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CYCLONITE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Cyclonite is a highly explosive compound used in munitions.

Specific Substances

    1) 1,3,5-trinitrohexahydro-s-triazine
    2) C4
    3) Cyclotrimethylenetrinitramine
    4) hexahydro-2,3,5-trinitro-1,3,5 triazine
    5) Hexogen
    6) Hexolite
    7) RDX
    8) T4
    9) CAS 121-82-4
    1.2.1) MOLECULAR FORMULA
    1) C3-H6-N6-O6

Available Forms Sources

    A) FORMS
    1) Cyclonite may exist as a white crystalline powder or as colorless crystals. It is a combustible solid and is considered a powerful high explosive (ACGIH, 1991a; Hathaway et al, 1996a).
    2) Impure military grades of this compound contain about 10% hexamethylenetetramine (HSDB, 2002).
    B) SOURCES
    1) Cyclonite is formed through a reaction of hexamethylenetetramine with concentrated nitric acid (Budavari, 1996; Lewis, 1997a).
    2) Using the Bachmann process, combining hexamethylenetetramine, ammonium nitrate, concentrated nitric acid, and para-formaldehyde will produce cyclonite(Ashford, 1994).
    3) Methenamine can be treated with fuming nitric acid to prepare cyclonite (Budavari, 2000).
    4) Cyclonite can also be made from hexamethylenetetramine through a direct nitrolysis process (Ashford, 1994).
    C) USES
    1) Cyclonite is used by the military as a powerful, high explosive; as a base charge for detonators; and as an ingredient of bursting-charge and plastic explosives. It has more shattering power than TNT (1.5 times more powerful) and can be mixed with TNT as a bursting charge for aerial bombs, mines, and torpedoes (ACGIH, 1991a; Ashford, 1994; Bingham et al, 2001a; Hathaway et al, 1996a; ITI, 1995; Lewis, 2000a; Lewis, 1997a; NIOSH, 2002).
    2) Cyclonite is also used in the manufacture of smokeless powders and as a rodenticide, particularly rat poison (ACGIH, 1991a; Budavari, 2000; Hathaway et al, 1996a; Kohler J and Meyer R, 1993).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Cyclonite does NOT have nitrate-like toxicity. It may be toxic by inhalation, ingestion, or skin and eye exposure.
    B) Cyclonite is a corrosive irritant of the eyes, skin, mucous membranes and respiratory tract, but it mainly affects the central nervous system, acting as a depressant.
    C) Exposure may result in dermatitis, mucous membrane ulceration, salivation, anorexia, nausea, vomiting, hematuria and renal tubular damage. Neurologic symptoms may include weakness, asthenia, dizziness, headache, insomnia, irritability, stupor, unconsciousness and seizures.
    D) Prominent signs and symptoms after ingestion have included staring into space, generalized seizures, lethargy, coma, muscular twitching, hyperreflexia, myalgias, headaches, vomiting, mild renal injury and hematuria.
    1) Additional effects following oral exposure have included: methemoglobinemia, metabolic acidosis with anion gap, hypokalemia, hyperglycemia, and increased liver enzymes. Onset is typically delayed for 3 to 12 hours after ingestion. Gastrointestinal effects are usually noted by 3 hours after ingestion, and central nervous system effects, 8 to 12 hours after ingestion.
    0.2.3) VITAL SIGNS
    A) Mild fever is common, lasting 24 to 48 hours.
    0.2.7) NEUROLOGIC
    A) Generalized seizures have been reported in workers exposed to cyclonite, as has confusion, loss of consciousness, exhaustion, vertigo and postictal coma. Irritability, insomnia, restlessness and anxiety were prodromal symptoms seen in workers who later became toxic. Ingestion has resulted in myoclonus, generalized seizures and status epilepticus.
    0.2.8) GASTROINTESTINAL
    A) Nausea and vomiting may occur in workers exposed to cyclonite by any route.
    0.2.10) GENITOURINARY
    A) Mild renal dysfunction occurs in about 16 percent of cases. Hemodialysis is rarely required. Hematuria is common.
    0.2.12) FLUID-ELECTROLYTE
    A) WITH POISONING/EXPOSURE
    1) Hypokalemia and hyperglycemia were reported with both inadvertent exposure and intentional ingestion of cyclonite.
    0.2.13) HEMATOLOGIC
    A) Leukocytosis and mild fever are common.
    0.2.14) DERMATOLOGIC
    A) Irritant and allergic contact dermatitis have been reported in workers who manufacture cyclonite.
    B) A petechial rash mimicking meningococcemia has been reported secondary to cyclonite-induced seizures.
    0.2.15) MUSCULOSKELETAL
    A) Muscle spasms were associated with ingestion of 1 tablespoonful of cyclonite by an adult. Myalgia and myoclonus are frequently noted.

