• Journal of The Korean Society of Clinical Toxicology
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• v.12 no.1
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• pp.22-30
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• 2014

Purpose: The purpose of this systematic review was to evaluate the evidence regarding injury and poisoning associated with the clinical mercury thermometer. Methods: Electronic literature searches were conducted for identification of relevant studies and case reports of injury and poisoning associated with the clinical mercury thermometer. The search outcomes were limited to literature with English and Korean languages published from 1966. Studies related to occupational mercury exposure, or mercury exposure from sphygmomanometer, barometer, and fluorescent light were excluded. Results: A total of 60 reports, including 59 case reports, were finally included. Of those, nine cases pertained to an intact thermometer as a foreign body, 25 injuries were related to a thermometer, and 26 cases involved exposures to mercury from a broken thermometer. Case reports were classified according to severity into 16 mild, 41 moderate, and two severe cases. Two cases of mortality were reported, one was deliberate intravenous injection of mercury and the other was acute vapor inhalation of mercury from broken thermometers. Conclusion: Findings of this systematic review suggested that the mercury thermometer could cause various forms of poisoning and injury. In particular, inhalation of mercury vapor from a broken thermometer can lead to systemic toxicity requiring chelating therapy.

• Journal of Oral Medicine and Pain
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• v.9 no.1
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• pp.29-33
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• 1984

Dental mercury was injected accidentally to left upper buccal mucosa of a 16-year-old girl by charlatan in order to anesthetize a tooth for extraction; thereafter,injected elemental mercury was almost removed by drug adimnistration and surgical operations.One year have passed, still, there are many scaffered small radiopaque white globular cimages in dental, maxillo-facial, and chest radiographs. Redish swollen gingiva and mobility of left upper central incisor which is adjacent to mercury injection site are oral manifestations in this mercury poisoning case. Recently, the patient complains of metallic taste, gastric discomfort and abdominal pain which are thought to be symptoms of mercury poisoning, but there seems to be no serious sequelae now.

• Journal of Preventive Medicine and Public Health
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• v.47 no.2
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• pp.74-83
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• 2014

Mercury exists naturally and as a man-made contaminant. The release of processed mercury can lead to a progressive increase in the amount of atmospheric mercury, which enters the atmospheric-soil-water distribution cycles where it can remain in circulation for years. Mercury poisoning is the result of exposure to mercury or mercury compounds resulting in various toxic effects depend on its chemical form and route of exposure. The major route of human exposure to methylmercury (MeHg) is largely through eating contaminated fish, seafood, and wildlife which have been exposed to mercury through ingestion of contaminated lower organisms. MeHg toxicity is associated with nervous system damage in adults and impaired neurological development in infants and children. Ingested mercury may undergo bioaccumulation leading to progressive increases in body burdens. This review addresses the systemic pathophysiology of individual organ systems associated with mercury poisoning. Mercury has profound cellular, cardiovascular, hematological, pulmonary, renal, immunological, neurological, endocrine, reproductive, and embryonic toxicological effects.

• Journal of Life Science
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• v.11 no.3
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• pp.259-265
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• 2001

Mercury vapor inhalation-induced acute respiratory failure(ARF) has been reported to be fatal. This study was designed to observe the possible mechanism of inhaled mercury vapor poisoning in the respiratory system. Sixty percent of rats(12/20) exposed to mercury vapor were dead within 72 hours of exposure whereas all the rats(20/20) exposed to mercury vapor combined with dithiothreitol(DTT) vapor survived. The histological observation showed that ARF was a direct cause of the death induced by mercury vapor inhalation, which was significantly circumvented by DTT vapor. Cyclic AMP mediated chloride secretion was inhibited by luminal side but not serosal side sulfhydryl blocking agents (Hf$^{2+}$ $\rho$-chloromercuribenzoic acid or $\rho$-chloromercuriphenyl sulfonic acid) in a dose-dependent manner in a primary cultured rat airway monolayer. The inhibitory component of cAMP induced chloride secretion was completely restored by luminal side DTT(0.5mM). these results suggest that the oxidized form(Hg$^{2+}$) of mercury vapor(Hg0) contribute to ARF and subsequent death. The finding is important as it can provide important information regarding emergency manipulation of ARF patients suffering from by mercury vapor poisoning.ing.

