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PubMed1995

[Liability in occupational asbestosis and its harmful sequelae].

A total of 139 cases of occupational asbestosis were registered in companies working with asbestosis in Croatia between the years 1985 and 1994. In the period from 1992 to 1994 thirty-five diseased workers sued in court for compensation of damage. In all suits and at all levels, the employer was judged to be responsible for the damage. Questioning the exclusiveness of responsibility, or at least co-responsibility for the other parties involved in the structure of occupational use of asbestos, the authors ascertained, in all the 35 cases of occupational asbestosis from the sample, that the full responsibility lay with the third party - the State - as representing the unity of the legal, executive and judicious powers.

Asbestosis↗

PubMed1997

An early study of pulmonary asbestosis among manufacturing workers: original data and reconstruction of the 1932 cohort.

A cross-sectional prevalence survey of asbestosis, including all 1,140 employees of a diversified asbestos products manufacturer, was conducted in 1932 by Drs. Anthony J. Lanza and Frank V. Meriwether. Occupational histories were obtained from workers in order to identify job tasks with exposure to asbestos and other fibrogenic dusts. Abbreviated medical histories, physical examinations, fluoroscopy, and chest radiographs were performed. Radiographs were interpreted according to applicable criteria for pneumoconiosis, the presence of which was confirmed in 327 subjects (29%). Among those, 64% had previous exposure to dusts in addition to asbestos, coal being the leading non-asbestos exposure. Thirty-six percent of cases had prior exposure only to asbestos dust. The original conclusions do not survive. Contemporaneous related documents suggest that the original authors believed asbestosis to be a milder form of lung disease than silicosis. It was subsequently recommended that the company institute pre-employment physicals, including chest radiographs; not hire people with prior coal-dust exposure; warn workers against excessive exposure to asbestos dust; remove those with disease to less dusty areas; and begin periodic medical surveillance for pneumoconiosis. The study, which has never appeared in the medical or scientific literature, holds important lessons for those concerned with occupational health today and in the future.

Asbestosis↗

PubMed1997

Cancer incidence and mortality among Finnish asbestos sprayers and in asbestosis and silicosis patients.

Cohorts of Finnish asbestos sprayers and of asbestosis and silicosis patients were followed for cancer with the aid of the Finnish Cancer Registry in the period 1967-1994. Compared with the cancer incidence of the total Finnish population, asbestos sprayers had an increased risk for total cancer (standardized incidence ratio [SIR] 6.7, 95% confidence interval [95% CI] 4.2-10); lung cancer (SIR 17.95% CI 8.2-31); and mesothelioma (SIR 263, 95% CI 85-614). The SIR of the asbestosis patients was 3.7 (95% CI 2.8-5.0) for all sites, 10 (95% CI 6.9-14) for lung cancer, and 65 (95% CI 13-188) for mesothelioma. The silicosis patients also had significantly high SIR values for all sites (1.5, 95% CI 1.0-2.1) and lung cancer (2.7, 95% CI 1.5-4.5). The values for the SIR and the standardized mortality ratio for all sites and lung cancer were very similar, and therefore it seems that both are reliable indicators of the occurrence of occupational cancer. It was concluded that pneumoconioses patients and asbestos-exposed workers have a markedly elevated risk for cancer. Asbestos-induced occupational cancers are not only diseases of the elderly, since the relative risk is high also for middle-aged people.

Adult↗

PubMed1997

Professor Matthew Stewart: asbestosis research 1929-1934.

Matthew Stewart, Professor of Pathology at Leeds University, developed an interest in asbestosis during the late 1920s. In 1929, the Medical Research Council (MRC), encouraged by an advisory committee, funded research into asbestosis at Leeds University. Stewart supported by physicians designed a program of clinical, radiological and physiological studies to follow up Merewether's affected asbestos workers. Unfortunately, this met with opposition from industry, and the Home Office Factory Department was reluctant to assist, so it was abandoned. Industry did, however, cooperate with Stewart's studies on the effects of exposing guinea pigs in the factory environment, but this led to little in the way of publication. The failure of the Leeds School to realize its potential in investigating the effects of asbestos in humans, results in part from the discouragement it received and in part from the limited time and energies available to persons with a wide range of active interests. Some 45 years were to elapse before the MRC were enabled to carry out an analysis of the clinical, radiological and physiological data of a population of asbestos workers.

