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PubMed1997

Asbestosis and silicosis.

Interstitial fibrosis resulting from workplace exposure to asbestos and crystalline silica persists throughout the world despite knowledge of the causes and effective means for prevention. Asbestosis and silicosis occurrence is predictable among people overexposed to dusts in various industries and occupations such as mining, construction, manufacturing, and building maintenance. Asbestosis and silicosis are incurable and may be progressive even after dust exposure has ceased, therefore early recognition and supportive interventions are important. Although current disease is a result of past exposures, effective control of current workplace exposures is the only way to prevent continued occurrence of these potentially debilitating diseases. Physicians can contribute to this effort through accurate diagnosis and disease reporting.

Asbestosis↗
PubMed1998

Histopathological changes in enlarged thoracic lymph nodes during the development of silicosis in rats.

Silicosis is primarily a fibrotic lung disease which also affects the draining lymph nodes. In the present study, we examined the lymph nodes of rats from 2 weeks to 52 weeks after an 8-day silica aerosol exposure. Parallel to the typical silicotic changes in the lungs, profound alterations occurred in both posterior mediastinal lymph nodes. The weight of the lymph nodes progressively increased from 3.5-fold to 35-fold at 52 weeks after silica exposure. The weight increase was accompanied by an early increase of T cells and preferentially of CD4+ cells at 2 weeks, which converted into a B cell increase at 6 weeks. Histologically, a leukocyte influx without apparent structural changes was noted at 2 weeks whereas at 6 weeks, germinal centers and T cell regions were disappearing and macrophages accumulated in granuloma-like structures which were randomly scattered throughout the lymphoid tissue. Within the granulomas, macrophages were detected that carried ingested silica particles without apparent signs of degeneration or apoptosis. At 52 weeks after silica exposure, macrophage granulomas persisted without induction of fibrosis in both lymph nodes, and T and B cells were now evenly distributed within the tissue. These data extend our previous findings on lymphocyte and macrophage activation and indicate that the early and marked disorganization of draining lymph node structures may contribute to the immune abnormalities in silicosis.

Animals↗
PubMed1994

[Acute silicosis caused by intentional inhalation of scouring powder].

A case of acute silicosis due to intentional inhalation of the scouring powder Ajax in a female patient suffering a sickle-cell trait (30% of S haemoglobin) is reported. It consisted of an acute immuno-allergic pneumonitis with fever and a respiratory distress syndrome. It was associated with a severe biological inflammatory syndrome and immunological disturbances with circulating immune complexes and antinuclear antibodies. The assessment of respiratory function demonstrated the presence of a restrictive syndrome with hypoxaemia and decreased CO transfer. The anatomopathological and mineralogical exams confirmed the diagnosis of silicosis and elicited birefringent particles in polarized light, some nodules, interstitial fibrosis and proteic deposits in favour of alveolar lipoproteinosis. The treatment included mechanical ventilation with PEEP, antibiotics and corticosteroids. Two pulmonary lavages were performed. The patient died of septic shock before a lung transplantation could be obtained.

Adolescent↗
PubMed2002

Pulmonary silicosis and systemic lupus erythematosus in men: a report of two cases.

We reporttwo cases of coexistence of pulmonary silicosis and systemic lupus erythematosus (SLE). The patients are two men with SLE exposed to silica for 20 years. The hypothesis that silica exposure is linked to a wide variety of known or suspected autoimmune diseases, including SLE, has been discussed in the last decade but few cases of pulmonary silicosis and SLE were reported. Our purpose was to bring attention to the increasing evidence that silica may also cause or stimulate SLE, and to suggest that the researchers look for occupational exposure, mainly in male SLE patients.

Adult↗
PubMed1997

Oxidative stress in silicosis: evidence for the enhanced clearance of free radicals from whole lungs.