• 월간산업보건
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• s.11
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• pp.7-12
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• 1989

A case of Occupational Mercury Poisoning Chung Yill Park, Chee Kyung Chung, Kwang Mook Lee and Seung Han Lee Catholic Industrial Medical Center,Catholic University Medical College, Seoul, Korea. The diagnosis of occupational mercury poisoning will depend on the exposure history, clininal symptoms and sings, laboratory findings and other informations such as laboratory results of other workers who have been worked under the same working condition. We diagnosed a 15 year-old male patient, who had been worked for 12 days at mercuny thermometer workshop, as occupational mercury poisoning by putting the above mentioned diagnostic bases together and reported here with brief rewiew of literature.

• Journal of The Korean Society of Clinical Toxicology
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• v.19 no.2
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• pp.127-132
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• 2021

Purpose: It is known that the most common cause of gas poisoning in Korea is suicide attempts by burning ignition coals. Ignition coals are made from waste wood, and studies have been reported that heavy metals are emitted when this coal is burned. However, there was no study on how much heavy metal poisoning occurs in the human body through this, so this study was planned to find out whether the concentration of heavy metals in the blood increased in patients exposed to ignition coal combustion. Methods: From April 2020 to April 2021, blood lead, mercury, and cadmium concentrations were investigated in carbon monoxide poisoning patients who visited one regional emergency medical center in Seoul, and their association with exposure time, source of poisoning, and rhabdomyolysis were investigated. Results: During the study period, a total of 136 carbon monoxide poisoning patients were tested for heavy metals, and 81 cases of poisoning by ignition coal were reported. When comparing poisoning caused by combustion of ignition coal and other substances, there was no difference in the concentrations of lead, mercury, and cadmium in the blood, and there was no difference in the number of patients above the reference range. However, the patients exposed to more than 5 hours of ignition coal gas exposure are more frequent than those in the group less than 5 hours in lead (51.4% vs. 23.9%, p=0.012). Conclusion: Compared to poisoning with other combustible substances, the blood concentration of lead, mercury, and cadmium does not increase further in patients with gas poisoning by ignition coal. However, prolonged exposure may result in elevated levels of lead.

• Journal of Ecology and Environment
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• v.47 no.2
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• pp.42-48
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• 2023

An adult male Eurasian river otter (Lutra lutra) with ataxia and lethargy was rescued. Through the necropsy of this otter with neurological symptoms, a broad range of vascular damage caused by mercury toxicity in several organs, hepatocellular necrosis, and vacuolation in the brain. In mercury examination, liver, kidney, and hair showed values of 0.878 ± 0.027, 1.807 ± 0.049, and 5.712 ± 0.102 ㎍/g, respectively. Compared with certified reference material, it was confirmed that the concentration of mercury were 6.7 times, 13.7 times, and 43.3 times higher, respectively. When the symptoms and diagnosis results were comprehensively reviewed, this otter's demise was revealed due to mercury poisoning. The mercury concentration in the liver does not exceed the lowest observed effect level of 3.4 ㎍/g. However, even at low concentrations, long-term accumulation can cause symptoms including neuropathy, and the possibility that these heavy metals have accumulated in other wild animals cannot be ruled out. It seems that continuous monitoring using sentinel animals is necessary.

