mercury poisoning mercury poisoning 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, numbness in the hands and feet, skin rashes, anxiety, memory problems, trouble speaking, trouble hearing, or trouble seeing. high-level exposure to methylmercury is known as minamata disease. 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. the effects of long-term low-dose exposure to methylmercury are unclear. mercury poisoningother namesmercury toxicity, mercury overdose, mercury intoxication, hydrargyria, mercurialismthe bulb of a mercury-in-glass thermometerspecialtytoxicologysymptomsmuscle weakness, poor coordination, numbness in the hands and feetcomplicationskidney problems, decreased intelligencecausesexposure to mercuryrisk factorsconsumption of fish, which may contain mercurydiagnostic methoddifficultpreventiondecreasing use of mercury, low mercury dietmedicationacute poisoning: dimercaptosuccinic acid (dmsa), dimercaptopropane sulfonate (dmps) forms of mercury exposure include metal, 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. tests of the blood, urine, and hair for mercury are available but do not relate well to the amount in the body. 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. in certain communities that survive on fishing, rates of mercury poisoning among children have been as high as 1.7 per 100. signs and symptoms common symptoms of mercury poisoning include peripheral neuropathy, presenting as paresthesia or itching, burning, pain, or even a sensation that resembles small insects crawling on or under the skin (formication); skin discoloration (pink cheeks, fingertips and toes); swelling; and desquamation (shedding or peeling of skin). mercury irreversibly inhibits selenium-dependent enzymes (see below) and may also inactivate s-adenosyl-methionine, which is necessary for catecholamine catabolism by catechol-o-methyl transferase. due to the body's inability to degrade catecholamines (e.g. adrenaline), a person with mercury poisoning may experience profuse sweating, tachycardia (persistently faster-than-normal heart beat), increased salivation, and hypertension (high blood pressure). affected children may show red cheeks, nose and lips, loss of hair, teeth, and nails, transient rashes, hypotonia (muscle weakness), and increased sensitivity to light. other symptoms may include kidney dysfunction (e.g. fanconi syndrome) or neuropsychiatric symptoms such as emotional lability, memory impairment, or insomnia. 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 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. exposure to mercury can occur from breathing contaminated air, from eating foods that have acquired mercury residues during processing, from exposure to mercury vapor in mercury amalgam dental restorations, 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. 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. 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. human-generated sources, such as coal-burning power plants emit about half of atmospheric mercury, with natural sources such as volcanoes responsible for the remainder. a 2021 publication investigating the mercury distribution in european soils found that high mercury concentrations are found close to abandoned mines (such as almadén (castilla-la mancha, spain), mt. amiata (italy), idrija (slovenia) and rudnany (slovakia)) and coal-fired power plants. 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. 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. 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 and traditional chinese medicine, contain mercury and other heavy metals. sources 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 and liver damage. the most dangerous mercury compound, dimethylmercury, is so toxic that even a few microliters spilled on the skin, or even on a latex glove, can cause death. methylmercury and related organomercury compounds methylmercury is the major source of organic mercury for all individuals. due to bioaccumulation it works its way up through the food web and thus biomagnifies, resulting in 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 170 g (6 oz) per week, and of all other fish and shellfish to no more than 340 g (12 oz) per week. 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. methylmercury exposure during rodent gestation, a developmental period that approximately models human neural development during the first two trimesters of gestation, 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 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. 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. 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 soluble 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 kidneys, 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. 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. the drug n-acetyl penicillamine has been used to treat mercury poisoning with limited success. 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. 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. 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. 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. 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). although it has many functions, thioredoxin reductase restores vitamins c and e, as well as a number of other important antioxidant molecules, back into their reduced forms, enabling them to counteract oxidative damage. 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