What chemical can i use to break down op's?


Organophosphates break down quickly in the environment without chemicals, and thus residues on crops are less likely to be a problem.

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Carbamates are organic compounds derived from carbamic acid (NH2COOH). A carbamate group, carbamate ester (e.g., ethyl carbamate), and carbamic acids are functional groups that are inter-related structurally and often are interconverted chemically. Carbamate esters are also called urethanes. Carbamic acids are derived from amines: Carbamic acid is about as acidic as acetic acid.][ Ionization of a proton gives the carbamate anion, the conjugate base of carbamic acid: Carbamates also arise via hydrolysis of chloroformamides: Carbamates may be formed from the Curtius Rearrangement, where isocyanates formed are reacted with an alcohol. Although most of this article concerns organic carbamates, the inorganic salt ammonium carbamate is produced on a large scale as an intermediate in the production of the commodity chemical urea from ammonia and carbon dioxide. N-terminal amino groups of valine residues in the α- and β-chains of deoxyhemoglobin exist as carbamates. They help to stabilise the protein, when it becomes deoxyhemoglobin and increases the likelihood of the release of remaining oxygen molecules bound to the protein. The influence of these carbamates on the affinity of hemoglobin for O2 is called the Bohr effect. The ε-amino groups of the lysine residues in urease and phosphotriesterase also feature carbamate. The carbamate derived from aminoimidazole is an intermediate in the biosynthesis of inosine. Carbamoyl phosphate is generated from carboxyphosphate rather than CO2. Perhaps the most important carbamate is the one involved in the capture of CO2 by plants since this process is relevant to global warming. The enzyme Ribulose 1,5-bisphosphate carboxylase/oxygenase fixes a molecule of carbon dioxide as a carbamate at the start of the Calvin cycle). At the active site of the enzyme, a Mg2+ ion is bound to glutamate and aspartate residues as well as a lysine carbamate. The carbamate is formed when an uncharged lysine side-chain near the ion reacts with a carbon dioxide molecule from the air (not the substrate carbon dioxide molecule), which then renders it charged, and, therefore, able to bind the Mg2+ ion. The so-called carbamate insecticides feature the carbamate ester functional group. Included in this group are aldicarb, carbofuran (Furadan), carbaryl (Sevin), ethienocarb, fenobucarb, oxamyl and methomyl. These insecticides kill insects by reversibly inactivating the enzyme acetylcholinesterase. The organophosphate pesticides also inhibit this enzyme, although irreversibly, and cause a more severe form of cholinergic poisoning. Fenoxycarb has a carbamate group but acts as a juvenile hormone mimic, rather than inactivating acetylcholinesterase. The insect repellent icaridin is a substituted carbamate. Polyurethanes contain multiple carbamate groups as part of their structure. The "urethane" in the name "polyurethane" refers to these carbamate groups; ethyl carbamate (common name "urethane") is neither a component of polyurethanes, nor is used in their manufacture. Polyurethane polymers have a wide range of properties and are commercially available as foams, elastomers, and solids. Typically, polyurethane polymers are made by combining diisocyanates, e.g. toluene diisocyanate, and diols, where the carbamate groups are formed by reaction of the alcohols with the isocyanates: Iodopropynyl butylcarbamate is a wood and paint preservative and used in cosmetics. Urethane or ethyl carbamate was once produced commercially in the United States as an antineoplastic agent and for other medicinal purposes. It was found to be toxic and largely ineffective. It is occasionally used as a veterinary medicine. In addition, some carbamates are used in human pharmacotherapy, for example, the cholinesterase inhibitors neostigmine and rivastigmine, whose chemical structure is based on the natural alkaloid physostigmine. Other examples are meprobamate and its derivatives like carisoprodol, felbamate, and tybamate, a class of anxiolytic and muscle relaxant drugs widely used in the 60s before the rise of benzodiazepines, and still used nowadays in some cases. The protease inhibitor darunavir for HIV treatment also contains a carbamate functional group. There are two oxygen atoms in a carbamate (1), ROC(=O)NR2, and either or both of them can be conceptually replaced by sulfur. Analogues of carbamates with only one of the oxygens replaced by sulfur are called thiocarbamates (2 and 3). Carbamates with both oxygens replaced by sulfur are called dithiocarbamates (4), RSC(=S)NR2. There are two different structurally isomeric types of thiocarbamate: O-thiocarbamates can isomerise to S-thiocarbamates, for example in the Newman-Kwart rearrangement. Carbamates-thiocarbamates-dithiocarbamates-general-2D.png

Tris(1,3-dichloropropan-2-yl) phosphate Tris, TDCP, TDCPP, Fyrol FR-2 O=P(OC(CCl)CCl)(OC(CCl)CCl)OC(CCl)CCl Tris(1,3-dichloro-2-propyl)phosphate is an organophosphate with the chemical formula OP(OCH(CH2Cl)2)3. Also known as "Tris", this phosphate ester is used as a flame retardant. The safety of this compound has been questioned.

