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. wood preservation in the us as of 2002, us-based industries consumed 19,600 metric tons of arsenic. ninety percent of this was used for treatment of wood with chromated copper arsenate (cca). in 2007, 50% of the 5,280 metric tons of consumption was still used for this purpose. in the united states, the voluntary phasing-out of arsenic in production of consumer products and residential and general consumer construction products began on 31 december 2003, and alternative chemicals are now used, such as alkaline copper quaternary, borates, copper azole, cyproconazole, and propiconazole. although discontinued, this application is also one of the most concerning to the general public. the vast majority of older pressure-treated wood was treated with cca. cca lumber is still in widespread use in many countries, and was heavily used during the latter half of the 20th century as a structural and outdoor building material. although the use of cca lumber was banned in many areas after studies showed that arsenic could leach out of the wood into the surrounding soil (from playground equipment, for instance), a risk is also presented by the burning of older cca timber. the direct or indirect ingestion of wood ash from burnt cca lumber has caused fatalities in animals and serious poisonings in humans; the lethal human dose is approximately 20 grams of ash. scrap cca lumber from construction and demolition sites may be inadvertently used in commercial and domestic fires. protocols for safe disposal of cca lumber are not consistent throughout the world. widespread landfill disposal of such timber raises some concern, but other studies have shown no arsenic contamination in the groundwater. mapping of industrial releases in the us one tool that maps the location (and other information) of arsenic releases in the united states is toxmap. toxmap is a geographic information system (gis) from the division of specialized information services of the united states national library of medicine (nlm) funded by the us federal government. with marked-up maps of the united states, toxmap enables users to visually explore data from the united states environmental protection agency's (epa) toxics release inventory and superfund basic research programs. toxmap's chemical and environmental health information is taken from nlm's toxicology data network (toxnet), pubmed, and from other authoritative sources. bioremediation physical, chemical, and biological methods have been used to remediate arsenic contaminated water. bioremediation is said to be cost-effective and environmentally friendly. bioremediation of ground water contaminated with arsenic aims to convert arsenite, the toxic form of arsenic to humans, to arsenate. arsenate (+5 oxidation state) is the dominant form of arsenic in surface water, while arsenite (+3 oxidation state) is the dominant form in hypoxic to anoxic environments. arsenite is more soluble and mobile than arsenate. many species of bacteria can transform arsenite to arsenate in anoxic conditions by using arsenite as an electron donor. this is a useful method in ground water remediation. another bioremediation strategy is to use plants that accumulate arsenic in their tissues via phytoremediation but the disposal of contaminated plant material needs to be considered. bioremediation requires careful evaluation and design in accordance with existing conditions. some sites may require the addition of an electron acceptor while others require microbe supplementation (bioaugmentation). regardless of the method used, only constant monitoring can prevent future contamination. toxicity and precautions main article: arsenic poisoning arsenic hazards ghs labelling: pictograms signal word danger hazard statements h301+h331, h315, h318, h350, h410 precautionary statements p273, p280, p301+p310, p302+p352, p304+p340+p311, p305+p351+p338 arsenic and many of its compounds are especially potent poisons. small amount of arsenic can be detected by pharmacopoial methods which includes reduction of arsenic to arsenious with help of zinc and can be confirmed with mercuric chloride paper. classification elemental 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 and arsenite ". legal limits, food, and drink in the united states since 2006, the maximum concentration in drinking water allowed by the environmental protection agency (epa) is 10 ppb 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, 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). 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. 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. reducing arsenic content in rice an improved rice cooking approach to maximise arsenic removal while preserving nutrient elements 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. occupational exposure limits country limit argentina confirmed human carcinogen australia twa 0.05 mg/m3 – carcinogen belgium twa 0.1 mg/m3 – carcinogen bulgaria confirmed human carcinogen canada twa 0.01 mg/m3 colombia confirmed human carcinogen denmark twa 0.01 mg/m3 finland carcinogen egypt twa 0.2 mg/m3 hungary ceiling concentration 0.01 mg/m3 – skin, carcinogen india twa 0.2 mg/m3 japan group 1 carcinogen jordan confirmed human carcinogen mexico twa 0.2 mg/m3 new zealand twa 0.05 mg/m3 – carcinogen norway twa 0.02 mg/m3 philippines twa 0.5 mg/m3 poland twa 0.01 mg/m3 singapore confirmed human carcinogen south korea twa 0.01 mg/m3 sweden twa 0.01 mg/m3 thailand twa 0.5 mg/m3 turkey twa 0.5 mg/m3 united kingdom twa 0.1 mg/m3 united states twa 0.01 mg/m3 vietnam confirmed human carcinogen ecotoxicity 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. toxicity in animals compound animal ld50 route arsenic rat 763 mg/kg oral arsenic mouse 145 mg/kg oral calcium arsenate rat 20 mg/kg oral calcium arsenate mouse 794 mg/kg oral calcium arsenate rabbit 50 mg/kg oral calcium arsenate dog 38 mg/kg oral lead arsenate rabbit 75 mg/kg oral compound animal ld50 route arsenic trioxide (as(iii)) mouse 26 mg/kg oral arsenite (as(iii)) mouse 8 mg/kg im arsenate (as(v)) mouse 21 mg/kg im mma (as(iii)) hamster 2 mg/kg ip mma (as(v)) mouse 916 mg/kg oral dma (as(v)) mouse 648 mg/kg oral im = injected intramuscularly ip = administered intraperitoneally biological mechanism 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. exposure risks and remediation 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 electronic semiconductor manufacturing. inorganic arsenic is also found in coke oven emissions associated with the smelter industry. the conversion between as(iii) and as(v) is a large factor in arsenic environmental contamination. according to croal, gralnick, malasarn and newman, " understanding what stimulates as(iii) oxidation and/or limits as(v) reduction is relevant for bioremediation of contaminated sites (croal). the study of chemolithoautotrophic as(iii) oxidizers and the heterotrophic as(v) reducers can help the understanding of the oxidation and/or reduction of arsenic. treatment 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