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BENOMYL

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Benomyl is a benzimidazole carbamate systemic foliar fungicide with a moderate to low degree of toxicity (Thomson, 1985). It does not inhibit cholinesterase and hence will not result in signs and symptoms of cholinergic stimulation (i.e., salivation, lacrimation, spontaneous urination, defecation, bradycardia etc) (Morgan, 1982).
    B) Benlate(R) has been contaminated with atrazine in the past; these products have been recalled. The "dry flowable" version of Benlate(R) (not the wettable powder) has negatively affected plant growth in plants sprayed with this material. No illness has been seen in animals or humans (Stipp D, 1991).

Specific Substances

    1) Methyl 1-(butylcarbamoyl)-2-benzimidazolecarbamal
    2) CAS 17804-35-2
    3) F-1,991
    4) BBC (BENOMYL)
    5) DUPONT 1991
    6) MBC (BENOMYL)
    1.2.1) MOLECULAR FORMULA
    1) C14-H18-N4-O3

Available Forms Sources

    A) FORMS
    1) Introduced in 1967 by E.I. du Pont de Nemours & Company (Hayes, 1982). Usually in the form of a wettable powder, for application to a wide range of vegetables, fruits, field crops, and ornamentals. Essentially insoluble in water or in oils.
    2) Benomyl, occupying 50 percent of the worldwide market, is one of the most widely used members of a family of systemic fungicides known as benzimidazoles (IPCS, 1993a).
    3) In aqueous solutions, benomyl decomposes to carbendazim (with the removal of butyl isocyanate) and ethyl analog. Carbendazim is thought to be the active component (Budavari, 1996) HSDB, 1999; (IPCS, 1993a).
    B) SOURCES
    1) Brand names include: Benlate, Tersan 1991 Turf Fungicide, Benlate T seed treatment, and Benex (Meister, 1987; Hayes, 1982).
    C) USES
    1) Benomyl is used on land surrounding airport runways to reduce the population of earthworms. This attracts fewer birds that interfere with air traffic. Benomyl was not toxic to birds and did not accumulate in the soil.
    2) Also used as an oxidizer in sewage treatment (Lewis, 1996; Budavari, 1996), in textile processing and paint pigment manufacture (ACGIH, 1996; HSDB, 1999). It is also effective against mites and is used for the control of storage rots (ACGIH, 1991; HSDB, 1999).
    3) Benomyl has been used in veterinary medicine as an anthelmintic (Budavari, 1996).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Benomyl may be irritating to the eyes, skin, and mucous membranes. Contact dermatitis has been reported from exposure.
    B) Benomyl is a carbamate fungicide with a low degree of toxicity. Exposure is NOT associated with signs and symptoms of cholinergic stimulation. Systemic symptoms have rarely, if ever, been reported following exposure.
    0.2.4) HEENT
    A) Rare eye irritation has been noted.
    0.2.6) RESPIRATORY
    A) Benomyl is a potential mild respiratory irritant.
    0.2.10) GENITOURINARY
    A) Hypospermatocytogenesis occurred in rats given benomyl.
    0.2.14) DERMATOLOGIC
    A) Skin irritation, eczema and contact dermatitis has been described.
    0.2.19) IMMUNOLOGIC
    A) HYPERSENSITIVITY - Benomyl may cause sensitization in some people.
    0.2.20) REPRODUCTIVE
    A) Benomyl has produced brain, eye and systemic malformations in rats, as well as adverse efffects on the male reproductive system of the rat.

Laboratory Monitoring

    A) Benomyl plasma levels are not clinically useful or readily available.
    B) No specific lab work (CBC, electrolytes, urinalysis) is needed unless otherwise clinically indicated.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    B) No systemic poisonings have been reported. Treatment should be symptomatic and supportive in patients demonstrating symptoms.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) The minimum toxic or lethal dose in humans is unknown. The acute oral LD50 in the rat is about 10,000 mg/kg.

Clinical Effects

Summary Of Exposure

    A) Benomyl may be irritating to the eyes, skin, and mucous membranes. Contact dermatitis has been reported from exposure.
    B) Benomyl is a carbamate fungicide with a low degree of toxicity. Exposure is NOT associated with signs and symptoms of cholinergic stimulation. Systemic symptoms have rarely, if ever, been reported following exposure.

