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Query: UMLS:C0037116 (silicosis)
1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective cohort study in 1794 male ceramic workers in the Netherlands was carried out to analyze the lung cancer risk in relation to crystalline silica exposure and silicosis. They had all been employed for two years or longer in ceramic industries between 1972 and 1982. During a health survey, 124 cases of simple pneumoconiosis were diagnosed; after 14 years of follow-up, 161 deaths had occurred. No increased overall and cause-specific mortality was found in the total group of ceramic workers, and a statistically significant cumulative dose-response relation for silica exposure and lung cancer did not emerge. An excess lung cancer mortality appeared among workers with simple pneumoconiosis. The authors conclude that the disease process resulting in silicosis in the ceramic industry carries an increased risk of lung cancer, which is supportive of a nongenotoxic pathway.
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PMID:Mortality and lung cancer in ceramic workers in The Netherlands: preliminary results. 883 78

The pathogenesis of mesenchymal and epithelial lung reactions was studied after a single intratracheal instillation of quartz into rats. Relationships between transforming growth factor beta1 (TGF-beta1) and the ras and p53 genes were investigated in silicosis and associated lung cancer. Immunohistochemical reactivity to mature TGF-beta1 was localized intracellularly in fibroblasts and macrophages at the periphery of silicotic granulomas and in stroma adjacent to hyperplastic alveolar type II cells and extracellularly in connective tissue matrix adjacent to hyperplastic alveolar type II cells. TGF-beta1 precursor was localized intracellularly in hyperplastic alveolar type II cells adjacent to granulomas and in the cells of adenomas, but not in carcinomas. Hematite-treated controls showed no reactivity to TGF-beta1. Immunohistochemical localization of pan-reactive p21 ras protein in quartz-treated rat lungs was increased in hyperplastic alveolar type II cells adjacent to granulomas, but not in adenomas and carcinomas. Foci of nuclear immunoreactivity to p53 protein were observed in 25% of the carcinomas.
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PMID:Transforming growth factor beta1, ras and p53 in silica-induced fibrogenesis and carcinogenesis. 892 85

A retrospective cohort mortality study was conducted for lung cancer among silica and clay brick workers at 11 refractory plants in China. The cohort included 6266 male workers employed before 1962 and followed between 1963 and 1985. The standardized rate ratios (SRR) were obtained by comparing the mortality rates of the silica-exposed cohort with those of a population of 11 470 male steel workers. As expected, significant excesses were observed for all deaths, all cancers, lung cancer, cardiorespiratory diseases, pulmonary heart diseases, and pulmonary tuberculosis. The lung cancer SRR was 1.49 (P < 0.01) for the total cohort. The increased lung cancer risk was attributed to the silicotics (SRR 2.10; P < 0.01) in the cohort. Higher lung cancer risk was found with increasing latency and severity of silicosis; this finding suggests that the excess was possibly related to occupational exposure to silica dust. Among the silicotics, there was a twofold excess of lung cancer risk among both the nonsmokers and the smokers.
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PMID:Lung cancer among workers exposed to silica dust in Chinese refractory plants. 892 95

Michigan and New Jersey in the United States maintain silicosis disease registers. In 1988-1992, 372 cases of silicosis were confirmed in Michigan, and, in 1979-1992, 288 were confirmed in New Jersey. A proportionate mortality ratio (PMR) analysis was performed on data from 292 deceased silicotics. Increases in PMR values were found for nonmalignant respiratory disease (NMRD) and lung cancer. The PMR values for NMRD were statistically elevated in all the analyses. The overall proportionate cancer mortality ratio (PCMR) for lung cancer was 1.78 [95% confidence interval (95% CI) 1.22-2.61]. For patients having ever smoked cigarettes, the PCMR for lung cancer was 1.82 (95% CI 1.8-2.81). Never smoking silicotics had a lung cancer PCMR of 1.48 (95% CI 0.43-2.86). For those who had never applied for workers' compensation the corresponding PCMR was higher, 2.10 (95% CI 1.21-3.69), than for those who had applied, 1.45 (95% CI 0.70-2.99).
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PMID:Mortality among persons with silicosis reported to disease surveillance systems in Michigan and New Jersey in the United States. 892 96

In 1940-1983, 760 cases of silicosis were identified among male North Carolina (NC) workers in dusty trades. Vital status was ascertained through 1983 for 714 silicotics, and death certificates were obtained for 546 of the 550 decedents. The standardized mortality ratio (SMR) for lung cancer based on United States rates was 2.6 [95% confidence interval (95% CI) 1.8-3.6] for whites, 2.3 (95% CI 1.5-3.4) for whites unexposed to other known occupational carcinogens, and 2.4 (95% CI 1.5-3.6) for whites with no other exposure and diagnosed with silicosis while still employed in dusty trades. In addition, the age- and smoking-adjusted rate for silicotics was 3.9 times higher (95% CI 2.4-6.4) than that of nonsilicotic metal miners. This analysis effectively controlled for confounding by age, cigarette smoking, exposure to other occupational carcinogens, and detection bias. The results congrue with the hypothesis of an association between silicosis and lung cancer.
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PMID:Silicosis and lung cancer among workers in North Carolina dusty trades. 892 98

Approximately 100 000 Finnish workers are currently employed in jobs and tasks that may involve exposure to airborne silica dust. The major industries involved are mining and quarrying; production of glass, ceramics, bricks and other building materials; metal industry, particularly iron and steel founding; and construction. Over 1500 cases of silicosis have occurred in Finland since 1935. Tuberculosis has been a frequent complication of silicosis. Results of studies from several countries strongly suggest that silica dust also causes lung cancer. The results of the relevant Finnish epidemiologic and industrial hygiene studies addressing cancer risk and exposure to quartz dust are summarized.
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PMID:Silica, silicosis and cancer in Finland. 892 99

