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PubMed2004

[Standardized CT/HRCT-classification of the German Federal Republic for work and environmental related thoracic diseases].

High resolution computed tomography (HRCT) plays an indispensable role in the diagnosis of pneumoconiosis and other lung damage arising from inhalation. Till now, however, there has been no agreed standardized convention for the use of the technique, or for documenting results uniformly. A task-group on Diagnostic Radiology in Occupational and Environmental Diseases of the German Radiological Society has produced a coding sheet based on experience gained in production of consultants' clinical reports, experts' examinations of patients seeking compensation for occupational lung disease, and physicians' professional development courses. The coding sheet has been used in a national multicenter study. It has been further developed and tested by an international working group comprising experts from Belgium (P.A. Gevenois), Germany (K.G. Hering, T. Kraus, S. Tuengerthal), Finland (L. Kivisaari, T. Vehmas), France (M. Letourneux), Great Britain (M.D. Crane), Japan (H. Arikawa, Y. Kusaka, N. Suganuma), and the USA (J. Parker). The intention is to standardize documentation of computertomographic findings in occupationally and environmentally related lung and pleural changes, and to facilitate international comparisons of results. Such comparisons were found to be achievable reproducibly with the help of CT/HRCT reference films. The classification scheme is purely descriptive (rather than diagnostic), so that all aspects of occupationally and environmentally related parenchymal and pleural abnormalities may be recorded. Although some of the descriptive terms used are associated with pneumoconiosis (e.g., rounded opacities in silicosis, or, in asbestosis, interlobular septal and intralobular non-septal lines, as well as honeycombing) many overlapping patterns that need to be considered for differential diagnosis are also included in the scheme.

Disability Evaluation↗
PubMed2003

CT findings and serum ca 125 levels in malignant peritoneal mesothelioma: report of 11 new cases and review of the literature.

The aim of this study was to review and reappraise the clinical and CT features of malignant peritoneal mesothelioma (MPM), and to discuss differential diagnosis. The history, clinical, and laboratory data, and imaging studies of 11 patients with a histologically proven diagnosis of MPM, were retrospectively reviewed. Our patients consisted of 7 women and 4 men, with a median age of 48 years (age range 40-55 years). There was a definite history of significant asbestos exposure in 6 patients. Abdominal swelling (9 of 11) was the most common presenting symptom. The mean serum CA-125 (normal value 1.2-32 U/ml) level was 230 U/ml (range 19-1000 U/ml). The most common radiological findings were extensive or moderate amounts ascites (11 of 11), irregular or nodular peritoneal thickening (11 of 11), omental involvement (10 of 11), mesentery involvement (9 of 11), pleural thickening, plaques or calcification (7 of 11), pleural effusion (6 of 11), and bowel wall thickening (5 of 11). Two patients had large upper abdominal masses. Computed tomography findings of MPM are nonspecific and inadequate to pinpoint specific diagnosis. The diagnosis requires histological demonstration which is commonly made by an image or laparoscopic-guided biopsy. Pleural changes suggesting asbestosis combined with CT findings and high CA-125 levels can suggest, but are not diagnostic of, mesothelioma. Suggesting the diagnosis of MPM is important because histological and immunohistochemical tests are needed for diagnostic accuracy.

Adult↗
PubMed2004

Asbestos induces tissue factor in Beas-2B human lung bronchial epithelial cells in vitro.

Asbestos has been implicated in the pathogenesis of interstitial lung diseases including asbestosis. Tissue factor (TF) initiates blood coagulation in vivo contributing to inflammation and tissue remodeling via extravascular fibrin deposition and signaling for profibrogenic mediators. We hypothesized that asbestos could induce TF expression by lung epithelial cells. We found that TF mRNA and TF-dependent procoagulant activity were induced in asbestos-treated Beas-2B human airway epithelial cells, which we used as a model system. The effect was increased by crocidolite and chrysotile versus control particulates, including titanium dioxide (TiO2) and Wollastonite (W). Transcription factors that bind the TF gene promoter, including NF-kappaB, AP1 and Sp1, were induced by asbestos while TF mRNA was unstable. TF mRNA was inhibited by mithramycin in asbestos-treated as well as control cells suggesting that Sp1 contributes to TF maintenance in Beas-2B cells. Sp1 knockdown with specific siRNA decreased TF antigen, which is consistent with Sp1-mediated control of TF in Beas-2B cells. The results demonstrate that asbestos induces TF expression in lung epithelial cells in vitro, representing a newly recognized potential mechanism by which asbestos may modulate epithelial cell responses germane to lung remodeling. The mechanism involves alterations in steady-state TF mRNA that do not involve posttranscriptional regulation, implicating control of TF gene expression at the transcriptional level through Sp1 or other transcription factors.

