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DICAMBA

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Dicamba is a translocation herbicide related to the chlorophenoxy compounds such as 2,4,D. It is a benzoic acid herbicide.

Specific Substances

    1) 3,6-Dichloro-2-methoxybenzoic acid
    2) 3,6-Dichloro-o-anisic acid
    3) Compound B
    4) Dicamba dimethylamine salt
    5) Dicamba monoethanolamine salt
    6) Dicamba potassium salt
    7) Dicamba diethanolamine salt
    8) MDBA
    9) Dianat
    10) Velsicol 58 CS-11
    11) CAS 1918-00-9
    12) MDBA (DICAMBA)
    13) VELSICOL
    1.2.1) MOLECULAR FORMULA
    1) C8-H6-Cl2-O3

Available Forms Sources

    A) FORMS
    1) Dicamba is an odorless, white or brown, crystalline solid. It has also been described as crystals from pentane. It is soluble in water and is resistant to hydrolysis and oxidation under normal environmental conditions (Harp, 2001; Budavari, 1996; CHRIS , 1992).
    B) SOURCES
    1) Dicamba is a component of many mixtures, some of which include: Cambilene, Banlene, Razol, Monkdak, Weedmaster, Banvel CST, Banvel D, Banvel XG, Banvel-K, Provel, and Scotlene (Thomson, 1981).
    2) Brand names include Banvel (Sandoz) and Mediben (Sandoz) (Budavari, 1996; Lewis, 1996).
    C) USES
    1) This herbicide has often been used for brush control along highways and is effective against broadleaf annuals and perennials (Gosselin et al, 1984; Thomson, 1981). Commercial use includes maintenance of pastures, forest lands, fence rows, and transportation and utility rights-of-way (Harp, 2001).
    2) Dicamba-containing herbicides have been considered viable alternatives for several of the suspended uses of silvex and 2,4,5-T, such as for home lawns, pastures, along ditch banks, and brush control in pastures (EPA, 1988). Weed reduction in grain/cereal crops is a primary agricultural use of dicamba (Harp, 2001).
    3) It is used to control dock in established grassland and to control bracken (Lewis, 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) USES: Dicamba is an aromatic acid herbicide and related to chlorophenoxy compounds, such as 2,4 D.
    B) TOXICOLOGY: Toxic effects reported are mostly topical irritation.
    C) EPIDEMIOLOGY: It is a commonly used herbicide, so exposures are frequent. However, serious toxicity is rare, especially with dicamba alone. Most exposures occur with a mixture of herbicides, including chlorophenoxy compounds. Fatalities reported are due to a mixture of herbicides, and not dicamba alone.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Mild to moderate toxicity consists of mild dermal and mucous membrane irritation. Burning of mucous membranes may occur with ingestion, along with gastrointestinal upset. Transient ECG abnormalities (ie, QT interval prolongation, tachycardia) have been reported with ingestion. Dyspnea and cyanosis can occur with respiratory exposure.
    2) SEVERE TOXICITY: Severe toxicity after large exposures can consist of CNS depression, metabolic acidosis, muscular weakness, dyspnea, and cyanosis. Shock with respiratory failure has been reported with large exposures.
    0.2.20) REPRODUCTIVE
    A) Dicamba was shown not to be teratogenic in rabbits and rats tested. When tested in rats over 3 generations, no reduction in reproduction capacity was noted.
    B) Lactating cows exposed to dicamba excreted about 0.02% in milk.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

