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Arsenic: the story on HearLore | HearLore
Arsenic
Arsenic has been known since ancient times to be poisonous to humans, yet it was frequently used for murder until the advent in the 1830s of the Marsh test, a sensitive chemical test for its presence. Owing to its use by the ruling class to murder one another and its potency and discreetness, arsenic has been called the poison of kings and the king of poisons. It became known as the inheritance powder due to its use in killing family members in the Renaissance era. The word arsenic has its origin in the Syriac word zarnika, from Arabic al-zarnīkh the orpiment, based on Persian zar gold from the word zarnikh, meaning yellow or literally gold-colored and hence yellow orpiment. It was adopted into Greek as arsenikon, a neuter form of the Greek adjective arsenikos, meaning male or virile. Latin-speakers adopted the Greek term as arsenicum, which in French ultimately became arsenic, whence the English word arsenic. Arsenic sulfides orpiment and realgar and oxides have been known and used since ancient times. Zosimos describes roasting sandarach realgar to obtain cloud of arsenic arsenic trioxide, which he then reduces to gray arsenic. During the Bronze Age, arsenic was melted with copper to make arsenical bronze. Jabir ibn Hayyan described the isolation of arsenic before 815 AD. Albertus Magnus Albert the Great, 1193, 1280 later isolated the element from a compound in 1250, by heating soap together with arsenic trisulfide. In 1649, Johann Schröder published two ways of preparing arsenic. Crystals of elemental native arsenic are found in nature, although rarely. Cadet's fuming liquid impure cacodyl, often claimed as the first synthetic organometallic compound, was synthesized in 1760 by Louis Claude Cadet de Gassicourt through the reaction of potassium acetate with arsenic trioxide. In the Victorian era, women would eat arsenic white arsenic or arsenic trioxide mixed with vinegar and chalk to improve the complexion of their faces, making their skin paler to show they did not work in the fields. The accidental use of arsenic in the adulteration of foodstuffs led to the Bradford sweet poisoning in 1858, which resulted in 21 deaths. From the late 18th century wallpaper production began to use dyes made from arsenic, which was thought to increase the pigment's brightness. One account of the illness and 1821 death of Napoleon implicates arsenic poisoning involving wallpaper. Two arsenic pigments have been widely used since their discovery , Paris Green in 1814 and Scheele's Green in 1775. After the toxicity of arsenic became widely known, these chemicals were used less often as pigments and more often as insecticides. In the 1860s, an arsenic byproduct of dye production, London Purple, was widely used. This was a solid mixture of arsenic trioxide, aniline, lime, and ferrous oxide, insoluble in water and very toxic by inhalation or ingestion. But it was later replaced with Paris Green, another arsenic-based dye. With better understanding of the toxicology mechanism, two other compounds were used starting in the 1890s. Arsenite of lime and arsenate of lead were used widely as insecticides until the discovery of DDT in 1942. In small doses, soluble arsenic compounds act as stimulants, and were once popular as medicine by people in the mid-18th to 19th centuries; this use was especially prevalent for sport animals such as race horses or work dogs and continued into the 20th century. A 2006 study of the remains of the Australian racehorse Phar Lap determined that its 1932 death was caused by a massive overdose of arsenic. Sydney veterinarian Percy Sykes stated, In those days, arsenic was quite a common tonic, usually given in the form of a solution Fowler's Solution ... It was so common that I'd reckon 90 per cent of the horses had arsenic in their system.
When was the Marsh test invented to detect arsenic?
The Marsh test was invented in the 1830s to detect the presence of arsenic. This sensitive chemical test allowed authorities to identify arsenic in bodies and food, ending its frequent use for murder.
What is the origin of the word arsenic?
The word arsenic originates from the Syriac word zarnika and the Arabic al-zarnīkh meaning orpiment. It derives from the Persian word zar meaning gold and the Greek arsenikos meaning male or virile before becoming the English term.
How did arsenic affect Napoleon Bonaparte?
One account of the 1821 death of Napoleon implicates arsenic poisoning involving wallpaper. The wallpaper production from the late 18th century used dyes made from arsenic to increase pigment brightness.
What is the current arsenic limit in US drinking water?
The Environmental Protection Agency set the maximum concentration in drinking water at 10 ppb effective the 23rd of January 2006. The FDA set the same standard for bottled water in 2005.
Which bacteria can substitute arsenic for phosphorus?
Researchers reported the discovery of a strain of the bacterium Halomonas designated GFAJ-1 in 2010 that was allegedly capable of substituting arsenic for phosphorus. Subsequent studies published in 2011 and 2012 contradicted these findings and the original paper was retracted in 2025.
