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CAMPHECHLOR

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Campheclor is a mixture of at least 670 chlorinated camphenes.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C10-H10-Cl8

Available Forms Sources

    A) FORMS
    1) Campheclor is a mixture of at least 670 chlorinated camphenes (Hathaway et al, 1996). The compound is composed of 67-69 percent chlorine (Budavari, 1996; Lewis, 1997).
    2) Campheclor is a mixture of at least 177 C10 polychloro derivatives produced by the chlorination of camphene. The compounds comprising campheclor contain 6-10 chlorine atoms each (Budavari, 1996).
    3) Campheclor was historically available as an emulsifiable concentrate, dustable powder, wettable powder, or oil solution (HSDB , 1999).
    B) USES
    1) The US Environmental Protection Agency has canceled registration of all formulations of campheclor. It is permissible to utilize existing stocks for pineapples in Puerto Rico, bananas in the Virgin Islands, cattle dip, and emergency use on corn, cotton, and small grains (Clayton & Clayton, 1994).
    2) Campheclor was used primarily as an insecticide on cotton and other crops. It is also utilized as a control against livestock pests (Budavari, 1996) Howard, 1991).
    3) Prior to its present status as a Restricted Use Pesticide (RUP), campheclor was used as a piscicide (fish toxicant) in lakes (Howard, 1991).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Camphechlor may be irritating to the eyes, skin, and mucous membranes. Signs and symptoms of exposure may include salivation, nausea, vomiting, asthenia, vertigo, allergic dermatitis, red skin, muscle cramps or spasms, headache, agitation, CNS depression, unconsciousness, tremors, seizures, respiratory tract irritation, bronchopneumonia, pulmonary edema, respiratory failure, and allergic dermatitis.
    B) Liver and kidney injury have been noted in experimental animals.
    0.2.3) VITAL SIGNS
    A) Respirations may decrease, then increase. Cyanosis precedes convulsions. Fever or hypothermia may occur.
    0.2.4) HEENT
    A) Hypersalivation may occur.
    0.2.5) CARDIOVASCULAR
    A) Cardiac dysrhythmias can occur from cardiac sensitization.
    0.2.6) RESPIRATORY
    A) Irritation, dyspnea, reduced gas exchange, chemical pneumonitis, bronchitis, lung inflammation, pulmonary edema, and allergic bronchopneumonia may occur. In the case of camphechlor, cyanosis may precede convulsions because respiration is arrested due to tetanic muscular contractions, then is increased as muscles relax.
    0.2.7) NEUROLOGIC
    A) Sensory disturbances, excitation with myoclonic jerking, convulsions, tremor, ataxia, agitation, nervousness, and amnesia may occur. In the case of camphechlor, cyanosis may precede convulsions because respiration is arrested due to tetanic muscular contractions, then is increased as muscles relax. Permanent damage may occur from acute exposure. Effects on behavior and learning have been reported.
    0.2.8) GASTROINTESTINAL
    A) Nausea or spontaneous vomiting may not exist prior to onset of convulsions in camphechlor poisoning. Diarrhea may occur.
    0.2.9) HEPATIC
    A) Camphechlor is a hepatic enzyme inducer.
    0.2.10) GENITOURINARY
    A) Renal insufficiency occurred in a case of mixed camphechlor exposure.
    0.2.11) ACID-BASE
    A) Severe metabolic acidosis may be a consequence of convulsions and an immediate cause of death.
    0.2.13) HEMATOLOGIC
    A) Aplastic anemia has occurred with camphechlor/lindane mixtures. Various blood dyscrasias including megaloblastic anemia have been reported with organochlorines.
    0.2.14) DERMATOLOGIC
    A) Extensive contact results in dermal irritation. Camphechlor can cause allergic dermatitis.
    0.2.15) MUSCULOSKELETAL
    A) Leg and back spasms, and tetanic muscular contractions of all skeletal muscles, have occurred with camphechlor poisoning.
    0.2.18) PSYCHIATRIC
    A) Alterations in mental function occur as a result of the neurotoxicity of organochlorine insecticides.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no reproductive studies were found for camphechlor in humans.
    B) Camphechlor did not affect reproduction, fertility, or lactation in multi-generation rodent studies. Stillbirths in sows were associated with gestational exposure. Camphechlor inhibited spermatogenesis in rats.
    0.2.21) CARCINOGENICITY
    A) Camphechlor has been carcinogenic in rats and mice, but not in hamsters. There is insufficient evidence to judge its potential carcinogenicity in humans.
    0.2.22) OTHER
    A) Camphechlor can cause systematic effects by any route of exposure. It is relatively rapidly metabolized and excreted.

