Summary Of Exposure |
A) PHARMACOLOGY: The spasmodic activity of lavender oil is due primarily to one of its constituents, linalool. In vitro studies have shown that the mechanism of action was mediated through an intracellular rise in cAMP.
B) TOXICOLOGY: Most essential oils cause mucous membrane irritation. aspiration is a risk from both the essential oil and from hydrocarbons or emulsifiers that are added to many preparations.
C) EPIDEMIOLOGY: Exposures are common but serious toxicity is rare. Most serious effects are related to aspiration.
D) WITH POISONING/EXPOSURE
1) OVERDOSE: MILD TO MODERATE: There is little published information regarding the toxicity of the many essential oils. Expected effects include mucous membrane irritation or numbness, gastrointestinal irritation, dermal irritation, and hypersensitivity. Ocular exposure can cause irritation, considerable erythema, pain, chemical conjunctivitis, and in severe cases corneal scarring.
2) SEVERE: Vertigo, ataxia, drowsiness, seizures, and coma can develop. Aspiration can cause severe pneumonitis. Rare, severe effects include respiratory depression, bradycardia, and hypotension.
3) EUCALYPTOL: Severe metabolic acidosis and multi-organ system failure, including cardiovascular collapse, respiratory failure, and hepatic failure.
4) FENNEL: Nausea, vomiting, seizure activity, pulmonary edema.
5) GERANIUM: Allergic contact chelitis.
6) LAVENDER: CNS depression, ataxia, photosensitizer that promotes hyperpigmentation, contact dermatitis.
7) LEMON MYRTLE: Skin irritation and corrosion.
8) THUJA (essential oil of the wormwood plant of the cedar family): Multiple tonic-clonic seizures.
9) WORMWOOD: Acidosis, acute renal failure, respiratory acidosis, rhabdomyolysis, visual alterations, delirium, restlessness, paranoia, tremor, and seizures.
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Heent |
3.4.3) EYES
A) WITH POISONING/EXPOSURE 1) IRRITATION: These materials are all very irritating to the eye, producing considerable erythema and pain, but seldom any long term damage (Gurr & Scroggie, 1965). 2) MENTHOL: Application to rabbit eyes has produced severe damage. Complete recovery was noted after application of 10 mg of menthol crystals (Grant & Schuman, 1993). 3) OLBAS OIL: Corneal scarring has been reported following intranasal use. a) CASE REPORT: A 4-month-old boy developed chemical conjunctivitis and corneal scarring after intranasal instillation of several drops of Olbas oil (Wyllie & Alexander, 1994). Olbas oil is a mixture of oils of peppermint, clove, eucalyptus, menthol and cajub.
4) OIL OF WORMWOOD: Chronic exposure to wormwood can result in visual alterations (Woolf, 1999). 3.4.5) NOSE
A) WITH POISONING/EXPOSURE 1) CILIARY BEAT FREQUENCY (CBF): Lavender oil and thyme oil were found to increase CBF in vitro at a concentration of 0.2% and to a lesser extent, 2%. Disturbed CBF has been associated with rhinosinusitis, bronchitis and otitis media (Neher et al, 2008).
3.4.6) THROAT
A) WITH POISONING/EXPOSURE 1) MUCOUS MEMBRANE IRRITATION: Essential oils are irritants, and commonly cause a burning sensation in the mouth, chest, and stomach after ingestion (Pilapil, 1989; Barkin et al, 1984).
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Cardiovascular |
3.5.2) CLINICAL EFFECTS
A) BRADYCARDIA 1) WITH POISONING/EXPOSURE a) Bradycardia has been observed in some cases of acute exposure to mentha species (Woolf, 1999).
B) CARDIOVASCULAR FINDING 1) WITH POISONING/EXPOSURE a) CASE REPORT: Cardiovascular and respiratory collapse occurred within 2 days after ingesting approximately 3 Lof a mouthwash containing ethanol 27%, eucalyptol 0.092% (total amount ingested: 2.76 g), menthol 0.042% (total amount ingested: 1.26 g), thymol 0.064% (total amount ingested: 1.92 g), and methyl salicylate 0.060% (total amount ingested: 1.8 g). The patient developed severe metabolic acidosis, disseminated intravascular coagulation, anuria, hepatic failure, and hypoxemia despite aggressive supportive care, and subsequently died 48 hours after hospital admission (approximately 4 days post-ingestion). Although the primary ingredient within the mouthwash is ethanol, the authors believed that the severity and progression of his illness was primarily due to the large ingestion of volatile essential oils present in the mouthwash (total amount of eucalyptol, menthol, and thymol ingested: 5.94 g) (Soo Hoo et al, 2003).
