Arsenic

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ArsenicAn overview

ContentsArticlesOverview 1

Arsenic 1

Isotopes 16

Isotopes of arsenic 16

Miscellany 20

Arsenic poisoning 20Arsenic contamination of groundwater 28Arsenic toxicity 35Carancas impact event 41Grainger challenge 45Marsh test 46Sono arsenic filter 49

ReferencesArticle Sources and Contributors 50Image Sources, Licenses and Contributors 51

Article LicensesLicense 52

1

Overview

Arsenic

Arsenic

Appearance

metallic grey

General properties

Name, symbol, number arsenic, As, 33

Pronunciation /ˈɑrsənɪk/ ar-sə-nik,also /ɑrˈsɛnɪk/ ar-sen-ik when attributive

Element category metalloid

Group, period, block 15, 4, p

Standard atomic weight 74.92160(2) g·mol−1

Electron configuration [Ar] 4s2 3d10 4p3

Electrons per shell 2, 8, 18, 5 (Image)

Physical properties

Phase solid

Density (near r.t.) 5.727 g·cm−3

Liquid density at m.p. 5.22 g·cm−3

Sublimation point 887 K,615 °C,1137 °F

Triple point 1090 K (817°C), 3628 [1]  kPa

Critical point 1673 K, ? MPa

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

Arsenic 2

Atomic properties

Oxidation states 5, 3, 2, 1,[2] -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 119 pm

Covalent radius 119±4 pm

Van der Waals radius 185 pm

Miscellanea

Crystal structure trigonal[3]

Magnetic ordering diamagnetic[4]

Electrical resistivity (20 °C) 333 nΩ·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

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 neutron

Arsenic  /ˈɑrsɪnɪk/ is a chemical element with the symbol As, atomic number 33 and relative atomic mass 74.92.Arsenic occurs in many minerals, usually in conjunction with sulfur and metals, and also as a pure elemental crystal.It was first documented by Albertus Magnus in 1250.[5]

Arsenic is a metalloid. It can exist in various allotropes, although only the grey form has important use in industry.The main use of metallic arsenic is for strengthening alloys of copper and especially lead (for example, in carbatteries). Arsenic is a common n-type dopant in semiconductor electronic devices, and the optoelectronic compoundgallium arsenide is the most common semiconductor in use after doped silicon.

Arsenic 3

A few species of bacteria are able to use arsenic compounds as respiratory metabolites, and are arsenic-tolerant.Arsenic is notoriously poisonous to multicellular life because of the interaction of arsenic ions with protein thiols.Arsenic and its compounds, especially the trioxide, are used in the production of pesticides (treated wood products),herbicides, and insecticides. These applications are declining, however, as many of these compounds are beingphased out.[6] Arsenic poisoning from naturally occurring arsenic compounds in drinking water remains a problem inmany parts of the world.

Characteristics

Physical characteristics

Crystal structure common to Sb, AsSb and greyAs

The three most common allotropes are metallic grey, yellow and blackarsenic, with grey being the most common.[7] Grey arsenic (α-As,space group R3m No. 166) adopts a double-layered structureconsisting of many interlocked ruffled six-membered rings. Because ofweak bonding between the layers, grey arsenic is brittle and has arelatively low Mohs hardness of 3.5. Nearest and next-nearestneighbors form a distorted octahedral complex, with the three atoms inthe same double-layer being slightly closer than the three atoms in thenext.[8] This relatively close packing leads to a high density of5.73 g/cm3.[9] Grey arsenic is a semimetal, but becomes asemiconductor with a bandgap of 1.2–1.4 eV if amorphized.[10] Yellowarsenic is soft and waxy, and somewhat similar to tetraphosphorus

(P4). Both have four atoms arranged in a tetrahedral structure in which each atom is bound to each of the other threeatoms by a single bond. This unstable allotrope, being molecular, is the most volatile, least dense and most toxic.Solid yellow arsenic is produced by rapid cooling of arsenic vapour, As4. It is rapidly transformed into the greyarsenic by light. The yellow form has a density of 1.97 g/cm3.[9] Black arsenic is similar in structure to redphosphorus.[9]

IsotopesNaturally occurring arsenic is composed of one stable isotope, 75As.[11] As of 2003, at least 33 radioisotopes havealso been synthesized, ranging in atomic mass from 60 to 92. The most stable of these is 73As with a half-life of80.3 days. Isotopes that are lighter than the stable 75As tend to decay by β+ decay, and those that are heavier tend todecay by β- decay, with some exceptions.At least 10 nuclear isomers have been described, ranging in atomic mass from 66 to 84. The most stable of arsenic'sisomers is 68mAs with a half-life of 111 seconds.[11]

ChemistryWhen heated in air, arsenic oxidizes to arsenic trioxide; the fumes from this reaction have an odour resemblinggarlic. This odour can be detected on striking arsenide minerals such as arsenopyrite with a hammer. Arsenic (andsome arsenic compounds) sublimes upon heating at atmospheric pressure, converting directly to a gaseous formwithout an intervening liquid state at 887 K (614 °C).[1] The triple point is 3.63 MPa and 1090 K (820 °C).[9] [1]

Arsenic makes arsenic acid with concentrated nitric acid, arsenious acid with dilute nitric acid, and arsenic trioxidewith concentrated sulfuric acid.[12]

Arsenic 4

Arsenic burning in the air

Compounds

Arsenic compounds resemble in some respects those of phosphorus,which occupies the same group (column) of the periodic table. Arsenicis less commonly observed in the pentavalent state, however. The mostcommon oxidation states for arsenic are: −3 in the arsenides, such asalloy-like intermetallic compounds; and +3 in the arsenites,arsenates(III), and most organoarsenic compounds. Arsenic also bondsreadily to itself as seen in the square As ions in the mineralskutterudite. In the +3 oxidation state, arsenic is typically pyramidal,owing to the influence of the lone pair of electrons.

Inorganic

Arsenic forms colourless, odourless, crystalline oxides As2O3 ("whitearsenic") and As2O5, which are hygroscopic and readily soluble inwater to form acidic solutions. Arsenic(V) acid is a weak acid. Its saltsare called arsenates, e.g., Paris Green (copper(II) acetoarsenite),calcium arsenate, and lead hydrogen arsenate. The latter three havebeen used as agricultural insecticides and poisons. The protonationsteps between the arsenate and arsenic acid are similar to those between phosphate and phosphoric acid. However,arsenite and arsenous acid contain arsenic bonded to three oxygen and not hydrogen atoms, in contrast to phosphiteand phosphonic acid, which contains a non-acidic P-H bond. Arsenous acid is genuinely tribasic, whereasphosphonic acid is not.

A broad variety of sulfur compounds of arsenic are known. Orpiment (As2S3) and realgar (As4S4) are somewhatabundant and were formerly used as painting pigments. Other sulfides include As4S3 and As4S10. Arsenic has aformal oxidation state of +2 in As4S4, which features As-As bonds so that the total covalency of As is still in factthree.[13]

The trifluoride, trichloride, tribromide, and triiodide of arsenic(III) are well known, whereas only AsF5 is the mainpentahalide. Arsenic pentafluoride is stable at room temperature, whereas the pentachloride is stable only below−50 °C.[9]

Organoarsenic compounds

Trimethylarsine

A large variety of organoarsenic compounds are known. Several were developed aschemical warfare agents during World War I, including vesicants such as lewisite andvomiting agents such as adamsite.[14] [15] [16] Cacodylic acid, which is of historic andpractical interest, arises from the methylation of arsenic trioxide, a reaction that has noanalogy in phosphorus chemistry.

Arsenic 5

AlloysArsenic is used as the group 5 element in the III-V semiconductors gallium arsenide, indium arsenide, andaluminium arsenide. The valence electron count of GaAs is the same as a pair of Si atoms, but the band structure iscompletely different, which results distinct bulk properties. Other arsenic alloys include the II-IV semiconductorcadmium arsenide.

Occurrence and production

A large sample of native arsenic

Minerals with the formula MAsS and MAs2 (M = Fe, Ni, Co) arethe dominant commercial sources of arsenic, together with realgar(an arsenic sulfide mineral) and native arsenic. An illustrativemineral is arsenopyrite (FeAsS), which is structurally related toiron pyrite. Many minor As-containing minerals are known.Arsenic also occurs in various organic forms in theenvironment.[17] Inorganic arsenic and its compounds, uponentering the food chain, are progressively metabolized to a lesstoxic form of arsenic through a process of methylation.[18]

Other naturally occurring pathways of exposure include volcanicash, weathering of arsenic-containing minerals and ores, anddissolved in groundwater. It is also found in food, water, soil, andair.[19] The most common pathway of exposure for humans isingestion, and the predominant source of arsenic in our diet is through seafood. An additional route of exposure isthrough inhalation.[20]

Arsenic output in 2006[21]

In 2005, China was the top producer of white arsenicwith almost 50% world share, followed by Chile, Peru,and Morocco, according to the British GeologicalSurvey and the United States Geological Survey.[21]

Most operations in the US and Europe have closed forenvironmental reasons. The arsenic is recovered mainlyas a side product from the purification of copper.Arsenic is part of the smelter dust from copper, gold,and lead smelters.[22]

On roasting in air of arsenopyrite, arsenic sublimes as arsenic(III) oxide leaving iron oxides,[17] while roastingwithout air results in the production of metallic arsenic. Further purification from sulfur and other chalcogens isachieved by sublimation in vacuum or in a hydrogen atmosphere or by distillation from molten lead-arsenicmixture.[23]

Arsenic 6

History

Realgar

Alchemical symbolfor arsenic

The word arsenic was borrowed from the Syriac word ܠܐ ܙܐܦܢܝܐ (al)zarniqa [24] and the Persian word زرنيخ Zarnikh, meaning "yelloworpiment", into Greek as arsenikon (Αρσενικόν). It is also related tothe similar Greek word arsenikos (Αρσενικός), meaning "masculine"or "potent". The word was adopted in Latin arsenicum and Old Frencharsenic, from which the English word arsenic is derived.[24] Arsenicsulfides (orpiment, realgar) and oxides have been known and usedsince ancient times.[25] Zosimos (circa 300 AD) describes roastingsandarach (realgar) to obtain cloud of arsenic (arsenious oxide), whichhe then reduces to metallic arsenic.[26] As the symptoms of arsenicpoisoning were somewhat ill-defined, it was frequently used formurder until the advent of the Marsh test, a sensitive chemical test forits presence. (Another less sensitive but more general test is theReinsch test.) Owing to its use by the ruling class to murder oneanother and its potency and discreetness, arsenic has been called thePoison of Kings and the King of Poisons.[27]

During the Bronze Age, arsenic was often included in bronze, which made the alloy harder (so-called "arsenicalbronze"[28] ). Albertus Magnus (Albert the Great, 1193–1280) is believed to have been the first to isolate the elementin 1250 by heating soap together with arsenic trisulfide.[5] In 1649, Johann Schröder published two ways ofpreparing arsenic.

Cadet's fuming liquid (impure cacodyl), often claimed as the first synthetic organometallic compound, wassynthesized in 1760 by Louis Claude Cadet de Gassicourt by the reaction of potassium acetate with arsenictrioxide.[29]

In the Victorian era, "arsenic" ("white arsenic" trioxide) was mixed with vinegar and chalk and eaten by women toimprove the complexion of their faces, making their skin paler to show they did not work in the fields. Arsenic wasalso rubbed into the faces and arms of women to "improve their complexion". The accidental use of arsenic in theadulteration of foodstuffs led to the Bradford sweet poisoning in 1858, which resulted in approximately 20deaths.[30]

Arsenic 7

Applications

Agricultural

Roxarsone is a controversial arseniccompound used as a nutritional

supplement for chickens

The toxicity of arsenic to insects, bacteria and fungi led to its use as a woodpreservative.[31] In the 1950s a process of treating wood with chromated copperarsenate (also known as CCA or Tanalith) was invented, and for decades thistreatment was the most extensive industrial use of arsenic. An increasedappreciation of the toxicity of arsenic resulted in a ban for the use of CCA inconsumer products; the European Union and United States initiated this processin 2004.[32] [33] CCA remains in heavy use in other countries however, e.g.Malaysian rubber plantations.[6]

Arsenic was also used in various agricultural insecticides, termination andpoisons. For example, lead hydrogen arsenate was a common insecticide onfruit trees,[34] but contact with the compound sometimes resulted in braindamage among those working the sprayers. In the second half of the 20thcentury, monosodium methyl arsenate (MSMA) and disodium methyl arsenate(DSMA) – less toxic organic forms of arsenic – have replaced lead arsenate inagriculture.

Arsenic is still added to animal food, in particular in the U.S. as a method of disease prevention[35] [36] and growthstimulation. One example is roxarsone, which is used as a broiler starter by about 70% of the broiler growers since1995.[37] The Poison-Free Poultry Act of 2009 proposes to ban the use of roxarsone in industrial swine and poultryproduction.[38]

Medical useDuring the 18th, 19th, and 20th centuries, a number of arsenic compounds have been used as medicines, includingarsphenamine (by Paul Ehrlich) and arsenic trioxide (by Thomas Fowler). Arsphenamine as well as neosalvarsanwas indicated for syphilis and trypanosomiasis, but has been superseded by modern antibiotics. Arsenic trioxide hasbeen used in a variety of ways over the past 500 years, but most commonly in the treatment of cancer. The US Foodand Drug Administration in 2000 approved this compound for the treatment of patients with acute promyelocyticleukemia that is resistant to ATRA.[39] It was also used as Fowler's solution in psoriasis.[40] Recently new researchhas been done in locating tumours using arsenic-74 (a positron emitter). The advantages of using this isotope insteadof the previously used iodine-124 is that the signal in the PET scan is clearer as the body tends to transport iodine tothe thyroid gland producing a lot of noise.[41]

In subtoxic doses, soluble arsenic compounds act as stimulants, and were once popular in small doses as medicine bypeople in the mid-18th century.[9]

AlloysThe main use of metallic arsenic is for alloying with copper and especially lead. Lead components in car batteries arestrengthened by the presence of a few percent of arsenic. Gallium arsenide is an important semiconductor material,used in integrated circuits. Circuits made from GaAs are much faster (but also much more expensive) than thosemade in silicon. Unlike silicon it is direct bandgap, and so can be used in laser diodes and LEDs to directly convertelectricity into light.[6]

Arsenic 8

MilitaryAfter World War I, the United States built up a stockpile of 20000tons of lewisite (ClCH=CHAsCl2), a chemicalweapon that is a vesicant (blister agent) and lung irritant. The stockpile was neutralized with bleach and dumped intothe Gulf of Mexico after the 1950s.[42] During the Vietnam War the United States used Agent Blue, a mixture ofsodium cacodylate and its acid form, as one of the rainbow herbicides to deprive the Vietnamese of valuable crops.

Other uses• Copper acetoarsenite was used as a green pigment known under many names, including 'Paris Green' and

'Emerald Green'. It caused numerous arsenic poisonings. Scheele's Green, a copper arsenate, was used in the 19thcentury as a coloring agent in sweets.[43]

• Also used in bronzing and pyrotechnics.• Up to 2% of arsenic is used in lead alloys for lead shots and bullets.[44]

• Arsenic is added in small quantities to alpha-brass to make it dezincification resistant. This grade of brass is usedto make plumbing fittings or other items that are in constant contact with water.[45]

• Arsenic is also used for taxonomic sample preservation.• Until recently arsenic was used in optical glass. Modern glass manufacturers, under pressure from

environmentalists, have removed it, along with lead.[46]

Biological role

Bacteria

Arsenobetaine

Some species of bacteria obtain their energy by oxidizing various fuelswhile reducing arsenate to arsenite. Under oxidative environmentalconditions some bacteria use arsenite, which is oxidized to arsenate asfuel for their metabolism.[47] The enzymes involved are known asarsenate reductases (Arr).

In 2008, bacteria were discovered that employ a version ofphotosynthesis in the absence of oxygen with arsenites as electrondonors, producing arsenates (just as ordinary photosynthesis uses wateras electron donor, producing molecular oxygen). Researchersconjecture that, over the course of history, these photosynthesizing organisms produced the arsenates that allowedthe arsenate-reducing bacteria to thrive. One strain PHS-1 has been isolated and is related to the γ-ProteobacteriumEctothiorhodospira shaposhnikovii. The mechanism is unknown, but an encoded Arr enzyme may function inreverse to its known homologues.[48]

HeredityArsenic has been linked to epigenetic changes that are heritable changes in gene expression that occur withoutchanges in DNA sequence and include DNA methylation, histone modification, and RNA interference. Toxic levelsof arsenic cause significant DNA hypermethylation of tumour suppressor genes p16 and p53, thus increasing risk ofcarcinogenesis. These epigenetic events have been observed in in vitro studies with human kidney cells and in vivotests with rat liver cells and peripheral blood leukocytes in humans.[49] Inductive coupled plasma mass spectrometry(ICP-MS) is used to detect precise levels of intracellular arsenic and its other bases involved in epigeneticmodification of DNA.[50] Studies investigating arsenic as an epigenetic factor will help in developing precisebiomarkers of exposure and susceptibility.

Arsenic 9

The Chinese brake fern (Pteris vittata) hyperaccumulates arsenic present in the soil into its leaves and has a proposeduse in phytoremediation.[51]

Arsenic reported substituting for phosphorus as a building block of lifeA NASA-funded astrobiology research team claimed on December 2, 2010 that the microbe strain GFAJ-1 of theGammaproteobacteria (designated Halomonadaceae) group has the ability to substitute arsenic for at least part of thephosphorus in the molecules of its cells, including DNA and ATP.[52] [53] Bacteria from Mono Lake, a naturallyarsenic-rich site in California, were cultured in an environment high in arsenic but low in phosphorus. This findinghas faced strong criticism from the scientific community; many scientists have argued that there is no evidence thatarsenic is actually incorporated into biomolecules.[54] [55] Independent confirmation of this finding has not yet beenpossible.

Biomethylation of arsenicInorganic arsenic and its compounds, upon entering the food chain, are progressively metabolised through a processof methylation.[56] For example, the mold Scopulariopsis brevicaulis produce significant amounts of trimethylarsineif inorganic arsenic is present.[57] The organic compound arsenobetaine is found in some marine foods such as fishand 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 ineating fish because this arsenic compound is nearly non-toxic.[58]

Environmental issues

Arsenic in drinking waterWidespread arsenic contamination of groundwater has led to a massive epidemic of arsenic poisoning inBangladesh[59] and neighbouring countries. As of this writing, 42 major incidents around the world have beenreported on groundwater arsenic contamination. It is estimated that approximately 57 million people are drinkinggroundwater with arsenic concentrations elevated above the World Health Organization's standard of 10 parts perbillion. However, a study of cancer rates in Taiwan[60] suggested that significant increases in cancer mortality appearonly at levels above 150 parts per billion. The arsenic in the groundwater is of natural origin, and is released from thesediment into the groundwater, owing to the anoxic conditions of the subsurface. This groundwater began to be usedafter local and western NGOs and the Bangladeshi government undertook a massive shallow tube welldrinking-water program in the late twentieth century. This program was designed to prevent drinking ofbacteria-contaminated surface waters, but failed to test for arsenic in the groundwater. Many other countries anddistricts in Southeast Asia, such as Vietnam and Cambodia have geological environments conducive to generation ofhigh-arsenic groundwaters. Arsenicosis was reported in Nakhon Si Thammarat, Thailand in 1987, and the dissolvedarsenic in the Chao Phraya River is suspected of containing high levels of naturally occurring arsenic, but has notbeen a public health problem owing to the use of bottled water.[61]

In the United States, arsenic is most commonly found in the ground waters of the southwest.[62] Parts of NewEngland, Michigan, Wisconsin, Minnesota and the Dakotas are also known to have significant concentrations ofarsenic 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.[63] According to a recent film funded by the USSuperfund, millions of private wells have unknown arsenic levels, and in some areas of the US, over 20% of wellsmay contain levels that exceed established limits.[64]

Low-level exposure to arsenic at concentrations found commonly in US drinking water compromises the initial immune response to H1N1 or swine flu infection according to NIEHS-supported scientists. The study, conducted in laboratory mice, suggests that people exposed to arsenic in their drinking water may be at increased risk for more

Arsenic 10

serious illness or death in response to infection from the virus.[65]

Epidemiological evidence from Chile shows a dose-dependent connection between chronic arsenic exposure andvarious forms of cancer, in particular when other risk factors, such as cigarette smoking, are present. These effectshave been demonstrated to persist below 50 parts per billion.[66]

Analyzing multiple epidemiological studies on inorganic arsenic exposure suggests a small but measurable riskincrease for bladder cancer at 10 parts per billion.[67] According to Peter Ravenscroft of the Department ofGeography at the University of Cambridge,[68] roughly 80 million people worldwide consume between 10 and 50parts per billion arsenic in their drinking water. If they all consumed exactly 10 parts per billion arsenic in theirdrinking water, the previously cited multiple epidemiological study analysis would predict an additional 2,000 casesof bladder cancer alone. This represents a clear underestimate of the overall impact, since it does not include lung orskin cancer, and explicitly underestimates the exposure. Those exposed to levels of arsenic above the current WHOstandard should weigh the costs and benefits of arsenic remediation.Early (1973) evaluations of the removal of dissolved arsenic by drinking water treatment processes demonstratedthat arsenic is very effectively removed by co-precipitation with either iron or aluminum oxides. The use of iron as acoagulant, in particular, was found to remove arsenic with efficiencies exceeding 90%.[69] [70] Several adsorptivemedia systems have been approved for point-of-service use in a study funded by the United States EnvironmentalProtection Agency (U.S.EPA) and the National Science Foundation (NSF). A team of European and Indian scientistsand engineers have set up six arsenic treatment plants in West Bengal based on in-situ remediation method (SARTechnology). This technology does not use any chemicals and arsenic is left as an insoluble form (+5 state) in thesubterranean zone by recharging aerated water into the aquifer and thus developing an oxidation zone to supportarsenic oxidizing micro-organisms. This process does not produce any waste stream or sludge and is relativelycheap.[71]

Another effective and inexpensive method to remove arsenic from contaminated well water is to sink wells 500 feetor deeper to reach purer waters. A recent 2011 study funded by the U.S. National Institute of Environmental HealthSciences' Superfund Research Program shows that deep sediments can remove arsenic and take it out of circulation.Through this process called adsorption in which arsenic sticks to the surfaces of deep sediment articles, arsenic canbe naturally removed from well water.[72]

Magnetic separations of arsenic at very low magnetic field gradients have been demonstrated in point-of-use waterpurification with high-surface-area and monodisperse magnetite (Fe3O4) nanocrystals. Using the high specificsurface area of Fe3O4 nanocrystals the mass of waste associated with arsenic removal from water has beendramatically reduced.[73]

Epidemiological studies have suggested a correlation between chronic consumption of drinking water contaminatedwith arsenic and the incidence of all leading causes of mortality. The literature provides reason to believe arsenicexposure is causative in the pathogenesis of diabetes.