    A) Most patients with inadvertent dicamba exposures do not need laboratory evaluation. Laboratory and radiographic evaluation can be targeted to symptoms (eg, chest).
    B) Obtain serum electrolytes, acetaminophen and salicylate concentrations after deliberate ingestion.
    C) Monitor vital signs and mental status and evaluate for respiratory distress.
    D) Dicamba serum concentrations are not routinely available and are not useful to guide management.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Symptomatic and supportive care is the mainstay for dicamba exposures. Rinse mouth and administer a small amount of water after ingestion.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treat respiratory distress symptomatically by administering oxygen and bronchodilators as needed for bronchospasm. If respiratory failure or severe CNS depression develops, airway protection may be indicated.
    C) DECONTAMINATION
    1) PREHOSPITAL: Do not induce vomiting if ingested. There is no role for activated charcoal.
    2) HOSPITAL: There is no role for lavage or charcoal. Rinse mouth and administer a small amount of water after ingestion.
    D) AIRWAY MANAGEMENT
    1) Treat according to symptoms. If cough develops, evaluate for pneumonitis or bronchospasm. Oxygen should be administered for hypoxia.
    E) ANTIDOTE
    1) None
    F) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with inadvertent low dose ingestions or exposures, who are asymptomatic or with minimal symptoms can be watched at home.
    2) OBSERVATION CRITERIA: Any patient who is symptomatic or has a deliberate or large ingestion should be referred to a healthcare facility for evaluation and treatment. Patients should be observed until symptoms resolve.
    3) ADMISSION CRITERIA: Toxicity is typically mild with dicamba exposure. However, patients who have severe toxicity, including persistent signs of respiratory irritation or failure, CNS depression, or shock, should be admitted for further evaluation.
    4) CONSULT CRITERIA: A toxicologist should be consulted in large exposures or with severe symptoms, or if the diagnosis is unclear.
    G) PITFALLS
    1) Pitfalls include not evaluating for other co-ingestants, such as solvents and surfactants, and other herbicides that are other ingredients included with this herbicide.
    H) TOXICOKINETICS
    1) There is no human kinetic data. In animal studies, dicamba has minimal dermal absorption, but is readily absorbed orally. It is rapidly and nonselectively distributed to most organ systems, and does not undergo appreciable metabolism. It is renally excreted.
    I) DIFFERENTIAL DIAGNOSIS
    1) Other herbicides, including chlorophenoxy herbicides such as 2,4 D.
    0.4.3) INHALATION EXPOSURE
    A) With inhalational exposure, move patients to fresh air. Treat respiratory distress symptomatically by administering oxygen and bronchodilators as needed for bronchospasm. If respiratory failure or severe CNS depression develops, airway protection may be indicated.
    0.4.4) EYE EXPOSURE
    A) For severe ocular exposure, irrigate eyes and perform a slit lamp exam.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Remove contaminated clothing and wash exposed skin with soap and water.

Range Of Toxicity

    A) A minimum lethal human dose and maximum tolerated human exposure dose have not been established. Patients, who intentionally ingested up to 300 mL of a pesticide containing 40% dicamba, were treated conservatively and were discharged within 7 days without sequelae.

Clinical Effects

Summary Of Exposure

    A) USES: Dicamba is an aromatic acid herbicide and related to chlorophenoxy compounds, such as 2,4 D.
    B) TOXICOLOGY: Toxic effects reported are mostly topical irritation.
    C) EPIDEMIOLOGY: It is a commonly used herbicide, so exposures are frequent. However, serious toxicity is rare, especially with dicamba alone. Most exposures occur with a mixture of herbicides, including chlorophenoxy compounds. Fatalities reported are due to a mixture of herbicides, and not dicamba alone.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Mild to moderate toxicity consists of mild dermal and mucous membrane irritation. Burning of mucous membranes may occur with ingestion, along with gastrointestinal upset. Transient ECG abnormalities (ie, QT interval prolongation, tachycardia) have been reported with ingestion. Dyspnea and cyanosis can occur with respiratory exposure.
    2) SEVERE TOXICITY: Severe toxicity after large exposures can consist of CNS depression, metabolic acidosis, muscular weakness, dyspnea, and cyanosis. Shock with respiratory failure has been reported with large exposures.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Dicamba is irritating to the eyes and may cause burns ((Anon, 2002); Harp, 2001; Gosselin et al, 1984). Conjunctival swelling and corneal clouding were noted when eyes were exposed to dicamba. Effects generally lasted 5 to 7 days. The dimethylamine salt is especially irritating ((Anon, 2002); Harp, 2001; Hayes & Laws, 1991). When working with concentrated solutions, more severe or permanent ocular damage may occur.
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) Dicamba is a mildly corrosive sensitizing agent. Ingestion may result in irritation of the mouth and throat ((Anon, 2002); Harp, 2001).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) BRADYCARDIA
    1) WITH POISONING/EXPOSURE
    a) Severe intoxications may result in bradycardia (Harp, 2001).
    B) PROLONGED QT INTERVAL
    1) WITH POISONING/EXPOSURE
    a) A retrospective review of cases from 2006 to 2013 was conducted of patients with dicamba poisoning who presented to a hospital in South Korea. There were 14 patients (ages ranging from 18 to 79 years) identified, who intentionally ingested dicamba herbicide only and presented to the emergency department within 24 hours postingestion. The amounts ingested ranged from 100 to 400 mL. QT interval prolongation was the most common ECG abnormality reported with an incidence of 71.4%, resolving by Day 1 after admission (Moon & Chun, 2014).
    C) TACHYCARDIA
    1) WITH POISONING/EXPOSURE
    a) A retrospective review of cases from 2006 to 2013 was conducted of patients with dicamba poisoning who presented to a hospital in South Korea. There were 14 patients (ages ranging from 18 to 79 years) identified, who intentionally ingested dicamba herbicide only and presented to the emergency department within 24 hours postingestion. The amounts ingested ranged from 100 to 400 mL. Sinus tachycardia was reported in 28.6% of patients, resolving by Day 1 after admission (Moon & Chun, 2014).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Dicamba is irritating to mucous membranes. Inhalation of the dust or fumes may result in upper respiratory irritation ((Anon, 2002); Harp, 2001).
    B) CYANOSIS
    1) WITH POISONING/EXPOSURE
    a) Following an ingestion of dicamba, dyspnea and cyanosis may occur. In severe poisonings, muscle weakness may lead to respiratory failure (Harp, 2001).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CYANOSIS
    a) Cyanosis and dyspnea were noted in experimental animals poisoned by dicamba (Gosselin et al, 1984; Edson & Sanderson, 1965).
    2) PULMONARY HEMORRHAGE
    a) Pulmonary hemorrhage was noted in a few cases of animal poisonings (Gosselin et al, 1984; Edson & Sanderson, 1965) .

