Asbestos fibre burden in gallbladder: A case study.

The methods conventionally used to determine the burden of asbestos fibres inhaled/incorporated in lung require chemical digestion of the biological matrix before counting/characterising the inorganic fibrous phases under scanning electron microscopy and energy dispersive spectroscopy (SEM/EDS). Asbestos fibres can also be present in extra-pulmonary organs, and we set out to quantify the fibres in gallbladder. Although the standardised procedure requires approximately 5 × 10-1 g of wet tissue, this amount of tissue is not always available. We applied the procedure on about 9 × 10-4 g of gallbladder from a patient with known environmental and workplace exposure to asbestos. The patient died of malignant pleural mesothelioma and was also affected by severe bile-tract problems. The traditional procedure of digesting tissue samples in NaClO and filtering the resulting suspension was carried out. The filter was then examined under SEM/EDS using two methods 1. following the standardised procedure to assess the fibre burden in lung by investigating only 2 mm2 of the filter (660 microscopic fields), and 2. analysing all the microscopic fields in one-quarter of the filter (about 82 mm2). In parallel, histological sections (prepared in the usual way for medical diagnosis) were analysed without digestion or manipulation of the sample using variable pressure SEM/EDS. The fibre counts obtained using the two methods were of the same order of magnitude, i.e., ∼105 fibres/g of wet tissue. We showed that the counting of fibres in human tissue may be successfully carried out even when a limited amount of tissue is available. We also found that, when exposure to asbestos is considerable, the number of asbestos fibres accumulating in the gallbladder may be significant.

Biological effects and comparative cytotoxicity of thermal transformed asbestos-containing materials in a human alveolar epithelial cell line.

Asbestos fibres can be transformed into potentially non-hazardous silicates by high-temperature treatment via complete solid-state transformation. A549 cells were exposed to standard concentrations of raw cement asbestos (RCA), chrysotile and cement asbestos subjected to an industrial process at 1200 degrees C (Cry_1200 and KRY.AS, respectively), raw commercial grey cement (GC). Cell growth rate and viability (MTT test) were detected in vitro. RCA and KRY.AS subjected to comprehensive microstructural study by electron microscopy were further in vitro assayed to compare their cytotoxic potential by morphostructural studies, proliferation index (Ki-67 antigen), apoptosis induction (AO/EB staining) assays and detection of intracellular reactive oxygen species (ROS) with the fluorescent DCFA dye. More severe cytotoxic damage was induced by RCA than by KRY.AS after each incubation period. Exposure to KRY.AS and GC resulted in comparable cell growth rates and cytotoxic effects. Cells incubated with RCA showed greater apoptotic induction and ROS production and a lower cell proliferation index than those exposed to KRY.AS. Chrysotile asbestos and RCA subjected to heat treatment underwent complete microstructure transformation. The final product of heat treatment of cement asbestos, KRY.AS, was considerably more inert and had lower cytotoxic potential than the original asbestos material in all in vitro tests.

Assessment of cancer risks due to environmental exposure to asbestos.

In a rural area widespread pollution of friable and non-friable waste products was present, used to harden dirt tracks, yards, and driveways during 1935-1974. Exposure to environmental asbestos was assessed by a site approach, based on number of polluted sites within postal code areas, and by a household approach, based on number of households in the close vicinity to polluted sites within postal code areas. Based on asbestos soil investigations, 293 sites were identified with asbestos waste material at the surface, of which 77% contained crocidolite fibres as well as chrysotile fibres. The 293 sites-at-risk varied from 5 m(2) to 2722 m(2) and were surrounded by 347 households within 100 m of these sites. Distance to the plant was associated with the number of sites (r=0.36), and with the number of households (r=0.52). However, categorization of postal code areas into low, intermediate or high likelihood of exposure to asbestos showed a modest agreement between the site and household approach. In the site approach a total of 2.3 million person-years at risk were estimated with an average exposure of 1674 fibres/m(3) and an expected 1.8 cases of malignant mesothelioma each year. The household approach resulted in estimates of 1.2 million person-years at risk, and 0.9 cases of malignant mesothelioma per year, respectively. This study illustrates that asbestos waste on the surface of roads and yards in an area with over 130,000 inhabitants may result in long-term exposure to asbestos that will cause several cases of malignant mesothelioma each year. Although distance to plant, number of polluted sites and number of exposed household were associated, the modest agreement among these measures of exposure indicate that the exposure assessment strategy chosen in a particular study may result in considerable misclassification. Without detailed information on individual behaviour within the polluted area, it is difficult to show that a more individually oriented approach will perform better than an ecological approach.