Laboratory Monitoring

    A) Analytical methods exist for determining levels of camphechlor in blood, urine, and other tissues. These determinations would be useful for confirmation of exposure. There is insufficient evidence to correlate levels in blood or urine with quantitative exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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) 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.
    F) Do not administer adrenergic amines, which may further increase myocardial irritability and produce refractory ventricular arrhythmias.
    G) CHOLESTYRAMINE - Oral administration may enhance the excretion of kepone and chlordane which are trapped 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) If clothing is contaminated remove, and wash skin and hair three times; do an initial soap washing followed by an alcohol washing followed by a soap washing. Leather absorbs pesticides. Hence, leather should not be worn in the presence of pesticides and all contaminated leather should be discarded.

Range Of Toxicity

    A) Camphechlor is considered among the most toxic organochlorine compounds. The estimated lethal dose is 2 to 7 g.

Clinical Effects

Summary Of Exposure

    A) Camphechlor may be irritating to the eyes, skin, and mucous membranes. Signs and symptoms of exposure may include salivation, nausea, vomiting, asthenia, vertigo, allergic dermatitis, red skin, muscle cramps or spasms, headache, agitation, CNS depression, unconsciousness, tremors, seizures, respiratory tract irritation, bronchopneumonia, pulmonary edema, respiratory failure, and allergic dermatitis.
    B) Liver and kidney injury have been noted in experimental animals.

Vital Signs

    3.3.1) SUMMARY
    A) Respirations may decrease, then increase. Cyanosis precedes convulsions. Fever or hypothermia may occur.
    3.3.2) RESPIRATIONS
    A) DEPRESSION - Camphechlor is a respiratory depressant. Respirations decrease at first, because of tetanic muscular contractions. Then, as muscles relax, respirations increase (CHRIS, 1999).
    B) CYANOSIS may precede convulsions in the case of camphechlor poisoning (EPA, 1985).
    3.3.3) TEMPERATURE
    A) FEVER occurred in a fatal case of endrin ingestion. Exposure to camphechlor has caused hyperthermia in experimental animals (Runhaar et al, 1985; HSDB , 1999).
    B) HYPOTHERMIA has occurred in experimental animals poisoned with camphechlor (Hayes & Laws, 1991).
    3.3.4) BLOOD PRESSURE
    A) Recurrent hypotension occurred in a fatal case of endrin ingestion (Runhaar et al, 1985).

Heent

    3.4.1) SUMMARY
    A) Hypersalivation may occur.
    3.4.3) EYES
    A) Exposure can cause eye irritation (Sittig, 1991; HSDB , 1999).
    3.4.6) THROAT
    A) HYPERSALIVATION has been reported with camphechlor poisoning (EPA, 1985) and with other chlorocyclodienes (Shemesh et al, 1988; Runhaar et al, 1985).

Cardiovascular

    3.5.1) SUMMARY
    A) Cardiac dysrhythmias can occur from cardiac sensitization.
    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) High concentrations of organochlorine insecticides may cause cardiac dysrhythmias by increasing myocardial irritability (Morgan, 1993).

