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ENDRIN

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Endrin is a cyclodiene insecticide.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C12-H8-Cl6-O

Available Forms Sources

    A) FORMS
    1) Endrin is non-flammable as the pure crystalline solid or powder. Its color varies from colorless or white, to tan. It usually is odorless, but sometimes it has mild chemical odor (ACGIH, 1991; CHRIS , 1999) Hathaway, 1996; (Sittig, 1991; HSDB , 1999; Lewis, 1996; NIOSH , 1999; Hartley & Kidd, 1987).
    2) "Endrin is a white crystalline, odorless solid dissolved in a liquid carrier." (AAR, 1998)
    3) Endrin is the stereoisomer of dieldrin, which is the endo-exoisomer, although, ICPS (1992) reports that endrin is the endo, endo stereoisomer of dieldrin (ACGIH, 1991).
    4) The compound in its technical grade is 95% to 98% pure with the following impurities: dieldrin, isodrin, aldrin, hepatachloronorbornadiene, hepatachloronorbornene, endrin aldehyde, and delta-ketoendrin. Dry and liquid formulations of endrin contain up to 75% and 25% pure endrin, respectively (CHRIS , 1999; HSDB , 1999).
    5) The minimum purity of endrin is 95% active ingredient with 55.57% chlorine content; less than 0.4% and 0.1% of free acid and water, respectively (HSDB , 1999).
    B) SOURCES
    1) Endrin is not found in nature (Howard, 1991).
    2) All uses of endrin in the United States have been voluntarily canceled by the manufacturer and manufacture of endrin has been discontinued in the US since 1986 (ACGIH, 1991).
    C) USES
    1) Endrin was used as a pesticide. Specifically, as an insecticide for Lepidoptera, grasshoppers, cutworms (Euxoa aoxiliaris, Agrotis orthogonia), and borers; as a rodenticide for voles (Microtus pinetorium, Microtus species); and as an avicide. Endrin was used on cotton, sugarcane, rice cereals, orchards, corn/maize, grain and on non-crop land as well (ACGIH, 1991) AAR, 1998; (HSDB , 1999; Hartley & Kidd, 1987).
    2) "All uses of endrin in the United States were canceled by the manufacturer in 1986." (Hathaway, 1996)

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Endrin is a chlorinated hydrocarbon (organochlorine) insecticide of the chlorinated ethane/cyclodiene/hexachlorocyclohexane type. It is extremely toxic and can be absorbed by any route of exposure.
    B) The primary target of action is the central nervous system (CNS). CNS excitation and convulsions may occur. Respiratory depression may occur concurrently with convulsions, and respiratory failure is the most common cause of death from endrin poisoning.
    C) Symptoms in less severe cases of endrin poisoning may include headache, dizziness, leg weakness, abdominal discomfort, nausea, vomiting, insomnia, agitation, and, occasionally, slight mental confusion.
    D) Pulmonary edema and renal insufficiency have been reported following endrin ingestion.
    E) Symptoms including headache, dizziness, weakness, lethargy, and weight loss may persist for 2 to 4 weeks.
    0.2.3) VITAL SIGNS
    A) Respiratory depression, hyperthermia, and recurrent hypotension have occurred in acute endrin poisoning.
    0.2.4) HEENT
    A) Hypersalivation and deafness may occur. White, foamy froth may emanate from the nose and mouth. Headache may persist for two to four weeks.
    0.2.5) CARDIOVASCULAR
    A) Cardiac dysrhythmias can occur.
    0.2.6) RESPIRATORY
    A) Reduced gas exchange, irritation, and chemical pneumonitis may occur.
    0.2.7) NEUROLOGIC
    A) Sensory disturbances, excitation with myoclonic jerking, convulsions, tremor, ataxia, agitation, nervousness, and amnesia may occur. Permanent damage may occur following acute exposure.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting, and diarrhea may occur following ingestion.
    0.2.9) HEPATIC
    A) Hepatic oxidative enzymes may be induced by endrin.
    0.2.10) GENITOURINARY
    A) Renal insufficiency occurred in a case of endrin ingestion.
    0.2.11) ACID-BASE
    A) Severe metabolic acidosis may be a consequence of convulsions and contributes to fatal outcomes.
    0.2.13) HEMATOLOGIC
    A) Rare cases of aplastic and megaloblastic anemia have been associated with organochlorine insecticides exposure. Thrombocytopenia has occurred with exposure to endrin.
    0.2.14) DERMATOLOGIC
    A) Extensive contact results in dermal irritation.
    0.2.18) PSYCHIATRIC
    A) Insomnia, anorexia, lethargy, weakness, and agressive confusion have been associated with endrin exposure.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no reproductive studies were found for endrin in humans. Endrin has been fetotoxic and embryotoxic in several species of experimental animals; other studies have not found teratogenic effects. Endrin is less likely to be transferred to breast milk than other organochlorine insecticides because it is metabolized relatively rapidly. Endrin has altered spermatogenesis in rats.
    0.2.21) CARCINOGENICITY
    A) There is inadequate evidence for assessing its carcinogenic potential in humans. In one study, workers exposed to endrin from 4 to 13 years did not show increased risk for any type of cancer. However, a significant increase in liver and biliary tract cancer was noted among workers at a facility where endrin and other organochlorine insecticides produced.
    0.2.22) OTHER
    A) Endrin can be absorbed by any route. Endrin is metabolized relatively rapidly by the hepatic cytochrome P-450 system.

