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Mercury poisoning

Mercury poisoning is a type of metal poisoning due to exposure to mercury.[3] Symptoms depend upon the type, dose, method, and duration of exposure.[3][4] They may include muscle weakness, poor coordination, numbness in the hands and feet, skin rashes, anxiety, memory problems, trouble speaking, trouble hearing, or trouble seeing.[1] High-level exposure to methylmercury is known as Minamata disease.[2] Methylmercury exposure in children may result in acrodynia (pink disease) in which the skin becomes pink and peels.[2] Long-term complications may include kidney problems and decreased intelligence.[2] The effects of long-term low-dose exposure to methylmercury are unclear.[6]

Not to be confused with Heavy metal poisoning.

Mercury poisoning

Mercury toxicity, mercury overdose, mercury intoxication, hydrargyria, mercurialism

Toxicology

Muscle weakness, poor coordination, numbness in the hands and feet[1]

Kidney problems, decreased intelligence[2]

Exposure to mercury[1]

Consumption of fish, which may contain mercury[3]

Difficult[3]

Decreasing use of mercury, low mercury diet[4]

Acute poisoning: dimercaptosuccinic acid (DMSA), dimercaptopropane sulfonate (DMPS)[5]

Forms of mercury exposure include metal, vapor, salt, and organic compound.[3] Most exposure is from eating fish, amalgam-based dental fillings, or exposure at a workplace.[3] In fish, those higher up in the food chain generally have higher levels of mercury, a process known as biomagnification.[3] Less commonly, poisoning may occur as a method of attempted suicide.[3] Human activities that release mercury into the environment include the burning of coal and mining of gold.[4][7] Tests of the blood, urine, and hair for mercury are available but do not relate well to the amount in the body.[3]


Prevention includes eating a diet low in mercury, removing mercury from medical and other devices, proper disposal of mercury, and not mining further mercury.[4][2] In those with acute poisoning from inorganic mercury salts, chelation with either dimercaptosuccinic acid (DMSA) or dimercaptopropane sulfonate (DMPS) appears to improve outcomes if given within a few hours of exposure.[5] Chelation for those with long-term exposure is of unclear benefit.[5] In certain communities that survive on fishing, rates of mercury poisoning among children have been as high as 1.7 per 100.[4]

Signs and symptoms[edit]

Common symptoms of mercury poisoning are peripheral neuropathy, presenting as paresthesia or itching, burning, pain, or even a sensation that resembles small insects crawling on or under the skin (formication); skin discoloration (pink cheeks, fingertips and toes); swelling; and desquamation (shedding or peeling of skin).[8]


Mercury irreversibly inhibits selenium-dependent enzymes (see below) and may also inactivate S-adenosyl-methionine, which is necessary for catecholamine catabolism by catechol-O-methyl transferase. Due to the body's inability to degrade catecholamines (e.g. adrenaline), a person with mercury poisoning may experience profuse sweating, tachycardia (persistently faster-than-normal heart beat), increased salivation, and hypertension (high blood pressure).[9]


Affected children may show red cheeks, nose and lips, loss of hair, teeth, and nails, transient rashes, hypotonia (muscle weakness), and increased sensitivity to light. Other symptoms may include kidney dysfunction (e.g. Fanconi syndrome) or neuropsychiatric symptoms such as emotional lability, memory impairment, or insomnia.[10]


Thus, the clinical presentation may resemble pheochromocytoma or Kawasaki disease. Desquamation (skin peeling) can occur with severe mercury poisoning acquired by handling elemental mercury.[11]

Mechanism[edit]

The toxicity of mercury sources can be expected to depend on its nature, i.e., salts vs. organomercury compounds vs. elemental mercury.