Asbestosis↗

PubMed2007

Radiographic readings for asbestosis: misuse of science--validation of the ILO classification.

BACKGROUND: Radiographic readings for pneumoconiosis (both asbestosis and silicosis), even those using the International Labour Office (ILO) Classification, have received widespread negative coverage in the media and strong judicial rebuke. METHODS: The medical literature over the past 90 years was reviewed for the relationships between radiographic severity (standardized as the ILO profusion score) and indices of exposure to silica or asbestos, tissue burden of silica particles or asbestos fibers, histologic fibrosis, various measurements of pulmonary function and mortality. RESULTS: Evidence from many different disciplines has demonstrated that the ILO profusion score correlates with occupational exposure, dust burden in the lung, histologic fibrosis and, more recently, with physiologic impairment and mortality. CONCLUSIONS: The ILO Classification has therefore been validated as a scientific tool. Its fraudulent misuse by "hired-gun" physicians, attorneys and elements of the compensation system to falsify claims of asbestosis and/or silicosis (often in the same claimant) must be condemned.

Asbestosis↗

PubMed1989

Diagnostic value of exercise testing in asbestosis.

The diagnostic value of simple exercise testing was examined in 81 current male asbestos-cement workers, divided into four groups according to the International Labour Office (ILO) category of irregular opacities: 0/0, 25; 1/1, 24; 1/2, 22; and 2/2, 10 men. An increasing X-ray score was accompanied by more severe functional abnormality in keeping with the development of a restrictive defect. Symptom-limited oxygen uptake (VO2SL) did not depend on the X-ray grade and was 76.7, 71.9, 68.7, and 73.5% pv, respectively, for the four groups. Subjects with ILO score 1/1 had significantly higher exercise ventilation at O2 uptake of 1.01.min-1 (VE 1.0) than those with grade 0/0. End-exercise tidal volume (VTSL in 1) decreased with an increasing X-ray score: 2.14, 1.98, 1.85, and 1.62, respectively. VTSL standardized for vital capacity (VTSL/VC) followed the same pattern. Asbestosis was diagnosed in 25 men, in whom VE 1.0 was significantly higher (p less than .02) and VTSL lower (p less than .01) than in the 0/0 group. VO2SL was similar in both groups. The findings suggest that VE 1.0 and VTSL may be early functional indicators of asbestos-related interstitial lung fibrosis. The measurement of both exercise indices may increase the certainty of clinical diagnosis of asbestosis in subjects with less advanced disease.

Adult↗

PubMed1993

A diagnostic approach to asbestosis, utilizing clinical criteria, high resolution computed tomography, and gallium scanning.

Seventy-five individuals known to have significant exposure to asbestos were evaluated by physical exam, pulmonary function tests (PFT), chest radiographs, high resolution computed tomography (HRCT), gallium-67 scanning, and various laboratory exams. Sixteen subjects met three of the following four criteria and were considered to have clinical asbestosis: 1) bibasilar rales, 2) FVC < 80% of predicted, 3) DLCO < 80% of predicted, and 4) an abnormal chest radiograph. Evaluations which included HRCT and Ga scanning detected pulmonary disease in these asbestos-exposed individuals in many cases where other modalities were unable to demonstrate significant abnormalities. While only 21% of the subjects satisfied commonly accepted criteria for the diagnosis of asbestosis, 75% had evidence of disease by both HRCT and gallium scanning. These data suggest that it may be time to include HRCT and Ga scanning when evaluating asbestos-exposed individuals, especially in cases where evaluations by physical exam, PFTs, and chest radiographs are non-diagnostic.

Adult↗

PubMed1993

Pulmonary function in asbestosis and asbestos-related pleural disease.

