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DIQUAT DIBROMIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Diquat dibromide is a bipyridyl herbicide.

Specific Substances

    1) DIQUAT DIBROMIDE
    2) DIPYRIDO(1,2-a;2',1'-c)PYRAZINEDIIUM, 6,7-DIHYDRO-,
    3) DIBROMIDE
    4) 1,1'-AETHYLEN-2,2'-BIPYRIDINIUM-DIBROMID (German)
    5) AQUACIDE
    6) CLEANSWEEP
    7) DEIQUAT
    8) DEXTRONE
    9) 9,10-DIHYDRO-8a,10,-DIAZONIAPHENANTHRENE DIBROMIDE
    10) 9,10-DIHYDRO-8a,10a-DIAZONIAPHENANTHRENE
    11) (1,1'-ETHYLENE-2, 2'-BIPYRIDYLIUM)DIBROMIDE
    12) 5,6-DIHYDRO-DIPYRIDO(1,2a;2,1c)PYRAZINIUM DIBROMIDE
    13) 6,7-DIHYDROPYRIDO(1,2-a;2',1'-c)PYRAZINEDIUM
    14) DIBROMIDE
    15) DIQUAT
    16) 1,1'-ETHYLENE-2,2'-BIPYRIDYLIUM DIBROMIDE
    17) ETHYLENE DIPYRIDYLIUM DIBROMIDE
    18) 1,1-ETHYLENE 2,2-DIPYRIDYLIUM DIBROMIDE
    19) 1,1'-ETHYLENE-2,2'-DIPYRIDYLIUM DIBROMIDE
    20) FB/2
    21) PREEGLONE
    22) REGLON
    23) REGLONE
    24) REGLOX
    25) SPECTRACIDE
    26) WEEDOL
    27) WEEDTRINE-D
    28) CAS 85-00-7
    29) CAS 2764-72-9
    30) DIQUAT ION
    1.2.1) MOLECULAR FORMULA
    1) C12-H12-N2.2Br C12-H12-N2

Available Forms Sources

    A) FORMS
    1) Diquat dibromide is available commercially as aqueous solutions (15% to 25% weight-to-volume) and as water soluble granules (2.5%) (Hathaway et al, 1991).

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: Herbicide.
    B) TOXICOLOGY: Diquat, functionally related to paraquat, is a potent oxidation-reduction cycler that readily generates a free radical in the presence of NADPH and cytochrome P450 reductase. The diquat radical reacts with oxygen to form a superoxide radical which is highly reactive. The superoxide radical generates a hydroxyl radical in the presence of iron and hydrogen peroxide. The hydroxyl radical initiates lipid peroxidation in biological membranes and can cause cell death. Human toxicity is primarily due to direct caustic effects and free radical injury in the kidneys.
    C) EPIDEMIOLOGY: From 1968 to 1999, only 30 cases of diquat poisoning were reported in detail in the literature, of which 13 (43%) were fatal.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Following ingestion of less than 1 gram of diquat, there is an initial burning sensation of the oral and pharyngeal mucosa. Nausea, repeated vomiting, and abdominal discomfort and pain may begin immediately, followed by extensive diarrhea. Renal impairment may develop, but recovery generally occurs after several days.
    2) SEVERE TOXICITY: May develop following ingestion of 1 to 12 grams; death has been reported with an ingestion of as little as 1.5 to 3 grams. Toxicity can affect all organ systems and result in death within 24 to 48 hours. Ulcerations of the gastrointestinal tract, pulmonary edema, acute liver and kidney failure, and rapid loss of consciousness may develop. Ileus can also occur, with abdominal distention, dehydration, and possible hypotension. Oliguria may occur early, with elevations of BUN and serum creatinine. A progressive decline in renal function may occur until the patient becomes anuric. This generally begins to reverse by days 7 to 10. Normal renal function returns about 2 to 3 weeks following ingestion. Hemodialysis may be required in the interim. Less common effects include pneumonia, ventricular dysrhythmias, seizures, and non-cardiogenic pulmonary edema. Liver injury may develop, but is generally mild and reversible. Approximately two-thirds of patients survive ingestions of up to 12 grams with good supportive care. The rapid onset of renal failure, ileus, ventricular dysrhythmias, coma or pulmonary complications requiring intubation/ventilation suggest a poor prognosis. Death occurs from multi-organ system failure.
    0.2.20) REPRODUCTIVE
    A) Diquat has not been associated with teratogenicity or adverse reproductive effects. However, results of reproductive studies with diquat have been conflicting.
    0.2.21) CARCINOGENICITY
    A) NOT CARCINOGENIC - Diquat is not considered to be a carcinogen. It has not been associated with any human cancer cases.

