AGRICULTURAL

POISONS

Dr. Sidharth. S
MD Forensic Medicine, PGDMLE
 ORGANOPHOSPHOROUS COMPONDS

• Consists of Central Phosphorus Molecule. With B & B’ Basic groups and another bond of
either Oxygen or Sulphur.
• The fourth bond is either Alkyl or Aryl Group.
• So they are either Alkyl or Aryl Phosphates.

• Parathion.
• Methyl Parathion.
• HETP (Hexa Ethyl Tetra Phosphate) • Paraoxon.
• TEPP ( Tetra Ethyl Pyrophosphate) • Diazinon.
• OMPA (Octa Methyl Pyrophosparamide)
• Malathion etc.
ABSORPTION OF OP Compounds:
• Absorbed through the intact skin and mucous membrane, gastro-intestinal tract and by
inhalation.
• Mixing it with AROMAX gives it a characteristic kerosene like odour.
MECHANISM OF ACTION:

• Acetyl Choline, produced in the body, is hydrolysed by Acetyl Cholinesterase (AChE) to Acetic
Acid and Choline.

True Cholinesterases PseudoCholinesterases

Red Cells, Neuro muscular Jn & Brain Plasma
• The OP Compounds inactivate the AChE by PHOPHORYLATION, resulting in accumulation od Acetyl Choline
in the body.
• AChE has two sites:
ANIONIC SITE
ESTERIC SITE

Organophosphates act on this site.

 Initially, the binding of organo Firm binding occurs when a H –ion
phosphorous is due to hydroststic is transferred from the complex.
attraction .

REVERSIBLE REACTION IRREVERSIBLE REACTION.

Treatment with antidote, if initiated, it has to be

done before firm binding.

Within 24 hours of poisoning.

 Signs & Symptoms:
• The clinical manifestations of Organophosphates are due to an overdose of Acetyl Choline in the body.

MUSACRINIC EFFECTS NICOTINIC EFFECTS CNS MANIFESTATIONS

Salivation
Lacrimation • Acts on Pre-ganglionic NMJ
Urination incontinence • Muscle twitching, cramps • Headache, Restlessness,
Defecation. and muscle fatigue. confusion, drowsiness, coma.
Gastro-intestinal distress. • Fasiculations. • Depression of Cardiac and
Emesis.
Respiratory centres.
• Death due to Respiratory Failure.
• Pupils constricted.
• In Eye, ciliary muscles are constricted & suspensory ligaments are relaxed; so lens bulges out into
anterior chamber- blurring of Vision.
• Severe Lacrimation in severe cases- Chromolachryorrhoea (due to inhibition of porphyrin metabolism
resulting in accumulation of porphyris in lacrimal glands).
• Respiratory system: Increased secretions, bronchoconstriction, dyspnoe, Pulmonary edema.
• CVS symptoms: Bradycardia, Hypotension.
 • Other Neurological Manifestations:
Type 3 Paralysis:

• 1-4 weeks after exposure to OP

Compounds.
Type 1 Paralysis:
• Sensory symptoms subside in 1-2
months, but paralysis persists.
• Acute paralysis within 24-48 Hours. • Do not respond to Atropine / Oximes.
• Due to persistent depolarization at
NMJ due to blockade of AChE.
• Fasiculations, Cramps, Weakness,
Paralysis of respiratory muscles & Type 2 Paralysis:
Respiratory failure.
• 2-4 days after resolution of acute cholinergic symptoms.
• Manifests as Paralysis & Respiratory distress.

• Rx: Atropine. • Due to Neuromuscular transmission defect or toxin induced

muscle instability or inadequate treatment.
• Weakness of Proximal Limb muscles, respiratory muscles &
Cranial nerve palsy.
• Delayed deaths +/-
• Do not respond to Atropine / Oximes.
OTHER SEQUELAE IN SURVIVORS:
1. Urinary incontinence, demyelination of optic nerve, visual defects, peripheral neuropathy, extra-pyramidal
symptoms, loss of memory and lethargy.
2. Chronic organophosphate induced neuropsychiatric disorder (COPIND)

Combination of psychiatric, neurological & extrapyramidal symptoms that occur late, but long lasting.
• Fatal Dose varies according to the type of OP Compound ingested.

• Fatal Period: death within 24 hours. (can occur as early as 30 mins after ingestion if dose is high).

