Diuron

Pesticide -> EPA IRIS

Herbicides

Active substance -> EU Pesticides database: Not approved

Pesticides -> Herbicides, Urea Derivative

Pesticide

Environmental transformation -> Pesticides (parent, predecessor)

log Kow = 2.68

2.85

White, crystalline solid

Colorless crystals

White powder

0.004 % (NIOSH, 2024)

In water, 42.0 mg/L at 25 °C

In water, 37.4 mg/L at 25 °C

Very low solubility in hydrocarbon solvents

In acetone 53, butyl stearate 1.4, benzene 1.2 (all in g/kg at 27 °C). Sparingly soluble in hydrocarbons.

0.004%

356 to 374 °F at 760 mmHg (USCG, 1999)

Decomposes at 180-190 °C

356 °F (decomposes)

356 °F (Decomposes)

Hazardous decomposition products formed under fire conditions: Carbon oxides, nitrogen oxides (NOx), hydrogen chloride gas.

Diuron, stable under normal conditions, decomposed on heating to 180 to 190 °C giving dimethylamine and 3,4-dichlorophenyl isocyanate.

When heated to decomposition it emits highly toxic fumes of /chlorine and nitrooxides/.

318.2 °F (USCG, 1999)

158-159 °C

MP: 159 °C. Decomposes at 180 °C

316 °F

316 °F

Danger

H350: May cause cancer [Danger Carcinogenicity]

P203, P260, P273, P280, P318, P319, P391, P405, and P501 (click each P-code to see the statement)

This chemical does not meet GHS hazard criteria for 0.1% (1 of 739) of reports.

Warning

H302 (99.9%): Harmful if swallowed [Warning Acute toxicity, oral]

Chemical: Urea, N'-(3,4-dichlorophenyl)-N,N-dimethyl-

Hazard Traits - Carcinogenicity; Environmental tox

Commission Regulation (EC) No 1490/2002

Urea, N'-(3,4-dichlorophenyl)-N,N-dimethyl- is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Urea, N'-(3,4-dichlorophenyl)-N,N-dimethyl- are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

08/91/EC, Reg (EU) 2019/707, Reg. (EU) 2022/801, Reg. (EU) No 2018/1262, Reg. (EU) No 540/2011

Status: Active Update: 21-10-2020 https://echa.europa.eu/registration-dossier/-/registered-dossier/13520

Urea-derived herbicides have low toxicity in animal feeding studies; May induce methemoglobinemia; [HSDB] Systemic toxicity unlikely unless large amounts ingested; [EPA Pesticides, p. 122] Skin and mucous membrane irritation have been reported with the use of diuron. [ACGIH]

The major hazards encountered in the use and handling of diuron stem from its toxicologic properties as a urea-based herbicide. Contact with diuron (particularly in concentrated form) may irritate the eyes, nose, throat, and skin. Exposure to diuron may even prove fatal if sufficient quantities are inhaled, swallowed, or absorbed through the skin. The ACGIH recommends a TLV-TWA of 10 mg/cu m of air to protect against the toxic effects of this odorless, crystalline herbicide. In addition, those who use or handle diuron should wash thoroughly with soap and water before smoking, eating, drinking, or using toilet facilities. In an emergency release situation, wear a positive-pressure breathing apparatus, and special protective clothing. Diuron will not ignite easily, but it may burn with the potential to produce irritating or poisonous gases. For small fires involving diuron, extinguish with dry chemical, CO2, water spray, or foam, and for large fires use water spray, fog, or foam. Runoff from fire control water may give off poisonous gases or cause water pollution and should, therefore, be diked for later disposal. Diuron is stable (to oxidation and moisture) under normal storage conditions, and is non-corrosive. The process of hydrolysis will be increased under acid or alkaline conditions, or elevated temperatures (with decomposition occurring at 180-190 °C). Diuron containers require no DOT label, and may be shipped via air, rail, road, or water. Small liquid spills of diuron should be reduced to a solid phase by evaporation, or taken up with a non-combustible absorbent material (eg, sand), and then placed in a container for later disposal. Small dry spills are carefully shovelled into a dry, lidded container. Large liquid spills on land first should be diked to prevent runoff from entering water sources and sewers. All spills on land should be deposited in excavated pits, ponds, or other holding areas which have been sealed with an impermeable, flexible membrane liner. Solids are then covered with a plastic sheet, while bulk liquids are absorbed with fly ash or cement powder. Spills of diuron into bodies of water are first treated with activated carbon, then the immobilized masses of pollutant and precipitates are removed with mechanical dredges or lifts. Before permanent land disposal of diuron, consult with environmental regulatory agencies. Also, releases or spills of diuron in amounts equal to, or greater than 100 lb, must be reported to the National Response Center.

