Mercury poisoning

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Mercury poisoning
Classification and external resources

ICD-10 T56.1
ICD-9 985.0
DiseasesDB 8057
MedlinePlus 002476
eMedicine emerg/813
MeSH D008630

Mercury poisoning (also known as hydrargyria or mercurialism) is a disease caused by exposure to mercury or its compounds. Mercury (chemical symbol Hg) is a heavy metal occurring in several forms, all of which can produce toxic effects in high enough doses. Its zero oxidation state Hg0 exists as vapor or as liquid metal, its mercurous state Hg22+ exists as inorganic salts, and its mercuric state Hg2+ may form either inorganic salts or organomercury compounds; the three groups vary in effects. Toxic effects include damage to the brain, kidney, and lungs.[1] Mercury poisoning can result in several diseases, including acrodynia (pink disease),[2] Hunter-Russell syndrome, and Minamata disease.[3]

Symptoms typically include sensory impairment (vision, hearing, speech), disturbed sensation and a lack of coordination. The type and degree of symptoms exhibited depend upon the individual toxin, the dose, and the method and duration of exposure.

Signs and symptoms

Common symptoms of mercury poisoning include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), swelling, and desquamation (shedding 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-methyl transferase. Due to the body's inability to degrade catecholamines (e.g. epinephrine), a person suffering from mercury poisoning may experience profuse sweating, tachycardia (persistently faster-than-normal heart beat), increased salivation, and hypertension (high blood pressure).

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, and / or insomnia.

Thus, the clinical presentation may resemble pheochromocytoma or Kawasaki disease.

An example of desquamation (skin peeling) of the hand of a child with severe mercury poisoning acquired by handling elemental mercury is this photograph in Horowitz, et al. (2002).[4]

Causes

The consumption of fish is by far the most significant source of ingestion-related mercury exposure in humans and animals, although plants and livestock also contain mercury due to bioconcentration of mercury from seawater, freshwater, marine and lacustrine sediments, soils, and atmosphere, and due to biomagnification by ingesting other mercury-containing organisms.[5] Exposure to mercury can occur from breathing contaminated air,[6] from eating foods that have acquired mercury residues during processing,[7] from exposure to mercury vapor in mercury amalgam dental restorations,[8] and from improper use or disposal of mercury and mercury-containing objects, for example, after spills of elemental mercury or improper disposal of fluorescent lamps.[9]

Consumption of whale and dolphin meat, as is the practice in Japan, is a source of high levels of mercury poisoning. Tetsuya Endo, a professor at the Health Sciences University of Hokkaido, has tested whale meat purchased in the whaling town of Taiji and found mercury levels more than 20 times the acceptable Japanese standard.[10]

Human-generated sources, such as coal-fired power plants, emit about half of atmospheric mercury, with natural sources such as volcanoes responsible for the remainder. An estimated two-thirds of human-generated mercury comes from stationary combustion, mostly of coal. Other important human-generated sources include gold production, nonferrous metal production, cement production, waste disposal, human crematoria, caustic soda production, pig iron and steel production, mercury production (mostly for batteries), and biomass burning.[11]

Small independent gold-mining operation workers are at higher risk of mercury poisoning because of crude processing methods. Such is the danger for the galamsey in Ghana and similar workers known as orpailleurs in neighboring francophone countries. While no official government estimates of the labor force have been made, observers believe 20,000-50,000 work as galamseys in Ghana, a figure including many women, who work as porters. Similar problems have been reported amongst the gold miners of Indonesia.[12]

Mercury and many of its chemical compounds, especially organomercury compounds, can also be readily absorbed through direct contact with bare, or in some cases (such as methylmercury) insufficiently protected, skin. 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.[13]

On the other hand, no scientific data supports the claim that mercury in vaccines causes autism[14] or its symptoms,[15]

Mechanism

Mercury is highly reactive with selenium, an essential dietary element required by about 25 genetically distinct enzyme types (selenoenzymes).[16] Among their numerous functions, selenoenzymes prevent and reverse oxidative damage in the brain and endocrine organs. The molecular mechanism of mercury toxicity involves its unique ability to irreversibly inhibit activities of selenoenzymes, such as thioredoxin reductase (IC50 = 9 nM).[17] Although it has many additional 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 within body cells.[18] 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,[19] 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. Mercury exposures in excess of dietary selenium intakes in young children can have severe neurological consequences, preventing nerve sheaths from forming properly. Mercury inhibits the formation of myelin.

According to some evidence, mercury poisoning may predispose to Young's syndrome (men with bronchiectasis and low sperm count).[20]

Because of differences in tissue distributions, mercury poisoning's effects will differ depending on whether it has been caused by exposure to elemental mercury, inorganic mercury compounds (as salts), or organomercury compounds.

