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HEXACHLOROCYCLOPENTADIENE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Hexachlorocyclopentadiene, also called C-56, is a chlorinated cyclic hydrocarbon.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C5-Cl6

Available Forms Sources

    A) FORMS
    1) Hexachlorocyclopentadiene is available in a technical grade (Lewis, 1997a).
    a) The technical grade may contain impurities, such as hexachlorobenzene and octachlorocyclopentene (HSDB, 2001).
    B) SOURCES
    1) Hexachlorocyclopentadiene occurs as an impurity in technical grade chlordane (Hayes & Laws, 1991).
    C) USES
    1) This compound is used as a chemical intermediate in the manufacture of chlorinated pesticides, fungicides, resins, dyes, flame retardants, shock proof plastics, esters, acids, ketones, fluorocarbons, and pharmaceuticals. It may be present in the end products in concentrations of 1% or less (ACGIH, 1992; Clayton & Clayton, 1982a; HSDB, 2001; Lewis, 1997a; Rand et al, 1982).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Hexachlorocyclopentadiene (C56) is highly irritating. Exposure effects may include cough, dyspnea, chest discomfort, headache, dizziness and burns. Proteinuria and elevated serum liver enzymes may occur. Pulmonary damage may range from bronchitis, chemical pneumonitis, bronchiolitis, and pulmonary edema to respiratory failure.
    B) Inhalation may cause coughing, difficult breathing, cyanosis, sneezing and salivation. Inhalation may be fatal because of bronchial spasm, inflammation, and edema of the larynx and bronchi. Degenerative changes of the brain, heart, liver (elevations in liver enzymes), adrenals, and kidneys have been reported.
    C) The compound is corrosive to tissues. Dermal and/or ocular contact ranges from irritation of the eyes, throat, nose and skin to dermatitis and burns.
    D) Other signs and symptoms of poisoning include: nausea, vomiting, hematemesis, abdominal cramps, diarrhea, nervousness, oliguria, proteinuria, hematuria, jaundice, hepatomegaly, optic neuritis, unconsciousness, coma, ventricular fibrillation.
    E) In experimental animals, the lung is the primary target organ for C56 toxicity even with oral administration. Degenerative changes were observed in multiple organ systems. Animal studies demonstrated the development of pulmonary edema, pulmonary hemorrhages, and necrotizing bronchitis and bronchiolitis. Diffuse degenerative changes of the central nervous system, heart, liver, adrenals, and kidneys have been observed. Even at the lowest exposure concentration (0.15 ppm) degenerative changes were observed in the liver and kidney.
    F) In human studies: workers noted eye and throat irritation, cough, chest discomfort and headache. Medical examination showed proteinuria and elevated serum lactic dehydrogenase (LDH) levels. Reported human cases have generally been mild.
    G) Hexachlorocyclopentadiene was negative in the Salmonella assay and the sex-linked recessive lethal mutation assay in Drosophila. This compound caused induction of chromosomal aberrations and sister chromatid exchange in cultured Chinese hamster ovary (CHO) cells.
    0.2.4) HEENT
    A) CONJUNCTIVITIS - Eye irritation is common. Irritation of the throat may be seen.
    0.2.5) CARDIOVASCULAR
    A) Degenerative cardiac changes have occurred in experimental animals.
    0.2.6) RESPIRATORY
    A) The major target organ for C56 toxicity is the lung, regardless of the exposure route. Cough, dyspnea, and chest discomfort have been reported in exposed humans. Experimental animals have developed pulmonary edema, pulmonary hemorrhages, and necrotizing bronchitis and bronchiolitis.
    0.2.7) NEUROLOGIC
    A) Headache is common. Degenerative CNS changes have been seen in experimental animals.
    0.2.8) GASTROINTESTINAL
    A) Nausea may occur.
    0.2.9) HEPATIC
    A) Exposed workers have developed reversible, subclinical elevations of serum liver function tests.
    0.2.10) GENITOURINARY
    A) Exposed workers have developed reversible proteinuria.
    0.2.14) DERMATOLOGIC
    A) Skin irritation may occur from direct contact or vapor exposure. Direct skin contact with the liquid can cause dermal blistering and burns.
    0.2.16) ENDOCRINE
    A) Degenerative adrenal gland changes have been observed in experimental animals.
    0.2.20) REPRODUCTIVE
    A) Hexachlorocyclopentadiene has been shown NOT to be teratogenic in mice and rabbits. Hexachlorocyclopentadiene was significantly toxic to rabbit dams, but showed little evidence of embryotoxicity.
    0.2.21) CARCINOGENICITY
    A) Several retrospective human mortality studies are inadequate because of lack of exposure information.

