Conium maculatum 18.May.2012-Expires: 7 days - Do not archive IDENTIFICATION The correct identification of this plant is imperative. If the identity is uncertain, seek clarification from a reliable source such as a garden center or botanist.   Different Conium species cause different toxic effects. Generalizations should never be made as to symptoms expected. “Hemlock” may refer to Conium maculatum or Cicuta spp.. Both are highly toxic but have very different effects.[1][2]   FAMILY NAME Umbelliferae SPECIES NAME Conium maculatum   COMMON NAME(S) California fern Carrot fern Deadly hemlock Giftkjets Hemlock Nebraska fern Poison hemlock Poison parsley Skarntyde Spotted hemlock Winter fern     NB: The common names of Conium maculatum are also used to refer to other genera in the Umbelliferae family. Botanic identification is crucial.   “Hemlock” most commonly refers to Conium maculatum (poison hemlock) but can refer to Cicuta spp. (water hemlock), which are related and significantly toxic, but contain different toxic components. Although many symptoms overlap, differentiation is important; in severe poisoning Conium maculatum causes respiratory paralysis, whereas Cicuta spp. plants result in profound seizures and potentially status epilepticus.[1][2]   IMAGE Click here for full-size image   Click here for full-size image   Click here for full-size image   HABITAT Grows in damp, cooler places and open woods. Weed of roadsides, ditches, edges of cultivated fields, and waste areas.[3][4][5]   Conium maculatum is native to Europe and West Asia. It has been introduced to America, North Africa, Australia, and New Zealand.   USES Extracts of this species were used both as a sedative and an antispasmodic. However, because of the plants toxicity, it was discontinued by the early 20th century.[6]   This species has no known uses and is classified as a weed. INTERVENTION CRITERIA Intervention Level Child and Adult Decontamination, if appropriate, and monitoring is recommended: For all known or suspected ingestions of hemlock With occupational or environmental exposures involving dermal contact, management depends on clinical presentation. Refer all symptomatic cases to an appropriate health care facility. Observation Period All patients require medical attention.   Medical Observation If medical observation is required the patient must be monitored for 4 hours following exposure for onset or worsening of symptoms.   If the patient is asymptomatic at the end of the observation period, and if they have been appropriately decontaminated and any investigations have been carried out, they may be: Discharged into the care of a reliable observer, or Referred for psychological assessment if the overdose was with intent of self-harm.   Investigations Levels A mousy odor is associated with Conium maculatum; this odor on the breath or in the urine can be used as a diagnostic clue. However, absence of this odor does not rule out exposure.   Coniine (or other plant alkaloids) blood levels are not readily available, nor necessary for clinical management. Admission Criteria Hospital admission is recommended: In all symptomatic cases   The admission hospital may require the following resources: Advanced care facilities/Intensive Care Unit   TREATMENT TREATMENT SUMMARY Activated charcoal may be useful up to 1 hour after ingestion, if the patient is not vomiting. There are no specific antidotes and no methods for enhancing elimination can be recommended.   Supportive care is the mainstay of management with primary emphasis on cardiovascular and respiratory support. In severe cases, particular care should be given to airways management and respiratory support is vital in obtaining a positive outcome, as death is usually due to respiratory paralysis. Routine supportive care should be used for the treatment of other effects.   Nausea and vomiting may persist requiring symptomatic care with IV rehydration or antiemetic drugs, appropriate fluid and electrolyte balance must be maintained. Hypotension usually responds to intravenous fluids, sympathomimetics may be needed. Rarely cardiac dysrhythmias occur and should be managed using standard electrical and/or pharmacological methods. Extreme agitation or seizures can be a complicating feature and should be treated with a benzodiazepine. Atropine may be used to control manifestations from parasympathetic stimulation, such as diarrhea, urination, bronchospasm, emesis, lacrimation and sweating. Rhabdomyolysis and acute renal failure should be monitored for.   