Laboratory Monitoring

    A) Cyclonite levels are not readily available in most clinical settings.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) EMESIS - Because of the probability of developing seizures, emesis is NOT recommended in cyclonite ingestions.
    B) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    C) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 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) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 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).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    D) SUPPORTIVE CARE - Symptomatic patients should be given adequate respiratory support during seizures. Monitor liver and renal function tests and urinalysis in patients with significant exposure.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) Most exposures to cyclonite have been in industrial or military settings. One adult worker who intentionally ingested 1 tablespoonful of cyclonite developed severe muscle spasms, but no seizures or CNS depression.
    B) Five adults ingested various amounts of cyclonite which ranged from 37 to 250 mg/kg; all made a complete recovery. Based on limited human exposure data, serum cyclonite levels appear to correlate with clinical presentation.

Clinical Effects

Summary Of Exposure

    A) Cyclonite does NOT have nitrate-like toxicity. It may be toxic by inhalation, ingestion, or skin and eye exposure.
    B) Cyclonite is a corrosive irritant of the eyes, skin, mucous membranes and respiratory tract, but it mainly affects the central nervous system, acting as a depressant.
    C) Exposure may result in dermatitis, mucous membrane ulceration, salivation, anorexia, nausea, vomiting, hematuria and renal tubular damage. Neurologic symptoms may include weakness, asthenia, dizziness, headache, insomnia, irritability, stupor, unconsciousness and seizures.
    D) Prominent signs and symptoms after ingestion have included staring into space, generalized seizures, lethargy, coma, muscular twitching, hyperreflexia, myalgias, headaches, vomiting, mild renal injury and hematuria.
    1) Additional effects following oral exposure have included: methemoglobinemia, metabolic acidosis with anion gap, hypokalemia, hyperglycemia, and increased liver enzymes. Onset is typically delayed for 3 to 12 hours after ingestion. Gastrointestinal effects are usually noted by 3 hours after ingestion, and central nervous system effects, 8 to 12 hours after ingestion.

Vital Signs

    3.3.1) SUMMARY
    A) Mild fever is common, lasting 24 to 48 hours.
    3.3.3) TEMPERATURE
    A) HYPERTHERMIA - Mild fever is common, lasting 24 to 48 hours (Ketel & Hughes, 1972).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) Sinus tachycardia has been observed after ingestion (Kucukardali et al, 2003; Stone et al, 1969).
    2) Bradycardia has been reported in one case series (2/17 patients) following intentional ingestion (Davies et al, 2007).
    B) ELECTROCARDIOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Frequent premature ventricular ectopy was reported in one patient following oral exposure (Kucukardali et al, 2003).

