Over 2,000 new cases of Mesothelioma are diagnosed each year in the United States (making up about 3 % of all cancer diagnoses).  The more research that is dedicated to finding a cure for this disease, the better.  One interesting study is called, "A Meta-Analysis of Colorectal Cancer and Asbestos Exposure" by David M. Horna, David H. Garabrant, and Brenda W. Gillespie -  American Journal of Epidemiology Vol. 139, No. 12: 1210-1222.  Here is an excerpt: "A meta-analysis of the relation between asbestos exposure and colorectal cancer mortality was conducted, using published reports of 20 asbestos-exposed cohorts. Summary standardized mortality ratios (SMRs) for colorectal cancer were examined in relation to asbestos type and estimates of dust exposure (as direct estimators of asbestos exposure) and in relation to lung cancer SMR and the proportion of all deaths due to mesothelioma (as proxy estimators of asbestos exposure). An elevated summary SMR was observed in cohorts exposed to amphibole asbestos (summary SMR = 1.47; 95% confidence interval (Cl) 1.09–2.00), but not in cohorts exposed to serpentine asbestos (summary SMR = 1.04; 95% Cl 0.81–1.33) or in cohorts exposed to both serpentine and amphibole asbestos (summary SMR = 1.03; 95% Cl 0.74–1.42). Cohorts having a lung cancer SMR greater than 2.00 had a summary SMR of 1.51 (95% Cl 1.29–1.76), and cohorts in which more than 1 % of all deaths were attributed to mesothelioma had a summary SMR of 1.24 (95% Cl 0.94–1.64), After stratifying the cohorts based on mortality due to all cancers excluding those known or suspected to be associated with asbestos exposure, lung cancer mortality was not clearly associated with colorectal cancer mortality, suggesting that the crude association between these factors may be due to misdiagnosis of lung cancer as other types of cancer in the reported causes of death. These results suggest that exposure to amphibole asbestos may be associated with colorectal cancer, but these findings may reflect an artifact of miscertification of cause of death. The results also suggest that serpentine asbestos is not associated with colorectal cancer."

A second study is called, "Association of Cigarette Smoking and Asbestos Exposure with Location and Histology of Lung Cancer" by BURTON W. LEE, JOHN C. WAIN, KARL T. KELSEY, JOHN K. WIENCKE, and DAVID C. CHRISTIANI - Am. J. Respir. Crit. Care Med., Volume 157, Number 3, March 1998, 748-755.  Here is an excerpt: "Prior studies have suggested that lung cancers that arise in association with cigarette smoking favor an upper-lobe location while those associated with asbestos exposure favor a lower-lobe location. An excess of adenocarcinomas has also been reported among cases not exposed to cigarette smoke as well as among those exposed to asbestos. However, these studies typically have not adjusted adequately for potential confounders such as the patient's age, sex, race, or family history of cancer. To better examine the effects of cigarette smoking and asbestos exposure on location and histology of lung cancer, we analyzed data from a large case-control study that included 456 patients with stage I or II lung cancer. Patients with upper-lobe tumors tended to have had more exposure to tobacco as assessed by pack-years smoked (54.7 versus 46.2, p = 0.07) and less time since quitting smoking (3.0 versus 5.5 yr, p = 0.05). In contrast to some prior reports, asbestos exposure was also associated with an upper-lobe location of tumor. Among those with upper-lobe tumors, 14.6% had a history of significant asbestos exposure compared with 5.4% of those with lower-lobe tumors (p < 0.01). The relationship between asbestos exposure and upper-lobe location of tumor was also statistically significant whether stratified by smoking or analyzed by multivariable logistic regression modeling. Adenocarcinomas were more likely among those with less exposure to cigarette smoke based on fewer pack-years smoked (41.5 versus 61.8, p = 0.0001) and more time since quitting smoking (5.0 versus 3.0 yr, p = 0.02). The proportion of patients with significant exposure to asbestos was lower among those with adenocarcinomas but was not statistically significant (9.5 versus 15.3%, p = 0.09). In multivariable logistic regression analysis, longer time since smoking exposure remained a significant predictor of adenocarcinomas (p < 0.02), but history of asbestos exposure did not predict tumor histology. Thus, in patients with lung cancer, both cigarette smoking and asbestos exposure histories favor an upper-lobe location of tumor. Longer time since smoking exposure favors adenocarcinomas, but the history of asbestos exposure does not appear to influence the tumor histology."