DEATH IN OP POISONING:
1. Respiratory failure due to paralysis of respiratory centre.
2. Paralysis of respiratory muscles & bronchospasm due to direct action of ACh here).
3. A-V Blockade leading to Cardiac Arrest.
Signs & Symptoms
with OP Poisoning.
 DIAGNOSIS

Cholinesterase Activity
Chemical Analysis

Estimation of cholinesterase activity- both red cell and • Detected in Blood using Thin Layer Chromatography
plasma cholinesterases. or Liquid Gas Chromatography.
• Estimation of para nitro phenol is diagnostic for
Parathion Poisoning.
Type of Cholinesterase Normal Value
Red cell Cholinesterase 77-142
Plasma Cholinesterase 41-140

• Ch-E activity reduced to 22 – 88 %.

• Pseudo ChE levels are more sensitive and falls rapidly than Red
Cell ChE.
• True ChE activity is better and of more diagnostic value.
• Prognosis based on the level of ChE Activity.
 Treatment
• In GENERAL, clothes of the patient to be removed, body to be washed with soap & water to prevent
cutaneous absorption of OPC.
• Irrigation of eyes, if contaminated.
• Maintain patent airway.
• Oxygen therapy if cyanosis +.
• Stomach wash with 1:1000 KMnO4 Soln. if the poison was ingested; with or without activated
• charcoal.

• Atropine Sulphate reverses effect of Ach. Acts as a PHYSIOLOGICAL ANTIDOTE.

§ Reverses the Muscarinic Effects of ACh at the Muscarinic receptors. So there is decreased
Parasympathetic activity.
§ No effect on Nicotinic symptoms as it do not act on those receptors. So, no action a
NMJ.
§ DOSE: 2-4 mg every 10-15 mintues till signs of atropinization appears.

§ Dilatation of pupil and decrease of secretions.

 • Treat with OXIMES (Specific Antidotes).

• React with phosphate moiety of OP-AChE complex and get phosphorylated.

• AChE is released from the complex and thus reactivated.

• Decreases the Muscarinic, nicotininc and CNS effects within 10-40 minutes.

• Oximes to be administered as early as possible, before the complex becomes irreversible.

Not beneficial if given after 48 hours of poisoning.

By this time, the complex will become irreversible.
Postmortem Appearence:
Brain: Congested.
Face: Congested
Lungs: Congested & edematous.
Conjunctivae: Congested

Stomach contents Froth in Mouth and nostrils.

smell of kerosene,
if the content
ingested contains
Aromax.
Heart: Petechial Hemorrhages
on Pericardial surface.

All Internal Organs are congested.

CHRONIC POISONING:

• Seen in persons spraying the compound in agricultural field, due to inhalation.

• Manufacture and packing of OPC.

• Symptoms: Muscle weakness lethargy, anxiety, confusion, muscle cramps, parasthesias.

CIRCUMSTANCES OF POISONING:

Accidental
Suicide Homicide In sprayers & children.
Most Common. Rare.
Can occur if mixed in alcohol
or other soft drinks.
 MEDICO LEGAL IMPORATNCE
OPC Poisoning

Suicide Alone or mixed with some other poison.

Homicide Rare- due to its strong smell and bad taste.
Accidental Quite common. Eg: Kerala Food Tragedy of 1958; Bihar mid-day meal tragedy of 2013.
Warfare Two main groups of OPCs used in Warfare are G & V series. (see War Gases).
• Organophosphate compounds resists PUTREFACTION.
• Can be detected in Viscera for some time even after death.
• OP Compounds are RESTRICTED USE PESTICIDES (RUP):
RUPs are pesticides that are available for purchase and use only by certified pesticide applicators or persons
under their direct supervision. This is assigned to those products that when not used according to directions, are
at a high potential of causing significant human and environmental hazard.
Examples: Diazinon, Fenthion, Methyl Parathion.
 CARBAMATES
• They are reversible Acetyl cholinesterase inhibitors.
• Examples: Carbaryl (sevin), carbofuran (furadan), methomyl (lannate), propoxur (hit spray), aprocarb
(baygon), aldicarb (temik).

Mechanism of Action:

• Carbamilate the serene moiety of the active site of AChE. So, Less Toxic.

• Reversible reaction.
• They are spontaneously hydrolysed from AChE enzyme site within 48 hours.
• CNS Effects are negligible. ( due to less penetration into CNS).
• Fatal Dose: 10-30 gm ( Carbofuran)
• Fatal period: 2-6 hours(Carbofuran)
SIGNS & SYMPTOMS:

• Same as that of OPC Poisoning.

• Less Prominent CNS Symptoms.