Respiratory

    3.6.1) SUMMARY
    A) Irritation, dyspnea, reduced gas exchange, chemical pneumonitis, bronchitis, lung inflammation, pulmonary edema, and allergic bronchopneumonia may occur. In the case of camphechlor, cyanosis may precede convulsions because respiration is arrested due to tetanic muscular contractions, then is increased as muscles relax.
    3.6.2) CLINICAL EFFECTS
    A) CYANOSIS
    1) REDUCED GAS EXCHANGE - Severe convulsions can limit pulmonary gas exchange, and this may be an immediate cause of death (Morgan, 1993). Cyanosis may precede convulsions in the case of camphechlor poisoning (EPA, 1985).
    B) DYSPNEA
    1) Dyspnea can occur suddenly with exertion in the case of camphechlor poisoning (EPA, 1985).
    C) PNEUMONITIS
    1) Aspiration of petroleum distillate solvent is likely to cause a hydrocarbon pneumonitis, which is potentially fatal.
    D) ACUTE RESPIRATORY INSUFFICIENCY
    1) Death from camphechlor overdose is usually from respiratory failure (Lewis, 1996).
    E) ACUTE LUNG INJURY
    1) Congestion and edema were seen in the lungs of four fatal poisonings in children (Clayton & Clayton, 1981).
    F) PNEUMONIA
    1) Heavy exposure to camphechlor spray produced extensive bilateral allergic bronchopneumonia with miliary shadows in two persons. The patients recovered with cortisone treatment (Warraki, 1963).
    G) BRONCHITIS
    1) Bronchitis and lung inflammation have occurred from inhalation of the spray (Sittig, 1991).

Neurologic

    3.7.1) SUMMARY
    A) Sensory disturbances, excitation with myoclonic jerking, convulsions, tremor, ataxia, agitation, nervousness, and amnesia may occur. In the case of camphechlor, cyanosis may precede convulsions because respiration is arrested due to tetanic muscular contractions, then is increased as muscles relax. Permanent damage may occur from acute exposure. Effects on behavior and learning have been reported.
    3.7.2) CLINICAL EFFECTS
    A) PARESTHESIA
    1) Early signs of organochlorine poisoning involve hyperesthesia and paresthesia of the face and extremities, headache, dizziness, and incoordination (Morgan, 1993).
    B) MYOCLONUS
    1) As the severity of the poisoning increases, myoclonic jerking movements appear (Morgan, 1993).
    C) SEIZURE
    1) Generalized tonic-clonic convulsions occur in severe poisonings. Coma and respiratory depression may ensue (Morgan, 1993). Camphechlor is a CNS excitant and convulsant.
    2) Convulsions may appear as an early sign, in the absence of the above symptoms, with the cyclodienes such as camphechlor (Morgan, 1993).
    a) Convulsions lasting for four days occurred in a fatal case of endrin ingestion (Runhaar et al, 1985).
    b) Seizures may recur over several days after an acute exposure (Morgan, 1993).
    3) Convulsions are characteristic of acute camphechlor poisoning and consist of tonic-clonic motions due to diffuse stimulation of the brain and spinal cord (Wells & Milhorn, 1983; ACGIH, 1991).
    a) Grand mal seizures and dysconjugate eye movements were seen in a patient who had ingested camphechlor. Intermittent seizure activity continued throughout the night, and the patient was recovered by the next morning (Wells & Milhorn, 1983).
    4) An outbreak of a convulsive disorder in Pakistan has been associated with endrin contamination of foodstuffs; there were 194 cases of convulsions with 19 deaths (Clinical Note, 1984; Rowley et al, 1987).
    5) A 20-year-old was unconscious and convulsing on admission one hour after ingesting 200 mL of 30 percent endosulfan (Shemesh et al, 1988).
    D) AMNESIA
    1) Amnesia following camphechlor ingestion has been reported (Dreisbach, 1983; Wells & Milhorn, 1983).
    E) SEQUELA
    1) PERMANENT DAMAGE - Severe mental impairment was evident one year after ingestion of endosulfan in one case. It is not clear if the brain damage was due to a direct effect of endosulfan, or to the hypoxemia accompanying convulsions and respiratory insufficiency (Shemesh et al, 1988).
    2) LEARNING - Effects on behavior and learning have been reported following toxaphene exposure (de Gues et al, 1999).
    F) SECONDARY PERIPHERAL NEUROPATHY
    1) Occasional reports have associated peripheral neuropathy with exposure to organochlorines.
    G) CENTRAL NERVOUS SYSTEM FINDING
    1) EFFECTS IN ANIMALS - Sows poisoned with camphechlor exhibited similar effects to those seen in humans: trembling, staggering, slobbering, vomiting, and recurring convulsions (Mount et al, 1980).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea or spontaneous vomiting may not exist prior to onset of convulsions in camphechlor poisoning. Diarrhea may occur.
    3.8.2) CLINICAL EFFECTS
    A) DIARRHEA
    1) Diarrhea may occur.
    B) LACK OF EFFECT
    1) In several cases of acute camphechlor poisoning, no nausea or spontaneous vomiting was present prior to development of convulsions (McGee et al, 1952; Wells & Milhorn, 1983).

