Mercury poisoning

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Mercury poisoning
Other namesMercury toxicity, mercury overdose, mercury intoxication, hydrargyria, mercurialism
Maximum thermometer close up 2.JPG
The bulb of a mercury-in-glass thermometer
Specialty Toxicology
Symptoms Muscle weakness, poor coordination, numbness in the hands and feet [1]
Complications Kidney problems, decreased intelligence [2]
CausesExposure to mercury [1]
Risk factors Consumption of fish, which may contain mercury [3]
Diagnostic method Difficult [3]
PreventionDecreasing use of mercury, low mercury diet [4]
Medication Acute poisoning: dimercaptosuccinic acid (DMSA), dimercaptopropane sulfonate (DMPS) [5]

Mercury poisoning is a type of metal poisoning due to exposure to mercury. [3] Symptoms depend upon the type, dose, method, and duration of exposure. [3] [4] 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. [1] High-level exposure to methylmercury is known as Minamata disease. [2] Methylmercury exposure in children may result in acrodynia (pink disease) in which the skin becomes pink and peels. [2] Long-term complications may include kidney problems and decreased intelligence. [2] The effects of long-term low-dose exposure to methylmercury are unclear. [6]

Contents

Forms of mercury exposure include metal, vapor, salt, and organic compound. [3] Most exposure is from eating fish, amalgam-based 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. [4] [2] 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. [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 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). [8]

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). [9]

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. [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

In 1862 soldier Carleton Burgan suffered severe facial disfigurement due to mercury poisoning after having an infection treated with calomel, a common medicine that contained mercury. Carleton Burgan (CP 1659), National Museum of Health and Medicine (3383372640).jpg
In 1862 soldier Carleton Burgan suffered severe facial disfigurement due to mercury poisoning after having an infection treated with calomel, a common medicine that contained mercury.

Historically, medicines could contain mercury and thus do more harm than good to patients. The popular Victorian medicine calomel contained mercury. In her 1859 autobiography, Scottish seamstress Elizabeth Storie describes her life as a disabled woman due to severe mercury poisoning when a doctor attempted to treat a mild childhood disease with prolonged administration of calomel. [12] In 1862 a soldier in the American civil war, Carleton Burgan, suffered a similar disfigurement when he was treated with calomel for an infection. [13]

Today, consumption of fish containing mercury is by far the most significant source of ingestion-related mercury exposure in humans, although plants and livestock also contain mercury due to bioconcentration of organic mercury from seawater, freshwater, marine and lacustrine sediments, soils, and atmosphere, and due to biomagnification by ingesting other mercury-containing organisms. [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 mercury amalgam dental restorations, [18] 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. [19]

All of these, except elemental liquid mercury, produce toxicity or death with less than a gram. Mercury's zero oxidation state (Hg 0) 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. [20] [21] [22]

Consumption of whale and dolphin meat, as is the practice in Japan, is a source of high levels of mercury poisoning. [23] 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. [24]

Human-generated sources, such as coal-burning power plants [25] 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. [26] 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. [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 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. [29]

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. [30]

Many traditional medicines, including ones used in Ayurvedic medicine, [31] [32] [33] [34] and in Traditional Chinese medicine, [35] contain mercury and other heavy metals.

Sources

Organic compounds of mercury tend to be much more toxic than either the elemental form or the salts. These compounds have been implicated in causing brain 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. [36] [37]

Methylmercury is the major source of organic mercury for all individuals. [38] 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. [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 excess coronary heart disease deaths and suboptimal neural 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 (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. [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 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. [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]

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. [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 also cyanide, leading to simultaneous cyanide poisoning. [46] The drug n-acetyl penicillamine has been used to treat mercury poisoning with limited success. [47]

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, [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 the respiratory tract, where it enters the circulatory 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 in case–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 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. [48]

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). [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 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, [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 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, such as those seen in Minamata disease. Mercury exposures in excess of dietary selenium intakes in young children can have severe neurological consequences, preventing nerve sheaths from forming properly.

Exposure to methylmercury causes increased levels of antibodies sent to myelin basic protein (MBP), which is involved in the myelination of neurons, and glial fibrillary acidic protein (GFAP), which is essential to many functions in the central nervous system (CNS). [56] This causes an autoimmmune response against MBP and GFAP and results in the degradation of neural myelin and general decline in function of the CNS. [57]

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. [58]

Diagnosis of organic mercury poisoning differs in that whole-blood or hair analysis is more reliable than urinary mercury levels. [58]

Prevention

Mercury poisoning can be prevented or minimized by eliminating or reducing exposure to mercury and mercury compounds. To that end, many governments and private groups have made efforts to heavily regulate the use of mercury, or to issue advisories about the use of mercury. Most countries have signed the Minamata Convention on Mercury.

