Contact Us    Contact Us     |     Feedback
MOBILE VIEW  | 

TURPENTINE OIL

Export To Excel

Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Turpentine is a volatile hydrocarbon compound. It contains terpenes; alpha-pinene is the primary constituent. It is used as a chemical intermediate for polyterpene resins, synthetic pine oil, and pinene-based flavors and perfumes. Turpentine is an irritant, CNS depressant and aspiration hazard.

Specific Substances

    1) Gum spirits
    2) Spirits of turpentine
    3) Oil of turpentine
    4) Oil of turpentine, rectified
    5) Terebenthine (French)
    6) Terpentin (German)
    7) Turpentine steam distilled
    8) CAS 8006-64-2 (turpentine oil)
    9) CAS 9005-90-7 (turpentine)
    10) OHM/TADS NUMBER 7217076 (TURPENTINE)
    11) TERBENTHINE (FRENCH)
    12) TERPENTINE (MISSPELLING OF TURPENTINE)
    13) TURPENTINE, COMBUSTIBLE LIQUID
    14) TURPENTINE, FLAMMABLE LIQUID
    1.2.1) MOLECULAR FORMULA
    1) C10-H16 (approximate)

Available Forms Sources

    A) FORMS
    1) Turpentine is a volatile hydrocarbon compound.
    2) Turpentine (i.e. wood turpentine) is a volatile, clear, colorless liquid with a characteristic odor described as aromatic, unpleasant, and penetrating. Gum turpentine is a volatile, yellowish, opaque, sticky mass with a characteristic odor (AAR, 1998) (ACGIH, 1991; Ashford, 1994; Budavari, 1996; Hathaway et al, 1996).
    3) Turpentine is a compound which contains the terpenes alpha-pinene, beta-pinene, and dipentene. Older North American preparations and preparations from other countries also contain 3-carene, delta-carene, and camphene (ACGIH, 1991; Ashford, 1994).
    B) SOURCES
    1) Wood turpentine is created through extraction or destructive distillation of wood. Gum turpentine is produced through steam distillation of turpentine gum (ACGIH, 1991).
    2) Turpentine is co-produced with dipentene, pine oil, rosin, and wood by the steam distillation of pinewood stumps. It is also produced by the fractionation of pyrolysis oil and pinewood and is co-produced with pine oil, wood pitch, tar oil, and wood (Ashford, 1999).
    3) This compound is prepared by distillation of volatile oil from oleoresin originating from Pinus palustris mill, pinaceae, and other terpene oil-yielding Pinus species (HSDB , 2000).
    4) Production of turpentine occurs through the use of aliphatic and aromatic solvents to extract aged pine stumps and distilling the extracts. The compound is also produced from the capture of condensed wood pulp vapors released when cooking the wood pulp during sulfate pulping (HSDB , 2000).
    C) USES
    1) Turpentine has been used as a solvent/thinner for pigment, varnishes, paints, oils, lacquers, resins, waxes, rubber, and polishes, as an insecticide, and in camphor and menthol synthesis (ACGIH, 1991; Budavari, 1996; Lewis, 1997; HSDB , 2000).
    a) More recently, turpentine oil has been largely replaced with white spirit or a turpentine substitute which are of relatively low toxicity when ingested (Riordan et al, 2002).
    2) Turpentine oil has been used in liniments, ointments, inks, deodorizers, and perfumes (ACGIH, 1991; Budavari, 1996; HSDB , 2000).
    3) Turpentine is used as a chemical intermediate for polyterpene resins, synthetic pine oil, and pinene-based flavors and perfumes (HSDB , 2000).
    4) MEDICAL/DENTISTRY USES
    a) Turpentine has been used topically as a rubefacient, counterirritant, and treatment for the elimination of parasitic infestations (Singh et al, 1993).
    b) This compound is used to dissolve gutta-percha, a plant-derived temporary filling material that is used in dentistry (Barbosa et al, 1994).
    c) Turpentine is a chemical intermediate for terpenes used in the pharmaceutical industry. It is used in expectorant formulations, and in veterinary medication (HSDB , 2000).

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: Turpentine has been often used as a paint thinner and solvent. In the past, it had been used as a diuretic and expectorant.
    B) TOXICOLOGY: Turpentine is an aliphatic hydrocarbon. Turpentine contains alpha-pinene as its primary constituent as well as beta-pinene, camphene, and limonene. Turpentine oil readily absorbed through the gastrointestinal tract or by inhalation.
    C) EPIDEMIOLOGY: Exposure has occurred; fatalities have been reported. However, turpentine oil has been largely been replaced with white spirit or a turpentine substitute which are of relatively low toxicity when ingested.
    D) WITH POISONING/EXPOSURE
    1) INGESTION: Ingestion is the most significant route of exposure. SYMPTOMS: Turpentine can produce burning, nausea, abdominal pain, vomiting, diarrhea, tachycardia, dyspnea, cyanosis and fever. Severe ingestions can cause glycosuria, hematuria, albuminuria, anuria, excitement, delirium, ataxia, vertigo, stupor, seizures and coma. A significant ingestion can lead to CNS depression that progresses from mild symptoms (ie, headache, dizziness and blurry vision) to lethargy and coma. ONSET: Usually 2 to 3 hours for systemic toxicity to develop. DURATION: GI and CNS symptoms generally resolve within 12 hours in patients with a moderate exposure. SEVERE EVENTS: Primary toxicity is due to the potential risk of aspiration causing a chemical pneumonitis; respiratory insufficiency and failure can develop.
    2) INHALATION: Inhalation of vapors may produce respiratory irritation. High vapor concentrations can cause mucous membrane irritation, hyperpnea, vertigo, tachycardia, headache, hallucinations, distorted perceptions, and seizures. PULMONARY EFFECT: Aspiration pneumonitis, pulmonary necrosis, pneumatocele or pulmonary edema can develop after ingestion, parenteral exposure, or the use of turpentine as a vaginal douche.
    3) DERMAL: Turpentine is absorbed through the skin. Topical application produces a rubefacient effect, with redness, warmth, blisters and burns. Long term or repeated exposure can result in irritation. Some turpentine preparations can cause contact dermatitis.
    4) OCULAR: Ocular exposure to liquid turpentine causes conjunctivitis, lid edema, and blepharospasm. Allergy has been reported.
    5) OTHER: Hemorrhagic cystitis has been associated with turpentine use. Turpentine exposure can produce the odor of violets in urine.
    0.2.20) REPRODUCTIVE
    A) The use of turpentine and water as a vaginal douche has resulted in abortion.
    0.2.21) CARCINOGENICITY
    A) The International Agency for Research on Cancer (IARC) has indicated that there is inadequate evidence for carcinogenicity of d-limonene (a constituent of turpentine oil) in humans. There is, however, evidence for carcinogenicity in experimental animals. Overall, the working group concluded that d-limonene produces renal tubular tumors in male rats by the non-DNA reactive alpha2u-globulin-associated responses that are not relevant to humans (National Toxicology Program (NTP), 2002). IARC has classified d-limonene (a constituent of turpentine) as a Group 3 chemical: not classifiable as to its carcinogenicity to humans (International Agency for Research on Cancer (IARC), 2016)

