Mercury poisoning is a type ofmetal poisoning due to exposure tomercury.[3] Symptoms depend upon the type, dose, method, and duration of exposure.[3][4] They may includemuscle weakness, poor coordination,numbness in the hands and feet, skin rashes, anxiety, memory problems, trouble speaking, trouble hearing, or trouble seeing.[1] High-level exposure tomethylmercury is known asMinamata disease.[2] Methylmercury exposure in children may result inacrodynia (pink disease) in which the skin becomes pink and peels.[2] Long-term complications may includekidney problems and decreased intelligence.[2] The effects of long-term low-dose exposure to methylmercury are unclear.[6]
Forms of mercury exposure includemetal,vapor,salt, andorganic compound.[3] Most exposure is fromeating fish,amalgam-baseddental fillings, or exposure at a workplace.[3] In fish, those higher up in thefood chain generally have higher levels of mercury, a process known asbiomagnification.[3] Less commonly, poisoning may occur as a method of attemptedsuicide.[3] Human activities that release mercury into the environment include the burning ofcoal and mining ofgold.[4][7] Tests of the blood, urine, and hair for mercury are available but do not relate well to the amount in the body.[3]
Prevention includes eating a diet low in mercury, removing mercury from medical and other devices, proper disposal of mercury, and not mining further mercury.[4][2] In those with acute poisoning from inorganic mercury salts,chelation with eitherdimercaptosuccinic acid (DMSA) ordimercaptopropane 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]
Common symptoms of mercury poisoning areperipheral neuropathy, presenting asparesthesia oritching, 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).[8] and the range ofneurological symptoms associated witherethism.
Thus, the clinical presentation may resemblepheochromocytoma orKawasaki disease. Desquamation (skin peeling) can occur with severe mercury poisoning acquired by handling elemental mercury.[11]
In 1862 soldier Carleton Burgan suffered severe facial disfigurement due to mercury poisoning after having an infection treated withcalomel, a common medicine that contained mercury.
Historically, medicines could contain mercury and thus do more harm than good to patients. The popular Victorian medicinecalomel contained mercury. In her 1859 autobiography, Scottish seamstressElizabeth 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.[12] In 1862 a soldier in theAmerican civil war, Carleton Burgan, suffered a similar disfigurement when he was treated with calomel for an infection.[13]
Today, consumption offish containing mercury is by far the most significant source of ingestion-related mercury exposure in humans, although plants and livestock also contain mercury due tobioconcentration of organic mercury from seawater, freshwater, marine and lacustrine sediments, soils, and atmosphere, and due tobiomagnification by ingesting other mercury-containing organisms.[14] Exposure to mercury can occur from breathing contaminated air,[15] from eating foods that have acquired mercury residues during processing,[16][17] from exposure to mercury vapor in mercurydental amalgam restorations,[18] and from improper use or disposal of mercury and mercury-containing objects, for example, after spills of elemental mercury or improper disposal offluorescent lamps.[19]
All of these, except elemental liquid mercury, produce toxicity or death with less than a gram. Mercury's zerooxidation state (Hg0) exists as vapor or as liquid metal, its mercurous state (Hg+) exists asinorganic salts, and its mercuric state (Hg2+) may form either inorganic salts ororganomercury compounds.[20][21][22]
Consumption of whale and dolphin meat, as is the practice inJapan, is a source of high levels of mercury poisoning.[23] Tetsuya Endo, a professor at the Health SciencesUniversity of Hokkaido, has testedwhale meat purchased in the whaling town ofTaiji and found mercury levels more than 20 times the acceptable Japanese standard.[24]
Human-generated sources, such ascoal-burning power plants[25] emit about half of atmospheric mercury, with natural sources such asvolcanoes 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 asAlmadén (Castilla-La Mancha, Spain), Mt. Amiata (Italy), Idrija (Slovenia) and Rudnany (Slovakia)) and coal-fired power plants.[26] An estimated two-thirds of human-generated mercury comes from stationary combustion, mostly ofcoal. Other important human-generated sources includegold production,nonferrous metal production,cement production,waste disposal, humancrematoria,caustic soda production,pig iron andsteel production, mercury production (mostly for batteries), and biomass burning.[27]
Small independent gold-mining operation workers are at higher risk of mercury poisoning because of crude processing methods.[28] Such is the danger for thegalamsey in Ghana and similar workers known asorpailleurs in neighboringfrancophone 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.[29]