Laboratory Monitoring

    A) Monitor renal function (BUN and serum creatinine) for at least 12 hours post-ingestion.
    B) Monitor CBC, liver enzymes, electrolytes and urine output in significantly symptomatic patients.
    C) Analysis for diquat in serum or urine is difficult and requires special expertise that may not be available in most laboratory facilities.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. Correct any significant fluid and/or electrolyte abnormalities in patients with severe diarrhea and/or vomiting.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. Treat seizures with benzodiazepines. Seizures refractory to benzodiazepines may respond to phenobarbital or propofol. Consider endoscopy in patients with oral burns, dysphagia, stridor or vomiting, or deliberate ingestions of concentrated solutions. Patients who develop renal failure may require hemodialysis.
    C) DECONTAMINATION
    1) PREHOSPITAL: Consider activated charcoal if the ingestion is recent, the patient is not vomiting, and is able to maintain their airway.
    2) HOSPITAL: Diquat irreversibly binds to clays and activated charcoal. Activated charcoal should be administered if the ingestion is recent, the patient is not vomiting, and is able to maintain their airway. BENTONITE CLAY (7% solution): DOSE: ADULT: 100 to 150 g; CHILD: 2 g/kg; or FULLER'S EARTH (30% solution) DOSE: ADULT: 100 to 150 g; CHILD: 2 g/kg.
    D) AIRWAY MANAGEMENT
    1) Ensure adequate ventilation and perform endotracheal intubation early in patients with significant CNS depression or pulmonary toxicity.
    E) ANTIDOTE
    1) There is NO antidote available for diquat toxicity.
    F) ENHANCED ELIMINATION PROCEDURE
    1) Hemodialysis has not been shown to be beneficial, but may be required in patients who develop renal failure.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with dermal exposures involving a small body surface area to intact skin that do not have local symptoms or mucous membrane involvement can be managed at home with simple soap and water decontamination.
    2) OBSERVATION CRITERIA: Following ingestion, patients should be sent to a health care facility for observation. If asymptomatic, monitor for symptoms and renal injury for 12 hours from time of exposure.
    3) ADMISSION CRITERIA: Symptomatic patients and those that develop renal injury should be admitted for further care.
    4) CONSULT CRITERIA: A toxicologist should be consulted for all ingestions and all dermal exposures involving more than minimal body surface area. Appropriate medical subspecialties should be consulted to aid in the support of specific organ dysfunction due to toxicity.
    H) PITFALLS
    1) Do not underestimate the potential for significant toxicity.
    I) TOXICOKINETICS
    1) Diquat is not readily absorbed across intact human skin. Diquat appears to be poorly absorbed from the gastrointestinal tract following ingestion. It is excreted in the feces and urine. Depending upon the dose and the functional state of the kidneys, the half-life of diquat is expected to be less than 24 hours.
    J) DIFFERENTIAL DIAGNOSIS
    1) Distinguish between paraquat and diquat exposures. Many other toxic exposures can result in immediate gastrointestinal symptoms and caustic injury.
    0.4.3) INHALATION EXPOSURE
    A) Administer oxygen and assist ventilation as needed. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) A chest x-ray may be indicated if edema or infiltrates are suspected on clinical exam.
    C) Exposure to diquat spray mist may result in upper respiratory tract irritation. Signs and symptoms remit once exposure has been discontinued. Proper respiratory protective equipment may prevent these effects.
    D) The vapor pressure of diquat is negligible; therefore, no adverse health effects are expected from exposure to the vapor or "fumes." No substantiated systemic poisonings have occurred from inhalation of spray mist.
    0.4.4) EYE EXPOSURE
    A) Diquat concentrate is a severe eye irritant.
    B) Remove contact lenses and irrigate eyes with room-temperature water for at least 15 minutes; continue if symptoms do not resolve. Cataracts and corneal scarring have been reported; patients with significant symptoms should be seen by an ophthalmologist.
    C) Depending upon the extent of exposure, transient corneal and conjunctival injury may develop and can be delayed for 12 to 24 hours after exposure. Healing may be slow.
    D) Obtain a detailed exposure history to be certain that none of the chemical was swallowed or came into contact with damaged skin.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Diquat is poorly absorbed through intact human skin. No substantiated cases of systemic human poisoning have been reported following dermal exposure (intact skin) with diquat.
    2) Diquat may cause skin irritation. In case of contact with diquat concentrate, Remove contaminated clothing and immediately wash skin with soap and water. Discard contaminated leather shoes.
    3) Nailbed contact with concentrate or repeated exposure to diluted diquat can result in a reversible discoloration or deformity of the finger and toenails. Decontaminate these areas thoroughly after direct contact with the herbicide.

Range Of Toxicity

    A) TOXICITY: Ingestion of 1 gram or less usually causes mild to moderate gastrointestinal and renal toxicity, with recovery following supportive care. Ingestion of 1 to 12 grams results in moderate to severe toxicity, with multiple organ dysfunction and acute renal failure, in particular, frequently occurring. Recovery has been reported in approximately two-thirds of cases, although a fatality has been reported following ingestion of 1.5 to 3 grams in an adult. Ingestion of greater than 12 grams results in multiple organ failure and death in the majority of patients within 24 to 48 hours.

