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Distant health effects of using asbestos in shipyards and in co-operating plants.

A survey was conducted during a 15-years period (1981-1994) among a group of workers employed in shipyards and in cooperating plants, who were exposed to asbestos. In a group of 681 people surveyed a growing incidence of asbestosis of the lung was revealed: from 3.9% in 1981 to 17.9% in 1994. Since 1990, 19 persons have been found to have malignant neoplasms, in that number in 9 cases the location of neoplasm was evidently associated with the effects of the asbestos dust (3 mesotheliomas of the pleura and 6 bronchial cancers of the lungs). The smoking habit was probably a contributing factor in the occurrence of these diseases.

Adult↗

Third wave of asbestos-related disease from secondary use of asbestos. A case report from industry.

An occupational health survey conducted in a workshop in which asbestos cement was used showed initial atmospheric asbestos levels ranging from 1.9 to 27.5 fibres per millilitre of air. Radiological changes suggestive of asbestos-related pleural disease were found in 2 workers (2.5%), while 3 (3.8%) had borderline features of asbestosis. The survey confirmed that uncontrolled and hazardous use of asbestos continues in industry despite public awareness of its dangers and the Asbestos Regulations of 1987.

Asbestos↗

Pneumoconioses in Bulgaria--prevalence, development, prognosis and prevention.

Prevalence of the basis types of pneumoconioses (silicosis, silicotuberculosis, asbestosis) in Bulgaria was studied during a 7-year period (1985-1991). Information was taken from reports of the Department for silicosis and other pneumoconioses control in the country. As a basis of the investigation serves the total number of workers endangered by dust exposure in different risk branches. The more rarely encountered pneumoconioses are referred to in absolute numbers. Trends in the development and prognosis of the most frequently encountered pneumoconiosis in Bulgaria could be followed. Recommendations are given for future preventive activity.

Asbestosis↗

[Health hazards: asbestos--a review (author's transl)].

The health hazards caused by asbestos are reviewed and some conclusions are drawn. Asbestos and the materials containing a high percentage of asbestos cannot completely be substituted by other materials without dangerous health effects. It is to be expected that the use of asbestos will still increase. An important health hazard has become evident among asbestos insulation workers. But also in other branches the application of asbestos is widespread. It seems to be difficult to find substitutes meeting the same requirements for using like asbestos. Rock-wool and glass fibres are used more and more in exchange for asbestos. Registers for asbestos workers and asbestos working places are established in several countries. The main causes of death induced by asbestos among asbestos workers are asbestosis. mesothelioma and cancer. For the evaluation and assessment of cancer risk due to asbestos epidemiological studies have to be conducted. Even a short period of exposure to low quantities of asbestos fibres proves to be a health hazard causing certain diseases (diffuse pulmonary fibrosis, pleural hyalinosis, pleural calcifications, mesothelioma) after more than 20 years. For avoiding occupational disease hazards among asbestos workers the dust level on the working place has to be lowered to acceptable concentrations (maximal allowable concentrations). The identification of dust sources of asbestos, the application of practice codes for handling of asbestos, the substitution of asbestos by materials without dangerous health effects, and dust control at source are the most effective directions of hygienic practice. The health protection requires annual medical examinations of all persons exposed to airborne concentrations of asbestos.

Adolescent↗

[Asbestos: past, present and future].

Owing to its particular properties asbestos has been widely used for the production of insulating material, for fire proofing, and for strengthening to other materials such as cements and plastics, and thus the story of this mineral was one of progressive commercial success until the middle of this century. However, serious health hazards were realized early: around the turn of the century a progressive form of diffuse fibrosis (asbestosis) in asbestos workers was observed and in 1950 an excess risk of lung cancer, while in 1960 the causal relationship between asbestos and mesothelioma were confirmed. In view of the known potential risks of asbestos and its widespread use in the building industry, more recently asbestos has caused considerable public concern and anxiety. Based on numerous experimental and epidemiological observations, present knowledge of the pathogenic effects of asbestos is sufficient for a number of broad conclusions to be drawn. (1) The amphibole types of asbestos are too dangerous for use as industrial material, and should be banned. (2) Chrysotile can probably be used safely if there is strict control of the workers' dust exposure. (3) It is very unlikely that the general public is at any measurable risk from asbestos in buildings. Exceptions are people working regularly on maintenance tasks involving removing or cutting of asbestos in buildings; such people are properly classified as asbestos workers and should be protected accordingly.(ABSTRACT TRUNCATED AT 250 WORDS)