The export from the European Union of mercury and some mercury compounds has been prohibited since 15 March 2011. [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]

US environmental limits [62]
CountryRegulating agencyRegulated activityMediumType of mercury compoundType of limitLimit
US Occupational Safety and Health Administration occupational exposureairelemental mercuryCeiling (not to exceed)0.1 mg/m3
USOccupational Safety and Health Administrationoccupational exposureairorganic mercuryCeiling (not to exceed)0.05 mg/m3
USFood and Drug Administrationeatingsea foodmethylmercuryMaximum allowable concentration1 ppm (1 mg/L)
US Environmental Protection Agency drinkingwaterinorganic mercuryMaximum contaminant level2 ppb (0.002 mg/L)

The United States Environmental Protection Agency (EPA) issued recommendations in 2004 regarding exposure to mercury 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.

Cleaning spilled mercury

EPA workers clean up residential mercury spill in 2004 EPA workers clean up residential mercury spill (3986684199).jpg
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, 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. [66]

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. [67] [68]

Chelation therapy

Chelation therapy for acute inorganic mercury poisoning, a formerly common method, was done with DMSA, 2,3-dimercapto-1-propanesulfonic acid (DMPS), D-penicillamine (DPCN), or dimercaprol (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 due to 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 and N-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, 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. [71]

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. [72] 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. [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 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 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]

History

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. [106] 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. [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]

Medicine

Mercury was once prescribed as a purgative. [110] Many mercury-containing compounds were once used in medicines. These include calomel (mercurous chloride), and mercuric chloride.

Thiomersal

In 1999, the Centers for Disease Control (CDC) and the American Academy of Pediatrics (AAP) asked vaccine makers to remove the organomercury compound thiomersal (spelled "thimerosal" in the US) from vaccines as quickly as possible, and thiomersal has been phased out of US and European vaccines, except for some preparations of influenza vaccine. [111] 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 thiomersal was a cause of autism. [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 2004 Institute 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 toxicity

Dental amalgam is a possible cause of low-level mercury poisoning due to its use in 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 skin whitening products contain the toxic mercury(II) chloride as the active ingredient. When applied, the chemical readily absorbs through the skin into the bloodstream. [116] 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. [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 amongst 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

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 the U.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 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. [125]

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, [126] while in 2010 journalists Viktor Kalashnikov and Marina Kalashnikova accused Russia's FSB of trying to poison them. [127]

In 2011, German Christoph Bulwin was poisoned with a mercury compound from a syringe attached to an umbrella.

See also

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<span class="mw-page-title-main">Mercury regulation in the United States</span>

Mercury regulation in the United States limit the maximum concentrations of mercury (Hg) that is permitted in air, water, soil, food and drugs. The regulations are promulgated by agencies such as the Environmental Protection Agency (EPA) and Food and Drug Administration (FDA), as well as a variety of state and local authorities. EPA published the Mercury and Air Toxics Standards (MATS) regulation in 2012; the first federal standards requiring power plants to limit emissions of mercury and other toxic gases.

<span class="mw-page-title-main">Selenium in biology</span> Use of Selenium by organisms

Selenium is an essential micronutrient for animals, though it is toxic in large doses. In plants, it sometimes occurs in toxic amounts as forage, e.g. locoweed. Selenium is a component of the amino acids selenocysteine and selenomethionine. In humans, selenium is a trace element nutrient that functions as cofactor for glutathione peroxidases and certain forms of thioredoxin reductase. Selenium-containing proteins are produced from inorganic selenium via the intermediacy of selenophosphate (PSeO33−).

<span class="mw-page-title-main">Marine mercury pollution</span> Mercury contamination in sea and sediments

Mercury is a heavy metal that cycles through the atmosphere, water, and soil in various forms to different parts of the world. Due to this natural mercury cycle, irrespective of which part of the world releases mercury it could affect an entirely different part of the world making mercury pollution a global concern. Mercury pollution is now identified as a global problem and awareness has been raised on an international action plan to minimize anthropogenic mercury emissions and clean up mercury pollution. The 2002 Global Mercury Assessment concluded that "International actions to address the global mercury problem should not be delayed". Among many environments that are under the impact of mercury pollution, the ocean is one which cannot be neglected as it has the ability to act as a "storage closet" for mercury. According to a recent model study the total anthropogenic mercury released into the ocean is estimated to be around 80,000 to 45,000 metric tons and two-thirds of this amount is estimated to be found in waters shallower than 1000m level where much consumable fish live. Mercury can bioaccumulate in marine food chains in the form of highly toxic methylmercury which can cause health risks to human seafood consumers. According to statistics, about 66% of global fish consumption comes from the ocean. Therefore, it is important to monitor and regulate oceanic mercury levels to prevent more and more mercury from reaching the human population through seafood consumption.

