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Pesticides

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Pesticides
Shared by: HC111129193212
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11/29/2011
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Pesticides

Definition of a Pesticide

 US EPA - any substance or mixture of

substances intended for preventing,

destroying, repelling, or mitigating any

pest. The term pest means any

harmful, destructive, or troublesome

animals, plants, or microorganisms.

History of Pesticides

 Sulfur used as a fumigant by the Chinese

before 1000 B.C. and as a fungicide in the

1800s in Europe against powdery mildew on

fruit; Sulfur containing compounds are still

used in CA today.



 The Chinese applied moderate amounts of

arsenic-containing compounds as insecticides

in the 16th century. In the 1800s arsenic

trioxide was used as a weed killer.

History (Continued)

 The 1930s ushered in the era of modern

synthetic chemistry.



 By the beginning of WWII there were a

number of synthetic pesticides.

Pesticides

 It is important to appreciate

 despite the modern day development of

second- and third- generation derivatives

of the early chemical pesticides, all

pesticides are inherently toxic to some

living organism, otherwise they would be

of no practical use.

 There is no such thing as a completely safe

pesticide.

Human Problems

 Target species and nontarget species can be

affected.

 On a world wide basis, intoxications due to

pesticides are estimated to be 3 million cases

of acute, severe poisoning annually with an

equal number of unreported cases, and some

220,000 deaths.

 In CA, ~ 25,000 cases of pesticide-related

illness occur annually among agricultural

workers. National ~ 80,000 cases per year.

Pesticide Regulation

 Federal Insecticide, Fungicide, and

Rodenticide Act of 1947.

 Taken over by EPA in 1972. Each pesticide

has a registration requirement that must

include appropriate chemical, toxicological,

and environmental impact studies. There are

label specifications, use restrictions and

tolerances for pesticide residues on raw

agricultural products. The EPA is responsible

for monitoring pesticide residue levels in

foods.

Pesticide Regulation

 Studies related to environmental impact on

birds, mammals, aquatic organisms, plants,

soils, environmental persistence, and

bioaccumulation are required.



 The average development cost for a new

pesticide is on the order of 30 - 50 million $.

Insecticides

 All of the chemical insecticides in use

today are neurotoxicants and they act

by poisoning the nervous system of

target (also non-target) organisms.

 Classes of Insecticides:

 Organochlorine Insecticides

 Organophosphate/Carbamate Insecticides

 Pyrethroid Insecticides

Organochlorine Insecticides

 The organochlorine (chlorinated hydrocarbon)

insecticides are a diverse group of agents

belonging to the following chemical classes:



 dichlorodiphenylethanes

 chlorinated cyclodienes

 chlorinated benzenes

 chlorinated cyclohexanes

Organochlorines (Continued)

 These agents were used extensively from the

mid 1940s to the mid 1960s in all aspects of

agriculture and forestry, building and

structural protection, and in human situations

to control a wide variety of insect pests.

Organochlorines (Continued)

 Properties which made them good

insecticides:

 low volatility

 chemical stability

 lipid solubility

 slow rate of biotransformation and

degradation

Organochlorines (Continued)

 These properties also led to their demise

because of their persistence in the

environment, bioaccumulation, and

biomagnification through the food chains.

Organochlorines (Continued)

 Studies in wildlife species and laboratory

animals have demonstrated potent estrogenic

and enzyme-inducing properties, which

interfere with fertility and reproduction.

 In birds, the interference is related to steroid

metabolism and the inability of the bird to mobilize

sufficient calcium to produce a strong eggshell.

Eggshell cracking allows bacteria into the egg,

which kills the embryo.

Organochlorines (Continued)

 Reproduction in fish is affected by the

bioconcentrations of these agents in the

yolk-sac of fry.





 The o,p'-isomer of DDT has been shown to

compete with estradiol for binding with the

estrogen receptor in rat uterine cells.

Typical Mechanism of Action

 For DDT Type Pesticides:

 periodic sequences of persistent tremoring and/or

convulsive seizures suggestive of repetitive

discharges in neurons.

 these tremors, seizures can be initiated by tactile

and auditory stimuli, indicating that the sensory

nervous system appears to be much more

responsive to stimuli.

Chlorinated Cyclodiene-, Benzene-

and Cyclohexane- type Insecticides

 These insecticides act in the CNS.

 (1) Mimic the action of the chemical

picrotoxin, a nerve excitant and antagonist

of the neurotransmitter GABA found in the

CNS.

 GABA induces the uptake of chloride ions by

neurons.

