Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

LAURYL SULFATE, MONOETHANOLAMINE SALT

NFPA

PRODUCT USE

Anionic surfactant.

SYNONYMS

C12-H26-O4-S.C2-H7-N-O, C12-H26-O4-S.C2-H7-N-O, "sulfuric acid, monododecyl ester,
compounded with 2-aminoethyl (1:1)", "sulfuric acid, monododecyl ester, compounded with
2-aminoethyl (1:1)", "ethanolamine dodecyl sulfate", "sulfuric acid mono C10-16 alkyl
esters with ethanolamine", "monoethanolamine lauryl sulfate", Empicol

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

Irritating to eyes, respiratory system and skin.

POTENTIAL HEALTH EFFECTS

ACUTE HEALTH EFFECTS

SWALLOWED

  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.  Ingestion of anionic surfactants may produce diarrhea, bloated stomach,and occasional vomiting.  

EYE

  This material can cause eye irritation and damage in some persons.  The material may produce moderate eye irritation leading to inflammation. Repeated or prolonged exposure to irritants may produce conjunctivitis.  Direct eye contact with some anionic surfactants in high concentration can cause severe damage to the cornea. Low concentrations can cause discomfort, excess blood flow, and corneal clouding and swelling. Recovery may take several days.  

SKIN

  This material can cause inflammation of the skin oncontact in some persons.  The liquid may produce skin discomfort following prolonged contact. Defatting and/or drying of the skin may lead to dermatitis.  The material may cause severe 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. Repeated exposures may produce severe ulceration.  Anionic surfactants can cause skin redness and pain, as well as a rash. Cracking, scaling and blistering can occur.  Repeated skin contact with some sulfonated surfactants has produced sensitization dermatitis in predisposed individuals.  

INHALED

  If inhaled, this material can irritate the throat andlungs of some persons.  Inhalation hazard is increased at higher temperatures.  Inhalation of vapor may aggravate a pre-existing respiratory condition.  Exposure to Sulfonates can cause an imbalance in cellular salts and therefore cellular function. Airborne sulfonates may be responsible for respiratory allergies and, in some instances, minor dermal allergies.  

CHRONIC HEALTH EFFECTS

  Principal routes of exposure are usually by skin contact/absorption and inhalation of vapor.  There is some evidence that inhaling this product is more likely to cause a sensitization reaction in some persons compared to the general population.  Alkyl-substituted sulfonates are thought to induce genetic mutations in cells.  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.