Paraquat is one of the most widely used herbicides in the world. It has
had a tarnished reputation because of its acute oral toxicity and ill-health
associated with operators - particularly in the plantation sectors of many
What is paraquat?
Paraquat is one of the most widely used herbicides,
and held the largest share of the global herbicide market until recently
overtaken by glyphosate. Paraquat is sold in about 130 countries for use on
large and small farms, plantations and estates and in non-agricultural weed
control. It is a quick acting, non-selective herbicide, which destroys green
plant tissue on contact and by translocation within the plant.
Paraquat was first synthesized in 1882.
Its herbicidal properties were discovered only in 1955 in the ICI (now Zeneca)
laboratories, who produced it commercially in 1961. This chemical type of
herbicide - a bipyridyl - is shared with few other pesticides. One, the related
diquat, is also a Zeneca product.
Although the patent protection on
paraquat has expired, Zeneca remains the world's major producer. The raw
bipyridyl and paraquat production take place in the UK (where a new £40 million
production plant at Huddersfield replaced the original Widnes plant in 1995), in
the US (Bayport, Texas) and Japan (Tal, 50% owned by Zeneca). Huddersfield is
Zeneca's main plant, producing 8,000 tonnes a year, of which 95% is exported(1).
In addition paraquat production takes place in Brazil and India. Final stage
manufacture takes place in Thailand and Kelang, Malaysia (Zeneca now has a
minority interest in the latter). The company has planned a US$80m. joint
venture in China (north of Shanghai) to come on stream in 1998 and has recently
said it will double the size of this plant to 6,000 tonnes a year(2).
Paraquat is made by other basic producers in Argentina, China, India, Spain,
Taiwan and the US.
Zeneca markets paraquat as Gramoxone
for agricultural use in formulations ranging between 24-36% active
ingredient and for home and garden use under the trade names Weedol and Pathclear
in formulations of about 2.5% paraquat. The biggest markets for the
company's paraquat products are the US, Japan, Malaysia, Thailand, Mexico,
France and Brazil and annual sales are still increasing(3).
For many years paraquat accounted for a big part of Zeneca's agro-chemical sales
(24% in 1987(4) ) and is still
a major product in the agrochemical portfolio.
Uses and usage
Paraquat is used to control broad-leaved weeds
and grasses, being less effective on deep rooted plants such as dandelions. It
does not harm mature bark, and is thus widely used for weed control in fruit
orchards and plantation crops, including coffee, cocoa, coconut, oil palms,
rubber, bananas, vines, olives and tea, ornamental trees and shrubs and in
forestry. Other uses include weed control in alfalfa, onion, leeks, sugar beet,
asparagus. It is used for weed control on non-crop land and can be used as a
defoliant for cotton and hops before harvesting. Paraquat is used as a desiccant
for pineapples, sugar cane, soya beans and sunflower(5). In pineapples, for
example, paraquat is applied after harvest to accelerate the drying out process
and enabling plants to be burnt after 3-5 weeks, compared to 13 weeks after the
alternative cutting and natural drying.
Paraquat is increasingly used to
destroy weeds in preparing land for planting in combination with no-till
agricultural practices which minimise ploughing and help prevent soil erosion.
Although toxic to fish, it is used as an aquatic herbicide where it is absorbed
by plant matter and silt.
Paraquat is highly toxic to animals and has
serious and irreversible delayed effects if absorbed. As little as one
teaspoonful of the active ingredient is fatal. Death occurs up to 30 days after
ingestion. Absorbed paraquat is distributed via the bloodstream to practically
all areas of the body. The lungs selectively accumulate paraquat, and therefore
contain higher concentrations than other tissues. This develops into pulmonary
oedema and other lung damage, leading to fibrosis. Liver damage occurs and renal
failure may follow as the kidneys remove absorbed paraquat.
At spray strength paraquat is of
relatively low acute toxicity. It is classified as a solid and with an acute
oral LD50 for rats of 157 mg/kg,
which puts it into WHO as Class II 'moderately hazardous'(6).
Paraquat is also toxic if absorbed through the skin, see 'health issues' below.
The minimum lethal dose by oral ingestion in human beings is about 35 mg/kg body
weight, although less could be lethal without treatment. In dogs the lethal dose
is 25-50 mg/kg and in cows and sheep 50-75 mg/kg(7).
