Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

UNIFRAX VARIFORM CASTABLE

NFPA

PRODUCT USE

Refractory castable insulation.

SYNONYMS

"refractory castable insulation", "thermal insulation", "Carbolane Variform", "Carbolane
Varicast", "Variform A", "Variform B", "Variform V14 Fiberfrax Variform", SMF, MMMF

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

Harmful: danger of serious damage to health by prolonged exposure through
inhalation.

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.  Considered an unlikely route of entry in commercial/industrial environments.  Ingestion may result in nausea, abdominal irritation, pain and diarrhea.  

EYE

  There is some evidence to suggest that this material can causeeye irritation and damage in some persons.  The dust may produce eye discomfort and abrasive eye inflammation.  

SKIN

  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.  The material is mildly abrasive and may produce discomfort which results in a temporary skin rash. Discomfort is accentuated by fiber adhering to sweaty skin at higher temperatures.  

INHALED

  There is some evidence to suggest that this material, if inhaled, can irritate the throat and lungs of some persons.  Although inhalation is not thought to produce harmful effects, the material may still produce health damage, especially where pre-existing organ (e.g. liver, kidney) damage is evident. Present definitions of harmful or toxic substances are generally confined to doses producing mortality (death) rather than those producing morbidity (disease, ill-  health).  The dust may produce upper respiratory tract discomfort. Nose and throat discomfort may be transitory. Cutting and trimming may result in fiber dislodgment and dust production.  Inhalation of dust may aggravate a pre-existing respiratory condition such as asthma, bronchitis, emphysema.  

CHRONIC HEALTH EFFECTS

  Principal routes of exposure are by accidental skin and eye contact andinhalation of generated dusts.  Inhalation of dusts containing crystalline silicas may lead to silicosis. Effects are cumulative, with scarring, impairment of breathing, emphysema, and restriction and obstruction of lung function. Chronic symptoms include decreased lung capacity and chest infections. Scarring often does not appear until after many months of exposure, and smoking increases the risk. Silicosis can progress even when exposure is removed. It has been claimed that silicosis can increase the risk of cancer of the lung and bronchi developing. Some jurisdictions require health surveillance be conducted on workers occupationally exposed to crystalline silica.  Inhaled synthetic mineral fibres (SMFs) generally exhibit some level of biopersistence, resisting changes in number, dimension, surface chemistry, chemical composition, surface area and other characteristics, depending on their composition. Alteration to any of these parameters, in turn, alters a fibre's residence in the lung, and as a result, the lung's long- term response to the fibre. Fibres, of sufficiently small length, may undergo macrophage-mediated clearance in the lung. For fibres that are too long to be dealt with by alveolar macrophages, principal alternate clearance mechanisms include translocation to other thoracic compartments, dissolution and/or transverse breakage into shorter segments. In vitro fibre dissolution experiments show a broad range of dissolution rate constants (K.dis = ng/cm2/hr) for the various synthetic vitreous (glass-  like) fibres. For refractory ceramic fibres (RCF) the K.dis is 3 whilst for slag wool the K.dis is greater than 400. In vitro fibre-degradation studies demonstrate a direct relationship between the fibre's rate of leaching (some components dissolve more rapidly than others leaving a depleted silica matrix) and its tendency to undergo transverse fragmentation. Synthetic mineral fibres tend to break transversely in contrast to asbestos which tends to split longitudinally. This is significant for pathogenesis because over a long period of time in the lung, the actual numbers of long asbestos fibre in the lung can increase due to splitting along the long axis whilst the number of long SMFs decrease as a result of splitting along the short axis. Lung clearance by macrophages and the mucociliary escalator has been found, experimentally, to be more efficient for shorter segments.  Fibres which exhibit a rapid rate of leaching and fragmentation in the lung are less biopersistent, even though they may not dissolve completely. Fiber toxicology tends to be dominated by physical characteristics such as shape and length whilst nonfibrous dusts exhibit a chemical origin of toxicity. Early rodent studies found no tumourigenesis as a result of inhalation exposure to several types of fibreglass other than transient lung inflammation that resolved after a brief recovery period. However, hamsters exposed to a special application glass of high durability (475 glass) developed minimal lung fibrosis; one animal out of 125 developed mesothelioma. This is the first published report of permanent lung damage in laboratory animals following inhalation of glass fibre compositions (albeit of a special type). Preliminary results from another study with another high durability glass (E glass) showed fibrosis and pulmonary tumours in rats exposed to high concentrations of inhaled microfibres. (E glass is now produced as a continuous filament that is too thick to be respirable and is no longer available as microfibres). Several studies have demonstrated that glass fibres, insulation glass in particular, clear the lung more rapidly than amosite asbestos. Early inhalation studies of the chronic toxicity of refractory ceramic fibre (RCF1) reported conflicting results. In more recent studies rodents were exposed to four types of RCF (RCF1-4) for 6 hours/day,  5 days/week, at a maximum dose of 30 mg/m3 (test fibres were selected to have dimensions close to 1 um x 20 um); in rats RCF1 induced lung fibrosis, lung tumours (13%) and pleural mesothelioma (1.6%). In hamsters RCF1 induced lung fibrosis, mesothelioma (38%) and no lung tumours. Species related differences also raise the issue of significance of these findings in humans. Early rodent inhalation studies reported no fibrosis or tumours with chronic exposure to mineral wool. More recent studies with two compositions of mineral wool,- rock wool (MMVF21) and slag wool (MMVF22), size selected to have average dimensions of 1 um x 20 um, showed that neither mineral wool was tumourigenic, in rats but that MMVF21 produced minimal lung fibrosis late in the inhalation period. Biopersistence, as represented by 90% clearance rate (T-90), has been shown, experimentally to agree well with toxicity; composition with long-fibre T-90s greater than 200 days were all fibrogenic and all but MMVF21 were associated with tumourigenesis. This relationship can be explained as follows; fibres too thick to be inhaled into the lower lung or short enough to be transported by alveolar macrophages, are quickly cleared from the respiratory tract and will probably produce no other response than transient pulmonary inflammation. Long fibres with diameters less than 3 um are able to penetrate into the lower lung but will become innocuous if they dissolve rapidly, can break transversely into smaller segments that can be cleared by alveolar macrophages and ciliated epithelium. Long thin fibres that reach the lower lung in sufficient quantities will be pathogenic if they do not dissolve or fragment. Surface chemistry may also play a role; In recent rat inhalation studies, E glass fibres but not 475 glass fibres were pathogenic in rats although both appeared to clear from the rat lung at about the same time. However during a year of post-exposure recovery 475 glass fibres underwent significant changes in chemistry due to leaching.