USEPA/Office of Prevention, Pesticides and Toxic Substances; Reregistration Eligibility Decision Document for Diuron. List A Case 0046 (September 2003). The RED summarizes the risk assessment conclusions and outlines any risk reduction measures necessary for the pesticide to continue to be registered in the U.S.[Available from, as of July 11, 2018: http://www.epa.gov/pesticides/reregistration/status.htm]

Section 8(a) of TSCA requires manufacturers of this chemical substance to report preliminary assessment information concerned with production, exposure, and use to EPA as cited in the preamble in 51 FR 41329. Effective date September 29, 2006; Reporting date: November 28, 2006.

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. Urea, N'-(3,4-dichlorophenyl)-N,N-dimethyl- is included on this list. Effective date September 29, 2006; Sunset date: November 28, 2006.

Tolerances are established for the combined residues of the herbicide diuron, 3-(3,4-dichlorophenyl)-1,1-dimethylurea and its metabolites convertible to 3,4-dichloroaniline in or on food commodities, as follows: [Table#1149]

Tolerances with a regional registration as defined in section 180.1(n) are established for the combined residues of the herbicide diuron (3-(3,4-dichlorophenyl)-1,1-dimethylurea and its metabolites convertible to 3,4-dichloroaniline) in or on the raw agricultural commodities:[Table#1150]

The Agency has completed its assessment of the occupational, residential, and ecological risks associated with the use of pesticide products containing the active ingredient diuron, as well as a diuron-specific dietary risk assessment. ... The Agency has determined that diuron products are eligible for reregistration provided that: (i) current data gaps and confirmatory data needs are addressed; (ii) the risk reduction measures outlined in this document are adopted; and (iii) label amendments are made to reflect these measures. ... Based on its evaluation of diuron, the Agency has determined that diuron products, unless labeled and used as specified in this document, would present risks inconsistent with FIFRA. Accordingly, should a registrant fail to implement any of the risk mitigation measures identified in this document, the Agency may take regulatory action to address the risk concerns from use of diuron. If all changes outlined in this document are incorporated into the product labels, then all current risks for diuron will be adequately mitigated for the purposes of this determination.

As the federal pesticide law FIFRA directs, EPA is conducting a comprehensive review of older pesticides to consider their health and environmental effects and make decisions about their continued use. Under this pesticide reregistration program, EPA examines newer health and safety data for pesticide active ingredients initially registered before November 1, 1984, and determines whether the use of the pesticide does not pose unreasonable risk in accordance to newer safety standards, such as those described in the Food Quality Protection Act of 1996. Diuron is found on List A, which contains most pesticides that are used on foods and, hence, have a high potential for human exposure. List A consists of the 194 chemical cases (or 350 individual active ingredients) for which EPA issued registration standards prior to FIFRA '88. Case No: 0046; Pesticide type: herbicide; Registration Standard Date: 09/30/83 PB84-210327; Case Status: OPP is reviewing data from the pesticide's producers regarding its human health and/or environmental effects, or OPP is determining the pesticide's eligibility for reregistration and developing the RED document.; Active ingredient (AI): diuron; Data Call-in (DCI) Date(s): 09/28/90, 07/26/95, 10/13/95; AI Status: The producers of the pesticide have made commitments to conduct the studies and pay the fees required for reregistration, and are meeting those commitments in a timely manner.

Excerpt from NIOSH Pocket Guide for Diuron:

(General first aid procedures)

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

Use dry chemical, CO2, water spray, or foam extinguishers ... If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters. Notify local health and fire officials and pollution control agencies. From a secure, explosion-proof location, use water spray to cool exposed containers. If cooling streams are ineffective (venting sound increases in volume and pitch, tank discolors or shows any digns of deforming), withdraw immediately to a secure position ... The only respirators recommended for fire fighting are self-contained breathing apparatuses that have full face-pieces and are operated in a pressure-demand or other positive-pressure mode.

If material involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.)

Keep container tightly closed in a dry and well-ventilated place. Keep in a dry place.

Store in tightly closed containers in a cool, well-ventilated area.

Avoid freezing liquid suspension. Dry formulations are stable under normal storage.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

Spill handling: Evacuate persons not wearing protective equipment from area of spill or leak until clean-up is complete. Remove all ignition sources. Collect powdered material in the most convenient and safe manner and deposit in sealed containers. Ventilate area after clean-up is complete. It may be necessary to contain and dispose of this chemical as a hazardous waste. If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters. Contact your local or federal environmental protection agency for specific recommendations.