We hypothesized that reactive oxygen species (ROS) may be involved in the pathogenesis of silicosis. To investigate ROS' dependent pathophysiological processes during silicosis we studied the kinetic clearance of instilled stable nitroxide radicals (TEMPO). Antioxidant enzymes' superoxide dismutase (SOD) and glutathione peroxidase (GPx), and lipid peroxidation were also studied in whole lungs of rats exposed to crystalline silica (quartz) and sham exposed controls. Low frequency L-band electron spin resonance spectroscopy was used to measure the clearance of TEMPO in whole-rat lungs directly. The clearance of TEMPO followed first order kinetics showing significant differences in the rate for clearance between the diseased and sham exposed control lungs. Comparison of TEMPO clearance rates in the sham exposed controls and silicotic rats showed an oxidative stress in the rats exposed to quartz. Studies on the antioxidant enzymes SOD and GPx in the lungs of silicotic and sham exposed animals supported the oxidative stress and accelerated clearance of TEMPO by up regulated levels of enzymes in quartz exposed animals. Increased lipid peroxidation potential in the silicotics also supported a role for enhanced generation of ROS in the pathogenesis of silica-induced lung injury. These in vivo experiments directly demonstrate, for the first time, that silicotic lungs are in a state of oxidative stress and that increased generation of ROS is associated with enhanced levels of oxidative enzymes and lipid peroxidation. This technique offers great promise for the elucidation of ROS induced lung injury and development of therapeutic strategies for the prevention of damage.

Animals↗
PubMed2002

Intramolecular epitope spreading among anti-caspase-8 autoantibodies in patients with silicosis, systemic sclerosis and systemic lupus erythematosus, as well as in healthy individuals.

Dysregulation of apoptosis through the Fas-Fas ligand pathway is relevant in autoimmune disease onset. We recently reported elevated serum levels of sFas in patients with silicosis, systemic sclerosis (SSC) and systemic lupus erythematosus (SLE), and proposed a block of apoptosis in the pathogenesis. The disturbance of apoptosis in lymphocytes including autoreactive clones could induce autoantibody production. Since autoantibodies directed against unknown antigens are present in the sera of these patients, the sera samples were examined for the presence of autoantibodies directed to caspase-8. Using Western blotting, autoantibodies against caspase-8 were detected in healthy individuals and in over 60% of patients. Using epitope mapping employing 12 amino acid polypeptides with SPOTs system, a minimum of 4 epitopes and a maximum of 13 were found, which implied that epitope spreading was in progress. It is noteworthy that two important catalytic cystein residues were included within the epitopes; firstly the active site cystein Cys287, and secondly Cys360 located in the unique pentapeptide motif QACQG. Using recombinant human caspase-8 linked protein chip array, autoantibodies were identified and molecular weight determined. The antibodies were mainly IgG; 80% were subclass IgG1(lambda); 20% were IgG4(kappa). Despite the ratio of human light chain kappa:lambda = 2:1, the predominance of IgG1(lambda) is noticeable. Anti-caspase-8 autoantibodies are detectable in healthy individuals and in patients suffering silicosis, SSc or SLE. A few epitopes were detected in healthy individuals compared to those suffering autoimmune diseases, indicating the intramolecular epitope spreading. Relationship of autoantibodies and the clinical background of the patients requires clarification.

Amino Acid Sequence↗
PubMed1996

[Miliary tuberculosis and silicosis with predominantly cerebral symptoms].

HISTORY AND CLINICAL FINDINGS: About 10 weeks before admission to hospital a 73-year-old woman developed a fever of up to 40 degrees C for three days. She then had subfebrile temperature for several weeks with some rises to 39 degrees C. She was known to have type II a diabetes mellitus and pulmonary silicosis, having worked in a porcelain and ceramic factory for many years. Before admission her cerebral functions were rapidly deteriorating, especially short-term memory. This was followed by increasing paraplegia of the legs with inability to walk. She finally had urinary and faecal incontinence and swallowing difficulties with tendency to aspiration, which necessitated hospitalisation. INVESTIGATIONS: Both lactate dehydrogenase (339 U/l) and C-reactive protein (112 mg/l) were elevated; the platelet count was low (73000/microliters). Cerebrospinal fluid was unremarkable, as was computed tomography of the skull. But magnetic resonance imaging revealed multiple spotty lesions with low contrast-medium uptake throughout the brain, pointing to a disseminated bacterial or mycotic infection. 3 days later the chest-ray showed small nodular soft shadows in the lungs, and lung functions had decreased. Mycobacteria were found in the urine and liver biopsy showed granulomatous hepatitis, establishing the diagnosis of miliary tuberculosis in the presence of silicosis. TREATMENT AND COURSE: Tuberculostatic treatment was instituted with four drugs (pyrazinamide, ethambutol, isoniazid and streptomycin. After 6 weeks the patient was again able to walk and continent of urine during the day. All cerebral functions gradually improved. CONCLUSION: Miliary tuberculosis should be included in the differential diagnosis of ill-defined feverish disease, especially in the elderly.

