# Mineral Fibres and Asbestos Bodies in Human Lung Tissue: A Case Study
## 1 Introduction
Moreover, the influence of ABs on the cytotoxicity of asbestos fibres is still a matter of debate [18; 19; 20; 21; 22; 23; 24; 25]. In particular, the potential toxicity of iron associated with ABs should be clarified [6; 9; 18]. The biological activity of mineral fibres is typically assessed by in vitro and in vivo studies [13; 17; 26; 27; 28; 29]. Recently, a comparative study on the biodurability of chrysotile and fibrous crocidolite was conducted using human mesothelial and broncho-alveolar cells [27]. In this study, after 96 h of contact with cell cultures, chrysotile fibres were partially dissolved and amorphised, whereas, after the same exposure time, crocidolite fibres showed very minor signs of amorphisation [27]. In the in vivo studies, dissolution of mineral fibres was monitored after injection (e.g., intratracheal, intraperitoneal) or inhalation in the animals' lungs [17; 28; 29]. [PERSON] et al. [17] reported the results of the first complete and accurate evaluation of biodurability/biopersistence of chrysotile and crocidolite asbestos found in the lung tissue of Sprague-Dawley rats subjected to intraperitoneal/intrapleural injection of fibres. Results of the in situ morpho-chemical evaluation [17] showed that crocidolite fibres display only a very thin amorphous layer after long contact times (93 weeks), whereas the chrysotile fibres are prone to dissolution, with leaching of Mg and production of a silica-rich relict. In vivo tests further showed that formation of asbestos coatings is a common feature in the lungs [9; 18]. ABs always coexist with non-coated fibres, which are invariably more abundant than coated fibres [18]. Most coated fibres seem to be amphibole asbestos [18]. ABs tend to form only on fibres longer than 20 \(\upmu\)m [25], and therefore, the infrequency of ABs forming on chrysotile core is probably due to the fragmentation of longer fibres into shorter fragments [25]. Even if there is a tradition of excellence in the use of animal models to help in understanding the fate of asbestos in the lung environment [17; 18; 19; 20; 21; 22; 23; 24; 25], for human studies the \"gold standard\" is the in vivo _ex post_ lung analysis of human subjects exposed to mineral fibres [6; 30; 31]. In vivo animal studies are of paramount importance for the understanding of asbestos-induced toxicity/pathogenicity, but they are not conclusive because of the differences in the tracheobronchial airway architecture between the rats and humans [32]. In fact, the differences in the lung geometry can lead to variationsin the particle-deposition pattern and hence the site-specific dosage [33]. Moreover, because rats used in in vivo tests have a life of about 3 y, the contact time of the fibres with the organic tissue is not comparable to the theoretical residence time of asbestos in the human lung. The present work reports the results of a combined scanning electron microscope (SEM), transmission electron microscope (TEM), and scanning transmission electron microscope (STEM) study of both fibres and ABs found in the lung tissue of a patient diagnosed with MM who died about 40 y after the first exposure to asbestos. Specifically, the main goals of this study are:  
(i) Assessing the biopersistence in vivo of the asbestos fibres by scrutinising the variation in the degree of crystallinity and chemical composition of the fibres that have remained in the human lung environment for about 40 y;  
(ii) Morphological, chemical and mineralogical characterisation of the ABs found in the lung tissue of the subject. These data are compared with the recently obtained results from an in vivo animal test [16; 17], in order to acquire more information on the nature and growth mechanism of human ABs and to validate the current knowledge, which is mostly based on animal models. These data are of paramount importance to unequivocally assess the effect of dissolution and coating processes on the different asbestos species and to improve our knowledge on the fate of these fibres in the human lungs.