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ISOBENZAN

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Isobenzan is a chlorinated hydrocarbon pesticide, a cyclodiene compound related to dieldrin, originally developed (1958) in Holland. Production was discontinued in 1965. Isobenzan was never registered for use in the USA (Hayes & Laws, 1991).

Specific Substances

    1) CP 14,957
    2) ENT 25,545-x
    3) Octachloro-hexahydromethanoisobenzofuran
    4) OMS-206
    5) OMS-618
    6) R 6700
    7) SD-4,402
    8) 1,3,4,5,6,7,10,10-Octachloro-endoMethylene-
    9) 4,7,8,9-Tetrahydrophthalan
    10) 1,3,4,5,6,7,8,8-Octachloro-2-Oxa-3a,4,7,7a-
    11) Tetrahydro-4,7-Methanoindene
    12) CAS 279-78-9
    1.2.1) MOLECULAR FORMULA
    1) C9-H4-Cl8-O

Available Forms Sources

    A) FORMS
    1) Isobenzan is a whitish to light-brown crystalline powder with a "chemical" odor (HSDB , 2001; Hayes & Laws, 1991).
    2) Isobenzan is a chlorinated hydrocarbon pesticide originally developed (1958) in Holland. Production was discontinued in 1965. It was supplied in the form of emulsifiable concentrate, dust, and granules (Hayes & Laws, 1991).
    3) Isobenzan was never registered for use in the USA (Hayes & Laws, 1991).
    B) USES
    1) Isobenzan is a chlorinated hydrocarbon insecticide (Budavari, 1996).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) There has been limited poisoning experience with this agent. The primary symptoms involve the CNS, with seizures, headache, dizziness, irritability, and paresthesias. Solvent toxicity should also be considered, as this compound is not water soluble and would be formulated with an organic solvent.
    0.2.5) CARDIOVASCULAR
    A) ECG changes have occurred in isobenzan exposures.
    0.2.6) RESPIRATORY
    A) Although not reported, pulmonary aspiration and lipoid pneumonitis may occur if a petroleum distillate-containing formulation is ingested.
    0.2.7) NEUROLOGIC
    A) Seizures and tremors have occurred in both poisoned experimental animals and humans. Other CNS effects include headache, dizziness, drowsiness, irritability, and paresthesias of the legs.
    0.2.8) GASTROINTESTINAL
    A) Vomiting may occur, especially if a petroleum distillate formulation is ingested.
    0.2.9) HEPATIC
    A) Hepatomegaly and necrosis have not been reported with isobenzan but have been caused by similar organochlorine pesticides.
    0.2.14) DERMATOLOGIC
    A) Isobenzan is not irritating to the skin.
    0.2.20) REPRODUCTIVE
    A) A dose of 1 ppm, administered daily for 120 days, failed to produce increased developmental abnormalities in mice. 2.5 ppm for 120 days was lethal to 80 percent of the test animals in this species.

Laboratory Monitoring

    A) Isobenzan may be measured in serum using gas-liquid chromatography. Interpretation of the resultant values is difficult due to limited human poisoning experience.
    B) Monitor liver function tests in patients with significant exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Inducing emesis is NOT RECOMMENDED due to potential CNS depression or seizures.
    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) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    D) 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.
    E) Do not give oils by mouth.
    F) Do not administer adrenergic amines, which may further increase myocardial irritability and produce refractory ventricular arrhythmias.
    G) CHOLESTYRAMINE - Oral administration has enhanced excretion of the similar compounds kepone and chlordane by trapping in the enterohepatic circulation.
    H) HEMODIALYSIS - Probably ineffective.
    I) EXCHANGE TRANSFUSION - Probably ineffective.
    J) HEMOPERFUSION - Probably ineffective.
    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) Blood levels less than 0.015 ppm are seldom, if ever, associated with poisoning. Blood levels as high as 0.03 ppm have been reported in patients with and without seizures.
    B) LD50 - dogs: 1.6 mg/kg; cats: 5 mg/kg.

