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PubMed1991

Idiopathic pulmonary fibrosis in asbestos-exposed workers.

Diffuse interstitial lung disease in asbestos-exposed workers is presumed to represent asbestosis. Among 176 asbestos-exposed persons for whom lung tissue was available, we found nine with clinical features consistent with asbestosis, but histologic sections failed to demonstrate asbestos bodies, the usual requirement for pathologic diagnosis of asbestosis (Group I). These nine were compared by analytic electron microscopy with nine persons with idiopathic pulmonary fibrosis (Group II), and with nine persons with all the criteria of asbestosis (Group III). The three groups did not differ significantly with respect to lung burden of chrysotile or tremolite and actinolite, but Group III had a lung burden of amosite and crocidolite that was three orders of magnitude greater than in Groups I and II, with no overlap. We conclude that (1) the American Thoracic Society criterion of "a reliable history of exposure" is sometimes difficult to define; (2) asbestos bodies are seen in tissue sections only when exposure has been reasonably high, and given the proper clinical setting, the presence of diffuse fibrosis and asbestos bodies in tissue sections are sensitive and specific criteria for a diagnosis of asbestosis; and (3) the prevalence here of 5.1% nonasbestos-induced interstitial lung disease among asbestos-exposed persons is artefactually high because of atypical case selection. However, because asbestosis is a disappearing disease, such cases will become more frequent. The identification of these other diseases is important because therapy and prognosis may differ from that of asbestosis.

Aged↗
PubMed1992

Influence of cigarette smoking on bronchoalveolar lavage cellularity in asbestos-induced lung disease.

To investigate the influence of cigarette smoking on bronchoalveolar lavage (BAL) cellularity in asbestos-induced lung disease, we compared BAL cells in asbestos-exposed, nondiseased subjects (n = 20) with those with either asbestosis (n = 25) or asbestos-induced pleural fibrosis (n = 28). Patients with asbestosis (ILO greater than or equal to 1/0) had higher concentrations of BAL macrophages (p = 0.04), neutrophils (p = 0.003), and eosinophils (p = 0.01), while patients with asbestos-induced pleural fibrosis (circumscribed plaques and diffuse pleural thickening) had higher concentrations of BAL lymphocytes (p = 0.02). Within our study population, however, cigarette smoking (smoking status or pack-years of smoking) was strongly associated with BAL macrophages, neutrophils, and eosinophils but was not associated with the concentration of BAL lymphocytes. Using multivariate analysis, we found that although asbestosis remained associated with higher concentrations of BAL macrophages, neutrophils, and eosinophils, cigarette smoking had a far greater contribution to the concentrations of BAL macrophages and eosinophils than did asbestosis. Although cigarette smoking accounted for 17 to 18% of the variance of BAL macrophages and eosinophils, asbestosis was associated with approximately 6% of the variance associated with these cells. In contrast, the concentration of BAL neutrophils remained associated with asbestosis and was not influenced by smoking behavior. We conclude that cigarette smoking strongly influences BAL cellularity (macrophages and eosinophils) in our patients with asbestosis but does not appear to affect the type or concentration of BAL cells in patients with asbestos-induced pleural fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Asbestosis↗
PubMed1988

Neutrophil chemotactic factor release and neutrophil alveolitis in asbestos-exposed individuals.

Alveolar neutrophil accumulation occurs in asbestosis. To evaluate a possible role for release of neutrophil chemotactic factor (NCF) in the pathogenesis of asbestosis, spontaneous NCF release from alveolar macrophages obtained by bronchoalveolar lavage (BAL) in eight individuals with asbestosis, 13 asbestos-exposed individuals without asbestosis, and five control subjects has been studied. Alveolar macrophages were incubated in medium (four hours; 37 degrees C), and neutrophil responses to the supernatants were assayed in a microchemotaxis chamber. Alveolar macrophages from subjects with asbestosis released more NCF (97 +/- 19 neutrophils per high-power field [N/HPF]) than controls (3 +/- 1 N/HPF; p less than 0.01). Alveolar macrophages from individuals with asbestos exposure and increased BAL neutrophil proportions (n = 7) released more NCF (93 +/- 24 N/HPF) than individuals with asbestos exposure and normal BAL neutrophil proportions (n = 6; 11 +/- 6 N/HPF; p less than 0.02). The results show that spontaneous NCF release occurs in asbestosis and that NCF release is associated with neutrophil alveolitis in asbestos-exposed individuals without asbestosis, suggesting a pathogenic role for NCF in mediating this neutrophil alveolitis. The results of the study also suggest that the presence of crackles is a better predictor of the presence of neutrophil alveolitis than is an abnormal chest x-ray film.

Asbestos↗
PubMed1992

[Biodemographic parameters as indicators of genetic adaptation to harmful occupational factors (e.g. asbestos)].

A total of 129 women working at asbestos-concentrating factories and asbestos articles manufacture plant, including 87 of them facing asbestosis and 42 exposed to asbestos without asbestosis were examined. There was no marked shifts in the reproductive function and pregnancy results of women facing asbestosis and those exposed to asbestos without asbestosis. Women facing asbestosis has infant mortality higher than other women. Parameters of potential selection (index Crow) in the studied population showed an unfavourable demographic situation in women facing asbestosis. Analysis of biodemographic data helped to suggest the possibility of genetic predisposition to asbestosis.

Abortion, Spontaneous↗
PubMed1997

Exposure-response analysis of risk of respiratory disease associated with occupational exposure to chrysotile asbestos.

