Diuron, N'-(3,4-dichlorophenyl)-N,N-dimethyl-urea (CAS number: 330-54-1), is a systemic herbicide derived from urea. It kills plants by blocking electron transport at photosystem II thus inhibiting photosynthesis. It is absorbed principally through the roots and is broad spectrum killing both broadleaf and grassy weeds along with mosses and algae.
Production and usage
Diuron was first reported in 1951(1) and first produced by E.I. du Pont de Nemours Co. in the US in
1966(2). This company no longer produces it but it is made by a number of generic manufacturers including Ancom, Bayer CropScience, Cedar, Crystal, Drexel, EMV, Griffin, Hegang Heyou, Hodogaya, Makhteshim-Agan, Milenia, Nufarm Ltd, Sannong, and United Phosphorus.
It is used to control weeds on hard surfaces, such as, roads, railway tracks, and paths (at around 3 kg/ha), and to control weeds in crops, such as, pear and apple trees, forestry, ornamental trees and shrubs, pineapples, sugar cane, cotton, alfalfa and wheat (at lower rates of around 1.8
kg/ha)(3). It can be used for both pre-emergent and knockdown weed control. Its use in some locations is becoming limited due to the development of resistant weed
species(4). In some products it is formulated with other active ingredients such as glyphosate, bromacil, hexazinone, amitrole and 2,4-D. In some countries diuron is also registered for aquatic weed control, as a cotton defoliant, and for use in home aquaria and fish ponds. It is used as a booster biocide in antifouling paints where its activity enhances the efficacy of copper in these products.
In the 1990's diuron accounted for 1-2% of the value of the non-crop market. Today diuron is worth around US$75 million at end user level, US$45 million at ex-manufacturer level, giving it a 0.6% share of the total non-crop market. This is equivalent to 8,400 metric tonnes of formulated product and 3,600 metric tonnes of active
ingredient(5). It is becoming less important as the use of other broad-spectrum herbicides, in particular glyphosate, expands. In France where its use has been limited since 1999 about 109 tonnes were made in 1996 and 133 tonnes in
1997(6). In the US between 907 and 1814 tonnes were used in 2001(7). In Denmark 20-25 tonnes per year were sold from 2001 to
2003(8).
Marketing takes place under a variety of trade names including Karmex, Diurex, Direx, and Lucenit. 'Inert' ingredients included in product formulations include ethylene glycol, the sodium salt of lignosulfonic acid, sodium polyphosphate, and
kaolin(9).
Manufacturing contaminants
Diuron contains two significant impurities from the manufacturing process 3,3',4,4'-tetrachloroazobenzene (TCAB) and 3,3',4,4'-tetrachloroazoxybenzene (TCAOB), both potent ‘dioxin-like’ substances. TCAB levels between 0.15 and 28 ppm have been found in diuron samples
tested(10). TCAOB is present at lower levels. Both TCAB and TCAOB cause chloracne a serious skin disease. The Australian National Registration Authority (NRA) is currently reviewing diuron registrations based partly on concern over the toxicity of these contaminants including their potential
carcinogenicity(11).
Fate in the environment
Persistence
Diuron is highly persistent in the environment. DT50 in soils varies from
90-180(12) days while other sources indicate it can range from one month to one
year(13). Further reports indicate that diuron-treated soils can continue to be toxic to plants at least three years after initial
treatment(14). The variability in calculated DT50s is likely due to differences in soil composition and other conditions. Degradation increases moderately in soils treated with diuron for many years. In one experiment where soils were treated at a rate of 3 kg/ha/year for 12 years the half-life decreased by 50% over this period suggesting that the soil microbial community was becoming increasingly able to degrade
it(15).
Diuron has a high soil organic fraction partition constant (Koc) of 485. This indicates it adsorbs tightly to soil organic matter and adsorption is directly affected by the amount of organic
matter(16). This means diuron leaches more readily from deeper soil with less organic matter giving it a higher likelihood of causing water pollution.
Diuron's octanol-water partition coefficient, Kow, is 2.6 indicating it has a low to medium propensity to accumulate in body fat.