Arsenic is a chemical element; it has the symbol As and atomic number 33. It is a metalloid and one of the pnictogens, and therefore shares many properties with its group 15 neighbors phosphorus and antimony. Arsenic is notoriously toxic. It occurs naturally in many minerals, usually in combination with sulfur and metals, but also as a pure elemental crystal. It has various allotropes, but only the grey form, which has a metallic appearance, is important to industry. The three most common arsenic allotropes are grey, yellow, and black arsenic, with grey being the most common. Grey arsenic α-As, space group Rm No. 166 adopts a double-layered structure consisting of many interlocked, ruffled, six-membered rings. Because of weak bonding between the layers, grey arsenic is brittle and has a relatively low Mohs hardness of 3.5. Nearest and next-nearest neighbors form a distorted octahedral complex, with the three atoms in the same double-layer being slightly closer than the three atoms in the next. This relatively close packing leads to a high density of 5.73 g/cm3. Grey arsenic is a semimetal, but becomes a semiconductor with a bandgap of 1.2, 1.4 eV if amorphized. Grey arsenic is also the most stable form. Yellow arsenic is soft and waxy, and somewhat similar to tetraphosphorus. Both have four atoms arranged in a tetrahedral structure in which each atom is bound to each of the other three atoms 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 vapor, . It is rapidly transformed into grey arsenic by light. The yellow form has a density of 1.97 g/cm3. Black arsenic is similar in structure to black phosphorus. Black arsenic can also be formed by cooling vapor at around and by crystallization of amorphous arsenic in the presence of mercury vapors. It is glassy and brittle. Black arsenic is also a poor electrical conductor. Arsenic sublimes upon heating at atmospheric pressure, converting directly to a gaseous form without an intervening liquid state at . However, at and 2.84 MPa, arsenic melts. The triple point is at 3.63 MPa and . Arsenic occurs naturally as a single stable isotope, 75As. Synthetic radioisotopes are known from 64As to 95As, as well as at least 11 isomers. The most stable of these are 73As with a half-life of 80.30 days and 74As with a half-life of 17.77 days, followed by 71As 65.30 hours, 77As 38.79 hours, 76As 26.24 hours, and 72As 26.0 hours. All others have half-lives under 100 minutes and most under one minute. Isotopes lighter than the stable one generally decay by positron emission or electron capture to germanium isotopes, while those heavier beta decay to selenium isotopes. A notable exception is that 74As decays both ways. Arsenic has a similar electronegativity and ionization energies to its lighter pnictogen congener phosphorus and therefore readily forms covalent molecules with most of the nonmetals. Though stable in dry air, arsenic forms a golden-bronze tarnish upon exposure to humidity which eventually becomes a black surface layer. When heated in air, arsenic oxidizes to arsenic trioxide; the fumes from this reaction have an odor resembling garlic. This odor can be detected on striking arsenide minerals such as arsenopyrite with a hammer. It burns in oxygen to form arsenic trioxide and arsenic pentoxide, which have the same structure as the more well-known phosphorus compounds, and in fluorine to give arsenic pentafluoride. Arsenic makes arsenic acid with concentrated nitric acid, arsenous acid with dilute nitric acid, and arsenic trioxide with concentrated sulfuric acid; however, it does not react with water, alkalis, or non-oxidising acids. Arsenic reacts with metals to form arsenides, though these are not ionic compounds containing the As3− ion as the formation of such an anion would be highly endothermic and even the group 1 arsenides have properties of intermetallic compounds. Like germanium, selenium, and bromine, which like arsenic succeed the 3d transition series, arsenic is much less stable in the +5 oxidation state than its vertical neighbors phosphorus and antimony, and hence arsenic pentoxide and arsenic acid are potent oxidizers. One of the simplest arsenic compounds is the trihydride, the highly toxic, flammable, pyrophoric arsine AsH3. This compound is generally regarded as stable, since at room temperature it decomposes only slowly. At temperatures of 523, 573 K 250, 300 °C decomposition to arsenic and hydrogen is rapid. Several factors, such as humidity, presence of light and certain catalysts namely aluminium facilitate the rate of decomposition. It oxidises readily in air to form arsenic trioxide and water, and analogous reactions take place with sulfur and selenium instead of oxygen. Arsenic forms colorless, odorless, crystalline oxides As2O3 white arsenic and As2O5 which are hygroscopic and readily soluble in water to form acidic solutions. Arsenic V acid is a weak acid and its salts, known as arsenates, are a major source of arsenic contamination of groundwater in regions with high levels of naturally occurring arsenic minerals. Synthetic arsenates include Scheele's Green cupric hydrogen arsenate, acidic copper arsenate, calcium arsenate, and lead hydrogen arsenate. These three have been used as agricultural insecticides and poisons. The protonation steps between the arsenate and arsenic acid are similar to those between phosphate and phosphoric acid. Unlike phosphorous acid, arsenous acid is genuinely tribasic, with the formula As OH 3. A broad variety of sulfur compounds of arsenic are known. Orpiment As2S3 and realgar As4S4 are somewhat abundant and were formerly used as painting pigments. In As4S10, arsenic has a formal oxidation state of +2 in As4S4 which features As-As bonds so that the total covalency of As is still 3. Both orpiment and realgar, as well as As4S3, have selenium analogs; the analogous As2Te3 is known as the mineral kalgoorlieite, and the anion As2Te− is known as a ligand in cobalt complexes. All trihalides of arsenic III are well known except the astatide, which is unknown. Arsenic pentafluoride AsF5 is the only important pentahalide, reflecting the lower stability of the +5 oxidation state; even so, it is a very strong fluorinating and oxidizing agent. The pentachloride is a kind of yellow solid that is only stable below −50 °C, at which temperature it decomposes to the trichloride, releasing chlorine gas. A large variety of organoarsenic compounds are known. Several were developed as chemical warfare agents during World War I, including vesicants such as lewisite and vomiting agents such as adamsite. Cacodylic acid, which is of historic and practical interest, arises from the methylation of arsenic trioxide, a reaction that has no analogy in phosphorus chemistry. Cacodyl was the first organometallic compound known even though arsenic is not a true metal and was named from the Greek κακωδία stink for its offensive, garlic-like odor; it is very toxic.