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor fluid status and electrolytes in patients with significant vomiting and/or diarrhea symptoms.
    C) No specific lab work (CBC, electrolytes, urinalysis) is needed unless otherwise clinically indicated.
    D) Monitor respiratory function including pulse oximetry and ABGs in patients at risk or suspected of aspiration.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) INGESTION: Treatment is symptomatic and supportive. Monitor vital signs, mental status and respiratory function. Monitor fluids and electrolytes if the patient develops significant vomiting and/or diarrhea. Treat with IV fluids as needed. Following a significant exposure, monitor for evidence of pulmonary aspiration. INHALATION: Immediately remove the patient from the source of exposure. Symptoms often improve following removal. Closely monitor respiratory function, provide oxygen and symptomatic and supportive care. DERMAL: After assuring that the patient is medically stable, remove contaminated clothing and wash exposed skin with soap and water.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) RESPIRATORY DISTRESS: Orotracheal intubation for airway protection should be performed early if a patient exhibits respiratory distress. Administer oxygen. Consider the use of a surfactant. Endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality in one study. RESPIRATORY FAILURE: Partial liquid ventilation, high frequency jet ventilation, extracorporeal membrane oxygenation (ECMO) and high frequency chest wall oscillation have all been used with apparent success in cases of severe hydrocarbon pneumonitis. SEIZURES: Following a large ingestion of turpentine, seizures, excitement and coma may develop. Initially treat seizures with benzodiazepines. OTHER: Prophylactic antibiotics and steroids are of no proven benefit following hydrocarbon pneumonitis. Monitor and treat significant dysrhythmias.
    C) DECONTAMINATION
    1) PREHOSPITAL: GI decontamination is not recommended because of the risk of aspiration. Activated charcoal is generally NOT indicated OR has limited utility as it may cause vomiting and subsequent aspiration. Remove contaminated clothing and wash exposed skin with soap and water.
    2) HOSPITAL: Studies fail to show if gastric emptying improves outcomes in patients with oral hydrocarbon ingestions. If a patient has ingested a large amount of a hydrocarbon that causes significant systemic toxicity shortly before presentation, it is reasonable to insert a small nasogastric tube and aspirate gastric contents. However, it should be reserved for patients with significant toxicity (ie, lethargy, coma, or seizures). Activated charcoal is generally NOT indicated OR has limited utility as it may cause vomiting and subsequent aspiration.
    D) AIRWAY MANAGEMENT
    1) Airway support is unlikely to be necessary following a minor or taste ingestion. However, perform orotracheal intubation to protect airway early in patients with severe intoxication (coma, dysrhythmias, respiratory distress).
    E) ANTIDOTE
    1) There is no known antidote.
    F) COMA
    1) Treatment is symptomatic and supportive. Perform orotracheal intubation to protect airway. Assess oxygenation, evaluate for hypoglycemia, and consider naloxone if coingestants are possible.
    G) TACHYCARDIA
    1) Tachycardia may occur from a combination of agitation and catecholamine release. Treat with IV fluids and benzodiazepine sedation if agitation is prominent.
    H) CONDUCTION DISORDER OF THE HEART
    1) Initiate ACLS protocols. Some solvents appear to sensitize the myocardium to catecholamines. Epinephrine and other sympathomimetics should be used with caution as ventricular dysrhythmias may be precipitated.
    I) ENHANCED ELIMINATION
    1) Hemodialysis and hemoperfusion are not of value.
    J) PATIENT DISPOSITION
    1) HOME CRITERIA: Asymptomatic patients with inadvertent exposures may be monitored at home, with particular attention to the development of any respiratory symptoms. Patients who develop symptoms during home monitoring should be referred to a medical facility.
    2) OBSERVATION CRITERIA: Patients with deliberate ingestions and symptomatic patients should be sent to a health care facility for observation for 6 to 8 hours. Although patients can develop a delayed pneumonitis, they are unlikely to do so if they have been completely asymptomatic during that time period. Obtain a mental health consult as appropriate.
    a) Patients with a deliberate ingestion, no initial symptoms and a normal chest x-ray obtained at least 6 hours after ingestion and who remain asymptomatic throughout the observation period (6 hours) can be safely discharged.
    3) ADMISSION CRITERIA: Patients with significant persistent central nervous system toxicity (somnolence, delirium), or respiratory symptoms of cough or tachypnea should be admitted. Patients with coma, dysrhythmias, or respiratory distress should be admitted to an intensive care setting.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity (ie, dysrhythmias, coma or respiratory distress), or in whom the diagnosis is not clear.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) TOXICITY: Turpentine is an irritant of the skin and mucous membranes and is a CNS depressant. A value range of 15 to 90 mL has been determined to be the mean oral lethal dose for humans through numerous reports of turpentine fatalities. ADULT: A dose of 120 to 180 mL may be fatal if no treatment is obtained. PEDIATRIC: A dose of 15 mL was fatal in a 2-year-old child; however, benzene was present in the mixture. Children have survived ingestions of 2 to 3 ounces.

Clinical Effects

Summary Of Exposure

    A) USES: Turpentine has been often used as a paint thinner and solvent. In the past, it had been used as a diuretic and expectorant.
    B) TOXICOLOGY: Turpentine is an aliphatic hydrocarbon. Turpentine contains alpha-pinene as its primary constituent as well as beta-pinene, camphene, and limonene. Turpentine oil readily absorbed through the gastrointestinal tract or by inhalation.
    C) EPIDEMIOLOGY: Exposure has occurred; fatalities have been reported. However, turpentine oil has been largely been replaced with white spirit or a turpentine substitute which are of relatively low toxicity when ingested.
    D) WITH POISONING/EXPOSURE
    1) INGESTION: Ingestion is the most significant route of exposure. SYMPTOMS: Turpentine can produce burning, nausea, abdominal pain, vomiting, diarrhea, tachycardia, dyspnea, cyanosis and fever. Severe ingestions can cause glycosuria, hematuria, albuminuria, anuria, excitement, delirium, ataxia, vertigo, stupor, seizures and coma. A significant ingestion can lead to CNS depression that progresses from mild symptoms (ie, headache, dizziness and blurry vision) to lethargy and coma. ONSET: Usually 2 to 3 hours for systemic toxicity to develop. DURATION: GI and CNS symptoms generally resolve within 12 hours in patients with a moderate exposure. SEVERE EVENTS: Primary toxicity is due to the potential risk of aspiration causing a chemical pneumonitis; respiratory insufficiency and failure can develop.
    2) INHALATION: Inhalation of vapors may produce respiratory irritation. High vapor concentrations can cause mucous membrane irritation, hyperpnea, vertigo, tachycardia, headache, hallucinations, distorted perceptions, and seizures. PULMONARY EFFECT: Aspiration pneumonitis, pulmonary necrosis, pneumatocele or pulmonary edema can develop after ingestion, parenteral exposure, or the use of turpentine as a vaginal douche.
    3) DERMAL: Turpentine is absorbed through the skin. Topical application produces a rubefacient effect, with redness, warmth, blisters and burns. Long term or repeated exposure can result in irritation. Some turpentine preparations can cause contact dermatitis.
    4) OCULAR: Ocular exposure to liquid turpentine causes conjunctivitis, lid edema, and blepharospasm. Allergy has been reported.
    5) OTHER: Hemorrhagic cystitis has been associated with turpentine use. Turpentine exposure can produce the odor of violets in urine.

Vital Signs

    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) FEVER and sweating may occur following exposure (Jacobziner & Raybin, 1961). Subcutaneous injection of 1.5 to 2 mL of turpentine caused fever within approximately 24 hours (Wedin & Jones, 1984).
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) A rapid, thready pulse may be present after exposure (Jacobziner & Raybin, 1961).

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) OCULAR IRRITATION: Eye contact with liquid turpentine causes conjunctivitis, eyelid edema and blepharospasm (Jacobziner & Raybin, 1961). Severe pain and conjunctival hyperemia and transient corneal injury can occur (Grant & Schuman, 1993). In severe cases of splash injury, temporary erosion of epithelium has occurred without damage to the corneal stroma (HSDB , 2000).
    a) High vapor concentrations of turpentine cause irritation.
    1) Turpentine vapor in air at concentrations of 75 to 200 ppm are moderately irritating, according to the OSHA (US DHHS, 1981). Another source reports perceptible irritation at 175 ppm, and uncomfortable irritation at 720 to 1,100 ppm (Grant & Schuman, 1993).
    2) PUPILLARY REACTIVITY: Pupils may be unreactive and dilated (Jacobziner & Raybin, 1961).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) IRRITATION: Coughing and irritation of the mucous membranes and throat occur with exposure to high vapor concentrations (HSDB , 2000).
    a) Burning pain in the mouth and throat occurs with ingestion. The breath may smell of turpentine or violets (Gosselin et al, 1984; Goldfrank, 1994).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) TACHYARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) Tachycardia may occur following turpentine ingestion or vapor inhalation (Gosselin et al, 1984). A rapid, thready pulse may be present following exposure (Jacobziner & Raybin, 1961).
    B) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Hypotension (50/40 mmHg) was reported in an elderly woman who was found comatose following a 200 mL (approximately) ingestion of turpentine. The patient made a complete recovery following supportive care (Troulakis et al, 1997).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) PNEUMONITIS
    1) WITH POISONING/EXPOSURE
    a) Aspiration of turpentine can result in chemical pneumonitis and pulmonary edema or aspiration pneumonia (Jacobziner & Raybin, 1961; Pande et al, 1994; Gosselin et al, 1984; HSDB , 2000).
    b) CASE REPORT: A 20-year-old man developed chemical pneumonitis after the accidental ingestion of unspecified quantity of turpentine at a lubricant manufacturing factory. Five days later he developed bilateral pleural effusions. On the hospital day 12 he became acutely short of breath and had a left sided pneumothorax. A chest tube was inserted, but he had a persistent air leak for 10 days because of a bronchopleural fistula. Following supportive treatment, he recovered completely (Rodricks et al, 2003).
    c) CASE SERIES: Dyspnea and coughing or choking occurred in 13 to 19% of a series of 450 cases in children. The incidence of aspiration pneumonitis was not reported, but several cases were described (Jacobziner & Raybin, 1961).
    B) ASTHMA
    1) WITH POISONING/EXPOSURE
    a) OCCUPATIONAL ASTHMA
    1) CASE REPORT: A 27-year-old woman, with a 7 year history as an art painter using balsamic turpentine as a thinner, developed a recurrent nonproductive cough and dyspnea with wheezing after 5 years of exposure. Symptoms usually occurred within 30 to 60 minutes of turpentine exposure. A resting spirometry test was positive when the patient was challenged using turpentine; all other clinical and laboratory findings were negative. Ten hours after the challenge the patient also reported mild dyspnea and chest tightness. Eosinophils were also observed in induced sputum 24 hours after turpentine exposure. The two specific findings confirmed the diagnosis of turpentine induced-asthma in this patient (Dudek et al, 2009).
    C) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Vapors may produce mucous membrane irritation of the respiratory tract (HSDB , 2000).
    D) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Intravenous injection of 5 mL of pure gum turpentine resulted in pulmonary edema and hypoxia in a 22-year-old man (Wason & Greiner, 1986).
    b) CASE REPORT: The use of turpentine (1:1 mixture with water) as a vaginal douche resulted in pulmonary edema in 1 case (Villalobos & Snodgrass, 1994).
    E) PULMONARY NECROSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: An 18-month-old child ingested an unknown amount of turpentine oil and subsequently presented with breathlessness and irritability approximately 14 hours later. An initial chest x-ray revealed a large infiltrate in the right lung with a small pleural effusion. Antibiotic treatment commenced; however, the patient developed increased breathlessness and a persistent fever. A repeat chest x-ray showed an increased amount of effusion, and a CT scan demonstrated right lower-lobe consolidation and atelectasis. A thoracotomy was performed, revealing necrosis of the right lung with multiple abscess cavities and requiring decortication of the right middle and lower lobes and segmental resection. The patient gradually recovered with resolution of the effusion and full expansion of the affected segments (Khan et al, 2006).
    F) APNEA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: An 85-year-old woman developed apnea and coma following an acute ingestion (approximately 200 mL) of turpentine (Troulakis et al, 1997). The patient made a complete recovery following mechanical ventilation and supportive care.