Aged↗
PubMed2001

Different distribution of HLA class II alleles in anti-topoisomerase I autoantibody responders between silicosis and systemic sclerosis patients, with a common distinct amino acid sequence in the HLA-DQB1 domain.

Autoantibodies against DNA topoisomerase I (anti-topo I) have been reported to be specific to systemic sclerosis (SSc), however, anti-topo I was detected in patients with silicone breast implants, SLE without features of SSc, and rheumatic diseases. We detected anti-topo I positive silicosis patients without any symptoms of autoimmune diseases. The correlation between anti-topo I autoantibody responses and HLA class II has been established. HLA-DRB1*1502; DQB1*0601 has been reported to be the most frequent anti-topo I associated haplotype among Japanese SSc patients. In this study, haplotype HLA-DR15; DQ6 was detected in all 4 anti-topo I positive Asian Japanese SSc patients randomly selected. Furthermore, HLA-DQB1*0402 was identified in 3 of 4 anti-topo I positive silicosis patients. These findings coincide with the results of a previous study, in which all 4 Japanese patients with anti-topo I had the DQB1*04 alleles, whereas no studies among Caucasian-Americans, African-Americans and Choctaw Indians found the involvement of DQB1*04. We investigated common features among various DQB 1 alleles. HLA-DQB I with a distinct characteristic is clearly involved in the anti-topo I response irrespective of ethnic groups, the main disease, or silica exposure. A common positioning of distinct amino acids, (i.e. positions 14, 30, 57 and 77 of the DQbeta1 domain are methionine, tyrosine, aspartic acid and threonine, respectively,) seems to be associated with anti-topo I response. The above-mentioned amino acid sequence is detected in alleles *0301, *0303, *0306, *0401, *0402, *0601 and *0602.

Alleles↗
PubMed1975

Identification of foreign material in lung by energy dispersive x-ray analysis. A new approach to silicosis.

Conventional methods for the detection of foreign material in the lungs are not only difficult but make it impossible to study any relationship between the material and the surrounding tissue. The present study employs energy dispersive x-ray analysis and scanning electron microscopy as the basis of a rapid and accurate method for determining the amount of silicon in the lungs of normal subjects and subjects with silicosis. A statistical evaluation of the data suggests that a silicon/sulfur ratio below 0.2 may be considered normal, whereas, a ratio above 0.3 may be considered to indicate silicosis.

Clinical Trials as Topic↗
PubMed1978

Silicosis in kaolin workers and firebrick makers.

Nine patients with disabling pneumoconiosis were selected over a three-year period for study because of a work history of kaolin exposure. All had worked in the Missouri firebrick industry. Chest roentgenograms from all nine and lung tissue from two were consistent with silicosis. Worksite analysis of airborne dust at several Missouri firebrick factories revealed that some current workers are exposed to both free silica (up to 4.5%) and cristobalite (up to 8.9%) at levels exceeding the threshold limit value (TLV). Analysis of airborne dust from several kaolin processing plants in South Carolina and Georgia revealed that a few workers are exposed to about 1% free silica at levels occasionally exceeding the TVL. We conclude that silicosis is a serious risk for Missouri kaolin workers and a potential risk for workers in South Carolina and Georgia. A prevalence survey is needed in Missouri to assess the problem.

Aged↗
PubMed1982

Mortality among miners receiving workmen's compensation for silicosis in Ontario: 1940-1975.