The King of Poisons
Some species of bacteria obtain their energy in the absence of oxygen by oxidizing various fuels while reducing arsenate to arsenite. Under oxidative environmental conditions some bacteria use arsenite as fuel, which they oxidize to arsenate. The enzymes involved are known as arsenate reductases Arr. In 2008, bacteria were discovered that employ a version of photosynthesis in the absence of oxygen with arsenites as electron donors, producing arsenates just as ordinary photosynthesis uses water as electron donor, producing molecular oxygen. Researchers conjecture that, over the course of history, these photosynthesizing organisms produced the arsenates that allowed the arsenate-reducing bacteria to thrive. One strain, PHS-1, has been isolated and is related to the gammaproteobacterium Ectothiorhodospira shaposhnikovii. The mechanism is unknown, but an encoded Arr enzyme may function in reverse to its known homologues. In 2010, researchers reported the discovery of a strain of the bacterium Halomonas designated GFAJ-1 that was allegedly capable of substituting arsenic for phosphorus in its biomolecules, including DNA, when grown in an arsenic-rich, phosphate-limited environment. This claim, published in Science, suggested that arsenic could potentially serve as a building block of life in place of phosphorus, challenging long-standing assumptions about biochemical requirements for life on Earth. The claim was met with widespread skepticism. Subsequent studies provided evidence contradicting the initial findings. One follow-up study published in Science in 2011 demonstrated that GFAJ-1 still requires phosphate to grow and does not incorporate arsenate into its DNA in any biologically significant way. Another independent investigation in 2012 used more sensitive techniques to purify and analyze the DNA of GFAJ-1 and found no detectable arsenate incorporated into the DNA backbone. The authors concluded that the original observations were likely due to experimental contamination or insufficient purification methods. Together, these studies reaffirmed phosphorus as an essential element for all known forms of life. In 2025, the journal Science formally retracted the original paper, citing a lack of sufficient experimental support for its key conclusions, though the authors continued to stand by their data. Arsenic may be an essential trace mineral in birds, involved in the synthesis of methionine metabolites. However, the role of arsenic in bird nutrition is disputed, as other authors state that arsenic is toxic in small amounts. Some evidence indicates that arsenic is an essential trace mineral in mammals. Anke M. 1986 Arsenic, pp. 347, 372 in Mertz W. ed., Trace elements in human and Animal Nutrition, 5th ed. Orlando, FL: Academic Press. Experimental studies in rodents and livestock have shown that arsenic deprivation can lead to impaired growth, reduced reproductive performance, and abnormal glucose metabolism, suggesting it may play a role in essential metabolic processes. Arsenic has been proposed to participate in methylation reactions, possibly influencing gene regulation and detoxification pathways. However, because the threshold between beneficial and toxic exposure is extremely narrow, arsenic is not currently classified as an essential element for humans, and its physiological role in higher animals remains uncertain. Arsenic has been linked to epigenetic changes, heritable changes in gene expression that occur without changes in DNA sequence. These include DNA methylation, histone modification, and RNA interference. Toxic levels of arsenic cause significant DNA hypermethylation of tumor suppressor genes p16 and p53, thus increasing risk of carcinogenesis. These epigenetic events have been studied in vitro using human kidney cells and in vivo using rat liver cells and peripheral blood leukocytes in humans. Inductively coupled plasma mass spectrometry ICP-MS is used to detect precise levels of intracellular arsenic and other arsenic bases involved in epigenetic modification of DNA. Studies investigating arsenic as an epigenetic factor can be used to develop precise biomarkers of exposure and susceptibility. The Chinese brake fern Pteris vittata hyperaccumulates arsenic from the soil into its leaves and has a proposed use in phytoremediation. Inorganic arsenic and its compounds, upon entering the food chain, are progressively metabolized through a process of methylation. For example, the mold Scopulariopsis brevicaulis produces trimethylarsine if inorganic arsenic is present. The organic compound arsenobetaine is found in some marine foods such as fish and algae, and also in mushrooms in larger concentrations. The average person's intake is about 10, 50 μg/day. Values about 1000 μg are not unusual following consumption of fish or mushrooms, but there is little danger in eating fish because this arsenic compound is nearly non-toxic. Naturally occurring sources of human exposure include volcanic ash, weathering of minerals and ores, and mineralized groundwater. Arsenic is also found in food, water, soil, and air. Arsenic is absorbed by all plants, but is more concentrated in leafy vegetables, rice, apple and grape juice, and seafood. An additional route of exposure is inhalation of atmospheric gases and dusts. During the Victorian era, arsenic was widely used in home decor, especially wallpapers. In Europe, an analysis based on 20,000 soil samples across all 28 countries show that 98% of sampled soils have concentrations less than 20 