Amphiboles - Crocidolite, Amosite

Mesothelioma Cancer Diagnosis

Mesothelioma Diagnosis

Our articles will give you a better understanding of the treatments available for anyone suffering from Mesothelioma.

Mesothelioma is a rare form of cancer. It affects the linings of the cavities around the lungs, stomach, and heart. It is caused by inhaling asbestos fibers, but the cancer usually does not appear until 10 to 40 years after a person first inhales asbestos.

The latest information about Mesothelioma diseases, their diagnoses, causes, treatments and the medical research currently underway to prevent and someday cure Mesothelioma. We want to help those potentially exposed to Mesothelioma to understand which materials contain Mesothelioma causing cancers and how exposures occur.

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Differences in pathogenic potential of fibre types

The results of human epidemiological studies and lung mineral content analyses demonstrate that amphiboles (crocidolite and amosite) are more strongly associated with mesothelioma than is chrysotile. Comparative analysis of fibre durability and chemical composition are helping to explain the greater toxicity of amphiboles.

Of the thousands of asbestos-related mesotheliomas reported, virtually all can be directly attributed to exposure to amphiboles. In his widely cited 1988 review of evidence related to mesothelioma causation, Dr. Andrew Churg found that only 53 cases of chrysotile-related mesothelioma had ever been reported from the tens of thousands of workers studied. Of these, ten cases were observed in secondary industry workers for which there was a strong suspicion of amphibole contamination, and 41 cases have occurred in individuals exposed to chrysotile mine dust, which contained traces of the naturally occurring amphibole; tremolite (Churg, 1988).

Other evidence of the extremely weak association between chrysotile exposure and mesothelioma has been revealed through the cohort study of some 11,000 Quebec chrysotile miners born between 1891 and 1920. The last follow-up of this cohort found that only 37 mesothelioma deaths had been identified among 8,000 deaths from all causes (McDonald et al., 1993). No cases were detected in workers with less than two years of exposure.

In addition, unlike crocidolite mining towns, there has been no indication of environmentally-related mesothelioma in chrysotile mining communities. Also in contrast to amphiboles, the risks to household members of chrysotile workers through non-occupational contact appear to be extremely low, as only 2 or 3 isolated cases allegedly related to this "second hand" exposure have been reported.

According to Churg, the research data indicates that although chrysotile asbestos can produce mesothelioma in man, the total number of such cases is small and the required doses extremely large. Another important factor is that while in general, amphiboles have been shown to cause lung disease and cancer after short but intense exposures, chrysotile-related illness is associated with very high, long-term exposures only.Greater toxicity of amphiboles linked to durability in the lung The greater durability of amphiboles compared to chrysotile appears to be one of the principle reasons for their greater carcinogenic potential.

Many researchers now believe that the longer a foreign substance persists in the body, the more likely it is to cause cellular damage and lead to accelerated cell reproduction and chromosomal damage, which are associated with tumour growth. Contrary to chrysotile fibres, which dissolve relatively quickly, amphiboles persist at sites of tumour development and serve as the stimulus for neoplastic (new tissue) growth (Jaurand, 1979; 1984). Because of chrysotile's rapid dissolution, particularly under conditions of low to moderate exposure, it may not persist in the human body over the extended period necessary for the development of tumours.

Several studies published in the early 1980s were conducted on lung tissue samples from workers whose deaths were considered to be asbestos related and compared to those of control groups. The results showed that the concentrations of amphiboles in their lungs were up to 100 times greater than those found in the control groups - while the amounts of chrysotile observed were similar for the subjects and the controls. Further-more, in asbestotic cases, the amounts of amphiboles, but not of chrysotile, related well quantitatively to the severity of the disease. These differences in biopersistence, according to fibre type, were particularly striking in cases of mesothelioma. For instance, several studies have shown that the mesothelioma cases are correlated with vastly increased lung burdens of amphiboles, but not chrysotile.

The most recent data available on the retention of asbestos fibres in lung tissue of asbestos workers is a Swedish study which shows different kinetics for amphibole and chrysotile fibres in human lung tissue (Albin et al., 1994). Amphibole fibre concentrations increase with duration of exposure, whereas chrysotile concentrations do not. Furthermore, the authors indicate that their study supports a former finding of a possible adaptive clearance of chrysotile, and conclude that they

"support the hypothesis that adverse effects are associated rather with the fibres that are retained (amphiboles), than with the ones being cleared (largely chrysotile).

"Amphiboles, iron and oxygen radicals In addition to the longer biopersistence of amphiboles, their iron-content particles appears to trigger an oxidative stress process - the generation of "Active Oxygen Species"

(AOS), which some researchers believe can cause membrane damage, induce the release of inflammatory compounds, which can lead to fibrosis, and even cause DNA strand breaks, which can lead to lung cancer. AOS production is normally held in check by protective agents and scavenger enzyme mechanisms. However, it is believed that high and sustained generation of AOS can eventually overwhelm scavenger mechanisms and lead to 'oxydative lung injury.'

Thus, studies of the impact of chemical composition on the carcinogenicity of fibrous materials have been undertaken. Iron-containing particles can produce AOS by oxidizing their iron (Guilianelli et al., 1993). Brooke Mossman, of the University of Vermont College of Medicine, suggests that the lower amounts and bio-availability of iron in chrysotile fibres may render them less biologically active over time. Other studies have confirmed the importance of fibre length and geometry in the generation of AOS by alveolar macrophages. Longer fibres such as crocidolite and erionite have been found to generate larger amounts of AOS, whereas short fibres and particles are generally relatively inactive (Hansen & Mossman, 1987).

Albin A, Pooley FD, Stromberg U, Attewell R, Mitha R and Welinder H, (1994) Retention patterns of asbestos fibres in lung tissue among asbestos cement workers. Occup. Environ. Med., 51: 205-211.

Churg, A. (1988) Chrysotile, Tremolite, and Malignant Mesothelioma in Man. Chest, 93: 621-628.

Guilianelli, C et al. Effect of Mineral Particles Containing Iron on Primary Cultures of Rabbit Trachael Epithelial Cells: Possible Implication of Oxidative Stress. Env. Health Persp., 1993; 101.

Hansen, K, Mossman, BT. Generation of superoxide from alveolar macrophages exposed to asbestiform and non-fibrous particles. Cancer Res. 1987;47:1681-6.

Jaurand, MC, Bignon, J, Sebastien, P, & Goni, J. Leaching of chrysotile asbestos in human lungs. Correlation within vitro studies using rabbit alveolar macrophages. Envir. Res. 1979; 14:245-54.

Jaurand, MC, Gaudichet, A, Halpern, S & Bignon, S. In Vitro biodegradation of chrysotile fibres by alveolar macrophages and mesothelial cells in culture: comparison with a pH effect. Br. J. Ind. Med. 1984;41:389-95.

McDonald, JC, Liddell, FD, Dufresne, A and McDonald, AD. The 1891-1920 birth cohort of Quebec chrysotile miners and millers: mortality 1976-88. Br. J. Ind. Med., 1993;60:1073.

Wagner, JC, Slegges, CA and Marchand, P. (1960) Diffuse pleural mesothelioma and asbestos exposure in the North Western Cape Province. Brit. J. Ind. Med. 17:260-271.

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