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[Total and partial O2 and CO2 ductances in workers exposed to inhalation of cement-asbestos].

The aim of the study was to assess the efficiency of the respiratory system in ensuring the correct dynamics of respiratory gases in subjects chronically exposed to the inhalation of asbestos-cement dust but not yet suffering from parenchymal asbestosis, via measurement of total and partial O2 and CO2 ductance coefficients (Du). Two groups of male workers of working age were selected, the first consisting of 22 workers employed on the manufacture of asbestos-cement products, the second consisting of 26 workers who had never been exposed to the inhalation of significant concentrations of occupational respiratory irritants. The two groups were comparable for age, smoking, and normal spirometric parameters for FVC, FEV1 and PEF, and were free of any type on interstitial lung disease according to ILO standards. In the exposed group, all O2 and CO2 ductance coefficients were significantly lower than in the non-exposed, except DuBCO2 (alveolar-capillary ductance for CO2). Measurement of O2 and CO2 lung ductances at rest thus revealed an impairment of the diffusion and of the interpulmonary exchange of blood and air in subjects chronically exposed to the inhalation of asbestos-cement dust. In the sample under study, such impairment preceded lung damage detectable by spirometric and radiological tests and was an obstacle not only to oxygen intake but also to the elimination of carbon dioxide.

Adult↗
PubMed1989

[The carcinogenic effect of asbestos].

There is a causal correlation between the inhaled dose of asbestos at the working place, the occurrence of asbestosis, and a 5-fold increased mortality rate of lung cancer. Mesothelioma, which appears to be very rare among the general population, is a specific sign of exposure to asbestos fibres. Malignant tumours of the urinary bladder, the gastro-intestinal tract, the larynx and the oesophagus in workers may also be ascribed to the specific exposure in some cases. After a brief outline of the epidemiology of these diseases the carcinogenic effects of asbestos on the cellular and subcellular level are described. It can be shown from most recent literature that asbestos fibres can also trigger epigenetic and genotoxic effects. Numeric mutation of chromosomes, damage of the plasma membrane, and a modification of the immune system are most significant. In the presence of PAH, asbestos acts as a cocarcinogen. Asbestos fibres are positive in the cellular transformation test. Due to its initiating and promoting effects, asbestos proves to be a complete carcinogen. Obviously, asbestos fulfils the criteria of the modern theory of carcinogenesis as a multicausal and multistep process.

Air Pollutants↗
PubMed1989

Malignant pleural mesothelioma in the southwestern part of The Netherlands.

This report is the result of an analysis of the medical records of 124 patients presenting with a malignant pleural mesothelioma. Information about asbestos exposure was available in 104 of them, which appeared to be positive in 95 (91%). The median duration of exposure was 34 yrs. The median latent period was 41 yrs. The median survival was 11 months while different ways of treatment could not prolong survival. The most common radiologic findings were pleural effusions, while in some patients contralateral effusions or pleural thickening was found. Pleural plaques or asbestosis were seen in a minority of the patients. In this series a relatively high percentage of mixed type mesotheliomas was found (56%). Large biopsies will often show both epithelial and connective tissue type elements. Concerning diagnostic procedures we recommend beginning with cytology of pleural fluid, which can easily be obtained together with an Abrams biopsy. If this does not give a definite diagnosis thoracoscopy or thoracotomy will be indicated.

Aged↗
PubMed1989

[Toxic organic damage].

