Mercury poisoning is a type of metal poisoning due to exposure to mercury.[ Symptoms depend upon the type, dose, method, and duration of exposure.][ They may include muscle weakness, poor coordination, paraesthesia, skin rashes, anxiety, memory problems, trouble speaking, trouble hearing, or trouble seeing.][ Methylmercury exposure in children may result in acrodynia (pink disease) in which the skin becomes pink and peels.][ Long-term complications may include kidney problems and decreased intelligence.]
Forms of mercury exposure include Heavy metals, vapor, salt, and organic compound.[ Most exposure is from eating fish, amalgam-based dental fillings, or exposure at a workplace.][ In fish, those higher up in the food chain generally have higher levels of mercury, a process known as biomagnification.][ Less commonly, poisoning may occur as a method of attempted suicide.][ Human activities that release mercury into the environment include the burning of coal and mining of gold.]
Prevention includes eating a diet low in mercury, removing mercury from medical and other devices, proper disposal of mercury, and not mining further mercury.[ 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.][ Chelation for those with long-term exposure is of unclear benefit.][
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Signs and symptoms
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; desquamation (shedding or peeling of skin).
Mercury irreversibly inhibits selenium-dependent enzymes (see below) and may also inactivate S-adenosyl methionine, which is necessary for catecholamine catabolism by catechol- O-methyltransferase. Due to the body's inability to degrade catecholamines (e.g. adrenaline), a person with mercury poisoning may experience profuse , tachycardia (persistently faster-than-normal heart beat), increased salivation, and hypertension (high blood pressure).
Affected children may show red , human 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 Labile affect, memory impairment, or insomnia.
Thus, the clinical presentation may resemble pheochromocytoma or Kawasaki disease. Desquamation (skin peeling) can occur with severe mercury poisoning acquired by handling elemental mercury.
Causes
Historically, medicines could contain mercury and thus do more harm than good to patients. The popular Victorian medicine calomel contained mercury. In her 1859 autobiography, Scottish seamstress Elizabeth Storie describes her life as a disabled woman due to severe mercury poisoning when a doctor attempted to treat a mild childhood disease with prolonged administration of calomel.
Today, consumption of fish containing mercury is by far the most significant source of ingestion-related mercury exposure in humans, although plants and livestock also contain mercury due to bioconcentration of organic mercury from seawater, freshwater, marine and lacustrine sediments, soils, and atmosphere, and due to biomagnification by ingesting other mercury-containing organisms.
All of these, except elemental liquid mercury, produce toxicity or death with less than a gram. Mercury's zero oxidation state (Hg0) exists as vapor or as liquid metal, its mercurous state (Hg+) exists as inorganic salts, and its mercuric state (Hg2+) may form either inorganic salts or organomercury compounds.
Consumption of whale and dolphin meat, as is the practice in Japan, is a source of high levels of mercury poisoning.[ Mercury danger in dolphin meat. 2009 ]
Human-generated sources, such as coal-burning power plants
Small independent gold-mining operation workers are at higher risk of mercury poisoning because of crude processing methods.[ How mercury poisons gold miners and enters the food chain , BBC News]
Some mercury compounds, especially organomercury compounds, can also be readily absorbed through direct skin contact. Mercury and its compounds are commonly used in chemical laboratories, hospitals, dental clinics, and facilities involved in the production of items such as fluorescent light bulbs, batteries, and explosives.
Many traditional medicines, including ones used in Ayurvedic medicine,
Sources
Organic compounds of mercury tend to be much more toxic than either the elemental form or the salts. These compounds have been implicated in causing brain damage and hepatitis. The most dangerous mercury compound, dimethylmercury, is so toxic that even a few spilled on the skin, or even on a latex glove, can cause death.[
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Methylmercury and related organomercury compounds
Methylmercury is the major source of organic mercury for all individuals.[ What you need to know about mercury in fish and shellfish – Advice for women who might become pregnant women who are pregnant nursing mothers young children. U.S. FDA and U.S. EPA Advisory EPA-823-F-04-009, March 2004.] A 2006 review of the risks and benefits of fish consumption found, for adults, the benefits of one to two servings of fish per week outweigh the risks, even (except for a few fish species) for women of childbearing age, and that avoidance of fish consumption could result in significant excess coronary heart disease deaths and suboptimal neural development in children.