Elemental mercury

Quicksilver (liquid metallic mercury) is poorly absorbed by ingestion and skin contact. It is hazardous due to its potential to release mercury vapor. 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 suffering from ileus. Cases of systemic toxicity from accidental swallowing are rare, and attempted suicide via intravenous injection does not appear to result in systemic toxicity.[21] 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.[22] Some mercury vapor is absorbed dermally, but uptake by this route is only about 1% of that by inhalation.[23]

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.[24] Chronic exposure by inhalation, even at low concentrations in the range 0.7–42 μg/m3, has been shown in case control studies to cause effects such as tremors, impaired cognitive skills, and sleep disturbance in workers.[25][26]

Acute inhalation of high concentrations causes a wide variety of cognitive, personality, sensory, and motor disturbances. The most prominent symptoms include tremors (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.[22]

Inorganic mercury compounds

Mercury occurs inorganically as salts such as mercury(II) chloride. Mercury salts affect primarily the gastrointestinal tract and the kidneys, and can cause severe kidney damage; however, as they cannot cross the blood–brain barrier easily, mercury salts inflict little neurological damage without continuous or heavy exposure.[27] As two oxidation states of mercury form salts (Hg22+ and Hg2+), mercury salts occur in both mercury(I) (or mercurous) and mercury(II) (mercuric) forms. Mercury(II) salts are usually more toxic than their mercury(I) counterparts because their solubility in water is greater; thus, they are more readily absorbed from the gastrointestinal tract.[27]

Mercuric cyanide

Mercuric cyanide (also known as Mercury (II) cyanide), Hg(CN)2, is a particularly toxic mercury compound. If ingested, both life-threatening mercury and cyanide poisoning can occur. Hg(CN)2 can enter the body via inhalation, ingestion, or passage through the skin. Inhalation of mercuric cyanide irritates the throat and air passages. Heating or contact of Hg(CN)2 with acid or acid mist releases toxic mercury and cyanide vapors that can cause bronchitis with cough and phlegm and/or lung tissue irritation. Contact with eyes can cause burns and brown stains in the eyes, and long-time exposure can affect the peripheral vision. Contact with skin can cause skin allergy, irritation, and gray skin color.[28]

Chronic exposure to trace amounts of the compound can lead to mercury buildup in the body over time; it may take months or even years for the body to eliminate excess mercury. Overexposure to mercuric cyanide can lead to kidney damage and/or mercury poisoning, leading to 'shakes' (ex: shaky handwriting), irritability, sore gums, increased saliva, metallic taste, loss of appetite, memory loss, personality changes, and brain damage. Exposure to large doses at one time can lead to sudden death.[28]

Mercuric cyanide has not been tested on its ability to cause reproductive damage. Although inorganic mercury compounds (such as Hg(CN)2) have not been shown to be human teratogens, they should be handled with care, as they are known to damage developing embryos and decrease fertility in men and women.[28]

According to one study, two people exhibited symptoms of cyanide poisoning within hours after ingesting mercuric cyanide or mercury oxycyanide, Hg(CN)2•HgO, in suicide attempts. The toxicity of Hg(CN)2 is commonly assumed to arise almost exclusively from mercury poisoning; however, the patient who ingested mercury oxycyanide died after five hours of cyanide poisoning before any mercury poisoning symptoms were observed. The patient who ingested Hg(CN)2 initially showed symptoms of acute cyanide poisoning, which were brought under control, and later showed signs of mercury poisoning before recovering. The degree to which cyanide poisoning occurs is thought to be related to whether cyanide ions are released in the stomach, which depends on factors such as the amount ingested, stomach acidity, and volume of stomach contents.[29] Given that Hg(CN)2 molecules remain undissociated in pure water and in basic solutions,[30] it makes sense that dissociation would increase with increasing acidity. High stomach acidity thus helps cyanide ions to become more bioavailable, increasing the likelihood of cyanide poisoning.

