Asbestos
is a commercial term indicating six natural silicates
with asbestiform crystal habit. Of these, five are double-chain silicates
(amphibole) and one is a layer silicate (serpentine asbestos or chrysotile).
Although all species are classified as human carcinogens, their degree
of toxicity is still a matter of debate. Amphibole asbestos species
are biopersistent in the human lungs and exert their chronic toxic
action for decades, whereas chrysotile is not biopersistent and transforms
into an amorphous silica structure prone to chemical/physical clearance
when exposed to the acidic environment created by the alveolar macrophages.
There is evidence in the literature of the toxicity of chrysotile,
but its limited biopersistence is thought to explain the difference
in toxicity with respect to amphibole asbestos. To date, no comprehensive
model describing the toxic action of chrysotile in the lungs is available,
as the structure and toxic action of the product formed by the biodissolution
of chrysotile are unknown. This work is aimed at fulfilling this gap
and explaining the toxic action in terms of structural, chemical,
and physical properties. We show that chrysotile’s fibrous
structure induces cellular damage, mainly through physical interactions.
Based on our previous work and novel findings, we propose the following
toxicity model: inhaled chrysotile fibers exert their toxicity in
the alveolar space by physical and biochemical action. The fibers
are soon leached by the intracellular acid environment into a product
with residual toxicity, and the dissolution process liberates toxic
metals in the intracellular and extracellular environment.