Mercury is a poisonous element found in various forms in Canada. It can be emitted in the atmosphere naturally and anthropogenically, the main cause of mercury emission in the environment. Mercury pollution has become a sensitive issue in Canada for the past few decades and many steps have been taken for prevention at local, national, and international levels. It has been found to have various negative health and environmental effects. Methylmercury is the most toxic form of mercury which is easily accessible as well as digestible by living organisms and it is this form of mercury causing serious harm to human and wildlife health.

<span class="mw-page-title-main">Mercury contamination in Grassy Narrows</span> Environmental & health disaster 1962 - 1970

Mercury contamination in Grassy Narrows was an uncontrolled discharge of between 9,000 kilograms (20,000 lb) and 11,000 kilograms (24,000 lb) of mercury from the Dryden Mill's chloralkali plant in Dryden into the headwaters of the Wabigoon River in the Kenora District of Northwestern Ontario from 1962 until 1970. It was described as "one of the worst cases of environmental poisoning in Canadian history." The contamination poisoned many people in the Grassy Narrows First Nation and Whitedog First Nation communities.

References

  1. 1 2 3 "Mercury". NIEHS. Archived from the original on 19 November 2016. Retrieved 19 November 2016.
  2. 1 2 3 4 5 Bose-O'Reilly S, McCarty KM, Steckling N, Lettmeier B (September 2010). "Mercury exposure and children's health". Current Problems in Pediatric and Adolescent Health Care. 40 (8): 186–215. doi:10.1016/j.cppeds.2010.07.002. PMC   3096006 . PMID   20816346.
  3. 1 2 3 4 5 6 7 8 9 Bernhoft RA (2012). "Mercury toxicity and treatment: a review of the literature". Journal of Environmental and Public Health. 2012: 460508. doi: 10.1155/2012/460508 . PMC   3253456 . PMID   22235210.
  4. 1 2 3 4 5 "Mercury and health". WHO. January 2016. Archived from the original on 20 November 2016. Retrieved 19 November 2016.
  5. 1 2 3 Kosnett MJ (December 2013). "The role of chelation in the treatment of arsenic and mercury poisoning". Journal of Medical Toxicology. 9 (4): 347–54. doi:10.1007/s13181-013-0344-5. PMC   3846971 . PMID   24178900.
  6. Hong YS, Kim YM, Lee KE (November 2012). "Methylmercury exposure and health effects". Journal of Preventive Medicine and Public Health = Yebang Uihakhoe Chi. 45 (6): 353–63. doi:10.3961/jpmph.2012.45.6.353. PMC   3514465 . PMID   23230465.
  7. Environment, U. N. (2019-03-04). "Global Mercury Assessment 2018". UNEP - UN Environment Programme. Retrieved 2022-01-12.
  8. Bernhoft, Robin A. (2012). "Mercury toxicity and treatment: a review of the literature". Journal of Environmental and Public Health. 2012: 460508. doi: 10.1155/2012/460508 . ISSN   1687-9813. PMC   3253456 . PMID   22235210.
  9. Spiller, Henry A. (May 2018). "Rethinking mercury: the role of selenium in the pathophysiology of mercury toxicity". Clinical Toxicology. 56 (5): 313–326. doi:10.1080/15563650.2017.1400555. ISSN   1556-9519. PMID   29124976. S2CID   4295652.
  10. Johnson-Arbor, Kelly; Tefera, Eshetu; Farrell, John (June 2021). "Characteristics and treatment of elemental mercury intoxication: A case series". Health Science Reports. 4 (2): e293. doi:10.1002/hsr2.293. ISSN   2398-8835. PMC   8177896 . PMID   34136656.
  11. Horowitz Y, Greenberg D, Ling G, Lifshitz M (June 2002). "Acrodynia: a case report of two siblings". Archives of Disease in Childhood. 86 (6): 453. doi:10.1136/adc.86.6.453. PMC   1762992 . PMID   12023189.
  12. Storie, Elizabeth (1859). he Autobiography of Elizabeth Storie, A Native of Glasgow, Who Was Subjected to Much Injustice at the Hands of Some Members of the Medical, Legal, and Clerical Professions. Glasgow: Richard Stobbs.
  13. Crumley, Roger L. (2003-01-01). "Some Pioneers in Plastic Surgery of the Facial Region". Archives of Facial Plastic Surgery. 5 (1): 9–15. doi:10.1001/archfaci.5.1.9. ISSN   1521-2491. PMID   12533132.
