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PLANTS-TULIPA

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) The genus Tulipa has more than 100 species and many more cultivars. They are common garden flowers throughout the world.

Specific Substances

    A) Tulipalin A
    1) Alpha-methylene-gamma-butyrolactone
    Tulipalin B
    1) Beta hydroxy-alphamethylene-gamma butyrolactone

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Toxicity from tulips takes 2 forms. The first is an allergic reaction most often called "tulip fingers" and the second is an acute ingestion of the bulb or other flower parts. The allergic reaction may produce a rash that may involve the fingers, eyelids, and nail beds.
    1) Nail brittleness, redness and swelling of the eyelids, nose, and face, and asthma-like symptoms may also occur. There is considerable variation in the allergic reaction based on cultivar of tulip.
    2) Allergenicity varies considerably from species to species and cultivar to cultivar.
    B) Ingestion may cause nausea, vomiting, dyspnea, palpitations, sweating, and salivation.
    C) Hoarseness, discomfort in the throat, and respiratory difficulties may be seen after exposure to the dust.
    0.2.4) HEENT
    A) Allergic conjunctivitis may be caused by the dust.
    0.2.5) CARDIOVASCULAR
    A) Palpitation may be caused by ingestion.
    0.2.6) RESPIRATORY
    A) Dyspnea and asthma-like symptoms may be seen after ingestion or exposure to dust.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting, and salivation may be seen after ingestion of bulbs.
    0.2.12) FLUID-ELECTROLYTE
    A) If vomiting is extensive, fluid, and electrolyte replacement may be required.
    0.2.13) HEMATOLOGIC
    A) Some lectins in tulips are known to agglutinate red blood cells in vitro.
    0.2.14) DERMATOLOGIC
    A) Various allergic rashes involving the fingers and fingernails have been reported. Nails may become brittle and split, fingers eczematous, blistered, fissured, and then crusted. Symptoms are generally related to handling the bulbs. This is a common occupational illness of gardeners and bulb handlers.
    0.2.19) IMMUNOLOGIC
    A) The dermatitis is allergic in nature. Patchtest with pure allergen down to 1:600 gave positive reactions in control patients, but in those individuals suffering from tulip dermatitis, positive reactions were seen down to 1:20,000.
    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.

Laboratory Monitoring

    A) No specific laboratory measures are indicated for ingestions.
    B) Patch or scratch testing is commonly done to test for allergenicity (Santucci et al, 1985; Hausen, 1982).

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) There is no specific antidote for these compounds. Cases of ingestion reported in the literature describe only mild to moderate symptoms requiring only supportive and symptomatic care.
    B) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    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 irrigate exposed areas with copious amounts of water. A physician may need to examine the area if irritation or pain persists.

Range Of Toxicity

    A) The minimum lethal human dose to this agent has not been delineated.
    B) No specific data is available. The dermal and eye irritant effects are allergic in nature and will depend on individual sensitivity. Moderate symptoms were seen in a family that ate a goulash made of 5 tulip bulbs.

Clinical Effects

Summary Of Exposure

    A) Toxicity from tulips takes 2 forms. The first is an allergic reaction most often called "tulip fingers" and the second is an acute ingestion of the bulb or other flower parts. The allergic reaction may produce a rash that may involve the fingers, eyelids, and nail beds.
    1) Nail brittleness, redness and swelling of the eyelids, nose, and face, and asthma-like symptoms may also occur. There is considerable variation in the allergic reaction based on cultivar of tulip.
    2) Allergenicity varies considerably from species to species and cultivar to cultivar.
    B) Ingestion may cause nausea, vomiting, dyspnea, palpitations, sweating, and salivation.
    C) Hoarseness, discomfort in the throat, and respiratory difficulties may be seen after exposure to the dust.

Vital Signs

    3.3.3) TEMPERATURE
    A) SWEATING INCREASED
    1) Sweating was seen within 10 minutes of eating a meal prepared with 5 tulip bulbs (Maretic et al, 1978).

