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PubMed1952

Asbestosis.

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Pneumoconiosis↗
PubMed1978

[Pulmonary silicosis (not including asbestosis and berylliosis].

The pleuro-pulmonary pathology of asbestos, top most of silicates, is today well known. Other silicates, talcum powder, clays, micas essentially, are exploited and commercialized. Their pathology is less well known and often contradictory because of the heterogeneity of the inhaled minerals. All can contain large quantities of quartz and some varieties of talcum and a considerable proportion of asbestos fibres. These minerals can provoke severe pneumoconioses, silicoses and asbestoses respectively. Some relatively pure products do not contain these contaminants. In case of intense and prolonged dust inhaling, they can produced an impressive pneumoconiosis with relatively mild clinical signs as shown by the series of 27 cases of pneumoconiosis from the french talcum powder as reported by the authors. The chemical nature and electronic structure of different silicates are very similar. It raises the question of the noxious effect of asbestos and the relative innocuousness of other minerals of the same family, and wether the fibrous structure alone is implicated.

Adult↗
PubMed1997

Relationship between Asbestos Exposures and 8-Hydroxydeoxyguanosine Levels in Leukocytic DNA of Workers at a Chinese Asbestos-material Plant.

The objective of the study was to evaluate the level of 8-hydroxydeoxyguanosine (8-OHdG) in DNA of peripheral-blood leukocytes as a biological marker of asbestos exposure and/or its fibrotic effects in an occupational population exposed to asbestos. The setting was a large-scale asbestos plant in China producing brake linings, asbestos rubber, and textile using chrysotile. From a base population of active and retired workers with various levels of cumulative exposure to asbestos and grades of asbestosis, 39 study subjects were randomly selected to reflect incremental grades of asbestosis based on Chinese diagnostic standards. They consisted of 19 "normal" (control) and ten "suspected" and ten "definite" asbestosis-grade subjects, group-matched for age and sex. Leukocytic DNA was extracted from 5-mL samples of peripheral blood and 8-OHdG level measured by high-pressure liquid chromatography. A cumulative asbestos exposure index (CEI) was calculated for each subject as the summed product of duration and level of asbestos exposure per job, incorporating a job-exposure matrix. Geometric mean 8-OHdG levels showed a positive gradient in relation to increasing grades of asbestosis (control: 1.78, suspected: 2.21, definite: 2.58), with a significant difference between the control and definite-asbestosis subgroups (p < 0.05). The 8-OHdG level of the two subgroups combined as one "asbestosis" group was significantly higher than that of the control group (control: 1.78, asbestosis: 2.39, p = 0.01). Further, 8-OHdG levels were moderately correlated with CEIs for all subjects (r = 0.35, p < 0.05) and with grades of asbestosis for all (r = 0.47, p < 0.01) and for male subjects (r = 0.43, p < 0.05). In multiple regression analyses, grade of asbestosis explained 27% of the total variation in 8-OHdG and was a better predictor than CEI or duration of exposure. Thus, the 8-OHdG level in leukocytic DNA is related to grade of asbestosis and to individual cumulative exposure and may serve as a biologic marker reflecting the status of oxidative DNA damage by asbestos.

Journal Article↗
PubMed2006

Association between polymorphisms of DNA repair gene XRCC1 and DNA damage in asbestos-exposed workers.