Emergency Stabilization Ensure adequate cardiorespiratory function Seizure Emergency monitoring Decontamination Ingestion Single dose activated charcoal Skin Irrigate Eye Irrigate immediately Antidote(s) None recommended Enhanced Elimination Not recommended Supportive Care Monitoring Gastrointestinal Gastrointestinal irritation Neurologic Coma Seizure Respiratory Respiratory failure Cardiovascular Bradycardia Musculoskeletal Rhabdomyolysis Renal Acute renal failure EMERGENCY STABILIZATION Ensure Adequate Cardiopulmonary Function Airway Ensure the airway is protected if compromised (intubation may be necessary).   Cardiovascular Immediately establish secure intravenous access.   Seizure Most toxic seizures are short-lived and often do not require intervention.   Administer a benzodiazepine as first-line treatment to patients with seizure activity.   Blood glucose concentration should be promptly determined. If the result indicates hypoglycemia, or is unobtainable, 50% dextrose should be administered IV (preceded by thiamine in adults).   Emergency Monitoring Heart rate Respiratory rate Seizure activity DECONTAMINATION Ingestion Single Dose Activated Charcoal Decontamination with activated charcoal is recommended for any suspected ingestion of hemlock, provided there is no evidence of CNS or respiratory depression.   Administer activated charcoal up to 1 hour following a potentially toxic ingestion.[7]   Single dose activated charcoal[8] CHILD 1 to 2 g/kg orally ADULT 50 to 100 g orally   Nasogastric Intubation Nasogastric instillation of activated charcoal is not recommended unless the ingestion is considered potentially severely toxic and oral administration is not successful. Accurate placement of the nasogastric tube and protection of the airway must be ensured.   Skin If necessary, remove contaminated clothing or jewellery. Flush the affected area with water as soon as possible. Continue to irrigate until all of the contaminant is removed.   Eye Remove contact lenses. Irrigate immediately with water or saline for at least 15 minutes. If the eye is contaminated with solid particles, the eyelid should be completely everted and any solid material removed as quickly as possible whilst continuing to irrigate. A topical anesthetic may be necessary in some patients, especially children, to enable the patient to open the lids sufficiently for effective irrigation.   If, following irrigation, any of the following are apparent: Ocular pain (other than mild and resolving) Erythema (other than mild and resolving) Decreased visual acuity Ocular discharge/crusting   A full ophthalmologic examination should be undertaken and any injury appropriately treated.   ANTIDOTE(S) There Are No Antidotes For This Substance There is no specific antidote for the treatment of this poisoning. Treatment is based on symptomatic and supportive care.   ENHANCED ELIMINATION Enhanced Elimination Not Recommended Dialysis or perfusion may be indicated for secondary complications, such as acidosis, or renal failure, but not for toxin removal alone.   SUPPORTIVE CARE Monitoring Heart rate Blood pressure ECG (12 lead) Cardiac monitoring Respiratory function Arterial blood gases (if compromised respiratory function) Neurological status Serum electrolytes Renal function On-set of paralysis   Gastrointestinal Gastrointestinal Irritation Due to nicotinic receptor over-stimulation gastrointestinal distress is common. Vomiting and diarrhea contribute to hypotension and fluid and electrolyte imbalances, potassium loss may increase the risk of cardiac dysrhythmia. Patients may require symptomatic care with antiemetic medication, IV fluids, and electrolyte replacement.[1]   Observe patient for: Nausea Vomiting Abdominal pain Hematemesis Diarrhea   Manage gastrointestinal irritation following standard treatment protocols.   Neurologic Coma The sedation phase of hemlock toxicity can lead to reduced levels of consciousness and coma.[9]   Closely monitor level of consciousness.   