Cohorts of Finnish asbestos sprayers and of asbestosis and silicosis patients were followed for cancer with the aid of the Finnish Cancer Registry in the period 1967-1994. Compared with the cancer incidence of the total Finnish population, asbestos sprayers had an increased risk for total cancer (standardized incidence ratio [SIR] 6.7, 95% confidence interval [95% CI] 4.2-10); lung cancer (SIR 17.95% CI 8.2-31); and mesothelioma (SIR 263, 95% CI 85-614). The SIR of the asbestosis patients was 3.7 (95% CI 2.8-5.0) for all sites, 10 (95% CI 6.9-14) for lung cancer, and 65 (95% CI 13-188) for mesothelioma. The silicosis patients also had significantly high SIR values for all sites (1.5, 95% CI 1.0-2.1) and lung cancer (2.7, 95% CI 1.5-4.5). The values for the SIR and the standardized mortality ratio for all sites and lung cancer were very similar, and therefore it seems that both are reliable indicators of the occurrence of occupational cancer. It was concluded that pneumoconioses patients and asbestos-exposed workers have a markedly elevated risk for cancer. Asbestos-induced occupational cancers are not only diseases of the elderly, since the relative risk is high also for middle-aged people.
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PMID:Cancer incidence and mortality among Finnish asbestos sprayers and in asbestosis and silicosis patients. 913 Dec 23

Iron oxides are present in many occupational atmospheres mainly in iron ore mines and in steel industry. Among these workers, epidemiological studies indicated an excess of lung cancer deaths. In mines, it was difficult to involve iron oxides exposure because there are other possible causes as radon, polycyclic aromatic hydrocarbon (PAH) present in diesel exhausts, silicosis or siderosis. The contradictory results of these studies are due to the differences of exposure levels or to the presence or not of these cofactors or of a sufficient prevention. But generally the results agree with an interaction of iron oxide dusts and smoking habits. It is unclear if this interaction supports an additive or multiplicative risk of lung cancer. Experimental studies with Fe2O3 showed that these particles are able to induce lung cancers only in the presence of PAH when administered to animals. In vitro studies permitted to observe an interaction in the metabolism of benzo(a)pyrene (BaP) leading to a higher level of precursors of the ultimate carcinogen. As this metabolism of BaP is known to be enhanced during lipoperoxidation, it is possible to involve this mechanism with Fe2O3. After phagocytosis and dissolution with production of ferric ions, Fe2O3 can enhance the production of reactive oxygen species responsible of damaging both lipidic constituents and DNA. Fe3O4 and mainly FeO may be more toxic, introducing directly ferrous ions in the cells after dissolution, but the cancerogenicity of the these compounds is unknown, making necessary to develop research.
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PMID:Interactive effects of polycyclic aromatic hydrocarbons and iron oxides particles. Epidemiological and fundamental aspects. 916 58

Data from nationwide registry-based cohorts of patients hospitalized for silicosis in Sweden from 1965 to 1983 and Denmark from 1977 to 1989 were linked to national cancer registries in both countries and to mortality data in Sweden to evaluate the risk of cancer and other disorders among hospitalized silicotic patients. The overall cancer standardized incidence ratio (SIR) was 1.5 (95% confidence interval [CI], 1.3 to 1.7) in Sweden and 1.7 (95% CI, 1.2 to 2.3) in Denmark, primarily because of elevations in primary lung cancer in both Sweden (SIR, 3.1; CI, 2.1 to 4.2) and Denmark (SIR, 2.9; CI, 1.5 to 5.2). For Sweden, the all-causes standardized mortality ratio (SMR) was 2.0 (1.9 to 2.2). The SMR for all malignancies was 1.5 (1.2 to 1.7), primarily because of excesses of lung cancer (SMR, 2.9; CI, 2.1 to 3.9). The significant increase in mortality for all infectious and parasitic conditions (SMR, 11.2) was primarily due to tuberculosis (SMR, 21.8). Significant excesses in mortality from silicosis (SMR, 523), bronchitis (SMR, 2.6) and emphysema (SMR, 6.7) contributed to the elevation in nonmalignant respiratory deaths (SMR, 8.8), whereas excess mortality from musculoskeletal disorders (SMR, 5.9) was due to six deaths from autoimmune diseases. Despite limitations of the available data, our findings are consistent with previous reports indicating that silicotic patients are at elevated risk of lung cancer, nonmalignant respiratory diseases, tuberculosis, and certain autoimmune disorders.
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PMID:Cancer risk and mortality patterns among silicotic men in Sweden and Denmark. 925 24

A total of 764 autopsy cases with a pathological diagnosis of nonasbestos pneumoconiosis were investigated in a search for lung cancer: 146 patients bore 148 lung cancers (19.1%). The incidence of a lung cancer was associated positively with aging longer occupational exposures, and smoking habits. A reverse correlation was found between carcinogenesis and the severity of pneumoconiosis. A statistically significant increase in the incidence of certain types of lung cancer (squamous cell carcinoma + small cell carcinoma) was found in silicotic lungs with massive fibrosis as compared to lungs with mixed dust pneumoconiosis of comparable severity. Although there appears to be no dose-response relationship in general between silicosis and lung cancer, it is advisable to consider the possibility that a presumptive silica-induced carcinogenesis might be masked by the severe fibrosis of a silicotic type, which obliterates the lung tissue in a different way from asbestosis, which is associated with epithelial proliferation.
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PMID:Silicosis, mixed dust pneumoconiosis, and lung cancer. 935 15


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