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PINE OIL

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Pine oil is used as a disinfectant/solvent in many cleaning agents.

Specific Substances

    1) Alpha Terpineol
    2) Aromatic Pine Oil
    3) Yarmor
    4) Oil of pine
    5) Arizole
    6) Oleum abietis
    7) Unipine
    8) Yarmour pine oil
    9) Terpentinoel (German)
    10) CAS 8002-09-3
    11) OIL, PINE

Available Forms Sources

    A) SOURCES
    1) Pine oil is available from natural sources. In 1958, 161 Sika deer perished on St. James Island in Maryland due to pine oil poisoning resulting from eating the bark of pine trees to avoid starvation.
    2) DERIVATION: Via steam distillation of wood from Pinus palustris and other pine species.
    3) PINE OIL CONSTITUENTS: Contains the monoterpenes alpha-pinene (57%), carene (26%), beta-pinene (8%), and limonene (6%) (Koppel et al, 1981).
    B) USES
    1) Pine oil is a common agent used in many household cleaners and disinfectants. It has also been used as a pure substance for its disinfectant properties.

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Pine oil is available from natural sources, such as the bark of pine trees. It is usually derived from the steam distillation of wood from Pinus palustris and other pine species. Pine oil contains monoterpenes alpha-pinene (57%), carene (26%), beta-pinene (8%), and limonene (6%). Pine oil is a common agent used in many household cleaners and disinfectants. It has also been used as a pure substance for its disinfectant properties.
    B) TOXICOLOGY: Unknown.
    C) EPIDEMIOLOGY: Poisoning by pine oil is relatively uncommon and is usually self-limiting in the vast majority of exposures. However, 3% of exposures that result in large amounts or high concentrations of pine oil can produce serious end-organ toxicity. Death has also been reported.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Mild symptoms such as mucous membrane irritation and gastroenteritis are common in small exposures. Erythema of the oral pharynx, lesions of the lips, and tonsillar pillars have been reported. ODOR: The smell of pine oil on the breath is a key diagnostic clue, even if the substance has been taken rectally. However, the lack of smell does not rule out the diagnosis or the presence of smell does not necessarily rule in the diagnosis.
    2) SEVERE TOXICITY: Large or highly concentrated exposures can cause aspiration pneumonitis, hypotension, bradycardia, respiratory depression, ataxia, headache, delirium, coma, nausea, vomiting (which may be bloody), diarrhea, renal failure, or myoglobinuria following the ingestion of large amounts.
    3) Cases describe hypotension, bradycardia, and respiratory failure. Gastrointestinal symptoms and CNS depression are reported in large overdoses. Moreover, in several of these cases patients developed pneumonitis, and hypoxemia. These patients can develop end organ failure, such as renal failure or respiratory failure.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    0.2.21) CARCINOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with hypoxia and respiratory symptoms.
    C) Monitor serum electrolytes, kidney function and liver enzymes in symptomatic patients.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. Patients with mild to moderate exposure, through dermal, oral, or inhalational exposure, usually require supportive care. Manage mild hypotension with IV fluids.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. Rarely, patients can become severely ill through either inhalational or oral exposure. Aggressive supportive care should be initiated for any patient exhibiting signs of toxicity. Treat severe hypotension with IV 0.9% NaCl at 10 to 20 mL/kg. Add dopamine or norepinephrine if unresponsive to fluids. Inhalational exposures should be watched for signs of pneumonitis, sinusitis, pharyngitis, and tonsillitis. While most exposures were self-limiting, there have been cases of patients requiring intubation from severe hypoxemia. Early intubation may be indicated to prevent aspiration in patients with large volume ingestions and CNS depression.
    C) DECONTAMINATION
    1) PREHOSPITAL: Prehospital gastrointestinal decontamination is generally not recommended because of the potential for CNS depression and subsequent aspiration. DERMAL EXPOSURE: Wash exposed areas with soap and water. EYE EXPOSURE: Irrigate exposed eyes with copious amounts of room temperature normal saline or water.
    2) HOSPITAL: Gastrointestinal decontamination is generally not recommended because of the potential for CNS depression and subsequent aspiration, but could be considered in rare cases (eg, large volume ingestions in which the patient is already intubated). DERMAL EXPOSURE: Wash exposed areas with soap and water. EYE EXPOSURE: Irrigate exposed eyes with copious amounts of room temperature normal saline or water.
    D) AIRWAY MANAGEMENT
    1) Large doses of pine oil have caused coma and respiratory distress in patients. Deaths have been reported in patients who develop significant pulmonary edema or pneumonitis from airway compromise. Moreover, some tests show that pine oil cause ciliary dysfunction, and early intubation might be warranted in patients that might be at risk of aspiration.
    E) ANTIDOTE
    1) None.
    F) ENHANCED ELIMINATION PROCEDURE
    1) Combination hemoperfusion and hemodialysis was begun about 14 hours postingestion in one patient. It is unknown whether this was of any benefit. Although patients who develop renal failure may require dialysis, there is no known role for dialysis to enhance the elimination of pine oil.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Asymptomatic patients can be managed at home. Any patient that intentionally ingested or inhaled a large amount of pine oil should be transferred to an emergency department for evaluation.
    2) OBSERVATION CRITERIA: Patients with confusion, listlessness, somnolence, and lethargy should be observed until their signs and symptoms have resolved. Approximately 95% of patients with these symptoms will have self-limiting courses and will be able to be safely discharged home from the emergency department.
    3) ADMISSION CRITERIA: Patients with end organ injury, such as hypoxia, renal injury, anuria, or persistent CNS depression should be admitted to hospital.
    4) CONSULT CRITERIA: If patients develop respiratory failure, hemodynamic instability, or any other symptoms that require hospitalization with this exposure, consult a toxicologist or regional poison center.
    H) PITFALLS
    1) Common errors for managing these patients include failing to screen electrolytes, failing to look for other exposures, and not identifying other similar presenting medical conditions. The lack of smell does not rule out the diagnosis or the presence of smell does not necessarily rule in the diagnosis.
    I) DIFFERENTIAL DIAGNOSIS
    1) Altered mental status may also produced by a wide range of toxic exposures (eg, alcohols, anticonvulsant, antidepressant, antipsychotic, hallucinogen, sedative-hypnotic, opioid withdrawal) and non-toxicologic causes (eg, CNS or systemic infection, hypercarbia, hypoglycemia, hypoxemia, intracranial bleeding, trauma). Pulmonary findings may be caused by other hydrocarbon aspirations, severe infections, and by cardiogenic and non-cardiogenic pulmonary edema.
    0.4.3) INHALATION EXPOSURE
    A) Inhalational exposures should be watched for signs of pneumonitis, sinusitis, pharyngitis, and tonsillitis. While most exposures were self-limiting, there have been cases of patients requiring intubation from severe hypoxemia. Early intubation may be indicated to prevent aspiration in patients with large volume ingestions and CNS depression.
    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: 14 grams (about 0.5 ounce) of pure pine oil has been fatal in a child, and 8 ounces (about 236 mL) of pine oil cleaner was fatal in an adult.

