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NORBORMIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Norbormide is a selective rodenticide lethal to rats but not other rodent species. It was developed by McNeil Laboratories in 1964 (Hayes, 1982). Because of its specificity, it is considered among the safest rodenticides.

Specific Substances

    1) 5-(alpha-hydroxy-alpha-2-pyridylbenzyl)-7-(alpha-2-
    2) pyridylbenzylidene)-norbor-5ene-2,3-dicarboximide
    3) McN-1,025
    4) S-6,999
    5) Molecular Formula: C33-H25-N3-O3
    6) CAS 991-42-4 (Norbormide)
    7) CAS 63907-08-4 (Norbormide hydrochloride)
    1.2.1) MOLECULAR FORMULA
    1) C33-H25-N3-O3

Available Forms Sources

    A) FORMS
    1) Norbormide is a white crystalline powder. It is stable at room temperature and to boiling. It is hydrolyzed by alkali; it is noncorrosive (Pelfrene, 1991). Brand names include Shoxin(R) and Raticate(R) (Pelfrene, 1991; Hayes, 1982).
    B) SOURCES
    1) It is usually found in cereal baits in concentrations of 5 to 10 g/kg. Baits should contain a warning dye (Pelfrene, 1991; Hayes, 1982).
    C) USES
    1) Norbormide is a selective rodenticide which is effective against most species of rats. It produces extreme irreversible peripheral vasoconstriction in the rats, resulting in death. Toxicity to other rodents is minimal (S Sweetman , 2001). Norbormide is apparently a unique agent. Many different analogs of norbormide have been evaluated, but none are as toxic to rats (Poos et al, 1966).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Human poisoning by norbormide is unlikely due to specificity for rats. Doses of 20 to 300 mg have been given to human volunteers with only minimal hypotensive effects. A dose of 300 mg corresponds to 60 grams of the 0.5% bait and 30 grams of the 1% bait.
    B) RATS given norbormide first present with a hunched position, followed by development of locomotor difficulties and weakness, but not paralysis of the hindlegs. Struggling, dyspnea, and mild seizures precede death which occurs within 15 minutes to 4 hours as a result of intense vasoconstriction.
    0.2.3) VITAL SIGNS
    A) Mild hypotension and fall in temperature may develop after ingestion.
    0.2.5) CARDIOVASCULAR
    A) The primary cause of death in rats is vasoconstriction. This effect has not been reported in humans.
    B) Mild reductions of systolic but not diastolic pressure were seen when 20 to 300 mg of norbormide was given orally to human volunteers. By 2 hours postingestion, the blood pressure levels were normal.
    0.2.14) DERMATOLOGIC
    A) Dermatitis has been reported following dermal exposure to a solution.
    B) Erythema with vascular injury due to an intradermal injection was observed in the rat.
    0.2.16) ENDOCRINE
    A) Hyperglycemia has been observed in rat studies.

Laboratory Monitoring

    A) No specific laboratory tests are needed unless otherwise clinically indicated. Monitor blood pressure in symptomatic patients. Rats develop hyperglycemia, but this has not been established as an effect in humans.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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.
    B) Poisoning cases should be treated with symptomatic and supportive care.
    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) Humans exposed to doses up to 300 mg have developed only mild reductions in systolic blood pressure.

Clinical Effects

Summary Of Exposure

    A) Human poisoning by norbormide is unlikely due to specificity for rats. Doses of 20 to 300 mg have been given to human volunteers with only minimal hypotensive effects. A dose of 300 mg corresponds to 60 grams of the 0.5% bait and 30 grams of the 1% bait.
    B) RATS given norbormide first present with a hunched position, followed by development of locomotor difficulties and weakness, but not paralysis of the hindlegs. Struggling, dyspnea, and mild seizures precede death which occurs within 15 minutes to 4 hours as a result of intense vasoconstriction.