Hepatic

    3.9.1) SUMMARY
    A) Camphechlor is a hepatic enzyme inducer.
    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) Camphechlor is a hepatic enzyme inducer (Wells & Milhorn, 1983).

Genitourinary

    3.10.1) SUMMARY
    A) Renal insufficiency occurred in a case of mixed camphechlor exposure.
    3.10.2) CLINICAL EFFECTS
    A) RENAL FAILURE SYNDROME
    1) A farmer who had received several exposures to camphechlor and other pesticides developed renal insufficiency. Weekly dialysis became necessary. The renal effects could not be attributed to camphechlor alone (Beat, 1970).

Acid-Base

    3.11.1) SUMMARY
    A) Severe metabolic acidosis may be a consequence of convulsions and an immediate cause of death.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) Severe metabolic acidosis may be a consequence of severe convulsions, and the acidosis may be an immediate cause of death (Morgan, 1993).

Hematologic

    3.13.1) SUMMARY
    A) Aplastic anemia has occurred with camphechlor/lindane mixtures. Various blood dyscrasias including megaloblastic anemia have been reported with organochlorines.
    3.13.2) CLINICAL EFFECTS
    A) APLASTIC ANEMIA
    1) Two cases of dermal exposure to camphechlor/lindane mixtures developed acute aplastic anemia; one case developed acute myelomonocytic leukemia (HSDB , 1999).
    B) MEGALOBLASTIC ANEMIA
    1) Megaloblastic anemia and blood dyscrasias have been associated with exposure to organochlorines (Infante et al, 1978; Sharp et al, 1986).
    C) THROMBOCYTOPENIC DISORDER
    1) Thrombocytopenia occurred in a fatal case of endrin ingestion (Runhaar et al, 1985).

Dermatologic

    3.14.1) SUMMARY
    A) Extensive contact results in dermal irritation. Camphechlor can cause allergic dermatitis.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) Some skin irritation, pain, and reddening may result from extensive contact with these agents or with petroleum distillates in which they are contained. In the Standard Draize Test, camphechlor caused moderate skin irritation in mammals (RTECS , 1999; Sittig, 1991).
    B) DERMATITIS
    1) Camphechlor can cause allergic contact dermatitis (Lewis, 1996).