Asbestos↗
PubMed2002

Three decades of pleural cancer and mesothelioma registration in Austria where asbestos cement was invented.

Recently, a new mesothelioma epidemic was predicted from observations made in Western Europe. From early observations in Austria the lower increase in cases of mesothelioma compared with neighbor countries had been related to different uses of asbestos. In order to test this hypothesis, incidence and mortality of pleural cancer [International Classification of Diseases (ICD)-8/9 163] were analyzed for three decades and supplemented by data from a cohort study in the factory that had been the largest consumer of asbestos imported to Austria and from all Austrian occupational diseases registered between 1990 and 2001. In men, mortality rates (based on 15 to 45 deaths/year) were lowest in 1980-1989, but similar in 1970-1979 and 1990-2001. No increase in younger-birth cohorts was detected. Incidence rates (based on 13 to 44 cases/year) increased (36%) non-significantly ( P=0.14). In women, a significant decrease in mortality and incidence rates ( P<0.01) was observed from 1970. Rates from work-related mesothelioma (based on only 0-7 men and 0-4 women/year) must be interpreted with caution. In the cohort of 2,816 asbestos cement workers 26 pleural mesotheliomas were registered from 1990 through mid-1999. Six of these cases (three male and three female) had not been registered as an occupational disease, but all of these cases had been encoded under ICD 163 in mortality statistics. One female cohort member registered as having asbestosis according to the death certificate had died from mesothelioma according to the statistics of occupational diseases. We conclude that no epidemic of mesothelioma due to past asbestos exposure is to be expected in Austria.

Asbestos↗
PubMed1980

Active pulmonary tuberculosis discovered at post-mortem examination of the lungs of black miners.

The prevalence of active pulmonary tuberculosis and pneumoconiosis in black mine workers who died while working on mines and came to autopsy is reported. All black mine workers are regularly examined radiologically during life and those with pulmonary tuberculosis or pneumoconiosis are compensated and sent home (after treatment in the case of tuberculosis) and would not enter this autopsy series. Details are given of the prevalence of tuberculosis separately for gold, coal and asbestos miners. Tuberculosis was age-related in all three cases. In black gold miners the presence of a slight degree of silicosis not detected radiologically in life was associated with a significantly increased prevalence of pulmonary tuberculosis compared to gold miners without silicosis. This was not found to be the case in those in whom asbestosis or coal workers' pneumoconiosis was found at autopsy.

Adolescent↗
PubMed1981

Diffuse malignant pleural mesothelioma in Glasgow.

Thirty-two patients seen in one area between 1974 and 1980 with a diagnosis of malignant pleural mesothelioma are reviewed retrospectively. Asbestos contact, often in the shipyards, was found in 80%. The average age at diagnosis was 64 years and chest pain or breathlessness were the most common initial symptoms. Radiology usually confirmed a pleural effusion, but rarely also showed pleural plaques or asbestosis. The most useful diagnostic investigation was pleural biopsy, with a 59% success rate. Post mortem examinations showed widespread infiltration of adjacent tissues in many, with haematogenous metastases in 52%. Prognosis was poor, with an average survival of 40 weeks from presentation. No treatment improved life expectancy. Thoracotomy was followed by painful chest wall masses. The incidence of mesothelioma in our area is six times higher than in the rest of Scotland. As the disease has a long latent period between asbestos exposure and appearance, it will be many years before this rate is significantly reduced.

Aged↗
PubMed1988

Bronchoalveolar lavage sampling of airway and alveolar cells.

