Arsenic poisoning [can cause arsenic skin lesions]

Arsenic poisoning

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Arsenic Poisoning
Classification and external resources
ICD–10	T57.0
ICD–9	985.1
eMedicine	emerg/42
MeSH	D020261

Arsenic Poisoning interferes with cellular longevity by allosteric inhibition of an essential metabolic enzyme pyruvate dehydrogenase (PDH) complex which catalyzes the oxidation of pyruvate to acetyl-CoA by NAD⁺. With the enzyme inhibited, the energy system of the cell is disrupted resulting in a cellular apoptosis episode. Biochemically, arsenic prevents use of thiamine resulting in a clinical picture resembling thiamine deficiency. Poisoning with arsenic can raise lactate levels and lead to lactic acidosis. Low potassium levels in the blood increase the risk of experiencing a life-threatening heart rhythm problem from arsenic trioxide. Arsenic in cells clearly stimulates the production of hydrogen peroxide (H₂O₂). When the H₂O₂ reacts with certain metals such as iron or manganese it produces a highly reactive hydroxyl radical. Inorganic Arsenic trioxide found in ground water particularly affects voltage-gated potassium channels,^[1] disrupting cellular electrolytic function resulting in neurological disturbances, cardiovascular episodes such as prolonged qt interval, neutropenia, high blood pressure,^[2] central nervous system dysfunction, anemia, Leukemia,^[3] and death. Arsenic trioxide is a ubiquitous molecule present in American drinking water.^[4]

“	Arsenic exposure plays a key role in the pathogenesis of vascular endothelial dysfunction as it inactivates endothelial nitric oxide synthase, leading to reduction in the generation and bioavailability of nitric oxide. In addition, the chronic arsenic exposure induces high oxidative stress, which may affect the structure and function of cardiovascular system. Further, the arsenic exposure has been noted to induce atherosclerosis by increasing the platelet aggregation and reducing fibrinolysis. Moreover, arsenic exposure may cause arrhythmia by increasing the QT interval and accelerating the cellular calcium overload. The chronic exposure to arsenic upregulates the expression of tumor necrosis factor-α, interleukin-1, vascular cell adhesion molecule and vascular endothelial growth factor to induce cardiovascular pathogenesis.	”
—Pitchai Balakumar1 and Jagdeep Kaur, “Arsenic Exposure and Cardiovascular Disorders: An Overview”, Cardiovascular Toxicology, December 2009[5]

Contents [show] 1 Toxicity 2 Symptoms of Arsenic Poisoning 3 Pathophysiology 4 Diagnosis 5 Treatment 6 Unintentional poisoning 6.1 Occupational exposures 6.2 Arsenicosis: chronic arsenic poisoning from drinking water 7 Intentional poisoning 7.1 Detection in biological fluids 8 Famous victims (known and alleged) 8.1 Francesco I de’ Medici, Grand Duke of Tuscany 8.2 George III of Great Britain 8.3 Napoleon Bonaparte 8.4 Simón Bolívar 8.5 Charles Francis Hall 8.6 Huo Yuan Jia 8.7 Clare Boothe Luce 8.8 Impressionist painters 8.9 The Emperor Guangxu 8.10 Phar Lap 9 See also 10 Footnotes 11 External links

[edit] Toxicity

Research has shown that the inorganic arsenites (trivalent forms) in drinking water have a much higher acute toxicity than organic arsenates (pentavalent forms).^[6] The acute minimal lethal dose of arsenic in adults is estimated to be 70 to 200 mg or 1 mg/kg/day.^[7] Most reported arsenic poisonings are caused by one of arsenic’s compounds, also found in drinking water, arsenic trioxide which is 500 times more toxic than pure arsenic.

Arsenic is related to the first five leading causes of non-accidental death in the United States, bringing the total to 1,525,675 related mortalities. EPA efforts are underway to reduce drinking water exposure to zero.^[8][9] heart disease^[10] (hypertension related cardiovascular), cancer,^[11] stroke^[12] (cerebrovascular diseases), chronic lower respiratory diseases,^[13] and diabetes. These diseases are all related to the alteration of voltage dependent potassium channels. Researchers, led by Ana Navas-Acien, MD, PhD, of the Johns Hopkins Bloomberg School of Health, studied 788 adults who had their urine tested for arsenic exposure in the 2003-2004 National Health and Nutrition Examination Survey. Participants with type 2 diabetes had a 26% higher level of total arsenic in their urine than those without the disease.^{[citation needed]} Diabetes is also related to alteration of voltage dependent potassium channels due in part to the function of insulin and potassium in the cellular metabolism of glucose. Due to the regular appearance of arsenic in public drinking water supplies, it is likely that arsenic plays a part in about thirty percent of total all cause mortality in the United States.^{[citation needed]} Arsenic prevalence in the water has been related to the occurrence of hypertension, erectile dysfunction and related conditions. Leading causes of mortality in the world are all related to arsenic. These are

Chronic exposure to inorganic arsenic may lead to hypertension, involuntary muscular dysfunction (including incontinence), diabetes, neuropathy, depression, obesity and any other condition related to the altered role of intercellular voltage-dependent potassium channels, including cutaneous hyperpigmentation.^[14]:859

[edit] Symptoms of Arsenic Poisoning

Symptoms of arsenic poisoning begin with headaches, confusion and drowsiness. As the poisoning develops, convulsions and changes in fingernail pigmentation may occur. When the poisoning becomes acute, symptoms may include diarrhea, vomiting, blood in the urine, cramping muscles, hair loss, stomach pain, and more convulsions. The organs of the body that are usually affected by arsenic poisoning are the lungs, skin, kidneys, and liver. The final result of arsenic poisoning is coma or death.