• Journal of Environmental Health Sciences
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• v.31 no.6
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• pp.451-456
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• 2005

Minamata disease made its first appearance in the world at Minamata City, Kumamoto Prefecture, in May 1956. In 1962 methyl mercury poisoning through the placenta was found for the first time in the world. This was called congenital Minamata disease. In all cases the clinical symptoms were consistent with those of cerebral palsy. The time and place of outbreak were the same as those for Minamata disease. Their mothers had eaten fish and shellfish during pregnancy. The principal symptoms of congenital Minamata disease are mentalretardation ($100\%$); primitive reflexes ($100\%$); disturbance of coordination ($100\%$); dysarthria ($100\%$); limb deformation (100%); growth disorders ($100\%$); nutritional disorders ($100\%$); chorea-athetose ($95\%$); and hypersalivation ($95\%$). However, today, when the world is polluted by mercury in various places and at various levels, the data we need is not represented by those severe cases, but rather by the chronic milder type. Even in Minamata, the issue of Minamata disease has not been resolved. And likewise, on a global scale the problem of Minamata disease is not yet over.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.28 no.6
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• pp.413-420
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• 2002

Mercury is one of the most frequently used heavy metal in dental clinic. Mercury poisoning rises up when someone is exposed to mercury chronically. In 1818, Amalgam was used for dental restorative procedure, and after then study about mercury toxicity has begun. Clinical signs of mercury toxicity in oral & maxillofacial area were increases of salivation, metallic taste, swelling and pain of tongue, redness and ulceration of oral mucosa, and increased mobility and loss of teeth. After we injected mercury($HgCl_{2}$) into intraperitoneum of rat, studied about histopathological changes of submandibular gland cell. Experimental group was divided into two groups by amount of mercury. (Group 1 was 0.5mg/Kg of mercury injection, group 2 was 1.0mg/Kg of mercury injection.) 1. After 3days of intraperitoneal injection, black granules were observed at macrophage cell in both group. In group 2, author found hyperchromatism of nucleus, and vacuolization of cellular matrix and nucleus of acinar cell. 2. After 1week of intraperitoneal injection, author found severe vacuolization of nucleus and cellular matrix, and irregular granules around nuclear membrane at mucous cell and serous cell in both group. Vacuolization of nucleus and cellular matrix was seen at duct cell in group 2. 3. After 2weeks of intraperitoneal injection, author could found severe vacuolization of cellular matrix, and sometimes nucleus was positioned in central area of cellular matrix at mucous and serous cell in both group. Vacuolization of nucleus and cellular matrix was found at vascular endothelial cell in group 2. 4. After 4weeks of intraperitoneal injection, destruction and distortion of gland cells were distinct. Vacuolization and destruction of nucleus and cellular matrix was found at duct cell in group 2. After intraperitoneal injection of mercury, we found equanimity of mercury and destruction of cellular matrix at serous cell, mucous cell, and duct cell of submandibular gland. So, we thought that metallic taste of mercury poisoning patient would be due to excretion of saliva containing mercury.

• Journal of Preventive Medicine and Public Health
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• v.22 no.4 s.28
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• pp.474-479
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• 1989

This research was conducted to evaluate the effect of improvement in work environment and of segregation in a fluorescent lamp manufacturing factory. Among the total of 80 workers, 8 workers whose mercury concentration in urine reached a hazardous level ($200-299{\mu}g/l$) were moved to mercury free workplace. The follow-up examination for their mercury concentration in urine was done three times ; on May 3, 1988, September 1, 1988 and April 3, 1989. The results were as follows : 1. Mercury concentration in the air was reduced from 0.140 to 0.107 $mg/m^3$ in 4 months, and to $0.087mg/m^3$ in one year after environmental improvement in workplace. However the level still exceeded the Threshold Limit Value. 2. The geometric mean of urinary mercury concentration among 80 workers was $173.0{\mu}g/l\;(5.1{\sim}458.6{\mu}g/l$). The distribution of workers according to urinary mercury concentration showed that 9 workers (11.2%) were above the mercury poisoning level ($300{\mu}g/l$), 24 workers (30.0%) were $200-299{\mu}g/l$, 35 workers (43.8%) were $50-199{\mu}g/l$, and 12 workers (15.0%) were below 50 ${\mu}g/l$. 3. Among the 24 workers whose urinary mercury concentration was 200-299 $50-199{\mu}g/l$, 8 were able to be followed up. Their mean urinary mercury concentration before segregation was $244.9{\mu}g/l$, but decreased to $151.4{\mu}g/l$ in four months, $128.8{\mu}g/l$ in six months, and $46.8{\mu}g/l$ in one year after segregation.