Various pests, fungi, weeds and rodents cause much harm to the production and storage of food grains A large number of pesticides including insecticides, rodenticides, herbicides and fungicides are available in the market.

1. Agricultural
Poisons
Dr Mohd Kaleem Khan
Assistant Professor
Department of Forensic Medicine
JNMCH AMU Aligarh

2. • Various pests, fungi, weeds and rodents cause much harm to the production
and storage of food grains
• A large number of pesticides including insecticides, rodenticides, herbicides
and fungicides are available in the market.
• They enable the farmers to control their crops, from being destroyed by
insects, diseases and weeds.
• As a result, though the yields of food crops have reached new high levels
• Extensive use by the agriculturists has resulted in poisoning of human
beings and domestic animals.

3. Fungicidal
• Fungicides preserve the seeds for seedling purposes.
• These are mainly mercurial compounds

4. Herbicidal orWeed Killers
• Since the growth of undesirable herbs and weeds in the field yields low
production, the herbicides or weed killers are used to protect the field.
These are:
• (i) Sulphuric acid (1%); is a corrosive acid
• (ii) Sodium chlorate; is irritant
• (iii) Potassium cyanide; causes tissue anoxia
• (iv) Paraquat.

5. Insecticides
• Insecticides are the compounds that are employed for killing insects, are
classified as:
• (1) Organophosphorus compounds
• (i) Alkyl phosphates
• (ii)Aryl phosphates
• 2. Halogenated hydrocarbons
• (i) Aldrine
• (ii)Endrine (iii) DDT

6. • 3. Miscellaneous compounds:
• (i) Mercurial salts
• (ii) Arsenic salts

7. • 4. Rodenticidal
• (i) Inorganic compounds
• Aluminium phosphide
• Zinc phosphide
• Thallium
• Phosphorus
• (ii) Organic compounds
• Fluoro-acetate
• (iii) Convulsants
• Strychnine
• (iv) Anticoagulant
• Warfarin.

8. Insecticides are further classified according to their
toxicity as:
• 1. Virtually Harmless
• (i) Pheno-oxalic acid
• (ii) Copper oxide—fungicide
• (iii) Lime sulphur—orchard fungicide
• (iv) Petroleum washes— orchard insecticide

9. Introduction
•Organophosphate compounds: are chemicals used in
both
• Domestic
• Industrial settings
• Potent nerve agents,

10. 2. Comparatively Harmless
• (i) Sulphuric acid20%—weed killer
• (ii) Sodium chlorate—mass herbicide
• 3. Mildly toxic (25-60gm)
• (i) Chlorinated hydrocarbons
• (ii) DDT
• (iii) Gammaxene
• (iv) Aldrin, dieldrin: used to control flies, louse, tick and as an agricultural
insecticide.

11. • 4. Moderately toxic (10-25 gm)
• (i) Diazinon

12. 5. Highly toxic
• (i) Sodium arsenite
• (ii) Lead and calcium arsenate
• (iii) Organic polyphosphates
• (iv) Organophosphorus compounds which include
• (a) HETP (Hexa Ethyl tetra phosphate)
• (b)TEPP (Tetra Ethyl pyro phosphate)
• (c) Parathion.

13. Contents
1.Introduction(What are Organophosphates?)
2.What is Organophosphate Poisoning?
3.MOA of Organophosphate Poisoning
4.Effects of Organophosphate poisoning
5.Management andTreatment OP poisoning
6.Medico legal aspect

14. Introduction
•Examples of organophosphates include;
• Insecticides (malathion, parathion, diazinon, fenthion, dichlorvos,
chlorpyrifos, ethion),
• Nerve gases (soman, soaring, tabun, vx),
• Ophthalmic agents (echothiophate, isoflurophate), and
• Anthelmintics (trichlorfon).
• Herbicides (tribufos [def], merphos) are tricresyl phosphate–
containing industrial chemicals.