[edit] Pathophysiology

Main article: Arsenic toxicity

Tissue culture studies have shown that arsenic blocks both IKr and Iks channels and, at the same time, activates IK-ATP channels. Arsenic also disrupts ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. These metabolic interferences lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. A post mortem reveals brick red colored mucosa, due to severe hemorrhage. Although arsenic causes toxicity, it can also play a protective role.^[15]

[edit] Diagnosis

There are tests available to diagnose poisoning by measuring arsenic in blood, urine, hair, and fingernails. The urine test is the most reliable test for arsenic exposure within the last few days. Urine testing needs to be done within 24–48 hours for an accurate analysis of an acute exposure. Tests on hair and fingernails can measure exposure to high levels of arsenic over the past 6–12 months. These tests can determine if one has been exposed to above-average levels of arsenic. They cannot predict, however, whether the arsenic levels in the body will affect health.^[16]

Hair is a potential bioindicator for arsenic exposure due to its ability to store trace elements from blood. Incorporated elements maintain their position during growth of hair. Thus for a temporal estimation of exposure, an assay of hair composition needs to be carried out with a single hair which is not possible with older techniques requiring homogenization and dissolution of several strands of hair. This type of biomonitoring has been achieved with newer microanalytical techniques like Synchroton radiation based X ray fluorescence (SXRF) spectroscopy and Microparticle induced X ray emission (PIXE).The highly focused and intense beams study small spots on biological samples allowing analysis to micro level along with the chemical speciation. In a study, this method has been used to follow arsenic level before, during and after treatment with Arsenious oxide in patients with Acute Promyelocytic Leukemia.^[17]

[edit] Treatment

Chemical and synthetic methods are now used to treat arsenic poisoning. Dimercaprol and dimercaptosuccinic acid are chelating agents which sequester the arsenic away from blood proteins and are used in treating acute arsenic poisoning. The most important side effect is hypertension. Dimercaprol is considerably more toxic than succimer.^[18]

In the journal Food and Chemical Toxicology, Keya Chaudhuri of the Indian Institute of Chemical Biology in Kolkata, and her colleagues reported giving rats daily doses of arsenic in their water, in levels equivalent to those found in groundwater in Bangladesh and West Bengal. Those rats which were also fed garlic extracts had 40 percent less arsenic in their blood and liver, and passed 45 percent more arsenic in their urine. The conclusion is that sulfur-containing substances in garlic scavenge arsenic from tissues and blood. The presentation concludes that people in areas at risk of arsenic contamination in the water supply should eat one to three cloves of garlic per day as a preventative.^[19][20][21]

Freddie Mercury

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Freddie Mercury
Mercury performing in New Haven, CT, 1977
Background information
Birth name	Farrokh Bulsara
Born	5 September 1946(1946-09-05) Stone Town, Zanzibar
Origin	London, England, UK[1]
Died	24 November 1991 (aged 45) Kensington , London, England, United Kingdom
Genres	Rock, Hard rock
Occupations	Musician, singer-songwriter, record producer
Instruments	Vocals, piano, keyboards, guitar
Years active	1969–91
Labels	Columbia, Polydor, EMI, Parlophone, Hollywood Records
Associated acts	Queen, Wreckage/Ibex, Montserrat Caballé

Freddie Mercury (born Farrokh Bulsara (Gujarati: ફ્રારુક બુલ્સારા‌), 5 September 1946 – 24 November 1991)^[2] was a British musician, best known as the lead vocalist and a songwriter of the rock band Queen. As a performer, he was known for his flamboyant stage persona and powerful vocals over a four-octave range.^[3][4][5] As a songwriter, Mercury composed many hits for Queen, including “Bohemian Rhapsody“, “Killer Queen“, “Somebody to Love“, “Don’t Stop Me Now“, “Crazy Little Thing Called Love” and “We Are the Champions“. In addition to his work with Queen, he led a solo career, penning hits such as “Barcelona“, “I Was Born to Love You” and “Living on My Own“. Mercury also occasionally served as a producer and guest musician (piano or vocals) for other artists.

Mercury, who was a Parsi born in Zanzibar and grew up there and in India until his mid-teens, has been referred to as “Britain’s first Asian rock star”.^[6] He died of bronchopneumonia brought on by AIDS on 24 November 1991, only one day after publicly acknowledging he had the disease. In 2006, Time Asia named him as one of the most influential Asian heroes of the past 60 years,^[7] and he continues to be voted one of the greatest singers in the history of popular music. In 2005, a poll organised by Blender and MTV2 saw Mercury voted the greatest male singer of all time.^[8] In 2009, a Classic Rock poll saw him voted the greatest rock singer of all time.^[9] In 2008, Rolling Stone editors ranked him number 18 on their list of the 100 greatest singers of all time.^[4] Allmusic has characterised Mercury as “one of the most dynamic and charismatic frontmen in rock history.”^[10]

Contents [show] 1 Early life 2 Career 2.1 Singer 2.2 Songwriter 2.3 Live performer 2.4 Instrumentalist 2.5 Solo career 3 Personal life 4 Illness and death 5 Criticism and controversy 5.1 Sexual orientation and HIV 5.2 Other controversies 6 Legacy 6.1 Continued popularity 6.2 Tributes 6.3 Importance in AIDS history 6.4 Appearances in lists of influential individuals 6.5 Portrayal in film 7 Discography 8 Notes 9 References 10 Bibliography 11 External links

Early life

The house in Zanzibar where Mercury lived in his early years

Mercury was born in the British protectorate of Zanzibar, East Africa. His parents, Bomi and Jer Bulsara,^[a]Parsis from the Gujarat region of the then province of Bombay Presidency in British India.^[11][b] The family surname is derived from the town of Bulsar (also known as Valsad) in southern Gujarat. As Parsis, Freddie and his family practised the Zoroastrian religion.^[12] The Bulsara family had moved to Zanzibar in order for his father to continue his job as a cashier at the British Colonial Office. He had one younger sister, Kashmira.^[13] were

In 1954, at the age of eight, Mercury was sent to study at St. Peter’s School,^[14] an English style boarding school for boys in Panchgani near Bombay (now Mumbai), India.^[15] At school, he formed a popular school band, The Hectics, for which he played piano. A friend from the time recalls that he had “an uncanny ability to listen to the radio and replay what he heard on piano”.^[16] It was also at St. Peter’s where he began to call himself “Freddie”. Mercury remained in India for most of his childhood, living with his grandmother and aunt. He completed his education in India at St. Mary’s School, Bombay.^[17]

At the age of 17, Mercury and his family fled from Zanzibar for safety reasons due to the 1964 Zanzibar Revolution.^[6] The family moved into a small house in Feltham, Middlesex, England. Mercury enrolled at Isleworth Polytechnic (now West Thames College) in West London where he studied art. He ultimately earned a Diploma in Art and Graphic Design at Ealing Art College, later using these skills to design the Queen crest. Mercury remained a British citizen for the rest of his life.