Because the process of mercury-dependent sequestration of selenium is slow, the period between exposure to methylmercury and the appearance of symptoms in adult poisoning cases tends to be extended. The longest recorded latent period is five months after a single exposure, in the Dartmouth case (see History); other latent periods in the range of weeks to months have also been reported. When the first symptom appears, typically paresthesia (a tingling or numbness in the skin), it is followed rapidly by more severe effects, sometimes ending in coma and death. The toxic damage appears to be determined by the peak value of mercury, not the length of the exposure.[
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Methylmercury exposure during rodent gestation, a developmental period that approximately models human neural development during the first two trimesters of gestation,
Ethylmercury is a breakdown product of the antibacteriological agent ethylmercurithiosalicylate, which has been used as a topical antiseptic and a vaccine preservative (further discussed under Thiomersal below). Its characteristics have not been studied as extensively as those of methylmercury. It is cleared from the blood much more rapidly, with a half-life of seven to ten days, and it is metabolized much more quickly than methylmercury. It is presumed not to have methylmercury's ability to cross the blood–brain barrier via a transporter, but instead relies on simple diffusion to enter the brain.[ Other exposure sources of organic mercury include phenylmercuric acetate and phenylmercuric nitrate. These compounds were used in indoor latex paints for their antimildew properties, but were removed in 1990 because of cases of toxicity.][
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Inorganic mercury compounds
Mercury occurs as salts such as mercuric chloride (HgCl2) and mercurous chloride (Hg2Cl2), the latter also known as calomel. Because they are more solubility in water, mercuric salts are usually more acutely toxic than mercurous salts. Their higher solubility lets them be more readily absorbed from the gastrointestinal tract. Mercury salts affect primarily the gastrointestinal tract and the , and can cause severe kidney damage; however, as they cannot cross the blood–brain barrier easily, these salts inflict little neurological damage without continuous or heavy exposure.[Emsley, John. The Elements of Murder. Oxford: Oxford University Press, 2005. ] The drug n-acetyl penicillamine has been used to treat mercury poisoning with limited success.["Mercuric Cyanide." 1987. (accessed April 2, 2009).]
Elemental mercury
Quicksilver (liquid metallic mercury) is poorly absorbed by ingestion and skin contact. Its vapor is the most hazardous form. Animal data indicate less than 0.01% of ingested mercury is absorbed through the intact gastrointestinal tract, though it may not be true for individuals with ileus. Cases of systemic toxicity from accidental swallowing are rare, and attempted suicide via intravenous injection does not appear to result in systemic toxicity,[ though it still causes damage by physically blocking blood vessels both at the site of injection and the lungs. Though not studied quantitatively, the physical properties of liquid elemental mercury limit its absorption through intact skin and in light of its very low absorption rate from the gastrointestinal tract, skin absorption would not be high.][ATSDR. 1999. Toxicological Profile for Mercury. Atlanta, GA:Agency for Toxic Substances and Disease Registry. ] Some mercury vapor is absorbed dermally, but uptake by this route is only about 1% of that by inhalation.
In humans, approximately 80% of inhaled mercury vapor is absorbed via the respiratory tract, where it enters the circulatory system and is distributed throughout the body.