15. Classification
•Alkyl Phosphate: Malathion, Dimefox, HETTP, TEPP,
Trichlorfos
•Aryl Phosphate: Parathion, Paraoxon, Chlorthion,
Diaznon

16. Examples of organophosphates include:
•Ophthalmic agents ( echothiophate, isoflurophate )
•Herbicides ( tribufos , merphos ) and
•tricresyl phosphate–containing, industrial chemicals

17. Organophosphate poisoning
• Organophosphate poisoning results from the exposure to
organophosphates (OPs), which causes
• Inhibition of the enzyme Acetylcholinesterase (AChE),
• Leading to the accumulation of acetylcholine(a neurotransmitter) (ACh)
in the body.
• Acetylcholinesterase (AChE) is an enzyme that degrades (breaks down) the
neurotransmitter Acetylcholine into Choline and Acetic Acid.
• The choline can be recycled and combine with Acetyl coA to form new
aceylcholine.

19. Mechanism of Action
• Organophosphates inactivate Acetylcholinesterase (AChE) by
phosphorylating (addition of a phosphate group) the serine
hydroxyl group located at the active site of acetylcholinesterase.
•Once AChE has been inactivated,
•Acetylcholine accumulates throughout the nervous system,
•Resulting in excessive stimulation of cholinergic receptors (muscarinic
and nicotinic receptors) at various organs
•Resulting in acute cholinergic crisis.

21. MECHANISM OF ACTION OF ORGANOPHOSPATE POISONING
•Irreversibly bind to serine-OH group at the active site of acetylcholinesterase (AChE)
establish covalent bond ( phosphorylation)
↓
•AGING: loss of alkyl group + strengthening of covalent bond
↓
•Phosphorylated AChE is very stable
↓
•Inhibition of enzyme activity
↓
•accumulation of ACh in the synapse and NMJ
↓
•Overstimulation of cholinergic receptors

23. Mechanism of Action

25. Effects of organophosphate poisoning
The effects of organophosphate (OP) poisoning can be divided
into 3 categories, including :
1. Muscarinic effects
2. Nicotinic effects and
3. CNS effects
Mnemonics used to remember the muscarinic effects of
organophosphates are:
• SLUDGE (Salivation, Lacrimation. Urination, Diarrhea, GI complaints,
Emesis)
• DUMBBELS (Diaphoresis (perspiration) and Diarrhea ; Urination, Miosis
(pupil constriction) , Bradycardia, Bronchospasm. Emesis, excess Lacrimation
(tears) and Salivation)

26. Muscarinic effects on organ systems include the following;
a) Cardiovascular system: Bradycardia, Hypotension
b) Respiratory: Rhinorrhea (runny nose), bronchorrhea ( production of
more than 100 mL per day of watery sputum), bronchospasm, cough,
severe respiratory distress.
c) Gastrointestinal: Hyper salivation, nausea and vomiting, abdominal
pain, fecal incontinence
d) Genitourinary: Urinary incontinence
e) Ocular: Blurred vision, Miosis (pupil constriction)
f) Glands: Increased lacrimation (tears), diaphoresis

27. • Autonomic nicotinic effects include;
oMuscle weakness and fasciculation,
oTachycardia
oCramping of skeletal muscle
oHypertension
oMydriasis, and pallor.
• Central Nervous System (CNS) effects include;
•anxiety, restlessness, confusion, ataxia, tremors, seizures, respiratory
failure and coma.

28. The clinical features depend on the route of entry ;
Ingestion :
Muscarinic effects(post
ganglionic parasympathetic
nerve ending)
• Bronchospasm(wheezing)
• Bronchorrhoea
• Cough
• Dyspnea
• Hypotension
• Bradycardia
• Cardiac arrhythmia
• Vomiting
• Salivation
• Miosis
• Lacrimation
• Blurred vision
Nicotinic effects (neuro
muscular junction)
• Muscle weakness
• Fasciculation
• Paralysis
• Muscle twitching