Laboratory Monitoring

    A) Endrin can be determined in biological samples by gas-liquid chromatography and in environmental samples by gas chromatography.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Emesis is not recommended due to potential CNS depression or seizures.
    B) 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.
    C) 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.
    D) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    E) Do not give oils by mouth.
    F) Do not administer adrenergic amines, which may further increase myocardial irritability and produce refractory ventricular arrhythmias.
    G) CHOLESTYRAMINE - Oral administration 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) As little as 0.2 mg/kg may cause symptoms, and 12 grams may be fatal based on the reported human LDLo.

Clinical Effects

Summary Of Exposure

    A) Endrin is a chlorinated hydrocarbon (organochlorine) insecticide of the chlorinated ethane/cyclodiene/hexachlorocyclohexane type. It is extremely toxic and can be absorbed by any route of exposure.
    B) The primary target of action is the central nervous system (CNS). CNS excitation and convulsions may occur. Respiratory depression may occur concurrently with convulsions, and respiratory failure is the most common cause of death from endrin poisoning.
    C) Symptoms in less severe cases of endrin poisoning may include headache, dizziness, leg weakness, abdominal discomfort, nausea, vomiting, insomnia, agitation, and, occasionally, slight mental confusion.
    D) Pulmonary edema and renal insufficiency have been reported following endrin ingestion.
    E) Symptoms including headache, dizziness, weakness, lethargy, and weight loss may persist for 2 to 4 weeks.

Vital Signs

    3.3.1) SUMMARY
    A) Respiratory depression, hyperthermia, and recurrent hypotension have occurred in acute endrin poisoning.
    3.3.2) RESPIRATIONS
    A) Respiratory arrest may be the immediate cause of death from acute exposure to endrin (EPA, 1985).
    3.3.3) TEMPERATURE
    A) Hyperthermia occurred in a fatal case of endrin ingestion (Runhaar et al, 1985).
    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 and deafness may occur. White, foamy froth may emanate from the nose and mouth. Headache may persist for two to four weeks.
    3.4.2) HEAD
    A) Headache is one of the symptoms of acute endrin poisoning. It may persist for 2 to 4 weeks (Sittig, 1991; EPA, 1985; Proctor et al, 1988; HSDB , 1996).
    3.4.4) EARS
    A) Deafness occurs in acute endrin poisonings (EPA, 1985).
    3.4.5) NOSE
    A) White, foamy froth emanating from the nostrils has frequently been seen in acute endrin poisonings (Reddy et al, 1966; Sittig, 1991).
    3.4.6) THROAT
    A) Foaming at the mouth was observed in a 20-year-old male one hour after ingestion of 200 mL of 30% endosulfan (Shemesh et al, 1988). Hypersalivation occurred in a fatal case of endrin ingestion (Runhaar et al, 1985).