An organophosphate (sometimes abbreviated OP) or phosphate ester is the general name for esters of phosphoric acid. Phosphates are probably the most pervasive organophosphorus compounds. Many of the most important biochemicals are organophosphates, including DNA and RNA as well as many cofactors that are essential for life. Organophosphates are the basis of many insecticides, herbicides, and nerve gases. The EPA lists organophosphates as very highly acutely toxic to bees, wildlife, and humans. Recent studies suggest a possible link to adverse effects in the neurobehavioral development of fetuses and children, even at very low levels of exposure. Organophosphates are widely used as solvents, plasticizers, and EP additives. Organophosphates are widely employed both in natural and synthetic applications because of the ease with which organic groups can be linked together. Being a triprotic acid, phosphoric acid can form triesters whereas carboxylic acids only form monoesters. Esterification entails the attachment of organic groups to phosphorus through oxygen linkers. The precursors to such esters are alcohols. Encompassing many thousands of natural and synthetic compounds, alcohols are diverse and widespread. The phosphate esters bearing OH groups are acidic and partially deprotonated in aqueous solution. For example, DNA and RNA are polymers of the type [PO2(OR)(OR')-]n. Polyphosphates also form esters; an important example of an ester of a polyphosphate is ATP, which is the monoester of triphosphoric acid (H5P3O10). Alcohols can be detached from phosphate esters by hydrolysis, which is the reverse of the above reactions. For this reason, phosphate esters are common carriers of organic groups in biosynthesis. In health, agriculture, and government, the word "organophosphates" refers to a group of insecticides or nerve agents acting on the enzyme acetylcholinesterase (the pesticide group carbamates also act on this enzyme, but through a different mechanism). The term is used often to describe virtually any organic phosphorus(V)-containing compound, especially when dealing with neurotoxic compounds. Many of the so-called organophosphates contain C-P bonds. For instance, sarin is O-isopropyl methylphosphonofluoridate, which is formally derived from phosphorous acid (HP(O)(OH)2), not phosphoric acid (P(O)(OH)3). Also, many compounds which are derivatives of phosphinic acid are used as neurotoxic organophosphates. Organophosphate pesticides (as well as sarin and VX nerve agent) irreversibly inactivate acetylcholinesterase, which is essential to nerve function in insects, humans, and many other animals. Organophosphate pesticides affect this enzyme in varied ways, and thus in their potential for poisoning. For instance, parathion, one of the first OPs commercialized, is many times more potent than malathion, an insecticide used in combatting the Mediterranean fruit fly (Med-fly) and West Nile Virus-transmitting mosquitoes. Organophosphate pesticides degrade rapidly by hydrolysis on exposure to sunlight, air, and soil, although small amounts can be detected in food and drinking water. Their ability to degrade made them an attractive alternative to the persistent organochloride pesticides, such as DDT, aldrin, and dieldrin. Although organophosphates degrade faster than the organochlorides, they have greater acute toxicity, posing risks to people who may be exposed to large amounts (see the Toxicity section below). Commonly used organophosphates have included parathion, malathion, methyl parathion, chlorpyrifos, diazinon, dichlorvos, phosmet, fenitrothion, tetrachlorvinphos, azamethiphos, and azinphos methyl. Malathion is widely used in agriculture, residential landscaping, public recreation areas, and in public health pest control programs such as mosquito eradication. In the US, it is the most commonly used organophosphate insecticide. Forty organophosphate pesticides are registered in the U.S., with at least 73 million pounds used in agricultural and residential settings. They are of concern to both scientists and regulators because they work by irreversibly blocking an enzyme that's critical to nerve function in both insects and humans. Even at relatively low levels, organophosphates may be most hazardous to the brain development of fetuses and young children. The EPA banned most residential uses of organophosphates in 2001, but they are still sprayed agriculturally on fruits and vegetables. They're also used to control pests like mosquitos in public spaces such as parks. They can be absorbed through the lungs or skin or by eating them on food. Early pioneers in the field include Jean Louis Lssaigne (early 19th century) and Philippe de Clermont (1854). In 1932, German chemist Willy Lange and his graduate student, Gerde von Krueger, first described the cholinergic nervous system effects of organophosphates, noting a choking sensation and a dimming of vision after exposure. This discovery later inspired German chemist Gerhard Schrader at company IG Farben in the 1930s to experiment with these compounds as insecticides. Their potential use as chemical warfare agents soon became apparent, and the Nazi government put Schrader in charge of developing organophosphate (in the broader sense of the word) nerve gases. Schrader's laboratory discovered the G series of weapons, which included Sarin, Tabun, and Soman. The Nazis produced large quantities of these compounds, though did not use them during World War II. British scientists experimented with a cholinergic organophosphate of their own, called diisopropylfluorophosphate (DFP), during the war. The British later produced VX nerve agent, which was many times more potent than the G series, in the early 1950s, almost 20 years after the Germans had discovered the G series. After World War II, American companies gained access to some information from Schrader's laboratory, and began synthesizing organophosphate pesticides in large quantities. Parathion was among the first marketed, followed by malathion and azinphosmethyl. The popularity of these insecticides increased after many of the organochlorine insecticides like DDT, dieldrin, and heptachlor were banned in the 1970s. Effective organophosphates have the following structural features: Thiophosphoryl compounds, those bearing the P=S functionality, are much less toxic than related phosphoryl derivatives, which include sarin, VX and tetraethyl pyrophosphate. Thiophosphoryl compounds are not active inhibitors of acetylcholinesterase in either mammals or insects; in mammals, metabolism tends to remove lipophilic side groups from the phosphorus atom while in insects it tends to oxidize the compound, thus removing the terminal sulfur and replacing it with a terminal oxygen, which allows the compound to more efficiently act as an acetylcholinesterase inhibitor. Within these requirements, a large number of different lipophilic and leaving groups have been used. The variation of these groups is one means of fine tuning the toxicity of the compound. A good example of this chemistry are the P-thiocyanate compounds which use an aryl (or alkyl) group and an alkylamino group as the lipophilic groups. The thiocyanate is the leaving group. It was claimed in a German patent that the reaction of 1,3,2,4-dithiadiphosphetane 2,4-disulfides with dialkyl cyanamides formed plant protection agents which contained six membered (P-N=C-N=C-S-) rings. It has been proven in recent times by the reaction of diferrocenyl 1,3,2,4-dithiadiphosphetane 2,4-disulfide (and Lawesson's reagent) with dimethyl cyanamide that, in fact, a mixture of several different phosphorus-containing compounds is formed. Depending on the concentration of the dimethyl cyanamide in the reaction mixture, either a different six membered ring compound (P-N=C-S-C=N-) or a