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JOHNSON MR MUSCLE HEAVY DUTY CAUSTIC OVEN C MSDS报告[下载][中文版]

Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

JOHNSON MR MUSCLE HEAVY DUTY CAUSTIC OVEN CLEANER

NFPA

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

PRODUCT USE

Application is by spray atomization from a hand held aerosol pack. Household oven cleaner.

SYNONYMS

"household oven cleaner"

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

May form explosive peroxides.
Harmful by inhalation.
Causes severe burns.
Risk of serious damage to eyes.
May impair fertility.
May cause harm to the unborn child.
Extremely flammable.
Risk of explosion if heated under confinement.

POTENTIAL HEALTH EFFECTS

ACUTE HEALTH EFFECTS

SWALLOWED

  The material can produce severe chemical burns within the oral cavity and gastrointestinal tract following ingestion.  Not normally a hazard due to physical form of product.  Considered an unlikely route of entry in commercial/industrial environments.  Ingestion of alkaline corrosives may produce burns around the mouth, ulcerations and swellings of the mucous membranes, profuse saliva production, with an inability to speak or swallow. Both the esophagus and stomach may experience burning pain; vomiting and diarrhea may follow. Epiglottal swelling may result in respiratory distress and asphyxia; shock can occur. Narrowing of the esophagus, stomach or stomach valve may occur immediately or after a long delay (weeks to years). Severe exposure can perforate the esophagus or stomach leading to infections of the chest or abdominal cavity, with low chest pain, abdominal stiffness and fever. All of the above can cause death.  

EYE

  The material can produce severe 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.  Direct eye contact with corrosive bases can cause pain and burns. There may be swelling, epithelium destruction, clouding of the cornea and inflammation of the iris. Mild cases often resolve; severe cases can be prolonged with complications such as persistent swelling, scarring, permanent cloudiness, bulging of the eye, cataracts, eyelids glued to the eyeball and blindness.  

SKIN

  The material can produce severe chemical burns following direct contactwith the skin.  Spray mist may produce discomfort.  Skin contact is not thought to produce harmful health effects (as classified using animal models). Systemic harm, however, has been identified following exposure of animals by at least one other route and the material may still produce health damage following entry through wounds, lesions or abrasions. Good hygiene practice requires that exposure be kept to a minimum and that suitable gloves be used in an occupational setting.  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 of aerosols (mists, fumes), generated by the material during the course of normal handling, may be harmful.  The material can cause respiratory irritation in some persons. The body's response to such irritation can cause further lung damage.  Inhaling corrosive bases may irritate the respiratory tract. Symptoms include cough, choking, pain and damage to the mucous membrane. In severe cases, lung swelling may develop, sometimes after a delay of hours to days. There may be low blood pressure, a weak and rapid pulse, and crackling sounds.  Inhalation of toxic gases may cause:  ·  Central Nervous System effects including depression, headache, confusion, dizziness, stupor, coma and seizures;  ·  respiratory: acute lung swellings, shortness of breath, wheezing, rapid breathing, other symptoms and respiratory arrest;  ·  heart: collapse, irregular heartbeats and cardiac arrest;  ·  gastrointestinal: irritation, ulcers, nausea and vomiting (may be bloody), and abdominal pain.  Material is highly volatile and may quickly form a concentrated atmosphere in confined or unventilated areas. Vapor is heavier than air and may displace and replace air in breathing zone, acting as a simple asphyxiant. This may happen with little warning of overexposure.  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.  WARNING: Intentional misuse by concentrating/inhaling contents may be lethal.  If exposure to highly concentrated solvent atmosphere is prolonged this may lead to narcosis, unconsciousness, even coma and possible death.  Exposure to Hydrocarbons may result in irregularity of heart beat. Symptoms of moderate poisoning may include dizziness, headache, nausea. Serious poisoning can result in decreased respiratory function, this may lead to unconsciousness and death. C4 hydrocarbons are especially dangerous to the nervous system. Inhalation of petroleum gases (partly due to olefin impurities) can induce sleep. Serious cases can result in cyanosis due to reduced oxygen concentration and hence asphyxiation, with symptoms of fast breathing, mental dullness, inco- ordination, poor judgment, nausea and vomiting; leading to unconsciousness and death.  The use of a quantity of material in an unventilated or confined space may result in increased exposure and an irritating atmosphere developing.Before starting consider control of exposure by mechanical ventilation.  

CHRONIC HEALTH EFFECTS

  Ample evidence exists from experimentation that reduced human fertility is directly caused by exposure to the material.  Ample evidence exists, from results in experimentation, that developmental disorders are directly caused by human exposure to the material.  
  Principal route of occupational exposure to the gas is by inhalation.  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.  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.  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.  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.  Chronic solvent inhalation exposures may result in nervous system impairment and liver and blood changes. [PATTYS].  
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