Spills of pesticides at any stage of their storage or handling should be treated with great care. Liquid formulations may be reduced to solid phase by evaporation. Dry sweeping of solids is always hazardous: These should be removed by vacuum cleaning or by dissolving them in water or other solvent in the factory environment. In the field they may be washed away with water into a suitable soak-hole. /Pesticides/

Cleaning glassware & spray equipment: flush tank, pump, hoses, & boom with several changes of water after removing nozzle tips & screens (clean these parts separately). Glassware can be cleaned by thorough washing with detergent followed by acetone rinse.

For more Cleanup Methods (Complete) data for Diuron (6 total), please visit the HSDB record page.

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contaminated packaging: Dispose of as unused product.

For terrestrial use, do not discharge effluent containing this product into lakes, streams, ponds, estuaries, oceans, or other waters unless in accordance with the requirements of a National Pollution Discharge Elimination System (NPDES) permit and the permitting authority has been notified in writing prior to discharge. ... For guidance contact your State Water Board or Regional Office of the EPA.

For more Disposal Methods (Complete) data for Diuron (9 total), please visit the HSDB record page.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed.

Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

For more Preventive Measures (Complete) data for Diuron (20 total), please visit the HSDB record page.

Tolerances are established for the combined residues of the herbicide diuron, 3-(3,4-dichlorophenyl)-1,1-dimethylurea and its metabolites convertible to 3,4-dichloroaniline in or on food commodities, as follows:[Table#1147]

Tolerances with a regional registration as defined in section 180.1(l) are established for the combined residues of the herbicide diuron (3-(3,4-dichlorophenyl)-1,1-dimethylurea and its metabolites convertible to 3,4-dichloroaniline) in or on the raw agricultural commodities:[Table#1148]

10.0 [mg/m3]

8 hr Time Weighted Avg (TWA): 10 mg/cu m

Peak Exposure Recommendation: Transient increases in workers' exposure levels may exceed 3 times the value of the TLV-TWA level for no more than 15 minutes at a time, on no more than 4 occasions spaced 1 hour apart during a workday, and under no circumstances should they exceed 5 times the value of the TLV-TWA level. In addition, the 8-hour TWA is not to be exceeded for an 8-hour work period.

A4: Not classifiable as a human carcinogen.

10 mg/m³ [1974]

Diuron and antimycin A act between both cytochromes b and cl of the respiratory chain, the rate of inhibition versus concentration of diuron yields hyperbolic kinetics whereas antimycin A shows a sigmoidal inhibition curve. Combined effects of antimycin A and diuron on yeast mitochondrial state 4 respiration as well as the apparent ki of diuron is significantly decreased in the presence of antimycin A. The interaction coefficient between antimycin A and diuron was 0.4, suggesting that antimycin A induced conformational change in the b-cl segment of the respiratory chain allows diuron to bind more tightly to its site of action.

Hematologic

Eyes, skin, respiratory system, blood

Diuron has reproductive, teratogenic effects and organ toxicity to mammals. Diuron induces urinary bladder cancer, mammary gland carcinoma and hepatocellular adenomas in mice, kidney toumors and testicular interstitial cell adenomas in rats. High level diuron exposure can cause central nervous system depression. Chronic exposure can affect bone marrow, spleen in rats. Anemia, increase mortality, growth retardation are also seen.

LD50; Species: Anas platyrhynchus (Mallard duck) oral > 2000 mg/kg

LD50; Species: Colinus virginianus (Northern Bobwhite quail) oral 940 mg/kg

LC50; Species: Anas platyrhynchus (mallard duck) subacute diet 1730 ppm

LC50; Species: Colinus virginianus (Bobwhite quail) subacute dietary >5000 ppm

For more Ecotoxicity Values (Complete) data for Diuron (46 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), measured Koc values ranging from 55.3 to 962(2-7) indicate that diuron is expected to have moderate to low mobility in soil(SRC). Volatilization of diuron from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 5.0X10-10 atm-cu m/mole(SRC), based upon its vapor pressure, 8.25X10-9 mm Hg(8), and water solubility, 37.5 mg/L(8). Diuron is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(8). Diuron is a highly persistent and fairly immobile herbicide(9). When applied to soil it has a mean half-life of approximately 330 days and will not leach below 5 to 10 cm from the surface(9). Metabolites of microbial degradation include the major metabolite, 3,4-dichloroaniline, and also 3-(3,4-dichlorophenyl)urea and 3-(3,4-dichlorophenyl)-1-methylurea(9). Utilizing the Japanese MITI test, 0% of the Theoretical BOD was reached in 4 weeks(10) indicating that biodegradation is not an important environmental fate process in soil(SRC). In field studies in Wyoming where fields were irrigated in different ways, diuron persisted for over 15 months at higher application levels(11). The half-life of diuron from field studies was 133-657 days with an average of 328 days(2).