Cardiovascular

    3.5.1) SUMMARY
    A) Cardiac dysrhythmias can occur.
    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) High concentrations of organochlorine insecticides can cause cardiac dysrhythmias by increasing myocardial irritability (Morgan, 1993; (HSDB , 1996).

Respiratory

    3.6.1) SUMMARY
    A) Reduced gas exchange, irritation, and chemical pneumonitis may occur.
    3.6.2) CLINICAL EFFECTS
    A) DISORDER OF RESPIRATORY SYSTEM
    1) Severe convulsions can limit pulmonary gas exchange, and this may be an immediate cause of death (Morgan, 1993).
    B) ACUTE LUNG INJURY
    1) Massive pulmonary edema occurred in one case of endrin ingestion. It was successfully treated with constant positive pressure ventilation with high-level PEEP (up to 28 cm H2O) (Jedeikin et al, 1979). Pulmonary edema may be due to the hydrocarbon solvents in commercial formulations.
    2) Refer to the "HYDROCARBONS" MEDITEXT(R) Medical Management for more information.
    C) PNEUMONITIS
    1) Aspiration of petroleum distillate solvent may cause potentially fatal lipoid pneumonitis.

Neurologic

    3.7.1) SUMMARY
    A) Sensory disturbances, excitation with myoclonic jerking, convulsions, tremor, ataxia, agitation, nervousness, and amnesia may occur. Permanent damage may occur following acute exposure.
    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) Endrin is a CNS excitant and convulsant (Clinical Note, 1984). Sudden epileptiform convulsions may be the first sign of endrin poisoning, with onset from 30 minutes to 10 hours after exposure (Coble et al, 1967; (EPA, 1985; Proctor et al, 1988; HSDB , 1996). A stuporous state may follow, and seizures may recur over several days (Proctor et al, 1988) Morgan, 1993). Coma and respiratory depression may ensue (Morgan, 1993).
    2) Convulsions may appear as an early sign in the absence of other symptoms with exposure to cyclodienes such as endrin (Morgan, 1993).
    3) Convulsions lasting for four days occurred in a fatal case of endrin ingestion (Runhaar et al, 1985).
    4) An outbreak of a convulsive disorder in Pakistan was associated with endrin contamination of foodstuffs; there were 194 patients with convulsions and 19 deaths (Clinical Note, 1984; Rowley et al, 1987).
    B) CENTRAL STIMULANT ADVERSE REACTION
    1) Kepone, mirex, endosulfan, and chlorbenzilate are more likely to produce tremors, ataxia, agitation, and nervousness than convulsions. Tremors have been reported from exposure to endrin (Proctor et al, 1988).
    C) AMNESIA
    1) Amnesia following camphechlor ingestion has been reported (Dreisbach, 1983; Wells & Milhorn, 1983). Amnesia may be possible with exposure to other organochlorine insecticides.
    D) ELECTROENCEPHALOGRAM ABNORMAL
    1) Acute endrin poisoning produced dysrhythmic changes in the EEG pattern preceding seizures. EEG generally returns to normal within 6 months after withdrawal from exposure (Proctor et al, 1988).
    E) ALTERED MENTAL STATUS
    1) In one case, severe mental impairment was evident one year after endosulfan ingestion. It is not clear if the brain damage was due to a direct effect of endosulfan, or to hypoxemia accompanying convulsions and respiratory insufficiency (Shemesh et al, 1988).
    F) NEUROPATHY
    1) Occasional reports have associated peripheral polyneuropathy with exposure to organochlorines.