Clinical Effects

Summary Of Exposure

    A) USES: Herbicide.
    B) TOXICOLOGY: Diquat, functionally related to paraquat, is a potent oxidation-reduction cycler that readily generates a free radical in the presence of NADPH and cytochrome P450 reductase. The diquat radical reacts with oxygen to form a superoxide radical which is highly reactive. The superoxide radical generates a hydroxyl radical in the presence of iron and hydrogen peroxide. The hydroxyl radical initiates lipid peroxidation in biological membranes and can cause cell death. Human toxicity is primarily due to direct caustic effects and free radical injury in the kidneys.
    C) EPIDEMIOLOGY: From 1968 to 1999, only 30 cases of diquat poisoning were reported in detail in the literature, of which 13 (43%) were fatal.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Following ingestion of less than 1 gram of diquat, there is an initial burning sensation of the oral and pharyngeal mucosa. Nausea, repeated vomiting, and abdominal discomfort and pain may begin immediately, followed by extensive diarrhea. Renal impairment may develop, but recovery generally occurs after several days.
    2) SEVERE TOXICITY: May develop following ingestion of 1 to 12 grams; death has been reported with an ingestion of as little as 1.5 to 3 grams. Toxicity can affect all organ systems and result in death within 24 to 48 hours. Ulcerations of the gastrointestinal tract, pulmonary edema, acute liver and kidney failure, and rapid loss of consciousness may develop. Ileus can also occur, with abdominal distention, dehydration, and possible hypotension. Oliguria may occur early, with elevations of BUN and serum creatinine. A progressive decline in renal function may occur until the patient becomes anuric. This generally begins to reverse by days 7 to 10. Normal renal function returns about 2 to 3 weeks following ingestion. Hemodialysis may be required in the interim. Less common effects include pneumonia, ventricular dysrhythmias, seizures, and non-cardiogenic pulmonary edema. Liver injury may develop, but is generally mild and reversible. Approximately two-thirds of patients survive ingestions of up to 12 grams with good supportive care. The rapid onset of renal failure, ileus, ventricular dysrhythmias, coma or pulmonary complications requiring intubation/ventilation suggest a poor prognosis. Death occurs from multi-organ system failure.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) IRRITATION: Concentrated diquat can cause severe eye irritation which develops gradually, reaching its maximum after 12 to 24 hours. There may be extensive stripping of superficial areas of corneal and conjunctival epithelium. Recovery is usually complete (Clark & Hurst, 1970; Grant & Schuman, 1993; Swan, 1968). No human cases of severe permanent eye damage have been reported following contact with diquat (Clark & Hurst, 1970; Grant & Schuman, 1993). Corneal scarring has been reported in a few cases, but is likely due to the surfactant contained in commercial solutions (Grant & Schuman, 1993). Exposure to diquat agricultural spray mist may cause minor eye irritation.
    2) CATARACTS: Results of subchronic and chronic laboratory toxicology studies indicate that diquat causes an increase in the onset and incidence of cataracts in high-doses (Hathaway et al, 1991). This finding has not been reported in humans (Clark & Hurst, 1970; FAO/WHO, 1978; pp 105-114; Pirie & Rees, 1970; Wojeck et al, 1983; Hathaway et al, 1991).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) IRRITATION: Exposure to diquat spray mist can result in mucosal irritation (nasal discharge, epistaxis, sneezing). These symptoms remit once exposure is discontinued. Protective equipment may help prevent these effects.
    2) LACK OF SYSTEMIC EFFECTS: No substantiated human cases of systemic poisoning or deaths have been reported from exposure to diquat spray mist. The vapor pressure of diquat is negligible, therefore no adverse health effects have been associated with exposure to diquat vapor or "fumes."
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) IRRITATION: Ingestion of diquat concentrate or strong solutions produces an initial burning sensation of the mouth and throat. Epistaxis and throat irritation have been reported following the inhalation of splashes or droplets caused by the careless mixing of diquat solutions (Clark & Hurst, 1970).
    2) ULCERATION: Severe oral and pharyngeal irritation or ulceration may develop within a few days following ingestion. The mucosa may slough; however, healing should be complete within 2 to 3 weeks (Tanen et al, 1999; Saeed et al, 2001).
    3) CASE REPORT: A 48-year-old man, who worked at an herbicide manufacturing plant, experienced tingling of the lips and tongue approximately 12 hours following direct exposure to diquat dust. Approximately 36 hours post-exposure, the patient developed severely swollen and ulcerated lips and tongue, that gradually resolved with symptomatic and supportive therapy (Adams et al, 2008).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) Ventricular dysrhythmias may develop in severe poisoning cases (Jones & Vale, 2000; Vanholder et al, 1981).
    b) CASE REPORTS: Ventricular dysrhythmias were reported in 2 cases of diquat ingestion. The first patient suffered from repeated attacks of ventricular fibrillation and died 24 hours post-ingestion. The second patient died 5 days post-ingestion from an uncorrectable ventricular dysrhythmia (Vanholder et al, 1981).
    c) POOR PROGNOSIS: Rapid onset of acute renal failure, development of intestinal ileus and subsequent fluid sequestration, ventricular dysrhythmias, respiratory dysfunction requiring intubation and mechanical ventilation, and coma are associated with a poor prognosis in patients following diquat exposure (Jones & Vale, 2000).
    B) SUBENDOCARDIAL ISCHEMIA
    1) WITH POISONING/EXPOSURE
    a) Subendocardial hemorrhage was reported on autopsy in one case; there were no clinical cardiac manifestations prior to death (McCarthy & Speth, 1983).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Extensive and continuous overexposure to diquat spray mist that produces severe irritation or damage to the respiratory tract mucosa may lead to poisoning (Charles et al, 1978).
    B) PNEUMONITIS
    1) WITH POISONING/EXPOSURE
    a) Pneumonia and ARDS have been reported after diquat ingestion (Schmidt et al, 1999; Saeed et al, 2001). The need for mechanical ventilation after diquat poisoning is associated with a poor prognosis (Jones & Vale, 2000).
    C) BURN
    1) WITH POISONING/EXPOSURE
    a) Upper airway irritation and laryngeal edema with airway narrowing have been reported after ingestion (Schmidt et al, 1999).
    D) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Severe pulmonary edema was noted during an autopsy of a 28-year-old man who developed multi-organ failure and died approximately 24 hours after ingesting approximately 120 to 240 mL of an herbicide containing 36.4% diquat dibromide (Schmidt et al, 1999).
    E) SEQUELA
    1) WITH POISONING/EXPOSURE
    a) LACK OF EFFECT: Under conditions of normal agricultural or product label uses of diquat, there have been no substantiated cases or reports of systemic poisoning or deaths associated with inhalation of spray mist. Agricultural spray equipment produces large spray droplets of about 100 to 200 microns in diameter which are primarily deposited in the upper airways. Diquat has a negligible vapor pressure, therefore no adverse health effects are expected from exposure to the vapor or "fumes"(Gage, 1968; Wojeck et al, 1983; Chester & Ward, 1984; Charles & Menzel, 1979).
    b) LACK OF PULMONARY FIBROSIS: Diquat has not been reported to cause pulmonary fibrosis in humans (Lam et al, 1980; Keeling et al, 1981; Olson, 1994).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) ALVEOLAR DAMAGE/FIBROSIS: Intratracheal administration of diquat in experimental animals has caused alveolar damage followed by pulmonary fibrosis (Manabe & Ogata, 1987). This effect has not be seen in exposed humans.