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Ingestion of large volumes of turpentine can cause excitement, ataxia, confusion, stupor, seizures and coma. Seizures may not develop for several hours after extremely high exposure Death has occurred in some cases (Gosselin et al, 1984; Jacobziner & Raybin, 1961).
    b) CASE REPORT: Status epilepticus occurred in a 16-year-old boy following ingestion of approximately 200 mL of turpentine oil (Pande et al, 1994). The patient was unresponsive to aggressive pharmacological intervention (phenobarbitone, phenytoin sodium, diazepam, corticosteroids and atropine) and mechanical ventilation. Postmortem exam revealed multiple small bleeding points of the meninges and cortical surface of the brain, and congestion of the lungs and kidneys.
    c) INCIDENCE: Seizures are infrequently reported following exposure (Haddad et al, 1998).
    B) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Lower levels of vapor exposure (750 to 1000 ppm X several hours) has produced headache and dizziness (US DHHS, 1981; HSDB , 2000).
    2) Lower levels of vapor exposure (750 to 1000 ppm X several hours) has produced headache and dizziness (US DHHS, 1981; HSDB , 2000).
    C) COMA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: An 85-year-old woman ingested approximately 200 mL of turpentine and was found comatose with a Glasgow coma score of 3 (reported shortly after admission) (Troulakis et al, 1997). Following supportive care which included mechanical ventilation for apnea and hemodynamic instability the patient became more alert over the next 10 hours. No permanent sequelae were reported.

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA, VOMITING AND DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting, abdominal pain, and diarrhea can occur following systemic toxicity (Jacobziner & Raybin, 1961; Haddad et al, 1998).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) GLOMERULONEPHRITIS
    1) WITH POISONING/EXPOSURE
    a) Fatal glomerulonephritis has been reported following vapor inhalation (Chapman, 1941). Chronic exposure to high vapor concentrations have caused nephritis (Jacobziner & Raybin, 1961).
    B) HEMORRHAGIC CYSTITIS
    1) WITH POISONING/EXPOSURE
    a) Hemorrhagic cystitis has been reportedly associated with turpentine use (Klein & Hackler, 1980).
    1) Hematuria and albuminuria may occur as a result of urinary tract irritation. The urine may have an odor of violets.
    C) LACK OF EFFECT
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: Kidney damage was NOT reported in a series of 450 cases of accidental turpentine ingestion (Jacobziner & Raybin, 1961).
    b) Renal effects following exposure to turpentine are rarely reported in more current literature, possibly because of the use of turpentine which has fewer impurities (Gosselin et al, 1984).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) BULLOUS ERUPTION
    1) WITH POISONING/EXPOSURE
    a) Erythema, blisters, urticaria, pain and burns may occur (Jacobziner & Raybin, 1961).
    B) ABSCESS
    1) WITH POISONING/EXPOSURE
    a) Injection of 1.5 to 5 mL of turpentine resulted in sterile abscesses in adults (Wedin & Jones, 1984; Wason & Greiner, 1986).
    b) A report from the 1960's described a procedure where chronic sterile abscesses from subcutaneously injected turpentine were deliberately produced in humans as an attempt to cause cancer remission (Szreder, 1968).
    C) CELLULITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Injection of 1.5 to 2 mL of turpentine resulted in cellulitis in an adult (Wedin & Jones, 1984). Intravenous injection of 5 mL of pure gum turpentine resulted in cellulitis and sterile abscess at the site of injection in another case (Wason & Greiner, 1986).
    D) CONTACT DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Turpentine oil can have an immediate irritant effect and cause contact dermatitis following dermal exposure to the liquid (Rudzki et al, 1991; HSDB , 2000), or skin exposure to turpentine vapors (Dooms-Goossens et al, 1986).
    b) Contact may also produce bullous dermatitis (HSDB , 2000).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) ACUTE ALLERGIC REACTION
    1) WITH POISONING/EXPOSURE
    a) Sensitization (Romaguera et al, 1986; Rudzki et al, 1991), allergy (Cachao et al, 1986), and occupational asthma (Hendy et al, 1985) have been reported.
    3.19.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ALLERGIC REACTION
    a) Injected turpentine induces inflammatory responses in rodents (Martins et al, 1992; Klett & Hackenthal, 1993; Min et al, 1991; Turnbull et al, 1994). Turpentine is used in laboratory investigations of the acute phase response.

Reproductive

    3.20.1) SUMMARY
    A) The use of turpentine and water as a vaginal douche has resulted in abortion.
    3.20.3) EFFECTS IN PREGNANCY
    A) HUMANS
    1) The use of a 1:1 mixture of turpentine and water as a vaginal douche resulted in abortion of a fetus (Villalobos & Snodgrass, 1994).
    2) Occupational exposure may affect the course of pregnancy and/or the development of the embryo and fetus (HSDB , 2000).
    B) REPRODUCTIVE AND DEVELOPMENT EFFECTS
    1) In a study conducted in Finland (1982) of children born with cleft palates to mothers possibly exposed to aromatic solvents, including lacquer petrol, methylene chloride, and turpentine, during their first trimester while working in the printing industry produced questionable findings, because of the small sample size (n=14) and potentially multiple chemical exposures (National Toxicology Program (NTP), 2002).
    C) ANIMAL STUDIES
    1) SUMMARY
    a) Inhalation exposure to turpentine vapors for 10 minutes twice daily on gestational days 17 through 21 increased fetal deaths and delayed fetal growth in surviving fetuses. The surviving pups developed dyspnea and severe CNS depression at birth; however, no gross histopathologic abnormalities were found in brain tissue (Gracia-Estrada et al, 1988).
    b) Subcutaneous injection of pregnant mice with turpentine produced plasma protein changes in response to the inflammation in both dams and fetuses (Vranckx, 1987).
    2) ABNORMAL BONE FORMATION
    a) d-Limonene is a constituent of turpentine and can be found in concentrations ranging form 0% to 20%. In an animal study, an increase in abnormal bone formation occurred in fetuses and a decrease in body weight gain in male offspring was found in mice dosed orally with 2363 mg/kg d-limonene on gestation days 7 through 12. A decrease in maternal body weight gain was also observed (National Toxicology Program (NTP), 2002).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS8006-64-2 (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
    3.21.2) SUMMARY/HUMAN
    A) The International Agency for Research on Cancer (IARC) has indicated that there is inadequate evidence for carcinogenicity of d-limonene (a constituent of turpentine oil) in humans. There is, however, evidence for carcinogenicity in experimental animals. Overall, the working group concluded that d-limonene produces renal tubular tumors in male rats by the non-DNA reactive alpha2u-globulin-associated responses that are not relevant to humans (National Toxicology Program (NTP), 2002). IARC has classified d-limonene (a constituent of turpentine) as a Group 3 chemical: not classifiable as to its carcinogenicity to humans (International Agency for Research on Cancer (IARC), 2016)
    3.21.3) HUMAN STUDIES
    A) SUMMARY
    1) The International Agency for Research on Cancer (IARC) has indicated that there is inadequate evidence for carcinogenicity of d-limonene (a constituent of turpentine oil) in humans. There is, however, evidence for carcinogenicity in experimental animals. Overall, the working group concluded that d-limonene produces renal tubular tumors in male rats by the non-DNA reactive alpha2u-globulin-associated responses that are not relevant to humans (National Toxicology Program (NTP), 2002).
    2) IARC has classified d-limonene (a constituent of turpentine) as a Group 3 chemical: not classifiable as to its carcinogenicity to humans (International Agency for Research on Cancer (IARC), 2016).
    3.21.4) ANIMAL STUDIES
    A) LACK OF EFFECT
    1) MELANOMA
    a) Mice treated with turpentine dermally produced an expected inflammatory response, but it did not promote the incidence of melanomas (National Toxicology Program (NTP), 2002).
    2) BENIGN HYPERPLASIA
    a) In animal studies, turpentine applied to the cheeks of animals produced chemically-induced benign epithelial hyperplasia with hyperkeratosis which does not have malignant potential (National Toxicology Program (NTP), 2002).

