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PubMed1991

Activated alveolar macrophages express the insulin-like growth factor-I receptor.

Alveolar macrophages (AM) recovered from the lower respiratory tract of individuals with interstitial lung disease (ILD) proliferate at a 2- to 15-fold increased rate (P.B. Bitterman et al. 1984. J. Clin. Invest. 74:460-469). Normal AM stimulated with immune complexes or asbestos release platelet-derived growth factor and insulin-like growth factor-I (IGF-I), and AM activated in vivo in ILD release these growth factors. We evaluated normal unstimulated and activated AM for the receptor for IGF-I to determine if macrophage IGF-I could be involved in the enhanced macrophage proliferation. Although normal AM did not have specific 125I-labeled recombinant IGF-I binding, AM activated by chrysotile asbestos or lipopolysaccharide in vitro or from individuals with ILD had detectable binding that could be inhibited by an anti-IGF-I receptor monoclonal antibody in a dose-dependent fashion. Autoradiography with 125I-labeled recombinant IGF-I revealed binding to the IGF-I receptor on the surface of activated AM, and the percentage of labeled cells was reduced with anti-IGF-I receptor monoclonal antibody or excess unlabeled recombinant IGF-I. Hybridization of total AM RNA to a 32P-labeled IGF-I receptor riboprobe using solution hybridization demonstrated IGF-I receptor mRNA transcripts in AM from an individual with asbestosis, consistent with active expression of the IGF-I receptor gene. In the context of the known role of IGF-I as a growth factor for many cells, these data are consistent with the concept that IGF-I and its receptor may play an important role in the proliferation of AM in the inflamed lower respiratory tract.

Adult↗
PubMed1991

In vitro bioactivity of asbestos for the human alveolar macrophage and its modification by IgG.

The alveolar macrophage (AM) is likely to play a central role in the initiation and development of the fibrosis associated with asbestos exposure due to its ability to produce factors that modulate cellular functions of the immune system of the lung. In this study, we examine the effects of IgG, albumin, and dipalmitoylphosphatidylcholine (DPPC), the major protein and lipid constituents of alveolar lining fluid, on the interaction between the human AM and chrysotile and crocidolite asbestos, silica, and aluminum beads. We show that both chrysotile and crocidolite asbestos, but not silica and aluminum beads, stimulate the human AM to produce superoxide anion. Preincubating chrysotile and crocidolite asbestos with IgG resulted in an enhancement of their ability to stimulate superoxide anion production. IgG subclasses were studied to determine the subclass specificity of this enhancing effect; on a molar basis, IgG1 was the most potent. After preincubation with IgG, both silica and aluminum also stimulated superoxide anion production to levels similar to the IgG-preincubated asbestos. When albumin and DPPC were included in the preincubation mixture, the IgG-mediated enhancement of superoxide anion production by asbestos was unaffected, while that of silica and aluminum was abolished. In summary, these results indicate that IgG can significantly enhance the bioactivity of particulates for human AM in vitro, and that chrysotile and crocidolite asbestos are unique in their ability to retain this enhancement in the presence of albumin and DPPC. These results are consistent with the suggestion that superoxide anion production by the AM may play an important role in the development of asbestosis.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1991

Human mononuclear phagocytes express the insulin-like growth factor-II/mannose-6-phosphate receptor.

The insulin-like growth factor (IGF)-II/mannose-6-phosphate (M6P) receptor, which targets acid hydrolases to lysosomes, is a multifunctional protein with separate binding sites for IGF-II and M6P. The purpose of this study was to determine if alveolar macrophages (AM) and their precursor cells, blood monocytes, expressed this receptor. AM expressed IGF-II/M6P receptors as detected by [125]IGF-II surface binding that was not reduced by recombinant IGF-I or IGF-I receptor monoclonal antibody (alpha IR3). Surface binding was also detected on blood monocytes and could be upregulated approximately 4-fold by incubation with lipopolysaccharide. There were no differences in surface binding by AM lavaged from individuals with asbestos exposure or from normal volunteers. Using the polymerase chain reaction and reverse transcriptase to reverse-transcribe mRNA from mononuclear phagocytes, specific IGF-II/M6P receptor cDNA was amplified and detected by agarose gel electrophoresis from both AM and blood monocytes. The IGF-II/M6P receptor has an intracellular transport role in many cells cycling from the cell surface to the cytoplasm, or binding to phosphorylated acid hydrolases in the Golgi and transporting them to an acidic prelysosomal site where they dissociate and fuse to the lysosomes and IGF-II/M6P recycles to the trans-Golgi. These functions may be particularly important in asbestosis and other interstitial lung diseases where AM are activated, intracellular lysosomes are a prominent morphologic feature, and acid hydrolases are found in recovered lavage fluid.