Following graduation, Mercury joined a series of bands and sold second-hand clothes in the Kensington Market in London. He also held a job at Heathrow Airport. Friends from the time remember him as a quiet and shy young man who showed a great deal of interest in music.^[18] In 1969 he joined the band Ibex, later renamed Wreckage. When this band failed to take off, he joined a second band called Sour Milk Sea. However, by early 1970 this group broke up as well.^[19]

In April 1970, Mercury joined guitarist Brian May and drummer Roger Taylor who had previously been in a band called Smile. Despite reservations from the other members, Mercury chose the name “Queen” for the new band. He later said about the band’s name, “I was certainly aware of the gay connotations, but that was just one facet of it”.^[1] At about the same time, he changed his surname, Bulsara, to Mercury.

Career

Singer

Although Mercury’s speaking voice naturally fell in the baritone range, he delivered most songs in the tenor^[20] His vocal range extended from bass low E (E2) to coloratura soprano E-natural (E6). His belting register soaring to tenor high F (F5).^[21] Biographer David Bret described his voice as “escalating within a few bars from a deep, throaty rock-growl to tender, vibrant tenor, then on to a high-pitched, perfect coloratura, pure and crystalline in the upper reaches”.^[22] Spanish soprano Montserrat Caballé, with whom Mercury recorded an album, expressed her opinion that “the difference between Freddie and almost all the other rock stars was that he was selling the voice”.^[23] As Queen’s career progressed, he would increasingly alter the highest notes of their songs when live, often harmonising with seconds, thirds or fifths instead. Mercury suffered from vocal fold nodules and claimed never to have had any formal vocal training.^[24] range.

Songwriter

Mercury wrote 10 of the 17 songs on Queen’s Greatest Hits album: “Bohemian Rhapsody“, “Seven Seas of Rhye“, “Killer Queen“, “Somebody to Love“, “Good Old-Fashioned Lover Boy“, “We Are the Champions“, “Bicycle Race“, “Don’t Stop Me Now“, “Crazy Little Thing Called Love” and “Play the Game“.

The most notable aspect of his songwriting involved the wide range of genres that he used, which included, among other styles, rockabilly, progressive rock, heavy metal, gospel and disco. As he explained in a 1986 interview, “I hate doing the same thing again and again and again. I like to see what’s happening now in music, film and theatre and incorporate all of those things.”^[25] Compared to many popular songwriters, Mercury also tended to write musically complex material. For example, “Bohemian Rhapsody” is acyclic in structure and comprises dozens of chords.^[26][27] He also wrote six songs from Queen II which deal with multiple key changes and complex material. “Crazy Little Thing Called Love”, on the other hand, contains only a few chords. Despite the fact that Mercury often wrote very intricate harmonies, he also claimed that he could barely read music.^[28] He wrote most of his songs on the piano and used a wide variety of different key signatures.^[26]

Mercury, performing live with his bottomless microphone stand

Live performer

Mercury was noted for his live performances, which were often delivered to stadium audiences around the world. He displayed a highly theatrical style that often evoked a great deal of participation from the crowd. A writer for The Spectator described him as “a performer out to tease, shock and ultimately charm his audience with various extravagant versions of himself”.^[29] David Bowie, who performed at the Freddie Mercury Tribute Concert and recorded the song “Under Pressure” with Queen, praised Mercury’s performance style, saying: “Of all the more theatrical rock performers, Freddie took it further than the rest… he took it over the edge. And of course, I always admired a man who wears tights. I only saw him in concert once and as they say, he was definitely a man who could hold an audience in the palm of his hand.”^[30]

One of Mercury’s most notable performances with Queen took place at Live Aid in 1985, during which the entire stadium audience of 72,000 people clapped, sang and swayed in unison. Queen’s performance at the event has since been voted by a group of music executives as the greatest live performance in the history of rock music. The results were aired on a television program called “The World’s Greatest Gigs”.^[31][32] In reviewing Live Aid in 2005, one critic wrote, “Those who compile lists of Great Rock Frontmen and award the top spots to Mick Jagger, Robert Plant, etc all are guilty of a terrible oversight. Freddie, as evidenced by his Dionysian Live Aid performance, was easily the most godlike of them all.”^[33]

Over the course of his career, Mercury performed an estimated 700 concerts in countries around the world with Queen. A notable aspect of Queen concerts was the large scale involved.^[25] He once explained, “We’re the Cecil B. DeMille of rock and roll, always wanting to do things bigger and better.”^[25] The band were the first ever to play in South American stadiums, breaking worldwide records for concert attendance in the Morumbi Stadium in São Paulo in 1981.^[34] In 1986, Queen also played behind the Iron Curtain, when they performed to a crowd of 80,000 in Budapest.^[35] Mercury’s final live performance with Queen took place on 9 August 1986 at Knebworth Park in England and drew an attendance estimated as high as 300,000.^[36]

Instrumentalist

Freddie Mercury playing guitar during a live concert with Queen in Frankfurt, 1984.

As a young boy in India, Mercury received formal piano training up to the age of nine. Later on, while living in London, he learned guitar. Much of the music he liked was guitar-oriented: his favourite artists at the time were The Who, The Beatles, Jimi Hendrix, David Bowie, and Led Zeppelin. He was often self-deprecating about his own skills on both instruments and from the early 1980s onward began extensively using guest keyboardists for both Queen and his solo career. Most notably, he enlisted Fred Mandel (a Canadian musician who also worked for Pink Floyd, Elton John and Supertramp) for his first solo project, and from 1985 onward collaborated with Mike Moran and Spike Edney, leaving most of the keyboard work exclusively to them.