mg/kg. In addition, the arsenic hotspots are related to both frequent fertilization and close distance to mining activities. Chronic exposure to arsenic, particularly through contaminated drinking water and food, has also been linked to long-term impacts on cognitive function, including reduced verbal IQ and memory. Extensive arsenic contamination of groundwater has led to widespread arsenic poisoning in Bangladesh and neighboring countries. It is estimated that approximately 57 million people in the Bengal basin are drinking groundwater with arsenic concentrations elevated above the World Health Organization's standard of 10 parts per billion ppb. However, a study of cancer rates in Taiwan suggested that significant increases in cancer mortality appear only at levels above 150 ppb. The arsenic in the groundwater is of natural origin, and is released from the sediment into the groundwater, caused by the anoxic conditions of the subsurface. This groundwater was used after local and western NGOs and the Bangladeshi government undertook a massive shallow tube well drinking-water program in the late twentieth century. This program was designed to prevent drinking of bacteria-contaminated surface waters, but failed to test for arsenic in the groundwater. Many other countries and districts in Southeast Asia, such as Vietnam and Cambodia, have geological environments that produce groundwater with a high arsenic content. Arsenicosis was reported in Nakhon Si Thammarat, Thailand, in 1987, and the Chao Phraya River probably contains high levels of naturally occurring dissolved arsenic without being a public health problem because much of the public uses bottled water. In Pakistan, more than 60 million people are exposed to arsenic polluted drinking water indicated by a 2017 report in Science. Podgorski's team investigated more than 1200 samples and more than 66% exceeded the WHO contamination limits of 10 micrograms per liter. Since the 1980s, residents of the Ba Men region of Inner Mongolia, China have been chronically exposed to arsenic through drinking water from contaminated wells. A 2009 research study observed an elevated presence of skin lesions among residents with well water arsenic concentrations between 5 and 10 μg/L, suggesting that arsenic-induced toxicity may occur at relatively low concentrations with chronic exposure. Overall, 20 of China's 34 provinces have high arsenic concentrations in the groundwater supply, potentially exposing 19 million people to hazardous drinking water. A study by IIT Kharagpur found high levels of Arsenic in groundwater of 20% of India's land, exposing more than 250 million people. States such as Punjab, Bihar, West Bengal, Assam, Haryana, Uttar Pradesh, and Gujarat have highest land area exposed to arsenic. In the United States, arsenic is most commonly found in the ground waters of
The Silent Killer
the southwest. Parts of New England, Michigan, Wisconsin, Minnesota and the Dakotas are also known to have significant concentrations of arsenic in ground water. Increased levels of skin cancer have been associated with arsenic exposure in Wisconsin, even at levels below the 10 ppb drinking water standard. According to a recent film funded by the US Superfund, millions of private wells have unknown arsenic levels, and in some areas of the US, more than 20% of the wells may contain levels that exceed established limits. Low-level exposure to arsenic at concentrations of 100 ppb i.e. above the 10 ppb drinking water standard 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 serious illness or death from the virus. Some Canadians are drinking water that contains inorganic arsenic. Private-dug, well waters are most at risk for containing inorganic arsenic. Preliminary well water analysis typically does not test for arsenic. Researchers at the Geological Survey of Canada have modeled relative variation in natural arsenic hazard potential for the province of New Brunswick. This study has important implications for potable water and health concerns relating to inorganic arsenic. Epidemiological evidence from Chile shows a dose-dependent connection between chronic arsenic exposure and various forms of cancer, in particular when other risk factors, such as cigarette smoking, are present. These effects have been demonstrated at contaminations less than 50 ppb. Arsenic is itself a constituent of tobacco smoke. Analyzing multiple epidemiological studies on inorganic arsenic exposure suggests a small but measurable increase in risk for bladder cancer at 10 ppb. According to Peter Ravenscroft of the Department of Geography at the University of Cambridge, roughly 80 million people worldwide consume between 10 and 50 ppb arsenic in their drinking water. If they all consumed exactly 10 ppb arsenic in their drinking water, the previously cited multiple epidemiological study analysis would predict an additional 2,000 cases of bladder cancer alone. This represents a clear underestimate of the overall impact, since it does not include lung or skin cancer, and explicitly underestimates the exposure. Those exposed to levels of arsenic above the current WHO standard should weigh the costs and benefits of arsenic remediation. Early 1973 evaluations of the processes for removing dissolved arsenic from drinking water demonstrated the efficacy of co-precipitation with either iron or aluminium oxides. In particular, iron as a coagulant was found to remove arsenic with an efficacy exceeding 90%. Several adsorptive media systems have been approved for use