Wood preservation in the USAs of 2002, US-based industries consumed 19,600 metric tons of arsenic. Ninety percent of this was used fortreatment of wood with chromated copper arsenate (CCA). In 2007, 50% of the 5,280 metric tons of consumptionwas still used for this purpose.[22] [74] In the United States, the use of arsenic in consumer products was discontinuedfor residential, and general consumer construction on December 31, 2003 and alternative chemicals are now used,such as Alkaline Copper Quaternary, borates, copper azole, cyproconazole, and propiconazole.[75]

Although discontinued, this application is also one of the 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

Arsenic 11

timber. The direct or indirect ingestion of wood ash from burnt CCA lumber has caused fatalities in animals andserious poisonings in humans; the lethal human dose is approximately 20 grams of ash. Scrap CCA lumber fromconstruction and demolition sites may be inadvertently used in commercial and domestic fires. Protocols for safedisposal of CCA lumber do not exist evenly throughout the world; there is also concern in some quarters about thewidespread landfill disposal of such timber.

Mapping of industrial releases in the USOne tool that maps releases of arsenic to particular locations in the United States[76] and also provides additionalinformation about such releases is TOXMAP. TOXMAP is a Geographic Information System (GIS) from theDivision of Specialized Information Services of the United States National Library of Medicine (NLM) that usesmaps of the United States to help users visually explore data from the United States Environmental ProtectionAgency's (EPA) Toxics Release Inventory and Superfund Basic Research Programs. TOXMAP is a resource fundedby the US Federal Government. TOXMAP's chemical and environmental health information is taken from NLM'sToxicology Data Network (TOXNET)[77] and PubMed, and from other authoritative sources.

Toxicity and precautions

Arsenic and many of its compounds are especially potent poisons. Many water supplies closeto mines are contaminated by these poisons. Arsenic disrupts ATP production through severalmechanisms. At the level of the citric acid cycle, arsenic inhibits lipoic acid, which is acofactor for pyruvate dehydrogenase; and by competing with phosphate it uncouplesoxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrialrespiration and ATP synthesis. Hydrogen peroxide production is also increased, which, it isspeculated, has potential to form reactive oxygen species and oxidative stress. These

metabolic interferences lead to death from multi-system organ failure, it is presumed from necrotic cell death, notapoptosis. A post mortem reveals brick-red-coloured mucosa, owing to severe haemorrhage. Although arsenic causestoxicity, it can also play a protective role.[78]

Elemental arsenic and arsenic compounds are classified as "toxic" and "dangerous for the environment" in theEuropean Union under directive 67/548/EEC. The International Agency for Research on Cancer (IARC) recognizesarsenic and arsenic compounds as group 1 carcinogens, and the EU lists arsenic trioxide, arsenic pentoxide andarsenate salts as category 1 carcinogens.Arsenic is known to cause arsenicosis owing to its manifestation in drinking water, “the most common species beingarsenate [HAsO4

2-; As(V)] and arsenite [H3AsO3 ; As(III)]”. The ability of arsenic to undergo redox conversionbetween 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 isrelevant for bioremediation of contaminated sites (Croal). The study of chemolithoautotrophic As(III) oxidizers andthe heterotrophic As(V) reducers can help the understanding of the oxidation and/or reduction of arsenic.[79]

Treatment of chronic arsenic poisoning is easily accomplished. British anti-lewisite (dimercaprol) is prescribed indosages of 5 mg/kg up to 300 mg each 4 hours for the first day. Then administer the same dosage each 6 hours forthe second day. Then prescribe this dosage each 8 hours for eight additional days.[80] However the Agency for ToxicSubstances and Disease Registry (ATSDR) states that the long-term effects of arsenic exposure cannot bepredicted.[20] Blood, urine, hair, and nails may be tested for arsenic; however, these tests cannot foresee possiblehealth outcomes from the exposure.[20] Excretion occurs in the urine and long-term exposure to arsenic has beenlinked to bladder and kidney cancer in addition to cancer of the liver, prostate, skin, lungs and nasal cavity.[81]

Occupational exposure and arsenic poisoning may occur in persons working in industries involving the use of inorganic arsenic and its compounds, such as wood preservation, glass production, nonferrous metal alloys, and

Arsenic 12

electronic semiconductor manufacturing. Inorganic arsenic is also found in coke oven emissions associated with thesmelter industry.[82]

Biochemical basis of arsenic toxicityThe high affinity of arsenic(III) oxides for thiols is usually assigned as the cause of the high toxicity. Thiols, in theform of cysteine residues, are situated at the active sites of many important enzymes.[6]

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Genetics 38: 175–206. doi:10.1146/annurev.genet.38.072902.091138. PMID 15568975.[80] The Psychiatric, Psychogenic ans Somatopsychic Disorders Handbook. New Hyde Park, NY: Medical Examination Publishing Co. 1978.

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Retrieved 2007-10-08.

Arsenic 15

External links• CTD's Arsenic page (http:/ / ctdbase. org/ detail. go?type=chem& acc=D001151) and CTD's Arsenicals page

(http:/ / ctdbase. org/ detail. go?type=chem& acc=D001152) from the Comparative Toxicogenomics Database• A Small Dose of Toxicology (http:/ / www. asmalldoseof. org/ )• Arsenic in groundwater (http:/ / www. hydrology. nl/ iahpublications/ 70-arsenic-in-groundwater. html) Book on

arsenic in groundwater by IAH's Netherlands Chapter and the Netherlands Hydrological Society• Contaminant Focus: Arsenic (http:/ / www. clu-in. org/ contaminantfocus/ default. focus/ sec/ arsenic/ cat/

Overview/ ) by the EPA.• Environmental Health Criteria for Arsenic and Arsenic Compounds, 2001 (http:/ / www. inchem. org/ documents/

ehc/ ehc/ ehc224. htm) by the WHO.• Evaluation of the carcinogenicity of arsenic and arsenic compounds (http:/ / www. informaworld. com/ smpp/

content~db=all?content=10. 1080/ 10934520600873571) by the IARC.• National Institute for Occupational Safety and Health – Arsenic Page (http:/ / www. cdc. gov/ niosh/ topics/

arsenic/ )• National Pollutant Inventory – Arsenic (http:/ / www. npi. gov. au/ database/ substance-info/ profiles/ 11. html)• origen.net – CCA wood and arsenic: toxicological effects of arsenic (http:/ / www. origen. net/ arsenic. html)

16

Isotopes

Isotopes of arsenicArsenic (As) has 33 known isotopes and at least 10 isomers. Only one of these isotopes, 75As, is stable; as such, it isconsidered a monoisotopic element. The longest-lived radioisotope is 73As has a half-life of 80 days. Arsenic hasbeen proposed as a "salting" material for nuclear weapons (cobalt is another, better-known salting material). A jacketof 75As, irradiated by the intense high-energy neutron flux from an exploding thermonuclear weapon, wouldtransmute into the radioactive isotope 76As with a half-life of 1.0778 days and produce approximately 1.13 MeV ofgamma radiation, significantly increasing the radioactivity of the weapon's fallout for several hours. Such a weaponis not known to have ever been built, tested, or used.Standard atomic mass: 74.92160(2) u.

Table

nuclidesymbol

Z(p) N(n) isotopic mass(u)

half-life decaymode(s)[1]

[2]

daughterisotope(s)[3]

nuclearspin

representativeisotopic

composition(mole

fraction)

range ofnatural

variation(mole

fraction) excitation energy

60As 33 27 59.99313(64)# p 59Ge 5+#

61As 33 28 60.98062(64)# p 60Ge 3/2-#

62As 33 29 61.97320(32)# p 61Ge 1+#

63As 33 30 62.96369(54)# p 62Ge (3/2-)#

64As 33 31 63.95757(38)# 40(30) ms[18(+43-7) ms]

β+ 64Ge 0+#

65As 33 32 64.94956(32)# 170(30) ms β+ 65Ge 3/2-#

66As 33 33 65.94471(73) 95.77(23) ms β+ 66Ge (0+)

66m1As 1356.70(17) keV 1.1(1) µs (5+)

66m2As 3023.9(3) keV 8.2(5) µs (9+)

67As 33 34 66.93919(11) 42.5(12) s β+ 67Ge (5/2-)

68As 33 35 67.93677(5) 151.6(8) s β+ 68Ge 3+

68mAs 425.21(16) keV 111(20) s[?107(+23-16)ns]

1+

69As 33 36 68.93227(3) 15.2(2) min β+ 69Ge 5/2-

70As 33 37 69.93092(5) 52.6(3) min β+ 70Ge 4(+#)

70mAs 32.008(23) keV 96(3) µs 2(+)

Isotopes of arsenic 17

71As 33 38 70.927112(5) 65.28(15) h β+ 71Ge 5/2-

72As 33 39 71.926752(5) 26.0(1) h β+ 72Ge 2-

73As 33 40 72.923825(4) 80.30(6) d EC 73Ge 3/2-

74As 33 41 73.9239287(25) 17.77(2) d β+ (66%) 74Ge 2-

β- (34%) 74Se

75As 33 42 74.9215965(20) Stable 3/2- 1.0000

75mAs 303.9241(7) keV 17.62(23) ms 9/2+

76As 33 43 75.922394(2) 1.0942(7) d β- (99.98%) 76Se 2-

EC (.02%) 76Ge

76mAs 44.425(1) keV 1.84(6) µs (1)+

77As 33 44 76.9206473(25) 38.83(5) h β- 77mSe 3/2-

77mAs 475.443(16) keV 114.0(25) µs 9/2+

78As 33 45 77.921827(11) 90.7(2) min β- 78Se 2-

79As 33 46 78.920948(6) 9.01(15) min β- 79mSe 3/2-

79mAs 772.81(6) keV 1.21(1) µs (9/2)+

80As 33 47 79.922534(25) 15.2(2) s β- 80Se 1+

81As 33 48 80.922132(6) 33.3(8) s β- 81mSe 3/2-

82As 33 49 81.92450(21) 19.1(5) s β- 82Se (1+)

82mAs 250(200) keV 13.6(4) s β- 82Se (5-)

83As 33 50 82.92498(24) 13.4(3) s β- 83mSe 3/2-#

84As 33 51 83.92906(32)# 4.02(3) s β-

(99.721%)84Se (3)(+#)

β-, n(.029%)

83Se

84mAs 0(100)# keV 650(150) ms

85As 33 52 84.93202(21)# 2.021(10) s β-, n(59.4%)

84Se (3/2-)#

β- (40.6%) 85Se86As 33 53 85.93650(32)# 0.945(8) s β- (67%) 86Se

β-, n (33%) 85Se87As 33 54 86.93990(32)# 0.56(8) s β- (84.6%) 87Se 3/2-#

β-, n(15.4%)

86Se

Isotopes of arsenic 18

88As 33 55 87.94494(54)# 300# ms[>300 ns]

β- 88Se

β-, n 87Se89As 33 56 88.94939(54)# 200# ms

[>300 ns]β- 89Se 3/2-#

90As 33 57 89.95550(86)# 80# ms[>300 ns]

91As 33 58 90.96043(97)# 50# ms[>300 ns]

3/2-#

92As 33 59 91.96680(97)# 30# ms[>300 ns]

[1] http:/ / www. nucleonica. net/ unc. aspx[2] Abbreviations:

EC: Electron capture[3] Bold for stable isotopes, bold italic for nearly-stable isotopes (half-life longer than the age of the universe)

Notes• Values marked # are not purely derived from experimental data, but at least partly from systematic trends. Spins

with weak assignment arguments are enclosed in parentheses.• Uncertainties are given in concise form in parentheses after the corresponding last digits. Uncertainty values

denote one standard deviation, except isotopic composition and standard atomic mass from IUPAC which useexpanded uncertainties.

References• Isotope masses from:

• G. Audi, A. H. Wapstra, C. Thibault, J. Blachot and O. Bersillon (2003). "The NUBASE evaluation of nuclearand decay properties" (http:/ / www. nndc. bnl. gov/ amdc/ nubase/ Nubase2003. pdf). Nuclear Physics A 729:3–128. Bibcode 2003NuPhA.729....3A. doi:10.1016/j.nuclphysa.2003.11.001.

• Isotopic compositions and standard atomic masses from:• J. R. de Laeter, J. K. Böhlke, P. De Bièvre, H. Hidaka, H. S. Peiser, K. J. R. Rosman and P. D. P. Taylor

(2003). "Atomic weights of the elements. Review 2000 (IUPAC Technical Report)" (http:/ / www. iupac. org/publications/ pac/ 75/ 6/ 0683/ pdf/ ). Pure and Applied Chemistry 75 (6): 683–800.doi:10.1351/pac200375060683.

• M. E. Wieser (2006). "Atomic weights of the elements 2005 (IUPAC Technical Report)" (http:/ / iupac. org/publications/ pac/ 78/ 11/ 2051/ pdf/ ). Pure and Applied Chemistry 78 (11): 2051–2066.doi:10.1351/pac200678112051. Lay summary (http:/ / old. iupac. org/ news/ archives/ 2005/atomic-weights_revised05. html).

• Half-life, spin, and isomer data selected from the following sources. See editing notes on this article's talk page.• G. Audi, A. H. Wapstra, C. Thibault, J. Blachot and O. Bersillon (2003). "The NUBASE evaluation of nuclear

and decay properties" (http:/ / www. nndc. bnl. gov/ amdc/ nubase/ Nubase2003. pdf). Nuclear Physics A 729:3–128. Bibcode 2003NuPhA.729....3A. doi:10.1016/j.nuclphysa.2003.11.001.

• National Nuclear Data Center. "NuDat 2.1 database" (http:/ / www. nndc. bnl. gov/ nudat2/ ). BrookhavenNational Laboratory. Retrieved September 2005.

• N. E. Holden (2004). "Table of the Isotopes". In D. R. Lide. CRC Handbook of Chemistry and Physics (85thed.). CRC Press. Section 11. ISBN 978-0849304859.

Isotopes of arsenic 19

• A.Shore, A. Fritsch, M. Heim, A. Schuh, M. Thoennessen. Discovery of the Arsenic Isotopes. arXiv:0902.4361(http:/ / arxiv. org/ abs/ 0902. 4361).

20

Miscellany

Arsenic poisoning

Arsenic poisoningClassification and external resources

Australian racehorse Phar Lap is suspected to have died from arsenic poisoning

ICD-10 T57.0 [1]

ICD-9 985.1 [2]

eMedicine emerg/42 [3]

MeSH D020261 [4]

Arsenic poisoning is a medical condition caused by increased levels of the element arsenic in the body. Arsenicinterferes with cellular longevity by allosteric inhibition of an essential metabolic enzyme. Symptoms of arsenicpoisoning include headache, confusion, convulsion, diarrhea, vomiting, and in severe cases coma and death.Routes of exposure include contaminated water, air, and food. Occupational exposure to arsenic may occur withcopper or lead smelting and wood treatment and among workers involved in the production or application ofpesticides.

Signs and symptomsSymptoms of arsenic poisoning begin with headaches, confusion, explosive diarrhea, implosive diarrhea, anddrowsiness. As the poisoning develops, convulsions and changes in fingernail pigmentation called leukonychia mayoccur. When the poisoning becomes acute, symptoms may include diarrhea, vomiting, blood in the urine, crampingmuscles, hair loss, stomach pain, and more convulsions. The organs of the body that are usually affected by arsenicpoisoning are the lungs, skin, kidneys, and liver. The final result of arsenic poisoning is coma to death.Arsenic is related to heart disease[5] (hypertension related cardiovascular), cancer,[6] stroke[7] (cerebrovasculardiseases), chronic lower respiratory diseases,[8] and diabetes.[9] [10]

Arsenic poisoning 21

Night blindnessLong term exposure to arsenic is related to vitamin A deficiency which is related to heart disease and nightblindness.[11]

CauseIn addition to its presence as a poison, for centuries arsenic was used medicinally. It has been used for over 2,400years as a part of traditional Chinese medicine.[12] In the western world, arsenic was used extensively to treatsyphilis before penicillin was introduced. It was eventually replaced as a therapeutic agent by sulfa drugs and then byantibiotics. Arsenic was also an ingredient in many tonics (or "patent medicines").In addition, during the Elizabethan era, some women used a mixture of vinegar, chalk, and arsenic applied topicallyto whiten their skin. This use of arsenic was intended to prevent aging and creasing of the skin, but some arsenic wasinevitably absorbed into the blood stream.Some pigments, most notably the popular Emerald Green (known also under several other names), were based onarsenic compounds. Overexposure to these pigments was a frequent cause of accidental poisoning of artists andcraftsmen. One of the biggest unintentional cases of arsenic poisoning via well water consumption is in Bangladeshand called by the World Health Organization as the "largest mass poisoning of a population in history."[13]

Research has shown that the inorganic arsenites (trivalent forms) in drinking water have a much higher acute toxicitythan organic arsenates (pentavalent forms).[14] The acute minimal lethal dose of arsenic in adults is estimated to be70 to 200 mg or 1 mg/kg/day.[15] Most reported arsenic poisonings are caused by one of arsenic's compounds, alsofound in drinking water, arsenic trioxide which is 500 times more toxic than pure arsenic.

Occupational exposuresIndustries that use inorganic arsenic and its compounds include wood preservation, glass production, nonferrousmetal alloys, and electronic semiconductor manufacturing. Inorganic arsenic is also found in coke oven emissionsassociated with the smelter industry.[16]

Occupational exposure to arsenic may occur with copper or lead smelting and wood treatment, among workersinvolved in the production or application of pesticides containing organic arsenicals. Humans are exposed to arsenicthrough air, drinking water, and food (meat, fish, and poultry); poultry is usually the largest source of food-basedarsenic ingestion due to usage of certain antibiotics in chicken feed. Arsenic was also found in wine if arsenicpesticides are used in the vineyard. Arsenic is well absorbed by oral and inhalation routes, widely distributed andexcreted in urine; most of a single, low-level dose is excreted within a few days after consuming any form ofinorganic arsenic. Remains of arsenic in nails (which show as white spots and lines) and hair can be detected yearsafter the exposure.

