Contact Us    Contact Us     |     Feedback
MOBILE VIEW  | 

CAMPHOR

Export To Excel

Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Camphor is a volatile, aromatic compound which is rapidly absorbed following ingestions and is highly toxic. Death generally results from respiratory depression or complications of seizures. A strong odor of camphor on the breath, or recent treatments with camphor-containing agents may suggest camphor poisoning. Absorption may also occur through topical or inhalation exposures.
    B) It has a familiar characteristic, fragrant, and penetrating odor and a slightly bitter and cooling taste.

Specific Substances

    1) 1,7,7-trimethylnorbornan-2-one
    2) 1,7,7-trimethylbicyclo[2,2,1]heptan-2-one
    3) 2-Boranone
    4) 2-Camphanone
    5) 2-keto-1,7,7-trimethylnorcamphane
    6) Bicyclo(2,2,1)heptan-2-one
    7) Bornan-2-one
    8) Camphor, natural
    9) Camphor, synthetic
    10) Camphora
    11) Camphre Droit (natural)
    12) Camphre du Japon (natural)
    13) Formosa camphor
    14) Gum camphor
    15) Japanese camphor
    16) Kamfer
    17) Laurel camphor
    18) Norcamphor, 1,7,7-trimethyll
    19) Matricaria camphor
    20) CAS 76-22-2 (Synthetic)
    21) CAS 464-49-3 (+)
    22) CAS 464-48-2 (-)
    23) CAS 21368-68-3 (+/-)
    1.2.1) MOLECULAR FORMULA
    1) C10-H16-O

Available Forms Sources

    A) FORMS
    1) Synthetic camphor is a colorless to white, translucent crystalline mass (O'Neil et al, 2006; Sax & Lewis, 1989).
    2) Camphor has the form of rhombohedral crystals from alcohol and cubic crystals by melting and chilling. It also has a familiar characteristic, fragrant, and penetrating odor and a pungent, aromatic taste (O'Neil et al, 2006).
    3) Camphor mothballs may be distinguished from naphthalene or paradichlorobenzene mothballs using a simple water test. Camphor mothballs will float in water, whereas naphthalene or paradichlorobenzene mothballs will sink in water (Koyama & Yamashita, 1991).
    4) Camphor mothballs are oilier than naphthalene or paradichlorobenzene mothballs. Camphor moth repellents are radiolucent, whereas naphthalene mothballs are faintly radiopaque, and paradichlorobenzene mothballs are densely radiopaque. Upon placement in a covered test tube in a 140 degrees F (60 degrees C) water bath, paradichlorobenzene melts, whereas camphor and naphthalene do not (Kuffner, 2006).
    5) All products containing camphor in oil or labeled camphorated oil, camphor oil, camphor liniment, or camphorated liniment have been taken off the US market (FDA, 1982). This does not include the camphor containing products such as Vicks Vaporub (4.8%), Vicks Vaposteam (6.2%) Camphophenique (11%), Absorbent Rub, etc. According to FDA regulations, as of 1982, nonprescription products may not contain greater than an 11% concentration of camphor.
    6) Triaminic vapor patches were removed from the US market in June 2006, following reports of seizures in children after chewing on the patches (Ragucci et al, 2007).
    B) SOURCES
    1) The natural form, derived from the gum of the camphor tree, Cinnamonum camphora, is optically active; otherwise it and the synthetic material appear to be identical (O'Neil et al, 2006; Sax & Lewis, 1989). Today it is produced synthetically from turpentine (Manoguerra, 2006).
    2) Camphor is an ingredient in liniments (0.3 to 20% camphor) and similar preparations designed to be applied externally for relief of muscular aches.
    3) Camphorated oils or liniments have usually contained 20% camphor by weight in cottonseed oil and are still available in these strengths outside of the U.S.
    4) Camphorated spirits (spirits of camphor) usually consist of 10% camphor by weight in isopropyl alcohol.
    5) Vicks Vaporub, Vicks Vaposteam and Camphophenique are commonly-used products containing camphor.
    6) Frequently, camphorated oils are mistaken for castor oil (Koeppel et al, 1982).
    C) USES
    1) Camphor has been used as a topical anti-infective, rubefacient, and antipruritic agent (Sax & Lewis, 1989). It has been used as an aphrodisiac, abortifacient, contraceptive, cold remedy, central nervous system and cardiovascular stimulant, lactation suppressant, and antiseptic (Manoguerra, 2006; Rabl et al, 1997).
    2) The American Academy of Pediatrics Committee on Drugs (1994) recommends that alternative therapeutic agents should be considered for all indications for camphor therapy - "no one" needs camphor (None Listed, 1994).
    3) Camphor may be abused for its stimulant effects (Koeppel et al, 1982).
    4) Camphor is still used rarely as a moth repellent in block or tablet form.
    5) It is used in the manufacture of plastics, especially celluloid; in lacquers and varnishes; in explosives; in pyrotechnics; as a moth repellent; in embalming fluids; in the manufacture of cymene; as a preservative in pharmaceuticals and cosmetics; and in camphorated parachlorophenol and paregoric (O'Neil et al, 2006; Proctor et al, 1988).
    6) Camphor is an excellent plasticizer for cellulose esters and ethers (O'Neil et al, 2006).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Camphor is used as a moth repellent, cold sore ointment, muscle cooling gel, anti-itch medication, and vapor-steam formulated cough suppressant. It is also used for industrial manufacture of plastics, embalming fluids, explosives, cosmetics, and varnishes. Over-the-counter products contain less than 11% camphor. Many herbal remedies and liniments contain camphor though the percentage is not well regulated.
    B) PHARMACOLOGY: The pharmacologic mechanism of camphor is not clear. Topical camphor may provide some relief of pruritic conditions or cooling of sore muscles; however, safer and more pharmacologically effective medications are available.
    C) TOXICOLOGY: Camphor acts as a CNS stimulant; the mechanism is not clear.
    D) EPIDEMIOLOGY: Toxicity from over-the-counter products is uncommon and severe toxicity is rare. Exposure to nonregulated products is rare but can produce severe toxicity.
    E) WITH THERAPEUTIC USE
    1) Headache, a feeling of warmth, and mild agitation can result from therapeutic uses of camphor. Asymptomatic transaminitis has been reported.
    F) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Camphor may lead to nausea and vomiting. Seizures may be the first clinical sign of severe toxicity; however, seizures are usually self-limited.
    2) SEVERE TOXICITY: Severe toxicity can result in delirium, visual hallucinations, cerebral edema, and status epilepticus. Systemic toxicity may include hypotension, tachycardia, respiratory failure and death.
    0.2.3) VITAL SIGNS
    A) Sinus tachycardia may occur following ingestion of camphor.
    0.2.20) REPRODUCTIVE
    A) Following ingestion, camphor crosses the placenta. Topical camphor is classified as FDA Pregnancy Category C. In one study, the topical use of camphorated oil in pregnancy was not associated with teratogenic effects.

Laboratory Monitoring

    A) Mild to moderate toxicity does not require laboratory evaluation.
    B) Monitor renal function, electrolytes, glucose, and calcium in patients with significant gastrointestinal effects or recurrent seizures.
    C) Monitor creatine phosphokinase concentration and venous blood gas in patients with recalcitrant seizures.
    D) Obtain a chest x-ray in symptomatic patients.
    E) Neuroimaging should be performed in patients with persistent confusion or recurrent seizures in order to rule out cerebral edema or alternative etiologies.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Supportive care with fluids and benzodiazepines will treat most toxic sequelae. Tachycardia is well-tolerated and no specific treatment, other than fluid resuscitation and benzodiazepines, is necessary.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Airway management may be necessary for severe CNS depression or recalcitrant seizures. Status epilepticus should be treated with high-dose benzodiazepines followed by propofol or phenobarbital, if benzodiazepines are ineffective. Fluid resuscitation should be the first line treatment for hypotension. Hypotension unresponsive to fluids should be treated with vasopressors.
    C) DECONTAMINATION
    1) PREHOSPITAL: Wash the skin thoroughly. Activated charcoal should not be administered since the main toxic effect is seizures.
    2) HOSPITAL: Gastric aspiration followed by activated charcoal should be attempted for severe toxicity from recent camphor ingestion that requires intubation.
    D) AIRWAY MANAGEMENT
    1) Airway management may be necessary for severe CNS depression or recalcitrant seizures.
    E) ANTIDOTE
    1) There is no antidote available.
    F) SEIZURES
    1) Agitation and seizures should be treated with benzodiazepines. Large doses may be necessary to suppress seizure activity, followed by propofol and phenobarbital, if benzodiazepines are ineffective.
    G) ENDOSCOPY
    1) Ingestion often leads to nausea, vomiting, diarrhea, and abdominal pain. Some camphor formulations are caustic and can lead to esophageal and gastric burns. Endoscopy is indicated for hematemesis or persistent dysphagia.
    H) ENHANCED ELIMINATION
    1) Neither hemodialysis nor hemoperfusion are effective in removing camphor because of its high lipid solubility and volume of distribution.
    I) PATIENT DISPOSITION
    1) HOME CRITERIA: Asymptomatic patients that inadvertently ingest less than 30 mg/kg, or patients who have remained asymptomatic for at least 4 hours after exposure, can be managed at home if someone is available to observe them. For a 10 kg child, this would permit home management for ingestion of less than: 2.8 mL of a product containing 108 mg of camphor/mL (10.8%), or 6.4 mL of an ointment with 4.8% camphor, or 7.6 mL of a cream with 4% camphor.
    2) OBSERVATION CRITERIA: Patients with deliberate ingestions, signs of moderate to severe toxicity (eg, convulsions, lethargy, ataxia, severe nausea and vomiting) by any route of exposure, and those who ingest 30 mg/kg or more should be referred to a health care facility for treatment (preferably by ambulance as seizures may develop abruptly). For a 10 kg child, this would require referral after ingestion of: 2.8 mL of a product containing 108 mg of camphor/mL (10.8%), or 6.4 mL of an ointment with 4.8% camphor, or 7.6 mL of a cream with 4% camphor. Patients who are asymptomatic or have only mild GI and CNS symptoms that resolve after 4 to 6 hours of observation may be discharged.
    3) ADMISSION CRITERIA: Patients with multiple seizures, severe GI symptoms, or systemic symptoms should be admitted.
    4) CONSULT CRITERIA: A medical toxicologist or poison center should be consulted for any patient with severe toxicity.
    J) PITFALLS
    1) Failure to use adequate doses of benzodiazepines for recurrent seizures. Failure to wash off topical exposures. Failure to inquire about herbal remedies. Failure to educate patients and families about potential toxicity of camphor.
    K) PHARMACOKINETICS
    1) Significant absorption occurs from inhalation, ingestion, dermal, or mucous membrane application. Absorption is rapid and peak concentration is within 90 minutes. Volume of distribution is 2 to 4 L/kg. Camphor is hepatically metabolized and renally cleared.
    L) TOXICOKINETICS
    1) Toxicity occurs rapidly following exposure, usually within 1 hour. Seizures may be the first manifestation of toxicity.
    M) DIFFERENTIAL DIAGNOSIS
    1) Many toxins can result in seizures (e.g., isoniazid, Gyromitra spp. mushrooms, bupropion, sympathomimetics). Other medical conditions must be considered if the history of exposure is questionable. Disorders such as intracranial hemorrhage, hypoglycemia, ethanol withdrawal, or meningitis should be considered and the appropriate workup pursued.

