Arsenic 

33 germanium ← arsenic → selenium
P
↑
As
↓
Sb
General
Name, Symbol, Number arsenic, As, 33
Element category metalloids
Group, Period, Block 15, 4, p
Appearance metallic grey
Standard atomic weight 74.92160(2)  g·mol−1
Electron configuration Ar 4s2 3d10 4p3
Electrons per shell 2, 8, 18, 5
Physical properties
Phase solid
Density (near r.t.) 5.727  g·cm−3
Liquid density at m.p. 5.22  g·cm−3
Melting point 1090 K
(817 °C, 1503 °F)
Boiling point subl. 887 K
(614 °C, 1137 °F)
Critical temperature 1673 K
Heat of fusion (grey) 24.44  kJ·mol−1
Heat of vaporization  ? 34.76  kJ·mol−1
Specific heat capacity (25 °C) 24.64  J·mol−1·K−1
Vapor pressure
P(Pa) 1 10 100 1 k 10 k 100 k
at T(K) 553 596 646 706 781 874
Atomic properties
Crystal structure rhombohedral
Oxidation states 5, 3, 1,1 -3
(mildly acidic oxide)
Electronegativity 2.18 (Pauling scale)
Ionization energies
(more)		 1st:  947.0  kJ·mol−1
2nd:  1798  kJ·mol−1
3rd:  2735  kJ·mol−1
Atomic radius 115  pm
Atomic radius (calc.) 114  pm
Covalent radius 119  pm
Van der Waals radius 185 pm
Miscellaneous
Magnetic ordering no data
Electrical resistivity (20 °C) 333 n Ω·m
Thermal conductivity (300 K) 50.2  W·m−1·K−1
Young's modulus 8  GPa
Bulk modulus 22  GPa
Mohs hardness 3.5
Brinell hardness 1440  MPa
CAS registry number 7440-38-2
Most-stable isotopes
Main article: Isotopes of arsenic
iso NA half-life DM DE (MeV) DP
73As syn 80.3 d ε - 73Ge
γ 0.05D, 0.01D, e -
74As syn 17.78 d ε - 74Ge
β+ 0.941 74Ge
γ 0.595, 0.634 -
β- 1.35, 0.717 74Se
75As 100% 75As is stable with 42 neutrons
References

Arsenic (pronounced /ˈɑrsənɪk/) is a chemical element that has the symbol As and atomic number 33. Arsenic was first documented by Albertus Magnus in 1250.2 Its atomic mass is 74.92. This is a notoriously poisonous metalloid that has many allotropic forms: yellow (molecular non-metallic) and several black and grey forms (metalloids) are a few that are seen. Three metalloidal forms of arsenic with different crystal structures are found free in nature (the minerals arsenic sensu stricto and the much rarer arsenolamprite and pararsenolamprite), but it is more commonly found as arsenide and arsenate compounds. Several hundred such mineral species are known. Arsenic and its compounds are used as pesticides, herbicides, insecticides and various alloys.

The most common oxidation states for arsenic are -3 (arsenides: usually alloy-like intermetallic compounds), +3 (arsenates(III) or arsenites, and most organoarsenic compounds), and +5 (arsenates(V): the most stable inorganic arsenic oxycompounds). Arsenic also bonds readily to itself, forming square As43- ions in the arsenide skutterudite. In the +3 oxidation state, the stereochemistry of arsenic is affected by possession of a lone pair of electrons.

Contents

History

The word arsenic is borrowed from the Persian word زرنيخ Zarnikh meaning "yellow orpiment". Zarnikh was borrowed by Greek as arsenikon, which means masculine or potent. Arsenic has been known and used in Persia and elsewhere since ancient times.3 As the symptoms of arsenic poisoning were somewhat ill-defined, it was frequently used for murder until the advent of the Marsh test, a sensitive chemical test for its presence. (Another less sensitive but more general test is the Reinsch test.) Due to its use by the ruling class to murder one another and its potency and discreetness, arsenic has been called the Poison of Kings and the King of Poisons.citation needed

During the Bronze Age, arsenic was often included in bronze, which made the alloy harder (so-called "arsenical bronze").

Arsenic was first isolated by Geber (721-815), an Arabian alchemist.4 Albertus Magnus (Albert the Great, 1193-1280) is believed to have been the first European to isolate the element in 1250.2 In 1649, Johann Schröder published two ways of preparing arsenic.