nonheterocylic compound (FcP(S)(NR2)(NCS)) is formed as the major product; the other compound is formed as a minor product. In addition, small traces of other compounds are also formed in the reaction. It is unlikely that the ring compound (P-N=C-S-C=N-) {or its isomer} would act as a plant protection agent, but (FcP(S)(NR2)(NCS)) compounds can act as nerve poisons in insects. Many organophosphates are potent nerve agents, functioning by inhibiting the action of acetylcholinesterase (AChE) in nerve cells. They are one of the most common causes of poisoning worldwide, and are frequently intentionally used in suicides in agricultural areas. Organophosphorus pesticides can be absorbed by all routes, including inhalation, ingestion, and dermal absorption. Their toxicity is not limited to the acute phase, however, and chronic effects have long been noted. Neurotransmitters such as acetylcholine (which is affected by organophosphate pesticides) are profoundly important in the brain's development, and many OPs have neurotoxic effects on developing organisms, even from low levels of exposure. Other organophosphates are not toxic, yet their main metabolites, such as their oxons are. Repeated or prolonged exposure to organophosphates may result in the same effects as acute exposure including the delayed symptoms. Other effects reported in workers repeatedly exposed include impaired memory and concentration, disorientation, severe depressions, irritability, confusion, headache, speech difficulties, delayed reaction times, nightmares, sleepwalking and drowsiness or insomnia. An influenza-like condition with headache, nausea, weakness, loss of appetite, and malaise has also been reported. Even at relatively low levels organophosphates may be hazardous to human health. The pesticides act on a set of brain chemicals closely related to those involved in ADHD, thus fetuses and young children, where brain development depends on a strict sequence of biological events, may be most at risk. They can be absorbed through the lungs or skin or by eating them on food. According to a 2008 report from the U.S. Department of Agriculture, in a representative sample of produce tested by the agency, 28 percent of frozen blueberries, 20 percent of celery, 27 percent of green beans, 17 percent of peaches, 8 percent of broccoli and 25 percent of strawberries contained traces of organophosphate. The United States Environmental Protection Agency lists the organophosphate parathion as a possible human carcinogen. A 2007 study linked the organophosphate insecticide chlorpyrifos, which is used on some fruits and vegetables, with delays in learning rates, reduced physical coordination, and behavioral problems in children, especially ADHD. An organic diet is an effective way to reduce exposure to the organophosphorus pesticides that are commonly used in agricultural production. Organophosphate metabolite levels rapidly drop and, for some metabolites, become undetectable in children's urine when an organic diet is consumed. A 2010 study has found that organophosphate exposure is associated with an increased risk of Alzheimer's disease. Another study from the same year found that each 10-fold increase in urinary concentration of organophosphate metabolites was associated with a 55% to 72% increase in the odds of ADHD in children. The study found that organophosphate exposure is associated with an increased risk of ADHD in children. Researchers analyzed the levels of organophosphate residues in the urine of more than 1,100 children aged 8 to 15 years old, and found that those with the highest levels of dialkyl phosphates, which are the breakdown products of organophosphate pesticides, also had the highest incidence of ADHD. Overall, they found a 35% increase in the odds of developing ADHD with every 10-fold increase in urinary concentration of the pesticide residues. The effect was seen even at the low end of exposure: children who had any detectable, above-average level of pesticide metabolite in their urine were twice as likely as those with undetectable levels to record symptoms of ADHD. Another 2010 study found that children who were exposed to organophosphate pesticides while still in their mother's womb were more likely to develop attention disorders years later. The researchers evaluated the children at age 3.5 and 5 years for symptoms of attention disorders and ADHD using maternal reports of child behavior, performance on standardized computer tests, and behavior ratings from examiners. Each tenfold increase in prenatal pesticide metabolites was linked to having five times the odds of scoring high on the computerized tests at age 5, suggesting a greater likelihood of a child having ADHD. The effect appeared to be stronger for boys than for girls. A 2012 study published in Environmental Health Perspectives found that prenatal organophosphate exposure had a significant impact on birthweight and gestational age. A 10-fold increase in organophosphates concentrations in the mother was associated with a 0.5 week decrease in the infant's gestational age and a birthweight decline of 151 grams (adjusted to account for changes in gestational age). "Diet and home pesticide use have been identified as important routes of exposure in non-agricultural populations," the researchers wrote, but noted that switching children from conventional to organic diets for several days reduced levels near or below the limit of detection, "suggesting that diet was the primary source of exposure in that study population." According to the non-governmental organisation Pesticide Action Network, the organophosphate parathion is one of the most dangerous pesticides. In the US alone more than 650 agricultural workers have been poisoned since 1966, of which 100 died. In underdeveloped countries many more people have suffered fatal and nonfatal intoxications. The World Health Organization, PAN and numerous environmental organisations propose a general and global ban. Its use is banned or restricted in 23 countries and its import is illegal in a total of 50 countries. Its use was banned in the U.S. in 2000 and it has not been used since 2003. Other than for agricultural use, the organophosphate diazinon has been banned in the U.S. Agriculturally, more than one million pounds of diazinon were used in California to control agricultural pests in 2000. The areas and crops on which diazinon are most heavily applied are structural pest control, almonds, head lettuce, leaf lettuce and prunes. In May 2006 the Environmental Protection Agency reviewed the use of the organophosphate dichlorvos and proposed its continued sale, despite concerns over its safety and considerable evidence suggesting it is carcinogenic and harmful to the brain and nervous system, especially in children. Environmentalists charge that the latest decision was the product of backroom deals with industry and political interference. In 2001 the EPA placed new restrictions on the use of the organophosphates phosmet and azinphos-methyl to increase protection of agricultural workers. The crop uses reported at that time as being phased out in four years included those for almonds, tart cherries, cotton, cranberries, peaches, pistachios, and walnuts. The crops with time-limited registration included apples/crab apples, blueberries, sweet cherries, pears, pine seed orchards, brussels sprouts, cane berries, and the use of azinphos-methyl by nurseries for quarantine requirements. The labeled uses of phosmet include alfalfa, orchard crops (e.g. almonds, walnuts, apples, cherries), blueberries, citrus, grapes, ornamental trees (not for use in residential, park, or recreational areas) and non-bearing fruit trees, Christmas trees and conifers (tree farms), potatoes and peas. Azinphos-methyl has been banned in Europe since 2006.