OBJECTIVE: To compare the asbestos-induced DNA damage and repair capacities of DNA damage between 104 asbestos-exposed workers and 101 control workers in Qingdao City of China and to investigate the possible association between polymorphisms in codon 399 of XRCC1 and susceptibility to asbestosis. METHODS: DNA damage levels in peripheral blood lymphocytes were determined by comet assay, and XRCC1 genetic polymorphisms of DNA samples from 51 asbestosis cases and 53 non-asbestosis workers with a similar asbestos exposure history were analyzed by PCR/RFLP. RESULTS: The basal comet scores (3.95 +/- 2.95) were significantly higher in asbestos-exposed workers than in control workers (0.10 +/- 0.28). After 1 h H2O2 stimulation, DNA damage of lymphocytes exhibited different increases. After a 4 h repair period, the comet scores were 50.98 +/- 19.53 in asbestos-exposed workers and 18.32 +/- 12.04 in controls. The residual DNA damage (RD) was significantly greater (P<0.01) in asbestos-exposed workers (35.62%) than in controls (27.75%). XRCC1 genetic polymorphism in 104 asbestos-exposed workers was not associated with increased risk of asbestosis. But compared with polymorphisms in the DNA repair gene XRCC1 (polymorphisms in codon 399) and the DNA damage induced by asbestos, the comet scores in asbestosis cases with Gln/Gln, Gln/Arg, and Arg/Arg were 40.26 +/- 18.94, 38.03 +/- 28.22, and 32.01 +/- 11.65, respectively, which were higher than those in non-asbestosis workers with the same genotypes (25.58 +/- 11.08, 37.08 +/- 14.74, and 29.38 +/- 10.15). There were significant differences in the comet scores between asbestosis cases and non-asbestosis workers with Gln/Gln by Student's t-test (P<0.05 or 0.01). The comet scores were higher in asbestosis workers with Gln/Gln than in those with Arg/Arg and in non-asbestosis workers exposed to asbestos, but without statistically significant difference. CONCLUSIONS: Exposure to asbestos may be related to DNA damage or the capacity of cells to repair H2O2-induced DNA damage. DNA repair gene XRCC1 codon 399 may be responsible for the inter-individual susceptibility in DNA damage and repair capacities.

Adult↗
PubMed1993

Asbestos-related disease in the workplace and the environment: controversial issues.

Asbestos-related diseases continue to be sources of controversy for epidemiologist, clinician, and pathologist. Most investigators agree that the different fiber types behave differently in the lung, with chrysotile being rapidly removed, and amphibole persisting. These differences in biologic behavior probably account for the much greater disease potential of amphibole (amosite and crocidolite) compared with chrysotile asbestos, particularly in regard to mesothelioma induction in man. Asbestosis is defined as diffuse interstitial fibrosis of the lung caused by asbestos exposure, and this is the only condition to which the term asbestosis should be applied. The classical pathologic diagnostic criteria for asbestosis, namely the presence of diffuse interstitial fibrosis resembling usual interstitial pneumonia, and asbestos bodies visible in ordinary tissue sections, have proved to withstand the test of time. Cases without asbestos bodies visible in routine or iron-stained tissue sections almost never turn out to be asbestosis. It should be remembered that workers with asbestos exposure develop all of the interstitial lung diseases to which the remainder of the populace is subject; some of these conditions are treatable and should not be misdiagnosed as asbestosis, which is not treatable. There is strong epidemiologic and pathologic evidence that the only association of asbestos exposure and lung cancer is the association of asbestosis and lung cancer. Thus, a lung cancer should only be attributed to asbestos exposure when asbestosis is present on clinical or pathologic grounds. The histologic type and location of the tumor are irrelevant in this regard. Analytical electron microscopy indicates that chrysotile asbestos does induce mesothelioma in man, but that extremely high levels of retained fibers, levels as high as those seen in cases of asbestosis, are required for this event to occur. The weight of the evidence suggests that exposure of the general population to the very low levels of chrysotile that are found in some public building (levels not greatly different from ambient air) will never produce mesothelioma, asbestosis, or lung cancer because these diseases all appear to require quite high-level occupational chrysotile exposure. Even if one accepts the ideas (probably wrong) that any level of asbestos exposure carries a risk of cancer, and that mathematical extrapolation of risk from high-level occupational exposure to low-level building exposure is scientifically valid, the calculated risks are much smaller than real everyday risks such as driving to work. Thus, exposure to asbestos at environmental levels appears to produce no real dangers to health.

Asbestos↗
PubMed1989

Health hazards from fine asbestos dusts. An analysis of 70,656 occupational preventive medical investigations from 1973 to the end of 1986.