Asbestos↗
PubMedDate not supplied

Clinical experience with pleuroscopy utilizing the bronchofiberscope.

The gas sterilized bronchofiberscope has been utilized as a pleuroscope for visual exploration of the pleural space and forceps biopsy of abnormal lesions in 16 patients with undiagnosed pleural disease. The instrument was inserted through a small (1-2 cm) incision. Aspiration of pleural fluid and instillation or aspiration of air to produce a controlled pneumothorax are easily accomplished through the instrument's suction channel. In eight patients with undiagnosed pleural effusion, biopsy of visualized nodules established the diagnosis of carcinoma. Three patients with bronchogenic carcinoma and pleural effusion had no pleural metastases at pleuroscopy which was confirmed in two patients who had thoracotomy and lung resection. Parenchymal subpleural nodules of metastatic carcinoma were confirmed by pleuroscopic biopsy in one patient. Biopsy via the pleuroscope was unsuccessful in two patients, one with pleural fibrosis, probably related to asbestosis, and one with mesothelioma. Both required open surgical biopsy of the pleura. There has been minimal patient discomfort and no serious complications.

Adenocarcinoma↗
PubMed1994

Usefulness of the Nd:YAG laser in parenchyma-sparing resection of pulmonary nodular lesions.

AIMS AND BACKGROUND: The neodymium:yttrium-aluminium-garnet (Nd:YAG) laser has been successfully employed in parenchyma-sparing resection of pulmonary nodular lesions. We report our experience with limited resection using a noncontact Nd:YAG laser applied through a thoracotomic approach. METHODS: During the period March 1987-October 1993, we performed parenchyma-sparing resections of 66 pulmonary nodular lesions with a noncontact Nd:YAG laser in 47 patients. Nodules were approached through postero-lateral thoracotomy (n = 40), median sternotomy (n = 5) or staged bilateral thoracotomy (n = 2). Fifty-two lesions were located in a peripheral position and the others (n = 14) at various depths within the parenchyma. RESULTS: Fifteen lesions were benign: hamartoma (n = 5), chronic pneumonic infiltrate (n = 3), tuberculoma (n = 3), asbestosis (n = 2), Wegener's granuloma (n = 1). Twelve lesions were attributable to primary lung cancer and 33 were metastatic lesions. Another 6 lesions turned out to be necrotic metastases following chemotherapy. There were no perioperative deaths. Pulmonary re-expansion was shortly obtained: mean drainage time was 4.31 +/- 3.9 days. Only one patient presented a prolonged drainage time (11 days); in this case, the air leak was successfully treated by tissue glue sealant trans-drainage infiltration. Follow-up ranged from 2 to 96 months. No case of relapse on the resection site has been observed. CONCLUSIONS: The results suggest that Nd:YAG laser resection is safe and worthwhile in patients with multiple lesions and borderline pulmonary function.

Adolescent↗
PubMed1994

Distribution of transforming growth factor-beta 1, fibronectin, and smooth muscle actin in asbestos-induced pulmonary fibrosis in rats.

We are studying the development of fibrogenic lesions in the lungs of rats exposed briefly to an aerosol of chrysotile asbestos fibers. This model of asbestosis has enabled us to establish very early cellular events at the specific locations where interstitial fibrosis will develop. These sites, the first alveolar duct bifurcations, are where the fibers are initially deposited and where macrophages first accumulate. In the studies presented here, we used immunohistochemical techniques to show that these macrophages exhibit strong localization of transforming growth factor-beta. In the adjacent developing fibrogenic lesions a clear increase in fibronectin staining was demonstrated and morphological analysis indicated a significant increase in amounts of smooth muscle actin. Such studies are essential in furthering our understanding of the distribution of potential mediators of the fibrogenic process and the cellular responses they elicit during the pathogenesis of disease.

Actins↗
PubMed1997

Occupational Exposures to Asbestos in Brazil.