Laboratory Monitoring

    A) C56 can be measured in air with gas chromatography.
    B) Baseline arterial blood gases, chest x-ray, liver and renal function tests, and urinalysis should be obtained in patients with significant exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Because of potential CNS depression, do NOT induce emesis.
    B) Significant esophageal or gastrointestinal tract irritation or burns may occur following ingestion. The possible benefit of early removal of some ingested material by cautious gastric lavage must be weighed against potential complications of bleeding or perforation.
    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) 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.
    E) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    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.
    B) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    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).
    2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

Range Of Toxicity

    A) Minimum lethal and maximum tolerated human exposures have not been well established.

Clinical Effects

Summary Of Exposure

    A) Hexachlorocyclopentadiene (C56) is highly irritating. Exposure effects may include cough, dyspnea, chest discomfort, headache, dizziness and burns. Proteinuria and elevated serum liver enzymes may occur. Pulmonary damage may range from bronchitis, chemical pneumonitis, bronchiolitis, and pulmonary edema to respiratory failure.
    B) Inhalation may cause coughing, difficult breathing, cyanosis, sneezing and salivation. Inhalation may be fatal because of bronchial spasm, inflammation, and edema of the larynx and bronchi. Degenerative changes of the brain, heart, liver (elevations in liver enzymes), adrenals, and kidneys have been reported.
    C) The compound is corrosive to tissues. Dermal and/or ocular contact ranges from irritation of the eyes, throat, nose and skin to dermatitis and burns.
    D) Other signs and symptoms of poisoning include: nausea, vomiting, hematemesis, abdominal cramps, diarrhea, nervousness, oliguria, proteinuria, hematuria, jaundice, hepatomegaly, optic neuritis, unconsciousness, coma, ventricular fibrillation.
    E) In experimental animals, the lung is the primary target organ for C56 toxicity even with oral administration. Degenerative changes were observed in multiple organ systems. Animal studies demonstrated the development of pulmonary edema, pulmonary hemorrhages, and necrotizing bronchitis and bronchiolitis. Diffuse degenerative changes of the central nervous system, heart, liver, adrenals, and kidneys have been observed. Even at the lowest exposure concentration (0.15 ppm) degenerative changes were observed in the liver and kidney.
    F) In human studies: workers noted eye and throat irritation, cough, chest discomfort and headache. Medical examination showed proteinuria and elevated serum lactic dehydrogenase (LDH) levels. Reported human cases have generally been mild.
    G) Hexachlorocyclopentadiene was negative in the Salmonella assay and the sex-linked recessive lethal mutation assay in Drosophila. This compound caused induction of chromosomal aberrations and sister chromatid exchange in cultured Chinese hamster ovary (CHO) cells.

Heent

    3.4.1) SUMMARY
    A) CONJUNCTIVITIS - Eye irritation is common. Irritation of the throat may be seen.
    3.4.3) EYES
    A) CONJUNCTIVITIS - Eye irritation and excessive lacrimation occur with vapor exposure (Kominsky et al, 1980; Hathaway et al, 1991).
    B) Hexachlorocyclopentadiene induced moderate to severe eye irritation in the rabbit in the Standard Draize Test (RTECS , 1996).
    3.4.6) THROAT
    A) MUCOSAL IRRITATION - Irritation of the throat has been described in workers exposed to hexachlorocyclopentadiene vapors (Kominsky et al, 1980).

Cardiovascular

    3.5.1) SUMMARY
    A) Degenerative cardiac changes have occurred in experimental animals.
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) DEGENERATIVE CHANGES - Diffuse degenerative changes have been described in the hearts of experimental animals exposed by inhalation to hexachlorocyclopentadiene (ACGIH, 1992). There are no human case reports of cardiac toxicity.