Drinking waterChronic arsenic poisoning results from drinking contaminated well water over a long period of time. This is due toarsenic contamination of aquifer water.[17] The World Health Organization recommends a limit of 0.01 mg/L(10ppb) of arsenic in drinking water. This recommendation was established based on the limit of detection ofavailable testing equipment at the time of publication of the WHO water quality guidelines. More recent findingsshow that consumption of water with levels as low as 0.00017 mg/L (0.17ppb) over long periods of time can lead toarsenicosis.[18]

From a 1988 study in China, the US protection agency quantified the lifetime exposure of arsenic in drinking water at concentrations of 0.0017 mg/L, 0.00017 mg/L, and 0.000017 mg/L are associated with a lifetime skin cancer risk of 1 in 10,000, 1 in 100,000, and 1 in 1,000,000 respectively. The World Health Organization contends that a level of 0.01 mg/L poses a risk of 6 in 10000 chance of lifetime skin cancer risk and contends that this level of risk is

Arsenic poisoning 22

acceptable.[19]

FoodChina is the only country to have set a standard for arsenic limits in food, as levels in rice exceed those in water[20] Ithas been found that rice is particularly susceptible to arsenic poisoning. Rice grown in US has an average 26 ppb ofarsenic according to a study.[21]

IntentionalArsenic became a favorite murder weapon of the Middle Ages and Renaissance, particularly among ruling classes inItaly allegedly. Because the symptoms are similar to those of cholera, which was common at the time, arsenicpoisoning often went undetected. By the 19th century, it had acquired the nickname "inheritance powder," perhapsbecause impatient heirs were known or suspected to use it to ensure or accelerate their inheritances.In ancient Korea, and particularly in Joseon Dynasty, arsenic-sulfur compounds have been used as a major ingredientof sayak (사약; 賜藥), which was a poison cocktail used in capital punishment of high-profile political figures andmembers of the royal family.[22]   Due to social and political prominence of the condemned, many of these eventswere well-documented, often in the Annals of Joseon Dynasty; they are sometimes portrayed in historical televisionminiseries because of their dramatic nature.[23]

On April 27, 2003, sixteen members of the Gustaf Adolph Lutheran Church in New Sweden, Maine, became illfollowing the church coffee hour; one man, Reid Morrill, died a short time later. It was found that the coffee hadbeen heavily laced with arsenic, setting off a flurry of local gossip and hysteria and worldwide media coverage. Asof the 2005 publication of journalist Christine Ellen Young's book, A Bitter Brew: Faith, Power and Poison in aSmall New England Town, no one had been charged with the crime, but Young's book revealed that lifelong churchmember Daniel Bondeson, who shot himself at his family farm five days after the poisoning, left a note confessingsole responsibility for the crime. Bondeson died while undergoing surgery, leaving Maine State Police and manychurch members convinced someone had helped Bondeson. Young's book rejected the conspiracy theory, citingevidence that the well-liked Bondeson had a dark side, harboring bitter grudges and battling emotional problems. In2006, the Maine Attorney General agreed that Bondeson had acted alone and closed the case.

PathophysiologyArsenic interferes with cellular longevity by allosteric inhibition of an essential metabolic enzyme pyruvatedehydrogenase (PDH) complex, which catalyzes the oxidation of pyruvate to acetyl-CoA by NAD+. With theenzyme 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 witharsenic can raise lactate levels and lead to lactic acidosis. Low potassium levels in the cells increases the risk ofexperiencing a life-threatening heart rhythm problem from arsenic trioxide. Arsenic in cells clearly stimulates theproduction of hydrogen peroxide (H2O2). When the H2O2 reacts with certain metals such as iron or manganese itproduces a highly reactive hydroxyl radical. Inorganic arsenic trioxide found in ground water particularly affectsvoltage-gated potassium channels,[24] disrupting cellular electrolytic function resulting in neurological disturbances,cardiovascular episodes such as prolonged QT interval, neutropenia, high blood pressure,[25] central nervous systemdysfunction, anemia, and death. Arsenic is a ubiquitous element present in American drinking water.[26]

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

Arsenic poisoning 23

to arsenic upregulates the expression of tumor necrosis factor-α, interleukin-1, vascular cell adhesion moleculeand vascular endothelial growth factor to induce cardiovascular pathogenesis.—Pitchai Balakumar1 and Jagdeep Kaur, "Arsenic Exposure and Cardiovascular Disorders: An Overview",Cardiovascular Toxicology, December 2009[27]

Tissue culture studies have shown that arsenic blocks both IKr and Iks channels and, at the same time, activatesIK-ATP channels. Arsenic also disrupts ATP production through several mechanisms. At the level of the citric acidcycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidativephosphorylation, 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, notapoptosis. A post mortem reveals brick red colored mucosa, due to severe hemorrhage. Although arsenic causestoxicity, it can also play a protective role.[28]

DiagnosisArsenic may be measured in blood or urine to monitor excessive environmental or occupational exposure, confirm adiagnosis of poisoning in hospitalized victims or to assist in the forensic investigation in a case of fatal over dosage.Some analytical techniques are capable of distinguishing organic from inorganic forms of the element. Organicarsenic compounds tend to be eliminated in the urine in unchanged form, while inorganic forms are largelyconverted to organic arsenic compounds in the body prior to urinary excretion. The current biological exposure indexfor U.S. workers of 35 µg/L total urinary arsenic may easily be exceeded by a healthy person eating a seafoodmeal.[29]

There are tests available to diagnose poisoning by measuring arsenic in blood, urine, hair, and fingernails. The urinetest is the most reliable test for arsenic exposure within the last few days. Urine testing needs to be done within24–48 hours for an accurate analysis of an acute exposure. Tests on hair and fingernails can measure exposure tohigh levels of arsenic over the past 6–12 months. These tests can determine if one has been exposed toabove-average levels of arsenic. They cannot predict, however, whether the arsenic levels in the body will affecthealth.[30] Chronic arsenic exposure can remain in the body systems for a longer period of time than a shorter term ormore isolated exposure and can be detected in a longer time frame after the introduction of the arsenic, important intrying to determine the source of the exposure.Hair is a potential bioindicator for arsenic exposure due to its ability to store trace elements from blood. Incorporatedelements maintain their position during growth of hair. Thus for a temporal estimation of exposure, an assay of haircomposition needs to be carried out with a single hair which is not possible with older techniques requiringhomogenization and dissolution of several strands of hair. This type of biomonitoring has been achieved with newermicroanalytical techniques like Synchroton radiation based X ray fluorescence (SXRF) spectroscopy andMicroparticle induced X ray emission (PIXE).The highly focused and intense beams study small spots on biologicalsamples allowing analysis to micro level along with the chemical speciation. In a study, this method has been used tofollow arsenic level before, during and after treatment with Arsenious oxide in patients with Acute PromyelocyticLeukemia.[31]

Arsenic poisoning 24

Treatment

ChelationChemical and synthetic methods are now used to treat arsenic poisoning. Dimercaprol and dimercaptosuccinic acidare chelating agents which sequester the arsenic away from blood proteins and are used in treating acute arsenicpoisoning. The most important side effect is hypertension. Dimercaprol is considerably more toxic than succimer.[32]

Mineral supplementsSupplemental potassium decreases the risk of experiencing a life-threatening heart rhythm problem from arsenictrioxide.[33]

Nutritional interventionIn the journal Food and Chemical Toxicology, Keya Chaudhuri of the Indian Institute of Chemical Biology inKolkata, and her colleagues reported giving rats daily doses of arsenic in their water, in levels equivalent to thosefound in groundwater in Bangladesh and West Bengal. Those rats which were also fed garlic extracts had 40 percentless arsenic in their blood and liver, and passed 45 percent more arsenic in their urine. The conclusion is thatsulfur-containing substances in garlic scavenge arsenic from tissues and blood. The presentation concludes thatpeople in areas at risk of arsenic contamination in the water supply should eat one to three cloves of garlic per day asa preventative.[34] [35] [36]

Notable casesArsenic poisoning, accidental or deliberate, has been implicated in the illness and death of a number of prominentpeople throughout history.

Francesco I de' Medici, Grand Duke of TuscanyRecent forensic evidence uncovered by Italian scientists suggests that Francesco and his wife were poisoned possiblyby his brother and successor Ferdinando.[37]

George III of Great BritainGeorge III's (1738–1820) personal health was a concern throughout his long reign. He suffered from periodicepisodes of physical and mental illness, five of them disabling enough to require the King to withdraw from hisduties. In 1969, researchers asserted that the episodes of madness and other physical symptoms were characteristic ofthe disease porphyria, which was also identified in members of his immediate and extended family. In addition, a2004 study of samples of the King's hair[38] revealed extremely high levels of arsenic, which is a possible trigger ofdisease symptoms. A 2005 article in the medical journal The Lancet[39] suggested the source of the arsenic could bethe antimony used as a consistent element of the King's medical treatment. The two minerals are often found in thesame ground, and mineral extraction at the time was not precise enough to eliminate arsenic from compoundscontaining antimony.

Napoleon BonaparteIt has been theorized that Napoleon Bonaparte (1769–1821) suffered and died from arsenic poisoning during his imprisonment on the island of Saint Helena. Forensic samples of his hair did show high levels, 13 times the normal amount, of the element. This, however, does not prove deliberate poisoning by Napoleon's enemies: copper arsenite has been used as a pigment in some wallpapers, and microbiological liberation of the arsenic into the immediate environment would be possible. The case is equivocal in the absence of clearly authenticated samples of the

Arsenic poisoning 25

wallpaper. As Napoleon's body lay for nearly 20 years in a grave on the island, before being moved to its presentresting place in Paris, arsenic from the soil could not have polluted the sample as the arsenic was found within hishair, which can only be possible when the arsenic was already in the body. Even without contaminated wallpaper orsoil, commercial use of arsenic at the time provided many other routes by which Napoleon could have consumedenough arsenic to leave this forensic trace.

Simón BolívarSouth American independence leader Simón Bolívar (1783–1830), according to Dr. Paul Auwaerter from theDivision of Infectious Diseases in the Department of Medicine at the Johns Hopkins University School of Medicine,may have died due to chronic arsenic poisoning further complicated by bronchiectasis and lung cancer.[40] [41] Dr.Auwaerter has considered murder and acute arsenic poisoning unlikely, arguing that gradual "environmental contactwith arsenic would have been entirely possible" as a result of drinking contaminated water in Peru or through themedicinal use of arsenic -which was common at the time- as Bolívar had reportedly resorted to it during thetreatment for some of his illnesses.[40]

Charles Francis HallAmerican explorer Charles Francis Hall (1821–1871) died unexpectedly during his third Arctic expedition aboardthe ship Polaris. After returning to the ship from a sledging expedition Hall drank a cup of coffee and fell violentlyill.[42] He collapsed in what was described as a fit. He suffered from vomiting and delirium for the next week, thenseemed to improve for a few days. He accused several of the ship's company, including ship's physician Dr. EmilBessels with whom he had longstanding disagreements, of having poisoned him.[42] Shortly thereafter, Hall againbegan suffering the same symptoms, died, and was taken ashore for burial. Following the expedition's return a USNavy investigation ruled that Hall had died from apoplexy.[43]

In 1968, however, Hall's biographer Chauncey C. Loomis, a professor at Dartmouth College, traveled to Greenlandto exhume Hall's body. Due to the permafrost, Hall's body, flag shroud, clothing and coffin were remarkably wellpreserved. Tissue samples of bone, fingernails and hair showed that Hall died of poisoning from large doses ofarsenic in the last two weeks of his life,[44] consistent with the symptoms party members reported. It is possible thatHall dosed himself with quack medicines which included the poison, but it is possible that he was murdered by Dr.Bessels or one of the other members of the expedition.[45]

Huo Yuan JiaHuo Yuan Jia made his name as a Chinese martial artist. There was rumour that he was poisoned in 1910.

Clare Boothe LuceA later case of arsenic poisoning is that of Clare Boothe Luce, (1903–1987) the American ambassador to Italy1953–1956. Although she did not die from her poisoning, she suffered an increasing variety of physical andpsychological symptoms until arsenic poisoning was diagnosed, and its source traced to the old, arsenic-ladenflaking paint on the ceiling of her bedroom. Another source (see below) explains her poisoning as resulting fromeating food contaminated by flaking of the ceiling of the embassy dining room.

Impressionist paintersEmerald Green, a pigment frequently used by Impressionist painters, is based on arsenic. Cézanne developed severediabetes, which is a symptom of chronic arsenic poisoning. Monet's blindness and Van Gogh's neurological disorderscould have been partially due to their use of Emerald Green. Poisoning by other commonly used substances,including liquor and absinthe, lead pigments, mercury-based Vermilion, and solvents such as turpentine, could alsobe a factor in these cases.

Arsenic poisoning 26

The Emperor GuangxuRecent testing in the People's Republic of China has confirmed that China's second-to-last emperor was poisonedwith a massive dose of arsenic; suspects include his dying aunt, the Empress Dowager Cixi, and her strongman,Yuan Shikai.

Phar LapThe famous and largely successful Australian racehorse Phar Lap died suddenly in 1932. Poisoning was consideredas a cause of death and several forensic examinations were completed at the time of death. In a recent examination,75 years after his death, forensic scientists determined that the horse had ingested a massive dose of arsenic shortlybefore his death.[46]

Footnotes[1] http:/ / apps. who. int/ classifications/ icd10/ browse/ 2010/ en#/ T57. 0[2] http:/ / www. icd9data. com/ getICD9Code. ashx?icd9=985. 1[3] http:/ / www. emedicine. com/ emerg/ topic42. htm[4] http:/ / www. nlm. nih. gov/ cgi/ mesh/ 2011/ MB_cgi?field=uid& term=D020261[5] Tseng CH, Chong CK, Tseng CP, et al. (January 2003). "Long-term arsenic exposure and ischemic heart disease in arseniasis-hyperendemic

villages in Taiwan". Toxicol. Lett. 137 (1–2): 15–21. doi:10.1016/S0378-4274(02)00377-6. PMID 12505429.[6] Smith AH, Hopenhayn-Rich C, Bates MN, et al. (July 1992). "Cancer risks from arsenic in drinking water". Environ. Health Perspect. 97:

259–67. doi:10.2307/3431362. PMC 1519547. PMID 1396465.[7] Chiou HY, Huang WI, Su CL, Chang SF, Hsu YH, Chen CJ (September 1997). "Dose-response relationship between prevalence of

cerebrovascular disease and ingested inorganic arsenic". Stroke 28 (9): 1717–23. doi:10.1161/01.STR.28.9.1717. PMID 9303014.[8] Hendryx M (January 2009). "Mortality from heart, respiratory, and kidney disease in coal mining areas of Appalachia". Int Arch Occup

Environ Health 82 (2): 243–9. doi:10.1007/s00420-008-0328-y. PMID 18461350.[9] Navas-Acien A, Silbergeld EK, Pastor-Barriuso R, Guallar E (August 2008). "Arsenic exposure and prevalence of type 2 diabetes in US

adults". JAMA 300 (7): 814–22. doi:10.1001/jama.300.7.814. PMID 18714061.[10] Kile ML, Christiani DC (August 2008). "Environmental arsenic exposure and diabetes". JAMA 300 (7): 845–6. doi:10.1001/jama.300.7.845.

PMID 18714068.[11] Hsueh YM, Wu WL, Huang YL, Chiou HY, Tseng CH, Chen CJ (December 1998). "Low serum carotene level and increased risk of

ischemic heart disease related to long-term arsenic exposure". Atherosclerosis 141 (2): 249–57. doi:10.1016/S0021-9150(98)00178-6.PMID 9862173.

[12] http:/ / www. ccmp. gov. tw/ en/ research/ result_detail. asp?relno=51& selno=0& no=95& detailno=1020[13] "Poisons in The Well: Exposure, Health Effects and Remediation of Arsenic and Manganese in Bangladesh" (http:/ / healthmad. com/

health/ poisons-in-the-well-exposure-health-effects-and-remediation-of-arsenic-and-manganese-in-bangladesh). Ebey Soman and HealthMad.. Retrieved 2009-11-01.

[14] Kingston RL, Hall S, Sioris L (1993). "Clinical observations and medical outcome in 149 cases of arsenate ant killer ingestion". J. Toxicol.Clin. Toxicol. 31 (4): 581–91. doi:10.3109/15563659309025763. PMID 8254700.

[15] Dart, RC (2004). Medical toxicology. Philadelphia: Williams & Wilkins. pp. 1393–1401. ISBN 0-7817-2845-2.[16] "OSHA Arsenic" (http:/ / www. osha. gov/ SLTC/ arsenic/ index. html). United States Occupational Safety and Health Administration. .

Retrieved 2007-10-08.[17] WHO Water-related diseases (http:/ / who. int/ water_sanitation_health/ diseases/ arsenicosis/ en/ )[18] "Water Sanitation and Health (WSH)" (http:/ / www. who. int/ water_sanitation_health/ diseases/ arsenicosis/ en/ ). WHO. .[19] "Towards an assessment of the socioeconomic impact of arsenic poisoning in Bangladesh: Health effects of arsenic in drinking water" (http:/

/ www. who. int/ water_sanitation_health/ dwq/ arsenic2/ en/ index2. html). Drinking Water Quality. WHO. . Retrieved 2009-12-03.[20] http:/ / www. speciation. net/ News/ China-Inorganic-Arsenic-in-Rice--An-Underestimated-Health-Threat--;~/ 2010/ 05/ 19/ 5027. html[21] http:/ / www. speciation. net/ News/ Surprisingly-high-concentrations-of-toxic-arsenic-species-found-in-US-rice-;~/ 2005/ 08/ 03/ 1561.

html[22] 공포의 '비소' 목재 (http:/ / imnews. imbc. com/ replay/ nwdesk/ article/ 2084429_2687. html)[23] 구혜선, '왕과 나' 폐비윤씨 사약받는 장면 열연 화제 (http:/ / spn. chosun. com/ site/ data/ html_dir/ 2008/ 02/ 18/ 2008021800711. html)[24] Zhou J, Wang W, Wei QF, Feng TM, Tan LJ, Yang BF (July 2007). "Effects of arsenic trioxide on voltage-dependent potassium channels

and on cell proliferation of human multiple myeloma cells". Chin. Med. J. 120 (14): 1266–9. PMID 17697580.[25] Konduri GG, Bakhutashvili, I, Eis A, Gauthier KM (2009). "Impaired Voltage Gated Potassium Channel Responses in a Fetal Lamb Model

of Persistent Pulmonary Hypertension of the Newborn". Pediatric Research 66 (3): 289–294. doi:10.1203/PDR.0b013e3181b1bc89.PMID 19542906.

[26] http:/ / water. usgs. gov/ nawqa/ trace/ arsenic/

Arsenic poisoning 27

[27] Balakumar, Pitchai; Kaur, Jagdeep (December 2009). "Arsenic Exposure and Cardiovascular Disorders: An Overview" (http:/ / www.springerlink. com/ content/ x0k1jtuj11745550/ ?p=ed19d21728b9483fbce43e4b4255802e& pi=1). Cardiovascular Toxicology 9 (4): 169–76.doi:10.1007/s12012-009-9050-6. PMID 19787300. .

[28] Klaassen, Curtis; Watkins, John (2003). Casarett and Doull's Essentials of Toxicology. McGraw-Hill. pp. 512. ISBN 978-0071389143.[29] R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 106-110.[30] "ToxFAQs for Arsenic" (http:/ / www. atsdr. cdc. gov/ tfacts2. html). Agency for Toxic Substances and Disease Registry. . Retrieved

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human hair". Biochimie 91 (10): 1260–7. doi:10.1016/j.biochi.2009.06.003. PMID 19527769.[32] Dimercaprol Drug Information, Professional (http:/ / www. drugs. com/ MMX/ Dimercaprol. html)[33] Arsenic Trioxide (Trisenox®)The Abramson Cancer Center of the University of Pennsylvania Last Modified: December 25, 2005[34] "Food and Chemical Toxicology - Elsevier" (http:/ / www. elsevier. com/ wps/ find/ journaldescription. cws_home/ 237/

description#description+ + ). . Retrieved 2009-03-05.[35] "Garlic combats arsenic poisoning - health - 14 January 2008 - New Scientist" (http:/ / www. newscientist. com/ article/ mg19726385.

100-garlic-combats-arsenic-poisoning. html). . Retrieved 2009-03-05.[36] Chowdhury, R; Dutta, A; Chaudhuri, S; Sharma, N; Giri, A; Chaudhuri, K (2008). "In vitro and in vivo reduction of sodium arsenite induced

toxicity by aqueous garlic extract". Food and Chemical Toxicology 46 (2): 740–51. doi:10.1016/j.fct.2007.09.108. PMID 17983699.[37] Mari F, Polettini A, Lippi D, Bertol E (December 2006). "The mysterious death of Francesco I de' Medici and Bianca Cappello: an arsenic

murder?" (http:/ / www. bmj. com/ cgi/ content/ full/ 333/ 7582/ 1299). BMJ 333 (7582): 1299–301. doi:10.1136/bmj.38996.682234.AE.PMC 1761188. PMID 17185715. .

[38] "King George III: Mad or misunderstood?" (http:/ / news. bbc. co. uk/ 1/ hi/ health/ 3889903. stm). BBC News. 2004-07-13. . Retrieved2010-04-25.

[39] Madness of King George Linked to Arsenic - AOL News (http:/ / aolsvc. news. aol. com/ news/ article. adp?id=20050722092109990013)[40] "Doctors Reconsider Health and Death of 'El Libertador,' General Who Freed South America" (http:/ / www. sciencedaily. com/ releases/

2010/ 04/ 100428110816. htm). Science Daily. April 29, 2010. . Retrieved July 17, 2010.[41] Simon Bolivar died of arsenic poisoning (http:/ / www. telegraph. co. uk/ news/ worldnews/ southamerica/ 7690928/

Simon-Bolivar-died-of-arsenic-poisoning. html) 7 May 2010. Nick Allen, The Telegraph. Retrieved on 17 July 2010.[42] Mowat Farley. 'The Polar Passion: The Quest for the North Pole'. Toronto: McClelland and Stewart Limited, 1967, p. 124[43] Parry, Richard. 'Trial By Ice: The True Story of Murder and Survival on the 1871 Polaris Expedition'. New York: Ballantine Books, 2001, p.

