Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

UNOCAL "WET" NATURAL GAS

NFPA

PRODUCT USE

Used according to manufacturer' s directions.

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

Toxic by inhalation.
Irritating to eyes and skin.
Extremely flammable.
Toxic to aquatic organisms.
Risk of explosion if heated under confinement.

POTENTIAL HEALTH EFFECTS

ACUTE HEALTH EFFECTS

SWALLOWED

  Not normally a hazard due to physical form of product.  Considered an unlikely route of entry in commercial/industrial environments.  

EYE

  There is some evidence to suggest that this material can causeeye irritation and damage in some persons.  

SKIN

  This material can cause inflammation of the skin oncontact in some persons.  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 vapors or aerosols (mists, fumes), generated by the material during the course of normal handling, may produce toxic effects.  There is some evidence to suggest that the material can cause respiratory irritation in some persons. The body's response to such irritation can cause further lung damage.  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.  Inhalation of vapours may cause drowsiness and dizziness. This may be accompanied by narcosis, reduced alertness, loss of reflexes, lack of coordination and vertigo.  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.  Hydrogen sulfide poisoning can cause increased secretion of saliva, nausea, vomiting, diarrhea, giddiness, headache, vertigo, memory loss, palpitations, heartbeat irregularities, weakness, muscle cramps, confusion, sudden collapse, unconsciousness and death due to paralysis of breathing (at levels above 300 parts per million). The "rotten egg" odor is not a good indicator of exposure since odor fatigue occurs and odor is lost at over 200 ppm. The gas can enter the body through a punctured ear drum and even wearing some respiratory protection. Immediate supportive care is essential. Ensure medical help is addressed as part of the site emergency plan and that employees who may be accidentally exposed are made aware of the existence of such a plan.  

CHRONIC HEALTH EFFECTS

  Principal route of occupational exposure to the gas is by inhalation.  Limited evidence suggests that repeated or long-term occupational exposure may produce cumulative health effects involving organs or biochemical systems.  There is some evidence to provide a presumption that human exposure to the material may result in impaired fertility on the basis of: some evidence in animal studies of impaired fertility in the absence of toxic effects, or evidence of impaired fertility occurring at around the same dose levels as other toxic effects but which is not a secondary non-  specific consequence of other toxic effects.  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.  Although prolonged exposure to carbon dioxide, at levels up to 1.5% in inhaled air, are well tolerated, calcium/ phosphorus metabolism may be affected. Serum levels of calcium and urinary phosphorus progressively fall. Prolonged exposure at 2% concentration, may produce deepened respiration. At 3%, impaired performance is evident. Tolerance may develop however following long exposure to low levels.  Reproductive effects may occur in animals.  Long term low level exposure to hydrogen sulfide may produce headache, fatigue, dizziness,  irritability and loss of sexual desire. These symptoms may also result when exposed to hydrogen sulfide at high concentration for a short period of time.