# Mineral Fibres and Asbestos Bodies in Human Lung Tissue: A Case Study
## 3 Results and Discussion
### Comparison with Literature Data  
In the last forty years, several studies focused on asbestos fibres found in lung tissue [52]. One of the universally accepted \"reference texts\" on this topic is [PERSON] et al. [53]. According to the so-called \"[PERSON] hypothesis\", carcinogenic asbestos fibres are longer than 8.0 \(\upmu\)m and thinner than 0.25 \(\upmu\)m (see Figure 4). Following that model, needle-shaped fibres with \"Stanton size\" cannot be removed by phagocytic cells like macrophages [53; 54], triggering the typical asbestos-induced patho-biological mechanisms (i.e., generation of free radicals, cell and DNA damage, chronic inflammatory reaction, delivery of chemical carcinogens) [15]. Of the amphibole fibres investigated in our work, 75% met the length criteria proposed by the [PERSON] hypothesis, whereas 50% were thicker than the \"Stanton-size thickness\". However, as mentioned above, these models are based on in vivo animal studies and are not always suitable for the study of human biomechanisms. In order to accurately identify the dimension of asbestos fibres that are biopersistent in the human lung, [PERSON] and [PERSON] [55] recently examined a wide range of morphologic data for asbestos fibres recovered from lungs of 91 human subjects. A statistically representative processing of this dataset indicated that the majority of amosite and crocidolite fibres that persisted in the lungs after being inhaled have L \(>\) 10 \(\upmu\)m and W \(<\) 1.0 \(\upmu\)m [55]. In general, amphibole fibres observed in our investigation met the width criteria proposed by [PERSON] and [PERSON] [55], but only 30% of the amphibole fibres had L \(<\) 10 \(\upmu\)m. As suggested by [PERSON] and [PERSON] [55], these shorter fibres (L \(<\) 10 \(\upmu\)m) should be classified as elongate cleavage fragments with little or no pathogenic effect. This hypothesis is also supported by the work of [PERSON] and [PERSON] [56] that through the statistical processing of the literature data showed that fibres with L \(>\) 10 \(\upmu\)m contribute most heavily to both asbestos-induced lung cancer and mesothelioma. However, there are still conflicting opinions on this issue and to date there are no conclusive studies proving the non-toxicity or non-pathogenicity of elongate cleavage fragments [57]. The findings of [PERSON] and [PERSON] [55] also confirm the difference between the size of crocidolite and amosite fibres observed in our investigations. Amosite fibres were systematically longer than crocidolite fibres, whereas crocidolite fibres were 30% thinner than amosite fibres.  
As proposed by several studies [18; 22; 55; 58] and confirmed by our results, the fibre length plays a key role in the development of ABs (Figure 4). ABs nucleate only at the surface of fibres longer than the Stanton size (Figure 4), which cannot be engulfed by human alveolar macrophages (generally assumed to have a size of \(\sim\)21 \(\upmu\)m [59]). These long fibres lead to frustrated phagocytosis and the release of highly reactive cyto- and genotoxic substances into the extracellular space. The formation of ABs represents the product of the exocytotic activity of macrophages aimed at the isolation of these reactive fibres [37]. However, the results of our investigation further suggest that the width of the fibres is also a controlling factor for the formation of ABs. Specifically, only very thin fibres (W \(<\) 0.5 \(\upmu\)m) were coated, and the average width of these coated fibres (0.25 \(\upmu\)m) has exactly the same value as that of Stanton-size fibres (Figure 4). It should be noted that some differences found between our results and those obtained in the in vivo tests with rats can be attributed to the intrinsic differences between human and other animal cells. For instance, the size of the phagocytes is species-dependent [59; 60] and this can undoubtedly influence the formation of ABs.