Mercury cyanide was used in two murders in New York in 1898. The perpetrator, Roland B. Molineux, sent poisoned medicines to his victims through the US mail. The first victim, Henry Barnett, died of mercury poisoning 12 days after taking the poison. The second victim, Catherine Adams, died of cyanide poisoning within 30 minutes of taking the poison. As in the suicide cases, the difference between the two cases may be attributed to differences in the acidities of the solutions containing the poison, or to differences in the acidities of the victims' stomachs.[31]

The drug n-acetyl penicillamine has been used to treat mercury poisoning with limited success.[28]

Organic mercury compounds

Compounds of mercury tend to be much more toxic than the elemental form, and organic compounds of mercury are often extremely toxic and have been implicated in causing brain and liver damage. The most dangerous mercury compound, dimethylmercury, is so toxic that even a few microliters spilled on the skin, or even a latex glove, can cause death, as in the case of Karen Wetterhahn.[32][33]

Methylmercury

Main article: Mercury in fish

Methylmercury is the major source of organic mercury for all individuals.[1] It works its way up the food chain through bioaccumulation in the environment, reaching high concentrations among populations of some species. Top predatory fish, such as tuna or swordfish, are usually of greater concern than smaller species. The US FDA and the EPA advise women of child-bearing age, nursing mothers, and young children to completely avoid swordfish, shark, king mackerel and tilefish from the Gulf of Mexico, and to limit consumption of albacore ("white") tuna to no more than 6 oz (170 g) per week, and of all other fish and shellfish to no more than 12 oz (340 g) per week.[34] 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.[35][35]

The period between exposure to methylmercury and the appearance of symptoms in adult poisoning cases is long. 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. No explanation for this long latent period is known. 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.[21]

Ethylmercury

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 10 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.[1]

Other sources

Other exposure sources of organic mercury include phenylmercuric acetate and phenylmercuric nitrate. These were used in indoor latex paints for their antimildew properties, but were removed in 1990 because of cases of toxicity.[1]

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 patients undergoing chelation therapy, as the therapy itself increases mercury levels in the samples.[36]

Diagnosis of organic mercury poisoning differs in that whole-blood or hair analysis is more reliable than urinary mercury levels.[36]

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 regulate heavily the use of mercury, or to issue advisories about its use. For example, the export from the European Union of mercury and some mercury compounds has been prohibited since the 15th of March, 2010.[37] The variability among regulations and advisories is at times confusing for the lay person as well as scientists.

[38]
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.[39] The EPA also developed the "Fish Kids" awareness campaign for children and young adults [40] on account of the greater impact of mercury exposure to that population.

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. Inorganic ingestion such as mercuric chloride should be approached as the ingestion of any other serious caustic. Immediate chelation therapy is the standard of care for a patient showing symptoms of severe mercury poisoning or the laboratory evidence of a large total mercury load.[1]

Chelation therapy for acute inorganic mercury poisoning can be done with DMSA, 2,3-dimercapto-1-propanesulfonic acid (DMPS), D-penicillamine (DPCN), or dimercaprol (BAL).[1] 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 due to mercury vapor.[41] No chelator for methylmercury or ethylmercury is approved by the FDA; DMSA is the most frequently used for severe methylmercury poisoning, as it is given orally, has fewer side-effects, and has been found to be superior to BAL, DPCN, and DMPS.[1] α-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.[42] Glutathione and N-acetylcysteine (NAC) are recommended by some physicians, but have been shown to increase mercury concentrations in the kidneys and the brain.[42] Experimental findings have demonstrated an interaction between selenium and methylmercury, but epidemiological studies have found little evidence that selenium helps to protect against the adverse effects of methylmercury.[43]

Chelation therapy can be hazardous if administered incorrectly. In August 2005, an incorrect form of EDTA used for chelation therapy resulted in hypocalcemia, causing cardiac arrest that killed a five-year-old autistic boy.[44]

Prognosis

Many of the toxic effects of mercury are partially or wholly reversible, either through specific therapy or through natural elimination of the metal after exposure has been discontinued.[45] However, heavy or prolonged exposure can do irreversible damage, in particular in fetuses, infants, and young children. Young's syndrome is believed to be a long term consequence of early childhood mercury poisoning.[46] Mercuric chloride may cause cancer as it has caused increases in several types of tumors in rats and mice, while methyl mercury has caused kidney tumors in male rats. 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 victims or to assist in the forensic investigation in a case of fatal overdosage. 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.[47]

History

  • The first emperor of unified China, Qin Shi Huang, it is reported, died of ingesting mercury pills that were intended to give him eternal life.[48]
  • The phrase mad as a hatter 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.)[49]
  • In 1810, two British ships, HMS Triumph 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 Burnet, MD published a report on the effects of Mercurial vapor.[50] The 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.[51]
  • Historically, gold amalgam was widely used in gilding, 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.[52][53]
  • 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.
  • On September 5, 1920, silent movie actress Olive Thomas ingested mercury capsules dissolved in an alcoholic solution at the Hotel Ritz in Paris. 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.
  • An early scientific study of mercury poisoning was in 1923–6 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—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.[54]
  • The term Hunter-Russell syndrome derives from a study of mercury poisoning among workers in a seed packing factory in Norwich, England in the late 1930s who breathed methylmercury that was being used as a seed disinfectant and preservative.[55]
  • 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.[3]
  • 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).[56]
  • 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 brain malfunction due to mercury intoxication.[32][33]
  • In April 2000, Alan Chmurny attempted to kill a former employee, Marta Bradley, by pouring mercury into the ventilation system of her car.[57]
  • 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.[58][59]
  • In December 2008, actor Jeremy Piven was diagnosed with mercury poisoning possibly resulting from eating sushi twice a day for twenty years or herbal remedies he was also taking.[60]
  • In India, a study by non-profit Centre for Science and Environment has found that in country's energy capital, Singrauli,[61] mercury is slowly entering people's homes, food, water and even blood.