Clinical Effects

Summary Of Exposure

    A) There has been limited poisoning experience with this agent. The primary symptoms involve the CNS, with seizures, headache, dizziness, irritability, and paresthesias. Solvent toxicity should also be considered, as this compound is not water soluble and would be formulated with an organic solvent.

Cardiovascular

    3.5.1) SUMMARY
    A) ECG changes have occurred in isobenzan exposures.
    3.5.2) CLINICAL EFFECTS
    A) ELECTROCARDIOGRAM ABNORMAL
    1) ECG changes have occurred in workers with isobenzan exposure and were observed to recover much more rapidly than neurologic effects when exposure ceased (Jager, 1970).

Respiratory

    3.6.1) SUMMARY
    A) Although not reported, pulmonary aspiration and lipoid pneumonitis may occur if a petroleum distillate-containing formulation is ingested.
    3.6.2) CLINICAL EFFECTS
    A) PNEUMONITIS
    1) Although isobenzan has not been shown to be exceptionally irritating, pulmonary aspiration of the petroleum distillate solvent may cause lipoid pneumonitis.
    B) ACUTE RESPIRATORY INSUFFICIENCY
    1) Respiratory depression has been reported in cases of poisoning with other chlorinated hydrocarbon pesticides (Hayes & Laws, 1991) and has been reported in animal studies (HSDB , 2001).

Neurologic

    3.7.1) SUMMARY
    A) Seizures and tremors have occurred in both poisoned experimental animals and humans. Other CNS effects include headache, dizziness, drowsiness, irritability, and paresthesias of the legs.
    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) Isobenzan is a CNS stimulant, resulting in seizures following absorption of toxic amounts (Tordoir & van Sittert, 1994). Seizures and tremors developed in poisoned rats within 1 hour of exposure to a lethal dose (HSDB , 2001; Hayes & Laws, 1991) and deaths occurred within 20 hours (Worden, 1969). Seizures have also been reported in occupationally exposed human workers (Jager, 1970).
    B) HEADACHE
    1) Headache has been reported in exposed workers (Jager, 1970) and appears to be common (HSDB , 2001).
    C) DIZZINESS
    1) Dizziness has been reported in exposed workers (HSDB , 2001; Jager, 1970).
    D) DROWSY
    1) Drowsiness, but not coma, has been reported in exposed workers (HSDB , 2001; Jager, 1970).
    E) FEELING NERVOUS
    1) Irritability has been reported in exposed workers (HSDB , 2001; Jager, 1970).
    F) PARESTHESIA
    1) Paresthesias of the legs have been reported in exposed workers (HSDB , 2001; Jager, 1970).
    G) ATAXIA
    1) Ataxia and muscle weakness have been reported as a consequence of chlorinated hydrocarbon pesticide toxicity and might occur in isobenzan poisoning (Tordoir & van Sittert, 1994); ataxia has been reported in animal studies (HSDB , 2001).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SEIZURES
    a) At isobenzan blood concentrations from 0.042 to 0.072 ppm, seizures developed in dogs (HSDB , 2001).

Gastrointestinal

    3.8.1) SUMMARY
    A) Vomiting may occur, especially if a petroleum distillate formulation is ingested.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) Vomiting was NOT a prominent sign in one group of exposed factory workers, but may occur, especially if an isobenzan-petroleum distillate formulation is ingested.

Hepatic

    3.9.1) SUMMARY
    A) Hepatomegaly and necrosis have not been reported with isobenzan but have been caused by similar organochlorine pesticides.
    3.9.2) CLINICAL EFFECTS
    A) LARGE LIVER
    1) Hepatomegaly and necrosis have NOT been reported in isobenzan poisoning, but have occurred in poisonings with other organochlorine pesticides.

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) HEMATOLOGY FINDING
    1) Prolonged exposure or massive ingestion of other organochlorines pesticides have resulted in various blood dyscrasias.

Dermatologic

    3.14.1) SUMMARY
    A) Isobenzan is not irritating to the skin.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) LACK OF EFFECT
    a) Isobenzan is NOT irritating to the skin (Worden, 1969).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MYOSITIS
    1) Although not reported in the literature, prolonged and untreated seizures due to isobenzan poisoning could result in muscle damage, including myositis or rhabdomyolysis.

