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PubMed2003

Previously undetected silicosis in New Jersey decedents.

BACKGROUND: Despite a reported decline in mortality and hospitalizations associated with silicosis [U.S. Department of Health and Human Services, 1999], this decline may be artifactual, stemming in part from underdiagnosis by physicians. METHODS: This study estimates, through radiological confirmation, the prevalence of unrecognized silicosis in a group of silica-exposed New Jersey decedents whose cause of death was chronic obstructive pulmonary disease (COPD), tuberculosis, or cor pulmonale. Two expert readers re-evaluated the chest X-rays of this group to determine the presence or absence of silicosis. The study population was considered to be presumptively exposed to silica dust by virtue of their usual industry of employment as listed on the death certificate. RESULTS: Radiographic evidence of silicosis was found in 8.5% of this population, and evidence of asbestosis was found in another 10.7%, for a total of 19.2%. CONCLUSIONS: The existence of previously unrecognized silicosis and asbestosis in 19.2% of this study group suggests that occupational lung disease is under-recognized and, hence, undercounted.

Aged↗
PubMed1985

Rapid progression of silicosis in slate pencil workers: II. A follow-up study.

Findings of the follow-up examination of slate-pencil workers after 16 months are described. The progression of silicosis with this short duration was very rapid with high mortality among those who had conglomerate silicosis at the initial examination. Twenty-three workers had died during this period at a mean age of only 34.7 years, with a mean duration of exposure of 11.9 years. This high mortality is attributed to exposure to high concentrations of silica dust leading to early onset of PMF at a relatively young age. The progression of silicosis within this period was related to the intensity and duration of dust exposure, and also to the severity of silicosis found at the initial examination. Smoking habits had an adverse, though statistically nonsignificant, effect on the evolution of silicosis.

Adult↗
PubMed2006

Role of exposure to radon and silicosis on the cell type of lung carcinoma in German uranium miners.

BACKGROUND: In East Germany, uranium mining was undertaken on a large scale from 1946 to 1990. Poor working conditions led to a high level of exposure to ionizing radiation and quartz dust. This analysis evaluates the histopathology of lung carcinoma in uranium miners in relation to radon exposure and silicosis. METHODS: A database developed for autopsy cases ascertained in a pathological tissue repository of German uranium miners was used to estimate odds ratios for developing lung carcinoma by major cell type with regard to radon exposure and silicosis. Silicosis information was extracted from autopsy protocols. Working level months (WLM) were calculated with a job-exposure matrix to assess lifetime radon exposure. Risk estimates were based on 3414 male miners who died from small cell lung carcinoma (SCLC, n = 1446), squamous cell carcinoma (SqCC, n = 1006), or adenocarcinoma (AC, n = 962) between 1957 and 1990. RESULTS: SCLC and SqCC seem more likely to be associated with high radon exposure than AC. Mean cumulative radon exposure was 868 (SD 631) WLM in SCLC, 871 (SD 652) WLM in SqCC, and 743 (SD 598) WLM in AC. Silicosis prevalence was 26% in SCLC, 38% in SqCC, and 30% in AC. In silicotics, AC and SqCC had a relatively higher frequency at the expense of SCLC. SCLC occurred earlier than AC and SqCC. CONCLUSION: High radon exposure was associated with a higher relative frequency of SCLC and SqCC than AC. Silicosis tended to increase the appearance of SqCC and AC.

Aged↗
PubMed1988

Prevalence of silicosis in the Dutch fine-ceramic industry.

In the nineteen-seventies a cross-sectional survey was conducted in the Dutch fine-ceramic industry. Workers employed in the ceramic industry (n = 3258) were examined for the presence of silicosis. In this article the results are reported for the area of Gouda and Maastricht. In Gouda the fine-ceramic industry consists of small workshops. The Maastricht working population comprises workers of two large, mechanized companies. The survey indicated that silicosis is still commonly present in Gouda (total prevalence of 13.3%), but is relatively rare in Maastricht (total prevalence of 1.7%). A clear dose-response relationship was found in both areas between duration of exposure to quartz-containing dust and the prevalence of silicosis. Furthermore it was noted that smoking was a risk factor for silicosis. However, this was restricted to workers who were heavy smokers and had had an occupational history of 20 years or more of exposure to quartz-containing dust. In this exposure category the prevalence of silicosis among heavy smokers was 50% higher than in light smokers and non-smokers.

