RECORD STATUS: None CITATION: Health Council of the Netherlands Gezondheidsraad. Asbestos diseases: asbestosis. The Hague: Health Council of the Netherlands/Gezondheidsraad (GR). 1999/04. 1999

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BACKGROUND: The carcinogenic effect of asbestos is accepted for lung cancer and mesothelioma, while conflicting opinions exist for other cancer sites. The aim of the present investigation is to study cause-specific mortality of women compensated for asbestosis who had certainly been exposed to high levels of asbestos fibers. METHODS: The cause-specific mortality of all Italian women compensated for asbestosis and alive December 31, 1979, was investigated through October 30, 1997. In the total cohort, which included 631 subjects, 277 deaths occurred. Cause-specific SMRs (Standardized Mortality Ratio) were computed using the national rates for comparison. RESULTS: A significantly increased mortality for all diseases related to asbestos exposure was observed. Mortality for all causes, all neoplasms, lung cancer, uterine cancer, ovarian cancer, and non-neoplastic respiratory diseases was significantly increased. Separate analyses for textile (n = 276) and asbestos-cement (n = 278) workers were performed. Women employed in the textile industry, mainly exposed to chrysotile, who are compensated at a younger age, showed higher SMRs for lung cancer and asbestosis. Women in the asbestos-cement industry, mainly exposed to crocidolite containing asbestos mixtures, experienced higher mortality for pleural malignancies. CONCLUSIONS: The role of asbestos exposure in the development of gastrointestinal and genital neoplasms is discussed.

The aim of the study was to assess the risk of asbestos-related malignancies among persons with diagnosed asbestosis. The study covered a cohort composed of 907 men and 490 women afflicted by asbestosis, diagnosed is 1970-1997. The follow-up of the cohort continued until 31 December 1999. In all, 421 deaths were registered and causes of death were retrieved for 93.3% of the deceased. A significantly increased mortality was observed both in the male 1300 deaths; SMR = 127; 95%CI: 113-142) and female (121 deaths, SMR = 150; 95%CI: 124-179) cohorts. The elevated number of deaths in the male and female cohorts were noted mainly due to respiratory diseases (men: 42 deaths; SMR = 344; 95%CI: 248-465; women: 20 deaths, SMR = 789; 95%CI: 482-1219) malignant neoplasms (men: 91 deaths, SMR = 146; 95%CI: 118-179; women: 34 deaths, SMR = 159; 95%CI: 110-222), including lung cancer (men: 39 deaths, SMR = 168; 95% CI: 119-230; women: 13 deaths, SMR = 621; 95%CI: 331-1062) and pleural mesothelioma (men: 3 deaths, SMR = 2680; 95%CI: 553-7832; women: 3 deaths, SMR = 7207; 95%CI: 1031-14612). Taking into account a cumulative dose of fibers, it was found that a significantly increased mortality from lung cancer and pleural mesothelioma applied to persons exposed to a dose above 25 f-y/ml. The results indicate that persons with asbestosis are at higher risk of developing malignant neoplasms, especially lung cancer and mesothelioma.

Annual chest radiographs, work history and mortality of 1,973 workers in an asbestos-cement factory were correlated with age and with duration and level of dust exposure. Degree of radiographic lung change was significantly related to fibre-years of exposure in the case of small lung opacities, pleural adhesions and pleural thickening. For 29 cases of asbestosis diagnosed between 1963 and 1977, a highly significant dose-response relationship was found. In comparison with national mortality rates, there was an excess of deaths due to cancer of the gastrointestinal tract, although there was no relationship to fibre-years.