Bronchoalveolar lavage (BAL) cell counts are used to assess 'alveolitis' in patients with interstitial lung diseases (ILD) but inflammatory cells from airways can contribute to the differential cell count. To determine what BAL volume samples airway cells in patients with ILD we measured the proportion of bronchial epithelial cells (BECs) in four successive 25 ml aliquots in a single lung subsegment in 23 patients with ILD (cryptogenic fibrosing alveolitis (CFA) four, rheumatoid lung (RL) three, asbestosis (ASB) 11, sarcoidosis (SARC) five). Cells recovered from the first two 25 ml lavages exhibited higher proportions of BECs (15 +/- 4% and 9 +/- 2% respectively) than those from the remaining two aliquots (3 +/- 1%, 3 +/- 1%, each P less than 0.01), suggesting that the first 50 ml BAL preferentially samples airway cells compared to the second 50 ml BAL. To evaluate airway and alveolar inflammatory cell proportions in ILD we performed two separate 50 ml BALs (samples I and II) in a single subsegment in 38 patients with ILD (CFA seven, RL five, ASB 19, SARC seven) and measured the proportions of recovered cells in each sample separately and combined. Seven control individuals were also studied. Sample I contained 1-67% (mean 26 +/- 3%) of the total recovered cells. Neutrophil (PMN) proportions were higher in sample I compared to sample II in CFA (20 +/- 6 vs 8 +/- 2%), RL (30 +/- 9 vs 8 +/- 2%) and ASB (12 +/- 2 vs 7 +/- 1%), P less than 0.05 for each, but were similar in samples I and II in patients with SARC (3 +/- 1 vs 2 +/- 1%) and controls (2 +/- 1 vs 2 +/- 1%). In combined samples (I + II), absolute PMN proportions were up to 8% higher than in sample II alone whereas absolute lymphocyte proportions were up to 8% less than in sample II alone. These data suggest that separate processing of the fluid recovered from the first 50 ml BAL in ILD patients provides information on the location of inflammatory cells and improves the accuracy of BAL cell counts.

Adult↗
PubMed1985

Selective exposure and analysis of the sheep tracheal lobe as a model for toxicological studies of respirable particles.

A conscious sheep model, recently developed to study sequentially the bronchoalveolar milieu, was further refined to use in the rapid in vivo assessment of the biological effects of respirable particles. In this model, the anatomically isolated tracheal lobe was selectively exposed to either 100 ml phosphate buffered saline (PBS) (control group of 12 sheep), 100 mg of 0.1-micron latex beads in 100 ml PBS (latex group of 12 sheep), or 100 mg of UICC Canadian chrysotile fibers in 100 ml PBS (asbestos group of 12 sheep). Bronchoalveolar lavages (BAL) of the tracheal lobe were obtained prior to exposure and at Days 1, 8, 15, 21, 29, 45, and 60 after exposure. Whole-lung detailed pulmonary function tests (PFT) were performed at the same times and the histopathology of the lobe was examined in six sheep in each group at Days 29 and 60. In the control sheep, there were no significant changes over time in any of the measures, and lung morphology remained normal. In the latex group, there was no significant change in PFT, the BAL analyses documented early transient increase in cellularity (macrophages and neutrophils at Day 1) and only macrophages after; lung histology documented an early macrophagic alveolitis which decreased to less than 10% of the initial inflammatory reaction at Day 60, without other distortion of the lung and airway architecture. In the asbestos sheep, the only change in whole-lung PFT was a 10-torr fall in arterial O2 pressure. BAL analyses documented persistent increases in macrophages, neutrophils, and lactate dehydrogenase as well as increasing gamma-globulins. Lung histology revealed a macrophagic and neutrophilic peribronchiolar alveolitis at Day 30, which regressed substantially by Day 60, but persistent peribronchiolar alveolitis, early fibrosis, and severe distortion of the small airways, lesions comparable to those of early asbestosis in sheep or humans. Thus selective exposure and sequential analyses of the sheep tracheal lobe in terms of BAL histomorphology should be valuable for rapid in vivo assessment of toxicity of respirable particles.

Air Pollutants↗
PubMed1982

The costs and effects of screening for cancer among asbestos-exposed workers.