at point-of-service in a study funded by the United States Environmental Protection Agency EPA and the National Science Foundation NSF. A team of European and Indian scientists and engineers have set up six arsenic treatment plants in West Bengal based on in-situ remediation method SAR Technology. This technology does not use any chemicals and arsenic is left in an insoluble form +5 state in the subterranean zone by recharging aerated water into the aquifer and developing an oxidation zone that supports arsenic oxidizing micro-organisms. This process does not produce any waste stream or sludge and is relatively cheap. Another effective and inexpensive method to avoid arsenic contamination is to sink wells 500 feet or deeper to reach purer waters. A recent 2011 study funded by the US National Institute of Environmental Health Sciences' Superfund Research Program shows that deep sediments can remove arsenic and take it out of circulation. In this process, called adsorption, arsenic sticks to the surfaces of deep sediment particles and is naturally removed from the ground water. Magnetic separations of arsenic at very low magnetic field gradients with high-surface-area and monodisperse magnetite Fe3O4 nanocrystals have been demonstrated in point-of-use water purification. Using the high specific surface area of Fe3O4 nanocrystals, the mass of waste associated with arsenic removal from water has been dramatically reduced. Epidemiological studies have suggested a correlation between chronic consumption of drinking water contaminated with arsenic and the incidence of all leading causes of mortality. The literature indicates that arsenic exposure is causative in the pathogenesis of diabetes. Chaff-based filters have recently been shown to reduce the arsenic content of water to 3 μg/L. This may find applications in areas where the potable water is extracted from underground aquifers. For several centuries, the people of San Pedro de Atacama in Chile have been drinking water that is contaminated with arsenic, and some evidence suggests they have developed some immunity. Genetic studies indicate that certain populations in this region have undergone natural selection for gene variants that enhance arsenic metabolism and detoxification. This adaptation is considered one of the few documented cases of human evolution in response to chronic environmental arsenic exposure. Around one-third of the world's population drinks water from groundwater resources. Of this, about 10 percent, approximately 300 million people, obtains water from groundwater resources that are contaminated with unhealthy levels of arsenic or fluoride. These trace elements derive mainly from minerals and ions in the ground. Arsenic is unique among the trace metalloids and oxyanion-forming trace metals e.g. As, Se, Sb, Mo, V, Cr, U, Re. It is sensitive to mobilization at pH values typical of natural waters pH 6.5, 8.5 under both oxidizing and reducing conditions. Arsenic can occur in the environment in several oxidation states −3, 0, +3 and +5, but in natural waters it is mostly found in inorganic forms as oxyanions of trivalent arsenite As III or pentavalent arsenate As V. Organic forms of arsenic are produced by biological activity, mostly in surface waters, but are rarely quantitatively important. Organic arsenic compounds may, however, occur where waters are significantly impacted by industrial pollution. Arsenic may be solubilized by various processes. When pH is high, arsenic may be released from surface binding sites that lose their positive charge. When water level drops and sulfide minerals are exposed to air, arsenic trapped in sulfide minerals can be released into water. When organic carbon is present in water, bacteria are fed by directly reducing As V to As III or by reducing the element at the binding site, releasing inorganic arsenic. The aquatic transformations of arsenic are affected by pH, reduction-oxidation potential, organic matter concentration and the concentrations and forms of other elements, especially iron and manganese. The main factors are pH and the redox potential. Generally, the main forms of arsenic under oxic conditions are, , and at pH 2, 2, 7, 7, 11 and 11, respectively. Under reducing conditions, is predominant at pH 2, 9. Oxidation and reduction affects the migration of arsenic in subsurface environments. Arsenite is the most stable soluble form of arsenic in reducing environments and arsenate, which is less mobile than arsenite, is dominant in oxidizing environments at neutral pH. Therefore, arsenic may be more mobile under reducing conditions. The reducing environment is also rich in organic matter which may enhance the solubility of arsenic compounds. As a result, the adsorption of arsenic is reduced and dissolved arsenic accumulates in groundwater. That is why the arsenic content is higher in reducing environments than in oxidizing environments. Zeng Zhaohua, Zhang Zhiliang 2002 The formation of As element in groundwater and the controlling factor. Shanghai Geology 87 3: 11, 15. The presence of sulfur is another factor that affects the transformation of arsenic in natural water. Arsenic can precipitate when metal sulfides form. In this way, arsenic is removed from the water and its mobility decreases. When oxygen is present, bacteria oxidize reduced sulfur to generate energy, potentially releasing bound arsenic. Redox reactions involving Fe also appear to be essential factors in the fate of arsenic in aquatic systems. The reduction of iron oxyhydroxides