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) TOXIC ENCEPHALOPATHY
    1) WITH POISONING/EXPOSURE
    a) Based on the results of animal toxicology studies and human case reports, diquat is not considered to be a neurotoxic chemical. It has not caused pathological changes or lesions in brain or nerve tissue in either experimental animal studies or human poisoning cases. However, through either indirect toxicological or treatment-related effects, in approximately 50% of human diquat poisoning cases, clinical signs of nervousness, irritability, restlessness, combativeness, disorientation, nonsensical statements, inability to recognize friends or family members, and diminished reflexes have been reported (O'Donoghue, 1985).
    b) CASE REPORT: A 25-year-old woman injected 20 mL of 6% diquat vaginally and presented 3 days later with somnolence, deviation of the head and eyes to the right, mydriasis and decreased pupillary light reflexes. Ten days after intoxication she was lethargic and dysarthric with spastic tetraparesis. Neither CT nor MRI was performed. Three months later she was able to walk and had normal function of the hands (Rudez et al, 1999).
    B) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) PROGRESSIVE NEUROLOGICAL EFFECTS: Some cases of poisoning have involved progressive development of neurological effects by 72 to 96 hours, consisting of decreased response to painful stimuli, somnolence, constriction and slight reactivity of pupils, decreased oculocephalic and caloric reflexes and lid retraction with down-beating nystagmus, cerebral hemorrhagic lesions, stupor, coma, and death (Saeed et al, 2001; Hantson et al, 2000; Jones & Vale, 2000; Mahieu et al, 1984; Pond et al, 1983; Powell et al, 1983; Schoenborn et al, 1971; Vanholder et al, 1981).
    b) The specific mechanism(s) responsible for these effects is not known.
    c) Lethargy and coma may occur in severe diquat intoxications (Vanholder et al, 1981). Coma is associated with a poor prognosis (Jones & Vale, 2000).
    d) Hemorrhagic cerebral and brainstem infarctions may occur (Olson, 1994).
    1) CASE REPORT: A 57-year-old woman intentionally ingested 4 to 8 ounces of Spectracide(R) Grass and Weed Killer (2.3% diquat; 1.26% diquat ion, 1.5 to 3 g diquat cation). Initially, the patient complained of throat irritation and was admitted for decontamination and observation. The patient had a transient rise in her liver transaminases, and by hospital day 4, renal function had deteriorated necessitating hemodialysis. That same day, the patient suffered cardiac arrest, and resuscitation measures were successful. However, the patient remained unresponsive, and CT of the head revealed brainstem swelling. Support was withdrawn on day 7. Autopsy revealed brainstem infarction (Ruha et al, 2001).
    e) Coma, seizures, and pontine hemorrhage may be seen in severe poisoning cases (Hantson et al, 2000; Jones & Vale, 2000; Schmidt et al, 1999; Saeed et al, 2001).
    f) POOR PROGNOSIS: Rapid onset of acute renal failure, development of intestinal ileus and subsequent fluid sequestration, ventricular dysrhythmias, respiratory dysfunction requiring intubation and mechanical ventilation, and coma are associated with a poor prognosis in patients following diquat exposure (Jones & Vale, 2000) .
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) NEUROLOGICAL EFFECTS: Aside from signs of renal and gastrointestinal involvement, other signs of toxicity, primarily in high dose groups, included depression, lethargy, collapse, coma, and death (Clark & Hurst, 1970; Cobb & Grimshaw, 1979).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Ingestion of toxic quantities of diquat results in vomiting and diarrhea with loss of fluids and electrolytes (Olson, 1994).
    B) GASTROINTESTINAL IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Diquat concentrate or strong solutions are corrosive to the lining of the digestive tract. Patients ingesting less than 1 g diquat usually experience a burning sensation of the mouth and the throat, followed by nausea, vomiting, abdominal pain, and diarrhea. Gastrointestinal distress may persist for 2 to 3 days following ingestion (Mahieu et al, 1984) (McCarthy & Speth, 1993)(Narita et al, 1978) (Okenek et al, 1976)(Oreopoulos & McEvoy, 1969; Pond et al, 1983; Schoenborn et al, 1971; Vanholder et al, 1981; Zilker et al, 1987; Olson, 1994; Jones & Vale, 2000).
    b) CASE REPORT: Gastrointestinal injury was reported following an ingestion of a diquat-based herbicide. Endoscopy revealed severe pan-esophagitis and a localized area of erosive hemorrhagic gastritis at the fundus; a large zone of disepithelization of the tongue mucosa appeared a few days later (Valiente et al, 1992).
    c) CASE REPORT: First- and second-degree burns of the esophagus and stomach were identified following ingestion of 200 mL diquat dibromide 1.84% (Tanen et al, 1999).
    C) DRUG-INDUCED ILEUS
    1) WITH POISONING/EXPOSURE
    a) Diquat has been associated with development of ileus in cases of systemic poisoning (Olson, 1994; Jones & Vale, 2000). Caution must be exercised in decontaminating the gut with either charcoal or clays to avoid formation of concretions in the intestinal lumen.
    b) CASE REPORT: Paralytic ileum has been reported in 4 cases; 3 of these were fatal. Death was felt to be the result of accumulation or sequestration of large amounts of fluid in the gut leading to hypovolemic shock (Jones & Vale, 2000).
    c) POOR PROGNOSIS: Rapid onset of acute renal failure, development of intestinal ileus and subsequent fluid sequestration, ventricular dysrhythmias, respiratory dysfunction requiring intubation and mechanical ventilation, and coma are associated with a poor prognosis in patients following diquat exposure (Jones & Vale, 2000) .

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) ABNORMAL LIVER FUNCTION
    1) WITH POISONING/EXPOSURE
    a) The liver may be affected to a minor degree during diquat poisoning (Schmidt et al, 1999; Gage, 1968; WHO, 1984).
    b) A rise in liver transaminase activities has been commonly reported in cases of diquat poisoning, but is usually mild, transient, and resolves spontaneously (Jones & Vale, 2000).
    c) CASE REPORT: A 57-year-old woman intentionally ingested 4 to 8 ounces of Spectracide(R) Grass and Weed Killer (2.3% diquat; 1.26% diquat ion, 1.5 to 3 g diquat cation). Initially, the patient complained of throat irritation and was admitted for decontamination and observation. On hospital day 3, the patient's AST and ALT peaked at 799 and 803 International Units/L, respectively, and normalized over the remainder of the hospitalization. By hospital day 4, renal function had deteriorated necessitating hemodialysis, and the patient suffered cardiac arrest. Resuscitation measures were successful, but support was withdrawn on day 7. Autopsy revealed brainstem infarction (Ruha et al, 2001).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) Diquat decreased glutathione and mRNA levels of cytochrome P450 CYP3A2 and glutathione transferases Ya1, Ya2, Yb1 and Yc1 in the liver in male Sprague-Dawley rats. Levels of CYP4A1 mRNA were increased. The net effect was depression of antioxidant enzymes and inhibition of glutathione synthesis (Gallagher et al, 1995).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) WITH POISONING/EXPOSURE
    a) The kidneys are primary target organs in diquat poisoning; the degree to which the renal tubules are affected depends upon the dose. There may be evidence of renal impairment following ingestions of less than 1 g diquat. The effect is generally transient (days), and typically becomes evident during the first 10 to 12 hours following ingestion, with elevated BUN and serum creatinine (Jones & Vale, 2000; Mahieu et al, 1984; Williams et al, 1986; Zilker et al, 1987).
    b) In some poisonings, urinary output declines progressively until the patient becomes anuric by days 7 to 10. The kidneys gradually return to normal function by the end of the second or third week (Hantson et al, 2000; Cobb & Grimshaw, 1979; Clark & Hurst, 1970; Mahieu et al, 1984; Williams et al, 1986; Zilker et al, 1987).
    B) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Multi-organ dysfunction, with acute renal failure in particular, can occur with diquat ingestions of 1 to 12 grams; recovery generally occurs in approximately two-thirds of cases (Jones & Vale, 2000).
    b) MULTI-ORGAN SYSTEM FAILURE: Ingestion of large amounts of diquat (greater than 3 ounces of concentrate) typically results in acute renal failure and death from multi-organ system failure within the first 24 to 48 hours (Jones & Vale, 2000; Saeed et al, 2001; McCarthy & Speth, 1983; Narita et al, 1978; Van Den Heede et al, 1982; Olson, 1994) (Hanston et al, 2000).
    c) CASE REPORT: A 57-year-old woman intentionally ingested 4 to 8 ounces of Spectracide(R) Grass and Weed Killer (2.3% diquat; 1.26% diquat ion; 1.5 to 3 g diquat cation). Initially, the patient complained of throat irritation and was admitted for decontamination and observation. On hospital day 2, the patient's renal function deteriorated (BUN 34 mg/dL; creatinine 4.6 mg/dL) and was anuric. By hospital day 4, hemodialysis was initiated, but the patient suffered cardiac arrest. Resuscitation measures were successful, but support was withdrawn on day 7. Autopsy revealed brainstem infarction (Ruha et al, 2001).
    d) POOR PROGNOSIS: Rapid onset of acute renal failure, development of intestinal ileus and subsequent fluid sequestration, ventricular dysrhythmias, respiratory dysfunction requiring intubation and mechanical ventilation, and coma are associated with a poor prognosis in patients following diquat exposure (Jones & Vale, 2000) .