Mercury played the piano in many of Queen’s most popular songs, including “Killer Queen“, “Bohemian Rhapsody“, “Good Old Fashioned Lover Boy“, “We Are the Champions“, “Somebody To Love” and “Don’t Stop Me Now“. He used concert grand pianos and, occasionally, other keyboard instruments such as the harpsichord. From 1980 onward, he also made frequent use of synthesizers in the studio. Queen guitarist Brian May claims that Mercury was unimpressed with his own abilities at the piano and used the instrument less over time because he wanted to walk around onstage and entertain the audience.^[37] Although he wrote many lines for the guitar, Mercury possessed only rudimentary skills on the instrument. Songs like “Ogre Battle” and “Crazy Little Thing Called Love” were composed on the guitar; the latter featured Mercury playing acoustic guitar both on stage and in the studio.

Lead poisoning

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Lead poisoning
Classification and external resources
An X ray demonstrating the characteristic finding of lead poisoning, dense metaphyseal lines.
ICD–10	T56.0
ICD–9	984.9
DiseasesDB	7307
MedlinePlus	002473
eMedicine	article/815399
MeSH	D007855

Lead poisoning (also known as plumbism, colica Pictonum, saturnism, Devon colic, or painter’s colic) is a medical condition caused by increased levels of the heavy metal lead in the body. Lead interferes with a variety of body processes and is toxic to many organs and tissues including the heart, bones, intestines, kidneys, and reproductive and nervous systems. It interferes with the development of the nervous system and is therefore particularly toxic to children, causing potentially permanent learning and behavior disorders. Symptoms include abdominal pain, headache, anemia, irritability, and in severe cases seizures, coma, and death.

Routes of exposure to lead include contaminated air, water, soil, food, and consumer products. Occupational exposure is a common cause of lead poisoning in adults. One of the largest threats to children is lead paint that exists in many homes, especially older ones; thus children in older housing with chipping paint are at greater risk. Prevention of lead exposure can range from individual efforts (e.g. removing lead-containing items such as piping or blinds from the home) to nationwide policies (e.g. laws that ban lead in products or reduce allowable levels in water or soil).

Elevated lead in the body can be detected by the presence of changes in blood cells visible with a microscope and dense lines in the bones of children seen on X-ray. However, the main tool for diagnosis is measurement of the blood lead level; different treatments are used depending on this level. The major treatments are removal of the source of lead and chelation therapy (administration of agents that bind lead so it can be excreted).

Humans have been mining and using this heavy metal for thousands of years, poisoning themselves in the process. Although lead poisoning is one of the oldest known work and environmental hazards, the modern understanding of the small amount of lead necessary to cause harm did not come about until the latter half of the 20th century. No safe threshold for lead exposure has been discovered—that is, there is no known amount of lead that is too small to cause the body harm.

Contents [show] 1 Classification 2 Signs and symptoms 2.1 Acute poisoning 2.2 Chronic poisoning 3 Exposure routes 3.1 Occupational exposure 3.2 Paint 3.3 Soil 3.4 Water 3.5 Lead-containing products 4 Pathophysiology 4.1 Enzymes 4.2 Neurons 5 Complications 5.1 Renal system 5.2 Cardiovascular system 5.3 Reproductive system 5.4 Nervous system 6 Diagnosis 6.1 Reference values 7 Prevention 8 Treatment 9 Prognosis 10 Epidemiology 11 History 12 Notable cases 13 In other species 13.1 Wildlife 14 References 15 Cited texts 16 External links

[edit] Classification

Classically, “lead poisoning” or “lead intoxication” has been defined as exposure to high levels of lead typically associated with severe health effects.^[1] Poisoning is a pattern of symptoms that occur with toxic effects from mid to high levels of exposure; toxicity is a wider spectrum of effects, including subclinical ones (those that do not cause symptoms).^[2] However, professionals often use “lead poisoning” and “lead toxicity” interchangeably, and official sources do not always restrict the use of “lead poisoning” to refer only to symptomatic effects of lead.^[2]

The amount of lead in the blood and tissues, as well as the time course of exposure, determine toxicity.^[3][4] Diagnosis and treatment of lead exposure are based on blood lead level (the amount of lead in the blood), measured in micrograms of lead per deciliter of blood (μg/dL). The US Centers for Disease Control and Prevention and the World Health Organization state that a blood lead level of 10 μg/dL or above is a cause for concern; however, lead may impair development and have harmful health effects even at lower levels, and there is no known safe exposure level.^[5][6] Authorities such as the American Academy of Pediatrics define lead poisoning as blood lead levels higher than 10 μg/dL.^[7] Lead poisoning may be acute (from intense exposure of short duration) or chronic (from repeat low-level exposure over a prolonged period), but the latter is much more common.

Lead forms a variety of compounds and exists in the environment in various forms.^[8] Features of poisoning differ depending on whether the agent is an organic compound (one that contains carbon), or an inorganic^[9] Organic lead poisoning is now very rare, because countries across the world have phased out the use of organic lead compounds as gasoline additives, but such compounds are still used in industrial settings.^[9]central nervous system^[9] one. Organic lead compounds, which cross the skin and respiratory tract easily, affect the predominantly.

[edit] Signs and symptoms

Lead poisoning can cause a variety of symptoms and signs which vary depending on the individual and the duration of lead exposure.^[10][11] Symptoms are nonspecific and may be subtle, and someone with elevated lead levels may have no symptoms.^[12] Symptoms usually develop over weeks to months as lead builds up in the body during a chronic exposure, but acute symptoms from brief, intense exposures also occur.^[13][14] Poisoning by organic lead compounds has symptoms predominantly in the central nervous system, such as insomnia, delirium, cognitive deficits, tremor, hallucinations, and convulsions.^[9] Symptoms from exposure to organic lead, which is probably more toxic than inorganic lead due to its lipid solubility, occur rapidly.