Respiratory

    3.6.1) SUMMARY
    A) The major target organ for C56 toxicity is the lung, regardless of the exposure route. Cough, dyspnea, and chest discomfort have been reported in exposed humans. Experimental animals have developed pulmonary edema, pulmonary hemorrhages, and necrotizing bronchitis and bronchiolitis.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) The major target organ for hexachlorocyclopentadiene toxicity in both experimental animals and humans is the lung (Clayton & Clayton, 1982; Lawrence & Dorough, 1982). Cough, chest discomfort, and dyspnea have been reported in workers exposed by inhalation (Kominsky et al, 1980).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Necrotizing bronchitis and bronchiolitis, pulmonary edema, and pulmonary hemorrhages have been described in experimental animals, even following oral administration (ACGIH, 1992; Lawrence & Dorough, 1982; Rand et al, 1982).

Neurologic

    3.7.1) SUMMARY
    A) Headache is common. Degenerative CNS changes have been seen in experimental animals.
    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) Headache and fatigue are commonly described following C56 exposure (Kominsky et al, 1980).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) DEGENERATIVE CHANGES - Diffuse central nervous system degenerative changes have been described in exposed experimental animals that died (ACGIH, 1992). There are no human case reports of serious central nervous system toxicity from hexachlorocyclopentadiene.

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea may occur.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA
    1) Workers exposed to vapors have complained of nausea (Kominsky et al, 1980).

Hepatic

    3.9.1) SUMMARY
    A) Exposed workers have developed reversible, subclinical elevations of serum liver function tests.
    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) Certain workers exposed to hexachlorocyclopentadiene vapors during a cleanup operation from a spill into a municipal wastewater treatment facility were noted to have reversible, subclinical elevations of liver function tests (Kominsky et al, 1980; Morse et al, 1979).
    2) No elevations in liver enzymes were seen in a group of 35 workers with mixed exposure to levels of hexachlorocylcopentadiene exceeding the MAK (Boogaard et al, 1993).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Experimental animals have had mild hepatotoxicity even with exposures to low concentrations of 0.15 ppm (Clayton & Clayton, 1982; ACGIH, 1992; Treon et al, 1955).

Genitourinary

    3.10.1) SUMMARY
    A) Exposed workers have developed reversible proteinuria.
    3.10.2) CLINICAL EFFECTS
    A) ALBUMINURIA
    1) Workers exposed to hexachlorocyclopentadiene vapors have developed reversible proteinuria (Clayton & Clayton, 1982). In one exposed group, albuminuria did not correspond with duration of employment (Boogaard et al, 1993).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Renal tubular necrosis, as well as diffuse degenerative changes in the kidneys, has been described in exposed experimental animals (Clayton & Clayton, 1982; ACGIH, 1992; Treon et al, 1955; Abdo et al, 1984). Female rats and mice were more sensitive than males (Abdo et al, 1984).

Dermatologic

    3.14.1) SUMMARY
    A) Skin irritation may occur from direct contact or vapor exposure. Direct skin contact with the liquid can cause dermal blistering and burns.
    3.14.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) Skin irritation has been noted with direct hexachlorocyclopentadiene contact and with dermal exposure to vapors (Clayton & Clayton, 1982; Kominsky et al, 1980; Hathaway et al, 1991). The liquid is extremely irritating and can cause blisters and burns (CHRIS, 1996).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Hexachlorocyclopentadiene induced severe skin irritation in the rabbit, mild skin irritation in the guinea pig, and severe skin irritation in the monkey in the Standard Draize Test (RTECS , 1996).

Endocrine

    3.16.1) SUMMARY
    A) Degenerative adrenal gland changes have been observed in experimental animals.
    3.16.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) DEGENERATIVE CHANGES - Diffuse degenerative changes in the adrenal glands have been reported in experimental animals (ACGIH, 1992). There are no human case reports of adrenal toxicity from hexachlorocyclopentadiene exposure.