Heent

    3.4.1) SUMMARY
    A) Allergic conjunctivitis may be caused by the dust.
    3.4.3) EYES
    A) The dust in tulip sheds may cause conjunctivitis (Van der Werff, 1959; (Hausen, 1982) and swelling of the eyelids.
    3.4.5) NOSE
    A) The dust in tulip sheds may cause an eosinophilic rhinitis (Van der Werff, 1959).

Cardiovascular

    3.5.1) SUMMARY
    A) Palpitation may be caused by ingestion.
    3.5.2) CLINICAL EFFECTS
    A) PALPITATIONS
    1) Palpitations were seen in a family who ingested a meal containing 5 tulip bulbs (Maretic et al, 1978).

Respiratory

    3.6.1) SUMMARY
    A) Dyspnea and asthma-like symptoms may be seen after ingestion or exposure to dust.
    3.6.2) CLINICAL EFFECTS
    A) DISORDER OF RESPIRATORY SYSTEM
    1) Difficulty in breathing was seen in individuals within 10 minutes of ingesting a goulash containing 5 tulip bulbs (Maretic et al, 1978).
    2) Hoarseness, discomfort in the throat, and respiratory difficulties may be seen after exposure to the dust (Lahti, 1986).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting, and salivation may be seen after ingestion of bulbs.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) A goulash meal made with 5 bulbs produced, within 10 minutes, nausea and vomiting in humans and a dog that ate the goulash (Maretic et al, 1978).
    B) EXCESSIVE SALIVATION
    1) Increased salivation was seen in the cases above after ingestion of the goulash containing tulip bulbs (Maretic et al, 1978).

Hematologic

    3.13.1) SUMMARY
    A) Some lectins in tulips are known to agglutinate red blood cells in vitro.
    3.13.2) CLINICAL EFFECTS
    A) ERYTHROCYTE AGGLUTINATION
    1) Tulip bulbs contain a lectin that can agglutinate human red blood cells at concentrations of 40 to 80 mcg/mL (Cammue & Peumans, 1985). There are also other lectins that agglutinate yeasts (Oda & Minami, 1986) and mouse and rat red blood cells, but not human blood cells (Oda et al, 1987).

Dermatologic

    3.14.1) SUMMARY
    A) Various allergic rashes involving the fingers and fingernails have been reported. Nails may become brittle and split, fingers eczematous, blistered, fissured, and then crusted. Symptoms are generally related to handling the bulbs. This is a common occupational illness of gardeners and bulb handlers.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Reaction to the tulipalin A in tulip may cause various erythematous hyperkeratotic rashes which may fissure, crust, and blister. Symptoms may be delayed for 12 hours (Illuminati et al, 1988; Gore, 1961) Caufield, 1936; (Rappaport & Welker, 1936).
    a) This dermatitis may spread beyond the hands to forearm and genital areas as well as the face, legs, lips, body trunk, and even affects speech (Hausen, 1982; Hjorth & Wilkinson, 1968).
    2) Up to 85% of the bulb handlers in Holland developed dermatitis in a 1935 report (Bertwistle, 1935). Occupational dermatitis due to Alstroemeria (tuliposide A) is becoming more common as the plant is more commonly available in the United States and Europe (Thiboutot et al, 1990).
    a) A 37-year-old woman developed erythema, edema and itching of the fingers, dorsa of hands and face, 20 minutes after cutting tulips (Lahti, 1986).
    3) Although there are several wild species of tulips, only the garden tulip is known to cause dermatitis in humans (Bruneton, 1999). The allergic contact dermatitis to (+) tulipalin B was shown to be enantiospecific. Sensitized animals did not react to (-) tulipalin B (Papageorgiou et al, 1988). Both the bulbs and the flowers may cause dermatitis (Slob & Varekamp, 1977).
    B) NAIL FINDING
    1) Nail brittleness may be seen in cases of tulip dermatitis (Fisher, 1986). Granulation tissue forms beneath the nail plate and is followed by onycholysis, transverse splitting of the nail and in serious cases, subungual abscesses (Mitchell & Rook, 1979; Overton, 1926; Bertwistle, 1935).
    C) PARESTHESIA
    1) Tingling of the fingertips is often an early symptom seen in tulip dermatitis (Bertwistle, 1935).