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) POISONING
    1) WITH POISONING/EXPOSURE
    a) POOR PERCUTANEOUS ABSORPTION: Diquat, a highly ionized molecule, is poorly absorbed through intact human skin. Findings from both animal and human studies indicate that diquat has a low rate of percutaneous absorption (Scott & Corrigan, 1990).
    b) Results of a human dermal penetration study, using radiolabeled diquat, demonstrated that a maximum of 0.3% of the applied dose penetrated through the skin over a 5 day observation period (Feldman & Maibach, 1974).
    B) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) Diquat has been associated with direct local corrosive effects (Hoffer & Taitelman, 1989; Smith, 1988; Manoguerra, 1990).
    b) CASE REPORT: A 51-year-old pesticide applicator developed full thickness burns on the plantar surface of the right foot and partial thickness burns on the sole of the left foot following exposure to diquat that leaked from a backpack sprayer and accumulated in the boots (Manoguerra, 1990).
    c) CASE REPORT: Chemical burns occurred in the perineal and scrotal regions of two pesticide appliers with dermal exposure to DUCATALON(R), a mixture of diquat and paraquat, leaking from faulty spraying equipment (Ronnen et al, 1995).
    d) CASE REPORT: Systemic toxicity with extensive mucosal necrosis of the vagina and vulva has been reported in a woman who instilled 20 mL of a 6% diquat solution intravaginally (Rudez et al, 1999).
    C) SYSTEMIC DISEASE
    1) WITH POISONING/EXPOSURE
    a) Prolonged or repeated contact with concentrated diquat solutions may cause moderate to severe skin irritation, which may result in systemic absorption and poisoning (Bainova, 1969; Clark & Hurst, 1970; Manoguerra, 1990).
    D) NAIL FINDING
    1) WITH POISONING/EXPOSURE
    a) Finger and toenail contact with diquat concentrate or strong solutions can result in discoloration and deformity of the nail. Normal nail regrowth occurs once exposure ceases (Samman & Johnson, 1969; Baran, 1974).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 57-year-old woman intentionally ingested 4 to 8 ounces of Spectracide(R) Grass and Weed Killer (2.3% diquat; 1.26% diquat ion, 1.5 to 3 g diquat cation). Initially, the patient complained of throat irritation and was admitted for decontamination and observation. On hospital day 2, the patient's renal function deteriorated (BUN 34 mg/dL; creatinine 4.6 mg/dL) and her creatine phosphokinase (CPK) peaked at 37,683 International Units/L. By hospital day 4, hemodialysis was initiated with subsequent decrease in CPK to 1436 International Units/L, but the patient suffered cardiac arrest. Resuscitation measures were successful, but support was withdrawn on day 7. Autopsy revealed brainstem infarction (Ruha et al, 2001).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) ACUTE ALLERGIC REACTION
    1) WITH POISONING/EXPOSURE
    a) LACK OF SENSITIZATION: Diquat has not been associated with allergic reactions and appears to have no adverse effects on the immune system in either laboratory animals or humans. No reports of allergic dermatitis or allergic respiratory effects have been reported in manufacturing, formulation, or field workers exposed to diquat (WHO, 1984).
    3.19.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) LACK OF SENSITIZATION: Results of animal skin sensitization studies indicate that diquat is not an allergen (WHO, 1984).

Reproductive

    3.20.1) SUMMARY
    A) Diquat has not been associated with teratogenicity or adverse reproductive effects. However, results of reproductive studies with diquat have been conflicting.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) Pregnant rats injected with 7 or 14 mg/kg of diquat dibromide on one of several days during organogenesis developed skeletal defects of the sternum and a lack of ossification or absence of one of the auditory ossicles in some fetuses (TH Shepard , 1995). One review stated that diquat caused reproductive disturbances in a three-generation experimental animal study (Clegg, 1979).
    2) A study of the effect of diquat bromide on the development of mallard embryos showed that exposure of eggs for 10 seconds to solutions of 0.88 to 56 g/L on days 4 and 21 resulted in malformations including brain, eye, bill, limb and pelvis defects, skeletal scoliosis and incomplete ossification. These concentrations indicate little effect in average water depth (diluted), but considerable effect if applied aboveground (Sewalk et al, 2001).
    3) Diquat caused increased resorptions and birth defects in mice (Selypes et al, 1980), and was more potent than paraquat in producing these effects (Bus et al, 1975).
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) FETOTOXICITY
    a) One study found that it was not embryotoxic in rats (Bogdanov, 1979). In another, it retarded fetal growth and was fetotoxic (effects became more pronounced later in gestation) (Khera et al, 1968). In experimental animals, maternal ingestion of toxic doses of the chemical can result in the death of the embryo or fetus depending upon the severity of the poisoning (Khera et al, 1968; Bus et al, 1975).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS85-00-7 (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
    B) IARC Carcinogenicity Ratings for CAS2764-72-9 (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) NOT CARCINOGENIC - Diquat is not considered to be a carcinogen. It has not been associated with any human cancer cases.
    3.21.3) HUMAN STUDIES
    A) LACK OF EFFECT
    1) NOT CARCINOGENIC - Diquat has not been associated with any human cancer cases. It is not considered to be a carcinogen (Clark & Hurst, 1970; Bainova & Vulcheva, 1978; WHO, 1984).
    3.21.4) ANIMAL STUDIES
    A) LACK OF EFFECT
    1) NOT CARCINOGENIC - Results of animal lifetime feeding studies indicate that there were no increased incidences in tumors in any of the treated animals, indicating that diquat is not an animal carcinogen. It was not carcinogenic in rats (Bainova & Vulcheva, 1978). Diquat is not considered to be or classed as a carcinogen (Clark & Hurst, 1970; Bainova & Vulcheva, 1978; WHO, 1984).