Range Of Toxicity

    A) TOXICITY: Gastrointestinal irritation and CNS depression may occur at doses over 10 mg/kg. Serious toxicity has not been reported below 30 mg/kg; however, ingestions at or above 30 mg/kg should be referred to an emergency department for evaluation. For a 10 kg child, this would require referral after ingestion of: 2.8 mL of a product containing 108 mg of camphor/mL (eg, campho-phenique), or 6.4 mL of an ointment with 4.% camphor (eg Vicks VapoRub Ointment) or 7.6 mL of a cream with 4% camphor (eg BenGay Ultra Strength Cream). As little as 1 g has been fatal in infants, and death has been reported with doses of 50 mg/kg or more. Exposures by any route resulting in moderate to severe toxicity (eg, convulsions, lethargy, ataxia, severe nausea and vomiting) should also be referred for evaluation.
    B) THERAPEUTIC DOSE: Varies depending upon the product used.

Clinical Effects

Summary Of Exposure

    A) USES: Camphor is used as a moth repellent, cold sore ointment, muscle cooling gel, anti-itch medication, and vapor-steam formulated cough suppressant. It is also used for industrial manufacture of plastics, embalming fluids, explosives, cosmetics, and varnishes. Over-the-counter products contain less than 11% camphor. Many herbal remedies and liniments contain camphor though the percentage is not well regulated.
    B) PHARMACOLOGY: The pharmacologic mechanism of camphor is not clear. Topical camphor may provide some relief of pruritic conditions or cooling of sore muscles; however, safer and more pharmacologically effective medications are available.
    C) TOXICOLOGY: Camphor acts as a CNS stimulant; the mechanism is not clear.
    D) EPIDEMIOLOGY: Toxicity from over-the-counter products is uncommon and severe toxicity is rare. Exposure to nonregulated products is rare but can produce severe toxicity.
    E) WITH THERAPEUTIC USE
    1) Headache, a feeling of warmth, and mild agitation can result from therapeutic uses of camphor. Asymptomatic transaminitis has been reported.
    F) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Camphor may lead to nausea and vomiting. Seizures may be the first clinical sign of severe toxicity; however, seizures are usually self-limited.
    2) SEVERE TOXICITY: Severe toxicity can result in delirium, visual hallucinations, cerebral edema, and status epilepticus. Systemic toxicity may include hypotension, tachycardia, respiratory failure and death.

Vital Signs

    3.3.1) SUMMARY
    A) Sinus tachycardia may occur following ingestion of camphor.
    3.3.3) TEMPERATURE
    A) HYPERTHERMIA: Mild hyperthermia may develop in patients with protracted seizures (Smith & Margolis, 1954; Goldfrank & Bresnitz, 1980).
    3.3.5) PULSE
    A) TACHYDYSRHYTHMIA: Sinus tachycardia may occur following ingestion of camphor (Koeppel et al, 1988; Benz, 1919; Smith & Margolis, 1954; Phelan, 1976; Goldfrank & Bresnitz, 1980).

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) MYDRIASIS: Mydriasis may occur with systemic camphor poisoning (Grant & Shuman, 1993).
    2) VISUAL DEFECTS: Flickering, darkening, or veiling of vision have been reported following oral doses of 0.06 to 4 grams (Grant & Shuman, 1993).
    3) SPLASH CONTACT: Eye exposure to camphor results in irritation, but no serious injuries have been reported (Grant & Shuman, 1993).
    4) IRRITATION: Ocular irritation occurred in workers exposed to approximately 2 ppm of camphor (Gronka et al, 1969; Proctor et al, 1988).
    5) KERATOCONJUNCTIVITIS
    a) CASE REPORT: A 61-year-old man who applied camphor oil presumably periorbitally secondary to delusions of parasitosis suffered severe corneal epithelial defects, ulceration, keratic precipitates, and mature cataract. This was complicated by secondary infection and corneal perforation, which required therapeutic penetrating keratoplasty (Lim et al, 2006).
    b) CASE REPORT: A 45-year-old man developed dermato-keratoconjunctivitis with corneal ulcer, corneal haze, conjunctival hyperemia, and lid edema after applying Vicks Vaporub around the eyes. The right eye required evisceration (Jaiwal, 1989).
    3.4.5) NOSE
    A) ANOSMIA: Workers exposed to approximately 2 ppm of camphor reported a loss of the sense of smell (Gronka et al, 1969).
    B) IRRITATION: Nasal irritation was described in workers exposed to 2 ppm of camphor (Gronka et al, 1969).
    3.4.6) THROAT
    A) IRRITATION: Burning of the mouth and throat mucosa are common following ingestion of camphor. Dry and sore throat occurred in 1 of 6 workers exposed to approximately 2 ppm of camphor (Gronka et al, 1969). A symptom of camphor poisoning typically includes the odor of camphor on the victim's breath.

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) TACHYARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) Sinus tachycardia may occur following camphor ingestion (Khine et al, 2009; Koeppel et al, 1988; Phelan, 1976; Smith & Margolis, 1954; Benz, 1919).
    b) CASE REPORT: Heart rates of 122 beats/min and 140 beats/min were reported in a 3-year-old girl and a 15-month-old boy, respectively, following ingestion of one teaspoonful and 20 mL of camphorated oil. Seizure activity occurred within 10 to 20 minutes of ingestion in both children (Theis & Koren, 1995).
    c) Unspecified dysrhythmias were noted in 5 patients ingesting a mean dose of 152 mg/kg (Geller et al, 1984).
    B) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Circulatory collapse is a rare effect that may develop with severe overdose (Vasey & Karayannopoulos, 1972).
    b) CASE REPORT: A blood pressure of 74/56 mm Hg was reported in a 15-month-old boy after ingestion of approximately 20 mL of 20% camphorated oil (Theis & Koren, 1995).
    C) MYOCARDITIS
    1) WITH POISONING/EXPOSURE
    a) Myocarditis is a rare effect.
    1) CASE REPORT: Ingestion of 8 grams of camphor was associated with QRS and QTc prolongation, and echocardiographic features of myocarditis, including decreased ejection fraction (40%). The changes resolved within 36 hours (Bhaya & Beniwal, 2007).
    D) CARDIAC ARREST
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 63-year-old man presented to the emergency department (ED) with apnea and in cardiac arrest following inadvertent administration of 4 ounces of a vaporizer fluid containing 6.2% (7.4 g) of camphor into his PEG tube. The estimated dose of camphor administered was 81 mg/kg. The patient's medical history included a cerebral aneurysm, left hemiparesis, dysphagia, ventriculoperitoneal shunt, and seizures. Following resuscitative efforts at the ED, the patient's circulation returned after 10 minutes of asystole. An ECG revealed a heart rate of 63 bpm with sinus rhythm, a QRS complex of 101, a QTc interval of 458, and t-wave flattening. Following intubation and mechanical ventilation, the patient experienced 2 more episodes of cardiac arrest. A repeat ECG indicated prolongation of the QTc interval to 540. Over the next several days, the patient's condition continued to deteriorate following a hospital course complicated by aspiration pneumonitis, hypotension, acidosis, atrial fibrillation, hypovolemia, bilateral cerebellar massive infarcts, and myoclonic jerking. Eleven days post-exposure, the patient died following a family decision to withdraw life support (Goertemoeller et al, 2015).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) ACUTE RESPIRATORY INSUFFICIENCY
    1) WITH POISONING/EXPOSURE
    a) Death is usually the result of postconvulsive respiratory depression with apnea (Emery & Corban, 1999; Reid, 1979). Respiratory depression necessitating intubation and ventilation is common following ingestions.
    b) Decreased respirations were reported in 2 children after ingestions of about 5 mL and 20 mL of camphorated oil. Both developed seizures and were treated with intravenous diazepam; one also received phenobarbital. Both children responded to respiratory assistance (Theis & Koren, 1995).
    B) PULMONARY ASPIRATION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 20-month-old child swallowed camphorated oil and aspirated. This produced profuse salivation resembling acute pulmonary edema and intermittent gasping respirations (LAURIE, 1950).
    b) Aspiration may also occur secondary to seizure activity (Kopelman et al, 1979a)