AQUATIC FATE: Based on a classification scheme(1), measured Koc values of 55.3-962(2-7) indicate that diuron is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(8) based upon an estimated Henry's Law constant of 5.0X10-10 atm-cu m/mole(SRC), derived from its vapor pressure, 8.25X10-9 mm Hg(9), and water solubility, 37.5 mg/L(9). According to a classification scheme(10), measured BCFs of <2.9-14(11), indicate that bioconcentration in aquatic organisms is low(SRC). The rate of diuron hydrolysis is negligible at neutral pH but increases as the conditions become strongly acidic or alkaline(12). Diuron was degraded 67-99% in 10 weeks under aerobic conditions by mixed cultures isolated from pond water and sediment(13), indicating that biodegradation may be an important environmental fate process in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), diuron, which has a vapor pressure of 8.25X10-9 mm Hg at 25 °C(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase diuron may be removed from the air by wet or dry deposition(SRC). The two main absorption bands for diuron are located at 247 nm and 284 nm; absorption is very low but not completely negligible between 320 and 370 nm(3) and therefore diuron may be susceptible to direct photolysis by sunlight(SRC).

Diuron was not detected (detection limit 0.01 ppm) in 59 composite Ontario-grown vegetable samples that were analyzed for phenylurea herbicides between 1980-1985(1). Diuron was not detected (detection limit 0.29 ug/L) in 100 raw milk, 30 full-fat milk, 20 half-skimmed milk and 20 skimmed milk samples(2). Raw milk was provided by a local farm and all other milk samples were obtained from local supermarkets in Shenyang, China(2).

Diuron was not detected (detection limit 0.29 ug/L) in 100 raw milk, 30 full-fat milk, 20 half-skimmed milk and 20 skimmed milk samples(1). Raw milk was provided by a local farm and all other milk samples were obtained from local supermarkets in Shenyang, China(1).

IDENTIFICATION AND USE: Diuron is a solid. Diuron is a photosynthesis inhibitor that is used mainly for general weed control on noncrop areas. It has also been used in the selective control of germinating broadleaf and grass weeds in sugarcane, citrus, pineapples, cotton, asparagus, and temperate climate tree and bush fruits. It is also used as a soil sterilant. HUMAN STUDIES: It may irritate the skin, eyes, or nose. Diuron is cytotoxic in vitro in human cells and oxidative stress contributes to its toxicity. The victim of a suicide attempt did not show signs of intoxication after ingesting diuron and amitrole preparation. ANIMAL STUDIES: It caused irritation to eyes and mucous membranes of rabbits but a 50% water paste was not irritating to intact skin of guinea pigs. Diuron at high dietary levels (2500 ppm) induces rat urinary bladder hyperplasia after 20 weeks of exposure. It was also noted that genes related to the aryl hydrocarbon receptor signaling were upregulated in rats exposed to the diuron high dose (1250 and 2500 ppm). Diuron induced high incidences of urinary bladder carcinomas and low incidences of kidney pelvis papillomas and carcinomas in rats exposed to high doses (2500 ppm) in a 2-year bioassay. The proposed rat urothelial mode of action for this herbicide consists of metabolic activation to metabolites that are excreted and concentrated in the urine, leading to cytotoxicity, urothelial cell necrosis and exfoliation, regenerative hyperplasia, and eventually tumors. At 2500 ppm for 2 years, both rats and dogs showed growth retardation, slight anemia, presence of abnormal pigment, increased erythropoiesis, and splenic hemosiderosis. Some rats showed splenic enlargement, and dogs showed liver enlargement. Diuron at 750 ppm induced male offspring toxicity but these alterations were not permanent, as evidenced by absence of reproductive-system alterations in adult rats. A dietary concentration of 125 ppm did not adversely affect reproduction in a three-generation rat study. In rat developmental studies, reduction in mean fetal weight at 500 mg/kg was noted, and 250 mg/kg increased the number of anomalous fetuses. In zebrafish studies, changes in behavior, such as decrease in spontaneous coiling movements of embryos and reduction of thigmotaxis in larvae, were pronounced for diuron. Diuron was active in vitro when tested for endocrine disrupting potential. Diuron was tested in Salmonella strains TA1535, TA97, TA98, and TA100 with metabolic activation at 0, 10, 25, 50, 100, or 250 ug/plate and without activation at 0, 0.5, 1, 2.5, 5, or 10 ug/plate. No increase in reversion rate reported. Cytotoxicity with TA1535. ECOTOXICITY STUDIES: Diuron metabolites had estrogenic effects potentially mediated through enhanced estradiol biosynthesis and accelerated the ovarian development of Nile tilapia females. Further studies indicated that biotransformation of diuron to active metabolites alter signaling pathways of the CNS which may impact androgen and the stress response as well as behavior necessary for social dominance, growth, and reproduction in fish. Exposure to a concentration of diuron that is frequently encountered in the field during the oyster's gametogenesis stage can impact the next generation and may result in fitness disturbance. Negative effect of diuron on oyster reproduction potentiated by inducing both structural and functional modifications of the DNA. Further in oysters, parental diuron exposure has an impact on the DNA methylation pattern of its progeny. The effect of the herbicide diuron was evaluated using a recycling multi compartment algae, Daphnia magna, bacteria microecosystem. A concentration of 0.2 ppm diuron was lethal to the Daphnia magna population. Diuron had an effect on newly born animals, and therefore these did not mature. Diuron was correlated with severe and widespread dieback of the dominant mangrove, Avicennia marina (Forsk.) Vierh. var. eucalyptifolia (Val.) N.C. Duke (Avicenniaceae), its reduced canopy condition, and declines in seedling health within three neighbouring estuaries in the Mackay region of NE Australia. The likely consequences of such dieback included declines in coastal water quality with increased turbidity, nutrients and sediment deposition, as well as further dispersal of the toxic chemicals.