We investigated mortality among 1,190 Ontario miners who received Workmen's Compensation awards for silicosis from 1940 through 1975. In comparison with the general population of Ontario these men had elevated all-cause mortality rates, with deaths attributed to nonmalignant respiratory diseases and tuberculosis being primarily responsible. The group of miners receiving their compensation awards between 1940 and 1959 has experienced more than twice as many lung cancer deaths as expected while men receiving compensation awards after 1959 have had lung cancer rates similar to the general population. It is concluded that silicosis is not a benign disease and that efforts must be continued to prevent its occurrence.

Adult↗
PubMed1993

Silicosis following employment in the manufacture of silica flour and industrial sand.

We describe silicosis in a patient with chronic obstructive pulmonary disease who worked as a maintenance mechanic for less than 5 years in a plant in South Carolina that manufactures silica flour and industrial sand. An open lung biopsy showed an early stage of silicosis manifested by perivascular and peribronchial collections of macrophages as well as early granuloma formation. An antinuclear antibody profile compatible with Sjogren's syndrome or systemic lupus erythematosus occurred with no symptoms of either disease. Excessive occupational exposure levels of respirable free silica were documented.

Biopsy↗
PubMed2006

Apoptosis and extracellular matrix remodelling in human silicosis.

AIMS: Silicosis is a chronic occupational disease caused by the inhalation of free crystalline silica particles which produce inflammation and tissue destruction followed by remodelling of the extracellular matrix. Apoptosis has been implicated in the development of the initial inflammation that triggers the remodelling process. Our aim was to elucidate the importance of Fas-ligand (Fas-L) in this disorder and to study the relationship between Fas-L and several other inflammatory and fibrotic remodelling markers. METHODS AND RESULTS: We analysed 23 lung biopsies from silicotic patients and five controls, quantifying Fas-L and Bcl-2 expression by inflammatory cells as well as mast cells and collagen and elastic fibres. We used immunohistochemistry and morphometry to evaluate the amount of Fas-L and Bcl-2. Our analysis revealed that the silicotic lung stage was significantly related to Fas-L, mast cell and extracellular matrix remodelling. Fas-L expression was inversely associated with mast cells, collagen/elastic deposition and the silicotic lung. CONCLUSION: Fas-L, mast cell staining and collagen/elastic fibre quantities in silicotic lungs are strongly related to silicosis progression.

Apoptosis↗
PubMedDate not supplied

Thoracic radiographic features of silicosis in 19 horses.

Clinical records and thoracic radiographs of 19 horses with a confirmed pathologic diagnosis of silicosis were reviewed. These horses had histories of varying degrees of chronic weight loss, exercise intolerance, and respiratory distress. At the time of presentation, two horses were asymptomatic. Ten horses were geldings and nine were female. The mean age of the 19 horses was 10.7 +/- 5.5 years. Fourteen horses were identified as being from the Monterey-Carmel Peninsula of midcoastal California. An abnormal, structured interstitial pulmonary pattern was identified on thoracic radiographs in each horse. The interstitial pulmonary changes were classified as miliary (13 horses), reticulonodular (4), or linear interstitial (2), and were best visualized dorsally and caudodorsally. In addition to the abnormal interstitial pulmonary pattern, areas of pulmonary consolidation were evident caudodorsally in seven horses. Other thoracic radiographic features included: hilar lymphadenopathy (4 horses), pleural effusion/thickening (4), cranial mediastinal lymphadenopathy (2), hyperinflation (1), and a discrete pulmonary mass (1). Necropsy findings in eight horses and results of lung biopsies in an additional five horses showed a diffuse, multifocal, granulomatous pneumonia with areas of pulmonary fibrosis. Cellular infiltrates included predominantly macrophages with intracellular and/or extracellular crystalline material, occasional lymphocytes, and giant cells. Similar cellular changes were also identified, during necropsy, in the hilar and tracheobronchial lymph nodes in each of the eight horses, although gross enlargement of the lymph nodes was present in only six horses. The radiographic and pathologic findings of these 19 horses are consistent with chronic or the accelerated forms of silicosis that are recognized in humans.