Neurologic

    3.7.1) SUMMARY
    A) Generalized seizures have been reported in workers exposed to cyclonite, as has confusion, loss of consciousness, exhaustion, vertigo and postictal coma. Irritability, insomnia, restlessness and anxiety were prodromal symptoms seen in workers who later became toxic. Ingestion has resulted in myoclonus, generalized seizures and status epilepticus.
    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) Generalized seizures (tonic-clonic) have been reported in individuals exposed to cyclonite (Kucukardali et al, 2003; Hett & Fichtner, 2002; Harrell-Bruder & Hutchins, 1995; Kaplan et al, 1965).
    2) CASE SERIES - Recurrent generalized seizures began a few to 16 hours after ingestion of cyclonite in 4 adults (Stone et al, 1969), and within 8 to 12 hours in 18 other cases. Seizures were often persistent and not controlled by phenytoin and phenobarbital. All resolved by 60 hours postingestion (Ketel & Hughes, 1972).
    3) In another case series, 5 adults inadvertently exposed to cyclonite developed symptoms within 4 to 16 hours after ingestion; 4 had recurrent tonic-clonic seizures. The frequency and duration of the seizures gradually declined over several days. Each patient was lethargic and comatose between episodes of seizure and hyperactive deep tendon reflexes were observed. Complete recovery was reported in all cases; discharge occurred between 7 and 21 days of admission (Kucukardali et al, 2003).
    4) CASE REPORT - Status epilepticus unresponsive to repeated IV doses of diazepam, phenytoin, and phenobarbital was reported in a 3-year-old boy several hours after the child was found chewing on clumps of plasticized cyclonite explosive carried into the home on the mother's clothing (Woody et al, 1986).
    5) Intentional ingestion of compound C-4, which contains cyclonite, caused generalized seizures (Davies et al, 2007; Hett & Fichtner, 2002; Harrell-Bruder & Hutchins, 1995).
    6) A 42-year-old-man had grand mal seizures after sieving granular hexogen (cyclonite) powder for 4 hours in an ammunition factory. Approximately six hours elapsed between completion of this task and seizure onset (Testud et al, 1996).
    B) MYOCLONUS
    1) CASE SERIES - Myoclonus was reported in 4 of 18 cases in one series. In 2 cases the onset was prior to development of generalized seizures, and in 2 it was interspersed between seizures (Ketel & Hughes, 1972).
    2) CASE REPORT - A 21-year-old soldier was noted to have myoclonic jerks following ingestion of a 1 cm x 1 cm x 1 cm cube. They occurred following two seizures, and resolved within 48 hours (Hett & Fichtner, 2002).
    C) HEADACHE
    1) Headache has been reported as an early symptom of acute cyclonite poisoning (Kucukardali et al, 2003; Kaplan et al, 1965).
    2) Headache was the most commonly reported symptom (82%) in a case series of 17 patients (Davies et al, 2007).
    D) CENTRAL NERVOUS SYSTEM DEFICIT
    1) Confusion, loss of consciousness, exhaustion, vertigo, and postictal coma have been seen in overexposed cyclonite plant workers and following ingestion (Harrell-Bruder & Hutchins, 1995; Stokinger, 1982; Kaplan et al, 1965) .
    E) FEELING NERVOUS
    1) Irritability, insomnia, restlessness, and anxiety were prodromal symptoms seen in workers who became toxic (Kaplan et al, 1965).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea and vomiting may occur in workers exposed to cyclonite by any route.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) Vomiting has been reported in several workers exposed to cyclonite. Ingestion is not required to produce nausea and vomiting (Kaplan et al, 1965).
    2) CASE SERIES - Five adult males were inadvertently exposed to food contaminated with cyclonite during a military training program, and developed initial symptoms that included: abdominal pain, nausea, vomiting, headache, myalgia and generalized weakness. Signs and symptoms were present within 3 hours of exposure (Kucukardali et al, 2003).
    3) CASE SERIES - Severe protracted vomiting occurred within 3 hours after ingestion of cyclonite in 4 adults (Stone et al, 1969).
    4) CASE SERIES - Vomiting was reported in 10/17 (58%) patients following the ingestion of C-4 by army commandos (Davies et al, 2007).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) Mild elevations of AST (SGOT) have been reported, and have been attributed to muscle trauma during seizures (Hollander & Colbach, 1969; Ketel & Hughes, 1972). Following oral exposure, elevated levels of AST and ALT have been reported (Kucukardali et al, 2003).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATITIS
    a) Experimental animals fed large amounts of cyclonite have developed fatty degeneration of the liver (von Oettingen et al, 1949). This has NOT been seen in human poisoning cases.

Genitourinary

    3.10.1) SUMMARY
    A) Mild renal dysfunction occurs in about 16 percent of cases. Hemodialysis is rarely required. Hematuria is common.
    3.10.2) CLINICAL EFFECTS
    A) RENAL TUBULAR DISORDER
    1) Mild renal tubular damage with elevated BUN and serum creatinine and proteinuria has been reported after cyclonite ingestion. The ingestion of the largest amount in this series (180 grams) produced only mild changes and no oliguria, but residual proteinuria was observed. Oliguria was present in two cases where the amount ingested was unknown (Stone et al, 1969).
    2) Renal toxicity occurred in 16 percent of patient in a series of 18 cases. Hemodialysis was required in one case (Ketel & Hughes, 1972).
    B) BLOOD IN URINE
    1) Gross and microscopic hematuria has been a characteristic finding after ingestion of cyclonite (Stone et al, 1969).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL TUBULAR DISORDER
    a) Renal tubular damage was seen in experimental animals fed large amounts of cyclonite (von Oettingen et al, 1949).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) METABOLIC ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) Severe metabolic acidosis with a high anion gap was reported in several patients following inadvertent oral exposure to cyclonite. Symptoms resolved following supportive care, which included hemodialysis (Kucukardali et al, 2003).

