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Searched by : Karint NymPh : 10 Dec 2006 วิสาหกิจชุมชนเรือนพระจันทร์
NERIUM OLEANDER Chemical Safety Poisons Information Monograph
1. NAME
1.1 Scientific name Nerium oleander L.
1.2 Family Apocynaceae
1.3 Common name(s) and synonyms
Adelfa (Puerto Rico, Spain); Alheli Extranjero (Puerto Rico);
Baladre (Catalunya-Spain); Espirradeira (Brazil);
Flor de Sao Jose (Brazil); Laurel de jardín (Argentina Uruguay);
Laurel rosa (Argentina, Uruguay); Laurier rose (France);
Loandro (Brazil); Loureiro rosa (Brazil); Oleana (Hawaii);
Oleander (Brazil, UK, USA); Oliwa (Hawaii); Rosa Francesa (Cuba);
Rosa Laurel (Mexico); Rose bay (UK).
 
 
 
2. SUMMARY
2.1 Main risks and target organs oleander ingestion causes both cardiac and gastrointestinal signs and symptoms. The main toxic principles are the glycosides, which induce cardiac arrhythmia and eventually death.
2.2 Summary of clinical effects The clinical picture usually starts with gastrointestinal signs: nausea, vomiting, abdominal pain and diarrhoea. Later, cardiovascular and neurological symptoms can occur. Sinus bradycardia or different degrees of atrioventricular (AV) block are the most frequent cardiac features. In severe cases, ectopic beats occur which may be followed by ventricular tachycardia and fibrillation. The main neurological symptoms are: tremor, drowsiness and ataxia. Hypotension and unconsciousness may also occur. Seizures have been described.
2.3 Diagnosis is based on the clinical features (malaise, vomiting, abdominal pain, bradycardia, dizziness), electrocardiographic changes and glycosides investigated by digoxin immunoassay. The triad of gastrointestinal distress, circumoral erythema and cardiac dysrhythmia should alert to the possibility of N. oleander poisoning. A plant specimen or parts obtained from gastric lavage or vomiting should be collected for botanical identification. N. oleander can be recognized by microscopic examination of its epidermis, where stoma cells are typical.
2.4 First-aid measures and management principles. Treatment should aim at:
- gut decontamination by means of emesis or lavage;
- correction of electrolyte imbalance;
- correction of severe bradycardia with atropine or electrical pacing
- corrections of ventricular dysrhythmias;
- administration of digoxin-specific Fab antibodies could be considered if available.
2.5 Poisonous parts : All parts, including the sap, either fresh, dried or boiled, are toxic.
A single leaf intensively chewed has been reported to be lethal.
2.6 Main Toxins Poisonous Principles are cardiac glycosides.
The one most studied is oleandrin, but there are more than ten other glycosides whose chemical structure is well known: 5 ß-cardenolides, such as oleandrine;
5 a-cardenolides, such as uzangenin-type;
oleandrigenin (16-Acetylgitoxigenin) (ol).
The "ol" being: oleandroside (oleandrin); glucose (glucosyloleandrin); gentiobioside (gentiobiosyl oleandrin); diginoside (nerigoside); digitoxigenin (digitalose/diginose); oleagenine - oleasides (A,E) (diginose, gentiobiose-diginose).
Adyregenin is a compound with no cardiac effect.
3. CHARACTERISTICS
3.1 Description of the plant
3.1.1 Special identification features oleander is an evergreen shrub reaching four metres in height. Leaves are 10 to 22 cm long, narrow, untoothed and short-stalked, dark or grey-green in colour. Some cultivars have leaves variegated with white or yellow. All leaves have a prominent mid rib, are "leathery" in texture and usually arise in groups of three from the stem. The plant produces terminal flower heads, usually pink or white, however, 400 cultivars have been bred and these display a wide variety of different flower colour: deep to pale pink, lilac, carmine, purple, salmon, apricot, copper, orange and white (Huxley, 1992). Each flower is about 5 cm in diameter and five-petalled. The throat of each flower is fringed with long petal-like projections. Occasionally double flowers are encountered amongst cultivars. The fruit consists of a long narrow capsule 10 to 12 cm long and 6 to 8 mm in diameter; they open to disperse fluffy seeds. Fruiting is uncommon in cultivated plants. The plant exudes a thick white sap when a twig or branch is broken or cut (Font-Quer, 1974; Schvartsman, 1979; Lampe & McCann, 1985; Pearn, 1987).
3.1.2 Habitat Where the species grows in the wild (i.e. in the Mediterranean), it occurs along watercourses, gravely places and damp ravines. It is widely cultivated particularly in warm temperate and subtropical regions where it grows outdoors in parks, gardens and along road sides. Elsewhere, where the plant is not frost-tolerant (e.g. in central and western Europe), it may be grown as a conservatory or patio plant.
3.1.3 Distribution Oleander is cultivated worldwide as an ornamental plant; it is native only in the Mediterranean region (Kingsbury, 1964; Hardin & Arena, 1974).
3.2 Poisonous parts of the plant - The whole plant, including the sap, is toxic.
3.3 The toxin(s)
3.3.1 Name(s) Oleandrin, a glycoside, is the main toxin. Its chemical name is
16b-acetoxy-3b-[(2,6 dideoxy-3-0-methyl-a2-L-arabino-hexopyranosyl) oxy]-14-hydroxy-5ß, 14ß-card-20(22)-enolide (Reynolds, 1989).