29. Nicotinic and muscarinic Ach
receptors in the CNS
• Confusion
• Agitation
• Respiratory failure
• Ataxia
• convulsion
Ach receptors in the
sympathetic system
• Excessive sweating
Other effects
• hyperglycemia
• Acute pancreatitis

31. Management
• In History taking: You have to find out;(Direct Answer Questions) What,
When, How much, andWhy
• Protect yourself using protective clothes and gloves and
decontaminate the patient by removing contaminated clothes and
washing the skin thoroughly with soap and water.
• Initial assessment: A B C (Airway, Breathing, Circulation)
• Look for and Recognize signs and sypmptoms of organophosphate
poisoning
oMIOSIS
oDIAPHORESIS
oPOOR AIR ENTRY or in severe cases, respiratory failure
oBRADYCARDIA
oHYPOTENSION

32. • Obtain IV access and give atrophine intravenously as soon as possible for a
symptomatic patient.
• Perform gastric decontamination with gastric lavage once the patient is
stabilized and within two hours of ingestion.
• Give activated charcoal while maintaining atrophine infusion
• Administer pralidoxime.

33. ATROPINE
• Used as an antidote to counter the muscarinic effects of acetylcholine; only
life saving antidote.
• Atropinisation, once achieved, should be maintained for 3-5 days,
depending upon the compound involved. When muscular paralysis
supervenes, mechanical ventilation is required.
• Atropinisation is evidenced by pupillary dilation, drying up of secretions and
pulse rate > 100. Atropine crosses the blood brain barrier and counters the
effect of excess acetylcholine on the extrapyramidal system.

34. PRALIDOXIME
• Oximes used as rejuvenators.
• The beneficial effect of oximes is exerted through the
• reactivation of enzyme cholinesterase by cleavage of the
phosphorylated site and by a direct
• detoxifying effect on the unbounded organophosphorous
compound.
• Additionally, oximes have an anticholinergic effect when used in normal
doses.
• The recommended dose is 1 gm every 8 hours by intravenous injection.

35. •Remove all clothing and gently
•Use personal protective equipment,
•such as neoprene gloves and gowns,
• Use charcoal cartridge masks for respiratory protection
•Irrigate the eyes of patients who have had ocular exposure
using isotonic sodium chloride

36. Post Mortem Findings
• External:
•Cyanosis of lips,fingers,and nose
•Deep staining
•Frothy discharge from nose and mouth
•Kerosene like smell
• Internal
•Mucosa congested
•Stomach content with kerosene like smell
•Edeme in lung
•Edemea of brain

37. Medico legal aspect
•Ahospitalisation4-6 days
•Differential diagnosis
•Acidental
•Suicidal
•Homicidal rare

38. Chlorinated Hydrocarbons
• The chlorinated hydrocarbons were developed beginning in the 1940s after
the discovery (1939) of the insecticidal properties of DDT.
• Other examples of this series are
• BHC, lindane, chlorobenzilate, methoxychlor,
• Cyclodienes ( aldrin, dieldrin, chlordane, heptachlor, and endrin).

39. Mechanism of Action
• Neurotoxins
•Behavioral changes,
• Involuntary muscle activity, and
• Depression of the respiratory center.
• Absorbed from the
•Gi tract,
•Across the skin, and by
•Inhalation.

40. •FD: 5-6 g
•FP: 1-2 h

41. Treatment
• Cholestyramine:16g / day increase faecal excretion
• Calcium gluconate
• Diazepam
• PM findings: Suggestive of Asphyxia

42. Medico Legal Aspect
• Suicidal
• Homicidal
• Accidental
• Chronic Poisoning
• Weight Loss, Mental Changes, Oligospermia, Tremors

43. Aluminum Phosphide (ALP)

44. Aluminium Phosphide (ALP)
• ALP is a solid fumigant and ideal pesticide
• Since 1940 as it is cheap, most efficacious and easy to use.
• Freely available on the counter in India (as alphos, celphos, quickphos,
phostek, phosfume and synfume),
• In form of chalky white or brown
• 3 gm. Tablets containing 56% of ALP and 44% of ammonium carbonate.