Pathohistological findings are playing an important role in the advice of toxic organ damages. After presentation of some details about the frequency of toxic organ damages, the pathways of toxic agents in the organism are discussed. In cells toxic damage may induce cell necrosis, functional disturbance, inhibition of cell proliferation or malignant transformation; in extracellular structures it may lead to degradation phenomena in the connective tissue matrix. As demonstrated in example of calciphylaxis, a combination of different noxes may not only add but even potentiate the effects of the single noxes. In intracellular reparation processes the lysosomal system is involved. In case of necrosis regeneration is possible in most kinds of tissues, if connective tissue rails are preserved. Otherwise an irreversible reparative fibrotic alteration of organ structure is induced which develops according to particular general and schematic rules. As mostly character and course of the tissue reaction is unspecific, pathohistological findings do not enable conclusions on the type of inducing toxic agent. The following presentation of some examples of toxic damages with pathognomonic histological appearance deals with asbestosis, silicosis, chloroquine-induced cardiomyopathy, aluminum-induced osteopathy and a recently described liver cirrhosis in early childhood induced by copper-containing drinking water. Some limits of traditional pathohistological evaluation of toxic organ damages have been overcome by application of new morphological techniques. Own investigations revealed that the immunocytochemical demonstration of the C5b-9-complement complex enables a better and earlier detection of irreversibly damaged cells. Discrimination of toxic and virus-induced tissue damage is facilitated by the technique of in-situ-hybridization. Sometimes a specific recognition and localization of toxic agents is achieved by X-ray microanalysis, electron-spectroscopic imaging (= ESI) resp. laser microprobe mass spectrometry (= LAMMA); comparing these techniques X-Ray microanalysis and ESI, both, enable specific identification of chemical elements, while LAMMA, in addition, offers some information about the involved molecules and isotopes.

Cells↗
PubMed1989

[Bronchoalveolar lavage in the assessment of lung diseases].

The bronchoalveolar lavage (BAL) is a new method of low risk for the differential diagnosis of pulmonary disorders. In the BAL cells, microorganisms, and non-corpuscular components derived from the alveolar space can be investigated. The analysis of the recovered cells delivers information about the diseases. Lymphocyte predominant disorders are sarcoidosis, hypersensitivity pneumonitis, alveolitis, tuberculosis, lymphangiosis carcinomatosa and pneumoconiosis. The prognosis of sarcoidosis depends on the ratio of the T-helper and T-suppressor cells. Neutrophil predominant disorders are seen in idiopathic pulmonary fibrosis, asbestosis and collagen vascular disorders. BAL has also become an established approach to the diagnosis of infections in the immunosuppressed patients. Also tumor cells and tumor markers can be detected. Phagocytosed particles are an indication of inhaled dust. Asbestos fibres and silica are visible by light microscopy and metals are detected by x-ray energy dispersive spectrometry.

Bronchoalveolar Lavage Fluid↗
PubMed1989

[Naf/nap-1, a new peptide which activates neutrophil leukocytes].

NAF/NAP-1 is a novel tissue-derived chemotactic peptide. It consists of 72 amino acids and has no sequence homology to known cytokines. NAF/NAP-1 is produced by a wide variety of cells after stimulation with interleukin-1, tumor necrosis factor or endotoxin, and has the properties of a local mediator of neutrophil recruitment into diseased tissues. There are indications that NAF/NAP-1 is important in the pathophysiology of inflammatory conditions such as psoriasis, idiopathic pulmonary fibrosis, asbestosis, adult respiratory distress syndrome and different forms of arthritis.

Amino Acid Sequence↗
PubMed1989

[Occupationally-induced pneumopathies].

Today chronic obstructive airways diseases rank amongst the most important occupational pneumopathies in Switzerland. As far as asthma is concerned, the baker's (flour) and the spray painter's (Isocyanates) types are the most important. Despite their frequent occurrence the two forms of asthma seem to differ in their pathogenetic mechanisms. Due to technical precautions another type of occupational pneumopathology namely pneumoconiosis was considerably reduced. Among asbestos induced diseases the cases of asbestosis are decreasing. However, there still are quite a lot of events of malignant mesotheliomas actually heading the list of occupational malignomas. The most numerous asbestos induced disturbances, however, are pleural plaques which seem to be of no considerable importance. Another group of occupational lung disorders is that of hypersensitivity pneumonitis (extrinsic allergic alveolitis), among which the "farmer's lung" and in more industrial settings the "humidifier lung" are most frequently seen. For the diagnosis and evaluation of occupational pneumopathies work related symptoms and individual work place exposure are of decisive importance.

