ORGANOCHLORINE

COMPOUNDS TOXICITY

INTRODUCTION
It is classified under Pesticides.
Used in Agricultural field food production

Sources of Toxicity
1. Accidental / Unintensional poisoning
Common
Storage tanks
Consumption of freshly sprayed cropsLA
Inhalation

Ingestion of contaminated concentrates.

Drinking of water from pesticide treated paddy

field .
Mosquito fogging, Aerial spray.
Consumption of intoxicated dairy products.
Spillage of pesticide.
Secondary poisoning (Dog-rat, Lawn ; BirdsSeeds )
Contaminated watering & feeding vessels
Exposure to Spray
Faulty storage
Higher concentration of pesticides

2. Malicious /Intensional poisoning

a. Intensional mixing in feed & fodder
b. Homicidal/Suicidal

3.Occupational poisoning
a. Pesticide industries
b. Faulty operation-leakage, naked hand
handling
c.Spraying by untrained workers

Pesticides
Insecticides- OPC , OCC, carbamate, Pyrethrins
Herbicide Inorganic & Organic
Fungicides - Captan
Fumigants Alliminium phosphide
Rodenticides - Warfarin
Molluscide Metaldehyde , CuSO4
Acaricides Amitraz
Avicides Chloralose , Endrin
Nematicide Acetoprole
Algicides Dichlone
Bird repellants Guazathine
Mammal repellants - Ziram

CLASSIFICATION OF INSECTICIDE
A.
B.
C.
D.
E.
F.
G.

OCC - DDT, BHC, Methoxychlor

OPC Malathion , Dichlorovos
Carbamate- Carbaryl, Propoxur
Pyrethroid Allethrin , Deltamethrin
Formamidine Amitraz
Neonicotinoid - Imidacloprid
Natural products Avermectins , Nicotine

Organochlorine Insecticide
are chlorinated hydrocarbons
First generation insecticide

OC TOXICOSIS
Used in

Agriculture
Malarial control programs
Ectoparasiticide
Used as Dusts, Wettable powder, Emulsions
,Suspe..

 DDT - First synthesized by a

German graduate student Othmar

Zeidler in 1873
Rediscovered by Paul Mueller, a
Swiss entomologist, in 1939
World War II, Use of DDT to
control typhus and
malaria.January 1, 1973
(EPA)Rachael Carson canceled all
uses of DDT in the US

Further classified on properties and Degree of

Toxicity

1. Diphenyl aliphatic compounds or DDT groupDDT,

Dicofol
2. Aryl hydrocarbons BHC, Mirex
3. Cyclodiene Endosulfan, Endrin, Aldrin

Properties
Lipid Soluble
poor Soluble in water
highly volatile exptn endosulfan and perthane
OC compounds-less toxic-when small dose absorbed

from gut or skin

Highly stable in enviroment because they resist chemical
or microbial decomposition in soil(1-12 yrs)
DDT; 3-10 yrs
Toxaphene; 10yrs
OCC+ Enviromental persistence = Bioaccumulation

DDT

GAMMA BHC

Methoxychlor

Factor affecting Toxicity

Young animals adult
Female-male
Fatty and lactating animal- Emaciated non

lactating
Stress or iIlness- se
OC in oily vehicle than suspension & dry
powder-Toxic
Cyclodiene group more toxic( DDT is least)
Cats more susceptible than other domestic
animal
Fishes > Mammals > Birds

Toxicity

Depends on ,
Type of compound Aliphatic , Aryl
Formulation - Oily,Dry
Species of animal
Route Ingestion, Inhalation, dermal
Toxicokinetics:
Absorption
It is lipid soluble absorbed through skin,oral
respiratory routes.
Intestinal absorption influenced by Fibre &fat
diet.
DDT-poorly absorption from skin & GIT except
oily preparation

Distribution
Entry into blood stream
Bind to Serum lipoproteins- Stored in body fat
Accumulate in Liver ,Kidney , Brain , Adrenal
Metabolism
Liver microsomal Cytochrome p-450 system
Conjugation with Glutathione / formation of
glucouronides
Cyclodiene
Epoxides
MFO
Diphenyl Aliphatics
Dechlorinated

Excretion
Bile, Milk, Urine, Faeces-Unchanged
Half life Days to weeks
Elimination
Two Compartment model
First phase - Rapid , 40-50% , 3-4 days
Second phase- Slow phase-Storage fat,
Months

Mechanism of action
Nonspecific stimulants to CNS
No Stereo receptors
No Known Competative Antagonist
Primary action - Interfere with Sodium Channel

kinetics in Nerve membranes

Diphenyl aliphatic OC- Lipid soluble enter nerve

membrane alters electrophysiological & Enzymatic

properties of nerve membrane
Change in Na+ & K+ flow (slowing down the Closure
of Na+ by inhibiting opening of K + - AP increase

Na+ Inflow - Increased

K+ Outflow Decreased

Ion Imbalance

Transmembrane resting Potential Action Potential -

se

se

Neuronal excitability
Senory nerves than Motor nerves
Depolarization of medullary neurons
Seizures, Respiratory failure

Cyclodiene
Primary target for Cyclodiene - GABA receptors
Cyclodiene & Aryl hydrocarbons- bind to site

close to
receptor

or in the Cl- channel on GABA

Inhibition of GABA depedent opening Cl - channel

Cl- influx into neurons
Partial Repolarization
Uncontrolled Excitation

 Inhibition of Some ion transporters like Na+/K+-

ATPase, Ca2+-ATPase, Ca-Mg ATPase.