There is no vapour toxicity, but it can cause nose bleeding if inhaled.
No antidote for poisoning exists
although it is recommended that the highly absorbent Fuller's Earth is
administered. Hospital care must be sought without delay.
The US EPA has classified paraquat as a
possible human carcinogen, but has concluded that the risks posed to individual
applicators are minimal and of no concern(8).
The EPA requested additional studies on
mutagenicity for re-registration in 1987. Of the studies of gene mutation
accepted eight were negative, four weakly positive and four were positive. Based
on these the EPA concluded that paraquat is weakly genotoxic.
Paraquat is less toxic to birds than to
mammals. Its toxicity to fish varies with the species, size of fish and the
softness or hardness of the water. Aquatic plants can concentrate high levels of
paraquat, and a recent study indicates that significant tadpole mortality
results from when they feed on paraquat-contaminated plant material. It also
resulted in tadpole tail abnormalities and affected swimming behaviour feeding
Key health issues
Being less acutely toxic at spray strength,
the greatest risk to workers of fatal and serious accidents is during mixing and
loading. Studies show high incidence of paraquat-related ill-health. For example
a study in Guápiles, one of the main plantation regions of Costa Rica,
identified 284 accident cases caused by paraquat between 1988 and 1990,
including 123 cases of systemic poisonings, burns, eye injuries and fingernail
Conditions of use in many developing
countries mean it is difficult to follow label instructions and recommendations
for use. Sprayers generally have no or inadequate protective clothing, lack
training, and have little knowledge of the specific effects of products they
use. Workers on estates are frequently employed as sprayers for 10 months of the
year, six days a week.
In occupational use the main route of
exposure is through the skin and the worst cases of exposure occur during
knapsack spraying. Continued exposure, as encountered by spray operators on
plantations, is reported to affect the skin, eyes, nose and finger nails. Skin
problems include mild irritation, blistering and ulceration, desquamation
(peeling of the outer layer of the skin), necrosis (cell-death in skin tissue),
dermatitis of the hands and in some cases scrotal areas (from leaking spray
machines soaking trousers)(11).
Severe exposure on hands has resulted in nail damage, ranging from localised
discoloration to temporary nail loss(12).
Eye splashes can result in irritation and inflamed eyelids (blepharitis) and
visual acuity can decrease(13). A
study in Thailand found clear indications of caustic burns on the feet after
working with spinning disk applicators(14).
While small farmers face some of the
same problems as estate workers (lacking training, distant washing medical
facilities), they are exposed to paraquat less regularly. A study of small
farmers in Kenya found no protective clothing was worn (the cost of a pair of
rubber gloves was equivalent to a day's wage)(15).
Intact human skin is relatively
impermeable to paraquat, although a number of fatalities resulting from dermal
exposure to intact skin have been documented(16).
The presence of scratches, cuts, sores or severe dermatitis on the skin
substantially increase the risks. Furthermore dermal exposure to paraquat can
lead to skin injury including severe dermatitis, second degree burns and itching
rash on the face, neck, hands or all over the body(17).
A study of Malaysian plantation sprayers cited health problems after exposure to
paraquat(18). An education worker
with banana plantation workers in Honduras sent reports of common nose bleeds,
diminishing eye sight, burning of skin, thinning of hair, nausea, loss of toe
and finger nails(19).
Incidents also occur in the North. In
1992, a UK agricultural worker died after being splashed in the face with
paraquat when he dropped an open container(20).
In 1994, a farmworker in the UK suffered a severe rash and infection to his
groin after applying paraquat with a knapsack sprayer(21).
A similar incident was confirmed in 1992.
Poisoning: suicides and accidents
Accidental or deliberate ingestion of paraquat
has been responsible for a large number of pesticide-related deaths. It is a
major suicide agent in many developing countries. In Sri Lanka a 1989 study of
669 poison incidents indicated that agrochemicals were responsible for 59% and
paraquat was the commonest poisoning agent with a fatality rate of 68%(22).
Paraquat poisonings are still common in the UK, where a study of pesticide
poisoning between 1990-1991 indicates 44 deaths with paraquat responsible for
75%(23). Many of these may be suicides. There is concern in developing countries
that the easy availability of pesticides leads to suicides which might not
otherwise occur. Most cases are self-poisoning, but not all intend to die(24).