Genotoxicity

    A) Diquat has demonstrated some mutagenic activity in vitro, but not in vivo.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor renal function (BUN and serum creatinine) for at least 12 hours post-ingestion.
    B) Monitor CBC, liver enzymes, electrolytes and urine output in significantly symptomatic patients.
    C) Analysis for diquat in serum or urine is difficult and requires special expertise that may not be available in most laboratory facilities.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Monitor renal function (BUN and serum creatinine) for at least 12 hours post-ingestion.
    2) Monitor CBC, liver enzymes, and electrolytes in significantly symptomatic patients.
    4.1.3) URINE
    A) Monitor urine output in significantly symptomatic patients.

Methods

    A) OTHER
    1) Analysis for diquat in serum or urine is difficult and requires special expertise that may not be available in most laboratory facilities (Baselt, 1988; Baselt & Cravey, 1989; Minakata et al, 1989).
    2) Specimens should be transferred to plastic containers because diquat binds to glass. Since diquat is a stable molecule, no special shipping conditions are required except that the container lids should fit tightly to prevent leakage and specimen contamination.
    SPECIMENQUANTITY REQUIRED
    Serum5 mL
    Urine50 to 100 mL
    Tissue25 grams

    B) CHROMATOGRAPHY
    1) TISSUE: Thin Layer Chromatography (TLC) has been used to detect diquat in tissues (Van Den Heede et al, 1982).
    2) SERUM/URINE/TISSUE: High-Performance Liquid Chromatography (HPLC) has been used to determine the presence of diquat in serum, urine, and human tissue (Nakagiri et al, 1989; Ito et al, 1993; Fuke et al, 1996).
    3) Diquat and its metabolites diquat-monopyridone and diquat-dipyridone can be analyzed simultaneously in serum or urine by ion-paired HPLC. Linear calibration was in the range of 0.1 to 10 mcg/mL (Ameno et al, 1995).
    C) SPECTROSCOPY/SPECTROMETRY
    1) SERUM/PLASMA: Other analytical techniques for measuring diquat in serum or plasma include: spectrophotometry (Sanchez-Sellero et al, 1993), spectroscopy (Fuke et al, 1992), spectrofluorometry (Perez-Ruiz et al, 1992), and a photokinetic method (Perez-Ruiz et al, 1990).
    2) URINE: Other analytical techniques for measuring diquat in urine include spectroscopy (Fuke et al, 1992), spectrofluorometry (Perez-Ruiz et al, 1991), and a photokinetic method (Perez-Ruiz et al, 1990).

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) Symptomatic patients and those that develop renal injury should be admitted for further care.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with dermal exposures involving a small body surface area to intact skin that do not have local symptoms or mucous membrane involvement can be managed at home with simple soap and water decontamination.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) A toxicologist should be consulted for all ingestions and all dermal exposures involving more than minimal body surface area. Appropriate medical subspecialties should be consulted to aid in the support of specific organ dysfunction due to toxicity.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Following ingestion, patients should be sent to a health care facility for observation. If asymptomatic, monitor for symptoms and renal injury for 12 hours from time of exposure.

Monitoring

    A) Monitor renal function (BUN and serum creatinine) for at least 12 hours post-ingestion.
    B) Monitor CBC, liver enzymes, electrolytes and urine output in significantly symptomatic patients.
    C) Analysis for diquat in serum or urine is difficult and requires special expertise that may not be available in most laboratory facilities.

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) EMESIS/NOT RECOMMENDED
    1) Do not induce emesis.
    B) ACTIVATED CHARCOAL
    1) Diquat binds irreversibly to clays and activated charcoal. Bentonite clay and Fuller's earth have been said to be preferable to activated charcoal, but aqueous suspensions of activated charcoal should be administered orally until clays are obtained (Akhavein & Linscott, 1968).
    2) 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.
    3) 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).
    C) CLAYS
    1) BENTONITE CLAY: DOSE: ADULT: 100 to 150 g; CHILD less than 12 years of age: 2 g/kg (7% suspension) (Bronstein, 2004)
    2) FULLER'S EARTH: DOSE: ADULT: 100 to 150 g; CHILD less than 12 years of age: 2 g/kg (30% suspension) (Bronstein, 2004).
    D) ILEUS: Diquat ingestion has been associated with the development of paralytic ileus, which may become evident by 24 to 48 hours. If this occurs, continued administration of clays or charcoal is CONTRAINDICATED because they may become impacted leading to obstruction or ischemia.
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive. Correct any significant fluid and/or electrolyte abnormalities in patients with severe diarrhea and/or vomiting.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment is symptomatic and supportive. Treat seizures with benzodiazepines. Seizures refractory to benzodiazepines may respond to phenobarbital or propofol. Consider endoscopy in patients with oral burns, dysphagia, stridor or vomiting, or deliberate ingestions of concentrated solutions. Patients who develop renal failure may require hemodialysis.
    B) MONITORING OF PATIENT
    1) Monitor renal function (BUN and serum creatinine) for at least 12 hours post-ingestion.
    2) Monitor CBC, liver enzymes, electrolytes and urine output in significantly symptomatic patients.
    3) Analysis for diquat in serum or urine is difficult and requires special expertise that may not be available in most laboratory facilities
    C) ENDOSCOPY
    1) Consider endoscopy in patients with oral burns, dysphagia, stridor or vomiting, or deliberate ingestions of concentrated solutions.
    D) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).