This review begins with the classic physiologic syndrome of interstitial lung disease (ILD) described in established asbestosis in the 1950s: reduced VC and pulmonary compliance, maintenance of airflow (measured indirectly), decreased diffusing capacity (a laborious undertaking in those years), and hyperventilation, increased dead space (VD/VT), and desaturation on exercise. Small airways dysfunction (SAD) was recognized in the 1960s and 1970s as the physiologic counterpart of the early peripheral bronchiolar inflammatory and fibrotic narrowing reported in experimental animals and in asbestos workers. SAD is nonspecific and is often overshadowed by more severe obstruction caused by smoking or by the countervailing effects of increased lung recoil caused by interstitial fibrosis. Airtrapping secondary to SAD may explain some of the reduction in VC in asbestos exposed workers whose FEV1/FVC is normal. There may be a greater frequency of obstructive airways disease in asbestos workers who smoke than in other smokers, suggesting an interaction between these two noxious inhalants. An interaction is seen in the greater frequency and severity of radiographic asbestosis in smokers at equivalent durations of exposure and in the greater reduction in FVC in smokers at equivalent ILO profusion scores. The functional importance of PT is well documented by lower values for FVC at equivalent profusions of parenchymal disease. This is true of circumscribed PT but much more so of diffuse PT, which can occasionally result in ventilatory failure and death. Incremental exercise testing often reveals evidence of excessive ventilation and abnormal gas exchange (VD/VT) attributable to ILD, when standard tests of pulmonary function and chest radiography are normal. These abnormalities help explain dyspnea in such patients.

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PubMed1998

Follow-up of asbestosis patients and predictors for radiographic progression.

OBJECTIVE: We followed a group of 85 Finnish asbestosis patients radiographically for an average of 6.5 (range 2-10) years to examine the progression of the disease and to assess possible explanations for the progression. METHODS: The examinations included full-size chest radiographs and a blood specimen analysis. The radiographs were classified according to the 1980 International Labor Office (ILO) classification. Progression was accepted if the second or third radiography was estimated (in a side-by-side comparison) to have more profusion of small opacities qualitatively than the first, even if the radiographs were classified into the same profusion category. RESULTS: In all, 38% of the patients showed progression during the follow-up period. The average progression of small opacities ranged from ILO 1/1 to ILO 2/2 (0.4 minor ILO categories/year). The asbestosis was progressive more often among the sprayers than among the insulators and asbestos factory workers [cross-tabulation, odds ratio (OR) 5.0, 95% confidence interval (95% CI) 1.2-20]. In the logistic regression model the ILO classification category at the beginning of the follow-up (OR 1.54; 95% CI 0.96-2.47), the fibronectin (OR 1.01; 95% CI 1.00-1.01) and angiotensin-converting enzyme (ACE; OR 1.10; 95% CI 1.00-1.20) levels, and the erythrocyte sedimentation rate (ESR; OR 1.05; 95% CI 1.00-1.10) were statistically associated with the radiographic progression of small opacities. Abnormalities of the pleura were found to progress more often among the patients with progressive parenchymal opacities. CONCLUSION: For the progression of small-opacity profusion the significant predictors in the logistic regression model were the ILO profusion category at the beginning of the follow-up period, the fibronectin level, the ACE value, and the ESR. The model correctly classified 94% of the patients with progression and 65% of those without progression. The differences in the mean values recorded for the biomarkers between the progressors and nonprogressors, however, were small and may therefore not be of any importance to the clinician.

Adult↗

PubMed1983

Lung mitochondria in experimental asbestosis.

Alterations in lung mitochondria were followed in guinea pigs at different periods after a single intratracheal injection of chrysotile dust. Cytochrome c oxidase and succinic dehydrogenase activities showed gradual increase after 90 days, whereas monoamine oxidase remained unaffected throughout the study. There was an increase in glutamate dehydrogenase activity in postmitochondrial as well as in mitochondrial fractions, the latter being accompanied by decreased latency of the enzyme. Mitochondria from asbestotic lung appeared to be more swollen than in normal animals at and after 90 days of exposure. There were fluctuations in the contents of different phospholipids as a result of asbestosis. Beyond 90 days, collagen and mucopolysaccharides also increased. The results confirm the contention that pulmonary mitochondria are among the major target sites in asbestosis.

Animals↗

PubMed1982

Current concepts about the pathogenesis of silicosis and asbestosis.

