Organophosphate

General chemical structure of an organophosphate

An organophosphate (sometimes abbreviated OP) or phosphate ester is the general name for 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.

OP(OH)3 + ROH → OP(OH)2(OR) + H2O
OP(OH)2(OR) + R'OH → OP(OH)(OR)(OR') + H2O
OP(OH)(OR)(OR') + R"OH → OP(OR)(OR')(OR") + H2O

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 biosynthesis.

Contents

  • Organophosphate pesticides 1
  • Organophosphates as nerve agents 2
    • History of nerve agents 2.1
    • Structural features of organophosphates 2.2
      • Terminal oxygen vs. terminal sulfur 2.2.1
      • Fine tuning 2.2.2
  • Organophosphate poisoning 3
  • Health effects 4
    • Chronic toxicity 4.1
    • Low level exposure 4.2
  • Proposal restrictions 5
  • See also 6
  • References 7
  • External links 8

Organophosphate pesticides

In health, agriculture, and government, the word "organophosphates" refers to a group of 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 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 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 [19]

Proposal restrictions

According to the non-governmental organisation

  • Costa LG (April 2006). "Current issues in organophosphate toxicology". Clin. Chim. Acta 366 (1-2): 1–13.  .
  • ATSDR Case Studies in Environmental Medicine: Cholinesterase Inhibitors, Including Pesticides and Chemical Warfare Nerve Agents U.S. Department of Health and Human Services
  • Organophosphates - an article by Frances M Dyro, MD
  • NYTimes: E.P.A. Recommends Limits On Thousands of Pesticides
  • EPA OP pesticide site
  • Epidemiological study of the relationships between exposure to organophosphate pesticides and indices of chronic peripheral neuropathy, and neuropsychological abnormalities in sheep farmers and dippers. Phase 3 Report Institute of Occupational Medicine TM/99/02c
  • Epidemiological study of the relationships between exposure to organophosphate pesticides and indices of chronic peripheral neuropathy, and neuropsychological abnormalities in sheep farmers and dippers. Phase 2 Report Institute of Occupational Medicine TM/99/0b
  • Epidemiological study of the relationships between exposure to organophosphate pesticides and indices of chronic peripheral neuropathy, and neuropsychological abnormalities in sheep farmers and dippers. Phase 1 Report Institute of Occupational Medicine TM/99/0a

