Mercury poisoning

Source: Wikipedia, the free encyclopedia.
(Redirected from
Mercury toxicity
)
Not to be confused with
Heavy metal poisoning
.
For the song by Graham Parker, see Mercury Poisoning.
Mercury poisoning
Other namesMercury toxicity, mercury overdose, mercury intoxication, hydrargyria, mercurialism
dimercaptopropane sulfonate (DMPS)[5]

Mercury poisoning is a type of

kidney problems and decreased intelligence.[2] The effects of long-term low-dose exposure to methylmercury are unclear.[6]

Forms of mercury exposure include

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.

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

Common symptoms of mercury poisoning are

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

sweating, tachycardia (persistently faster-than-normal heart beat), increased salivation, and hypertension (high blood pressure).[9]

Affected children may show red

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]

Causes

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.[12] Exposure to mercury can occur from breathing contaminated air,[13] from eating foods that have acquired mercury residues during processing,[14][15] from exposure to mercury vapor in mercury amalgam dental restorations,[16] 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.[17]

All of these, except elemental liquid mercury, produce toxicity or death with less than a gram. Mercury's zero

organomercury compounds.[18][19][20]

Consumption of whale and dolphin meat, as is the practice in

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.[22]

Human-generated sources, such as

caustic soda production, pig iron and steel production, mercury production (mostly for batteries), and biomass burning.[25]

Small independent gold-mining operation workers are at higher risk of mercury poisoning because of crude processing methods.

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.[27]

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.[28]

Many traditional medicines, including ones used in

Ayurvedic medicine and Traditional Chinese medicine, contain mercury and other heavy metals.[29][30]

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

microliters spilled on the skin, or even on a latex glove, can cause death.[31][32]

Methylmercury and related organomercury compounds

Main article: Mercury in fish

neural development in children.[35]

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.[36]

Methylmercury exposure during rodent gestation, a developmental period that approximately models human neural development during the first two trimesters of gestation,[37][38] has long-lasting behavioral consequences that appear in adulthood and, in some cases, may not appear until aging. Prefrontal cortex or dopamine neurotransmission could be especially sensitive to even subtle gestational methylmercury exposure[39] and suggests that public health assessments of methylmercury based on intellectual performance may underestimate the impact of methylmercury in public health.

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.[33] 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.[33]

Inorganic mercury compounds

Mercury occurs as salts such as

Mercuric cyanide (Hg(CN)2) is a particularly toxic mercury compound that has been used in murders, as it contains not only mercury but also cyanide, leading to simultaneous cyanide poisoning.[41] The drug n-acetyl penicillamine has been used to treat mercury poisoning with limited success.[42]

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,[36] 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.[43] Some mercury vapor is absorbed dermally, but uptake by this route is only about 1% of that by inhalation.[44]

In humans, approximately 80% of inhaled mercury vapor is absorbed via the

case–control studies to cause effects such as tremors, impaired cognitive skills, and sleep disturbance in workers.[46][47]

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

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.[43]

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

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,[50]
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

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

autoimmmune response against MBP and GFAP and results in the degradation of neural myelin and general decline in function of the CNS.[52]

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.[53]

Diagnosis of organic mercury poisoning differs in that whole-blood or hair analysis is more reliable than urinary mercury levels.[53]

Prevention

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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.[54] The European Union has banned most uses of mercury.[55] Mercury is allowed for fluorescent light bulbs because of pressure from countries such as Germany, the Netherlands and Hungary, which are connected to the main producers of fluorescent light bulbs: General Electric, Philips and Osram.[56]

US environmental limits[57]
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.[58] The EPA also developed the "Fish Kids" awareness campaign for children and young adults [59] on account of the greater impact of mercury exposure to that population.