3.3.2 Description, chemical structure, stability Oleandrin:
CAS number: 465-16-7
Structural formula: C32H48O9
Molecular weight: 576.7
Structural name: oleandrin
3.3.3 Other physico-chemical characteristics Oleandrin forms colourless, odourless, acicular crystals which are very bitter (Shaw & Pearn, 1979). The concentration of oleandrin in the plant tissues is approximately 0.08% (Schvartsman, 1979).
Solubility: insoluble in water; it has little resistance to light but it is heat-stable (Pearn, 1987; Reynolds, 1989).
3.4 Other chemical contents of the plant : Oleander contains at least 2% cardiac glycosides.
Rosagenin may be extracted from the bark and has a strychnine-like action.
Several flavones (0.5%) and volatile oils (unimportant amount), as well as rubber, fats, sugars and hydrocyanic acid, can be isolated from its leaves (Schvartsman, 1979; Shaw & Pearn, 1979; Pearn, 1987).
4. USES/CIRCUMSTANCES OF POISONING
4.1 Uses
4.1.1 Uses
Miscellaneous pharmaceutical product. Other therapeutic preparation
4.1.2 Description
Preparations containing the active principles were used formerly as rodenticides, insecticides, and as remedies for indigestion, fever, ringworm, malaria, leprosy, venereal diseases and as abortifacients. Therapeutic use of oleander glycosides as cardiac drugs were assessed and documented in the 1930s (Shaw & Pearn, 1979; Osterloh et al., 1982). The USSR pharmacopoeia contains an oleandrin solution (solution Neriolini) and oleandrin tablets, and oleandrin solution (oleandrin 22 mg, alcohol 74 mL, distilled water to 100 mL). This contains 7 to 9 'frog units' per mL (1 mg oleandrin = 34 to 44 frog units). Oleandrin tablets each contain 100 mg of the active principle (Reynolds, 1989).
4.2 High risk circumstances
The high risk circumstances of exposure are: children playing with the ornamental shrub (tasting, chewing, ingesting portions of the plant), and inappropriate medicinal use of plant infusion. Intentional poisoning by ingestion of plant infusions has been reported.
4.3 High risk geographical areas
Although the plant is native to the Mediterranean basin,
it has been introduced as an ornamental shrub in many tropical and subtropical countries (Mahin et al., 1984). The plant is common in Australia and southern Africa and ingestion of plant parts is one of the major causes of childhood admission to hospital (Shaw & Pearn, 1979).
5. ROUTES OF EXPOSURE
5.1 Oral
Parts of the plant can be ingested accidentally or in suicide attempts (Jouglard et al., 1973; Pronczuk & Laborde, 1988). Extracts or herbal teas made of N. oleander have been ingested for suicidal or medicinal purposes (Haynes et al., 1985; Blum & Rieders, 1987). Ingestion of water contaminated with N. oleander leaves (from a flower bowl), meat cooked or stirred with the stems, and honey made by bees visiting the flowers have produced toxic effects (Hardin & Arena, 1974).
5.2 Inhalation
Smoke from burning N. oleander may be toxic (Hardin & Arena, 1974; Shaw & Pearn, 1979).
5.3 Dermal
No data available.
5.4 Eye
No data available.
5.5 Parenteral
No data available.
5.6 Others
A fatal case, following rectal and oral administration of N. oleander extract, has been described (Blum & Rieders, 1987).
6. KINETICS
6.1 Absorption by route of exposure. Oleandrin is well absorbed orally (Schvartsman, 1979).
6.2 Distribution by route of exposure.
Wide body distribution is expected: high concentrations of oleandrin have been measured in blood, liver, heart, lung, brain, spleen and kidney in a fatal case of N. oleander extract poisoning (Blum & Rieders, 1987).
6.3 Biological half-life by route of exposure
No data available.
6.4 Metabolism
No data available.
6.4 Elimination and excretion.
Oleandrin is eliminated very slowly from the body (one to two weeks)
(Shaw & Pearn, 1979).
7. TOXINOLOGY
7.1 Mode of Action
The cardiac effects of the glycosides are due to direct cardiotoxicity and an indirect effect via the vagal nerve. The direct effect is due to the inhibition of the Na-K ATP-ase pump sodium-potassium adenosine triphosphatase enzyme system). This specific action increases intracellular sodium ion and serum potassium concentrations. The sodium influx lowers the membrane potential threshold, increasing excitability. The chronotropic effect is primarily central, mediated by an increase of vagal tone which decreases the rate of sinoatrial node depolarization (Osterloh et al., 1982).
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults : Between 7 to 20, or a "handful", of the leaves have been ingested by adult patients who were intoxicated but recovered completely; the dose of oleandrin in this sample is not known (Pronczuk & Laborde, 1988; Shumaik et al., 1988).
7.2.1.2 Children : A single leaf may be lethal to a child (Shaw & Pearn, 1979).
7.2.2 Relevant animal data
One leaf of N. oleander may be sufficient to kill a sheep (Shaw & Pearn, 1979). The lethal dose of N. oleander leaves reported for several animal species is about 0.5 mg/kg. Animals poisoned by eating the plant often develop bloody diarrhoea, due to a direct effect on the gastrointestinal tract. The bitter and astringent taste of the plant's leaves means that all but starving creatures are likely to be exposed. (Szabuniewicz et al., 1971; Pearn, 1987).
7.2.3 Relevant in vitro data
No data available.
7.3 Carcinogenicity
No data available.
7.4 Teratogenicity
No data available.
7.5 Mutagenicity
No data available.
7.6 Interactions : Pre-medication with digoxin or other cardiac glycosides may increase the severity of poisonings. The well-known interaction between digoxin and quinidine (increasing digoxin levels) should be considered.
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
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