Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

OIL OF CLOVES

NFPA

PRODUCT USE

Microscopy (histology) reagent; therapeutic for toothache, carminative; in confectionery,
tooth powders, soaps, perfumery. Synthetic

SYNONYMS

"clove oil", "caryophyllus oil", "clove oil BP", "clove bud oil", "oil of clove bud",
"nelken oel", "oleum caryophylli"

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

Harmful if swallowed.
Irritating to skin.
May cause SENSITIZATION by skin contact.

POTENTIAL HEALTH EFFECTS

ACUTE HEALTH EFFECTS

SWALLOWED

  Accidental ingestion of the material may be harmful; animal experiments indicate that ingestion of less than 150 gram may be fatal or may produce serious damage to the health of the individual.  Ingestion of eugenol and eugenol-containing oils may produce gastroenteritis. Systemic toxicity is similar but less than that of phenol, perhaps because of its relatively insolubility. Aqueous emulsions by mouth induce vomiting in man and dog and promote gastric secretion of mucin.  Poisoned rats exhibited paresis of hind legs and jaw with eventual prostration and coma. Death is believed t have been due to peripheral vascular collapse. Surviving rats showed haematuria (blood in the urine),  

EYE

  There is some evidence to suggest that this material can causeeye irritation and damage in some persons.  

SKIN

  The material may cause moderate inflammation of the skin either following direct contact or after a delay of some time. Repeated exposure can cause contact dermatitis which is characterized by redness, swelling and blistering.  Skin contact with the material may damage the health of the individual; systemic effects may result following absorption.  Eugenol produces local anaesthesia and is a local antiseptic. Contact dermatitis has been produced in dental surgeons during exposure in an occupational setting.  Entry into the blood-stream, through, for example, cuts, abrasions or lesions, may produce systemic injury with harmful effects. Examine the skin prior to the use of the material and ensure that any external damage is suitably protected.  

INHALED

  Inhalation may produce health damage*.  Inhalation of aerosols (mists, fumes), generated by the material during the course of normal handling, may be damaging to the health of the individual.  There is some evidence to suggest that the material can cause respiratory irritation in some persons. The body's response to such irritation can cause further lung damage.  Inhalation hazard is increased at higher temperatures.  Inhalation of essential oil volatiles may cause dizziness, rapid, shallow breathing, increased heart rate, respiratory irritation, loss of consciousness or convulsions. Urination may stop, and there may be swelling and inflammation of the lungs.  