  14. United States Environmental Protection Agency (December 1997). Mercury Study Report to Congress (PDF). Vol. 3. Washington, D.C.: United States Environmental Protection Agency. Archived (PDF) from the original on 2011-02-03.
  15. ATSDR Mercury ToxFAQ (April 1999). "ToxFAQs: Mercury" (PDF). Agency for Toxic Substances and Disease Registry . Retrieved 2007-07-25.
  16. Dufault R, LeBlanc B, Schnoll R, Cornett C, Schweitzer L, Wallinga D, et al. (January 2009). "Mercury from chlor-alkali plants: measured concentrations in food product sugar". Environmental Health. 8 (1): 2. Bibcode:2009EnvHe...8....2D. doi: 10.1186/1476-069X-8-2 . PMC   2637263 . PMID   19171026.
  17. "Mercury in High-Fructose Corn Syrup?".
  18. Levy M (August 1995). "Dental amalgam: toxicological evaluation and health risk assessment". Journal. 61 (8): 667–8, 671–4. PMID   7553398.
  19. Goldman LR, Shannon MW (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.
  20. "Just how dangerous is mercury, anyway? – DW – 01/24/2023". dw.com. Retrieved 2024-02-16.
  21. Smith, Jeremy (2014-04-15). Molecular Mechanisms of Bacterial Mercury Transformation (Report). Univ. of Tennessee, Knoxville, TN (United States). OSTI   1127445.
  22. "The Toxicology of Mercury".{{cite web}}: Missing or empty |url= (help)
  23. Project, International Marine Mammal (2023-08-28). "New Tests Confirm Poisons in Dolphin Meat". International Marine Mammal Project. Retrieved 2024-02-16.
  24. Mercury danger in dolphin meat. 2009 Archived 2012-06-30 at archive.today
  25. "Mercury". 2013-07-08. Archived from the original on 2015-04-08. Retrieved 2015-04-08.
  26. Ballabio C, Jiskra M, Osterwalder S, Borrelli P, Montanarella L, Panagos P (May 2021). "A spatial assessment of mercury content in the European Union topsoil". The Science of the Total Environment. 769: 144755. Bibcode:2021ScTEn.76944755B. doi:10.1016/j.scitotenv.2020.144755. PMC   8024745 . PMID   33736262.
  27. Pacyna EG, Pacyna JM, Steenhuisen F, Wilson S (2006). "Global anthropogenic mercury emission inventory for 2000". Atmos. Environ. 40 (22): 4048–63. Bibcode:2006AtmEn..40.4048P. doi:10.1016/j.atmosenv.2006.03.041.
  28. Esdaile, L. J.; Chalker, J. M. (2018). "The Mercury Problem in Artisanal and Small-Scale Gold Mining". Chemistry – A European Journal. 24 (27): 6905–6916. doi:10.1002/chem.201704840. PMC   5969110 . PMID   29314284.
  29. How mercury poisons gold miners and enters the food chain Archived 2013-09-23 at the Wayback Machine , BBC News
  30. United States Environmental Protection Agency (December 1997). Mercury Study Report to Congress (PDF). Vol. 4. Washington, D.C.: United States Environmental Protection Agency. Archived (PDF) from the original on 2011-02-03.
  31. "Metal Toxicity from Ayurvedic Medications - MN Dept. of Health". www.health.state.mn.us. Retrieved 2024-04-26.
  32. Mikulski, Marek A.; Wichman, Michael D.; Simmons, Donald L.; Pham, Anthony N.; Clottey, Valentina; Fuortes, Laurence J. (July 2017). "Toxic metals in ayurvedic preparations from a public health lead poisoning cluster investigation". International Journal of Occupational and Environmental Health. 23 (3): 187–192. doi: 10.1080/10773525.2018.1447880 . ISSN   1077-3525. PMC   6060866 . PMID   29528276.
  33. Breeher, Laura; Mikulski, Marek A.; Czeczok, Thomas; Leinenkugel, Kathy; Fuortes, Laurence J. (October 2015). "A cluster of lead poisoning among consumers of Ayurvedic medicine". International Journal of Occupational and Environmental Health. 21 (4): 303–307. doi: 10.1179/2049396715Y.0000000009 . ISSN   1077-3525. PMC   4727589 . PMID   25843124.
  34. Lynch E, Braithwaite R (July 2005). "A review of the clinical and toxicological aspects of 'traditional' (herbal) medicines adulterated with heavy metals". Expert Opinion on Drug Safety. 4 (4): 769–78. doi:10.1517/14740338.4.4.769. PMID   16011453. S2CID   19160044.
  35. Ching FM (2007). Chinese Herbal Drug Research Trends. Nova Publishers. ISBN   9781600219283.
  36. 1 2 The Karen Wetterhahn story Archived 2012-05-30 at the Wayback Machine – University of Bristol web page documenting her death, retrieved December 9, 2006.