Reproductive

    3.20.1) SUMMARY
    A) A dose of 1 ppm, administered daily for 120 days, failed to produce increased developmental abnormalities in mice. 2.5 ppm for 120 days was lethal to 80 percent of the test animals in this species.
    3.20.2) TERATOGENICITY
    A) DEATH
    1) MICE - A dose of 1 ppm, administered daily for 120 days, failed to produce increased developmental abnormalities in mice. 2.5 ppm for 120 days was lethal to 80 percent of the test animals in this species (Ware & Good, 1967).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS297-78-9 (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
    3.21.4) ANIMAL STUDIES
    A) NEOPLASM
    1) Isobenzan was found to be an equivocal tumorigenic agent in mice by RTECS criteria (RTECS , 2001).
    B) LACK OF EFFECT
    1) Innes et al (1969) administered the maximum tolerated dose in mice for 18 months but failed to increase tumor incidence.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Isobenzan may be measured in serum using gas-liquid chromatography. Interpretation of the resultant values is difficult due to limited human poisoning experience.
    B) Monitor liver function tests in patients with significant exposure.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Although hepatic damage has not specifically been mentioned in isobenzan overdose, patients with significant exposure may require monitoring of liver function tests.

Methods

    A) CHROMATOGRAPHY
    1) Isobenzan, like other organochlorines, may be measured in serum using gas-liquid chromatography.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Isobenzan may be measured in serum using gas-liquid chromatography. Interpretation of the resultant values is difficult due to limited human poisoning experience.
    B) Monitor liver function tests in patients with significant exposure.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED -
    1) Inducing emesis is NOT recommended due to potential for CNS depression or 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) Inducing emesis is NOT RECOMMENDED due to potential CNS depression or seizures.
    B) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    C) 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) 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, 2010; 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).
    B) CONTRAINDICATED TREATMENT
    1) Do NOT give oils by mouth. They tend to increase intestinal absorption of these lipophilic toxicants.
    2) Do NOT administer adrenergic amines, which further increase myocardial irritability and produce refractory ventricular arrhythmias (Dreisbach, 1983; Bryson, 1986).
    C) CHOLESTYRAMINE
    1) Cholestyramine (4 grams every eight hours) accelerated excretion of the similar compounds kepone and chlordane in excessively exposed workers, and probably would have a similar effect on other slowly excreted organochlorines by trapping them in the enterohepatic circulation (Cohn et al, 1978) Garrettson et al, 1984, 1985; (Boylan et al, 1978).
    D) PULMONARY ASPIRATION
    1) Evaluate the patient for pulmonary complications, especially if the ingested product contained a petroleum solvent.
    E) EXPERIMENTAL THERAPY
    1) Peters et al (1982) report that symptoms of chronic exposure to hexachlorobenzene improved following treatment with intravenous and oral edetic acid therapy.

Inhalation Exposure

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

Eye Exposure

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

Dermal Exposure

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

Enhanced Elimination

    A) EXTRACORPOREAL ELIMINATION
    1) HEMODIALYSIS: Has not proven effective.
    2) HEMOPERFUSION: Effectiveness not known.

Range Of Toxicity

Summary

    A) Blood levels less than 0.015 ppm are seldom, if ever, associated with poisoning. Blood levels as high as 0.03 ppm have been reported in patients with and without seizures.
    B) LD50 - dogs: 1.6 mg/kg; cats: 5 mg/kg.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.
    B) CHRONIC
    1) There is a marked species difference in susceptibility to repeated doses of isobenzan.
    2) Rats given 2.5 mg/kg/day for a week died in a week or less. In another experiment, 20 percent of rats who received 30 ppm died, although none died in the group given 17.5 ppm (Worden, 1969).
    3) Mice were much more susceptible; 80 percent of those given 2.5 ppm died within 120 days (Ware & Good, 1967).
    4) Dogs were also more sensitive than rats (Worden, 1969) Brown et al, 1962).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to this agent has not been delineated.
    B) CONCENTRATION LEVEL
    1) TOXIC SERUM/PLASMA/BLOOD CONCENTRATIONS -
    a) HUMANS - Blood levels less than 0.015 ppm are seldom if ever associated with poisoning (Hayes & Laws, 1991). Blood levels as high as 0.03 ppm have been reported in patients with and without seizures.
    b) ANIMALS - Beagle dogs developed seizures at blood levels of 0.042 to 0.072 ppm (HSDB , 2001) Brown et al, 1962).
    C) CHRONIC
    1) Workers employed in an isobenzan production facility for as many as 9 years complained of dizziness, headache, drowsiness, irritability, and paresthesias with slow recovery following exposure cessation (Jager, 1970).
    D) ANIMAL DATA
    1) Ware and Good (1967) fed this polychlorinated insecticide in the diet to mice. A dietary level of 1 ppm had no effect on fertility or litter size.

