Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

TALL OIL DIETHANOLAMIDE

NFPA

PRODUCT USE

Foam booster, surfactant; widely used in neutralised, diluted form in products such as
hair shampoos.

SYNONYMS

"tall oil, reaction products with diethanolamine", "tallate diethanolamide"

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

Harmful if swallowed.
Risk of serious damage to eyes.
Harmful: danger of serious damage to health by prolonged exposure if swallowed.
Irritating to respiratory system and skin.

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.  Considered an unlikely route of entry in commercial/industrial environments.  Ingestion may result in nausea, pain, vomiting. Vomit entering the lungs by aspiration may cause potentially lethal chemical pneumonitis.  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.  The material may produce severe irritation to the eye causing pronounced inflammation. Repeated or prolonged exposure to irritants may produce conjunctivitis.  The material may produce moderate eye irritation leading to inflammation. Repeated or prolonged exposure to irritants may produce conjunctivitis.  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.  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.  

SKIN

  This material can cause inflammation of the skin oncontact in some persons.  Skin contact is not thought to have harmful health effects, however the material may still produce health damage following entry through wounds, lesions or abrasions.  The liquid may produce skin discomfort following prolonged contact. Defatting and/or drying of the skin may lead to dermatitis.  Many amine compounds are sensitizers and some are absorbed through intactskin.  The material may cause skin irritation after prolonged or repeated exposure and may produce on contact skin redness, swelling, the production of vesicles, scaling and thickening of the skin.  

INHALED

  If inhaled, this material can irritate the throat andlungs of some persons.  Although inhalation is not thought to produce harmful effects, the material may still produce health damage, especially where pre-existing organ (e.g. liver, kidney) damage is evident. Present definitions of harmful or toxic substances are generally confined to doses producing mortality (death) rather than those producing morbidity (disease, ill-  health).  Inhalation hazard is increased at higher temperatures.  Inhalation of vapor may aggravate a pre-existing respiratory condition.  

CHRONIC HEALTH EFFECTS

  Principal routes of exposure are usually by skin contact/absorption and inhalation of vapor.  Repeated application of a formulation containing coconut diethanolamide  to rabbit skin produced changes in blood biochemical markers.  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.