Several million workers previously exposed to asbestos are at risk each year for developing asbestosis or cancer as a result of this exposure. We have reviewed the data on the general effectiveness of screening for the two most common cancers found in these workers (lung cancer and colo-rectal cancer) and have compared the relative benefits expected from screening workers for colon or lung cancer 10, 15, 20 or 25 yr after their initial exposure. Although lung cancer is common, there is little evidence at present that screening for this disease is effective in reducing mortality. Colon cancer is less common, there is more evidence that screening is effective, and the relatively high risk of dying from this disease in asbestos workers makes screening useful. The cost per additional year of life extended by screening is only a few hundreds of dollars, making colon cancer screening programs for asbestos workers considerably more cost-effective than most other screening programs. We conclude that occupational safety agencies should consider implementing screening programs for colon cancer in workers exposed to asbestos over 10 yr ago.

Asbestos↗
PubMed1984

Bone marrow alterations induced in mice with inhalation of chrysotile asbestos.

The effect of chrysotile asbestos exposure on bone marrow and immune parameters was examined in mice at 2, 12, and 26 weeks following a 3-day inhalation exposure. Ultrastructural examination revealed that the fibers were deposited primarily at alveolar duct bifurcations within the centriacinar region of the lung. Histological pulmonary changes were minimal, but by 26 weeks early asbestosis characterized by clusters of macrophages and minimal fibrosis were present in the centriacinar region of the lung. Lymphoproliferative responses, antibody levels, and number of plaque forming cells were not significantly altered in exposed mice. Pulmonary macrophages, but not peritoneal macrophages, showed evidence of activation in the chrysotile-exposed mice at 26 weeks following exposure. The most striking change was the depression of the number of bone marrow pluripotent stem cells (CFU-S) and marrow granulocyte macrophage progenitors (CFU-GM) which were lower at all three postexposure examinations. It is felt that the depression of bone marrow progenitors in asbestos-exposed mice may have relevance to the leukopenia reported in workers with occupational history of asbestos exposure.

Animals↗
PubMed1982

The industrial physician and occupational lung disease.

Prevention and management of chronic occupational illnesses requires that they first be recognized as such. This appears to be particularly difficult in the case of occupational lung disease and doubly so in the case of occupational immunologic lung disease. It took years to recognize asbestosis, byssinosis, and other chronic lung diseases as being occupational in origin. Trimellitic anhydride is particularly interesting in that it took a variety of purely clinical perceptions to arouse the suspicion that an immunologic response was involved. Increased cooperation of industry managements, occupational physicians, and researchers can lead to the elucidation of causes, which, in turn, can led to the goals we all share, the discovery, the treatment, and, even better, the prevention of disease.

Humans↗
PubMed1996

Iron-induced carcinogenesis: the role of redox regulation.

Redox cycling is a characteristic of transition metals such as iron. Iron is hypothesized to have been actively involved in the birth of primitive life on earth through the generation of reducing equivalents in the presence of UV light. Iron is an essential metal in mammals for oxygen transport by hemoglobin and for the function of many enzymes including catalase and cytochromes. However, the "free" or "catalytic" form of iron mediates the production of reactive oxygen species via the Fenton reaction and induces oxidative stress. Serum "free" iron is observed in rare situations such as in severe hemochromatosis in which serum transferrin is saturated. However, it is known that superoxide can release "free" iron from ferritin and hemosiderin in the cell. "Free" iron is quite cytotoxic as well as mutagenic and carcinogenic. Iron compounds were first reported to induce sarcomas in rats by Richmond in 1959. Thereafter, several iron-induced carcinogenesis models were established, including the ferric nitrilotriacetate model by Okada and colleagues. Iron may have a role in the carcinogenic process of other transition metals such as copper and nickel, or other kinds of carcinogens such as nitrosamine and even virus-induced carcinogenesis. In humans, genetic hemochromatosis and asbestosis are two major diseases associated with iron-induced carcinogenesis. There is an increasing number of reports of an association between increased body iron stores and increased risk of cancer. Iron-induced oxidative stress results in two possible consequences: (1) redox regulation failure that leads to lipid peroxidation and oxidative DNA and protein damage; (2) redox regulation that activates a variety of reducing and oxystress-protective mechanisms via signal transduction. Both consequences appear to play a role in iron-induced carcinogenesis.