Reproductive

    3.20.1) SUMMARY
    A) Hexachlorocyclopentadiene has been shown NOT to be teratogenic in mice and rabbits. Hexachlorocyclopentadiene was significantly toxic to rabbit dams, but showed little evidence of embryotoxicity.
    3.20.2) TERATOGENICITY
    A) LACK OF EFFECT
    1) Hexachlorocyclopentadiene has been shown NOT to be teratogenic in mice and rabbits (Murray et al, 1980).
    2) A dose of 45 mg/kg was not toxic to mice before or after birth, and the F1 generation reproduced normally (Chernoff & Kavlock, 1982; Gray & Kavlock, 1984).
    3.20.3) EFFECTS IN PREGNANCY
    A) PREGNANCY DISORDER
    1) MATERNAL TOXICITY - Hexachlorocyclopentadiene was significantly toxic to rabbit dams administered 75 mg/kg/day, but showed little evidence of embryotoxicity (Murray et al, 1980).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS77-47-4 (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
    3.21.2) SUMMARY/HUMAN
    A) Several retrospective human mortality studies are inadequate because of lack of exposure information.
    3.21.3) HUMAN STUDIES
    A) HUMANS
    1) Several retrospective human mortality studies are inadequate because of lack of exposure information.
    2) In one retrospective mortality study of 783 workers at Velsicol Chemical Corporation who used hexachlorocyclopentadiene as an intermediate in the manufacture of chlorinated hydrocarbon insecticides for at least 3 months between 1946 and 1979, no excess deaths were seen in relation to job class or individual chemical (Shindell & Associates, 1980).
    3) A nonsignificant increase in deaths from lung cancer was seen in a group of 1115 Velsicol workers employed for at least 3 months between 1952 and 1979 (Shindell & Associates, 1981).
    4) A nonsignificant increase in lung cancer deaths occurred in 1403 Velsicol workers employed from 1946 to 1976, but there was no relationship with duration of exposure or latency (Wang & MacMahon, 1979).
    5) Deaths from all cancers were fewer than expected in a group of 341 workers at Hooker Chemical Corporation employed between 1953 and 1978 (Buncher CR, Moomaw C & Sirkeski B, 1980).
    3.21.4) ANIMAL STUDIES
    A) LACK OF EFFECT
    1) LACK OF EFFECT
    a) ANIMAL STUDIES
    1) There was no evidence of carcinogenicity in rats and mice exposed by the inhalation route (NTP, 1994).

Genotoxicity

    A) Hexachlorocyclopentadiene was not genotoxic in several test systems.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) C56 can be measured in air with gas chromatography.
    B) Baseline arterial blood gases, chest x-ray, liver and renal function tests, and urinalysis should be obtained in patients with significant exposure.
    4.1.2) SERUM/BLOOD
    A) ACID/BASE
    1) Baseline arterial blood gases should be obtained in victims with significant exposure or respiratory irritation.
    B) BLOOD/SERUM CHEMISTRY
    1) Baseline liver and renal function tests should be obtained in victims with significant exposure.
    4.1.3) URINE
    A) URINALYSIS
    1) Baseline urinalysis should be obtained in victims with significant exposure.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Baseline chest x-ray should be obtained in victims with significant exposure or respiratory irritation.

Methods

    A) CHROMATOGRAPHY
    1) C56 can be measured in air by gas chromatography (Kominsky et al, 1980).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) C56 can be measured in air with gas chromatography.
    B) Baseline arterial blood gases, chest x-ray, liver and renal function tests, and urinalysis should be obtained in patients with significant exposure.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) OVERVIEW
    1) Remove victims from the toxic environment and supply supplemental humidified oxygen with assisted ventilation as required. Exposed eyes and skin should be flushed copiously with water. Patients should be carefully observed for any signs of central nervous system involvement.
    B) INHALATION EXPOSURE
    1) 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.
    2) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    C) DERMAL EXPOSURE
    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).
    2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    D) EYE EXPOSURE
    1) 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.
    E) ORAL EXPOSURE
    1) Because of potential CNS depression, do not induce emesis.
    2) 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.
    a) 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.
    3) 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.
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Because of potential CNS depression, do NOT induce emesis.
    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/CATHARTIC
    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) MONITORING OF PATIENT
    1) Obtain baseline chest x-ray and arterial blood gases as pulmonary injury may occur with oral ingestion.
    2) Obtain baseline liver and renal function tests and urinalysis.
    B) OXYGEN
    1) If signs of pulmonary toxicity are noted, supplemental humidified oxygen with assisted ventilation as required should be supplied.
    C) SUPPORT
    1) Should hepatic or renal failure occur, supportive treatment should be administered.
    D) OBSERVATION REGIMES
    1) Patients should be observed carefully for any signs of central nervous system involvement.
    E) IRRITATION SYMPTOM
    1) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.