Symptoms may be different in adults and children; the main symptoms in adults are headache, abdominal pain, memory loss, kidney failure, male reproductive problems, and weakness, pain, or tingling in the extremities.^[15] The classic signs and symptoms in children are loss of appetite, abdominal pain, vomiting, weight loss, constipation, anemia, kidney failure, irritability, lethargy, learning disabilities, and behavior problems.^[15] Children may also experience hearing loss, delayed growth, drowsiness, clumsiness, or loss of new abilities, especially speech skills.^[12] Symptoms may appear in children at lower blood lead levels than in adults.^[16]

Early symptoms of lead poisoning in adults are commonly nonspecific and include depression, loss of appetite, intermittent abdominal pain, nausea, diarrhea, constipation, and muscle pain.^[17] Other early signs in adults include malaise, fatigue, decreased libido, and problems with sleep.^[10] An unusual taste in the mouth and personality changes are also early signs.^[18] In adults, symptoms can occur at levels above 40 μg/dL, but are more likely to occur only above 50–60 μg/dL.^[10] Symptoms begin to appear in children generally at around 60 μg/dL.^[19] However, the lead levels at which symptoms appear vary widely depending on unknown characteristics of each individual.^[20] At blood lead levels between 25 and 60 μg/dL, neuropsychiatric effects such as delayed reaction times, irritability, and difficulty concentrating, as well as slowed motor nerve^[21] Anemia may appear at blood lead levels higher than 50 μg/dL.^[17] In adults, Abdominal colic, involving paroxysms of pain, may appear at blood lead levels greater than 80 μg/dL.^[11] Signs that occur in adults at blood lead levels exceeding 100 μg/dL include wrist drop and foot drop, and signs of encephalopathy (a condition characterized by brain swelling), such as those that accompany increased pressure within the skull, delirium, coma, seizures, and headache.^[22] In children, signs of encephalopathy such as bizarre behavior, discoordination, and apathy occur at lead levels exceeding 70 μg/dL.^[22] For both adults and children, it is rare to be asymptomatic if blood lead levels exceed 100 μg/dL.^[11] conduction and headache can occur.

[edit] Acute poisoning

In acute poisoning, typical neurological signs are pain, muscle weakness, paraesthesia, and, rarely, symptoms associated with encephalitis.^[15] Abdominal pain, nausea, vomiting, diarrhea, and constipation are other acute symptoms.^[23] Lead’s effects on the mouth include astringency and a metallic taste.^[23] Gastrointestinalconstipation, diarrhea, poor appetite, or weight loss, are common in acute poisoning. Absorption of large amounts of lead over a short time can cause shock (insufficient fluid in the circulatory system) due to loss of water from the gastrointestinal tract.^[23] Hemolysis (the rupture of red blood cells) due to acute poisoning can cause anemia and hemoglobin in the urine.^[23] Damage to kidneys can cause changes in urination such as decreased urine output.^[23] People who survive acute poisoning often go on to display symptoms of chronic poisoning.^[23] problems, such as

[edit] Chronic poisoning

Chronic poisoning usually presents with symptoms affecting multiple systems,^[9] but is associated with three main types of symptoms: gastrointestinal, neuromuscular, and neurological.^[15] Central nervous system and neuromuscular symptoms usually result from intense exposure, while gastrointestinal symptoms usually result from exposure over longer periods.^[23] Signs of chronic exposure include loss of short-term memory or concentration, depression, nausea, abdominal pain, loss of coordination, and numbness and tingling in the extremities.^[18] Fatigue, problems with sleep, headaches, stupor, slurred speech, and anemia are also found in chronic lead poisoning.^[15] A “lead hue” of the skin with pallor is another feature.^[24] A blue line along the gum, with bluish black edging to the teeth is another indication of chronic lead poisoning.^[25] Children with chronic poisoning may refuse to play or may have hyperkinetic or aggressive behavior disorders.^[15]

[edit] Exposure routes

Lead is a common environmental pollutant.^[7] Causes of environmental contamination include industrial use of lead, such as is found in plants that process lead-acid batteries or produce lead wire or pipes, and metal recycling and foundries.^[26] Children living near facilities that process lead, such as smelters, have been found to have unusually high blood lead levels.^[27] In August 2009, parents rioted in China after lead poisoning was found in nearly 2000 children living near zinc and manganese smelters.^[28] Lead exposure can occur from contact with lead in air, household dust, soil, water, and commercial products.^[5]

Mercury poisoning [can also cause red, white blood and immune cell abnormalities]

Mercury poisoning

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Mercury poisoning
Classification and external resources
Elemental mercury
ICD–10	T56.1
ICD–9	985.0
DiseasesDB	8057
MedlinePlus	002476
eMedicine	emerg/813

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

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

Contents [show] 1 Signs and symptoms 1.1 Causes 2 Mechanism 2.1 Elemental mercury 2.2 Inorganic mercury compounds 2.3 Organic mercury compounds 3 Diagnosis 4 Prevention 5 Treatment 6 Prognosis 6.1 Detection in biological fluids 7 History 7.1 Infantile Acrodynia 7.2 Medical procedures 7.2.1 Thiomersal 7.2.2 Dental amalgam 7.3 Cosmetics 7.4 Fluorescent lamps 8 See also 9 References 10 External links

[edit] Signs and symptoms

Common symptoms of mercury poisoning include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), swelling, and desquamation (shedding of skin).

Because mercury blocks the degradation pathway of catecholamines, epinephrine excess causes profuse sweating, tachycardia (persistently faster-than-normal heart beat), increased salivation, and hypertension (high blood pressure). Mercury is thought to inactivate S-adenosyl-methionine, which is necessary for catecholamine catabolism by catechol-o-methyl transferase.

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 kidneyFanconi syndrome) or neuropsychiatric symptoms (Bradley Coyne Syndrome) such as emotional lability, memory impairment, or insomnia. disfunction (e.g.