For the period from 1973 to the end of 1986, 70,656 data sets on occupational preventive medical examinations in employees exposed occupationally to asbestos dust (G 1.2) were made available to us by the Central Registry for Employees Exposed to Asbestos Dust (ZAS). On the basis of this data, an analysis of asbestosis risk was to be made in relation to specific areas of work, taking into consideration the beginning and duration of exposure. Proceedings for declaratory appraisal in accordance with occupational disease no. 4103 were instituted in 1760 cases in the report period. In accordance with the character of the available data, the X-ray findings in the lungs were available from the persons investigated as parameters of possible asbestosis risk on the basis of coding consistent with the International Pneumoconiosis Classification (ILO U/C 1971 and/or ILO 1980 West Germany). The major result of the statistical analyses on the mainframe macrocomputer of the University of Erlangen-Nuremberg was that the relatively highest risk of asbestosis was present in persons whose exposure began before 1955. On the other hand, with increasing duration of exposure, an unequivocal rise of the asbestosis risk could not be detected on the basis of the overall population. In relation to the individual fields of work, the relatively highest risk of asbestosis was shown to be in the asbestos textile and paper industry, as well as in the asbestos cement industry. No detectable risk of asbestosis was present in the fields of mining, traffic and health service and for women in the industrial sectors of building material, gas and water, catering trade, building, commerce as well as banking and insurance. Accordingly, it can be assumed that certain fields of work are or were exposed to such a small extent or not at all that a risk of asbestosis which is relevant in terms of occupational medicine is no longer to be assumed or was not to be assumed. This applies above all to certain work in the frictional coating (brake lining) and asbestos paper industry. Furthermore, the analysis of the data material did not provide any unequivocal indications that inhalative smoking habits have a negative effect on the risk of asbestosis. In principle, it can be stated that the occupational preventive medical investigations according to G 1.2 are effective.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1989

Alveolar macrophages from patients with asbestos exposure release increased levels of leukotriene B4.

The alveolar influx and subsequent activation of inflammatory cells such as neutrophils and eosinophils are believed to be important in the pathogenesis of many interstitial lung disorders, including asbestosis. Indices of lower respiratory tract abnormalities detected by bronchoalveolar lavage (BAL) were investigated in 93 asbestos-exposed workers as well as in smoking (n = 12) and nonsmoking (n = 10) control subjects. Patients with clinical asbestosis (n = 12) exhibited increases in both BAL neutrophils and BAL eosinophils, expressed as both percentage of total cells and total numbers, when compared to asbestos-exposed workers without asbestosis (n = 81) and control subjects. Significantly greater numbers of BAL neutrophils were also found in asbestos-exposed workers without asbestosis than in either smoking or nonsmoking control subjects. These abnormalities correlated significantly with in vitro BAL alveolar macrophage production of the potent leukocyte chemotaxin, leukotriene B4 (LTB4). For example, basal, unstimulated LTB4 production was 3.1 +/- 0.8 ng/10(6) alveolar macrophages for patients with asbestosis, 1.05 +/- 0.2 ng/10(6) cells in asbestos workers without asbestosis, 0.9 +/- 0.2 ng/10(6) cells in control nonsmokers, and 0.2 +/- 0.05 ng/10(6) cells in control smokers. Stimulated LTB4 release from BAL alveolar macrophages (A23187 or arachidonate) was even more pronounced in asbestos workers with or without asbestosis, suggesting an in vivo priming effect on alveolar macrophage synthesis of LTB4. Cell-free BAL supernatants from asbestos-exposed patients with or without asbestosis also contained significantly greater amounts of LTB4 than did those from control subjects, indicating enhanced in vivo production of this inflammatory mediator.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

High-resolution CT of benign asbestos-related diseases: clinical and radiographic correlation.

We prospectively analyzed benign asbestos-related pleural and parenchymal abnormalities on high-resolution CT scans and correlated them with clinical diagnoses in 100 asbestos-exposed workers. All subjects had high-resolution CT scans in conjunction with conventional CT at the time of clinical evaluation. To evaluate for asbestosis, we ranked high-resolution CT scans as high, intermediate, or low probability of asbestosis on the basis of the multiplicity and extent of observed parenchymal changes. By linear regression analysis, the most distinctive high-resolution CT features of asbestosis included thickened nondependent interstitial short lines and parenchymal bands. In 45 subjects satisfying clinical criteria of asbestosis, high-resolution CT probability of asbestosis was high in 38 (84%), intermediate in five (11%), and low in two (4%). In 20 (36%) of 55 subjects without clinical asbestosis, parenchymal abnormalities indicative of a high probability of asbestosis were observed on high-resolution CT. High-resolution CT probability scores had a strong positive correlation with chest radiographic profusion scores (p less than .0001) and asbestos-related pleural thickening (p less than .0001). Significant inverse correlations were seen with forced vital capacity (p less than .006) and single-breath diffusing capacity (p less than .03), both functional measures of restrictive interstitial lung disease. Neither clubbing nor rales were sufficiently prevalent to have statistical correlation with high-resolution CT scores. High-resolution CT is sensitive in detecting both pleural and parenchymal abnormalities in the asbestos-exposed subject. Asbestos-related pleural changes are observed more frequently on high-resolution CT than on conventional CT or chest radiography. The probability of asbestosis based on high-resolution CT parenchymal features has a significant correlation with existing clinical determinants of disease, and high-resolution CT can detect abnormality when other methods are not diagnostic.

