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CHLOROPHACINONE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Chlorophacinone is an indandione COUMARIN DERIVATIVE.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C23-H15-Cl-O3

Available Forms Sources

    A) FORMS
    1) Chlorophacinone is a crystalline solid. The commercial product is an oil concentrate or dust concentrate (EPA, 1985; Budavari, 1989). Chlorophacinone is an indandione COUMARIN DERIVATIVE.
    B) SOURCES
    1) Chlorophacinone is produced using para-chlorobenzophenone, sodium cyanide, methyl acetate, and dimethyl phthalate in a series of reactions including cyanohydrin formation, alcohol reduction, and condensation (Ashford, 2001).
    C) USES
    1) It is used as a rodenticide because of its anticoagulant properties.

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) In massive overdose, these agents have produced rapid and persistent hypoprothrombinemia and associated bleeding diathesis. Chlorophacinone produces especially prolonged periods of hypocoagulability. Once coagulation defects occur, they may persist for 6 weeks to many months. Because it has an elimination half-life of several days, daily exposures would produce cumulative toxicity. No chronic data were found for chlorophacinone in humans, however.
    B) Cardiopulmonary injury and neurologic toxicity have been reported with the indandiones in animals but not humans.
    0.2.4) HEENT
    A) Epistaxes may be noted. Burns to the eyes may be produced by direct contact.
    0.2.7) NEUROLOGIC
    A) Neurologic damage has been seen in experimental animals, but not in a case of human overdose. Intracranial hemorrhage may occur.
    0.2.8) GASTROINTESTINAL
    A) Spontaneous emesis may occur. Blood may be present in the feces.
    0.2.10) GENITOURINARY
    A) Hematuria may occur.
    0.2.13) HEMATOLOGIC
    A) Hemorrhage is the most common toxic sign and may be manifested by epistaxis, gum bleeding, hemoptysis, intracranial hemorrhage, hematuria, GI bleeding, ecchymosis, bloody or melenotic stools, bruising, abdominal and flank pain. Lengthened prothrombin time may be evident within 24 hours and maximal in 36 to 72 hours. In overdose PT prolongation and clinical bleeding have persisted for 45 days to 8 months.
    0.2.14) DERMATOLOGIC
    A) Ecchymoses and hematomas occur due to reduced clotting capacity.
    0.2.20) REPRODUCTIVE
    A) Spontaneous abortion occurred in a case of brodifacoum ingestion. Some coumarin derivatives, principally warfarin, are known human teratogens.
    B) Central nervous system defects, including hydrocephaly and microcephaly are linked with exposure during the second or third trimester.
    C) At the time of this review, no data were available to assess the potential effects of exposure to this agent during lactation.
    0.2.21) CARCINOGENICITY
    A) No studies on the possible carcinogenicity of chlorophacinone were found.
    0.2.22) OTHER
    A) Chlorophacinone may be hazardous by the dermal and oral route. No information is available on its hazard by inhalation, but its high toxicity makes it likely that some effect would be obtained by the latter route. Phenobarbital increased the rate of elimination of chlorophacinone in one case.

Laboratory Monitoring

    A) Monitor prothrombin time or INR and PTT. Obtain PT or INR at 24 and 48 hours postingestion. If any prolongation is observed, repeat PT or INR every 6 to 12 hours.
    B) Factor assays (II, VII, IX, X) may be abnormal in patients with a normal PT, INR, and PTT. Vitamin K therapy should not be discontinued until factor assays are normal.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Emesis and gastric lavage are not generally recommended. Gastric decontamination is unnecessary after accidental "taste" ingestions in children. Lavage may increase the risk of bleeding after deliberate ingestions in adults.
    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) VITAMIN K1 (PHYTONADIONE) - Is a specific antidote and should be administered to any patient with a prolonged PT or INR. Menadione (vitamin K3) should NOT be used. Oral therapy may be indicated in small ingestions or mild coagulopathy. Administer 15 to 25 mg in adult and 5 to 10 mg in children. Daily maintenance doses of 100 to 125 mg/day may be required for 1.5 to 8 months in severe cases.
    1) IV injection is preferable in severe cases where rapid correction is required. DOSE: ADULTS 10 mg IV diluted in saline or glucose at a rate not exceeding 5% of the total dose/min. Subcutaneous injection may be indicated in patients with less severe coagulopathy where the risk of hematoma is low, DOSE: ADULT 5 to 10 mg. CHILD 1 to 5 mg.
    D) There is no specific therapeutic maneuver other than restoration of PT and factor levels to normal if toxicity occurs. Administer fresh frozen plasma and/or factor concentrates in addition to packed red blood cells and vitamin K in patients with active bleeding.
    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) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) Acute ingestion of between 100 mg and 250 mg has caused prolonged anticoagulation in adults.

