It must be noted that the issue of a Data Sheet for a particular pesticide does not imply endorsement of the pesticide by WHO or FAO for any particular use, or exclude its use for other purposes not stated. While the information provided is believed to be accurate according to data available at the time when the sheet was compiled, neither WHO nor FAO are responsible for any errors or omissions, or any consequences therefrom.

The issue of this document does not constitute formal publication. It should not be reviewed, abstracted or quoted without the agreement of the Food and Agriculture Organization of the United Nations or of the World Health Organization.

Ce document ne constitue pas une publication. Il ne doit faire l'objet d'aucun compte rendu ou résumé ni d'aucune citation sans l'autorisation de l'Organisation des Nations Unies pour l'Alimentation et l'Agriculture ou de l'Organisation Mondiale de la Santé.

carbendazim (BSI, E-ISO), carbendasime (F-ISO), carbendazol (JMAF), BMC (USSR)

Aimcozim; BAS 346F; Bavistin^R; BCM; Bendazim; BMC; carbendazole; Carbendor; Cekudazim; Corbel; Custos^R; Delsene^R; Derosal^R; Derosalin; Equitdazin^R; Focal; Hoe 017411; Kemdazin^R; Kombat; Konker; Lignasan; MBC; MCAB; MCB; Pillarstin^R; Triticol.

Carbendazim is a broad spectrum benzimidazole carbamate fungicide with systemic activity. Acute toxicity is low and excretion is rapid. At high dose levels, repeated exposure causes spermatogenic effects in rats and hepatic tumours in mice. Foetotoxic and teratogenic effects were observed in laboratory animals following bolus oral dosing, but not following dietary exposure.

Pure carbendazim is a colourless, white crystaline, odourless solid which decomposes on melting at approximately 250ºC. Technical grade is >98% pure (FAO specification). Carbendazim is not corrosive.

(at 20 ºC)

8 mg/litre water (at pH7)

68 mg/litre dichloromethane

100 mg/litre chloroform

300 mg/litre acetone

5 g/litre dimethylformamide

300 g/litre ethanol

Stable in storage at 35-50 ºC. Slowly decomposes in alkaline solution. Stable in acid, forming water soluble salts.

<100 nPa (20 ºC)

Wettable powder (500 g/kg and 600 g/kg), oil dispersion (200 g/litre), aqueous dispersion (500 g/litre), aqueous suspension (200 g/litre), water-soluble liquid (as phosphate salt, 7 g/litre). Also available as suspension concentrate and dry seed dressing and in combination with many other fungicides in liquid, wettable powder or seed treatment powder formulations.

Controls a wide range of fungal pathogens on cereals, fruits, cotton, tobacco, turf, ornamentals and vegetables.

Soil treatment and foliage application on appearance of disease. Absorbed by roots and has some foliar penetration. Soluble acid salts give some control of Dutch elm disease when injected into the bark. May be used as a seed dressing or as a post-harvest dip. In many countries its use is restricted to certain specific uses with strict limitations.

Toxic to some fish. May decrease earthworm feeding and populations.

No recommended usage.

No recommended usage.

Well absorbed (80-85%) from the gastro-intestinal tract. Carbendazim may also be absorbed from the lungs or from intact skin, but there are no published quantitative data available.

Carbendazim inhibits fungal mitotic microtubule formation. A similar mode of action has been postulated for mammalian cells.

In the rat more than 98% of an oral dose of 50 mg radio-labelled carbendazim was recovered in the urine and faeces within 72 hours. Urinary excretion accounted for approximately 65% of the given dose. The major metabolite was free methyl-5-hydroxy-benzimidazol-2-ylcarbamate, minor metabolites were the glucuronide and/or sulphate conjugates of this metabolite.

A single gavage dose of 1,000 mg a.i./kg b.w. to Wistar rats resulted in mitotic abnormalities in bone-marrow samples taken four hours after dosing.

Gross and histopathological changes were observed in the testes and epididymides of rats receiving oral doses of  1000 mg/kg b.w. (Section 2.1.7).

Transient reddening of rabbit conjunctival sacs was observed following instillation of 10 mg carbendazim. No adverse effects were noted at 5 mg. Dermal application of 500 mg carbendazim/day for five days to intact rabbit skin did not produce any irritation.

Carbendazim either technical material or a 75% wettable powder formulation presented no evidence of dermal sensitization following either intradermal injections or repeated applications to shaved intact skin of albino guinea-pigs.

