Paraquat Presented by Jason Kujawa CHEM 471

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ParaquatPresented byJason Kujawa CHEM 471
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Outline Discovery Use Chemical Properties Environm
ental Effects Toxicity Exposure Toxicity Tests
Neonatal Toxicity Tests Mechanism of
Action Treatment
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Discovery -first synthesized in 1882.
-herbicidal properties discovered in 1955.
-first commercially used as herbicide in 1961.
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Use -kills broad-leaved weeds and grasses.
-weed control in orchards. -desiccant
for pineapples, sugar cane, and sunflowers.
-used by ATF for large scale destruction of
marijuana.
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Chemical Properties -IUPAC name is
1,1-dimethyl-4-4-bipyridium. -belongs to the
bipyridylium herbicide class. -highly water
soluble and highly polar. -stable to light
and heat, but inactivated on contact with soil.
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Environmental Effects -binds tightly to
clay in soil and renders paraquat inactive.
-no long term build-up in soil. -lethal to
wildlife especially aquatic species.
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Toxicity Exposure -usually ingested by
accident and through dermal contact with weed
application. Dose -dose of lt20 mg/kg results
in vomiting and diarrhea. -dose of 20-50 mg/kg
results in pharyngeal burns, vomiting, diarrhea,
acute kidney and liver insufficiency, and
necrosis of the liver. -dosegt50 mg/kg results
in death in 72 hours because of multiple organ
failure. -LD50 for humans is 30 mg/kg or
equivalent to a few ml. of concentrated paraquat.
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Toxicity Tests -acute toxicity tests
within 10 to 14 days reveal impaired breathing.
-the lungs selectively accumulate paraquat and
contain the highest concentrations.
-paraquat causes destruction of type I and type
II alveolar epithelial cells. -no chronic
toxicity tests because death occurs up to 30 days
after ingestion. -neonatal toxicity tests
with European starlings reveal considerately
higher levels of paraquat than those of
the adult species.
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Mechanism of Action -mechanism not fully
understood. -hypothesized mechanism of
action is phase I through oxidation and
reduction reactions accompanied by phase I
oxidation of NADPH and NADP. -formation of
superoxide ions, hydrogen peroxide, and hydroxyl
radicals. -lipids of cellular membranes
peroxidized and cellular death results.
-no phase II biotransformation processes occur
for paraquat.
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Treatment -no
treatment of paraquat poisoning.
-prevent further GI absorption of paraquat by
inducing gastric lavage and
administering activated charcoal with magnesium
citrate to absorb paraquat.
-oxygen therapy avoided because
increasing oxygen level is believed to
increase phase I oxidation and cause higher
toxicity.
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References
1. Pesticides News. No.32 (1996, June).
Pesticides News
Homepage of Pesticides News, Online.
Available
http//pan-uk.org/pestnews/actives/paraquat.htm
2. Viccelio, Peter, 1993.
Handbook of Medical Toxicology.
Little, Brown, and Company, New York.
pgs. 315-316 3.
Ashton, F.M., Crafts, A.S. 1973. Mode of Action
of Herbicides. John
Wiley Sons, Inc., New York. pg. 185
4. Klassen, C.D. 1996/2001.
Casarett and Doulls Toxicology
The basic science of poisons (CD).
5th/6th Edition. McGraw-Hill,
New York. pgs.130, 674.
5. Haley, T.J., Berndt, W.O. 1987.
Toxicology. Hempshire,
Washington. pgs. 147-149, 609.
6. Hoffman, D.J., Rattner, B.A., Burton,
G.A., Cairns, J. 199 5/2001.
Handbook of Ecotoxicology. Lewis, Boca
Raton. pg.55.