To prevent accidental deaths, Zeneca
added three alerting agents in the formulations. A stenching agent, was added to
some formulations in 1975, an emetic to induce vomiting in 1977, and a blue dye
to prevent confusion with cola, black coffee or other beverages was added from
1977. These are included in most but not all formulations depending on cultural
acceptance and product registration.
Incidents in the UK do include paraquat (14
cases [11%] in 1994)(25), some of which are deliberate baiting of animals, while
others involve exposure during or after spraying.
Measures to reduce exposure
In the US paraquat is a restricted use
pesticide, and may be purchased and used only by certified applicators. In the
UK there are no such restrictions and Pathclear and Weedol are
allowed for amateur use in household gardens. Professional users should wear a
protective face shield, wash splashes immediately, avoid spray drift and remove
contaminated clothes immediately. The WHO Health and Safety Guide adds that
normal personal protection and hygienic measures should be rigorously observed;
paraquat should not be sprayed with inadequate dilution, nor used by people
suffering dermatitis or with wounds(26).
Residues in food are generally not detectable,
except when it is used as a pre-harvest desiccant in food crops (e.g. cereals)
where levels of up to 0.2 mg/kg of plant matter have been reported(27). The
Acceptable Daily Intake is recommended as 0.004 mg/kg/day body weight(28).
Paraquat binds rapidly and tightly to clay
materials in soils, and when adsorbed it is biologically inactive. It also binds
to humus and other organic material: this results in no, or very low soil
residues or leaching into water sources.
Multiple spray trials showed paraquat
residues in soil from 22-58 mg/kg. Under field conditions, the residual paraquat
is slowly redistributed. Long-term field studies have shown degradation rates of
5-10% per annum, which is thought to prevent saturation of the carrying capacity
of the soil and to prevent adverse effects on microflora and other soil
organisms or on crop growth. In sandy soils with a low organic content paraquat
may be more readily released into ground water(29) .
The German federal biological institute
(BBA) asserted in 1983 that repeated treatments of paraquat led to an
accumulation in the soil and damage to crops. It refused to re-register paraquat
products, but this was challenged in the courts by ICI. In 1992 the Court ruled
that the BBA was justified but also ruled that registration should be granted to
a new ICI formulation of only 10% paraquat, which was re-approved later that
year. Field crop applications are permitted only once every four years, and only
in areas at risk from erosion. Wider registrations were refused because of
effects on the environment(30).
In contrast to less widely used herbicides,
resistance has only occurred in 18 minor species on 50 sites, and nowhere is it
of any agronomic or economic significance(31).
As paraquat is absorbed and binds quickly to
soil, leaching into water sources is not generally a problem and its use as a
herbicide does not lead to food residues. A major concern centres on accidental
and deliberate ingestion of the active ingredient, where even small quantities
are fatal. Exposure to the concentrated active ingredient is a problem during
mixing and loading sprayers. In developing countries the conditions of use make
safe use very difficult. Although not fatal at spray strength, regular use, such
as required on plantations, leads to health problems.
Finland and Sweden banned
paraquat because of its high toxicity.
Austria banned because of high toxicity and
high frequency of poisonings(32).
Hungary severely restricted because accidental
poisoning rate was unacceptably high(33).
Norway voluntary cancellation.
Limited registration in Germany. Concern with
residues in soil has led to registration for field crop applications only once
every four years, and only in areas at risk from erosion.
US Restricted use pesticide - purchase and use
only by certified applicators.
Europe Under EC Registration Directive 91/414
the UK will review paraquat on behalf of Member States by mid 1997(34).
1. 'Zeneca points to strong results', Agrow, No. 225,
3 February 1995.
2. 'Zeneca to boost herbicide plant, Financial Times,
22 May 1996.
3. 'Zeneca defends independence as agrochemicals
advance', Agrow, No. 252, 15 March 1996.
4. Dinham, Barbara, ICI Limited, Paraquat Production -
Starting the Chain, a report for Greenpeace International, December 1989.