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.
    6.7.2) TREATMENT
    A) SUPPORT
    1) Administer oxygen and assist ventilation as needed. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    2) LACK OF CASES: There have been NO substantiated cases of systemic diquat poisoning associated with exposure to agricultural spray mist or inhalation of vapor or "fumes."
    a) Inhalation of spray mist can occur, but the droplets are usually large (100 to 200 microns in diameter) and deposit in the upper respiratory tract. Exposure to spray mist can result in localized irritation of the respiratory tract.
    3) Administration of supplemental oxygen has been recommended when the pO2 falls to less than 50 mmHg (Pond, 1994).
    4) HYPEROXIA/INCREASED MORTALITY
    a) ANIMAL STUDIES
    1) In rats, hyperoxia (supplemental oxygen) enhances the toxic effects of diquat (Pratt et al, 1980; Kehrer et al, 1979).
    2) Although diquat poisoning has not caused pulmonary fibrosis in humans, it HAS caused this effect in experimental animals in an hyperoxic environment (Winchester, 1990).
    3) In view of the fact that diquat generally does NOT cause pulmonary fibrosis in humans, low-flow, low-concentration humidified supplemental oxygen to alleviate upper airway irritant symptoms is NOT contraindicated.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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).
    6.8.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Concentrated diquat can cause severe eye irritation which develops gradually, reaching its maximum after 12 to 24 hours. Patients with eye contact involving diquat concentrate or strong solutions should be examined by a physician.
    2) Prolonged flushing and early ophthalmological consultation may be advisable.
    3) Treatment is supportive and healing may be slow.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) Remove contaminated clothing and immediately wash skin with soap and water. Discard contaminated leather shoes.
    6.9.2) TREATMENT
    A) SUPPORT
    1) IRRITATION/SYSTEMIC ABSORPTION: Diquat can be irritating to human skin, and in cases involving dermal exposure where the chemical has not been removed from the skin and irritation is present, systemic poisoning could potentially occur.
    a) However, dermal contact with only slightly irritated skin should not result in systemic absorption and poisoning.
    2) Patients presenting with exposure histories involving contact of diquat concentrate or strong solutions with damaged skin should be immediately hospitalized and evaluated, with medical management directed towards supportive care.
    a) In all cases, the patient should be questioned regarding possible ingestion of the chemical and examined to determine whether any dermal lesions or cuts are present. The patient should be instructed to avoid or minimize dermal contact with the chemical by wearing protective clothing or modifying the spraying procedure.
    B) IRRITATION SYMPTOM
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    2) Topical silver sulfadiazine and systemic antibiotics were effective in treating severe skin burns caused by DUCATALON(R), a mixture of diquat and paraquat (Ronnen et al, 1995).
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EXTRACORPOREAL ELIMINATION
    1) SUMMARY
    a) There is no evidence that charcoal hemoperfusion, hemodialysis, or forced diuresis remove significant quantities of diquat from the body or alter patient outcome after poisoning. Routine use is NOT recommended. Some clinicians believe that early in the course of intoxication (within the first 2 to 4 hours) these modalities may be useful, but there is no data to support this practice.
    b) For removal of diquat from the blood, hemoperfusion is more effective than hemodialysis (Winchester, 1990).
    2) HEMOPERFUSION
    a) In general, hemoperfusion is NOT EFFECTIVE in altering the course of the poisoning unless it can be started within 4 hours of ingestion and continued for at least 6 to 8 hours (Pond, 1994).
    3) HEMODIALYSIS
    a) Hemodialysis, which is much less effective than hemoperfusion, can be used in tandem with charcoal hemoperfusion and continued in between hemoperfusions (Okonek & Hofmann, 1975; (Okonek et al, 1976; Okonek, 1981; Williams et al, 1986).

Range Of Toxicity

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) Data concerning toxic levels of diquat in human serum following ingestion of the chemical are limited. However, based on data from the Chevron Emergency Information Center, it appears that diquat serum levels greater than 0.5 micrograms/milliliter during the first 24 hours have typically been associated with systemic poisoning.
    b) Diquat serum levels in one FATAL CASE (Litovitz et al, 1989) -
    (a = BEFORE Hemoperfusion/Hemodialysis; b = AFTER Hemoperfusion/Hemodialysis)
    TIME POSTINGESTION (H = Hours/D = Days)SERUM LEVEL (mcg/dL)
    3 H7.6 (a)
    3.5 H9.6 (a)
    1 D1.3 (b)
    2 D1.45 (a)
    2 D0.48 (b)
    3 D0.38 (a)
    3 D0.067 (b)
    4 D0.11 (a)
    4 D0.074 (b)
    6 D0.017 (b)

    1) The above data demonstrate a REBOUND phenomenon of serum diquat levels following extracorporeal elimination measures.
    c) The diquat serum concentration of 64 mcg/mL in a patient 4 hours after the ingestion of diquat 60 g was probably the highest level recorded in the literature (Hantson et al, 2000).

Workplace Standards

    A) ACGIH TLV Values for CAS85-00-7 (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) Diquat
    a) TLV:
    1) TLV-TWA: 0.5 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4, A4
    2) Codes: I, I, Skin, Skin
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    c) I: Inhalable fraction; see Appendix C, paragraph A (of TLV booklet).
    d) I: Inhalable fraction; see Appendix C, paragraph A (of TLV booklet).
    e) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    f) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): LRT irr; cataract
    d) Molecular Weight: Varies
    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) Adopted Value
    1) Diquat
    a) TLV:
    1) TLV-TWA: 0.1 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4, A4
    2) Codes: R, R, Skin, Skin
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    c) R: Respirable fraction; see Appendix C, paragraph C (of TLV booklet).
    d) R: Respirable fraction; see Appendix C, paragraph C (of TLV booklet).
    e) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    f) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): LRT irr; cataract
    d) Molecular Weight: Varies
    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) ACGIH TLV Values for CAS2764-72-9 (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) Diquat
    a) TLV:
    1) TLV-TWA: 0.5 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4, A4
    2) Codes: I, I, Skin, Skin
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    c) I: Inhalable fraction; see Appendix C, paragraph A (of TLV booklet).
    d) I: Inhalable fraction; see Appendix C, paragraph A (of TLV booklet).
    e) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    f) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): LRT irr; cataract
    d) Molecular Weight: Varies
    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) Adopted Value
    1) Diquat
    a) TLV:
    1) TLV-TWA: 0.1 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4, A4
    2) Codes: R, R, Skin, Skin
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    c) R: Respirable fraction; see Appendix C, paragraph C (of TLV booklet).
    d) R: Respirable fraction; see Appendix C, paragraph C (of TLV booklet).
    e) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    f) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): LRT irr; cataract
    d) Molecular Weight: Varies
    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:

    C) NIOSH REL and IDLH Values for CAS85-00-7 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Diquat (Diquat dibromide)
    2) REL:
    a) TWA: 0.5 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH: Not Listed

