2. “Any substance or mixture of substances
intended for preventing, destroying, repelling,
or mitigating any insects, rodents, nematodes,
fungi, or weeds, or any other forms of life
declared to be pests; any substance or mixture
of substances intended for use as a plant
regulator, defoliant, or desiccant.”
--Federal Insecticide, Fungicide, and
Rodenticide Act (US EPA)
3. Historical background:
- Alkaloids nicotine and anabasine contained in
tobacco – insecticides
- Pyrethrines contained in plants of the genus
Pyrethrum – insecticides
Pyrethrines later became the prototype for
synthetic pyrethroids
- Rotenon – is highly toxic to all forms of life, is from
roots of lianas. Rotenon was used as a piscicide and
insecticide
- An important milestone was introduction of
phenyl mercury in 1913 for the protection of seed –
fungicide
- Insecticidal effect of DDT was discovered in 1939
by the Swiss Paul Müller
8. Pesticide degradation
- in abiotic environment
the most important factors are light, temperature,
photolysis, free radicals produced in
photochemical reactions, hydrolysis
- in biotic environment
1. phase 2. phase
XH X – OH X – O – conjugate
The final products are inactive and are
excreted.
9. Pesticide transformation
- mostly detoxicative nature
- result may even be a more toxic substances
(desulphuration of organophosphates)
parathion paraoxon – a powerful ACHE
inhibitor
trichlorfon dichlorvos
diazinon diazooxon
DDT DDE (extremely persistent and
xenoestrogenic)
10. Dose/Response
DoseTerminology
LD50 = Lethal Dose50% TestPopulation
LD0 = Highest Dose with no Lethality in the Test Population
LD100 = Lethal Dose100% Test Population
LC50 = Lethal Concentration50% TestPopulation
LOAEL =Lowest Observed AdverseEffect Level
NOAEL = No ObservedAdverseEffect Level
11. Dose/Response
Exposure Terminology
Acute:Short term, highdose, usually measured in minutesto days, can be multiple
doses within a short period (burst hose on a azinphos-methylapplicationor a B.T.
Collins Cocktail).
SubChronic:Intermediate term, moderate to low dose, measured in weeks tomonths
(exposure to a seasonal use material,e.g.triadimefonon grapes) .
Chronic:Long term, low dose, measured in monthsto years (exposure toa constant
use material,e.g. sulfuryl fluoride for home fumigation).
12. Pesticides:
- Organochlorine pesticides
- Organophosphates
- Carbamate pesticides
- Pyrethroids
- Phenoxyacetic acid – based pesticides
- Urea – based pesticides
- Diazine and triazine pesticides
- Bipyridil – based pesticides
- Phenylpyrazoles
- Metal – based pesticides
13. Organophosphates
- insecticides
- antiparasitics
Mechanism of toxic action – irreversible
inhibition of enzymes, particularly of
acetylcholinesterase on nerve synapses (by
phosphorylation of hydroxyl group of serine
bound in the active centre of ACHE).
16. Carbamate pesticides
- insecticides
- herbicides
- fungicides
Mechanism of the toxic action – reversible
inhibition of acetylcholinesterase (by carboxylation
of hydroxyl group of serine bound in the active
centre of ACHE).
Carbofuran is very up-to-date substance in
toxicology. It is used to control vermin (foxes) and is
used in baits. Birds are 10 times more sensitive to
carbofuran than mammals (LD50 for mammals 3 –
19 mg/kg body weight). Frequent carbofuran
poisoning cases among predatory birds.
20. Pyrethroids
- insecticides
- antiparasitics
Mechanism of the toxic action -
- pyrethroids T (tremor) – contain no α-cyano group
cause reversible block of sodium channels (e.g.
permethrin)
- pyrethroids CS (choreoatetosis, salivation) –
contain α-cyano group
cause reversible block of sodium channels and
inhibition of GABA (e.g. deltamethrin)
21. Pyrethroids are
- highly toxic for fish (LC50 below 0,1 mg/l)
- toxic for bees (LD50 2 – 11 µg/bee)
- not very toxic for mammals
Cats are most sensitive mammals to pyrethroids.
Why?
- Pyrethroids’ detoxification, similarly to other organic
toxicants, takes place in two phases. Activity of
conjugation enzyme, especially of glucuronyl transferase,
is very low in cats.
22.