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.[62] The word is derived from the Greek, where άκρο means end (as in: upper extremity) and οδυνη means pain. Also known as pink disease, Swift disease, Feer disease, Selter disease, erythroderma, erythroderma polyneuritis, dermatopolyneuritis, trophodermatoneurosis, erythema arthricum epidemicum,[63] vegetative neurosis, and vegetative encephalitis.[2] These terms describe different aspects of the syndrome. Acrodynia was relatively commonplace among children in the first half of the 20th century.[64] At first, the cause of the acrodynia epidemic among infants and young children was unknown;[65] however, mercury poisoning, primarily from calomel in teething powders, began to be widely accepted as its cause in the 1950s and 60s.[2][64] The prevalence of acrodynia decreased greatly after calomel was excluded from most teething powders in 1954.[2][64]

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."[66]

Medical procedures

Because elemental mercury often passes through the GI tract without being absorbed, it was used medically for various purposes until the dangers of mercury poisoning became known. For example, elemental mercury was used to mechanically clear intestinal obstructions (due to its great weight and fluidity), and it was a key ingredient in various medicines throughout history, such as blue mass. The toxic effects often were either not noticed at all or so subtle or generic that they were attributed to other causes and were not recognized as poisoning caused by mercury. While the usage of mercury in medicine has declined, mercury-containing compounds are still used medically in vaccines and dental amalgam, both of which have been the subject of controversy regarding their potential for mercury poisoning.

Thiomersal

For more details on this topic, see Thiomersal controversy.

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.[67] The CDC and the AAP followed the precautionary principle, which assumes that there is no harm in exercising caution even if it later turns out to be unwarranted, but their 1999 action sparked confusion and controversy that has diverted attention and resources away from efforts to determine the causes of autism.[67] 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.[68] A 2004 Institute of Medicine (IOM) committee favored rejecting any causal relationship between thiomersal-containing vaccines and autism.[69] Autism incidence rates increased steadily even after thiomersal was removed from childhood vaccines.[70] Currently there is no accepted scientific evidence that exposure to thiomersal is a factor in causing autism.[71]

Dental amalgam

For more details on this topic, see Dental amalgam controversy.

Dental amalgam, an alloy of about 50 percent elemental mercury, was first introduced in France in the early 19th century.[72] Chosen for its cost-effective durability, this amalgam is a source of low-level exposure to mercury vapour, and an enormous amount of controversy. Although the vast majority of patients with amalgam fillings are exposed to levels believed to be too low to pose any risk to health, many patients (i.e., those in the upper 99.9 percentile) exhibit urine test results that are comparable to those at the maximum allowable legal limits for workplace (occupational) safety.[73][74][75] Nonetheless, in the United States the National Institutes of Health has stated that amalgam fillings pose no personal health risk, and that replacement by non-amalgam fillings is not indicated.[1] In Norway, amalgam fillings are banned due to concerns over public health and environmental pollution.[76]

In 2002, Maths Berlin, Professor Emeritus of Environmental Medicine and chair of the 1991 World Health Organization Task Group on Environmental Health Criteria for Inorganic Mercury, published an overview and assessment of the scientific literature published between November 1997 and 2002 as part of a special investigation for the Swedish Government on amalgam-related health issues. The report concluded: "With reference to the fact that mercury is a multipotent toxin with effects on several levels of the biochemical dynamics of the cell, amalgam must be considered to be an unsuitable material for dental restoration."[77]

Cosmetics

Some skin whitening products contain the toxic chemical mercury(II) chloride as the active ingredient. When applied, the chemical readily absorbs through the skin into the bloodstream.[78] The use of mercury in cosmetics is illegal in the United States. However, cosmetics containing mercury are often illegally imported. Following a certified case of mercury poisoning resulting from the use of an imported skin whitening product, the United States Food and Drug Administration warned against the use of such products.[79][80] Symptoms of mercury poisoning have resulted from the use of various mercury-containing cosmetic products.[21][81][82] The use of skin whitening products is especially popular amongst Asian women.[83] In Hong Kong in 2002, two products were discovered to contain between 9,000 to 60,000 times the recommended dose.[84]