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Camphor poisoning classically produces seizures, including status epilepticus (Khine et al, 2009; Guilbert et al, 2007; Emery & Corban, 1999; Bridge, 1995; Nishimori et al, 1994; Koeppel et al, 1988; Reid, 1979; Antman et al, 1978; Phelan, 1976; Aronow & Spigiel, 1976; Vasey & Karayannopoulos, 1972).
    1) Seizures may occur suddenly and without warning (Kopelman et al, 1979) or may be preceded by fasciculations, mental confusion and irritability (Phelan, 1976), neuromuscular hyperactivity, and jerky movements of extremities (Michiels & Mazor, 2010; Gibson et al, 1989; Antman et al, 1978; Craig, 1953).
    b) Large series of camphor poisonings totaling 748 patients mostly children, have shown an incidence of seizures of 4% to 42% following ingestion of 700 to 6000 mg (Phelan, 1976). Seizures were reported in one patient with a camphor concentration of 14.5 mg/L (Winter et al, 1991).
    c) Seizure may be delayed as long as 9 hours post-ingestion (Ruha et al, 2003).
    d) CASE REPORTS
    1) ADULT
    a) Grand mal seizures occurred within 5 to 10 minutes of ingestion of 4.75 grams (68 mg/kg) of camphor in an adult (Lahoud et al, 1997).
    b) A 52-year-old man, with a history of ingesting small amounts of pure camphor crystals to help with his nasal allergies and to aid in digestion, developed nausea, abdominal pain, palpitations, headache, confusion, and 2 witnessed seizures after ingesting a large teaspoonful of camphor crystals. The patient had no history of seizures or recent head trauma. Following hospital presentation, his vital signs and neurological examination, including a noncontrast head CT scan, were normal. Because the patient had not mentioned his history of camphor ingestion, phenytoin therapy was initiated and the patient was discharged 24 hours later without recurrence of seizures. After his camphor ingestion history was known, phenytoin therapy was discontinued and, at his 4-month follow-up examination, the patient remained seizure-free. It was estimated that the patient had ingested 10 g of camphor, as a single ingestion, prior to onset of symptoms (MacKinney et al, 2015).
    2) PEDIATRIC
    a) Theis & Koren (1995) reported two children, a 3-year-old and a 15-month-old, who developed generalized tonic-clonic seizures within 20 minutes of ingestion of one teaspoonful and 20 mL, respectively, of 19% and 20% camphorated oil. Both children developed a second seizure upon arrival at a hospital, which responded to diazepam (Theis & Koren, 1995).
    b) TOPICAL EXPOSURE: Generalized tonic-clonic seizures, developing into status epilepticus, occurred in a 4-month-old child approximately 72 hours following dermal exposure to a camphor-containing solution given as an abdominal massage to the child. The solution was reported to have anti-flatulence effects. The seizures stopped and the child recovered without neurologic deficits following symptomatic treatment with clonazepam and phenobarbital (Guilbert et al, 2007). Chan et al (2009) reported that camphor is rapidly absorbed transcutaneously and causes rapid onset of seizures, usually within the first few hours. Therefore, it is unlikely that camphor was the cause of seizures in this patient (Chan et al, 2009).
    c) Generalized seizures were reported in 3 children (ages ranging from 15 months to 3 years) following exposure to camphor. Two of the children (ages 15 months and 22 months) had ingested camphor cubes within one hour prior to onset of symptoms. The 3-year-old child developed seizures after camphor ointment was applied to her upper chest, forehead, and back every hour for 10 hours for treatment of cold symptoms. Camphor-containing products had also been used in various areas within the child's bedroom. All 3 children recovered with supportive therapy. On follow-up 10 weeks post-discharge, no additional seizure episodes were reported (Khine et al, 2009).
    d) A 3-year-old girl ingested at least 1 tablet containing 0.5 to 1 g of camphor and, 45 minutes later, experienced a seizure, characterized by unresponsiveness, teeth grinding, eye blinking, and posturing. On presentation to the emergency department, the patient experienced 3 more seizures, with each seizure lasting 2 to 3 minutes. With supportive treatment, the patient recovered and was discharged without sequelae (Michiels & Mazor, 2010).
    e) A 1.5-year-old child presented with 30 minutes of recurrent vomiting and generalized tonic-clonic seizures. At admission, the patient was drowsy (Glasgow Coma Scale score of 10), but vital signs were normal; however, there was a noticeable aromatic odor from the patient's breath and vomitus. With administration of lorazepam and phenobarbital, the seizures resolved. Laboratory parameters, CT scan of the head and an EEG were normal. Interview of the mother revealed that the patient had ingested approximately 2 teaspoonfuls of an oil containing an unknown concentration of camphor to treat joint pains approximately 1 hour before presentation. With supportive care, the patient completely recovered within 24 hours and was discharged on day 3. There was no evidence of the recurrence of seizures at his follow up exams 4 weeks and 12 weeks later (Marwah & Marwah, 2014).
    B) PSYCHOMOTOR AGITATION
    1) WITH POISONING/EXPOSURE
    a) Hallucinations and agitation may occur (Koeppel et al, 1982).
    C) CLOUDED CONSCIOUSNESS
    1) WITH POISONING/EXPOSURE
    a) Confusion, headache, dizziness, twitching of facial muscles, spasticity, and anxiety may occur after heavy inhalation exposures (Proctor et al, 1988).
    b) Chronic poisoning may cause CNS depression (Jimenez et al, 1983).
    c) Confusion persisted for 3 days in a patient augmenting dermabrasive therapy ("coining") with camphor balm (Rampini et al, 2002).
    D) COMA
    1) WITH POISONING/EXPOSURE
    a) Seizures may be followed by coma and apnea (Kopelman et al, 1979; Smith & Margolis, 1954).
    b) In the absence of seizures, coma may progress to death (Jimenez et al, 1983a).
    E) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 10-year-old boy presented to the emergency department with lethargy, nausea, vomiting, and rigors, as well as complaining of neck pain and stiffness, approximately 24 hours after ingesting 3 medicated patches. Each patch contained 4.7% camphor (95.37 mg) and 2.6% menthol. Physical examination revealed tremors, hyperreflexia, clonus, and pain on flexion of his neck. With supportive care, the patient recovered and was discharged 4 days post-admission (Ragucci et al, 2007).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Oral and epigastric burning, nausea, and vomiting usually occur shortly after ingestion and are common effects (MacKinney et al, 2015; Michiels & Mazor, 2010; Khine et al, 2009; Antman et al, 1978; Craig, 1953).
    b) CASE REPORT: A 10-year-old boy presented to the emergency department with lethargy, nausea, vomiting, and rigors, as well as complaining of neck pain and stiffness, approximately 24 hours after ingesting 3 medicated patches. Each patch contained 4.7% camphor (95.37 mg) and 2.6% menthol. With supportive care, the patient recovered and was discharged 4 days post-admission (Ragucci et al, 2007).
    c) CASE REPORT: A 1.5-year-old child presented with 30 minutes of recurrent vomiting and generalized tonic-clonic seizures. At admission, the patient was drowsy (Glasgow Coma Scale score of 10), but vital signs were normal; however, there was a noticeable aromatic odor from the patient's breath and vomitus. With administration of lorazepam and phenobarbital, the seizures resolved. Laboratory parameters, CT scan of the head and an EEG were normal. Interview of the mother revealed that the patient had ingested approximately 2 teaspoonfuls of an oil containing an unknown concentration of camphor to treat joint pains approximately 1 hour before presentation. With supportive care, the patient completely recovered within 24 hours and was discharged on day 3. There was no evidence of the recurrence of seizures at his follow up exams 4 weeks and 12 weeks later (Marwah & Marwah, 2014).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) A mild poisoning can produce a transiently elevated AST, ALT, and lactic dehydrogenase (LDH) (Theis & Koren, 1995; Reid, 1979; Antman et al, 1978; Weiss & Catalano, 1973) .
    b) Elevations in AST (peak 1550), ALT (peak 568), LDH (peak 738), and alkaline phosphatase (peak 296) were reported following daily dermal application of a cold remedy containing camphor (4.8%) in a 2-month-old baby (Uc et al, 2000).
    c) Mildly elevated AST (169) and ALT (183) followed dermabrasive therapy ("coining") augmented with camphor balm (Rampini et al, 2002).
    B) ABNORMAL LIVER FUNCTION
    1) WITH POISONING/EXPOSURE
    a) CHRONIC TOXICITY
    1) Chronic ingestion may cause granulomatous hepatitis (McCollam et al, 1989) or fatty metamorphosis (Jimenez et al, 1983a).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) WITH POISONING/EXPOSURE
    a) Leukocyte counts may become elevated following poisoning with camphor. A leukocyte count of 18.2 x10(9)/L was reported in a 15-month-old boy after ingestion of 20 mL of 20% camphorated oil (Theis & Koren, 1995). A mild lymphocytosis was reported in a 20-month-old girl after ingestion of an unknown amount of camphor (Emery & Corban, 1999).
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) PORPHYRIN PRODUCTION
    a) Camphor exposure has resulted in an increase in porphyrin production in primary cultures of chick embryo liver cells. This may have an implication in toxicities of persons with known underlying defects in hepatic heme synthesis (Bonkovsky et al, 1992).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) CONTACT DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Two cases of contact allergy have been reported as a result of exposure to a sunscreen agent containing 3-(4-methylbenzylidene)-d-1-camphor (Bilsland & Ferguson, 1993). Buckley et al (1993) report a case of contact and photocontact allergy to methylbenzylidene camphor with presentation including pruritic, blistering, erythematous rash on body areas exposed to sunlight.
    B) PARESTHESIA
    1) WITH POISONING/EXPOSURE
    a) Green (1990) has demonstrated a 20% camphor solution on skin to be a weak sensory irritant with modest excitatory effect on thermosensitive cutaneous fibers. It produced a significant increase in the frequency of reports of topical burning (Green, 1990).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) Uncontrolled, camphor-induced seizures might precipitate rhabdomyolysis.