O,O-Diethyl O-3,5,6-trichloropyridin-2-yl phosphorothioate Brodan, Detmol UA, Dowco 179, Dursban, Empire, Eradex, Lorsban, Paqeant, Piridane, Scout, Stipend and Tricel. Clc1c(OP(=S)(OCC)OCC)nc(Cl)c(Cl)c1 InChI=1S/C9H11Cl3NO3PS/c1-3-14-17(18,15-4-2)16-9-7(11)5-6(10)8(12)13-9/h5H,3-4H2,1-2H3Yes 
Key: SBPBAQFWLVIOKP-UHFFFAOYSA-NYes  InChI=1/C9H11Cl3NO3PS/c1-3-14-17(18,15-4-2)16-9-7(11)5-6(10)8(12)13-9/h5H,3-4H2,1-2H3
Key: SBPBAQFWLVIOKP-UHFFFAOYAG 42 °C Chlorpyrifos (IUPAC name: O,O-diethyl O-3,5,6-trichloropyridin-2-yl phosphorothioate) is a crystalline organophosphate insecticide. It was introduced in 1965 by Dow Chemical Company and is known by many trade names (see table), including Dursban and Lorsban. It acts on the nervous system of insects by inhibiting acetylcholinesterase. Chlorpyrifos is moderately toxic to humans and chronic exposure has been linked to neurological effects, developmental disorders, and autoimmune disorders. Exposure during pregnancy retards the mental development of children, and most use in homes has been banned since 2001 in the U.S. In agriculture, it remains "one of the most widely used organophosphate insecticides", according to the United States Environmental Protection Agency (EPA). Chlorpyrifos is produced via a multistep synthesis from 3-methylpyridine, eventually reacting 3,5,6-trichloro-2-pyridinol with diethylthiophosphoryl chloride. The crops with the most intense chlorpyrifos use are cotton, corn, almonds, and fruit trees including oranges, bananas and apples. Chlorpyrifos is normally supplied as a 23.5% or 50% liquid concentrate. The recommended concentration for direct-spray pin point application is 0.5% and for wide area application a 0.03 – 0.12% mix is recommended (US). First registered in 1965 and marketed by Dow Chemical under the tradenames Dursban, Lorsban and Renoban, chlorpyrifos was a well known home and garden insecticide, and at one time it was one of the most widely used household pesticides in the US. In 1995, Dow was fined US$732,000 for not sending the EPA reports it had received on 249 chlorpyrifos poisoning incidents. Facing impending regulatory action by the EPA, Dow agreed to withdraw registration of chlorpyrifos for almost all use (except child-proof containerized insect baits) in homes and other places where children could be exposed, and severely restricted its use on crops. These changes took effect on Dec 31, 2001. It is still widely used in agriculture, and Dow continues to market Dursban for home use in developing countries. Dow's sales literature claimed Dursban has "an established record of safety regarding humans and pets." In 2003, Dow agreed to pay US$2 million – the largest penalty ever in a pesticide case – to the state of New York, in response to a lawsuit filed by the Attorney General to end Dow's illegal advertising of Dursban as "safe". On July 31, 2007, a coalition of farmworker and advocacy groups filed a lawsuit against the EPA seeking to end agricultural use of chlorpyrifos. The suit claims that the continued use of chlorpyrifos poses an unnecessary risk to farmworkers and their families. The suit was still pending as of August 2012. In August 2007, Dow's Indian offices were raided by Indian authorities for allegedly bribing officials to allow chlorpyrifos to be sold in the country. In 2008, the National Marine Fisheries Service (NMFS) imposed 1000 ft buffer zones around salmon habitat to protect endangered salmon and steelhead species. Aerial applications of chlorpyrifos will be prohibited within these zones. Chlorpyrifos is an organophosphate, with potential for both acute toxicity at larger amounts and neurological effects in fetuses and children even at very small amounts. For acute effects, the EPA classifies chlorpyrifos as Class II: moderately toxic. The oral LD50 for chlorpyrifos in experimental animals is 32 to 1000 mg/kg. The dermal LD50 in rats is greater than 2000 mg/kg and 1000 to 2000 mg/kg in rabbits. The 4-hour inhalation LC50 for chlorpyrifos in rats is greater than 200 mg/m3. Chlorpyrifos poisoning has been described by New Zealand scientists as the likely cause of death of several tourists in Chiang Mai, Thailand who developed myocarditis in 2011. Thai investigators have come to no conclusion as to what caused the deaths, but maintain that chlorpyrifos was not responsible, and that the deaths were not linked. Research indicated in 2006 that children exposed to chlorpyrifos while in the womb have an increased risk of delays in mental and motor development at age 3 and an increased occurrence of pervasive developmental disorders such as ADHD. An earlier study had demonstrated a correlation between prenatal chlorpyrifos exposure and lower weight and smaller head circumference at birth. Among 50 farm pesticides studied, chlorpyrifos was one of two found to be associated with higher risks of lung cancer among frequent pesticide applicators than among infrequent or non-users. Pesticide applicators as a whole were found to have a 50% lower cancer risk than the general public, which is attributable to the nearly 50% lower smoking rate found among farm workers. However, applicators of chlorpyrifos had a 15% lower cancer risk than the general public, which the study suggests indicates a likely link between chlorpyrifos application and lung cancer. A 2010 study found that each 10-fold increase in urinary concentration of organophosphate metabolites was associated with a 55% to 72% increase in the odds of ADHD in children. Studies have shown evidence of "deficits in Working Memory Index and