Genotoxicity

    A) At the time of this review, no genotoxicity studies were found for turpentine (National Toxicology Program (NTP), 2002).
    B) d-Limonene, a constituent of turpentine, was not mutagenic in 4 strains of Salmonella typhimurium or in the mouse lymphoma L5178Y/TK+/- assay (National Toxicology Program (NTP), 2002).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) Monitor fluid status and electrolytes in patients with significant vomiting and/or diarrhea symptoms.
    C) No specific lab work (CBC, electrolytes, urinalysis) is needed unless otherwise clinically indicated.
    D) Monitor respiratory function including pulse oximetry and ABGs in patients at risk or suspected of aspiration.

Methods

    A) CHROMATOGRAPHY
    1) Turpentine can be analyzed by gas chromatography, within a range of 264 to 1107 mg/m(3) (NIOSH, 1988).
    2) Troulakis et al (1997) reported the use of gas chromatography to determine blood and urine levels in an adult following an acute ingestion of turpentine.
    B) OTHER
    1) SCREENING TEST: Extract (chloroform) of serum plus freshly made reagent (100 mg K3Fe(CN)6 + 40 mg FeCl3 + 100 mL water) yields a green-blue turbidity (Kaye, 1973).

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 with significant persistent central nervous system toxicity (somnolence, delirium), or respiratory symptoms of cough or tachypnea should be admitted. Patients with coma, dysrhythmias, or respiratory distress should be admitted to an intensive care setting.
    B) If a patient is symptomatic, admission is indicated. Asymptomatic patients can be observed for 6 hours and discharged if no symptoms develop. In a series of 184 cases of accidental hydrocarbon ingestions, none of the 120 patients with no initial symptoms developed later complications (Machado et al, 1988).
    6.3.1.2) HOME CRITERIA/ORAL
    A) Asymptomatic patients with inadvertent exposures may be monitored at home, with particular attention to the development of any respiratory symptoms. Patients who develop symptoms during home monitoring should be referred to a medical facility.
    B) Accidental ingestions of small quantities of hydrocarbons can safely be handled at home by home monitoring provided the patient is asymptomatic, there is access to a follow-up mechanism, and no suspicious indications of child abuse or attempted suicide exist (Machado et al, 1988).
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity (ie, dysrhythmias, coma or respiratory distress), or in whom the diagnosis is not clear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with deliberate ingestions and symptomatic patients should be sent to a health care facility for observation for 6 to 8 hours. Although patients can develop a delayed pneumonitis, they are unlikely to do so if they have been completely asymptomatic during that time period. Obtain a mental health consult as appropriate.
    1) Patients with a deliberate ingestion, no initial symptoms and a normal chest x-ray obtained at least 6 hours after ingestion and who remain asymptomatic throughout the observation period (6 hours) can be safely discharged (Gummin, 2011).

Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor fluid status and electrolytes in patients with significant vomiting and/or diarrhea symptoms.
    C) No specific lab work (CBC, electrolytes, urinalysis) is needed unless otherwise clinically indicated.
    D) Monitor respiratory function including pulse oximetry and ABGs in patients at risk or suspected of aspiration.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) PREHOSPITAL: GI decontamination is not recommended because of the risk of aspiration. Activated charcoal is generally NOT indicated OR has limited utility as it may cause vomiting and subsequent aspiration. Remove contaminated clothing and wash exposed skin with soap and water.
    6.5.2) PREVENTION OF ABSORPTION
    A) NASOGASTRIC SUCTION
    1) Nasogastric suction lavage should be reserved for patients with lethargy, coma, or seizures, and should be preceded by intubation with a cuffed endotracheal tube (Gummin, 2011; Ng et al, 1974).
    2) Because these products are liquid, a small bore nasogastric tube should be sufficient to remove pine oil and perform gastric lavage if this is deemed appropriate.
    B) ACTIVATED CHARCOAL
    1) Activated charcoal is generally NOT indicated OR has limited utility as it may cause vomiting and subsequent aspiration (Gummin, 2011). It may be considered in rare patients with ingestions of highly toxic hydrocarbons (e.g., halogenated hydrocarbons, carbon tetrachloride) and for hydrocarbons which contain very toxic additives (e.g., heavy metals, pesticides). Should be given within 1 to 2 hours of ingestion. Questionable efficacy thereafter.
    2) Activated charcoal adsorbs kerosene, turpentine, and benzene in vitro and in animal models (Chin et al, 1969; Laass, 1974; Laass, 1980; Decker et al, 1981).
    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) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) INGESTION: Treatment is symptomatic and supportive. Monitor vital signs, mental status and respiratory function. Monitor fluids and electrolytes if the patient develops significant vomiting and/or diarrhea. Treat with IV fluids as needed. Following a significant exposure, monitor for evidence of pulmonary aspiration. INHALATION: Immediately remove the patient from the source of exposure. Symptoms often improve following removal. Closely monitor respiratory function, provide oxygen and symptomatic and supportive care. DERMAL: After assuring that the patient is medically stable, remove contaminated clothing and wash exposed skin with soap and water.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) RESPIRATORY DISTRESS: Orotracheal intubation for airway protection should be performed early if a patient exhibits respiratory distress. Administer oxygen. Consider the use of a surfactant. Endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality in one study. RESPIRATORY FAILURE: Partial liquid ventilation, high frequency jet ventilation, extracorporeal membrane oxygenation (ECMO) and high frequency chest wall oscillation have all been used with apparent success in cases of severe hydrocarbon pneumonitis. SEIZURES: Following a large ingestion of turpentine, seizures, excitement and coma may develop. Initially treat seizures with benzodiazepines. OTHER: Prophylactic antibiotics and steroids are of no proven benefit following hydrocarbon pneumonitis. Monitor and treat significant dysrhythmias.
    B) MONITORING OF PATIENT
    1) Monitor vital signs and mental status. Blood concentrations are not readily available or useful to guide management.
    2) Obtain an ECG and institute continuous cardiac monitoring in patients with moderate to severe toxicity. Obtain CBC, basic chemistry panel, serum creatinine and liver enzymes in severe overdoses.
    3) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests and obtain chest radiograph in patients with any respiratory symptoms. NOTE: The chest radiograph may be normal early in the clinical course.
    4) Standard urine toxicology screen does not detect hydrocarbons.
    5) Monitor fluid and electrolyte status in patients with significant vomiting and/or diarrhea.
    6) Head CT should be obtained in patients with altered mental status.
    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, 2010; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    D) PULMONARY ASPIRATION
    1) If the patient is symptomatic upon arrival at the medical facility, aspiration has probably already occurred. Monitor pulse oximetry and obtain arterial blood gases as needed in cases of severe aspiration pneumonitis to ensure adequate ventilation.
    2) Admit and obtain chest x-ray in all symptomatic patients.
    3) Observe patient for 6 hours. Discharge if asymptomatic and no radiographic evidence of pneumonitis (Gummin, 2011).
    E) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    8) PARTIAL LIQUID VENTILATION
    a) ANIMAL DATA: In a rat model of kerosene aspiration and subsequent pneumonitis, mortality was significantly greater in the rats who received partial liquid ventilation (PLV) with perfluorocarbon as compared to the rats who did not receive PLV (Burns et al, 1999).
    9) HIGH FREQUENCY JET VENTILATION
    a) A 13-month-old boy with severe hydrocarbon pneumonitis required high PEEP to maintain oxygenation and developed high peak inspiratory pressures and barotrauma (pneumomediastinum and subcutaneous emphysema) (Bysani et al, 1994). Changing the patient from a conventional ventilator to a high frequency jet ventilator allowed adequate oxygenation with lower peak inspiratory pressures and eventual recovery from the pneumonitis.
    F) EXTRACORPOREAL MEMBRANE OXYGENATION
    1) Extracorporeal membrane oxygenation may be beneficial in patients that develop severe pulmonary toxicity as noted by severe ventilation-perfusion mismatch despite PEEP and high frequency jet ventilation (HFJV) (Gummin, 2011).
    G) CORTICOSTEROID
    1) Steroids have NOT been shown to be of benefit in treating the early phase of hydrocarbon pneumonitis, however pulse steroid therapy may be useful in the late phase of adult respiratory distress syndrome following hydrocarbon ingestion. Two children with naphtha-induced chemical pneumonia were successfully treated with nebulized budesonide.
    a) CASE REPORT: A 23-year-old woman developed severe respiratory distress, requiring mechanical ventilation, after ingesting 1000 milliliters of petroleum naphtha. Chest x-ray showed progressively worsening of infiltrates and diffuse interstitial consolidation of both lungs with a large pneumatocele in the right upper lobe. Pulse steroid therapy was initiated, on hospital day 17, with hydrocortisone 1000 milligrams/day IV for the first three days, followed by gradually decreasing prednisolone doses over 7 weeks, and concurrent administration of piperacillin sodium 2 grams IV every 12 hours. A follow-up chest x-ray showed rapid improvement of interstitial consolidation 3 days after beginning therapy, and, despite an enlargement of the pneumatocele, as well as, the appearance of several smaller pneumatoceles, the patient was successfully extubated six days later (Kamijo et al, 2000).
    1) The patient's enlarging pneumatocele; however, became infected and subsequently ruptured, leading to recurrent respiratory distress. The patient gradually recovered following a protracted illness (hospitalized for 67 days) with no permanent sequelae after administration of antibiotics and open thoracic surgery for a bronchopleural fistula repair.
    b) After ingesting naphtha, two 3-year-old boys developed chemical pneumonia with severe symptoms (dyspnea, suppressed breath sounds, crackles, hypoxemia, and cyanosis) unresponsive to supportive measures (Gurkan & Bosnak, 2005).
    1) On the first day of hospitalization, radiographic exam revealed pneumonic infiltration; severe pulmonary symptoms developed on the second and fourth days, respectively. Despite supportive care, their symptoms worsened; chest radiographs showed localized consolidation and bilateral diffuse reticulonodular infiltration. Both patients were successfully treated with nebulized budesonide (0.5 mg every 12 hours for 4 days). A response (improvement in oxygen saturation and decrease in symptoms) was noted within 6 hours of budesonide administration. They were discharged after a week of hospitalization (Gurkan & Bosnak, 2005).

