Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

WHITECARE XTRA STRIPPER

NFPA

PRODUCT USE

Heavy duty, multi- purpose floor stripper.

SYNONYMS

"Extra Stripper (misspelling) floor stripper"

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

May form explosive peroxides.
Causes burns.
Risk of serious damage to eyes.
Harmful by inhalation, in contact with skin and if swallowed.

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 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.  At sufficiently high doses the material may be hepatotoxic(i.e. poisonous to the liver).  

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.  This material can cause eye irritation and damage in some persons.  The material may produce severe irritation to the eye causing pronounced inflammation. Repeated or prolonged exposure to irritants may produce conjunctivitis.  

SKIN

  The material can produce chemical burns following direct contactwith the skin.  Skin contact with the material may be harmful; systemic effects may resultfollowing absorption.  This material can cause inflammation of the skin oncontact in some persons.  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.  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.  Not normally a hazard due to non-volatile nature of product.  Inhalation of vapors, aerosols (mists, fumes) or dusts, generated by the material during the course of normal handling, may be harmful.  If exposure to highly concentrated solvent atmosphere is prolonged this may lead to narcosis, unconsciousness, even coma and possible death.  Acute effects from inhalation of high vapor concentrations may be chest and nasal irritation with coughing, sneezing, headache and even nausea.  

CHRONIC HEALTH EFFECTS

  Limited evidence suggests that repeated or long-term occupational exposure may produce cumulative health effects involving organs or biochemical systems.  Asthma-like symptoms may continue for months or even years after exposure to the material ceases. This may be due to a non-allergenic condition known as reactive airways dysfunction syndrome (RADS) which can occur following exposure to high levels of highly irritating compound. Key criteria for the diagnosis of RADS include the absence of preceding respiratory disease, in a non-atopic individual, with abrupt onset of persistent asthma-like symptoms within minutes to hours of a documented exposure to the irritant. A reversible airflow pattern, on spirometry, with the presence of moderate to severe bronchial hyperreactivity on methacholine challenge testing and the lack of minimal lymphocytic inflammation, without eosinophilia, have also been included in the criteria for diagnosis of RADS. RADS (or asthma) following an irritating inhalation is an infrequent disorder with rates related to the concentration of and duration of exposure to the irritating substance. Industrial bronchitis, on the other hand, is a disorder that occurs as result of exposure due to high concentrations of irritating substance (often particulate in nature) and is completely reversible after exposure ceases. The disorder is characterised by dyspnea, cough and mucus production.  There is some evidence that inhaling this product is more likely to cause a sensitization reaction in some persons compared to the general population.  There is some evidence that human exposure to the material may result in developmental toxicity. This evidence is based on animal studies where effects have been observed in the absence of marked maternal toxicity, or at around the same dose levels as other toxic effects but which are not secondary non-specific consequences of the other toxic effects.  Ethylene glycol esters and their ethers cause wasting of the testicles, reproductive changes, infertility and changes to kidney function. Shorter chain compounds are more dangerous. They are also associated with the formation of stones in the urine.  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.  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.