Full-Scale IQ as a function of prenatal [chlorpyrifos] exposure [as measured when the children reach] 7 years of age." A 2012 study showed that the insecticide is more harmful to the mental development of boys than to that of girls. A 2011 study on the neurotoxic effects of chlorpyrifos showed that chlorpyrifos and its more toxic metabolite, chlorpyrifos oxon, altered firing rates in the locus coeruleus. These results indicate that the pesticide may be involved in Gulf War Syndrome and other neurodegenerative disorders. Chlorpyrifos is highly toxic to amphibians, and a recent study by the United States Geological Survey found that its main breakdown product in the environment, chlorpyrifos oxon, is even more toxic to these animals. The substance is very toxic for aquaculture fishand bees. A body burden study conducted by the Centers for Disease Control and Prevention found TCPy, a metabolite specific to chlorpyrifos, in the urine of 91% of people tested. An independent analysis of the CDC data claims that Dow has contributed 80% of the chlorpyrifos body burden of people living in the US. A 2008 study found dramatic drops in the urinary levels of chlorpyrifos metabolites when children switched from conventional to organic diets. Air monitoring studies conducted by the California Air Resources Board (CARB) have documented chlorpyrifos in the air of California communities. Analyses of the CARB data indicate that children living in areas of high chlorpyrifos use are often exposed to levels of the insecticide that exceed levels considered acceptable by the EPA. Recent air monitoring studies in Washington and Lindsay, CA have yielded comparable results. Grower and pesticide industry groups have argued that the air levels documented in these studies are not high enough to cause significant exposure or adverse effects, but a follow-up biomonitoring study in Lindsay, CA has shown that people there have higher than normal chlorpyrifos levels in their bodies. A study of the effects of chlorpyrifos on humans exposed over time showed that people exposed to high levels have autoimmune antibodies that are common in people with autoimmune disorders. There is a strong correlation to chronic illness associated with autoimmune disorders after exposure to chlorpyrifos. Before it was banned from residential use in the US, chlorpyrifos was detected in 100% of personal indoor air samples and 70% of umbilical-cord blood collected from pregnant women 18–35 years old who self-identified as African American or Dominican and living in New York City public housing.

VX (nerve agent)
Ethyl ({2-[bis(propan-2-yl)amino]ethyl}sulfanyl)(methyl)phosphinate Ethyl ({2-[bis(propan-2-yl)amino]ethyl}sulfanyl)(methyl)phosphinate VX
[2-(Diisopropylamino)ethyl]-O-ethyl methylphosphonothioate
Ethyl {[2-(diisopropylamino)ethyl]sulfanyl}(methyl)phosphinate CCOP(C)(=O)SCCN(C(C)C)C(C)C O=P(OCC)(SCCN(C(C)C)C(C)C)C InChI=1S/C11H26NO2PS/c1-7-14-15(6,13)16-9-8-12(10(2)3)11(4)5/h10-11H,7-9H2,1-6H3Yes 
Key: JJIUCEJQJXNMHV-UHFFFAOYSA-NYes  InChI=1/C11H26NO2PS/c1-7-14-15(6,13)16-9-8-12(10(2)3)11(4)5/h10-11H,7-9H2,1-6H3
Key: JJIUCEJQJXNMHV-UHFFFAOYAV -50 °C, 223 K, -58 °F 298 °C, 571 K, 568 °F VX, IUPAC name O-ethyl S-[2-(diisopropylamino)ethyl] methylphosphonothioate, is an extremely toxic substance that has no known uses except in chemical warfare as a nerve agent. As a chemical weapon, it is classified as a weapon of mass destruction by the United Nations in UN Resolution 687. The production and stockpiling of VX was outlawed by the Chemical Weapons Convention of 1993. The VX nerve agent is the best-known of the V-series of nerve agents and is considered an area denial weapon due to its physical properties. Ranajit Ghosh, a chemist at the Plant Protection Laboratories of Imperial Chemical Industries based in the United States was investigating a class of organophosphate compounds (organophosphate esters of substituted aminoethanethiols). Like Gerhard Schrader, an earlier investigator of organophosphates, Ghosh found that they were quite effective pesticides. In 1954, ICI put one of them on the market under the trade name Amiton. It was subsequently withdrawn, as it was too toxic for safe use. The toxicity did not go unnoticed, and samples of it had been sent to the British Armed Forces research facility at Porton Down for evaluation. After the evaluation was complete, several members of this class of compounds became a new group of nerve agents, the V agents. The best known of these is probably VX, assigned the UK Rainbow Code Purple Possum, with the Russian V-Agent coming a close second (Amiton is largely forgotten as VG). This class of compounds is also sometimes known as Tammelin's esters, after Lars-Erik Tammelin of the Swedish Defence Research Agency. Tammelin was also conducting research on this class of compounds in 1952, but did not publicize his work widely. With its high viscosity and low volatility, VX has the texture and feel of motor oil. This makes it especially dangerous, as it has a high persistence in the environment. It is odorless and tasteless, and can be distributed as a liquid, both pure and as a mixture with a polymer in the form of thickened agent, or as an aerosol. VX is an acetylcholinesterase inhibitor, i.e. it works by blocking the function of the enzyme acetylcholinesterase. Normally, an electric nerve pulse would cause the release of acetylcholine over a synapse that would stimulate muscle contraction. The acetylcholine is then broken down to non-reactive substances (acetic acid and choline) by the