Immunologic

    3.19.1) SUMMARY
    A) The dermatitis is allergic in nature. Patchtest with pure allergen down to 1:600 gave positive reactions in control patients, but in those individuals suffering from tulip dermatitis, positive reactions were seen down to 1:20,000.
    3.19.2) CLINICAL EFFECTS
    A) ACUTE ALLERGIC REACTION
    1) The dermatitis is allergic in nature. Patchtest with pure allergen down to 1:600 gave positive reactions in control patients, but in those individuals suffering from tulip dermatitis, positive reactions were seen down to 1:20,000 (Hjorth & Wilkinson, 1968).

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

    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic or mutagenic potential of this agent.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No specific laboratory measures are indicated for ingestions.
    B) Patch or scratch testing is commonly done to test for allergenicity (Santucci et al, 1985; Hausen, 1982).
    4.1.2) SERUM/BLOOD
    A) OTHER
    1) No specific laboratory measures are indicated for ingestions.
    4.1.4) OTHER
    A) OTHER
    1) DERMAL
    a) Patch or scratch testing is commonly done to test for allergenicity (Santucci et al, 1985; Hausen, 1982).

Methods

    A) CHROMATOGRAPHY
    1) Tuliposides can be identified by paper and gas chromatography, but this is generally not done in clinical practice (Slob, 1973).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) No specific laboratory measures are indicated for ingestions.
    B) Patch or scratch testing is commonly done to test for allergenicity (Santucci et al, 1985; Hausen, 1982).

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) 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) There is no specific treatment. Cases have been treated with symptomatic and supportive care.
    B) FLUID/ELECTROLYTE BALANCE REGULATION
    1) If vomiting is extensive, fluid, and electrolyte replacement may be required.

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).
    6.9.2) TREATMENT
    A) DERMATITIS
    1) Several authors have mentioned the use of topical steroids to help reduce the rashes caused by this family. A dermatologist should be consulted before long-term topical steroids are recommended.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) SUMMARY
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent.

Abstracts

Case Reports

    A) CHRONIC EFFECTS
    1) A 40-year-old man developed skin lesions that became worse when he handled tulip bulbs. Two years after his first outbreak, the eczematous lesions spread to axillae, lips, the area around the waist, behind the knees, legs, and the fingertips became furrowed with rhagades.
    2) Each year the symptoms became worse, finally affecting the entire integument with facial and eyelid swelling, and impediment of speech. After 4 years the lesions were chronic with little or no improvement during times the bulbs were not handled.
    3) Topical steroids had little effect after an initial improvement. The only relief was obtained by totally removing himself from all exposure to tulips, including tulip dust (Hausen, 1982).
    B) ACUTE EFFECTS
    1) A 54-year-old woman had worked as a gardener for 18 years, working primarily with tulips, narcissus, and chrysanthemums. She started working with Alstroemeria and was exposed to the sap of cut stem through a hole in a rubber glove.
    2) Two days later she developed itching and urticaria-like lesions on her right thumb, index finger, and forearm. A few days later the lesions had become eczematous with scaling and vesicles. She was treated with a week of topical steroids and healed completely.
    3) Two months later she noted spotty depigmentation of sites on her hand and arm where she had had the dermatitis (Bjorkner, 1982).
    C) ADULT
    1) DERMATITIS - A 35-year-old male who handled tulip bulbs developed itching and swelling which started at the fingertips and moved down the fingers. Edema and pruritus became more intense each day.
    2) Within a few days the fingers were raw, swollen, and most of the fingertips were almost black. The superficial skin on the fingers was exfoliated in irregular patches producing areas of superficial ulceration. It took a week for the lesions to subside.
    3) Treatment was to wear gloves while handling the bulbs (Rappaport & Welker, 1936).