293[44] Fleming, Fergus. 'Ninety Degrees North: The Quest for the North Pole'. New York: Grove Press, 2001, p. 142[45] Chauncey Loomis. "Charles Francis Hall 1821–1871" (http:/ / pubs. aina. ucalgary. ca/ arctic/ Arctic35-3-442. pdf). .[46] "Phar Lap 'died from arsenic poisoning'" (http:/ / news. theage. com. au/ national/ phar-lap-died-from-arsenic-poisoning-20080619-2t3m.

html). The Age. 19 June 2008. . Retrieved 2008-01-09.

Further reading• Atlas (color) of Chronic Arsenic Poisoning (2010), Nobuyuki Hotta, Ichiro Kikuchi, Yasuko Kojo, Sakuragaoka

Hospital, Kumamoto, ISBN 978-4-9905256-0-6.• A 2011 article in the journal Social Medicine (http:/ / www. socialmedicine. info) discusses community

interventions to combat arsenic poisoning: Beyond medical treatment, arsenic poisoning in rural Bangladesh(http:/ / socialmedicine. info/ index. php/ socialmedicine/ article/ view/ 472/ 1082).

External links• Arsenic poisoning (http:/ / www. dmoz. org/ Science/ Environment/ Environmental_Health/ Toxic_Substances/

Arsenic/ / ) at the Open Directory Project• Subterranean Arsenic Removal (SAR) Technology in West Bengal (http:/ / www. insituarsenic. org)• Arsenic Removal in West Bengal, India (http:/ / www. worstpolluted. org/ projects_reports/ display/ 76)• Drinking Death in Groundwater: Arsenic Contamination as a Threat to Water Security for Bangladesh (http:/ /

acdis. illinois. edu/ publications/ 207/publication-DrinkingDeathinGroundwaterArsenicContaminationasaThreattoWaterSecurityforBangladesh. html),by Mustafa Moinuddin, ACDIS Occasional Paper, Program in Arms Control, Disarmament, and InternationalSecurity, University of Illinois, May 2004.

Arsenic contamination of groundwater 28

Arsenic contamination of groundwaterArsenic contamination of groundwater is a natural occurring high concentration of arsenic in deeper levels ofgroundwater, which became a high-profile problem in recent years due to the use of deep tubewells for water supplyin the Ganges Delta, causing serious arsenic poisoning to large numbers of people. A 2007 study found that over 137million people in more than 70 countries are probably affected by arsenic poisoning of drinking water.[1] Arseniccontamination of ground water is found in many countries throughout the world, including the USA. [2]

Approximately 20 incidents of groundwater arsenic contamination have been reported from all over the world. [3] Ofthese, four major incidents were in Asia, including locations in Thailand, Taiwan, and Mainland China.[4] [5] SouthAmerican countries like Argentina and Chile have also been affected. There are also many locations in the UnitedStates where the groundwater contains arsenic concentrations in excess of the Environmental Protection Agencystandard of 10 parts per billion adopted in 2001. According to a recent film funded by the US Superfund, "In SmallDoses" [6]., millions of private wells have unknown arsenic levels, and in some areas of the US, over 20% of wellsmay contain levels that are not safe.Arsenic is a carcinogen which causes many cancers including skin, lung, and bladder as well as cardiovasculardisease.Some research concludes that even at the lower concentrations, there is still a risk of arsenic contamination leadingto major causes of death. A study conducted in a contiguous six-county area of southeastern Michigan investigatedthe relationship between moderate arsenic levels and 23 selected disease outcomes. Disease outcomes includedseveral types of cancer, diseases of the circulatory and respiratory system, diabetes mellitus, and kidney and liverdiseases. Elevated mortality rates were observed for all diseases of the circulatory system. The researchersacknowledged a need to replicate their findings.[7]

A preliminary study shows a relationship between arsenic exposure measured in urine and Type II diabetes. Theresults supported the hypothesis that low levels of exposure to inorganic arsenic in drinking water may play a role indiabetes prevalence.[8]

Arsenic in drinking water may also compromise immune function "Scientists link influenza A (H1N1) susceptibilityto common levels of arsenic exposure" [9]..

Contamination specific nations and regions

Groundwater arsenic contamination areas

Bangladesh and West Bengal

The story of the arsenic contamination of the groundwater inBangladesh is a tragic one. Many people have died from thiscontamination. Diarrheal diseases have long plagued the developingworld as a major cause of death, especially in children. Prior to the1970s, Bangladesh had one of the highest infant mortality rates in theworld. Ineffective water purification and sewage systems as well asperiodic monsoons and flooding exacerbated these problems. As asolution, UNICEF and the World Bank advocated the use of wells to tap into deeper groundwater for a quick andinexpensive solution. Millions of wells were constructed as a result. Because of this action, infant mortality anddiarrheal illness were reduced by fifty percent. However, with over 8 million wells constructed, it has been foundover the last two decades that approximately one in five of these wells is now contaminated with arsenic above thegovernment's drinking water standard.

Arsenic contamination of groundwater 29

In the Ganges Delta, the affected wells are typically more than 20 m and less than 100 m deep. Groundwater closerto the surface typically has spent a shorter time in the ground, therefore likely absorbing a lower concentration ofarsenic; water deeper than 100 m is exposed to much older sediments which have already been depleted of arsenic.[4]

[10]

Dipankar Chakraborti from West Bengal brought the crisis to international attention in 1995.[11] [12] [13] Beginninghis investigation in West Bengal in 1988, he eventually published, in 2000, the results of a study conducted inBangladesh, which involved the analysis of thousands of water samples as well as hair, nail, and urine samples. Theyfound 900 villages with arsenic above the government limit.Chakraborti has criticized aid agencies, saying that they denied the problem during the 1990s while millions of tubewells were sunk. The aid agencies later hired foreign experts who recommended treatment plants which were notappropriate to the conditions, were regularly breaking down, or were not removing the arsenic.[14]

Chakraborti says that the arsenic situation in Bangladesh and West Bengal is due to negligence. He also adds that inWest Bengal water is mostly supplied from rivers. Groundwater comes from deep tubewells, which are few innumber in the state. Because of the low quantity of deep tubewells, the risk of arsenic patients in West Bengal iscomparatively less.[15]

According to the World Health Organisation, “In Bangladesh, West Bengal (India), and some other areas mostdrinking-water used to be collected from open dug wells and ponds with little or no arsenic, but with contaminatedwater transmitting diseases such as diarrhoea, dysentery, typhoid, cholera, and hepatitis. Programmes to provide‘safe’ drinking-water over the past 30 years have helped to control these diseases, but in some areas they have had theunexpected side-effect of exposing the population to another health problem—arsenic.” [16] The acceptable level asdefined by WHO for maximum concentrations of arsenic in safe drinking water is 0.01 mg/L. The Bangladeshgovernment's standard is at a slightly higher rate, at 0.05 mg/L being considered safe. WHO has defined the areasunder threat: Seven of the nineteen districts of West Bengal have been reported to have ground water arsenicconcentrations above 0.05 mg/L. The total population in these seven districts is over 34 million while the numberusing arsenic-rich water is more than 1 million (above 0.05 mg/L). That number increases to 1.3 million when theconcentration is above 0.01 mg/L. According to a British Geological Survey study in 1998 on shallow tube-wells in61 of the 64 districts in Bangladesh, 46 percent of the samples were above 0.01 mg/L and 27 percent were above0.050 mg/L. When combined with the estimated 1999 population, it was estimated that the number of peopleexposed to arsenic concentrations above 0.05 mg/L is 28-35 million and the number of those exposed to more than0.01 mg/L is 46-57 million (BGS, 2000).[16]

Throughout Bangladesh, as tube wells get tested for concentrations of arsenic, ones which are found to have arsenicconcentrations over the amount considered safe are painted red to warn residents that the water is not safe to drink.The solution, according to Chakraborti, is “By using surface water and instituting effective withdrawal regulation.West Bengal and Bangladesh are flooded with surface water. We should first regulate proper watershedmanagement. Treat and use available surface water, rain-water, and others. The way we're doing [it] at present is notadvisable."[15]

United StatesThere are many locations across the United States where the groundwater contains naturally high concentrations ofarsenic. Cases of groundwater-caused acute arsenic toxicity, such as those found in Bangladesh, are unknown in theUnited States where the concern has focused on the role of arsenic as a carcinogen. The problem of high arsenicconcentrations has been subject to greater scrutiny in recent years because of changing government standards forarsenic in drinking water.Some locations in the United States, such as Fallon, Nevada, have long been known to have groundwater with relatively high arsenic concentrations (in excess of 0.08 mg/L).[17] Even some surface waters, such as the Verde River in Arizona, sometimes exceed 0.01 mg/L arsenic, especially during low-flow periods when the river flow is

Arsenic contamination of groundwater 30

dominated by groundwater discharge.[18]

A drinking water standard of 0.05 mg/L (equal to 50 parts per billion, or ppb) arsenic was originally established inthe United States by the Public Health Service in 1942. The Environmental Protection Agency (EPA) studied thepros and cons of lowering the arsenic Maximum Contaminant Level (MCL) for years in the late 1980s and 1990s.No action was taken until January 2001, when the Clinton administration in its final weeks promulgated a newstandard of 0.01 mg/L (10 ppb) to take effect January 2006.[19] The incoming Bush administration suspended themidnight regulation, but after some months of study, the new EPA administrator Christine Todd Whitman approvedthe new 10 ppb arsenic standard and its original effective date of January 2006.[20]

Many public water supply systems across the United States obtained their water supply from groundwater that hadmet the old 50 ppb arsenic standard but exceeded the new 10 ppb MCL. These utilities searched for either analternative supply or an inexpensive treatment method to remove the arsenic from their water. In Arizona, anestimated 35 percent of water-supply wells were put out of compliance by the new regulation; in California, thepercentage was 38 percent .[21]

The proper arsenic MCL continues to be debated. Some have argued that the 10 ppb federal standard is still too high,while others have argued that 10 ppb is needlessly strict. Individual states are able to establish lower arsenic limits;New Jersey has done so, setting a maximum of 0.005 mg/L for arsenic in drinking water.[22]

A study of private water wells in the Appalachian mountains found that six percent of the wells had arsenic abovethe U.S. MCL of 0.010 mg/L.[23]

NepalIn Nepal there is a serious problem with arsenic contamination particularly in Terai region, the worst being nearNawalparasi District, where 26 percent of shallow wells failed to meet WHO standard of 10 ppb. A study by JapanInternational Cooperation Agency and the Environment in the Kathmandu Valley showed that 72% of deep wellsfailed to meet the WHO standard, and 12% failed to meet the Nepali standard of 50 ppb.[24]

Water purification solutions

Small-scale water treatmentA review of methods to remove arsenic from groundwater in Pakistan summarizes the most technically viableinexpensive methods [25] .Chakraborti claims that arsenic removal plants (ARPs) installed in Bangladesh by UNDP and WHO were a colossalwaste of funds due to breakdowns, inconvenient placements and, lack of quality control.[15]

A simpler and less expensive form of arsenic removal is known as the Sono arsenic filter, using three pitcherscontaining cast iron turnings and sand in the first pitcher and wood activated carbon and sand in the second.[26]

Plastic buckets can also be used as filter containers.[27] It is claimed that thousands of these systems are in use andcan last for years while avoiding the toxic waste disposal problem inherent to conventional arsenic removal plants.Although novel, this filter has not been certified by any sanitary standards such as NSF, ANSI, WQA and does notavoid toxic waste disposal similar to any other iron removal process.In the United States small "under the sink" units have been used to remove arsenic from drinking water. This optionis called "point of use" treatment. The most common types of domestic treatment use the technologies of adsorption(using media such as Bayoxide E33, GFH, or titanium dioxide) or reverse osmosis. Ion exchange and activatedalumina have been considered but not commonly used.

Arsenic contamination of groundwater 31

Large-scale water treatmentIn some places, such as the United States, all the water supplied to residences by water utilities must meet primary(health-based) drinking water standards. This may necessitate large-scale treatment systems to remove arsenic fromthe water supply. The effectiveness of any method depends on the chemical makeup of a particular water supply.The aqueous chemistry of arsenic is complex, and may affect the removal rate that can be achieved by a particularprocess.Some large utilities with multiple water supply wells could shut down those wells with high arsenic concentrations,and produce only from wells or surface water sources that meet the arsenic standard. Other utilities, however,especially small utilities with only a few wells, may have no available water supply that meets the arsenic standard.Coagulation/filtration (also known as flocculation) removes arsenic by coprecipitation and adsorption using ironcoagulants. Coagulation/filtration using alum is already used by some utilities to remove suspended solids and maybe adjusted to remove arsenic. But the problem of this type of filtration system is that it gets clogged very easily,mostly within two to three months. The toxic arsenic sludge are disposed of by concrete stabilization, but there is noguarantee that they won't leach out in future.Iron oxide adsorption filters the water through a granular medium containing ferric oxide. Ferric oxide has a highaffinity for adsorbing dissolved metals such as arsenic. The iron oxide medium eventually becomes saturated, andmust be replaced. The sludge disposal is a problem here too.Activated alumina is an adsorbent that effectively removes arsenic. Activated alumina columns connected toshallow tube wells in India and Bangladesh have successfully removed both As(III) and As(V) from groundwater fordecades. Long-term column performance has been possible through the efforts of community-elected watercommittees that collect a local water tax for funding operations and maintenance[28] . It has also been used to removeundesirably high concentrations of fluoride.Ion Exchange has long been used as a water-softening process, although usually on a single-home basis. Traditionalanion exchange is effective in removing As(V), but not As (III), or arsenic trioxide, which doesn't have a net charge.Effective long-term ion exchange removal of arsenic requires a trained operator to maintain the column.Both Reverse osmosis and electrodialysis (also called electrodialysis reversal) can remove arsenic with a net ioniccharge. (Note that arsenic oxide, As2O3, is a common form of arsenic in groundwater that is soluble, but has no netcharge.) Some utilities presently use one of these methods to reduce total dissolved solids and therefore improvetaste. A problem with both methods is the production of high-salinity waste water, called brine, or concentrate,which then must be disposed of.Subterranean Arsenic Removal (SAR) Technology SAR Technology [29]

In subterranean arsenic removal (SAR), aerated groundwater is recharged back into the aquifer to create an oxidationzone which can trap iron and arsenic on the soil particles through adsorption process. The oxidation zone created byaerated water boosts the activity of the arsenic-oxidizing microorganisms which can oxidize arsenic from +3 to +5state SAR Technology [29]. No chemicals are used and almost no sludge is produced during operational stage sinceiron and arsenic compounds are rendered inactive in the aquifer itself. Thus toxic waste disposal and the risk of itsfuture mobilization is prevented. Also, it has very long operational life, similar to the long lasting tube wells drawingwater from the shallow aquifers.Six such SAR plants, funded by the World Bank and constructed by Ramakrishna Vivekananda Mission,Barrackpore & Queen's University Belfast, UK are operating in West Bengal. Each plant has been delivering morethan 3,000 litres of arsenic and iron-free water daily to the rural community. The first community water treatmentplant based on SAR technology was set up at Kashimpore near Kolkata in 2004 by a team of European and Indianengineers led by Dr. Bhaskar Sen Gupta of Queen's University Belfast for TiPOT.[30] [31] [32] [33]

SAR technology had been awarded Dhirubhai Ambani Award, 2010 from IChemE UK for Chemical Innovation. Again, SAR was the winner of the St. Andrews Award for Environment, 2010 [34]. The SAR Project was selected by

Arsenic contamination of groundwater 32

the Blacksmith Institute - New York & Green Cross- Switzerland as one of the "12 Cases of Cleanup & Success" inthe World's Worst Polluted Places Report 2009. (Refer: www.worstpolluted.org [35]).Currently, large scale SAR plants are being installed in USA, Malaysia, Cambodia & Vietnam.

Dietary intakeResearchers from Bangladesh and the United Kingdom have recently claimed that dietary intake of arsenic adds asignificant amount to total intake where contaminated water is used for irrigation.[36] [37] [38]

Notes[1] "Arsenic in drinking water seen as threat" (http:/ / www. usatoday. com/ news/ world/ 2007-08-30-553404631_x. htm,). Associated Press.

2007-08-30. .[2] Twarakavi, N. K. C., Kaluarachchi, J. J. (2006). "Arsenic in the shallow ground waters of conterminous United States: assessment, health

risks, and costs for MCL compliance" (http:/ / www3. interscience. wiley. com/ journal/ 118632836/ abstract?CRETRY=1& SRETRY=0).Journal of American Water Resources Association 42 (2): 275–294. doi:10.1111/j.1752-1688.2006.tb03838.x. .

[3] Mukherjee A., Sengupta M. K., Hossain M. A. (2006). "Arsenic contamination in groundwater: A global perspective with emphasis on theAsian scenario" (http:/ / 202. 136. 7. 26/ images/ jhpn242_Arsenic-contamination. pdf). Journal of Health Population and Nutrition 24 (2):142–163. .

[4] The UNESCO Courier, Bangladesh's arsenic poisoning: who is to blame? (http:/ / www. unesco. org/ courier/ 2001_01/ uk/ planet. htm)[5] Chowdhury U. K., Biswas B. K., Chowdhury T. R. (2000). "Groundwater arsenic contamination in Bangladesh and West Bengal, India"

(http:/ / www. ehponline. org/ members/ 2000/ 108p393-397chowdhury/ chowdhury-full. html). Environmental Health Perspectives (Brogan&#38) 108 (4): 393–397. doi:10.2307/3454378. JSTOR 3454378. .

[6] http:/ / www. youtube. com/ watch?v=hi5DfRy01vE[7] , Jaymie R. Meliker, Arsenic in drinking water and cerebrovascular disease, diabetes mellitus, and kidney disease in Michigan: a

standardized mortality ratio analysis (http:/ / www. ehjournal. net/ content/ 6/ 1/ 4) Environmental Health Magazine. Volume 2:4. 2007.Accessed 9 Sept. 2008.

[8] Ana Navas-Acien, "Arsenic Exposure and Prevalence of Type 2 Diabetes in US Adults," Journal of American Medical Association, v.300,n.7 (August 2008).

[9] http:/ / www. eurekalert. org/ pub_releases/ 2009-05/ mbl-sli052009. php[10] Singh A. K. (2006). "Chemistry of arsenic in groundwater of Ganges-Brahmaputra river basin" (http:/ / www. ias. ac. in/ currsci/ sep102006/

599. pdf). Current Science 91 (5): 599–606. .[11] David Bradley, "Drinking the water of death", The Guardian, 5 January 1995[12] Amit Chatterjee, Dipankar Das, Badal K. Mandal, Tarit Roy Chowdhury, Gautam Samanta and Dipankar Chakraborti (1995). "Arsenic in

ground water in six districts of West Bengal, India: the biggest arsenic calamity in the world. Part I. Arsenic species in drinking water andurine of the affected people". Analyst 120 (3): 643–651. doi:10.1039/AN9952000643.

[13] Dipankar Das, Amit Chatterjee, Badal K. Mandal, Gautam Samanta, Dipankar Chakraborti and Bhabatosh Chanda (1995). "Arsenic inground water in six districts of West Bengal, India: the biggest arsenic calamity in the world. Part 2. Arsenic concentration in drinking water,hair, nails, urine, skin-scale and liver tissue (biopsy) of the affected people". Analyst 120 (3): 917–925. doi:10.1039/AN9952000917.PMID 7741255.

[14] New Scientist, Interview: Drinking at the west's toxic well (http:/ / www. newscientist. com/ article/ mg19025450. 600. html) 31 May 2006.[15] The Times of India, 'Use surface water. Stop digging' (http:/ / timesofindia. indiatimes. com/ articleshow/ 864169. cms), interview, 26 Sep,

2004.[16] World Health Organization, Arsenic in Drinking Water (http:/ / www. who. int/ mediacentre/ factsheets/ fs210/ en/ index. html), accessed 5

Feb 2007.[17] Frederick Rubel Jr. and Steven W. Hathaway (1985) Pilot Study for removal of arsenic from drinking water at the Fallon, Nevada, Naval

Air Station, Environmental Protection Agency, EPA/600/S2-85/094.[18] M. Taqueer A. Qureshi (1995) Sources of Arsenic in the Verde River and Salt River Watersheds, Arizona, M.S. thesis, Arizona State

University, Tempe.[19] The history of arsenic regulation, Southwest Hydrology, May/June 2002, p.16.[20] EPA announces arsenic standard for drinking water of 10 parts per billion, EPA press release, 10/31/2001.[21] Alison Bohlen (2002) States move forward to meet new arsenic standard, Southwest Hydrology, May/June 2002, p.18-19.[22] Megan A. Ferguson and others, Lowering the detection limit for arsenic: implications for a future practical quantitation limit, American

Water Works Association Journal, Aug. 2007, p.92-98.[23] John G. Shiber, "Arsenic in domestic well water and health in Central Appalachia, USA" (http:/ / cat. inist. fr/ ?aModele=afficheN&

cpsidt=16437433)[24] http:/ / southasia. oneworld. net/ todaysheadlines/ nepal-filters-to-provide-arsenic-free-drinking-water

Arsenic contamination of groundwater 33

[25] Fatima Hashmi and Joshua M. Pearce, “Viability of Small-Scale Arsenic-Contaminated Water Purification Technologies for SustainableDevelopment in Pakistan”, Sustainable Development, 19(4), pp. 223-234, 2011. pdf (http:/ / www3. interscience. wiley. com/ journal/122394419/ abstract?CRETRY=1& SRETRY=0) Open access full text (http:/ / hdl. handle. net/ 1974/ 6828)

[26] Evaluation of Performance of Sono 3-Kolshi Filter for Arsenic Removal from Groundwater Using Zero Valent Iron Through Laboratory andField Studies (http:/ / www. unu. edu/ env/ Arsenic/ Munir. pdf)PDF (272 KiB)

[27] SONO ARSENIC FILTER FROM BANGLADESH - 1 (http:/ / phys4. harvard. edu/ ~wilson/ arsenic/ remediation/ SONO/ As filtrationpictures. pdf)PDF (102 KiB) - pictures with descriptions.