INVESTIGATIONS:
• Blood is drawn to look for presence of poison.
• AChE levels is not reliable, as it comes to normal within hours.
TREATMENT:

• Atropine is the Drug Of Choice.

• Oximes – NOT RECOMMENDED.
• As it is a reversible reaction.
• Also, it may form CARBAMYLATED OXIMES,
which is a much more potent AChE Inhibitor.

• However, Oximes can be given during mass causalities when the nature. Of the poison is not known.

POST MORETM APPEARENCES: same as that of OPC.

 ORGANOCHLORINES

Examples: DDT, BHC, Lindane, Endrin, Endosulphan etc.

MEDICO LEGAL IMPORTANCE
Suicide Very Common.
Homicide Rare, due to strong smell and bad taste.
Accidental Quite common; Eg. Qatar & Saudi Arabia poisoning tragedy of 1967.
Occupational Exposure- is possible.
Endrin resists PUTREFACTION.- So detected in the body for sometime after death.
Restriced use OC In India: DDT, Endosulfan, Lindane.
 ZINC PHOSPHIDE
• Used as rodenticide.
• Garlicky odour.
• When ingested, it reacts with HCl in the stomach and forms phosphine(PH3). This gets
absorbed into the blood.
• Inhibits the enzyme Cytochrome Oxidase C & hence affects cellular respiration.

SYMPTOMS
GIT RESPIRATORY SYSTEM CNS
Burning sensation, nausea & Dyspnea, Cyanosis, Coma, convulsion and death
vomiting. Breathlessness, fever &
respiratory distress.
CVS
Dysrhythmia, Circulatory
collapse.
• HEPATIC SYMPTOMS:
• If the person survives more than 24 hours, complications
like hepatic failure may occur.
• Fatty change and necrosis of the liver.
• Patient will be deeply jaundiced.
• Death will be due to hepato-renal failure.
• RENAL SYMPTOMS:
• Renal Tubular Necrosis & Renal failure.
• Post-mortem appearances:
• Garlicky smell in the stomach and stomach contents.
• All internal organs will be congested.
• Lungs are congested and edematous.
• Fatty change and centrilobular necrosis in the liver.
• Yellowish discoloration of all the membranes, meninges and costal cartilages due to
jaundice.
• Renal capsule may be adherent to the renal mass.

• Death is due to HEPATO-RENAL FAILURE.

• MEDICOLEGALLY,
• ZINC PHOSPHIDE is the main content of rat poison.
• Used for suicidal and homicidal purposes.
• Accidental poisoning may occur in children.
 ALUMINIUM PHOSPHIDE
• Used as both pesticide & rodenticide.
• Garlicky odour.

• When in contact with moisture, it liberates PHOSPHINE.

The production of phosphine is accelerated in the
presence of HCl.

• Phosphine is a toxic gas that gets absorbed into the

system & inhibits the respiratory chain enzymes
especially Cytochrome Oxidase C & produces Tissue
anoxia.
• Also, affects the liver by producing necrosis of the liver
tissue.

• Fatal period is generally 1-24 hours.

 SIGNS & SYMPTOMS
• May enter the body by inhalation or ingestion.
• If inhaled, it will cause headache, nausea, vomiting, dizziness, respiratory distress, ARDS,
convulsion, coma & death.
• If ingested,

GIT
Burning sensation, nausea &
vomiting & epigastric pain.
Fatty change, Hepatitis, Jaundice, Hepatomegaly, Liver necrosis, hepatic encephalopathy.
SYMPTOMS
RENAL SYSTEM CNS
Renal Tubular necrosis, renal Coma, convulsion and death
failure
CVS
Dysrhythmia, myocarditis,
pericarditis, hypotension,
Circulatory collapse, shock.
Hepatic symptoms:
• Post-mortem appearances:
• Garlicky smell in the stomach and stomach contents.
• When stomach is opened, the contents when on contact with water will FUMIGATE. Stomach
mucosa may show corrosion.
• All internal organs will be congested.
• Lungs are congested and edematous. Hence, froth may be present at the mouth and nostrils.
• Adrenals may be congested, sometime hemorrhagic.
• Fatty change and centrilobular necrosis in the liver.
• Yellowish discoloration of all the membranes, meninges and costal cartilages due to
jaundice.
• Renal capsule may be adherent to the renal mass.

• Death is due to HEPATO-RENAL FAILURE.

• MEDICOLEGALLY,
• Used for suicidal purposes generally and rarely for homicidal purposes.
• Accidental poisoning may occur in children.
• Due to its fumigant properties, it is a potential agent of chemical terrorism.
Thank You