European and Canadian asbestos companies have long taken advantage of the lack of regulation of the asbestos industry in developing countries. Their activities exploit vulnerable workers whose lack of medical care may result in a silent epidemic of asbestos-related diseases. At this time, virtually all cases of asbestosis and asbestos-related cancers are not identified, reported, or compensated in developing countries. Brazil provides a compelling example of this growing problem. To stem the epidemic of asbestos-related diseases, Brazil, and many other countries, must adopt the total ban on asbestos use now in effect in more developed countries. Obstacles to accomplishing this in developing countries are daunting.

Journal Article↗
PubMed2004

Assessment of 18F-fluorodeoxyglucose dual-head gamma camera in asbestos lung diseases.

The purpose of this study was to evaluate the performance of 18F-fluorodeoxyglucose (18FDG) imaging via coincidence detection emission tomography (CDET) in identifying malignant lesions in subjects exposed to asbestos. A total of 30 patients exposed to asbestos underwent 18FDG-CDET between January 2000 and June 2003. A CDET scan of the thorax and abdomen was performed 60 min after injection of 18FDG in fasting patients, and results were obtained in slices in three axes. The CDET results were compared to those from computed tomography (CT), and pleural or surgical biopsy in patients with positive 18FDG-CDET results. All primary malignant mesotheliomas accumulated 18FDG (n=6), and, in two patients, CDET findings were superior to those of CT, allowing early detection. In two cases, lung carcinomas with malignant pleural effusion were also detected. There were five false positive CDET results: three unilateral pleural thickening, one rounded atelectasis, and one benign lung nodule. All patients with pleural plaques showed no significant 18FDG uptake. Malignant diseases were detected by 18FDG-CDET imaging with a sensitivity of 89% and specificity of 71%. Coincidence detection emission tomography can identify malignant mesothelioma in selected subjects exposed to asbestos. Coincidence detection emission tomography appears to be a useful noninvasive method for the follow-up of subjects with exposure risk of asbestosis.

Adult↗
PubMed2005

Nonmalignant pleural lesions due to environmental exposure to asbestos: a field-based, cross-sectional study.

The aim of the present study was to investigate the frequencies of asbestos-related benign pleural diseases in villagers environmentally exposed to asbestos and the factors affecting these frequencies. A field-based, cross-sectional study was designed. In total, 991 villagers from 10 villages, randomly chosen from 67 villages with known use of asbestos-containing white soil in central Anatolia (Turkey), were investigated. The type of asbestos in the white soil was determined for each village, as well as air-borne fibre concentrations. The villagers were investigated with small-size chest roentgenograms and epidemiological features were recorded. The air-borne fibre levels were generally low. Despite this, pleural plaques were found in 14.4% of the villagers, 10.4% had diffuse pleural fibrosis and 0.4% asbestosis. The significant variables for plaques were age, sex, type of asbestos fibre, e.g. actinolite and tremolite, and exposure duration, while there was a negative relationship with cumulative exposure. The variables affecting diffuse pleural fibrosis were age, exposure duration and cumulative exposure. In conclusion, villagers exposed to environmental asbestos have high frequencies of pleural plaques and diffuse pleural fibrosis, similar to occupationally exposed asbestos cohorts. Different types of asbestos appear to result in different frequencies of pleural lesions.

Adult↗
PubMed1998

Interstitial lung disease more than 40 years after a 5 year occupational exposure to talc.

A 62 yr old woman was initially diagnosed with sarcoidosis until a thoracoscopic biopsy revealed the presence of numerous birefringent particles in fibrotic areas of the centrilobular lung zones. These particles were examined by electron microscopy and X-ray spectrometry and characterized as impure talc. Further inquiry into her occupational history revealed that she had worked from the age of 14-18 yrs in a factory making rubber hoses, where she had had an intense exposure to talc. There was no evidence of silicosis or asbestosis, and other significant causes of interstitial lung disease were excluded. This case emphasizes the importance of a thorough occupational history, which may reveal a remote and forgotten exposure to a significant cause of interstitial lung disease. Although this presentation of talcosis is unusual, this case suggests that even a relatively short, but presumably intense exposure to talc more than 40 yrs previously may be a cause of progressive lung fibrosis.

Female↗
PubMed2006

Measurements of asbestos burden in tissues.