Follow standard protocols for the management of coma.   Seizures Seizures may develop after the ingestion of hemlock,[6] though this has not been described in most case reports. Seizures should be treated with a benzodiazepine.   Observe the patient closely for onset of seizure activity.   Toxic seizure may be managed following these (hyperlinked) recommendations.   Respiratory Respiratory Failure The sedation phase of hemlock toxicity will cause weakness and paralysis, which includes muscle weakness. This can lead to respiratory arrest.[9] Intense respiratory support, when needed, constitutes the most vital supportive measure in preventing a poor outcome. Respiratory failure is usually the most common cause of death.   Monitoring for respiratory failure should include: Chest auscultation Oxygen saturation Arterial blood gases   Treat using standard protocols for respiratory failure.   Cardiovascular Bradycardia The late inhibitory phase of conium toxicity will result in bradycardia.[9]   Monitor: Heart rate/rhythm Blood pressure ECG   Manage bradycardia following standard treatment protocols.   Musculoskeletal Rhabdomyolysis The toxic effect of conium may result in the paralysis of skeletal muscles, which may lead to rhabdomylosis;[10] this is characterized by an increase in muscle enzymes and the urine becoming red-brown, due to the presence of myoglobin.   Examine patient for muscle tenderness/pain and weakness. Monitor: Serum creatine kinase (increased CK-MM isoenzyme) Urinalysis: Myoglobin pH   Rhabdomyolysis may be managed following these (hyperlinked) recommendations.   Renal Acute Renal Failure Acute renal failure can occur as a result of rhabdomylosis.   Patients should be monitored for the onset of renal failure: Urine output Creatinine Blood urea nitrogen (urea) Proteinuria Hematuria Loin pain may occur   Manage following standard treatment protocols for acute renal failure.   DISCHARGE CRITERIA Patients may be discharged from hospital care when clearly asymptomatic and fully recovered from any complications. Appropriate psychiatric intervention may be necessary depending on the circumstances of the exposure.   FOLLOW UP Medical follow-up is unlikely to be required. Psychiatric intervention may be necessary depending on the circumstances of the exposure.   SIGNS AND SYMPTOMS The effects of coniine are similar to those of nicotine, but with more pronounced CNS and curare-like actions.   General signs are salivation, vomiting, dilation of the pupils, blurred vision, incoordination, myalgia, muscle fasciculations or flaccid paralysis, coldness of the extremities, and slow weak pulse. The patients pulse later becoming rapid and thready followed by coma, convulsions, and eventually death from respiratory paralysis.[11][12] Rhabdomyolysis and subsequent renal failure have also been reported.[10]   Routes of Exposure Systemic symptoms can occur after ingestion of fresh hemlock plant material; drying is thought to somewhat reduce toxicity, but poisonings have still occurred. Seeds of hemlock are toxic whether fresh or dried. Although the active alkaloids are oily volatile liquids, deaths have been reported after drinking liquid from boiling hemlock leaves.[11] Poisoning has also transpired from use of the hollow stem as a musical instrument or pea shooter.[13] Meat of birds, which eat hemlock seeds during migratory flights, is also poisonous to humans.[14]   Onset/Duration of Symptoms Symptoms could be expected to appear quite promptly, due to rapid absorption and the onset of similar compounds such as nicotine. One report describes the onset of symptoms occurring within 30 minutes of eating hemlock leaves[15] whereas another case reports the death of a child 3 hours after ingesting plant leaves.[11] Effects usually persist for between 4 to 24 hours.[15][16]   Animal studies have shown an onset of 0.5 to 2 hours with duration of 3 to 7 hours.[17][18]   Severity of Poisoning Mild Conium maculatum Toxicity Moderate Conium maculatum Toxicity Severe Conium maculatum Toxicity GI effects Thirst Nausea Vomiting Agitation Severe GI effects Salivation Abdominal pain Mydriasis Muscle weakness Muscle fasciculations Myalgia Drowsiness Tachycardia Tachypnea Respiratory depression Bradycardia Hypotension Seizures Paralysis Rhabdomyolysis Renal failure Respiratory failure Coma    ACUTE EFFECTS (ROUTE OF EXPOSURE) Skin Local dermatitis[19] (with or without blisters) Burning sensation[19] Numbness[19]   Systemic symptoms have not been reported following skin exposure.   