Eye Exposure

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

Dermal Exposure

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

Range Of Toxicity

Summary

    A) TOXICITY: Turpentine is an irritant of the skin and mucous membranes and is a CNS depressant. A value range of 15 to 90 mL has been determined to be the mean oral lethal dose for humans through numerous reports of turpentine fatalities. ADULT: A dose of 120 to 180 mL may be fatal if no treatment is obtained. PEDIATRIC: A dose of 15 mL was fatal in a 2-year-old child; however, benzene was present in the mixture. Children have survived ingestions of 2 to 3 ounces.

Minimum Lethal Exposure

    A) ADULT
    1) A value range of 15 to 90 mL has been determined to be the mean oral lethal dose for humans through numerous reports of turpentine fatalities (ACGIH, 1991). Other reports indicate that doses between 120 to 180 mL may be fatal if no treatment is obtained (HSDB , 2000).
    B) PEDIATRIC
    1) As little as 15 mL has been fatal to a 2-year-old child; however, benzene was present in the mixture (Gosselin et al, 1984; HSDB , 2000).
    2) Ingestion of approximately 200 mL of turpentine oil was fatal in a 16-year-old boy (Pande et al, 1994).
    C) SUMMARY
    1) Turpentine is an irritant of the skin and mucous membranes and is a CNS depressant. In addition to the high toxicity of low oral doses, turpentine can be toxic if aspirated leading to chemical pneumonitis with pathogenic dyspnea, acute pulmonary edema, cyanosis, and even death from respiratory failure (ACGIH, 1991; Hathaway et al, 1996).

Maximum Tolerated Exposure

    A) ADULT
    1) There has been a report of human recovery from a turpentine dose of 120 g (Clayton & Clayton, 1994).
    2) CASE REPORT: An 85-year-old woman survived an estimated ingestion of 200 mL turpentine and developed CNS depression which included coma. Following supportive care the patient made a complete recovery (Troulakis et al, 1997).
    3) Volunteers exposed to turpentine vapors for 3-5 minutes reported that 75 ppm caused nose and throat irritation, and 175 ppm was intolerable. The majority of these subjects estimated 100 ppm to be the highest tolerable 8-hour exposure. Workers exposed to 750 to 1000 ppm turpentine vapors for several hours reported eye irritation, headache, dizziness, nausea, and tachycardia.
    a) Case reports indicated that chronic occupational exposure can result in respiratory irritation, renal injury, and death. Dermal contact can result in eczema and contact dermatitis. Splashes of turpentine into the eye can result in severe pain and blepharospasm followed by conjunctival hyperemia and slight transient injury of the corneal epithelium (ACGIH, 1991) (Grant & Schumann, 1993) (Harbison, 1998; Hathaway et al, 1996).
    B) PEDIATRIC
    1) Children have survived doses of approximately 3 ounces (HSDB , 2000).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CASE REPORTS
    a) CASE REPORT - An 85-year-old female survived a 200 mL turpentine ingestion and had initial serum blood and urine levels of 28 mcg/mL and 15 mcg/mL, respectively (Troulakis et al, 1997).

Workplace Standards

    A) ACGIH TLV Values for CAS8006-64-2 (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) Turpentine
    a) TLV:
    1) TLV-TWA: 20 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: SEN
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) SEN: The designation SEN refers to the potential for an agent to produce sensitization, as confirmed by human or animal data. The notation does not imply that this is the critical effect or that this is the sole basis for the TLV. Although, for those TLVs that are based on sensitization, the TLV is meant to protect workers from induction of this effect, but cannot protect workers who have already become sensitized. The notation should be used to assist in identifying sensitization hazards and reducing respiratory, dermal, and conjunctival exposures to sensitizing agents in the workplace. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): URT and skin irr; CNS impair; lung dam
    d) Molecular Weight: 136
    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) Adopted Value
    1) Turpentine and selected monoterpenes
    a) TLV:
    1) TLV-TWA: 20 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: SEN
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) SEN: The designation SEN refers to the potential for an agent to produce sensitization, as confirmed by human or animal data. The notation does not imply that this is the critical effect or that this is the sole basis for the TLV. Although, for those TLVs that are based on sensitization, the TLV is meant to protect workers from induction of this effect, but cannot protect workers who have already become sensitized. The notation should be used to assist in identifying sensitization hazards and reducing respiratory, dermal, and conjunctival exposures to sensitizing agents in the workplace. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): URT and skin irr; CNS impair; lung dam
    d) Molecular Weight: Varies
    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 CAS8006-64-2 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Turpentine
    2) REL:
    a) TWA: 100 ppm (560 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: 800 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS8006-64-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Turpentine
    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) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Turpentine and selected monoterpenes
    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.
    3) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    4) 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
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Turpentine
    6) MAK (DFG, 2002): Category 3A ; Listed as: Turpentine
    a) Category 3A : Substances for which the criteria for classification in Category 4 or 5 are fulfilled but for which the database is insufficient for the establishment of a MAK value.
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS8006-64-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Turpentine
    2) Table Z-1 for Turpentine:
    a) 8-hour TWA:
    1) ppm: 100
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 560
    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) Reference: HSDB, 2000; Lewis, 1996; RTECS, 2000
    1) LD50- (ORAL)RAT:
    a) 5760 mg/kg
    2) TCLo- (INHALATION)HUMAN:
    a) 175 ppm -- Conjunctive irritation; changes in respiratory system; changes in sense organs and special senses
    b) 6 g/m(3) for 3H -- Hallucinations, distorted perceptions; headache; changes in sense organs and special senses

Pharmacology Toxicology

Toxicologic Mechanism

    A) Spirit of turpentine or wood turpentine varies in composition according to its source and method of production. A typical analysis yields the following: alpha-pinene, 82.4%; camphene, 8.7%; beta-pinene, 2.1%; unidentified natural turpenes, 6.8% (Hathaway et al, 1996).