    D) NIOSH REL and IDLH Values for CAS2764-72-9 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    E) Carcinogenicity Ratings for CAS85-00-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Diquat
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Diquat
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    3) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Diquat
    4) 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
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Diquat (Diquat dibromide)
    6) MAK (DFG, 2002): Not Listed
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    F) Carcinogenicity Ratings for CAS2764-72-9 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Diquat
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Diquat
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    3) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    4) 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
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    6) MAK (DFG, 2002): Not Listed
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    G) OSHA PEL Values for CAS85-00-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    H) OSHA PEL Values for CAS2764-72-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) (Budavari, 2000; Clayton & Clayton, 1981 Finkel, 1983 Gaines & Linder, 1986 Gosselin et al, 1984 Hartley & Kidd, 1987 Lewis, 2000 Morgan, 1989 ) Sine, 1987 Sittig, 1985 RTECS, 2001
    1) LD50- (ORAL)MOUSE:
    a) 233 mg/kg
    b) 125 mg/kg (Budavari, 2000)
    2) LD50- (ORAL)RAT:
    a) 120 mg/kg
    b) 231 mg/kg (Budavari, 2000)
    c) 600-810 mg salt/kg
    3) LD50- (SKIN)RAT:
    a) 433 mg/kg
    4) LD50- (SUBCUTANEOUS)RAT:
    a) 20 mg/kg (Lewis, 2000)
    b) 11 mg/kg -- mydriasis, dyspnea, and somnolence
    5) TCLo- (INHALATION)RAT:
    a) 1900 mcg/m(3) for 4H/19W- intermittent -- structural changes or functional change to trachea or bronchi, changes in tubules, affected phosphatases

Summary

    A) TOXICITY: Ingestion of 1 gram or less usually causes mild to moderate gastrointestinal and renal toxicity, with recovery following supportive care. Ingestion of 1 to 12 grams results in moderate to severe toxicity, with multiple organ dysfunction and acute renal failure, in particular, frequently occurring. Recovery has been reported in approximately two-thirds of cases, although a fatality has been reported following ingestion of 1.5 to 3 grams in an adult. Ingestion of greater than 12 grams results in multiple organ failure and death in the majority of patients within 24 to 48 hours.

Minimum Lethal Exposure

    A) ACUTE
    1) Based on limited clinical reports, the estimated adult minimum lethal oral dose of diquat concentrate is probably near 20 to 50 mL (Pond et al, 1983; Schoenborn et al, 1971; Vanholder et al, 1981).
    2) CASE REPORT: A 57-year-old woman intentionally ingested 4 to 8 ounces of Septracide(R) Grass and Weed Killer containing 2.3% diquat dibromide (1.26% diquat ion, 1.5 to 3 g diquat ion (25 to 50 mg/kg for a 60 kg person)). Severe toxicity ensued and death resulted 7 days later (Ruha et al, 2001).
    3) Severe toxicity and death have been reported following ingestion of as little as 20 mL of Reglone(R) containing 20 g/100 mL diquat (67 mg/kg for a 60 kg person) (Vanholder et al, 1981).
    4) Over the period 1968 to 1999, 30 cases of diquat poisoning were reported in detail in the literature, of which 13 (43%) were fatal (Jones & Vale, 2000).
    5) Ingestion of greater than 12 grams results in multiple organ failure and death in the majority of patients within 24 to 48 hours (Jones & Vale, 2000).

Maximum Tolerated Exposure

    A) ACUTE
    1) Ingestion of 1 gram or less usually causes mild to moderate gastrointestinal and renal toxicity, with recovery following supportive care. Ingestion of 1 to 12 grams results in moderate to severe toxicity, with multiple organ dysfunction and acute renal failure, in particular, frequently reported. Recovery has been reported in approximately two-thirds of cases (Jones & Vale, 2000).
    2) Human systemic poisoning and deaths have been reported from ingestion of 20 to 50 mL of diquat concentrate (Narita et al, 1978; Schoenborn et al, 1971; Vanholder et al, 1981), while one report to the Chevron Emergency Information Center indicates a patient surviving alleged ingestion of approximately 300 mL of diquat concentrate.
    a) One patient survived without sequelae following ingestion of 30 mL of a 20% diquat formulation (Mahieu et al, 1984; Ellenhorn & Barceloux, 1988).
    b) A review of human diquat exposure cases reported to the Chevron Emergency Information Center revealed that ingestion of approximately 5 mL of diquat concentrate or less (1200 mg diquat ion or less) resulted in only minor gastrointestinal involvement and detection of diquat in the serum. None of the cases developed into actual systemic poisonings.
    B) ANIMAL DATA
    1) In chronic oral toxicity tests, rats were not killed by a dietary level of 1000 ppm for two years, but their food consumption and growth declined. A dietary level of 500 ppm (about 25 mg/kg/day) does not affect food intake, growth, blood, or urine findings, or cause pathological changes except in the eyes.
    a) Cataracts show a clear dose-response relationship, appearing earlier, more severely, and more frequently at higher dietary levels. At a dietary level of 1000 ppm, complete opacities appear in one or both lenses within six months in one-fourth of the animals (ACGIH, 1986).
    b) A dietary level of 10 ppm (about 0.5 mg/kg/day) did not produce cataracts in a 2 year test (ACGIH, 1986).
    2) Lens opacities developed within 11 months in dogs fed 15 mg/kg/day and within 17 months at 5 mg/kg/day. Dogs tolerated 1.7 mg/kg/day for 4 years without developing cataracts (ACGIH, 1986; Proctor et al, 1988).
    3) Diquat applied to the skin of rabbits at 40 mg/kg killed 4 of 6 rabbits after 8 to 20 applications (Proctor et al, 1988).

Pharmacology Toxicology

Toxicologic Mechanism

    A) Diquat is a potent oxidation-reduction cycler that readily generates a free radical in the presence of NADPH and cytochrome P450 reductase. The diquat radical reacts with oxygen to form a superoxide radical which is highly reactive. The superoxide radical generates hydroxyl radical in the presence of iron and hydrogen peroxide. The hydroxyl radical initiates lipid peroxidation in biological membranes and can cause cell death (Jones & Vale, 2000). The exact mechanism of diquat associated renal toxicity is unknown.
    B) In humans, diquat does not accumulate in the pneumatocytes as does paraquat. Therefore, the lung is generally not injured in diquat poisoning (Lam et al, 1980; Keeling et al, 1981).

Physicochemical

Physical Characteristics

    A) Diquat is a pale yellow or yellow reddish-brown crystalline solid (pure salt monohydrate) (Budavari,2000; (CHRIS , 2001; Hayes & Laws, 1991; HSDB , 2001); or dark reddish-brown liquid (CHRIS , 1992; HSDB , 2001).
    B) Diquat is odorless because there is virtually no measurable vapor pressure (Hayes & Laws, 1991).
    C) It has a salty taste (Budavari, 1989).

Molecular Weight

    A) 345.17

References

General Bibliography

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