Clinical Effects

Summary Of Exposure

    A) USES: Pine oil is available from natural sources, such as the bark of pine trees. It is usually derived from the steam distillation of wood from Pinus palustris and other pine species. Pine oil contains monoterpenes alpha-pinene (57%), carene (26%), beta-pinene (8%), and limonene (6%). Pine oil is a common agent used in many household cleaners and disinfectants. It has also been used as a pure substance for its disinfectant properties.
    B) TOXICOLOGY: Unknown.
    C) EPIDEMIOLOGY: Poisoning by pine oil is relatively uncommon and is usually self-limiting in the vast majority of exposures. However, 3% of exposures that result in large amounts or high concentrations of pine oil can produce serious end-organ toxicity. Death has also been reported.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Mild symptoms such as mucous membrane irritation and gastroenteritis are common in small exposures. Erythema of the oral pharynx, lesions of the lips, and tonsillar pillars have been reported. ODOR: The smell of pine oil on the breath is a key diagnostic clue, even if the substance has been taken rectally. However, the lack of smell does not rule out the diagnosis or the presence of smell does not necessarily rule in the diagnosis.
    2) SEVERE TOXICITY: Large or highly concentrated exposures can cause aspiration pneumonitis, hypotension, bradycardia, respiratory depression, ataxia, headache, delirium, coma, nausea, vomiting (which may be bloody), diarrhea, renal failure, or myoglobinuria following the ingestion of large amounts.
    3) Cases describe hypotension, bradycardia, and respiratory failure. Gastrointestinal symptoms and CNS depression are reported in large overdoses. Moreover, in several of these cases patients developed pneumonitis, and hypoxemia. These patients can develop end organ failure, such as renal failure or respiratory failure.