[28] SARKAR, S; GUPTA, A, BISWAS, R, DEB, A, GREENLEAF, J, SENGUPTA, A (1 May 2005). "Well-head arsenic removal units inremote villages of Indian subcontinent: Field results and performance evaluation". Water Research 39 (10): 2196–2206.doi:10.1016/j.watres.2005.04.002.

[29] http:/ / www. insituarsenic. org[30] 12 Cases of Cleanup & Success (http:/ / www. worstpolluted. org/ )[31] "World's Worst Polluted Places Report 2009" (http:/ / www. worstpolluted. org/ projects_reports/ display/ 76)[32] Scientific American (http:/ / www. scientificamerican. com/ podcast/ episode. cfm?id=can-the-worlds-most-polluted-places-09-10-29&

SID=mail& sc=emailfriend)[33] Reuters Global (http:/ / uk. reuters. com/ article/ idUKTRE59R4BE20091028?pageNumber=1& virtualBrandChannel=0)[34] http:/ / www. thestandrewsprize. com/ lists/ 2010. htm[35] http:/ / www. worstpolluted. org/ files/ FileUpload/ files/ 2009-report/ Blacksmith-Institute-Green-Cross-Switzerland-WWPP-Report-2009.

pdf[36] Mustak Hossain (2006-07-13). "Toxic rice harvested in southwestern Bangladesh" (http:/ / www. scidev. net/ News/ index.

cfm?fuseaction=readNews& itemid=2975& language=1). SciDev.Net. .[37] Williams, P.N.; Islam, M. R.; Adomako, E. E.; Raab, A.; Hossain, S. A.; Zhu, Y. G.; Feldmann, J.; Meharg, A. A. (2006). "Increase in Rice

Grain Arsenic for Regions of Bangladesh Irrigating Paddies with Elevated Arsenic in Groundwaters". Environ. Sci. Technol 40 (16):4903–4908. doi:10.1021/es060222i.

[38] *Raghvan T. "Screening of Rice Cultivars for Grain Arsenic Concentration and Speciation". American Society of Agronomy Proceeding.

References• Smedley PL, Kinniburgh DG (2002). "A review of the source, behaviour and distribution of arsenic in natural

waters". Applied Geochemistry 17 (5): 517–568. doi:10.1016/S0883-2927(02)00018-5.• Nickson RT, McArthur JM, Ravenscroft P (2000). "Mechanism of arsenic release to groundwater, Bangladesh

and West Bengal". Applied Geochemistry 15 (4): 403–413. doi:10.1016/S0883-2927(99)00086-4.• Korte N. E., Fernando Q. (1991). "A Review of Arsenic(III) in Groundwater". Critical Reviews in Environmental

Control 21 (1): 1–39. doi:10.1080/10643389109388408.• Smith AH, Lingas EO, Rahman M (2000). "Contamination of drinking-water by arsenic in Bangladesh: a public

health emergency" (http:/ / www. scielosp. org/ scielo. php?script=sci_arttext&pid=S0042-96862000000900005& lng=en& nrm=iso). Bulletin of the World Health Organization 78 (9):1093–1103. doi:10.1590/S0042-96862000000900005. PMC 2560840. PMID 11019458.

• Harvey CF, Swartz CH, Badruzzaman ABM (2002). "Arsenic mobility and groundwater extraction inBangladesh". Science 298 (5598): 1602–1606. doi:10.1126/science.1076978. PMID 12446905.

• Raghvan T. "Screening of Rice Cultivars for Grain Arsenic Concentration and Speciation". American Society ofAgronomy Proceeding.

• Hossain MF (2006). "Arsenic contamination in Bangladesh - An overview". Agriculture Ecosystem &Environment 113 (1-4): 1–16. doi:10.1016/j.agee.2005.08.034.

Arsenic contamination of groundwater 34

External links• ATSDR - Case Studies in Environmental Medicine: Arsenic Toxicity (http:/ / www. atsdr. cdc. gov/ csem/

arsenic/ )• Arsenic in groundwater (http:/ / www. igrac. net/ publications/ 142) IGRAC International Groundwater Resources

Assessment Centre• Arsenic in Groundwater: A World Problem (http:/ / www. hydrology. nl/ iahpublications/

70-arsenic-in-groundwater. html) - IAH publication, Netherlands National Chapter, 2008• SOS-Arsenic.net (http:/ / www. sos-arsenic. net) - information and awareness raising site, focused on Bangladesh.• Contamination of drinking-water by arsenic in Bangladesh: a public health emergency (http:/ / www. sos-arsenic.

net/ english/ contamin/ smith. html) - at SOS-Arsenic.net• Subterranean Arsenic Treatment Technology in West Bengal (http:/ / www. insituarsenic. org)• 12 Cases of Cleanup & Success (http:/ / www. worstpolluted. org/ projects_reports/ display/ 76)• www.wbphed.gov.in (http:/ / www. wbphed. gov. in/ PHEDTables/ arsenicbackground. html) - Arsenic Scenario

of West Bengal• Drinking Death in Groundwater: Arsenic Contamination as a Threat to Water Security for Bangladesh (http:/ /

www. acdis. uiuc. edu/ Research/ OPs/ Moinuddin/ MoinuddinOP. pdf), ACDIS Occasional Paper by MustafaMoinuddin

• St Andrews Prize for Environment 2010 (http:/ / www. st-andrews. ac. uk/ news/ archive/ 2010/ Title,51258,en.html)

Arsenic toxicity 35

Arsenic toxicity

Arsenic toxicityClassification and external resources

ICD-10 T57.0 [1]

ICD-9 985.1 [2]

Arsenic and many of its compounds are especially potent poisons. Arsenic disrupts ATP production through severalmechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing withphosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrialrespiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygenspecies and oxidative stress. These metabolic interferences lead to death from multi-system organ failure (see arsenicpoisoning) probably from necrotic cell death, not apoptosis. A post mortem reveals brick red colored mucosa, due tosevere hemorrhage. Although arsenic causes toxicity, it can also play a protective role.[1]

ExposureOrganic arsenic exposure can occur by eating food. Organic arsenic is 500 times less harmful than inorganicarsenic.[2] Food is a source of the less toxic organic arsenic, with the predominant source being seafood.Inorganic arsenic trioxide is a component of geologic formations and can be washed out into the ground water.Arsenic poisoning can be related to human activities such as mining and ore smelting but is more often associatedwith dissolved solids naturally endemic in the aquifer environment. Unlike the organic form, inorganic arsenic isquite harmful even in minute quantities.

KineticsThe two forms of inorganic arsenic, reduced (trivalent As (III)) and oxidized (pentavalent As(V)), can be absorbed,and accumulated in tissues and body fluids.[3] In the liver, the metabolism of arsenic involves enzymatic andnon-enzymatic methylation, the most frequently excreted metabolite (≥ 90%) in the urine of mammals isdimethylarsinic acid(or Cacodylic acid) (DMA(V)).[4] Dimethylarsenic acid is also known as Agent Blue and wasused as herbicide in the American war in the South-East Asian country of Viet Nam.In humans inorganic arsenic is reduced nonenzymatically from pentoxide to trioxide, using glutathione (GSH) or it ismediated by enzymes. Reduction of arsenic pentoxide to arsenic trioxide increases its toxicity and bio availability, .Methylation occurs through methyltransferase enzymes. S-adenosylmethionine (SAM) may serve as methyl donor.Various pathways are used, the principal route being dependent on the current environment of the cell.[5] Resultingmetabolites are monomethylarsonous acid (MMA(III)) and dimethylarsinous acid (DMA(III)).Methylation had been regarded as a detoxification process. While in fact reduction from +5 As to +3 As may beconsidered as a bioactivation instead.[6] Another suggestion is that methylation might be a detoxification if "As[III]intermediates are not permitted to accumulate" because the pentavalent organoarsenics have a lower affinity to thiolgroups than inorganic pentavalent arsenics.[5] Gebel (2002) stated that methylation is a detoxification throughaccelerated excretion.[7] With regard to carcinogenicity it has been suggested that methylation should be regarded asa toxification.[8] [9] [10]

Arsenic, especially +3 As, binds to single, but with higher affinity to vicinal sulfhydryl groups, thus reacts with a variety of proteins and inhibits their activity. It was also proposed that binding of arsenite at nonessential sites might contribute to detoxification.[11] Arsenite inhibits members of the disulfide oxidoreductase family like glutathione

Arsenic toxicity 36

reductase[12] and thioredoxin reductase.[13]

The remaining unbound arsenic (≤ 10%) accumulates in cells, which over time may lead to skin, bladder, kidney,liver, lung, and prostate cancers.[4] Other forms of arsenic toxicity in humans have been observed in blood, bonemarrow, cardiac, central nervous system, gastrointestinal, gonadal, kidney, liver, pancreatic, and skin tissues.[4]

MechanismArsenite inhibits not only the formation of Acetyl-CoA but also the enzyme succinic dehydrogenase. Arsenate canreplace phosphate in many reactions. It is able to form Glc-6-Arsenate in vitro; therefore it has been argued thathexokinase could be inhibited.[14] (Eventually this may be a mechanism leading to muscle weakness in chronicarsenic poisoning.) In the glyceraldehyde-3-P-dehydrogenase reaction arsenate attacks the enzyme-bound thioester.The formed 1-arseno-3-phosphoglycerate is unstable and hydrolyzes spontaneously. Thus, ATP formation inGlycolysis is inhibited while bypassing the phosphoglycerate kinase reaction. (Moreover, the formation of2,3-bisphosphoglycerate in erythrocytes might be affected, followed by a higher oxygen affinity of hemoglobin andsubsequently enhanced cyanosis) As shown by Gresser (1981), submitochondrial particles synthesizeAdenosine-5’-diphosphate-arsenate from ADP and arsenate in presence of succinate. Thus, by a variety ofmechanisms arsenate leads to an impairment of cell respiration and subsequently diminished ATP formation.[15] Thisis consistent with observed ATP depletion of exposed cells and histopathological findings of mitochondrial and cellswelling, glycogen depletion in liver cells and fatty change in liver, heart and kidney.Experiments demonstrated enhanced arterial thrombosis in a rat animal model, elevations of serotonin levels,thromboxane A[2] and adhesion proteins in platelets, while human platelets showed similar responses.[16] The effecton vascular endothelium may eventually be mediated by the arsenic-induced formation of nitric oxide. It wasdemonstrated that +3 As concentrations substantially lower than concentrations required for inhibition of thelysosomal protease cathepsin L in B cell line TA3 were sufficient to trigger apoptosis in the same B cell line, whilethe latter could be a mechanism mediating immunosuppressive effects.[17]

CarcinogenicityIt is still a matter of debate whether DNA repair inhibition or alterations in the status of DNA methylation areresponsible for the carcinogenic potential of As. As vicinal sulfhydryl groups are frequently found in DNA-bindingproteins, transcription factors and DNA-repair proteins, interaction of arsenic with these molecules appears to belikely. However, in vitro, most purified DNA repair enzymes are rather insensitive to As, but in cell culture, Asproduces a dose-dependant decrease of DNA ligase activity. This might indicate that inhibition of DNA repair is anindirect effect due to changes in cellular redox levels or alterated signal transduction and consequent geneexpression.[18] In spite of its carcinogenicity, the potential of arsenic to induce point mutations is weak. Ifadministered with point mutagens it enhances the frequency of mutations in a syngergistic way.[19]

Its comoutagenic effects may be explained by interference with base and nucleotide excision repair, eventuallythrough interaction with zinc finger structures.[20] DMA showed to effectuate DNA single stand breaks resultingfrom inhibition of repair enzymes at levels of 5 to 100 mM in human epithelial type II cells.[21] [22]

+3 MMA and +3 DMA were also shown to be directly genotoxic by effectuating scissions in supercoiled ΦX174DNA.[23] Increased arsenic exposure is associated with an increased frequency of chromosomal aberrations,[24]

micronuclei[25] [26] and sister-chromatid exchanges. An explanation for chromosomal aberrations is the sensitivity ofthe protein tubulin and the mitotic spindle to arsenic. Histological observations confirm effects on cellular integrity,shape and locomotion.[27]

+3 DMA is able to form reactive oxygen species (ROS) by reaction with molecular oxygen. Resulting metabolites are the dimethylarsenic radical and the dimethylarsenic peroxyl radical.[28] Both +5 DMA and +3 DMA were shown to release iron from horse spleen as well as from human liver ferritin if ascorbic acid was administered

Arsenic toxicity 37

simultaneously. Thus, formation of ROS can be promoted.[29] Moreover, Arsenic could cause oxidative stress bydepleting the cell’s antioxidants, especially the ones containing thiol groups. The accumulation of ROS like the citedabove and hydroxyl radicals, superoxide radicals and hydrogen peroxides causes aberrant gene expression at lowconcentrations and lesions of lipids, proteins and DNA in higher concentrations which eventually lead to cellulardeath. In a rat animal model, urine levels of 8-hydroxy-2’-desoxyguanosine (as a biomarker of ROS DNA damage)were measured after treatment with DMA. In comparison to control levels, they turned out to be significantlyincreased.[30] This theory is further supported by a cross-sectional study which found elevated mean serum lipidperoxides (LPO) in the As exposed individuals which correlated with blood levels of inorganic arsenic andmethylated metabolites and inversely correlated with nonprotein sulfhydryl (NPSH) levels in whole blood.[31]

Another study found an association of As levels in whole blood with the level of reactive oxidants in plasma and aninverse relationship with plasma antioxidants.[32] A finding of the latter study indicates that methylation might in factbe a detoxification pathway with regard to oxidative stress: the results showed that the lower the As methylationcapacity was, the lower the level of plasma antioxidant capacity. As reviewed by Kitchin (2001), the oxidative stresstheory provides an explanation for the preferred tumor sites connected with arsenic exposure.[8] Considering that ahigh partial pressure of oxygen is present in lungs and +3 DMA is excreted in gaseous state via the lungs this seemsto be a plausible mechanism for special vulnerability. The fact that DMA is produced by methylation in the liver,excreted via the kidneys and latter on stored in the bladder accounts for the other tumor localizations.Regarding DNA methylation, some studies suggest interaction of As with methyltransferases which leads to aninactivation of tumor suppressor genes through hypermethylation, others state that hypomethylation might occur dueto a lack of SAM resulting in aberrant gene activation.[33] An experiment by Zhong et al. (2001) witharsenite-exposed human lung A549, kidney UOK123, UOK109 and UOK121 cells isolated eight different DNAfragments by methylation-sensitive arbitrarily primed PCR.[34] It turned out that six of the fragments were hyper-and two of them were hypomethylated.[34] Higher levels of DNA methltransferase mRNA and enzyme activity werefound.[34]

Kitchin (2001) proposed a model of altered growth factors which lead to cell proliferation and thus tocarcinogenesis.[8] From observations it is known that chronic low-dose arsenic poisoning can lead to increasedtolerance to its acute toxicity.[19] [35] MRP1-overexpressing lung tumor GLC4/Sb30 cells poorly accumulate arseniteand arsenate. This is mediated through MRP-1 dependent efflux.[36] The efflux requires GSH, but no As-GSHcomplex formation.[37]

Although a lot of mechanisms have been proposed, no definite model can be given for the mechanisms of chronicarsenic poisoning. The prevailing events of toxicity and carcinogenicity might be quite tissue-specific. Currentconsensus on the mode of carcinogenesis is that it acts primarily as a tumor promoter. Its co-carcinogenicity has beendemonstrated in several models. However, the finding of several studies that chronically arsenic-exposed Andeanpopulations (as most extremely exposed to UV-light) do not develop skin cancer with chronic arsenic exposure, ispuzzling.[38]

Heat shock responseAnother aspect is the similarity of arsenic effects to the heat shock response. Short-term arsenic exposure has effectson signal transduction inducing heat shock proteins with masses of 27,60,70,72,90,110 kDa as well asmetallotionein, ubiquitin, mitogen-activated [MAP] kinases, extracellular regulated kinase [ERK], c-jun terminalkinases [JNK] and p38.[27] [39] Via JNK and p38 it activates c-fos, c-jun and egr-1 which are usually activated bygrowth factors and cytokines[27] [40] [41] The effects are largely dependant on the dosing regime and may be as wellinversed.As shown by some experiments reviewed by Del Razo (2001), ROS induced by low levels of inorganic arsenic increase the transcription and the activity of the activator protein 1 (AP-1) and the nuclear factor-κB (NF-κB) (maybe enhanced by elevated MAPK levels), which results in c-fos/c-jun activation, over-secretion of

Arsenic toxicity 38

pro-inflammatory and growth promoting cytokines stimulating cell proliferation.[39] [42] Germolec et al. (1996)found an increased cytokine expression and cell proliferation in skin biopsies from individuals chronically exposedto arsenic-contaminated drinking water.[43]

Increased AP-1 and NF-κB obviously also result in an up-regulation of mdm2 protein, which decreases p53 proteinlevels.[44] Thus, taking into account p53’s function, a lack of it could cause a faster accumulation of mutationscontributing to carcinogenesis. However, high levels of inorganic arsenic inhibit NF-κB activation and cellproliferation. An experiment of Hu et al. (2002) demonstrated increased binding activity of AP-1 and NF-κB afteracute (24 h) exposure to +3 sodium arsenite, whereas long-term exposure (10–12 weeks) yielded the oppositeresult.[45] The authors conclude that the former may be interpreted as a defense response while the latter could leadto carcinogenesis.[45] As the contradicting findings and connected mechanistic hypotheses indicate, there is adifference in acute and chronic effects of arsenic on signal transduction which is not clearly understood yet.

Oxidative stressStudies have demonstrated that the oxidative stress generated by arsenic may disrupt the signal transductionpathways of the nuclear transcriptional factors PPAR’s, AP-1, and NF-κB,[4] [45] [46] as well as the pro-inflammatorycytokines IL-8 and TNF-α.[4] [45] [46] [47] [48] [49] [50] [51] The interference of oxidative stress with signal transductionpathways may affect physiological processes associated with cell growth, metabolic syndrome X, glucosehomeostasis, lipid metabolism, obesity, insulin resistance, inflammation, and diabetes-2.[52] [53] [54] Recent scientificevidence has elucidated the physiological roles of the PPAR’s in the ω- hydroxylation of fatty acids and theinhibition of pro-inflammatory transcription factors (NF-κB 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 factors.[4] [47] [52] [54] [55]

Epidemiological studies have suggested a correlation between chronic consumption of drinking water contaminatedwith arsenic and the incidence of Type 2-diabetes.[4] The human liver after exposure to therapeutic drugs may exhibithepatic non-cirrhotic portal hypertension, fibrosis, and cirrhosis.[4] However, the literature provides insufficientscientific evidence to show cause and effect between arsenic and the onset of diabetes mellitus Type 2.[4]

References[1] Klaassen, Curtis; Watkins, John (2003). Casarett and Doull's Essentials of Toxicology. McGraw-Hill. p. 512. ISBN 978-0-07-138914-3.[2] Medicine net.com july,2 2010 definition of arsenic[3] Ueki K, Kondo T, Tseng YH, Kahn CR (July 2004). "Central role of suppressors of cytokine signaling proteins in hepatic steatosis, insulin

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[4] Vigo, J. B., and J. T. Ellzey (2006). "Effects of Arsenic Toxicity at the Cellular Level: A Review". Texas Journal of Microscopy 37 (2):45–49.

[5] Thompson DJ (September 1993). "A chemical hypothesis for arsenic methylation in mammals". Chemico-biological Interactions 88 (2-3):89–14. doi:10.1016/0009-2797(93)90086-E. PMID 8403081.

[6] Vahter M, Concha G (July 2001). "Role of metabolism in arsenic toxicity". Pharmacology & Toxicology 89 (1): 1–5.doi:10.1034/j.1600-0773.2001.d01-128.x. PMID 11484904.

[7] Gebel TW (October 2002). "Arsenic methylation is a process of detoxification through accelerated excretion". International Journal ofHygiene and Environmental Health 205 (6): 505–8. doi:10.1078/1438-4639-00177. PMID 12455273.