Breakdown products
Diuron in waters is stable to hydrolysis only breaking down very slowly under neutral conditions. Photodegradation does occur in waters but is also very slow. Diuron breaks down more rapidly when microorganisms are present, such as in soils. A number of pathways of both aerobic and anaerobic degradation have been
identified(17). Most involve initial breakdown to 3,4-dichloroaniline (3,4-DCA), a substance also formed during breakdown of the related herbicides linuron and propanil. Although the data are limited, studies indicate that 3,4-DCA may be considerably more toxic than diuron (see below).
Health
Acute toxicity
Diuron is absorbed readily through the gut and lungs while uptake through the skin is more limited. It is slightly toxic to mammals but juveniles are more susceptible than
adults(18). The oral LD50 in rats is 3.4 g/kg and the dermal LD50 is > 2 g/kg(19). An early study indicated that animals fed protein-deficient diets were considerably more vulnerable to diuron toxicity: rats fed a diet of 3% protein were five times more sensitive to
diuron(20).
Exposure to sub-lethal doses of diuron causes formation of methaemoglobin, an abnormal form of the protein haemoglobin which carries oxygen in the
blood(21). Diuron can decrease the number of red blood cells (RBCs), increase the number of abnormally shaped RBCs, and increase the number of white blood cells. Diuron may cause the spleen to become congested due to the increased demand to remove damaged RBCs. Increases in liver size are also observed and are indicative of the extra load placed on this organ, the body’s major site of detoxification. Diuron can also cause eye and skin
irritation(22).
Carcinogenicity
The US Environmental Protection Agency (EPA) has classified diuron as a 'known/likely' carcinogen since 1997 based on the results of two studies. One study on rats indicated that both males and females fed diuron had a higher incidence of bladder cancer than control animals. The male rats in this study also had a higher incidence of kidney cancer than the control animals. In a study of mice animals with higher exposures had more breast
cancer(23).
Mutagenicity
There is conflicting evidence on whether diuron can cause mutations. The National Institute for Occupational Safety and Health in the US categorised diuron as a mutagen based on old
studies(24). Some recent studies support this finding(25) while others have not found evidence of mutagenicity.
Developmental Toxicity
Rats fed relatively high levels (125 mg/kg/day) of diuron produced offspring with delayed bone
formation(26) and other studies indicate that similar levels of diuron reduce birth weight. The US Toxics Release Inventory list diuron as a developmental toxin.
Health effects of 3,4-DCA
The main breakdown product of diuron is 3,4-DCA. The oral LD50 of 3,4-DCA in rats is around 60 mg/kg and by the inhalation route the LC50 ranges from 2.8 to 4.7 mg/l/4hrs indicating that 3,4-DCA is considerably more toxic than diuron itself. Dermal and inhalation absorption is rapid leading to formation of methaemoglobin. A marked species difference is dermal toxicity is noted with rabbit considerably more sensitive than rats. No human data is available but by extrapolating from other aromatic amines humans could be considerably more sensitive to methaemoglobin formation than rats. 3,4-DCA should be regarded as a potential respiratory
sensitizer(27). The carcinogenic potential of 3,4-DCA remains uncertain.
Wildlife
Diuron is of low toxicity to birds but moderately toxic to
fish(28). In the waters around the Queensland coast of Australia diuron is found at concentrations known to be harmful to seagrass, an important component of the marine ecosystems and the major food source for the dugong, a protected mammal. Mangroves have been dying back along parts of this coastline and diuron has been found contaminating sediments in these areas. While the sensitivity of mangroves to diuron has not been determined it is suspected that diuron contamination may be contributing to this dieback. There is also concern that terrestrial run-off containing diuron may be impacting the health of the Great Barrier
Reef(29).
