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WHAT IS PARAQUAT?
An Introduction to Paraquat. Mary O'Brien.
Dirty Dozen Campaigner, September 1989.
Dirty Dozen Campaigner
A Publication of the
Pesticide Action Network
An Introduction to Paraquat
"Paraquat is probably the most effective herbicide that exists
right now on the Earth. It is also one of the world's worst
poisons." -Edward Block, lung specialist at the University of
Paraquat is a nonselective contact herbicide, defoliant,
desiccant, and plant growth regulator manufactured by Imperial
Chemical Industries (ICI, United Kingdom) and produced by a
number of other companies in other countries (e.g. Chevron
Chemical Company in the United States). It is used for
desiccation of cotton, potato vines, and other crops; for weed
control in rubber and coffee plantations, rice paddies,
industrial sites and rights-of-way, and among fruit trees, shade
trees and ornamentals; for pasture renovation; and for aquatic
weed control. Paraquat is sold worldwide (i.e., in over 130
countries); its damage to humans is similarly worldwide.
Paraquat's acute toxicity is extreme; 3-5 g (approximately
3-5 ml, or less than a teaspoon) is the approximate lethal dose
(LD50) of paraquat for an adult male. Death results from lung
failure within weeks of ingestion. This is because paraquat
concentrates in lung tissue, causing cells critical to oxygen
exchange to die and be replaced by connective tissue cells,
suffocating the victim. If very large doses of paraquat are
ingested (as in suicide cases), death will occur within a few
days from damage to several vital organs, including the brain,
adrenals, liver, kidney, and lungs.
There is no antidote for paraquat poisoning, so survival
depends on the amount ingested and time before beginning
intensive medical measures to inactivate and eliminate the
paraquat from the gut and blood. Severe paraquat poisoning is
Absorbed following skin exposure, inhalation, or ingestion,
paraquat is toxic to epithelial tissues such as skin, nails,
cornea, liver, kidneys, and the linings of the gastrointestinal
and respiratory tracts. Systemic damage can result from skin
contact. Symptoms of systemic illness include pain and burning in
the chest and throat, weight loss, aching joints, pain in the
eyes, nervousness and rash, dizziness and nausea. Symptoms of eye
injury include conjunctivitis (inflammation of the inner surface
of the eyelid), marked swelling, and eye irritation.
At very low levels of exposure, paraquat can cause skin
injury, including severe dermatitis, second degree burns, a rash
all over the body, discolored or itching hands, and an itching
rash on the face and neck. Premalignant skin lesions develop
where skin exposed to paraquat is also exposed to sunlight.
Given paraquat's extreme acute toxicity and its potential
for chronic toxicity, it is callous to export it to hot southern
countries where worker protection is minimal or nonexistent and
the essential protective clothing is unbearable.
A California Department of Food and Agriculture report on
paraquat poisonings of California workers during 1975 repeatedly
notes that the workers were not wearing every piece of protective
equipment required for mixing and loading of paraquat: "a rubber
apron, rubber gloves, a full face shield, rubber boot coverings,
and a waterproof hat or helmet." Is this likely to be the
protection a Malaysian plantation worker receives? Could the
worker function in high heat and humidity wearing that clothing?
The continued use of paraquat worldwide is a testament to
the senseless addiction of agriculture to murderous toxins and
the willingness of the chemical industry to congratulate itself
for making a profit on a pesticide, even as people are dying from
it. Paraquat use is not necessary anywhere; it is environmentally
dangerous and a human health hazard everywhere; and its sale in
Third World countries is unconscionable.
Mary O'Brien is Staff Scientist with the Northwest Coalition for
Alternatives to Pesticides (NCAP), and editor of the Journal for
Pesticide Reform. She has worked with diverse agencies to develop
pest management policies, and serves on the PAN North America
This article was excerpted from a longer piece which appeared in
the Summer 1989 issue of the Journal of Pesticide Reform. For a
copy of the original article or the entire issue, contact NCAP at
P.O. Box 1393; Eugene, OR 97440; USA.
Pesticide Action Network North America Regional Center
116 New Montgomery Street,#810
San Francisco CA, 94105