Diuron has been reported to bind to androgen receptors. This suggests that diuron may block the receptors and result in the toxicity on the reproductive system.

/AQUATIC SPECIES/ Fertilization and embryo development that occur in sea water are sensitive to xenobiotics from anthropogenic sources. In this work, we evaluated the influence of two antifouling biocides, tributyltin (TBT) and diuron, on the reproductive mechanisms of the marine invertebrate Ciona intestinalis. By using electrophysiological techniques, we examined the impact of these compounds on the electrical properties of the mature oocytes and of events occurring at fertilization. With different toxicity assays, we studied the effect of the two biocides on the gametes by evaluating fertilization rate and embryo development. Results show that sodium (Na+) currents were significantly reduced by either of the two biocides, whereas conductance was significantly increased. The fertilization current frequency and amplitude, fertilization rate and larval development were affected only by TBT. This study suggests that: (i) the two biocides affect either the electrical properties of the oocyte plasma membrane and the reproductive success representing a risk factor for the survival of the species exposed to environmental pollution; (ii) the ascidian Ciona intestinalis may represent a good model organism to test toxicity of marine pollutants. Possible mechanisms of action of the two biocides are discussed.

/AQUATIC SPECIES/ Some endocrine disrupting chemicals (EDCs) can alter the estrogenic activities of the organism by directly interacting with estrogen receptors (ER) or indirectly through the hypothalamus-pituitary-gonadal axis. Recent studies in male Nile tilapia (Oreochromis niloticus) indicated that diuron may have anti-androgenic activity augmented by biotransformation. In this study, the effects of diuron and three of its metabolites were evaluated in female tilapia. Sexually mature female fish were exposed for 25 days to diuron, as well as to its metabolites 3,4-dichloroaniline (DCA), 3,4-dichlorophenylurea (DCPU) and 3,4-dichlorophenyl-N-methylurea (DCPMU), at concentrations of 100 ng/L. Diuron metabolites caused increases in E2 plasma levels, gonadosomatic indices and in the percentage of final vitellogenic oocytes. Moreover, diuron and its metabolites caused a decrease in germinative cells. Significant differences in plasma concentrations of the estrogen precursor and gonadal regulator 17alpha-hydroxyprogesterone (17alpha-OHP) were not observed. These results show that diuron metabolites had estrogenic effects potentially mediated through enhanced estradiol biosynthesis and accelerated the ovarian development of O. niloticus females.

/AQUATIC SPECIES/ The Pacific oyster Crassostrea gigas is the main oyster species produced in the world, and a key coastal economic resource in France. High mortalities affect Pacific oysters since 2008 in France and Europe. Their origins have been attributed to a combination of biotic and abiotic factors, underlining the importance of environment quality. The impact of water pollution has been pointed out and one of the pollutants, the genotoxic herbicide diuron, occurs at high concentrations all along the French coasts. Previous work has revealed that a parental exposure to diuron had a strong impact on hatching rates and offspring development even if spats were not exposed to diuron themselves. In this study, we explored for the first time the transcriptional changes occurring in oyster spats (non exposed) originating from genitors exposed to an environmentally relevant concentration of diuron during gametogenesis using the RNAseq methodology. We identified a transcriptomic remodeling revealing an effect of the herbicide. Different molecular pathways involved in energy production, translation and cell proliferation are particularly disturbed. This analysis revealed modulated candidate genes putatively involved in response to oxidative stress and mitochondrial damage in offspring of genitors exposed to diuron. Complementary measures of the activity of enzymes involved in these latter processes corroborate the results obtained at the transcriptomic level. In addition, our results suggested an increase in energy production and mitotic activity in 5-month-spats from diuron-exposed genitors. These results could correspond to a "catch-up growth" phenomenon allowing the spats from diuron-exposed genitors, which displayed a growth delay at 3 months, to gain a normal size when they reach the age of 6 months. These results indicate that exposure to a concentration of diuron that is frequently encountered in the field during the oyster's gametogenesis stage can impact the next generation and may result in fitness disturbance.

