1. Herbicides
Domina Petric, MD

2. Herbicides can be devided into
Chlorophenoxy herbicides
Glyphosate
Bipyridyl herbicides

3. Chlorophenoxy herbicides
2,4-dichlorophenoxyacetic acid (2,4-D)
2,4,5-trichlorophenoxyacetic acid (2,4,5-T)
Their salts and esters

4. Chlorophenoxy herbicides
2,4-D and 2,4,5-T and their salts and esters are herbicides used for the destruction of weeds.
Probable human lethal dosages are at mg/kg.

5. Chlorophenoxy herbicides
2,4,5-T (Agent Orange) is no longer used because it caused severe agricultural damage and social disruption.

6. Chlorophenoxy herbicides
2,4-D in large doses can cause coma and generalized muscle hypotonia in humans.
Muscle weakness and marked hypotonia may persist for several weeks.

7. Chlorophenoxy herbicides
There is causal link between 2,4-D exposure and non-Hodgkin´s lymphoma.
Chemical contaminants (dioxins) produced during the manufacturing process are also very important human carcinogens.

8. Glyphosate It is now the most widely used herbicide in the world.
Gylphosate-related poisoning incidents are commonly reported: from minor injuries (most common) to lethal outcomes.

9. Glyphosate Glyphosate is a significant eye and skin irritant.
It has caused lethal outcomes.
Commercial formulations often contain surfactants and other active compounds that complicate glyphosate toxicity.

10. No specific treatment is available for glyphosate toxicity.

11. Bipyridyl Herbicides: Paraquat
Mechanism of action: single-electron reduction of the herbicide to free radical species.
Human lethal dosage is mg/kg.
Lethal human intoxications have been reported.

12. Paraquat
Paraquat accumulates slowly in the lung by an active process and causes:
lung oedema
alveolitis
progressive fibrosis

13. Paraquat
It inhibits superoxide dismutase resulting in intracellular free radical oxygen toxicity.

14. Paraquat
The first signs and symptoms after oral exposure are hematemesis and bloody stools.
Within a few days, delayed toxicity occurs, with respiratory oedema accompanied by widespread cellular proliferation.

15. Paraquat Hepatic, renal and myocardial involvement may also occur.
The interval between ingestion and death may be several weeks.
Because of delayed pulmonary toxicity, prompt removal of paraquat from the digestive tract is important.

16. Paraquat intoxication treatment
gastric lavage
cathartics
adsorbents

17. Paraquat intoxication treatment
Oxygen should be used cautiously for dyspnoea and cyanosis.
Oxygen may aggravate the pulmonary lesions.

18. Paraquat intoxication treatment
Patients require prolonged observation.
Proliferative phase begins 1-2 weeks after ingestion.

19. Katzung, Masters, Trevor. Basic and clinical pharmacology.