Range Of Toxicity

Summary

    A) The minimum lethal human dose to this agent has not been delineated.
    B) No specific data is available. The dermal and eye irritant effects are allergic in nature and will depend on individual sensitivity. Moderate symptoms were seen in a family that ate a goulash made of 5 tulip bulbs.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) No specific data are available. The dermal and eye irritant effects are allergic in nature and will depend on individual sensitivity. Moderate symptoms were seen in a family that ate a goulash made of 5 tulip bulbs (Maretic et al, 1978)

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (INTRAPERITONEAL)MOUSE:
    1) 6.1 mg/kg -- the glycoprotein, not the glycoside or lactone (Gasperi-Campani, 1987)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Tuliposides A and B have little antibiotic action, but on invasion by a fungus they are converted to the lactones tulipalin A and B which are fungitoxic. These compounds complex with SH groups and inhibit enzymatic activities in the invading fungus (Bruneton, 1999; Keeler & Tu, 1983; Beijersbergen & Lemmer, 1972; Hutchinson, 1974).

Toxicologic Mechanism

    A) Tulip bulbs contain a lectin that agglutinates human red blood cells at concentrations of 40 to 80 mcg/mL. It shows pronounced specificity for type O red cells (Cammue & Peumans, 1985).
    B) A glycoprotein (proposed name tulipin, but not related to the above mentioned glycosides or lactones) has been isolated from tulip bulbs. It is a DNA synthesis-inhibiting protein which does not inhibit RNA or protein synthesis(Bruneton, 1999) Gasper-Campani et al, 1987).
    1) It is found in tulips as 3.4% to 4.1% of the total protein content and inhibits DNA synthesis in cells up to an ID50 (concentration that would inhibit 50% of synthesis) of 400 ng/mL. The ID varied in intact cells according to cell type (Gasper-Campani et al, 1987).
    C) Tulipalin A (not B) is allergenic and produces the various forms of dermatitis (Bruneton, 1999; Santucci et al, 1985). Studies indicate that the presence of a methylene group in the alpha position of the tulipalin is important for allergenic activity (Santucci et al, 1985).

