The toxicology of chrysotile which rapidly falls apart in the lung into many small particles can best be understood in comparison to
other non-fibrous minerals, while that of amphibole asbestos is clearly a response to the insoluble fibrous structure of this mineral.
Chrysotile is mineralogically distinct from the amphiboles with a very different chemical structure. This structure leads to the ability of the lung to decompose the chrysotile fibers once inhaled as seen in the biopersistence studies of commercial chrysotiles.
The chronic inhalation toxicity studies that have been performed on chrysotile in animals have unfortunately been performed at very high exposure concentrations and so under conditions of lung overload. In consequence their relevance to human exposures is extremely limited.
Chrysotile following subchronic inhalation at a mean exposure of 76 Wbers L > 20 m/cm3 (3413 total Wbers/cm3) resulted in no fibrosis (Wagner score 1.8–2.6) at any time point and no difference with controls in BrdU response or biochemical and cellular parameters. The long chrysotile fibers were observed to break apart into small particles and smaller fibers.
The value of the present and other similar studies is that they show that low exposures to pure chrysotile do not present a detectable risk to health. Since total dose over time decides the likelihood of disease occurrence and progression, they also suggest that the risk of an adverse outcome may be low if even any high exposures experienced were of short duration.