The interaction between healthy cells and exposure to asbestos fibers has been studied in earnest. Unfortunately, the environmental exposure commonly encountered by the certain populations in industrial countries has been unacceptably high. One interesting study on point is called, +Asbestos Fibres in the Lungs of Chrysotile Miners and Millers + a Preliminary Report+ by N. Rowlands, GW Gibbs, and AD McDonald .
Here is an excerpt: +Transmission electron microscope examination of 47 autopsy lung samples from Quebec miners and millers showed that tremolite was present in approximately similar quantities to chrysotile (with crocidolite and amosite in much smaller amounts), although the quantity of tremolite compared with chrysotile in the ore worked was extremely small. These findings suggest to remove chrysotile from the lungs and to retain the tremolite. However, in spite of this removal, it seems that the chrysotile content of lung tissue can serve as an indicator of past exposure. The effect of the interval between exposure and death will be examined later. The design of the study does not permit evaluation of the contribution of tremolite to pulmonary fibrosis in Quebec miners and millers.
A second study entitled mRNA expression patterns in different stages of asbestos-induced carcinogenesis in rats+ by H. Sandhu, W. Dehnen, M. Roller, J. Abel and K. Here is an excerpt: Human malignant mesotheliomas are induced almost exclusively by fibrous dusts. The nature of interactions between fibers and target cells, and the molecular mechanisms leading to tumorigenesis, are not yet understood. Here, the mRNA expression patterns at different stages of asbestos-induced carcinogenesis in rats were monitored by suppression subtractive hybridization (SSH) and array assay. Several genes were upregulated in pretumorous tissues from asbestos-treated rats, in asbestos-induced tumors and in cells treated with asbestos in vitro. The upregulation of the proto-oncogene c-myc, fra-1 and egfr in fiber-induced carcinogenesis was demonstrated at different stages of carcinogenesis. A dose-dependent expression in in mesothelial cells treated with asbestos in vitro substantiates a possible role of Fra-1 as one of the dimeric proteins generating the AP-1 transcription. The upregulation of osteopontin (an extracellular matrix protein) and of zyxin and integrin-linked kinase (intracellular proteins associated with the focal adhesion contact), indicate that fibers may affect integrin-linked signal transduction and extracellular matrix proteins
A third study called “Environmental exposure to asbestos and risk of pleural mesothelioma: review and meta-analysis” by Valirie Bourdis, Paolo Boffetta and Paola Pisani. Here is an excerpt: A number of epidemiological studies have addressed the risk of pleural mesothelioma from environmental (household and neighborhood) exposure to asbestos, but no overall risk estimate is available. The researchers reviewed the epidemiological studies on risk of pleural mesothelioma and household or neighborhood exposure to asbestos then identified eight relevant studies; most were conducted in populations with relatively high exposure levels. The risk estimates in a meta-analysis were combined based on the random-effects model. The relative risks (RRs) of pleural mesothelioma for household exposure ranged between 4.0 and 23.7, and the summary risk estimate was 8.1 (95% confidence interval [CI]: 5.3 12). For neighborhood exposure, RRs ranged between 5.1 and 9.3 (with a single RR of 0.2) and the summary estimate was 7.0 (95% CI: 4.7 11).
If you found any of these excerpts interesting, please read the studies in their entirety.