Alveolitis, Extrinsic Allergic↗
PubMed1989

[Pulmonary opacities in the shape of ribbon streamers. Apropos of a case].

The authors report a case of chronic interstitial pneumonia with a very unusual appearance (on plain films and CT); in fact such ribbon-like linear opacities with concentric and pseudo-cavitary disposition have not been previously described. They are comparable but different from the linear opacities described by Carrington in some cases of chronic eosinophilic interstitial pneumonia, which are vertical and peripheral. They are also different from the curvilinear sub-pleural opacities reported in some cases of asbestosis. On the basis of the anatomic findings they discuss the specificity of such radiologic patterns or their sole value as an evolutive state.

Female↗
PubMed1989

Estimations of risk from environmental asbestos in perspective.

Because very recent data on asbestos in the environment are available, some fairly firm conclusions can now be drawn regarding current exposure to asbestos fibres. If account is taken of occupational exposure data (where past exposure levels were very high indeed, leading to a very significant risk to workers at the time), it is possible to make some reasoned estimates of the risk from ambient air. In the past, there was considerable confusion regarding the degree of risk for both occupational and environmental conditions. In estimating the risk, account needs to be taken, in particular, of the fact that: (a) occupational exposures in the past were frequently higher than reported; (b) asbestosis (a disease only associated with very heavy occupational exposures) would seem to be mechanistically involved in the development of lung cancer associated with asbestos exposure; (c) chrysotile asbestos is now the commonest form of fibre used unlike in the past, when greater quantities of crocidolite and amosite were used, the latter types being much more closely associated with mesothelioma than chrysotile; (d) overall levels of asbestos in environmental ambient air are lower than they used to be; (e) ingested asbestos seems to be associated with a negligible degree of risk as indicated by animal and human studies. The estimated values of risk provided here are smaller than those published some years ago but are similar to those given in very recent key publications. The level of environmental lifetime risk from exposure to airborne asbestos would appear to be about 1 in 100,000 or even lower. Such a level of risk is exceedingly low, and bearing in mind the criteria of both WHO and the Royal Society of London, it would appear to represent an acceptable 'rare-event' extremely low-level risk, like the cancer risk from the cosmic radiation adsorbed when flying across the Atlantic or from eating charcoal broiled meat, or the risk of being killed by lightning.

Air Pollutants↗
PubMed1989

[Health damage caused by asbestos and other mineral fibers].

Occupational exposure to asbestos is associated with malignant tumors in the lung and malignant mesothelioma in the pleura and peritoneum. Tumors at other sites have also been reported. The benign asbestos-related disorders are asbestosis and pleural fibrosis, effusion and plaques. Chronic bronchitis may be associated with previous asbestos exposure. Fiber dimensions and durability are main factors for carcinogenicity. For practical reasons, long and thin fibers like asbestos should be considered carcinogenic. The diagnosis of asbestos-related disease is based upon information on occupational exposure. Analysis of lung fiber burden supports information given by the occupational history and gives valuable information on dose-response and dose-effect relationships. Building materials with good maintainance of the surfaces do not release asbestos fibers, whereas materials subject to mechanical stress should be replaced by nonasbestos-containing materials to avoid the stipulated very low increase in cancer risk.

Asbestos↗
PubMed1989

The interaction of asbestos and neutrophils injures cultured human pulmonary epithelial cells: role of hydrogen peroxide.

