WATTYL SIGMA HULLRITE HARDENER
Flammability | 2 | |
Toxicity | 2 | |
Body Contact | 3 | |
Reactivity | 1 | |
Chronic | 3 | |
SCALE: Min/Nil=0 Low=1 Moderate=2 High=3 Extreme=4 |
Hardener or Part B of a 2 pack. epoxy coating system. Requires that the two parts be mixed
by hand or mixer before use, in accordance with manufacturers directions. Mix only as much
as is required. Do not return the mixed material to the original containers. 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.
Irritating to skin.
Risk of serious damage to eyes.
Limited evidence of a carcinogenic effect.
HARMFUL - May cause lung damage if swallowed.
Harmful by inhalation and in contact with skin.
Flammable.
Harmful to aquatic organisms.
Accidental ingestion of the material may be damaging to the health of the individual. Overexposure to non-ring alcohols causes nervous system symptoms. These include headache, muscle weakness and inco-ordination, giddiness, confusion, delirium and coma. Digestive symptoms may include nausea, vomiting and diarrhea. Aspiration is much more dangerous than ingestion because lung damage can occur and the substance is absorbed into the body. Alcohols with ring structures and secondary and tertiary alcohols cause more severe symptoms, as do heavier alcohols. Not a likely route of entry into the body in commercial or industrial environments. The liquid may produce considerable gastrointestinal discomfort and be harmful or toxic if swallowed. Ingestion may cause nausea, pain and vomiting. Vomit entering the lungs by aspiration can cause inflammation of the lungs, which can lead to death. 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. Ingestion of amine epoxy-curing agents (hardeners) may cause severe abdominal pain, nausea, vomiting or diarrhea. The vomitus may contain blood and mucous. If death does not occur within 24 hours there may be an improvement in the patients condition for 2-4 days only to be followed by the sudden onset of abdominal pain, boardlike abdominal rigidity or hypo- tension; this indicates that delayed gastric or esophageal corrosive damage has occurred.
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. 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. The material may produce severe irritation to the eye causing pronounced inflammation. Repeated or prolonged exposure to irritants may produce conjunctivitis.
Skin contact with the material may be harmful; systemic effects may resultfollowing absorption. The material may cause moderate inflammation of the skin either following direct contact or after a delay of some time. Repeated exposure can cause contact dermatitis which is characterized by redness, swelling and blistering. Toxic effects may result from skin absorption. Exposure limits with "skin" notation indicate that vapor and liquid may be absorbed through intact skin. Absorption by skin may readily exceed vapor inhalation exposure. Symptoms for skin absorption are the same as for inhalation. Contact with eyes and mucous membranes may also contribute to overall exposure and may also invalidate the exposure standard. 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.
Inhalation of vapors or aerosols (mists, fumes), generated by the material during the course of normal handling, may be harmful. Headache, fatigue, lassitude, irritability and gastrointestinal disturbances (e.g., nausea, anorexia and flatulence) are the most common symptoms of xylene overexposure. Injury to the heart, liver, kidneys and nervous system has also been noted amongst workers. Transient memory loss, renal impairment, temporary confusion and some evidence of disturbance of liver function was reported in three workers overcome by gross exposure to xylene (10000 ppm). One worker died and autopsy revealed pulmonary congestion, oedema and focal alveolar haemorrhage. Volunteers inhaling xylene at 100 ppm for 5 to 6 hours showed changes in manual coordination reaction time and slight ataxia. Tolerance developed during the workweek but was lost over the weekend. Physical exercise may antagonise this effect. Xylene body burden in humans exposed to 100 or 200 ppm xylene in air depends on the amount of body fat with 4% to 8% of total absorbed xylene accumulating in adipose tissue. The material can cause respiratory irritation in some persons. The body's response to such irritation can cause further lung damage. If exposure to highly concentrated solvent atmosphere is prolonged this may lead to narcosis, unconsciousness, even coma and possible death. Xylene is a central nervous system depressant.
There has been 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 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. Exposure to the material for prolonged periods may cause physical defects in the developing embryo (teratogenesis). Chronic solvent inhalation exposures may result in nervous system impairment and liver and blood changes. [PATTYS]. 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. 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. Prolonged or repeated contact with xylenes may cause defatting dermatitis with drying and cracking. Chronic inhalation of xylenes has been associated with central nervous system effects, loss of appetite, nausea, ringing in the ears, irritability, thirst anaemia, mucosal bleeding, enlarged liver and hyperplasia. Exposure may produce kidney and liver damage. In chronic occupational exposure, xylene (usually mix ed with other solvents) has produced irreversible damage to the central nervous system and ototoxicity (damages hearing and increases sensitivity to noise), probably due to neurotoxic mechanisms. Industrial workers exposed to xylene with a maximum level of ethyl benzene of 0.06 mg/l (14 ppm) reported headaches and irritability and tired quickly. Functional nervous system disturbances were found in some workers employed for over 7 years whilst other workers had enlarged livers. Xylene has been classed as a developmental toxin in some jurisdictions. Small excess risks of spontaneous abortion and congenital malformation were reported amongst women exposed to xylene in the first trimester of pregnancy. In all cases, however, the women were also been exposed to other substances. Evaluation of workers chronically exposed to xylene has demonstrated lack of genotoxicity. Exposure to xylene has been associated with increased risks of haemopoietic malignancies but, again, simultaneous exposure to other substances (including benzene) complicates the picture. A long-term gavage study to mixed xylenes (containing 17% ethyl benzene) found no evidence of carcinogenic activity in rats and mice of either sex.