Silicosis and asbestosis are two forms of fibrotic lung disease resulting from the inhalation of inert materials indigestible by pulmonary alveolar macrophages. Results of studies of the host response to these particulates have not always been consistent. It is clear, however, that after phagocytosis, both cause alveolar macrophage damage, with resultant release of macrophage products, including fibrogenic factors and chemotactic factors for neutrophils. The latter cells also release lysosomal enzymes and free radicals when exposed to silica and asbestos. The net effect of these observations suggests that the combination of tissue damage and fibroblast stimulation results in the pulmonary fibrosis characterizing these diseases. Patients with silicosis and asbestosis have normal or decreased cell-mediated and increased humoral immunity with a high incidence of circulating immune complexes and autoantibodies. Whether these abnormalities are related to the pathogenesis of pulmonary fibrosis or are epiphenomena remains to be determined.

Animals↗

PubMed1983

Immunologic aberrations in asbestos cement workers: dissociation from asbestosis.

Immunoregulatory disorders have been implicated in the pathogenesis of asbestosis. We therefore compared the immunologic status of a well-characterized group of 31 current and former asbestos-cement workers with that of a group of 52 healthy controls, after adjustments had been made for the possible confounding effects of age, race, and smoking. The asbestos workers had significantly decreased percentages and numbers of both B and T lymphocytes in peripheral blood and a paradoxical IgG hypergammaglobulinemia. Analysis of T-lymphocyte subpopulations revealed that total T-cell numbers (OKT3+), helper-inducer T-cell numbers (OKT4+), and suppressor-cytotoxic T cell numbers (OKT8+) were decreased by similar proportions. These decreases were negatively correlated with time elapsing since the end of exposure to asbestos. In both workers and controls, lymphocyte proliferative responses to phytohemagglutinin (PHA) were correlated positively with the number of OKT4+ cells and negatively with age and serum IgG levels. When adjustments had been made for these confounding variables, no differences in PHA responses were noted between workers and controls. No relationship was detected in the workers between any of the immunologic aberrations noted and (1) radiographic category of pneumoconiosis, (2) estimates of cumulative asbestos exposure, or (3) abnormalities of pulmonary function. These data suggest that the immunologic perturbations we have noted in asbestos-exposed individuals are epiphenomena, unrelated to the pathogenesis of asbestosis itself.

Adult↗

PubMed1997

Asbestosis and silicosis.

Interstitial fibrosis resulting from workplace exposure to asbestos and crystalline silica persists throughout the world despite knowledge of the causes and effective means for prevention. Asbestosis and silicosis occurrence is predictable among people overexposed to dusts in various industries and occupations such as mining, construction, manufacturing, and building maintenance. Asbestosis and silicosis are incurable and may be progressive even after dust exposure has ceased, therefore early recognition and supportive interventions are important. Although current disease is a result of past exposures, effective control of current workplace exposures is the only way to prevent continued occurrence of these potentially debilitating diseases. Physicians can contribute to this effort through accurate diagnosis and disease reporting.

Asbestosis↗

PubMed1987

[Asbestosis and the rheumatic lung. Medical insurance assessment of combined lung diseases].

A fibrosing pulmonary disease, which could not be further classified, was diagnosed in a 76-year-old woman who for 40 years had worked as a seamstress in the textile industry. For the last 16 years she had suffered from progressively increasing shortness of breath. She died three weeks after hospitalization during which she received intensive respiratory and circulatory supportive treatment. At post-mortem examination there was evidence of minimal asbestosis, of pulmonary manifestations of rheumatoid arthritis and of recurrent pulmonary thromboembolism, as well as of the consequences of two weeks of artificial ventilation during the terminal period. This constellation of histopathological findings was assessed in relation to the part played by her occupational disease. She had been previously awarded a pension as a recognized sufferer form asbestosis (50% reduction of earning power). The histopathological findings were not such--in view of the difficult diagnostic constellation while she was alive--as to contradict with a high degree of probability the finding that she had suffered from an occupational disease.

Aged↗

PubMedDate not supplied

Asbestos fiber analysis in seven asbestosis cases.