 The blockage of this uptake results in only

partial repolarization of the neuron and a

state of uncontrolled excitation.

(Continued)

 (2) Inhibitors of Na/K ATPase and Ca/Mg

ATPase that is essential for the transport of

Ca++ across membranes.

 The inhibition of Ca/Mg ATPase located in

synaptic terminals of neurons results in an

accumulation of intracellular free Ca++ which

stimulates neurotransmitter release,

depolarization of adjacent neurons, and

propagation of stimuli throughout the CNS.

Metabolism of Compounds

 Very slow rate for DDT due to complex

aromatic ring structure and chlorination.

Half-life is 335 days in cattle.



 DDT broken down to DDE both

nonenzymatically and by cytochrome P450

reductive dechlorination. All metabolites are

highly lipophilic.

Metabolism (Continued)

 Biotransformation is also slow for cyclodiene-

type insecticides.



 Aldrin and Heptachlor are converted by

cytochrome P450 oxidation reactions to

dieldrin and heptachlor epoxide without a

change in lipid solubility or toxicity.

Organophosphate /

Carbamate Pesticides



 ~ 200 different organophosphate insecticides



 ~ 25 different carbamate insecticides



 These two types of insecticides are

considered together because they have a

similar mechanism of action.

(Continued)

 Organophosphorus insecticides were first

synthesized in 1937 by German chemists as

potential chemical warfare agents.

 Sarin is an organophosphate compound that was

used against Kurdish people in northern Iraq in

1988.





 The first carbamates were synthesized in the

1930s as fungicides.

Mechanism of Action

 Both organophosphate and carbamate

insecticides act by inhibiting the action of

acetylcholinesterase (AchEase) at the

synapse between two neurons or between a

motor neuron and a muscle.

 AChEase is the enzyme responsible for the

breakdown of the neurotransmitter acetylcholine

(ACh).

 Organophosphate compounds are irreversible

inhibitors of AChEase while carbamate compounds

are reversible inhibitors of AChEase.

Mechanism (Continued)

 The reaction between an organophosphate

and the active site on AChEase (a serine

hydroxyl group) results in the formation of an

intermediate that undergoes partial hydroylsis

with the loss of the "Z" group, leaving a

stable, phosphorylated, permanently inhibited

enzyme.

 Signs and symptoms are prolonged and

persistent. Without intervention, the toxicity

will persist until sufficient amounts of "new"

AChEase are synthesized in 20 to 30 days.

Mechanism (Continued)

 Carbamate compounds attach to the

serine hydroxyl group, the "X" group is

removed by hydrolysis forming a

carbamylated enzyme, and then

decarbamylation occurs regenerating

free, active AChEase.

 Carbamate pesticides are really just poor

substrates for AChEase.

Metabolism

 Both types of insecticides undergo extensive

metabolism in all forms of life. The routes

and rates are highly species specific. Both

phase I and phase II mechanisms are

involved.

 One reaction, oxidative desulphuration, results in

a significant increase in toxicity. In parathion,

methyl parathion and malathion, the presence of

the P = S reduces the AChEase inhibiting

properties of the compound.

Mechanism (Continued)

 There is a characteristic prolongation of the

falling phase of the action potential. The

nerve membrane remains in a partially

depolarized state and is extremely sensitive

to complete depolarization again by very

small stimuli.



 See handout

Why Prolonged Repolarization

 (1) DDT affects the permeability of the nerve

cell membrane to K+ ions reducing K+

transport across the membrane.

 (2) DDT alters the Na+ channels, they open

normally but are closed (inactivated) slowly.

 (3) DDT inhibits neuronal ATPase activity

particularly Na/K ATPase and Ca ATPase

which play a role in repolarization of the

neuron.

Why (Continued)

 All of these factors reduce the rate at

which repolarization occurs and

increase the sensitivity of the neurons

to small stimuli that would not elicit a

response in a fully repolarized neuron.

Pyrethroid Insecticides

 This is the newest class of insecticides, a

group of chemicals that entered the

marketplace in 1980 but by 1982 accounted

for approx. 30% of worldwide insecticide use.

 These synthetic chemicals are similar to the

insecticides extracted from pyrethrum or

chrysanthemum flowers.

Pyrethroids (Continued)

 Type I pyrethroids affect Na+ channels in

nerve membranes (both sensory and motor)

and gives long afterpotential similar to DDT.

 Type II pyrethroids cause persistent

depolarization and prolonged repetitive firing

of sensory receptors and muscle fibers.

 Both types also inhibit Ca/Mg ATPase

resulting in increased intracellular Ca++

levels and increased neurotransmitter

release.


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