Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

OLEIC DIETHANOLAMIDE

NFPA

PRODUCT USE

Fatty acid amides are nonionic substances which have a strong tendency to reduce friction
on various surfaces by forming a layer on surfaces. This coating action may be attributed
to their hydrophobic character and strong hydrogen bonding. Primary, secondary, and
bisamides are widely used as lubricating or slip agents and alkanolamides. Their
ethoxylated counterparts are commonly used as surfactants in personal care and detergent
applications. The dehydration of amides that produces nitriles is of great commercial
value. The most widely used synthetic route for primary amides is the reaction of a fatty
acid with anhydrous ammonia. Typical uses of fatty acid amides include lubricants for
synthetic resins (polyethylene, polypropylene, etc.), anti- blocking agents, mold release
agents, printing ink additives, and pigment/dye dispersants. Foam booster, surfactant;
widely used in neutralised, diluted form in products such as hair shampoos. Intermediate

SYNONYMS

C22-H43-N-O3, C22-H43-N-O3, "N, N'-bis(2-hydroxyethyl)dodecanamide", "N, N'-bis(2-
hydroxyethyl)dodecanamide", "9-octadecenamide, N-N'(2-hydroxyethyl)", "9-octadecenamide,
N-N'(2-hydroxyethyl)", "N, N-bis(2-hydroxyethyl)oleoamide", "N, N-bis(2-
hydroxyethyl)oleoamide", "N, N-diethanololeoamide", "N, N-diethanololeoamide", "N, N-
diethanololeamide", "N, N-diethanololeamide", "N, N-diethanololeic acid amide", "N, N-
diethanololeic acid amide", "oleylamide DEA", "oleic acid diethanolamide",
diethanololeamide, "oleamide DEA", "Amisol ODE", "Clindrol 2000", 2020, "Emid 6545",
"Mackamide O", "Schercomid ODA", Steinamid, "Witcamide 511C"

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

None

EMERGENCY OVERVIEW

RISK

Harmful if swallowed.
Risk of serious damage to eyes.
May cause SENSITIZATION by skin contact.
Harmful: danger of serious damage to health by prolonged exposure if swallowed.
Irritating to respiratory system and skin.
Very toxic to aquatic organisms, may cause long- term adverse effects in the
aquatic environment.

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.  Nonionic surfactants may produce localized irritation of the oral or gastrointestinal lining and induce vomiting and mild diarrhea.  

EYE

  If applied to the eyes, this material causes severe eye damage.  Low concentrations (0.6%) of fatty acid amides such as cocoamide DEA are severely irritating to the eyes of rabbits.  Eye contact with fatty acid diethanolamides (C8-18) and fatty acid monoethanolamides may lead to a risk of serious damage to eyes (CESIO).  Vapors of volatile amines irritate the eyes, causing excessive secretion of tears, inflammation of the conjunctiva and slight swelling of the cornea, resulting in "halos" around lights. This effect is temporary, lasting only for a few hours. However this condition can reduce the efficiency of undertaking skilled tasks, such as driving a car. Direct eye contact with liquid volatile amines may produce eye damage, permanent for the lighter species.  Non-ionic surfactants can cause numbing of the cornea, which masks discomfort normally caused by other agents and leads to corneal injury. Irritation varies depending on the duration of contact, the nature and concentration of the surfactant.  

SKIN

  The material may cause mild but significant 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.  A 30% fatty acid amide (cocoamide DEA solution) was a moderate skin irritant in rabbits. Test sites were scored for irritation according to Draize, and the Primary Irritation Index (PII) was 3.1 (maximum irritation is indicated by the score of 8). In products intended for prolonged contact with the skin, the concentration of cocoamide DEA should not exceed 5%. Fatty acid diethanolamides (C8-C18) and monoethanolamides are classified by CESIO as irritating.  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*.  The material can cause respiratory irritation in some persons. The body's response to such irritation can cause further lung damage.  Inhalation of vapors or aerosols (mists, fumes), generated by the material during the course of normal handling, may be damaging to the health of the individual.  Inhalation hazard is increased at higher temperatures.  Inhalation of amine vapors may cause irritation of the mucous membrane of the nose and throat, and lung irritation with respiratory distress and cough. Swelling and inflammation of the respiratory tract is seen in serious cases; with headache, nausea, faintness and anxiety There may also be wheezing.  