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Respiratory |
3.6.2) CLINICAL EFFECTS
A) PULMONARY ASPIRATION 1) WITH POISONING/EXPOSURE a) CITRONELLA OIL: In a review of 5 cases of citronella oil ingestion, aspiration pneumonitis developed in the only child treated with gastric lavage (uncuffed endotracheal tube in place during lavage) and in 1 of the 2 children in whom vomiting was induced (Temple et al, 1991).
B) PULMONARY EDEMA 1) WITH POISONING/EXPOSURE a) FENNEL OIL: Oral ingestion may produce pulmonary edema (Anon, 1994).
C) DYSPNEA 1) WITH POISONING/EXPOSURE a) OLBAS OIL: A 4-month-old boy developed severe respiratory distress with hypoxia, cyanosis, tachypnea (80 to 90 breaths/minute) wheezing, inspiratory stridor and profuse oral and nasal secretions after intranasal instillation of several drops of Olbas oil (Wyllie & Alexander, 1994). Olbas oil is a mixture of oils of peppermint, clove, eucalyptus, menthol and cajub.
D) RESPIRATORY FAILURE 1) WITH POISONING/EXPOSURE a) CASE REPORT: Cardiovascular and respiratory collapse occurred within 2 days after ingesting approximately 3 L of a mouthwash containing ethanol 27%, eucalyptol 0.092% (total amount ingested: 2.76 g), menthol 0.042% (total amount ingested: 1.26 g), thymol 0.064% (total amount ingested: 1.92 g), and methyl salicylate 0.060% (total amount ingested: 1.8 g). The patient developed severe metabolic acidosis, disseminated intravascular coagulation, anuria, hepatic failure, and hypoxemia despite aggressive supportive care, and subsequently died 48 hours after hospital admission (approximately 4 days postingestion). Although the primary ingredient within the mouthwash was ethanol, the authors believed that the severity and progression of his illness was primarily due to the large ingestion of volatile essential oils present in the mouthwash (total amount of eucalyptol, menthol, and thymol ingested: 5.94 g) (Soo Hoo et al, 2003).
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Neurologic |
3.7.2) CLINICAL EFFECTS
A) CENTRAL NERVOUS SYSTEM DEFICIT 1) WITH POISONING/EXPOSURE a) Effects may be extremely variable depending on the amount, type, and concentration of the essential oil. Vertigo, ataxia, drowsiness, and coma have been noted.
b) ONSET: CNS depression may have a rapid onset and many cases have progressed to coma within 30 minutes, although onset may be delayed for up to 4 hours and depression may persist for up to 3 days. Dizziness, giddiness, and disorientation usually occur in the first 30 minutes as well.
c) LAVENDER OIL: A 19-month-old boy developed ataxia after ingesting an unknown amount of lavender oil (Wilkinson, 1991).
d) LAVANDIN EXTRACT: An 18-month-old boy developed deep drowsiness and CNS depression approximately 3 hours after ingesting a small amount of lavandin extract. Upon presentation to the emergency department, motor responses were inducible only with painful stimulation, and the boy's breath had a distinctive lavender odor. The patient made a full recovery spontaneously in approximately 6 hours (Landelle et al, 2008).
B) SEIZURE 1) WITH POISONING/EXPOSURE a) Between 1976 and 1981, 8 cases of toxicity involving essential oils (sage, hyssop, thuja, and cedar leaves) resulting in seizure activity were reported to the Poison Control Center in Marseille, France. In 7 cases the essential oil was ingested for supposed therapeutic reasons; one case involved occupational exposure through pipetting. Recurrent seizures were observed in most cases. Neurologic investigation ruled out organic causes for the seizures in 6 cases but 2 patients had been on long-term anticonvulsant therapy. The seizure activity resolved spontaneously in 6 cases. In 2 cases, intensive respiratory care and anticonvulsant treatment was required (Millet et al, 1981). b) CEDAR LEAVES OIL 1) A 32-year-old man developed seizures after ingesting 10 mL of cedar leaves oil to improve digestion. No residual complications were reported (Millet et al, 1981).
c) FENNEL OIL 1) FENNEL OIL: Oral exposure may produce seizures (Anon, 1994).
d) HYSSOP OIL 1) CASE REPORT: PEDIATRIC: A 6-year-old girl was medicated with hyssop oil, 2 to 3 drops/day by mouth to treat asthma. In addition, she was administered a single, 1/2 teaspoon dose infused in thyme for respiratory distress. The girl developed multiple seizures, metabolic acidosis, and required respiratory intensive care. She recovered after treatment (Millet et al, 1981).