Reproductive

    3.20.1) SUMMARY
    A) Following ingestion, camphor crosses the placenta. Topical camphor is classified as FDA Pregnancy Category C. In one study, the topical use of camphorated oil in pregnancy was not associated with teratogenic effects.
    3.20.2) TERATOGENICITY
    A) LACK OF EFFECT
    1) Following exposure to topical camphor in the first four lunar months of pregnancy, 168 mother-child pairs evaluated as part of the Collaborative Perinatal Project, had no increase risk of malformation; 763 patients who used camphor or any time during pregnancy had no increased risk of malformation (Heinonen et al, 1977).
    3.20.3) EFFECTS IN PREGNANCY
    A) PREGNANCY CATEGORY
    1) Camphor is classified as FDA pregnancy category C (Briggs et al, 1998).
    B) FETAL DEATH
    1) ORAL - Following oral ingestion, camphor crosses the placenta and has been associated with one fetal death (Riggs et al, 1965), but 2 other cases resulted in apparently healthy babies (Weiss & Catalano, 1973).
    C) FETAL LIVER ENZYMES ABNORMAL
    1) Weiss & Catalano (1973) reported uncomplicated delivery which occurred within 24 hours of ingestion of 2 ounces of camphorated oil (10 days pre-estimated day of confinement). In the infant, AST and ALT were transiently and mildly elevated. Both infant and amniotic fluid had an odor of camphor. (Weiss & Catalano, 1973).
    D) LACK OF EFFECT
    1) ORAL
    a) Weiss & Catalano (1973) reported uncomplicated delivery which occurred within 24 hours of ingestion of 2 ounces of camphorated oil (10 days pre-estimated day of confinement). Both infant and amniotic fluid had an odor of camphor (Weiss & Catalano, 1973). In another case, a healthy baby was born 6 months after ingestion of 45 mL of camphorated oil which produced seizures in the mother (Blackmon & Curry, 1957).
    b) Thirty grams of camphor in 250 mL of red wine was used in an intentional attempt to induce abortion at 6 weeks gestation. The patient recovered and underwent elective termination of pregnancy. There was no toxicological evaluation of the fetus (Rabl et al, 1997).
    c) A 17-year-old woman drank 60 mL of camphorated oil in order to induce abortion. She recovered and the fetus remained viable, although no further information was provided (Jacobziner & Raybin, 1962).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS76-22-2 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.3) HUMAN STUDIES
    A) LACK OF EFFECT
    1) Carcinogenicity tests using only camphor alone have been negative (ACGIH, 1996).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Mild to moderate toxicity does not require laboratory evaluation.
    B) Monitor renal function, electrolytes, glucose, and calcium in patients with significant gastrointestinal effects or recurrent seizures.
    C) Monitor creatine phosphokinase concentration and venous blood gas in patients with recalcitrant seizures.
    D) Obtain a chest x-ray in symptomatic patients.
    E) Neuroimaging should be performed in patients with persistent confusion or recurrent seizures in order to rule out cerebral edema or alternative etiologies.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Tests for qualitative and quantitative determination of camphor concentrations are not generally available. Very little information has been published on the dose-plasma concentration relationship in camphor poisoning (Koeppel et al, 1988; Kopelman, 1990).
    2) Monitor renal function, electrolytes, glucose, and calcium in patients with significant gastrointestinal effects or recurrent seizures.
    3) Monitor creatine phosphokinase concentration and venous blood gas in patients with recalcitrant seizures.
    4.1.3) URINE
    A) Tests for urine qualitative and quantitative determination of camphor concentrations are not generally available. Very little information has been published on the dose-urine concentration relationship in camphor poisoning.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor ECG in symptomatic patients.
    b) Provide continuous cardiopulmonary monitoring and obtain a chest radiograph in patients with prolonged CNS depression or respiratory symptoms.
    2) NEUROIMAGING
    a) Neuroimaging should be performed in patients with persistent confusion or recurrent seizures in order to rule out cerebral edema or alternative etiologies.

Methods

    A) CHROMATOGRAPHY
    1) Camphor has been measured by flame ionization gas chromatography, following extraction by hexane and using acetophenone (Kelly et al, 1979) or bornyl acetate (Koeppel et al, 1988; Koeppel et al, 1982; Winter et al, 1991) as an internal standard. The method has a detection limit of 0.1 microgram/milliliter.
    2) Plasma camphor concentrations in an 84-year-old woman were determined by HPLC (Nishimori et al, 1994).

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) Patients who have developed either severe gastrointestinal or neurologic symptoms of poisoning should also be admitted regardless of the amount ingested (Manoguerra, 2006).
    1) Patients should be observed in a monitored setting where immediate anticonvulsant therapy and respiratory support can be provided.
    6.3.1.2) HOME CRITERIA/ORAL
    A) An asymptomatic patient who has reported an inadvertent exposure of less than 30 mg/kg of camphor can be managed at home if someone is available to observe them (Manoguerra, 2006; Geller et al, 1984). For a 10 kg child, this would permit home management for ingestion of less than: 2.8 mL of a product containing 108 mg of camphor/mL (eg campho-phenique), or 6.4 mL of an ointment with 4.8% camphor (eg Vicks VapoRub Ointment) or 7.6 mL of a cream with 4% camphor (eg BenGay Ultra Strength Cream) (Manoguerra, 2006).
    B) Patients who have a reported ingestion of camphor and have remained asymptomatic for 4 hours can be observed at home (Manoguerra, 2006).
    C) Clinically significant camphor toxicity has not been reported below 30 mg/kg of camphor and is uncommon below 50 mg/kg of camphor in asymptomatic patients (Geller et al, 1984).
    D) Patients reportedly ingesting between 10 to 30 mg/kg appear to be at risk for the development of minor symptoms, but still at low risk for seizures (Geller et al, 1984).
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) A medical toxicologist or poison center should be consulted for any patient with severe toxicity.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with deliberate ingestions, signs of moderate to severe toxicity (eg, convulsions, lethargy, ataxia, severe nausea and vomiting) by any route of exposure, and those who ingest 30 mg/kg or more should be referred to a health care facility for treatment (preferably by ambulance as seizures may develop abruptly). For a 10 kg child, this would require referral after ingestion of: 2.8 mL of a product containing 108 mg of camphor/mL (eg campho-phenique), or 6.4 mL of an ointment with 4.8% camphor (eg Vicks VapoRub Ointment) or 7.6 mL of a cream with 4% camphor (eg BenGay Ultra Strength Cream) (Manoguerra, 2006).
    1) Consider transportation via ambulance following any acute ingestion. Seizures may occur within minutes after ingestion without warning while en route to the emergency department (Gibson et al, 1989).
    2) Patients should be observed in a monitored setting where immediate anticonvulsant therapy and respiratory support can be provided.
    3) Patients who have remained asymptomatic for a period of 4 to 6 hours since ingestion may be discharged.

Monitoring

    A) Mild to moderate toxicity does not require laboratory evaluation.
    B) Monitor renal function, electrolytes, glucose, and calcium in patients with significant gastrointestinal effects or recurrent seizures.
    C) Monitor creatine phosphokinase concentration and venous blood gas in patients with recalcitrant seizures.
    D) Obtain a chest x-ray in symptomatic patients.
    E) Neuroimaging should be performed in patients with persistent confusion or recurrent seizures in order to rule out cerebral edema or alternative etiologies.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL
    1) Activated charcoal is not recommended for prehospital management of camphor ingestions.
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) No human study has been reported that demonstrates activated charcoal is or is not effective as a gastrointestinal decontaminant in camphor poisoning. Dean et al (1992) showed no difference in the absorption of camphor when activated charcoal was used in a rat model (Dean et al, 1992).
    2) Due to the rapid absorption of liquid camphor, fast onset of action, and risk of seizure from camphor ingestion, activated charcoal is not generally recommended after camphor ingestion. It may be considered in selected cases if other toxic substances have been coingested (Manoguerra, 2006; Kuffner, 2002).
    3) 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.
    4) 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) AIRWAY MANAGEMENT
    1) Adequacy of respirations and oxygenation must be assured. Supplemental oxygenation, assisted respirations, and endotracheal intubation may be necessary.
    B) MONITORING OF PATIENT
    1) Mild to moderate toxicity does not require laboratory evaluation.
    2) Monitor renal function, electrolytes, glucose, and calcium in patients with significant gastrointestinal effects or recurrent seizures.
    3) Monitor creatine phosphokinase concentration and venous blood gas in patients with recalcitrant seizures.
    4) Obtain a chest x-ray in symptomatic patients.
    5) Neuroimaging should be performed in patients with persistent confusion or recurrent seizures in order to rule out cerebral edema or alternative etiologies.
    C) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    7) RECURRING SEIZURES
    a) If seizures are not controlled by the above measures, patients will require endotracheal intubation, mechanical ventilation, continuous EEG monitoring, a continuous infusion of an anticonvulsant, and may require neuromuscular paralysis and vasopressor support. Consider continuous infusions of the following agents:
    1) MIDAZOLAM: ADULT DOSE: An initial dose of 0.2 mg/kg slow bolus, at an infusion rate of 2 mg/minute; maintenance doses of 0.05 to 2 mg/kg/hour continuous infusion dosing, titrated to EEG (Brophy et al, 2012). PEDIATRIC DOSE: 0.1 to 0.3 mg/kg followed by a continuous infusion starting at 1 mcg/kg/minute, titrated upwards every 5 minutes as needed (Loddenkemper & Goodkin, 2011).
    2) PROPOFOL: ADULT DOSE: Start at 20 mcg/kg/min with 1 to 2 mg/kg loading dose; maintenance doses of 30 to 200 mcg/kg/minute continuous infusion dosing, titrated to EEG; caution with high doses greater than 80 mcg/kg/minute in adults for extended periods of time (ie, longer than 48 hours) (Brophy et al, 2012); PEDIATRIC DOSE: IV loading dose of up to 2 mg/kg; maintenance doses of 2 to 5 mg/kg/hour may be used in older adolescents; avoid doses of 5 mg/kg/hour over prolonged periods because of propofol infusion syndrome (Loddenkemper & Goodkin, 2011); caution with high doses greater than 65 mcg/kg/min in children for extended periods of time; contraindicated in small children (Brophy et al, 2012).
    3) PENTOBARBITAL: ADULT DOSE: A loading dose of 5 to 15 mg/kg at an infusion rate of 50 mg/minute or lower; may administer additional 5 to 10 mg/kg. Maintenance dose of 0.5 to 5 mg/kg/hour continuous infusion dosing, titrated to EEG (Brophy et al, 2012). PEDIATRIC DOSE: A loading dose of 3 to 15 mg/kg followed by a maintenance dose of 1 to 5 mg/kg/hour (Loddenkemper & Goodkin, 2011).
    4) THIOPENTAL: ADULT DOSE: 2 to 7 mg/kg, at an infusion rate of 50 mg/minute or lower. Maintenance dose of 0.5 to 5 mg/kg/hour continuous infusing dosing, titrated to EEG (Brophy et al, 2012)
    b) Endotracheal intubation, mechanical ventilation, and vasopressors will be required (Brophy et al, 2012) and consultation with a neurologist is strongly advised.
    c) Neuromuscular paralysis (eg, rocuronium bromide, a short-acting nondepolarizing agent) may be required to avoid hyperthermia, severe acidosis, and rhabdomyolysis. If rhabdomyolysis is possible, avoid succinylcholine chloride, because of the risk of hyperkalemic-induced cardiac dysrhythmias. Continuous EEG monitoring is mandatory if neuromuscular paralysis is used (Manno, 2003).
    D) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    E) ENDOSCOPY
    1) Ingestion often leads to nausea, vomiting, diarrhea, and abdominal pain. Some camphor formulations are caustic and can lead to esophageal and gastric burns. Endoscopy is indicated for hematemesis or persistent dysphagia.
    F) CONTRAINDICATED TREATMENT
    1) Never administer oils, alcohols or fats to a person who has ingested camphor. These substances promote gastrointestinal absorption.
    G) OBSERVATION REGIMES
    1) Close observation for symptoms in the patient is the primary consideration in treatment.
    H) SMELL OF BREATH - FINDING
    1) Odor of camphor on the breath - may assist in diagnosis of camphor poisoning.