/AQUATIC SPECIES/ Genitors of the Pacific oyster Crassostrea gigas were submitted during gametogenesis to a short pulse exposure to the herbicide diuron at a realistic environmental concentration. Histological analysis showed no effect of diuron on gametogenesis course, sex ratio and reproductive effort. A non-significant increase in testosterone and progesterone levels was observed in genitors exposed to the herbicide. At cell level, diuron exposure was shown to modulate the phagocytic activity of circulating hemocytes. The results of a transcriptional analysis showed that diuron affected the expression of genes belonging to functions known to play a major role during oyster gametogenesis such as gene transcription regulation, DNA replication and repair, DNA methylation and cytokinesis. Taking into account the results we previously obtained on the same genitors, this study showed a negative effect of diuron on oyster reproduction by inducing both structural and functional modifications of the DNA.

For more Ecotoxicity Excerpts (Complete) data for Diuron (53 total), please visit the HSDB record page.

Section 8(a) of TSCA requires manufacturers of this chemical substance to report preliminary assessment information concerned with production, exposure, and use to EPA as cited in the preamble in 51 FR 41329. Effective date September 29, 2006; Reporting date: November 28, 2006.

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. Urea, N'-(3,4-dichlorophenyl)-N,N-dimethyl- is included on this list. Effective date September 29, 2006; Sunset date: November 28, 2006.

Tolerances are established for the combined residues of the herbicide diuron, 3-(3,4-dichlorophenyl)-1,1-dimethylurea and its metabolites convertible to 3,4-dichloroaniline in or on food commodities, as follows: [Table#1149]

Tolerances with a regional registration as defined in section 180.1(n) are established for the combined residues of the herbicide diuron (3-(3,4-dichlorophenyl)-1,1-dimethylurea and its metabolites convertible to 3,4-dichloroaniline) in or on the raw agricultural commodities:[Table#1150]

The Agency has completed its assessment of the occupational, residential, and ecological risks associated with the use of pesticide products containing the active ingredient diuron, as well as a diuron-specific dietary risk assessment. ... The Agency has determined that diuron products are eligible for reregistration provided that: (i) current data gaps and confirmatory data needs are addressed; (ii) the risk reduction measures outlined in this document are adopted; and (iii) label amendments are made to reflect these measures. ... Based on its evaluation of diuron, the Agency has determined that diuron products, unless labeled and used as specified in this document, would present risks inconsistent with FIFRA. Accordingly, should a registrant fail to implement any of the risk mitigation measures identified in this document, the Agency may take regulatory action to address the risk concerns from use of diuron. If all changes outlined in this document are incorporated into the product labels, then all current risks for diuron will be adequately mitigated for the purposes of this determination.

As the federal pesticide law FIFRA directs, EPA is conducting a comprehensive review of older pesticides to consider their health and environmental effects and make decisions about their continued use. Under this pesticide reregistration program, EPA examines newer health and safety data for pesticide active ingredients initially registered before November 1, 1984, and determines whether the use of the pesticide does not pose unreasonable risk in accordance to newer safety standards, such as those described in the Food Quality Protection Act of 1996. Diuron is found on List A, which contains most pesticides that are used on foods and, hence, have a high potential for human exposure. List A consists of the 194 chemical cases (or 350 individual active ingredients) for which EPA issued registration standards prior to FIFRA '88. Case No: 0046; Pesticide type: herbicide; Registration Standard Date: 09/30/83 PB84-210327; Case Status: OPP is reviewing data from the pesticide's producers regarding its human health and/or environmental effects, or OPP is determining the pesticide's eligibility for reregistration and developing the RED document.; Active ingredient (AI): diuron; Data Call-in (DCI) Date(s): 09/28/90, 07/26/95, 10/13/95; AI Status: The producers of the pesticide have made commitments to conduct the studies and pay the fees required for reregistration, and are meeting those commitments in a timely manner.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 100 lb or 45.4 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

Diuron is designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance.

(AZ) ARIZONA 14 ug/L

(FL) FLORIDA 14 ug/L

(ME) MAINE 14 ug/L

/Chlorophyll/ fluorescence measurements indicated significant electron transport inhibition in /intact soybean/ leaves 1 hr after treatment with 40 mM solutions of ... diuron.