Some mercury compounds, especiallyorganomercury 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.[30]
Organic compounds of mercury tend to be much more toxic than either the elemental form or the salts. These compounds have been implicated in causingbrain andliver damage. The most dangerous mercury compound,dimethylmercury, is so toxic that even a fewmicroliters spilled on the skin, or even on a latex glove, can cause death.[36][37]
Methylmercury is the major source of organic mercury for all individuals.[38] Due tobioaccumulation, it works its way up through thefood web and thus biomagnifies, resulting in high concentrations among populations of some species. Top predatory fish, such astuna orswordfish, are usually of greater concern than smaller species. The USFDA and theEPA advise women of child-bearing age, nursing mothers, and young children to completely avoidswordfish,shark,king mackerel andtilefish from the Gulf of Mexico, and to limit consumption ofalbacore ("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.[39] 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 excesscoronary heart disease deaths and suboptimalneural development in children.[40]
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 (seeHistory); other latent periods in the range of weeks to months have also been reported. When the first symptom appears, typicallyparesthesia (a tingling or numbness in the skin), it is followed rapidly by more severe effects, sometimes ending incoma and death. The toxic damage appears to be determined by the peak value of mercury, not the length of the exposure.[41]
Methylmercury exposure during rodent gestation, a developmental period that approximately models human neural development during the first two trimesters of gestation,[42][43] 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[44] 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 underThiomersal below). Its characteristics have not been studied as extensively as those of methylmercury. It is cleared from the blood much more rapidly, with ahalf-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 theblood–brain barrier via a transporter, but instead relies on simple diffusion to enter the brain.[38] 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.[38]
Mercury occurs as salts such asmercuric chloride (HgCl2) and mercurous chloride (Hg2Cl2), the latter also known as calomel. Because they are moresoluble 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 thekidneys, and can cause severe kidney damage; however, as they cannot cross theblood–brain barrier easily, these salts inflict little neurological damage without continuous or heavy exposure.[45]Mercuric cyanide (Hg(CN)2) is a particularly toxic mercury compound that has been used in murders, as it contains not only mercury but alsocyanide, leading to simultaneouscyanide poisoning.[46] The drug n-acetyl penicillamine has been used to treat mercury poisoning with limited success.[47]
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 intactgastrointestinal tract, though it may not be true for individuals withileus. Cases of systemic toxicity from accidental swallowing are rare, and attempted suicide via intravenous injection does not appear to result in systemic toxicity,[41] 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.[48] Some mercury vapor is absorbed dermally, but uptake by this route is only about 1% of that by inhalation.[49]
In humans, approximately 80% of inhaled mercury vapor is absorbed via therespiratory tract, where it enters thecirculatory system and is distributed throughout the body.[50] Chronic exposure by inhalation, even at low concentrations in the range 0.7–42 μg/m3, has been shown incase–control studies to cause effects such as tremors, impaired cognitive skills, and sleep disturbance in workers.[51][52]
Acute inhalation of high concentrations causes a wide variety of cognitive, personality, sensory, and motor disturbances. The most prominent symptoms includetremors (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.[48]
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 asthioredoxin reductase (IC50 = 9 nM).[53] Although it has many functions, thioredoxin reductase restores vitamins C and E, as well as a number of other important antioxidant molecules, back into their reduced forms, enabling them to counteract oxidative damage.[54] Since the rate of oxygen consumption is particularly high in brain tissues, production of reactive oxygen species (ROS) is accentuated in these vital cells, making them particularly vulnerable tooxidative damage and especially dependent upon theantioxidant protection provided by selenoenzymes. High mercury exposures deplete the amount of cellular selenium available for the biosynthesis of thioredoxin reductase and other selenoenzymes that prevent and reverse oxidative damage,[55] which, if the depletion is severe and long lasting, results in brain cell dysfunctions that can ultimately cause death.