ACUTE EFFECTS (ORGAN SYSTEM) Gastrointestinal Burning mouth or throat[15] Nausea[20] Vomiting[15][11] Salivation[15] Thirst[21] Abdominal pain[22]   Neurologic Tremor[6] Nervousness[6] Dizziness[16] Headache[16] Double vision[16] CNS depression[15] Dysarthria[16] Muscle paralysis[22] Seizures[6] Coma[6]   Respiratory Tachypnea[6] (initially) Dyspnea[16] Respiratory depression[16] Respiratory paralysis[6] Respiratory failure[16][12][22]   Cardiovascular Tachycardia[15] (initially) Bradycardia[12] Weak and thready pulse[6] Asystole[12]   Musculoskeletal Muscle fasciculations[15] Myalgia[15] Muscle edema[23] Muscle weakness[22][16] Skeletal muscle paralysis[22] Rhabdomyolysis[24][10]   Renal Urination[6] Acute tubular necrosis[24][10] Renal failure[23] (secondary to rhabdomyolysis)   Ocular Mydriasis[21][20] Double vision[16] Amblyopia[20]   TOXICITY The toxic content of plants may vary from year to year due to various factors that affect growth such as available moisture and spring temperatures. Thus, it is difficult to establish an association between the severity of symptoms and the ingestion of a specific amount of plant material.   HUMAN The primary toxic effects of this plant are due to coniine, but the toxicity of this plant may vary considerable from that of its toxic component, due a number of different considerations, including toxic concentration, and growth factors of this plant. Poison hemlock has been responsible for many human fatalities because of the resemblance of the seed to Anise, the leaves to parsley or carrot, and the roots to parsnips. All parts, especially the seeds, should be regarded as poisonous, even when dried.    An adult lethal dose is 100 to 300 mg of the toxic alkaloids. [24]   This approximately corresponds to:   Root 40 g in a 60 kg adult 10 g in a 15 kg child Shoots 29 to 1000 g in a 60 kg adult 7 to 250 g in a 15 kg child Leaves 13 to 67 g in a 60 kg adult 3 to 17 g in a 15 kg child Flowers 20 g in a 60 kg adult 5 g in a 15 kg child Unripe fruit 7 to 30 g in a 60 kg adult 2 to 8 g in a 15 kg child Ripe fruit 20 to 100 g in a 60 kg adult 5 to 25 g in a 15 kg child Seeds 22 to 100 g in a 60 kg adult 6 to 25 g in a 15 kg child   Child Toxicity is likely to occur after any ingestion of this plant.   An estimated lethal dose in a 3 year old male has been reported to be approximately 142 g of leaf material. [11] The child died approximately 3 hours after ingesting the plant.   A 4 year old male developed CNS depression 30 minutes after ingesting hemlock leaves and could not be roused after a further 2 hours. Following decontamination and supportive care, he became conscious 6.5 hours post ingestion. [15]   Adult Two adults died after ingesting an unknown amount of hemlock, which was prepared by boiling the leaves in water.[11]   Adults have become poisoned after ingesting the meat from birds that have ingested hemlock buds.[24] The birds themselves (robins, skylarks, chaffinches) were not susceptible to the alkaloids.   A 19 year old female required intubation 40 minutes after ingesting an unknown quantity of plant material. After 25 hours her breathing had improved sufficiently to discontinue this support.[16]   ANIMAL Acute Coniceine: LD50 Oral, Mouse 12 mg/kg12 mg/kg/[14] Coniine: LD50 Oral, Mouse 100 mg/kg100 mg/kg/[14] N-methylconiine: LD50 Oral, Mouse 204.5 mg/kg204.5 mg/kg/ Birds   Some small birds are not susceptible to coniine poisoning, consuming the seeds as a food source, and therefore may have the potential to cause toxicity in any species ingesting them. In contrast, deaths have resulted in other larger birds such as chickens and turkeys.[17][25]   Farm Animals   Severe poisoning and fatalities in cattle, goats, horses, sheep, and pigs have resulted from poison hemlock exposure. Symptoms generally involve movement problems, increased salivation and urination, tremor, vocalization, muscle weakness, and respiratory problems, all which can occur quite rapidly.