Vital Signs

    3.3.1) SUMMARY
    A) Mild hypotension and fall in temperature may develop after ingestion.
    3.3.3) TEMPERATURE
    A) TEMPERATURE REDUCTION is cited as an effect based on a human study (Pelfrene, 1991; Hayes, 1982). The largest fall in temperature, 0.7 degree Centigrade, occurred at doses of 20 and 80 milligrams.
    3.3.4) BLOOD PRESSURE
    A) In a human study, 20 to 300 mg norbormide were given orally to volunteers. Mild reductions of systolic but not diastolic pressure were seen (HSDB , 2001) Pelgrene, 1991; (Hayes, 1982).

Cardiovascular

    3.5.1) SUMMARY
    A) The primary cause of death in rats is vasoconstriction. This effect has not been reported in humans.
    B) Mild reductions of systolic but not diastolic pressure were seen when 20 to 300 mg of norbormide was given orally to human volunteers. By 2 hours postingestion, the blood pressure levels were normal.
    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) CASE SERIES - In a human study, 20 to 300 mg norbormide were given orally to human volunteers. Mild reductions of systolic but not diastolic pressure were seen. The most significant changes were from 132/76 to 100/74 after a 200-mg dose and from 120/80 to 96/80 with a 300-mg dose, about 1 hour postingestion. By 2 hours postingestion, blood pressures were normal (HSDB , 2001; Pelfrene, 1991; Hayes, 1982)
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) VASOSPASM
    a) RATS - The primary cause of death in rats is vasoconstriction. This effect is also seen when 0.1 mL of a 0.1% solution is injected intradermally in rats. In humans this same injection produced no response (Roszkowski, 1965).

Neurologic

    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) COMA
    a) RATS - Coma developed 0.5 to 2 hours after oral or intraperitoneal doses of 1,020 mg/kg in rats (Patil & Radhakrishnamurty, 1973).
    2) SEIZURES
    a) RATS - Animals given norbormide first present with a hunched position; then, they develop locomotor difficulties and weakness, but not paralysis of the hindlegs. Struggling, dyspnea, and mild seizures precede death which occurs within 15 minutes to 4 hours because of intense vasoconstriction (Roszkowski et al, 1964).

Dermatologic

    3.14.1) SUMMARY
    A) Dermatitis has been reported following dermal exposure to a solution.
    B) Erythema with vascular injury due to an intradermal injection was observed in the rat.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) A case of dermatitis following accidental skin exposure was reported in an adult. Signs of acute skin inflammation with a clinical picture of chronic dermatosis were noted (HSDB , 2001).
    B) LACK OF EFFECT
    1) Following intradermal injections (0.1 mL of 0.1% norbormide solution) in human volunteers, no skin reactions or lesions were reported (HSDB , 2001).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SKIN NECROSIS
    a) RATS - Erythema with vascular injury due to an intradermal injection of 0.1 mL of 0.1% solution occurs in rats. Erythema develops 6 hours later and becomes maximal in 24 to 48 hours, occasionally progressing to necrosis (Hayes, 1982).

Endocrine

    3.16.1) SUMMARY
    A) Hyperglycemia has been observed in rat studies.
    3.16.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HYPERGLYCEMIA
    a) RATS - Doubling of blood glucose levels and a decrease of liver and muscle glycogen were noted after an oral or intraperitoneal dose of 1,020 mg/kg in rats. Coma began 0.5 to 2 hours after treatment. Insulin counteracted the hyperglycemic effect but did not protect against toxic manifestations and death (Patil & Radhakrishnamurty, 1973).
    b) MICE - No similar effects were elicited in 2 strains of mice (Hayes, 1982).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS991-42-4 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No specific laboratory tests are needed unless otherwise clinically indicated. Monitor blood pressure in symptomatic patients. Rats develop hyperglycemia, but this has not been established as an effect in humans.