23. Phenoxyacetic acid – based pesticides (MCPA)
- herbicides
Mechanism of the toxic action –
disruption of oxidation and phosphorylation processes
(drop in the ATP production and disruption of energy
metabolism).
They are little toxic for mammals, fish, bees.
Symptoms of poisoning: hypotermia, hypodynamia,
paresis, paralysis, tympania in ruminants.
But: In the production and use of those herbicides (2,
4-D; 2,4,5-T) dioxin was produced.
24. They cause damage of the thyroid gland and diuron
may cause methaemoglobinemia.
In mammals linuron reduces haematopoiesis
In dogs triasulfuron causes cystic hyperplasia of the
prostate, vacuolisation of liver cells, anaemia and
accumulation of pigment in the liver
25. Diazine and triazine pesticides
- herbicides
Diazine pesticides are less toxic than triazine ones
Mechanism of the toxic action –
- triazines are antimetabolites of pirimidine bases -
components of nucleic acids and folic acid
- atrazine damages the liver detoxication functions
- simazine, prometryne, terbutryne – inhibit
haematopoiesis
Toxicity: toxic for fish
relatively harmless for bees
LD50 for mammals exceeds 1000 mg.kg-1
live weight
26. Serious risk of triazine – based pesticides
1. very low biodegradability (risk for drinking water)
2. triazines are secondary amines (secondary amines +
nitrosation agents
nitrosamines)
3. atrazine has xenoestrogenic effects (causes
abnormal development of gonads, turns amphibians
into hermaphrodites)
27. Bipyridil – based pesticides
- herbicides
- desiccant
They are very rapidly deactivated in soil, but leave
residues in plants: diquat for 3 – 5 days,
paraquat for 21 days.
Diquat (Reglone)
LD50 for cattle 30 – 50 mg.kg-1 l.w.
for rabbit 280 mg.kg-1 l.w.
Symptoms of poisoning – pulmonary oedema,
damage of liver and
kidneys, arthritis,
periarthritis
28. Paraquat (Gramoxone)
LD50 for man 40 mg.kg-1 l.w.
for cattle and pigs 30 – 70 mg.kg-1 l.w.
for dogs and cats 25 – 50 mg.kg-1 l.w.
Mechanism of toxic action – is mediated by
- free oxygen radicals
- proteolytic enzymes formed by active
neutrophilic leucocytes
Symptoms of poisoning – pulmonary oedema,
fibrotic pneumonia
fetotoxicity,retardation of ossification
29. Metal – based pesticides
arsenic compounds – insecticides, rodenticides
phenylmercury – fungicide for treatment of seed (1913 –
1993)
tributyltin – fungicide (xenoestrogenic effect)
thalium compounds – rodenticides
Today
Copper compounds – copper sulphate
- copper oxichloride
fungicides, algicides, molluscocides
Toxicity for fish – LC50 1 – 10 mg.l-1 depending on water
quality
30. Phenylpyrazoles
- insecticides
- antiparasitics
Mechanism of the toxic action – inhibition of
GABA
Fipronil is very toxic for bees (LD50 is 5 ng/bee)
It causes secondary toxicity in bees.
Its residua persists for 21 days.
It produces the „knock down“ effect.
31. Diagnosis of Pesticide Illness
Exposure history most important
Occupational and environmental history
Duration, dose, route of potential exposure
Symptom review
Physical exam & lab findings
Health effects may be due to any component of
pesticide formulations
31
32. Aspects of History that Suggest
Pesticide Illness
Multiple cases
Similar symptoms, exposure history
History of chemical application
Home or office
Accidental ingestion, esp. children
Suicide, homicide attempts
32
34. Pesticide Illness May Mimic
Common Medical Conditions
Mild:
Upper respiratory tract infection/influenza
Food-borne illness
Asthma
Plant-induced irritant or allergic dermatitis
Severe:
Cerebrovascular accident
Psychiatric dysfunction
Heat stroke
34
35. Treatment of Pesticide Illness
Decontamination
Shower, shampoo
Scrub under fingernails
Contain contaminated
clothing, body fluids
Save for residue analysis
Protect treating staff
Body fluid precautions
Personal protective
equipment if appropriate
35
36. Pesticide Illness
Medical Treatment
Symptomatic treatment
Respiratory distress
Maintain airway, breathing, circulation
Oxygen, bronchodilators if indicated
Ingestion
Gastric lavage, charcoal if indicated
Specific antidotes where applicable
36
