Glufosinate ammonium fact sheet
Glufosinate is produced by AgrEvo, a joint venture
established by the German chemical corporations Hoechst and Schering. Current
usage levels raise concern because of the marketing of genetically engineered
crops resistant to this herbicide.
Glufosinate is produced at Hoechst's Frankfurt plant in
Germany where work began in 1995 to double production capacity in anticipation
of the launch of genetically engineered glufosinate resistant crops.
The herbicide was first introduced into
Japan in 1984. In the UK, glufosinate was first considered in 1984. It was not
approved then for toxicological reasons, but was given provisional approval in
1991 (see below). US registration was achieved in 1993. The product is now
registered for use in more than forty countries and is marketed under a number
of trade names including Basta, Rely, Finale and Challenge.
In the UK agriculture, relatively small
amounts of glufosinate are used: 25 tonnes on 60,000 ha. The main crops are
oilseed rape and potatoes(1). These
figures may change dramatically if genetically engineered, glufosinate resistant
crops are commercialised.
In North America, commercialisation has
already begun. AgrEvo recently launched a formulation called Liberty, a
glufosinate product for use on crops resistant to glufosinate. In Canada,
Liberty Link canola has been on sale since 1995. In 1997, Liberty Link soybean
and maize were approved in the US. The US maize and soybean herbicide markets
account for 40% of all US pesticide sales(2).
AgrEvo expects glufosinate to become
its linchpin product by 2000, with an annual turnover of about US$680 million by
2001-2(3). AgrEvo aims to promote
the fast spread of glufosinate resistance into popular crop varieties, including
sugar beet. The profits could be considerable: introduction of Liberty Link
varieties is expected to increase sales of glufosinate to over US$300 million(4).
What is glufosinate
Glufosinate is a short name for the ammonium salt,
glufosinate-ammonium. It is a broad-spectrum contact herbicide and is used to
control a wide range of weeds after the crop emerges or for total vegetation
control on land not used for cultivation. Glufosinate herbicides are also used
to desiccate (dry off) crops before harvest.
Glufosinate is a natural compound
isolated from two species of Streptomyces fungi. It inhibits the activity of an
enzyme, glutamine synthetase, which is necessary for the production of glutamine
and for ammonia detoxification. The application of glufosinate leads to reduced
glutamine and increased ammonia levels in the plant tissues. This causes
photosynthesis to stop and the plant dies within a few days(5).
Glufosinate also inhibits the same enzyme in animals.
Hoechst claims that under conditions of recommended
use of glufosinate ammonium, a "detrimental effect on the health of both
users and consumers is extremely unlikely" (6). Glufosinate ammonium
structurally resembles glutamic acid, a natural amino acid that can stimulate
the central nervous system. It is recognised that excess release of glutamic
acid results in the death of nerve cells in the brain(7).
The surfactant, AES, which is used in
formulations, has also been found to cause toxic effects and may be a cause of
some of the clinical symptoms observed in suicide cases involving glufosinate.
The metabolite, MPPA-3, is, like glufosinate, a neurotoxin. The US EPA reported
that MPPA-3 injected into the brain of rats caused severe convulsions(8).
The toxicity of glufosinate varies in different
laboratory animals. The oral LD50 is 436-464 mg/kg in mice and 1,510-1,660 mg/kg
in rats. Dogs are the most sensitive. They can be twice as susceptible as mice
(the LD50 for beagles is 200-400 mg/kg(9)). The LD50 of the surfactant, AES, is
1,995-2,138 mg/kg in rats. The World Health Organisation (WHO) classifies
glufosinate in toxicity Class III, "slightly hazardous". The WHO
classification system is based on the LD50 for rats and aims to take account of
the sensitivities of more vulnerable test animals.
The dermal LD50
for glufosinate is about the same as for oral exposures. However, through the
skin, glufosinate formulations can be 2.5 times more toxic than glufosinate
alone(10). Glufosinate was first
considered by the UK Ministry of Agriculture, Fisheries and Food (MAFF)
Scientific Sub-Committee in 1984. The herbicide was refused approval because of
the toxicity of the formulation (containing 30% surfactant) when absorbed
through the skin(11).