Mercury in its various forms is particularly harmful tofetuses as anenvironmental toxin in pregnancy, as well as toinfants. 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 seriousbirth defects, such as those seen inMinamata disease. Mercury exposures in excess of dietary selenium intakes in young children can have severe neurological consequences, preventing nerve sheaths from forming properly.
Diagnosis of elemental or inorganic mercury poisoning involves determining the history of exposure, physical findings, and an elevatedbody 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 undergoingchelation therapy, as the therapy itself increases mercury levels in the samples.[58]
Diagnosis of organic mercury poisoning differs in that whole-blood or hair analysis is more reliable than urinary mercury levels.[58]
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 theMinamata Convention on Mercury.
The export from theEuropean Union of mercury and some mercury compounds has been prohibited since 15 March 2011.[59] The European Union has banned most uses of mercury.[60] 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.[61]
TheUnited States Environmental Protection Agency (EPA) issued recommendations in 2004 regarding exposure tomercury in fish and shellfish.[63] The EPA also developed the "Fish Kids" awareness campaign for children and young adults[64] on account of the greater impact of mercury exposure to that population.
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.[65] If available, powderedsulfur may be applied to the spill, in order to create a solid compound that is more easily removed from surfaces than liquid mercury.[66]
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 ofiodide were given orally, such as heavily popularized byLouis Melsens and many nineteenth and early twentieth century doctors.[67][68]
Chelation therapy for acute inorganic mercury poisoning, a formerly common method, was done withDMSA,2,3-dimercapto-1-propanesulfonic acid (DMPS),D-penicillamine (DPCN), ordimercaprol (BAL).[38] 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.[69] 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.[38]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.[70]Glutathione andN-acetylcysteine (NAC) are recommended by some physicians, but have been shown to increase mercury concentrations in the kidneys and the brain.[70]
Chelation therapy can be hazardous if administered incorrectly. In August 2005, edetate disodium, an incorrect form ofEDTA for chelation therapy, resulted inhypocalcemia leading tocardiac arrest that killed a five-year-old autistic boy.[71]
Experimental animal and epidemiological study findings have confirmed the interaction betweenselenium 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.[72] For example, increased ocean fish consumption during pregnancy was associated with 4-6 point increases in child IQs.
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.[73] Autopsy findings point to a half-life of inorganic mercury in human brains of 27.4 years.[74] 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.[75]
Mercuric chloride maycause cancer as rats and mice treated with the substance have gone on to develop several types of tumors, while male rats treated withmethyl mercury have gone on to develop kidney tumors. The EPA has classified mercuric chloride and methyl mercury as possible human carcinogens (ATSDR, EPA)
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.[76]
Neolithic artists usingcinnabar show signs of mercury poisoning.[77]
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.[78]
Emperor Xuānzong of Tang, one of the emperors of the lateTang dynasty of China, was prescribed "cinnabar that had been treated and subdued by fire" to achieve immortality.[79] 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.[79] Xuānzong became irritable and paranoid, and he seems to have ultimately died in 859 from the poisoning.[79]
In hisNatural 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 ofPPE.[80]
Carl Scheele, a significant 18th centurySwedish pioneer of chemical research, died from mercury poisoning arising from his work, at the relatively early age of 43.[81]
The phrasemad as a hatter is likely a reference to mercury poisoning amongmilliners (so-called "mad hatter disease"), as mercury-based compounds were once used in the manufacture offelt hats in the 18th and 19th century. (TheMad Hatter character ofAlice in Wonderland was, it is presumed, inspired by an eccentric furniture dealer namedTheophilus Carter. Carter was not a victim of mad hatter disease althoughLewis Carroll would have been familiar with the phenomenon of dementia that occurred among hatters.)[82][83]
In 1810, two British ships,HMSTriumph andHMS 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 1823William Burnett, M.D. published a report on the effects of mercurial vapor.[84]Triumph'ssurgeon, 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 theorlop was forbidden; and no men slept in the lower deck if they were at all symptomatic. Windsails were set to channel fresh air into the lower decks day and night.[85]
Historically, gold-mercury amalgam was widely used ingilding, 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 ofSaint Isaac's Cathedral alone, 60 men died from the gilding of the main dome.[86][87]