CHRONIC HEALTH EFFECTS

  Harmful: danger of serious damage to health by prolonged exposure if swallowed.  This material can cause serious damage if one is exposed to it for long periods. It can be assumed that it contains a substance which can produce severe defects. This has been demonstrated via both short- and long-term experimentation.  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.  Prolonged or chronic exposure to alkanolamines may result in liver, kidney or nervous system injury. Repeated inhalation may aggravate asthma and inflammatory or fibrotic pulmonary disease.Results of repeated exposure tests with diethanolamine (DEA) in laboratory animals include anaemia (rats) and effects on the kidneys (rats and mice) and liver (mice). DEA produces nervous system injury in dogs and rats. Heart and salivary gland lesions have also been seen in mice treated cutaneously with DEA and in mice receiving DEA in drinking water. Rats given high doses of DEA developed anaemia and testicular lesions.Exaggerated doses of DEA produced heart and nervous system effects in other animals. Changes in other organs were judged to be secondary due to the poor health of animals subjected to extremely high doses of DEA. Rats, rabbits and guinea pigs exposed to high vapour concentrations of volatile monoethanolamine (MEA) (up to 1250 ppm) for periods of up to 5 weeks developed pulmonary, hepatic and renal lesions. Dogs, rats and guinea pigs exposed to 100 ppm MEA for 30 days, became apathetic and developed poor appetites. Animal tests also indicate that inhalation exposure to MEA may result in nervous system injury. All species exposed to airborne MEA experienced dermal effects, varying from ulceration to hair loss probably resulting from contact with the cage.An increased incidence of skeletal variations, suggestive of a slight developmental delay was seen in the foetuses of rats given 1500 mg/kg/day DEA cutaneously; this also produced significant maternal toxicity. No foetal malformations, however, were seen in rats nor in rabbits receiving identical treatment. The foetus of rats given high doses of MEA by gavage, showed an increased rate of embryofoetal death, growth retardation, and some malformations including hydronephrosis and hydroureter. The high doses required to produce these effects bring into question the relevance of this finding to humans. There is some evidence that embryofoetotoxicity and teratogenicity does not occur in rats when MEA is administered by dermal application to the mother.The National Toxicology Program (NTP) concluded that there is clear evidence of liver tumours and some evidence of kidney tumours in mice exposed dermally to DEA over their lifetime. Chronic skin painting studies in mice of both sexes produced liver tumours and an increased incidence of kidney tumours in male mice. The significance of these findings to humans is unclear as DEA is neither genotoxic, mutagenic nor clastogenic, and did not induce tumours in rats or transgenic mice similarly treated. Alkanolamines (especially those containing a secondary amine moiety) may react with nitrites or other nitrosating agents to form carcinogenic N-  nitrosamines. Alkanolamines are metabolised by biosynthetic routes to ethanolamine and choline and incorporated into phospholipids. They are excreted predominantly unchanged with a half-life of approximately one week. In the absence of sodium nitrite, no conversion to carcinogenic N-nitrosamines was observed.Diethanolamine competitively inhibits the cellular uptake of choline, in vitro, and hepatic changes in choline homeostasis, consistent with choline deficiency, are observed in vivo.Many amines are potent skin and respiratory sensitisers and certain individuals especially those described as "atopic" (i.e. those predisposed to asthma and other allergic responses) may show allergic reactions when chronically exposed to alkanolamines.In a study with coconut diethanolamide, the National Toxicology Program (Technical Report Series 479), showed clear evidence of carcinogenic activity in male B6C3F1 mice based on increased incidences of hepatic and renal tubule neoplasms and in female B6C3F1 mice based on increased incidences of hepatic neoplasms. There was equivocal evidence of carcinogenic activity in female F344/N rats based on a marginal increase in the incidence of renal tube neoplasms. These increases were associated with the concentration of free diethanolamine present as a contaminant in the diethanolamine condensate. Exposure to rats to coconut oil diethanolamine condensate by dermal application in ethanol for 2 years resulted in epidermal hyperplasia, sebaceous gland hyperplasia, hyperkeratosis and parakeratosis in males and females and ulcer in females at the site of application. There were increases in the incidences of chronic inflammation, epithelial hyperplasia, and epithelial ulcer in the forestomach of female rats. The severity of nephropathy in dosed female rats were increased. Exposure of mice to coconut oil diethanolamine condensate by dermal application for 2 years resulted in increased incidences of eosinophilic foci of the liver in males. Increased incidences of epidermal hyperplasia, sebaceous gland hyperplasia, and hyperkeratosis in males and females, ulcer in males, and parakeratosis and inflammation in females at the site of application and of follicular cell hyperplasia in the thyroid gland of males and females, were chemical related.  Prolonged or repeated skin contact may cause drying with cracking,irritation and possible dermatitis following.  Unless exposure is prolonged irritation effects are reversible.