Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

WORMALD INERGEN

NFPA

PRODUCT USE

Used according to manufacturer' s directions.

SYNONYMS

"inert gases"

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

Risk of explosion if heated under confinement.

POTENTIAL HEALTH EFFECTS

ACUTE HEALTH EFFECTS

SWALLOWED

  Although ingestion is not thought to produce harmful effects, the material may still be damaging to the health of the individual following ingestion, especially where pre-  existing organ (e.g. liver, kidney) damage is evident. Present definitions of harmful or toxic substances are generally based on doses producing mortality (death) rather than those producing morbidity (disease, ill-health). Gastrointestinal tract discomfort may produce nausea and vomiting. In an occupational setting however, ingestion of insignificant quantities is not thought to be cause for concern.  Overexposure is unlikely in this form.  Not normally a hazard due to physical form of product.  Considered an unlikely route of entry in commercial/industrial environments.  

EYE

  Although the material is not thought to be an irritant, direct contact with the eye may produce transient discomfort characterized by tearing or conjunctival redness (as with windburn).  

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 is not thought to produce adverse health effects or skin irritation following contact (as classified using animal models). Nevertheless, good hygiene practice requires that exposure be kept to a minimum and that suitable gloves be used in an occupational setting.  

INHALED

  The material is not thought to produce adverse health effects or irritation of the respiratory tract (as classified using animal models). Nevertheless, good hygiene practice requires that exposure be kept to a minimum and that suitable control measures be used in an occupational setting.  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 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 vapours may cause drowsiness and dizziness. This may be accompanied by narcosis, reduced alertness, loss of reflexes, lack of coordination and vertigo.  Inhalation of non-toxic gases may cause:  ·  CNS effects: headache, confusion, dizziness, stupor, seizures and coma;  ·  respiratory: shortness of breath and rapid breathing;  ·  cardiovascular: collapse and irregular heart beats;  ·  gastrointestinal: mucous membrane irritation, nausea and vomiting.  The material is not thought to produce respiratory irritation (as classified using animal models). Nevertheless inhalation of the material, especially for prolonged periods, may produce respiratory discomfort and occasionally, distress.  Nitrogen is non-toxic but may replace oxygen in the inhaled air producing asphyxiation.  As the amount of inhaled oxygen is reduced from 21% to 14% (by volume), pulse rate and volume of breathing, increase.  Nitrogen inhaled under increased atmospheric pressure (>1.5 atmospheres), may dissolve in fat-containing brain-cells producing anaesthesia and causing narcosis. Individuals exposed to increased pressures for some time and who are suddenly released from the pressure may develop decompression sickness. Repeated exposures, without complete decompression, may result in decompression sickness.  Carbon dioxide is an odourless gas which gives very poor warning of exposure. The gas can produce rapid unconsciousness and death from oxygen deficiency at concentrations of 10% in air. Even concentrations of 3% may produce shortness of breath and headache.  Carbon dioxide is the most powerful cerebral vasodilator known. High levels, even in the presence of sufficient oxygen may produce rapid circulatory insufficiency leading to coma and death.  Continuous exposure to 1.5% carbon dioxide may cause changes in some physiological processes. Increased concentrations of carbon dioxide in blood affect the rate of breathing. Even at low concentrations, regular exposure to carbon dioxide is potentially harmful as a consequence of cellular membrane effects and biochemical alterations; these may result in increased concentration of bicarbonate ions and acidosis.  High concentrations of carbon dioxide (2-10%) may produce an acidic taste, dyspnoea, headache, vertigo, nausea, laboured breathing, weakness, drowsiness, mental confusion, and increased blood pressure, pulse and respiratory rate. Exposure to 10% for a few minutes reportedly produces visual disturbances, tinnitus, tremors, profuse perspiration, restlessness, paraesthaesia, general feeling of discomfort, loss of consciousness, and coma. Concentrations of 25-50% may cause coma and convulsions within one minute. Tachycardia and arrhythmias are possible. Concentrations of 50% may cause symptoms of hypocalcaemia including carpopedal spasms. Excessive carbon dioxide for a period of time (not more than five minutes) was reported to cause visual effects, enlargement of the blind spot, photophobia, loss of convergence and accommodation, and deficient dark adaptation as well as headache, insomnia and personality changes (largely depression and irritability). Even when there is sufficient oxygen present to prevent simple asphyxiation, high concentrations of carbon dioxide may cause adverse effects by interfering with its normal elimination from the body. Initial overexposure to carbon dioxide results in an compensatory increase in both rate and depth of ventilation. Beyond a certain point, however, this may reverse to hypoventilation resulting in respiratory acidosis. Death from asphyxia may occur if the concentration and duration of exposure are sufficient.  

CHRONIC HEALTH EFFECTS

  Principal route of occupational exposure to the gas is by inhalation.  Long-term exposure to the product is not thought to produce chronic effects adverse to the health (as classified using animal models); nevertheless exposure by all routes should be minimized as a matter of course.