[8] Kitchin KT (May 2001). "Recent advances in arsenic carcinogenesis: modes of action, animal model systems, and methylated arsenicmetabolites". Toxicology and Applied Pharmacology 172 (3): 249–61. doi:10.1006/taap.2001.9157. PMID 11312654.

[9] Kenyon EM, Fea M, Styblo M, Evans MV (2001). "Application of modelling techniques to the planning of in vitro arsenic kinetic studies".Alternatives to Laboratory Animals 29 (1): 15–33. PMID 11178572.

[10] Styblo M, Thomas DJ (April 2001). "Selenium modifies the metabolism and toxicity of arsenic in primary rat hepatocytes". Toxicology andApplied Pharmacology 172 (1): 52–61. doi:10.1006/taap.2001.9134. PMID 11264023.

[11] Aposhian HV, Maiorino RM, Dart RC, Perry DF (May 1989). "Urinary excretion of meso-2,3-dimercaptosuccinic acid in human subjects".Clinical Pharmacology and Therapeutics 45 (5): 520–6. doi:10.1038/clpt.1989.67. PMID 2541962.

Arsenic toxicity 39

[12] Rodríguez VM, Del Razo LM, Limón-Pacheco JH, et al. (March 2005). "Glutathione reductase inhibition and methylated arsenicdistribution in Cd1 mice brain and liver". Toxicological Sciences 84 (1): 157–66. doi:10.1093/toxsci/kfi057. PMID 15601678.

[13] Rom, William N.; Markowitz, Steven B. (2007). Environmental and Occupational Medicine (http:/ / books. google. com/?id=H4Sv9XY296oC& pg=RA2-PA1014& lpg=RA2-PA1014#PRA2-PA1014,M1). Lippincott Williams & Wilkins. pp. 1014–5.ISBN 978-0-7817-6299-1. .

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[16] Lee MY, Bae ON, Chung SM, Kang KT, Lee JY, Chung JH (March 2002). "Enhancement of platelet aggregation and thrombus formationby arsenic in drinking water: a contributing factor to cardiovascular disease". Toxicology and Applied Pharmacology 179 (2): 83–8.doi:10.1006/taap.2001.9356. PMID 11884240.

[17] Harrisson JW, Packman EW, Abbott DD (February 1958). "Acute oral toxicity and chemical and physical properties of arsenic trioxides".A.M.A. Archives of Industrial Health 17 (2): 118–23. PMID 13497305.

[18] Hu Y, Su L, Snow ET (September 1998). "Arsenic toxicity is enzyme specific and its affects on ligation are not caused by the directinhibition of DNA repair enzymes". Mutation Research 408 (3): 203–18. doi:10.1016/S0921-8777(98)00035-4. PMID 9806419.

[19] Gebel TW (March 2001). "Genotoxicity of arsenical compounds". International Journal of Hygiene and Environmental Health 203 (3):249–62. doi:10.1078/S1438-4639(04)70036-X. PMID 11279822.

[20] Hartwig A, Schwerdtle T (February 2002). "Interactions by carcinogenic metal compounds with DNA repair processes: toxicologicalimplications". Toxicology Letters 127 (1-3): 47–54. doi:10.1016/S0378-4274(01)00482-9. PMID 12052640.

[21] Yamanaka K, Hayashi H, Tachikawa M, et al. (November 1997). "Metabolic methylation is a possible genotoxicity-enhancing process ofinorganic arsenics". Mutation Research 394 (1-3): 95–101. PMID 9434848.

[22] Bau DT, Wang TS, Chung CH, Wang AS, Wang AS, Jan KY (October 2002). "Oxidative DNA adducts and DNA-protein cross-links are themajor DNA lesions induced by arsenite". Environmental Health Perspectives 110 (Suppl 5): 753–6. PMC 1241239. PMID 12426126.

[23] Mass MJ, Tennant A, Roop BC, et al. (April 2001). "Methylated trivalent arsenic species are genotoxic". Chemical Research in Toxicology14 (4): 355–61. doi:10.1021/tx000251l. PMID 11304123.

[24] Mäki-Paakkanen J, Kurttio P, Paldy A, Pekkanen J (1998). "Association between the clastogenic effect in peripheral lymphocytes andhuman exposure to arsenic through drinking water". Environmental and Molecular Mutagenesis 32 (4): 301–13.doi:10.1002/(SICI)1098-2280(1998)32:4<301::AID-EM3>3.0.CO;2-I. PMID 9882004.

[25] Warner ML, Moore LE, Smith MT, Kalman DA, Fanning E, Smith AH (1994). "Increased micronuclei in exfoliated bladder cells ofindividuals who chronically ingest arsenic-contaminated water in Nevada" (http:/ / cebp. aacrjournals. org/ cgi/ pmidlookup?view=long&pmid=7827589). Cancer Epidemiology, Biomarkers & Prevention 3 (7): 583–90. PMID 7827589. .

[26] Gonsebatt ME, Vega L, Salazar AM, et al. (June 1997). "Cytogenetic effects in human exposure to arsenic". Mutation Research 386 (3):219–28. doi:10.1016/S1383-5742(97)00009-4. PMID 9219560.

[27] Bernstam L, Nriagu J (2000). "Molecular aspects of arsenic stress". Journal of Toxicology and Environmental Health. Part B, CriticalReviews 3 (4): 293–322. doi:10.1080/109374000436355. PMID 11055208.

[28] Yamanaka K, Hoshino M, Okamoto M, Sawamura R, Hasegawa A, Okada S (April 1990). "Induction of DNA damage by dimethylarsine, ametabolite of inorganic arsenics, is for the major part likely due to its peroxyl radical". Biochemical and Biophysical ResearchCommunications 168 (1): 58–64. doi:10.1016/0006-291X(90)91674-H. PMID 2158319.

[29] Ahmad R, Alam K, Ali R (February 2000). "Antigen binding characteristics of antibodies against hydroxyl radical modified thymidinemonophosphate". Immunology Letters 71 (2): 111–5. doi:10.1016/S0165-2478(99)00177-7. PMID 10714438.

[30] Yamanaka K, Mizol M, Kato K, Hasegawa A, Nakano M, Okada S (May 2001). "Oral administration of dimethylarsinic acid, a mainmetabolite of inorganic arsenic, in mice promotes skin tumorigenesis initiated by dimethylbenz(a)anthracene with or without ultraviolet B as apromoter". Biological & Pharmaceutical Bulletin 24 (5): 510–4. doi:10.1248/bpb.24.510. PMID 11379771.

[31] Pi J, Yamauchi H, Kumagai Y, et al. (April 2002). "Evidence for induction of oxidative stress caused by chronic exposure of Chineseresidents to arsenic contained in drinking water". Environmental Health Perspectives 110 (4): 331–6. doi:10.1289/ehp.02110331.PMC 1240794. PMID 11940449.

[32] Wu MM, Chiou HY, Wang TW, et al. (October 2001). "Association of blood arsenic levels with increased reactive oxidants and decreasedantioxidant capacity in a human population of northeastern Taiwan". Environmental Health Perspectives (Brogan &#38) 109 (10): 1011–7.doi:10.2307/3454955. JSTOR 3454955. PMC 1242077. PMID 11675266.

[33] Goering PL, Aposhian HV, Mass MJ, Cebrián M, Beck BD, Waalkes MP (May 1999). "The enigma of arsenic carcinogenesis: role ofmetabolism". Toxicological Sciences 49 (1): 5–14. doi:10.1093/toxsci/49.1.5. PMID 10367337.

[34] Zhong CX, Mass MJ (July 2001). "Both hypomethylation and hypermethylation of DNA associated with arsenite exposure in cultures ofhuman cells identified by methylation-sensitive arbitrarily-primed PCR". Toxicology Letters 122 (3): 223–34.doi:10.1016/S0378-4274(01)00365-4. PMID 11489357.

[35] Brambila EM, Achanzar WE, Qu W, Webber MM, Waalkes MP (September 2002). "Chronic arsenic-exposed human prostate epithelialcells exhibit stable arsenic tolerance: mechanistic implications of altered cellular glutathione and glutathione S-transferase". Toxicology andApplied Pharmacology 183 (2): 99–107. doi:10.1016/S0041-008X(02)99468-8. PMID 12387749.

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[36] Vernhet L, Allain N, Bardiau C, Anger JP, Fardel O (January 2000). "Differential sensitivities of MRP1-overexpressing lung tumor cells tocytotoxic metals". Toxicology 142 (2): 127–34. doi:10.1016/S0300-483X(99)00148-1. PMID 10685512.

[37] Salerno M, Petroutsa M, Garnier-Suillerot A (April 2002). "The MRP1-mediated effluxes of arsenic and antimony do not requirearsenic-glutathione and antimony-glutathione complex formation". Journal of Bioenergetics and Biomembranes 34 (2): 135–45.doi:10.1023/A:1015180026665. PMID 12018890.

[38] Gebel T (April 2000). "Confounding variables in the environmental toxicology of arsenic". Toxicology 144 (1-3): 155–62.doi:10.1016/S0300-483X(99)00202-4. PMID 10781883.

[39] Del Razo LM, Quintanilla-Vega B, Brambila-Colombres E, Calderón-Aranda ES, Manno M, Albores A (December 2001). "Stress proteinsinduced by arsenic". Toxicology and Applied Pharmacology 177 (2): 132–48. doi:10.1006/taap.2001.9291. PMID 11740912.

[40] Cavigelli M, Li WW, Lin A, Su B, Yoshioka K, Karin M (November 1996). "The tumor promoter arsenite stimulates AP-1 activity byinhibiting a JNK phosphatase". The EMBO Journal 15 (22): 6269–79. PMC 452450. PMID 8947050.

[41] Ludwig S, Hoffmeyer A, Goebeler M, et al. (January 1998). "The stress inducer arsenite activates mitogen-activated protein kinasesextracellular signal-regulated kinases 1 and 2 via a MAPK kinase 6/p38-dependent pathway". The Journal of Biological Chemistry 273 (4):1917–22. doi:10.1074/jbc.273.4.1917. PMID 9442025.

[42] Simeonova PP, Luster MI (2000). "Mechanisms of arsenic carcinogenicity: genetic or epigenetic mechanisms?". Journal of EnvironmentalPathology, Toxicology and Oncology 19 (3): 281–6. PMID 10983894.

[43] Germolec DR, Yoshida T, Gaido K, et al. (November 1996). "Arsenic induces overexpression of growth factors in human keratinocytes".Toxicology and Applied Pharmacology 141 (1): 308–18. doi:10.1006/taap.1996.0288. PMID 8917704.

[44] Hamadeh HK, Vargas M, Lee E, Menzel DB (September 1999). "Arsenic disrupts cellular levels of p53 and mdm2: a potential mechanismof carcinogenesis". Biochemical and Biophysical Research Communications 263 (2): 446–9. doi:10.1006/bbrc.1999.1395. PMID 10491313.

[45] Hu Y, Jin X, Snow ET (July 2002). "Effect of arsenic on transcription factor AP-1 and NF-κB DNA binding activity and related geneexpression". Toxicology Letters 133 (1): 33–45. doi:10.1016/S0378-4274(02)00083-8. PMID 12076508.

[46] Walton FS, Harmon AW, Paul DS, Drobná Z, Patel YM, Styblo M (August 2004). "Inhibition of insulin-dependent glucose uptake bytrivalent arsenicals: possible mechanism of arsenic-induced diabetes". Toxicology and Applied Pharmacology 198 (3): 424–33.doi:10.1016/j.taap.2003.10.026. PMID 15276423.

[47] Black PH (October 2003). "The inflammatory response is an integral part of the stress response: Implications for atherosclerosis, insulinresistance, type II diabetes and metabolic syndrome X". Brain, Behavior, and Immunity 17 (5): 350–64. doi:10.1016/S0889-1591(03)00048-5.PMID 12946657.

[48] Carey AL, Lamont B, Andrikopoulos S, Koukoulas I, Proietto J, Febbraio MA (March 2003). "Interleukin-6 gene expression is increased ininsulin-resistant rat skeletal muscle following insulin stimulation". Biochemical and Biophysical Research Communications 302 (4): 837–40.doi:10.1016/S0006-291X(03)00267-5. PMID 12646246.

[49] Dandona P, Aljada A, Bandyopadhyay A (January 2004). "Inflammation: the link between insulin resistance, obesity and diabetes". Trendsin Immunology 25 (1): 4–7. doi:10.1016/j.it.2003.10.013. PMID 14698276.

[50] Fischer CP, Perstrup LB, Berntsen A, Eskildsen P, Pedersen BK (November 2005). "Elevated plasma interleukin-18 is a marker ofinsulin-resistance in type 2 diabetic and non-diabetic humans". Clinical Immunology 117 (2): 152–60. doi:10.1016/j.clim.2005.07.008.PMID 16112617.

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[52] Kota BP, Huang TH, Roufogalis BD (February 2005). "An overview on biological mechanisms of PPARs". Pharmacological Research 51(2): 85–94. doi:10.1016/j.phrs.2004.07.012. PMID 15629253.

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Carancas impact event 41

Carancas impact event

impact site

Location in the Puno Region in Peru where the meteorite struck.16°39′52″S 69°02′38″W[1]

The Carancas impact event refers to the fall of the Carancas chondritic meteorite on September 15, 2007, near thevillage of Carancas in Peru, close to the Bolivian border and Lake Titicaca.[2] [3] [4] [5] The impact created a craterand scorched earth around its location.[6] A local official, Marco Limache, said that “boiling water started coming outof the crater, and particles of rock and cinders were found nearby”, as “fetid, noxious” gases spewed from thecrater.[7] [8]

After the impact, villagers who had approached the impact site grew sick from a then-unexplained illness, with awide array of symptoms.[9] [10] [11] Two days later, Peruvian scientists confirmed that there had indeed been ameteorite strike, quieting widespread speculation that it may have been a geophysical rather than a celestial event. Atthat point, no further information on the cause of the mystery illness was known.[5] The ground water in the localarea is known to contain arsenic compounds, and the illness is now believed to have been caused by arsenicpoisoning incurred when residents of the area inhaled the vapor of the boiling arsenic-contaminated water.[12]

The impact eventAt 11:45 local time (16:45 GMT) on September 15, 2007, a chondritic meteorite crashed near the village of Carancasin the Puno Region, Peru, near the Bolivian border and Lake Titicaca (see map box on right).[2] [] [4] [5] The impactcreated a crater larger than 4.5 m (15 ft) deep, 13 m (43 ft) wide, with visibly scorched earth around the impactsite.[6] A local official, Marco Limache, said that “boiling water started coming out of the crater, and particles of rockand cinders were found nearby”, as “fetid, noxious” gases spewed from the crater.[7] [8] The crater size was given as13.80 by 13.30 meters (45.28 by 43.64 feet), with its greatest dimensions in an east-west direction. The fireball hadbeen observed by the locals as strongly luminous with a smoky tail, and seen from just 1000 meters (3280.84 ft)above the ground. The object moved in a direction toward N030E. The strong explosion at impact shattered thewindows of the local health center 1-kilometer (0.62 mi) away. A smoke column was formed at the site that lastedseveral minutes, and boiling water was seen in the crater.Soon after the impact, over 600 villagers who had visited the site began to fall ill from unexplained causes, including symptoms of dermal injuries, nausea, headaches, diarrhea and vomiting.[9] [] [11] On September 20, Peruvian scientists confirmed that there had been a meteorite strike, but no further information on the cause of the illnesses was known.[5] Impact crater specialists have called the impact unusual, and have stated that the meteorite was at least 3 m (10 ft) in diameter before breaking up.[13] The ground water in the area is known to contain arsenic compounds,

Carancas impact event 42

and the illness was believed to have been caused by arsenic poisoning incurred when residents of the area inhaled thevapor of the boiling arsenic-contaminated water.[12] However, further investigations have led to the conclusion thatthe arsenic content in the groundwater did not differ from that of the local drinking supply, and that the illnessreported was likely caused by the vaporization of troilite, a sulfur-bearing compound present within the meteorite inlarge amounts, and which would have melted at relatively low temperatures and high pressures created by such animpact.According to cosmochemist Larry Grossman of the University of Chicago, the aerial lights and explosions reportedwere consistent with extraterrestrial material.[14]

The loud noise and explosive impact originally led Peruvians to think that the neighboring nation of Chile hadlaunched an attack.[15]

Nature of the object

27.70g fragment of the Carancas meteorite fallrecovered several days after the fall. The scale

cube is 1cm3

A report from three geologists at Peru’s Geophysics Institute wasreleased on Thursday, September 20. Astrophysicist Jose Ishitsukaconfirmed that there had been a meteorite strike.[5] [13]

On September 20, the X-Ray Laboratory at the Faculty of GeologicalSciences, Mayor de San Andres University, La Paz, Bolivia, publisheda report of their analysis of a small sample of material recovered fromthe impact site. They detected iron, nickel, cobalt, and traces of iridium— elements characteristic of the elemental composition of meteorites.The quantitative proportions of silicon, aluminum, potassium, calcium,magnesium, and phosphorus are incompatible with rocks that arenormally found at the surface of the Earth.[16]

INGEMMET (Instituto Geológico Minero y Metalúrgico) of Perureleased internally on September 21 a report on the Carancas meteoritefall. The release of the document to the public was delayed for oneweek. The researchers found that the fragments from the crater zone had a chondritic texture and the followingmineral composition: pyroxene (1) 40%, olivine 20%, feldspar 10%, pyroxene (2) 10%; kamacite 15%, troilite 5%,and traces of chromite and native copper. Kamacite occurs naturally only in meteorites.

The official classification of the Carancas meteorite, accepted by the Meteoritical Society[17] was done by a team ofscientists working at the University of Arizona. The meteorite is an ordinary chondrite, an H chondrite breccia,containing clasts of petrologic types 4 to 5. The formal classification is H4-5. The meteoroid had experienced aconsiderable amount of shock before its ultimate encounter with Earth. Further results are expected, and material isalso going to be studied by NASA, British, and Japanese researchers according to media reports.[1]

Illness complaintsAfterwards, local townspeople went to see what happened, and 100 to 200 people who got near to the meteoritecrater soon reported feeling sick.[4] [5] First responding police officers arriving to investigate the scene also fell ill.[18]

After the initial event of September 15, the number of people falling ill increased, requiring physicians to establishauxiliary medical tents for the Carancas health center.[11] Patients were treated for dermal injuries, nausea,headaches, diarrhea and vomiting.[] [11] The death of nearby livestock was also reported.[19] Locals made thedecision to stop drinking from nearby water sources for fear of contamination and authorities considered declaring astate of emergency.[7] [11] Four days after the meteorite impact and the unexplained illness, most villagers reportedhaving recovered.[12]

Carancas impact event 43

Reported details about the event, such as water boiling in the muddy crater for ten minutes from the heat of theimpact, presented a problem for experts. Because the impact site is at a high altitude of more than 3800 m (12467 ft),the meteoroid may not have been slowed down as much as it ordinarily would have been by passage through theEarth’s denser lower atmosphere, and kinetic energy at impact may have been unusually high for a terrestrial impactof an object of this size and mass. Most larger meteorites are cold in their bulk mass when they land on Earth, sincetheir heated outer layers ablate from the objects before impacting.[13] It was later confirmed that the meteorite hadhigh degrees of iron and possessed magnetic properties common to similar metallic objects, which contributed to itscapacity to retain heat during atmospheric entry.[20]

Government responseIn contrast with other international media reports, Peruvian health officials downplayed the incident. Jorge LópezTejada, the Regional Health Director for Puno, Peru, denied any serious medical situation existed. However, a healthbrigade arrived with personnel and medication to the site on September 18, reporting that the odors rising from thecrater were causing medical issues.[21] Earlier, Tejada had stated that the officers were dizzy, nauseous and somewere vomiting.[22]

On September 19, Andina, Peru’s official government news agency, reported that the sick villagers appeared to berecovering somewhat.[23] "They are recovering, there aren't any critical cases. A total of 200 people with differentsymptoms have been seen," stated López Tejada.[23] Government officials also specifically asked people to avoid the"glowing object that fell from the sky."[23]

Suspected etiologyScientists initially ruled out radiation as the cause of the illness. Renan Ramirez of the Peruvian Nuclear EnergyInstitute stated that the medical conditions could have been caused by sulfur, arsenic or other toxins that may havemelted in the extreme heat produced by the meteorite strike.[24] Some unnamed Peruvian sources stated soon afterthe event occurred that it was indeed a meteorite.[4] [25] Later on September 18, a Peruvian vulcanologist stated thatthe impact was caused by a chondrite meteorite arrival.[26]

