Many have examined the association between asbestos exposure and disease development such as mesothelioma or lung cancer.  Some factors that are strongly associated with cellular abnormalities are increased age, being male, and working for certain employers during a certain time period.

One important study is called, "Radiographic abnormalities and exposure to asbestos-contaminated vermiculite in the community of Libby, Montana, USA." By Lucy A. Peipins, Michael Lewin, Sharon Campolucci, Jeffrey A. Lybarger, Aubrey Miller, Dan Middleton, Christopher Weis, Michael Spence, Brad Black, and Vikas Kapil - Environmental Health Perspectives, Vol. 111, 2003.  Here is an excerpt: "Mining, handling, processing, and personal or commercial use of asbestos-contaminated vermiculite have led to widespread contamination of the Libby, Montana, area. We initiated a medical testing program in response to reports of respiratory illness in the community. The purpose of this analysis was to identify and quantify asbestos-related radiographic abnormalities among persons exposed to vermiculite in Libby and to examine associations between these outcomes and participants' self-reported exposures. A cross-sectional interview and medical testing were conducted in Libby from July through November 2000 and from July through September 2001. A total of 7,307 persons who had lived, worked, or played in Libby for at least 6 months before 31 December 1990 completed the interview. Of those, 6,668 participants [greater than or equal to] 18 years of age received chest radiographs to assess the prevalence of pleural and interstitial abnormalities.

We observed pleural abnormalities in 17.8% of participants and interstitial abnormalities in < 1% of participants undergoing chest radiography. We examined 29 occupational, recreational, household, and other exposure pathways in the analysis. The prevalence of pleural abnormalities increased with increasing number of exposure pathways, ranging from 6.7% for those who reported no apparent exposures to 34.6% for those who reported [greater than or equal to] 12 pathways. The factors most strongly associated with pleural abnormalities were being a former W.R. Grace worker, being older, having been a household contact of a W.R. Grace worker, and being a male. In addition to being a former W.R. Grace worker, environmental exposures and other nonoccupational risk factors were also important predictors of asbestos-related radiographic abnormalities."

Another interesting study is called, "Asbestos causes translocation of p65 protein and increases NF-kappa B DNA binding activity in rat lung epithelial and pleural mesothelial cells." By Y. M. Janssen, K. E. Driscoll, B. Howard, T. R. Quinlan, M. Treadwell, A. Barchowsky, and B. T. Mossman - Department of Pathology, University of Vermont, Burlington, USA. - Am J Pathol. 1997 August; 151(2): 389–401.   Here is an excerpt:
"The mechanisms of cell signaling and altered gene expression by asbestos, a potent inflammatory, fibrogenic, and carcinogenic agent, are unclear. Activation of the transcription factor, nuclear factor (NF)-kappa B, is critical in up-regulating the expression of many genes linked to inflammation and proliferation. Inhalation models of crocidolite- and chrysotile-induced inflammation and asbestosis were used to study the localization of p65, a protein subunit of the NF-kappa B transcription factor, in sham control rats and those exposed to asbestos. In addition, we investigated, using electrophoretic mobility shift analysis, whether in vitro exposure of rat lung epithelial cells and rat pleural mesothelial cells to asbestos increased binding of nuclear proteins, including p65, to the NF-kappa B DNA response element. Furthermore, translocation of p65 into the nucleus was determined by confocal microscopy. In comparison with sham animals, striking increases in p65 immunofluorescence were observed in airway epithelial cells of rats at 5 days after inhalation of asbestos. These increases were diminished by 20 days, the time period necessary for development of fibrotic lesions. In contrast, although inter-animal variability was observed, immunoreactivity for p65 was more dramatic in the interstitial compartment of asbestos-exposed rat lungs at both 5 and 20 days. Changes in p65 expression in pleural mesothelial cells exposed to asbestos in inhalation experiments were unremarkable. Exposure to asbestos also caused significant increases in nuclear protein complexes that bind the NF-kappa B consensus DNA sequence in both rat lung epithelial and rat pleural mesothelial cells. Using confocal microscopy, we observed partial nuclear translocation of p65 in rat pleural mesothelial cells exposed to asbestos. This partial response contrasted with the effects of lipopolysaccharide, which caused rapid and complete translocation of p65 from cytoplasm to nucleus. Our studies are the first to show the presence of the NF-kappa B system in lung tissue and evidence of activation in vitro and in vivo after exposure to a potent inflammatory, fibrinogenic, and carcinogenic environmental agent."

If you found any of these excerpts interesting, please read the studies in their entirety.  We all owe a great debt to these researchers for their important work.