JOHNSON SOLUTIONS CENTER 8: WASHROOM CLEANER & DISINFECTAN
Flammability | 1 | |
Toxicity | 2 | |
Body Contact | 4 | |
Reactivity | 1 | |
Chronic | 3 | |
SCALE: Min/Nil=0 Low=1 Moderate=2 High=3 Extreme=4 |
Washroom cleaner and disinfectant.
Causes burns.
Risk of serious damage to eyes.
May cause CANCER by inhalation.
Harmful by inhalation, in contact with skin and if swallowed.
Very toxic to aquatic organisms.
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. The material can produce chemical burns within the oral cavity and gastrointestinal tract following ingestion. There is some evidence to suggest that this material can cause, if swallowed once, irreversible damage of organs. The material can produce severe chemical burns within the oral cavity and gastrointestinal tract following ingestion. Concentrated solutions of many cationics may cause corrosive damage to mucous membranes and the esophagus. Nausea and vomiting (sometimes bloody) may follow ingestion. Serious exposures may produce an immediate burning sensation of the mouth, throat and abdomen with profuse salivation, ulceration of mucous membranes, signs of circulatory shock (hypotension, labored breathing, and cyanosis) and a feeling of apprehension, restlessness, confusion and weakness. Weak convulsive movements may precede central nervous system depression. Erosion, ulceration, and petechial hemorrhage may occur through the small intestine with glottic, brain and pulmonary edema. Death may result from asphyxiation due to paralysis of the muscles of respiration or cardiovascular collapse. Fatal poisoning may arise even when the only pathological signs are visceral congestion, swallowing, mild pulmonary edema or varying signs of gastrointestinal irritation. Individuals who survive a period of severe hypertension may develop kidney failure. Cloudy swelling, patchy necrosis and fatty infiltration in such visceral organs as the heart, liver and kidneys shows at death. Concentrated solutions of cationic surfactants may cause destruction of the tissue lining the mouth, throat and gullet, and may cause nausea and vomiting. In sufficient quantity may produce restlessness, confusion, low blood pressure, muscle weakness, collapse, convulsion, labored breathing, blue coloration of the lips and coma. Death may occur in 1- 4 hours. Fatal dose is estimated at 1-3 grams for certain cationics.
The material can produce chemical burns to the eye following direct contact. Vapors or mists may be extremely irritating. 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. The material may produce moderate eye irritation leading to inflammation. Repeated or prolonged exposure to irritants may produce conjunctivitis.
The material can produce chemical burns following direct contactwith the skin. Skin contact with the material may damage the health of the individual; systemic effects may result following absorption. The material can produce severe chemical burns following direct contactwith the skin. 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.
The material can cause respiratory irritation in some persons. The body's response to such irritation can cause further lung damage. The material is not thought to produce adverse health effects following inhalation (as classified using animal models). Nevertheless, adverse effects have been produced following exposure of animals by at least one other route and good hygiene practice requires that exposure be kept to a minimum and that suitable control measures be used in an occupational setting. Inhalation of vapours may cause drowsiness and dizziness. This may be accompanied by narcosis, reduced alertness, loss of reflexes, lack of coordination and vertigo. The material may produce respiratory tract irritation, and result in damage to the lung including reduced lung function.
On the basis of epidemiological data, it has been concluded that prolonged inhalation of the material, in an occupational setting, may produce cancer in humans.
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. There has been some concern that this material can cause cancer or mutations but there is not enough data to make an assessment. 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 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. Respiratory sensitization may result in allergic/asthma like responses; from coughing and minor breathing difficulties to bronchitis with wheezing, gasping. Injection of EDTA and it salts can cause severe kidney damage with tissue death and internal bleeding, bone marrow depression and critically low levels of calcium.