Asbestos↗

[Asbestos-related lesions detected by high-resolution CT scanning in asymptomatic workers. Specificity, relation to the duration of exposure and cigarette smoking].

The possibility to detect initial "preclinical" pulmonary lesions related to asbestos is under debate. The aim of this study is to report our experience. We have submitted to HRCT 70 shipyard workers with chest X-ray judged "normal" by "outside" readers (mean age 44.5 +/- 6.1 ys) with a similar grade of (low-level) exposure to amosite (mean duration of "direct"/"heavy" exposure was 4.2 +/- 4.9 ys; "environmental"/"light" exposure was 8.4 +/- 5.9 ys). Among the 70 workers, in 34 pleural plaques were shown, in 6 subjects parenchymal abnormalities alone and in 13 parenchymal and pleural abnormalities were found; in the last 17 workers no pathological finding was shown. In six subjects the presence of a combination of parenchymal abnormalities permitted us to diagnose asbestosis. The difference in the duration of exposure to asbestos for the subjects with both pleural and parenchymal involvement compared to all other groups of workers was statistically significant; also the difference in duration of exposure between workers with or without parenchymal involvement resulted significant. In a control group (20 subjects without any known professional exposure to asbestos) HRCT permitted us to identify 5 cases with small pleural plaques while only one case presented parenchymal bands; lesion frequency was significantly lower in comparison with the exposed group. Calcified plaques have been proved to be more common in the workers with heavier exposure, and no one of the reference group had calcified plaques. The CT-determined emphysema score was found to optimally correlate with smoking habit (pack/years). In conclusion our study suggests that pulmonary or pleural involvement can be shown by HRCT before the onset of any clinical symptomatology with high sensitivity and specificity. Furthermore the results seem to indicate that the prevalence of HRCT-shown parenchymal lesions and the severity of lung involvement among asbestos-exposed workers are related to the duration of exposure, as in most of clinically evident asbestos-related lung disorders, in contrast with previous observations.

Adult↗

[The role of pulmonary macrophages in the development of pulmonary fibrosis caused by asbestos].

The role of alveolar and interstitial macrophages in asbestos-induced pulmonary fibrosis is discussed. Asbestosis is thought to result from a series of cellular interaction involving the pulmonary macrophages and lung fibroblasts. Inhaled asbestos fibres activate serum complement-dependent chemoattractant for macrophages which accumulate at alveolar duct bifurcations playing a central role in phagocytosis fibers and forming early pulmonary lesions. After phagocytic stimulation macrophages release various chemotactic factors for neutrophils and other inflammatory cells including TNF, neutrophil chemotactic factor and many proinflammatory mediators such as prostaglandins, leukotrienes, thromboxane. Apart from that, macrophages produce free radical oxygen and release lysosome enzymes which may cause lung tissue injury. There is also concomitant accumulation of fibroblasts proliferating in response to macrophages-derived growth factors, interleukin-1 and fibronectin. As a result of those processes collagen production increase and pulmonary fibrosis develops.

Animals↗

[The role of pulmonary epithelial cells in lung cellular reaction to asbestos exposure].

The damage of pulmonary alveolar epithelial cells occurs in many inflammatory conditions caused by various agents, e.g. asbestos, that involve interstitial lung disease in experimental animals and in humans. After exposure to asbestos alveolar epithelial cells contain significant amount of asbestos fibers and show histologic changes which indicate a marked epithelial injury. The alveolar epithelial injury is manifested by swelling, debris and patchy necrosis of type I cells partly detached from its basement membrane. Besides, regenerative hyperplasia of type II pneumocytes with ultrastructurally cisternal dilation of the rough endoplastic reticulum and significantly greater number of lamellar bodies are found. Following the cessation of exposure, epithelial cells are cleared out of asbestos fibers and return to the normal condition. These data provide insight into pathogenesis of diffuse lung disease and the role of alveolar cells in early and late phases of asbestosis.