Methods

    A) SPECTROSCOPY/SPECTROMETRY
    1) UV spectrophotometry has been employed for analysis of products and residues (Hartley & Kidd, 1987).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) No specific laboratory tests are needed unless otherwise clinically indicated. Monitor blood pressure in symptomatic patients. Rats develop hyperglycemia, but this has not been established as an effect in humans.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Since so little is known of norbormide's toxicity in humans, decontamination should be considered in patients with ingestions of amounts in excess of 300 mg of norbormide.
    B) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) Since little is known of norbormide's toxicity in humans, activated charcoal should be considered for ingestion of amounts in excess of 300 mg norbormide.
    2) 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.
    3) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) Significant toxicity after overdose is not expected due to the specificity of this compound for rats. Since no specific effect has been identified other than mild reduction of systolic blood pressure, only symptomatic and supportive care has been recommended.
    2) Since mild reductions of systolic blood pressure were reported in human volunteers, symptomatic patients should have blood pressures monitored for the first 2 hours postingestion.
    3) Although rats have shown hyperglycemia, this was not reported in tests on humans. Clinicians may wish to check blood glucose in ingestions of significant amounts.

Eye Exposure

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

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

Summary

    A) Humans exposed to doses up to 300 mg have developed only mild reductions in systolic blood pressure.

Minimum Lethal Exposure

    A) ACUTE
    1) Toxic hazard rating for humans involves a probable oral lethal dose between 5 to 15 grams/kilogram (between 1 pint and 1 quart for a 70-kilogram person) and 5 to 50 milligrams/kilogram (between 7 drops and 1 teaspoonful for a 70-kilogram person) (Gosselin et al, 1984).

Maximum Tolerated Exposure

    A) CASE REPORTS
    1) Doses up to 300 milligrams have been given to human volunteers with only mild reduction in systolic blood pressure (Hayes, 1982).
    2) No ill effects were noted in 3 adult male volunteers who received 15 milligrams/kilogram daily for 3 days (Worthing & Walker, 1983).
    B) ANIMAL DATA
    1) Dogs tolerated the equivalent of 1,000 parts per million for 60 days without ill effect. When given a dose corresponding to 10,000 parts per million for 15 to 60 days they looked "sick" and lost weight (Roszkowski et al, 1964). Animals receiving intravenous injections of 40 milligrams/kilogram showed no detectable responses (Hayes, 1982).
    2) At a dose of 1 gram/kilogram there was no detectable effect in cats, dogs, monkeys, sheep, and pigs (Roszkowski, et al, 1964; (Niu, 1970).
    3) A single oral dose of 1,000 milligrams/kilogram had no effect on monkeys or turkeys nor was it lethal to any of 40 other animal species tested (Worthing & Walker, 1983).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) Not established.

Workplace Standards

    A) ACGIH TLV Values for CAS991-42-4 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS991-42-4 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS991-42-4 :
    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 CAS991-42-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 2001 Hayes, 1982
    1) LD50- (ORAL)MOUSE:
    a) 2250 mg/kg
    2) LD50- (INTRAPERITONEAL)RAT:
    a) 20 mg/kg
    3) LD50- (ORAL)RAT:
    a) 3800 mcg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) RATS -
    1) VASOCONSTRICTION -
    a) Norbormide causes an extreme and irreversible peripheral vasoconstriction resulting from both systemic or local (in laboratory experiments) administration.
    b) This effect and the subsequent complications such as reduced coronary flow rate and arrhythmias, appears to be the cause of death.
    c) This vasoconstrictive effect was not seen even at high doses in animals other than the rat (Roszkowski, 1965; Niu, 1970).
    2) HYPERGLYCEMIA -
    a) Doses of about 1 g/kg produced a doubling of blood glucose with a decrease in both liver and muscle glycogen (Patil & Radhakrish, 1973).
    b) Coma began 0.5 to 2 hours post treatment.
    c) Insulin reversed the hyperglycemia, but the rats still died, suggesting the hyperglycemia is a secondary toxic effect (Patil & Radhakrish, 1973).

Physicochemical

Physical Characteristics

    A) Norbormide is a white crystalline powder. It is stable at room temperature and to boiling. It is hydrolyzed by alkali; it is noncorrosive (Pelfrene, 1991; Hayes, 1982).

Molecular Weight

    A) NORBORMIDE: 511.6 (S Sweetman , 2001)
    B) NORBORMIDE HYDROCHLORIDE: 547.06

References

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