Adult↗
PubMed2004

Factors associated with early-stage pulmonary fibrosis as determined by high-resolution computed tomography among persons occupationally exposed to asbestos.

OBJECTIVES: Asbestosis remains difficult to diagnose, particularly in its early stages. The aim of this study was to determine criteria for independently associated features of pulmonary fibrosis in high-resolution computed tomograms among persons occupationally exposed to asbestos. METHODS: Retired persons with documented occupational asbestos exposure and no known asbestos-related diseases were assessed for occupational, clinical, functional respiratory, and chest X-ray criteria. In addition, they all underwent high-resolution computed tomography (HRCT) in the prone position. RESULTS: Altogether 51 (7.2%) of the 706 enrolled participants had features of pulmonary fibrosis consistent with asbestosis in the HRCT. Among those with small irregular opacities of <1/0 according to the 1980 International Labour Office Classification (ILO-C) in their X-rays, 5% had asbestosis in the HRCT. In a multivariate analysis, only age [odds ratio (OR) per year 1.08, 95% confidence interval (95% CI) 1.02-1.14], cumulative-exposure index (CEI) for asbestos (OR 6.4, 95% CI 1.5-28.4 for a CEI of > or =100 fibers/ml x years), and the presence of small irregular X-ray opacities of > or =1/0 ILO-C (OR 3.0, 95% CI 1.6-6.0) were independently associated with HRCT asbestosis. No combinations of these criteria simultaneously yielded high sensitivity and specificity for the diagnosis of early-stage HRCT asbestosis. Moreover, only 2% of the persons with a CEI of <25 fibers/ml x years had HRCT asbestosis, the finding confirming the low incidence of asbestosis for such low exposure, as previously reported on the basis of X-ray data. CONCLUSIONS: Additional research is needed to better identify the persons most likely to benefit from HRCT screening for asbestosis.

Aged↗
PubMed1989

Monocyte-derived growth factors in asbestos-induced interstitial fibrosis.

Asbestos-induced pulmonary fibrosis is thought to result from a series of cellular interactions involving the alveolar macrophage and the lung fibroblast. Although a dose-response relation has been established between asbestos exposure and the development of interstitial fibrosis, the majority of workers exposed even to high concentrations of asbestos do not develop radiographically evident interstitial fibrosis. As a means of understanding the pathogenesis of asbestos-induced fibrosis and the differential host response to the asbestos fiber, we studied the production of monocyte-derived growth factors in subjects with asbestosis (N = 5) and normal exposure-matched controls (N = 5). Under unstimulated culture conditions, the conditioned medium (CM) from monocytes from control subjects had a greater proliferative effect on fibroblasts than monocyte CM from patients with asbestosis. With CM from concanavalin A-stimulated monocytes, the proliferative response of the fibroblast was similar in those with asbestosis and control subjects. Freshly isolated monocytes from both normal subjects and patients with asbestosis did not express the gene for the B chain of platelet-derived growth factor (PDGF) as evaluated by hybridization with a PDGF-specific human cDNA probe. After 20 hr of culture in concanavalin A, monocytes from normal subjects expressed the gene for the B chain of PDGF while, under the same culture conditions, none of the monocyte preparations from patients with asbestosis produced mRNA for this growth factor. These data indicate that peripheral blood monocytes from patients with asbestosis compared to exposure-matched controls have a reduced capacity to produce growth factor activity as measured by mitogenic activity and mRNA levels for the B chain of PDGF. These results suggest that peripheral blood monocytes from patients with asbestosis may comprise a less mature population of cells compared to exposure-matched controls.

Animals↗
PubMed1993

The importance of lung function, non-malignant diseases associated with asbestos, and symptoms as predictors of ischaemic heart disease in shipyard workers exposed to asbestos.