2) CASE REPORT: An 18-year-old woman developed seizures after ingesting 30 drops of hyssop oil to treat a cold. No residual complications were reported (Millet et al, 1981).
3) CASE REPORT: A 26-year-old woman developed a tonic seizure on day 2 after ingesting hyssop oil 10 mL/day for 2 days to treat the flu. No residual complications were reported (Millet et al, 1981).
e) OIL OF WORMWOOD 1) Acute toxicity of wormwood poisoning includes seizures (Woolf, 1999).
2) CASE REPORT: PEDIATRIC: A 7-month-old infant experienced a total of 8 tonic-clonic seizures in a 3-week period. The infant had been receiving thuja for 4 weeks as a calming agent around immunization times. All seizure activity ceased after stopping the thuja (derived from the WORMWOOD plant), and the child had no permanent neurologic or developmental complications (Stafstrom, 2007).
3) CASE REPORT: A 31-year-old man ingested approximately 10 mL of essential oil of wormwood used in aromatherapy. Paramedics reported tonic-clonic seizures with decorticate posturing. There was no further seizure activity, and no focal neurologic abnormalities were reported (Weisbord et al, 1997).
4) CASE REPORT: A 40-year-old woman developed seizure activity after ingesting 10 mL of thuja essential oil to enhance fitness. No residual complications were reported (Millet et al, 1981).
5) CASE REPORT: A 50-year-old woman developed seizures 10 days after ingesting 25 drops/day of undiluted thuja oil, which was intended for dilution. During the seizure she sustained an occipito-parietal fracture. She recovered after treatment (Millet et al, 1981).
f) SAGE OIL 1) CASE REPORT: PEDIATRIC: A 33-day-old infant without risk for or history of seizure developed generalized tonic-clonic seizures 20 minutes after he was inadvertently exposed to an unreported amount of oral sage oil (Salvia officinalis). The seizure duration was 20 minutes. He presented to the emergency department after the seizure. Upon examination his heart rate was 120 beats/minute, rectal temperature 37.3 C, and respiratory rate 44 breaths/minute. Vertical nystagmus, irritability, and hyperreflexia were observed. He responded to treatment with rectal diazepam and was admitted for observation. He experienced a recurrent tonic-clonic seizure lasting about 1 minute 3 hours after admission and was treated with one dose of IV midazolam. He was discharged 3 days after admission and 1 year later remained seizure free (Halicioglu et al, 2011).
2) CASE REPORT: PEDIATRIC: A 5-year-old girl without history of epilepsy developed a generalized tonic-clonic seizure lasting 10 minutes shortly after an inadvertent exposure to oral sage oil (amount undetermined). Upon presentation to the emergency department, she was treated with gastric lavage and active charcoal and then admitted to the pediatric intensive care unit. She did not develop recurrent seizures and was discharged in good health 48 hours after admission. One year later she remained seizure free (Halicioglu et al, 2011).
C) CENTRAL NERVOUS SYSTEM FINDING 1) WITH POISONING/EXPOSURE a) OIL OF WORMWOOD: Acute effects of wormwood poisoning may include symptoms of restlessness, delirium and paranoia (Woolf, 1999).
b) CASE REPORT: A 31-year-old man accidentally ingested approximately 10 mL of oil of wormwood believing it was absinthe liqueur and several hours later was found in an agitated state, incoherent, and disoriented. Mental status improved with haloperidol. Lumbar puncture and head CT were within normal limits (Weisbord et al, 1997).
D) CHRONIC POISONING 1) WITH POISONING/EXPOSURE a) OIL OF WORMWOOD: Chronic exposure can lead to deteriorating mental status, seizures, tremors and coma (Woolf, 1999).
