PARAQUAT

• Dole Food Company announced in October
2007 that it was discontinuing the use of paraquat
worldwide in its operations (Dole 2008).
• Chiquita has also stopped using paraquat in
banana plantations (Gochez 2009).
• United Plantations has announced it will
cease use of paraquat on all its plantations
by January 1st, 2011 (UP 2010). United
Plantations is one of the largest oil palm
plantation companies in Malaysia; it also has
some coconut plantations, and oil palm in
Indonesia.
• The Danish company AarhusKarlshamn,
a leading producer of speciality vegetable
oils and fats and a founding member of the
Roundtable for Sustainable Palm Oil has
stated that paraquat should be minimised
or phased out “as soon as possible” (Frank
2010).
2. Toxicological Assessment
2.1 Absorption and distribution
Paraquat can be rapidly absorbed by inhalation
and through the intestine after ingestion.
Absorption after oral intake is about 10% (EC
2003).
Absorption through intact skin is generally low,
0.5% according to EC (2003), but is substantially
increased if the skin is damaged, and has lead
to death in humans (Kemi 2006).
After oral intake, there is high initial concentration
in the liver and kidneys, which then reduces.
Plasma concentration is relatively stable for 30
hrs, and concentration in the lungs increases.
It is actively concentrated in the lungs (Kemi
2006).
Low levels of paraquat may be retained in
muscle tissue after skin exposure and slowly
released into the blood (Lee 2008a).
Metabolism of paraquat is limited, and it is largely
(69-96%) excreted in the faeces unchanged. One
study showed a degree of microbial degradation
in the gut (US EPA 1997).
2.2 Acute toxicity
WHO (2010) Recommended Classification of
Pesticides by Hazard: Class II Moderately toxic.
However, it is argued that paraquat, because of
its acute toxicity, delayed effects, and absence
of an antidote should be in WHO Class 1a or 1b
(Isenring 2006).
US EPA (1997) Hazard Classifi cation:
• Acute toxicity by inhalation = Category I,
highly toxic
• Acute toxicity from oral intake = Category II,
moderately toxic
• Systemic toxicity from dermal absorption =
Category III, slightly toxic
• Eye irritation = Category II, moderate to
severe
• Skin irritation = Category IV, minimal
Lethal doses
The lethal dose, LD 50 , is the dose that kills 50%
of test animals.
A wide variety of lethal doses have been
reported, some expressed in terms of paraquat
ion and some technical grade paraquat
dichloride, others not identifying which but
presumed to be in terms of paraquat ion.
Oral:
FAO (2008):
• Oral LD 50 rat, male = 113.5 mg/kg body
weight (paraquat ion), which is 344 (range
246-457) mg/kg bw of paraquat dichloride
technical
• Oral LD 50 rat, female = 93.4 mg/kg bw
(paraquat ion), 40-200 mg/kg bw of paraquat
dichloride technical
Kemi (2006):
• Oral LD 50 rat = 40-200 mg/kg
• Oral LD 50 mouse = 120 mg/kg
• Oral LD 50 guinea pig = 22-80 mg/kg
• Oral LD 50 rabbit = 49-150 mg/kg
• Oral LD 50 sheep = 50-75 mg/kg
• Oral LD 50 cat = 26-50 mg/kg
• Oral LD 50 dog = 25-50 mg/kg
• Oral LD 50 monkey = 50 mg/kg
• Oral LD 50 human = 40-60 mg/kg
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