Alchemical symbol for arsenic

Cadet's fuming liquid, the first organometalic compound, was synthesized in 1760 by Louis Claude Cadet de Gassicourt by the reaction of potassium acetate with arsenic trioxide.5

In the Victorian era, "arsenic" (colourless, crystalline, soluble "white arsenic") was mixed with vinegar and chalk and eaten by women to improve the complexion of their faces, making their skin paler to show they did not work in the fields. Arsenic was also rubbed into the faces and arms of women to "improve their complexion". The accidental use of arsenic in the adulteration of foodstuffs led to the Bradford sweet poisoning in 1858, which resulted in approximately 20 deaths and 200 people taken ill with arsenic poisoning.6

Characteristics

Arsenic is very similar chemically to its predecessor, phosphorus. Like phosphorus, it forms colourless, odourless, crystalline oxides As2O3 and As2O5 which are hygroscopic and readily soluble in water to form acidic solutions. Arsenic (V) acid, like phosphorous acid, is a weak acid. Like phosphorus, arsenic forms an unstable, gaseous hydride: arsine (AsH3). The similarity is so great that arsenic will partly substitute for phosphorus in biochemical reactions and is thus poisonous. However, in subtoxic doses, soluble arsenic compounds act as stimulants, and were once popular in small doses as medicinals by people in the mid 18th century.

When heated in air it oxidizes to arsenic trioxide; the fumes from this reaction have an odor resembling garlic. This odor can be detected on striking arsenide minerals such as arsenopyrite with a hammer. Arsenic (and some arsenic compounds) sublimes upon heating at atmospheric pressure, converting directly to a gaseous form without an intervening liquid state. The liquid state appears at 20 atmospheres and above, which explains why the melting point is higher than the boiling point 7.

Allotropes

Structure of yellow arsenic As4 and white phosphorus P4

Like phosphorus, arsenic is an excellent example of an element that exhibits allotropy, as its various allotropes have strikingly different properties. The three most common allotropes are metallic grey, yellow and black arsenic.8

The most common allotrophe of arsenic is grey arsenic. It has a similar structure to black phosphorus (β-metallic phosphorus) and has a structure somewhat resembling that of graphite. It consists of many six-membered rings which are interlinked. Each atom is bound to three other atoms in the layer and is coordinated by each 3 arsenic atoms in the upper and lower layer. This close package leads to a high density of 5.73 g/cm³.7

Yellow arsenic (As4) is soft and waxy, not unlike P4. Both have four atoms arranged in a tetrahedral structure in which each atom is bound to the other three atoms by a single bond, resulting in very high ring strain and instability. This form of the elements are the least stable, most reactive, more volatile, less dense, and more toxic than the other allotropes. Yellow arsenic is produced by rapid cooling of arsenic vapour with liquid nitrogen. It is rapidly transformed into the grey arsenic by light The yellow form has a density of 1.97 g/cm³.7

The black arsenic is similar in structure to red phosphorus.7

Applications

Wood preservation

The toxicity of arsenic to insects, bacteria and fungi makes it an ideal component for the preservation of wood. World wide the treatment with chromated copper arsenate, also known as CCA or Tanalith was the largest consumer of arsenic since the introduction of the process in the 1950s. Due to the environmental problems caused by the arsenic most countries banned the use of chromated copper arsenate on consumer products. The ban began in the European Union and in the United States in 2004.910

In 2002 in the United States 90% of the 19,600 metric tons of arsenic compounds were used to preserve wood, in 2007 still 50% of the 5,280 metric tons of consumption was used for this purpose.1112 In the European Union the use of arsenic in consumer products According to the USEPA's website, CCA lumber was discontinued for residential and general consumer construction on December 31, 2003 and alternative methods are now used like ACQ, Borates, Copper Azole, Cyproconazole, and Propiconazole.

Although discontinued this application is also the one of most concern to the general public. The vast majority of older pressure-treated wood was treated with CCA. CCA lumber is still in widespread use in many countries, and was heavily used during the latter half of the 20th century as a structural and outdoor building material. Although the use of CCA lumber was banned in many areas after studies showed that arsenic could leach out of the wood into the surrounding soil (from playground equipment, for instance), a risk is also presented by the burning of older CCA timber. The direct or indirect ingestion of wood ash from burnt CCA lumber has caused fatalities in animals and serious poisonings in humans; the lethal human dose is approximately 20 grams of ash. Scrap CCA lumber from construction and demolition sites may be inadvertently used in commercial and domestic fires. Protocols for safe disposal of CCA lumber do not exist evenly throughout the world; there is also concern in some quarters about the widespread landfill disposal of such timber.