  37. 1 2 OSHA update following Karen Wetterhahn's death Archived 2015-07-11 at the Wayback Machine
  38. 1 2 3 4 5 Clifton JC (April 2007). "Mercury exposure and public health". Pediatric Clinics of North America. 54 (2): 237–69, viii. doi:10.1016/j.pcl.2007.02.005. PMID   17448359.
  39. 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. Archived 2013-05-17 at the Wayback Machine U.S. FDA and U.S. EPA Advisory EPA-823-F-04-009, March 2004.
  40. Mozaffarian D, Rimm EB (October 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.
  41. 1 2 3 Clarkson TW, Magos L (September 2006). "The toxicology of mercury and its chemical compounds". Critical Reviews in Toxicology. 36 (8): 609–662. doi:10.1080/10408440600845619. PMID   16973445. S2CID   37652857.
  42. Bayer SA, Altman J, Russo RJ, Zhang X (1993). "Timetables of neurogenesis in the human brain based on experimentally determined patterns in the rat". Neurotoxicology. 14 (1): 83–144. PMID   8361683.
  43. Rice D, Barone S (June 2000). "Critical periods of vulnerability for the developing nervous system: evidence from humans and animal models". Environmental Health Perspectives. 108 Suppl 3 (3): 511–33. doi:10.2307/3454543. JSTOR   3454543. PMC   1637807 . PMID   10852851.
  44. Newland MC, Reed MN, Rasmussen E (May 2015). "A hypothesis about how early developmental methylmercury exposure disrupts behavior in adulthood". Behavioural Processes. 114: 41–51. doi:10.1016/j.beproc.2015.03.007. PMC   4407818 . PMID   25795099.
  45. Langford N, Ferner R (October 1999). "Toxicity of mercury". Journal of Human Hypertension. 13 (10): 651–6. doi:10.1038/sj.jhh.1000896. PMID   10516733. S2CID   37322483.
  46. Emsley, John. The Elements of Murder. Oxford: Oxford University Press, 2005. ISBN   0-19-280599-1
  47. "Mercuric Cyanide." 1987. "Mercuric Cyanide". Archived from the original on 2011-05-11. Retrieved 2011-02-22. (accessed April 2, 2009).
  48. 1 2 ATSDR. 1999. Toxicological Profile for Mercury. Atlanta, GA:Agency for Toxic Substances and Disease Registry. "Archived copy" (PDF). Archived (PDF) from the original on 2011-07-21. Retrieved 2011-02-22.{{cite web}}: CS1 maint: archived copy as title (link)
  49. Hursh JB, Clarkson TW, Miles EF, Goldsmith LA (1989). "Percutaneous absorption of mercury vapor by man". Archives of Environmental Health. 44 (2): 120–7. doi:10.1080/00039896.1989.9934385. PMID   2494955.
  50. Cherian MG, Hursh JB, Clarkson TW, Allen J (1978). "Radioactive mercury distribution in biological fluids and excretion in human subjects after inhalation of mercury vapor". Archives of Environmental Health. 33 (3): 109–14. doi:10.1080/00039896.1978.10667318. PMID   686833.
  51. Ngim CH, Foo SC, Boey KW, Jeyaratnam J (November 1992). "Chronic neurobehavioural effects of elemental mercury in dentists". British Journal of Industrial Medicine. 49 (11): 782–90. doi:10.1136/oem.49.11.782. PMC   1039326 . PMID   1463679.
  52. Liang YX, Sun RK, Sun Y, Chen ZQ, Li LH (February 1993). "Psychological effects of low exposure to mercury vapor: application of a computer-administered neurobehavioral evaluation system". Environmental Research. 60 (2): 320–7. Bibcode:1993ER.....60..320L. doi:10.1006/enrs.1993.1040. PMID   8472661.
  53. Carvalho CM, Chew EH, Hashemy SI, Lu J, Holmgren A (May 2008). "Inhibition of the human thioredoxin system. A molecular mechanism of mercury toxicity". The Journal of Biological Chemistry. 283 (18): 11913–23. doi: 10.1074/jbc.m710133200 . PMID   18321861. S2CID   1318126.
  54. Linster CL, Van Schaftingen E (January 2007). "Vitamin C. Biosynthesis, recycling and degradation in mammals". The FEBS Journal. 274 (1): 1–22. doi: 10.1111/j.1742-4658.2006.05607.x . PMID   17222174. S2CID   21345196.
  55. Ralston NV, Raymond LJ (November 2010). "Dietary selenium's protective effects against methylmercury toxicity". Toxicology. 278 (1): 112–23. Bibcode:2010Toxgy.278..112R. doi:10.1016/j.tox.2010.06.004. PMID   20561558.
