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]