Hazard and Precautionary Statements (GHS)

Chenopodium oil Chemical Properties,Usage,Production

Chemical Properties

Colorless or yellowish oil; characteristic penetrating odor; bitterish burning taste. Soluble in 3–10 volumes of 70% alcohol (inferior and adulterated oils do not yield a clear solution).

Occurrence

Found in the flowers and fruit of the plant C. ambrosioides and C. ambrosioides L. var. anthelminticum (L.) A. Gray (Fam. Chenopodiaceae) (Guenther, 1952).

Uses

Medicine (anthelmintic).

Uses

Chenopodium Oil may cause an increase in the erythrocyte count by provoking contraction of the spleen. Chenopodium Oil has been used for the treatment of strongylidosis in horses.

Preparation

By steam distillation from the overground parts of the flowering and fruiting plant, C. ambrosioides (Guenther, 1952).

Toxicity evaluation

The acute oral LD₅₀ in rats was reported as 0.255 g/kg while the acute dermal LD₅₀ in rabbits was reported as 0.415 g/kg (McGee. 1974). At full strength, chenopodium oil applied to the backs of hairless mice was toxic (Urbach & Forbes, 1974). The acute oral LD₅₀ in mice was found to be 0.38 ml/kg (Kasahara, 1956). The lethal dose of chenopodium oil for the hen was reported as 0.6ml/kg; toxic signs were seen in hens at 0.3 ml/kg and in dogs as 0.28-0.4 ml/kg (Szakall, 1940). When 23 rats were given a single ip injection of 0.12 ml/kg, the toxic effects seen included disturbances of balance and generalized tetanic contractions; all animals died within 18 hr. In a further group of ten rats given four ip injections each of 0.07 ml/kg on alternate days, disturbances of balance and orientation were milder than in the previous group and were accompanied by torpor, anorexia and weight loss but no fatalities occurred. Autopsy revealed cerebral hyperaemia and oedema with degeneration of the nerve cells together with loss of RNA. A primary action on the CNS was suggested (Cheli & Soragni, 1953). Acute poisoning of rats with chenopodium oil produced an increase in liver lipids, but no change in liver RNA content (Rezza & Soragni, 1951). Human toxicity and fatal poisoning. Toxic effects include skin and mucous-membrane irritation, headache, vertigo, nausea, vomiting, constipation, tinnitus, temporary deafness, diplopia and blindness, transient stimulation followed by depression of the CNS leading to delirium and coma, occasional convulsions, circulatory collapse due to vasomotor paralysis and sometimes pulmonary oedema. Chenopodium oil is also toxic to the kidneys and liver and haematuria, albuminuria and jaundice have been observed. Doses of 0.2-1.2 ml have been used but the usual adult dose is 1 ml (Gleason, Gosselin, Hodge & Smith. 1969; Goodman & Gilman, 1960; M art Male, The Extra Pharmacopoeia, 1972). Several reports of fatal poisoning followed the therapeutic use of chenopodium oil in man (Campagne, 1939; Ibru-M??r. 1932; Kr?ber. 1936; Meie, 1952; Wolf, 1935). For example, a 14-month-old baby given one teaspoonful of chenopodium oil exhibited vomiting, convulsions, weakness, sleepiness and cardiac and respiratory disturbances followed by death 12hr later (Meie, 1952). Autopsy showed hyperaemia of the CNS, pulmonary oedema with bronchopneumonic foci, changes in the myocardium and the kidneys, fatty liver degeneration and gastritis.In another case of fatal poisoning, a 2-yr-old child suffering from sickle-cell anaemia was given 16 minims of oil of chenopodium in divided doses over 3 wk; she became comatose and died after a further 2 days. Albuminuria, degenerative changes in the liver and kidneys and cerebral oedema were evident (Wolf, 1935).

Pharmacology

In tests of antispasmodic activity, a saturated aqueous solution of chenopodium oil showed musculotropic spasmolytic activity against BaCl2-induced spasms in rat duodenum, had a clear antihistaminic action in guinea-pig ileum and inhibited nicotine-induced spasms in rabbit jejunum (Debelmas & Rochat, 1967). Frogs, toads and guinea-pigs responded to chenopodium oil by a decrease in the rate and amplitude of the heart beat, ascribed to vagus excitation and myocardium intoxication (Donatelli, 1935).

Metabolism

The oil is readily absorbed from the gastro-intestinal tract. It is partially eliminated in the lungs, but excretion via the urine or faeces does not appear to have been reported (Goodman & Gilman, 1960). Traces of ascaridole were found in the stomach and intestinal tract of a 14-monthold baby who died from poisoning with chenopodium oil (Meie, 1952).