  56. da Silva, Diane Cleydes Baía; Bittencourt, Leonardo Oliveira; Baia-da-Silva, Daiane Claydes; Chemelo, Victoria Santos; Eiró-Quirino, Luciana; Nascimento, Priscila Cunha; Silva, Márcia Cristina Freitas; Freire, Marco Aurelio M.; Gomes-Leal, Walace; Crespo-Lopez, Maria Elena; Lima, Rafael Rodrigues (2022-03-29). "Methylmercury Causes Neurodegeneration and Downregulation of Myelin Basic Protein in the Spinal Cord of Offspring Rats after Maternal Exposure". International Journal of Molecular Sciences. 23 (7): 3777. doi: 10.3390/ijms23073777 . ISSN   1422-0067. PMC   8998727 . PMID   35409136.
  57. el-Fawal HA, Gong Z, Little AR, Evans HL (1996). "Exposure to methyl mercury results in serum autoantibodies to neurotypic and gliotypic proteins". Neurotoxicology. 17 (1): 267–76. PMID   8784838.
  58. 1 2 Ibrahim D, Froberg B, Wolf A, Rusyniak DE (March 2006). "Heavy metal poisoning: clinical presentations and pathophysiology". Clinics in Laboratory Medicine. 26 (1): 67–97, viii. doi:10.1016/j.cll.2006.02.003. PMID   16567226.
  59. "Export-ban of mercury and mercury compounds from the EU by 2011" (Press release). European Parliament. 2008-05-21. Archived from the original on 2008-09-25. Retrieved 2008-06-10.
  60. "Mercury - Industry - Environment -European Commission". 22 April 2024.
  61. "EU states clash over use of toxic mercury in light bulbs". TheGuardian.com . 7 February 2020.
  62. ATSDR – Mercury – Regulations and Advisories Archived 2011-06-06 at the Wayback Machine
  63. FDA/EPA 2004 Advice on What You Need to Know About Mercury in Fish and Shellfish Archived 2009-03-08 at the Wayback Machine
  64. EPA Fish Kids Flash-based movie Archived 2008-10-11 at the Wayback Machine
  65. Cleaning Up Spilled Mercury Archived 2016-04-03 at the Wayback Machine
  66. "What to Do if a Mercury Thermometer Breaks". US Environmental Protection Agency. 2015-08-18. Retrieved 2018-03-22.
  67. "Sur l'emploi de l'iodure de potassium pour combattre les affections saturnines et mercurielles", in Annales de chimie et de physique, t. 26, 3e série, 1849.
  68. "On the Employment of Iodide of Potassium as a Remedy for the Affections Caused by Lead and Mercury", in Br Foreign Med Chir Rev. 1853 Jan; 11(21): 201–224.
  69. Risher JF, Amler SN (August 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. Bibcode:2005NeuTx..26..691R. doi:10.1016/j.neuro.2005.05.004. PMID   16009427.
  70. 1 2 Rooney JP (May 2007). "The role of thiols, dithiols, nutritional factors and interacting ligands in the toxicology of mercury". Toxicology. 234 (3): 145–56. Bibcode:2007Toxgy.234..145R. doi:10.1016/j.tox.2007.02.016. PMID   17408840.
  71. Hazards of chelation therapy:
  72. Spiller HA (May 2018). "Rethinking mercury: the role of selenium in the pathophysiology of mercury toxicity". Clinical Toxicology. 56 (5): 313–326. doi:10.1080/15563650.2017.1400555. PMC   4856720 . PMID   29124976.
  73. Ralston NV, Kaneko JJ, Raymond LJ (September 2019). "Selenium health benefit values provide a reliable index of seafood benefits vs. risks". Journal of Trace Elements in Medicine and Biology. 55 (5): 50–57. Bibcode:2019JTEMB..55...50R. doi: 10.1016/j.jtemb.2019.05.009 . PMID   31345365. S2CID   190878923.
  74. Rooney JP (February 2014). "The retention time of inorganic mercury in the brain--a systematic review of the evidence". Toxicology and Applied Pharmacology. 274 (3): 425–35. Bibcode:2014ToxAP.274..425R. doi:10.1016/j.taap.2013.12.011. hdl: 2262/68176 . PMID   24368178.
  75. 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.
  76. R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 923–927.
  77. Kindy, David (19 November 2021). "Earliest Evidence of Mercury Poisoning in Humans Found in 5,000-Year-Old Bones". Smithsonian . Retrieved 3 December 2021.
  78. Zhao HL, Zhu X, Sui Y (August 2006). "The short-lived Chinese emperors". Journal of the American Geriatrics Society. 54 (8): 1295–6. doi: 10.1111/j.1532-5415.2006.00821.x . PMID   16914004. S2CID   31630319.
  79. 1 2 3 Chris Stewart (22 January 2017). "#116-Tang 28: I, Xuānzong". The History of China (Podcast). Agora Podcast Network. Event occurs at 29:30. Archived from the original on 6 March 2017. Retrieved 24 January 2017.
