4 ± 3.2 years. A total of 42.7% of cases were symptomatic, with headache being the most common symptom (26.8%). Significant reductions in blood and urine mercury levels were observed after treatment ( p  < 0.001). Adverse effects of the drug were reported in 43.9% of cases, with nausea (50%) and itching (25%) being the most frequent. Conclusion : Chelation therapy was effective in significantly reducing mercury levels in cases of mercury poisoning. Adverse effects must be carefully managed, and long-term follow-up is essential. This study provides significant contributions to the literature on mass mercury poisoning cases. What is Known: • Symptoms of mercury poisoning. What is New: • Long-term outcomes of DMPS therapy in 82 patients.

Mercury intoxication is not uncommon and often presents with diverse symptoms of multiple systems. While neurological disorders and renal impairments have been examined in isolation, the concurrent occurrence of systemic symptoms linked to immune dysregulation is infrequently observed. Here, we report an unusual case that a 55-year-old male patient, who is a scrap merchant, was admitted to our center for neuropsychiatric disturbances, including incoherent speech and hallucinations. He was initially diagnosed with autoimmune encephalitis (AE) because of double positivity for CASPR2 and LGl1 antibodies in serum. The patient later presented with pruritus and nephrotic syndrome, where renal biopsy revealed membranous nephropathy (MN). In view of the mercury exposure history and elevated urinary mercury level, AE and MN were suspected to be related to mercury poisoning. The patient achieved a full recovery following a four-month treatment regimen comprising immunosuppressants and mercury-chelating agents, underscoring the significance of recognizing environmental toxins such as mercury in the coexisting diseases of different systems such as AE and MN.

Although high mercury levels (> 100 μg/L in blood) have occasionally been reported in Canadian adults since the 1970s, mercury-induced signs and symptoms have never been comprehensively studied. Consequently, it is virtually impossible to establish diagnostic criteria for mercury intoxication at exposure levels relevant to northern Canada. Moreover, the evidence base for the health effects of long-term mercury exposure in Canadian adults is limited in scope and methodology. For example, among 135 Quebec Cree adults less than 40 years old, tremor was significantly associated with increasing mercury concentrations when measured by a general clinical examination but not by a specialized neurologic examination.40 The study was the result of a lawsuit, which may have compromised internal validity because participants with symptoms may have self-selected into the study. In a crosssectional study with a control group of nonexposed Japanese residents, First Nations adults from Grassy Narrows, Ontario, exhibited neurologic symptoms consistent with mercury poisoning, but the study lacked biomarker data of actual mercury exposure.41 Other cross-sectional studies conducted outside of Canada have also documented neurologic abnormalities in fisheating populations with comparable mercury exposure levels.42 In contrast to children, in whom the developing brain is a critical target of mercury toxicity, the cardiovascular system may be most sensitive in adults.1 Representative surveys of Nunavik Inuit and Cree adults documented associations between increasing blood mercury concentrations and risk markers for cardiovascular disease.43,44 Although the studies used crosssectional designs and had low response rates (< 50%), they had large samples (> 600) and adjusted extensively for confounders.43,44 It is possible that chronic conditions influence mercury metabolism and excretion, and thus affect exposure concentrations observed in crosssectional studies (e.g., reverse causality). In addition, cross-sectional studies cannot determine whether the observed mercury-induced cardiovascular damage occurred prenatally or postnatally. Two well-conducted nested case-control studies analyzing data from large prospective US cohorts found no association between mercury exposure and hypertension, nonfatal myocardial infarction, coronary artery disease or stroke in adults free of cardiovascular disease at baseline; however, exposure levels in these cohorts were lower than those typically observed in northern Canada.45,46 In the absence of prospective studies among adults with greater exposure levels, it may be justifiable to advise people with elevated cardiovascular risk to reduce mercury exposure as a precaution. We searched Embase, MEDLINE, Scopus and Google Scholar from 1994 to 2015 for English- and French-language epidemiologic studies conducted in Canada using the following search terms: \"mercury\" or \"methylmercury,\" and \"Canada,\" \"Nunavik,\" \"Nunavut,\" \"Northwest Territories,\" \"Yukon,\" \"Inuit,\" \"Cree,\" \"Dene,\" \"Metis,\" \"First Nations,\" \"indigenous,\" \"Aboriginal\" and \"fishermen.\" We conducted a cited reference search on all review articles on the topic. In addition, we reviewed books and technical reports from the National Academy of Sciences, the Arctic Monitoring and Assessment Programme and the World Health Organization.

Chelation for heavy metal intoxication began more than 70 years ago with the development of British anti-lewisite (BAL; dimercaprol) in wartime Britain as a potential antidote the arsenical warfare agent lewisite (dichloro[2-chlorovinyl]arsine). DMPS (unithiol) and DMSA (succimer), dithiol water-soluble analogs of BAL, were developed in the Soviet Union and China in the late 1950s. These three agents have remained the mainstay of chelation treatment of arsenic and mercury intoxication for more than half a century. Animal experiments and in some instances human data indicate that the dithiol chelators enhance arsenic and mercury excretion. Controlled animal experiments support a therapeutic role for these chelators in the prompt treatment of acute poisoning by arsenic and inorganic mercury salts. Treatment should be initiated as rapidly as possible (within minutes to a few hours), as efficacy declines or disappears as the time interval between metal exposure and onset of chelation increases. DMPS and DMSA, which have a higher therapeutic index than BAL and do not redistribute arsenic or mercury to the brain, offer advantages in clinical practice. Although chelation following chronic exposure to inorganic arsenic and inorganic mercury may accelerate metal excretion and diminish metal burden in some organs, potential therapeutic efficacy in terms of decreased morbidity and mortality is largely unestablished in cases of chronic metal intoxication.

Cinnabar is a natural mercury sulfide (HgS) mineral of volcanic or hydrothermal origin that is found worldwide. It has been mined prehistorically and historically in China, Japan, Europe and the Americas to extract metallic mercury (Hg 0 ) for use in metallurgy, as a medicinal, a preservative and as a red pigment for body paint and ceramics. Processing cinnabar via combustion releases Hg 0 vapor that can be toxic if inhaled. Mercury from cinnabar can also be absorbed through the gut and skin, where it can accumulate in organs and bone. Here, we report moderate to high levels of total mercury (THg) in human bone from three Late Neolithic/Chalcolithic (5400–4100 B.P.) sites in southern Portugal that were likely caused by cultural use of cinnabar. We use light stable isotope and Hg stable isotope tracking to test three hypotheses on the origin of mercury in this prehistoric human bone. We traced Hg in two individuals to cinnabar deposits near Almadén, Spain and conclude that use of this mineral likely caused mild to severe mercury poisoning in the prehistoric population. Our methods have applications to bioarchaeological investigations worldwide and for tracking trade routes and mobility of prehistoric populations where cinnabar use is documented.