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 actressOlive Thomas ingested mercury capsules dissolved in an alcoholic solution at the Hotel Ritz in Paris.[88] There is still controversy over whether it was suicide, or whether she consumed the external preparation by mistake. Her husband,Jack Pickford (the brother ofMary Pickford), hadsyphilis, and the mercury was used as a treatment of the venereal disease at the time. She died a few days later at the American Hospital in Neuilly.[89]
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—diffusion pumps,float valves, andmanometers—all of which contained mercury, and also from mercury that had been accidentally spilt and remained in cracks in thelinoleum 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 termmicromercurialism.[90]
The termHunter-Russell syndrome derives from a study of mercury poisoning among workers in a seed-packaging factory inNorwich, England in the late 1930s who breathedmethylmercury that was being used as a seed disinfectant and pesticide.[91]
Outbreaks ofmethylmercury 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 inMinamata andNiigata. In Minamata alone, more than 600 people died due to what became known asMinamata disease. More than 21,000 people filed claims with the Japanese government, of which almost 3000 became certified as having the disease. In 22 documented cases, pregnant women who consumed contaminated fish showed mild or no symptoms but gave birth to infants with severe developmental disabilities.[92]
Widespread mercury poisoning occurred in ruralIraq in 1971–1972, when grain treated with a methylmercury-basedfungicide 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 (seeBasra poison grain disaster).[97]
In April 2000, Alan Chmurny attempted to kill a former employee, Marta Bradley, by pouring mercury into theventilation system of her car.[98][99]
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.[100][101]
In December 2008, actorJeremy Piven was diagnosed with mercury poisoning possibly resulting from eating sushi twice a day for twenty years or from taking herbal remedies.[102]
In India, a study byCentre for Science and Environment and Indian Institute of Toxicology Research has found that in the country's energy capitalSingrauli, mercury is slowly entering people's homes, food, water and even blood.[103]
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.[104]
In August 2024, chess player Amina Abakarova allegedly attempted to poison her rival, Umayganat Osmanova, by coating chess pieces in mercury from a thermometer.[105]
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.[106] The word is derived from theGreek, where άκρο meansend orextremity, and οδυνη meanspain. Acrodynia resulted primarily fromcalomel in teething powders and decreased greatly after calomel was excluded from most teething powders in 1954.[107][108]
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."[109]
Mercury was once prescribed as a purgative.[110] Many mercury-containing compounds were once used in medicines. These includecalomel (mercurous chloride), andmercuric chloride.
In 1999, theCenters for Disease Control (CDC) and theAmerican Academy of Pediatrics (AAP) asked vaccine makers to remove theorganomercury compoundthiomersal (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 ofinfluenza vaccine.[111] The CDC and the AAP followed theprecautionary 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 thiomersal was a cause ofautism.[111]
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.[112] A 2004Institute of Medicine (IOM) committee favored rejecting any causal relationship between thiomersal-containing vaccines and autism.[113] Autism incidence rates increased steadily even after thiomersal was removed from childhood vaccines.[114] Currently there is no accepted scientific evidence that exposure to thiomersal is a factor in causing autism.[115]
Dental amalgam is a possible cause of low-level mercury poisoning due to its use indental fillings. Discussion on the topic includes debates on whether amalgam should be used, with critics arguing that its toxic effects make it unsafe.
Someskin whitening products contain the toxic mercury(II) chloride as the active ingredient. When applied, the chemical readily absorbs through the skin into the bloodstream.[116] The use ofmercury 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 StatesFood and Drug Administration warned against the use of such products.[117][118] Symptoms of mercury poisoning have resulted from the use of various mercury-containing cosmetic products.[41][119][120] The use of skin whitening products is especially popular among Asian women.[121] In Hong Kong in 2002, two products were discovered to contain between 9,000 and 60,000 times the recommended dose.[122]
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.[123] When broken indoors, bulbs may emit sufficient mercury vapor to present health concerns, and theU.S. Environmental Protection Agency recommends evacuating and airing out a room for at least 15 minutes after breaking a fluorescent light bulb.[124] Breakage of multiple bulbs presents a greater concern. A 1987 report described a 23-month-old toddler who hadanorexia, 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.[125]
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