Organo-phosphorus Poisoning

Organo-phosphorus compounds

According to the World Health Organization (WHO), 3 million instances of pesticide poisoning (mostly OP compounds) occur each year, resulting in over 250,000 fatalities. One million are unintentional poisonings, while two million are suicidal poisonings. The frequency has progressively grown in recent years, and it has reached a point in developing nations where it may be referred to be a “social tragedy.” Clinical criteria are used to make a diagnosis. Atropine and oximes are well-known antidotes for OP poisoning. While the effectiveness of atropine has been clinically confirmed, clinical experience with pralidoxime has been inconclusive. Many innovative treatment techniques, such as K-oximes, hemoperfusion, and fresh frozen plasma, are being investigated. Prevention appears to be the most effective management strategy.


  • Organo-phosphorus compound as poisons have become common only in the past few decades.
  • They are alkyl and aryl phosphates.
  • Organo phosphorus compounds are available as dusts, granules, or liquids.
  • Some products need to be diluted with water before use.
  • Some products are burnt to make smoke that kills insects.
  • They are powerful insecticides and deadly poisons.
  • They are complex organic compounds containing sulphur, phosphorus and other organic radicles mostly in the form of alkyl and aryl phosphate.
  • Organophosphorus compounds are available as dust powder or liquid.
  • Organophosphorus compounds are classified into 2 forms: Alkyl and Aryl compounds.

1.Alkyl compounds – such as tetraethyl pyrophosphate (TEPP), hexa-ethyl tetraphosphate (HETP), octa- methyl pyrophosphate (OMPA), malathion etc.

2. Aryl compounds – such as parathion, chlorothion, diazinon (Tik-20), paraoxon etc.


  • These compounds are used as pesticides extensively in agriculture and horticulture.
  • They are also used to kill household bugs, flies and other pests.

Fatal Dose

The organophosphates can be classified according to toxicity:

Mild Toxic: Chlorothion and malathion are mild toxics as fatal dose is more than 25 gm.

Moderately Toxic: Diazinon has a fatal dose of 10–25 gm.

Highly Toxic: The fatal dose is less than 5 gm. Examples are parathion (15–30 mg), methyl parathion (15 mg) and TEPP (5 gm).

Fatal Period

Symptoms start within 30 minutes and death may occur within 4 hours. In non-fatal cases, effects may last for 30–72 hours.


  • These substances are given or taken in food or inhaled accidently.
  • They are also administered through injection also.
  • As they are very strong poisons, they are being used increasingly for homicidal and suicidal purposes.

Absorption, Metabolism and Excretion

● Organophosphorus compounds are absorbed by any route such as skin, conjunctiva, inhalation, oral or by direct injection.

● Some compounds such as parathion are stored in body fat and are released slowly in the circulation thus prolonging the duration of toxic action.

● Parathion is first metabolized to paraoxon, which is the active toxic agent and then to paranitrophenol that is excreted into urine. Malathion is metabolized in liver by esterases and part of this metabolized product is excreted in urine as phosphate.

Mechanism of Action

●Organophosphates are powerful inhibitors of acetylcholinesterase which is responsible for hydrolysing acetylcholine to choline and acetic acid after its release and completion of function (i.e. propagation of action potential). As a result, there is accumulation of acetylcholine with continued stimulation of local receptors and eventual paralysis of nerve or muscle.

●Although organophosphates differ structurally from acetylcholine, they can bind to the acetylcholinesterase molecule at the active site and phosphorylate the serine moiety. When this occurs, the resultant conjugate is infinitely more stable than the acetylcholine-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 exacerbating the situation. As this occurs, the enzyme can no longer spontaneously hydrolyse and becomes permanently inactivated.

● Apart from acetylcholinesterase, organophosphates exert powerful inhibitory action over other carboxylic ester hydrolases such as chymotrypsin, butyrlcholinesterase (pseudocholinesterase), plasma and hepatic carboxylesterases, paraoxonases, and other non-specific proteases.

It has been proposed that delayed peripheral neuropathy caused by organophosphates is due to phosphorylation of some esterase(s) other than acetylcholinesterase, such as neurotoxic esterase, also known as neuropathy target esterase (NTE). Neuropathy caused by inhibition of NTE may develop 2 to 5 weeks after an acute poisoning.

Sign and Symptoms

  • Headache
  • Giddiness
  • Nausea
  • Salivation
  • Vomiting
  • Diarrhoea
  • Spasm
  • Abdominal cramps
  • Mental confusion
  • Delirium
  • Paralysis
  • Coma
  • Death

Acute Poisoning

Muscarinic effects

Due to muscarinic like action, following clinical features are observed:

Bronchial tree: Cough, increased secretions, bronchoconstriction, wheezing, dyspnea, pulmonary edema.

Gastrointestinal: Nausea, vomiting, abdominal cramp, diarrhea.

Sweat glands: Increased sweating.

Salivary glands: Increased salivation.

Lacrimal glands: Increased lacrimation and Chromodacryorrhea (shedding of red tears) due to accumulation of porphyrin in the lachrymal glands is seen very rarely.

Eyes: Miosis, blurring of vision or dimness of vision. Miosis develops due to the inhibition of cholinesterase and marked parasympathomimetic stimulation of iris. However, dilatation of pupil in organophosphate intoxication has been recorded, therefore, it is essential not to rely only on pupillary size as diagnostic criteria for organophosphate compound poisoning.

