Pesticides

Pesticides
• A substance or mixture of substances intended for
preventing, destroying or repelling a pest.

• It is a physical, chemical, or biological agent that kills

undesirable plant or animal pest.

• Pests include harmful, destructive, or troublesome

animals, plants or microorganisms.
• They are non-target specific in most cases.
 Methods of pests control
Chemical control (Pesticides): Natural or
synthetic agents can be used to reduce the
population of a pest species temporary.
Genetic Control: by breeding resistant host
species particularly for pathogenic bacteria,
fungi, and viruses.
Biological Control: Insect pests are controlled by
introducing their predators and parasites
 Methods of pests control
Integrated Pest Management :
• various combinations of chemical, biological, and
physical controls are employed.
• might reduce pesticide use by as much as 50 percent.
 Classification of pesticides
• Insecticides
• Rodenticides
• Fumigants
• Fungicides
• Herbicides
 Insecticides
• Neurotoxicants affecting the nervous systems of the
target organisms.

• The CNS of the insects is highly developed while the

PNS of insects is not as complex as that of mammals but
still bears similarities to the mammalian NS.

• Common classes are

 Organochlorines
 Anti choline-estrases
 Pyrethroids
 Botanical insecticides
 1- Organochlorine compounds
Several structural classes: Low volatility, chemical stability, lipid solubility, slow
rate of biotransformation
Dichlorodiphenylethanes … ex: DDT and Methoxychlor
Cyclodienes … ex: Aldrin, Heptachlor and Chlordane
Cyclohexanes … ex: Lindane
Others … ex: Chlodecone and Mirex.
Mechanism of action:
• DDT reduces the potassium transport across the membrane.
• DDT interferes the active transport of sodium.
• DDT also inhibits Na+-K+ ATPase and Ca+ ATPase, which play vital roles in
neuronal repolarization.
• It also inhibits the ability of calmodulin to transport calcium ions.
 Chlorinated cyclodienes and cycohexanes affects the CNS rather than the
PNS. Cyclodienes antagonize the action of GABA; they block GABA-induced
uptake of chloride ions, besides the inhibition of Na+-K+ ATPase and Ca+
ATPase.
 Organochlorine compounds
• Dichlorodiphenylethanes high oral doses of DDT results in
parasthesia of the tongue, lips, and face; hypersusceptibility to
external stimuli; irritability; dizziness, and vertigo; tremors and tonic
and clonic convulsions. Symptoms usually appear several (4-6 hours)
after exposure to large doses. Major pathological changes may be
observed in the liver and reproductive organs and an increase in
hepatic tumors. Little toxicity is seen following dermal exposure to
DDT due to poor absorption.
• Cyclodienes are efficiently absorbed through the skin and therefore
pose an appreciable hazard to occupationally exposed individuals. In
addition, aldrin and dieldrin were shown in several studies to
interfere with reproduction and have teratologic effects.
• Cyclohexanes lindane is used medicinally to treat scabies. Similar to
that caused by DDT. In severe cases of acute poisoning, violent tonic
and clonic convulsions occur and degenerative changes in liver and
renal tubules occur.
 Organochlorines
Treatment:
• General decontamination
• Supportive treatment
• Diazepam (0.3 mg/kg IV or phenobarbital (15
mg/kg IV) may be administered by slow
injection to control the convulsions.
 2- Anticholine esterase agents
Includes two main classes:
 Organophosphorus insecticides: Parathion, Malathion, Leptofos, Diazinon,
Dichlorvos and trichlorofon
 Carbamate insecticides: Carbaryl (Sevin), Propoxur and Aldicarb.
Mechanism of toxicity: stimulation of the muscarinic receptors; the junctions between
nerves and muscles the CNS
• Carbamate toxicity is seen more rapid than organophosphates (15 min-2 hours
while it takes 12-24 hrs in case of organophosphates). Carbamates toxicity usually
resolves within 24 hours regardless of treatment while in case of
organophosphates within 10 days.
• Delayed peripheral neuropathy (DPN or OPIDN) can occur 1 to 5 weeks after
exposure to certain organophosphates. The neuropathy typically begins with
parathesias and pain followed by ataxia, weakness and "toe drop" which rapidly
progress to flaccid paralysis, diminished reflexes and sensory dysfunction. The
disease may progress for 2 to 3 months.
Management
• General measures.
• Atropine
• Oxime Pralidoxime chloride (2-PAM)
 3- Pyrethroids
Synthetic insecticides derived from pyrethrum with a little storage or
accumulation in the body due to efficient detoxification by ester
hydrolysis.
• They exert Skin, Pulmonary, GIT, Neurologic symptoms.
• They cause allergic reactions:
 Type I syndromes caused by some pyrethroids as Allethrin,
Pyrethrin 1 and tetramethrin is characterized by restlessness,
hyperexcitation and tremors.
 Type II syndromes caused by othe pyrethroids as cypermethrin and
deltamethrin is characterized by dermal tingling, clonic seizures,
and profuse salivation.
Mechanism of toxic action
They delay sodium inactivation and interfere with GABA transmission.
They are excitatory neurotoxins keeping the nerve in the
deplolarized state
 FUMIGANTS
• Fumigation uses gaseous pesticides
to kill pests ( insects, nematodes,
weed seeds and fungi) in areas
difficult to access.
• These chemicals are nonselective,
highly reactive and cytotoxic.
• Examples are cyanide, carbon
tetrachloride, phosphine and
methylbromide.
 Cyanide
• It has a high affinity for the mitochondrial cytochrome oxidase
in the ferric state leading to cytotoxic hypoxia.
• Toxicity is characterized by transient state of CNS stimulation
and respiratory stimulation followed by hypoxic convulsions
and death due to respiratory failure.
• Diagnosis is aided by the odor of bitter almond.
• Treatment must be very rapid:
 Amyl nitrite inhalation and IV sodium nitrite must be given as
quickly as possible to create methemoglobinemia to bind to
cyanide ion.
 Sodium thiosulfate forms thiocyanate with the cyanide ion a
reaction catalyzed by Rhodanase enzyme. SCN is more
excretable.
An alternative regimen is to give cobalt EDTA or
hydroxycobolamine.
 Methyl bromide
• Colorless, odorless, non-inflammable but
highly toxic insecticide.
• Cloropicrin is added as a warning sign as
it is a powerful lacrimator.
• Toxicity signs may be delayed: CNS
stimulation, malaise, headache, vomiting,
visual disturbances and convulsion.
• Methyl bromide has high affinity for SH
group. This may be responsible for its
toxicity.
 Phosphine
• Used as a grain fumigant.
• It is applied in the form of aluminum phosphide, zinc
phosphide and calcium phosphide pellets that
release phosphine upon contact with atmospheric
moisture. The pellets decrease the chance of
explosion and ignition of the released phosphine.
• Symptoms of poisoning include shortness of breath,
cough and pulmonary irritation, nausea, headache,
jaundice and fatigue
• The main target is the respiratory tract
• Exposure to large quantities can cause olfactory
fatigue
 Zinc phosphide
• On contact with water and weak acids (gastric acid),
phosphine gas will be released
• Phosphine will cause wide spread cellular toxicity
with necrosis of the GIT and damage to the liver and
the kidney
• Treatment by decontamination and supportive
measures