Oral: Gavage administration of 500 mg/kg b.w./day for four days resulted in hypoplastic changes and mitotic arrest in the bone-marrow of Wistar rats. Degenerative changes in the thymus, gut, testes, and blood were also apparent. In rats gavage administration of up to 40 mg/kg b.w./day for two weeks had no effect on the bone-marrow, behaviour, mortality or weight gain. An increased relative and absolute liver weight was observed at doses of 40 mg/kg b.w./day.

Dermal: Repeated application of 2000 mg/kg of carbendazim as a 50% aqueous paste to the skin of New Zealand albino rabbits over ten days have produced necrosis of epidermis and polymorphonuclear cell infiltration of the dermis in five out of six exposed rabbits. No other effects were observed.

Cumulation of effects: No published data available, however, studies on pesticides with metabolic profiles similar to that of carbendazim show no cumulation of effects.

Short-term: Dietary administration of 2,000, 4,000 or 8,000 mg/kg/diet for 28 days had no adverse effects on the haematology, blood chemistry or urinalysis in Sprague Dawley rats. At doses of 4,000 and 8,000 mg/kg/diet food consumption and growth were depressed. At these two doses degeneration of the testes and effects on spermatogenesis or oogenesis were observed. Relative and absolute liver weights were increased at all dose levels but no histopathological changes were recorded.

Increased absolute and/or relative liver weights were observed in rats following three months dietary exposure to carbendazim. In Sprague Dawley rats increased liver weights were observed in both sexes at concentrations of 1350 mg/kg. A second study with an unspecified strain of rat reported increased liver weights in female rats at 80 mg/kg/diet and in male rats at 400 mg/kg/diet. No adverse histopathology accompanied these changes in either study. The increases in liver weight were reversed on cessation of exposure, although reversal was only partial in female rats after a 12 day recovery period.

Three months dietary exposure of dogs to levels of carbendazim up to 2500 mg/kg/diet did not result in mortality or adverse clinical signs. Histological examination of liver, kidney and testes did not indicate compound-related effects.

In the separate study, the dose of 2000 mg/kg carbendazim in the diet over 13 weeks has resulted in slight increase in relative liver and thyroid weights and decrease in relative heart weights.

Male CD-1 mice showed increased food consumption but decreased food efficiency when exposed to diet containing 7500 mg/kg of carbendazim. Exposure was reduced to 3750 mg/kg/diet at 66 weeks, but increased mortality required that this group be terminated at week 73. Dose levels of 1500 mg/kg/diet also decreased longevity of male mice. Male mice receiving diet containing 1500 mg/kg of carbendazim showed centilobular hypertrophy, necrosis and swelling of the liver, lymphoid depletion of the thymus, deposition of yellow-brown pigment in the kidney tubules and decreased thymus and kidney weights. In females lymphoid depletion of the thymus was observed at  1500 mg/kg. Reduced erythrocyte counts, a marginally reduced blood haemoglobin concentration, accumulation of pigment in the renal tubules and macrophages, and cystic renal tubules were observed at 7500 mg/kg diet group. Kidney and thymus absolute weights were decreased in 500 and 1500 mg/kg diet group but not at 7500 mg/kg. The effects on tumour incidence are reported in 2.1.10 below.

Female Wistar rats receiving a diet containing 10 000 mg/kg of carbendazim for two years showed increased relative liver weights, reduced blood haemoglobin concentration, reduced blood packed-cell volume and proliferation of the parafollicular cells of the thyroid. A no observed adverse effect level of 300 mg/kg was established on the basis of this study.

Carcinogenicity: Carbendazim increased the incidence of benign and malignant hepatic tumours in both sexes of CD-1 mice during a two year feeding study (See 2.1.9). A dose-related decrease in the latency of tumour formation was also apparent. In female mice, dose-related hepatic oncogenic changes were observed starting at 500 mg/kg/diet. In males, carcinogenic changes were observed in the livers at 1500 mg/kg/diet. The high dose group of this sex was terminated at 73 weeks and the hepatic histopathology is not reported.

Similar findings were reported in Swiss mice, where an increased incidence of malignant liver tumours (male) and benign liver tumours (female) was reported after an 80 week exposure to 5000 mg/kg/diet. In contrast, other workers report hepatotoxicity but not carcinogenicity in HOE NMR mice receiving feed containing 5000 mg/kg/diet of carbendazim for two years.

The carcinogenic effect in some of the studies was shown to be related to impurities mainly 2,3 diaminophenazine (DAP) and 2-amino-3-hydroxyphenazine (HAP).

Carbendazim caused an increase in malformations and anomalies in rats when administrated daily dose levels greater than 10 mg/kg b.w. on days 7-16 of gestation. There was a slightly decreased rate of implantation in rabits administered 20 and 125 mg/kg b.w. per day on days 7-19 of gestation and an increased incidence of resorption at 125 mg/kg b.w. per day.

