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Organophosphate poisoning

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Organophosphate poisoning
SpecialtyEmergency medicine Edit this on Wikidata

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. Organophophate poisoning may cause what is known as the 'suicide impulse' which may lead to the high level of suicides in some sectors of the agricultural industry.[1]

Examples

Effects

The effects of organophosphate poisoning are recalled using the mnemonic SLUDGEM (Salivation, Lacrimation, Urination, Defecation, Gastrointestinal motility, Emesis, miosis)[2]

These side effects occur because of the excess acetylcholine that results from blocking acetylcholinesterase. In addition, bronchospasm, blurred vision and bradycardia may result.

An additional mnemonic is DUMBELLS: Diarrhea, Urination, Miosis, Bradycardia, Bronchoconstriction, Emesis, Lacrimation, Salivation, Sweating, Secretion.[citation needed]

Treatment

Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime),[3] though the use of "-oximes" has been found to be of no benefit, or possibly harmful, in at least two meta-analyses.[4][5] Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.

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 currently being researched. Aerotoxic Syndrome is a medical condition allegedly caused by exposure to contaminated bleed air.

Purdey (1998) suggested that organophosphates, in particular Phosmet, induced the transmissible spongiform encephalopathy epidemic of BSE.[6] A European Union food safety Scientific Steering Committee examined the evidence and did not find a link.[7]

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. [8]

Ginger Jake

Main article: 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.[9]

Effects

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,"[10] and Abou Donia the term, OPICN, or Organophosphate-Induced Chronic Neuropathy for describing these effects.[11]

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

Governmental review

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. [12]

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.[13]

See also

Organophosphate Pesticides Reports

References

  1. ^ http://www.pan-uk.org/pestnews/Actives/organoph.htm
  2. ^ Toxicity, Organophosphate and Carbamate at eMedicine
  3. ^ Jokanović M, Prostran M (2009). "Pyridinium oximes as cholinesterase reactivators. Structure-activity relationship and efficacy in the treatment of poisoning with organophosphorus compounds". Curr. Med. Chem. 16 (17): 2177–88. doi:10.2174/092986709788612729. PMID 19519385.
  4. ^ Rahimi R, Nikfar S, Abdollahi M (2006). "Increased morbidity and mortality in acute human organophosphate-poisoned patients treated by oximes: a meta-analysis of clinical trials". Hum Exp Toxicol. 25 (3): 157–62. doi:10.1191/0960327106ht602oa. PMID 16634335. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  5. ^ Peter JV, Moran JL, Graham P (2006). "Oxime therapy and outcomes in human organophosphate poisoning: an evaluation using meta-analytic techniques". Crit. Care Med. 34 (2): 502–10. doi:10.1097/01.CCM.0000198325.46538.AD. PMID 16424734. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  6. ^ Purdey M (1998). "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. 50 (2): 91–111. doi:10.1016/S0306-9877(98)90194-3. PMID 9572563. {{cite journal}}: Unknown parameter |month= ignored (help)
  7. ^ "Health and Consumer Protection – Scientific Steering Committee – Outcome of discussions 18". Retrieved 2007-07-30.
  8. ^ 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.
  9. ^ Morgan JP, Tulloss TC (1976). "The Jake Walk Blues. A toxicologic tragedy mirrored in American popular music". Ann. Intern. Med. 85 (6): 804–8. PMID 793467. {{cite journal}}: Unknown parameter |month= ignored (help)
  10. ^ Jamal GA (1997). "Neurological syndromes of organophosphorus compounds". Adverse Drug React Toxicol Rev. 16 (3): 133–70. PMID 9512762. {{cite journal}}: Unknown parameter |month= ignored (help)
  11. ^ Abou-Donia MB (2003). "Organophosphorus ester-induced chronic neurotoxicity". Arch. Environ. Health. 58 (8): 484–97. doi:10.3200/AEOH.58.8.484-497. PMID 15259428. {{cite journal}}: Unknown parameter |month= ignored (help)
  12. ^ Janofsky, Michael. "E.P.A. Recommends Limits On Thousands of Pesticides", The New York Times, August 4, 2006, accessed April 1, 2008.
  13. ^ Slotkin TA, Levin ED, Seidler FJ (2006). "Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity". Environ. Health Perspect. 114 (5): 746–51. doi:10.1289/ehp.8828. PMC 1459930. PMID 16675431. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
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