Medical

Arsphenamine (Salvarsan)

During the 18th, 19th, and 20th centuries, a number of arsenic compounds have been used as medicines, including arsphenamine (by Paul Ehrlich) and arsenic trioxide (by Thomas Fowler). Arsphenamine as well as Neosalvarsan was indicated for syphilis and trypanosomiasis, but has been superseded by modern antibiotics. Arsenic trioxide has been used in a variety of ways over the past 200 years, but most commonly in the treatment of cancer. The US Food and Drug Administration in 2000 approved this compound for the treatment of patients with acute promyelocytic leukemia that is resistant to ATRA.13 It was also used as Fowler's solution in psoriasis.14

Recently new research has been done in locating tumours using arsenic-74 (a positron emitter). The advantages of using this isotope instead of the previously used iodine-124 is that the signal in the PET scan is clearer as the iodine tends to transport iodine to the thyroid gland producing a lot of noise.15

Pigments

Copper acetoarsenite was used as a green pigment known under many different names, including 'Paris Green' and 'Emerald Green'. It caused numerous arsenic poisonings. Scheele's Green, a copper arsenate, was used in the 19th century as a coloring agent in sweets.16

Military

After World War I the United States built up a stockpile 20,000 tons of Lewisite; a chemical weapon, acting as a vesicant (blister agent) and lung irritant. The stockpile was neutralized with bleach and dumped into the Gulf of Mexico after the 1950s.17 During the Vietnam War the United States used Agent Blue a mixture of Na cacodylate) and dimethyl arsinic acid (cacodylic acid as one of the rainbow herbicides to deprive the Vietnamese of valuable crops.

Other uses

Occurrence

See also Arsenide minerals, Arsenate minerals.

A large sample of native arsenic.

Arsenopyrite, also unofficially called mispickel,22 (FeAsS) is the most common arsenic-bearing mineral.

Realgar

The most important compounds of arsenic are arsenic (III) oxide, As2O3, ("white arsenic"), the yellow sulfide orpiment (As2S3) and red realgar (As4S4), Paris Green, calcium arsenate, and lead hydrogen arsenate. The latter three have been used as agricultural insecticides and poisons. Orpiment and realgar were formerly used as painting pigments, though they have fallen out of use due to their toxicity and reactivity. Although arsenic is sometimes found native in nature, its main economic source is the mineral arsenopyrite mentioned above; it is also found in arsenides of metals such as silver, cobalt (cobaltite: CoAsS and skutterudite: CoAs3) and nickel, as sulfides, and when oxidised as arsenate minerals such as mimetite, Pb5(AsO4)3Cl and erythrite, Co3(AsO4)2. 8H2O, and more rarely arsenites ('arsenite' = arsenate(III), AsO33- as opposed to arsenate (V), AsO43-).

In addition to the inorganic forms mentioned above, arsenic also occurs in various organic forms in the environment.

Production

Arsenic output in 200623

In 2005, China was the top producer of white arsenic with almost 50% world share, followed by Chile, Peru and Morocco, reports the British Geological Survey and the United States Geological Survey.23. The arsenic was recovered mostly during mining operations, for example the production from Peru comes mostly from copper mining and the production in China is due to gold mining. The arsenic is there part of the smelter dust from copper, gold, and lead smelters.12

On roasting in air of arsenopyrite, the arsenic sublimes as arsenic (III) oxide leaving iron oxides.24 While roasting without air results in the production of metallic arsenic. For further purification of the arsenic from sulfur and other chacogenes is sublimed in vacuum or in a hydrogen atmosphere or by distilling it from molten lead arsenic mixture.25

Biological role

Trimethylarsine
Arsenobetaine

Inorganic arsenic and its compounds, upon entering the food chain, are progressively metabolised to a less toxic form of arsenic through a process of methylation. For example certain the mold Scopulariopsis brevicaulis produce significant amounts of trimethylarsine if inorganic arsenic is present.26 The organic compound arsenobetaine is found in some marine foods such as fish and algae, and also in mushrooms in larger concentrations. The average person's intake is about 10-50 µg/day. Values about 1000 µg are not unusual following consumption of fish or mushrooms. But there is little danger in eating fish because this arsenic compound is nearly non-toxic.27

Some species of bacteria obtain their energy by oxidizing various fuels while reducing arsenate to arsenite. The enzymes involved are known as arsenate reductases (Arr).

In 2008, bacteria were discovered that employ a version of photosynthesis in the absence of oxygen with arsenites as electron donors, producing arsenates (just like ordinary photosynthesis uses water as electron donor, producing molecular oxygen). Researchers conjecture that historically these photosynthesizing organisms produced the arsenates that allowed the arsenate-reducing bacteria to thrive. One strain PHS-1 has been isolated and is related to the γ-Proteobacterium Ectothiorhodospira shaposhnikovii. The mechanism is unknown, but an encoded Arr enzyme may function in reverse to its known homologues.28

Precautions

Main article: Arsenic poisoning

Arsenic and many of its compounds are especially potent poisons. Arsenic 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 (see arsenic poisoning) 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.29.