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Asbestos is a naturally occurring mineral that was widely used in a variety of products.  Asbestos only becomes dangerous when it is broken into small pieces that become airborne.  When these small pieces of asbestos dust are inhaled they settle into the lungs and can cause life threatening diseases.  One interesting study is called, "Screening for asbestos-induced diseases in Finland" by Kari Koskinen, MD, Jouko-Pekka Rinne, MD, Anders Zitting, MD, Antti Tossavainen, DTech, Jukka Kivekäs, MD, Kari Reijula, MD, Pekka Roto, MD, MIH, Matti S. Huuskonen, MD, MSc - Finnish Institute of Occupational Health, Helsinki, Finland - American Journal of Industrial Medicine - Volume 30 Issue 3, Pages 241 – 251.  Here is an excerpt: "Abstract - Screening for asbestos-induced diseases in Finland was carried out in 1990-1992 as a part of the Asbestos Program of the Finnish Institute of Occupational Health. The aim of the present study was to find the workers who had developed an asbestos-induced disease in certain occupations. Examination of active or retired workers included a personal interview on work history and asbestos exposure, and a chest X-ray. The target group for the screening comprised workers under 70 years of age who had worked at least for 10 years in construction, 1 year in a shipyard or in the manufacture of asbestos products. A preliminary questionnaire was sent to 54,409 workers, 18,943 of whom finally participated in the screening examination. The mean age of the workers was 53 years; 95% were employed in construction, 2% in shipyards, and 3% in the asbestos industry. The criteria for a positive screening result were (1) a radiographic finding clearly indicating lung fibrosis (at least ILO category 1/1), (2) a radiographic finding indicating mild lung fibrosis (ILO category I/O) with unilateral or bilateral pleural plaques, (3) marked abnormalities of the visceral pleura (marked adhesions with or without pleural thickening), or (4) bilateral pleural plaques. The positive cases totalled 4,133 (22%) and were sent for further investigation. In addition to the screening, information on the presence of asbestos in the work environment, prevention of asbestos exposure, as well as on the health effects of asbestos exposure and smoking were given to the participating workers. The screening acted as a preliminary survey to prompt further national follow-up of asbestos-induced diseases among the workers who have been exposed to asbestos. This article presents the material, methods, and overall results of the screening.  

A second study is called, "Clara cell protein (CC-16) and surfactant-associated protein A (SP-A) in asbestos-exposed workers." By Lesur O, Bernard AM, Bégin RO - Unité de Recherche Pulmonaire, Université de Sherbrooke, Québec, Canada.  Chest. 1996 Feb;109(2):467-74.  Here is an excerpt: "Abstract - Asbestos-exposed workers (Asb) can sometimes develop lung impairments resembling idiopathic pulmonary fibrosis (IPF). Smoking is often a troubling confounder in the natural history of these lung diseases. Distal airspace epithelial cells, which are also altered in asbestosis, secrete Clara cell protein (CC-16, also designated CC-10) and surfactant-associated protein A (SP-A). By inhibiting phospholipase A2 (PLA2), CC-16 and SP-A are putative candidates for controlling lung inflammatory events. Both were measured with PLA2 activity in alveolar fluids (and sera for CC-16) of smoker and nonsmoker Asb and compared with smoking-matched normal subjects (N). CC-16 (in mg/L) was slightly increased in Asb and affected by smoking: nonsmoker Asb: 3.1 +/- 0.5 vs nonsmoker N: 1.9 +/- 0.2 (p < 0.05), smoker Asb: 1.7 +/- 0.3 vs smoker N: 0.6 +/- 0.1 (p < 0.05). SP-A (in microgram/mL) was enhanced in Asb but not affected by smoking: 5.4 +/- 1.5 in Asb vs 1.6 +/- 0.4 in N (p < 0.05), whereas SP-A to phosphorus ratio was increased in Asb but affected by smoking. CC-16 to albumin and CC-16 in serum to alveolar fluid ratios were altered by cigarette consumption in Asb (p < 0.05 vs N). Secretory PLA2 activity was slightly enhanced in Asb (p < 0.05 vs N). All data were similar between stages of disease. In summary, alveolar CC-16, SP-A, and secretory PLA2 activity were increased in Asb. Smoking affected several parameters. By this habit, Asb might reinforce lung profibrotic factors and increase their risk in developing lung alterations resembling IPF."