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) Following a severe intoxication, CNS depression may occur ((Anon, 2002); Harp, 2001).
    B) ALTERED MENTAL STATUS
    1) WITH POISONING/EXPOSURE
    a) A retrospective review of cases from 2006 to 2013 was conducted of patients with dicamba poisoning who presented to a hospital in South Korea. There were 14 patients (ages ranging from 18 to 79 years) identified, who intentionally ingested dicamba herbicide only and presented to the emergency department within 24 hours postingestion. The amounts ingested ranged from 100 to 400 mL. Depressed mental state, irritability, or confusion were reported in 35.7% of patients. The mental status of all patients normalized without specific treatment 20.6 +/- 12.3 hours after presentation (Moon & Chun, 2014).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Vomiting has been reported with human exposure to the dimethylamine salt (Beste, 1983; HSDB , 1999; Harp, 2001; (Anon, 2002)).
    b) A retrospective review of cases from 2006 to 2013 was conducted of patients with dicamba poisoning who presented to a hospital in South Korea. There were 14 patients (ages ranging from 18 to 79 years) identified, who intentionally ingested dicamba herbicide only and presented to the emergency department within 24 hours postingestion. The amounts ingested ranged from 100 to 400 mL. Nausea and vomiting were reported in 28.6% of patients (Moon & Chun, 2014).
    B) LOSS OF APPETITE
    1) WITH POISONING/EXPOSURE
    a) Anorexia and weight loss have been reported after human exposure to the dimethylamine salt (HSDB , 1999; Beste, 1983) .
    b) A retrospective review of cases from 2006 to 2013 was conducted of patients with dicamba poisoning who presented to a hospital in South Korea. There were 14 patients (ages ranging from 18 to 79 years) identified, who intentionally ingested dicamba herbicide only and presented to the emergency department within 24 hours postingestion. The amounts ingested ranged from 100 to 400 mL. Anorexia was reported in 14.3% of patients (Moon & Chun, 2014).
    C) ESOPHAGITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 40-year-old man presented with a burning sensation in his substernal area and hematemesis approximately 1 hour after intentionally ingesting 300 mL of dicamba herbicide. An upper endoscopy revealed Grade IIa corrosive esophagitis as well as several mucosal defects down the length of the esophagus, and atrophic gastritis. With supportive therapy, including administration of a proton-pump inhibitor for approximately 1 week, the patient recovered. A follow-up endoscopy 18 days postadmission showed complete healing of the esophageal lesions (Moon & Chun, 2014).