Fluorescent lamps

Fluorescent lamps contain mercury which is released when bulbs are broken. Mercury in bulbs is typically present as either elemental mercury liquid, vapor, or both, since the liquid evaporates at ambient temperature.[85] When broken indoors, bulbs may emit sufficient mercury vapor to present health concerns, and the U.S. Environmental Protection Agency recommends evacuating and airing out a room for at least 15 minutes after breaking a fluorescent light bulb.[86] Breakage of multiple bulbs presents a greater concern. A 1987 report described a 23-month-old toddler who suffered anorexia, weight loss, irritability, profuse sweating, and peeling and redness of fingers and toes. This case of acrodynia was traced to exposure of mercury from a carton of 8-foot fluorescent light bulbs that had broken in a potting shed adjacent to the main nursery. The glass was cleaned up and discarded, but the child often used the area for play.[87]

Assassination

Mercury has 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,[88] while in 2010 journalists Viktor Kalashnikov and Marina Kalashnikova accused Russia's FSB of trying to poison them.[89]

See also

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 Clifton JC 2nd (2007). "Mercury exposure and public health". Pediatr Clin North Am 54 (2): 237–69, viii. doi:10.1016/j.pcl.2007.02.005. PMID 17448359. 
  2. ↑ 2.0 2.1 2.2 2.3 Bjørklund G (1995). "Mercury and Acrodynia". Journal of Orthomolecular Medicine 10 (3 & 4): 145–146. 
  3. ↑ 3.0 3.1 Davidson PW, Myers GJ, Weiss B (2004). "Mercury exposure and child development outcomes". Pediatrics 113 (4 Suppl): 1023–9. doi:10.1542/peds.113.4.S1.1023. PMID 15060195. 
  4. ↑ Horowitz Y, Greenberg D, Ling G, Lifshitz M (2002). "Acrodynia: a case report of two siblings". Arch Dis Child 86 (6): 453. doi:10.1136/adc.86.6.453. PMC 1762992. PMID 12023189. 
  5. ↑ United States Environmental Protection Agency (December 1997). Mercury Study Report to Congress (PDF) 3. Washington, D.C.: United States Environmental Protection Agency. 
  6. ↑ ATSDR Mercury ToxFAQ (April 1999). "ToxFAQs: Mercury". Agency for Toxic Substances and Disease Registry. Retrieved 2007-07-25. 
  7. ↑ Dufault R, LeBlanc B, Schnoll R et al. (2009). "Mercury from chlor-alkali plants: measured concentrations in food product sugar". Environ Health 8 (1): 2. doi:10.1186/1476-069X-8-2. PMC 2637263. PMID 19171026. Lay summary – Medscape Today (2009-01-27). 
  8. ↑ Levy M. (1995). "Dental Amalgam: toxicological evaluation and health risk assessment". J Cdn Dent Assoc 61: 667–8, 671–4. 
  9. ↑ Goldman LR, Shannon MW; American Academy of Pediatrics: Committee on Environmental Health (July 2001). "Technical report: mercury in the environment: implications for pediatricians". Pediatrics 108 (1): 197–205. doi:10.1542/peds.108.1.197. PMID 11433078. Retrieved 2007-07-25. 
  10. ↑ url = http://search.japantimes.co.jp/cgi-bin/nn20090923f2.html
  11. ↑ Pacyna EG, Pacyna JM, Steenhuisen F, Wilson S (2006). "Global anthropogenic mercury emission inventory for 2000". Atmos Environ 40 (22): 4048–63. doi:10.1016/j.atmosenv.2006.03.041. 
  12. ↑ How mercury poisons gold miners and enters the food chain, BBC News
  13. ↑ United States Environmental Protection Agency (December 1997). Mercury Study Report to Congress (PDF) 4. Washington, D.C.: United States Environmental Protection Agency. 
  14. ↑ Doja A, Roberts W (2006). "Immunizations and autism: a review of the literature". Can J Neurol Sci 33 (4): 341–6. PMID 17168158. 
  15. ↑ Thompson WW, Price C, Goodson B et al. (2007). "Early thimerosal exposure and neuropsychological outcomes at 7 to 10 years". N Engl J Med 357 (13): 1281–92. doi:10.1056/NEJMoa071434. PMID 17898097. 
