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PubMed1991

Silicosis and lung cancer among Chinese granite workers.

Of the 184 cases of silicosis registered between 1 January 1970 and 31 December 1984 in Singapore, all the relevant information was available for 159, which were linked to the population-based National Cancer Register for lung cancer. Nine cases of lung cancer were found. The standardized incidence ratio (SIR) was computed with the age- and calendar-specific incidence of lung cancer rates of Chinese males in Singapore as a basis. Excess risk of lung cancer was found (SIR 2.01, 95% confidence interval 0.92-3.81). Adjustment for smoking showed that it alone could not account for the excess lung cancer risk. There was an increasing, but not significant, trend with increasing severity of silicosis and exposure duration. The results suggest that the severity of silicosis and possibly exposure to free silica may have contributed to the excess of lung cancer among the cases of silicosis studied.

Cohort Studies↗
PubMed2005

Meta-analysis of silicosis and lung cancer.

OBJECTIVES: This study examined the association between silicosis and lung cancer in a systematic review (and meta-analysis) of the epidemiologic literature, with special reference to the methodological quality of observational studies. METHODS: We searched Medline, Toxline, BIOSIS and Embase (1966-May 2004) for original articles published in any language and systematically reviewed the bibliographies of the retrieved articles. Observational studies (cohort and case-control studies) were selected if they reported a measure of association [standardized mortality ratio (SMR), relative risk or odds ratio] relating lung cancer to silicosis. RESULTS: Thirty-one studies (27 cohort studies, 4 case-control studies) met the inclusion criteria of the meta-analysis. Without any adjustment for smoking, the meta-analysis of the cohort studies indicated that the common SMR was 2.45 [95% confidence interval (95% CI) 1.63-3.66; homogeneity P<0.0001]. When the results of the cohorts for which mortality data were adjusted for smoking were pooled, the common SMR was 1.60 (95% CI 1.33-1.93; homogeneity P=0.52). In a "dose-response" analysis, the profusion of small and large opacities found in chest X-rays correlated with the risk of death from lung cancer. Overall, the case-control studies were more conservative in their conclusions. CONCLUSIONS: Because of biases inherent to observational studies, it is likely that the risk of lung cancer among silicosis patients is overestimated in the current literature. There is nevertheless evidence, from data restricted to never-smokers and from a "dose-response" analysis, that silicosis and lung cancer are associated.

Bias↗
PubMed1998

[Changes in blood levels of nitric oxide, oxidation and lipoperoxidation in patients with silicosis].

OBJECTIVE: To explore the relationship between nitric oxide, oxidation, lipoperoxidation and silicosis. METHODS: Blood plasma levels of nitric oxide (P-NO), vitamin C (P-VC), vitamin E (P-VE), beta-carotene (P-beta-CAR), lipoperoxidase (P-LPO), and erythrocyte activities of superoxide dismutase (E-SOD), catalase (E-CAT), glutathione peroxidase (E-GSH-Px) and lipoperoxidase (E-LPO) were measured in 73 patients with silicosis and 60 healthy subjects. RESULTS: The average levels of P-VC, P-VE, P-beta-CAR, E-SOD, E-CAT and E-GSH-Px were significantly lower and the average levels of P-NO, P-LPO and E-LPO significantly increased in the silicosis with varied severity of the disease and lung function status more than in the controls. There was linear relationship between all the above indices and length of the disease. Stepwise regression analysis showed that the severity of the disease and lung function status correlated most closely with the levels of P-NO, P-VE, E-SOD and E-LPO. CONCLUSION: Metabolism of nitric oxide was abnormal, balance between oxidation and antioxidation was disturbed seriously, and oxidation and lipoperoxidation reaction pathologically exacerbated in the bodies of the patient with silicosis.

Adult↗
PubMedDate not supplied

[Pulmonary fibrosis caused by inhalation: silicosis].