Hepatic

    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATIC FUNCTION ABNORMAL
    a) When dicamba was fed to rats in varying concentrations over a 3 week period, no change in liver weights or feed efficiency was noted. However, a statistically significant increase in peroxisomal B-oxidation activity in liver homogenates was noted in rats fed the highest (1%) concentration of dicamba (Espandiari et al, 1995).

Genitourinary

    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) URINARY INCONTINENCE
    a) Incontinence was noted in animals poisoned experimentally (Gosselin et al, 1984).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) A retrospective review of cases from 2006 to 2013 was conducted of patients with dicamba poisoning who presented to a hospital in South Korea. There were 14 patients (ages ranging from 18 to 79 years) identified, who intentionally ingested dicamba herbicide only and presented to the emergency department within 24 hours postingestion. The amounts ingested ranged from 100 to 400 mL. Metabolic acidosis (pH less than 7.35, HCO3 less than 20 mmol/L) was reported in 21.4% of patients. The patients recovered with supportive care (Moon & Chun, 2014).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) DEFICIENCY OF CHOLINESTERASE
    1) WITH POISONING/EXPOSURE
    a) Anticholinesterase activity has been reported with dicamba. In a case series of 14 dicamba herbicide applicators, 6 were found to have significant reductions (greater than 20%) in red blood cell (RBC) acetylcholinesterase (AChE) activity. Reductions in plasma butyrylcholinesterase levels, however, were not seen. It was suggested that contamination of commercial-grade dicamba with impurities capable of cholinesterase inhibition may have occurred, or, dicamba itself may have the ability to inhibit RBC AChE due to its structural similarity to a group of amphiphilic agents known to inhibit cholinesterase (Harp, 2001).
    B) LEUKOCYTOSIS
    1) WITH POISONING/EXPOSURE
    a) A retrospective review of cases from 2006 to 2013 was conducted of patients with dicamba poisoning who presented to a hospital in South Korea. There were 14 patients (ages ranging from 18 to 79 years) identified, who intentionally ingested dicamba herbicide only and presented to the emergency department within 24 hours postingestion. The amounts ingested ranged from 100 to 400 mL. Leukocytosis (white blood cell count ranging from 11.1 x 10(3) to 30 x 10(3)/mm(3)) was reported in 64.3% of patients (Moon & Chun, 2014).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Dicamba is irritating to the skin (Gosselin et al, 1984). Skin irritation or burns may occur following dermal exposures. This herbicide is a mildly corrosive sensitizing agent ((Anon, 2002); Harp, 2001).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ALLERGIC REACTION
    a) Dicamba has been shown to be a moderate skin sensitizer in guinea pigs (Hartley & Kidd, 1987).
    2) NECROSIS
    a) When injected subcutaneously in animals, necrosis or fluid filled abscesses were noted (Hayes & Laws, 1991; Gosselin et al, 1984).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE WEAKNESS
    1) WITH POISONING/EXPOSURE
    a) Severe intoxications may result in muscular weakness/exhaustion subsequent to muscle spasms (myotonia) (Harp, 2001).
    b) Muscular weakness was reported after human exposure to the dimethylamine salt (Beste, 1983).
    3.15.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) TWITCHING
    a) Experimental animals that were poisoned experienced myotonic muscular spasms (Gosselin et al, 1984).
    2) MYOTONIA
    a) Myotonia developed in a dog given 86.7 milligrams/kilogram of dicamba orally (Beasley et al, 1991).

Reproductive

    3.20.1) SUMMARY
    A) Dicamba was shown not to be teratogenic in rabbits and rats tested. When tested in rats over 3 generations, no reduction in reproduction capacity was noted.
    B) Lactating cows exposed to dicamba excreted about 0.02% in milk.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) Dicamba was shown not to be teratogenic in rabbits and rats tested (Hartley & Kidd, 1987). When tested in rats over 3 generations, no reduction in reproduction capacity was noted (Beste, 1983).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) BREAST MILK
    1) Lactating cows exposed to dicamba excreted about 0.02% in milk (Oehler, 1980).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS1918-00-9 (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
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    2) The U.S. EPA has classified dicamba as a group D carcinogen (not classifiable as to human carcinogenicity) ((Anon, 2002)).