Physicochemical

Physical Characteristics

    A) Turpentine (i.e. wood turpentine) is a volatile, clear, colorless liquid with a characteristic odor described as aromatic, unpleasant, and penetrating. Gum turpentine is a volatile, yellowish, opaque, sticky mass with a characteristic odor (AAR, 1998; (ACGIH, 1991; Ashford, 1994; Budavari, 1996; Hathaway et al, 1996).

Molecular Weight

    A) 136 (approximate)(ACGIH, 2000)

Other

    A) ODOR THRESHOLD
    1) 100 ppm (wood turpentine) (ACGIH, 1991)

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 Indices, 6th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1991.
    14) AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
    15) AMA Department of DrugsAMA Department of Drugs: AMA Evaluations Subscription, American Medical Association, Chicago, IL, 1992.
    16) 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.
    17) Ansell-Edmont: SpecWare Chemical Application and Recommendation Guide. Ansell-Edmont. Coshocton, OH. 2001. Available from URL: http://www.ansellpro.com/specware. As accessed 10/31/2001.
    18) Artigas A, Bernard GR, Carlet J, et al: The American-European consensus conference on ARDS, part 2: ventilatory, pharmacologic, supportive therapy, study design strategies, and issues related to recovery and remodeling.. Am J Respir Crit Care Med 1998; 157:1332-1347.
    19) Ashford R: Ashford's Dictionary of Industrial Chemicals, Wavelength Publications Ltd, London, England, 1994.
    20) Barbosa SV, Burkard DH, & Spangberg LSW: Cytotoxic effects of gutta-percha solvents. J Endodontics 1994; 20:6-8.
    21) Bata Shoe Company: Industrial Footwear Catalog, Bata Shoe Company, Belcamp, MD, 1995.
    22) Best Manufacturing: ChemRest Chemical Resistance Guide. Best Manufacturing. Menlo, GA. 2002. Available from URL: http://www.chemrest.com. As accessed 10/8/2002.
    23) Best Manufacturing: Degradation and Permeation Data. Best Manufacturing. Menlo, GA. 2004. Available from URL: http://www.chemrest.com/DomesticPrep2/. As accessed 04/09/2004.
    24) Boss Manufacturing Company: Work Gloves, Boss Manufacturing Company, Kewanee, IL, 1998.
    25) Brophy GM, Bell R, Claassen J, et al: Guidelines for the evaluation and management of status epilepticus. Neurocrit Care 2012; 17(1):3-23.
    26) Brower RG, Matthay AM, & Morris A: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Eng J Med 2000; 342:1301-1308.
    27) Budavari S: The Merck Index, 12th ed, Merck & Co, Inc, Whitehouse Station, NJ, 1996.
    28) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    29) Burns MJ, Dickson EW, & Sivilotti MLA: Enhanced mortality from perfluorocarbon administration in a rat model of kerosene aspiration. Clin Toxicol 1999; 37:855-859.
    30) Bysani GK, Rucoba RJ, & Noah ZL: Treatment of hydrocarbon pneumonitis - high frequency jet ventilation as an alternative to extracorporeal membrane oxygenation. Chest 1994; 106:300-303.
    31) CHRIS : CHRIS Hazardous Chemical Data. US Department of Transportation, US Coast Guard. Washington, DC (Internet Version). Edition expires 4/30/2000; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    32) Cachao P, Menezes Brandao F, & Carmo M: Allergy to oil of turpentine in Portugal. Contact Dermatitis 1986; 14:205-208.
    33) Cataletto M: Respiratory Distress Syndrome, Acute(ARDS). In: Domino FJ, ed. The 5-Minute Clinical Consult 2012, 20th ed. Lippincott Williams & Wilkins, Philadelphia, PA, 2012.
    34) 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.
    35) Chapman EM: Observations on the effect of paint on the kidneys with particular reference to the role of turpentine. J Ind Hyg Toxicol 1941; 23:277-289.
    36) ChemFab Corporation: Chemical Permeation Guide Challenge Protective Clothing Fabrics, ChemFab Corporation, Merrimack, NH, 1993.
    37) Chin L, Picchioni AL, & Duplisse BR: Comparative antidotal effectiveness of activated charcoal, Arizona montmorillonite, and evaporated milk. J Pharm Sci 1969; 58:1353.
    38) 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.
    39) Choonara IA & Rane A: Therapeutic drug monitoring of anticonvulsants state of the art. Clin Pharmacokinet 1990; 18:318-328.
    40) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    41) Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Vol 2B, Toxicology, 4th ed, John Wiley & Sons, New York, NY, 1994.
    42) Comasec Safety, Inc.: Chemical Resistance to Permeation Chart. Comasec Safety, Inc.. Enfield, CT. 2003. Available from URL: http://www.comasec.com/webcomasec/english/catalogue/mtabgb.html. As accessed 4/28/2003.
    43) Comasec Safety, Inc.: Product Literature, Comasec Safety, Inc., Enfield, CT, 2003a.
    44) 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.
    45) Decker WJ, Corby DG, & Hilburn RE: Adsorption of solvents by activated charcoal, polymers, and mineral sorbents. Vet Hum Toxicol 1981; 23(Suppl 1):44-45.
    46) Dooms-Goossens AE, Debusschere KM, & Gevers DM: Contact dermatitis caused by airborne agents. J Am Acad Dermatol 1986; 15:1-10.
    47) DuPont: DuPont Suit Smart: Interactive Tool for the Selection of Protective Apparel. DuPont. Wilmington, DE. 2002. Available from URL: http://personalprotection.dupont.com/protectiveapparel/suitsmart/smartsuit2/na_english.asp. As accessed 10/31/2002.
    48) DuPont: Permeation Guide for DuPont Tychem Protective Fabrics. DuPont. Wilmington, DE. 2003. Available from URL: http://personalprotection.dupont.com/en/pdf/tyvektychem/pgcomplete20030128.pdf. As accessed 4/26/2004.
    49) DuPont: Permeation Test Results. DuPont. Wilmington, DE. 2002a. Available from URL: http://www.tyvekprotectiveapprl.com/databases/default.htm. As accessed 7/31/2002.
    50) Dudek W , Wittczak T , Swierczynska-Machura D , et al: Occupational asthma due to turpentine in art painter--case report. Int J Occup Med Environ Health 2009; 22(3):293-295.
    51) 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/.
    52) 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.
    53) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    54) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    55) Falk AA, Hagberg MT, & Lof AE: Uptake, distribution and elimination of alpha-pinene in man after exposure by inhalation. Scand J Work Environ Health 1990; 16:372-378.
    56) Filipsson AF: Short term inhalation exposure to turpentine - toxicokinetics and acute effects in men. Occup Environ Med 1996; 53:100-105.
    57) Finkel AJ: Hamilton and Hardy's Industrial Toxicology, 4th ed, John Wright, PSG, Inc, Boston, MA, 1983.
    58) Goldfrank LR: Hydrocarbons, in: Goldfrank LR, Flomenbaum NE, Lewin NA et al (Eds), Goldfrank's Toxicologic Emergencies, 5th ed, Appleton & Lange, Norwalk, CT, 1994.
    59) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    60) Gosselin RE, Smith RP, & Hodge HC: Clinical Toxicology of Commercial Products, 5th ed, Williams & Wilkins, Baltimore, MD, 1984.
    61) Gracia-Estrada J, Segura AR, & Garzon P: Cerebral cortex and body growth development of progeny of rats exposed to thinner and turpentine inhalation. Gen Pharmacol 1988; 19:467-470.
    62) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    63) Grant WM & Schuman JS: Toxicology of the Eye, 4th ed, Charles C Thomas, Springfield, IL, 1993.
    64) Grant WM: Toxicology of the Eye, 3rd ed, Charles C Thomas, Springfield, IL, 1986.
    65) Guardian Manufacturing Group: Guardian Gloves Test Results. Guardian Manufacturing Group. Willard, OH. 2001. Available from URL: http://www.guardian-mfg.com/guardianmfg.html. As accessed 12/11/2001.
    66) Gummin DD: Hydrocarbons. In: Nelson LS, Lewin NA, Howland MA et al, eds. Goldfrank's Toxicologic Emergencies, 9th ed. McGraw Hill, New York, NY, 2011.
    67) Gurkan F & Bosnak M: Use of nebulized budesonide in two critical patients with hydrocarbon intoxication. Am J Ther 2005; 12(4):366-367.
    68) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2000; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    69) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 7/31/1996; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    70) Haas CF: Mechanical ventilation with lung protective strategies: what works?. Crit Care Clin 2011; 27(3):469-486.
    71) Haddad LM, Shannon MW, & Winchester JF: Clinical Management of Poisoning and Drug Overdose, 3rd Ed., W.B, Saunders Co, Philadelphia, PA, 1998.
    72) Harbison RD: Hamilton & Hardy's Industrial Toxicology, 5th ed, Mosby-Year Books, St. Louis, MO, 1998.
    73) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    74) Hathaway GJ, Proctor NH, & Hughes JP: Chemical Hazards of the Workplace, 3rd ed, Van Nostrand Reinhold Company, New York, NY, 1991.
    75) Hathaway GJ, Proctor NH, & Hughes JP: Chemical Hazards of the Workplace, 4th ed, Van Nostrand Reinhold Company, New York, NY, 1996.
    76) Hegenbarth MA & American Academy of Pediatrics Committee on Drugs: Preparing for pediatric emergencies: drugs to consider. Pediatrics 2008; 121(2):433-443.
    77) Hendy MS, Beattie BE, & Burge PS: Occupational asthma due to an emulsified oil mist. Br J Ind Med 1985; 42:51-54.
    78) Hvidberg EF & Dam M: Clinical pharmacokinetics of anticonvulsants. Clin Pharmacokinet 1976; 1:161.
    79) 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.