Musculoskeletal

    3.15.1) SUMMARY
    A) Leg and back spasms, and tetanic muscular contractions of all skeletal muscles, have occurred with camphechlor poisoning.
    3.15.2) CLINICAL EFFECTS
    A) INCREASED MUSCLE TONE
    1) Leg and back muscle spasms, and tetanic contractions of all skeletal muscles, have occurred with camphechlor poisoning (Clayton & Clayton, 1981; (EPA, 1985).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no reproductive studies were found for camphechlor in humans.
    B) Camphechlor did not affect reproduction, fertility, or lactation in multi-generation rodent studies. Stillbirths in sows were associated with gestational exposure. Camphechlor inhibited spermatogenesis in rats.
    3.20.2) TERATOGENICITY
    A) MALFORMATION
    1) Behavioral effects on newborns, musculoskeletal system developmental abnormalities, fetotoxicity, change in growth statistics and delayed physical effects on newborns have been observed in rodent studies (RTECS , 1999).
    2) Camphechlor, at doses at or above the LD50, induced malformations in mallard chicks (Hoffman & Eastin, 1982). It induced supernumerary ribs in rats when given at maternally toxic levels on days 6 to 15 of gestation (Chernoff et al, 1990).
    B) FETOTOXICITY
    1) Camphechlor induced decreased ossification in rats, and induced encephalocele in mice (Chernoff & Carver, 1976; Kavlock et al, 1985; Schardein, 1993). These effects were interpreted as fetotoxic, and maternal toxicity was seen in both species (Clayton & Clayton, 1982).
    C) CHOLINESTERASE INHIBITION
    1) Fetal cholinesterase activity and differentiation of cardiac neural elements were impeded in rats exposed to 12 mg/kg/day for 2 weeks prenatally (HSDB , 1999).
    D) CONGENITAL ANOMALY
    1) Camphechlor was slightly teratogenic in hamsters and rats (HSDB , 1999).
    2) Camphechlor, at doses at or above the LD50, induced malformations in mallard chicks (Hoffman & Eastin, 1982). The implications of this finding to the human situation are not known.
    3.20.3) EFFECTS IN PREGNANCY
    A) STILLBIRTH
    1) ANIMAL STUDIES
    a) A litter of stillborn pigs was born to a sow who had been acutely poisoned by camphechlor during gestation (Mount et al, 1980).
    B) LACK OF EFFECT
    1) ANIMAL STUDIES
    a) No effects on reproduction, fertility, or lactation were seen in a 3-generation dietary study in rats at doses up to 100 ppm (Kennedy et al, 1973), or 500 ppm (Chu et al, 1988), or in a 5-generation study in mice at 25 ppm (Clayton & Clayton, 1981).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) BREAST MILK
    1) Highly lipophilic compounds which are stored in body fat such as dieldrin are likely to be transferred to breast milk. Those chlorinated hydrocarbon insecticides which are more rapidly metabolized, such as camphechlor, are less likely to be detected in breast milk (Morgan, 1993).
    a) Camphechlor has not occurred to a significant extent in human breast milk, but it has been detected in cow's milk (Cairns et al, 1981) at concentrations proportional to the level in body fat (Clayton & Clayton, 1981). It cannot be assumed that there would be no risk of camphechlor in breast milk after a significant exposure.
    2) The daily intake of total organochlorine pesticides residues calculated for the suckling infant was significantly higher when compared with the acceptable daily intake (ADI) as recommended by FAO/WHO (FAO/WHO, 1970).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS8001-35-2 (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) IARC Classification
    a) Listed as: Toxaphene (Polychlorinated camphenes)
    b) Carcinogen Rating: 2B
    1) The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    3.21.2) SUMMARY/HUMAN
    A) Camphechlor has been carcinogenic in rats and mice, but not in hamsters. There is insufficient evidence to judge its potential carcinogenicity in humans.
    3.21.3) HUMAN STUDIES
    A) HUMANS
    1) With few exceptions, the delayed effects of pesticides on human health have been difficult to detect. Perhaps the health risks are sufficiently small that they are below the power of epidemiologic studies to detect (Sharp et al, 1986).
    2) A survey of 199 employees working with camphechlor showed no undue deaths from cancer (IARC, 1979).
    3) One case of acute myelomonocytic leukemia developed in a person who had dermal exposure to mixtures of camphechlor and LINDANE (HSDB, 1993).
    3.21.4) ANIMAL STUDIES
    A) ANIMAL STUDIES
    1) In the rat, camphechlor was found to be an equivocal tumorigenic agent by RTECS criteria for the blood system and carcinogenic by RTECS criteria with liver tumors present (RTECS , 1999). It induced liver tumors in mice and neoplastic thyroid lesions in rats in chronic feeding studies (Anon, 1979; Hathaway et al, 1996; Proctor et al, 1988).
    2) Camphechlor was not carcinogenic in hamsters (Clayton & Clayton, 1981).
    3) In the NCI Carcinogenesis Bioassay (Feed), clear evidence for carcinogenicity was found in the mouse and equivocal evidence in the rat (RTECS , 1999).