Ceramics↗
PubMed1993

Surfactant-associated proteins (SP-A, SP-B) are increased proportionally to alveolar phospholipids in sheep silicosis.

In silicosis, a profile of surfactant overproduction associated with type II epithelial cell hypertrophy and hyperplasia has been documented. In addition, enhanced accumulation of surfactant-associated protein A (SP-A) has been seen in the rat model of acute silicosis by 2 independent groups, but the exact role of these surfactant changes in silicosis are incompletely understood. In this study we measured in lung lavage surfactant total phospholipids and surfactant-associated proteins A and B (SP-A, SP-B). In addition, the surface tension reducing activities of lipid extracts of bronchoalveolar lavage fluids (BALFs) in the sheep silicosis model were examined using a pulsating bubble surfactometer. Two groups of animals (n = 18) were investigated: a saline-exposed (PBS-PBS) group and a silica-exposed (Si-PBS) group. Total surfactant phospholipids in the silicotic sheep increased 2-fold over the control sheep values (p < 0.05), as previously reported. In addition, we found a substantial rise in total surfactant-associated proteins, with significant increase in SP-A (1.16 +/- 0.22 micrograms/ml Si-PBS group vs. 0.70 +/- 0.07 micrograms/ml PBS-PBS group, p < 0.05) and a parallel but not significant increase in SP-B (2.68 +/- 0.90 micrograms/ml Si-PBS group vs. 1.10 +/- 0.30 micrograms/ml PBS-PBS group). The surface-tension-reducing activities of alveolar fluid lipid extracts did not differ significantly between the groups (Si-PBS group at maximal bubble radius [Rmax]: 27.0 +/- 1.6 and at minimal bubble radius [Rmin]: 1.0 +/- 0.7 milli Newton/m, vs. PBS-PBS group Rmax: 27.0 +/- 2.2 and Rmin: 0.7 +/- 0.3 milli Newton/m at 4 min pulsation). The ratios of SP-A and SP-B to lipid phosphorus levels document a proportional enhancement of surfactant-associated proteins and phospholipids, thus suggesting a co-ordinated upregulation of both surfactant-associated proteins and phospholipids in this model of silicosis. However, on an individual basis, these changes were not related, suggesting a more complex model of regulation. This study documents significant increases of the surfactant apoproteins proportional to changes in phospholipids in the lung of silicotic sheep. In spite of these alterations of surfactant components, organic solvent lipid extracts of BAPLFs surfactant remained equally effective in reducing surface tension.

Animals↗
PubMed1996

Technegas ventilation SPECT for evaluating silicosis in comparison with computed tomography.

To compare the subtle pulmonary parenchymal morphologic changes with ventilation function in patients with silicosis, the conventional CT, high resolution CT and technegas ventilation SPECT were performed. In 25 silicotic patients and six controls, the pulmonary ventilation state was evaluated by an index called the coefficient of variation (CV), which expresses the subliminal heterogeneous distribution of technegas in the lungs. The results showed that with silicosis the CV value is significantly higher than that without silicosis. The CV value was proved by multifactorial analysis to independently reflect the extent of the appearance of small scattered interstitial findings such as nodules, septal thickening and bulla, which were typical findings for silicosis. The CV value calculated from the technegas SPECT correlated well with the severity of silicosis. It is considered that the CV value can also express the functional state of the silicotic lung.

Adult↗
PubMed1986

Silicosis and risk of lung cancer or lung tuberculosis: a cohort study.

This is a study of cancer mortality, cancer incidence, and incidence of lung tuberculosis among cases of silicosis reported to the National Swedish Pneumoconiosis Register during 1959-1977. Two occupational categories were extracted--"mining, tunneling, and quarrying" (n = 284) and "iron and steel foundries" (n = 428), respectively. Control groups were drawn from a national register of persons undergoing periodic health examinations with regard to silicosis risk. The controls were matched for occupation, age, and time of first exposure. The follow-up was performed through record-linkage operations to computerized information in Swedish Death Statistics, Swedish Cancer Register, and the Swedish Tuberculosis Index. End of follow-up was set at December 31, 1980. In cases drawn from mining, quarrying, and tunneling workers seven deaths in lung cancer were observed and two among the controls. Among iron and steel foundry workers the corresponding numbers were 10 and 6. The values for expected numbers, based on general population statistics, were 1.3 and 2.6, respectively, for these two occupational groups. When cancer incidence statistics were used, the case/control ratio for lung cancer was 2.1 for "mining, quarrying, and tunneling" and 0.6 for "iron and steel foundries." There were 29 cases of lung tuberculosis registered among the silicosis cases during the follow-up period. Only one tuberculosis case was observed among the controls. The results demonstrate that persons with silicosis contracted in the mining, quarrying, and tunneling occupations are subject to an increased risk of lung cancer. The risk is observed when both the general population and a closely matched control population from the same occupations are used for values of reference. The results also demonstrate the high risk of persons with silicosis to contract lung tuberculosis.