    80) 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.
    81) 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.
    82) 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.
    83) 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.
    84) 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.
    85) ICAO: Technical Instructions for the Safe Transport of Dangerous Goods by Air, 2003-2004. International Civil Aviation Organization, Montreal, Quebec, Canada, 2002.
    86) ILC Dover, Inc.: Ready 1 The Chemturion Limited Use Chemical Protective Suit, ILC Dover, Inc., Frederica, DE, 1998.
    87) ITI: Toxic and Hazardous Industrial Chemicals Safety Manual, The International Technical Information Institute, Tokyo, Japan, 1995.
    88) 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.
    89) 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.
    90) Jacobziner H & Raybin HW: Turpentine poisoning. Arch Pediatr 1961; 357-364.
    91) Kamijo Y, Soma K, & Asari Y: Pulse steroid therapy in adult respiratory distress syndrome following petroleum naphtha ingestion. Clin Toxicol 2000; 38:59-62.
    92) Kappler, Inc.: Suit Smart. Kappler, Inc.. Guntersville, AL. 2001. Available from URL: http://www.kappler.com/suitsmart/smartsuit2/na_english.asp?select=1. As accessed 7/10/2001.
    93) Kaye S: Handbook of Emergency Toxicology, 3rd ed, CC Thomas, Springfield, IL, 1973.
    94) Khan AJ, Akhtar RP, & Faruqui ZS: Turpentine oil inhalation leading to lung necrosis and empyema in a toddler. Pediatr Emerg Care 2006; 22(5):355-357.
    95) Kimberly-Clark, Inc.: Chemical Test Results. Kimberly-Clark, Inc.. Atlanta, GA. 2002. Available from URL: http://www.kc-safety.com/tech_cres.html. As accessed 10/4/2002.
    96) Klein FA & Hackler RH: Hemorrhagic gastritis associated with turpentine ingestion. Urology 1980; 16:187.
    97) Klett C & Hackenthal E: The response of hepatic angiotensinogen secretion to experimental inflammatory stimula. Agents Actions 1993; 38:220-230.
    98) Kollef MH & Schuster DP: The acute respiratory distress syndrome. N Engl J Med 1995; 332:27-37.
    99) LaCrosse-Rainfair: Safety Products, LaCrosse-Rainfair, Racine, WI, 1997.
    100) Laass W: Suitability of using activated charcoal for the treatment of acute oral poisoning with organic solvents. Pharmazie 1974; 29:728.
    101) Laass W: Therapy of acute oral poisonings by organic solvents: treatment by activated charcoal in combination with laxatives. Arch Toxicol 1980; 4(Suppl):406-409.
    102) Lewis RJ: Hawley's Condensed Chemical Dictionary, 13th ed, John Wiley & Sons, Inc, New York, NY, 1997.
    103) Lewis RJ: Sax's Dangerous Properties of Industrial Materials, 9th ed, Van Nostrand Reinhold Company, New York, NY, 1996.
    104) Liu JK & Couldwell WT: Contemporary management of prolactinomas. Neurosurg Focus 2004; 16(4):E2-.
    105) Loddenkemper T & Goodkin HP: Treatment of Pediatric Status Epilepticus. Curr Treat Options Neurol 2011; Epub:Epub.
    106) MAPA Professional: Chemical Resistance Guide. MAPA North America. Columbia, TN. 2003. Available from URL: http://www.mapaglove.com/pro/ChemicalSearch.asp. As accessed 4/21/2003.
    107) MAPA Professional: Chemical Resistance Guide. MAPA North America. Columbia, TN. 2004. Available from URL: http://www.mapaglove.com/ProductSearch.cfm?id=1. As accessed 6/10/2004.
    108) Machado B, Cross K, & Snodgrass WR: Accidental hydrocarbon ingestion cases telephoned to a regional poison center. Ann Emerg Med 1988; 17:804-807.
    109) Manno EM: New management strategies in the treatment of status epilepticus. Mayo Clin Proc 2003; 78(4):508-518.
    110) Mar-Mac Manufacturing, Inc: Product Literature, Protective Apparel, Mar-Mac Manufacturing, Inc., McBee, SC, 1995.
    111) Marigold Industrial: US Chemical Resistance Chart, on-line version. Marigold Industrial. Norcross, GA. 2003. Available from URL: www.marigoldindustrial.com/charts/uschart/uschart.html. As accessed 4/14/2003.
    112) Martins B, Kouyoumdjian M, & Limaos EA: The clearance rate of plasma kallikrein by the liver increases during the acute-phase response to inflammation. Agents Actions 1992; 37:111-113.
    113) Memphis Glove Company: Permeation Guide. Memphis Glove Company. Memphis, TN. 2001. Available from URL: http://www.memphisglove.com/permeation.html. As accessed 7/2/2001.
    114) Min K, Terano Y, & Onosaka S: Induction of hepatic metallothionein by nonmetallic compounds associated with acute-phase response in inflammation. Toxicol Appl Pharmacol 1991; 111:152-162.
    115) Montgomery Safety Products: Montgomery Safety Products Chemical Resistant Glove Guide, Montgomery Safety Products, Canton, OH, 1995.
    116) NFPA: Fire Protection Guide to Hazardous Materials, 13th ed., National Fire Protection Association, Quincy, MA, 2002.
    117) NHLBI ARDS Network: Mechanical ventilation protocol summary. Massachusetts General Hospital. Boston, MA. 2008. Available from URL: http://www.ardsnet.org/system/files/6mlcardsmall_2008update_final_JULY2008.pdf. As accessed 2013-08-07.
    118) NIOSH : Pocket Guide to Chemical Hazards. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2000; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    119) NOAA: Chemical Reactivity Worksheet v12 (Turpentine). Developed by the CAMEO Team at the Hazardous Materials Response and Assessment Division, ORCA/NOS/NOAA, and the Chemical Emergency Preparedness Office of EPA, NOAA Hazmat, Seattle, WA, 2000.
    120) NPS: Environmental Contaminants Encyclopedia (Turpentine), RJ Irwin, (ed), National Park Service Water Resources Divisions, Water Operations Branch, Fort Collins, CO, 1997.
    121) 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.
    122) 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.
    123) 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.
    124) 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.
    125) Naradzay J & Barish RA: Approach to ophthalmologic emergencies. Med Clin North Am 2006; 90(2):305-328.
    126) Nat-Wear: Protective Clothing, Hazards Chart. Nat-Wear. Miora, NY. 2001. Available from URL: http://www.natwear.com/hazchart1.htm. As accessed 7/12/2001.
    127) 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.
    128) 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.
    129) 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.
    130) 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.
    131) 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.
    132) 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.
    133) 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.
    134) 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.
    135) 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.
    136) 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.
    137) 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.
    138) 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.
    139) 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.
    140) 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.
    141) 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.
    142) 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.
    143) 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.
    144) 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.
    145) 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.
    146) 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.
    147) 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.
    148) 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.
    149) 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.
    150) 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.
    151) 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.
    152) 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.
    153) 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.
    154) 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.
    155) 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.
    156) 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.
    157) 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.
    158) 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.
    159) 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.
    160) 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.
    161) 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.
    162) 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.
    163) 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.
    164) 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.
    165) 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.
    166) 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.
    167) 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.
    168) 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.
    169) 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.
    170) 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.
    171) 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.
    172) 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.
    173) 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.
    174) 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.