In 1991, The Scientific Sub-Committee
recommended "Provisional Approval for six products for five years with a
data submission deadline of three years subject to a number of specific
conditions and label amendments" (12).
However, the Sub-Committee remained concerned about the dermal toxicity of one
of the six formulations, requiring the applicants to submit further studies.
Glufosinate has been found to cause a number of
neurological symptoms in laboratory animals following both oral and dermal
exposure. At lethal doses, overt signs of toxicity include: convulsions,
salivation, hypersensitivity, irregular breathing, and trembling(13). Some of
the behavioural changes lasted several days(14).
At sub-lethal doses, glufosinate can
have significant, but not so easily observable impacts. For example, a recent
study found that low doses of glufosinate affected central nervous system
development in young rats. One-day old rats were exposed to a dose of 1, 2 or 5
mg/kg of glufosinate daily for seven days. At six weeks they were tested for the
'wet-dog shakes' induced by administering kainic acid. Kainic acid stimulates
glutamate receptors in the brain. The frequency of wet-dog shakes decreased
significantly in all the glufosinate exposed rats. The results suggested that
exposure to even low doses of glufosinate in the infantile period in rats causes
changes in the kainic acid receptor in the brain(15).
Teratogenic effects (birth defects)
In recent studies, sub-lethal doses of glufosinate
ammonium was found to cause abnormalities in the development of embryos in
mammals both in vitro and in vivo. Deformities in the brain were
the main finding of these studies:
- Mouse embryos exposed to glufosinate in vitro
developed apoptosis (fragmentation of the cells leading to cell death) in
the neuroepithelium of the brain(16). An earlier study found that all the
embryos in the treated groups had specific defects including overall growth
retardation, increased death of embryos, hypoplasia (incomplete development)
of the forebrain at 10 mg/ml,
and cleft lips at 20 mg/ml(17).
- The effects on embryos after exposure of pregnant rats to
glufosinate during the time of neurogenesis (central nervous system
development) was determined. Pregnant rats were injected subcutaneously with
3 or 5 mg/kg of glufosinate once daily from days 13-20 of gestation. The
results suggested that glufosinate exposure at a crucial stage in pregnancy
causes a decrease in the number of glutamate receptors in offspring(18).
Residues in food and water
Residues in food are an area of concern, especially
when glufosinate is used as a pre-harvest desiccant. MAFF in the UK states that
adult consumers are most likely to be exposed to residues of glufosinate in
potatoes and dried (or processed) peas and in liver and kidney from animals fed
on contaminated cereal straw(19). The WHO/FAO recommended acceptable daily
intake (ADI) for glufosinate is 0.02 mg/kg.
MAFF's 1990 evaluation document on
glufosinate states that when it is used as a desiccant, glufosinate residues
will be found in dried peas, field beans, wheat, barley, oilseed rape, and
linseed. The highest likely residue levels in commodities for human consumption
were considered to be: 3 mg/kg in peas, 1 mg/kg in wheat grain, and 0.5 mg/kg in
oilseed rape. The reported residue levels in animal feed were high, including 50
mg/kg in barley straw and pea stalks and 20 mg/kg in wheat straw and field bean
MAFF reported that when wheat grain
containing residues was turned into flour, 10-100% of the residue was retained.
Residue levels in bran were 10-600% of those in grain. In addition, MAFF found
that the use of glufosinate as a herbicide and/or a desiccant in potato crops
can lead to residues in the tubers in the order of 0.1 mg/kg.
In 1991, the MAFF Advisory Committee on
Pesticides, the body responsible for registering pesticides in the UK, was
concerned that significant residues of glufosinate were found in the crops at
the time of harvest(20). In
particular, they were concerned that residues of 'additive ingredient' and the
metabolite, MPPA-3, were found in milk and the tissues of animals fed treated
straw. The Sub-Committee proposed a restriction on straw feeding to reduce
health risks to livestock and consumer intakes of residues in animal products.
