Organophosphate ( OP ) compounds are a diverse group of chemicals used in both domestic and industrial settings .
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.
Massive organophosphate intoxication from suicidal and accidental events, such as the Jamaican ginger palsy incident in 1930, led to the discovery of the mechanism of action of organophosphates. In 1995, a religious sect, Aum Shinrikyo, used sarin to poison people on a Tokyo subway.
Mass poisonings still occur today; in 2005, 15 victims were poisoned after accidentally ingesting ethion-contaminated food in a social ceremony in Magrawa, India.
Nerve agents have also been used in battle, notably in Iraq in the 1980s. Additionally, chemical weapons still pose a very real concern in this age of terrorist activity.
Exposure to organophosphates (OPs) is also possible via intentional or unintentional contamination of food sources. Although no clinical effects of chronic, low-level organophosphates (OPs) exposure from a food source have been shown, advancements in risk assessment and preparedness are ongoing
The primary mechanism of action of organophosphate pesticides is inhibition of carboxyl ester hydrolases, particularly acetylcholinesterase ( AChE ). AChE is an enzyme that degrades the neurotransmitter acetylcholine ( ACh ) into choline and acetic acid . ACh is found in the central and peripheral nervous system, neuromuscular junctions, and red blood cells ( RBCs).
Organophosphates inactivate AChE by phosphorylating the serine hydroxyl group located at the active site of AChE . The phosphorylation occurs by loss of an organophosphate leaving group and establishment of a covalent bond with AChE .
Organophosphates can be absorbed cutaneously, ingested, inhaled, or injected. Although most patients rapidly become symptomatic, the onset and severity of symptoms depend on the specific compound, amount, route of exposure, and rate of metabolic degradation
In 2007, The American Association of Poison Control Centers' received 96,307 calls (3.4% of all human exposures) related to pesticide exposures, many of which involved organophosphate (OP) agents and 80 uses of 2-PAM.
However, poison center – recorded exposures to organophosphates (OPs) from 1995 to 2004 have declined because of the United States Environmental Protection Agency phasing out commonly used household and agricultural organophosphate (OP) agents.
Pesticide poisonings are among the most common modes of poisoning fatalities. In countries such as India and Nicaragua, organophosphates (OPs) are easily accessible and, therefore, a source of both intentional and unintentional poisonings.
The incidence of international organophosphate-related human exposures appears to be underestimated.
-Worldwide mortality studies report mortality rates from 3-25%. The compounds most frequently involved include malathion, dichlorvos, trichlorfon, and fenitrothion/malathion.
-Mortality rates depend on the type of compound used, amount ingested, general health of the patient, delay in discovery and transport, insufficient respiratory management, delay in intubation, and failure in weaning off ventilatory support.
-Complications include severe bronchorrhea, seizures, weakness, and neuropathy. Respiratory failure is the most common cause of death.
Signs and symptoms of organophosphate poisoning can be divided into 3 broad categories, including ( 1 ) muscarinic effects, ( 2 ) nicotinic effects, and ( 3 ) CNS effects .
1- Mnemonic devices used to remember the muscarinic effects of organophosphates are SLUDGE ( salivation, lacrimation, urination, diarrhea, GI upset, emesis ) and DUMBELS ( diaphoresis and diarrhea; urination; miosis; bradycardia, bronchospasm, bronchorrhea; emesis; excess lacrimation; and salivation ).
Cont.. Muscarinic effects by organ systems include the following Cardiovascular : Bradycardia, hypotension Respiratory : Rhinorrhea, bronchorrhea, bronchospasm, cough, severe respiratory distress Gastrointestinal : Hypersalivation, nausea and vomiting, abdominal pain, diarrhea, fecal incontinence Genitourinary : Incontinence Ocular : Blurred vision, miosis Glands : Increased lacrimation, diaphoresis signs and symptoms include muscle fasciculations, cramping, weakness, and diaphragmatic failure .