Elemental arsenic and arsenic compounds are classified as "toxic" and "dangerous for the environment" in the European Union under directive 67/548/EEC.

The IARC recognizes arsenic and arsenic compounds as group 1 carcinogens, and the EU lists arsenic trioxide, arsenic pentoxide and arsenate salts as category 1 carcinogens.

Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of “pins and needles” in hands and feet.

Arsenic is known to cause arsenicosis due to its manifestation in drinking water, “the most common species being arsenate [HAsO42- ; As(V)] and arsenite [H3AsO3 ; As(III)]”. The ability of arsenic to undergo redox conversion between As(III) and As(V) makes its availability in the environment more abundant. According to Croal, Gralnick, Malasarn, and Newman, “[the] understanding [of] what stimulates As(III) oxidation and/or limits As(V) reduction is relevant for bioremediation of contaminated sites (Croal). The study of chemolithoautotrophic As(III) oxidizers and the heterotrophic As(V) reducers can help the understanding of the oxidation and/or reduction of arsenic.30

Treatment of chronic arsenic poisoning is easily accomplished. British antilewisite (dimercaprol) is prescribed in dosages of 5mg/kg up to 300mg each 4 hours for the first day. Then administer the same dosage each 6 hours for the second day. Then prescribe this dosage each 8 hours for eight additional days. 31

Arsenic in drinking water

Main article: Arsenic contamination of groundwater

Arsenic contamination of groundwater has led to a massive epidemic of arsenic poisoning in Bangladesh32 and neighbouring countries. Presently 42 major incidents around the world have been reported on groundwater arsenic contamination. It is estimated that approximately 57 million people are drinking groundwater with arsenic concentrations elevated above the World Health Organization's standard of 10 parts per billion. However, a study of cancer rates in Taiwan 33 suggested that significant increases in cancer mortality appear only at levels above 150 parts per billion. The arsenic in the groundwater is of natural origin, and is released from the sediment into the groundwater due to the anoxic conditions of the subsurface. This groundwater began to be used after western NGOs instigated a massive tube well drinking-water program in the late twentieth century. This program was designed to prevent drinking of bacterially contaminated surface waters, but failed to test for arsenic in the groundwater.(2) Many other countries and districts in South East Asia, such as Vietnam, Cambodia, and Tibet, China, are thought to have geological environments similarly conducive to generation of high-arsenic groundwaters. Arsenicosis was reported in Nakhon Si Thammarat, Thailand in 1987, and the dissolved arsenic in the Chao Phraya River is suspected of containing high levels of naturally occurring arsenic, but has not been a public health problem due to the use of bottled water.34

The northern United States, including parts of Michigan, Wisconsin, Minnesota and the Dakotas are known to have significant concentrations of arsenic in ground water. Increased levels of skin cancer have been associated with arsenic exposure in Wisconsin, even at levels below the 10 part per billion drinking water standard.35

Epidemiological evidence from Chile shows a dose dependent connection between chronic arsenic exposure and various forms of cancer, particularly when other risk factors, such as cigarette smoking, are present. These effects have been demonstrated to persist below 50 parts per billion. 36

Analyzing multiple epidemiological studies on inorganic arsenic exposure suggests a small but measurable risk increase for bladder cancer at 10 parts per billion.37 According to Peter Ravenscroft of the Department of Geography at the University of Cambridge 38 roughly 80 million people worldwide consume between 10 and 50 parts per billion arsenic in their drinking water. If they all consumed exactly 10 parts per billion arsenic in their drinking water, the previously cited multiple epidemiological study analysis would predict an additional 2,000 cases of bladder cancer alone. This represents a clear underestimate of the overall impact, since it does not include lung or skin cancer, and explicitly underestimates the exposure. Those exposed to levels of arsenic above the current WHO standard should weigh the costs and benefits of arsenic remediation.

Arsenic can be removed from drinking water through coprecipitation of iron minerals by oxidation and filtering. When this treatment fails to produce acceptable results, adsorptive arsenic removal media may be utilized. Several adsorptive media systems have been approved for point-of-service use in a study funded by the United States Environmental Protection Agency (U.S.EPA) and the National Science Foundation (NSF).

Magnetic separations of arsenic at very low magnetic field gradients have been demonstrated in point-of-use water purification with high-surface-area and monodisperse magnetite (Fe3O4) nanocrystals. Using the high specific surface area of Fe3O4 nanocrystals the mass of waste associated with arsenic removal from water has been dramatically reduced. 39

Occupational Exposures

Industries that use inorganic arsenic and its compounds include wood preservation, glass production, nonferrous metal alloys, and electronic semiconductor manufacturing. Inorganic arsenic is also found in coke oven emissions associated with the smelter industry. 40

Occupational exposure to arsenic may occur with copper or lead smelting and wood treatment, among workers involved in the production or application of pesticides containing organic arsenicals. Humans are exposed to arsenic through air, drinking water, and food (meat, fish, and poultry); this food is usually the largest source of arsenic. Arsenic was also found in wine if arsenic pesticides are used in the vineyard. Arsenic is well absorbed by oral and inhalation routes, widely distributed and excreted in urine; most of a single, low-level dose is excreted within a few days after consuming any form of inorganic arsenic. Remains of arsenic in nails and hair can be detected even after years and years after the exposure.