Vital Signs

    3.3.2) RESPIRATIONS
    A) TACHYPNEA may occur (Brook et al, 1989).
    3.3.3) TEMPERATURE
    A) FEVER: Temperatures of 100 to 104 degrees F have occurred (Koppel et al, 1981).

Heent

    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) CILIARY BEAT FREQUENCY (CBF): Exposure to pine oil vapors was found to significantly decrease CBF in vitro at a concentration of 8.3 g/m(3), 9.4 g/m(3), and 10 g/m(3) (p<0.0001) in a dose dependent manner. The authors note that effects may be diminished in vivo where respiratory cells have a protective mucus layer; however disturbed CBF has been associated with rhinosinusitis, bronchitis and otitis media (Riechelmann et al, 1997).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) ERYTHEMA of the oral pharynx, lesions of the lips, and tonsillar pillars has been reported (Hill et al, 1975) Conrad et al, 1986).
    2) CASE SERIES: Oral erythema or pain was described in 7 of 17 adult ingestions of pine oil cleaners (Brook et al, 1989).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) BRADYCARDIA
    1) WITH POISONING/EXPOSURE
    a) Bradycardia may be see with ingestion of large quantities of pine oil.
    b) CASE REPORT: Ingestion of an unknown amount of a 20% pine oil containing product produced bradycardia which resolved within 24 hours (Conrad et al, 1986).
    B) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypotension may be seen with ingestion of large quantities of pine oil (Koppel et al, 1981; Welker & Zaloga, 1999).
    b) CASE REPORT: Hypotension requiring vasopressors occurred in one fatal case (Litovitz et al, 1988).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) RESPIRATORY ARREST
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 3-week-old infant had a cold preparation which contained: levomenthol, terpineol, pumilio pine oil, and pine oil sylvestris incorrectly applied to the nose, and developed symptoms of respiratory difficulty and had a respiratory arrest (Blake, 1993). The infant was intubated for several hours and made a complete recovery.
    B) HYPOVENTILATION
    1) WITH POISONING/EXPOSURE
    a) Respiratory depression and coughing have occurred in humans (Hill et al, 1975; Welker & Zaloga, 1999).
    C) PNEUMONITIS
    1) WITH POISONING/EXPOSURE
    a) Chemical and aspiration pneumonitis have been reported, as has adult respiratory distress syndrome.
    b) CHEMICAL PNEUMONITIS: Signs and symptoms include hyperpnea, noisy respirations, and radiographic abnormalities.
    1) CASE SERIES: These signs occurred in 3 of 5 children with a history of accidental ingestion of pine oil cleaners. Improvement or resolution occurred within 24 hours (Brook et al, 1989).
    2) CASE SERIES: Three comatose adults developed pneumonitis; two developed bacterial superinfection (Brook et al, 1989).
    c) ASPIRATION PNEUMONITIS and ARDS have resulted in death in a few cases (Litovitz et al, 1988; Welker & Zaloga, 1999).
    D) BRONCHOSPASM
    1) WITH POISONING/EXPOSURE
    a) Occupational exposure may result in asthma.
    b) CASE REPORT: Occupational asthma was reported in a 63-year-old exposed to an emulsified oil mist containing pine oil and colophony (a pine tree constituent) (Hendy et al, 1985).
    E) SMELL OF BREATH - FINDING
    1) WITH POISONING/EXPOSURE
    a) A violet-like breath odor was noted in 11 of 78 children who ingested pine oil (Koppel et al, 1981).
    b) The smell of pine oil on the breath is a key diagnostic clue (Welker & Zaloga, 1999), even if the substance has been taken rectally (Tauscher & Polich, 1959).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) PULMONARY EDEMA
    a) Injection in animal studies produced pulmonary edema as a prime toxic effect (Tobin et al, 1976).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) WITH POISONING/EXPOSURE
    a) Listlessness, somnolence, and lethargy may proceed to coma in serious ingestions.
