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 environment risk.

What is 2,4-D?
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.

Production
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 tonnes).

Use
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 weeds.

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).

Acute toxicity
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 chemical hypersensitivity(11). 

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)

Chronic effects
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 intoxication(13). 

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 the acid.

Cancer
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).

Reproductive effects
Abnormal foetal skeletal development, increased foetal mortality and other reproductive effects are fairly conclusively associated with exposure to phenoxy-acid herbicide and their dioxin contaminants(20). 

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.

Wildlife
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."

Conclusions
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 pollution.

References
1. The Pesticide Manual 10th Edition, British Crop Protection Council/Royal Society of Chemistry, 1994.
2. Generic Pesticides-the markets. Agrow report DS100, PJB Publications, Richmond, UK, 1994.
3. Post-emergence herbicides, Agrow report, PJB Publications Ltd, Richmond, UK, 1995.
4. Chemical Regulation Reporter, p 44, Bureau of National Affairs, US, 4 September 1993.
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.
9. International 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.
15. Interdepartmental Executive Committee on Pest Management, 2,4-D Re-evaluation update and label improvement program, Plant Industry Directorate, Canada, 23 November, 1994.
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, 1996.
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, 1993.
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, March 1997.
28. Op. cit. 10.

[This article first appeared in Pesticides News No.37, September 1997, p20]