Hematologic

    3.13.1) SUMMARY
    A) Leukocytosis and mild fever are common.
    3.13.2) CLINICAL EFFECTS
    A) METHEMOGLOBINEMIA
    1) CASE SERIES - Five adult males were inadvertently exposed to food contaminated with cyclonite during a military training program, and developed laboratory evidence of methemoglobinemia. MetHb levels ranged from 14% to 20%. Ascorbic acid and methylene blue were given for levels of 14% or above. Clinical and laboratory abnormalities resolved and no permanent sequelae occurred (Kucukardali et al, 2003).
    a) Previously, methemoglobinemia had not been reported in human cases or seen in experimental animal studies (Kaplan et al, 1965; von Oettingen et al, 1949).
    B) LEUKOCYTOSIS
    1) Transient leukocytosis was reported in 72% of patients in one series of 18 cases (Ketel & Hughes, 1972). It was also reported in 5 adults inadvertently exposed to cyclonite (Kucukardali et al, 2003).

Dermatologic

    3.14.1) SUMMARY
    A) Irritant and allergic contact dermatitis have been reported in workers who manufacture cyclonite.
    B) A petechial rash mimicking meningococcemia has been reported secondary to cyclonite-induced seizures.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Irritant and allergic contact dermatitis were reported in workers who manufactured cyclonite. The areas primarily affected were the face and eyelids. The exact offending agent is unknown, but appears to be related to fumes released from the reaction mixture during cyclonite production (Stokinger, 1982).
    2) Although dermatitis from the pure material is possible, cyclonite is not a strong contact irritant. Patch testing with moistened cyclonite did not produce irritation (von Oettingen et al, 1949).
    B) PURPURA
    1) CASE REPORT - Presenting signs in a 19-year-old male who ingested a piece of plastic explosive containing cyclonite included a disseminated petechial rash, frontal headache, and seizures; meningococcal disease was ruled out (Goldberg et al, 1992).

Musculoskeletal

    3.15.1) SUMMARY
    A) Muscle spasms were associated with ingestion of 1 tablespoonful of cyclonite by an adult. Myalgia and myoclonus are frequently noted.
    3.15.2) CLINICAL EFFECTS
    A) SPASM
    1) Severe muscle spasms were associated with ingestion of 1 tablespoonful of cyclonite by an adult male worker (Kaplan et al, 1965).
    B) ASTHENIA
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES - Generalized weakness and myalgia developed within 3 hours of inadvertent exposure to cyclonite in 5 adult males (Kucukardali et al, 2003).
    C) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) Rhabdomyolysis developed in several patients inadvertently exposed to food contaminated with cyclonite. Recurrent seizures were also noted in these patients. In two patients, CK levels peaked at 73,420 and 82,400, respectively. Although elevated CK levels may have been due to repeated seizure activity, the authors suggested that elevated CK levels may have been the result of primary toxic effects of cyclonite on muscle tissue (Kucukardali et al, 2003).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS121-82-4 (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

Genotoxicity

    A) Soils contaminated with TNT and cyclonite have been mutagenic in bacterial test systems and cultured mammalian cells.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Cyclonite levels are not readily available in most clinical settings.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) In a small case series, serum cyclonite concentrations strongly correlated with clinical and laboratory presentation (Kucukardali et al, 2003).
    2) Obtain a baseline CBC, electrolytes (in particular potassium and glucose), methemoglobin levels following a significant exposure. Creatine kinase is also indicated in patients with seizures or significant toxicity.
    3) Monitor liver and kidney function tests and urinalysis in patients with significant exposure.
    4) Monitor arterial blood gases in patients with metabolic acidosis.

Methods

    A) CHROMATOGRAPHY
    1) An HPLC method was used to obtain plasma levels in 5 patients acutely exposed to cyclonite. In this study, plasma levels strongly correlated with clinical and laboratory presentation (Kucukardali et al, 2003).
    2) An HPLC method with UV detection was used to detect cyclonite in serum and urine (Turley & Brewster, 1987).
    3) Cyclonite can be determined in contaminated soil and water with an automated multiple development high performance thin layer chromatography technique (Steuckart et al, 1994).
    4) An HPLC method using reverse phase C18 column and UV-DAD using Tox-clean RC cartridge for SPC was successful at detecting cyclonite (RDX) with a lower limit of detection of 0.005 mcg/mL (Ozhan et al, 2003).