    175) 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.
    176) 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.
    177) 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.
    178) 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.
    179) 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.
    180) 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.
    181) 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.
    182) 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.
    183) 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.
    184) 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.
    185) 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.
    186) 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.
    187) 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.
    188) 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.
    189) 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.
    190) 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.
    191) 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.
    192) 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.
    193) 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.
    194) 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.
    195) 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.
    196) 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.
    197) 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.
    198) 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.
    199) 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.
    200) 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.
    201) 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.
    202) National Research Council : Acute exposure guideline levels for selected airborne chemicals, 5, National Academies Press, Washington, DC, 2007.
    203) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 6, National Academies Press, Washington, DC, 2008.
    204) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 7, National Academies Press, Washington, DC, 2009.
    205) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 8, National Academies Press, Washington, DC, 2010.
    206) National Toxicology Program (NTP): Turpentine (turpentine oil, wood turpentine, sulfate turpentine, sulfite turpentine): review of toxicological literature. National Toxicology Program (NTP), National Institute of Environmental Health Sciences (NIEHS). Research Triangle Park, NC. 2002. Available from URL: https://ntp.niehs.nih.gov/ntp/htdocs/chem_background/exsumpdf/turpentine_508.pdf. As accessed 2016-08-19.
    207) Neese Industries, Inc.: Fabric Properties Rating Chart. Neese Industries, Inc.. Gonzales, LA. 2003. Available from URL: http://www.neeseind.com/new/TechGroup.asp?Group=Fabric+Properties&Family=Technical. As accessed 4/15/2003.
    208) Ng RC, Darwish H, & Stewart DA: Emergency treatment of petroleum distillate and turpentine ingestion. Can Med Assoc J 1974; 111(6):537-538.
    209) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    210) North: Chemical Resistance Comparison Chart - Protective Footwear . North Safety. Cranston, RI. 2002. Available from URL: http://www.linkpath.com/index2gisufrm.php?t=N-USA1. As accessed April 30, 2004.
    211) North: eZ Guide Interactive Software. North Safety. Cranston, RI. 2002a. Available from URL: http://www.northsafety.com/feature1.htm. As accessed 8/31/2002.
    212) Pande TK, Sidhartha P, & Hiran S: Turpentine poisoning: a case report. Forens Sci Internat 1994; 65:47-49.
    213) Peate WF: Work-related eye injuries and illnesses. Am Fam Physician 2007; 75(7):1017-1022.
    214) Playtex: Fits Tough Jobs Like a Glove, Playtex, Westport, CT, 1995.
    215) Pohanish RP & Greene SA: Rapid Guide to Chemical Incompatibilities, Van Nostrand Reinhold Company, New York, NY, 1997.
    216) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    217) Product Information: diazepam IM, IV injection, diazepam IM, IV injection. Hospira, Inc (per Manufacturer), Lake Forest, IL, 2008.
    218) Product Information: lorazepam IM, IV injection, lorazepam IM, IV injection. Akorn, Inc, Lake Forest, IL, 2008.
    219) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2000; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    220) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    221) Riordan M, Rylance G, & Berry K: Poisoning in children 4: household products, plants, and mushrooms. Arch Dis Child 2002; 87(5):403-406.
    222) River City: Protective Wear Product Literature, River City, Memphis, TN, 1995.
    223) Rodricks A, Satyanarayana M, D'Souza GA, et al: Turpentine-induced chemical pneumonitis with broncho-pleural fistula. JAPI 2003; 51:729-730.
    224) Romaguera C, Alomar A, & Conde Salazar L: Turpentine sensitization. Contact Dermatitis 1986; 14:197.
    225) Rudzki E, Berova N, & Czernielewski Z: Contact allergy to oil of turpentine: a 10-year retrospective view. Contact Dermatitis 1991; 24:317-318.
    226) Safety 4: North Safety Products: Chemical Protection Guide. North Safety. Cranston, RI. 2002. Available from URL: http://www.safety4.com/guide/set_guide.htm. As accessed 8/14/2002.
    227) 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.
    228) Servus: Norcross Safety Products, Servus Rubber, Servus, Rock Island, IL, 1995.
    229) Singh I, Gathwala G, & Yadav SPS: Myiasis in children: the Indian perspective. J Pediatr Otorhinolaryngol 1993; 25:127-131.
    230) Sittig M: Handbook of Toxic and Hazardous Chemicals and Carcinogens, 3rd ed, Noyes Publications, Park Ridge, NJ, 1991.
    231) 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 2010; 14(2):162-168.
    232) Standard Safety Equipment: Product Literature, Standard Safety Equipment, McHenry, IL, 1995.
    233) Stolbach A & Hoffman RS: Respiratory Principles. In: Nelson LS, Hoffman RS, Lewin NA, et al, eds. Goldfrank's Toxicologic Emergencies, 9th ed. McGraw Hill Medical, New York, NY, 2011.
    234) Szreder W: Effect of chronic sterile abscess on neoplastic disease in man. Neoplasm 1968; 15(4):427-431.
    235) Tingley: Chemical Degradation for Footwear and Clothing. Tingley. South Plainfield, NJ. 2002. Available from URL: http://www.tingleyrubber.com/tingley/Guide_ChemDeg.pdf. As accessed 10/16/2002.
    236) Trelleborg-Viking, Inc.: Chemical and Biological Tests (database). Trelleborg-Viking, Inc.. Portsmouth, NH. 2002. Available from URL: http://www.trelleborg.com/protective/. As accessed 10/18/2002.
    237) Trelleborg-Viking, Inc.: Trellchem Chemical Protective Suits, Interactive manual & Chemical Database. Trelleborg-Viking, Inc.. Portsmouth, NH. 2001.
    238) Troulakis G, Tsatsakis AM, & Tzatzarakis M: Acute intoxication and recovery following massive turpentine ingestion: clinical and toxicological data. Vet Human Toxicol 1997; 3:155-157.
    239) Turnbull AV, Dow RC, & Hopkins SJ: Mechanisms of activation of the pituitary-adrenal axis by tissue injury in the rat. Psychoneuroendocrinology 1994; 165-178.
    240) 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.
    241) 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.
    242) 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-.
    243) 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.
    244) 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.
    245) 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.
    246) 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.
    247) 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-.
    248) U.S. Occupational Safety, and Health Administration (OSHA): Process safety management of highly hazardous chemicals. 29 CFR 2010 2010; 29(1910.119):348-.
    249) US DHHS: Occupational Health Guideline for Turpentine, in: NIOSH/OSHA Occupational Health Guidelines for Chemical Hazards, volume 2, Publication No 81-123, DHHS(NIOSH), Washington, DC, 1981.
    250) 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.
    251) Villalobos D & Snodgrass W: Fulminant non-cardiogenic pulmonary edema from vaginal turpentine douche (abstract), AAPCC Annual Scientific Meeting, Salt Lake City, UT, 1994.
    252) Vranckx R: Alpha-fetoprotein and transcortin behave as acute phase reactants in the maternal and fetal compartments of the inflammatory pregnant mouse. Endocrinology 1987; 120:1782-1789.
    253) Wason S & Greiner PT: Intravenous hydrocarbon abuse. Am J Emerg Med 1986; 4:543-544.
    254) Wedin GP & Jones RR: Parenteral administration of hydrocarbons. Clin Toxicol 1984; 22:485-492.
    255) Wells Lamont Industrial: Chemical Resistant Glove Application Chart. Wells Lamont Industrial. Morton Grove, IL. 2002. Available from URL: http://www.wellslamontindustry.com. As accessed 10/31/2002.
    256) Willson DF, Truwit JD, Conaway MR, et al: The adult calfactant in acute respiratory distress syndrome (CARDS) trial. Chest 2015; 148(2):356-364.
    257) Wilson DF, Thomas NJ, Markovitz BP, et al: Effect of exogenous surfactant (calfactant) in pediatric acute lung injury. A randomized controlled trial. JAMA 2005; 293:470-476.
    258) Workrite: Chemical Splash Protection Garments, Technical Data and Application Guide, W.L. Gore Material Chemical Resistance Guide, Workrite, Oxnard, CA, 1997.