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) Absorption may be both dermal and inhalational from topical application of the medication. Pulmonary edema may develop with systemic toxicity though there is no direct pulmonary toxicity from camphor inhalation.
    B) PULMONARY ABSORPTION
    1) Inhalation of camphor via a vaporizer preparation resulted in a seizure in a child who had previously developed seizures following a dermal exposure (Skoglund et al, 1977).
    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) IRRITATION SYMPTOM
    1) Camphor is an eye irritant.
    2) Keratitis (inflammation of the cornea) is normally transient, but if it persists an ophthalmic examination should be performed.
    B) 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 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).
    6.9.2) TREATMENT
    A) SUPPORT
    1) Dermal exposure can lead to systemic symptoms. The skin should be washed thoroughly when history of topical application is elicited. Some camphor formulations can be directly caustic. Contact dermatitis has been reported and should be treated with topical steroids.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EXTRACORPOREAL ELIMINATION
    1) Neither hemodialysis nor hemoperfusion are effective in removing camphor because of its high lipid solubility and volume of distribution.
    B) HEMODIALYSIS
    1) Aqueous hemodialysis is ineffective in removing camphor.
    2) Lipid dialysis using soybean oil has been shown in one patient to effectively remove camphor with a successful patient outcome (Ginn et al, 1968).
    3) Lipid dialysis is not routinely recommended following camphor poisoning.
    C) HEMOPERFUSION
    1) A 37-year-old man, who displayed recurrent seizures following ingestion of camphorated oil, was treated with combined Amberlite XAD-4 resin hemoperfusion and lipid (Wesson Oil) hemodialysis. This treatment resulted in only 60% extraction of plasma camphor by lipid hemodialysis.
    a) The combination of resin hemoperfusion and lipid hemodialysis resulted in complete plasma camphor extraction with good patient outcome (Kopelman, 1990; Kopelman et al, 1979).
    2) Koeppel et al (1988) reported no obvious clinical benefit of hemoperfusion (Amberlite XAD4) in a 54-year-old woman following an ingestion of 10% camphor spirit. Plasma clearance was 122 to 123 milliliters/minute at a plasma flow rate of 136 milliliters/minute (Koeppel et al, 1988).
    a) While the plasma compartment was almost completely cleared of camphor, only approximately 35 milligrams was removed, presumably due to its high apparent volume of distribution.
    3) Charcoal hemoperfusion cleared the blood of camphor efficiently in a 60-year-old woman who ingested a toxic dose of camphorated oil.
    a) However, the fraction of ingested dose retrieved was less than 1 percent and the treatment was thought to have no clinical benefit (Mascie-Taylor et al, 1981).
    b) The relative importance of plasma to total body camphor has not been defined (Kopelman, 1990).
    4) An in vitro study showed that Amberlite XAD-4 resin was superior to activated charcoal in removing camphor from blood (Koeppel et al, 1982).
    D) DIURESIS
    1) Ineffective in removing camphor.

Abstracts

Case Reports

    A) Numerous case reports and case series document camphor's gastrointestinal, neurological, and cardiopulmonary effects.
    B) ADULT
    1) A 72-year-old woman presented to a community hospital with complaints of weakness, fever, intense pruritus, anorexia, weight loss, and hepatomegaly. Liver biopsy revealed granulomatous hepatitis with necrosis and eosinophils. The patient was discharged, and returned 4 months later with identical symptoms.
    a) She reported ingesting Vicks Vapo-Rub(R) 5 small bottles over the last 5 years. Following cessation of ingestion, her liver abnormalities slowly resolved and she symptomatically improved. No neurotoxic signs or sequelae were evident (McCollam et al, 1989).
    2) An 84-year-old woman ingested an unknown amount of moth balls and developed seizures and hypotension. Seizures continued and she died about 40 hours post-ingestion (Nishimori et al, 1994).
    C) PEDIATRIC
    1) A 3-year-old girl ingested approximately 700 mg of camphor from one tablespoon of Vicks VapoRub(R) (4.81% camphor). She had also had this product placed in her nares twice a day for 5 months. Two hours after the ingestion she had a grand mal seizure. Confusion, irritability, and vomiting preceded the seizure. Coma and respiratory depression lasted for 21 hours. The child recovered fully (Phelan, 1976).
    2) A 2-year-old child ingested 9.5 mL of Camphophenique(R) containing 1,026 mg of camphor and 446.5 mg of phenol. Seizures occurred in route to the emergency department within 10 minutes after ingestion. Upon arrival he was floppy, listless, and unresponsive to pain, with intermittent twitching of the extremities. Orogastric lavage was performed and phenobarbital and activated charcoal were given. No further seizures occurred and the mental status cleared over 24 hours (Gibson et al, 1989).
    3) INFANTS
    a) A 6-month-old boy who had received a total dosage of camphor of (3 grams/kg) over a 5 month period presented with clinical symptoms consistent with Reye's syndrome, including prodromal viral illness, rapid neurologic deterioration, hepatomegaly, elevated AST, ALT, ammonia, prolonged prothrombin time, and low blood glucose (Jimenez et al, 1983).
    b) A 15-month-old child crawled through a spill of 10% spirits-of-camphor. Over the next 48 hours, the child developed ataxia and generalized major motor seizures which persisted for two days in spite of treatment. He recovered fully. Upon repeat exposure one year later to a camphor vaporizer preparation (4.81%), seizure again occurred (Skoglund et al, 1977).
    c) A 2-month-old child receiving thrice-daily application of camphor (4.8%) for 5 days experienced hepatotoxicity which normalized following cessation of product usage (Uc et al, 2000).

Range Of Toxicity

Summary

    A) TOXICITY: Gastrointestinal irritation and CNS depression may occur at doses over 10 mg/kg. Serious toxicity has not been reported below 30 mg/kg; however, ingestions at or above 30 mg/kg should be referred to an emergency department for evaluation. For a 10 kg child, this would require referral after ingestion of: 2.8 mL of a product containing 108 mg of camphor/mL (eg, campho-phenique), or 6.4 mL of an ointment with 4.% camphor (eg Vicks VapoRub Ointment) or 7.6 mL of a cream with 4% camphor (eg BenGay Ultra Strength Cream). As little as 1 g has been fatal in infants, and death has been reported with doses of 50 mg/kg or more. Exposures by any route resulting in moderate to severe toxicity (eg, convulsions, lethargy, ataxia, severe nausea and vomiting) should also be referred for evaluation.
    B) THERAPEUTIC DOSE: Varies depending upon the product used.

Minimum Lethal Exposure

    A) ADULT
    1) Probable human adult lethal dose of liquid camphor is reported to be 50 to 500 mg/kg. Clinically significant toxicity has not been reported with ingestions of less than 30 mg/kg and is uncommon with ingestions of less than 50 mg/kg (Gleason et al, 1976).
    2) Median lethal dose in a review of 6 fatalities was 113 mg/kg (Geller et al, 1984).
    3) CASE REPORT: A 63-year-old man presented to the emergency department (ED) with apnea and in cardiac arrest following inadvertent administration of 4 ounces of a vaporizer fluid containing 6.2% (7.4 g) of camphor into his PEG tube. The estimated dose of camphor administered was 81 mg/kg. The patient's medical history included a cerebral aneurysm, left hemiparesis, dysphagia, ventriculoperitoneal shunt, and seizures. Following resuscitative efforts in the ED, the patient's circulation returned after 10 minutes of asystole. An ECG revealed a heart rate of 63 bpm with sinus rhythm, a QRS complex of 101, a QTc interval of 458, and t-wave flattening. Following intubation and mechanical ventilation, the patient experienced 2 more episodes of cardiac arrest. A repeat ECG indicated prolongation of the QTc interval to 540. Over the next several days, the patient's condition continued to deteriorate following a hospital course complicated by aspiration pneumonitis, hypotension, acidosis, atrial fibrillation, hypovolemia, bilateral cerebellar massive infarcts, and myoclonic jerking. Eleven days post-exposure, the patient died following a family decision to withdraw life support (Goertemoeller et al, 2015).
    B) PEDIATRIC
    1) In infants, less than 1 g of ingested camphor may be fatal and less can produce toxic symptoms (Manoguerra, 2006; Varano, 1980).
    2) A lethal dose of camphorated oil (as liniment) of about 5 mL (1 g camphor) was reported in a 19-month-old child (Smith & Margolis, 1954).
    3) Death has been reported in a 6-month-old infant following chronic ingestion of camphor 3 g/kg total dose over a 5 month period (Jimenez et al, 1983).