Acute inhalation of high concentrations causes a wide variety of cognitive, personality, sensory, and motor disturbances. The most prominent symptoms include (initially affecting the hands and sometimes spreading to other parts of the body), emotional lability (characterized by irritability, excessive shyness, confidence loss, and nervousness), insomnia, memory loss, neuromuscular changes (weakness, muscle atrophy, muscle twitching), headaches, polyneuropathy (paresthesia, stocking-glove sensory loss, hyperactive tendon reflexes, slowed sensory and motor nerve conduction velocities), and performance deficits in tests of cognitive function.
Mechanism
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).
Mercury in its various forms is particularly harmful to as an environmental toxin in pregnancy, as well as to . 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).
Diagnosis
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.[
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Diagnosis of organic mercury poisoning differs in that whole-blood or hair analysis is more reliable than urinary mercury levels.
Prevention
Mercury poisoning can be prevented or minimized by eliminating or reducing exposure to mercury and mercury compounds. To that end, many governments and private groups have made efforts to heavily regulate the use of mercury, or to issue advisories about the use of mercury. Most countries have signed the Minamata Convention on Mercury.
The export from the European Union of mercury and some mercury compounds has been prohibited since 15 March 2011.
+US environmental limits[ ATSDR – Mercury – Regulations and Advisories ]
!Country
!Regulating agency
!Regulated activity
!Medium
!Type of mercury compound
!Type of limit
!Limit |
| US | Occupational Safety and Health Administration | occupational exposure | air | elemental mercury | Ceiling (not to exceed) | 0.1 mg/m3 |
| US | Occupational Safety and Health Administration | occupational exposure | air | organic mercury | Ceiling (not to exceed) | 0.05 mg/m3 |
| US | Food and Drug Administration | eating | sea food | methylmercury | Maximum allowable concentration | 1 ppm (1 mg/L) |
| US | Environmental Protection Agency | drinking | water | inorganic mercury | Maximum contaminant level | 2 ppb (0.002 mg/L) |
The United States Environmental Protection Agency (EPA) issued recommendations in 2004 regarding exposure to mercury in fish and shellfish.[ FDA/EPA 2004 Advice on What You Need to Know About Mercury in Fish and Shellfish ] The EPA also developed the "Fish Kids" awareness campaign for children and young adults [ EPA Fish Kids Flash-based movie ] on account of the greater impact of mercury exposure to that population.
Cleaning spilled mercury
Mercury thermometers and mercury light bulbs are not as common as they used to be, and the amount of mercury they contain is unlikely to be a health concern if handled carefully. However, broken items still require careful cleanup, as mercury can be hard to collect and it is easy to accidentally create a much larger exposure problem.[ Cleaning Up Spilled Mercury ] If available, powdered sulfur may be applied to the spill, in order to create a solid compound that is more easily removed from surfaces than liquid mercury.
Treatment
Identifying and removing the source of the mercury is crucial. Decontamination requires removal of clothes, washing skin with soap and water, and flushing the eyes with saline solution as needed.
Before the advent of organic chelating agents, salts of iodide were given orally, such as heavily popularized by Louis Melsens and many nineteenth and early twentieth century doctors.[ "Sur l'emploi de l'iodure de potassium pour combattre les affections saturnines et mercurielles", in Annales de chimie et de physique, t. 26, 3e série, 1849.][ "On the Employment of Iodide of Potassium as a Remedy for the Affections Caused by Lead and Mercury", in Br Foreign Med Chir Rev. 1853 Jan; 11(21): 201–224.]
Chelation therapy
Chelation therapy for acute inorganic mercury poisoning, a formerly common method, was done with DMSA, 2,3-dimercapto-1-propanesulfonic acid (DMPS), penicillamine (DPCN), or dimercaprol (BAL).[ Only DMSA is FDA-approved for use in children for treating mercury poisoning. However, several studies found no clear clinical benefit from DMSA treatment for poisoning caused by mercury vapor.][ Lipoic acid (ALA) has been shown to be protective against acute mercury poisoning in several mammalian species when it is given soon after exposure; correct dosage is required, as inappropriate dosages increase toxicity. Although it has been hypothesized that frequent low dosages of ALA may have potential as a mercury chelator, studies in rats have been contradictory.][ Glutathione and acetylcysteine (NAC) are recommended by some physicians, but have been shown to increase mercury concentrations in the kidneys and the brain.]