  16. ↑ Reeves, M.A.; Hoffman, P.R. (2009). "The human selenoproteome: recent insights into functions and regulation.". Cell Mol Life Sci. 66 (15): 2457–2478. doi:10.1007/s00018-009-0032-4. PMC 2866081. PMID 19399585. 
  17. ↑ Carvalho, C.M.L.; Hashemy, S.I., Lu, J., Holmgren A. (2008). "Inhibition of the human thioredoxin system: A molecular mechanism of mercury toxicity.". Journal of Biological Chemistry. 283 (18): 11913–11923. 
  18. ↑ Linster, C.L.; Van Schaftingen, E. (2007). "Vitamin C: Biosynthesis, recycling and degradation in mammals.". FEBS Journal 274 (1): 1–22. doi:10.1111/j.1742-4658.2006.05607.x. PMID 17222174. 
  19. ↑ Ralston, Nicholas V.C.; Raymond, Laura J. (2010). "Dietary selenium's protective effects against methylmercury toxicity.". Toxicology 278: 112–123. doi:10.1016/j.tox.2010.06.004. 
  20. ↑ Hendry WF, A'Hern FPA, Cole PJ (1993). "Was Young's syndrome caused by mercury exposure in childhood?". BMJ 307 (6919): 1579–82. doi:10.1136/bmj.307.6919.1579. PMC 1697782. PMID 8292944. 
  21. ↑ 21.0 21.1 21.2 Clarkson TW, Magos L (2006). "The toxicology of mercury and its chemical compounds". Crit Rev Toxicol 36 (8): 609–62. doi:10.1080/10408440600845619. PMID 16973445. 
  22. ↑ 22.0 22.1 ATSDR. 1999. Toxicological Profile for Mercury. Atlanta, GA:Agency for Toxic Substances and Disease Registry. http://www.atsdr.cdc.gov/toxprofiles/tp46.pdf
  23. ↑ Hursh JB, Clarkson TW, Miles E, Goldsmith LA (1989). "Percutaneous absorption of mercury vapor by man". Arch. Environ. Health 44 (2): 120–127. doi:10.1080/00039896.1989.9934385. PMID 2494955. 
  24. ↑ Cherian MG, Hursh JG, Clarkson TW (1978). "Radioactive mercury distribution in biological fluids and excretion in human subjects after inhalation of mercury vapor". Archives of Environmental Health 33: 190–214. 
  25. ↑ Ngim CH, Foo SC, Boey KW, and Keyaratnam J (1992). "Chronic neurobehavioral effects of elemental mercury in dentists". British Journal of Industrial Medicine 49 (11): 782–790. PMC 1039326. PMID 1463679. 
  26. ↑ Liang YX, Sun RK, Chen ZQ, and Li LH (1993). "Psychological effects of low exposure to mercury vapor: Application of computer-administered neurobehavioral evaluation system". Environmental Research 60 (2): 320–327. doi:10.1006/enrs.1993.1040. PMID 8472661. 
  27. ↑ 27.0 27.1 Langford NJ, Ferner RE (1999). "Toxicity of mercury" (PDF). Journal of Human Hypertension 13 (10): 651–6. doi:10.1038/sj.jhh.1000896. PMID 10516733. Retrieved 2007-07-31. 
  28. ↑ 28.0 28.1 28.2 28.3 "Mercuric Cyanide." 1987. http://www.gulflink.osd.mil/m256/m256_refs/n17en111/164.htm (accessed April 2, 2009).
  29. ↑ Benaissa M.L., Hantson P., Bismuth C., Baud F.J. (1995). "Mercury oxycyanide and mercuric cyanide poisoning: two cases.". Intensive Care Med. 21 (12): 1051–1053. doi:10.1007/BF01700673. PMID 8750135. 
  30. ↑ Aylett, B.J. "Mercury (II) Pseudohalides: Cyanide, Thiocyanate, Selenocyanate, Azide, Fulminate." Comprehensive Inorganic Chemistry 3:304-306. J.C. Bailar, H.J. Emeléus, Sir Ronald Nyholm, and A.F. Trotman-Dickenson, ed. Oxford: Pergamon Press, 1973; distributed by Compendium Publishers (Elmsford, NY), p. 304.
  31. ↑ Emsley, John. The Elements of Murder. Oxford: Oxford University Press, 2005. ISBN 0-19-280599-1
  32. ↑ 32.0 32.1 The Karen Wetterhahn story - University of Bristol web page documenting her death, retrieved December 9, 2006.
  33. ↑ 33.0 33.1 OSHA update following Karen Wetterhahn's death
  34. ↑ 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.
  35. ↑ 35.0 35.1 Mozaffarian D, Rimm EB (2006). "Fish intake, contaminants, and human health: evaluating the risks and the benefits". JAMA 296 (15): 1885–99. doi:10.1001/jama.296.15.1885. PMID 17047219. 