References

General Bibliography

    1) Alaspaa AO, Kuisma MJ, Hoppu K, et al: Out-of-hospital administration of activated charcoal by emergency medical services. Ann Emerg Med 2005; 45:207-12.
    2) Beijersbergen JCM & Lemmer CBG: Enzymic and non-enzymic liberation of tulipalin A in extracts of tulip. Physiol Plant Pathol 1972; 2:265-270.
    3) Bertwistle AP: Tulip fingers. Br Med J 1935; 2:255.
    4) Bjorkner BE: Contact allergy and depigmentation from Alstroemeria. Contact Dermatitis 1982; 8:178-184.
    5) Bruneton J: Toxic plants. Dangerous to humans and animals, Lavoisier publishing, Paris, France, 1999, pp 363-365.
    6) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    7) Cavallito CJ & Haskell TH: Alpha methylene butyrolactone from Erythronium americanum. J Am Chem Soc 1946; 68:23-32.
    8) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    9) Dagnone D, Matsui D, & Rieder MJ: Assessment of the palatability of vehicles for activated charcoal in pediatric volunteers. Pediatr Emerg Care 2002; 18:19-21.
    10) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    11) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    12) Fisher AA: Contact Dermatitis, 3rd ed, Lea & Febiger, Philadelphia, PA, 1986.
    13) Frohne P & Pfander HJ: A Colour Atlas of Poisonous Plants, Wolfe Publishing Ltd, London, England, 1983.
    14) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    15) Gore HC Jr: "Tulip fingers" (Dermatitis venenata due to constituent in tulip bulb). NY Acad Med (Derm & Syphil) 1961; 798.
    16) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    17) Guenther Skokan E, Junkins EP, & Corneli HM: Taste test: children rate flavoring agents used with activated charcoal. Arch Pediatr Adolesc Med 2001; 155:683-686.
    18) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    19) Hausen BM, Pratter E, & Schubert H: The sensitizing capacity of Alstroemeria cultivars in man and guinea pig. Contact Dermatitis 1983; 9:46-54.
    20) Hausen BM: Airborne contact dermatitis caused by tulip bulbs. J Am Acad Dermatol 1982; 7:500-503.
    21) Hjorth N & Wilkinson DS: Contact dermatitis IV. Tulip fingers, hyacinth itch, lily rash. Br J Dermatol 1968; 80:696-698.
    22) Hutchinson CR: A synthesis of tulipalin A and B and the acylglucoside tuliposide A, fungitoxic agents from Tulipa gesneriana. Carbon-13 nuclear magnetic resonance analysis of anomeric configuration in acylglucosides. J Org Chem 1974; 39:1854-1858.
    23) Illuminati R, Russo R, & Guerra L: Occupational airborne contact dermatitis in a florist. Contact Dermatitis 1988; 19:246.
    24) Keeler RF & Tu A: Handbook of Natural Toxins, vol 1: Plant and Fungal Toxins, Marcel Dekker Inc, New York, NY, 1983.
    25) Lahti A: Contact urticaria and respiratory symptoms from tulips and lilies. Contact Dermetitis 1986; 14:317-318.
    26) Maretic Z, Russel FE, & Ladavac J: Tulip bulb poisoning. Peroid Biol 1978; 80:141-143.
    27) Marks JG Jr: Allergic contact dermatitis to Alstroemeria. Arch Dermatol 1988; 124:914-916.
    28) Mitchell J & Rook A: Botanical Dermatology, Greengrass, Vancouver, BC, 1979.
    29) Naradzay J & Barish RA: Approach to ophthalmologic emergencies. Med Clin North Am 2006; 90(2):305-328.
    30) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    31) Oda Y & Minami K: Isolation and characterization of a lectin from tulip bulbs, Tulipa gesneriana. Eur J Biochem 1986; 159:239-245.
    32) Oda Y, Minami K, & Ichida S: A new agglutinin from the Tulipa gesneriana bulbs. Eur J Biochem 1987; 165:297-302.
    33) Overton SG: Dermatitis from handling flower bulbs. Lancet 1926; 2:1003.
    34) Papageorgiou C, Stampf JL, & Benezra C: Allergic contact dermatitis to tulips: an example of enantio-specificity. Arch Dermatol Res 1988; 280:5-7.
    35) Peate WF: Work-related eye injuries and illnesses. Am Fam Physician 2007; 75(7):1017-1022.
    36) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    37) Rappaport BZ & Welker WH: Tulip bulb dermatitis. J Allergy 1936; 8:379-380.
    38) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    39) Santucci B, Picardo M, & Iavarone C: Contact dermatitis to Alstroemeria. Contact Dermatitis 1985; 12:215-219.
    40) Slob A & Varekamp HQ: Tuliposide contents of tulip (Tulipa) species and cultivars during the flowering stage. Proc K Med Akad Wetensch 1977; C80:201-211.
    41) Slob A, Jekel B, & de Jong B: On the occurrence of tuliposides in the liliflorae. Phytochem 1975; 14:1997-2005.
    42) Slob A: Tulip allergens in Alstroemeria and some other Liliflorae. Phytochem 1973; 12:811-815.
    43) Spiller HA & Rogers GC: Evaluation of administration of activated charcoal in the home. Pediatrics 2002; 108:E100.
    44) Thakore S & Murphy N: The potential role of prehospital administration of activated charcoal. Emerg Med J 2002; 19:63-65.
    45) Thiboutot DM, Hamory BH, & Marks JG Jr: Dermatoses amoung floral shop workers. J Am Acad Dermatol 1990; 22:54-58.
    46) Tschesche R, Kammerer FJ, & Wulff G: Uber die Struker der antibiotisch aktinen substanzen der Tulpe. Chem Ber 1969; 102:2057-2071.