    b) INCIDENCE: 3 of 22 adult patients who ingested pine cleaners developed coma (Brook et al, 1989). Koppel et al (1981) found 4 of 78 patients developed somnolence (Koppel et al, 1981).
    c) TOXIC AMOUNTS: Two patients with coma drank 12 to 28 ounces of products containing 35% to 57% pine oil, which represents 126 to 479 mL pine oil, respectively (Brook et al, 1989).
    d) CASE REPORT: An 88-year-old woman with Alzheimer's disease accidentally ingested 10 ounces of a cleaning solution containing pine oil and isopropyl alcohol (Welker & Zaloga, 1999). CNS and respiratory depression occurred, which temporarily improved with symptomatic care; baseline mental status returned by day 2. The hospital course, however, was complicated by ongoing pulmonary dysfunction, multiorgan failure, and sepsis with death occurring on day 16.
    B) ATAXIA
    1) WITH POISONING/EXPOSURE
    a) Ataxia may occur after ingestion.
    b) INCIDENCE: Ataxia in reported studies is variable. In two studies, Koppel et al (1981) found an incidence of only 3 of 78 (3.8%) in adults, while Brook et al (1989) found 4 of 5 (80%) children to be affected (Koppel et al, 1981; Brook et al, 1989).
    c) TOXIC AMOUNTS: Brooks et al (1989) reported a range from 1 to 3 ounces of cleaners, which contained 30% to 35% pine oil (9 to 31.5 mL of oil, respectively) (Brook et al, 1989).
    C) SYNCOPE
    1) WITH POISONING/EXPOSURE
    a) Syncope has been reported (Gornel & Goldman, 1968).
    D) CENTRAL STIMULANT ADVERSE REACTION
    1) WITH POISONING/EXPOSURE
    a) Transient CNS excitement or delirium may be seen in non-fatal doses (Tobin et al, 1976; Koppel et al, 1981).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Spontaneous vomiting, bloody vomiting, nausea, and cramping have occurred (Gornel & Goldman, 1968).
    b) INCIDENCE (PEDIATRIC): 4 of 5 (80%) (Brook et al, 1989); 12 of 78 (15%) (Koppel et al, 1981).
    c) INCIDENCE (ADULT): 9 of 17 (53%) (Brook et al, 1989); 4 of 6 (67%) (Koppel et al, 1981).
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea has been seen (Koppel et al, 1981).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) Metabolic acidosis may occur in conjunction with renal failure (Litovitz et al, 1988).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Pine oil may be irritating to the skin if left in contact for a prolonged period of time (Lewis, 1996).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS8002-09-3 (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) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ANURIA
    1) WITH POISONING/EXPOSURE
    a) Anuria was seen after pine oil was used as an abortifacient.
    b) CASE REPORT: A woman instilled 3 to 6 ounces of a 70% pine oil solution diluted 2:1 intravaginally as an abortifacient. Anuria developed.
    B) MYOGLOBINURIA
    1) WITH POISONING/EXPOSURE
    a) Myoglobinuria may proceed to renal failure.
    b) CASE REPORT: Eight ounces of pine oil cleaner produced myoglobinuria, then renal failure (Litovitz et al, 1988).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL TUBULAR DISORDER
    a) Mild segmental degeneration of some renal epithelial tubular cells have been seen (Tobin et al, 1976).
    b) CATS: Tubular cell degeneration was seen in one cat poisoning (Rousseaux et al, 1986).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with hypoxia and respiratory symptoms.
    C) Monitor serum electrolytes, kidney function and liver enzymes in symptomatic patients.
    4.1.2) SERUM/BLOOD
    A) TOXICITY
    1) There are no therapeutic or toxic levels established for either pine oil or alpha terpineol. Levels are not clinically useful. Monitor acid-base status and renal function.
    4.1.3) URINE
    A) URINALYSIS
    1) Renal function may need to be monitored for those patients following large acute exposures or chronic use.
    B) OTHER
    1) Myoglobin may be present in severe cases and may precipitate renal failure (Litovitz et al, 1988).