Animals↗

[Epidemiology of chronic, precancerous and oncologic diseases in workers of asbestos and cement industry].

Hygienic, clinical and epidemiologic screening was performed in staff of asbestos and cement goods production enterprise. Various dystrophic processes of pharynx and nasal cavity appeared to prevail among upper respiratory tract diseases. Average exposure to dust during 22 years at the stated production can lead to asbestosis 0-I stage, average exposure during 20.5 years can result in dust bronchitis and occupational allergic dermatosis can result from average exposure to dust during 21 years. Retrospective cohort study of mortality within 1949-1988 failed to find oncologic risk in workers engaged into asbestos and cement goods production higher than in general population.

Adult↗

High-resolution CT of the lung in asbestos-exposed subjects. Comparison of low-dose and high-dose HRCT.

The lowest possible mAs settings for high-resolution CT (HRCT) were studied on 45 individuals with suspected asbestos-related lung disease. All patients were investigated with 5 to 6 high-dose HRCT images (120 kVp/160 mA/2 s) at 3-cm intervals. At a selected level 4 additional low-dose images were obtained on each patient with lower mAs settings (100 mA/2 s, 80 mA/2 s, 60 mA/2 s, 30 mA/2 s). Thirty-seven subjects out of 45 had HRCT lesions compatible with asbestosis. HRCT images obtained with as low as 60 mA/2 s settings clearly showed pleural tractions and thickenings, parenchymal bands, honeycombing and subpleural curvilinear shadows, whereas in the evaluation of subpleural short lines and ground glass findings 80 mA/2 s were required. The lowest setting, 30 mA/2 s, was sufficient only in detecting and evaluating pleural tractions and thickenings. We conclude that 160 mAs yield good quality HRCT images, with substantial decrease of radiation dose, for the evaluation of asbestos-related lesions.

Adult↗

[Computed tomography of pneumoconioses].

Thoracic computed tomography is now used in the assessment of occupational diseases. Coal miner's pneumoconiosis, silicosis and benign asbestosis constitute the principal indications. The specific contribution of computed tomography techniques, their methodology and their signs are presented.

Asbestosis↗

Hyaline splenic and hepatic plaques. Correlation with cirrhosis, pulmonary tuberculosis, and asbestos exposure.

Nine hundred twenty-five unselected autopsies were investigated for the presence or absence of hyaline peritoneal (splenic or hepatic) plaques, hyaline pleural plaques, asbestos, liver cirrhosis, heart failure, previous peritoneal dialysis or abdominal surgery, chronic peritonitis, splenomegaly, splenic infarcts, and pulmonary or abdominal tuberculosis. Lung asbestos body concentrations were calculated in 570 subjects. Peritoneal plaques were recorded in 163 cases. In both univariate and multivariate analyses, they were associated with cirrhosis, pulmonary nonactive tuberculosis, pleural plaques, and asbestosis. Association with asbestos body counts was also found, with a significant trend. Peritoneal plaques were described long ago in different pathologic conditions, for some of which (cirrhosis and nonactive pulmonary tuberculosis) the association is confirmed by the present analysis. It is suggested that they are significantly associated, moreover, with indicators of asbestos exposure.

Adult↗

[Interleukin-1 beta production by alveolar macrophages in cases of asbestos exposure].

In order to investigate the role of interleukin-1 beta secreted by alveolar macrophages in the pathogenesis of pulmonary asbestosis, we performed bronchoalveolar lavage on 12 asbestos-exposed subjects and 10 control subjects, and measured interleukin-1 beta secreted by alveolar macrophages. Interleukin-1 beta production was increased in the asbestos-exposed subjects compared to control subjects (3.1 +/- 2.2 ng/ml versus 0.8 +/- 0.4 ng/ml, p < 0.05). The period after retirement was inversely correlated with interleukin-1 beta production (r = -0.67, p < 0.05). We divided non-smoking asbestos-exposed subjects into two subgroups based on the radiographical profusion according to the ILO classification. The advanced group was defined as grade 2 or greater profusion, and the early group was defined as grade 1 or lower profusion. We found higher production of IL-1 beta in the early group than in the advanced group.