Animals↗
PubMed1992

The mineral dust diseases.

The mineral dust diseases, also called the pneumoconioses, comprise a wide spectrum of conditions ranging from diseases characterized by diffuse collagenous pulmonary reactions to relatively small lung burdens of bioactive dusts (e.g. silicosis, asbestosis) to diseases characterized by largely non-collagenous reactions in the face of heavy lung dust burdens (e.g. coal workers pneumoconiosis). According to information submitted to the International Labour Office, which is however incomplete, substantial numbers of individuals are still at risk for the mineral dust diseases in the workplaces of the world. An overview of their epidemiology in industrialized and industrializing countries reveals more commonalities than contrasts. Commonalities include the major determinants of disease (including exposure level, intensity and particle size distribution), their clinical manifestations and, probably, secular trends towards less clinically severe disease, at least in the larger, better controlled workplaces. Still a risk however, in both industrializing as well as industrialized countries, are the small, uncontrolled workplaces, often the source of mini-epidemics. Contrasts relate to the incidence and/or prevalence rates of tuberculosis amongst workforces at risk for the mineral dust diseases. Rates, which are invariably higher in industrializing than in industrialized economies, usually reflect the background tuberculosis rates in the populations which furnish the industrial workforces and they should be the target for control measures. Research in the industrialized countries should focus on disease mechanisms and on the bioactivity of workplace contaminants, old and new, and in the industrializing countries on the distribution and determinants of mineral dust diseases in their workplaces.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed2004

Proposed criteria for mixed-dust pneumoconiosis: definition, descriptions, and guidelines for pathologic diagnosis and clinical correlation.

We defined mixed-dust pneumoconiosis (MDP) pathologically as a pneumoconiosis showing dust macules or mixed-dust fibrotic nodules (MDF), with or without silicotic nodules (SN), in an individual with a history of exposure to mixed dust. We defined the latter arbitrarily as a mixture of crystalline silica and nonfibrous silicates. According to our definition of MDP, therefore, MDF should outnumber SN in the lung to make a pathologic diagnosis of MDP. In the absence of confirmation of exposure, mineralogic analyses can be used to support the pathologic diagnosis. The clinical diagnosis of MDP requires the exclusion of other well-defined pneumoconioses, including asbestosis, coal workers' pneumoconiosis, silicosis, hematite miners' pneumoconiosis, welders' pneumoconiosis, berylliosis, hard metal disease, silicate pneumoconiosis, diatomaceous earth pneumoconiosis, carborundum pneumoconiosis, and corundum pneumoconiosis. Typical occupations associated with the diagnosis of MDP include metal miners, quarry workers, foundry workers, pottery and ceramics workers, and stonemasons. Irregular opacities are the major radiographic findings in MDP (ILO 1980), in contrast to silicosis, in which small rounded opacities predominate. Clinical symptoms of MDP are nonspecific. MDP must be distinguished from a variety of nonoccupational interstitial pulmonary disorders.

Dust↗
PubMed2004

Induction of CD69 antigen expression in peripheral blood mononuclear cells on exposure to silica, but not by asbestos/chrysotile-A.

While cases of silicosis are often complicated by various autoimmune disorders, patients with asbestosis develop malignant tumors such as lung cancer and malignant mesothelioma. These differences may derive from different biological effects, particularly on immunological cells, of silica and asbestos. To find differences between silica and asbestos, the early activation antigen, CD69, on T cells was examined because dysregulated and continuous activation of T cells may promote the survival of self-recognizing T cells. After cultivation of peripheral blood mononuclear cells with or without silica or chrysotile-A, an asbestos, only silica induced CD69 expression on the lymphocytes. This induction of CD69 expression was mediated by protein kinase C activation. In addition, cell-cell contact mediated by HLA-DR was more important than soluble factors secreted from silica-phagocytosed cells such as IL-1beta, IL-6, and IL-8, even though IL-6 and IL-8 were produced during the culture of PBMCs with silica and chrysotile-A. It should be examined how these activated, CD69-expressing lymphocytes affect other immune systems as well as alter themselves in terms of cytokine production and cell-cell interaction, leading to autoimmune disorders in silicosis patients.