5. Tomlin, Clive (ed), The Pesticide Manual,
incorporating The Agrochemicals Handbook, Tenth Edition, British Crop
Protection Council and the Royal Society of Chemistry, Farnham UK, 1994.
6. WHO Recommended Classification of Pesticides by
Hazard and Guidelines to Classification 1996-97,WHO/PCS/96.3, WHO, Geneva,
7. Bismuth, C., et. al., 'Prognosis and treatment of
paraquat poisoning. A review of 28 cases', Journal of Toxicol. Clinical.
Toxicol. 19, pp 461-474, 1982, quoted in International Programme on Chemical
Safety, Environmental Health Criteria 39, Paraquat and Diquat, WHO, Geneva,
8. EPA, Paraquat Fact Sheet No. 131, 1987.
9. Bauer Dial, C.A. and Dial, N.A., 'Lethal effects of
the consumption of field levels of paraquat-contaminated plants on frog
tadpoles', Bulletin of Environmental Contamination and Toxicology, 1995,
10. Vergara, A. Accidentes con productos agroqu'micos
reportados al Instituto Nacional de Seguros durante 1990, cant - n de Pococ'
y Guácimo: un análisis preliminar: Ajuste Estructural: Mujer, Salud y
Empleo, Jan José, Costa Rica, 1991.
11. Ongom et al 1994, Binns 1976, Newhouse et al 1978,
Waight and Wheather 1979, Levin et al 1979, Horiuchi et al 1980 cited in EHC
12. Samman and Johnston 1969, Howard 1979b, cited in
13. Studies reported in EHC39, p. 90.
14. Howard, J.K., Paraquat spraying. Comparative risks
from high and low volume application methods. In Proceedings of 10th Asian
Conference on Occupa-tional Health, Singapore, pp. 1-7. (EHC39, p86).
15. Craig, Ian and Chris Mbevi, 'Contamination in the
Tropics', Pesticides News, 19, March 1993, p. 5.
16. Smith, J.G., Paraquat poisoning by skin
absorption:a review', Human Toxicology, 7:15-19, 1988.
18. Arumugam, V., Victims Without Voice, Tenaganita
and PAN Asia Pacific, 1992.
19. Brady, Christopher, US worker on a health and
literacy project, Honduras, interview material and letter to the Pesticides
Trust [now PAN UK], 18 March 1992.
20. Health and Safety Executive, Pesticide Incidents
Investigated in 1992/93, UK.
21. Health and Safety Executive, Pesticide Incidents
Investigated in 1994/95, UK.
22. Hettiarachchi, J. and G.C.S. Kodithuwakku,
'Pattern of Poisoning in Rural Sri Lanka', International Journal of
Epidemiology, Vol 18 No 2, UK.
23. Pesticide Monitoring Unit, Surveillance of Human
Acute Poisoning from Pesticides 1 October 1990-30 September 1993, National
Poisons Information Service (Birmingham Centre).
24. Hettiarachchi, J. and G.C.S. Kodithuwakku,
'Self-poisoning in Sri Lanka: factors determining the choice of the
poisoning agents', Human Toxicology, 8, 1989, pp 507-510.
25. Report of the Environmental Panel of the Advisory
Committee on Pesticides, Pesticide Poisoning of Animals in 1994,
Investigations of Suspected Incidents in the UK (and for 1993), MAFF, and
Scottish agricultural Science Agency, UK, 1995.
26. International Programme on Chemical Safety,
Paraquat Health and Safety Guide No. 51 WHO, Geneva, 1991.
27. Draft Decision Guidance Document for paraquat,
FAO, 10 April 1993.
28. JMPR/CODEX, established in 1986.
29. Op. cit 26 and EHC39, op cit.
30. 'German paraquat decision endorsed but ICI to gain
new registration', Agrow, 166, 28 August 1992, p. 1 and Agrow 175 8 January
1993, p. 9.
31. Holt, et al, Mechanisms and agronomic aspects of
herbicide resistance, Annual Review of Plant Physiology & Molecular
Biology, 1993, vol.44:203-229.
32. UNEP/FAO Information exchange on banned and
severely restricted chemicals in international trade, control actions to ban
or severely restrict chemicals, 1996.
34. Pesticide Safety Directorate, UK, 10 May 1996,
[This article first
appeared in Pesticides News No.32, June 1996, p20-21]