The mechanism and kinetics of the extraction of iron ions from crocidolite asbestos have been investigated over long periods of time (30 days). Various chelators (endogenous, analytical reagents and iron sequestering drugs) have been employed. The various chelators extracted iron to different extents. Their potency was unrelated to the thermodynamic stability constant but appears linked to a sort of fitting of the molecule at the particle surface. The mechanism of extraction reveals a fast release of surface iron followed by slow ion diffusion, whereby iron flows out of the fibres. Substitution of iron by other ions present in the solution causes structural instability and collapse of the silica framework, confirmed by a parallel release of silicon into the supernatant at the end of the process. The surface shrinks and partly loses its original reactivity, however, new layers are progressively brought to the solid-liquid interface. Conversely, when the original fibres were in contact with iron bound to a weak chelator, such as Fe-NTA, the surface acts as a chelating agent and withdraws iron from the complex. This suggests that in vivo iron cycling may continuously take place at the particle surface. Modifications of the redox state of iron, following incubation in deferoxamine, are evident from cyclic voltammetry. Although deprived of iron, the deferoxamine-treated fibres exhibited a higher amount of redox cycling iron ions than the original ones.