Antibodies↗
PubMed2005

Biomarkers in risk assessment of asbestos exposure.

Developments in the field of molecular epidemiology and toxicology have given valuable tools for early detection of impending disease or toxic condition. Morbidity due to respiratory distress, which may be due to environmental and occupational exposure, has drawn attention of researchers worldwide. Among the occupational exposure to respiratory distress factors, fibers and particles have been found to be main culprits in causing diseases like asbestosis, pleural plaques, mesotheliomas and bronchogenic carcinomas. An early detection of the magnitude of exposure or its' effect using molecular end points is of growing importance. The early inflammatory responses like release of the inflammatory cells collected by non-invasive methods give an indication of the unwanted exposure and susceptibility to further complications. Since free radicals like O2-, OH, OOH, NO, NOO, etc. are involved in the progression of asbestos-related diseases and lead to cytogenetic changes, an evaluation of antioxidant states reducing equivalents like GSH and ROS generation can be a good biomarker. The cytogenetic end points like chromosomal aberration, micronucleus formation and sister chromatid exchange give indication of genetic damage, hence they are used as effective biomarkers. New techniques like fluorimetric analysis of DNA unwinding, alkaline elution test, fluorescent in situ hybridization and comet assay are powerful tools for early detection of initiation of disease process and may help in planning strategies for minimizing morbidity related to asbestos fiber exposure. The present review article covers in detail possible biomarkers for risk assessment of morbidity due to fibers/particles in exposed population.

Asbestos↗
PubMed2005

Poly(ADP-ribosyl)ation in asthma and other lung diseases.

Inhibition of poly(ADP-ribosyl)ation in oxidative stress-related pathologies has recently emerged as a very effective anti-inflammatory intervention in animal models of arthritis, colitis, diabetes and shock. Recent data from three laboratories also support the role of poly(ADP-ribose) polymerase-1 (PARP-1) activation in asthma. Similarly to other inflammatory conditions, the protective effects of PARP inhibition and the PARP-1 knock out phenotype in asthma models have been attributed to inhibition of inflammatory signal transduction (mainly via NF-kappaB) and of oxidative stress-induced cell dysfunction and tissue injury. Here I discuss the complex role of poly(ADP-ribosyl)ation in the regulation of inflammatory cell migration, chemokine and cytokine production and expression of other inflammatory mediators (inducible nitric oxide synthase, matrix metalloproteinases) in asthma. The role of PARP-1 in other oxidative stress-related lung diseases such as asbestosis, silicosis, acute respiratory distress syndrome and ischemia-reperfusion injury is also reviewed.

Animals↗
PubMed2005

Malignant mesothelioma in Hong Kong.

Malignant mesothelioma (mesothelioma) is rare. We conducted the first systematic study of the epidemiology of mesothelioma in Hong Kong from 1988 to May 2002 by reviewing medical records. Mesothelioma patients were identified from the database of 12 out of 20 hospitals that would have admitted mesothelioma patients territory-wide. These 12 hospitals served 73% of the total hospital bed-years of the 20 hospitals. We identified 67 mesothelioma patients. The estimated annual incidence was one per million, which was similar to the background incidence of one to two per million among Caucasians. Occupational history was available in 43 subjects. Three quarters of mesothelioma patients with available occupational history had occupational asbestos exposure. Restricting analysis to 48 patients with accessible medical records and using 67 occupational asbestosis patients for comparison, the epidemiology of mesothelioma in Hong Kong shares similarities with the literature: mean age of 63 years upon diagnosis, mean latency of 46 years, median survival of 9.5 months, male predominance, selective presentation among women, high prevalence among workers in ships and dockyards, predominantly epithelioid type, lower prevalence of asbestos bodies, and negative association with pleural plaques. Asbestos consumption in Hong Kong rose in the 1970s and peaked in early 1980s and late 1990s. Hong Kong may encounter an epidemic of mesothelioma in the 2010s if effective occupational asbestos control measures are not in place.

Adult↗