Aged↗

[Study on correlation between chest X-P course findings and change in antinuclear antibody in asbestos plant employees].

In order to investigate the correlation between a course of chest radiograms and changes in antinuclear antibody (ANA), 140 asbestos workers who had a chest radiogram and measurement of ANA in 1987 and had been working in the same plant were given the same examination again in 1992. In the group who showed a change in ANA to positive, the progression of pulmonary asbestosis was significantly higher than in the group who remained negative. Progression in pleural lesions was not significantly correlated.

Antibodies, Antinuclear↗

[Characteristics of respiratory and cardiovascular systems of workers with extended length of service at asbestos plants].

Examination of 72 individuals (including 62 workers of asbestos production and 10 silicosis patients) revealed that asbestos dust primarily causes hypoxemia followed by pulmonary ventilation disorders and characteristic X-ray signs of asbestosis. Hypoxemia is associated by reliable changes in functioning of left ventricle and central hemodynamics. Degree of hypoxemia appeared to correlate with echocardiographic signs of malfunction of left ventricle and chronic heart failure.

Adult↗

[Lung cancers attributable to asbestos on a pathological basis].

More than 1,000 asbestos bodies/gram dry weight (AB/gdw) were found by light microscopy in lung tissues, out of 429 non selected cases of pulmonary carcinoma (264 from surgery and 165 from autopsy). Asbestosis was detected by histology in 28% of the cases with AB > 1,000/gdw (in 19% of the surgical cases, and in 38% of the autopsy cases). A proportion of 4% of the total cases may be related to asbestos exposure.

Air Pollutants, Occupational↗

[Asbestos fiber count in extra-pulmonary tissues].

Most autoptic tissues of three men (two with pulmonary asbestosis and one without any exposure to asbestos) were analyzed by transmission electron microscopy and energy dispersion spectrometry for the quantitative and qualitative evaluation of asbestos fibers. Preliminary results indicate that only in cases with occupational exposure were found asbestos fibers (in lung, pleura , bladder, kidney and liver). These results allow interesting speculations on some environmental pathogenetic questions and deserve further investigations.

Aged↗

The clinical aspects of mesothelioma.

Three hundred and twenty-seven cases of mesothelioma accepted by a panel of pathologists have been used to construct a clinical picture of the disease. The cases analysed died between 1 January 1960 and 31 December 1969 and consisted of 267 pleural, 37 peritoneal, and 23 cases which could have arisen in either site. Two hundred and sixty-eight were in men and 59 in women and the disease appeared to be the same in women as in men. The mean age at death was 59-37 (+/- SD 9-89) years but ranged from 29 to 88 years. The mode of onset was insidious in all but a few cases and the mean interval before reaching the hospital was 3-39 (+/- SD 4-64) months for pleural and 3-08 (+/- SD 3-22) for peritoneal cases. Patients usually noticed a dull non pleuritic pain first but suffered some breathlessness, lassitude and weight loss by the time they reached hospital. On examination there was little evidence of disease apart from the signs of pleural effusion or thickening or ascites. Clubbing and signs of asbestosis were rare except in the peritoneal cases who more frequently gave an occupational history of heavy exposure and showed the radiological consequences of this. At the time when these patients were investigated diagnostic procedures were unrewarding and many patients were only diagnosed in retrospect. The prognosis was somewhat better for patients shown to have mainly epithelial cell tumours, 17-89 (+/- SD 18-26) months, predominantly spindle cell lesions surviving on the average only 7-98 (+/- SD 8-55) months and mixed tumours 11-3 months. The criteria for the early clinical diagnosis are described with a view of facilitating the search for effective treatment.

Adult↗