Silicosis is an important disease not only for its prevalence and the degree of pulmonary insufficiency it entails but also because it provides a natural model of interstitial fibrotic disease in the lung which is of known origin. This can, in turn, help us understand the pathogenic nature of a great number of pulmonary fibroses whose cause is unknown. The fifty postmortem studies which we describe correspond to miners who had worked in underground mines in the mountainous region near Cartagena (SE Spain) for times ranging from 5 to 36 years. The autopsies showed that they had been exposed to dust containing abundant metallic particles, particularly iron oxide (mixed dust). Although the pathogenic action was related with silica, it was also clearly modified by the composition of the dust associated with it. The basic lesions which are produced in the lung after inhalation of silica (< 5 microns diameter) are coniosis, fibroconiosis and sclerohyalinosis. The sclerohyalino nodules are characterized by abundant collagenization and hyalinization, different types of which can be distinguished according to the disposition of the collagenous fibres. Nodular lesions gradually grow in size even when exposure to dust has ceased. As they grow they get nearer until they join to form conglomerate masses. When the diameter exceeds 3 cm this is called massive fibrosis. Pulmonary tuberculosis was found in 27% of cases. This took the form of lesions, which could be associated to or independent of silicotic lesions. Besides evolutive nodular lesions, a patient suffering from silicosis may show other unspecific lesions which must be correctly evaluated for a more correct clinical-pathological assessment, since, clinically, the respiratory function may be profoundly affected although such silicotic damage may be not very noticeable by radiological examination. Silicosis of the liver and spleen was not infrequent in the autopsies carried out, with basic lesions in all evolutive states being observed, the most evolved in the spleen. This means that silicosis should be considered as a systemic illness.

Animals↗
PubMedDate not supplied

Considerations on the changes of certain immunologic cells in silicosis.

Cell-mediated immunity was estimated in a group of 68 patients divided into three subgroups according to the evolutive stage of disease. It was demonstrated that in silicosis there is a disturbance of immunity. The detection of E rosettes and of activated rosettes was carried out according to the classical method. The mean percentage of total T lymphocytes was found lower in silicosis (62 +/- 2% statistically significant for p < 0.05), compared to the control group (66 +/- 4.6%). The study revealed a decrease of T helper lymphocytes, an increase of T suppressor/cytotoxic lymphocytes and a decrease of the T helper/T suppressor ratio (1.96 +/- 0.13) in silicosis as compared to the control group (2.83 +/- 0.31). The presence of these changes in silicotic patients suggested the participation of cell-mediated immunity in the pathogenesis of disease, the cell mediated immunity being directly responsible for the evolution of silicosis.

Adult↗
PubMed2000

[Application of monocyte strains (THP-1 cells) in study on silicosis in vitro].

OBJECTIVE: To explore the application of human blood monocyte strain (THP-1 cells) with properties of pulmonary alveolar macrophage in study on pathogenesis of silicosis in vitro. METHODS: Effects of cell culture supernatant of THP-1 stimulated by silica or induced and differentiated by phorbol ester (PMA) on proliferation of fibroblast (CHL), formation of Ag-NORs granule, migration of pulmonary alveolar epithelium (CCL-64) and occurrence of silicosis-like pathological changes were observed in rats. Chemo-illuminescence stimulated by silica in PMA-primed THP-1 cells was studied, as compared with that by PMA. RESULTS: Supernatant of silica-stimulated THP-1 cell culture could effectively enhance proliferation of CHL cells and increase the mean number of Ag-NORs granule and their dispersion, with a good dose-response relationship, which correlated highly with cytotoxicity index, pulmonary alveolar macrophage (PAM), caused by silica. And, they could also inhibit the migration of CCL-64 and the repair of epithelial damage. The supernatants from silica-stimulated PAM and THP-1 cell culture could cause early silicotic nodule-like lesions in rats. Chemo-illuminescence response in PMA-primed THP-1 cells and PAM was enhanced by stimulation with silica in a dose-dependent pattern. CONCLUSION: PMA-primed THP-1 cells may have a prospect of wide application in study on pathogenesis of silicosis and production of silicosis-related cytokine and oxygen free radicals in vitro.

Animals↗
PubMed2001

[A case of silicosis with MPO-ANCA-associated glomerulonephritis and alveolar hemorrhage].