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with hypoxia and respiratory symptoms.
    2) CASE SUMMARY: In 2 fatal cases, chest x-rays were abnormal 1 to 5 hours postingestion (Litovitz et al, 1988).

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 end organ injury, such as hypoxia, renal injury, anuria, or persistent CNS depression should be admitted to hospital.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Asymptomatic patients can be managed at home. Any patient that intentionally ingested or inhaled a large amount of pine oil should be transferred to an emergency department for evaluation.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) If patients develop respiratory failure, hemodynamic instability, or any other symptoms that require hospitalization with this exposure, consult a toxicologist or regional poison center.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with confusion, listlessness, somnolence, and lethargy should be observed until their signs and symptoms have resolved. Approximately 95% of patients with these symptoms will have self-limiting courses and will be able to be safely discharged home from the emergency department.

Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with hypoxia and respiratory symptoms.
    C) Monitor serum electrolytes, kidney function and liver enzymes in symptomatic patients.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ORAL EXPOSURE: Prehospital gastrointestinal decontamination is generally not recommended because of the potential for CNS depression and subsequent aspiration.
    B) DERMAL EXPOSURE: Wash exposed areas with soap and water.
    C) EYE EXPOSURE: Irrigate exposed eyes with copious amounts of room temperature normal saline or water.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Gastrointestinal decontamination is generally not recommended because of the potential for CNS depression and subsequent aspiration, but could be considered in rare cases (eg, large volume ingestions in which the patient is already intubated).
    2) VOMITING/ASPIRATION: Pure pine oil or pine oil cleaners may be aspirated (Litovitz et al, 1988).
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive. Patients with mild to moderate exposure, through dermal, oral, or inhalational exposure, usually require supportive care. Manage mild hypotension with IV fluids.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment is symptomatic and supportive. Rarely, patients can become severely ill through either inhalational or oral exposure. Aggressive supportive care should be initiated for any patient exhibiting signs of toxicity. Treat severe hypotension with IV 0.9% NaCl at 10 to 20 mL/kg. Add dopamine or norepinephrine if unresponsive to fluids. Inhalational exposures should be watched for signs of pneumonitis, sinusitis, pharyngitis, and tonsillitis. While most exposures were self-limiting, there have been cases of patients requiring intubation from severe hypoxemia. Early intubation may be indicated to prevent aspiration in patients with large volume ingestions and CNS depression.
    B) MONITORING OF PATIENT
    1) Monitor vital signs and mental status.
    2) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with hypoxia and respiratory symptoms.
    3) Monitor serum electrolytes, kidney function and liver enzymes in symptomatic patients.
    C) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    D) 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).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) PULMONARY ASPIRATION
    1) If cough persists, consider physician evaluation and chest x-ray. Coughing may be due to aspirated substance.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

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

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).

Enhanced Elimination

    A) SUMMARY
    1) Combination hemoperfusion and hemodialysis was begun about 14 hours postingestion in one patient. It is unknown whether this was of any benefit. Although patients who develop renal failure may require dialysis, there is no known role for dialysis to enhance the elimination of pine oil.
    B) EXCHANGE TRANSFUSION
    1) CASE REPORT: One case of rectally administered pine oil poisoning in a 4-year-old was successfully treated with exchange transfusion. Exchanging the estimated blood volume over a 3 hour and 15 minute period significantly improved CNS and respiratory depression (Tauscher & Polich, 1959).
    C) HEMOPERFUSION
    1) CASE REPORT: Charcoal hemoperfusion, resin hemoperfusion, and hemodialysis were performed in an adult who ingested 400 to 500 milliliters of pine oil. The clearance of alpha-pinene was greater during resin hemoperfusion (133 milliliters/minute) than during charcoal hemoperfusion (46 milliliters/minute).
    a) EFFICACY: Minimal, presumably due to high tissue concentration (Koppel et al, 1981).
    D) HEMOPERFUSION AND HEMODIALYSIS
    1) CASE REPORT: A 49-year-old man ingested 400 to 500 mL. Upon admission one hour postingestion, psychomotor agitation, headache, breath odor, mouth and larynx erythema, facial flushing, ataxia, and hyperventilation were noted. Gastric lavage with mineral oil was performed. At 10 hours postingestion impaired consciousness and hypotension were noted, and vasopressors were given. Combination hemoperfusion and hemodialysis was begun about 14 hours postingestion. On the second day, leukocytosis, slight elevation in LFTs, and decreased pseudocholinesterase were noted. Transient oliguria during the hypotensive episode was the only renal effect. The patient recovered fully (Koppel et al, 1981).

