Surface Properties of Respirable Silicate and Aluminosilicate Dusts Affecting Bioavailability

Pure respirable quartz is a known pathogenic agent for lung disease. However, for mixed dusts, neither mineralogical nor in vitro cytotoxicity assays unequivocally predict the contribution of quartz to their pathogenic potential.First, although Coal Workers' Pneumoconiosis (CWP) and Progressive Massive Fibrosis (PMF) prevalence have been found to correlate with total respirable coal mine dust exposure, and with coal rank (Attfield and Morring, 1992), epidemiological studies generally have not found the quartz component of coal mine dust as measured by X-ray diffraction or infrared spectroscopy (each of which essentially measures the mass-percent quartz in a bulk sample) to be clear predictors of CWP prevalence or incidence (Walton et al., 1971). Second, the properties which distinguish the extreme fibrogenic potential of quartz are not revealed by conventional in vitro bioassay comparison with other silicate mineral dusts. As an example, quartz and kaolin (aluminosilicate) clay in vitro cytotoxicities are comparable for lavaged primary pulmonary macrophages.The studies discussed here address these two anomalies from a general hypothesis that the pathogenic activity of respired quartz particles is associated with properties of, and interactions with, the particle surfaces. One factor in the expression of toxic activity by a particle surface is the biological availability of that surface. Anomalous lack of correlation of disease prevalence with mass percent quartz in exposures to some mixed composition respirable-sized dusts suggests that individual particle surface features, invisible by bulk sample mass analysis, may alter the biological availability of a fraction of quartz particles in a dust. For pure-surfaced mineral particles, the comparably strong prompt membranolytic activities of quartz and kaolin in vitro suggest that upon deposition of such particles in the lung there must be other interactions with particle surfaces which distinguish quartz. This might be due to toxic surface-associated sites specific to silica, or to interactions of other sites on other mineral particles which affect the biological availability of their toxic functional groups. For example, alurninol groups on clays affect the availability or activity of adjacent silanol groups. Surface activities which distinguish quartz pathogenici ty might be manifest in one or more of the sequential interactions upon deposition in the lung; first with the pulmonary surfactant system, then with extracellular and phagolysosomal enzymatic digestive processes, or with subsequent cytotoxic processes.