The mortality from ischaemic heart disease was studied in a prospective cohort of 1725 shipyard workers exposed to asbestos. The analyses were stratified for age and smoking habits and restricted to men. In agreement with other findings, men with impaired lung function had a significantly higher risk (relative risk (RR) = 3.5) of dying from ischaemic heart disease than men with normal lung function. Men with asbestosis or suspected asbestosis had a significantly higher risk (RR = 3.1) of dying from ischaemic heart disease than men without asbestosis. Thus asbestosis or suspected asbestosis also seemed to be a risk factor for ischaemic heart disease. This finding was independent of respiratory function. There was no increased risk for ischaemic heart disease in men with compared with men without pleural plaques. Men with production of phlegm or sputum and wheezing or whistling had no increased risk for ischaemic heart disease compared with men without these symptoms. In the group with normal lung function men with dyspnoea had a significantly higher risk of dying from ischaemic heart disease than men without dyspnoea. The findings for men with asbestosis or suspected asbestosis indicated a further risk factor besides impaired lung function, in persons exposed to asbestos. Perhaps this risk factor is due to lesions of the pericardium with consequences for heart function.

Aged↗
PubMed1984

Asbestos related pleuropulmonary lesions and the erythrocyte sedimentation rate.

Asbestos related lesions of the lung parenchyma and the pleura can be divided into three main types: parietal pleural plaques, diffuse interstitial fibrosis ("classical asbestosis"), and a third type of reaction affecting both the pleura and the lung parenchyma. The last type includes such lesions as acute pleurisy, diffuse pleural thickening, and rounded atelectasis. Among 1344 patients with asbestos related pleural lesions, 1190 had pleural plaques, 29 of whom also had pulmonary fibrosis (asbestosis); 83 had unilateral sequelae of pleurisy, of whom nine had asbestosis; and 71 had bilateral sequelae of pleurisy, of whom 23 also suffered from asbestosis. The erythrocyte sedimentation rate (ESR) was measured in 184 patients--79 with pleural plaques, 44 with unilateral sequelae of pleurisy, and 61 with bilateral sequelae. In patients with pleural plaques with or without asbestosis the ESR was usually normal, the mean being 9.6 mm in one hour. Among patients with sequelae of pleurisy, however, many had a raised ESR. The mean ESR was 25.7 mm in one hour in those with bilateral changes and 13.2 in those with unilateral changes. Statistical analysis showed that in this group of subjects the presence of sequelae of pleurisy was a highly significant determining factor for the ESR (p less than 0.0001). Asbestosis alone was not a significant determining factor but there was a low grade of significance for the combined effect of asbestosis and sequelae of pleurisy (p less than 0.05). These findings suggest that the pathogenesis of the various changes is different.

Asbestos↗
PubMed1991

Abnormal lung function associated with asbestos disease of the pleura, the lung, and both: a comparative analysis.

The impairment of lung function associated with different types of asbestos related disease was examined in 1298 men. The 310 men with circumscribed pleural lesions (plaques) or diffuse pleural thickening without asbestosis were compared with 596 men with asbestosis only and with 322 men with pleural abnormalities and asbestosis, as classified from chest radiographs by ILO pneumoconiosis criteria. Spirometric indices and total lung capacity (TLC; determined by planimetry) were measured and expressed as percentages of predicted values. Non-smoking men with pleural disease only had reduced values of mid and terminal expiratory flows (80.6 and 69.9% predicted) and a reduced FEV1 (89% predicted) with a forced vital capacity (FVC) of 94% predicted. TLC was 104% predicted. Thus they had airways obstruction with-out restriction. Non-smoking men with pulmonary asbestosis (ILO profusion of opacities mostly 1/0 and 1/1) had pulmonary function similar to that of men with pleural disease. FEV1 and FVC and flow rates at other lung volumes were lower in smokers with asbestosis (after adjustment for duration of smoking) than in the non-smokers with asbestosis. Airflow limitation was worse in the men with both pleural abnormalities and pulmonary asbestosis with lower values for mid expiratory flow, FEV1 and FVC (but not TLC) than those with either abnormality alone, in both non-smokers and current smokers. Men with diffuse pleural thickening that included the costophrenic angles had more airways obstruction and air trapping and lower FVC values than those with circumscribed pleural disease.

Aged↗