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

An example of desquamation of the hand of a child with severe mercury poisoning acquired by handling elemental mercury is this photograph in Horowitz, et al. (2002).^[3]

[edit] Causes

The consumption of fish is by far the most significant source of ingestion-related mercury exposure in humans and animals, although plants and livestock also contain mercury due to bioaccumulation of mercury from soil, water and atmosphere, and due to biomagnification by ingesting other mercury-containing organisms.^[4]. Exposure to mercury can occur from breathing contaminated air;^[5] from eating foods containing mercury residues from processing, such as can occur with high-fructose corn syrup;^[6] from exposure to mercury vapor in mercury amalgam dental restorations;^[7] 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.^[8]

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 that are more than 20 times acceptable Japanese standards. ^[9]

Human-generated sources such as coal plants emit approximately half of atmospheric mercury, with natural sources such as volcanoes responsible for the remainder. An estimated two-thirds of human-generated mercury comes from stationary combustion, mostly of coal. Other important human-generated sources include gold production, non-ferrous metal production, cement production, waste disposal, human crematoria, caustic soda production, pig iron and steel production, mercury production (mostly for batteries), and biomass burning.^[10]

Small independent gold mining operations employ workers who are exposed to more risk to 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 there are no official government estimates of the labor force, observers believe twenty thousand to fifty thousand work as galamseys in Ghana, a figure that includes many women, who work as porters.

Mercury and many of its chemical compounds, especially organomercury compounds, can also be readily absorbed through direct contact with bare, or in some cases (such as dimethylmercury) insufficiently protected, skin. Mercury and its compounds are commonly used in chemical laboratories, hospitals, dental clinics, and facilities involved in the production of items such as fluorescent light bulbs, batteries, and explosives.^[11]

[edit] Mechanism

Mercury is such a highly reactive toxic agent that it is difficult to identify its specific mechanism of damage, and much remains unknown about the mechanism.^[12] It damages the central nervous system, endocrine system, kidneys, and other organs, and adversely affects the mouth, gums, and teeth. Exposure over long periods of time or heavy exposure to mercury vapor can result in brain damage and ultimately death. Mercury and its compounds are particularly toxic to fetuses and infants. Women who have been exposed to mercury in pregnancy have sometimes given birth to children with serious birth defects (see Minamata disease).

Mercury exposure in young children can have severe neurological consequences, preventing nerve sheaths from forming properly. Mercury inhibits the formation of myelin.

There is some evidence that mercury poisoning may predispose to Young’s syndrome (men with bronchiectasis and low sperm count).^[13]

Mercury poisoning’s effects partially depend on whether it has been caused by exposure to elemental mercury, inorganic mercury compounds (as salts), or organomercury compounds.

[edit] Elemental mercury

Quicksilver (liquid metallic mercury) is poorly absorbed by ingestion and skin contact. It is hazardous due to its potential to release mercury vapour. Animal data indicate that less than 0.01% of ingested mercury is absorbed through the intact gastrointestinal tract; though it may not be true for individuals suffering from ileus. Cases of systemic toxicity from accidental swallowing are rare, and attempted suicide via intravenous injection does not appear to result in systemic toxicity.^[12] 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.^[14] Some mercury vapour is absorbed dermally but uptake by this route is only approximately 1% of that by inhalation.^[15]

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.^[16] 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.^[17][18] 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.^[14]

[edit] Inorganic mercury compounds

Mercury occurs inorganically as salts such as mercury(II) chloride. Mercury salts primarily affect the gastro-intestinal tract and the kidneys, and can cause severe kidney damage; however, as they can not cross the blood-brain barrier easily, mercury salts inflict little neurological damage without continuous or heavy exposure.^[19] As two oxidation states of mercury form salts (Hg⁺ and Hg²⁺), mercury salts occur in both mercury(I) (or mercurous) and mercury(II) (mercuric) forms. Mercury(II) salts are usually more toxic than their mercury(I) counterparts because their solubility in water is greater; thus, they are more readily absorbed from the gastrointestinal tract.^[19]

Hg(CN)₂ is a particularly toxic mercury compound. If ingested, both life-threatening mercury and cyanide poisoning can occur. Hg(CN)₂ can enter the body via inhalation, ingestion, or passage through the skin. Inhalation of mercuric cyanide irritates the throat and air passages. Heating or contact of Hg(CN)₂ with acid or acid mist releases toxic mercury and cyanide vapors that can cause bronchitis with cough and phlegm and/or lung tissue irritation. Contact with eyes can cause burns and brown stains in the eyes, and long time exposure can affect the peripheral vision. Contact with skin can cause skin allergy, irritation, and gray skin color.^[20]

Chronic exposure to trace amounts of the compound can lead to mercury buildup in the body over time; it may take months or even years for the body to eliminate excess mercury. Overexposure to mercuric cyanide can lead to kidney damage and/or mercury poisoning, leading to ‘shakes’ (ex: shaky handwriting), irritability, sore gums, increased saliva, metallic taste, loss of appetite, memory loss, personality changes, and brain damage. Exposure to large doses at one time can lead to sudden death.^[20]

Mercuric cyanide has not been tested on its ability to cause reproductive damage. Although inorganic mercury compounds (such as Hg(CN)₂) have not been shown to be human teratogens, they should be handled with care as they are known to damage developing embryos and decrease fertility in men and women.^[20]

According to one study, two people exhibited symptoms of cyanide poisoning within hours after ingesting mercuric cyanide or mercury oxycyanide, Hg(CN)₂•HgO, in suicide attempts. The toxicity of Hg(CN)₂ is commonly assumed to arise almost exclusively from mercury poisoning; however, the patient who ingested mercury oxycyanide died after 5 hours of cyanide poisoning before any mercury poisoning symptoms were observed. The patient who ingested Hg(CN)₂ initially showed symptoms of acute cyanide poisoning which were brought under control, and later showed signs of mercury poisoning before recovering. It is thought that the degree to which cyanide poisoning occurs is related to whether cyanide ions are released in the stomach, which depends on factors such as the amount ingested, stomach acidity, and volume of stomach contents.^[21]₂ molecules remain undissociated in pure water and in basic solutions,^[22] it makes sense that dissociation would increase with increasing acidity. High stomach acidity thus helps cyanide ions to become more bioavailable, increasing the likelihood of cyanide poisoning. Given that Hg(CN)

Mercury cyanide was used in two murders in New York in 1898. The perpetrator, Roland B. Molineux, sent poisoned medicines to his victims through the US mail. The first victim, Henry Barnett, died of mercury poisoning twelve days after taking the poison. The second victim, Catherine Adams, died of cyanide poisoning within 30 minutes of taking the poison. As in the suicide cases, the difference between the two cases may be attributed to differences in the acidities of the solutions containing the poison, or to differences in the acidities of the victims’ stomachs.^[23]