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Gastrointestinal |
3.8.2) CLINICAL EFFECTS
A) NAUSEA AND VOMITING 1) WITH POISONING/EXPOSURE a) Heartburn, epigastric and oral pain, reflux, nausea, vomiting, and abdominal pain may occur shortly after ingestion (Antman et al, 1978; Craig, 1953; Pilapil, 1989; Perry et al, 1990; Grande & Dannewitz, 1987).
b) EUCALYPTOL: CASE REPORT: Nausea, vomiting, and epigastric pain occurred in a 45-year-old man following ingestion of approximately 3 L of a mouthwash containing volatile essential oils, including eucalyptol (total amount ingested: 2.76 g), menthol (total amount ingested: 1.26 g), and thymol (total amount ingested: 1.92 g) (Soo Hoo et al, 2003).
c) FENNEL OIL: Ingestion of the volatile oil can produce nausea and vomiting (Anon, 1994).
d) OIL OF WORMWOOD: Vomiting is likely to occur following acute toxicity (Woolf, 1999).
B) DIARRHEA 1) WITH POISONING/EXPOSURE a) Diarrhea may occur. The fats, waxes, and oil could contribute to the diarrhea.
C) CHRONIC POISONING 1) WITH POISONING/EXPOSURE a) OIL OF WORMWOOD: Chronic exposure to the oil can result in gastritis and pica (Woolf, 1999).
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Hepatic |
3.9.2) CLINICAL EFFECTS
A) TOXIC LIVER DISEASE 1) WITH POISONING/EXPOSURE a) COPAIBA: CASE REPORT: A 79-year-old woman who was taking Hypericum perforatum, copaiba, levothyroxine, omega 3, glucosamine and chondroitin, presented with a 1-month history of jaundice. On presentation, she was also tachycardic (100 beats/min) and laboratory results revealed elevated liver enzymes and hyperbilirubinemia. Following the discontinuation of all medications, except for levothyroxine, her laboratory results normalized (Agollo et al, 2014).
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Genitourinary |
3.10.2) CLINICAL EFFECTS
A) ACUTE RENAL FAILURE SYNDROME 1) WITH POISONING/EXPOSURE a) OIL OF WORMWOOD: A 31-year-old man developed acute renal failure following an accidental ingestion of 10 mL of oil of wormwood. On day 3, the patient's serum creatinine peaked at 4.4 mg/dL. The patient was hydrated and given sodium bicarbonate; oliguria, hypocalcemia, or hypophosphatemia did not develop. By day 17, serum creatinine and electrolytes were within normal limits (Weisbord et al, 1997).
B) NEPHRITIS 1) WITH POISONING/EXPOSURE a) The essential oils are excreted in the urine. Irritation may rarely cause nephritis (Heng, 1987).
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Acid-Base |
3.11.2) CLINICAL EFFECTS
A) ACIDOSIS 1) WITH POISONING/EXPOSURE a) OIL OF WORMWOOD: A 31-year-old man initially developed an anion gap metabolic and respiratory acidosis following a 10 mL ingestion of oil of wormwood. ABGs while receiving oxygen were: pH 7.27; PCO2, 43 mm Hg; and PO2 133 mm Hg, serum bicarbonate 7.7 mmol/L (Weisbord et al, 1997).
b) CASE REPORT: A 45-year-old man presented to the ED with nausea, vomiting, lethargy, and hyperventilation 2 days after ingesting approximately 3 L of a mouthwash containing ethanol 27%, eucalyptol 0.092% (total amount ingested: 2.76 g), menthol 0.042% (total amount ingested: 1.26 g), thymol 0.064% (total amount ingested: 1.92 g), and methyl salicylate 0.060% (total amount ingested: 1.8 g). Arterial blood gases showed severe metabolic acidosis (pH 6.95, PaCO2 12 mmHg, PaO2 97 mmHg) with a calculated anion gap of 38 mmol/L. Hemodialysis resulted in initial correction of the patient's metabolic acidosis; however, he continued to deteriorate leading to respiratory and cardiovascular collapse and necessitating mechanical ventilation and vasopressor support. Progressive acidosis, hepatic failure, and hypoxemia ensued, despite aggressive supportive care, and the patient subsequently died 48 hours after hospital admission (approximately 4 days postingestion). Although ethanol is the primary ingredient in the mouthwash, the authors believed that the severity and progression of his illness was primarily due to the large ingestion of volatile essential oils present in the mouthwash (total amount of eucalyptol, menthol, and thymol ingested: 5.9 g) (Soo Hoo et al, 2003).