Water contamination
Diuron's potential to pollute water is of particular concern. Herbicides used for weed control on hard surfaces are washed down drains into water supplies by rainfall. In addition, diuron in antifouling paint on ships has contributed to contamination of marine and estuarine waters, and of marine sediments. As abiotic breakdown in waters is extremely slow this contamination will likely persist for years despite regulatory action withdrawing antifouling uses of diuron in a number of countries. In the Japanese aquatic environment 86% of tested samples showed a 3.05 µg/litre concentration of
diuron(30). In Dutch coastal waters a higher level than the permitted 430 ng/litre was
detected(31). According to the French Environmental Institute diuron is detected in 34.6% of surface waters in France where it was the fifth most frequently detected pesticides. It was also found in 6.4% of groundwater samples where it was the seventh most frequently detected
pesticide(32). In the UK diuron is consistently one of the pesticides most frequently found exceeding the non-statutory Environmental Quality Standard of 0.1 µg/litre(33). Many other studies have reported contamination of water by diuron in antifouling
paint(34).
Regulation
The Australian NRA is currently reconsidering registrations and approvals related to
diuron(35). Their main concern is the impacts of marine contamination raised by studies mainly focusing on the Queenland area (see above) along with concern over the toxicology of the two impurities TCAB and TCAOB (see above), including their potential carcinogenicity. Their review should be published shortly.
A review of the booster biocidal uses of diuron in antifouling paint by the UK's Advisory Committee on Pesticides in 2000 resulted in its withdrawal from use in antifouling paints mainly due to concern over operator
exposure(36). Inclusion of diuron in a list of Priority Hazard Substances is being considered by the European
Commission(37). Substances on the list are those that have been shown to be of major concern for European Waters and which must be phased out under the Water Framework Directive. Diuron use is also being reviewed under Directive 91/414/EEC. The European Diuron Task Force (including Griffin and Bayer) have presented data to defend its continued use in Europe. A decision is expected later this year. Diuron's registration in Sweden was cancelled in 1992 due to concerns about its carcinogenicity. It was banned in the Netherlands in 1999 due to problems with water
quality(38). (RM)
1. Science, 1951 (114) p493.
2. Guidance for the reregistration of manufacturing-use and certain end-use pesticide products containing diuron as the active ingredient, US EPA Office of Pesticide Programs, Washington DC, 30 September 1983, p3.
3. Giacomazzi S, Cochet N, Environmental impact of diuron transformation, Chemosphere, 2004, 56:1021-1032.
4. Ureas and amides resistant weeds, Herbicide Resistance Action Committee, North American Herbicide Resistance Action Committee and the Weed Science Society of America, 2003, www.weedscience.org/Summary/UspeciesMOA.asp
5. Parker R, Agricultural Information Services Ltd., pers comm.
6. Reseau Ferre de France, http://www.rff.fr
7. www.epa.gov/oppbead1/pestsales/01pestsales/
market-estimates2001.pdf
8. Gravesen L, pers comm.
9. Cox C, Diuron, Journal of Pesticide Reform, Spring 2003, 23(1)12-20.
10. Singh J, Bingley R, Levels of 3,3',4,4'-tetrachloroazobenzene in diuron and linuron herbicide formulations, Journal of the Association Official Analytical Chemists 1990, 73(5):749-51; National Toxicology Program report on the toxicity studies of 3,3',4,4'-tetrachloroazobenzene, http://ehp.niehs.nih.gov/ntp/docs/toxreports.html
11. Diuron Review Scope Document, NRA, Canberra, Australia, December 2002.
12. Tomlin CDS, The Pesticide Manual (13th Ed), British Crop Protection Council, 2003, p347.
13. Field JA, Reed RL, Sawyer TE, Griffiths SM, Wigington PJ, Diuron occurrence and distribution in soil and surface and ground water associated with grass seed production, Journal of Environmental Quality, 2003, 32:171-179; Okamura H, Aoyama I, Ono Y, Nichida T, Antifouling herbicides in the coastal waters of western Japan, 2003, Japanese Marine Pollution Bulletin.
14. Op. Cit. 11; Marriage PB, Saidak WJ, von Stryk FG, Residues of atrazine, simazine, linuron and diuron after repeated annual applications in a peach orchard, Weed Research 15:373-379; Elder VA et al, Dissipation of phytotoxic diuron residues in Hawaii pineapple soils, University of Hawaii, College of Tropical Agriculture and Human Resources, Res. Ser 006.
