2,4-D fact sheet
The herbicide 2,4-D was
first identified in 1942 and marketed in 1944. Despite
its decades of usage, there are still data gaps
concerning 2,4-D's effects on human health and
This highly selective herbicide is toxic to broad
leafed plants but less harmful to grasses(1). One
of the hormone weedkillers, 2,4-D
(2,4-dichlorophenoxy acetic acid) is an
aryloxyalkanoic acid known also as a 'phenoxy
herbicide', which includes MCPA, mecoprop,
triclopyr and 2,4,5-T. These chemicals have
complex mechanisms of action against weeds,
resembling those of auxins (growth hormones).
Once absorbed 2,4-D is translocated within the
plant and accumulates at the growing points of
roots and shoots where it inhibits growth.
Introduced in 1942, 2,4-D has been off patent for
many years and is manufactured and sold by many
different companies around the world.
The global market is estimated
to be over US$300 million and the main producers
are Agrolinz, Atanor, Dow, AH Marks (UK), Nufarm
(Australia), Polikemia, Rhône-Poulenc, Sanachem,
Sinochem (China) and Ufa, together with four
other producers in Turkey(2) .
Ufa (Russia) produced about
49,000 tonnes of different formulations until
production was discontinued some years ago due to
'environmental problems'. Production has resumed
at lower levels. Dow (US) is now the largest
producer with a capacity of 20,000 tonnes.
Rhône-Poulenc is the largest European producer
(7,000 tonnes pa), followed by Agrolinz (4,000
The principal use is for
the control of broad leaf weeds in cereal
crops-including wheat, maize, rice and
sorghum-and grassland and turf areas. It is also
widely used in mixtures with other herbicides to
provide weed control in forestry, orchards and
non-crop areas, and for the control of aquatic
The phenoxy acid group of
herbicides are probably one of the widest used
herbicide chemcial classes. The US, South
America, Europe and the former Soviet Union are
major markets for 2,4-D-weed control on US wheat
relies on little else-and global use is predicted
to grow over the next decade(3). In the US where it was the third most
used pesticide in the early to mid 1990s, over
31,000 tonnes of 2,4-D was used annually(4). In the UK it
is among the top six herbicides used by UK local
authorities, and it ranked seventh among
herbicides used on grassland and fodder crops and
twentieth among herbicides used in orchards in
1992(5,6). Overall the area of land treated with
2,4-D in UK agriculture (excluding amenity use)
declined by 83% during the period 1984-1994(7). 2,4-D is
also used widely in developing countries: India,
for example, used 1,300 tonnes in 1994-5(8).
2,4-D is a WHO Class II
'moderately hazardous' pesticide. This places it
in the same class as endosulfan, lindane,
paraquat and toxaphene. It has an LD50 of 375
mg/kg in the rat with evidence suggesting a
similar level of toxicity in humans(9).
Occupational exposure to 2,4-D
has produced serious eye and skin irritation.
Other symptoms of 2,4-D poisoning include nausea,
weakness and fatigue, and in some cases
neurotoxic effects including inflammation of
nerve endings(10). Some medical reports from practitioners
who have treated victims of acute exposure to
2,4-D mention severe and sometimes long lasting
or even permanent symptoms. These include, as
well as those listed above, diarrhoea, temporary
loss of vision, respiratory tract irritation,
confusion, numbness and tingling, bleeding and
A recent review of 2,4-D by the
UK Advisory Committee on Pesticides (ACP) noted
that "Approval holders must generate a
number of toxicology/operator exposure studies to
allow a full risk assessment to be made."(12)
It seems that long term
exposure to 2,4-D can affect different animals in
a wide variety of ways. Rats for example were
found to be largely unaffected when fed
moderately large amounts in their diet over long
periods, although signs of kidney pathology were
demonstrated. Dogs however died when fed smaller
amounts over shorter periods. A human fed 16.3
grammes over 32 days showed severe symptoms of
It also seems that the various
chemical forms of 2,4-D can have different toxic
effects. Acid, salt and various esters differ in
all their measured toxic effects to some extent,
but the majority of toxicity data relates only to
Phenoxy acid herbicides
have been linked with soft tissue sarcomas, but
the UK ACP has concluded that 'the data do not
suggest a positive link with 2,4-D'14 as
have the Canadian authorities(15). However, the
International Agency for Research on Cancer
(IARC) has classified 2,4-D among the phenoxy
acid herbicides MCPA and 2,4,5-T as a class 2B
carcinogen-possibly carcinogenic to humans(16)
(concluding that there was limited evidence in
humans, inadequate evidence in animals).
The US authorities have also
been reluctant to declare 2,4-D as a potential
human carcinogen, but the US courts decided that
a forestry worker contracted cancer and died as a
direct result of his exposure to 2,4-D during the
course of his work(17).
One concern about 2,4-D has
related to dioxin contamination. 2,4-D was in the
past frequently co-formulated with the herbicide
2,4,5-T. Production of 2,4,5-T was contaminated
with the carcinogenic dioxin TCDD. Those who were
exposed to the mixed formulations might therefore
have been exposed to TCDD. The most notorious
mixed formulation was Agent Orange, used first by
the UK military in Malaysia and later extensively
by the US military to defoliate jungle regions in
Vietnam. In the UK, 2,4-D + 2,4,5-T formulations
were in use until 1994(18). 2,4-D has been produced with
contaminant dioxins, but not the harmful TCDD(19).
