The genus Cinnamomum

Pharmacology and Toxicology of Cinnamon and Cassia 277
were more susceptible than larvae. Cinnamaldehyde also exhibited good antifeedant
activity. The toxicity of the oil on Ceratitis capitata (an amphibian pest which causes
serious damage to fruit crops) was investigated by Moretti et al. (1998). Toxicity
produced by oral administration of emulsions containing the active constituent was
assessed and it was found that over 90% mortality was obtained with 5% emulsion.
The pesticidal effect was caused by the irreversible damage caused by the active
constituent to the gut of the organism.
Cinnamon wood exhibits considerable termiticidal activity. The wood meal was
used for a study and compared with other pine wood meals. It was found that cinnamon
wood meal exhibited a significantly higher effect than other wood meal studied
(Hashimoto et al., 1997). Morallo Rejeus and Punzalan (1997) reported on the
molluscicidal action of cinnamon oil. The LC 100 value was assessed to be less than
200 ppm. Another study by Roger and Hamraoui (1994) on Acanthoscelides oblectus,
a storage pest that damages its host plant Phaseolus vulgaris (kidney bean), showed
that cinnamon oil exhibited fumigant toxicity to adults and inhibited reproduction
through ovicidal and larvicidal action. These actions can be combined to improve
the management of this bruchid. The antignawing activity of cinnamon bark was
studied using laboratory reared mice and it was found to be very effective (Hoiseon
et al., 1999). Both cinnamaldehyde and cinnamylalcohol were the active constituents
which produced the action. They exhibited potent activity at a concentration
of 5 and 2.5%.
Toxicology
Cinnamon bark and cinnamon oil are non-toxic and generally considered as safe
(GRAS) substances. The ADI (allowable daily intake) recommended by WHO/FAO is
700 g/kg body weight when used as food additives (FAO/WHO Tech. Report, 1984).
Allergic reactions, mainly contact sensitivity, to cassia oil and bark have been reported.
Cinnamaldehyde in toothpastes and perfumes has also been reported to cause contact
sensitivity. In a double blind placebo-controlled personal study Minimaki (1995)
reported that out of 29 patients studied six positive cases were obtained. Allen and
Blozis (1988) reported the formation of oral lesions induced by contact allergy with cinnamon
flavoured chewing gum. The symptoms subsided two days after discontinuing
the product containing cinnamon. Sensitivity reactions due to cinnamaldehyde in
toothpaste have also been reported (Lamey et al., 1990). Cassia oil is stated to cause
dermal and mucous membrane irritation. The irritant and sensitising properties of
cassia oil have been attributed to cinnamaldehyde. The LD 50 value of cinnamaldehyde
was assessed to be 132, 6110 and 2225 mg/kg body weight in mice by intravenous,
intraperitonial and oral administration, respectively. The intravenous LD 50 of the
decoction of the herb was 18.48 1.80 g/kg (Wang, 1983). The LD 50 of the oil in
an oral toxicity study was assessed to be 5.36 ml/kg in mice (Yadav et al., 1999).
Cinnamaldehyde at low dosage caused inhibition of the activity of animals and at high
dosage caused strong spasms, motor disturbances, shortness of breath and lastly death
from respiratory paralysis (Wang, 1983). However, no human study has been reported
which assessed the acute and chronic toxicity at high doses. Because of the pungent
taste of the bark and oil, ingestion of high doses is highly unlikely. The recommended
dose as a food additive is 10–20 ppm.