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) Patients suspected of ingesting or inhaling cyclonite should be observed in a health care facility for a minimum of 18 to 24 hours. Seizures may occur suddenly, and typically are delayed for 4 to 16 hours after exposure (Kucukardali et al, 2003; Ketel & Hughes, 1972).

Monitoring

    A) Cyclonite levels are not readily available in most clinical settings.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/ NOT RECOMMENDED
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for seizures.
    B) 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) Because of the probability of developing seizures, inducing emesis is NOT RECOMMENDED in cyclonite ingestions.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) Treatment is symptomatic and supportive. Based on limited human data, significant exposure has resulted in seizures, rhabdomyolysis, metabolic acidosis, and alterations in electrolyte status (Kucukardali et al, 2003).
    B) SEIZURE
    1) In a small case series (n=5), seizures developed within 4 to 16 hours of oral exposure. Recurrent seizures were observed in patients with the highest plasma cyclonite levels (Kucukardali et al, 2003).
    2) 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).
    3) 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 .
    4) 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).
    5) 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, 2010; Chin et al, 2008).
    6) 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).
    7) 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).
    8) RECURRING SEIZURES
    a) If seizures are not controlled by the above measures, patients will require endotracheal intubation, mechanical ventilation, continuous EEG monitoring, a continuous infusion of an anticonvulsant, and may require neuromuscular paralysis and vasopressor support. Consider continuous infusions of the following agents:
    1) MIDAZOLAM: ADULT DOSE: An initial dose of 0.2 mg/kg slow bolus, at an infusion rate of 2 mg/minute; maintenance doses of 0.05 to 2 mg/kg/hour continuous infusion dosing, titrated to EEG (Brophy et al, 2012). PEDIATRIC DOSE: 0.1 to 0.3 mg/kg followed by a continuous infusion starting at 1 mcg/kg/minute, titrated upwards every 5 minutes as needed (Loddenkemper & Goodkin, 2011).
    2) PROPOFOL: ADULT DOSE: Start at 20 mcg/kg/min with 1 to 2 mg/kg loading dose; maintenance doses of 30 to 200 mcg/kg/minute continuous infusion dosing, titrated to EEG; caution with high doses greater than 80 mcg/kg/minute in adults for extended periods of time (ie, longer than 48 hours) (Brophy et al, 2012); PEDIATRIC DOSE: IV loading dose of up to 2 mg/kg; maintenance doses of 2 to 5 mg/kg/hour may be used in older adolescents; avoid doses of 5 mg/kg/hour over prolonged periods because of propofol infusion syndrome (Loddenkemper & Goodkin, 2011); caution with high doses greater than 65 mcg/kg/min in children for extended periods of time; contraindicated in small children (Brophy et al, 2012).
    3) PENTOBARBITAL: ADULT DOSE: A loading dose of 5 to 15 mg/kg at an infusion rate of 50 mg/minute or lower; may administer additional 5 to 10 mg/kg. Maintenance dose of 0.5 to 5 mg/kg/hour continuous infusion dosing, titrated to EEG (Brophy et al, 2012). PEDIATRIC DOSE: A loading dose of 3 to 15 mg/kg followed by a maintenance dose of 1 to 5 mg/kg/hour (Loddenkemper & Goodkin, 2011).
    4) THIOPENTAL: ADULT DOSE: 2 to 7 mg/kg, at an infusion rate of 50 mg/minute or lower. Maintenance dose of 0.5 to 5 mg/kg/hour continuous infusing dosing, titrated to EEG (Brophy et al, 2012)
    b) Endotracheal intubation, mechanical ventilation, and vasopressors will be required (Brophy et al, 2012) and consultation with a neurologist is strongly advised.
    c) Neuromuscular paralysis (eg, rocuronium bromide, a short-acting nondepolarizing agent) may be required to avoid hyperthermia, severe acidosis, and rhabdomyolysis. If rhabdomyolysis is possible, avoid succinylcholine chloride, because of the risk of hyperkalemic-induced cardiac dysrhythmias. Continuous EEG monitoring is mandatory if neuromuscular paralysis is used (Manno, 2003).
    C) MONITORING OF PATIENT
    1) Following a significant exposure, monitor CBC, serum electrolytes (including potassium, glucose), liver enzymes and creatine kinase.
    2) Monitor methemoglobin levels following significant exposure. Based on limited human data, methemoglobinemia can occur following acute exposure (Kucukardali et al, 2003).
    D) ACIDOSIS
    1) Monitor serum electrolytes. Obtain ABGs when patients are symptomatic or acidotic. Metabolic acidosis with a high anion gap has been reported in a limited number of adults orally exposed to cyclonite(Kucukardali et al, 2003).
    2) Intravenous sodium bicarbonate should NOT routinely be administered. Sodium bicarbonate should not be administered prophylactically or for the treatment of mild to moderate acidosis or acidemia. Sodium bicarbonate administration may be useful to manage cases of severe or life-threatening acidosis and acidemia. DOSE: ADULT: 1 to 2 milliequivalents/kilogram; CHILDREN: 1 milliequivalent/kilogram) Repeat dosing of sodium bicarbonate should be guided by the response to therapy as indicated by electrolyte and ABG monitoring.
    3) CASE REPORT - Five adults were inadvertently exposed to oral cyclonite and 4 patients developed metabolic acidosis (pH ranged between 7.0 to 7.12; anion gap ranged between 35 to 41). Treatment included sodium bicarbonate, but 3 patients required hemodialysis due to a lack of response following sodium bicarbonate (Kucukardali et al, 2003).