INTRODUCTION AND METHODS: We investigated the diagnostic and prognostic value of soluble mesothelin-related proteins (SMRP) in sera from patients with newly diagnosed malignant pleural mesothelioma (MPM) (n = 100), MPM patients at tumor relapse (n = 29), primary lung cancer (n = 139), and benign asbestosis (n = 75) using Mesomark--enzyme-linked immunosorbent assay kit (Fujirebio Diagnostics, Malvern, PA). RESULTS: SMRP concentrations were significantly higher in MPM compared with benign asbestosis (p < 0.001) or lung cancer (p < 0.001). The median values were 1.4 nM, 0.9 nM, and 0.8 nM, respectively. The best statistical cutoff was found to be 1.35 nM resulting in a sensitivity of 53% and a specificity of 82.7%. Receiver operating characteristics curves gave an area under curve of 0.72 for the discrimination between MPM and non-MPM patients (p < 0.001). No significant differences in SMRP levels were found among histologies and stages of MPM. The highest median SMRP levels (4.2 nM) were measured in 29 MPM patients with relapse/progression (75.8% > 1.35 nM). Univariately, SMRP discriminated significantly (p < 0.003) between favorable (n = 71, median survival: 17.1 month; 1-year survival: 63.1%) and worse prognosis (n = 20, median survival: 8.4 months, 1-year survival: 32%) at 3.5 nM. In multivariate analysis, histology, therapy, and SMRP were shown to be independent prognostic factors in all MPM patients (hazard ratio for SMRP: 1.96; p = 0.025). Nevertheless, subtype-driven reanalysis showed only a trend in epithelial MPM. CONCLUSION: In conclusion, SMRP add limited information to the diagnosis of MPM. Nevertheless, SMRP might be a useful measure in treatment and monitoring of MPM. The prognostic impact of SMRP in MPM is not conclusive and needs further evaluation.

The clinical and pathoanatomical findings from a 46 year old man with peritoneal mesothelioma in pulmonary asbestosis are described. The tumor arose 13 years after termination of a 10 year professional exposure to asbestos dust. The findings of asbestos bodies in the hilar and tracheobronchial lymph nodes is interpreted as evidence for transport of asbestos bodies in the lymphatic vessels from the lungs to the peritoneal cavity. In the case in question, numerous histological slides showed no asbestos bodies in the tumor tissue itself. The pathogenesis of mesotheliomas following exposure to asbestos is discussed.

Eleven cases of diffuse abdominal tumours in association with exposure to asbestos were discovered in the years 1958 to 1963. There were eight men and three women, all of whom had worked at the same factory. In seven of the men the age at death ranged from 38 to 78 years; one man is still alive at the age of 46. The women died at 44, 61, and 67. The survival time after the first exposure varied from 20 to 46 years. The shortest period of exposure was 10 months and the longest 32 years. All three of the main commercial types of asbestos had been involved in their working operations. Histological confirmation of the nature of the tumour has been obtained at necropsy in nine of the 10 deceased and at biopsy in six, including the survivor. A remarkable feature of these cases is the minimal fibrosis found in the lungs. In three men and one woman, asbestosis was not diagnosed during life, and no patient was completely disabled by pulmonary fibrosis.

OBJECTIVES: A recent review or meta-analysis of epidemiologic studies concluded that persons with asbestos-related pleural plaques do not have an increased risk of lung cancer in the absence of parenchymal asbestosis. The reviewer inferred that this conclusion provided indirect supportive evidence for the proposition that asbestosis is a necessary precursor of asbestos-related lung cancer. The objective of the present communication is to contest these claims. METHODS: Finnish epidemiologic data and population statistics were used to estimate the apparent risk ratio of lung cancer associated with radiographic signs of pleural plaques. Power calculations were applied to compute the needed population sizes to demonstrate that the association is statistically significant. RESULTS: Unrealistically large population studies would be needed to observe the statistical relation between pleural plaques and lung cancer, quantitated as a risk ratio of 1.1, resulting from relatively low levels of environmental asbestos exposure. In realistic and valid epidemiologic studies on heavily exposed subpopulations, a two- or threefold risk can be identified. CONCLUSIONS: Uninformative studies should not be interpreted as providing suppressive evidence that pleural plaques are a noncausal risk indicator of lung cancer. Even for the null hypothesis, the inference that asbestosis is a necessary causal link between asbestos and lung cancer is illogical.

The patient had been employed in an asbestos factory for four years from the age of 16. Five years ago, she complained of sputum and cough, and she was treated for chronic bronchitis. From March, 1977, when she was 53 years old, hydrothorax and ascites increased, her weight decreased and she was hospitalized for cachexia. The clinical diagnosis of malignant diffuse mesothelioma was made on the presence of atypical cells in the effusions. Atypical cells showed a positive colloidal iron staining test and positive hyaluronidase digestion test. Asbestos bodies were found in the sputum. The patient died on February 1978. Postmortem confirmed asbestosia and mesothelioma which was scattered over the pleura, pericardial sac, diaphragma, peritoneum and pancreas. In addition, bronchiolo-alveolar cell type lung cancer was found localized in the lower lobe of the left lung. The electron beam diffraction disclosed the asbestos as amosite (brown asbestos).