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting, and diarrhea may occur following ingestion.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA, VOMITING AND DIARRHEA
    1) When ingested, these agents cause nausea and vomiting and diarrhea (Sittig, 1991; HSDB , 1996).

Hepatic

    3.9.1) SUMMARY
    A) Hepatic oxidative enzymes may be induced by endrin.
    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) ENZYME INDUCER - DDT, camphechlor (Wells & Milhorn, 1983) and chlordane (Garrettson et al, 1984-85) are hepatic enzyme inducers. This probably is the basis for an estrogenic effect of DDT in rodents.

Genitourinary

    3.10.1) SUMMARY
    A) Renal insufficiency occurred in a case of endrin ingestion.
    3.10.2) CLINICAL EFFECTS
    A) RENAL FAILURE SYNDROME
    1) RENAL INSUFFICIENCY occurred in a fatal case of endrin ingestion (Runhaar et al, 1985).

Acid-Base

    3.11.1) SUMMARY
    A) Severe metabolic acidosis may be a consequence of convulsions and contributes to fatal outcomes.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) Severe metabolic acidosis may be a consequence of convulsions, and may contribute to fatal outcomes (Morgan, 1993).

Hematologic

    3.13.1) SUMMARY
    A) Rare cases of aplastic and megaloblastic anemia have been associated with organochlorine insecticides exposure. Thrombocytopenia has occurred with exposure to endrin.
    3.13.2) CLINICAL EFFECTS
    A) ANEMIA
    1) DYSCRASIAS - Rare cases of aplastic and megaloblastic anemia have been attributed to exposure to organochlorine insecticides (Morgan, 1993; (Infante et al, 1978; Sharp et al, 1986), but a causal relationship has not been proven.
    B) 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.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) Some skin irritation results from extensive contact with these agents or with the petroleum distillates in which they are formulated (CHRIS , 1996).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no reproductive studies were found for endrin in humans. Endrin has been fetotoxic and embryotoxic in several species of experimental animals; other studies have not found teratogenic effects. Endrin is less likely to be transferred to breast milk than other organochlorine insecticides because it is metabolized relatively rapidly. Endrin has altered spermatogenesis in rats.
    3.20.2) TERATOGENICITY
    A) CONGENITAL ANOMALY
    1) ANIMAL STUDIES
    a) In rodent studies, fetotoxicity, increased pre-implantation mortality, change in litter size, change in growth statistics, changes in behavior, change in weaning or lactation index, specific developmental abnormalities, and fetal death have been observed (RTECS , 1996).
    b) Open-eye and cleft palate were induced in mice by endrin. Open-eye, cleft palate, syndactyly, and embryotoxicity were seen in hamsters. Behavioral alterations were found in rats from prenatal exposure (Schardein, 1985) Gray et al, 1983; (Gray et al, 1981).
    c) Endrin was fetotoxic and induced a low incidence of defects in mice (Kavlock et al, 1985).
    d) Endrin produced fused ribs and meningoencephaloceles in fetal hamsters following a single maternal dose of 5 mg/kg on day 8 of gestation (Chernoff et al, 1979).
    e) Endrin was fetotoxic and teratogenic in hamsters when given at the LD50 dose on days 7 to 9 of gestation (Ottolenghi et al, 1974).
    f) Endrin did not produce cleft palate or hydro-nephrosis in C57BL/6J and DBA/2J mice after a single oral dose of 4.5 or 6 mg/kg on day 12 of gestation; fetal and placental weights were decreased in both strains, and thymic weight was lower only in C57BL/6J fetuses (Hassoun & Stohs, 1996).
    g) Fetal rats and mice had reduced survival, and mice had increased incidence of club foot deformity when given endrin at a dose of 0.58 mg/kg four times per week prior to conception (Noda et al, 1972).
    B) MENTAL STATUS CHANGES
    1) Behavioral changes (increased activity) were seen in rats and hamsters prenatally exposed to endrin (Gray et al, 1981).
    C) LACK OF EFFECT
    1) ANIMAL STUDIES
    a) Endrin was not teratogenic in mice given garage doses up to 2 mg/kg/day, where maternal toxicity was observed (HSDB , 1996). It was not teratogenic in rats or mice at doses up to 1 mg/kg/day (Kavlock et al, 1981).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) BREAST MILK
    1) Highly lipophilic compounds which are stored in body fat are likely to be transferred to breast milk. Clorinated hydrocarbon insecticides which are more rapidly metabolized, such as endrin, are less likely to be detected in breast milk (Morgan, 1993).
    2) Endrin residues were not detected in human breast milk from Brazilian women, under conditions where several other organochlorine insecticides were measurable (Matuo et al, 1992).
    3) 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 CAS72-20-8 (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) IARC Classification
    a) Listed as: Endrin
    b) Carcinogen Rating: 3
    1) The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    3.21.2) SUMMARY/HUMAN
    A) There is inadequate evidence for assessing its carcinogenic potential in humans. In one study, workers exposed to endrin from 4 to 13 years did not show increased risk for any type of cancer. However, a significant increase in liver and biliary tract cancer was noted among workers at a facility where endrin and other organochlorine insecticides produced.
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) With few exceptions, the delayed effects of pesticides on human health have been difficult to detect. The health risks may be sufficiently small that they are below the power of epidemiologic studies to detect (Sharp et al, 1986).
    2) OCCUPATIONAL - A significant increase in liver and biliary tract cancer was noted among workers at a facility where endrin and other organochlorine insecticides produced (Brown, 1992).
    3) However, workers exposed to endrin from 4 to 13 years did not show increased risk for any type of cancer (ACGIH, 1991).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Endrin induced neoplasms of the liver, as well as carcinomas and sarcomas in other organs, in rats and induced high incidences of carcinoma of the liver in mice (Reuber, 1987). However, Endrin was not carcinogenic in mice or rats in an NCI Carcinogenesis bioassay feeding study (RTECS , 1996; HSDB , 1996).