Cleaning spilled mercury

EPA workers clean up residential mercury spill in 2004

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.[60] 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.[61]

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.[62][63]

Chelation therapy

DMSA, 2,3-dimercapto-1-propanesulfonic acid (DMPS), D-penicillamine (DPCN), or dimercaprol (BAL).[33] 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.[64] 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.[33] 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.[65] Glutathione and N-acetylcysteine (NAC) are recommended by some physicians, but have been shown to increase mercury concentrations in the kidneys and the brain.[65]

Chelation therapy can be hazardous if administered incorrectly. In August 2005, an incorrect form of EDTA (edetate disodium) used for chelation therapy resulted in hypocalcemia, causing cardiac arrest that killed a five-year-old autistic boy.[66]

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.[67] For example, increased ocean fish consumption during pregnancy was associated with 4-6 point increases in child IQs.

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.[68] Autopsy findings point to a half-life of inorganic mercury in human brains of 27.4 years.[69] 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.[70]

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 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.[71]

History

  • Neolithic artists using cinnabar show signs of mercury poisoning.[72]
  • 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:
    • 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.[73]
    • 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.[74] Concerns that the prescription was having ill effects on the emperor's health and sanity were waved off by the imperial alchemists, who cited medical texts listing a number of the emperor's conditions (including itching, formication, swelling, and muscle weakness), today recognized as signs and symptoms of mercury poisoning, as evidence that the elixir was effectively treating the emperor's latent ailments.[74] Xuānzong became irritable and paranoid, and he seems to have ultimately died in 859 from the poisoning.[74]
  • 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.[75]
  • Carl Scheele, a significant 18th century Swedish pioneer of chemical research, died from mercury poisoning arising from his work, at the relatively early age of 43.[76]
  • The phrase
    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.)[77][78]
  • In 1810, two British ships,
    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.[80]
  • 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.[81][82]
  • 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.[83] 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.[84]
  • An early scientific study of mercury poisoning was in 1923–1926 by the German inorganic chemist,
    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.[85]
  • 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.[86]
  • 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.[87]
  • Mercury poisoning of generations of
    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.[88][89][90][91]
  • Widespread mercury poisoning occurred in rural
    Basra poison grain disaster).[92]
  • 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[31][32]
  • In April 2000, Alan Chmurny attempted to kill a former employee, Marta Bradley, by pouring mercury into the ventilation system of her car.[93][94]
  • 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.[95][96]
  • 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.[97]
  • 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.[98]
  • 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.[99]

Infantile acrodynia

Further information: 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.[100] The word is derived from the Greek, where άκρο means end or extremity, and οδυνη means pain. Acrodynia resulted primarily from calomel in teething powders and decreased greatly after calomel was excluded from most teething powders in 1954.[101][102]

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."[103]

Medicine

Further information: Mercury (element) § Medicine

Mercury was once prescribed as a purgative.[104] Many mercury-containing compounds were once used in medicines. These include calomel (mercurous chloride), and mercuric chloride.

Thiomersal

Further information:
Thiomersal controversy

In 1999, the

autism.[105]

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.

Institute of Medicine (IOM) committee favored rejecting any causal relationship between thiomersal-containing vaccines and autism.[107] Autism incidence rates increased steadily even after thiomersal was removed from childhood vaccines.[108] Currently there is no accepted scientific evidence that exposure to thiomersal is a factor in causing autism.[109]

Dental amalgam toxicity

Further information:
Dental amalgam toxicity

dental fillings
. Discussion on the topic includes debates on whether amalgam should be used, with critics arguing that its toxic effects make it unsafe.

Cosmetics

Some

Food and Drug Administration warned against the use of such products.[111][112] Symptoms of mercury poisoning have resulted from the use of various mercury-containing cosmetic products.[36][113][114] The use of skin whitening products is especially popular amongst Asian women.[115] In Hong Kong in 2002, two products were discovered to contain between 9,000 and 60,000 times the recommended dose.[116]

Fluorescent lamps

U.S. Environmental Protection Agency recommends evacuating and airing out a room for at least 15 minutes after breaking a fluorescent light bulb.[118] Breakage of multiple bulbs presents a greater concern. A 1987 report described a 23-month-old toddler who had 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 to play in.[119]

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,[120] while in 2010 journalists Viktor Kalashnikov and Marina Kalashnikova accused Russia's FSB of trying to poison them.[121]

See also

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External links

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