Clinical Effects

Summary Of Exposure

    A) In massive overdose, these agents have produced rapid and persistent hypoprothrombinemia and associated bleeding diathesis. Chlorophacinone produces especially prolonged periods of hypocoagulability. Once coagulation defects occur, they may persist for 6 weeks to many months. Because it has an elimination half-life of several days, daily exposures would produce cumulative toxicity. No chronic data were found for chlorophacinone in humans, however.
    B) Cardiopulmonary injury and neurologic toxicity have been reported with the indandiones in animals but not humans.

Heent

    3.4.1) SUMMARY
    A) Epistaxes may be noted. Burns to the eyes may be produced by direct contact.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) BURNS - Chlorophacinone may burn the eyes upon direct contact (EPA, 1985; Sittig, 1991).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) EPISTAXIS may be noted (Sittig, 1991).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) CARDIOVASCULAR FINDING
    1) WITH POISONING/EXPOSURE
    a) Cardiopulmonary injury has been described in experimental animals (Hayes & Laws, 1991).

Neurologic

    3.7.1) SUMMARY
    A) Neurologic damage has been seen in experimental animals, but not in a case of human overdose. Intracranial hemorrhage may occur.
    3.7.2) CLINICAL EFFECTS
    A) NEUROPATHY
    1) WITH POISONING/EXPOSURE
    a) Neurologic toxicity has been described with the indandiones in laboratory rats, however no neurologic symptoms occurred in one massive overdose of chlorophacinone in an adult (Murdoch, 1983).
    B) INTRACRANIAL HEMORRHAGE
    1) WITH POISONING/EXPOSURE
    a) Death due to massive hemorrhage, preceded by headache, loss of consciousness, and seizures, has been described after massive brodifacoum ingestion (Basehore LM & Mowry JM, 1987; Helmuth et al, 1989).

Gastrointestinal

    3.8.1) SUMMARY
    A) Spontaneous emesis may occur. Blood may be present in the feces.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Spontaneous emesis may occur (Smolinske et al, 1989).
    B) GASTROINTESTINAL HEMORRHAGE
    1) WITH POISONING/EXPOSURE
    a) Blood may be present in the feces (Sittig, 1991).

Genitourinary

    3.10.1) SUMMARY
    A) Hematuria may occur.
    3.10.2) CLINICAL EFFECTS
    A) BLOOD IN URINE
    1) WITH POISONING/EXPOSURE
    a) Hematuria may occur (Sittig, 1991).

Hematologic

    3.13.1) SUMMARY
    A) Hemorrhage is the most common toxic sign and may be manifested by epistaxis, gum bleeding, hemoptysis, intracranial hemorrhage, hematuria, GI bleeding, ecchymosis, bloody or melenotic stools, bruising, abdominal and flank pain. Lengthened prothrombin time may be evident within 24 hours and maximal in 36 to 72 hours. In overdose PT prolongation and clinical bleeding have persisted for 45 days to 8 months.
    3.13.2) CLINICAL EFFECTS
    A) HEMORRHAGE
    1) WITH POISONING/EXPOSURE
    a) Hemorrhage is the most common toxic sign and may be manifested by epistaxis, gum bleeding, hemoptysis, intracranial hemorrhage, hematuria, gastrointestinal bleeding, ecchymoses, bloody or melenotic stools (Sittig, 1991).
    b) Lengthened prothrombin time may be evident within 24 hours of ingestion and maximal in 36 to 72 hours. Larger doses produce a more rapid prolongation of PT than smaller doses (Leck & Park, 1981). In overdose, PT prolongation and clinical bleeding have persisted for 45 days to 8 months (Barlow et al, 1982; Lipton & Klass, 1984; Murdoch, 1983).
    c) While the onset of prolonged prothrombin times occurs generally within 48 hours, the first clinical signs of bleeding may be delayed until one week after ingestion (Burucoa et al, 1989).
    d) Prolonged hypocoagulability has been shown to occur with ingestion of chlorophacinone (Chataigner et al, 1989). In one case, where approximately 100 mg had been ingested, prothrombin time was not normalized until seven weeks after exposure (Vogel et al, 1988). Acute ingestion of 625 mg in a 37-year-old resulted in anticoagulation lasting 59 days (Murdoch, 1983).
    B) INTRACRANIAL HEMORRHAGE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - A 59-year-old male presented with cervical-dorsal subdural hematoma associated with accidental poisoning with difenacoum (Nighoghossian et al, 1990).