In addition to decreased pregnancy rate and increased early resorptions in the rat, there were significant reductions in foetal weights at 20 and 90 mg/kg b.w. per day and a significant increase in foetal malformations at 90 mg/kg b.w. per day. However, in the rabbit no significant malformations were observed.

ChR-CD rats fed 500 mg/kg diet showed no adverse effects in a three generation reproduction study. Reduced average litter weights at weaning, in all generations, were the only adverse findings at 5000 and 10,000 mg/kg/diet dose levels.

A single oral dose of 300 mg/kg b.w. to adult Sprague Dawley rats caused premature exfoliation of late spermatids in the testes, two hours after administration. Nine hours after an oral dose of 150 mg/kg b.w. effects on mitosis leading to cell death were apparent. Decreased spermatogenesis or oogenesis were reported after rats were fed on a diet containing 4000 or 8000 mg/kg of carbendazim for 28 days.

Several in vitro and in vivo tests suggest that carbendazim is probably not a mutagen. The in vivo effects indicate that carbendazim may act as a mitotic spindle poison in mammalian cells. A dose related increase in abnormal cell nuclei was seen in the bone marrow cells of mice receiving two gavage doses of 50 - 1000 mg/kg b.w./day. The cells characteristically resembled those seen following exposure to mitotic-spindle poisons. Similar marrow cell abnormalities were seen following a single gavage or intraperitoneal dose of 1000 mg/kg b.w. The serum from these rats, collected 30 minutes after dosing, was cytotoxic to a human cell line (Chang cells) in vitro. Dietary administration of  1000 mg/kg/diet for 300 days did not cause chromosomal aberrations in the bone marrow of male rats.

No adverse effects in dominant lethal mutation tests were observed following intraperitoneal administration of 1280 mg/kg b.w. to mice or after feeding rats for a period of four months with a diet containing 1000 mg/kg of carbendazim.

No published data available, however, based on animal data it is anticipated that carbendazim is absorbed from the gastro-intestinal tract. Carbendazim may also be slowly absorbed by inhalation and across intact skin.

No published information available.

Selected blood profiles, including white blood cell count, red blood cell count, haemoblogin and haematocrit values were comparable among 50 factory workers involved in the manufacture of carbendazim and control groups of workers who were not exposed to the fungicide.

The fertility of 298 male manufacturing workers was not affected compared with matched control group.

No published information available. With good agricultural practice the public should not be exposed to hazardous amounts of carbendazim.

No published information available.

No published information available.

Toxic to some species.

LC₅₀ (96 hours):

Oral LD₅₀:

Not toxic to honey bees. May diminish earthworm populations.

(For definition of categories see the "Introduction to data sheets".)

The potential of single exposures to cause foetotoxic or teratogenic effects in laboratory animals necessitates classification into a category more restrictive than that computed by oral LD₅₀ data alone.

All formulations - Category 4.

All formulations: Should be transported in clearly labelled, leakproof containers, out of reach of children, and away from food and drink.

All formulations: A dust mask must be worn when handling solid formulations in amounts of 2 kg or above. Contact with skin should be minimized by the wearing of gloves. Hands should be washed after handling of the pesticide and before eating, drinking or smoking.

Decontamination of containers is probably not practical due to the low solubility of carbendazim. Containers must be burned or crushed and buried below topsoil. Care must be taken to avoid contamination of water sources.

All formulations: Warning of workers to minimize contact is essential. Women of childbearing age should be informed of the foetotoxic and teratogenic potential of carbendazim. Pregnant women should avoid contact with carbendazim formulations.

All formulations: Pilots and loaders should have special training in application methods and recognition of early warning symptoms of pesticide poisoning. All workers must wear a dust mask to minimize inhalation exposure. Additionally loaders must wear clean overalls and impermeable gloves. Flagmen should wear a dust mask, overalls and an impermeable broad brimmed hat, and should be located away from the dropping zone.

All formulations - minimum cautionary statement:

This formulation contains the fungicide carbendazim which is poisonous if swallowed. During pregnancy, ingestion or inhalation of this formulation may cause harm to the unborn child. Use of a dust mask is essential when handling quantities in excess of 2 kg of solid formulation. Keep out of reach of children and pets, and well away from foodstuffs or animal feed.

Maximum levels have been recommended for a variety of foodstuffs by the FAO/WHO Joint Meeting on Pesticide Residues. An acceptable daily intake of 0-0.03 mg/kg b.w. was set by the JMPR in 1995.