External links

  1. ^ "Basic Information". Clothianidin – Registration Status and Related Information. U.S. EPA. 27 July 2012. 
  2. ^ "FENITROTHION". Pesticide Information Profiles. Extension Toxicology Network. Sep 1995. 
  3. ^ Malathion for mosquito control, US EPA
  4. ^ Bonner MR, Coble J, Blair A, et al. (2007). "Malathion Exposure and the Incidence of Cancer in the Agricultural Health Study". American Journal of Epidemiology 166 (9): 1023–34.  
  5. ^ Maugh II, Thomas H. (16 May 2010). "Study links pesticide to ADHD in children". Los Angeles Times. 
  6. ^ Goodman, Brenda (21 Apr 2011). "Pesticide Exposure in Womb Linked to Lower IQ". Health & Pregnancy. WebMD. 
  7. ^ "PARATHION". Pesticide Information Profiles. Extension Toxicology Network. Sep 1993. 
  8. ^ Jurewicz, Joanna; Hanke, Wojciech (9 Jul 2008). "Prenatal and Childhood Exposure to Pesticides and Neurobehavioral Development: Review of Epidemiological Studies". International Journal of Occupational Medicine and Environmental Health (Versita, Warsaw) 21 (2): 121–132.  
  9. ^ metaanalysis and inconclusive. 
  10. ^ "Study: ADHD linked to pesticide exposure". CNN. 17 May 2010. 
  11. ^ "Parathion (CASRN 56-38-2)". IRIS Summaries. U.S. EPA. 9 Aug 2012. 
  12. ^ Study Links Organophosphate Insecticide Used on Corn With ADHD. Beyond Pesticides. 5 January 2007.
  13. ^ a b Lu, Chensheng; Toepel, Kathryn; Irish, Rene; Fenske, Richard A.; Barr, Dana B.; Bravo, Roberto (2006). "Organic Diets Significantly Lower Children's Dietary Exposure to Organophosphorus Pesticides". Environmental Health Perspectives 114 (2): 260–3.  
  14. ^ Hayden, K.; Norton, M.; Darcey, D.; Ostbye, T.; Zandi, P.; Breitner, J. , E. A. ; Welsh-Bohmer, K. A.; For the Cache County Study Investigators (2010). "Occupational exposure to pesticides increases the risk of incident AD: the Cache County study". Neurology 74 (19): 1524–1530.  
  15. ^ Bouchard, Maryse F.; Bellinger, David C.; Wright, Robert O.; Weisskopf, Marc G. (17 May 2010). "Attention-Deficit/Hyperactivity Disorder and Urinary Metabolites of Organophosphate Pesticides" (PDF). Pediatrics (American Academy of Pediatrics) 125 (6): e1270–e1277.  
  16. ^ Megan, Brooks (17 May 2010). "Organophosphate Pesticides Linked to ADHD". Environmental AirTechs. 
  17. ^ Klein, Sarah. Study: ADHD linked to pesticide exposure. CNN. 17 May 2010.
  18. ^ Marks, Amy R.; Harley, Kim; Bradman, Asa; Kogut, Katherine; Boyd Barr, Dana; Johnson, Caroline; et al. (19 Aug 2012). "Organophosphate Pesticide Exposure and Attention in Young Mexican-American Children: The CHAMACOS Study". Environmental Health Perspectives 118 (12): 1768–1774.  
  19. ^ Rauch, SA; Braun, JM; Barr, DB; Calafat, AM; Khoury, J; Montesano, AM; et al. (20 Mar 2012). "Associations of prenatal exposure to organophosphate pesticide metabolites with gestational age and birth weight.". Environ Health Perspect. 120 (7): 1055–60.  
  20. ^ S. Kegley, B. Hill, S. Orme. "Parathion - Identification, toxicity, use, water pollution potential, ecological toxicity and regulatory information".  
  21. ^ a b "Parathion (Ethyl) - Remaining Use Canceled 9/00". Pesticide Active Ingredient Information. Cornell University. 13 Oct 2000. 
  22. ^ "Diazinon". Agrochemicals. Great Vista Chemicals. 
  23. ^ Raeburn, Paul (14 Aug 2006). "Slow-Acting".  
  24. ^ Hess, Glenn (1 Nov 2011). "US EPA restricts pesticides azinphos-methyl, phosmet". ICIS.com. 
  25. ^ Peck, Chuck; Aubee, Catherine (29 Mar 2010). "Risks of Phosmet Use to the Federally Threatened and Endangered California Tiger Salamander (Ambystoma californiense)" (PDF). Pesticide Effects Determinations. Environmental Fate and Effects Division, Office of Pesticide Programs. 
  26. ^ Scott, Alex (4 Aug 2008). "Europe Rejects Appeal for Use of Azinphos-methyl Pesticide". IHS Chemical Week. 

References

See also

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.[24] 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.[25] Azinphos-methyl has been banned in Europe since 2006.[26]

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.[23]

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.[22]

[21] Its use was banned in the U.S. in 2000 and it has not been used since 2003.[21] A 2012 study published in

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.[18]

A 2010 study has found that organophosphate exposure is associated with an increased risk 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.

An organic diet is an effective way to reduce exposure to the organophosphorus pesticides that are commonly used in agricultural production.[13] Organophosphate metabolite levels rapidly drop and, for some metabolites, become undetectable in children's urine when an organic diet is consumed.[13]

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.[12]

The carcinogen.[11]

Even at relatively low levels organophosphates may be hazardous to human health. The pesticides act on a set of brain chemicals Which 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.[8][9]Metaanalysis can't make causal statements 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, ″detectable″ traces of organophosphate were found 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.[10]

Low level exposure

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.[7]

Chronic toxicity

Health effects

Many organophosphates are potent nerve agents, functioning by inhibiting the action of acetylcholinesterase (AChE) in nerve oxons are. Treatment includes both a pralidoxime binder and an anticholinergic such as atropine.

Organophosphate poisoning

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.

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.

One of the products of the reaction of Fc2P2S4 with dimethyl cyanamide

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.

Fine tuning

Thiophosphoryl compounds, those bearing the P=S functionality, are much less toxic than related phosphoryl derivatives. 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.

Terminal oxygen vs. terminal sulfur

  • A terminal oxygen connected to phosphorus by a double bond, i.e. a phosphoryl group
  • Two lipophilic groups bonded to the phosphorus
  • A leaving group bonded to the phosphorus, often a halide

Effective organophosphates have the following structural features:

Structural features of organophosphates

After World War II, American companies gained access to some information from Schrader's laboratory, and began synthesizing organophosphate pesticides in large quantities. DDT, dieldrin, and heptachlor were banned in the 1970s.

Early pioneers in the field include 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.

History of nerve agents

Organophosphates as nerve agents

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.[6]

[5]

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