Genotoxicity

    A) Dicamba was shown to be positive in bacterial toxicity assays (pp 89-113).
    B) Hrelia et al (1994) found dicamba to have no clastogenic activity in vivo in rodents.
    C) In vitro experiments, using human peripheral blood lymphocytes, showed dicamba to induce unscheduled DNA synthesis, and it slightly increased the frequency of sister chromatid exchange (Harp, 2001).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Most patients with inadvertent dicamba exposures do not need laboratory evaluation. Laboratory and radiographic evaluation can be targeted to symptoms (eg, chest).
    B) Obtain serum electrolytes, acetaminophen and salicylate concentrations after deliberate ingestion.
    C) Monitor vital signs and mental status and evaluate for respiratory distress.
    D) Dicamba serum concentrations are not routinely available and are not useful to guide management.

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) Dicamba can be determined using infrared spectrophotometry, gas liquid chromatography, and high pressure liquid chromatography (Smith, 1965; Lee & Chau, 1983; Worthing & Walker, 1983; Grorud & Forrette, 1983; Perez, 1983).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Toxicity is typically mild with dicamba exposure. However, patients who have severe toxicity, including persistent signs of respiratory irritation or failure, CNS depression, or shock, should be admitted for further evaluation.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with inadvertent low dose ingestions or exposures, who are asymptomatic or with minimal symptoms can be watched at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) A toxicologist should be consulted in large exposures or with severe symptoms, or if the diagnosis is unclear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Any patient who is symptomatic or has a deliberate or large ingestion should be referred to a healthcare facility for evaluation and treatment. Patients should be observed until symptoms resolve.

Monitoring

    A) Most patients with inadvertent dicamba exposures do not need laboratory evaluation. Laboratory and radiographic evaluation can be targeted to symptoms (eg, chest).
    B) Obtain serum electrolytes, acetaminophen and salicylate concentrations after deliberate ingestion.
    C) Monitor vital signs and mental status and evaluate for respiratory distress.
    D) Dicamba serum concentrations are not routinely available and are not useful to guide management.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Do not induce vomiting if ingested. With inhalational exposures, move patient to fresh air. With dermal exposures, remove clothing and wash exposed areas with soap and water. If ocular exposure occurs, irrigate thoroughly.
    6.5.2) PREVENTION OF ABSORPTION
    A) There is no role for lavage or charcoal. Rinse mouth and administer a small amount of water after ingestion.
    6.5.3) TREATMENT
    A) SUPPORT
    1) Symptomatic and supportive care is the mainstay for dicamba exposures. There is no antidote available.
    B) MONITORING OF PATIENT
    1) Most patients with dicamba exposures do not need laboratory evaluation. Laboratory and radiographic evaluation can be targeted to symptoms (eg, chest).
    2) Monitor vital signs and mental status and evaluate for respiratory distress.
    3) Dicamba serum concentrations are not routinely available and are not useful to guide management.
    C) AIRWAY MANAGEMENT
    1) Treat according to symptoms. If cough develops, evaluate for pneumonitis or bronchospasm. Oxygen should be administered for hypoxia.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) With inhalational exposure, move patients to fresh air. Treat respiratory distress symptomatically by administering oxygen and bronchodilators as needed for bronchospasm. If respiratory failure or severe CNS depression develops, airway protection may be indicated.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) For severe ocular exposure, irrigate eyes and perform a slit lamp exam.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) Remove contaminated clothing and wash exposed skin with soap and water.

Abstracts

Case Reports

    A) ADULT
    1) A 61-year-old woman committed suicide when she ingested Killex(R) in an unknown amount. Killex has 100 grams/liter of 2,4,D; 50 grams/liter of mecoprop; and 9 grams/liter of dicamba (amine salt). The level of dicamba in the blood was 140 mg/liter (Fraser et al, 1984).

Range Of Toxicity

Summary

    A) A minimum lethal human dose and maximum tolerated human exposure dose have not been established. Patients, who intentionally ingested up to 300 mL of a pesticide containing 40% dicamba, were treated conservatively and were discharged within 7 days without sequelae.