Inhalation Exposure

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

Eye Exposure

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

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) 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.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) HEMODIALYSIS
    1) Hemodialysis was used to treat 3 patients that developed severe metabolic acidosis following inadvertent oral exposure to cyclonite. The patients were initially treated with sodium bicarbonate without improvement. Of note, the patients clinically improved following therapy, but cyclonite levels did not significantly decrease. At 72 hours, serum levels rose 2 fold in 2 of 3 patients treated. The authors concluded that cyclonite is not dialyzable, and absorption from the gastrointestinal tract may be slow (Kucukardali et al, 2003).

Abstracts

Case Reports

    A) ROUTE OF EXPOSURE
    1) ORAL: A three-year-old child developed status epilepticus unresponsive to repeated doses of diazepam, phenytoin (20 mg/kg), and phenobarbital (30 mg/kg). The mother associated this seizure activity and a previous similar episode with finding the child chewing on clumps of plasticized cyclonite explosive brought into the home from her workplace by adhering to her boots and clothing. Cyclonite concentrations in serum, stool, urine, and cerebral spinal fluid confirmed this observation (Woody et al, 1986).
    2) ORAL: A 19-year-old male developed frontal headache and seizures 4 hours after deliberate ingestion of a "piece" of plastic explosive containing cyclonite. A progressively disseminating petechial rash began immediately following the first seizure. A second seizure occurred, followed by spontaneous uneventful recovery (Goldberg et al, 1992).

Range Of Toxicity

Summary

    A) Most exposures to cyclonite have been in industrial or military settings. One adult worker who intentionally ingested 1 tablespoonful of cyclonite developed severe muscle spasms, but no seizures or CNS depression.
    B) Five adults ingested various amounts of cyclonite which ranged from 37 to 250 mg/kg; all made a complete recovery. Based on limited human exposure data, serum cyclonite levels appear to correlate with clinical presentation.

Minimum Lethal Exposure

    A) The minimum lethal human dose to this agent has not been delineated.
    B) ANIMAL DATA
    1) The toxicity of cyclonite is dependent on the exposure route and the chemical's granulation. The LD50 of a coarse granular cyclonite is three times higher than that of a fine powder at 100 mg/kg mixed in a solution or slurry (Bingham et al, 2001).
    2) An oral dose of 100 mg/kg or greater resulted in rat mortality (Bingham et al, 2001).
    3) Eight rats died after an oral exposure of cyclonite in an isotonic saline slurry at 20 mg/kg/day between days 42 and 77 (EPA, 1990).
    4) Seven female dogs were fed a diet of cyclonite at 50 mg/kg/day (molded into a moistened pellet) for 6 days/6 weeks. One died at the end of the fifth week from excessive congested areas on the walls of the small intestines (ACGIH, 1991; Bingham et al, 2001) EPA, 1990).
    5) Rats ingesting repeated doses of cyclonite at 25, 50, 100 mg/kg displayed hyperirritability, convulsions, and mortality in 40%, 60%, and 87% of the animals, respectively (ACGIH, 1991).