Some reports indicated initial suspicions that the illnesses may have been psychosomatic in nature.[13] DonYeomans, head of the Near Earth Object Program at NASA’s Jet Propulsion Laboratory in Pasadena, California,said, “Statistically, it’s far more likely to have come from below than from above. The noxious fumes that havesupposedly sickened curious locals who went to examine the crater would seem to indicate hydrothermal activity,such as a local gas explosion, because meteorites don't give off odors.”By September 21, it was believed that the illness was caused by arsenic poisoning. Luisa Macedo of Peru’s Mining,Metallurgy, and Geology Institute said gases were created when the meteorite’s hot surface reacted with anunderground water supply tainted with arsenic. Natural arsenic deposits in ground water are not uncommon insouthern Peru. José Ishitsuka of the Peruvian Geophysics Institute said, “If the meteorite arrives incandescent and ata high temperature because of friction in the atmosphere, hitting water can create a column of steam.”[12] Meteorites,however, often impact the earth at low temperatures, making this an unusual event.[13]

Carancas impact event 44

References[1] Luisa Macedo F. & José Macharé O., INGEMMET, "The Carancas Meteorite Fall, 15 September 2007" (http:/ / www. ingemmet. gob. pe/

paginas/ pl01_quienes_somos. aspx?opcion=320), September 21, 2007. Retrieved October 10, 2007.[2] Planetario Max Schreier "Meteorito por el Desaguadreo" (http:/ / fcpn. umsa. bo/ fcpn/ app?service=page/ Planetarium_PublicationList),

September 24, 2007. Retrieved October 10, 2007.[3] RSOE Emergency and Disaster Information Service, Budapest, Hungary, "Cosmic Event - South-America" (http:/ / hisz. rsoe. hu/ alertmap2/

woalert_read. php?cid=13424& lang=eng), September 18, 2007. Retrieved October 10, 2007.[4] Teresa Cespedes, Reuters, "Peruvians get sick from apparent meteorite crater" (http:/ / uk. reuters. com/ article/ scienceNews/

idUKN1843987520070918), September 18, 2007. Retrieved October 10, 2007.[5] Ed Sutherland, All Headline News, "Experts Confirm Peru Meteorite Site" (http:/ / www. allheadlinenews. com/ articles/ 7008582242),

September 20, 2007. Retrieved October 10, 2007.[6] Rory Carroll, The Guardian UK, "Peru meteorite crash 'causes mystery illness'" (http:/ / www. guardian. co. uk/ space/ article/ 0,,2171920,00.

html), September 18, 2007. Retrieved October 10, 2007.[7] MSNBC, "Villagers fall ill after fireball hits Peru" (http:/ / www. msnbc. msn. com/ id/ 20838944/ ), September 18, 2007. Retrieved October

10, 2007.[8] BBC News, "Scores ill in Peru 'meteor crash'" (http:/ / news. bbc. co. uk/ 2/ hi/ americas/ 7001897. stm), September 18, 2007. Retrieved

October 10, 2007.[9] Lester Haines, The Register, "Peruvian 'meteorite' strike provokes noxious gas attack" (http:/ / www. theregister. co. uk/ 2007/ 09/ 18/

peruvian_gas_attack/ ), September 18, 2007. Retrieved October 10, 2007.[10] Australian Broadcasting Corporation, "Locals fall sick after meteorite lands in Peru" (http:/ / abc. net. au/ news/ stories/ 2007/ 09/ 19/

2037244. htm?section=justin), September 18, 2007. Retrieved October 10, 2007.[11] Living in Peru, LIP-ir, "Doctors Aid in Rising Number of Illnesses after Meteorite Crash" (http:/ / www. livinginperu. com/ news/ 4732),

September 19, 2007. Retrieved October 10, 2007.[12] José Orozco, National Geographic News, "Meteor Crash in Peru Caused Mysterious Illness" (http:/ / news. nationalgeographic. com/ news/

2007/ 09/ 070921-meteor-peru. html), September 21, 2007. Retrieved October 10, 2007.[13] Monty Hayes, Associated Press/Google, "Meteorite Likely Caused Crater in Peru" (http:/ / ap. google. com/ article/

ALeqM5isWWHSxCh_u0yUNU9Gpk1qfg996A), September 20, 2007. Retrieved October 10, 2007.[14] Andrea Thompson, Space.com, "Scientists Doubt Meteorite Sickened Peruvians " (http:/ / www. space. com/ scienceastronomy/

070919_peru_meteorite. html), September 19, 2007. Retrieved October 10, 2007.[15] Liubomir Fernandez and Patrick J. McDonnell, Los Angeles Times, "Meteorite causes a stir in Peru" (http:/ / www. latimes. com/ news/

nationworld/ world/ la-fg-meteor21sep21,1,5605341. story?ctrack=1& cset=true), September 21, 2007 (registration is required). RetrievedOctober 10, 2007.

[16] Mario Blanco Cazas, "Informe Laboratorio de Rayos X — FRX-DRX" (http:/ / fcpn. umsa. bo/ fcpn/ app?service=external/PublicationDownload& sp=227) (in Spanish), Universidad Mayor de San Andres, Facultad de Ciencias Geologicas, Instituto deInvestigaciones Geologicas y del Medio Ambiente, La Paz, Bolivia, September 20, 2007. Retrieved October 10, 2007.

[17] Meteoritical Bulletin: Entry for Carancas (http:/ / www. lpi. usra. edu/ meteor/ index. php?code=45817)[18] Agence France Presse, "Peruvian scientists probe fumes from meteorite crater" (http:/ / afp. google. com/ article/

ALeqM5gDC5TNcMdGoRuHqJTzPpeyU8ZJ2Q), September 18, 2007 (first published report of event). Retrieved October 10, 2007.[19] CBC News, "600 sick in Peru after 'meteorite' crashes" (http:/ / www. cbc. ca/ world/ story/ 2007/ 09/ 19/ peru-meteorite. html), September

19, 2007. Retrieved October 10, 2007.[20] Living in Peru, LIP-ir, "Astrophysicist in Peru Identifies Properties in Meteorite" (http:/ / www. livinginperu. com/

news-4758-environmentnature-astrophysicist-peru-identifies-properties-meteorite), September 21, 2007, 17:00. Retrieved October 10, 2007.[21] Living in Peru, LIP-ir, "Regional Health Director Reports on Health Near Meteorite Crash Site" (http:/ / www. livinginperu. com/

news-4728-health-peru-regional-health-director-reports-health-near-meteorite-crash-site), September 18, 2007, 15:00. Retrieved October 10,2007.

[22] Living in Peru, LIP-ir, "Police Officers Hospitalized After Collecting Meteorite Samples in Peru" (http:/ / www. livinginperu. com/news-4724-environmentnature-police-officers-hospitalized-after-collecting-meteorite-samples-peru), September 18, 2007, 11:00. RetrievedOctober 10, 2007.

[23] Living in Peru, LIP-ir, "Peru's Geophysicists Test for Radiation, Meteorite Sickness Caused by Toxic Gases" (http:/ / www. livinginperu.com/ news-4736-health-perus-geophysicists-test-for-radiation-meteorite-sickness-caused-by-toxic-gases), September 19, 2007, 16:00.Retrieved October 10, 2007.

[24] Agence France Presse, "Peru meteor illness deepens" (http:/ / www. theage. com. au/ news/ world/ peru-meteor-illness-deepens/ 2007/ 09/18/ 1189881490291. html), September 18, 2007. Retrieved October 10, 2007.

[25] Associated Press, " Peru Links Illness to Supposed Meteorite" (http:/ / ap. google. com/ article/ALeqM5isWWHSxCh_u0yUNU9Gpk1qfg996A), September 18, 2007. Retrieved October 10, 2007.

[26] Living in Peru, LIP-ir, "Scientist Confirms Meteorite in Puno, Peru is a Chondrite" (http:/ / www. livinginperu. com/news-4730-environmentnature-scientist-confirms-meteorite-in-puno-peru-is-a-chondrite), September 18, 2007, 18:30. Retrieved October 10,2007.

Carancas impact event 45

External links• Brief account on the impact event and photos of Carancas meteorite fragments (http:/ / www. meteorite-recon.

com/ en/ meteorite_carancas. htm)• Brown Scientist Answers How Peruvian Meteorite Made It to Earth (http:/ / media. www. browndailyherald. com/

media/ storage/ paper472/ news/ 2008/ 04/ 04/ Features/ Professor. Solves. A. Meteor. Mystery-3304236. shtml)

Grainger challengeThe Grainger challenge is a scientific competition to find an economical way to remove arsenic fromarsenic-contaminated groundwater. This competition is being funded by the United States National Academy ofEngineering and the Grainger Foundation and is meant to help provide safe drinking water to countries such asBangladesh, India, and Cambodia.In 2007, the winner of the Gold Award ($1,000,000) was Dr. Abul Hussam, for his invention of the Sono arsenicfilter. The Silver Award ($200,000) was awarded to Dr. Arup K Sengupta for his invention and implementation ofArsenXnp [1] hybrid anion exchange (HAIX) resin.[2] The Children's Safe Drinking Water Program at Procter &Gamble Co. (P&G), Cincinnati, received the Bronze Award of US$ 100,000 for the PUR™ Purifier of Water [3]

coagulation and flocculation water treatment system.

External links• Grainger challenge page at the National Academy of Engineering [4]

• Grainger Foundation [5]

References[1] http:/ / www. systematixusa. com/ products/ media/ active_media/ arsenx. htm[2] Pfitzer, Kurt. "Arsenic-removal system wins NAE award" (http:/ / www3. lehigh. edu/ News/ RCEASnews_story. asp?iNewsID=2013).

Arsenic-removal system wins NAE award. Lehigh University. . Retrieved 23 April 2011.[3] http:/ / www. purwater. com/ clean-drinking-water-for-the-world. html[4] http:/ / www. nae. edu/ nae/ grainger. nsf[5] http:/ / www. ee. washington. edu/ energy/ apt/ grainger/

Marsh test 46

Marsh testThe Marsh test is a highly sensitive method in the detection of arsenic, especially useful in the field of forensictoxicology when arsenic was used as a poison. It was developed by the chemist James Marsh and first published in1836.Arsenic, in the form of white arsenic trioxide As2O3, was a highly favored poison, for it is odorless, easilyincorporated into food and drink, and before the advent of the Marsh test, untraceable in the body. In France, it cameto be known as poudre de succession ("inheritance powder"). For the untrained, arsenic poisoning would havesymptoms similar to cholera.

Precursor methodsThe first breakthrough in the detection of arsenic poisoning was in 1775 when Carl Wilhelm Scheele discovered away to change arsenic trioxide to garlic-smelling arsine gas (AsH3), by treating it with nitric acid (HNO3) andcombining it with zinc.

As2O3 + 6 Zn + 12 HNO3 → 2 AsH3 + 6 Zn(NO3)2 + 3 H2OIn 1787, Johann Metzger discovered that if arsenic trioxide was heated in the presence of charcoal, a shiny blackpowder (arsenic mirror) would be formed over it. This is the reduction of As2O3 by carbon:

2 As2O3 + 3 C → 3 CO2 + 4 AsIn 1806, Valentin Rose took the stomach of a victim suspected of being poisoned and treated it with potassiumcarbonate (K2CO3), calcium oxide (CaO) and nitric acid. Any arsenic present would appear as arsenic trioxide andthen could be subjected to Metzger's test.However, the most common test (and used even today in water test kits) was discovered by Samuel Hahnemann. Itwould involve combining a sample fluid with hydrogen sulfide (H2S) in the presence of hydrochloric acid (HCl). Ayellow precipitate, arsenic trisulfide (As2S3) would be formed if arsenic were present.

Circumstances and methodologyEven so, these tests have proven not to be sensitive enough. In 1832, a certain John Bodle was brought to trial forpoisoning his grandfather by putting arsenic in his coffee. James Marsh, a chemist working at the Royal Arsenal inWoolwich was called by the prosecution to try to detect its presence. He performed the standard test by passinghydrogen sulfide through the suspect fluid. While Marsh was able to detect arsenic, the yellow precipitate did notkeep very well, and by the time it was presented to the jury it deteriorated. The jury was not convinced, and JohnBodle was acquitted.Angered and frustrated by this, especially when John Bodle confessed later that he indeed killed his grandfather,Marsh decided to devise a better test to demonstrate the presence of arsenic. Taking Scheele's work as a basis, heconstructed a simple glass apparatus capable of not only detecting minute traces of arsenic but also measuring itsquantity. Adding a sample of tissue or body fluid to a glass vessel with zinc and acid would produce arsine gas ifarsenic was present, in addition to the hydrogen that would be produced regardless by the zinc reacting with the acid.Igniting this gas mixture would oxidize any arsine present into arsenic and water vapor. This would cause a coldceramic bowl held in the jet of the flame to be stained with a silvery-black deposit of arsenic, physically similar tothe result of Metzger's reaction. The intensity of the stain could then be compared to films produced using knownamounts of arsenic.[1] Not only could minute amounts of arsenic be detected (as little as 0.02 mg), the test was veryspecific for arsenic. Although antimony (Sb) could give a false-positive test by forming a similar black deposit, itwould not dissolve in a solution of sodium hypochlorite (NaOCl), while arsenic would.

Marsh test 47

Specific reactions involvedThe Marsh test treats the sample with sulfuric acid and arsenic-free zinc. Even if there are minute amounts of arsenicpresent, the zinc reduces the trivalent arsenic (As3+ ). Here are the two half-reactions:

Oxidation: Zn → Zn2+ + 2 e−

Reduction: As2O3 + 12 e− + 6 H+ → 2 As3− + 3 H2OOverall, we have this reaction:

As2O3 + 6 Zn + 6 H+ → 2 As3− + 6 Zn2+ + 3 H2OIn an acidic medium, As3− is protonated to form arsine gas (AsH3), so adding sulfuric acid (H2SO4) to each side ofthe equation we get:

As2O3 + 6 Zn + 6 H+ + 6 H2SO4 → 2 As3− + 6 H2SO4 + 6 Zn2+ + 3 H2OAs the As3− combines with the H+ to form arsine:

As2O3 + 6 Zn + 6 H+ + 6 H2SO4 → 2 AsH3 + 6 ZnSO4 + 3 H2O + 6 H+

By eliminating the common ions:As2O3 + 6 Zn + 6 H2SO4 → 2 AsH3 + 6 ZnSO4 + 3 H2O

First notable applicationAlthough the Marsh test was efficacious, its first publicly documented use — in fact, the first time evidence fromforensic toxicology was ever introduced — was in Tulle, France in 1840 with the celebrated LaFarge poisoning case.Charles LaFarge, a foundry owner, was suspected of being poisoned with arsenic by his wife Marie. Thecircumstantial evidence was great: it was shown that she brought arsenic trioxide from a local chemist, supposedly tokill rats which infested their home. In addition, their maid swore that she had mixed a white powder into his drink.Although the food was found to be positive for the poison using the old methods as well as the Marsh test, when thehusband's body was exhumed and tested, the chemists assigned to the case were not able to detect arsenic. MathieuOrfila, the renowned toxicologist retained by the defence and an acknowledged authority of the Marsh test examinedthe results. He performed the test again and demonstrated that the Marsh test was not at fault for the misleadingresults but rather those who performed it did it incorrectly. Orfila thus proved the presence of arsenic in LaFarge'sbody using the test. As a result of this, Marie was found guilty and sentenced to life imprisonment.

Effects of the Marsh testThe case proved to be controversial, for it divided the country into factions who were convinced or otherwise ofMme. LaFarge's guilt; nevertheless, the impact of the Marsh test was great. The French press covered the trial andgave the test the publicity it needed to give the field of forensic toxicology the legitimacy it deserved, although insome ways it trivialized it: Marsh test assays were actually done in salons, public lectures and even in some playsthat recreated the LaFarge case.The existence of the Marsh test also served a deterrent effect: deliberate arsenic poisonings became rarer because ofthe fear of discovery became more present.

Marsh test 48

References[1] http:/ / www. chm. bris. ac. uk/ motm/ arsine/ arsineh. htm

Apparatus for the Marsh test

• Marsh J. (1836). "Account of a method of separating smallquantities of arsenic from substances with which it may be mixed".Eddinburgh New Philosophical Journal 21: 229–236.

• Marsh J. (1837). "Arsenic; nouveau procédé pour le découvrir dansles substances auxquelles il est mêlé". Journal de Pharmacie 23:553–562.

• Marsh, James (1837). "Beschreibung eines neuen Verfahrens, umkleine Quantitäten Arsenik von den Substanzen abzuscheiden,womit er gemischt ist". Liebigs Annalen der Chemie 23 (2): 207.doi:10.1002/jlac.18370230217.

• Mohr C. F. (1837). "Zusätze zu der von Marsh angegebenen Methode, den Arsenik unmittelbar im regulinischenZustande aus jeder Flüssigkeit auszuscheiden". Annalen der Pharmacie und Chemie 23 (2): 217–225.doi:10.1002/jlac.18370230218.

• Lockemann, Georg (1905). "Über den Arsennachweis mit dem Marshschen Apparate". Angewante Chemie 18(11): 416. doi:10.1002/ange.19050181104.

• Harkins, W. D. (1910). "The Marsh test and Excess Potential (First Paper.1) The Quantitative Determination ofArsenic". Journal of the American Chemical Society 32 (4): 518–530. doi:10.1021/ja01922a008.

• Campbell W. A. (1965). "Some landmarks in the history of arsenic testing". Chemistry in Britain 1: 198–202.

External links• McMuigan, Hugh (1921). An Introduction to Chemical Pharmacology (http:/ / books. google. com/

?id=n4I6AAAAMAAJ& pg=PA396& dq=arsenic+ test+ apparatus). Philadelphia: P. Blakiston's Son & Co..pp. 396–397. Retrieved 2007-12-16.

• Wanklyn, James Alfred (1901). Arsenic (http:/ / books. google. com/ ?id=GyAVfFrjAfwC& pg=PA39&dq=james+ marsh+ test). London: Kegan Paul, Trench, Trübner & Co. Ltd.. pp. 39–57. Retrieved 2007-12-16.

Sono arsenic filter 49

Sono arsenic filterThe Sono arsenic filter was invented in 2006 by Abul Hussam, who is a chemistry professor at George MasonUniversity (GMU) in Fairfax, Virginia. It was developed to deal with the problem of arsenic contamination ofgroundwater. The filter is now in use in Hussam's native Bangladesh.

DevelopmentFarmers had been drinking fresh groundwater from wells, whereas previously they had had to use ponds andmudholes which were contaminated with bacteria and viruses. However, the wells were also contaminated withnaturally occurring high concentrations of poisonous arsenic, causing skin ailments and cancers. Awareness of theproblem developed through the 1990s.Allan Smith, an epidemiologist at the University of California at Berkeley, observed that the arsenic problem affectsmillions of people worldwide:

You can't see it or taste or smell it. The idea that crystal-clear drinking water would end up causing lungdisease in 20 or 30 years is a little weird. It's unbelievable to people.

Hassam developed his filter after years of testing hundreds of prototypes. The final version contains 20 pounds ofshards of porous iron, which bonds chemically with arsenic. It also includes charcoal, sand and bits of brick. It filtersnearly all of the arsenic from the well water.

AwardsHassam was awarded the 2007 Grainger challenge Prize for Sustainability by the National Academy ofEngineering.[1] Hussam plans to use 70% of the $1 million engineering prize to distribute filters to needycommunities.[2]

References[1] National Academies Press Release (http:/ / www8. nationalacademies. org/ onpinews/ newsitem. aspx?RecordID=02012007), accessed 5 Feb

2007.[2] Professor wins $1 million for arsenic filter (http:/ / www. enn. com/ sci. html?id=833& ref=rss), Associated Press, 2/3/07.

External links• A simple and effective arsenic filter based on composite iron matrix: Development and deployment studies

forgroundwater of Bangladesh (http:/ / chemistry. gmu. edu/ faculty/ hussam/ Arsenic Filters/ ESH ARSENICFILTER PAPER 2007. pdf) - (PDF file)

• DWC-Water: Arsenic filtration (http:/ / www. dwc-water. com/ technologies/ arsenic-filtration/ index. html) -description and test results.

• Invention description at GMU website (http:/ / chemistry. gmu. edu/ faculty/ hussam/ Arsenic Filter. html)• Manob Sakti Unnayan Kendro (MSUK) (http:/ / www. msuk-bd. org/ image/ Arsenic_Contamination . htm) -

development and distribution.