The potent inhibitory effect of substituted ureas on the photosynthetic mechanism of ... plants ... /is exerted through inhibition of/ Hill reaction, ie, evolution of oxygen in presence of living chloroplasts & suitable hydrogen acceptor. /Substituted ureas/

Diuron is carcinogenic to the rat urinary bladder at high dietary levels. The proposed mode of action (MOA) for diuron is urothelial cytotoxicity and necrosis followed by regenerative urothelial hyperplasia. Diuron-induced urothelial cytotoxicity is not due to urinary solids. Diuron is extensively metabolized, and in rats, N-(3,4-dichlorophenyl)urea (DCPU) and 4,5-dichloro-2-hydroxyphenyl urea (2-OH-DCPU) were the predominant urinary metabolites; lesser metabolites included N-(3,4-dichlorophenyl)-3-methylurea (DCPMU) and trace levels of 3,4-dichloroaniline (DCA). In humans, DCPMU and DCPU have been found in the urine after a case of product abuse. To aid in elucidating the MOA of diuronand to evaluate the metabolites that are responsible for the diuron toxicity in the bladder epithelium, we investigated the urinary concentrations of metabolites in male Wistar rats treated with 2500 ppm of diuron, the urothelial cytotoxicity in vitro of the metabolites and their gene expression profiles. DCPU was found in rat urine at concentrations substantially greater than the in vitro IC50 and induced more gene expression alterations than the other metabolites tested. 2-OH-DCPU was present in urine at a concentration approximately half of the in vitro IC50, whereas DCPMU and DCA were present in urine at concentrations well below the IC50. For the diuron-induced MOA for the rat bladder, we suggest that DCPU is the primary metabolite responsible for the urothelial cytotoxicity with some contribution also by 2-OH-DCPU. This study supports a MOA for diuron-induced bladder effects in rats consisting of metabolism to DCPU (and 2-OH-DCPU to a lesser extent), concentration and excretion in urine, urothelial cytotoxicity, and regenerative proliferation.

This study was designed to investigate diuron biotransformation and disposition ... . The only metabolic pathway detected by liquid chromatography/mass spectometry in human liver homogenates and seven types of mammalian liver microsomes including human was demethylation at the terminal nitrogen atom. No other phase I or phase II metabolites were observed. The rank order of N-demethyldiuron formation in liver microsomes based on intrinsic clearance (V(max)/K(m)) was dog > monkey > rabbit > mouse > human > minipig > rat. All tested recombinant human cytochrome P450s (P450s) catalyzed diuron N-demethylation and the highest activities were possessed by CYP1A1, CYP1A2, CYP2C19, and CYP2D6. Relative contributions of human CYP1A2, CYP2C19, and CYP3A4 to hepatic diuron N-demethylation, based on average abundances of P450 enzymes in human liver microsomes, were approximately 60, 14, and 13%, respectively. Diuron inhibited relatively potently only CYP1A1/2 (IC(50) 4 uM)...

3,4-dichloroaniline (3,4-DCA) is a metabolite of diuron as well as two other pesticides, linuron and propanil. However, EPA's Metabolism Assessment Review Committee (MARC) concluded that residues of 3,4-DCA should not be aggregated for the diuron, linuron, and propanil risk assessments because 3,4-DCA is significant residue of concern for propanil, but is not a residue of concern per se for diuron or linuron. Although the analytical method for quantifying residues of concern from diuron converts all residues to 3,4-DCA as a convenience, 3,4-DCA was not a significant residue in any metabolism or hydrolysis study.

... In ... a woman poisoned with Diuron, 1-(3,4-dichlorophenyl)-3,3-dimethylurea, plus 3-amino-1,2,4-triazole, 1-(3,4-dichlorophenyl)-3-methylurea, and 1-(3,4-dichlorophenyl)urea were isolated from urine. The urine probably contained small amt of 3,4-dichloroaniline, but no unchanged herbicide.

For more Metabolism/Metabolites (Complete) data for Diuron (12 total), please visit the HSDB record page.

Diuron has known human metabolites that include N-demethyldiuron.

Diuron is readily absorbed through the gastrointestinal tract in rats and dogs. Tissue level of diuron were positively correlated with dosage. No apparent storage of diuron in tissues was noted ... Diuron is also partially excreted unchanged in feces and urine.

Root uptake of (14)C-Diuron from solution was studied. ... small amount of the monomethyl and demethylated derivatives were found in nutrient solution from ... soybeans, ... oat, and corn tops.

Diuron is most readily absorbed through the root system; less so through foliage & stems. Translocation is primarily upward in xylem.

Diuron was fed to five dairy cows at 0-550 ppm concentration levels. About 50% of the diuron was detected in the urine, 10% in the feces and 5% in the blood. Milk samples did not contain diuron. A positive correlation was noted between the concn of diuron products in urine and blood and a negative correlation between urine and feces. It is suggested that the remaining diuron is absorbed in the body or degraded into undetectable metabolites.