Inhibition of Calmodulin- Ca2+ binding.centration
It produce changes in concentration of various
biogenic amines- Serotonin ,nor adrenaline Hyperthermia
Ach-tremors & Convulsions
Small concentrations - depress mitochondrial
respiration.
Large concentration of OC cause lysis of
mitochodrial membrane,uncoupling
phosphorylation & blockade
of ETS/ETC.(Neurotoxicity)

They have endocrine disrupting properties

perhaps act either as endogenous harmone

mimetics or harmone blockers
DDT- Estrogen agonist
DDE- Estrogen Partial agonist & antagonist
Anti-androgen by bind to androgen receptor
(disrupt Reproductive development)
DDT - potent inducers of mixed function

oxidase

DDT, Pasture Grass, and Milk Per Cow

DDT retained on
pasture grass

10 percent

Van Nostrand Enc. of Science and

Technology (1995), p1725

DDT ingested by
cow and excreted in
cow's milk

25 percent

Modern Toxicology (1997), p114

Milk per cow per

year
Pasture required for
one cow

2,769 kg
3.5 acres

Encyclopedia Britannica (1906)

Encyclopedia Britannica (1906)

Lethal dose-50 (mg/kg)

Clinical Signs
Accute toxicity: ( Within 24 hr )
Fever(108 F)
Nausea
Vomiting
Diarrhoea , Urination, Salivation
Bradycardia or Tachycardia
Restlessness, staggers , Tremor
Intermittent clonic seizures- convulsion
Abnormal postures, Head pressing
Opisthotonus , Mydriasis
Paddling, Clamping of jaws.
Intoxicated bird-Sudden death
Respiratory Failure
Coma , Death

Emaciated

Resting on sternum

DDT toxicity

Chronic Toxicity:
Sometimes death
Acute nervous signs-

sed milk, egg, appetite,

weight
Interupted oestrous cycle, Reproductive
problems
Birds Thinning of egg shells, sed Hatchability
Teratogenicity- endocrine disruption

Carcinogenicity

Endosulfan
toxicity

What effects does DDT have on wildlife?

DDT is slightly to moderately toxic to birds when eaten

DDE decreases the reproductive rate of birds by

causing
eggshell thinning and embryo deaths
DDT is highly toxic to aquatic animals (15)-affects the

heart and brain

DDT is highly toxic to fish .Fish have a poor ability to

detect DDT in water .

DDT moderately toxic to amphibians like frogs, toads, and

salamanders. Immature amphibians are more sensitive to

the effects of DDT than adults (15).

Post mortem findings

Nonspecific & unreliable
Carcass- bruised, Lacerated, & dirty due to

convulsions
Rigor is prominent
Pale musculature after seizures, Hyperthermia
Congestion & odema of different organs
Diffused endocardial haemorrhage, exceesive
pericardial fluid, Congestion of lungs
Petechiae on heart, Intestine, lungs
Odema of brain & spinal cord
Dog liver centrilobular necrosis & Adrenal
gland haemorrhage

Diagnosis
History
Clinical signs & Clinical lesions
Chemical analysis-Milk, Blood, Liver, Kidney
Samples- suspected sources, stomach

contents, vomitus, milk fat and adipose

tissues

Differential diagnosis
NaCl Poisoning -no increase in temperature
Lead poisoning Not cause abnormal posture

Convulsions are less

Urea poisoning- no abnormal posture ,no colic
Strychnine poisoning- convulsions -not tonic
Fluroacetate poisoning- no convulsion
Anticholinesterase poisoning OPC & Carbamate

poisoning responds to it but not OCC

Comparison between organophosphates,

organochlorines, and pyrethroids

Treatment
CNS Depressants :

Sedatives- 24-48 hr
Dog
Benzodiapines- Diazepam (0.1-0.5 mg/kg),
Ca
(0.3-1.0 mg/kg)
t
Barbiturates- Phenobarbitone
Cattle & Horses 3-6 g I/V
Sheep /Goat,Pig 1-2 g I/V
Dog cat 2 mg/kg PO bid or tid

Xylazine
Dog cat- 1 mg/kg I/V or 1-3 mg/kg I/M
Cattle 0.05-0.3 mg/kg I/M
Horses 0.6- 1 mg/kg I/V or 2.2-3 mg/kg I/M
Sheep goat 0.05-0.1 mg/kg I/V or 0.1-0.2
mg/kg I/M
Chloral hydrate
Horses, Cattle 40-60 g PO or 30-40g I/V
Sheep goat 2-4 gI/V
Note : IF Animal is already depressed, CNS
depressants contraindicated

Calcium borogluconate (LA-200-400 ml)-prevent

liver damage &neutralise preconvulsive

hyperkalemia
Activated charcoal-GI contamination
Cholestyramine high lipophillic agents
Saline purgatives or Gastric lavage- oil

purgatives contraindicated
If dermal route exposed-scribble gently with soap
Anmal placed in warm & comfortable place

Prognosis
Guarded or good

Public health and Control

Accumulation of OCC in edible tissues of food

animals
Consumption/ immediate sale of such toxic
animals is avoided
Excessive contamination of ecosystem should
be prohibited/restricted
Less usage of insecticides

THANK
YOU!