Carbendazim is a benzimidazole carbamate fungicide without anti-cholinesterases activity. The oral and dermal acute toxicity of carbendazim is low. However, spermatogenic effects and effects on the foetus may be observed in laboratory animals following administration of a single dose. To reduce the risk of inhalation exposure, use of a dust mask is recommended when handling larger amounts of solid formulations.

The Russian Federation gives a TLV of 0.1 mg/m³ for carbendazim. Closed systems and forced ventilation should be used to reduce inhalation exposure. Protective equipment for respiratory tract and skin is usually necessary.

Respiratory protection must be used at all times. When opening the container and when mixing, care should be taken to avoid contact with the eyes and mouth. Mixing if not mechanical, should always be carried out with a paddle of appropriate length. The applicator should avoid working in spray mist and avoid contact with the mouth. Splashes must be washed from the skin or eyes immediately, using large volumes of water. Before eating, drinking, or smoking, hands and other exposed skin should be washed.

Persons exposed to carbendazim and associated with its application should wear protective clothing and observe the precautions described above in 4.1.3. under "Mixers and Applicators".

With good agricultural practice other populations should not be exposed to hazardous amounts of carbendazim.

The general population should be kept out of the treated areas until the applied formulation has dried.

Residues in containers should be emptied in diluted form into a deep pit taking care to avoid contamination of water sources. Low solubility and high stability of carbendazim makes decontamination of containers impractical. Spillage of liquid formulations should be contained with absorbent material. This material, or spillage of dry formulations, should be collected and burned or buried in a deep pit. The spillage area should then be decontaminated by thorough washing with detergent and water. Care must be taken to avoid contamination of all water sources.

No reported cases, but the symptoms would probably include nausea, diarrhoea, vomiting and headache.

The person should stop work immediately, remove contaminated clothing and wash contaminated skin with soap and water, and flush the skin with large quantities of water. If contaminated, eyes should be flushed with copious amounts of clean water. Unless oil dispersion formulations have been ingested, vomiting may be induced if the patient is fully conscious.

Carbendazim is a benzimidazole carbamate fungicide without anticholinesterase activity. Ingestion and inhalation are the most likely routes of systemic exposure. The acute toxicity is low but in laboratory animals oral doses may elicit effects on the sperm and on the foetus.

No cases of human poisoning published, however, the symptoms would probably include headache, nausea, diarrhoea and vomiting.

Direct measurement of carbendazim in the blood or its metabolites in the urine and faeces confirms exposure but is not specific for this pesticide alone.

Following ingestion, rapid gastric lavage should be performed. Some formulations contain oils and solvents and care must be taken to avoid pulmonary complications if the patient is vomiting. In the case of skin contamination the exposed area should be washed with soap and water. If the compound has entered the eyes they should be washed with isotonic saline or water.

Treatment is mainly symptomatic and there is no specific antidote.

Good, the acute toxicity is low and there are no other adverse health effects for the user. Exposure during pregnancy may however produce foetotoxic and teratogenic effects in the unborn child.

No published information on cases available.

There are no readily available field techniques to determine the degree of exposure.

Aharonson N and Ben-Aziz A (1973), J Assoc Off Anal Chem 56:1330-1334.

Kirkland JJ, Holt RH, Pease HL (1973), J Agric Food Chem 21(3):368-371.

Pressley TA and Longbottom JE (1982), The Determination of Benomyl and Carbendazim in Industrial and Municipal Wastewater, Method 61. EPA-600/4-82-012. PB82-156068.

Pesticide Residues in Food - 1995 Evaluations, Part II - Toxicology and Environment. World Health Organization document WHO/PCS/96.-- (In press).

The Pesticide Manual, A World Compendium (10th edition 1994), Tomlin, C., ed., British Crop Protection Council, 20 Bridport Road, Thornton Heath, CR4 7QG, U.K.

    See Also:
       Toxicological Abbreviations
       Carbendazim (EHC 149, 1993)
       Carbendazim (HSG 82, 1993)
       Carbendazim (ICSC)
       Carbendazim (WHO Pesticide Residues Series 3)
       Carbendazim (Pesticide residues in food: 1976 evaluations)
       Carbendazim (Pesticide residues in food: 1977 evaluations)
       Carbendazim (Pesticide residues in food: 1978 evaluations)
       Carbendazim (Pesticide residues in food: 1983 evaluations)
       Carbendazim (Pesticide residues in food: 1985 evaluations Part II Toxicology)
       Carbendazim (Pesticide residues in food: 1995 evaluations Part II Toxicological & Environmental)
       Carbendazim (Pesticide residues in food: 1995 evaluations Part II Toxicological & Environmental)
       Carbendazim (JMPR Evaluations 2005 Part II Toxicological)