AgroEvo claims that glufosinate is
unlikely to leach into groundwater(21),
but independent evidence suggests otherwise. Glufosinate is highly soluble in
water and is also classified as persistent and mobile (see below). The dangers
of soluble pesticides contaminating water supplies as a result of recommended
agricultural use is recognised by both the industry and governments throughout
the European Union.
The US Environmental Protection Agency (US EPA)
classifies glufosinate ammonium as 'persistent' and 'mobile'. Degradation of
glufosinate is largely by microbial activity. The half life has been determined
in numerous laboratory studies and varies from 3 to 42 days in some studies(22)
and up to 70 days in others(23). The shortest half life tends to be in soils
with a high clay and organic matter content(24).
In one study, residues of glufosinate
were found in spinach, radishes, wheat and carrots planted 120 days after
glufosinate had been applied(25). In
sandy soils, which overlie many aquifers, glufosinate has been found to be
highly persistent due to lack of biodegradation. Its transport through the soil
was also determined to be 'essentially unretarded' (26).
Glufosinate's metabolite, MPPA-3, has been found to be more persistent and more
mobile than glufosinate(27).
Effects on wildlife
Very little information is available on the effects
of glufosinate on aquatic and terrestrial wildlife. Most of the experimental
work to date has been produced as a requirement of registration and has focused
on the lethal dose rates for different organisms. Information on the sub-lethal
effects of glufosinate on plants or animals is sparse. Researchers at the
Department of Animal Ecology, Justus-Liebig University, Germany, are concerned
about the lack of data on the impacts of glufosinate in the environment. They
are particularly concerned about the commercialisation of glufosinate resistant
crops and say "it has become a matter of urgency to make a study of the
behaviour of this substance [glufosinate] in conjunction with natural
Glufosinate is toxic to a number of
aquatic animals including the larvae of clams and oysters(29),
daphnia and some freshwater fish species(30).
The commercial formulations are more toxic than the technical grade glufosinate.
For example, for the aqueous formulation, the LC50s
for the fish tested were between 12.3 and 79 mg/l and for the active ingredient
they were between 320 and 1,000 mg/l(31).
The rainbow trout, Oncorhynchus mykiss, was the most sensitive species in
The acute oral LD50
for birds is 2,000 mg/kg. 4 day old partridges given a dose of 2,000 mg/kg of
96% glufosinate showed signs of central nervous system damage including ataxia,
disequilibrium, convulsions, trembling, and wing flapping(32).
Effects on non-target plants
Glufosinate is a broad spectrum herbicide and is
damaging to most plants that it comes into contact with. The US EPA has stated
that glufosinate is "expected to adversely affect non-target terrestrial
plant species" (33).
The development of herbicide resistant crops is a
strategy developed by a number of chemical companies to increase profits and
ensure that key product lines can compete in the market place. AgrEvo has
targeted the broad spectrum herbicide, glufosinate, as their linchpin product
for the future and initiated a fast track programme to produce a range of crops
resistant to glufosinate. However, studies demonstrate that it causes adverse
health effects in animal studies, is likely to leach to drinking water sources,
could increase nitrate leaching, and is toxic to beneficial soil
micro-organisms. The introduction of glufosinate resistant crops and a greater
exposure to glufosinate increases the likelihood of these harmful effects in
humans and the environment. Glufosinate resistance will tend to intensify and
increase dependency on herbicide use rather than lead to significant reductions.
This fact sheet is taken from Health and Environmental
Effects of Glufosinate (in press) written by Topsy Jewell for Friends of the
1. Pers. Comm., MAFF, Pesticides Usage Survey
Group. MAFF, York.
2. Agrow No. 273 January 31st 1997, p. 21.
3. S. Watkins, 1995. Agrow's Top Twenty Five.
Report ref: DS 106, PJB Publications, London.
4. Agrow, 1997, Agrow's Top 25 1997 edition.
5. E. Rasche, J. Cremer, G. Donn, J, Zink.
1995, The Development of Glufosinate Ammonium Tolerant Crops into the
Market. In Brighton Crop Protection Conference, Weeds, 1995, BCPC, Farnham,
6. Hack, R. , E Ebert, G. Ehling, and K.H.
Leist, Glufosinate-ammonium - some aspects of its mode of action in mammals,
Food and Chemical Toxicology, 1994,Vol. 32, No. 5, pp. 461-470.
