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TALLOW ALKYL/ ISOPROPANOLAMINE-N-DIPROPYLAM MSDS报告[下载][中文版]

Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

TALLOW ALKYL/ ISOPROPANOLAMINE-N-DIPROPYLAMIDE DERIVATIVE

NFPA

Flammability 1
Toxicity 2
Body Contact 3
Reactivity 1
Chronic 2
SCALE: Min/Nil=0 Low=1 Moderate=2 High=3 Extreme=4

PRODUCT USE

Ore flotation. Asphalt emulsifier. Corrosion inhibitor. Petroleum product additive

SYNONYMS

"2-propanol, 1-[bis(3-aminopropyl)amino]-N-tallowalkyl derivatives", "2-propanol, 1-
[bis(3-aminopropyl)amino]-N-tallowalkyl derivatives", "N-dipropylamineisopropanolamine
fatty acid polyamides", "N-dipropylamineisopropanolamine fatty acid polyamides", "tallow
alkanolamine"

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

Causes burns.
Risk of serious damage to eyes.

POTENTIAL HEALTH EFFECTS

ACUTE HEALTH EFFECTS

SWALLOWED

  The material can produce chemical burns within the oral cavity and gastrointestinal tract following ingestion.  Accidental ingestion of the material may be damaging to the health of the individual.  Amines without benzene rings when swallowed are absorbed throughout the gut. Corrosive action may cause damage throughout the gastrointestinal tract. They are removed through the liver, kidney and intestinal mucosa by enzyme breakdown.  Nonionic surfactants may produce localized irritation of the oral or gastrointestinal lining and induce vomiting and mild diarrhea.  

EYE

  The material can produce chemical burns to the eye following direct contact. Vapors or mists may be extremely irritating.  If applied to the eyes, this material causes severe eye damage.  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

  The material can produce chemical burns following direct contactwith the skin.  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.  Volatile amine vapors produce irritation and inflammation of the skin. Direct contact can cause burns. They may be absorbed through the skin and cause similar effects to swallowing, leading to death. The skin may exhibit whiteness, redness and wheals.  Open cuts, abraded or irritated skin should not be exposed to this material.  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*.  If inhaled, this material can irritate the throat andlungs of some persons.  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 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.  Inhalation of quantities of liquid mist may be extremely hazardous, even lethal due to spasm, extreme irritation of larynx and bronchi, chemical pneumonitis and pulmonary edema.  

CHRONIC HEALTH EFFECTS

  Repeated or prolonged exposure to corrosives may result in the erosion of teeth, inflammatory and ulcerative changes in the mouth and necrosis (rarely) of the jaw. Bronchial irritation, with cough, and frequent attacks of bronchial pneumonia may ensue. Gastrointestinal disturbances may also occur. Chronic exposures may result in dermatitis and/or conjunctivitis.  Limited evidence suggests that repeated or long-term occupational exposure may produce cumulative health effects involving organs or biochemical systems.  There is limited evidence that, skin contact with this product is more likely to cause a sensitization reaction in some persons compared to the general population.  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.  
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