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Organophosphate poisoning

Organophosphate poisoning
Classification & external resources
ICD-10 T60.0
ICD-9 989.3

Many organophosphates are potent neurotoxins, 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.



The effects of organophosphate poisoning are recalled using the mnemonic SLUDGE (Salivation, Lacrimation, Urination, Diaphoresis (or Defecation), Gastrointestinal motility, Emesis)[1]


Atropine can be used as an antidote in conjunction with pralidoxime, though the use of "-oximes" has been found to be of no benefit, or possibly harmful, in at least two meta-analyses.[2][3]

Potential effects of environmental organophosphates

The use of the organophosphates in aviation lubricating oils and hydraulic fluids and its impact on health and flight safety is a matter of some debate. Airline employees set up a non profit group in 2001 to highlight their concerns called the Aviation Organophosphate Information Site (AOPIS).[4]

Purdey (1998) suggested that organophosphates, in particular Phosmet, induced the transmissible spongiform encephalopathy epidemic of BSE.[5] An European Union food safety Scientific Steering Committee examined the evidence and did not find a link.[6]

As opposed to the two examples given above, the toxicological literature on persistent chronic toxicity from acute poisonings or long-term low level exposure is quite extensive. The phenomenon of OPIDP (organophosphate induced delayed polyneuropathy, also OPIDN), which causes degeneration of the peripheral nerves, has been noted to occur several weeks after exposure to some organophosphates. [7]

Ginger Jake

A striking example of OPIDN occurred during the 1930s Prohibition Era when thousands of men in the American South and Midwest developed arm and leg weakness and pain after drinking a "medicinal" alcohol substitute. The drink, called "Ginger Jake," contained an adulterated Jamaican ginger extract containing tri-ortho-cresyl phosphate (TOCP) which resulted in partially reversible neurologic damage. The damage resulted in the limping "Jake Leg" or "Jake Walk" which were terms frequently used in the blues music of the period. Europe and Morocco both experienced outbreaks of TOCP poisoning from contaminated abortifacients and cooking oil, respectively.[8]


Other studies suggest a link between chronic low level organophosphate exposure and neuropsychiatric and behavioral effects. Jamal has suggested the term COPIND, or "Chronic Organophosphate-Induced Neurologic Dysfunction,"[9] and Abou Donia the term, OPICN, or Organophosphate-Induced Chronic Neuropathy for describing these effects.[10]

Low-level effects on the developing brains of fetuses, infants, and children have been documented as well.


The U.S. Food Quality Protection Act (FQPA), passed in 1996, designated the United States Environmental Protection Agency (EPA) to conduct a 10 year review process of the health and environmental effects of all pesticides, beginning with the Organophosphates. The process has taken longer than expected, but was recently concluded and eliminated or modified thousands of uses. NYTimes Aug 4, 2006

Many non-governmental and research groups, as well as the EPA's Office of Inspector General, have published concerns that the review did not take into account possible neurotoxic effects on developing fetuses and children, an area of developing research. OIG report. A group of leading EPA scientists sent a letter to the chief administrator, Stephen Johnson, decrying the lack of developmental neurotoxicity data in the review process. EPA Letter EHP article New studies have shown toxicity to developing organisms during certain "critical periods" at doses much lower than those previously suspected to cause harm.[11]

See also


  1. ^ eMedicine - Toxicity, Organophosphate and Carbamate : Article by Daniel K Nishijima, MD. Retrieved on 2007-08-22.
  2. ^ Rahimi R, Nikfar S, Abdollahi M. Increased morbidity and mortality in acute human organophosphate-poisoned patients treated by oximes: a meta-analysis of clinical trials. Hum Exp Toxicol. 2006 Mar;25(3):157-62. PMID 16634335
  3. ^ Peter JV, Moran JL, Graham P. Oxime therapy and outcomes in human organophosphate poisoning: an evaluation using meta-analytic techniques. Crit Care Med. 2006 Feb;34(2):502-10. Review. PMID 16424734
  4. ^ Aviation Organophoshate Information Site: Informing crews to the potential of organophosphate exposure due to the contamination of the aircraft air conditioning system.. Retrieved on 2007-07-30.
  5. ^ Purdey M. High-dose exposure to systemic phosmet insecticide modifies the phosphatidylinositol anchor on the prion protein: the origins of new variant transmissible spongiform encephalopathies? Med Hypotheses 1998;50:91-111. PMID 9572563.
  6. ^ Health and Consumer Protection - Scientific Steering Committee - Outcome of discussions 18. Retrieved on 2007-07-30.
  7. ^ Costa LG (2006). "Current issues in organophosphate toxicology". Clin. Chim. Acta 366 (1-2): 1-13. doi:10.1016/j.cca.2005.10.008. PMID 16337171.
  8. ^ Morgan JP, Tulloss TC. The Jake Walk Blues. A toxicologic tragedy mirrored in American popular music. Annals of Internal Medicine. 1976 Dec;85(6):804-8. PMID: 793467.
  9. ^ Jamal GA. "Neurological syndromes of organophosphorus compounds." Adverse Drug React Toxicol Rev. 1997 Aug;16(3):133-70. PMID: 9512762
  10. ^ Abou-Donia MB. "Organophosphorus ester-induced chronic neurotoxicity." Arch Environ Health. 2003 Aug;58(8):484-97. PMID: 15259428
  11. ^ Slotkin TA, Levin ED, Seidler FJ. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Environ Health Perspect. 2006 May;114(5):746-51. PMID: 16675431
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Organophosphate_poisoning". A list of authors is available in Wikipedia.
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