Article Sources and Contributors 50

Article Sources and ContributorsArsenic  Source: http://en.wikipedia.org/w/index.php?oldid=464268394  Contributors: *drew, 05C4RK1NR055, 08prl, 123123john, 21655, 25or6to4, 28bytes, 2D, 2over0, 5 albert square,A8UDI, ACSE, ATSDR, Abductive, Abw87, Acolorpink1, Acroterion, Adacus12, Adam Krellenstein, Adashiel, Addshore, Aerogami, Ahoerstemeier, Alansohn, Alex earlier account,Alguienboga, Alibb, Alvis, Amble, Amorelli, Ams80, Amsibert, AnakngAraw, Andre Engels, Andres, Andrew Rodland, Anetode, Angrynight, Anonymous101, Anonymous26, Antandrus,Anwar saadat, Arakunem, Aramgutang, Arbitrarily0, Arcadian, Archimerged, ArielGold, Arpingstone, Ascorbic, Ask123, Astatine-210, Atokoy, Audiosmurf, Aussie Alchemist, Austiwang,Australian Matt, Avanu, Avono, Awesome91, AxelBoldt, Axiosaurus, Axl, Az1568, Bantman, BarretBonden, BatteryIncluded, Bdodo1992, Bedrupsbaneman, Beetstra, Beland, Belizefan,Belovedfreak, Ben Ben, BenFrantzDale, Benbest, Bender235, Bendzh, Benwildeboer, Bhny, BiT, Bigheadedboy, Bikeable, Billibongofong, Bkell, BlueEarth, Bobo192, Bobépierre, Bogey97,Boing! said Zebedee, Bongwarrior, Booksworm, BoomerAB, Borislav.dopudja, Bossrat, Brandmeister (old), Breakoneout, Brianski, Brim, Bryan Derksen, Bryandn321, Bubba hotep,Bubbachuck, Buleemem3, Burntsauce, C3o, CHADMEISTER, CYD, Cacycle, Cadwaladr, CalicoCatLover, Camembert, CanadianLinuxUser, Carnildo, Cdang, Ceyockey, Cflm001,CharlotteWebb, Chasingsol, ChemNerd, Chemicalinterest, Chinaexports, Chris.urs-o, Christopher Parham, Chriswaterguy, CiTrusD, Cjw22, Ck lostsword, ClamDip, Closedmouth, Cmdrjameson,Cmichael, Cnmetaltrade, ColetteHoch, Conversion script, Courcelles, Cpaton, Crestville, Crohnie, Cryptic C62, Cxz111, Cybercobra, Cyde, Cyrusuryc, DARTH SIDIOUS 2, DJBullfish, DVD RW, DanielCD, Dark Lord of the Sith, Darrien, DaveGorman, David Latapie, David Pierce, David spector, Dawn Bard, Dcandeto, Dead3y3, December21st2012Freak, Deflective, Deli nk,Delirium, Delta G, Devon.pottle, Djr5353, Dlae, Doc Tropics, Don4of4, Donarreiskoffer, Donhoraldo, Doniago, Donna914, Doulos Christos, Dr. Dunglison, Drbillellis, Drbogdan, Dreadstar,Drjohntoconnorpe, Drmies, Drphilharmonic, Duderusia, ESkog, Eaw9184, Ed Poor, Edgar181, Edward, Edwy, Egmonster, El C, Elassint, Eldin raigmore, Eliotsmith, Ellafb, Elwood j blues,Emperorbma, Environmentsver, Epbr123, Epolk, EricWesBrown, Erifneerg, Erik Zachte, Euchiasmus, Evice, Excirial, Explicit, Fallatio, Faradayplank, Favonian, Fconaway, Femto, Floria L,Floul1, Frank Lofaro Jr., Fredbauder, Freddyd945, Fun3tubs, Funnyfarmofdoom, Garrettett, Gcsuchemistry, Gdhfidhfihs, Geht, Gelzo, Giftlite, Gjd001, Gmaxwell, Gobonobo, Gogo Dodo,Graham87, Grassfire, Greatestqueen, Grendelkhan, Grim23, Gsayles, Gscshoyru, Guanaco, Gumba gumba, Guoguo12, Gurch, H1bhaska, Hak-kâ-ngìn, Hamiltondaniel, Harish2k1vet, Hburg,Headbomb, Hellbus, Heron, HexaChord, Hippietrail, HokieRNB, Hu12, Hydrogen Iodide, IW.HG, Ianbon, Ibreiwish93, Icairns, Ideal gas equation, Ideyal, Iepeulas, Igodard, ImperatorExercitus,Inka 888, Inkypaws, Insanity Incarnate, Inspector08, InverseHypercube, Ioeth, Iridescent, Isis, J.delanoy, J7890bigman, J8079s, JForget, JFreeman, JNW, JRPG, Ja 62, Jac16888, Jackcsk, Jagged85, James500, Jamesontai, Jan.Smolik, Jannikkappel, Jaraalbe, Jason ost, JavierMC, Jeffrey O. Gustafson, Jermantowicz, Jimjamjak, Jimokay, Jjron, Jkl, Joanjoc, Johann Wolfgang, John,JohnCD, Johnbibby, Jonny-mt, Jordan042, Jose77, Josh Grosse, Joshschr, Jossi, Joyous!, Jpe77, JuneGloom07, Jusdafax, Karlhahn, Katieh5584, Kazvorpal, Kbrose, Keegan, Keilana, KeithH,Kichigoro12, Killiondude, Koalaman520, Kolkata culture, Kooo, Kpjas, Kralizec!, Kreatureuk, Krich, Ktsquare, Kubigula, Kukini, Kuru, Kurykh, Kwamikagami, L Kensington, LFaraone, LeeDaniel Crocker, Leiem, Lightdarkness, LilHelpa, Limulus, Link2joon, Logicman1966, LuigiManiac, Luk, MER-C, MFago, MMS2013, Magepure892, Magister Mathematicae, Mai-tai-guy,Malcolm Farmer, Manette, Mani1, Manny 7, Marcelo.84, Marcelo1229, Marek69, Marnanel, Masoninman, Master Jay, Materialscientist, Matt.T, MattieTK, Mav, Mclause, Mcrosenstein,Melis610, Mencha833, Mgimpel, Michaelkourlas, Micru, MightyWarrior, Mimihitam, Minesweeper, Mini-Geek, Mlinan, Mr Bungle, Mr Stephen, Mr. Lefty, MrMunky, Mschel, Mschiffler,MuVo100, Mufka, Muhandes, Munozdj, N2e, Natalie Erin, Nburden, NellieBly, Nergaal, Neverquick, NewEnglandYankee, Nibuod, Nick Y., Nick88, Nickj, Nihiltres, Nitchell, Noctibus,Northumbrian, Novaprospekt, Number 57, Oajsn, Off2riorob, Ojay123, Oliver202, Oneslowlx, Onions and liver, Opelio, Ottawa4ever, OwenX, Oxymoron83, PDH, PP Jewel, PStatic, Pacific66,Panoptical, PatVanHove, Pedometer+1, Perseus, Son of Zeus, Peter Karlsen, Pfahlstrom, Pharaoh of the Wizards, Philip Baird Shearer, Philip Trueman, Physchim62, Phædrus, Piano non troppo,PierreAbbat, Pinethicket, Pishogue, Plasmic Physics, Poolkris, Poor Yorick, Pras, Pstanton, Pstudier, Quebec99, Qwertymasterfull101, Qxz, RG2, RTC, RainbowOfLight, Rainbowwrasse,Raven4x4x, Reach Out to the Truth, Redux, Remember, Requiems, Reuben, RexNL, Reyk, Rgfjdsf, Riana, Rich Farmbrough, Rifleman 82, Ripfester, Rizzardi, Rjwilmsi, Rmhermen, Rob Hooft,Robert McClenon, RobertMfromLI, Roberta F., Rolen2ws, Romanm, Roscelese, RoyBoy, Rtyq2, Rummmy, SJFriedl, SQGibbon, Sander123, Saperaud, Sapphirine, Sbharris, Schneelocke,Sciurinæ, Screen317, Sehsuan, Sengkang, Serinoah, SexyBern, Shaddack, Shadowjams, Shanel, Shirik, Shizane, Shootbamboo, Silentlight, Sionus, Sir-Restriction, Sixstix1, Sjö, Skatebiker,Skizzik, Sl, Sleigh, Smallverm, Smartse, Smokefoot, Smokizzy, Snottywong, SoCalSuperEagle, Sole Soul, Squids and Chips, Squirepants101, Staeiou, StaticGull, StaticVision, Steloukos,Stemonitis, StephanieM, Stephenb, Steven Zhang, Stevenfruitsmaak, Stifynsemons, Stone, StradivariusTV, Sunborn, Syrthiss, Taivo, Tassedethe, Tehehhehehhe, Tempodivalse, Terence,Tetracube, The Minister of War, The Nut, The Thing That Should Not Be, TheKMan, TheSuperBrain2, Themerejoy, Theseeker4, Thorwald, Thricecube, Thue, Thumperward, Tiddly Tom, Tiderolls, Tim Starling, Tiptoety, Tisdalepardi, Titoxd, Tizzybag, Tkynerd, Tom harrison, Tombadog, Tommy2010, Tone, Topdeck, Trevor MacInnis, Triforce of Power, Trovatore, Trusilver, Ttsalo,Turmeric3, Twonernator, Ucanlookitup, Utility Monster, Vanished user 39948282, Velella, Versus22, Victor falk, Vildricianus, Viriditas, Vogon77, Voyagerfan5761, Vsmith, Vuong Ngan Ha,WJBscribe, Wancheseblondie, Warut, Watch37264, Wfructose, Whyipee, Wiki Raja, Wikieditor06, Wikimedes, WikipedianMarlith, William Avery, Wknight94, Wolfrock, Xeworlebi, Xiaoyu ofYuxi, Yath, Yiplop stick stop, YixilTesiphon, Yyy, Zedla, Zephyris, Zigger, ZooPro, Zoofroot, Zsinj, Äpple, Δζ, Александър, 1207 anonymous edits

Isotopes of arsenic  Source: http://en.wikipedia.org/w/index.php?oldid=458897763  Contributors: Bryan Derksen, Colinho22, DGaw, DenverRedhead, Donarreiskoffer, DragonflySixtyseven,Elium2, Femto, Headbomb, Pgk, Rjwilmsi, V1adis1av, Waggers, XinaNicole, 4 ,حسن علي البط anonymous edits

Arsenic poisoning  Source: http://en.wikipedia.org/w/index.php?oldid=464284649  Contributors: 08prl, ABF, Alvis, Alynna Kasmira, Amcfreely, Andreworkney, Andros 1337, Anglius,Angrynight, Antrikshy, Arcadian, Archaeogenetics, Astralblue, Aussie Alchemist, Axeman89, BD2412, Bansal palash, BatteryIncluded, Beetstra, Belizefan, Ben.c.roberts, Boccobrock, Bodil,Bronsonboy, Bryan Derksen, C9, CanadianLinuxUser, Captain-tucker, Catgut, Chowbok, Chris 73, ChrisCork, Chriswaterguy, Chuunen Baka, Circeus, Cmprince, Costela.ardelean, CrackDragon,CzarB, DabMachine, Daedae, Daniel Medina, DeadEyeArrow, Dialacina, Dichloride, Diderot, Digger212, DocKrin, DocWatson42, Dominus, Donreed, Dr. Dunglison, DragonflySixtyseven,Drbogdan, Drmies, Dtremenak, Dumbo1, ESkog, Earlypsychosis, Eastlaw, Ebyabe, Edward321, Element16, Erianna, Evanirvana500, Excirial, Fabiform, Fixmanius, Freestyle-69, Funnyhat,GFLewis, Gawaxay, Gegnome, Gobonobo, Googoodal, GregorB, Grey noise, Guanaco, Gurch, Headbomb, Hemanshu, Heron, Humphreys7, Huo Xin, ILikeGeology, IanManka, Ichiro Kikuchi,Ido50, Il barese, ImperatorExercitus, Into The Fray, Itub, Ixfd64, J8079s, Jaeger5432, Jeanie821, Jimbo Wales, Jmh649, Jomasecu, Jonabbey, Jordgette, Jrockley, Juancarlos2004, Justincon6420,Kairos, Karlhahn, Klausok, Kpjas, Kungfuadam, Law Lord, Lawrence Cohen, Lepidoptera, Limulus, Longhair, Luchano's, Maestrosync, Mav, Maximus Rex, McSly, Mellowymaiden,Mephistophelian, Midnightcomm, Mikespedia, Mirasmus, Miss Madeline, Moonraker12, Mouse Nightshirt, Mr Bungle, Mr. Stradivarius, MrFish, My Core Competency is Competency, NeveDan, Nipisiquit, NiteSensor23, NuclearWarfare, Onebravemonkey, Oxymoron83, PaperTruths, Park3r, Paul D. Anderson, Pcampsie, PeterSymonds, Peterlewis, PhilKnight, Philip Trueman,Physchim62, Pibwl, Pinethicket, Plrk, Plutonium27, Puppy8800, QuasiAbstract, Raga, Ratel, Rbaselt, Rdunn, Redsaph, RexNL, Rich Farmbrough, Rivertorch, Rjwilmsi, Ruggiero, Rursus,Saintnazaire2000, Saxophobia, Scottalter, Seaphoto, Senator Palpatine, Serchdf, Shad0, Shaddack, SimonP, Smalljim, Snezzy, Snowolfd4, Southernwolfie, Spinningspark, Spondoolicks, Stone,Storm Rider, Suffusion of Yellow, Superm401, Tea with toast, Tetraedycal, Tide rolls, Timotheus Canens, Tom harrison, Topbanana, Trevor MacInnis, Uberfruk, Ufinne, Ulric1313, Vacuum,Velella, Versus22, Vfp15, Vreejack, WBardwin, Wackyvorlon, WhatamIdoing, Woohookitty, Wouterstomp, Wtshymanski, XLerate, Zatoichi26, Zeimusu, 362 ,55דוד anonymous edits

Arsenic contamination of groundwater  Source: http://en.wikipedia.org/w/index.php?oldid=457309116  Contributors: Adam Krellenstein, Adilliwallah, Alan Liefting, Alksentrs, Beetstra,Blutfink, Bogdangiusca, Bryan Derksen, Carcharoth, Ccgrimm, Chaser, Chowbok, Chriswaterguy, Closedmouth, Colonies Chris, David Pierce, Doseiai2, Ed Poor, Enviro1, Euryalus, Fourdee,Groganus, H1bhaska, KJRehberg, Kaarel, Karlhahn, Kemcolian, Kornerep, Leontios, LilHelpa, Margin1522, Michael Devore, Mike2vil, NiteSensor23, P.K.Niyogi, Pasha123, Planetbitter,Plazak, PokeYourHeadOff, Raven in Orbit, Rifleman 82, Rjohnstonunicef, Rjwilmsi, Rxnd, Sbandrews, Sm8900, Smallverm, Soumenkumar, Stone, Styrofoam1994, Tombadog, Warut,Wavelength, Woohookitty, 77 anonymous edits

Arsenic toxicity  Source: http://en.wikipedia.org/w/index.php?oldid=461071410  Contributors: Alguienboga, Chris Capoccia, Chris the speller, Darth Mike, Drbogdan, LilHelpa, Maralia, MildBill Hiccup, Mr Bungle, Nergaal, Purser123, Rich Farmbrough, Stone, Time9, 8 anonymous edits

Carancas impact event  Source: http://en.wikipedia.org/w/index.php?oldid=453956448  Contributors: A.Savin, Accurizer, AgainErick, Akedahllof, Allstarecho, Amwyll Rwden, Art LaPella,Astrogeo, Aucahuasi, Basilicofresco, Bentley4, Bevo, Bmrbarre, Bog4rt, Brandmeister (old), Carnildo, Cla68, David Shankbone, Davidovic, Deconstructhis, Dinosaur puppy, Dmmaus,Downwards, Edgar181, Electron9, Eric, Fg2, Frankie816, GregU, GregorB, Igorberger, Jaraalbe, Jersey Devil, Jgristy, Jngrossman, Jusdafax, Kauczuk, Korg, Kozuch, Kurieeto, Lawrence Cohen,Lightmouse, Malintex Terek, Mannheim 34, Meteoritekid, Michael Devore, Montrealais, Ms2ger, Nightstallion, NurseryRhyme, Nv8200p, Peteretherden, Piperh, RidinHood25, Rjwilmsi,Rmhermen, Sajani Rheka, Saudade7, Sharkwelder, Sijo Ripa, Simongar, SkyWalker, Smithbrenon, The Haunted Angel, Timwi, Toussaint, Tuxedo junction, Vendrov, Victor12, Viriditas,Woohookitty, Yellowdesk, Zamphuor, Zazaban, 80 anonymous edits

Grainger challenge  Source: http://en.wikipedia.org/w/index.php?oldid=450742575  Contributors: Bryan Derksen, Dirac1933, Headbomb, Kurieeto, Msgerman1, Pfahlstrom, Sm8900

Marsh test  Source: http://en.wikipedia.org/w/index.php?oldid=453687594  Contributors: AaronY, After Midnight, Arcadian, Arimareiji, Astrochemist, Bemoeial, Bryan Derksen, F.chiodo,Groyolo, Headbomb, Heron, Hohenloh, Kaini, Micahmn, RashBold, Richwales, Rifleman 82, Ronhjones, Securiger, Shinkolobwe, Stone, Suisui, Tetracube, Wtshymanski, Zinnmann, 17anonymous edits

Sono arsenic filter  Source: http://en.wikipedia.org/w/index.php?oldid=451905931  Contributors: Chriswaterguy, Giftlite, Hooperbloob, Mbell, Mercury, Mr.Z-man, Rifleman 82, Sm8900,Timurite, Tyrenius, Vegaswikian, Wkped2007utah, Yworo, 5 anonymous edits

Image Sources, Licenses and Contributors 51

Image Sources, Licenses and Contributorsfile:Arsen 1a.jpg  Source: http://en.wikipedia.org/w/index.php?title=File:Arsen_1a.jpg  License: Creative Commons Attribution-ShareAlike 3.0 Unported  Contributors: Arsen_1.jpg: Originaluploader was Tomihahndorf at de.wikipedia derivative work: Materialscientist (talk)File:Loudspeaker.svg  Source: http://en.wikipedia.org/w/index.php?title=File:Loudspeaker.svg  License: Public Domain  Contributors: Bayo, Gmaxwell, Husky, Iamunknown, Mirithing,Myself488, Nethac DIU, Omegatron, Rocket000, The Evil IP address, Wouterhagens, 16 anonymous editsFile:SbAs lattice.png  Source: http://en.wikipedia.org/w/index.php?title=File:SbAs_lattice.png  License: Creative Commons Attribution-Sharealike 3.0  Contributors: MaterialscientistFile:Burn arsenic.jpg  Source: http://en.wikipedia.org/w/index.php?title=File:Burn_arsenic.jpg  License: Creative Commons Attribution-Sharealike 3.0  Contributors: User:LeiemImage:Trimethylarsine-2D.png  Source: http://en.wikipedia.org/w/index.php?title=File:Trimethylarsine-2D.png  License: Public Domain  Contributors: Benjah-bmm27Image:Native arsenic.jpg  Source: http://en.wikipedia.org/w/index.php?title=File:Native_arsenic.jpg  License: Public domain  Contributors: Aram Dulyan (User:Aramgutang)Image:World Arsenic Production 2006.svg  Source: http://en.wikipedia.org/w/index.php?title=File:World_Arsenic_Production_2006.svg  License: Public Domain  Contributors: SchtoneImage:Mineraly.sk - realgar.jpg  Source: http://en.wikipedia.org/w/index.php?title=File:Mineraly.sk_-_realgar.jpg  License: unknown  Contributors: Helix84, Saperaud, Wela49Image:Arsenic alchemical symbol.svg  Source: http://en.wikipedia.org/w/index.php?title=File:Arsenic_alchemical_symbol.svg  License: Public Domain  Contributors: User:Bryan DerksenImage:Roxarsone.png  Source: http://en.wikipedia.org/w/index.php?title=File:Roxarsone.png  License: Public Domain  Contributors: Edgar181, Ephemeronium, Leyo, SmokefootImage:ArsenobetainePIC.svg  Source: http://en.wikipedia.org/w/index.php?title=File:ArsenobetainePIC.svg  License: Public Domain  Contributors: Original uploader was V8rik at en.wikipediaImage:Skull and crossbones.svg  Source: http://en.wikipedia.org/w/index.php?title=File:Skull_and_crossbones.svg  License: Public Domain  Contributors: unknownFile:Phar Lap.jpg  Source: http://en.wikipedia.org/w/index.php?title=File:Phar_Lap.jpg  License: Public Domain  Contributors: Charles Daniel Pratt, 1893-1968File:Weltkarte arsenrisikogebiete.gif  Source: http://en.wikipedia.org/w/index.php?title=File:Weltkarte_arsenrisikogebiete.gif  License: GNU Free Documentation License  Contributors:Original uploader was Matze6587 at de.wikipediafile:Peru location map.svg  Source: http://en.wikipedia.org/w/index.php?title=File:Peru_location_map.svg  License: Creative Commons Attribution-Sharealike 3.0  Contributors:Peru_-_(Template).svg: Huhsunqu derivative work: SpischotFile:Blue_pog.svg  Source: http://en.wikipedia.org/w/index.php?title=File:Blue_pog.svg  License: Public Domain  Contributors: Andux, Antonsusi, Droll, Juiced lemon, STyx, TwoWings,WikipediaMaster, 6 anonymous editsImage:Carancas Meteorite 2.jpg  Source: http://en.wikipedia.org/w/index.php?title=File:Carancas_Meteorite_2.jpg  License: Creative Commons Attribution-Sharealike 3.0,2.5,2.0,1.0 Contributors: Meteorite ReconFile:Marsh test apparatus.jpg  Source: http://en.wikipedia.org/w/index.php?title=File:Marsh_test_apparatus.jpg  License: Public Domain  Contributors: Hugh McMuigan

License 52

LicenseCreative Commons Attribution-Share Alike 3.0 Unported//creativecommons.org/licenses/by-sa/3.0/