acetylcholinesterase enzyme. If more muscle tension is needed the nerve must release more acetylcholine. VX blocks the action of acetylcholinesterase, thus resulting in initial violent contractions, followed by sustained supercontraction restricted to the subjunctional endplate sarcoplasm and prolonged depolarizing neuromuscular blockade, the latter resulting in flaccid paralysis of all the muscles in the body. Sustained paralysis of the diaphragm muscle causes death by asphyxiation. VX is produced via the "transester process". This entails a series of steps whereby phosphorus trichloride is methylated to produce methyl phosphonous dichloride. The resulting material is reacted with ethanol to form a diester. This is then transesterified with -diisopropylaminoethanolN,N to produce the mixed phosphonite. Finally, this immediate precursor is reacted with sulfur to form VX. VX TransesterProcess.png VX can also be delivered in binary chemical weapons which mix in-flight to form the agent prior to release. Binary VX is referred to as VX2, and is created by mixing O-(2-diisopropylaminoethyl) O′-ethyl methylphosphonite (Agent QL) with elemental sulfur (Agent NE) as is done in the Bigeye aerial chemical bomb. It may also be produced by mixing with sulfur compounds, as with the liquid dimethyl polysulfide mixture (Agent NM) in the canceled XM-768 8-inch binary projectile program.][ Like other organophosphorus nerve agents, VX may be destroyed by reaction with strong nucleophiles such as pralidoxime. The reaction of VX with concentrated aqueous sodium hydroxide results in competing cleavage of the P-O and P-S esters, with P-S cleavage dominating. This is somewhat problematic, since the product of P-O bond cleavage (named EA 2192) remains toxic. In contrast, reaction with the anion of hydrogen peroxide (hydroperoxidolysis) leads to exclusive cleavage of the P-S bond., VX is the most toxic nerve agent ever synthesized for which activity has been independently confirmed. The median lethal dose (LD50) for humans is estimated to be about 10 milligrams through skin contact and the LCt50 for inhalation is estimated to be 30–50 mg·min/m³. Early symptoms of percutaneous exposure (skin contact) may be local muscular twitching or sweating at the area of exposure followed by nausea or vomiting. Some of the early symptoms of a VX vapor exposure to nerve agent may be rhinorrhea (runny nose) and/or tightness in the chest with shortness of breath (bronchial constriction). Miosis (pinpointing of the pupils) may be an early sign of agent exposure but is not usually used as the only indicator of exposure. Primary consideration should be given to removal of the liquid agent from the skin before removal of the individual to an uncontaminated area or atmosphere. After removal from the contaminated area, the casualty will be decontaminated by washing the contaminated areas with household bleach and flushing with clean water. After decontamination, the contaminated clothing is removed and skin contamination washed away. If possible, decontamination is completed before the casualty is taken for further medical treatment. An individual who has received a known nerve-agent exposure or who exhibits definite signs or symptoms of nerve-agent exposure should immediately have the nerve agent antidote drugs atropine, pralidoxime (2-PAM), and a sedative/antiepileptic such as diazepam injected. In several nations the nerve agent antidotes are issued for military personnel in the form of an autoinjector such as the United States military Mark I NAAK. Atropine works by binding and blocking a subset of acetylcholine receptors (known as muscarinic acetylcholine receptor, mAchR), so that the build up of acetylcholine produced by loss of the acetylcholinesterase function can no longer affect their target. The injection of pralidoxime regenerates bound acetylcholinesterase. Controlled studies in humans have shown that minimally toxic doses cause 70-75% depression of erythrocyte cholinesterase within several hours of exposure. The serum level of ethyl methylphosphonic acid (EMPA), a VX hydrolysis product, was measured to confirm exposure in one poisoning victim. The chemists Ranajit Ghosh and J.F. Newman discovered the V-series nerve agents at ICI in 1952, patenting diethyl S-2-diethylaminoethyl phosphono- thioate (agent VG) in November, 1952. Further commercial research on similar compounds ceased in 1955 when its lethality to humans was discovered. The US went into production of large amounts of VX in 1961 at Newport Chemical Depot. There was evidence of a combination of chemical agents having been used by Iraq against the Kurds at Halabja in 1988 under Saddam Hussein. Hussein later testified to UNSCOM that Iraq had researched VX, but had failed to weaponize the agent due to production failure. After U.S. and allied forces had invaded Iraq, no VX agent or production facilities were found. However, UNSCOM laboratories detected traces of VX on warhead remnants. In December 1994 and January 1995, Masami Tsuchiya of Aum Shinrikyo synthesized 100 to 200 grams of VX which was used to attack three persons. Two persons were injured and one 28-year-old man died, who is believed to be the only fully documented victim of VX ever in the world. The VX victim, whom Shoko Asahara had suspected as a spy, was attacked at 7:00 am on December 12, 1994 on the street in Osaka by Tomomitsu Niimi and another AUM member, who sprinkled the nerve agent on his neck. He chased them for about 100 yards (90 metres) before collapsing, dying 10 days later without ever coming