Genotoxicity

    A) Endrin may be genotoxic at the chromosomal level.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Endrin can be determined in biological samples by gas-liquid chromatography and in environmental samples by gas chromatography.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Concentrations of endrin found in the blood of acutely poisoned persons who survived ranged from 0.007 to 0.053 mg/L (Baselt, 1988). The toxic level in human blood is 0.003 mcg/L (HSDB , 1990).
    4.1.3) URINE
    A) URINARY LEVELS
    1) Urinary concentrations of endrin in survivors of acute poisonings ranged from less than 0.004 to 0.020 mg/L (Baselt, 1988).
    4.1.4) OTHER
    A) OTHER
    1) POSTMORTEM
    a) Concentrations of endrin found in various tissues following fatal poisonings have been 0.685 mg/kg in liver, 0.116 mg/kg in kidney, 0.45 mg/L in blood (4 hours after ingestion), and 90 mg/kg postmortem in adipose tissue (Baselt & Cravey, 1989).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Endrin can be determined in biological samples by gas-liquid chromatography and in environmental samples by gas chromatography.

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) 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).
    B) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2010; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    C) CONTRAINDICATED TREATMENT
    1) Do NOT give oils by mouth. They tend to increase intestinal absorption of these lipophilic toxicants.
    2) Do NOT administer adrenergic amines, which further increase myocardial irritability and produce refractory ventricular arrhythmias (Dreisbach, 1983; Bryson, 1986).
    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.
    F) EXPERIMENTAL THERAPY
    1) Peters et al (1982) report that symptoms of chronic exposure to hexachlorobenzene improved following treatment with intravenous and oral edetic acid therapy.