Dermatologic

    3.14.1) SUMMARY
    A) Ecchymoses and hematomas occur due to reduced clotting capacity.
    3.14.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) Chlorophacinone may burn the skin upon direct contact (EPA, 1985; Sittig, 1991).
    B) ECCHYMOSIS
    1) WITH POISONING/EXPOSURE
    a) Ecchymoses have been reported (Sittig, 1991).

Reproductive

    3.20.1) SUMMARY
    A) Spontaneous abortion occurred in a case of brodifacoum ingestion. Some coumarin derivatives, principally warfarin, are known human teratogens.
    B) Central nervous system defects, including hydrocephaly and microcephaly are linked with exposure during the second or third trimester.
    C) At the time of this review, no data were available to assess the potential effects of exposure to this agent during lactation.
    3.20.2) TERATOGENICITY
    A) CONGENITAL ANOMALY
    1) At the time of this review, no human data were available to assess the teratogenic potential of chlorophacinone.
    2) HUMAN TERATOGEN - Some coumarin anticoagulants, primarily WARFARIN, have been linked with human birth defects. Characteristic skeletal defects, called FETAL WARFARIN SYNDROME, arise when exposure is during the first trimester (Schardein, 1993).
    3) Hypoplastic nose, often flattened and sunken into the face, radiological stippling of the spinal column, and punctate calcification are characteristic effects of exposure during the first trimester (Schardein, 1993).
    4) Central nervous system defects, including hydrocephaly and microcephaly, are linked with exposure during the second or third trimester (Schardein, 1993).
    5) The risk of malformation when a pregnant woman is exposed to therapeutic levels of coumarin anticoagulants appears to be approximately 1 in 5 (Schardein, 1993). Risks from high acute exposures are not known.
    3.20.3) EFFECTS IN PREGNANCY
    A) ABORTION
    1) CASE REPORT - Spontaneous abortion occurred in a 31-year-old woman who ingested 1500 g of Talon(R) (containing 75 mg of brodifacoum) approximately five weeks earlier (Lipton & Klass, 1984).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) LACK OF INFORMATION
    1) No studies were found on the possible effects of chlorophacinone on lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS3691-35-8 (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) No studies on the possible carcinogenicity of chlorophacinone were found.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Genotoxicity

    A) Chlorophacinone did not induce chromosome aberrations or impair spermatogenesis in mice.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor prothrombin time or INR and PTT. Obtain PT or INR at 24 and 48 hours postingestion. If any prolongation is observed, repeat PT or INR every 6 to 12 hours.
    B) Factor assays (II, VII, IX, X) may be abnormal in patients with a normal PT, INR, and PTT. Vitamin K therapy should not be discontinued until factor assays are normal.
    4.1.2) SERUM/BLOOD
    A) COAGULATION STUDIES
    1) PROTHROMBIN TIME OR INTERNATIONAL NORMALIZED RATIO (INR) is helpful in diagnosis and monitoring of antidotal therapy. Any prolongation of PT or INR when compared to normal controls indicates toxicity. Prothrombin times or INRs may be normal 24 hours postingestion, and become prolonged at 48 hours or later, therefore a 24-hour and a 48-hour PT or INR is recommended (Smolinske et al, 1989). If any prolongation is observed, repeat PT or INR every 6 to 12 hours to assess efficacy of therapy. PTT has also been prolonged in overdose.
    2) FACTOR ASSAYS - Determination of blood clotting factors II, VII, IX, and X may be helpful in guiding therapy in symptomatic patients. Since clotting factors may be abnormal with a normal PT and INR, they are a more sensitive measure of toxicity and may be more useful in guiding vitamin K1 therapy (Hoffman et al, 1988).
    B) BLOOD/SERUM CHEMISTRY
    1) CHLOROPHACINONE LEVELS - In a series of 4 adult poisonings (in 3 patients) where multiple plasma levels were obtained, the risk of bleeding was minimal when the plasma level was below 1 mcg/mL. The levels at presentation with clinical bleeding were 6.3, 12.9, 13.3, and 15.2 mcg/mL in these cases (Burucoa et al, 1989).
    C) HIGH PERFORMANCE LIQUID CHROMATOGRAPHY
    1) Measurement of chlorophacinone blood levels in 20 intoxicated persons, using high performance liquid chromatography, revealed that no risk of bleeding was present when chlorophacinone levels were below 1 mcg/mL (Mura et al, 1992).
    4.1.4) OTHER
    A) OTHER
    1) FECAL
    a) Check for the presence of blood in the stools in symptomatic patients or in patients with a prolonged PT or INR.
    2) OTHER
    a) Most of these products contain a water-soluble dye (usually blue or green). However, evidence of dye in the mouth was not predictive of which children developed a prolonged PT in a prospective study of 110 accidental pediatric ingestions (Smolinske et al, 1989).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Coagulopathy commonly persists for 6 weeks or longer in patients who ingest large amounts in suicidal attempts. Premature discharge of such patients at 3 to 4 weeks postingestion prior to full normalization of factor levels has resulted in fatality in 3 cases (Basehore LM & Mowry JM, 1987; Helmuth et al, 1989) Kruse & Carlson, 1992).
    B) Frequent outpatient monitoring should be done on patients discharged on oral vitamin K1 to ensure compliance and adequacy of treatment. Factor assays should be normal prior to discontinuation of vitamin K1.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Children with a history of accidental ingestion of less than a few grains or pellets can be observed at home. Outpatient evaluation of the prothrombin time or INR at 48 hours postingestion should be done. Larger or unknown ingestions should prompt consideration of gastric decontamination, along with clinical and laboratory evaluation (Smolinske et al, 1989).