The primary mechanism of mercury toxicity involves its irreversible inhibition of selenoenzymes, such as thioredoxin reductase (IC50 = 9 nM).[53] Although it has many functions, thioredoxin reductase restores vitamins C and E, as well as a number of other important antioxidant molecules, back into their reduced forms, enabling them to counteract oxidative damage.[54] Since the rate of oxygen consumption is particularly high in brain tissues, production of reactive oxygen species (ROS) is accentuated in these vital cells, making them particularly vulnerable to oxidative damage and especially dependent upon the antioxidant protection provided by selenoenzymes. High mercury exposures deplete the amount of cellular selenium available for the biosynthesis of thioredoxin reductase and other selenoenzymes that prevent and reverse oxidative damage,[55] which, if the depletion is severe and long lasting, results in brain cell dysfunctions that can ultimately cause death.


Mercury in its various forms is particularly harmful to fetuses as an environmental toxin in pregnancy, as well as to infants. Women who have been exposed to mercury in substantial excess of dietary selenium intakes during pregnancy are at risk of giving birth to children with serious birth defects, such as those seen in Minamata disease. Mercury exposures in excess of dietary selenium intakes in young children can have severe neurological consequences, preventing nerve sheaths from forming properly.


Exposure to methylmercury causes increased levels of antibodies sent to myelin basic protein (MBP), which is involved in the myelination of neurons, and glial fibrillary acidic protein (GFAP), which is essential to many functions in the central nervous system (CNS).[56] This causes an autoimmmune response against MBP and GFAP and results in the degradation of neural myelin and general decline in function of the CNS.[57]

Diagnosis[edit]

Diagnosis of elemental or inorganic mercury poisoning involves determining the history of exposure, physical findings, and an elevated body burden of mercury. Although whole-blood mercury concentrations are typically less than 6 μg/L, diets rich in fish can result in blood mercury concentrations higher than 200 μg/L; it is not that useful to measure these levels for suspected cases of elemental or inorganic poisoning because of mercury's short half-life in the blood. If the exposure is chronic, urine levels can be obtained; 24-hour collections are more reliable than spot collections. It is difficult or impossible to interpret urine samples of people undergoing chelation therapy, as the therapy itself increases mercury levels in the samples.[58]


Diagnosis of organic mercury poisoning differs in that whole-blood or hair analysis is more reliable than urinary mercury levels.[58]

Neolithic artists using show signs of mercury poisoning.[77]

cinnabar

Qin Shi Huang

In his , Pliny the Elder writes that "it is a fact generally admitted that [cinnabar] is a poison" and warns against using it in medicine, also noting that workers polishing it "tie on their face loose masks of bladder-skin, to prevent their inhaling the dust in breathing", one of the earliest mentions of PPE.[80]

Natural History

a significant 18th century Swedish pioneer of chemical research, died from mercury poisoning arising from his work, at the relatively early age of 43.[81]

Carl Scheele

The phrase is likely a reference to mercury poisoning among milliners (so-called "mad hatter disease"), as mercury-based compounds were once used in the manufacture of felt hats in the 18th and 19th century. (The Mad Hatter character of Alice in Wonderland was, it is presumed, inspired by an eccentric furniture dealer named Theophilus Carter. Carter was not a victim of mad hatter disease although Lewis Carroll would have been familiar with the phenomenon of dementia that occurred among hatters.)[82][83]

mad as a hatter

In 1810, two British ships, and HMS Phipps, salvaged a large load of elemental mercury from a wrecked Spanish vessel near Cadiz, Spain. The bladders containing the mercury soon ruptured. The element spread about the ships in liquid and vapor forms. The sailors presented with neurologic compromises: tremor, paralysis, and excessive salivation as well as tooth loss, skin problems, and pulmonary complaints. In 1823 William Burnett, M.D. published a report on the effects of mercurial vapor.[84] Triumph's surgeon, Henry Plowman, had concluded that the ailments had arisen from inhaling the mercurialized atmosphere. His treatment was to order the lower deck gun ports to be opened, when it was safe to do so; sleeping on the orlop was forbidden; and no men slept in the lower deck if they were at all symptomatic. Windsails were set to channel fresh air into the lower decks day and night.[85]

HMS Triumph

Historically, gold-mercury amalgam was widely used in , applied to the object and then heated to vaporize the mercury and deposit the gold, leading to numerous casualties among the workers. It is estimated that during the construction of Saint Isaac's Cathedral alone, 60 men died from the gilding of the main dome.[86][87]

gilding

For years, including the early part of his presidency, took a common medicine of his time called "blue mass", which contained significant amounts of mercury.