Genotoxicity

    A) Camphechlor has been genotoxic at the mutational and chromosomal level.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Analytical methods exist for determining levels of camphechlor in blood, urine, and other tissues. These determinations would be useful for confirmation of exposure. There is insufficient evidence to correlate levels in blood or urine with quantitative exposure.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Blood chlorinated hydrocarbon levels are not clinically useful following acute exposure. For most compounds they reflect cumulative exposure over a period of months or years rather than recent exposure (Coye et al, 1986). In the case of camphechlor, there is insufficient evidence in the literature to permit quantitative correlation of blood levels with exposure.
    4.1.3) URINE
    A) URINALYSIS
    1) Camphechlor was not detected in the urine of persons exposed to 1.3 to 17.5 ppm in soil while harvesting onions (Munn et al, 1985). In the case of camphechlor, there is insufficient evidence in the literature to permit quantitative correlation of urinary levels with exposure.
    4.1.4) OTHER
    A) OTHER
    1) POSTMORTEM
    a) Levels of camphechlor found in various tissues in a case of fatal poisoning in a 9-month-old infant were liver: 7.85 ppm; kidney: 6.75 ppm; brain: 14.03 ppm (Haun & Cueto, 1967).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Analytical methods exist for determining levels of camphechlor in blood, urine, and other tissues. These determinations would be useful for confirmation of exposure. There is insufficient evidence to correlate levels in blood or urine with quantitative exposure.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Emesis is not recommended due to potential CNS depression or seizures.
    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).
    C) 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.
    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, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    B) 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).
    C) CONTRAINDICATED TREATMENT
    1) Administer adrenergic amines with caution as they may increase myocardial irritability and produce refractory ventricular arrhythmias (Dreisbach, 1983; Bryson, 1986).
    D) CHOLESTYRAMINE
    1) Cholestyramine (4 grams every eight hours) accelerated excretion of kepone and chlordane in excessively exposed workers, and probably would have a similar effect on other slowly excreted organochlorines which are trapped in the enterohepatic circulation (Cohn et al, 1978) Garrettson et al, 1984, 1985; (Boylan et al, 1978).
    E) PULMONARY ASPIRATION
    1) Evaluate the patient for pulmonary complications, especially if the ingested product contained a petroleum solvent.

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 been proven effective.
    2) HEMOPERFUSION - The effectiveness is not known due to limited experience.
    3) Exchange transfusion, extracorporeal, and peritoneal dialysis have not proven effective in management of these poisonings. There has been little or no experience with charcoal hemoperfusion in organochlorine poisonings.

Range Of Toxicity

Summary

    A) Camphechlor is considered among the most toxic organochlorine compounds. The estimated lethal dose is 2 to 7 g.