A photosynthesis inhibitor, diuron is used for general weed control and to kill emerging weeds in sugarcane, citrus, pineapple, cotton, and asparagus crops. [ACGIH]

Farming (Pesticides) [Category: Industry]

For Diuron (USEPA/OPP Pesticide Code: 035505) ACTIVE products with label matches. /SRP: Registered for use in the U.S. but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./

N'-(3,4-Dichlorophenyl)-N,N-dimethylurea, diuron is a broad-spectrum algicide, which acts by interrupting the photosynthetic electron transport in algae. The main applications are paints, coatings and plasters. In practice, dry-film preservatives contain a combination of algicides and fungicides, such as diuron, carbendazim and OIT /2-n-octylisothiazol-3-one/, or diuron, zinc pyrithione and OIT.

Systemic herbicide. Total control of weeds and mosses on non-crop areas. Selective control of germinating grass and broad-leaved weeds in many crops, including asparagus, tree fruit, bush fruit, citrus fruit, vines, olives, pineapples, bananas, sugar cane, cotton, peppermint, alfalfa, forage legumes, cereals, maize, sorghum, and perennial grass-seed crops.

Pre-emergence herbicide, sugar cane flowering suppressant.

The presence of 3,3',4,4'-tetrachloroazobenzene (TCAB) was determined in 3,4-dichloroaniline and its herbicidal derivatives /propanil, diuron, linuron, and neburon,/ using high-pressure liquid chromatography. The concn was in the range of 9-1400 ug/g.

(1977) 4.15X10+7 G

(1982) 3.68X10+8 G

2023: 25,000 - <50,000 lb

(1981) 2.7X10+9 G (SALES)

Urea, N'-(3,4-dichlorophenyl)-N,N-dimethyl- is listed as a High Production Volume (HPV) chemical (65FR81686). Chemicals listed as HPV were produced in or imported into the U.S. in >1 million pounds in 1990 and/or 1994. The HPV list is based on the 1990 Inventory Update Rule. (IUR) (40 CFR part 710 subpart B; 51FR21438).

Production volumes for non-confidential chemicals reported under the Inventory Update Rule. [Table#1154]

Non-confidential 2016 Chemical Data Reporting (CDR) information on the production and use of chemicals manufactured or imported into the United States. Chemical: Diruon:

Industrial commercial uses-eg, on railroad rights-of-way, 57%; cotton, 19%; citrus crops, 12%; deciduous fruits & nuts, 3%; wheat, 3%; vegetables, 2%; other field crops, eg, alfalfa & sugarcane, 4% (1978 herbicide use)

(1978) 2.63X10+9 G (CONSUMPTION)

The annual agricultural use of diuron as a herbicide in the United States was estimated as approximately 3.6X10+6 lbs for 1992.

Diuron is produced by reaction of 3,4-dichlorophenyl isocyanate with dimethylamine.

... Prepared by the reaction of an appropriate mono- or dihalo-substituted phenyl isocyanate with dimethyl or methylethyl amine. ... The amine-isocyanate reaction is most readily carried out in the presence of an inert solvent, such as toluene, anisole, benzene, chlorobenzene, or dioxane. No catalyst is needed, and since the reaction is exothermic it is ordinarily unnecessary to supply heat. ... The reaction is conveniently carried out by first mixing the isocyanate with the inert solvent at room temperature to increase through the range of 25 to 75 °C. The tri-substituted urea products are generally quite insoluble in the solvent used and, therefore, precipitate out as formed and are readily separated from the reaction mass.

Preparation: Jones, United States of America patent 2768971 (1956 to I.C.I.)

The National Pesticide Information Retrieval System (NPIRS) identifies 31 companies with active labels for products containing the chemical diuron. To view the complete list of companies, product names and percent diuron in formulated products click the following url and enter the CAS Registry number in the Active Ingredient field.

Sahara DG Herbicide (BASF Corporation): Active ingredient: diuron 62.22% and imazapyr 7.78%.

Topsite 2.5G Herbicide (BASF Corporation): Active ingredient: diuron 2.0% and imazapyr 0.5%.

Ginstar EC Cotton Defoliant (Bayer CropScience LP): Active ingredient: diuron 6.0% and imazapyr 12.0%.

For more Formulations/Preparations (Complete) data for Diuron (29 total), please visit the HSDB record page.

Pesticides -> Herbicides -> Urea herbicides -> Phenylurea herbicides

Herbicides

Environmental transformation -> Pesticides (parent, predecessor)

HERBICIDES

Plastics Material and Resin Manufacturing

Urea, N'-(3,4-dichlorophenyl)-N,N-dimethyl-: ACTIVE

Laboratory method of purification: by recrystallization three times from absolute ethanol.

... Involves the use of (14)carbon arylamines, eg for the synthesis of diuron, with dimethylcarbamoyl chloride.