One group that has been profoundly impacted by asbestos are iron workers. In fact, they have one of the highest rates of mesothelioma of any trade group because the use of asbestos was so ubiquitous during their work day. Exposure resulted in a variety of ways. Workers could inhale asbestos paint that was sprayed onto the iron beams. They could also inhale asbestos dust during sanding or drilling. Even some of their clothing was made from asbestos materials.

If we are ever going to find a cure for mesothelioma or lung cancer, we are going to need to fully fund medical research and raise public awareness. One interesting study is called, "Asbestos, chromosomal deletions, and tumor suppressor gene alterations in human malignant mesothelioma" by Siva S. Murthy, and Joseph R. Testa - Program of Molecular Oncology, Fox Chase Cancer Center, Philadelphia, Pennsylvania. Funded by: National Cancer Institute; Grant Number: CA-45745, CA-06927 - Commonwealth of Pennsylvania. Here is an excerpt: " Abstract - Exposure to the carcinogen asbestos is considered to be a major factor contributing to the development of most malignant mesotheliomas (MMs). We highlight the role of asbestos in MM and summarize cytogenetic and molecular genetic findings in this malignancy.

The accumulation of numerous clonal chromosomal deletions in most MMs suggests a multistep process of tumorigenesis, characterized by the loss and/or inactivation of multiple tumor suppressor genes (TSGs). Cytogenetic and loss of heterozygosity (LOH) analyses of MMs have demonstrated frequent deletions of specific sites within chromosome arms 1p, 3p, 6q, 9p, 13q, 15q, and 22q. Furthermore, TSGs within two of these regions, i.e., p16/CDKN2A-p14ARF at 9p21 and NF2 at 22q12, are frequently altered in MMs. Homozygous deletion appears to be the major mechanism affecting p16/CDKN2A-p14ARF, whereas inactivating mutations coupled with allelic loss occur at the NF2 locus. Finally, recent studies have demonstrated the presence and expression of simian virus 40 (SV40) in many MMs. SV40 large T antigen has been shown to inactivate the TSG products Rb and p53, suggesting the possibility that asbestos and SV40 could act as cocarcinogens in MM. The frequent occurrence of homozygous deletions of p16/CDKN2A-p14ARF and the ability of SV40 Tag to bind TSG products suggest that perturbations of both Rb- and p53-dependent growth-regulatory pathways are critically involved in the pathogenesis of MM. J. Cell. Physiol. 180:150-157, 1999. © 1999 Wiley-Liss, Inc."

Another interesting study is called, "Asbestos induces selective release of lysosomal enzymes from mononuclear phagocytes" by Philip Davies, Anthony C. Allison, Jill Ackerman, Ann Butterfield and Susan Williams. - Division of Cell Pathology, MRC Clinical Research Centre, Watford Road, Harrow, Middlesex HA1 3UJ, UK. Here is an excerpt: "THE association of asbestos inhalation and lung disease has been recognised for many years1. Asbestosis is a chronic inflammatory reaction in the terminal bronchioles and alveoli of the lung with considerable fibrosis leading to distortion and eventual obliteration of the alveoli. There is also an association between asbestosis and the development of bronchogenic cancer2 and Wagner et al. 3 have noted the occurrence of diffuse pleural and peritoneal mesotheliomas in individuals occupationally exposed to asbestos dust and in experimental animals following intrapleural injection of asbestos."

If you found either of these excerpts helpful, please read them in their entirety.