The drug NAP (n-acetyl penicillamine) has been used to treat mercury poisoning with limited success.^[20]

[edit] Organic mercury compounds

Compounds of mercury tend to be much more toxic than the element itself, and organic compounds of mercury are often extremely toxic and have been implicated in causing brain and liver damage. The most dangerous mercury compound, dimethylmercury, is so toxic that even a few microliters spilled on the skin, or even a latex glove, can cause death.^[24][25]

Methylmercury is the major source of organic mercury for all individuals.^[1] It works its way up the food chainbioaccumulation in the environment, reaching high concentrations among populations of some species. Larger species of fish, such as tuna or swordfish, are usually of greater concern than smaller species. The U.S. Food and Drug Administration (FDA) and the U.S. Environmental Protection Agency (EPA) advise women of child-bearing age, nursing mothers, and young children to completely avoid swordfish, shark, king mackereltilefish from the Gulf of Mexico, (Golden Tilefish from the Mid- and North-Atlantic present no risk), to limit consumption of albacore (“white”) tuna to no more than 6 oz (170 g) per week, and of all other fish and shellfish to no more than 12 oz (340 g) per week.^[26] A 2006 review, conducted by Dr. Dariush Mozaffarian and Dr. Eric B. Rimm, of the risks and benefits of fish consumption found that 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.^[27] (Dr. Rimm has reported in the past that he has received payment or honoraria for presentations about food and diets from both the Culinary Institute of America and the International Chefs Association, among others.)^[27] through and

There is a long latent period between exposure to methylmercury and the appearance of symptoms in adult poisoning cases. The longest recorded latent period is five months after a single exposure, in the Dartmouth case (see History); other latent periods in the range of weeks to months have also been reported. No explanation for this long latent period is known. When the first symptom appears, typically paresthesia (a tingling or numbness in the skin), it is followed rapidly by more severe effects, sometimes ending in coma and death. The toxic damage appears to be determined by the peak value of mercury, not the length of the exposure.^[12]

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 7 to 10 days, and it is metabolized much more quickly than methylmercury. It probably does not have methylmercury’s ability to cross the blood-brain barrier via a transporter, but instead relies on simple diffusion to enter the brain.^[1]

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

[edit] Diagnosis

Diagnosis of elemental or inorganic mercury poisoning involves determining the history of exposure, physical findings, and an elevated body burden of mercury. Although whole blood mercury concentrations are typically less than 6 μg/L, diets rich in fish can result in blood mercury concentrations higher than 200 μg/L; it is not that useful to measure these levels for suspected cases of elemental or inorganic poisoning because of mercury’s short half-life in the blood. If the exposure is chronic, urine levels can be obtained; 24-hour collections are more reliable than spot collections. It is difficult or impossible to interpret urine samples of patients undergoing chelation therapy, as the therapy itself increases mercury levels in the samples.^[28]

Diagnosis of organic mercury poisoning differs in that whole-blood or hair analysis is more reliable than urinary mercury levels.^[28]

[edit] Prevention

Mercury poisoning can be prevented (or minimized) by eliminating or reducing exposure to mercury and mercury compounds. To that end, many governments and private groups have made efforts to regulate the use of mercury heavily, or to issue advisories about its use. For example, the export from the European Union^[29] The variability among regulations and advisories is at times confusing for the lay person as well as scientists. of mercury and some mercury compounds has been prohibited since 2010-03-15.

^[30]

Country	Regulating agency	Regulated activity	Medium	Type of mercury compound	Type of limit	Limit
US	Occupational Safety and Health Administration	occupational exposure	air	elemental mercury	Ceiling (not to exceed)	0.1 mg/m³
US	Occupational Safety and Health Administration	occupational exposure	air	organic mercury	Ceiling (not to exceed)	0.05 mg/m³
US	Food and Drug Administration	drinking	water	inorganic mercury	Maximum allowable concentration	2 ppb (0.002 mg/L)
US	Food and Drug Administration	eating	sea food	methylmercury	Maximum allowable concentration	1 ppm
US	Environmental Protection Agency	drinking	water	inorganic mercury	Maximum contaminant level	2 ppb (0.002 mg/L)

The United States Environmental Protection Agency‎ (EPA) issued recommendations in 2004 regarding exposure to mercury in fish and shellfish.^[31] The EPA also developed the “Fish Kids” awareness campaign for children and young adults ^[32] on account of the greater impact of mercury exposure to that population.

[edit] Treatment

Identifying and removing the source of the mercury is crucial. Decontamination requires removal of clothes, washing skin with soap and water, and flushing the eyes with saline solution as needed. Inorganic ingestion such as mercuric chloride should be approached as the ingestion of any other serious caustic. Immediate chelation therapy is the standard of care for a patient showing symptoms of severe mercury poisoning or the laboratory evidence of a large total mercury load.^[1]

Chelation therapy for acute inorganic mercury poisoning can be done with DMSA, 2,3-dimercapto-1-propanesulfonic acid (DMPS), D-penicillamine (DPCN), or dimercaprol (BAL).^[1] Only DMSA is FDA-approved for use in children for treating mercury poisoning. However, several studies found no clear clinical benefit from DMSA treatment for poisoning due to mercury vapor.^[33] No chelator for methylmercury or ethylmercury is approved by the FDA; DMSA is the most frequently used for severe methylmercury poisoning, as it is given orally, has fewer side effects, and has been found to be superior to BAL, DPCN, and DMPS.^[1] Alpha-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.^[34] Glutathione and N-acetylcysteine^[34] Experimental findings have demonstrated an interaction between selenium and methylmercury, but epidemiological studies have found little evidence that selenium helps to protect against the adverse effects of methylmercury.^[35] (NAC) are recommended by some physicians, but have been shown to increase mercury concentrations in the kidneys and the brain.

