Investigation of Crystalline Phases in Silica Fume

Silicosis is a debilitating lung disease, believed to be caused by the inhalation of crystalline silica.  Despite intervention in exposure of workers over many decades, silicosis is still recognised internationally as a major occupational disease of special concern.  Because of the ongoing health problems associated with silicosis, it appears that simply measuring airborne levels of crystalline silica using the standard occupational hygiene techniques may not in all situations provide the information necessary to assess and manage silicosis risks in industries.  One of the issues that have been controversial for many years relates to the possible link between amorphous silica and silicosis.   

Silica fume, generally described as amorphous silica, is likely to be associated with the development of fibrotic effects in exposed individuals.  If microcrystalline phases were present in thermally generated silica fume, this might lead to the development of silicosis.  Microcrystalline phases are however difficult to detect with routine X-ray diffraction in the ultrafine matrix.  It may therefore be possible that silica fume that appears to be amorphous in occupational hygiene surveys, might have the potential to cause silicosis because it contains a small proportion of crystalline silica.  In order to further clarify this issue, this SIMRAC study was initiated to confirm whether crystalline phases could in fact be present in silica fume and if so, at what levels.  Furthermore, the role of the ultrafine nature of silica fume in its overall toxicity was considered to require better clarification.  

Samples of airborne silica fume were collected on filters at various locations in a typical silicon smelter plant.  Collected particles were transferred to carbon grids and used for transmission electron microscopic (TEM) analyses of particle sizes, crystallinity and of the composition of crystalline phases.  The TEM techniques used were bright field (to count particles), conical dark field (to determine the crystallinity of the particles) and EDS (energy dispersive spectroscopy) to evaluate the composition of the crystalline particles. 

The transmission electron microscopy evidence presented in this report leaves no doubt that crystalline particles are present in silica fume that forms when oxygen is bubbled through molten silicon.  The concentration of crystalline particles was low (less than 1 per cent of silica particles were crystalline), but its potential impact on the development of lung fibrosis should not be dismissed.  Particle sizes were not quantitatively characterised, but a general estimate could be made from evidence on the electron microscopy photographs.  The needle-shaped crystalline particles were approximately 200 nm and less in length and approximately 20 nm wide.  Amorphous silica fume particles in all of the samples were smoothly spherical in shape and the diameter appeared to be almost exclusively in the order of 100 nm and less.  This places silica fume clearly in the category of ultrafine particles.    
In humans, occupational exposure to amorphous silica generally did not show a silicotic effect.  In most cases in the literature where silicosis was reported after exposure to amorphous silica, it was acknowledged that exposures were mixed, with both amorphous and crystalline silica being present in the dusts/fumes.  A major limitation in most of the studies is that exposure levels were not known accurately and, where dust levels were measured, the crystalline content was uncertain.  Furthermore, many of the studies considered other types of amorphous silica, and not silica fume.  It is, however, clear that even small contaminations of crystalline silica in the order of 0.1 per cent of the total amorphous content, is known to result in fibrotic effects. 
Clinical diagnoses of lung fibrosis and decreased lung function parameters were described for uncontaminated amorphous silica in the occupational setting.  Inflammatory responses such as bronchitis, airway obstruction and emphysema were described, but the importance of confounders has not been sufficiently quantified.   
More recent work on ultrafine particles has added to the evidence that ultrafine particles clearly have respiratory effects that include inflammatory responses, while amorphous silica exposure can clearly result in lung fibrosis.  The aetiology of silicosis involves both of these physiological processes.  It is possible that co-exposure to ultrafine particles might sensitise the lung to silicotic effects by stimulating recruitment and activation of inflammatory cells and the amplified release of fibrogenic factors, preparing the scene for low concentrations of crystalline particles to trigger a silicotic effect.  The dose-effect relationship for the development of silicosis under such conditions is not known, and it is therefore difficult to estimate an appropriate occupational exposure threshold level.  It has now been confirmed unambiguously, however, that small concentrations of crystalline silica can be present in amorphous silica under certain process conditions, and this fact should affect the overall interpretation of the association between exposure to silica fume and the potential for development of silicosis.    
The current scientific understanding of the fibrogenic effects of ultrafine amorphous silica fume, irrespective of the potential for development of silicosis, also suggests a re-assessment of the guidelines that have been promulgated in the interest of protection of occupational health.  The fibrogenic effects associated with exposure to amorphous silica fume may be transient, but they still classify as adverse.  Both the U.S. National Institute for Occupational Safety and Health (NIOSH) and the U.S. Occupational Safety and Health Administration (OSHA) have set guidelines for various amorphous forms of silica, but not for silica fume per se.  The ACGIH occupational exposure guideline for silica fume is 2 mg/m3, but certain specialists have questioned this guideline.  The German Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area has set a guideline (MAK) value of 0.3 mg/m3 for fine dust for several forms of amorphous silica together.  The guideline concentration used in South Africa for assessment of exposure to respirable amorphous SiO2 is 3 mg/m3, which is actually at the level recommended for diatomaceous earth in the ACGIH TLVs.  There appears to be insufficient justification to retain this guideline in view of the available evidence on adverse health effects of ultrafine silica fume.  It is therefore apparent from this SIMRAC study that the occupational exposure guideline for amorphous silica fume should be reassessed.  Setting a new guideline has to follow a specific regulatory process, and has to be initiated by the Department of Minerals and Energy.   
PDF icon SIM 02-06-01 Final Report.pdf11.73 MB