Heent

    3.4.1) SUMMARY
    A) Rare eye irritation has been noted.
    3.4.3) EYES
    A) CONJUNCTIVITIS - Benomyl has caused temporary mild conjunctival irritation in rabbits (ACGIH, 1991).
    3.4.5) NOSE
    A) Male and female rats exposed to 50 to 200 mg/cubic meter inhaled benomyl for 90 days showed olfactory epithelium degeneration on necropsy (Warheit et al, 1989).

Respiratory

    3.6.1) SUMMARY
    A) Benomyl is a potential mild respiratory irritant.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Benomyl is a potential mild respiratory tract irritant (Morgan, 1982).

Genitourinary

    3.10.1) SUMMARY
    A) Hypospermatocytogenesis occurred in rats given benomyl.
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) TESTIS DISORDER
    a) RATS - Pre-pubertal or pubertal rats given at least 250 mg/kg/day showed diffuse hypospermatocytogenesis (Carter et al, 1984).

Dermatologic

    3.14.1) SUMMARY
    A) Skin irritation, eczema and contact dermatitis has been described.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) Cases of eczematous dermatitis have been reported (van Joost et al, 1983). In one case, dermatitis was observed in Japanese women but not in Japanese men or women of Mexican ancestry (Hayes, 1982).
    2) A 0.1 percent concentration caused mild irritation (RTECS , 2000).
    3) Benomyl is among the most common causes of pesticide associated skin disease (Zenz, 1994).
    B) DISCOLORATION OF SKIN
    1) Hyperpigmentation has been seen in women exposed to benomyl. It is said to be a photosensitizor producing significant irritation, redness, or itching (Binder, 1976).
    C) CONTACT DERMATITIS
    1) CASE SERIES - In one study of 62 benomyl-exposed workers in Denmark, none were found to be sensitized to benomyl on a patch test (Larsen et al, 1990).

Immunologic

    3.19.1) SUMMARY
    A) HYPERSENSITIVITY - Benomyl may cause sensitization in some people.
    3.19.2) CLINICAL EFFECTS
    A) ACUTE ALLERGIC REACTION
    1) Benomyl may cause sensitization of some individuals. Sensitized individuals may demonstrate an increased irritation to Benomyl (van Ketel, 1977).