Chelation therapy can be hazardous if administered incorrectly. In August 2005, edetate disodium, an incorrect form of EDTA for chelation therapy, resulted in hypocalcemia leading to cardiac arrest that killed a five-year-old autistic boy.[Hazards of chelation therapy:
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Other
Experimental animal and epidemiological study findings have confirmed the interaction between selenium and methylmercury. Instead of causing a decline in neurodevelopmental outcomes, epidemiological studies have found that improved nutrient (i.e., omega-3 fatty acids, selenium, iodine, vitamin D) intakes as a result of ocean fish consumption during pregnancy improves maternal and fetal outcomes.
Prognosis
Some of the toxic effects of mercury are partially or wholly reversible provided specific therapy is able to restore selenium availability to normal before tissue damage from oxidation becomes too extensive.
Mercuric chloride may Carcinogen as rats and mice treated with the substance have gone on to develop several types of tumors, while male rats treated with methyl mercury have gone on to develop kidney tumors. The EPA has classified mercuric chloride and methyl mercury as possible human carcinogens (ATSDR, EPA)
Detection in biological fluids
Mercury may be measured in blood or urine to confirm a diagnosis of poisoning in hospitalized people or to assist in the forensic investigation in a case of fatal over dosage. Some analytical techniques are capable of distinguishing organic from inorganic forms of the metal. The concentrations in both fluids tend to reach high levels early after exposure to inorganic forms, while lower but very persistent levels are observed following exposure to elemental or organic mercury. Chelation therapy can cause a transient elevation of urine mercury levels.[R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 923–927.]
History
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Neolithic artists using cinnabar show signs of mercury poisoning.
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Several Chinese emperors and other Chinese nobles are known or suspected to have died or been sickened by mercury poisoning after alchemists administered them "elixirs" to promote health, longevity, or immortality that contained either elemental mercury or (more commonly) cinnabar. Among the most prominent examples:
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The first emperor of unified China, Qin Shi Huang, it is reported, died in 210 BC of ingesting mercury pills that were intended to give him eternal life.
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Emperor Xuānzong of Tang, one of the emperors of the late Tang dynasty of China, was prescribed "cinnabar that had been treated and subdued by fire" to achieve immortality.
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In his Natural History, 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.
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Carl Scheele, a significant 18th century Sweden pioneer of chemical research, died from mercury poisoning arising from his work, at the relatively early age of 43.
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The phrase mad as a hatter is likely a reference to mercury poisoning among (so-called "Erethism"), as mercury-based compounds were once used in the manufacture of Felt 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.)
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In 1810, two British ships, HMS Triumph and , 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.
[An Account of the Effect of Mercurial Vapors on the Crew of His Majesty's Ship Triumph, in the year 1810. By Wm. Burnett, M.D. one of the Medical Commissioners of the Navy, formerly Physician and Inspector of Hospitals to the Mediterranean Fleet.] Triumph 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.[Michael J. Doherty MD: The Quicksilver Prize: Mercury vapor poisoning aboard HMS Triumph and HMS Phipps (2003).]
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Historically, gold-mercury amalgam was widely used in gilding, 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.
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For years, including the early part of his presidency, Abraham Lincoln took a common medicine of his time called "blue mass", which contained significant amounts of mercury.
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On September 5, 1920, silent movie actress Olive Thomas ingested mercury capsules dissolved in an alcoholic solution at the Hotel Ritz in Paris.
[Foster, Charles (2000). Stardust and Shadows: Canadians in Early Hollywood, page 257. Toronto, Canada: Dundurn Press, 2000. .]