Asbestos bodies and fibers deposited in the lungs of seven asbestosis cases were counted after tissue digestion. The types and sizes of 100 asbestos fibers for each case were also analyzed. Asbestos bodies were counted with an optical microscope at 100x magnification, and asbestos fibers were counted with a transmission electron microscope (TEM) at 2000x magnification. Most asbestos fibers detected with TEM were longer than 3 microns (92.5%) and thicker than 0.1 microns (92.3%). Short fibers less than 2 microns--both chrysotile and amphiboles, as well as long, thin fibers less than 0.06 microns--would be missed at 2000x (TEM). An average of 1.37 (0.081-5.5) x 10(6) asbestos bodies and 164.8 (0.55-610) x 10(6) asbestos fibers per 5 g wet (0.88 g dry) lung tissue were found, and these values are higher than what was reported in mesothelioma cases without asbestosis that were reported previously. More than 13 (average = 266.2) asbestos bodies were found in a 4-micron-thick tissue section (average area = 3.24 cm2). One asbestos body in a section equaled approximately 5,000 per 5 g wet lung tissue. The intensity of fibrosis was minimal in one case, mild in four, moderate and severe in one each, and the intensity was correlated with the number of asbestos bodies and fibers. The fibrosis in the severe case may have been intensified by repeated infection. Crocidolite fibers were found most frequently (84.7%), were thin, and had a high aspect ratio by our counting rules. Crocidolite with a high aspect ratio may be most fibrogenic in the lung.

Adult↗

PubMedDate not supplied

Pulmonary function of nonsmoking female asbestos workers without radiographic signs of asbestosis.

Researchers disagree about whether exposure to asbestos causes significant respiratory impairments and airway obstruction in the absence of radiographic asbestosis and smoking. To obtain confirmatory information, the authors examined pulmonary function of 208 nonsmoking female asbestos workers who did not have asbestosis and 136 controls. The authors observed an overall lower single-breath carbon monoxide diffusing capacity in the asbestos workers than in controls. In addition, significant decreases in percentage vital capacity, percentage forced vital capacity, and percentage mean forced expiratory flow during the middle half of the forced vital capacity were evident in the older workers. Logistic regression analysis revealed that asbestos exposure was associated with abnormal single-breath carbon monoxide diffusing capacity, vital capacity, and mean forced expiratory flow during the middle half of the forced vital capacity among the older workers. The age-related decline in vital capacity, forced vital capacity, and mean forced expiratory flow during the middle half of the forced vital capacity was significantly greater in the asbestos workers than the controls. The findings imply that asbestos-exposure per se contributes predominantly to restricted lung volume and reduced single-breath carbon monoxide diffusing capacity. Asbestos may also cause slight airway obstruction, especially in workers who are heavily exposed.

Adult↗

PubMed2005

Asbestos, asbestosis, and lung cancer: a critical assessment of the epidemiological evidence.

The question of whether lung cancer can be attributed to asbestos exposure in the absence of asbestosis remains controversial. Nine key epidemiological papers are reviewed in a point/counterpoint format, giving the main strengths and limitations of the evidence presented. Of the nine papers, two concluded that asbestosis was necessary and seven that it was not. However, the study design, nature and circumstances of exposure and method of analysis of the studies differed considerably, and none was considered definitive. It is concluded that, because of the relative insensitivity of chest radiography and the uncertain specificity of findings from histological examinations or computed tomography, it is unlikely that epidemiology alone can put either the strict scientific or practical medicolegal questions beyond doubt. It is probable that the issue may depend critically on asbestos fibre type, an aspect not so far addressed.

Asbestos↗

PubMed1986

Pulmonary asbestosis: CT study of subpleural curvilinear shadow. Work in progress.

High-resolution computed tomographic scans of 19 patients with pulmonary asbestosis revealed a subpleural curvilinear shadow (SCLS) parallel to the inner chest wall in the lungs of 15 (78.9%) patients. Most (46.7%) SCLS measured greater than 5 cm but less than 10 cm in length and occurred less than 1 cm from the inner chest wall in all cases. SCLS was distributed mainly in the lower lobe in patients with mild pulmonary fibrosis and in segments where fibrosis was mild in patients with honeycomb shadows. This may reflect initiation of pulmonary fibrosis leading to the formation of a honeycomb shadow. Radiologic-pathologic correlation, achieved in one postmortem specimen, seemed to indicate that SCLS was associated with the initial change of fibrosing bronchioloalveolitis, which is characteristic of pulmonary asbestosis.

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