plays a key role in the release of arsenic to water. So arsenic can be enriched in water with elevated Fe concentrations. Under oxidizing conditions, arsenic can be mobilized from pyrite or iron oxides especially at elevated pH. Under reducing conditions, arsenic can be mobilized by reductive desorption or dissolution when associated with iron oxides. The reductive desorption occurs under two circumstances. One is when arsenate is reduced to arsenite which adsorbs to iron oxides less strongly. The other results from a change in the charge on the mineral surface which leads to the desorption of bound arsenic. Thomas, Mary Ann 2007 The Association of Arsenic With Redox Conditions, Depth, and Ground-Water Age in the Glacial Aquifer System of the Northern United States. U.S. Geological Survey, Virginia. pp. 1, 18. Some species of bacteria catalyze redox transformations of arsenic. Dissimilatory arsenate-respiring prokaryotes DARP speed up the reduction of As V to As III. DARP use As V as the electron acceptor of anaerobic respiration and obtain energy to survive. Other organic and inorganic substances can be oxidized in this process. Chemoautotrophic arsenite oxidizers CAO and heterotrophic arsenite oxidizers HAO convert As III into As V. CAO combine the oxidation of As III with the reduction of oxygen or nitrate. They use obtained energy to fix produce organic carbon from CO2. HAO cannot obtain energy from As III oxidation. This process may be an arsenic detoxification mechanism for the bacteria. Equilibrium thermodynamic calculations predict that As V concentrations should be greater than As III concentrations in all but strongly reducing conditions, i.e. where sulfate reduction is occurring. However, abiotic redox reactions of arsenic are slow. Oxidation of As III by dissolved O2 is a particularly slow reaction. For example, Johnson and Pilson 1975 gave half-lives for the oxygenation of As III in seawater ranging from several months to a year. In other studies, As V/As III ratios were stable over periods of days or weeks during water sampling when no particular care was taken to prevent oxidation, again suggesting relatively slow oxidation rates. Cherry found from experimental studies that the As V/As III ratios were stable in anoxic solutions for up to 3 weeks but that gradual changes occurred over longer timescales. Sterile water samples have been observed to be less susceptible to speciation changes than non-sterile samples. Oremland found that the reduction of As V to As III in Mono Lake was rapidly catalyzed by bacteria with rate constants ranging from 0.02 to 0.3-day−1. Arsenic and many of its compounds arsine, for instance are potent poisons. Element arsenic and arsenic sulfate and trioxide compounds are classified as toxic and dangerous for the environment in the European Union under directive 67/548/EEC. The International Agency for Research on Cancer IARC recognizes arsenic and inorganic arsenic compounds as group 1 carcinogens, and the EU lists arsenic trioxide, arsenic pentoxide, and arsenate salts as category 1 carcinogens. Arsenic is known to cause arsenicosis when present in drinking water, the most common species being arsenate As V and arsenite As III. In the United States since 2006, the maximum concentration in drinking water allowed by the Environmental Protection Agency EPA is 10 ppbArsenic Rule. U.S. Environmental Protection Agency. Adopted the 22nd of January 2001; effective the 23rd of January 2006 and the FDA set the same standard in 2005 for bottled water. The Department of Environmental Protection for New Jersey set a drinking water limit of 5 ppb in 2006. The IDLH immediately dangerous to life and health value for arsenic metal and inorganic arsenic compounds is 5 mg/m3 5 ppb. The Occupational Safety and Health Administration has set the permissible exposure limit PEL to a time-weighted average TWA of 0.01 mg/m3 0.01 ppb, and the National Institute for Occupational Safety and Health NIOSH has set the recommended exposure limit REL to a 15-minute constant exposure of 0.002 mg/m3 0.002 ppb. The PEL for organic arsenic compounds is a TWA of 0.5 mg/m3 0.5 ppb. In 2008, based on its ongoing testing of a wide variety of American foods for toxic chemicals,Total Diet Study and Toxic Elements Program the U.S. Food and Drug Administration set the level of concern for inorganic arsenic in apple and pear juices at 23 ppb, based on non-carcinogenic effects, and began blocking importation of products in excess of this level; it also required recalls for non-conforming domestic products. In 2011, the national Dr. Oz television show broadcast a program highlighting tests performed by an independent lab hired by the producers. Though the methodology was disputed it did not distinguish between organic and inorganic arsenic the tests showed levels of arsenic up to 36 ppb. In response, the FDA tested the worst brand from the Dr. Oz show and found much lower levels. Ongoing testing found 95% of the apple juice samples were below the level of concern. Later testing by Consumer Reports showed inorganic arsenic at levels slightly above 10 ppb, and the organization urged parents to reduce consumption. In July 2013, on consideration of consumption by children, chronic exposure, and carcinogenic effect, the FDA established an action level of 10 ppb for apple juice, the same as the drinking water standard. Concern about arsenic in rice in Bangladesh was raised in 2002, but at the time only Australia had a legal limit for food one milligram per kilogram, or 