Animals↗
PubMed1998

Shenjincao (Palhinhaea cernua) injection for treatment of experimental silicosis of rats.

Shenjincao injection is a traditional Chinese medicine prepared from Palhinhaea cernua (L.) A. Franco et Vasc. by ultrafiltration. Its anti-silicosis action has been investigated both as a prophylactic and for treatment of the disease. Wistar rats were injected intra-tracheally with quartz dust and then divided randomly into groups-treatment and control prophylactic groups and treatment and control disease groups. After five days or eight weeks, respectively, the silica-exposed rats of the two treatment groups were injected intraperitoneally three times a week with shenjincao injection, dose 2.0 mL, for five weeks or 11 weeks, respectively. The rats were then dissected, and the ceruloplasmin content of the serum and the fresh weight, dry weight, collagen content and pathological grade of the lungs were measured. Compared with the corresponding exposed control groups for the same treatment periods the values of these parameters were reduced by 62.8% to 30.7% for rats in the prophylactic treatment group (P < 0.01 for all) and by 50.8% to 30.2% for the diseased group (P < 0.01 for all). The values for the disease-treatment group were also reduced by 37.9% to 25.9% compared with values for the exposed control group before treatment (P < 0.01 or P < 0.05). The effective coefficients for prophylactic treatment were 82.6% to 56.0%; for disease treatment they were 68.8% to 39.8%. These results show that shenjincao injection is efficacious against experimental silicosis not only when used prophylactically but also when used to treat the disease.

Animals↗
PubMed1985

Silica, silicosis, and progressive systemic sclerosis.

An inquiry into the relation between exposure to silica dust, the presence of silicosis, and progressive systemic sclerosis was conducted in white South African gold miners by means of a case-control study. Seventy nine cases of progressive systemic sclerosis were matched by year of birth with an equal number of control miners selected randomly but bearing in mind the administrative channel through which the case had come to be identified. Analysis showed no association between silicosis and PSS but did show that the cumulative life time silica exposure was significantly higher in the cases compared with controls. This difference was due to a difference in the intensity of exposure to silica during mining service rather than a difference in duration of service. The results are discussed in the context of current thought on the aetiology of progressive systemic sclerosis, particularly in relation to autoimmune and genetic factors.

Dose-Response Relationship, Drug↗
PubMed1987

Mortality among workers receiving compensation awards for silicosis in Ontario 1940-85.

The mortality experience of 1190 miners and 289 surface industry workers receiving workers' compensation awards for silicosis in Ontario since 1940 has been studied up to mid-1985. Both groups were found to have a significantly increased mortality from lung cancer (miners' SMR: 230; surface workers' SMR: 302) and stomach cancer (miners' SMR: 188; surface workers' SMR: 366). Adjustment for smoking and country of origin did not explain the excesses observed. The lung cancer findings are consistent with observations from silicosis registries in Europe. Possible explanatory factors are discussed.

Cause of Death↗
PubMed1989

Histocompatibility antigens in a population based silicosis series.

Individual susceptibility to silicosis is suggested by the lack of a uniform dose response relation and by the presence of immunological epiphenomena, such as increased antibody levels and associated diseases that reflect altered immune regulation. Human leucocyte antigens (HLA) are linked with immune response capability and might indicate a possible genetic susceptibility to silicosis. Forty nine silicotic subjects were identified from chest radiographs in a population based study in Leadville, Colorado. They were interviewed for symptoms and occupational history and gave a blood specimen for HLA-A, -B, -DR, and -DQ typing and for antinuclear antibody, immune complexes, immunoglobulins, and rheumatoid factor. Silicotic subjects had twice the prevalence of B44 (45%) of the reference population and had triple the prevalence of A29 (20%), both of which were statistically significant when corrected for the number of comparisons made. No perturbations in D-region antigen frequencies were detected. B44-positive subjects were older at diagnosis and had less dyspnoea than other subjects. A29-positive subjects were more likely to have abnormal levels of IgA and had higher levels of immune complexes. This study is the first to find significant HLA antigen excesses among a series of silicotic cases and extends earlier reported hypotheses that were based on groups of antigens of which B44 and A29 are components.

Adult↗