Even if the patient has no symptoms or documented history of mercury exposure, a minority of physicians (predominantly those in alternative medicine) use chelation to “rid” the body of mercury, which they believe to cause neurological and other disorders. A common practice is to challenge the patient’s body with a chelation agent, collect urine samples, and then use laboratory reports to diagnose the patient with toxic levels of mercury; often no pre-chelation urine sample is collected for comparison. The patient is then advised to undergo further chelation.^[33] No scientific data supports the claim that the mercury in vaccines causes autism^[36] or its symptoms,^[37] and there is no scientific support for chelation therapy as a treatment for autism.^[38]

Chelation therapy can be hazardous. In August 2005, an incorrect form of EDTA used for chelation therapy resulted in hypocalcemia, causing cardiac arrest that killed a five-year-old autistic boy.^[39]

[edit] Prognosis

Many of the toxic effects of mercury are partially or wholly reversible, either through specific therapy or through natural elimination of the metal after exposure has been discontinued.^[40] However, heavy or prolonged exposure can do irreversible damage, particularly in fetuses, infants, and young children. Young’s syndrome is believed to be a long term consequence of early childhood mercury poisoning.^[41] 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)

[edit] Detection in biological fluids

Mercury may be measured in blood or urine to confirm a diagnosis of poisoning in hospitalized victims or to assist in the forensic investigation in a case of fatal overdosage. Some analytical techniques are capable of distinguishing organic from inorganic forms of the metal. The concentrations in both fluids tend to reach high levels early after exposure to inorganic forms, while lower but very persistent levels are observed following exposure to elemental or organic mercury. Chelation therapy can cause a transient elevation of urine mercury levels.^[42]

[edit] History

• The first emperor of unified China, Qin Shi Huang, reportedly died of ingesting mercury pills that were intended to give him eternal life.^[43]
• The phrase mad as a hatter is likely a reference to mercury poisoning, as mercury-based compounds were once used in the manufacture of felt hats in the 18th and 19th century. (The Mad Hatter character of Alice in Wonderland was almost certainly inspired by an eccentric furniture dealer, not by a victim of mad hatter disease.)^[44]
• In 1810, two British ships, HMS Triumph and HMS Phipps, salvaged a large load of elemental mercury from a wrecked Spanish vessel near Cadiz, Spain. The bladders containing the mercury soon ruptured. The element spread about the ships in liquid and vapour forms. The sailors presented with neurologic compromises: tremor, paralysis, and excessive salivation as well as tooth loss, skin problems, and pulmonary complaints. In 1823 William Burnet, MD published a report on the effects of Mercurial vapour.^[45] The Triumph’s surgeon, Henry Plowman, had concluded that the ailments had arisen from inhaling the mercurialized atmosphere. His treatment was to order the lower deck gun ports to be opened, when it was safe to do so; sleeping on the orlop was forbidden; and no men slept in the lower deck if they were at all symptomatic. Windsails were set to channel fresh air into the lower decks day and night.^[46]
• For years, including the early part of his presidency, Abraham Lincoln took a common medicine of his time called “blue mass” which contained significant amounts of mercury.
• On September 5, 1920, silent movie actress Olive Thomas ingested mercury capsules dissolved in an alcoholic solution at the Hotel Ritz in Paris. There is still controversy over whether it was suicide, or whether she consumed the external preparation by mistake. Her husband, Jack Pickford (the brother of Mary Pickford), had syphilis, and the mercury was used as a treatment of the venereal disease at the time. She died a few days later at the American Hospital in Neuilly.
• An early scientific study of mercury poisoning was in 1923–6 by the German inorganic chemist, Alfred Stock, who himself became poisoned, together with his colleagues, by breathing mercury vapour that was being released by his laboratory equipment—diffusion pumps, float valves, and manometers—all of which contained mercury, and also from mercury that had been accidentally spilt and remained in cracks in the linoleum floor covering. He published a number of papers on mercury poisoning, founded a committee in Berlin to study cases of possible mercury poisoning, and introduced the term micromercurialism.^[47]
• The term Hunter-Russell syndrome derives from a study of mercury poisoning among workers in a seed packing factory in Norwich, England in the late 1930s who breathed methylmercury that was being used as a seed disinfectant and preservative.^[48]
• Outbreaks of methylmercury poisoning occurred in several places in Japan during the 1950s due to industrial discharges of mercury into rivers and coastal waters. The best-known instances were in Minamata and Niigata. In Minamata alone, more than 600 people died due to what became known as Minamata disease. More than 21,000 people filed claims with the Japanese government, of which almost 3000 became certified as having the disease. In 22 documented cases, pregnant women who consumed contaminated fish showed mild or no symptoms but gave birth to infants with severe developmental disabilities.^[2]
• Widespread mercury poisoning occurred in rural Iraq in 1971-1972, when grain treated with a methylmercury-based fungicide that was intended for planting only was used by the rural population to make bread, causing at least 6530 cases of mercury poisoning and at least 459 deaths (see Basra poison grain disaster).^[49]
• On August 14, 1996, Karen Wetterhahn, a chemistry professor working at Dartmouth College, spilled a small amount of dimethylmercury on her latex glove. She began experiencing the symptoms of mercury poisoning five months later and, despite aggressive chelation therapy, died a few months later from brain malfunction due to mercury intoxication.^[24][25]
• In April 2000, Alan Chmurny attempted to kill a former employee, Marta Bradley, by pouring mercury into the ventilation system of her car.^[50]
• On March 19, 2008, Tony Winnett, 55, inhaled mercury vapors while trying to extract gold from computer parts, and died ten days later. His Oklahoma residence became so contaminated that it had to be gutted.^[51][52]
• In December 2008, actor Jeremy Piven was diagnosed with hydrargyria resulting from eating sushi twice a day for twenty years.^[53]

[edit] 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.^[54]Greek, where άκρο means end (as in: upper extremity) and οδυνη means pain. Also known as pink disease, erythredema, Selter’s disease, or Swift-Feer disease, acrodynia was relatively commonplace amongst children in the first half of the 20th century.^[55] Initially, the cause of the acrodynia epidemic among infants and young children was unknown^[56]; however, mercury poisoning, primarily from calomel in teething powders, began to be widely accepted as its cause in the 1950s and 60s.^[55] The prevalence of acrodynia decreased greatly after calomel was excluded from most teething powders in 1954.^[55] The word is derived from the

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.”^[57]