Adult↗
PubMed2002

A case-control study of lung cancer in relation to silica exposure and silicosis in a rural area in Japan.

PURPOSE: In southeast Okayama Prefecture, Japan, there have been reports of a high prevalence of silicosis among refractory brick production workers. Recently, a high mortality rate of lung cancer among the local residents has been observed. Therefore, a population based case-control study was conducted concerning the relationship between silica, silicosis, and lung cancer using multiple cancer controls. METHODS: Cases and controls were restricted to male subjects and information was obtained from death certificates from 1986 to 1993 in the area. Three categories of deceased control groups were selected: a series of deaths from liver cancer, colon cancer, and cancers of other organs, which was assumed not to be related to silica exposure. Age and smoking habits were adjusted by stratified analysis using the Mantel-Haenszel odds ratio estimates. Unconditional logistic regression analysis was also conducted to control potential confounding factors; such as age and smoking habits. RESULTS: The age-, smoking-adjusted odds ratios were 1.94 (0.94-4.43) for the colon cancer control group, 2.13 (1.19-3.85) for the other cancer control group related to silica exposure, and 2.94 (1.30-8.90) and 2.69 (1.43-5.37) related to silicosis, respectively. The direct weighted average using the estimates for colon and the other cancer controls was 2.06 (1.29-3.29) for silica exposure, and 2.77 (1.60-4.77) for silicosis. Histological or cytological types of lung cancer cases were obtained from 64.1% of the subjects (118/184). As for the histologic type of lung cancer, small cell carcinoma was higher among those who had been silica-exposed workers than the unexposed lung cancer cases and the data from the general Japanese population. On chest x-ray findings, elevated lung cancer mortality compared with cancers other than lung cancer was demonstrated among patients without large opacities. CONCLUSIONS: Silica exposure increased the lung cancer mortality in the area. A high lung cancer mortality rate in the area could be explained by silica exposure and silicosis prevalence in this area.

Adult↗
PubMed2001

Fas ligand triggers pulmonary silicosis.

We investigated the role of Fas ligand in murine silicosis. Wild-type mice instilled with silica developed severe pulmonary inflammation, with local production of tumor necrosis factor (TNF)-alpha, and interstitial neutrophil and macrophage infiltration in the lungs. Strikingly, Fas ligand-deficient generalized lymphoproliferative disease mutant (gld) mice did not develop silicosis. The gld mice had markedly reduced neutrophil extravasation into bronchoalveolar space, and did not show increased TNF-alpha production, nor pulmonary inflammation. Bone marrow chimeras and local adoptive transfer demonstrated that wild-type, but not Fas ligand-deficient lung macrophages recruit neutrophils and initiate silicosis. Silica induced Fas ligand expression in lung macrophages in vitro and in vivo, and promoted Fas ligand-dependent macrophage apoptosis. Administration of neutralizing anti-Fas ligand antibody in vivo blocked induction of silicosis. Thus, Fas ligand plays a central role in induction of pulmonary silicosis.

Adoptive Transfer↗
PubMed2002

Silicosis and lung function decrements among female ceramic workers in Italy.

It is well known that male ceramic workers have elevated risks of chronic silicosis. The objective of this study was to assess whether female ceramic workers also have an increased risk of silicosis and whether these women have decreased lung function related to silica exposure. Ceramic workers from Civitacastellana, Italy, were enrolled in health surveillance during the 1970s. A total of 642 women were under surveillance; a respiratory monitoring program was conducted from 1974 to 1987, with follow-up through 1991 that included annual chest radiography and measurement of lung function. Radiography findings were defined as silicosis if the chest films were > or =1/0 with small, rounded opacities. Multiple linear regression models for repeated measures (generalized estimating equations) were run to evaluate associations of forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV(1)) with years of exposure and radiograph opacities. Nine cases of silicosis were identified on the basis of radiographic evidence. Silicosis risk was not associated with smoking but was related to employment before 1970 and demonstrated a dose-response gradient for years of exposure. FVC and FEV(1) both showed significant (p < 0.05) associations with duration of exposure and with positive radiography findings. The results for female ceramic workers are consistent with those for male employees regarding exposure to fibrogenic dusts.