Toxicity

Exposure to arsenic can occur from the environment and food consumption 41. The two forms of arsenic, reduced (As (III)) and oxidized (As(V)), can be absorbed, and accumulated in diverse tissues and body fluids41. In the liver, the metabolism of arsenic involves enzymatic and non-enzymatic methylation, in which the most frequently excreted metabolite (≥ 90%) in the urine of mammals is dimethylarsinic acid (DMA(V)). The remaining non-excreted arsenic (≤ 10%) accumulates in cells, which over time may lead to skin, bladder, kidney, liver, lung, and prostate cancers42. Other forms of arsenic toxicity in humans have been observed in blood, bone marrow, cardiac, central nervous system, gastrointestinal, gonadal, kidney, liver, pancreatic, and skin tissues42. The human liver after exposure to therapeutic drugs may exhibit hepatic non-cirrhotic portal hypertension, fibrosis, and cirrhosis42.

Epidemiological studies have suggested a correlation between chronic consumption of drinking water contaminated with arsenic and the incidence of Type 2-diabetes42. The human liver after exposure to therapeutic drugs may exhibit hepatic non-cirrhotic portal hypertension, fibrosis, and cirrhosis42. However, the literature provides insufficient scientific evidence to show cause and effect between arsenic and the onset of diabetes mellitus Type 242. The human liver after exposure to therapeutic drugs may exhibit hepatic non-cirrhotic portal hypertension, fibrosis, and cirrhosis42. Studies have demonstrated that the oxidative stress generated by arsenic may disrupt the signal transduction pathways of the nuclear transcriptional factors PPAR’s, AP-1, and NFκB43,44,45, as well as the pro-inflammatory cytokines IL-8 and TNF-α46,47,48,49,50,51,42,52. Table 1 (which will be posted later because it is still under construction) summarizes a number of rodent hepatic genes with differential expression associated with arsenic. These genes have been grouped according to functions such as oxidative stress, signal transduction, inflammation, and growth factor/hormone receptors53. The interference of oxidative stress with signal transduction pathways may affect physiological processes associated with cell growth, metabolic syndrome X, glucose homeostasis, lipid metabolism, obesity, insulin resistance, inflammation, and diabetes-254,55,56. Recent scientific evidence has elucidated the physiological roles of the PPAR’s in the ω- hydroxylation of fatty acids and the inhibition of pro-inflammatory transcription factors (NFκB and AP-1), pro-inflammatory cytokines (IL-1, -6, -8, -12, and TNF-α), cell4 adhesion molecules (ICAM-1 and VCAM-1), inducible nitric oxide synthase, proinflammatory nitric oxide (NO), and anti-apoptotic factors57,58,59,60,61.


Testing for Exposure in Humans to Arsenic

There are tests available to measure arsenic in your 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 you have been exposed to above-average levels of arsenic. They cannot predict whether the arsenic levels in your body will affect your health. [1]

62

Compounds

Arsenic compounds resemble in many respects phosphorus compounds, as arsenic and phosphorus occur in the same group (column) of the periodic table.

Arsenic also has a formal oxidation state of +2 in As4S4, realgar.63

See also Arsenic compounds.