  80. "Pliny the Elder's Contribution to Toxicology & Occupational Health & Safety". Online Safety Trainer. 2023-03-29. Retrieved 2024-01-03.
  81. Castle, Frederick A.; Rice, Charles, eds. (1886). "Carl Wilhelm Scheele". American Druggist. 15 (August). New York: 157–158. Retrieved 15 August 2023.
  82. Waldron HA (1983). "Did the Mad Hatter have mercury poisoning?". British Medical Journal. 287 (6409): 1961. doi:10.1136/bmj.287.6409.1961. PMC   1550196 . PMID   6418283.
  83. Kitzmiller KJ. "The Not-So-Mad Hatter: Occupational Hazards of Mercury". Archived from the original on 2013-12-02.
  84. An Account of the Effect of Mercurial Vapors on the Crew of His Majesty's Ship Triumph, in the year 1810. By Wm. Burnett, M.D. one of the Medical Commissioners of the Navy, formerly Physician and Inspector of Hospitals to the Mediterranean Fleet.
  85. Michael J. Doherty MD: The Quicksilver Prize: Mercury vapor poisoning aboard HMS Triumph and HMS Phipps (2003).
  86. "An article about the cathedral". Archived from the original on 2011-08-28.
  87. "An article about gilding". Archived from the original on 2013-10-23.
  88. "Bichloride of Mercury Killed Olive Thomas". The Toronto World. September 15, 1920. p. 6. Retrieved August 27, 2018.
  89. Foster, Charles (2000). Stardust and Shadows: Canadians in Early Hollywood, page 257. Toronto, Canada: Dundurn Press, 2000. ISBN   978-1550023480.
  90. Stock A (1926). "Die Gefaehrlichkeit des Quecksilberdampfes". Zeitschrift für Angewandte Chemie. 39 (15): 461–466. Bibcode:1926AngCh..39..461S. doi:10.1002/ange.19260391502.
  91. Hunter D, Bomford RR, Russell DS (1940). "Poisoning by methylmercury compounds". Quarterly Journal of Medicine. 9: 193–213.
  92. Davidson PW, Myers GJ, Weiss B (April 2004). "Mercury exposure and child development outcomes". Pediatrics. 113 (4 Suppl): 1023–9. doi:10.1542/peds.113.S3.1023. PMID   15060195. S2CID   6597018. Archived from the original on 2012-12-16.
  93. McDonald A. "Indigenous peoples' vulnerabilities exposed: Lessons learned from Canada's Minamata incident: An Environmental analysis based on the case study of methyl-mercury pollution in northwestern Ontario, Canada". JACS Conference 2007 (PDF). Japanese Association for Canadian Studies. Archived from the original (PDF) on October 14, 2007. Retrieved December 14, 2007.
  94. D'ltri PA, D'ltr FM (January 1, 1978). "Mercury contamination: A human tragedy". Environmental Management. 2 (1): 3–16. Bibcode:1978EnMan...2....3D. doi:10.1007/BF01866442. ISSN   1432-1009. S2CID   153666705 . Retrieved March 6, 2021.
  95. Bruser D, Poisson J (November 11, 2017). "Ontario knew about Grassy Narrows mercury site for decades, but kept it secret". The Toronto Star. ISSN   0319-0781 . Retrieved 2017-12-16.
  96. Porter J (2016). "Children of the poisoned river". CBC News. Retrieved March 3, 2021.
  97. Engler R (April 27, 1985). "Technology out of Control". The Nation. 240. Archived from the original on March 17, 2011.
  98. Vargas JA (2007-01-26). "'Mad Scientist': On Court TV, Fatal Chemistry". The Washington Post . Archived from the original on 2012-11-08. Retrieved 2007-01-28.
  99. Perl, Peter (2002-02-03). "Obsession". The Washington Post . Retrieved 2021-08-28.
  100. Swearengin, M. (2008-04-01). "Man dies from mercury poisoning after trying to extract gold". Durant Daily Democrat.
  101. "Colbert man dies from mercury poisoning". Tulsa World. Associated Press. 2008-04-01. Retrieved 2019-05-18.
  102. Tiffany McGee (2009-01-15). "Jeremy Piven Explains His Mystery Ailment". People . Archived from the original on 2009-01-21. Retrieved 2009-01-15.
  103. "Death in India lurks in poisoned water on the rim of coal fields". 5 December 2014. Archived from the original on 2017-10-15. Retrieved 2017-10-15.
  104. Coulter MA (January 20, 2017). "Minamata Convention on Mercury". Cambridge. 55 (3). Cambridge University Press: 582–616. doi:10.5305/intelegamate.55.3.0582. S2CID   132189787.