Inhalation Exposure

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

Eye Exposure

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

Dermal Exposure

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

Enhanced Elimination

    A) EXTRACORPOREAL ELIMINATION
    1) HEMODIALYSIS: Has not proven effective.
    2) HEMOPERFUSION: Effectiveness 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) As little as 0.2 mg/kg may cause symptoms, and 12 grams may be fatal based on the reported human LDLo.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) Quantitative dose-response data are not available for endrin in humans, but some poisonings have occurred from eating contaminated food at doses in the range of 0.2 mg/kg body weight (Sittig, 1985).
    2) The minimum lethal dose for humans is approximately 7 g (Lewis, 1998).
    3) Oral lethal dose has been estimated at 10 mg/L (IPCS, 1995).

Maximum Tolerated Exposure

    A) The maximum tolerated human exposure to this agent has not been delineated.

Workplace Standards

    A) ACGIH TLV Values for CAS72-20-8 (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) Endrin
    a) TLV:
    1) TLV-TWA: 0.1 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: Skin
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): Liver dam; CNS impair; headache
    d) Molecular Weight: 380.93
    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 CAS72-20-8 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Endrin
    2) REL:
    a) TWA: 0.1 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: [skin]
    1) Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.
    f) Note(s):
    3) IDLH:
    a) IDLH: 2 mg/m3
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS72-20-8 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Endrin
    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): D ; Listed as: Endrin
    a) D : Not classifiable as to human carcinogenicity.
    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): 3 ; Listed as: Endrin
    a) 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Endrin
    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 CAS72-20-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Endrin
    2) Table Z-1 for Endrin:
    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: 0.1
    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: ACGIH, 1991 Budavari, 1996 Hartley & Kidd, 1987 ITI, 1995 Hayes & Laws, 1991 Clayton & Clayton, 1993; IPCS, 1992 Lewis, 1996 RTECS, 2003
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 5 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 1.3 mg/kg
    b) 1.37 mg/kg
    c) 1370 mcg/kg
    d) Male, 8.6 mg/kg
    e) 13 mg/kg
    3) LD50- (ORAL)RAT:
    a) 5.3 mg/kg
    b) 3 mg/kg
    c) 7-15 mg/kg
    d) 13 mg/kg
    e) Female, 4 mg/kg
    f) Female, 7.5 mg/kg
    g) Female (4-5 weeks), 16.8 mg/kg
    h) Female (6 months), 7.3 mg/kg
    i) Female (12-14 weeks), 5.3 mg/kg -- endrin 99% pure
    j) Female (12-13 weeks), 4.0 mg/kg
    k) Male, 4 mg/kg
    l) Male, 9.0 mg/kg
    m) Male, 18 mg/kg
    n) Male (4-5 weeks), 28.8 mg/kg
    o) Male (6 months), 43.4 mg/kg
    p) Male (6 months), 40.0 mg/kg
    q) Male (adult), 17.8 mg/kg
    r) Male (7 weeks), 27 mg/kg
    s) Male (12-14 weeks), 5.6 mg/kg -- endrin 99% pure
    t) Male (12-13 weeks), 8.9 mg/kg
    4) LD50- (SKIN)RAT:
    a) 12 mg/kg
    b) 18 mg/kg
    c) Female, 15 mg/kg
    d) Male, 18 mg/kg

Physicochemical

Physical Characteristics

    A) Endrin is non-flammable as the pure, crystalline solid or powder. Its color varies from colorless or white, to tan. It usually is odorless, but sometimes it has mild chemical odor (AAR, 1998; (ACGIH, 1991; CHRIS , 1999) Hathaway, 1996; (Sittig, 1991; HSDB , 1999; Lewis, 1996; NIOSH , 1999; Hartley & Kidd, 1987).
    B) The technical grade contains 85-90% endrin; the balance is made up of related compounds (ACGIH, 1991).
    C) When burned or heated to decomposition, endrin emits phosgena and hydrogen chloride (AAR, 1994).

Molecular Weight

    A) 380.91

Other

    A) ODOR THRESHOLD
    1) 1.80x10(-2) ppm (perfume/flavor grade purity) (HSDB , 1999)

References

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