Abstracts

Case Reports

    A) ADULT
    1) A 20-year-old man who ingested 8 ounces of a pine oil cleaner developed respiratory distress, ARDS, and hypotension one hour postingestion. Complications of rhabdomyolysis, renal failure, and metabolic acidosis preceded cardiac arrest; and death occurred 40 hours postingestion (Litovitz et al, 1988).
    2) A 49-year-old male ingested 400 to 500 mL. Upon admission one hour postingestion, psychomotor agitation, headache, breath odor, mouth and larynx erythema, facial flushing, ataxia, and hyperventilation were noted. Gastric lavage with mineral oil was performed. At 10 hours postingestion impaired consciousness and hypotension were noted, and vasopressors were given. Combination hemoperfusion and hemodialysis was begun about 14 hours postingestion. On the second day, leukocytosis, slight elevation in LFTs, and decreased pseudocholinesterase were noted. Transient oliguria during the hypotensive episode was the only renal effect. The patient recovered fully (Koppel et al, 1981).
    3) A 70-year-old man accidentally ingested an unknown amount of pine oil cleaner and developed somnolence, lethargy, and spontaneous vomiting. Gastric lavage and activated charcoal were given. The baseline chest x-ray and blood gases were normal at 2 hours postingestion. At 5 hours postingestion metabolic acidosis and rales were noted. At 18 hours postingestion, a right lung infiltrate and fever indicated aspiration pneumonitis. Death occurred due to cardiopulmonary arrest 20 hours postingestion (Litovitz et al, 1988).

Range Of Toxicity

Summary

    A) TOXICITY: 14 grams (about 0.5 ounce) of pure pine oil has been fatal in a child, and 8 ounces (about 236 mL) of pine oil cleaner was fatal in an adult.

Minimum Lethal Exposure

    A) CASE REPORTS
    1) PEDIATRIC
    a) Fourteen grams (about 0.5 ounce) of pure pine oil was reported fatal in a child (Hill et al, 1975). This is equivalent to 70 mL of a 20% solution.
    2) ADULT
    a) Ingestion of 8 ounces of a pine oil cleaner (concentration of pine oil unknown) resulted in respiratory distress, ARDS, renal failure, metabolic acidosis with death occurring 40 hours post ingestion due to cardiac arrest (Litovitz et al, 1988).

Maximum Tolerated Exposure

    A) CONCENTRATION LEVEL
    1) Toxicity is dependent on concentration and volume of pine oil ingested.
    2) Accidental ingestions of products with concentrations under 20% seldom produced significant symptoms. When concentrations exceeded this, ingestions sometimes produced bradycardia, vomiting, lethargy, coma, pneumonitis, oral erythema, and respiratory distress.
    B) CASE REPORTS
    1) CONCENTRATIONS UNDER 20 PERCENT
    a) One patient who ingested a large amount (15 to 28 ounces of cleaner) of a 5% product, developed only vomiting and lethargy (Brook et al, 1989).
    b) CASE STUDIES: Ingestion of household cleaners containing less than 20% pine oil did not result in signs or symptoms of toxicity in a series of 62 exposures (Conrad et al, 1986).
    2) CONCENTRATIONS OVER 20 PERCENT
    a) CASE STUDIES: Ingestion of products containing greater than 20% pine oil resulted in mild signs of toxicity (ie vomiting, lethargy, asymptomatic bradycardia, mucous membrane erythema) in 7 of 62 cases (Conrad et al, 1986).
    3) PEDIATRIC
    a) Four children who ingested 1 to 3 ounces of 30% to 35% pine oil cleaners developed ataxia (4), lethargy (4), spontaneous vomiting (3), and pneumonitis (3) (Brook et al, 1989).
    4) ADULTS
    a) Six of 8 obtunded adults ingested less than 6 ounces of pine oil cleaner (Brook et al, 1989).
    b) In a series of 16 adult cases of ingestion of pine oil cleaners containing 30% to 57% pine oil, significant manifestations (coma, pneumonitis) were seen in 3 patients who ingested 12 to 28 ounces. In the remaining patients who ingested 1 to 16 ounces, symptoms were minor, including vomiting, lethargy, and oral erythema or pain (Brook et al, 1989).
    5) CONCENTRATIONS UNKNOWN
    a) ADULT
    1) Survival has been reported with ingestions of up to 400 to 500 mL (Koppel et al, 1981).
    2) Mild respiratory distress occurred in an adult following an intentional ingestion of 250 to 500 mL of pine oil (concentration not specified) (Popiel et al, 1989).
    3) Ingestion of 250 to 500 mL in a suicide attempt resulted in mild respiratory distress, but no serious CNS or respiratory problems (Erickson et al, 1990).