  36. ↑ 36.0 36.1 Ibrahim D, Froberg B, Wolf A, Rusyniak DE (2006). "Heavy metal poisoning: clinical presentations and pathophysiology". Clin Lab Med 26 (1): 67–97, viii. doi:10.1016/j.cll.2006.02.003. PMID 16567226. 
  37. ↑ "Export-ban of mercury and mercury compounds from the EU by 2011" (Press release). European Parliament. 2008-05-21. Retrieved 2008-06-10. 
  38. ↑ ATSDR - Mercury - Regulations and Advisories
  39. ↑ What You Need to Know about Mercury in Fish and Shellfish
  40. ↑ EPA Fish Kids Flash-based Movie
  41. ↑ Risher JF, Amler SN (2005). "Mercury exposure: evaluation and intervention the inappropriate use of chelating agents in the diagnosis and treatment of putative mercury poisoning". Neurotoxicology 26 (4): 691–9. doi:10.1016/j.neuro.2005.05.004. PMID 16009427. 
  42. ↑ 42.0 42.1 Rooney JP (2007). "The role of thiols, dithiols, nutritional factors and interacting ligands in the toxicology of mercury". Toxicology 234 (3): 145–56. doi:10.1016/j.tox.2007.02.016. PMID 17408840. 
  43. ↑ Watanabe C (2002). "Modification of mercury toxicity by selenium: practical importance?" (PDF). Tohoku J Exp Med 196 (2): 71–7. doi:10.1620/tjem.196.71. PMID 12498318. 
  44. ↑ Hazards of chelation therapy:
  45. ↑
  46. ↑ Hendry WF, A'Hern RP, Cole PJ (1993). "Was Young's syndrome caused by exposure to mercury in childhood?". BMJ 307 (6919): 1579–82. doi:10.1136/bmj.307.6919.1579. PMC 1697782. PMID 8292944. 
  47. ↑ R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 923-927.
  48. ↑ Zhao HL, Zhu X, Sui Y (2006). "The short-lived Chinese emperors". J Am Geriatr Soc 54 (8): 1295–6. doi:10.1111/j.1532-5415.2006.00821.x. PMID 16914004. 
  49. ↑ Waldron HA (1983). "Did the Mad Hatter have mercury poisoning?". Br Med J (Clin Res Ed) 287 (6409): 1961. doi:10.1136/bmj.287.6409.1961. PMC 1550196. PMID 6418283. 
  50. ↑ An Account of the Effect of Mercurial Vapors on the Crew of His Majesty's Ship Triumph, in the year 1810. By Wm. Burnet, M.D. one of the Medical Commissioners of the Navy, formerly Physician and Inspector of Hospitals to the Mediterranean Fleet.
  51. ↑ Michael J. Doherty MD: The Quicksilver Prize: Mercury vapor poisoning aboard HMS Triumph and HMS Phipps (2003).
  52. ↑ "An article about the cathedral.". Archived from the original on 2011-08-25. 
  53. ↑ "An article about gilding.". 
  54. ↑ Stock A (1926). "Die Gefaehrlichkeit des Quecksilberdampfes". Zeitschrift für angewandte Chemie 39 (15): 461–466. doi:10.1002/ange.19260391502. 
  55. ↑ Hunter D, Bomford RR, Russell DS (1940). "Poisoning by methylmercury compounds". Quart. J. Med. 9: 193–213. 
  56. ↑ Engler R (April 27, 1985). "Technology out of Control". The Nation 240. 
  57. ↑ Vargas JA (2007-01-26). "'Mad Scientist': On Court TV, Fatal Chemistry". The Washington Post. Retrieved 2007-01-28. 
  58. ↑ Swearengin M (2008-04-01). "Man dies from mercury poisoning after trying to extract gold". Durant Daily Democrat. 
  59. ↑ (Associated Press) (2008-04-01). "Colbert man dies from mercury poisoning". Tulsa World. Retrieved 2008-04-20. 
  60. ↑ Tiffany McGee (2009-01-15). "Jeremy Piven Explains His Mystery Ailment". People. Retrieved 2009-01-15. 
  61. ↑ Down To Earth: India's Minimata
  62. ↑ James WD, Berger TG, Elston DM (2006). Andrews' diseases of the skin: clinical dermatology (10th ed.). Saunders. p. 134. ISBN 0-7216-2921-0. 
  63. ↑ The name erythema arthricum epidemicum more commonly describes Haverhill fever (rat-bite fever).
  64. ↑ 64.0 64.1 64.2 Dally A (1997). "The rise and fall of pink disease". Soc Hist Med 10 (2): 291–304. doi:10.1093/shm/10.2.291. PMID 11619497. 