Heart: slow pulse, hypotension.

Urinary bladder: frequency of micturation, urinary incontinence.

► Nicotinic effects:

The nicotinic effects are as follows:-

  • Striated muscles — easy fatigue, weakness, muscular twitching, fasciculation, cramps.
  • Sympathetic ganglia — pallor, occasional elevation of blood pressure (hypertension), tachycardia.
  • Increased adrenal medulla activity.

CNS effects:

The CNS effects are:

  • Irritability
  • Apprehension
  • Restlessness
  • Fine fibrillary tremors of hands, eyelids, face or tongue.
  • Muscular weakness
  • Convulsions — the convulsions may be tonic (limbs stretched and rigid) or may be clonic (rapid repetitive movement). Clonic convulsions are more common.
  • Mental confusion progressing to stupor to coma.
  • Depression of respiratory and circulatory centers.

Causes of Death

  • Respiratory failure
  • Cerebral hypoxia
  • Hyperthermia
  • Hepatic failure
  • Renal failure

Post-Mortem Findings

  • Nothing characteristics through signs of asphyxial death are seen in many cases.
  • Pulmonary odema.
  • Insecticide like smell.
  • sometimes garlicky or kerosene like smell.
  • Froth at mouth and nostrils.
  • Cyanosis
  • Constricted pupils
  • Stomach contents have insecticide like smell. Mucosa stained with compound color, congested and eroded.
  • Congestion of organs.
  • Cerebral edema
  • Features of toxic myocarditis had also been seen.
  • Microscopic examination of heart reveals dilatation of pericardial blood vessels with hemorrhages in the surrounding tissues, interstitial edema of myocardium, inflammatory cells, hemosiderin-laden macrophages and fatty infiltration of the myocardium.


The organo-phosphorus compounds are steam volatile. The tissues and other biological materials are acidified with phosphoric acid and steam distilled. The distillate is extracted with hexane which on evaporation gives organo-phosphorus insecticide.

Forensic Examination and Detection

● Parathon, Sumithion etc having para-nitro-phenyl group gives yellow colour on heating with alakali.

● The nitro group in the compound is reduced to amino group which after diazotization and coupling with B- naphthol etc. gives intense coloured dyes.

● Cholinesterase level- Depression of RBC cholinesterase level more than 50 percent of normal indicates organophosphate poisoning. The decrease is due to binding by phosphate group of pesticide. It is better parameter than plasma cholinesterase.

● Depression of plasma (serum) cholinesterase activity more than 50 percent of normal indicates Organophosphate poisoning. This test is not specific as plasma cholinesterase activity is also depressed in cirrhosis of liver, neoplasia, malnutrition, septicemia due to burns, obstructive jaundice.

● Colorimetric method-1 ml sample urine is taken and 1 ml of NBB {45% in acetone 4-(nitrobenzyl) pyridine} added and mixed for 30 seconds in vortex mixer. Then the mixture is heated at 100o C for 20 minutes. Organophosphate insecticide shows a characteristic purplish blue color that can be read using spectrophotometer.

● P-nitrophenol test

Paper chromatography

Gas chromatography (GC)

● Gas chromatography-mass spectrometry (GC-MS)

High performance liquid chromatography (HPLC)

● ECG may show right axis deviation, ST segment depression and T wave inversion.

Thin Layer Chromatography on silica gel-G using rhodamine B spray followed by exposure to bromine vapours gives purple spots against white background. Rf values are characteristics for each individual organo-phosphorus compounds.

● UV Spectrophotometry.


  • Stabilization of patient.
  • Decontamination.
  • Antidote administration.
  • Supportive measures.
  • Nursing care.

Antidote Administration

Atropine is competitive antagonist of acetylcholine and blocks muscarinic manifestations of Organophosphate. It does not reverse peripheral muscular paralysis, which is nicotinic action. The atropine should be given 2 mg intravenous promptly with dose repeated every 10 minutes till pupil dilates (up to 200 mg has been administered in a day).

Some authorities recommend administration of atropine until bronchial and other secretions have dried. According to them pupil size and heart rate cannot be used as end-points. Continued treatment with maintenance doses may be required for 1 to 2 weeks.

Oximes are used as they helps to regenerate acetylcholinesterase at muscarinic, nicotinic and CNS sites.

Pralidoxime (2-PAM) is given intravenously as 500- mg/20 ml infusion in a dose of 1 to 2 gm (children 20 to 40 mg/kg).

Supportive Measures

  • Oxygen administration.
  • Ventilator assistance.
  • Maintain vital parameters
  • Hydration and urine output.
  • Convulsions should be controlled with judicious use of diazepam.

Toxicological Materials

  • Vomitus
  • Urine
  • Blood
  • Stomach contents
  • Liver

Medicolegal Importance

  • Accidental poisoning may occur in farmers while spraying in the fields or opening the lid of the containers.
  • Suicidal poisoning is common with this insecticide.
  • Homicidal is rare as it is difficult to mask the smell of insecticide.


  1. Dr. K.S. Narayan Reddy. The essential of forensic medicine and toxicology.34th edition.
  2. VV Pillay. Modern medical toxicology.4th edition.
  3. R.K.Sharma. Concise textbook of forensic medicine and toxicology. 3rd edition.
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