Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

KODAK FIXER & DEVELOPER MIXED - WASTE

NFPA

PRODUCT USE

Waste product from the mixture of Kodak photographic fixer and developer solutions.

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

May cause SENSITIZATION by inhalation and skin contact.
Limited evidence of a carcinogenic effect.
Possible risk of irreversible effects.
Harmful by inhalation and if swallowed.
Irritating to eyes, respiratory system and skin.
Toxic to aquatic organisms.

POTENTIAL HEALTH EFFECTS

ACUTE HEALTH EFFECTS

SWALLOWED

  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.  

EYE

  This material can cause eye irritation and damage in some persons.  

SKIN

  This material can cause inflammation of the skin oncontact in some persons.  The material may accentuate any pre-existing dermatitis condition.  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 be harmful.  The material can cause respiratory irritation in some persons. The body's response to such irritation can cause further lung damage.  

CHRONIC HEALTH EFFECTS

  There has been concern that this material can cause cancer or mutations, but there is not enough data to make an assessment.  Inhaling this product is more likely to cause a sensitization reaction in some persons compared to the general population.  Skin contact with the material is more likely to cause a sensitization reaction in some persons compared to the general population.  Exposure to the material may result in a possible risk of irreversible effects. The material may produce mutagenic effects in man. This concern is raised, generally, on the basis ofappropriate studies using mammalian somatic cells in vivo. Such findings are often supported by positive results from in vitro mutagenicity studies.  Limited evidence suggests that repeated or long-term occupational exposure may produce cumulative health effects involving organs or biochemical systems.  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.  Respiratory sensitization may result in allergic/asthma like responses; from coughing and minor breathing difficulties to bronchitis with wheezing, gasping.  Sulfites and bisulfites can cause narrowing of the airways, stomach upset, flushing, low blood pressure. tingling sensation, itchy wheal, swelling and shock, and asthmatics are especially prone. They induce allergic-like reactions which can occur on first contact with the material.  Repeated exposure of animals to airborne sulfur dioxide (SO2) can produce a thickening of the mucous layer in the trachea and an increase in goblet cells and mucous glands similar to pathological changes found in chronic human bronchitis.  Chronic exposure to sulfur dioxide (SO2) particulate complexes, present in polluted air, have been associated with the aggravation of chronic cardiovascular diseases such as asthma, chronic pulmonary disease, and coronary artery disease (this may occur at levels of 6-10 ug/m3 for 24 hours), An association exists between persistent cough and sputum production, particularly in women and non-smokers. A 10-year follow study on workers exposed to a mean sulfur dioxide concentration of up to 33 ppm did not reveal an increased prevalence of chronic respiratory disease or decreased pulmonary function.  By contrast, studies of smelter workers, exposed to concentrations below 2 ppm, suggest that chronic respiratory disease may develop and that workers exposed at concentrations exceeding 1 ppm show accelerated loss of pulmonary function.  Although SO2 is not a carcinogen, the apparent increases in mortalities amongst arsenic-  exposed smelter workers was greater when exposures included both high arsenic concentrations and moderate to high SO2 exposures, suggesting that SO2 might act as a promoter.  Intermittent exposure of rats to benz[a]pyrene along with inhalation of SO2 at 4-10 ppm, 1-6 hours per day, 5 days per week, produced substantial increases in respiratory tract squamous cell carcinomas compared to that associated with exposure to B[a]P or SO2 alone.