  105. Culture, Billie Schwab Dunn Pop; Reporter, Entertainment (2024-08-08). "Chess player caught on camera attempting to poison rival with mercury". Newsweek. Retrieved 2024-08-09.
  106. James WD, Berger TG, Elston DM (2006). Andrews' diseases of the skin: clinical dermatology (10th ed.). Saunders. p.  134. ISBN   978-0-7216-2921-6.
  107. Bjørklund G (1995). "Mercury and Acrodynia" (PDF). Journal of Orthomolecular Medicine. 10 (3 & 4): 145–146. Archived (PDF) from the original on 2011-07-21.
  108. Dally A (August 1997). "The rise and fall of pink disease". Social History of Medicine. 10 (2): 291–304. doi:10.1093/shm/10.2.291. PMID   11619497.
  109. Ford M, Delaney KA, Ling L, Erickson T (2000). Clinical Toxicology (1st ed.). Saunders. ISBN   978-0-7216-5485-0.
  110. Bartholow, Roberts (1879). A practical treatise on materia medica and therapeutics. Appleton. p. 200.
  111. 1 2 Offit PA (September 2007). "Thimerosal and vaccines – a cautionary tale". The New England Journal of Medicine. 357 (13): 1278–79. doi: 10.1056/NEJMp078187 . PMID   17898096.
  112. Sugarman SD (September 2007). "Cases in vaccine court – legal battles over vaccines and autism". The New England Journal of Medicine. 357 (13): 1275–1277. doi: 10.1056/NEJMp078168 . PMID   17898095.
  113. Immunization Safety Review Committee (2004). Immunization Safety Review: Vaccines and Autism. The National Academies Press. doi:10.17226/10997. ISBN   978-0-309-09237-1. PMID   20669467. Archived from the original on 2012-07-04.
  114. Gerber JS, Offit PA (February 2009). "Vaccines and autism: a tale of shifting hypotheses". Clinical Infectious Diseases. 48 (4): 456–461. doi:10.1086/596476. PMC   2908388 . PMID   19128068.
  115. Doja A, Roberts W (November 2006). "Immunizations and autism: a review of the literature". The Canadian Journal of Neurological Sciences. 33 (4): 341–346. doi: 10.1017/s031716710000528x . PMID   17168158.
  116. Counter SA (December 16, 2003). Whitening skin can be deadly. The Boston Globe. Archived from the original on September 1, 2009.
  117. "FDA Proposes Hydroquinone Ban". Archived from the original on 2007-07-03.FDA bans hydroquinone in skin whitening products
  118. "NYC Health Dept. Warns Against Use of 'Skin-lightening' Creams Containing Mercury or Similar Products Which Do Not List Ingredients". January 27, 2005. Archived from the original on May 24, 2007.
  119. Counter SA, Buchanan LH (2004). "Mercury exposure in children: a review". Toxicology and Applied Pharmacology. 198 (2): 209–230. Bibcode:2004ToxAP.198..209C. doi:10.1016/j.taap.2003.11.032. PMID   15236954.
  120. Mahaffey KR (2005). "Exposure to Mercury in the Americas". Dynamics of Mercury Pollution on Regional and Global Scales. Springer. pp. 345–384. doi:10.1007/0-387-24494-8_15. ISBN   978-0-387-24493-8.
  121. In a survey, 28% of Koreans and 50% of Philippians say that they use skin whitening products. "Skin lightening in Asia? A bright future?". Archived from the original on 2007-05-25.
  122. Bray M (2002-05-15). SKIN DEEP: Dying to be white. CNN. Archived from the original on 2010-04-08. Retrieved 2010-05-12.
  123. Aucott M, McLinden M, Winka M (February 2003). "Release of mercury from broken fluorescent bulbs". Journal of the Air & Waste Management Association. 53 (2): 143–51. Bibcode:2003JAWMA..53..143A. doi: 10.1080/10473289.2003.10466132 . PMID   12617289. S2CID   9263443.
  124. "Spills, disposal and site cleanup". U.S. Environmental Protection Agency. 2009-07-13. Archived from the original on 2009-07-01. Retrieved 2009-06-30.
  125. Tunnessen WW, McMahon KJ, Baser M (May 1987). "Acrodynia: exposure to mercury from fluorescent light bulbs". Pediatrics. 79 (5): 786–789. doi:10.1542/peds.79.5.786. PMID   3575038. S2CID   36523101.
  126. Gutterman, Steve (15 October 2008). "Russian lawyer suspects mercury poisoning". USA Today. Associated Press. Archived from the original on 2011-12-17.
  127. Allen, Nick (27 December 2010). "German inquiry into 'poisoning' of Russian dissidents". The Telegraph. Archived from the original on 2010-12-29.