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.
    6.7.2) TREATMENT
    A) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    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).

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).

Abstracts

Case Reports

    A) ROUTE OF EXPOSURE
    1) INHALATION
    a) Kominsky et al (1980) reported results from evaluation of a group of workers at a wastewater treatment facility who were exposed to C56 vapors from a spill that contaminated a municipal sewer.
    1) Workers initially reported an objectionable odor, headache, and tracheobronchial irritation. During cleanup procedures, airborne levels of C56 reached from 27 to 1920 times the recommended threshold limit value.
    2) Workers complained (in decreasing frequency) of eye irritation, headache, chest discomfort, fatigue, sore throat, cough, nausea, and skin irritation. Transient confusion and memory loss were reported by a few workers. Subclinical elevations of liver function tests were noted in 18 of 97 of these cleanup workers.
    3) These signs and symptoms slowly declined over six months following cessation of exposure.

Range Of Toxicity

Summary

    A) Minimum lethal and maximum tolerated human exposures have not been well established.

Minimum Lethal Exposure

    A) ACUTE
    1) The probable human lethal dose is 50 to 500 mg/kg, or between 1 teaspoon and 1 ounce for a 150 lb (70 kg) person (EPA, 1985).
    B) ANIMAL DATA
    1) An acute inhalation toxicity study was conducted with groups of male and female rats (5/sex/exposure) receiving whole body exposure to hexachlorocyclopentadiene in a dynamic air flow chamber (Huntingdon Research Center, 1987).
    2) Groups of animals received a single exposure to the test substance at mean analytical concentrations of 0, 18.8, 20.5, 37.1 or 38.9 micrograms per liter resulting in the following mortality data (number animals dead/number animals tested): 0/10, 2/10, 2/10, 6/10 and 6/10, respectively. Most of the rats died within the first 14 days of the 28 day observation period (Huntingdon Research Center, 1987).
    3) The LC50 of hexachlorocyclopentadiene was calculated to be 41.2 micrograms per liter 14 days after exposure, and 32.7 micrograms per liter 28 days after exposure (Huntingdon Research Center, 1987).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to this agent has not been delineated.
    B) OCCUPATIONAL
    1) In March 1977, a large volume of industrial chemical hexachlorocyclopentadiene was dumped into a municipal sewage system in Kentucky, causing immediate tracheobronchial irritation among sewage treatment plant workers. The contaminant was dispersed in about 6 tons of fuel-oil (Kominsky & Wisseman, 1978; Morse et al, 1979).
    2) AIR SAMPLES obtained 4 days after initial worker exposure showed hexachlorocyclopentadiene concentrations between 270 and 970 parts per billion (ppb); the 8-hour time weighted average limit recommended by the American Conference of Governmental Industrial Hygienists was 10 ppb (Kominsky & Wisseman, 1978; Morse et al, 1979).
    3) A study of the HEALTH EFFECTS of exposure to this compound in 145 of the sewage treatment plant workers found that 59% had noted eye irritation, 45% had headaches, and 27% had throat irritation. Skin irritation, cough, nausea, and abdominal cramps were also reported. Symptoms occurred throughout the plant; however, highest attack rates occurred in primary sewage treatment areas (Kominsky & Wisseman, 1978; Morse et al, 1979).
    4) As long as 6 weeks following exposure, 15-46% of the workers still reported fatigue, respiratory tract irritation, headaches, and eye irritation (Kominsky & Wisseman, 1978; Morse et al, 1979).
    5) Maximum time-concentrations by volume in air survived (Clayton & Clayton, 1981) -
    a) GUINEA PIGS -
    MAXIMUM TIME CONCENTRATIONS
    0.25 h20.2 ppm
    1 h7.2 ppm
    3.5 h3.1 ppm
    7 h1.5 ppm