Maximum Tolerated Exposure

    A) SUMMARY: Serious toxicity has not been reported below 30 mg/kg; however, ingestions at or above 30 mg/kg should be referred to an emergency department for evaluation. Exposures by any route resulting in moderate to severe toxicity (eg, convulsions, lethargy, ataxia, severe nausea and vomiting) should also be referred for evaluation (Manoguerra, 2006).
    B) ADULT
    1) Acute camphor poisoning secondary to tasting (or unintentional ingestion of small amounts i.e., less than a teaspoonful) of Vicks Vaporub, or similar products, is unlikely (Alsop, 1993).
    2) No ill effects occurred following an oral ingestion of 200 mg of camphor with and without 10 mL of Tween 80 (Koeppel et al, 1988).
    3) Psychomotor agitation and hallucinations occurred in 2 men following an ingestion of 6 to 10 g of camphor (Koeppel et al, 1982).
    4) Major symptoms (syncope, cyanosis, hypotension, dysrhythmias, and mental status changes) were associated with a mean reported dose exposure of 152 mg/kg (range 59 to 475 mg/kg) (Geller et al, 1984).
    5) CASE REPORT: Lahoud et al (1997) reported grand mal seizures within 5 to 10 minutes of ingestion of 4.75 g (68 mg/kg) of camphor by an adult (Lahoud et al, 1997).
    6) CASE REPORT: A 52-year-old man developed nausea, abdominal pain, palpitations, headache, confusion, and 2 witnessed seizures after ingesting approximately 10 g of camphor crystals. With supportive care, the patient recovered without neurologic sequelae (MacKinney et al, 2015).
    C) PEDIATRIC
    1) Serious toxicity has not been reported below 30 mg/kg; however, ingestions at or above 30 mg/kg should be referred to an emergency department for evaluation. For a 10 kg child, this would require referral after ingestion of: 2.8 mL of a product containing 108 mg of camphor/mL (eg, campho-phenique), or 6.4 mL of an ointment with 4% camphor (eg, Vicks VapoRub Ointment) or 7.6 mL of a cream with 4% camphor (eg, BenGay Ultra Strength Cream) (Manoguerra, 2006).
    2) Seizures, apparent within 20 minutes, occurred in a 3-year-old girl after ingestion of one teaspoonful (5 mL, 1.7 g) of 19% camphorated oil, and in a 15-month-old boy after ingestion of about 20 mL of 20% camphorated oil (Theis & Koren, 1995).
    3) CASE REPORT: Seizures occurred in a 3-year-old girl approximately 45 minutes after ingesting at least one tablet containing 0.5 to 1 g of camphor. With supportive treatment, the patient recovered without sequelae (Michiels & Mazor, 2010).
    4) CAMPHOR-PHENOL: Ingestion of 9.5 mL of Camphophenique(R) containing 1,026 mg of camphor and 446.5 mg of phenol, resulted in seizures in a 2-year-old child (Gibson et al, 1989).
    D) MINIMUM SYMPTOMATIC EXPOSURE
    1) In adults, 2 grams can produce toxic effect, although 20 grams may be compatible with survival. Twenty grams of Vicks Vaporub(R), 10 mL of Camphophenique(R) and 16 mL of Vicks Vaposteam(R) contain about 1 g of camphor.
    2) Camphor dissolved in alcohol (camphorated spirits) is absorbed most readily, hence is more liable to induce toxic effects.
    3) The smallest reported dose associated with mild toxicity was 500 mg (18.5 mg/kg) in a 6-year-old boy with mumps (Manoguerra, 2006).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) ADULT
    a) An adult, who ingested about 5 grams of camphor and who developed seizures, had a plasma camphor concentration of 3.1 milligrams/liter, 3 hours post-ingestion (Mascie-Taylor et al, 1981).
    b) An adult who ingested 18 grams of camphor and was severely poisoned had a plasma camphor concentration of 1.7 milligrams/liter 12 hours post-ingestion (Kopelman et al, 1979).
    c) A patient who had a blood camphor concentration of 14.5 milligrams/liter developed seizures (Winter et al, 1991).
    d) Plasma camphor concentrations in an 84-year-old woman who ingested an unknown amount of moth balls were 11.40 mcg/mL on the day of admission, 7.61 mcg/mL on day 2, 5.7 mcg/mL on day 3 as determined by HPLC (Nishimori et al, 1994).
    e) URINE - Urine camphor concentration in a 20-year-old man who ingested 68 mg/kg of camphor was 1.5 mcg/mL (Lahoud et al, 1997).
    2) PEDIATRIC
    a) Seven hours following a reported ingestion of 0.7 gram of camphor which produced projectile vomiting and seizure in a 3-year-old girl, a camphor plasma concentration was 19.5 milligrams/liter (Phelan, 1976).
    b) At 20 minutes following a reported ingestion of 0.54 to 1.08 grams of camphor which produced immediate vomiting and anxiety in a 2-year-old girl, a camphor serum concentration was 15 micrograms/liter (Phelan, 1976).
    c) A 20-month-old girl who developed tonic clonic seizures and respiratory depression following ingestion of an unknown quantity of camphor was reported to have serum and urine camphor concentrations of 3.3 and 1.1 milligrams/milliliter, respectively (Emery & Corban, 1999).
    d) Plasma camphor concentration in a 4-year-old girl at 12 hours after ingestion of approximately 175 mg/kg was 4.1 mg/L (Ruha et al, 2003).

Workplace Standards

    A) ACGIH TLV Values for CAS76-22-2 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Camphor, synthetic
    a) TLV:
    1) TLV-TWA: 2 ppm
    2) TLV-STEL: 3 ppm
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: Not Listed
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    c) TLV Basis - Critical Effect(s): Eye and URT irr; anosmia
    d) Molecular Weight: 152.23
    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 CAS76-22-2 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Camphor (synthetic)
    2) REL:
    a) TWA: 2 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 200 mg/m3
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS76-22-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Camphor, synthetic
    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): 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 ; Listed as: Camphor (synthetic)
    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 CAS76-22-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Camphor, synthetic
    2) Table Z-1 for Camphor, synthetic:
    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: 2
    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: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (INTRAPERITONEAL)MOUSE:
    1) 3000 mg/kg (RTECS, 2006)
    B) LD50- (ORAL)MOUSE:
    1) 1310 mg/kg (RTECS, 2006)
    C) LD50- (SUBCUTANEOUS)RAT:
    1) 70 mg/kg (RTECS, 2006)

Pharmacology Toxicology

Toxicologic Mechanism

    A) Camphor is a cyclic terpene having a ketone structure. Terpenes are lipophilic, rapid-acting neurotoxins that have both excitatory and depressant actions, which form the basis for camphor's mechanism of toxicity. Camphor is a CNS stimulant whose effects range from mild excitation to grand mal seizures or status epilepticus (Gleason et al, 1976). It is also a rubefacient (topical irritant).
    B) Sensations of warmth appear to be modulated by camphor agonism at Transient Receptor Potential (TRP) V3 ion channels. Camphor also has mild activity at the cool-sensitive channel TRP M8 (Vogt-Eisele et al, 2007).

Physicochemical

Physical Characteristics

    A) Translucent crystalline mass, blocks, or powdery masses, with characteristic penetrating aromatic odor and pungent aromatic taste. Produces a sensation of cold (International Programme on Chemical Safety INCHEM, 1989).

Ph

    1) No information found at the time of this review.