Monitoring

    A) Monitor prothrombin time or INR and PTT. Obtain PT or INR at 24 and 48 hours postingestion. If any prolongation is observed, repeat PT or INR every 6 to 12 hours.
    B) Factor assays (II, VII, IX, X) may be abnormal in patients with a normal PT, INR, and PTT. Vitamin K therapy should not be discontinued until factor assays are normal.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) 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).
    B) GASTRIC LAVAGE
    1) Not recommended as it may induce bleeding in adults with significant coagulopathy and is not necessary in children after accidental ingestion.
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Monitor prothrombin time or INR routinely. A PT or INR obtained prior to 48 hours post-ingestion may not be predictive of subsequent coagulopathy. A 24 hour AND a 48 hour PT is therefore recommended (Smolinske et al, 1989). If any prolongation is observed, repeat PT or INR every 6 to 12 hours to assess efficacy of therapy.
    2) PATIENT CURRENTLY ON THERAPEUTIC ANTICOAGULATION - Get prothrombin time or INR immediately. If patient is anticoagulated for prosthetic valve or other procedure requiring absolute anticoagulation, do not give vitamin K unless anticoagulation is excessive. Only a small intravenous dose (1 to 5 milligrams) titrated to return PT or INR to THERAPEUTIC (not normal) should be utilized. Substitution of heparin as an anticoagulant may be necessary until PT or INR is therapeutic.
    3) Follow hematocrit closely, at least a reading every four hours until it is stable.
    4) All stools and vomitus should be Hematest for occult blood.
    B) PHYTONADIONE
    1) VITAMIN K 1 (phytonadione, AquaMEPHYTON(R), Mephyton(R)): is a specific antidote and should be administered to any patient with a prolonged PT or INR. Menadione (Vitamin K 3, Synkayvite(R)) SHOULD NOT be used.
    a) ORAL VITAMIN K INDICATIONS - Oral phytonadione may be indicated in small ingestions or when the amount is uncertain, but presumed to be small. Administer 15 to 25 milligrams in adults and 5 to 10 milligrams in children.
    b) ORAL DOSE - Absorption is inconsistent. Large daily maintenance doses (100 to 125 milligrams/day) were required for prolonged therapy in severe overdose (75 milligrams of brodifacoum) (1.5 to 8 months) (Lipton & Klass, 1984). 20 to 100 milligrams/day was adequate to prevent bleeding in 4 adult cases where less amounts were ingested (2.15 to 10 milligrams) (Jones et al, 1984; (Chong et al, 1986; Hoffman et al, 1988) Ross et al, 1992), and in two young children with chronic Bromadine poisoning (Greeff et al, 1987).
    c) INTRAVENOUS INJECTION
    1) INTRAVENOUS VITAMIN K INDICATIONS - Intravenous phytonadione is preferable in SEVERE cases where rapid correction is required.
    2) DOSE - Adults: A minimum of 10 milligrams intravenously diluted in saline or glucose at a rate not exceeding 5 percent of the total dose per minute. In maximally anticoagulated individuals, repeat doses at six to eight hour intervals may be required. Initial intravenous doses of 25 milligrams, 100 milligrams, 150 milligrams, 160 milligrams, and 400 milligrams have been required (Hoffman et al, 1988; Vogel et al, 1988; Burucoa et al, 1989) in actively hemorrhaging patients.
    3) ADVERSE EFFECTS
    a) Rapid intravenous infusion may produce flushing, cyanosis, dizziness, hypotension, and bronchoconstriction.
    d) INTRAMUSCULAR INJECTION - May be indicated in MILD ingestions where the risk of hematoma is low (Dose: Adult 5 to 10 milligrams; Child 1 to 5 milligrams).
    e) SUBCUTANEOUS INJECTION - Maintenance doses of 50 to 100 milligrams/day were required in an adult who ingested 10 milligrams of brodifacoum (Hoffman et al, 1988).
    f) MENADIONE/MENADIOL - (Vitamin K 3) requires metabolism by the liver to Vitamin K 1. The ability of the liver to utilize menadione in the face of generalized hemorrhagic disease is doubtful. Menadione was ineffective as maintenance therapy in one human overdose (Murdoch, 1983), and as initial parenteral therapy in an acute overdose (Kruse & Carlson, 1992).
    C) PHENOBARBITAL
    1) Phenobarbital, 100 to 180 milligrams/day has been administered to adults in an attempt to induce liver microsomal enzymes and hasten metabolism of brodifacoum, but its efficacy has not been proven (Jones et al, 1984; (Lipton & Klass, 1984) Kruse & Carlson, 1992).
    2) Administration of phenobarbital to an adult poisoned with chlorophacinone resulted in a decrease in the apparent elimination half-life from 22.8 days to 5.9 days (Burucoa et al, 1989).
    3) In rats pretreated with phenobarbital, hypoprothrombinemia was only partially antagonized (Bachmann & Sullivan, 1983).
    D) TRANSFUSION
    1) There is not a specific therapeutic maneuver other than restoration of prothrombin level to normal if toxicity occurs. Administer fresh frozen plasma and/or factor concentrates in addition to packed red blood cells and vitamin K in patients with active bleeding.
    E) TELEPHONE CONSULTATION
    1) National pesticide telecommunications network:
    2) The National Pesticide Information Center (NPIC) is a cooperative effort of Oregon State University and the US EPA. NPIC provides consultation to poison centers and other health care professionals for the management of pesticide poisoning. Calls regarding emergency cases requiring immediate medical response will be transferred to the Oregon Poison Center.
    a) NPIC contact information: phone: 1-800-858-7378. email: npic@ace.orst.edu Hours: 8 AM to 12 PM Pacific time Monday through Friday, excluding holidays.

