Exploring Cancer And The Asbestos Burden

The overwhelming majority of experts agree that there is a causal relationship between asbestos exposure the development of cancers such as mesothelioma. One interesting study that explores this issue is called, Asbestos burden and the pathology of lung cancer. By Warnock ML, Isenberg W. - Chest. 1986 Jan;89(1):20-6. Here is an excerpt: Abstract - To determine whether we could distinguish asbestos-related lung cancers from unrelated ones, we typed and quantified by electron-optical methods the asbestos fibers in the lungs of 75 men with lung cancer. All but eight men had some history of asbestos exposure. On the basis of combined amosite and crocidolite (AC) concentrations, we divided the subjects into three groups (AC fibers per gram of dry lung): low (less than 10(5)); intermediate (10(5) to 10(6)); and high (greater than 10(6)). Age, smoking history, latent period, and type and location of tumors were similar in all three groups. Of 62 evaluated subjects, zero of 14 in the low group, seven of 29 in the intermediate group, and five of 19 in the high group had asbestosis. Epidemiologic studies suggest that persons exposed to concentrations of asbestos that can cause asbestosis are at increased risk for lung cancer. Thus, the subjects in our intermediate and high concentration groups may have been at increased risk for cancer, even when they did not have asbestosis. Because large burdens of asbestos do not always cause pulmonary fibrosis, asbestosis may be a poor marker of fiber-related lung cancer.

Another interesting study is called, Two-stage carcinogenesis studies with asbestos in Fisher 344 rats by Topping, D.C. ; Nettesheim, P. - J. Natl. Cancer Inst.; (United States); Journal Volume: 65:3 - 1980 Sep 01. Here is an excerpt: The cocarcinogenic effect of chrysotile asbestos was investigated in heterotopic tracheal transplants of F344 rats. Tracheal transplants were first exposed to graded doses of dimethylbenz(a)anthracene (DMBA) contained in intraluminal pellets. Four weeks after the start of DMBA the spent pellets were removed, and 200 ..mu..g chrysotile, a nontumorigenic dose of asbestos, was introduced into the lumina of the preexposed tracheas. No significant enhancement of the tumor response was seen with 100 ..mu..g DMBA, a dose that was tumorigenic by itself. However, with 50 and 25 ..mu..g DMBA, nontumorigenic dose levels, a 15 and 23% incidence of tracheal carcinomas occurred when DMBA exposure was followed by a nontumorigenic dose of chrysotile. At 12.5..mu..g DMBA, this effect was not observed.

A third study worth examining is called, Changing patterns in asbestos-induced lung disease Chest. 2004 Feb;125(2):744-53. by Ohar J, Sterling DA, Bleecker E, Donohue J. Here is an excerpt: Abstract - STUDY OBJECTIVES: To determine patterns in asbestos-induced lung diseases found in older, less exposed workers. DESIGN: Review of a database evaluating lung function, smoking status, form of asbestos-induced lung disease, and radiograph abnormalities. SETTING: Outpatient clinic. PARTICIPANTS: A total of 3383 asbestos-exposed workers referred for independent medical evaluation, including control subjects who lacked asbestos-specific radiograph abnormalities (n = 243), subjects with low International Labor Organization (ILO) scores (n = 2,685), high ILO scores (n = 312), bronchogenic cancer (n = 63), and mesothelioma (n = 80). Of these, 3,327 workers have specific smoking status information and 3,312 workers have lung volume measures. INTERVENTIONS: Chest radiographs were interpreted by a certified B-reader, and abnormalities were quantified according to the ILO scoring system. Spirometry and lung volume measurement were performed. Subjects completed a self-administered questionnaire that was reviewed at the time of examination. Control subjects were screened on two separate occasions at least 10 years apart to exclude subclinical or slowly progressive asbestos-induced lung disease. MEASUREMENTS AND RESULTS: The mean age of the population was 65.1 +/- 9.9 years, and the latency was 41.4 +/- 10.1 years (+/- SD). Most subjects (41.8%) had normal pulmonary function. Obstruction was the most common pulmonary function abnormality (25.4%), followed by restriction (19.3%) and a mixed pattern (6.0%). Most subjects (79.4%) had low ILO scores. Benign pleural abnormalities were the only findings in 54% of subjects with low ILO score. Subjects with high ILO scores were older, smoked more, and had a longer latency than subjects with low ILO scores and control subjects. Smokers were younger, had a shorter latency, and had paradoxically greater ILO scores than nonsmokers. Subjects with bronchogenic cancer and mesothelioma had longer latencies than control subjects and subjects with benign asbestos-induced lung disease. CONCLUSIONS: Asbestos-induced lung disease today is characterized by low ILO scores, long latencies, greater disease magnitude in smokers, and a normal or obstructive pattern of pulmonary function abnormality. Spirometric evaluation in the absence of lung volume measurements caused misclassification that resulted in overestimation of the presence of a restrictive pattern of pulmonary function.

We all owe a great debt to these fine researchers for doing this important work.

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