A 63-year-old man was referred to our hospital for rapid deterioration of his renal function. He had worked as a metal founder for more than 40 years, and had been diagnosed as having silicosis. Laboratory data on admission showed severe anemia, thrombocytopenia, and end-stage renal failure (BUN 88.8 mg/dl, serum creatinine 9.0 mg/dl). Myeloperoxidase anti-neutrophil cytoplasmic antibody(MPO-ANCA) was also detected in his sera. On the next day after admission, he complained of sudden dyspnea and hemoptysis. Mechanical ventilation with pure oxygen was insufficient to improve hypoxia without concomitant use of percutaneous cardio-pulmonary support(PCPS) and continuous hemofiltration(CHF). We diagnosed his condition as MPO-ANCA-associated rapidly progressive glomerulonephritis with diffuse alveolar hemorrhage. Treatment with plasmapheresis, pulse methylprednisolone and pulse cyclophosphamide effectively improved his hemoptysis as well as chest X-ray findings and blood gas analysis. However on his later clinical course, he was complicated with superimposed complex infection and passed away. Autopsy findings showed crescentic glomerulonephritis in the kidneys and silica nodules in the lungs. Recently it has been postulated that some relationship exists between ANCA-associated(especially MPO-ANCA-associated) glomerulonephritis and silica exposure. The reported cases of glomerulonephritis in the patients with silica exposure showed a rapidly progressive clinical course and pauci-immune necrotizing crescentic glomerulonephritis in their histology. Gregorini et al. reported that 12 of 37 (32%) male patients with RPGN had either silicosis or significant silica exposure, and 7 of 8 patients examined were ANCA-positive(6 of 7 were MPO-ANCA-positive). Therefore silica seems to cause glomerulonephritis by disrupting the immune response. Including this case mentioned above, we have experienced 10 cases of MPO-ANCA-associated glomerulonephritis, at least 3 cases out of which had suffered from silicosis in the past(30%). These results indicate that silicosis should be considered a relevant pathogen of MPO-ANCA-associated glomerulonephritis beyond the race.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed2001

[Hereditary polymorphism features in patients with silicosis associated with chronic bronchitis].

Chronic bronchitis frequently accompanies silicosis in metallurgy workers. Association of the two diseases significantly lowers life quality and disables the patients. Prophylactic measures for the diseases are elimination of the etiologic factors and detection of genetic markers for propensity and insusceptibility to silicosis and chronic bronchitis. Phenotypes of Lewis a-b- system, of Hp2-1 haptoglobin and of group-specific component Gc2-2 could be risk factors for chronic bronchitis in silicosis patients. Those of Lewis a-b+ system, of Hp2-2 haptoglobin and group-specific component Gc1-2 are resistant to chronic bronchitis on silicosis background.

Adult↗
PubMed2001

Lymphocytes, lymphokines, and silicosis.

Silicosis is characterized by mononuclear cell aggregation with mineral particles and fibrosis. Lymphocytes are abundant in these lesions. We exposed inbred strains of mice to a respirable aerosol of cristobalite silica (70 mg/m3, 5 h/d, 12 d) or shamair. Silicosis evolved over months after exposure. The silica-exposed mice showed the accumulation of lymphocytes in alveolar spaces (seen in bronchoalveolar lavage), in lung parenchymal lesions and nodules, and in enlarged bronchial-associated lymphoid tissues and thoracic lymph nodes. The lung lymphocytes were predominantly CD4+ T cells, but numerous CD8+ T cells, natural killer cells, and CD4- gammadelta-TCR+ T cells were present as well. Interferon-gamma (IFN-gamma) production was upregulated, suggesting a THelper-1-like response in silicosis. In silicotic lung tissue, mRNA transcripts for the macrophage-derived cytokines IL-12 and -18 were increased. IFN-gamma gene-deleted mice (C57Bl/6-Ifngtm1 Ts) exposed to silica developed less extensive silicosis and less lung collagen accumulation than wild-type mice. We hypothesize that there is a reiterative amplification cycle in which macrophages with silica may produce cytokines, such as IL-12 and -18, that attract and activate lymphocytes. These activated lymphocytes may then produce additional mediators that in turn attract and activate an expanded secondary population of macrophages. IFN-gamma would be a likely cause of macrophage activation in this cycle. More work is needed to understand the biological events that lead from the inhaled dust to the scarred lung, and to clarify the role of lymphocytes in this process.

Air Pollutants, Occupational↗
PubMed2001

IgG subclass responses in experimental silicosis.