Reproductive

    3.20.1) SUMMARY
    A) Benomyl has produced brain, eye and systemic malformations in rats, as well as adverse efffects on the male reproductive system of the rat.
    3.20.2) TERATOGENICITY
    A) CNS CONGENITAL ANOMALY
    1) ANIMAL STUDIES
    a) Malformations of the brains of fetal rats have been reported when pregnant mothers were treated with benomyl on 7th to 21st day of gestation (Grant, 1993).
    b) Benomyl produced craniocerebral and systemic malformations in rats at doses of 31 to 125 mg/kg (Ellis et al, 1987).
    c) When 62.5 mg/kg/day of benomyl was given continuously to pregnant rats beginning at day 7 of gestation, craniocerebral anomalies were reported in fetuses at day 16 or day 20 (Harbison, 1998; Hathaway et al, 1996).
    B) FETOTOXICITY
    1) ANIMAL STUDIES
    a) When given per os in rats, benomyl induced multiple malformations. In the same study, the same amounts of benomyl were given in the diet of rats and caused fetotoxicity but not teratogenicity (Kavlock et al, 1982).
    b) It induced hydrocephalus, retinal dysplasia, cleft palate, hydronephrosis, and skeletal defects in rats and mice at doses of 31 to 250 mg/kg/day (Kavlock et al, 1982) Zeman et al, 1986; (Ellis et al, 1987) 1988; (Hoogenboom et al, 1991). All rat fetuses were affected at a dose of 125 mg/kg on days 7 to 21 of gestation (Ellis et al, 1987).
    c) Multiple malformations were produced with oral dosing, but equivalent doses in the diet were only fetotoxic (Kavlock et al, 1982). Dietary levels as high as 0.5% on days 6 through 15 did not affect pregnancies or outcomes in rats (Sherman et al, 1975). Higher frequencies of malformations were produced in dams fed protein-deficient diets (Hoogenboom et al, 1991).
    C) EYE ANOMALY
    1) Recently, there have been anecdotal reports in the British press that exposure to benomyl may be associated with central nervous system defects in humans. Apparent clusters of children born with anophthalmia or microphthalmia seemed to be linked to benomyl use (Gilbert, 1993) Dolk & Elliot, 1993).
    2) These reports have not been borne out in large epidemiological studies, however. In a study of over 940,000 cases, there was no association between geographical areas with high use of benomyl and two specific anomalies, anophthalmia (absence of eyes) and microphthalmia (small eyes) (Spagnole et al, 1994).
    3) Similarly, no evidence of an association between exposure to benomyl and anophthalmia or microphthalmia has been found in several large birth defects registries (Gilbert, 1993; Bianchi et al, 1994; Castilla, 1994; Kristensen & Irgens, 1994). Birth defects registries are fairly insensitive for detecting previously unknown human teratogens, however.
    4) In an analysis of 3 large birth defects registries, 849 cases of anophthalmia and microphthalmia were seen out of approximately 5.7 million births. Prevalence at birth varied between 0.92 and 2.29 per 10,000, with differences due mainly to whether or not infants with chromosome abnormalities were included (mainly trisomy 13). Risk increased with high maternal age (Kallen et al, 1996).
    5) ANIMAL STUDIES
    a) Malformations of the eyes of fetal rats have been reported when pregnant mothers were treated with benomyl on 7th to 21st day of gestation (Grant, 1993).
    1) Reported eye malformations include retinal dysplasia, cataract, microphthalmia, and anophthalmia (Grant, 1993).
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) Benomyl is embryotoxic and teratogenic in animals (Shtenberg & Torchinsky, 1977; (Berezovskaya & Torchinsky, 1979). Dose-dependent postimplantation mortalities and malformations were seen in offspring of rats injected with 250 or 750 mg/kg of benomyl on day 12 of gestation (Berezovskaya & Torchinsky, 1979).
    2) In a study presented by EI duPont de Nemours and Company to the United States Environmental Protection Agency, the only effects seen in a 3-generation rat feeding study from doses as high as 125 mg/kg/day in the diet were decreased weanling weights at the higher doses (IRIS , 1996; Sherman et al, 1975).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS17804-35-2 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.4) ANIMAL STUDIES
    A) LYMPHOMA-LIKE DISORDER
    1) ANIMAL STUDIES
    a) Female, but not male, mice that received 500 mg/kg/day benomyl via gavage experienced an increased incidence of lymphosarcoma. The mice were also exposed to 500 ppm sodium nitrite in the drinking water, so the cause of this effect is ambiguous (Hayes, 1982; Borzsonyi & Pinter, 1977; Hayes & Laws, 1991).
    b) Benomyl was not carcinogenic in rats, mice or dogs in 2-year feeding studies at doses up to 62.5, 125, or 750 mg/kg/day, respectively (IRIS , 1996).

Genotoxicity

    A) Benomyl is genotoxic in a variety of short-term genetic tests. Because its mechanism of action is inhibition of DNA synthesis by interfering with microtubules in the cell division apparatus, it would be expected to be active in many kinds of genetic tests, especially in eukaryotic cells. The basis for its fungicidal activity is induction of numerical chromosome aberrations or aneuploidy.
    B) Benomyl is a mutagen in E. coli and S. typhimurium. It produces no dominant lethal mutations in rats. It does result in increased frequencies of chromosome aberrations in rat, not human, lymphocytes and in cultured cell lines. It may or may not produce aneuploidy. Benomyl may result in the formation of micronuclei and may produce sister chromatid exchanges.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Benomyl plasma levels are not clinically useful or readily available.
    B) No specific lab work (CBC, electrolytes, urinalysis) is needed unless otherwise clinically indicated.

Methods

    A) CHROMATOGRAPHY
    1) Chromatographic methods are available for measuring benomyl and its metabolites in various media (Zweig & Gao, 1983), but they have not been utilized in exposure situations.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Benomyl plasma levels are not clinically useful or readily available.
    B) No specific lab work (CBC, electrolytes, urinalysis) is needed unless otherwise clinically indicated.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) No systemic poisonings have been reported.
    2) Monitor for any toxic effects and treat symptomatically.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. Rescue personnel and bystanders should avoid direct contact with contaminated skin, clothing, or other objects (Burgess et al, 1999). Since contaminated leather items cannot be decontaminated, they should be discarded (Simpson & Schuman, 2002).
    2) A physician may need to examine the exposed area if irritation or pain persists after the area is washed.