[26][17][27]   Other animals including rabbits and elk are affected in a similar way to farm animals.   REPRODUCTION PREGNANCY It is unknown whether coniine crosses the placenta but poison hemlock is likely to affect the infant. Any exposure to poison hemlock should be avoided during pregnancy.   No human information is available however Conium maculatum appears to act as a teratogen and abortifacient in animal poisonings.   Malformations have been found in multiple species including cattle, sheep, horse, pigs, and goats after exposure to poison hemlock. These include limb and joint malformations, as well as cleft palate.[27][28][26]   LACTATION It is unknown if exposure to, or ingestion of, this plant results in excretion of toxic substances into breast milk.   FERTILITY It is unknown if exposure to, or ingestion of, this plant causes impaired fertility.   TOXIC COMPONENTS Piperazine plant alkaloids include: Conhydrine Coniine Gamma-Coniceine N-Methylconiine Pseudoconhydrine   Coniine and gamma-coniceine are found in the largest amounts and combined account for most of the plant’s toxic activity. Coniine is about 8 times more toxic than gamma-coniceine.[14]   These alkaloids are structurally related to nicotine, and could be expected to produce similar symptoms.   Plant Content All parts of the plant contain toxic piperidine alkaloids. Before flowering, the leaves contain the most alkaloids, but the greatest concentrations are found in the flowers and fruits/seeds. The roots, at all times, contain the least. Younger plants have 0.3 to 0.6% in leaves and 0.15% in other plant material (excluding flowers and fruit). Older plants contain approximately 1% in all parts of the plant.[29] The alkaloid content, however, does vary with the climatic conditions. In good growing seasons, the average weight of the fruits and thus the quantity of alkaloids can be twice that of normal. Drying the plant reduces the alkaloid content. TOXIC MECHANISM Coniine alkaloids affect the neurological junction where they act as non-depolarising neuromuscular blockers, similar to curare.[30] However, they also act on autonomic nervous system ganglia with varying degrees of stimulator, and inhibitor (biphasic) effects (resembling the effects of nicotine).   BIOLOGICAL LEVELS - TOXIC Coniine (or other plant alkaloids) blood levels are not readily available, nor necessary for clinical management. KINETICS No human pharmacokinetic data were found in the literature.   DESCRIPTION PLANT ATTRIBUTES General A coarse, erect, branched plant, that can be biennial (lives for two years and flowers in the second year), sometimes annual (lifecycle completed in one year) or perennial (lasting several years). It may exceed 2 m in height. The stem is hairless, slightly ridged and hollow with characteristic irregular purple blotches.   When the plant is crushed or bruised, it emits a mousy odor.[3][31][5] Leaves Leaves are up to 30 cm long, triangular in outline, with finely divided leaflets, arranged on either side of the stem, with deeply serrated edges. This gives the plant a delicate, lacy, fernlike appearance. Leaves lack hairs and are described as large and carrot-like.[32][31][5] Flowers Appear in almost flat-topped clusters of 2 mm white flowers. Each cluster is 2 to 5 cm in diameter.[3] Fruit Fruit consist of a pair of flattened, greyish-brown seeds, with five prominent wavy longitudinal ridges, which are about 3 mm long when ripe.[33][31][5] The root is generally a thick yellow or white tap root (similar to a parsnip), which may or may not have branches.[33] REFERENCES [1] Schep LJ, Slaughter RJ, Beasley DM. Nicotinic plant poisoning. Clin Toxicol (Phila) 2009 Sep; 47 (8): 771-81. [2] Schep LJ, Slaughter RJ, Becket G, Beasley DM. Poisoning due to water hemlock. Clin Toxicol (Phila) 2009 Apr; 47 (4): 270-8. [3] Cooper MR, Johnson AW. Poisonous plants in Britain and their effects on animals and man. London: Crown Copyright; 1984. p. 229. [4] Kingsbury JM. Poisonous plants of the United States and Canada. Englewood Cliffs (NJ): Prentice-Hall; 1964. p. 381. [5] Everist SL. Poisonous plants of Australia. Sydney: Angus & Robertson Publishers; 1981. p. 718. [6] Vetter J. Poison hemlock (Conium maculatum L.). Food Chem Toxicol 2004 Sep; 42 (9): 1373-82. [7] Chyka PA, Seger D, Krenzelok EP, Vale JA. Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43 (2): 61-87. [8] Fountain JS, Beasley DM. Activated charcoal supercedes ipecac as gastric decontaminant. N Z Med J 1998 Oct 23; 111 (1076): 402-4. [9] Brent J, Wallace KL, Burkhart KK, Phillips SD, Donovan JW, editors. Critical Care Toxicology. Philadelphia (PA): Elsevier Mosby; 2005. p. 1321. [10] Rizzi D, Basile C, Di Maggio A, Sebastio A, Introna F Jr, Rizzi R, Scatizzi A, De Marco S, Smialek JE. Clinical spectrum of accidental hemlock poisoning: neurotoxic manifestations, rhabdomyolysis and acute tubular necrosis. Nephrol Dial Transplant 1991; 6 (12): 939-43. [11] Drummer OH, Roberts AN, Bedford PJ, Crump KL, Phelan MH. Three deaths from hemlock poisoning. Med J Aust 1995 Jun 5; 162 (11): 592-3. [12] Foster PF, McFadden R, Trevino R, Galliardt S, Kopczewski LA, Gugliuzza K, Gonzalez Z, Wright F. Successful transplantation of donor organs from a hemlock poisoning victim. Transplantation 2003 Sep 15; 76 (5): 874-6. [13] Everist SL. Poisonous plants of Australia. Sydney: Angus & Robertson Publishers; 1981. p. 717-20. [14] Lopez TA, Cid MS, Bianchini ML. Biochemistry of hemlock (Conium maculatum L.) alkaloids and their acute and chronic toxicity in livestock. A review. Toxicon 1999 Jun; 37 (6): 841-65. [15] Frank BS, Michelson WB, Panter KE, Gardner DR. Ingestion of poison hemlock (Conium maculatum). West J Med 1995 Dec; 163 (6): 573-4. [16] Biberci E, Altuntas Y, Cobanoglu A, Alpinar A. Acute respiratory arrest following hemlock (Conium maculatum) intoxication. [Letter] J Toxicol Clin Toxicol 2002; 40 (4): 517-8. [17] Short SB, Edwards WC. Accidental Conium maculata poisoning in the rabbit. Vet Hum Toxicol 1989 Feb; 31 (1): 54-7. [18] Jessup DA, Boermans HJ, Kock ND. Toxicosis in tule elk caused by ingestion of poison hemlock. J Am Vet Med Assoc 1986 Nov 1; 189 (9): 1173-5. [19] Mitchell J, Rook A. Botanical dermatology: plants and plant products injurious to the skin. Vancouver: Greengrass; 1979. [20] Ober WB. Did Socrates die of hemlock poisoning? N Y State J Med 1977 Feb; 77 (2): 254-8. [21] Bruneton J. Toxic plants dangerous to humans and animals. Paris: Lavoisier Publishing; 1999. p. 108-13. [22] West PL, Horowitz BZ, Montanaro MT, Lindsay JN. Poison hemlock-induced respiratory failure in a toddler. Pediatr Emerg Care 2009 Nov; 25 (11): 761-3. [23] Scatizzi A, Di Maggio A, Rizzi D, Sebastio AM, Basile C. Acute renal failure due to tubular necrosis caused by wildfowl-mediated hemlock poisoning. Ren Fail 1993; 15 (1): 93-6. [24] Rizzi D, Basile C, Di Maggio A, Sebastio A, Introna F Jr, Rizzi R, Bruno S, Scatizzi A, De Marco S. Rhabdomyolysis and acute tubular necrosis in coniine (hemlock) poisoning. [Letter] Lancet 1989 Dec 16; 2 (8677): 1461-2. [25] Frank AA, Reed WM. Conium maculatum (poison hemlock) toxicosis in a flock of range turkeys. Avian Dis 1987 Apr-Jun; 31 (2): 386-8. [26] Panter KE, Bunch TD, Keeler RF, Sisson DV, Callan RJ. Multiple congenital contractures (MCC) and cleft palate induced in goats by ingestion of piperidine alkaloid-containing plants: reduction in fetal movement as the probable cause. J Toxicol Clin Toxicol 1990; 28 (1): 69-83. [27] Keeler RF. Coniine, a teratogenic principle from Conium maculatum producing congenital malformations in calves. Clin Toxicol 1974 Apr; 7 (2): 195-206. [28] Keeler RF, Balls LD. Teratogenic effects in cattle of Conium maculatum and conium alkaloids and analogs. Clin Toxicol 1978; 12 (1): 49-64. [29] CROMWELL BT. The separation, micro-estimation and distribution of the alkaloids of hemlock (Conium maculatum L.). Biochem J 1956 Oct; 64 (2): 259-66. [30] BOWMAN WC, SANGHVI IS. Pharmacological actions of hemlock (Conium maculatum) alkaloids. J Pharm Pharmacol 1963 Jan; 15 (): 1-25. [31] Kingsbury JM. Poisonous plants of the United States and Canada. Englewood Cliffs (NJ): Prentice-Hall; 1964. p. 379. [32] Cooper MR, Johnson AW. Poisonousp in Britain and their effects on animals and man. London: Crown Copyright; 1984. p. 229. [33] Cooper MR, Johnson AW. Poisonous plants in Britain and their effects on animals and man. London: Crown Copyright; 1984. p. 229-32. Do Not Archive. This document is current on day of issue, NZ: 18.May.2012

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