Adult↗
PubMed2002

Silicosis compensation in Western Australian gold miners since the introduction of an occupational exposure standard for crystalline silica.

UNLABELLED: Occupational exposure limits for crystalline silica are under review worldwide because of the large numbers of exposed people and, especially, because of the recent International Agency for Research on Cancer classification of silica as a human carcinogen. OBJECTIVES: The aims of this study were to (i) re-examine the incidence of silicosis in Western Australian gold miners and, using estimates of the total population at risk, (ii) estimate the upper confidence limit for the risk of silicosis in Western Australian gold miners since 1974, when the current exposure standard for crystalline silica was implemented. METHODS: Work histories of cases compensated for pneumoconiosis after 1974 were examined. Numbers of workers in the total workforce likely to be exposed to crystalline silica in Western Australia were estimated as the population at risk. RESULTS: There were no cases of compensated silicosis in Western Australian miners whose first dust exposure began during or after 1974. The upper 95% confidence interval for this zero rate was estimated to be 4.8 per 100,000 person-yr. CONCLUSIONS: There have been no compensated cases of silicosis in Western Australia among miners first exposed to crystalline silica after introduction of the current exposure standard. A rate of compensated silicosis higher than five cases per 100,000 person-yr is unlikely.

Adult↗
PubMed1996

Silicosis among foundry workers. Implication for the need to revise the OSHA standard.

To evaluate the risk of pneumoconiosis among workers in a Midwestern automotive foundry, medical records and silica sand exposure data were analyzed for 1,072 current and retired employees with at least 5 years of employment as of June 1991. Approximately half of these employees had worked at the foundry for 20 or more years. Sixty workers were found to have radiographic evidence of pneumoconiosis. Twenty-eight workers had radiographs consistent with silicosis, of which 25 were consistent with simple silicosis and three with progressive massive fibrosis. The prevalence of radiographic changes consistent with silicosis increased with: number of years worked at the foundry (6% for 20-29 years and 12% for 30 or more years); cigarette smoking (12.2% among smokers with high silica exposure vs. 4.4% among never smokers with high silica exposure); work area within the foundry (cleaning room, core room, mold area, core knockout); and quantitative silica exposure (0.3-2.7% of workers at the current Occupational Safety and Health Administration (OSHA) standard and 4.9-9.9% of workers above the OSHA standard). In addition, the odds of developing radiographic changes consistent with silicosis were increased for African Americans (odds ratio = 2.14, 95% confidence interval 0.85-5.60) in comparison with whites. (The risk was similar when silica exposure was equal, but African-American workers on average had greater exposure to silica, despite having a similar duration of work as white workers.) Another eight workers had radiographic evidence of asbestosis, and 24 had pleural plaques. These asbestos-related changes were not associated with increasing exposure to silica but rather were associated with being in the maintenance department and performing repair work. After controlling for cigarette smoking, race, and exposure to silica at another job besides the foundry, the authors found a 1.45 increased risk of developing a radiograph consistent with silicosis after 20 years of work at the current OSHA standard, and a 2.10 increased risk after 40 years of work at the current OSHA standard. On the basis of these findings, the authors recommend maintaining silica air levels no higher than the exposure level of 0.05 mg/m3 recommended by the National Institute for Occupational Safety and Health.

Black People↗
PubMed2005

Basic pathogenetic mechanisms in silicosis: current understanding.

PURPOSE OF REVIEW: Silicosis continues to be a common cause of chronic lung diseases, despite evidence that these diseases can be prevented by environmental dust control. Silicosis has been studied extensively by basic and clinical scientists, yet little is known about the crucial cellular and molecular mechanisms that initiate and propagate the process of inflammation and scarring. RECENT FINDINGS: Recent in vivo, in vitro, and human studies have focused on several main areas of investigation into the causes and processes of the development of silicosis. These areas of investigation include the variability of pathogenic potential of different varieties of silica; the role of activated alveolar macrophages products in the development and progression of silicosis; and the direct role played by the silica particle surface in triggering adverse biologic reactions, such as generating ROS and RNS. The generation of oxidants by silica particles and by silica-activated cells results in cell and lung damage; increased expression of inflammatory cytokines, including TNF-alpha, IL 1 beta, and TGF-beta; activation of cell signaling pathways, including the MAP kinase pathways; and phosphorylation and activation of specific transcription factors (e.g., NFkB). The ROS, RNS, and NO generated by the silica particles also induce apoptosis in macrophages and other cells. SUMMARY: Further research on the molecular mechanisms involved in the inflammatory processes important for progression to fibrotic diseases is needed for the development of effective treatment of silicosis. Potential therapeutic strategies include inhibition of cytokines such as IL-1, TNF alpha, the use of anti-oxidants, and the inhibition of apoptosis.