Maximum Tolerated Exposure

    A) HUMAN DATA
    1) Most exposures to cyclonite have been in industrial settings. One adult worker who intentionally ingested 1 tablespoonful of cyclonite developed severe muscle spasms, but no seizures or CNS depression (Kaplan et al, 1965).
    2) Five adults were inadvertently exposed to cyclonite contaminated food during military training and developed seizures, rhabdomyolysis, hypokalemia, methemoglobinemia, hyperglycemia and metabolic acidosis. Plasma levels ranged from 37 to 250 mg/kg. Serum levels appeared to correlate with clinical presentation. All patients made a complete recovery (Kucukardali et al, 2003).
    3) Ingestion of a "marble-sized" piece of C4 has been reported to cause seizures (Hollander & Colbach, 1969). C-4 was the name of a plastic explosive used by the military in Vietnam. It was a malleable solid that was used as a cooking fuel when other sources were unavailable and also ingested to produce an ethanol-like state of intoxication. The constituents of this product included cyclonite 91%, polyisobutylene 2.1%, motor oil 1.6%, and di-(2 ethylhexyl) sebacate 5.3% (Stone et al, 1969).
    4) CASE REPORT - Serum levels were obtained in a three-year-old child found chewing on clumps of plasticized cyclonite. Using pharmacokinetic curve fitting and back extrapolation, the ingested dose was estimated to be 84.82 mg/kg (1.23 grams) (Woody et al, 1986).
    5) CASE REPORT - Seizures were reported in two young men who ingested 25 grams each, and in one man who ingested 180 grams. All survived with no sequelae (Stone et al, 1969).
    6) CASE REPORT - Seizures were reported in 18 men who had used C4 as a cooking fuel. Small amounts adhering to the knife used to cut the fuel may have been ingested, but it is likely that the major exposure was by inhalation of the fumes (Ketel & Hughes, 1972).
    7) CASE REPORT - Two generalized seizures followed by an uneventful recovery were reported in a 19-year-old male who ingested a "piece" of cyclonite-containing plastic explosive (Goldberg et al, 1992).
    B) ANIMAL DATA
    1) Spontaneous seizures were induced in rats, with a peak at 2 hours, after administration of as little as 10 mg/kg. Audiogenic seizures could not be elicited until 8-16 hours after ingestion (Burdette et al, 1988).
    2) Rats administered doses of cyclonite experienced spontaneous seizures at doses as low as 12.5 mg/kg (Hathaway et al, 1996).
    3) Rats administered oral doses of cyclonite have the following lowest observed adverse effect level (LOAEL) based on specific criteria (EPA, 1990):
    a) LOAEL
    1) (ORAL) RAT, Male: 1.5, 8.0, 40.0 mg/kg/day for 2Y was 1.5 mg/kg/day - based on prostate inflammation
    2) (ORAL) RAT, Male and Female: 0, 40, 60, 80 mg/kg/day for 2W followed by 0, 80, 160, or 320 mg/kg/day for 11W was 160 mg/kg/day - based on anemia in the males
    3) (ORAL) RAT, Male and Female: 0, 10, 14, 20, 28, or 40 mg/kg/day for 13W was 28 mg/kg/day - based on anemia
    4) (ORAL) RAT: 0, 10, 30, 100, 300, or 600 mg/kg/day for 13W was 100 mg/kg/day - based on the liver weight
    5) (ORAL) RAT: 0, 15, 50, or 100 mg/kg/day for 10W was 50 mg/kg/day - based on the CNS effects
    6) (ORAL) RAT: 0, 15, 25, or 50 mg/kg/day for 12W was 25 mg/kg/day - based on the mortality and body weight loss
    7) (ORAL) RAT, Male and Female: 0, 1.0, 3.1, or 10 mg/kg/day for 2Y was 3.1 mg/kg/day - based on decreased body weight in females
    8) (ORAL) RAT, Male and Female: 0, 1.5, 7.0, 35.0 or 100 mg/kg/day for 2Y was 35 mg/kg/day - based on testicular degeneration in males
    9) (ORAL) MONKEY: 0, 0.1, 1, or 10 mg/kg in a 1% aqueous solution of methylcellulose for 90D was 10 mg/kg/day - based on CNS effects
    C) LACK OF EFFECT
    1) Tests evaluating chronic oral exposures documented no observed effects at 0.3 mg/kg per day (EPA, 1990).
    2) No oncogenic effects were noted in male and female rats fed doses of RDX at 1.0, 3.1 or 10 mg/kg/day for 2 years. Another 2 year study on rats also confirmed this information; rats were fed 0.3, 1.5, 8.0, or 40.0 mg/kg/day (EPA, 1990).
    3) No signs of toxicity were observed in dogs fed 0, 0.1, 1, or 10 mg/kg/day for 3 months (EPA, 1990).
    4) Rats ingesting 15 mg/kg for 10 weeks had no observed effects (ACGIH, 1991).
    5) Rats administered oral doses of cyclonite have the following no-observed adverse effect level (NOAEL) based on specific criteria:
    a) NOAEL
    1) (ORAL) RAT: 10 mg/kg/day (Bingham et al, 2001)
    2) (ORAL) RAT, Male: 1.5, 8.0, 40.0 mg/kg/day for 2Y was 0.3 mg/kg/day -- based on prostate inflammation (EPA, 1990)
    3) (ORAL) RAT, Male and Female: 0, 40, 60, 80 mg/kg/day for 2W followed by 0, 80, 160, or 320 mg/kg/day for 11W was 80 mg/kg/day -- based on anemia in the males (EPA, 1990)
    4) (ORAL) RAT, Male and Female: 0, 10, 14, 20, 28, or 40 mg/kg/day for 13W was 20 mg/kg/day -- based on anemia (EPA, 1990)
    5) (ORAL) RAT: 0, 10, 30, 100, 300, or 600 mg/kg/day for 13W was 30 mg/kg/day -- based on the liver weight (EPA, 1990)
    6) (ORAL) RAT: 0, 15, 50, or 100 mg/kg/day for 10W was 15 mg/kg/day -- based on the CNS effects (EPA, 1990)
    7) (ORAL) RAT: 0, 15, 25, or 50 mg/kg/day for 12W was 15 mg/kg/day -- based on the mortality and body weight loss (EPA, 1990)
    8) (ORAL) RAT, Male and Female: 0, 1.0, 3.1, or 10 mg/kg/day for 2Y was 1 mg/kg/day -- based on decreased body weight in females (EPA, 1990)
    9) (ORAL) RAT, Male and Female: 0, 1.5, 7.0, 35.0 or 100 mg/kg/day for 2Y was 7.0 mg/kg/day -- based on testicular degeneration in males (EPA, 1990)
    10) (ORAL) MONKEY: 0, 0.1, 1, or 10 mg/kg in a 1% aqueous solution of methylcellulose for 90D was 1 mg/kg/day - based on CNS effects (EPA, 1990)