Silicosis is a crippling fibrotic lung disease induced by inhaling crystalline silica. In addition to fibrosis, silica inhalation by humans is associated with a number of immunological effects including increased levels of serum immunoglobulins (in particular IgG), increased prevalence of autoantibodies, and autoimmune disease. Recent studies using rodent models have shown that experimental silicosis is associated with a T-helper (TH)1 pattern of T-cell activation in the lungs and lung-associated lymph nodes after silica inhalation, which are also the sites of increased IgG production. We therefore hypothesized that the subclass distribution of IgG production occurring in experimental silicosis would suggest TH1 activation as the primary stimulus for IgG production. Using an ELISPOT assay, we found increased IgG-secreting spot-forming cells of all IgG subclasses in lung-associated lymph nodes taken from silica-exposed rats 3 to 4 months after aerosol exposure to silica. Neither TH1- nor TH2-dependent IgG subclass-secreting cells were selectively enhanced. Our findings suggest that TH1 activation alone does not account for increased production of IgG in experimental silicosis.

Administration, Inhalation↗
PubMedDate not supplied

Pulmonary function in sandblasters' silicosis.

Lung function was examined in 55 patients with sandblasters' silicosis. In this type of silicosis, patients with simple nodular disease had normal function. Restrictive and obstructive impairment was present in patients with large opacities, and was more marked in patients with radiographic evidence of contraction or cavitation. In the last group, striking average annual declines in ventilatory function occurred. Compared to patients with classical silicosis, these patients were younger and had intense, short exposures to free crystalline silica. The pattern of functional abnormalities suggested that restriction of lung volumes is a fundamental abnormality in this form of silicosis.

Adult↗
PubMed1992

Lung function in relation to silicosis and silica exposure in granite workers.

Lung function tests (forced expiratory volume in one second (FEV1), forced vital capacity (FVC) and FEV1/FVC %) were related to silica exposure and the extent of radiological opacities in a study of 206 active and 132 previously employed granite workers from two quarries. The investigations included detailed personal interviews, spirometric testing and radiographic examination of the chest. The chest X-ray films were read randomly and independently by three readers, using International Labour Office (ILO) standard films. Cumulative exposure to respirable silica (mg.m-3-yr) and total granite dust (million particles per cubic foot (mppcf-yr)) were estimated for each subject based on his years of employment at various jobs and historical and current measurements of quarry-, period- and job-specific exposures. The results suggest that chronic simple silicosis, especially for profusion category 2 and 3, was associated with significant lung function loss. As expected, mixed dust fibrosis was associated with little or no functional disturbance. Massive fibrosis was associated with significant obstructive and restrictive impairment. No additional effect of exposure to respirable silica on lung function loss was found after allowing for the presence of "silicosis". However, exposure to total dust (mppcf-yr) appeared to be associated with some lung function loss independent of silicosis. Our results indicate that chronic simple silicosis is not a benign disease; silica exposure is the primary cause, but the lung function loss in silicotics is directly attributable to the fibrotic lung disease. However, exposure to total granite dust beyond the respirable size range may separately produce additional lung function loss.

Adult↗
PubMed1992

[The cytokinetics of the bronchoalveolar lavage fluid from workers in silicosis-hazardous jobs].

Cytogram of pulmonary lavage fluid was studied in 50 workers al risk of developing silicosis. Workers with long length of service showing no radiographic signs of silicosis had normal cytogram of pulmonary lavage fluid, except for slightly increased neutrophil counts. Cytogram of patients with first recognized silicosis were characterized by elevated lymphocyte count. Neutrophil level increased in chronic silicosis. Cytogram of pulmonary lavage fluid is considered valuable for the diagnosis and prognosis.

Adult↗
PubMed2003

[Epidemiological study of gem worker's silicosis].

OBJECTIVE: To study the hazards of gem dusts and the epidemiological features of the occurrence of gem worker's silicosis (GWS). METHODS: Epidemiological investigation in a gem factory in Guangdong province was carried out. RESULTS: The average dusts concentration in workshop was 2.3 mg/m(3), average free silica content was 94.64%. There were 47 patients diagnosed as silicosis. The prevalence of GWS was 4.58% (47/ 1,027). The age of patients suffering from silicosis and the duration of dust exposure were (27.04 +/- 3.25) years and (4.67 +/- 1.17) years respectively. Chest radiographic examination showed mainly small round opacities "q". The incidences of GWS complicated by pulmonary tuberculosis, spontaneous pneumothorax and pulmonary emphysema were 10.64%, 10.64%, 44.68% respectively. CONCLUSION: The hazards of gem dust to workers might be serious. Higher incidence, younger age suffered from silicosis, shorter duration of dust exposure, more complications, and poorer prognosis in gem workers appeared to be the main epidemiological features of GWS in Guangdong.

