Some asbestiform minerals may cause lung disease in humans such as asbestosis, mesothelioma, and lung cancer. Crocidolite, the asbestiform counterpart of the amphibole riebeckite, is particularly dangerous in cases of chronic exposure. Its pathogenic activity may result from the interaction of the fiber surfaces with physiological fluids. Fe removed from the fiber surface by molecular chelators present in the body can promote a series of reactions that yield the hydroxyl radicals (•OH) which are known to cause DNA damage. This breakdown of DNA may be part of the mechanism for crocidolite-induced pathogenesis.

X-ray photoelectron spectroscopy (XPS) and solution chemistry were used to monitor the changes in surface composition of crocidolite fibers in a 50 mM NaCl solution at pH= 7.5 and 25°C in the presence of Fe chelators (citrate, EDTA, or desferrioxamine) for up to 30 days. The data show that the introduction of Fe chelators dramatically increases the rate at which Fe is released from the surface when compared to a control group where no chelators were added. In particular, XPS shows that Fe(III) is more effectively removed in the presence of the chelators.

Past studies of the dissolution of Fe-containing silicates generally indicate that Fe removal is the rate-limiting step. Fe(III) is particularly insoluble under circumneutral conditions. However, our work suggests that crocidolite undergoes enhanced dissolution in the presence of a chelator. Therefore, based on our XPS and solution data, and assuming a typical fiber diameter, we can estimate that a crocidolite fiber will survive on the order of hundreds of years in lung-like conditions. This is at least two orders of magnitude longer than a chrysotile fiber of the same size, and corresponds well with the fiber content observed in human lung tissue.