out of a deep coma. Doctors in the hospital suspected at the time he had been poisoned with an organophosphate pesticide. But the cause of death was pinned down only after cult members arrested for the subway attack confessed to the killing. Ethyl methylphosphonate, methylphosphonic acid and diisopropyl-2-(methylthio) ethylamine were later found in the body of the victim. Unlike the cases for sarin (Matsumoto incident and Sarin gas attack on the Tokyo subway), VX was not used for mass murder. The only countries known to possess VX are the United States and Russia. A Sudanese pharmaceutical facility was bombed by the U.S. in 1998 acting on information that it used VX and that the origin of the agent was associated with both Iraq and Al Qaeda. The chemical in question was later identified as -ethyl hydrogen methylphosphonothioateO (EMPTA), used as a precursor in the production of VX. In the late 1960s, the US canceled its chemical weapons programs and began the destruction of its stockpiles of agents by a variety of methods. Early disposal included the US Army's CHASE (Cut Holes And Sink 'Em) program, in which old ships were filled with chemical weapons stockpiles and then scuttled. CHASE 8 was conducted on June 15, 1967, in which the S.S. Cpl. Eric G. Gibson was filled with 7,380 VX rockets and scuttled in 7,200 feet (2,200 m) of water, off the coast of Atlantic City, New Jersey. As of FY2008 the US Department of Defense reported dumping at least 124 tons][ of VX into the Atlantic Ocean off the coasts of New York/New Jersey and Florida. This material consisted of nearly 22,000 M55 rockets, 19 bulk containers holding 1,400 pounds (640 kg) each, and one M23 chemical landmine. Incineration was used for VX stockpile destruction starting in 1990 with Johnston Atoll Chemical Agent Disposal System in the North Pacific with other incineration plants following at Deseret Chemical Depot, Pine Bluff Arsenal, Umatilla Chemical Depot and Anniston Army Depot with the last of the VX inventory destroyed on December 24, 2008. The Newport Chemical Depot began VX stockpile elimination using chemical neutralization in 2005. VX was hydrolyzed to much less toxic byproducts by using concentrated caustic solution, and the resulting waste was then shipped off-site for further processing. Technical and political issues regarding this secondary byproduct resulted in delays, but the depot completed their VX stockpile destruction in August, 2008. The remaining VX stockpile in the US will be treated by the Blue Grass Chemical Agent-Destruction Pilot Plant, part of the Program Executive Office, Assembled Chemical Weapons Alternatives program. The program was established as an alternative to the incineration process successfully used by the Army Chemical Materials Agency, which completed its stockpile destruction activities in March 2012. The Blue Grass Pilot Plant has been plagued by repeated cost over-runs and schedule slippages since its inception. Worldwide, VX disposal has continued since 1997 under the mandate of the Chemical Weapons Convention. In Russia, the US is providing support for these destruction activities with the Nunn-Lugar Global Cooperation Initiative.  The Initiative has been able to convert a former chemical weapons depot at Shchuchye, Kurgan Oblast, into a facility to destroy those chemical weapons. The new facility, which opened in May 2009, has been working on eliminating the nearly 5,950 tons][ of nerve agents held at the former storage complex. However, this facility only holds about 14% of Russian chemical weapons that are stored throughout][ seven sites. Another such destruction plant for Russia, built for €140 million and paid for by Germany, is to open][ at Potshep, Bryansk Oblast, in 2009. The use and effects of VX nerve agent have been portrayed in the film The Rock, in an episode of the American science-based drama television series Eleventh Hour and on the History Channel's television series Modern Marvels episode "Deadliest Weapons"

O,O-Diethyl O-(4-nitrophenyl) phosphorothioate E605 S=P(Oc1ccc(cc1)[N+]([O-])=O)(OCC)OCC InChI=1S/C10H14NO5PS/c1-3-14-17(18,15-4-2)16-10-7-5-9(6-8-10)11(12)13/h5-8H,3-4H2,1-2H3Yes 
Key: LCCNCVORNKJIRZ-UHFFFAOYSA-NYes  InChI=1/C10H14NO5PS/c1-3-14-17(18,15-4-2)16-10-7-5-9(6-8-10)11(12)13/h5-8H,3-4H2,1-2H3
Key: LCCNCVORNKJIRZ-UHFFFAOYAR 6 °C, 279 K, 43 °F in xylene and butanol Parathion, also called parathion-ethyl or diethyl parathion, is an organophosphate compound. It is a potent insecticide and acaricide. It was originally developed by IG Farben in the 1940s. It is highly toxic to non-target organisms, including humans. Its use is banned or restricted in many countries, and there are proposals to ban it from all use. Closely related is "methyl parathion" (see below). "Parathion-methyl" (CAS#298-00-0), also known as methyl parathion or dimethyl parathion, was also developed and is marketed for similar uses. It is a distinct compound with diminished toxicity. Some trade names of parathion-methyl include Bladan M, Metaphos, ME605, and E601. Parathion was developed by Gerhard Schrader for the German trust IG Farben in the 1940s. After the war and the collapse of IG Farben due to the war crime trials, the Western allies seized the patent, and parathion was marketed worldwide by different companies and under different brand names. The most common German brand was E605 (banned in Germany after 2002); this was not a food-additive "E number" as used in the EU today. "E" stands for Entwicklungsnummer (German for "development number"). When pure, parathion