CHRONIC HEALTH EFFECTS

  Skin contact with the material is more likely to cause a sensitization reaction in some persons compared to the general population.  There has been some concern that this material can cause cancer or mutations but there is not enough data to make an assessment.  Limited evidence suggests that repeated or long-term occupational exposure may produce cumulative health effects involving organs or biochemical systems.  There is some evidence that inhaling this product is more likely to cause a sensitization reaction in some persons compared to the general population.  Some phenol-based naturally occurring substances, (e.g. phenol, guaiacol, tannic acid, eugenol) undergo conversion to produce derivatives which produce skin (and possibly respiratory) sensitisation. Each of these compounds has phenolic hydroxyl groups which are readily oxidized to produce reactive quinone-like compounds. Phenol is converted in the body to quinone whilst guaiacol (ortho-methoxyphenol) and eugenol (2-allylguaiacol) are converted to the ortho-quinone. Both eugenol and isoeugenol (4-propenylguaiacol) are pro-haptens that require biotransformation to become protein-reactive haptens. Although they are close structural isomers they show markedly different levels of sensitisation and are weakly cross-reactive in in vivo tests. Isoeugenol is a strong sensitiser and eugenol is moderate. It appears that neither share a common mechanism for sensitisation although structural similarities exist. This relates to different mechanisms of biotransformation.  Cinnamaldehyde and cinnamic acid are structurally related to eugenol and isoeugenol; they seen to generate a common hapten and appear to produce simultaneous sensitisation to eugenol and isoeugenol despite being metabolised via different pathways. Buckley et al British Jnl of Dermatology 2006 Vol 154 pp 885-884  The phenolics and related substances permeate the dermis where they undergo bio-  distribution. Phenolic permeation is related to liphophilicity and molecular volume. Phenols are metabolised by cutaneous enzymes or other processes to form reactive metabolites or may be chemically modified through the reaction of UV light. The skin has a wide-ranging metabolic capability which can perform essentially all the metabolic transformation which are know to be carried out in the liver. Metabolic by- products may be haptens and produce sensitisation. Eugenol although a weak sensitiser, in its own right, is oxidised to the highly reactive ortho-quinone. The sensitising principal in poison ivy, a catechol know as urishiol, appears to undergo similar oxidation to produce a reactive hapten. These reactive haptens bind to dermal proteins (haptens are often electrophilic and bind covalently with -NH2 and -SH groups on proteins, modifying the protein which when exposed to the immune system, will react with antigen-presenting cells in the dermis.  Axillary dermatitis is common and over represented in people with contact allergy to fragrances. Many people suspect their deodorants to be the incriminating products. In order to investigate the significance of isoeugenol in deodorants for the development of axillary dermatitis when used by people with and without contact allergy to isoeugenol, patch tests with deodorants and ethanol solutions with isoeugenol), as well as repeated open application tests (ROAT) with roll-on deodorants with and without isoeugenol at various concentrations, were performed in 35 dermatitis patients, 10 without and 25 with contact allergy to isoeugenol. A positive ROAT was observed only in patients hypersensitive to isoeugenol and only in the axilla to which the deodorants containing isoeugenol had been applied. Deodorants containing isoeugenol in the concentration range of 0.0063-0.2% used 2 times daily on healthy skin can thus elicit axillary dermatitis within a few weeks in people with contact allergy to isoeugenol. Bruze et al ; Contact Dermatitis Vol 52, May 2005 pp 7.  Certain substances, commonly found in perfumes or perfumed products, produce hypersensitivity. Sensitising constituents have been classified as Class A (common sensitisers) or Class B (rare sensitisers) in a Japanese study (Nakayama 1998). Contact allergy to perfumes occurs with a relatively high incidence, such incidence only surpassed by nickel allergy in the community. In a Danish study, it was found that about 1.1% of the population was allergic to Peru balsam or "fragrance mix".  There is no cure for perfume allergy. Once sensitised, exposure to even minute amounts of the perfume, gives rise to eruptions and eczema. These symptoms may be treated with steroid creams, although frequent recourse to this treatment produces unwanted side-  effects.  Intolerance to perfumes, by inhalation, may occur if the perfume contains a sensitising principal. Symptoms may vary from general illness, coughing, phlegm, wheezing, chest-  tightness, headache, exertional dyspnoea, acute respiratory illness, hayfever, and other respiratory diseases (including asthma). Perfumes can induce hyper-reactivity of the respiratory tract without producing an IgE-mediated allergy or demonstrable respiratory obstruction. This was shown by placebo-controlled challenges of nine patients to "perfume mix". The same patients were also subject to perfume provocation, with or without a carbon filter mask, to ascertain whether breathing through a filter with active carbon would prevent symptoms. The patients breathed through the mouth, during the provocations, as a nose clamp was used to prevent nasal inhalation. The patient's earlier symptoms were verified; breathing through the carbon filter had no protective effect. The symptoms were not transmitted via the olfactory nerve but they may have been induced by trigeminal reflex via the respiratory tract or by the eyes.  Cases of occupational asthma induced by perfume substances such as isoamyl acetate, limonene, cinnamaldehyde and benzaldehyde, tend to give persistent symptoms even though the exposure is below occupational exposure limits.  Inhalation intolerance has also been produced in animals. The emissions of five fragrance products, for one hour, produced various combinations of sensory irritation, pulmonary irritation, decreases in expiratory airflow velocity as well as alterations of the functional observational battery indicative of neurotoxicity in mice. Neurotoxicity was found to be more severe after mice were repeatedly exposed to the fragrance products, being four brands of cologne and one brand of toilet water.