1000 ppb. Concern was raised about people who were eating U.S. rice exceeding WHO standards for personal arsenic intake in 2005. In 2011, the People's Republic of China set a food standard of 150 ppb for arsenic. In the United States in 2012, testing by separate groups of researchers at the Children's Environmental Health and Disease Prevention Research Center at Dartmouth College early in the year, focusing on urinary levels in children and Consumer Reports in November found levels of arsenic in rice that resulted in calls for the FDA to set limits. Lawmakers Urge FDA to Act on Arsenic Standards. Foodsafetynews.com the 24th of February 2012. Retrieved 2012-05-23. The FDA released some testing results in September 2012, and as of July 2013, is still collecting data in support of a new potential regulation. It has not recommended any changes in consumer behavior. Consumer Reports recommended That the EPA and FDA eliminate arsenic-containing fertilizer, drugs, and pesticides in food production; That the FDA establish a legal limit for food; That industry change production practices to lower arsenic levels, especially in food for children; and That consumers test home water supplies, eat a varied diet, and cook rice with excess water, then draining it off reducing inorganic arsenic by about one third along with a slight reduction in vitamin content. Evidence-based public health advocates also recommend that, given the lack of regulation or labeling for arsenic in the U.S., children should eat no more than 1.5 servings per week of rice and should not drink rice milk as part of their daily diet before age 5. They also offer recommendations for adults and infants on how to limit arsenic exposure from rice, drinking water, and fruit juice. A 2014 World Health Organization advisory conference was scheduled to consider limits of 200, 300 ppb for rice. In 2020, scientists assessed multiple preparation procedures of rice for their capacity to reduce arsenic content and preserve nutrients, recommending a procedure involving parboiling and water-absorption. Arsenic's toxicity comes from the affinity of arsenic III oxides for thiols. Thiols, in the form of cysteine residues and cofactors such as lipoic acid and coenzyme A, are situated at the active sites of many important enzymes. Arsenic disrupts ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits lipoic acid, which is a cofactor for pyruvate dehydrogenase. By competing with phosphate, arsenate uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration and ATP synthesis. Hydrogen peroxide production is also increased, which, it is speculated, has potential to form reactive oxygen species and oxidative stress. These metabolic interferences lead to death from multi-system organ failure. The organ failure is presumed to be from necrotic cell death, not apoptosis, since energy reserves have been too depleted for apoptosis to occur. Treatment of chronic arsenic poisoning is possible. British anti-lewisite dimercaprol is prescribed in doses of 5 mg/kg up to 300 mg every 4 hours for the first day, then every 6 hours for the second day, and finally every 8 hours for 8 additional days. However the USA's Agency for Toxic Substances and Disease Registry ATSDR states that the long-term effects of arsenic exposure cannot be predicted. Blood, urine, hair, and nails may be tested for arsenic; however, these tests cannot foresee possible health outcomes from the exposure. Long-term exposure and consequent excretion through urine has been linked to bladder and kidney cancer in addition to cancer of the liver, prostate, skin, lungs, and nasal cavity. Arsenic is bioaccumulative in many organisms, marine species in particular, but it does not appear to biomagnify significantly in food webs. In polluted areas, plant growth may be affected by root uptake of arsenate, which is a phosphate analog and therefore readily transported in plant tissues and cells. In polluted areas, uptake of the more toxic arsenite ion found more particularly in reducing conditions is likely in poorly drained soils. Arsenic and many of its compounds arsine, for instance are potent poisons. Element arsenic and arsenic sulfate and trioxide compounds are classified as toxic and dangerous for the environment in the European Union under directive 67/548/EEC. The International Agency for Research on Cancer IARC recognizes arsenic and inorganic arsenic compounds as group 1 carcinogens, and the EU lists arsenic trioxide, arsenic pentoxide, and arsenate salts as category 1 carcinogens. Arsenic is known to cause arsenicosis when present in drinking water, the most common species being arsenate As V and arsenite As III. In the United States since 2006, the maximum concentration in drinking water allowed by the Environmental Protection Agency EPA is 10 ppbArsenic Rule. U.S. Environmental Protection Agency. Adopted the 22nd of January 2001; effective the 23rd of January 2006 and the FDA set the same standard in 2005 for bottled water. The Department of Environmental Protection for New Jersey set a drinking water limit of 5 ppb in 2006. The IDLH immediately dangerous to life and health value for arsenic metal and inorganic arsenic compounds is 5 mg/m3 5 ppb. The Occupational Safety and Health Administration has set the permissible exposure limit PEL to a time-weighted average TWA of 0.01 mg/m3 0.01 ppb, and the National Institute for Occupational Safety and Health NIOSH has set the recommended exposure limit REL to a 15-minute constant exposure of 0.002 mg/m3 0.002 ppb. The