Adult↗
PubMed2004

Silicosis in dental laboratory technicians--five states, 1994-2000.

Silicosis is a debilitating, sometimes fatal, yet preventable occupational lung disease caused by inhaling respirable crystalline silica dust. Although crystalline silica exposure and silicosis have been associated historically with work in mining, quarrying, sandblasting, masonry, founding, and ceramics, certain materials and processes used in dental laboratories also place technicians at risk for silicosis. During 1994--2000, occupational disease surveillance programs in five states identified nine confirmed cases of silicosis among persons who worked in dental laboratories; four persons resided in Michigan, two in New Jersey, and one each in Massachusetts, New York, and Ohio. This report describes three of the cases and underscores the need for employers of dental laboratory technicians to ensure appropriate control of worker exposure to crystalline silica.

Aged↗
PubMed1978

Electrocardiographic signs of chronic cor pulmonale in 40 376 patients with silicosis.

The records of all patients who were examined for silicosis at the Fund of Occupational Diseases between 1972 and 1976 are reviewed. In 3627 cases the mechanographical record was incomplete leaving 40 376 patients in the study. Electrocardiographic signs of chronic cor pulmonale (C.C.P.) were detected in 5.58 per cent. The severity of C.C.P. was evaluated and the prevalence of the different electrocardiographic signs was examined. The presence and severity of C.C.P. was compared to the radiological stage of silicosis, to the pulmonary function, to the duration of professional exposure to the risk of silicosis and to the use of tobacco. The value of the electrocardiographic signs of C.C.P. was evaluated. It is concluded that the mechanographical record obtained in insurance medicine is a valuable tool for statistical analysis of a disease and that C.C.P. is an infrequent and mostly late complication of silicosis.

Belgium↗
PubMed2006

[A case of HLA-B54 positive silicosis with rheumatoid arthritis and lung cancer].

In the same environment or workplace, some people contract pneumoconiosis, including silicosis, and some do not. This suggests the important role of constitutional predisposition. In Japanese cases with silicosis, the frequency of HLA-B54 was increased and disease susceptibility gene (s) may exist near the HLA-B locus. It is well known that silicosis is frequently accompanied with rheumatoid arthritis, probably due to the effects of silica on the immunological system. We encountered a case of silicosis with rheumatoid arthritis and lung cancer, who was found to have HLA-B54.

Aged↗
PubMed1991

Leukocyte immunophenotypes in bronchoalveolar lavage fluid and peripheral blood of paracoccidioidomycosis, sarcoidosis and silicosis.

Leukocyte subsets in bronchoalveolar lavage (BAL) fluid and peripheral blood of patients with paraccoccidioidomycosis, sarcoidosis and silicosis were characterized using monoclonal antibodies and an immunoperoxidase technique. In paraccocidioidomycosis, the number of T-helper/inducer CD4-positive lymphocytes was lower in peripheral blood than in BAL fluid. Additional analysis showed that the expression of HLA-DR was very similar in alveolar macrophages, lung and blood T-cells. In sarcoidosis and silicosis there were higher proportions of T-helper/inducer cells in peripheral blood than in BAL fluid. The alterations in the T-helper/inducer/T-suppressor/cytoxic CD4/CD8 ratio in sarcoidosis and silicosis were more appreciable in peripheral blood than in BAL fluid, contrasting with the results in paracoccidioidomycosis. The expression of HLA-DR by alveolar macrophages in sarcoidosis was the highest of all the disease studied. No statistically significant differences were observed between chronic multifocal and chronic unifocal paracoccidioidomycosis disease, stage II and stage III sarcoidosis, and chronic and accelerated silicosis. The three granulomatous diseases analyzed had a few alveolar macrophages expressing the CD4 molecule on their surface. These findings and the technique of analyzing both peripheral blood and BAL leukocyte subsets may help to understand the pathogenesis of interstitial lung diseases.

Bronchoalveolar Lavage Fluid↗