Workplace Standards

    A) ACGIH TLV Values for CAS8002-09-3 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS8002-09-3 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS8002-09-3 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS8002-09-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (ORAL)RAT:
    1) 3200 mg/kg (RTECS , 1999)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Pine oil contains various monoterpenes which have spasmolytic, bactericidal, and CNS effects.

Physicochemical

Physical Characteristics

    A) Pine oil is a colorless to pale yellow or amber liquid with a penetrating, piny or turpentine-like odor (Lewis, 1996; CHRIS , 1999).
    B) The major constituent of pine oil is alpha-terpineol (Tobin et al, 1976), but borneol and other terpene ethers are also present.
    C) Pine oil was found to contain the monoterpenes alpha-pinene 57%, carene 26%, beta-pinene 8%, and limonene 6% (Koppel et al, 1981).

Molecular Weight

    A) 154.25 (alpha terpenol primary component) (CHRIS , 1999)

Other

    A) ODOR THRESHOLD
    1) Currently not available (CHRIS , 2002)

Animal Toxicology

Clinical Effects

    11.1.5) EQUINE/HORSE
    A) After injection into animals, the primary site of toxicity was the lungs, and the main cause of death was pulmonary edema (Tobin et al, 1976).
    B) Mild segmental degeneration of renal tubular cells has been noted (Tobin et al, 1976).
    11.1.6) FELINE/CAT
    A) A cat who ingested about 100 mL of Pinesol(R), containing 20% pine oil and 10.9% isopropanol, developed severe depression, ataxia, and unresponsive pupils and died.
    1) Autopsy revealed pulmonary edema, acute centrilobular hepatic necrosis, and total renal cortical necrosis (Rousseaux et al, 1986).
    11.1.13) OTHER
    A) OTHER
    1) Clinical signs may include oral and pharyngeal irritation, vomiting, CNS depression, tachycardia, nephritis, and fever (Coppock et al, 1988).
    2) Ocular exposure results in severe irritation with blephorospasm, lacrimation, conjunctivitis, and photosensitivity (Coppock et al, 1988).

Treatment

    11.2.2) LIFE SUPPORT
    A) GENERAL
    1) MAINTAIN VITAL FUNCTIONS: Secure airway, supply oxygen, and begin supportive fluid therapy if necessary.
    11.2.4) DECONTAMINATION
    A) GASTRIC DECONTAMINATION
    1) GENERAL TREATMENT
    a) Since aspiration pneumonitis may occur, gastric lavage, followed by activated charcoal (2 g/kg) and sorbitol (1 to 2 g/kg) is preferable.
    11.2.5) TREATMENT
    A) GENERAL TREATMENT
    1) Maintain fluid and electrolyte balance. Observe for a minimum of 24 hours. Chest x-rays should be obtained.

Continuing Care

    11.4.2) DECONTAMINATION
    11.4.2.2) GASTRIC DECONTAMINATION
    A) GASTRIC DECONTAMINATION
    1) GENERAL TREATMENT
    a) Since aspiration pneumonitis may occur, gastric lavage, followed by activated charcoal (2 g/kg) and sorbitol (1 to 2 g/kg) is preferable.

Kinetics

    11.5.1) ABSORPTION
    A) LACK OF INFORMATION
    1) There was no specific information on absorption at the time of this review.
    11.5.2) DISTRIBUTION
    A) HORSE
    1) Tobin (1976) found that horses had no alpha terpineol in their plasma within 2 hours, and none in other tissues at 24 hours.

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