Animals↗
PubMed2002

Exposure to crystalline silica, silicosis, and lung disease other than cancer in diatomaceous earth industry workers: a quantitative risk assessment.

OBJECTIVES: To estimate excess lifetime risk of (a) mortality from lung disease other than cancer (LDOC), and, (b) onset of radiographic silicosis, arising from occupational exposure to respirable crystalline silica dust. METHODS: Data from a cohort of California diatomaceous earth mining and processing workers exposed to crystalline silica dust (mainly as cristobalite) were reanalyzed with Poisson regression methods with internal and external adjustments for potential confounding by calendar time, age, smoking, Hispanic ethnicity, and time since first observation. Model fit was evaluated by comparing deviances and fitting cubic spline models. Lifetime risks of death from LDOC and radiographic silicosis were estimated up to age 85 with an actuarial approach accounting for competing causes of death. RESULTS: For deaths due to LDOC, a linear relative rate model gave the best fit in Poisson regression analyses. At the mean cumulative exposure of LDOC cases to silica, after adjustment for smoking, the estimated rate ratio was 4.2 (p<0.0001); at the maximum cumulative exposure of cases, the rate ratio was 18.4. The excess lifetime risk for white men exposed to respirable cristobalite dust for 45 years at the current permissible exposure limit (PEL; about 0.05 mg/m(3)) of the Occupational Safety and Health Administration was 54/1000 (95% confidence interval (95% CI) 17 to 150). For 70 incident cases of radiographic silicosis largely manifest before the end of employment, the best fit was also the linear relative rate model, predicting a rate ratio of 25.6 for silicosis at the mean cumulative exposure of the cases (p<0.0001). The excess lifetime risk for silicosis at the current PEL was 75/1000. CONCLUSION: Current occupational health standards for crystalline silica permit risks of lung disease other than cancer far in excess of what is usually considered acceptable by the Occupational Safety and Health Administration (a lifetime risk of less than one in a thousand deaths).

Adult↗
PubMed1997

Lung cancer in relation to exposure to silica dust, silicosis and uranium production in South African gold miners.

BACKGROUND: A nested case-control study for lung cancer was performed on a cohort of 2260 South African gold miners in whom an association between exposure to silica dust and risk of lung cancer was previously reported. The objective was to investigate an expanded set of risk factors and also cancer cell type. METHODS: The 78 cases of lung cancer found during the follow up period from 1970 to 1986 were matched with 386 controls. Risk of lung cancer was related to smoking, exposure to silica dust, incidence of silicosis, and uranium production and the uranium content of the mine ore. RESULTS: The risk of lung cancer was associated with tobacco smoking, cumulative dust exposure, duration of underground mining, and with silicosis. The best predictive model included pack years of cigarette consumption (adjusted relative risk (RR) = 1.0 for < 6.5 pack years, 3.5 (95% confidence interval (CI) 0.7 to 16.8) for 6.5-20 pack years, 5.7 (95% CI 1.3 to 25.8) for 21-30 pack years, and 13.2 (95% CI 3.1 to 56.2) for more than 30 pack years) and silicosis (RR = 2.45 (95% CI 1.2 to 5.2)). No association was found with uranium production. The lung tumour cell type distribution was 40.3% small cell carcinoma, 38.8% squamous cell, 16.4% adenocarcinoma, and 4.5% large cell carcinoma. Small and large cell cancer combined were associated with exposure to dust. CONCLUSIONS: The results cannot be interpreted definitively in terms of causal association. Possible interpretations are: (1) subjects with high dust exposure who develop silicosis are at increased risk of lung cancer; (2) high levels of exposure to silica dust on its own is important in the pathogenesis of lung cancer and silicosis is coincidental; and (3) high levels of silica dust exposure may be a surrogate for the exposure to radon daughters.

Adenocarcinoma↗
PubMed1998

Pemphigus vulgaris associated with silicosis.