Asbestos exposure causes diffuse interstitial pulmonary fibrosis. Since alveolar epithelial cell injury is hypothesized to precede the fibrotic response in asbestosis, we investigated whether asbestos, either alone or in conjunction with neutrophils (PMNs), injured cultured human pulmonary epithelial cells (HPECs). HPEC cytotoxicity was assessed with a standard 51chromium release assay after a 16-hour incubation with asbestos and PMNs. Negligible HPEC cytotoxicity was observed after incubation with either amosite asbestos (500 micrograms/ml) or PMNs alone in serum-free media. However, incubation with both asbestos and PMNs caused significant HPEC injury, which was asbestos dose-dependent; causing 25% +/- 4% detachment and 52% +/- 8% 51chromium release with 500 micrograms/ml asbestos. The cytotoxic effects of asbestos plus PMNs were nearly completely attenuated with serum (20%) or catalase (100 micrograms/ml) but were not prevented with scavengers of superoxide anion, hydroxyl radical, or hypochlorous acid. A role for hydrogen peroxide (H2O2) in mediating HPEC injury was also suggested by the demonstration of asbestos-induced generation of H2O2 by PMNs. Furthermore, H2O2 alone (10(-4)mol/L) caused significant HPEC damage. Intimate contact between asbestos-activated PMNs and HPECs was a necessary requirement for PMN-mediated HPEC cytotoxicity. These data suggest that pulmonary epithelial cell injury is mediated in part by H2O2 release from asbestos-activated PMNs as well as intimate contact between the epithelial cell, PMNs, and asbestos.

Asbestos↗
PubMed1985

Angiotensin-converting enzyme activity in sarcoidosis and other disorders.

A review is given on S-angiotensin-converting enzyme (SACE) and its clinical value, based upon 327 sarcoidosis patients and 1,274 patients with various disorders. SACE was elevated in 55% of the sarcoidosis patients, although with a higher frequency in those with active disease. Erythema nodosum was associated with normal initial SACE, subsequently rising, and sarcoid hypercalcaemia was consistently followed by elevated SACE. In non-sarcoid patients, elevated SACE was observed in only 10 cases. The sensitivity and specificity were 0.55 and 0.99, respectively, and the positive and negative predictive values were 0.95 and 0.90, respectively. Elevated SACE pointed strongly towards the presence of sarcoidosis, although reservations must be made in patients with liver disorders, diabetes mellitus, hyperthyroidism, asbestosis or silicosis which are rather common disorders also associated with elevated SACE. Normal SACE does not exclude sarcoidosis.

Berylliosis↗
PubMed1988

[Pathologic analysis of 302 primary bronchogenic adenocarcinomas].

Pathomorphology of 302 primary bronchogenic adenocarcinomas resected in our hospital from 1957 to 1984 was studied. It consisted of 23.5% of the total lung cancers. Gross findings are: central type 15.9%, peripheral type 82.4%, and disseminated type. 1.7%. Cancerous cavity was observed in 13.2%. According to the histologic classification of lung tumor, WHO, 1981, adenocarcinoma was divided into four subtypes: 1. acinar adenocarcinoma (132 cases); 2. papillary adenocarcinoma (73 cases); 3. bronchiolo-alveolar carcinoma (74 cases) and 4. solid carcinoma with mucus formation (23 cases). Among them, there were 16.6% of scar carcinoma and 1 case associated with asbestosis. 15 cases were studied by electron microscope. The 5-year survival rate was 19.6% (peripheral type 21.7%, central type 12.5% and disseminated type 0%). There was no significant difference in the prognoses of the histologic subtypes. The patients without metastasis to the hilum, mediastinum or positive stump had better prognosis. The relationship between adenocarcinoma and bronchiolo-alveolar carcinoma is discussed.

Adenocarcinoma↗
PubMed1988

Smoking and pulmonary fibrosis.

A review of the relevant literature provides evidence that cigarette smoking causes microscopic diffuse interstitial pulmonary fibrosis in humans at autopsy. The association shows a dose-response relationship and the fibrosis is often severe. Experimental animal studies have confirmed these observations when the exposure to inhaled smoke was prolonged or heavy. Six published and one unpublished cross-sectional chest x-ray surveys of adults have shown low profusion of small irregular opacities related to smoking with a dose-response relationship when this has been studied. Although information on radiographic-pathologic correlation is deficient, these studies support the hypothesis that smoking causes diffuse interstitial pulmonary fibrosis which is radiologically visible with low profusion in low prevalence. The x-ray manifestations may be confused with early pneumoconiosis such as asbestosis.