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An early scientific study of mercury poisoning was in 1923–1926 by the German inorganic chemist, Alfred Stock, who himself became poisoned, together with his colleagues, by breathing mercury vapor that was being released by his laboratory equipment—, , and —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.
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The term Hunter-Russell syndrome derives from a study of mercury poisoning among workers in a seed-packaging factory in Norwich, England in the late 1930s who breathed methylmercury that was being used as a seed disinfectant and pesticide.
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Outbreaks of methylmercury 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.
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Mercury poisoning of generations of Grassy Narrows 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 of mercury directly into the Wabigoon River–English River system and continued with mercury air pollution until 1975.
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Widespread mercury poisoning occurred in rural Iraq 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).
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On August 14, 1996, Karen Wetterhahn, 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.
[ The Karen Wetterhahn story – University of Bristol web page documenting her death, retrieved December 9, 2006.][ OSHA update following Karen Wetterhahn's death ]
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In April 2000, Alan Chmurny attempted to kill a former employee, Marta Bradley, by pouring mercury into the ventilation system of her car.
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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.
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In December 2008, actor Jeremy Piven was diagnosed with mercury poisoning possibly resulting from eating sushi twice a day for twenty years or from taking herbal remedies.
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In India, a study by Centre for Science and Environment 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.
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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—Earth Day. It was the sixtieth anniversary of the discovery of the disease.
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In August 2024, chess player Amina Abakarova allegedly attempted to poison her rival, Umayganat Osmanova, by coating chess pieces in mercury from a thermometer.
Infantile acrodynia
Infantile acrodynia (also known as "calomel disease", "erythredemic polyneuropathy", and "pink disease") is a type of mercury poisoning in children characterized by pain and pink discoloration of the hands and feet.
Acrodynia is difficult to diagnose; "it is most often postulated that the etiology of this syndrome is an idiosyncratic hypersensitivity reaction to mercury because of the lack of correlation with mercury levels, many of the symptoms resemble recognized mercury poisoning."
Medicine
Mercury was once prescribed as a purgative.
Thiomersal
In 1999, the Centers for Disease Control (CDC) and the American Academy of Pediatrics (AAP) asked vaccine makers to remove the organomercury compound thiomersal (spelled "thimerosal" in the US) from vaccines as quickly as possible, and thiomersal has been phased out of US and European vaccines, except for some preparations of influenza vaccine.
Since 2000, the thiomersal in child vaccines has been alleged to contribute to autism, and thousands of parents in the United States have pursued legal compensation from a federal fund.
Dental amalgam toxicity
Dental amalgam is a possible cause of low-level mercury poisoning due to its use in . Discussion on the topic includes debates on whether amalgam should be used, with critics arguing that its toxic effects make it unsafe.
Cosmetics
Some skin whitening products contain the toxic mercury(II) chloride as the active ingredient. When applied, the chemical readily absorbs through the skin into the bloodstream.[FDA bans hydroquinone in skin whitening products][In a survey, 28% of Koreans and 50% of Philippians say that they use skin whitening products.] In Hong Kong in 2002, two products were discovered to contain between 9,000 and 60,000 times the recommended dose.
Fluorescent lamps
contain mercury, which is released when bulbs break. Mercury in bulbs is typically present as either elemental mercury liquid, vapor, or both, since the liquid evaporates at ambient temperature.
Assassination attempts
Mercury has, allegedly, been used at various times to assassinate people. In 2008, Russian lawyer Karinna Moskalenko claimed to have been poisoned by mercury left in her car,
In 2011, German Christoph Bulwin was poisoned with a mercury compound from a syringe attached to an umbrella.
See also
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Environmental impact of the coal industry
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Got Mercury?, a public awareness campaign
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Mercury vacuum
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Mercury-Containing and Rechargeable Battery Management Act
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Niigata Minamata disease
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Ontario Minamata disease
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Mercury contamination in Grassy Narrows, Ontario, Canada
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Mercury cycle
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Mercury methylation
External links