See also

Notes

  1. ^ "Stabilized Arsenic(I) Iodide: A Ready Source of Arsenic Iodide Fragments and a Useful Reagent for the Generation of Clusters". ACS Publications. Retrieved on 2007-12-10.
  2. ^ a b Emsley, John (2001). Nature's Building Blocks: An A-Z Guide to the Elements. Oxford: Oxford University Press. pp. 43,513,529. ISBN 0-19-850341-5. 
  3. ^ Bentley, Ronald; Chasteen, Thomas G. (2002). "Arsenic Curiosa and Humanity". The Chemical Educator 7 (2): 51. doi:10.1007/s00897020539a, http://192.129.24.144/licensed_materials/00897/sbibs/s0007002/spapers/720051rb.pdf. 
  4. ^ George Sarton, Introduction to the History of Science (cf. Dr. A. Zahoor and Dr. Z. Haq (1997), Quotations From Famous Historians of Science, Cyberistan)
  5. ^ Seyferth, Dietmar (2001). "Cadet's Fuming Arsenical Liquid and the Cacodyl Compounds of Bunsen". Organometallics 20 (8): 1488–1498. doi:10.1021/om0101947, http://pubs.acs.org/cgi-bin/abstract.cgi/orgnd7/2001/20/i08/abs/om0101947.html. 
  6. ^ Turner, Alan (1999). "Viewpoint: the story so far: An overview of developments in UK food regulation and associated advisory committees". British Food Journal 101 (4): 274–283., http://www.emeraldinsight.com/Insight/ViewContentServlet?Filename=Published/EmeraldFullTextArticle/Pdf/0701010401.pdf. 
  7. ^ a b c d Holleman, Arnold F.; Wiberg, Egon; Wiberg, Nils; (1985). "Arsen" (in German). Lehrbuch der Anorganischen Chemie (91–100 ed.), Walter de Gruyter. pp. 699–672. ISBN 3110075113. 
  8. ^ Norman, Nicholas C. (1998). Chemistry of Arsenic, Antimony and Bismuth, Springer. pp. 50. ISBN 9780751403893, http://books.google.de/books?id=vVhpurkfeN4C. 
  9. ^ Lichtfouse, Eric; Schwarzbauer, Jan; Robert, Didier, ed. (2004). "Electrodialytical Removal of Cu, Cr and As from Threaded Wood". Environmental Chemistry: Green Chemistry and Pollutants in Ecosystems. ISBN 9783540228608, http://books.google.com/books?id=IDGLh_cWAIwC. 
  10. ^ Mandal, Badal Kumar; Suzuki, Kazuo T. (2002). "Arsenic round the world: a review". Talanta 58 (1): 201–235. doi:10.1016/S0039-9140(02)00268-0. 
  11. ^ Reese, Jr., Robert G.. "Commodity Summaries 2002: Arsenic". United States Geological Survey. Retrieved on 2008-11-08.
  12. ^ a b Brooks, William E.. "Minerals Yearbook 2007: Arsenic". United States Geological Survey. Retrieved on 2008-11-08.
  13. ^ Antman, Karen H. (2001). "The History of Arsenic Trioxide in Cancer Therapy". Introduction to a supplement to The Oncologist' 6 (Suppl 2): 1–2. PMID 11331433, http://theoncologist.alphamedpress.org/cgi/content/full/6/suppl_2/1. 
  14. ^ Huet et.al (1975). "Noncirrhotic presinusoidal portal hypertension associated with chronic arsenical intoxication.". Gastroenterology 68' (5 Pt 1): 1270–1277. PMID 1126603. 
  15. ^ Jennewein, Marc; Lewis,Matthew A.; Zhao, Dawen; Tsyganov, Edward; Slavine, Nikolai; He, Jin; Watkins, Linda; Kodibagkar, Vikram D.; O'Kelly, Sean; Kulkarni, Padmakar; Antich, Peter P.M; Hermanne, Alex; Rösch, Frank; Mason Ralph P.; Thorpe, Philip E. (2008). "Vascular Imaging of Solid Tumors in Rats with a Radioactive Arsenic-Labeled Antibody that Binds Exposed Phosphatidylserine". Journal of Clinical Cancer 14: 1377–1385. doi:10.1158/1078-0432.CCR-07-1516. 
  16. ^ Timbrell, John (2005). "Butter Yellow and Scheele's Green". The Poison Paradox: Chemicals as Friends and Foes, Oxford University Press. ISBN 9780192804952, http://books.google.de/books?id=qYYOtQU37jcC. 
  17. ^ Code Red - Weapons of Mass Destruction [Online Resource - Blister Agents]
  18. ^ Peryea F.J. 1998. Historical use of lead arsenate insecticides, resulting in soil contamination and implications for soil remediation. Proceedings, 16th World Congress of Soil Science, Montpellier, France. 20-26. Aug. Available online: http://soils.tfrec.wsu.edu/leadhistory.htm
  19. ^ Nachman, Keeve E.; Graham, Jay P.; Price, Lance B.; Silbergeld, Ellen K. (2005). "Arsenic: A Roadblock to Potential Animal Waste Management Solutions". Environmental Health Perspective 113 (9): 1123–1124. doi:10.1289/ehp.7834.. 