    b) RATS -
    MAXIMUM TIME CONCENTRATIONS
    0.25 h20.2 ppm
    0.5 h7.2 ppm
    1 h3.1 ppm
    7 h0.33 ppm

    c) Guinea pigs, rabbits, and rats were subjected to 150 7-hour exposures over 216 days. They survived at 0.15 ppm by volume in air, but mild liver and kidney damage were noted (Clayton & Clayton, 1981).
    d) A dose of 500 mg/4H (Standard Draize Test-skin route) caused severe skin irritation in test rabbits (RTECS , 2001).
    e) A dose of 20 mg (Standard Draize Test-skin route) caused mild skin irritation in test guinea pigs (Lewis, 2000; RTECS , 2001).
    f) A dose of 10 mg (Standard Draize Test-skin route) caused severe skin irritation in test monkeys (Lewis, 2000; RTECS , 2001).
    g) A dose of 20 mg/24H (Standard Draize Test-eye route) caused moderate eye irritation in test rabbits (Lewis, 2000; RTECS , 2001).
    h) A dose of 100 mg/5min (Standard Draize Test-eye route) caused severe eye irritation in test rabbits (Lewis, 2000; RTECS , 2001).
    i) The threshold for toxic effects in rats was 0.11-0.5 ppm in a 14-day range-finding study (Rand et al, 1982).
    j) The acceptable daily intake for a 70-kg adult is 0.00462 mg (EPA, 1984).

Workplace Standards

    A) ACGIH TLV Values for CAS77-47-4 (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) Hexachlorocyclopentadiene
    a) TLV:
    1) TLV-TWA: 0.01 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: Not Listed
    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.
    c) TLV Basis - Critical Effect(s): URT irr
    d) Molecular Weight: 272.75
    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 CAS77-47-4 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Hexachlorocyclopentadiene
    2) REL:
    a) TWA: 0.01 ppm (0.1 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

    C) Carcinogenicity Ratings for CAS77-47-4 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Hexachlorocyclopentadiene
    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): E ; Listed as: Hexachlorocyclopentadiene (HCCPD)
    a) E : Evidence of non-carcinogenicity for humans.
    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: Hexachlorocyclopentadiene
    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 CAS77-47-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: Clayton & Clayton, 1994 HSDB, 2001 Lewis, 2000 OHM/TADS, 2001 RTECS, 2001
    1) LD50- (ORAL)MOUSE:
    a) 505 mg/kg
    2) LD50- (ORAL)RAT:
    a) 1300 mg/kg (Lewis, 2000)
    b) 113 mg/kg (OHM/TADS, 2001)
    c) 315 mg/kg
    d) 4g/kg (Clayton & Clayton, 1994)
    e) 500 mg/kg (OHM/TADS, 2001)
    f) Albino, 300-630 mg/kg (HSDB, 2001)
    3) TCLo- (INHALATION)MOUSE:
    a) 340 ppb for 7H/6W-intermittent decreased weight gain or weight loss; chronic pulmonary edema; death
    b) 150 ppb for 6H/13W- intermittent -- respiratory changes; death
    4) TCLo- (INHALATION)RAT:
    a) 500 ppb for 6H/2W-intermittent -- pigmented or necleated red blood cells; weight loss or decreased weight gain; lung weight altered
    b) 100 ppb for 6H/30W-intermittent -- change in erythrocyte count and spleen weight; pigmented or nucleated RBC
    c) 400 ppb for 6H/13W-intermittent -- changes to sense organs and lung weight; trachea and bronchi structural and functional changes

Pharmacology Toxicology

Toxicologic Mechanism

    A) C56 is a potent irritant of the skin, eyes, and mucous membranes, particularly in the respiratory tract (ACGIH, 1992; Clayton & Clayton, 1982).

Physicochemical

Physical Characteristics

    A) Hexachlorocyclopentadiene is a greenish-yellow to amber-colored, dense, oily liquid with a pungent, unpleasant odor (HSDB , 2001; Lewis, 2000; Sittig, 1991).

Molecular Weight

    A) 272.77

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