Abnormal foetal skeletal
development, increased foetal mortality and other
reproductive effects are fairly conclusively
associated with exposure to phenoxy-acid
herbicide and their dioxin
2,4-D has also been classified
as an endocrine disrupter(21), and significant chromosomal damage
occurred in human cells cultured in the presence
of 2,4-D. At the same time no evidence for
mutagenicity has been found and 2,4-D did not
damage DNA in human lung cells(22).
Fate in the environment
2,4-D has low soil sorbtion
and a high potential for leachability(23). Indeed
2,4-D residues have been recorded many times both
in water company monitoring programmes and by the
UK Department of the Environment(24,25). It has
also been detected in groundwater supplies in a
number of US States and in Canada(26). In
1994, 3% of groundwater samples, and in 1995, 4%
of surface water samples in England and Wales
exceeded the EU standard(27).
Its high potential for water
contamination has led to the inclusion of 2,4-D
in the EC Priority Candidate List of chemicals to
be considered for inclusion among the chemicals
most tightly controlled to prevent water
pollution. 2,4-D is also a priority candidate for
inclusion in the UK Department of the Environment
Red List which has a similar function.
Some formulations of 2,4-D are highly toxic to
fish while others are less so. Aquatic
invertebrates do not in general seem to be very
sensitive to 2,4-D. Moderate exposure of honey
bees to 2,4-D severely impaired reproduction.
Toxicity to birds is low to moderate(28).
However, the ACP noted "Insufficient data
are available to fully assess the safety of in or
near water uses to aquatic life" and
"Approval holders must generate a number of
studies using 2,4-D and its derivatives in order
to allow a full assessment of the risk to
wildlife to be made."
2,4-D is a pesticide that has been heavily used
in agriculture all over the world for some fifty
years or more. Alarmingly the ACP Evaluation has
highlighted a large number of major data
gaps-covering human health effects, aquatic and
wider environmental risk. In addition to the
number and the range of these data gaps, there
continue to be concerns about long term adverse
effects of 2,4-D on human health and water
1. The Pesticide Manual
10th Edition, British Crop Protection
Council/Royal Society of Chemistry, 1994.
Pesticides-the markets. Agrow report DS100, PJB
Publications, Richmond, UK, 1994.
herbicides, Agrow report, PJB Publications Ltd,
Richmond, UK, 1995.
4. Chemical Regulation
Reporter, p 44, Bureau of National Affairs, US, 4
5. Produce Studies, Non
agricultural use of pesticides in England and
Wales, DoE, November 1996.
6. Pesticide usage
survey report 119: Grassland and fodder crops in
Great Britain 1993; and Pesticide usage survey
report 115: Orchards and fruit stores in Great
Britain 1992, MAFF, 1994.
7. Pesticide usage
survey report 100: Review of usage of pesticides
in agriculture and horticulture throughout Great
Britain 1984-94, MAFF, 1997.
8. Op cit. 3.
Programme on Chemical Safety, The WHO recommended
classification of pesticide by hazard and
guidelines to classification 1996-97.
10. Extoxnet data sheet
on 2,4-D, Pesticide Mange-ment Programme, Cornell
University, US, 1994.
11. Shearer, Ruth W,
Health effects of 2,4-D herbicide, in 2,4-D
Information Packet, North West Coalition for
Alternatives to Pesticides, January 1990.
12. Evaluation on
2,4-dichlorophenoxyacetic acid salts and esters,
MAFF, March 1993.
13. Op. cit. 10.
14. Op. cit. 12.
Executive Committee on Pest Management, 2,4-D
Re-evaluation update and label improvement
program, Plant Industry Directorate, Canada, 23
16. IARC monographs on
the evaluation of carcinogenic risks to humans:
An updating of IARC Monographs volumes 1 to 42.
Supplement 7, WHO, Lyon, France 1987.
17. O'Brien, Mary, Jury
Charges Dow $1.5 million for 2,4-D caused death
of forest worker, Journal of Pesticide Reform,
1987, 7: 4(30).
18. Veterans and Agent
Orange-Update 1996, National Academy Press, US,
19. Ibid, pp35-87.
20. Environmental Health
Criteria 29, 2,4-Dichlorophenoxyacetic acid
(2,4-D), IPCS, Geneva, 1984.
21. Colborn, T, et al.
Developmental effects of endocrine disrupting
chemicals in wildlife and humans, Env. Health
Perspectives 101:378-384, 1993.
22. Op. cit. 10.
23. Montgomery, John H,
Agrochemicals desk reference, Lewis Publishers,
24. Pesticides in water:
Report of the working party on the incidence of
pesticides in water, HMSO, May 1996.
25. Drinking Water
Inspectorate, Drinking water 1953: A report of
the Chief Inspector, HMSO, 1996.
26. Op. cit. 10.
27. Pesticides in the
Aquatic Environment, 1995, Environment Agency,
28. Op. cit. 10.
[This article first
appeared in Pesticides News No.37, September 1997, p20]