Chemical research in toxicology | 2019
Structure model and toxicity of the product of bio-dissolution of chrysotile asbestos in the lungs.
Abstract
Asbestos is a commercial term indicating six natural silicates with asbestiform crystal habit. Of these, five are double-chain silicates (amphibole) and one (serpentine asbestos or chrysotile) is a layer silicate. Although all species are classified as human carcinogens, their degree of toxicity is still 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 it transforms into an amorphous silica structure prone to chemical/physical clearance when exposed to an 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 metastable product formed by the bio-dissolution of chrysotile are unknown. This work is aimed at fulfilling this gap and to explain the toxic action in terms of structural, chemical and physical properties. We show that chrysotile s fibrous metastable 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 bio-chemical action. The fibers are soon leached by the intracellular acid environment into a metastable product with residual toxicity, and the dissolution process liberates toxic metals in the intracellular and extracellular environment.