Organophosphorus Poisoning: Action, Symptoms, Causes and Uses

Organophosphorus poisoning

Pesticides are chemical and biological substances such as bacteria, viruses, or disinfectants that are meant to detect or kill pests. Organophosphorus can be classified according to its origin. It can be further divided into Organic and Inorganic.

Inorganic pesticides do not comprise carbon and are generally extracted from mineral ores extracted from the earth. Examples of inorganic pesticides comprise Copper Sulphate, Ferrous Sulphate, Copper, and sulfur. On the other hand, Organic pesticides include carbon in their chemical structure.

Organophosphates are a common class of insecticides. Actually, its large doses of organophosphates can also harm people and other animals. It can occur when you’re exposed to them for too long or at high levels. They are typically colorless-to-brown liquids at room temperature. Some may be odorless, while others have a fruit-like smell.

According to research, it says as many as 25 million agricultural workers across the developing world have at least one episode of organophosphate poisoning per year. It’s being seen with more frequency in areas where there is limited access to insecticide safety gear, such as suits and breathing apparatuses.

Organophosphates are among the most widely used insecticides in India as well as in the whole world. Organophosphorus can be derived from phosphoric acid or phosphonic acid. It can broadly be classified into four sub-categories i.e.,

  1. Phosphoric acid
  2. Thio-phosphoric
  3. Di-Thio phosphoric
  4. Miscellaneous
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During the decade of 1930- 1940, Gerhard Schrader and his co-workers realized the insecticidal properties of these compounds and by the end of the World War II they were successful to make many of the insecticidal Organophosphates used at present.

Organophosphorus is derived from

  1. Phosphoric Acid

*Phosphates has more pesticidal properties than phosphites.

2. Phosphonic Acid

Examples of phosphoric acid are:-

a) Dichlorofos/ dichlorovos

b) Bromochlorophos

3. Thio-phosphoric acid

Example of Thio-phospheric acid is Parathion.

4. Di-thiophosphric acid

Example of di-thiophosphoric acid is Malathion.

Mode of Action

Organophosphates are powerful inhibitors of acetylcholinesterase which is liable for hydrolyzing acetylcholine to choline and acetic acid after its release and completion of function. As a result, there is a build-up of acetylcholine with continuous stimulation of local receptors and ultimately paralysis of nerves or muscles.

Although organophosphates differ structurally from acetylcholine, they can bind to the acetylcholinesterase molecule at the active site and phosphorylate the serine. When this occurs, the consequential conjugate is infinitely more stable than the acetylcholinesterase conjugate, although endogenous hydrolysis does occur.

Depending on the amount of stability and charge distribution, the time to hydrolysis is increased. Phosphorylated enzymes degrade very slowly over days to weeks, making the acetylcholinesterase essentially inactive.

Once the acetylcholinesterase is phosphorylated, over the next 24 to 48 hours an alkyl group is eventually lost from the conjugate, further worsening the situation. As this occurs, the enzyme can no longer spontaneously hydrolyze and becomes permanently inactivated. Apart from acetylcholinesterase, organophosphates exert powerful inhibitory action over other carboxylic ester hydrolases such as chymotrypsin, plasma, and hepatic carboxylesterases, and another nonspecific protease.

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Causes of Organophosphorus Poisoning

The people most at-risk for organophosphorus poisoning are those who live or work on or near farms. You can also get organophosphate poisoning by intense contaminated food or water. The most common involuntary exposure routes are through breathing and contact with the skin. People who intentionally expose themselves to organophosphates tend to inhale and ingest it. These concentrated, high doses are often fatal.

Toxicokinetics

Organophosphates can be absorbed by any route including transconjunctival, transdermal, inhalational, across the GI and GU mucosa, and through direct injection. Appearances usually begin within a few minutes to few hours, but may be delayed up to 12 hours or more in the case of certain compounds (e.g. Parathion).

Fatal Dose

Extremely Toxic:- (LD50: 1 – 50 mg/kg) to highly toxic (LD50: 51 to 500 mg/kg) – Chlorfenvinphos, Chlorpyriphos, Dichlorvos, Dimethoate, Disulfoton, Ethion,  Fensulfothion, Fenthion, Fonophos, Formothion, Methyl Parathion, Mevinphos, Monocrotophos, Oxydemeton Methyl, Phenthoate, Phorate, Phosphamidon, Quinalphos, TEPP and Thiometon.

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Moderately toxic:- (LD50: 501 to 5000 mg/kg) to slightly toxic (LD50: >5000mg/kg)- Abate, Acephate, Coumaphos, Crufomate, Famphur, Glyphosate, Malathion, Phenthoate, Primiphos Methyl, Ronnel, Temephos, Triazophos, and Trichlorphon.

Fatal Period

In fatal doses symptoms starts within half an hour and death occurs within three hours. In non-fatal cases, effect last for 36 hours and fade off in 48-72 hours to 3 weeks.

Symptoms of Organophosphorus Poisoning

  1. Glands like sweat gland, lacrimal gland and excessive salivation (ptyalism) can be seen.
  2. Cyanosis (lack of oxygen in blood).
  3. Miosis (constriction of pupil of eye).
  4. Tremors.
  5. Slurred speech.
  6. Weakness (ATP formation not occurred).

Medicolegal Importance

  1. They are mostly seen in Homicidal, suicidal and accidental poisoning cases.
  2. Hospitalizing all patients for at least 4-6 days to notice out the symptoms, because of the risk of development of respiratory depression or immediate syndrome.
  3. The symptoms of OPC poisoning can mimic other diseases.

Uses of Organophosphorous

  1. It can be sprayed on crops and plants.
  2. They are used in agriculture, home gardens, and veterinary practice

Conclusions

Organophosphorus insecticide poisoning is a serious condition that requires rapid diagnosis and treatment. Since respiratory failure is the major reason for death, careful monitoring, appropriate management. Early recognition of this complication may decrease the mortality rate among these patients.

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