Abstracts

Case Reports

    A) ROUTE OF EXPOSURE
    1) INHALATION/DERMAL - A possible report of benomyl toxicity involved an Australian man who cleaned out silos filled with benomyl-"pickled" wheat. After three such exposures, the worker experienced lethargy and somnolence, weight loss, dizziness and sweating, and an overall "pins-and-needles" feeling. Exposure occurred dermally and by inhalation; the worker wore no protective gear or clothing. Resolution of the symptoms occurred over the next two years (Gale, 1988). However, this report is unsubstantiated and other experts postulate that the described toxicity was probably not due to benomyl (Christophers, 1989).

Range Of Toxicity

Summary

    A) The minimum toxic or lethal dose in humans is unknown. The acute oral LD50 in the rat is about 10,000 mg/kg.

Minimum Lethal Exposure

    A) The minimum lethal human dose to this agent has not been delineated.

Workplace Standards

    A) ACGIH TLV Values for CAS17804-35-2 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Benomyl
    a) TLV:
    1) TLV-TWA: 1 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A3
    2) Codes: I, SEN
    3) Definitions:
    a) A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    b) I: Inhalable fraction; see Appendix C, paragraph A (of TLV booklet).
    c) SEN: The designation SEN refers to the potential for an agent to produce sensitization, as confirmed by human or animal data. The notation does not imply that this is the critical effect or that this is the sole basis for the TLV. Although, for those TLVs that are based on sensitization, the TLV is meant to protect workers from induction of this effect, but cannot protect workers who have already become sensitized. The notation should be used to assist in identifying sensitization hazards and reducing respiratory, dermal, and conjunctival exposures to sensitizing agents in the workplace. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): URT irr; male repro and testicular dam; embryo/fetal dam
    d) Molecular Weight: 290.32
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS17804-35-2 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Benomyl
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix D
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS17804-35-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Benomyl
    a) A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Benomyl
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Benomyl
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS17804-35-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Benomyl (Total dust)
    2) Table Z-1 for Benomyl (Total dust):
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 15
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed
    3) Listed as: Benomyl (Respirable fraction)
    4) Table Z-1 for Benomyl (Respirable fraction):
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 5
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) NOTES: Specific references are included below when differing values are reported for the same animal and route.
    1) LD50- (ORAL)MOUSE:
    a) 5600 mg/kg
    2) LD50- (ORAL)RAT:
    a) >10,000 mg/kg
    3) LD50- (SKIN)RAT:
    a) >1 g/kg
    4) TCLo- (INHALATION)RAT:
    a) 200 mg/m(3) for 6 H/14 W-I
    b) Male, 1.2 mg/m(3) for 4 H -- at 72D prior to mating, affected spermatogenesis
    B) NOTES: Specific references are included below when differing values are reported for the same animal and route.
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 1225 mg/kg -- caused respiratory depression and behavioral changes (RTECS, 2000)
    b) >15,000 mg/kg (Clayton & Clayton, 1994)
    2) LD50- (ORAL)MOUSE:
    a) 7700 mg/kg
    3) LD50- (INTRAPERITONEAL)RAT:
    a) Male, >7230 mg/kg (Clayton & Clayton, 1994)
    b) Female, >15,000 mg/kg (Clayton & Clayton, 1994)
    c) 1720 mg/kg -- caused respiratory depression and behavioral changes (RTECS, 2000)
    4) LD50- (ORAL)RAT:
    a) >10,000 mg/kg (Clayton & Clayton, 1994)
    b) 6400 mg/kg (RTECS, 2000)
    5) LD50- (SKIN)RAT:
    a) 2 g/kg
    6) TCLo- (INHALATION)RAT:
    a) Male, 1200 mcg/M(3) for 4H -- at 72D prior to mating, affected spermatogenesis

Pharmacology Toxicology

Pharmacologic Mechanism

    A) There is very little evidence of benomyl toxicity in mammals, probably due largely to its limited absorption. There is minimal tissue storage of benomyl or metabolites. Metabolites do not appear to be any more acutely toxic than the unmetabolized fungicide.
    B) Benomyl does emit toxic fumes of nitrogen oxides when heated to decomposition (Lewis, 1996) or exposed to strong acid or alkali (Pohanish & Greene, 1997).

Physicochemical

Physical Characteristics

    A) Benomyl is an oil-dispersible powder with faint acrid odor (HSDB, 1999).
    B) Benomyl is a white crystalline solid insoluble in oil (Budavari, 1996).
    C) Benomyl is a tan crystalline solid marketed as a wettable powder or as dry flowable, dispersible granules (IPCS, 1993b).

Molecular Weight

    A) 290.32

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