Age Factors↗
PubMed1987

[Clinical evaluation of primary lung cancer induced by exposure to asbestos].

Upon autopsy, asbestos was found in the lungs of 7 primary lung cancer patients out of 70. These seven-patients were men over 60 years old. All of them had occupational histories of exposure to asbestos. In histological classification, 4 of the cases were adenocarcinoma and the others were squamous. Six of them were in the peripheral area. According to chest X-rays two of the patients showed lung fibrosis (asbestosis), and all of them showed pleural plaque. Thus, we concluded that ten percent of the primary lung cancer cases autopsied in our hospital might be induced by exposure to asbestos.

Adenocarcinoma↗
PubMed1986

[Asbestos carcinogenesis from clinical and hypothetical viewpoints].

On the basis of a case of mesothelioma of the pleura in a 28-year-old female who among our patients had the longest survival time after establishment of the diagnosis (31 months) the authors adopt a definite attitude to the problems of asbestosis. It can be regarded as ascertained that after asbest exposition a systemic contamination of the organism occurs. Apart from the inhalative intake further possibilities of the asbest fibre incorporation and the elimination are referred to. As to the cancerogenesis of asbest-induced malignomas the existing theories appear at present still insufficient; analogies to Virchow's irritation theory are possible in the serosa tumours.

Adult↗
PubMed1985

Benign and malignant pleural mesothelioma.

Malignant mesotheliomas have assumed an importance in the medical and lay literature out of proportion to their incidence in the American population, chiefly due to the known association of pleural mesothelioma with asbestos exposure. Data from the Connecticut tumor registry suggest that this tumor is increasing in incidence. Based on exposures between 1940 and approximately 1970, when industrial precautions were first instituted, epidemiologists estimate that the number of new cases of mesothelioma will peak sometime in the 1990s and that mesothelioma will thereafter become less common. These models generally assume that asbestos exposures after 1970 will be insignificant. While industrial levels that are legal today will almost certainly prevent the development of severe asbestosis in most workers, unfortunately a threshold of exposure below which there is no risk of mesothelioma has not been documented. Asbestos continues to be used in floor and ceiling tiles, in automobile brake linings, and in a variety of other products. At the present time, construction workers who maintain or remove asbestos constitute one of a number of groups with continued exposure. The diagnosis of a malignant pleural mesothelioma is not difficult provided that the physicians caring for such a patient consider mesothelioma in the differential diagnosis. Patients present with chest pain or shortness of breath, or both, and the initial chest x-ray film most often reveals a large unilateral pleural effusion. The tumor characteristically remains localized until late in its course, and thus extensive workup at the time of diagnosis is seldom required. Generally, a large piece of tissue obtained via an open biopsy is required for adequate histologic diagnosis. Investigational approaches include taking numerous needle biopsies with samples sent for electron microscopy as well as for immunoperoxidase staining for keratin and CEA. The treatment of this disease remains unsatisfactory. Occasional patients have remained disease-free for periods in excess of 5 years after intensive treatment, however. The conclusion that mesothelioma is untreatable is clearly untenable since palliation and a response rate of 30 per cent to various chemotherapeutic regimens have been reported by a number of investigators. While many authors have advocated supportive care alone because "current treatments have not demonstrated increased survival," we believe patients with mesothelioma should be offered investigational therapy.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1979

Schistosomiasis--cancer: etiological considerations. A review.

Evidence for a causal connection between Schistosoma haematobium-infection and carcinoma of the urinary bladder is discussed. A group relationship of schistosomiasis cancer to cancers as+sociated with asbestosis, foreign body implants, and cicatrization is suggested on the basis of several criteria. Results of experimental foreign body tmuorigenesis in mice are presented and elaborated in relationship to schistosomiasis cancer. Carcinogenic development at the cellular level is discussed with emphasis on the essential role of tissue-environmental conditions, especially fibrotic changes and macrophage quiescence.

Adult↗