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When pieces of asbestos are inhaled or swallowed, they can lead to life threatening diseases.  To date, over 730,000 people have filed claims for asbestos related injuries in the United States alone. One interesting study that examples the link between exposure and Mesothelioma disease is called, "Analysis of asbestos fibers and asbestos bodies in tissue samples from human lung. An international interlaboratory trial." by Gylseth B, Churg A, Davis J.M., Johnson N, Morgan A, Mowe G, Rogers A, Roggli V. - Scand J Work Environ Health. 1985 Apr;11(2):107-10.  Here is an excerpt: "Abstract - In order to compare methods of counting asbestos fibers in lung tissue, seven laboratories participated in an interlaboratory trial in which tissue samples from five human lungs were analyzed. In some laboratories, fiber concentrations were assessed with the light microscope and, in others, with either scanning or transmission electron microscopes. Within each laboratory the ranking of the results was similar, but there were marked differences in the absolute values obtained by the different laboratories. It is concluded that the laboratories participating in this trial appear to produce internally consistent results, but there is difficulty in directly comparing results from one laboratory to the next."

A second study is called, "Reduced Fhit protein expression and loss of heterozygosity at FHIT gene in tumours from smoking and asbestos-exposed lung cancer patients." By Pylkkanen L, Wolff H, Stjernvall T, Tuominen P, Sioris T, Karjalainen A, Anttila S, Husgafvel-Pursiainen K.  Int J Oncol. 2002 Feb;20(2):285-90.  Here is an excerpt: "Abstract - The FHIT gene, at 3p14.2, has been suggested to form a molecular target to damage induced by human lung carcinogens. We examined aberrant expression of the Fhit protein and allele loss at the FHIT gene in a series of lung cancer cases, mainly of non-small cell carcinoma (NSCLC) histology. We had detailed data on tobacco smoke exposure and occupational asbestos exposure available for the cases. The principal aim of the present study was to investigate whether absent or reduced Fhit expression or FHIT allele loss was associated with exposure to these pulmonary carcinogens. We detected reduced Fhit expression in 62% (33/53) of the cases analysed. Prevalence of allele loss at the FHIT locus was 22% (20/89). Reduced protein expression was common both in the asbestos-exposed (67%) and non-exposed cases (59%); [odds ratio (OR) 1.4, 95% confidence interval (CI) 0.4-4.9]. LOH frequencies differed somewhat between the two groups and were 25% vs. 16%, respectively (OR 1.8; 95% CI 0.5-5.9). Absent or reduced expression was common in smokers, with no significant difference found between current smokers and non-smokers (mainly former smokers) (OR 1.4, 95% CI 0.5-4.5). NSCLCs with squamous cell histology exhibited both aberrant [removed]OR 3.1, 95% CI 0.9-10.3) and allele loss (OR 3.3, 95% CI 0.9-12.7) more frequently than adenocarcinoma. Finally, we found that FHIT allele loss was increased in stage II or more advanced disease (OR 2.5, 95% CI 0.9-7.4), and in poorly differentiated tumours (grade 3, OR 2.6, 95% CI 0.8-8.1). In conclusion, our present data support significance of FHIT inactivation in development of lung cancer."

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