  20. ^ Jones, F. T. (2007). "A Broad View of Arsenic". Poultry Science 86: 2–14, http://ps.fass.org/cgi/content/abstract/86/1/2. 
  21. ^ Guruswamy, Sivaraman (1999). "XIV. Ammunition". Engineering Properties and Applications of Lead Alloys, CRC Press. pp. 569–570. ISBN 9780824782474, http://books.google.de/books?id=TtGmjOv9CUAC. 
  22. ^ King, R. J. (2002). "Minerals explained 35: Arsenopyrite". Geology Today 18 (2): 72–75. doi:10.1046/j.1365-2451.2002.t01-1-00006.x. 
  23. ^ a b Brooks, William E.. "Mineral Commodity Summaries 2007: Arsenic". United States Geological Survey. Retrieved on 2008-11-25.
  24. ^ Matschullat, Jörg (2000). "Arsenic in the geosphere — a review". The Science of the Total Environment 249: 297–312. doi:10.1016/S0048-9697(99)00524-0. 
  25. ^ Whelan, J. M.; Struthers, J. D.; Ditzenberger, J. A. (1960). "Separation of Sulfur, Selenium, and Tellurium from Arsenic". Journalof the Electrochemical Society 107 (12): 982–985. doi:10.1149/1.2427585. 
  26. ^ Bentley, Ronald; Chasteen, Thomas G. (2002). "Microbial Methylation of Metalloids: Arsenic, Antimony, and Bismuth". Microbiology and Molecular Biology Reviews 66 (2): 250–271. doi:10.1128/MMBR.66.2.250-271.2002. 
  27. ^ Cullen, William R.; Reimer, Kenneth J. (1989;). "Arsenic speciation in the environment". Chemical Reviews 89 (4): 713–764. doi:10.1021/cr00094a002. 
  28. ^ Kulp, T. R. et al (2008). "Arsenic(III) fuels anoxygenic photosynthesis in hot spring biofilms from Mono Lake, California.". Science 321 (5891): 967–970. doi:10.1126/science.1160799. Lay summary – Chemistry World, 15 August 2008. 
  29. ^ Klaassen, Curtis; Watkins, John (2003). Casarett and Doull's Essentials of Toxicology, McGraw-Hill. pp. 512. ISBN 978-0071389143. 
  30. ^ Croal, Laura R., Jeffrey A. Gralnick, Davin Malasarn, and Dianne K. Newman. "The Genetics of Geochemisty." Annual Review of Genetics 38.1 (2004): 175-206. 24 April 2006. <http://web103.epnet.com>
  31. ^ AJ Giannini. The Psychiatric, Psychogenic ans Somatopsychic Disorders Handbook New Hyde Park, NY. Medical Examination Publishing Co.1978, pp.pp.81-82.
  32. ^ Andrew Meharg, Venomous Earth - How Arsenic Caused The World's Worst Mass Poisoning, Macmillan Science, 2005.
  33. ^ Lamm SH, Engel A, Penn CA, Chen R, Feinleib M (2006). "Arsenic cancer risk confounder in southwest Taiwan data set". Environ. Health Perspect. 114 (7): 1077–82. PMID 16835062. 
  34. ^ http://wedc.lboro.ac.uk/conferences/pdfs/28/Kohnhorst.pdf
  35. ^ Knobeloch LM, Zierold KM, Anderson HA (2006). "Association of arsenic-contaminated drinking-water with prevalence of skin cancer in Wisconsin's Fox River Valley". J Health Popul Nutr 24 (2): 206–13. PMID 17195561. 
  36. ^ Ferreccio C, Sancha AM (2006). "Arsenic exposure and its impact on health in Chile". J Health Popul Nutr 24 (2): 164–75. PMID 17195557. 
  37. ^ Chu HA, Crawford-Brown DJ (2006). "Inorganic arsenic in drinking water and bladder cancer: a meta-analysis for dose-response assessment". Int J Environ Res Public Health 3 (4): 316–22. PMID 17159272. 
  38. ^ "Arsenic in drinking water seen as threat - USATODAY.com". Retrieved on 2008-01-01.
  39. ^ Yavuz et al., Low-Field Magnetic Separation of Monodisperse Fe3O4 Nanocrystals Science, 2005.
  40. ^ "OSHA Arsenic". United States Occupational Safety and Health Administration. Retrieved on 2007-10-08.
  41. ^ a b Ueki, K.; Kondo, T.; Tseng, Y.-H.; Kahn, R. C. (2004). "Central role of suppressors of cytokine signaling proteins in hepatic steatosis, insulin resistance, and the metabolic syndrome in the mouse". Proceedings of the National Academy of Sciences of the United States of America 101 (28): 10422–10427. doi:10.1073/pnas.0402511101. 
  42. ^ a b c d e f g h Vigo, J. B., and J. T. Ellzey. Effects of Arsenic Toxicity at the Cellular Level: A Review. Texas Journal of Microscopy, 37(2) (2006) 45-49.