15. Rouchard J, Neus R, Bulcke K, Cools K, Eelen H, Deckers T, Soil dissipation of diuron, chlorotoluron, simazine, propyzamide and diflufenican herbicides after repeated applications in fruit tree orchards, Archives of Environmental Contamination and Toxicology, 2000, 39:60-65.
16. Alva AK and Singh M, Sorption of bromocil, diuron, norfluron, and simazine at various horizons in two soils, Bulletin of Environmental Contamination and Toxicology, 1990, 45:365-374.
17. Giacomazzi S, op. cit. 3.
18. Hayes WJ Jr, Pesticides studied in man, 1982, Williams and Wilkins, Baltimore, MD.
19. EXtension TOXicology NETwork: http://ace.orst.edu/info/extoxnet/pips/diuron.htm
20. Boyd EM and Krupa V, Protein-deficient diet and diuron toxicity Journal of Agriculture and Food Chemistry, 1970, 18:1104-1107.
21. Griffin LLC, Material Safety Data Sheet: Direx 80 DF, 2002, www.cdms.net
22. Cox C, Diuron, Journal of Pesticide Reform, Spring, 2003, 23(1) pp12-20.
23. US EPA Office of Pesticide Programs, Health Effects Division, 1999, Tox Oneliners, EPA chem code 035505 - diuron, 12 March 2003 update.
24. National Institute for Occupational Safety and Health. The registry of toxic effects of chemical substances. Urea, 3-(3,4-dichlorophenyl)-1,1-dimethyl-.www.cdc.niosh/rtecs/ys882148.html; JP Seiler, Herbicidal phenylalkylureas as possible mutagens I. Mutagenicity tests with some urea herbicides 1978 Mutation Research 58:353-359.
25. Cox C, op. cit. 9.
26. KS Khera et al, Teratogenicity studies of pesticidal formulations of dimethoate, diuron, and lindane, 1979, Bulletin of Environmental Contamination and Toxicology 22:522-529.
27. Opinion of the results of the Risk Assessment of: 3,4-Dichloroaniline Human Health Part, Scientific Committee on Toxicity, Ecotoxicity and Environment, November 2003, http://europa.eu.int/comm/health/ph_risk/committees/sct/documents/out205_en.pdf
28. EXTOXNET, Op. cit. 19.
29. www.apvma.gov.au/gazette/gazette0212p24.pdf; Op. Cit. 11.
30. Okamura H, Aoyama I, Ono Y, Nichida T, Antifouling herbicides in the coastal waters of western Japan 2003, Japanese Marine Pollution Bulletin.
31. Lamoree MH, Swart CP, van der Horst A, van Hattum B, Determination of diuron and the antifouling paint biocide Irgarol 1051 in Dutch marinas and coastal waters, Journal of Chromatography, 2002, 970:183-190.
32. IFEN The French Institute of the Environment. Les pesticides dans les eaux, 6čme annuel 2002.
33. Pesticides 2002: a summary of monitoring of the aquatic environment in England and Wales, Environment Agency.
34. Boxall ABA, Comber SD, Conrad AU, Howcroft J, Zaman N, Inputs, monitoring and fate modelling of antifouling biocides in UK estuaries, Marine Pollution Bulletin, 2000, 40:898-905; Thomas KV, Fileman TW, Readman JW, Waldock M, Antifouling paint booster biocides in the UK coastal environment and potential risks of biological effects, Marine Pollution Bulletin, 2001, 42:677-688.
35. Op. cit. 29.
36. Evaluation on Diuron: Use as a Booster Biocide in Antifouling Products, Advisory Committee on Pesticides.
37. http://europa.eu.int/comm/environ
ment/water/water-framework/priority_substances.htm
38. Bannink AD, How Dutch drinking water production is affected by the use of herbicides on pavements, Water Science and Technology, 49:173-181.[This article first appeared in Pesticides News No. 67, March 2005, page 20-21]