7. Fujii, T., Transgenerational effects of
maternal exposure to chemicals on the functional development of the brain in
the offspring. Cancer Causes and Control, 1997, Vol. 8, No. 3, pp. 524-528.
8. Cox, C., Herbicide Fact Sheet: Glufosinate,
Journal of Pesticide Reform, North West Coalition for Alternatives to
Pesticides, Oregan, US, 1996.
9. MAFF, Evaluation No. 33 : HOE 399866
(Glufosinate-ammonium), Ministry of Agriculture Fisheries and Food, London,
10. US EPA, Office of Pesticides and Toxic
Substances, Experimental Use permit (6340-EUP-RN) and Temporary Tolerance
Petition (4G3156) for HOE 39866. Memo from D.S. Saunders to R. Mountfort,
Registration Division, 18th April 1985.
11. MAFF, Health and Safety Executive, 1991.
Advisory Committee on Pesticides Annual Report 1991, HMSO, London.
13. Op. cit. 9.
14. Op. cit. 8.
15. Fujii, T., T. Ohata, M. Horinaka,
Alternations in the response to kainic acid in rats exposed to
glufosinate-ammonium, a herbicide, during infantile period. Proc. Of the
Japan Acad. Series B-Physical and Biological Sciences, 1996, Vol. 72, No. 1,
16. Watanabe, T. , Apoptosis induced by
glufosinate ammonium in the neuroepithelium of developing mouse embryos in
culture. Neuroscientific Letters, 1997, Vol. 222, No. 1, pp.17-20.
17. Watanabe, T. and T. Iwase, Development and
dymorphogenic effects of glufosinate ammonium on mouse embryos in culture.
Teratogenesis carcinogenesis and mutagenesis, 1996, Vol. 16, No. 6, pp.
18. Op. cit. 7.
19. Op. cit. 9.
20. MAFF, Health and Safety Executive, 1991.
Advisory Committee on Pesticides Annual Report 1991, HMSO, London.
21. Pesticides Trust [now PAN UK], Crops Resistant to
Glutamine Synthetase Inhibitors. Pesticides Trust, London, 1997.
22. Op. cit. 9.
23. Op. cit. 8.
24. B.S. Ismail, and A.R. Ahmed, Attenuation
of the herbicidal activities of glufosinate-ammonium and imazapyr in 2
soils. Agric. Ecosystems and Environ., 1994, Vol. 47, No. 4, pp. 279-285.
25. US EPA, Glufosinate Ammonium: Review and
assessment of individual studies and environmental fate assessment .
Submitted by Dynamac Corp, Sept 8 1988 Cited in Cox, C. 1996. Op. cit. 8.
26. Allenking, R.M., B.J. Butler. and B.
Reichert, Fate of the herbicide glufosinate-ammonium in the sandy, low
organic-carbon aquifer at CFB Borden, Ontario, Canada, Journal of
Contaminant Hydrology, 1995, Vol 18, No 2, pp161-179.
27. Gallina, M.A. and G.R. Stevenson,
Dissipation of [c-14] glufosinate ammonium in 2 Ontario soils, J. of Agric.
And Food Chem., 1992, Vol. 40, No. 1., pp.165-168.
28. Meyer, H., and V. Wolkers, (unpublished)
Herbicides Containing glufosinate-ammonium and their effect on
micro-organisms and animals in both terrestrial and aquatic eco-systems.
29. Op. cit. 8.
30. Op. cit. 9.
31. Op. cit. 9.
32. Op. cit. 9.
33. US EPA, EEB review of glufosinate/ignite
herbicide . Memo from D. Urban, Ecological Effects Branch, to J. Miller
Registration Div. , June 16th 1993, Cited in Cox, C. 1996. Op. cit. 8.
[This article first
appeared in Pesticides News No.42, December 1998, p20-21]