Minimum Lethal Exposure

    A) 2 to 7 grams is the estimated lethal ingestion dose for humans (Hathaway et al, 1996; Lewis, 1996).
    B) CARCINOGENICITY - Camphechlor is a confirmed carcinogen with experimental carcinogenic and tumorigenic data. According to the International Agency for Research on Cancer (IARC), there is Human Limited Evidence and Animal Sufficient Evidence to term camphechlor carcinogenic (Lewis, 1996). In experimental animals, camphechlor is carcinogenic (Hathaway et al, 1996).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Toxic doses of organochlorine compounds vary enormously with route and rate of absorption. Based on reports of poisonings and laboratory studies, camphechlor would be considered in the group of HIGHEST toxicity.
    B) CASE REPORTS
    1) In one controlled study, 25 human volunteers were exposed to 500 mg/m(3) for 30 minutes for 10 days, and no adverse effects were evident (Hathaway et al, 1996).
    2) A dose of 10 mg/kg may cause convulsions in some persons, but not in others (ACGIH, 1991).
    C) ANIMAL DATA
    1) The no-effect oral dose in subchronic studies was 0.2 gm/kg for dogs and 4.0 ppm (0.35 mg/kg) for rats (Chu et al, 1986).
    2) Monkeys tolerated a dietary dose of 10 ppm with no apparent effects (ACGIH, 1986).
    3) Guinea pigs and rats tolerated a dietary dose of 800 ppm for 6 months with no apparent effects (ACGIH, 1986). Some rats had minor changes in the liver when fed 50 ppm for 6 to 9 months (Clayton & Clayton, 1981).

Workplace Standards

    A) ACGIH TLV Values for CAS8001-35-2 (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) Chlorinated camphene
    a) TLV:
    1) TLV-TWA: 0.5 mg/m(3)
    2) TLV-STEL: 1 mg/m(3)
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A3
    2) Codes: Skin
    3) Definitions:
    a) A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    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): CNS convul; liver dam
    d) Molecular Weight: 414
    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 CAS8001-35-2 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Chlorinated camphene
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    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): See Appendix A
    3) IDLH:
    a) IDLH: 200 mg/m3
    b) Note(s): Ca
    1) Ca: NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A).

    C) Carcinogenicity Ratings for CAS8001-35-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Chlorinated camphene
    a) A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    2) EPA (U.S. Environmental Protection Agency, 2011): B2 ; Listed as: Toxaphene
    a) B2 : Probable human carcinogen - based on sufficient evidence of carcinogenicity in animals.
    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): 2B ; Listed as: Toxaphene (Polychlorinated camphenes)
    a) 2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Chlorinated camphene
    a) Ca : NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    5) MAK (DFG, 2002): Category 2 ; Listed as: Chlorinated camphene
    a) Category 2 : Substances that are considered to be carcinogenic for man because sufficient data from long-term animal studies or limited evidence from animal studies substantiated by evidence from epidemiological studies indicate that they can make a significant contribution to cancer risk. Limited data from animal studies can be supported by evidence that the substance causes cancer by a mode of action that is relevant to man and by results of in vitro tests and short-term animal studies.
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): R ; Listed as: Toxaphene
    a) R : RAHC = Reasonably anticipated to be a human carcinogen

    D) OSHA PEL Values for CAS8001-35-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Chlorinated camphene
    2) Table Z-1 for Chlorinated camphene:
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.5
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: Yes
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: Budavari, 1996 Clayton & Clayton, 1994 ITI, 1995 Lewis, 1996 RTECS, 1999
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 47 mg/kg
    b) 42 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 112 mg/kg
    3) LD50- (ORAL)RAT:
    a) 50 mg/kg
    b) 60 mg/kg
    c) 85 mg/kg
    d) Male, 90 mg/kg
    e) Female, 80 mg/kg
    4) LD50- (SKIN)RAT:
    a) 80 mg/kg
    b) 600 mg/kg
    c) Male, 1075 mg/kg
    d) Female, 780 mg/kg

Physicochemical

Physical Characteristics

    A) Campheclor exists as an amber/yellow, waxy solid with a mild pine-, chlorine-, and camphor-like odor (Budavari, 1996; Hathaway et al, 1996; Lewis, 1993; Sittig, 1991).

Molecular Weight

    A) 413.81

Other

    A) ODOR THRESHOLD
    1) In water: 0.14 mg/L ((EPA, 1998))
    2) In water: 0.140 ppm (HSDB , 1999)
    3) 2.3660 mg/m(3) (medium not specified) (HSDB , 1999)

References

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