Abraham Lincoln

On September 5, 1920, silent movie actress ingested mercury capsules dissolved in an alcoholic solution at the Hotel Ritz in Paris.[88] There is still controversy over whether it was suicide, or whether she consumed the external preparation by mistake. Her husband, Jack Pickford (the brother of Mary Pickford), had syphilis, and the mercury was used as a treatment of the venereal disease at the time. She died a few days later at the American Hospital in Neuilly.[89]

Olive Thomas

An early scientific study of mercury poisoning was in 1923–1926 by the German inorganic chemist, , who himself became poisoned, together with his colleagues, by breathing mercury vapor that was being released by his laboratory equipment—diffusion pumps, float valves, and manometers—all of which contained mercury, and also from mercury that had been accidentally spilt and remained in cracks in the linoleum floor covering. He published a number of papers on mercury poisoning, founded a committee in Berlin to study cases of possible mercury poisoning, and introduced the term micromercurialism.[90]

Alfred Stock

The term Hunter-Russell syndrome derives from a study of mercury poisoning among workers in a seed-packaging factory in , England in the late 1930s who breathed methylmercury that was being used as a seed disinfectant and pesticide.[91]

Norwich

Outbreaks of poisoning occurred in several places in Japan during the 1950s due to industrial discharges of mercury into rivers and coastal waters. The best-known instances were in Minamata and Niigata. In Minamata alone, more than 600 people died due to what became known as Minamata disease. More than 21,000 people filed claims with the Japanese government, of which almost 3000 became certified as having the disease. In 22 documented cases, pregnant women who consumed contaminated fish showed mild or no symptoms but gave birth to infants with severe developmental disabilities.[92]

methylmercury

Mercury poisoning of generations of and Whitedog native people in Ontario, Canada who were exposed to high levels of mercury by consuming mercury-contaminated fish when Dryden Chemical Company discharged over 9,000 kilograms (20,000 lb) of mercury directly into the Wabigoon–English River system and continued with mercury air pollution until 1975.[93][94][95][96]

Grassy Narrows

Widespread mercury poisoning occurred in rural in 1971–1972, when grain treated with a methylmercury-based fungicide that was intended for planting only was used by the rural population to make bread, causing at least 6530 cases of mercury poisoning and at least 459 deaths (see Basra poison grain disaster).[97]

Iraq

On August 14, 1996, , a chemistry professor working at Dartmouth College, spilled a small amount of dimethylmercury on her latex glove. She began experiencing the symptoms of mercury poisoning five months later and, despite aggressive chelation therapy, died a few months later from a mercury induced neurodegenerative disease[36][37]

Karen Wetterhahn

In April 2000, Alan Chmurny attempted to kill a former employee, Marta Bradley, by pouring mercury into the system of her car.[98][99]

ventilation

On March 19, 2008, Tony Winnett, 55, inhaled mercury vapors while trying to extract gold from computer parts (by using liquid mercury to separate gold from the rest of the alloy), and died ten days later. His Oklahoma residence became so contaminated that it had to be gutted.[101]

[100]

In December 2008, actor was diagnosed with mercury poisoning possibly resulting from eating sushi twice a day for twenty years or from taking herbal remedies.[102]

Jeremy Piven

In India, a study by and Indian Institute of Toxicology Research has found that in the country's energy capital Singrauli, mercury is slowly entering people's homes, food, water and even blood.[103]

Centre for Science and Environment

The Minamata Convention on Mercury in 2016 announced that the signing of the "international treaty designed to protect human health and the environment from anthropogenic releases and emission of mercury and mercury compounds" on April 22, 2016—. It was the sixtieth anniversary of the discovery of the disease.[104]

Earth Day

at Curlie

Hazardous Substances: Mercury

at Curlie

Toxic Substances: Mercury