Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

UNIFRAX FIBERFRAX DURAFLEX

NFPA

PRODUCT USE

Thermal insulation.

SYNONYMS

"thermal insulation", "AL 1300", "aluminosilicate vitreous fibres", "Carbolane Flexiform",
"Duraboard FX", "Ceramic Fibre", "Refractory Fibre", MMVF, SMF

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

Limited evidence of a carcinogenic effect.
Harmful: danger of serious damage to health by prolonged exposure through
inhalation.
Irritating to eyes, respiratory system and skin.

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.  

EYE

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

SKIN

  This material can cause inflammation of the skin oncontact in some persons.  Skin contact is not thought to have harmful health effects, however the material may still produce health damage following entry through wounds, lesions or abrasions.  Irritating to skin.  

INHALED

  If inhaled, this material can irritate the throat andlungs 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).  Not normally a hazard due to non-volatile nature of product.  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.  Irritating to respiratory system.  

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.  

  Principal routes of exposure are by accidental skin and eye contact andinhalation of generated dusts.  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.  As with any chemical product, contact with unprotected bare skin; inhalation of vapor, mist or dust in work place atmosphere; or ingestion in any form, should be avoided by observing good occupational work practice.  Limited evidence of a carcinogenic effect.