PEL for organic arsenic compounds is a TWA of 0.5 mg/m3 0.5 ppb. In 2008, based on its ongoing testing of a wide variety of American foods for toxic chemicals,Total Diet Study and Toxic Elements Program the U.S. Food and Drug Administration set the level of concern for inorganic arsenic in apple and pear juices at 23 ppb, based on non-carcinogenic effects, and began blocking importation of products in excess of this level; it also required recalls for non-conforming domestic products. In 2011, the national Dr. Oz television show broadcast a program highlighting tests performed by an independent lab hired by the producers. Though the methodology was disputed it did not distinguish between organic and inorganic arsenic the tests showed levels of arsenic up to 36 ppb. In response, the FDA tested the worst brand from the Dr. Oz show and found much lower levels. Ongoing testing found 95% of the apple juice samples were below the level of concern. Later testing by Consumer Reports showed inorganic arsenic at levels slightly above 10 ppb, and the organization urged parents to reduce consumption. In July 2013, on consideration of consumption by children, chronic exposure, and carcinogenic effect, the FDA established an action level of 10 ppb for apple juice, the same as the drinking water standard. Concern about arsenic in rice in Bangladesh was raised in 2002, but at the time only Australia had a legal limit for food one milligram per kilogram, or 1000 ppb. Concern was raised about people who were eating U.S. rice exceeding WHO standards for personal arsenic intake in 2005. In 2011, the People's Republic of China set a food standard of 150 ppb for arsenic. In the United States in 2012, testing by separate groups of researchers at the Children's Environmental Health and Disease Prevention Research Center at Dartmouth College early in the year, focusing on urinary levels in children and Consumer Reports in November found levels of arsenic in rice that resulted in calls for the FDA to set limits. Lawmakers Urge FDA to Act on Arsenic Standards. Foodsafetynews.com the 24th of February 2012. Retrieved 2012-05-23. The FDA released some testing results in September 2012, and as of July 2013, is still collecting data in support of a new potential regulation. It has not recommended any changes in consumer behavior. Consumer Reports recommended That the EPA and FDA eliminate arsenic-containing fertilizer, drugs, and pesticides in food production; That the FDA establish a legal limit for food; That industry change production practices to lower arsenic levels, especially in food for children; and That consumers test home water supplies, eat a varied diet, and cook rice with excess water, then draining it off reducing inorganic arsenic by about one third along with a slight reduction in vitamin content. Evidence-based public health advocates also recommend that, given the lack of regulation or labeling for arsenic in the U.S., children should eat no more than 1.5 servings per week of rice and should not drink rice milk as part of their daily diet before age 5. They also offer recommendations for adults and infants on how to limit arsenic exposure from rice, drinking water, and fruit juice. A 2014 World Health Organization advisory conference was scheduled to consider limits of 200, 300 ppb for rice. In 2020, scientists assessed multiple preparation procedures of rice for their capacity to reduce arsenic content and preserve nutrients, recommending a procedure involving parboiling and water-absorption. Arsenic's toxicity comes from the affinity of arsenic III oxides for thiols. Thiols, in the form of cysteine residues and cofactors such as lipoic acid and coenzyme A, are situated at the active sites of many important enzymes. Arsenic disrupts ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits lipoic acid, which is a cofactor for pyruvate dehydrogenase. By competing with phosphate, arsenate uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration and ATP synthesis. Hydrogen peroxide production is also increased, which, it is speculated, has potential to form reactive oxygen species and oxidative stress. These metabolic interferences lead to death from multi-system organ failure. The organ failure is presumed to be from necrotic cell death, not apoptosis, since energy reserves have been too depleted for apoptosis to occur. Treatment of chronic arsenic poisoning is possible. British anti-lewisite dimercaprol is prescribed in doses of 5 mg/kg up to 300 mg every 4 hours for the first day, then every 6 hours for the second day, and finally every 8 hours for 8 additional days. However the USA's Agency for Toxic Substances and Disease Registry ATSDR states that the long-term effects of arsenic exposure cannot be predicted. Blood, urine, hair, and nails may be tested for arsenic; however, these tests cannot foresee possible health outcomes from the exposure. Long-term exposure and consequent excretion through urine has been linked to bladder and kidney cancer in addition to cancer of the liver, prostate, skin, lungs, and nasal cavity. Arsenic is bioaccumulative in many organisms, marine species in particular, but it does not appear to biomagnify significantly in food webs. In polluted areas, plant growth may be affected by root uptake of arsenate, which is a phosphate analog and therefore readily transported in plant tissues and cells. In polluted areas, uptake of the more toxic arsenite ion found more particularly in reducing conditions is likely in poorly drained soils.