Asbestos inhaled into the lung is recognized as a potential causal agent for the development of diseases in man. The diseases induced by asbestos include lung cancer, fibrosis of the lung (asbestosis), and extrapulmonary tumors including mesothelioma (a tumor of the serosal membrane), as well as fibrosis and other changes in the pleura linings. The cause of these diseases can often be more specifically linked to asbestos exposure once tissue burden of asbestos is established. The asbestos burden in tissue can be defined as the number of asbestos bodies and/or the numbers and types of asbestos fibers found in the tissue. In either of these cases the quality of information is directly dependent on the preparative techniques and instrumentation used in the analysis. The present article will discuss the significance of findings of tissue burden based on both these variables.

Asbestos↗
PubMed1983

Malignant mesothelioma following radiation exposure.

Mesothelioma developed in proximity to the field of therapeutic radiation administered 10-31 years previously in four patients. In three, mesothelioma arose within the site of prior therapeutic radiation for another cancer. Mesothelioma in the fourth patient developed adjacent to the site of cosmetic radiation to a thyroidectomy scar. None of these four patients recalled an asbestos exposure or had evidence of asbestosis on chest roentgenogram. Lung tissue in one patient was negative for ferruginous bodies, a finding considered to indicate no significant asbestos exposure. Five other patients with radiation-associated mesothelioma have been reported previously, suggesting that radiation is an uncommon cause of human mesothelioma. Problems in the diagnosis of radiation-associated mesotheliomas are considered.

Adenocarcinoma↗
PubMed1999

Occupational cancer in central European countries.

The countries of central Europe, including Poland, the Czech Republic, Slovakia, Hungary, Romania, and Bulgaria, suffer from environmental and occupational health problems created during the political system in place until the late 1980s. This situation is reflected by data on workplace exposure to hazardous agents. Such data have been systematically collected in Skovakia and the Czech Republic since 1977. The data presented describe mainly the situation in the early 1990s. The number of workers exposed to risk factors at the workplace represent about 10% of the working population in Slovakia and 30% in Poland. In Slovakia in 1992 the percentage of persons exposed to chemical substances was 16.4%, to ionizing radiation 4.3%, and to carcinogens 3.3% of all workers exposed to risk factors. The total number of persons exposed to substances proven to be carcinogens in Poland was 1.3% of the employees; 2.2% were exposed to the suspected carcinogens. The incidence of all certified occupational diseases in the Slovak Republic was 53 per 100,000 insured employees in 1992. Cancers certified as occupational cancers are skin cancer caused by occupational exposure to carcinogens, lung cancer caused by ionizing radiation, and asbestosis together with lung cancer. Specific information on occupational cancers from Romania and Bulgaria was not available for this paper. It is difficult to predict a trend for future incidences of occupational cancer. Improved control technology, governmental regulatory activity to reduce exposure, surveillance of diseases and risk factors, and vigilant use of preventive measures should, however, ultimately reduce occupational cancer.

Carcinogens↗
PubMed1983

Epidemiologic basis for the asbestos standard.

The current standard for occupational exposure to asbestos is 2 fibers/cm3 averaged over an 8-hr day. A NIOSH/OSHA committee has recently concluded that the 2 fiber/cm3 standard is grossly inadequate to protect workers from asbestos-related disease, and that all levels of asbestos exposure studied thus far have demonstrated asbestos-related disease. The committee recommends that a 0.1 fiber/cm3 limit replace the current 2 fiber/cm3 standard on the grounds that this is the lowest level detectable with currently available analytical techniques. Thus a 0.1 fiber/cm3 limit is not based on epidemiological data but on the presumption that any level of exposure is disease producing. This paper addresses the question of whether it would be possible to detect health effects of exposure below the current 2 fiber/cm3 standard. Five studies are reviewed which provide evidence on the strength of the relationship between asbestos fiber exposure and lung cancer. Calculation of sample sizes needed to be 95% certain of detecting the kind of excess probably associated with exposure to 2 fibers/cm3 suggests that epidemiology is not likely to be useful in detecting lung cancer below the current standard. Some outcome measures other than lung cancer or clinical asbestosis will be needed if observations on humans are to be used as evidence for a lowering of the present standard.

Asbestos↗
PubMed1984

Particles causing lung disease.