is a white crystalline solid, however it is commonly distributed as a brown liquid that smells of rotting eggs or garlic. The insecticide is more or less stable, although it darkens when exposed to sunlight. Parathion is synthesized from diethyl dithiophosphoric acid (C2H5O)2PS2H, which is obtained by treatment of 5S2P with ethanol (methanol is used to prepare methyl parathion). Diethyl dithiophosphoric acid is chlorinated to generate diethylthiophosphoryl chloride, which is then treated with sodium 4-nitrophenolate (the sodium salt of 4-nitrophenol). As a pesticide, parathion is generally applied by spraying. It is often applied to cotton, rice and fruit trees. The usual concentrations of ready-to-use solutions are 0.05 to 0.1%. The chemical is banned for use on many food crops. Parathion acts on the enzyme acetylcholinesterase, but indirectly. After being ingested by insects (and unintentionally, by humans), the parathion becomes oxidized by oxidases to give paraoxon, replacing the double bonded sulfur with oxygen. The phosphate ester is more reactive in organisms than the phosphorothiolate ester, as the phosphorus atoms become much more electronegative. Degradation of parathion leads to more water soluble products. Hydrolysis, which deactivates the molecule, occurs at the aryl ester bond resulting in diethyl thiophosphate and 4-nitrophenol. Degradation proceeds differently under anaerobic conditions: the nitro group on parathion is reduced to the amine. Parathion is a cholinesterase inhibitor. It generally disrupts the nervous system by inhibiting acetylcholinesterase. It is absorbed via skin, mucous membranes, and orally. Absorbed parathion is rapidly metabolized to paraoxon, as described above. Paraoxon exposure can result in headaches, convulsions, poor vision, vomiting, abdominal pain, severe diarrhea, unconsciousness, tremor, dyspnea, and finally lung-edema as well as respiratory arrest. Symptoms of poisoning are known to last for extended periods of time, sometimes months. The most common and very specific antidote is atropine, in doses of up to 100 mg daily. Because atropine may also be toxic, it is recommended that small frequently repeated doses be used in treatment. If human poisoning is detected early and the treatment is prompt (atropine and artificial respiration), fatalities are infrequent. Insufficient oxygen will lead to cerebral hypoxia and permanent brain damage. Peripheral neuropathy including paralysis is noticed as late sequelae after recovery from acute intoxication. Parathion has been used for committing suicide and deliberately poisoning other persons. It is known as "Schwiegermuttergift" (mother-in-law poison) in Germany. For this reason, most formulations contain a blue dye providing warning. Parathion has been used as a chemical weapon, most notably by the Selous Scouts during the Rhodesian Bush War. Based on animal studies, parathion is considered by the U.S. Environmental Protection Agency to be a possible human carcinogen. Studies show that parathion is toxic to fetuses, but does not cause birth defects. It is classified as a UNEP Persistent Organic Pollutant and WHO Toxicity Class, "Ia, Extremely Hazardous". Parathion is very toxic to bees, fish, birds, and other forms of wildlife. Parathion can be replaced by many safer and less toxic alternatives (less toxic organophosphates, carbamates, or synthetic pyrethroids). To provide the end user with a minimum standard of protection, suitable protective gloves, clothing, and a respirator with organic-vapour cartridges must be worn. Industrial safety during the production process requires special ventilation and continuous measurement of air contamination in order not to exceed PEL levels, as well as paying careful attention to personal hygiene. Frequent analysis of workers' serum acetylcholinesterase activity is also helpful with regards to occupational safety, because the action of parathion is cumulative. If an area of the body is contaminated with parathion, the contamination should be removed immediately and thoroughly. Also, atropine has been used as a specific antidote. According to the non-governmental organisation Pesticide Action Network or PAN, parathion is one of the most dangerous pesticides. This organization lists parathion also as a 'bad actor chemical'. In the US alone more than 650 agricultural workers have been poisoned since 1966, of which 100 died. In underdeveloped countries many more people have suffered fatal and nonfatal intoxications. The World Health Organization, PAN and numerous environmental organisations propose a general and global ban. Its use is banned or restricted in 23 countries and its import is illegal in a total of 50 countries.

Oxon (chemical)
An oxon is an organic compound derived from another chemical in which a phosphorus-sulfur bond in the parent chemical has been replaced by a phosphorus-oxygen bond in the derivative. Important examples of oxons can be found in the family of pesticides known as organophosphates. Some of these chemicals, such as chlorpyrifos, diazinon, and parathion, do not manifest their main toxicity in their original form. Rather, an animal's liver replaces a phosphorus-sulfur bond with a phosphorus-oxygen bond, turning these chemicals into oxons. The oxons then inhibit an enzyme that breaks down acetylcholine, an important neurotransmitter. Acetylcholine starts to accumulate uncontrollably, wreaking havoc on the animal's nervous system.
chemicals chemical can Organophosphate Environment

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