46. • On coming into contact with water or moisture or OH radical of air or
hydrochloric acid in stomach,
•AlP+3H20 = Al(OH)3+PH3
•AlP+3HC1 = AlC13+PH3
•The residue, Al (OH)3 is non-toxic
•The tablet has typical odor of garlic.
3 gm. tablet of ALP liberates 1gm. of phosphine or phosphorus
hydrogen.

47. Mechanism Of Action
• The systemic toxic effects appear in 0-60 minutes after ingestion.
• PH3, inhibits the electron transport resulting from preferential inhibition of
cytochrome oxidase leading .
• To respiratory chain inhibition which leads to cellular hypoxia
• Small vessel injury which is further potentiated by cardiotoxicity due to
anoxic myocardial damage and shock.
• Direct toxic effect of alp on myocardium or hypomagnesaemia brought on
by focal myocardial damage leads to arrhythmias.
• Hypotension and shock ensue within 3-6 hours of ingestion of Alp.

48. Sign and Symptom
• GIT System: Nausea, vomiting, diarrhea (20%), pain
epigastrium, retrosternal pain and epigastric burning sensation
(60%),
• Hepatobiliary System: Acute hepatic failure (6%), jaundice,
hepatitis and soft tender hepatomegaly.

49. • Cardiovascular System (60-100'%): Increased JVP, feeble
heart sounds, S3 gallop and muffled 5" hypotension, shock,
arrhythmias, myocarditis and pericarditis
• Respiratory System (within 2 to 3 hours) :Cough, dyspnoea,
cyanosis,, respiratory failure and ARDS,
• Renal System: Acute (oliguric or nonoliguric) renal failure.

50. • Central Nervous System (50%):
•Headache, Dizziness, Diplopia, Paraesthesias, Ataxia, Altered
Sensorium, Restlessness, Intention Tremors, Convulsion,
•Hypoxic Encephalopathy, Coma and Delayed Hemorrhagic Stroke.
• Muscular System:
•Muscle Pain, Severe Muscle Weakness,
•Myopathy With Muscle Wasting
•Proximal Muscle Weakness.

51. • Haemopoietie System: Bleeding diathesis, DIC and jaundice.
• Endocrinal System: Hypoglycemia and hyperglycemia.
• Shock.

52. Management(To Decrease PH3 Absorption)
• Gastric lavage with KMNO4, ( 1:10,000) immediately after admission and
to be repeated twice or thrice.
• Activated charcoal 100 gm orally for absorbing PH3 from GIT.
• Medicated liquid paraffin and vegetable oils to accelerate the excretion of
ALP and PH3, from the gut and inhibit release of PH3, from ALP.

53. • Reduction of organ toxicity
•By using membrane stabilizer like mgso4,
• Enhancing PH3 excretion
•Renal perfusion with I /V fluids.
• Detoxication of absorbed PH3, can't be done as there is no
specific antidote

54. • MgS04
• Is effective in first 24 hours
• In dose of 1gm. I /V stat after dissolving in 100 ml of 5% dextrose and 1
gm. Every hour for next 3 hours and then 1 gm. Every 6 hours for 5-7
days in continuous IV infusion in 5% dextrose .
•It corrects cardiac arrhythmias by modulating
sympathetic, parasympathetic and slow channel
kinetics

55. • Metabolic Acidosis: The presence of moderate to severe acidosis
with HCO, level less than 15 mmol/l is corrected by
• 1N Sodabicarb to raise HCO, level to 18 to 20 mmol/l for 3 to 4 days till
PH3, is excreted.
• The peritoneal or haemodialysis is useful in case, if metabolic acidosis
persists in haemodynamically stable patients.

56. Specific Preventive Measures
• Availability of single tablet pack encased in hard plastic material with
spikes
• By restricting the free sale of the chemical.
• Social awareness regarding handling of the substance and its lethality.
• Some emetic substance may be added in it.