  65. ↑ No Given Author or Editor. (1935). Everybody's Family Doctor. London, UK: Odhams Press LTD. p. 16. 
  66. ↑ Ford M, Delaney KA, Ling L, Erickson T (2000). Clinical Toxicology (1st ed.). Saunders. ISBN 0-7216-5485-1. 
  67. ↑ 67.0 67.1 Offit PA (2007). "Thimerosal and vaccines—a cautionary tale". N Engl J Med 357 (13): 1278–9. doi:10.1056/NEJMp078187. PMID 17898096. 
  68. ↑ Sugarman SD (2007). "Cases in vaccine court—legal battles over vaccines and autism". N Engl J Med 357 (13): 1275–7. doi:10.1056/NEJMp078168. PMID 17898095. 
  69. ↑ Immunization Safety Review Committee (2004). Immunization Safety Review: Vaccines and Autism. The National Academies Press. ISBN 0-309-09237-X. 
  70. ↑ Gerber, Jeffrey S.; Paul A. Offit (2009). "Vaccines and Autism: A Tale of Shifting Hypotheses". Clinical Infectious Diseases 48 (4): 456–451. doi:10.1086/596476. PMC 2908388. PMID 19128068. 
  71. ↑ Doja A, Roberts W (2006). "Immunizations and autism: a review of the literature". Can J Neurol Sci 33 (4): 341–6. PMID 17168158. 
  72. ↑ Ferracane JL (2001). Materials in Dentistry: Principles and Applications (2nd ed.). Lippincott Williams & Wilkins. p. 3. ISBN 0-7817-2733-2. 
  73. ↑ L. Barregard. (2005) Occupational and Environmental Medicine, June 1, 2005. no. 62 pg. 352-353. Mercury From Dental Amalgam: Looking Beyond the Average. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1741026/pdf/v062p00352.pdf
  74. ↑ Occupational Safety and Health Guideline for Mercury, OSHA, US Department of Labor http://www.osha.gov/SLTC/healthguidelines/mercuryvapor/recognition.html
  75. ↑ Diana Echeverria, et al. (1998) The FASEB Journal vol. 12, no. 11, pg. 971-980. Neurobehavioral Effects from Exposure to Dental Amalgam (Hg0): new distinctions between recent exposure and Hg body burden. http://www.fasebj.org/content/12/11/971.full retrieved:19/10/2011.
  76. ↑ Edlich RF, Cochran AA, Cross CL, Wack CA, Long WB, Newkirk AT (2008). "Legislation and informed consent brochures for dental patients receiving amalgam restorations". Int J Toxicol 27 (4): 313–6. doi:10.1080/10915810802366851. PMID 18821394. 
  77. ↑ Berlin, Maths. "Mercury in dental-filling materials –– an updated risk analysis in environmental medical terms". Dental Material Commission. p. 25. Retrieved 23 October 2013. 
  78. ↑ Counter SA (December 16, 2003). Whitening skin can be deadly. The Boston Globe. 
  79. ↑ "FDA Proposes Hydroquinone Ban". FDA bans hydroquinone in skin whitening products
  80. ↑ "NYC Health Dept. Warns Against Use of "Skin-lightening" Creams Containing Mercury or Similar Products Which Do Not List Ingredients". January 27, 2005. 
  81. ↑ Counter SA, Buchanan LH. Mercury exposure in children: a review (PDF). 
  82. ↑ Mahaffey KR. "Dynamics of Mercury Pollution on Regional and Global Scales". 
  83. ↑ In a survey, 28% of Koreans and 50% of Philippians say that they use skin whitening products."Skin lightening in Asia? A bright future?". 
  84. ↑ Bray M (2002-05-15). SKIN DEEP: Dying to be white. CNN. Retrieved 2010-05-12. 
  85. ↑ Aucott M, McLinden M, Winka M (2003). "Release of mercury from broken fluorescent bulbs". J Air Waste Manag Assoc 53 (2): 143–51. PMID 12617289. 
  86. ↑ "Spills, disposal and site cleanup". U.S. Environmental Protection Agency. 2009-07-13. Retrieved 2009-06-30. 
  87. ↑ Tunnessen WW Jr, McMahon KJ, Baser M (1987). "Acrodynia: exposure to mercury from fluorescent light bulbs". Pediatrics 79 (5): 786–9. PMID 3575038. 
  88. ↑ Russian lawyer suspects mercury poisoning, USA Today.com
  89. ↑ German inquiry into 'poisoning' of Russian dissidents, Telegraph

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