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL/SUMMARY
    a) Blood levels less than 0.015 parts per million are seldom if ever associated with poisoning (Hayes & Laws, 1991). Blood levels as high as 0.03 parts per million have been reported in patients with and without seizures.
    2) ANIMAL DATA
    a) Beagle dogs developed seizures at blood levels of 0.042 to 0.072 parts per million (Brown et al, 1962).

Workplace Standards

    A) ACGIH TLV Values for CAS297-78-9 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS297-78-9 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS297-78-9 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS297-78-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: Lewis, 1996 RTECS, 2001
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 8170 mcg/kg
    2) LD50- (ORAL)MOUSE:
    a) 8400 mcg/kg
    3) LD50- (INTRAPERITONEAL)RAT:
    a) 3560 mcg/kg LD50 - (IV) RAT: 1800 mcg/kg
    4) LD50- (ORAL)RAT:
    a) 4800 mcg/kg
    5) LD50- (SKIN)RAT:
    a) 5 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) The principal neurotoxic action of these compounds is that of an "axon poison", affecting primarily CNS neurons.
    1) The organochlorines pesticides interfere with the normal flux of Na+ and K+ ions across the axon membrane as nerve impulses pass. This results in irritability, disturbance of mental processes, sensory aberrations, and seizures.
    2) Depression of the medullary respiratory center drive often occurs concurrently, leading to respiratory depression.
    3) Depending on dose, these effects may be fatal or entirely reversible within minutes or hours.
    4) The organochlorine pesticides do not inhibit cholinesterases.

Physicochemical

Physical Characteristics

    A) Crystals from heptane (Budavari, 1996).
    B) ODOR: Mild "chemical" smell (Hayes & Laws, 1991).
    C) COLOR: White to light-brown crystalline powder (HSDB , 2001; Hayes & Laws, 1991)

Ph

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

Molecular Weight

    A) 411.79 (Budavari, 1996)

Animal Toxicology

Range Of Toxicity

    11.3.2) MINIMAL TOXIC DOSE
    A) RODENT
    1) RAT - 0.25 mg/kg/day: No effect level (Worden, 1969)
    2) RAT - 17.5 ppm (0.86 mg/kg/day) given orally for 2 years: Immediate irritability and seizures; No mortality (Worden, 1969)
    3) RAT - 30 ppm (1.5 mg/kg/day) given orally for 2 years: Immediate irritability and seizures; 20% mortality (Worden, 1969)
    4) RAT - 2.5 mg/kg/day given orally: Death within a week (Worden, 1969)
    5) MOUSE - 2.5 ppm (0.3 mg/kg/day): 80 percent fatality within 20 days (Ware & Good, 1967)
    6) MOUSE - 5 ppm: 100 percent mortality within 64 days (Hayes & Laws, 1991)
    7) MOUSE - 10 ppm: 100 percent mortality within 24 days (Hayes & Laws, 1991)
    B) DOG
    1) DOG - 0.025 to 0.08 mg/kg/day: No effect level (Worden, 1969) Brown et al, 1962)
    2) DOG - 0.08 mg/kg/day: No effect level (Brown et al, 1962)
    3) DOG - 0.1 mg/kg/day for 2 years: Slow growth, slight increase in serum alkaline phosphatase, and increases in relative weights of liver, lung, and kidney (Worden, 1969)

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