  43. ^ Hu Y., X. Jin, and E. Snow. Effect of arsenic on transcription factor AP-1 and NF- K B. Toxicology Letters, 133 (2002) 33-45.
  44. ^ Vigo, J. B., and J. T. Ellzey. Effects of Arsenic Toxicity at the Cellular Level: A Review. Texas Journal of Microscopy, 37(2) (2006) 45-49.
  45. ^ Walton, F., A. Harmon, D. Paul, Z. Drobna, Y. Patel, and M. Styblo. Inhibition of insulin-dependent glucose uptake by trivalent arsenicals: possible mechanisms of arsenic-induced diabetes. Toxicology and Applied Pharmacology, 198(3) (2004) 424-433.
  46. ^ Black, P. The inflammatory response is an integral part of the stress response: Implications for atherosclerosis, insulin resistance, type II diabetes and metabolic syndrome X. Brain, Behavior, and Immunity, 17 (2003) 350-364.
  47. ^ Carey, A., B. Lamont, S. Andrikopoulos, I. Koukoulas, J. Proietto, and M. Febbraio. Interleukin-6 gene expression is increased in insulin-resistant rat skeletal muscle following insulin stimulation. Biochemical and Biophysical Research Communications, 302 (2003) 837-840.
  48. ^ Dandona, P., A. Aljada, and A. Bandyopadhyay. Inflammation: the link between insulin resistance, obesity and diabetes. Trends in Immunology, 25(1) (2004) 4-7.
  49. ^ Fischer, C., L. Perstrup, A. Berntsen, P. Eskildsen, and B. Pedersen. Elevated plasma interleukin-18 is a marker of insulin-resistance in type 2 diabetic and non-diabetic humans. Clinical Immunology, 117(2) (2005) 152-160.
  50. ^ Gentry, P., T. Covington, S. Mann, A. Shipp, J. Yager, and H. Clewell. Physiologically based pharmacokinetic modeling of arsenic in the mouse. Journal of Toxicology and Environmental Health A, 67 (2004) 43-71.
  51. ^ Hu Y., X. Jin, and E. Snow. Effect of arsenic on transcription factor AP-1 and NF- KB. Toxicology Letters, 133 (2002) 33-45.
  52. ^ Walton, F., A. Harmon, D. Paul, Z. Drobna, Y. Patel, and M. Styblo. Inhibition of insulin-dependent glucose uptake by trivalent arsenicals: possible mechanisms of arsenic-induced diabetes. Toxicology and Applied Pharmacology, 198(3) (2004) 424-433.
  53. ^ Chen, H., J. Liu, B. Merrick, and M. Waalkes. Genetic events associated with arsenic induced malignant transformation: applications of cDNA micro array technology. Molecular Carcinogenesis, 30(2) (2001) 79-87.
  54. ^ Kota, P., H. Hsun-Wei, and B. Roufogalis. An overview on biological mechanisms of PPAR's. Pharmacological Research 51 (2005) 85-94.
  55. ^ Luquet, S., C. Gaudel, D. Holst, J. Lopez-Soriano, C. Jehl-Pietri, A. Fredenrich, and the treatment of type 2 diabetes. Biochimica et Biophysica Acta 1740 (2005) 313-317.
  56. ^ Moraes, L., L. Piqueras, and D. Bishop-Bailey. Peroxisome proliferator-activated receptors and inflammation. Pharmacology and Therapeutics 110(3) (2006) 371-385.
  57. ^ Black, P. The inflammatory response is an integral part of the stress response: Implications for atherosclerosis, insulin resistance, type II diabetes and metabolic syndrome X. Brain, Behavior, and Immunity, 17 (2003) 350-364.
  58. ^ Hara K., O. Terumasa, K. Tobe, K. Yasuda, Y. Mori, H. Kadowaki, R. Hagura, Y. Akanuma, S. Kimura, C. Ito, and T. Kadowaki. The Pro12Ala Polymorphism in PPAR-2 may confer resistance to type 2 diabetes. Biochemical and Biophysical Research Communications, 271 (2000) 212-216.
  59. ^ Kota, P., H. Hsun-Wei, and B. Roufogalis. An overview on biological mechanisms of PPAR's. Pharmacological Research 51 (2005) 85-94.
  60. ^ Moraes, L., L. Piqueras, and D. Bishop-Bailey. Peroxisome proliferator-activated receptors and inflammation. Pharmacology and Therapeutics 110(3) (2006) 371-385.
  61. ^ Vigo, J. B., and J. T. Ellzey. Effects of Arsenic Toxicity at the Cellular Level: A Review. Texas Journal of Microscopy, 37(2) (2006) 45-49.
  62. ^ http://www.atsdr.cdc.gov/tfacts2.html
  63. ^ "Arsenic: arsenic(II) sulfide compound data". WebElements.com. Retrieved on 2007-12-10.

References

External links

Sister project Wikimedia Commons has media related to: Arsenic
Look up arsenic in Wiktionary, the free dictionary.