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Dermatologic |
3.14.2) CLINICAL EFFECTS
A) CONTACT URTICARIA 1) WITH THERAPEUTIC USE a) SPEARMINT OIL (R-CARVONE): An adult reported a 6-month history of swelling of the lips a few minutes after contact with toothpaste, followed by gingival swelling and shortness of breath a short time later. He switched toothpaste brands several times with similar symptoms; an absence of symptoms was only observed with children's fruit-flavored toothpaste. Skin testing was strongly reactive with a wheal after 2 minutes with R-carvone (the main ingredient in spearmint oil) and S-carvone. No further symptoms were reported after the avoidance of spearmint gum or toothpaste. Cheilitis has been well documented with toothpaste containing carvone (Hansson et al, 2011)
2) WITH POISONING/EXPOSURE a) These substances cause a redness and burning sensation of the skin (Spoerke et al, 1989). Although no actual burns usually result, skin irritation and urticaria have been noted with menthol-containing products (Parys, 1983). b) ANISE OIL: A 2% solution in a petrolatum base did not produce dermal reactions on human skin (Anon, 1994). 1) Anethole (primary component of the oil) has caused sensitization which resulted in irritation, erythema, scaling, and vesication (Anon, 1973).
2) When used in dental products, contact sensitivity has produced stomatitis and cheilitis (Duke, 1985).
B) PHOTOSENSITIVITY 1) WITH POISONING/EXPOSURE a) OIL OF LAVENDER: Lavender oil is a photosensitizer and may produce hyperpigmentation (Fisher, 1986).
C) CONTACT DERMATITIS 1) WITH THERAPEUTIC USE a) Contact dermatitis has been reported after chronic exposure to a number of essential oils including: lavender oil, sandalwood, lemon oil, eugenol, tea tree oil, chamomile oil, myrrh, frankincense, rosewood, geranium, vetiver, basil, marjoram, peppermint, sage, bergamot, orange, benzoin, ylang-ylang, laurel oil, pomerance flower oil, jasmine oil (Schaller & Korting, 1995; Selvaag et al, 1994; Selvaag et al, 1995; McGeorge & Steele, 1991; Sharma et al, 1987; Brandao, 1986).
b) OIL OF LAVENDER: A 9 year study in Japan reported that 13.9% of exposures to lavender oil resulted in contact dermatitis (Cavanagh & Wilkinson, 2002).
D) SKIN IRRITATION 1) WITH POISONING/EXPOSURE a) LEMON MYRTLE OIL: Dermal exposure to neat lemon myrtle oil in vitro and subsequent absorption caused cellular necrosis (15%), vacuolation (25%) and loss of skin integrity. Similar effects, although to a lesser severity, were seen with a 1% lemon myrtle solution in vitro. The patho-histological skin alterations reported are indicative of skin irritation and corrosion (Hayes & Markovic, 2003).
E) CHEILITIS 1) WITH THERAPEUTIC USE a) GERANIUM OIL: Allergic contact cheilitis developed in an adult female following use of a lip balm product that contained geranium oil. Patch testing was positive, and gradual healing occurred after the product was stopped (Chang & Maibach, 1997).
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Musculoskeletal |
3.15.2) CLINICAL EFFECTS
A) RHABDOMYOLYSIS 1) WITH POISONING/EXPOSURE a) OIL OF WORMWOOD: A 31-year-old man developed leg muscle soreness and a markedly elevated creatine kinase (serum CK greater than 80,000 Units/L) which peaked on day 3 of his hospital admission after oil of wormwood poisoning. Treatment consisted of sodium bicarbonate and saline. Further urine studies indicated a positive tetramethylbenzidine reaction suggestive of myoglobinuria; however, ammonium sulfate precipitation test was negative. By day 17, serum creatine kinase and other laboratory values were within normal limits (Weisbord et al, 1997).
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Reproductive |
3.20.1) SUMMARY
A) Oil from Juniperus sabina when injected subcutaneously in pregnant mice induces resorptions. This oil is a well known abortifacient. Oil from Plectrantus fruticosus when given orally to pregnant rats induced resorptions and ocular malformations.
3.20.2) TERATOGENICITY
A) ABORTION 1) MICE - Oil from Juniperus sabina: when injected subcutaneously in pregnant mice, at doses of 15, 45 or 135 mg/kg it induces resorptions (Pages et al, 1989). This oil is a well known abortifacient (Banthrope et al, 1975; (Koedam & Looman, 1980; Schilcher, 1985). This oil is approximately 50% sabinyl acetate (Fournier et al, 1988).
2) RATS - Oil from Plectrantus fruticosus: contains approximately 50% sabinyl acetate (Fournier et al, 1986a). When given orally to pregnant rats at doses of 5 or 20 mg/kg, it induced resorptions and ocular malformations (Pages et al, 1988; Fournier et al, 1986b; Pages et al, 1991; Dumitresco & Boudene, 1988).
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