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) SUPPORT
    1) It is not known if exposure by the inhalation route can cause systemic toxicity. Systemic toxicity is likely, however, given the high toxicity of this substance.
    B) OBSERVATION REGIMES
    1) All patients with inhalation exposure should be carefully observed for the possible development of systemic signs and symptoms. Follow treatment recommendations in the ORAL EXPOSURE section where appropriate.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) SUPPORT
    1) It is not known if exposure by the ocular route can cause systemic toxicity. Systemic toxicity is likely, however, given the high toxicity of this substance.
    B) OBSERVATION REGIMES
    1) All patients with ocular exposure should be carefully observed for the possible development of systemic signs and symptoms. Follow treatment recommendations in the ORAL EXPOSURE section when appropriate.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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).

Range Of Toxicity

Summary

    A) Acute ingestion of between 100 mg and 250 mg has caused prolonged anticoagulation in adults.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The probable oral lethal dose for humans is less than 5 mg/kg to 50 mg/kg (between less than 7 drops and 1 teaspoon for a 150 pound (70 kg) person) (Sittig, 1991).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The actual maximum tolerated exposure in any individual case would depend primarily on the agressiveness of the medical treatment.
    B) CASE REPORTS
    1) Acute ingestion of 100 mg (1.6 mg/kg) in an 18-year-old woman resulted in asymptomatic anticoagulation lasting 7 weeks (Vogel et al, 1988).
    2) Ingestion of 250 milligrams resulted in anticoagulation lasting 49 days in a 20-year-old woman (Burucoa et al, 1989).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) HIGH PERFORMANCE LIQUID CHROMATOGRAPHY
    a) Measurement of chlorophacinone blood levels in 20 intoxicated persons, using high performance liquid chromatography, revealed that no risk of bleeding was present when chlorophacinone levels were below 1 mcg/mL (Mura et al, 1992).

Workplace Standards

    A) ACGIH TLV Values for CAS3691-35-8 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS3691-35-8 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS3691-35-8 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS3691-35-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 1999
    1) LD50- (ORAL)MOUSE:
    a) 1060 mcg/kg
    2) LD50- (ORAL)RAT:
    a) 2100 mcg/kg

Physicochemical

Physical Characteristics

    A) Yellow crystalline solid (Harbison, 1998)

Molecular Weight

    A) 374.82 (Budavari, 1996)

References

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