Pemphigus vulgaris has never before been associated with silicosis, although there are many reports of silicosis accompanied by several autoimmune diseases such as progressive systemic sclerosis, systemic lupus erythematosus, dermatomyositis or rheumatoid arthritis. We observed a patient with pemphigus vulgaris accompanied with silicosis. The patient was a 75-year-old man with a 2-month history of repeated oral erosions and blisters on the back, thighs and axillas. Histological examination showed suprabasal cleavage with acantholysis. Immunoblotting analysis demonstrated binding of the patient's serum to the 130-kD pemphigus vulgaris antigen (desmoglein 3) and the 160-kD pemphigus foliaceus antigen (desmoglein 1). The patient has radiographically been diagnosed as having silicosis. An elevated serum IgG, antinuclear antibody, anti-ssDNA, antimicrosomal antibodies and a biologically false-positive reaction to the Wassermann test were also detected. Although the clinical symptoms improved after treatment with systemic steroids, the patient died due to pneumonia. This is the first reported case in which the characteristics of both pemphigus vulgaris and silicosis could be detected.

Aged↗
PubMed2001

Antidesmoglein autoantibodies in silicosis patients with no bullous diseases.

BACKGROUND: Pemphigus is an autoimmune bullous disease characterized by the presence of antidesmoglein autoantibodies. However, the mechanism of its autoantibody production remains unknown. In previous reports, we have described rare cases of pemphigus and pemphigoid associated with silicosis. It is well known that during long-term silicosis, some autoimmune diseases, such as systemic sclerosis, systemic lupus erythematosus or rheumatoid arthritis, can occur. OBJECTIVE: The aim of this study was to explore the presence of pemphigus or pemphigoid autoantibodies in silicosis patients without clinical bullous diseases or collagen diseases. METHOD: The presence of pemphigus antibodies was examined in 54 silicosis patients with no associated bullous diseases, using immunofluorescence, the enzyme-linked immunosorbent assay (ELISA) for desmoglein 1 and 3, and immunoblotting methods. In the antibody-positive cases, HLA genotyping of peripheral lymphocytes was performed with PCR-RFLP. RESULTS: Seven out of the 54 patients were found to be positive for pemphigus antibodies and 1 for bullous pemphigoid by immunofluorescence. In addition, by ELISA, 6 patients were found to be positive against the desmoglein 1 antigen, 2 against the desmoglein 3 antigen and 2 against both desmoglein 1 and desmoglein 3. CONCLUSION: The results of the present study strongly suggest the occurrence of pemphigus and pemphigoid autoantibodies in patients with silicosis. It remains unclear whether such patients will develop an autoimmune bullous disease in the future. Accordingly, long-term follow-up of antibody-positive patients is required.

Aged↗
PubMed1996

Transforming growth factor-beta (TGF-beta) in silicosis.

Silicosis is characterized by fibrosing nodular lesions that may eventually develop into progressive massive fibrosis (PMF). Cytokines (interleukin-1beta [IL-1beta], tumor necrosis factor-alpha [TNF-alpha] and growth factors insulin-like growth factor-1 [IGF-1] platelet-derived growth factor [PDGF]) have been implicated in the formation of these lesions. TGF-beta promotes extracellular matrix accumulation by upregulating collagen and fibronectin gene expression, and inhibits matrix degradation by decreasing secretion of proteases and increasing secretion of protease inhibitors. We hypothesized that TGF-beta is associated with matrix deposition and fibrosis in silicosis. To test this hypothesis we studied early and late nodular lesions and PMF (11 cases and two controls) with immunohistochemistry, using rabbit polyclonal antibody to the purified whole molecule of TGF-beta in Bouin's fixed lung tissue. This antibody is reactive with both intra- and extracellular forms of TGF-beta. In the control lungs, small amounts of TGF-beta were present in the bronchial epithelium, macrophages, bronchial and vascular smooth muscle, and bronchial glands. There was minimal to moderate staining in the early silicotic peribronchiolar lesions. In the nodular lesions of silicosis, central hyalinized areas contained the maximum staining for TGF-beta. Fibroblasts in the periphery of the nodular lesions were also positive. In acute silicosis, there was marked staining of hyperplastic alveolar epithelium. Macrophages were markedly positive. In the PMF lesions, large areas of scar tissue contained TGF-beta. These data suggest a major role for TGF-beta in silicosis, particularly in the formation of silicotic nodules and the development of PMF.

Adult↗