Molecular Weight

    A) 152.23

References

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
    4) 49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.
    5) 62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.
    6) 65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    7) 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    8) 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    9) 66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.
    10) 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
    11) 68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.
    12) 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
    13) ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices, 6th ed (Supplement), Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1996.
    14) ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices, 6th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1991.
    15) AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
    16) AMA Department of DrugsAMA Department of Drugs: AMA Evaluations Subscription, American Medical Association, Chicago, IL, 1992.
    17) Alsop JA: Camphor toxicity from accidental ingestions (abstract). Vet Human Toxicology 1993; 35:346.
    18) American Conference of Governmental Industrial Hygienists : ACGIH 2010 Threshold Limit Values (TLVs(R)) for Chemical Substances and Physical Agents and Biological Exposure Indices (BEIs(R)), American Conference of Governmental Industrial Hygienists, Cincinnati, OH, 2010.
    19) Antman E, Jacob G, & Volpe B: Camphor overdosage: therapeutic considerations. State J Med 1978; 78:896-897.
    20) Aronow R & Spigiel RW: Implications of camphor poisoning. Drug Intell Clin Pharm 1976; 10:631-634.
    21) Benz RW: Camphorated oil poisoning with no mortality. JAMA 1919; 72:1217-1218.
    22) Bhaya M & Beniwal R: Camphor induced myocarditis: a case report. Cardiovasc Toxicol 2007; 7(3):212-214.
    23) Bilsland D & Ferguson J: Contact allergy to sunscreen chemicals in photo- sensitivity dermatitis/actinic reticuloid syndrome (PD/AR) and polymorphic light eruption (PLE). Contact Derm 1993; 29:70-73.
    24) Blackmon WP & Curry HB: Camphor poisoning; report of case occurring during pregnancy. J Fla Med Assoc 1957; 43(10):999-1000.
    25) Bonkovsky HL, Cable EE, & Cable JW: Porphyrogenic properties of the terpenes camphor, pinene, and thujone. Biochem Pharmacology 1992; 43:2359-2368.
    26) Bridge CK: Hazards of camphorated oil (letter). Can Med Assoc J 1995; 153:881.
    27) Briggs GG, Freeman RK, & Yaffe SJ: Drugs in Pregnancy and Lactation, 5th ed, Williams & Wilkins, Baltimore, MD, 1998, pp 582-83.
    28) Brophy GM, Bell R, Claassen J, et al: Guidelines for the evaluation and management of status epilepticus. Neurocrit Care 2012; 17(1):3-23.
    29) Budavari S: The Merck Index, 11th ed, Merck & Co, Inc, Rahway, NJ, 1989, pp 261-262.
    30) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    31) Chamberlain JM, Altieri MA, & Futterman C: A prospective, randomized study comparing intramuscular midazolam with intravenous diazepam for the treatment of seizures in children. Ped Emerg Care 1997; 13:92-94.
    32) Chan CK, Chan YC, & Lau FL: Status epilepticus after topical application of a solution containing camphor. Emerg Med J 2009; 26(1):76-.
    33) Chin RF , Neville BG , Peckham C , et al: Treatment of community-onset, childhood convulsive status epilepticus: a prospective, population-based study. Lancet Neurol 2008; 7(8):696-703.
    34) Choonara IA & Rane A: Therapeutic drug monitoring of anticonvulsants state of the art. Clin Pharmacokinet 1990; 18:318-328.
    35) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    36) Craig JO: Poisoning by the volatile oils in childhood. Arch Dis Child 1953; 28:475-483.
    37) DFG: List of MAK and BAT Values 2002, Report No. 38, Deutsche Forschungsgemeinschaft, Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, Wiley-VCH, Weinheim, Federal Republic of Germany, 2002.
    38) Dean BS, Burdick JD, & Geotz CM: In vivo evaluation of the adsorptive capacity of activated charcoal for camphor. Vet Hum Toxicol 1992; 34:297-300.
    39) EPA: Search results for Toxic Substances Control Act (TSCA) Inventory Chemicals. US Environmental Protection Agency, Substance Registry System, U.S. EPA's Office of Pollution Prevention and Toxics. Washington, DC. 2005. Available from URL: http://www.epa.gov/srs/.
    40) ERG: Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident, U.S. Department of Transportation, Research and Special Programs Administration, Washington, DC, 2004.
    41) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    42) Emery DP & Corban JG: Camphor toxicity. J Paediatr Child Health 1999; 35:105-106.
    43) FDA: New drugs; camphorated oil drug products for human use. FDA: Fed Register 1982; 47:41716-41720.
    44) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    45) Geller RJ, Spyker DA, & Garrettson LK: Camphor toxicity: development of a triage strategy. Vet Hum Toxicol 1984; 26(Suppl 2):8-10.
    46) Gibson DE, Moore GP, & Pfaff JA: Camphor ingestion. Am J Emerg Med 1989; 7:41-43.
    47) Ginn HE, Anderson KE, & Mercier RK: Camphor intoxication treated by lipid dialysis. JAMA 1968; 203:230-231.
    48) Gleason MN, Gosselin RE, & Hodge HC: Clinical toxicology of commercial products, 4th ed, Williams & Wilkins, Baltimore, MD, 1976, pp 77-79.
    49) Goertemoeller S, Yin S, & Haver D: Cardiac arrest following camphor administration via a PEG tube: 2015 Annual Meeting of the North American Congress of Clinical Toxicology (NACCT). Clin Toxicol 2015; 53(7):742-742.
    50) Goldfrank L & Bresnitz E: Camphor. Hosp Physician 1980; 45-54.
    51) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    52) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    53) Grant WM & Shuman JS: Toxicology of the Eye, 4th ed, Charles C Thomas, Springfield, IL, 1993.
    54) Green HG: Sensory characteristics of camphor. J Investigative Dermatology 1990; 94:662-666.
    55) Gronka PA, Bobkoskie RL, & Tomchick GH: Camphor exposures in a packaging plant. Am Ind Hyg Assoc J 1969; 30:276-279.
    56) Guilbert J, Flamant C, Hallalel F, et al: Anti-flatulence treatment and status epilepticus: a case of camphor intoxication. Emerg Med J 2007; 24(12):859-860.
    57) Gyoubu K & Miyazawa M: In vitro metabolism of (-)-camphor using human liver microsomes and CYP2A6. Biol Pharm Bull 2007; 30(2):230-233.
    58) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 1992; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    59) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    60) Hegenbarth MA & American Academy of Pediatrics Committee on Drugs: Preparing for pediatric emergencies: drugs to consider. Pediatrics 2008; 121(2):433-443.
    61) Heinonen OP, Slone D, & Shapiro S: Birth Defects and Drugs in Pregnancy, Publishing Sciences Group, Littleton, MA, 1977.
    62) Hvidberg EF & Dam M: Clinical pharmacokinetics of anticonvulsants. Clin Pharmacokinet 1976; 1:161.
    63) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: 1,3-Butadiene, Ethylene Oxide and Vinyl Halides (Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide), 97, International Agency for Research on Cancer, Lyon, France, 2008.
    64) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol, 88, International Agency for Research on Cancer, Lyon, France, 2006.
    65) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Household Use of Solid Fuels and High-temperature Frying, 95, International Agency for Research on Cancer, Lyon, France, 2010a.
    66) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Smokeless Tobacco and Some Tobacco-specific N-Nitrosamines, 89, International Agency for Research on Cancer, Lyon, France, 2007.
    67) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Some Non-heterocyclic Polycyclic Aromatic Hydrocarbons and Some Related Exposures, 92, International Agency for Research on Cancer, Lyon, France, 2010.
    68) IARC: List of all agents, mixtures and exposures evaluated to date - IARC Monographs: Overall Evaluations of Carcinogenicity to Humans, Volumes 1-88, 1972-PRESENT. World Health Organization, International Agency for Research on Cancer. Lyon, FranceAvailable from URL: http://monographs.iarc.fr/monoeval/crthall.html. As accessed Oct 07, 2004.
    69) ICAO: Technical Instructions for the Safe Transport of Dangerous Goods by Air, 2003-2004. International Civil Aviation Organization, Montreal, Quebec, Canada, 2002.
    70) International Agency for Research on Cancer (IARC): IARC monographs on the evaluation of carcinogenic risks to humans: list of classifications, volumes 1-116. International Agency for Research on Cancer (IARC). Lyon, France. 2016. Available from URL: http://monographs.iarc.fr/ENG/Classification/latest_classif.php. As accessed 2016-08-24.
    71) International Agency for Research on Cancer: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. World Health Organization. Geneva, Switzerland. 2015. Available from URL: http://monographs.iarc.fr/ENG/Classification/. As accessed 2015-08-06.
    72) International Programme on Chemical Safety INCHEM: Camphor. International Programme on Chemical Safety INCHEM. Hamilton, Ontario, Canada. 1989. Available from URL: http://www.inchem.org/documents/pims/pharm/camphor.htm. As accessed December 5, 2007.
    73) Jacobziner H & Raybin HW: Camphor poisoning. Arch Pediatr 1962; 79:28-30.
    74) Jaiwal A: Vick's Vaporub induced dermo kerato conjunctivitis--a case report. Indian J Ophthalmol 1989; 37(3):154.
    75) Jimenez JF, Brown AL, & Arnold WC: Chronic camphor ingestion mimicking Reye's syndrome. Gastroenterology 1983; 84:394-398.
    76) Jimenez JF, Brown AL, Arnold WC, et al: Chronic camphor ingestion mimicking Reye's syndrome.. Gastroenterology 1983a; 84:394-398.
    77) Kelly RC, Kopelman RC, & Sunshine I: A simple gas chromatographic procedure for the determination of camphor in plasma. J Anal Toxicol 1979; 3:76-77.
    78) Khine H, Weiss D, Graber N, et al: A cluster of children with seizures caused by camphor poisoning. Pediatrics 2009; 123(5):1269-1272.
    79) Kleinman ME, Chameides L, Schexnayder SM, et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 14: pediatric advanced life support. Circulation 2010; 122(18 Suppl.3):S876-S908.
    80) Koeppel C, Martens F, & Schirop T: Hemoperfusion in acute camphor poisoning. Intensive Care Med 1988; 14:431-433.
    81) Koeppel C, Tenezer J, & Schirop T: Camphor poisoning: abuse of camphor as a stimulant. Arch Toxicol 1982; 51:101-106.
    82) Kopelman R, Miller S, & Kelly R: Camphor intoxication treated by resin hemoperfusion. JAMA 1979; 241:727-728.
    83) Kopelman R, Mitler S, & Kelley R: Camphor intoxication treated by resin hemoperfusion. JAMA 1979a; 241:727-728.
    84) Kopelman RC: Camphor. In: LM Haddad & JF Winchester: Clinical Management of Poisoning & Drug Overdose, 2nd ed, Saunders, Philadelphia, PA, 1990, pp 1451-1455.
    85) Koyama K & Yamashita M: A simple test for mothball component differentiation using water and a saturated solution of table salt: its utilization for poison information service. Vet Hum Toxicol 1991; 33:425-427.
    86) Kuffner EK: Camphor and moth repellents. In Flomenbaum NE, Goldfrank LR, Hoffman RS, et al, eds. Goldfrank's Toxicologic Emergencies, 8th ed. 8th ed, New York, NY, 2006, pp -.
    87) Kuffner EK: Camphor and moth repellents. In: Goldfrank LR, Flomenbaum NE, Levin NA, et al, eds. Goldfrank's Toxicologic Emergencies, 7th ed, McGraw-Hill Medical Pub Division, New York, NY, 2002, pp 1295-1296.
    88) LAURIE NM: Camphorated oil asphyxia. Can Med Assoc J 1950; 63(3):298-298.
    89) Lahoud CA, March JA, & Proctor DD: Campho-phenique ingestion: an intentional overdose. So Med J 1997; 90:647-648.
    90) Lim GC, Chen Y, Liu L, et al: Camphor-related self-inflicted keratoconjunctivitis complicating delusions of parasitosis. Cornea 2006; 25(10):1254-1256.
    91) Loddenkemper T & Goodkin HP: Treatment of Pediatric Status Epilepticus. Curr Treat Options Neurol 2011; Epub:Epub.
    92) MacKinney TG, Soti KR, Shrestha P, et al: Camphor: an herbal medicine causing grand mal seizures. BMJ Case Rep 2015; 2015:Epub.
    93) Manno EM: New management strategies in the treatment of status epilepticus. Mayo Clin Proc 2003; 78(4):508-518.
    94) Manoguerra AS, Erdman AR, Wax PM, et al.: Camphor Poisoning: an Evidence-Based Consensus Guideline for Out-of-Hospital Management*. American Association of Poison Control Centers. Washington, DC. 2006. Available from URL: http://www.aapcc.org/FinalizedPMGdlns/Camphor%20guideline%20for%20AAPCC%202006-2-16.pdf. As accessed 04/25/06.
    95) Martin D, Valdez J, Boren J, et al: Dermal absorption of camphor, menthol, and methyl salicylate in humans. J Clin Pharmacol 2004; 44(10):1151-1157.
    96) Marwah P & Marwah A: Camphor poisoning: a rare but preventable cause of status epilepticus. Indian J Pediatr 2014; 81(9):956.
    97) Mascie-Taylor BH, Widdop B, & Davison AM: Camphor intoxication treated by charcoal hemoperfusion. Postgrad Med J 1981; 57:725-726.
    98) McCollam A, Block R, & Lipscomb JW: Chronic camphor ingestion: A case report of granulomatous hepatitis (abstract 32). Vet Hum Toxicol 1989; 31:337.
    99) Michiels EA & Mazor SS: Toddler with seizures due to ingesting camphor at an Indian celebration. Pediatr Emerg Care 2010; 26(8):574-575.
    100) NFPA: Fire Protection Guide to Hazardous Materials, 13th ed., National Fire Protection Association, Quincy, MA, 2002.
    101) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 1, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2001.
    102) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 2, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2002.
    103) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 3, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2003.
    104) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 4, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2004.
    105) Naradzay J & Barish RA: Approach to ophthalmologic emergencies. Med Clin North Am 2006; 90(2):305-328.
    106) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,3-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    107) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,4-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    108) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Butylene Oxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648083cdbb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    109) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Dibromoethane (Proposed). United States Environmental Protection Agency. Washington, DC. 2007g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802796db&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    110) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,3,5-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    111) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 2-Ethylhexyl Chloroformate (Proposed). United States Environmental Protection Agency. Washington, DC. 2007b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037904e&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    112) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Acrylonitrile (Proposed). United States Environmental Protection Agency. Washington, DC. 2007c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648028e6a3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    113) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Adamsite (Proposed). United States Environmental Protection Agency. Washington, DC. 2007h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    114) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Agent BZ (3-quinuclidinyl benzilate) (Proposed). United States Environmental Protection Agency. Washington, DC. 2007f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ad507&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    115) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Allyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039d9ee&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    116) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    117) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Arsenic Trioxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480220305&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    118) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Automotive Gasoline Unleaded (Proposed). United States Environmental Protection Agency. Washington, DC. 2009a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cc17&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    119) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Biphenyl (Proposed). United States Environmental Protection Agency. Washington, DC. 2005j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1b7&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    120) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bis-Chloromethyl Ether (BCME) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648022db11&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    121) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Boron Tribromide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae1d3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    122) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromine Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2007d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039732a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    123) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromoacetone (Proposed). United States Environmental Protection Agency. Washington, DC. 2008e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187bf&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    124) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Calcium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    125) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae328&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    126) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Sulfide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037ff26&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    127) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Chlorobenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803a52bb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    128) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Cyanogen (Proposed). United States Environmental Protection Agency. Washington, DC. 2008f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187fe&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    129) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Dimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbf3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    130) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Diphenylchloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    131) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091884e&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    132) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Phosphorodichloridate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480920347&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    133) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809203e7&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    134) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    135) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Germane (Proposed). United States Environmental Protection Agency. Washington, DC. 2008j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963906&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    136) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Hexafluoropropylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1f5&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    137) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ketene (Proposed). United States Environmental Protection Agency. Washington, DC. 2007. