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Toxicity of pesticides

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Toxicity of pesticides

  1. 1. Abdulrahman Mohammed L-2012-V-21-D School of Public Health & Zoonoses GADVASU, Ludhiana
  2. 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. 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
  4. 4. Classification of pesticides General Classes Insecticides 1. Organophosphates(OP) 2. Carbamates 3. ChlorinatedHydrocarbons(CHC) 4. Pyrethroids 5. Biologicals 6. Metals/Elementals 7. Insect Growth Regulators(IGR)
  5. 5. Fungicides 1. Substitutedbenzenes 2. Thiocarbamates 3. EBDC(Ethylenebisdithiocarbamates) 4. Phthalates 5. Metals/Elements 6. Others
  6. 6. Rodenticides 1. Coumarins 2. Indandiones 3. Metals/Inorganics 4. Convulsants
  7. 7. Herbicides 1. Chlorophenoxy 2. Nitro-phenolic/cresolic 3. Dipyridyls 4. Triazines 5. Thiocarbamates 6. Phosphonates 7. Others
  8. 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. 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. 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. 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. 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. 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).
  14. 14. Action of Acetylcholine & Cholinesterase
  15. 15. - acetylcholine - cholinesterase - acetate - choline - organophosphate - 2-PAM nerve cell muscle Normal Electrical Nerve Impulse Transmission
  16. 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.
  17. 17. Pesticides Insecticide Toxicology OP Carbamates Parathion Propoxur Azinphos-methyl Methomyl Diclorvos Carbofuran Naled Aldicarb Fenamiphos Carbaryl Methidathion Fenoxycarb Oxydemeton-methyl Thiodicarb malathion Oxamyl
  18. 18. Pesticides OPs and Carbamates CarbarylParathion
  19. 19. Pesticides CHCs Dieldrin DDT
  20. 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. 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. 22. 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.
  23. 23. 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
  24. 24. 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
  25. 25. 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)
  26. 26. 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
  27. 27. 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
  28. 28. 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
  29. 29. 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.
  30. 30. 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
  31. 31. 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
  32. 32. Pesticide Illness Nonspecific Symptoms & Signs  Rash  Flu-like symptoms  Dizziness, malaise, respiratory tract irritation  Gastrointestinal symptoms  Seizures  Odor-related effects  Not toxicological effects of active ingredient 33
  33. 33. 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
  34. 34. 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
  35. 35. 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
  36. 36. THANK YOU FOR LISTENING

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