The lung has a limited number of patterns of reaction to inhaled particles. The disease observed depends upon the location: conducting airways, terminal bronchioles and alveoli, and upon the nature of inflammation induced: acute, subacute or chronic. Many different agents cause narrowing of conducting airways (asthma) and some of these cause permanent distortion or obliteration of airways as well. Terminal bronchioles appear to be particularly susceptible to particles which cause goblet cell metaplasia, mucous plugging and ultimately peribronchiolar fibrosis. Cancer is the last outcome at the bronchial level and appears to depend upon continuous exposure to or retention of an agent in the airway and failure of the affected cells to be exfoliated which may be due to squamous metaplasia. Alveoli are populated by endothelial cells, Type I or pavement epithelial cells and metabolically active cuboidal Type II cells that produce the lungs specific surfactant, dipalmytol lecithin. Disturbances of surfactant lead to edema in distal lung while laryngeal edema due to anaphylaxis or fumes may produce asphyxia. Physical retention of indigestible particles or retention by immune memory responses may provoke hyaline membranes, stimulate alveolar lipoproteinosis and finally fibrosis. This later exuberant deposition of connective tissue has been best studied in the occupational pneumoconioses especially silicosis and asbestosis. In contrast emphysema a catabolic response, appears frequently to result from leakage or release of lysosomal proteases into the lung during processing of cigarette smoke particles. The insidious and probably most important human lung disease due to particles is bronchiolar obstruction and obliteration, producing progressive impairment of air flow. The responsible particle is the complex combination of poorly digestive lipids and complex carbohydrates with active chemicals which we call cigarette smoke. More research is needed to perfect, correct and quantify our preliminary picture of the pathogenesis of lung disease by particles, but a useful start has been made.

Animals↗
PubMed1984

Inhaled particles in human disease and animal models: use of electron beam instrumentation.

The mineral pneumoconioses (lung disease caused by inhalation of inorganic dust) have been an important disease entity for centuries. In the last several decades, the electron microscope has been used to elucidate the distribution and identification of inhaled minerals, to aid in establishing etiologic factors, and less commonly, to determine the basic biologic mechanisms through which inhaled minerals cause lung disease. In this section, I review the instrumentation and tissue preparation currently used to address some modern problems in particle-induced lung disease. For example, human pneumoconioses of undetermined etiology can be clarified by electron microscopy and X-ray energy spectrometry. In addition, the initial deposition patterns of asbestos and silica are demonstrated in animal models, and the contributions of electron microscopy in establishing the initial lesions of asbestosis are described.

Animals↗
PubMed1993

Asbestos-induced lung disease.

This review attempts to deal with two major questions concerning asbestos-induced lung disease: How does inhaled asbestos cause cell proliferation and fibrosis? and Will there continue to be risk from exposure to asbestos in schools and public buildings? The first is a scientific question that has spawned many interesting new experiments over the past 10 years, and there appear to be two hypothetical schemes which could explain, at least in part, the fibroproliferative effects of asbestos fibers. One supports the view that toxic oxygen radicals generated on fiber surfaces and/or intracellularly are the central mediators of disease. The second hypothesis is not mutually exclusive of the first, but, in my opinion, may be integral to it, i.e., the cellular injury induced by oxygen radicals stimulates the elaboration of multiple varieties of growth factors and cytokines that mediate the pathogenesis of asbestosis. There is increasing evidence that molecules such as platelet-derived growth factor and transforming growth factor beta, both synthesized and secreted by activated lung macrophages, are responsible, respectively, for the increased interstitial cell populations and extracellular matrix proteins that are the hallmarks of asbestos-induced fibrosis. The challenge today is to establish which combinations of the many factors released actually are playing a role in disease pathogenesis. The issue of continued risk currently is more a question of policy and perception than science because a sufficient database has not yet been established to allow full knowledge of the circumstances under which asbestos in buildings constitutes an ongoing health hazard. The litigious nature of this question does not help its resolution. In as much as public policy statements and risk assessment are not within my purview, I have focused on the state-of-the-art of asbestos as a complete carcinogen. It appears to be generally nongenotoxic, but all asbestos fiber types can induce chromosomal mutations and aneuploidy, perhaps through their ability to disrupt normal chromosome segregation.

Asbestos↗
PubMed2002

Asbestos-related disease.

Until the 1980s, asbestos was widely used throughout the UK. The incidence of asbestos-related disease is still climbing because of the long delay in developing the disease from the initial exposure. The spectrum of diseases encompasses malignant mesothelioma, asbestosis, asbestos-related lung carcinoma and benign pleural disease, including pleural plaques.

Asbestos↗