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ee7c&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    138) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    139) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    140) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Malathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2009k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809639df&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    141) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Mercury Vapor (Proposed). United States Environmental Protection Agency. Washington, DC. 2009b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a087&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    142) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Isothiocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a03&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    143) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a57&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    144) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl tertiary-butyl ether (Proposed). United States Environmental Protection Agency. Washington, DC. 2007a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802a4985&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    145) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methylchlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5f4&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    146) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    147) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c646&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    148) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN1 CAS Reg. No. 538-07-8) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    149) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN2 CAS Reg. No. 51-75-2) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    150) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN3 CAS Reg. No. 555-77-1) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    151) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Tetroxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091855b&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    152) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Trifluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e0c&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    153) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008o. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e32&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    154) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perchloryl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e268&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    155) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perfluoroisobutylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2009d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26a&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    156) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008p. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dd58&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    157) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2006d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020cc0c&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    158) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    159) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phorate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008q. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dcc8&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    160) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene (Draft-Revised). United States Environmental Protection Agency. Washington, DC. 2009e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a08a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    161) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene Oxime (Proposed). United States Environmental Protection Agency. Washington, DC. 2009f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26d&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    162) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    163) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    164) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Propargyl Alcohol (Proposed). United States Environmental Protection Agency. Washington, DC. 2006e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec91&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    165) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Selenium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec55&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    166) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Silane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d523&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    167) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    168) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    169) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Strontium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    170) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sulfuryl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec7a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    171) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tear Gas (Proposed). United States Environmental Protection Agency. Washington, DC. 2008s. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e551&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    172) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tellurium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e2a1&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    173) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tert-Octyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2008r. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5c7&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    174) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tetramethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-17.
    175) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    176) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7d608&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    177) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethylacetyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008t. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5cc&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    178) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Zinc Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    179) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for n-Butyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064808f9591&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    180) National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
    181) National Institute for Occupational Safety and Health: NIOSH Pocket Guide to Chemical Hazards, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Cincinnati, OH, 2007.
    182) National Research Council : Acute exposure guideline levels for selected airborne chemicals, 5, National Academies Press, Washington, DC, 2007.
    183) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 6, National Academies Press, Washington, DC, 2008.
    184) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 7, National Academies Press, Washington, DC, 2009.
    185) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 8, National Academies Press, Washington, DC, 2010.
    186) Nishimori S, Shimizu K, & Honma M: Camphor intoxication by mouth in an old female. Nihon Kyukyu Igakukai Kanto Chihoukaishi 1994; 15:346-347.
    187) None Listed: Camphor revisited: focus on toxicity. Committee on Drugs. American Academy of PediatricsNone. Pediatrics 1994; 94(1):127-128.
    188) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    189) O'Neil MJ, Heckelman PE, Koch CB, et al: The Merck Index. 14th ed., 14th ed. 14th ed, Whitehouse Station, NJ, 2006, pp -.
    190) OHM/TADS : Oil and Hazardous Materials/Technical Assistance Data System. US Environmental Protection Agency. Washington, DC (Internet Version). Edition expires 1992; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    191) Peate WF: Work-related eye injuries and illnesses. Am Fam Physician 2007; 75(7):1017-1022.
    192) Peberdy MA , Callaway CW , Neumar RW , et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science. Part 9: post–cardiac arrest care. Circulation 2010; 122(18 Suppl 3):S768-S786.
    193) Phelan WJ III: Camphor poisoning: over the counter dangers. Pediatrics 1976; 57:428-431.
    194) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    195) Proctor NH, Hughes JP, & Fischman ML: Chemical Hazards of the Workplace, 2nd ed, JB Lippincott Co, Philadelphia, PA, 1988.
    196) Product Information: diazepam IM, IV injection, diazepam IM, IV injection. Hospira, Inc (per Manufacturer), Lake Forest, IL, 2008.
    197) Product Information: dopamine hcl, 5% dextrose IV injection, dopamine hcl, 5% dextrose IV injection. Hospira,Inc, Lake Forest, IL, 2004.
    198) Product Information: lorazepam IM, IV injection, lorazepam IM, IV injection. Akorn, Inc, Lake Forest, IL, 2008.
    199) Product Information: norepinephrine bitartrate injection, norepinephrine bitartrate injection. Sicor Pharmaceuticals,Inc, Irvine, CA, 2005.
    200) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 1992; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    201) RTECS: Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2006; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    202) Rabl W, Katzgraber F, & Steinlechner M: Camphor ingestion for abortion (case report). Forensic Sci Int 1997; 89(1-2):137-140.
    203) Ragucci KR, Trangmar PR, Bigby JG, et al: Camphor ingestion in a 10-year-old male. South Med J 2007; 100(2):204-207.
    204) Rampini SK, Schneemann M, Rentsch K, et al: Camphor intoxication after cao gio (coin rubbing). JAMA 2002; 288(1):45-45.
    205) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    206) Reid FM: Accidental camphor ingestion (letter). JACEP 1979; 8:339-340.
    207) Riggs J, Hamilton R, & Homel S: Camphorated oil intoxication during pregnancy. Obstet Gynecol 1965; 25:255-258.
    208) Ruha AM, Graeme KA, & Field A: Late seizure following ingestion of Vicks VapoRub. Acad Emerg Med 2003; 10(6):691-691.
    209) Sax NI & Lewis RJ: Dangerous Properties of Industrial Materials, 7th ed, Van Nostrand Reinhold Company, New York, NY, 1989, pp 688.
    210) Scott R, Besag FMC, & Neville BGR: Buccal midazolam and rectal diazepam for treatment of prolonged seizures in childhood and adolescence: a randomized trial. Lancet 1999; 353:623-626.
    211) Skoglund RR, Ware LL, & Schanberger IE: Prolonged seizures due to contact and inhalation exposure to camphor: a case report. Clin Pediatr 1977; 16:901-902.
    212) Smith AG & Margolis G: Camphor poisoning: anatomical and pharmacologic study; report of a fatal case; experimental investigation of protective action of barbiturate. Am J Pathol 1954; 30:857-868.
    213) Sreenath TG, Gupta P, Sharma KK, et al: Lorazepam versus diazepam-phenytoin combination in the treatment of convulsive status epilepticus in children: A randomized controlled trial. Eur J Paediatr Neurol 2009; Epub:Epub.
    214) Theis JGW & Koren G: Camphorated oil: still endangering the lives of Canadian children. Can Med Assoc J 1995; 152:1821-1824.
    215) U.S. Department of Energy, Office of Emergency Management: Protective Action Criteria (PAC) with AEGLs, ERPGs, & TEELs: Rev. 26 for chemicals of concern. U.S. Department of Energy, Office of Emergency Management. Washington, DC. 2010. Available from URL: http://www.hss.doe.gov/HealthSafety/WSHP/Chem_Safety/teel.html. As accessed 2011-06-27.
    216) U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project : 11th Report on Carcinogens. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Washington, DC. 2005. Available from URL: http://ntp.niehs.nih.gov/INDEXA5E1.HTM?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932. As accessed 2011-06-27.
    217) U.S. Environmental Protection Agency: Discarded commercial chemical products, off-specification species, container residues, and spill residues thereof. Environmental Protection Agency's (EPA) Resource Conservation and Recovery Act (RCRA); List of hazardous substances and reportable quantities 2010b; 40CFR(261.33, e-f):77-.
    218) U.S. Environmental Protection Agency: Integrated Risk Information System (IRIS). U.S. Environmental Protection Agency. Washington, DC. 2011. Available from URL: http://cfpub.epa.gov/ncea/iris/index.cfm?fuseaction=iris.showSubstanceList&list_type=date. As accessed 2011-06-21.
    219) U.S. Environmental Protection Agency: List of Radionuclides. U.S. Environmental Protection Agency. Washington, DC. 2010a. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    220) U.S. Environmental Protection Agency: List of hazardous substances and reportable quantities. U.S. Environmental Protection Agency. Washington, DC. 2010. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    221) U.S. Environmental Protection Agency: The list of extremely hazardous substances and their threshold planning quantities (CAS Number Order). U.S. Environmental Protection Agency. Washington, DC. 2010c. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-part355.pdf. As accessed 2011-06-17.
    222) U.S. Occupational Safety and Health Administration: Part 1910 - Occupational safety and health standards (continued) Occupational Safety, and Health Administration's (OSHA) list of highly hazardous chemicals, toxics and reactives. Subpart Z - toxic and hazardous substances. CFR 2010 2010; Vol6(SEC1910):7-.
    223) U.S. Occupational Safety, and Health Administration (OSHA): Process safety management of highly hazardous chemicals. 29 CFR 2010 2010; 29(1910.119):348-.
    224) Uc A, Bishop WP, & Sanders KD: Camphor hepatotoxicity. South Med J 2000; 93(6):596-598.
    225) United States Environmental Protection Agency Office of Pollution Prevention and Toxics: Acute Exposure Guideline Levels (AEGLs) for Vinyl Acetate (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6af&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    226) Varano C: Hazards of camphorated oil. Pharmacy Int 1980; 1:5-6.
    227) Vasey RH & Karayannopoulos SJ: Camphorated Oil. Brit Med J 1972; 1:112.
    228) Vogt-Eisele AK, Weber K, Sherkheli MA, et al: Monoterpenoid agonists of TRPV3. Br J Pharmacol 2007; 151(4):530-540.
    229) Weiss J & Catalano P: Camphorated oil intoxication during pregnancy. Pediatrics 1973; 52:713-714.
    230) Winter ML, Rice BS, & Snodgrass WR: Seizures and serum camphor concentration in man (Abstract). Vet Hum Toxicol 1991; 33:375.