Maximum Tolerated Exposure

    A) According to a review of medical records involving 12 patients who were admitted after intentionally ingesting up to 300 mL of a pesticide containing 40% dicamba, 8 patients were discharged without sequelae following conservative supportive treatment, including 1 session each of hemodialysis and hemoperfusion. Of the other 4 patients requiring hospital stays longer than 7 days, 1 patient developed pneumonia and paralytic ileus, 1 patient developed a catheter-related infection, elevated aminotransferase concentrations were reported in the third patient and ultimately attributed to hepatitis C infection, and microscopic hematuria was noted on the urinalysis of the fourth patient (Park et al, 2011).
    B) A retrospective review of cases from 2006 to 2013 was conducted of patients with dicamba poisoning who presented to a hospital in South Korea. There were 14 patients (ages ranging from 18 to 79 years) identified, who intentionally ingested dicamba herbicide only and presented to the emergency department within 24 hours postingestion. The amounts ingested ranged from 100 to 400 mL. Nausea, vomiting, anorexia, metabolic acidosis, leukocytosis, tachycardia, and QT interval prolongation were reported following ingestion. All patients recovered with supportive care (Moon & Chun, 2014).
    C) CASE REPORT: A 40-year-old man presented with a burning sensation in his substernal area and hematemesis approximately 1 hour after intentionally ingesting 300 mL of dicamba herbicide. An upper endoscopy revealed Grade IIa corrosive esophagitis as well as several mucosal defects down the length of the esophagus, and atrophic gastritis. With supportive therapy, including administration of a proton-pump inhibitor for approximately 1 week, the patient recovered. A follow-up endoscopy 18 days after admission showed complete healing of the esophageal lesions (Moon & Chun, 2014).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CASE REPORTS
    a) A 61-year-old female committed suicide when she ingested Killex(R) in an unknown amount. Killex has 100 grams/liter of 2,4,D; 50 grams/liter of mecoprop; and 9 grams/liter of dicamba (amine salt). The level of dicamba in the blood was 140 milligrams/liter (Fraser, 1984).

Workplace Standards

    A) ACGIH TLV Values for CAS1918-00-9 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS1918-00-9 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS1918-00-9 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Dicamba
    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
    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 CAS1918-00-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: HSDB, 1992 RTECS, 2002
    1) LD50- (ORAL)MOUSE:
    a) 1190 mg/kg
    2) LD50- (INTRAPERITONEAL)RAT:
    a) 80 mg/kg
    3) LD50- (ORAL)RAT:
    a) 1039 mg/kg
    b) Male, 757 mg/kg
    c) Female, 1414 mg/kg
    4) LD50- (SKIN)RAT:
    a) >1 g/kg

Pharmacology Toxicology

Pharmacologic Mechanism

    A) A selective translocation herbicide, dicamba is absorbed by the weed and distributed throughout the plant via the symplastic and apoplastic systems. Its primary action is to act like an auxin growth regulator (Hartley & Kidd, 1987).

Physicochemical

Physical Characteristics

    A) This compound exists as odorless, colorless crystals (Hartley & Kidd, 1987; HSDB , 1992).
    B) pale buff crystalline solid (technical product) (HSDB , 1999)
    C) brown crystalline solid (technical acid) (HSDB , 1999)
    D) white crystalline solid (reference grade) (HSDB , 1999)

Ph

    1) No information found at the time of this review.

Molecular Weight

    A) 221.04 (Budavari, 1996)

Other

    A) ODOR THRESHOLD
    1) 250.8 ppm (HSDB , 1999)

Animal Toxicology

Clinical Effects

    11.1.3) CANINE/DOG
    A) Dogs fed 50 milligrams/kilogram in their diet for 2 years showed no ill effects (Hartley & Kidd, 1987).

Kinetics

    11.5.1) ABSORPTION
    A) LACK OF INFORMATION
    1) There was no specific information on absorption at the time of this review.
    11.5.4) ELIMINATION
    A) CATTLE
    1) When tested in the cow, over 73 percent of a dose was detected in the urine, with none in either milk or feces. The excretion pattern was unusual in that the amount excreted remained fairly constant for 6 days, then dropped radically in the seventh (St John & Lisk, 1969). This may indicate there is a maximal rate of excretion (Hayes & Laws, 1991).
    2) In another study done on lactating cows, 89% of a dose was excreted in urine, 2% in feces and 0.02% in milk (Oehler, 1980).

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