Workplace Standards

    A) ACGIH TLV Values for CAS121-82-4 (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) Cyclonite
    a) TLV:
    1) TLV-TWA: 0.5 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: 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) 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): Liver dam
    d) Molecular Weight: 222.26
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS121-82-4 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Cyclonite
    2) REL:
    a) TWA: 1.5 mg/m(3)
    b) STEL: 3 mg/m(3)
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: [skin]
    1) Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.
    f) Note(s):
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS121-82-4 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Cyclonite
    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) EPA (U.S. Environmental Protection Agency, 2011): C ; Listed as: Hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX)
    a) C : Possible human carcinogen.
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Cyclonite
    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 CAS121-82-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: ACGIH, 1991 Bingham et al, 2001 HSDB, 2002 Kaplan et al, 1965 RTECS, 2002
    1) LD50- (ORAL)MOUSE:
    a) 59 mg/kg -- convulsions or affected seizure threshold; dyspnea
    b) 59-97 mg/kg (Bingham et al, 2001)
    c) 500 mg/kg (Kaplan et al, 1965)
    2) LD50- (ORAL)RAT:
    a) 100 mg/kg -- convulsions or affected seizure threshold
    b) 200 mg/kg - (4% solution) nonfasting (ACGIH, 1991; HSDB, 2002; ITI, 1995; Kaplan et al, 1965)
    c) 71-300 mg/kg (Bingham et al, 2001)
    d) 50-100 mg/kg -- fasting (Kaplan et al, 1965)

Physicochemical

Physical Characteristics

    A) Cyclonite may exist as a white crystalline powder or as colorless crystals. It is a combustible solid and is considered a powerful high explosive. Orthorhombic crystals are formed when it comes in contact with acetone (ACGIH, 1991; Budavari, 2000; Hathaway et al, 1996; NIOSH , 2002).

Molecular Weight

    A) 222.12

Animal Toxicology

Clinical Effects

    11.1.3) CANINE/DOG
    A) Generalized seizures were reported 8 to 9 hours after ingestion of cyclonite by a German shepherd dog (Berry et al, 1983).

References

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