OBJECTIVES: To evaluate alternative models and estimate risk of mortality from lung cancer and asbestosis after occupational exposure to chrysotile asbestos. METHODS: Data were used from a recent update of a cohort mortality study of workers in a South Carolina textile factory. Alternative exposure-response models were evaluated with Poisson regression. A model designed to evaluate evidence of a threshold response was also fitted. Lifetime risks of lung cancer and asbestosis were estimated with an actuarial approach that accounts for competing causes of death. RESULTS: A highly significant exposure-response relation was found for both lung cancer and asbestosis. The exposure-response relation for lung cancer seemed to be linear on a multiplicative scale, which is consistent with previous analyses of lung cancer and exposure to asbestos. In contrast, the exposure-response relation for asbestosis seemed to be nonlinear on a multiplicative scale in this analysis. There was no significant evidence for a threshold in models of either the lung cancer or asbestosis. The excess lifetime risk for white men exposed for 45 years at the recently revised OSHA standard of 0.1 fibre/ml was predicted to be about 5/1000 for lung cancer, and 2/1000 for asbestosis. CONCLUSIONS: This study confirms the findings from previous investigations of a strong exposure-response relation between exposure to chrysotile asbestos and mortality from lung cancer, and asbestosis. The risk estimates for lung cancer derived from this analysis are higher than those derived from other populations exposed to chrysotile asbestos. Possible reasons for this discrepancy are discussed.

Adult↗
PubMed2001

Non-malignant asbestos-related diseases in Brazilian asbestos-cement workers.

BACKGROUND: Production of asbestos-cement products in Brazil started in the 1940s, peaked in the 60-70s and is still an active industry. This study was designed to assess the non-malignant effects of asbestos exposure in the asbestos-cement industry in Brazil. METHODS: A group of 828 former asbestos-cement workers enrolled in a cross-sectional and cohort study of respiratory morbidity, submitted to a detailed occupational history, respiratory symptoms questionnaire, spirometry, PA chest x-ray, and high resolution computed chest tomography (HRCT). Asbestos exposure was assessed by years of exposure, cumulative exposure (a semi-quantitative method), and latency time from first exposure. Asbestosis and pleural thickening were assessed according to HRCT criteria. RESULTS: Asbestosis was present in 74 (8.9%) and pleural thickening in 246 (29.7%). Using the HRCT as the "best available evidence", it was shown that were more false negatives than false positives in the x-ray readings for parenchymal (21.6% false negatives, 4.2% false positives) and pleural (26.0% false negatives, 14.4% false positives) diseases due to asbestos. Latency time from first exposure was the best predictor for both asbestosis and pleural thickening. Subjects in the higher exposure groups presented lower levels of lung function. Obstructive defects were significantly related to smoking, shortness of breath, body mass index, and age, whereas restrictive defects were related to asbestosis, shortness of breath, and latency time. Chronic bronchitis increased with latency time in the three smoking groups and was significantly related to pleural thickening (OR 1.56 (1.00-2.42)). Shortness of breath was significantly associated with body mass index and pleural thickening (OR 1.30 (1.24-2.09)). CONCLUSIONS: Pleural thickening and asbestosis showed a significant association with latency time and exposure. FVC and FEV(1) decreased across increasing profusion with an added effect of pleural thickening. There was a significant and independent effect of exposure on lower levels of FVC and FEV(1). Obstructive defects were mainly related to smoking and restriction to asbestosis. Dust exposure and smoking were synergistic in increasing chronic bronchitis and shortness of breath report. Shortness of breath report was also related to pleural thickening and higher body mass index.

Adult↗
PubMed1985

Clinical features to stage alveolitis in asbestos workers.

To analyze the clinical features of asbestos-induced alveolitis and stage its activity, we evaluated 217 asbestos workers by the usual clinical, radiological, and functional parameters and computerized gallium 67(Ga) lung scan; we obtained bronchoalveolar lavage (BAL) in 33 and lung biopsy in 6. In addition, we scored the profusion of lung rales and correlated it with other parameters of severity of asbestosis. In the 55 workers without asbestosis and normal 67Ga scan, BAL analyses were comparable to those of controls. Of the 56 without asbestosis but increased 67Ga lung uptake, BAL analyses in 8 documented a predominantly macrophagic alveolitis (confirmed on lung biopsy in 3), with the highest levels of BAL fibronectin. In the 106 workers with asbestosis, 67Ga lung uptake was increased in 75; BAL in 17 demonstrated a macrophagic and neutrophilic alveolitis with elevated fibronectin levels. Lung biopsy in 3 of the latter workers documented peribronchiolar fibrosing alveolitis. Rale scores in all workers or in those without asbestosis did not correlate with 67Ga scores; they correlated fairly well with profusion of parenchymal opacities (Rs = 0.42) and rigidity of the lung pressure-volume curve (Rs = 0.39). Thus, 67Ga lung uptake is an early indicator of chronic macrophagic alveolitis in asbestos workers, which usually progresses to asbestosis. In the disease, profusion of lung rales constitutes a simple clinical mode of assessment of disease severity that correlates better with radiological and functional parameters than with parameters of alveolitis.

Adult↗
PubMed1994

Biological effects: asbestos-cement manufacturing.

Fourteen cohorts of asbestos-cement workers have been studied. These studies have demonstrated exposure-response relationships for lung cancer, mesothelioma and asbestosis. For lung cancer, relatively consistent results have been observed, with risk two-fold or less in 13 of the 14 cohorts. Among New Orleans workers, excess risk was restricted to those with X-ray evidence of asbestosis. Workers employed at least 21 years but without X-ray abnormalities, experienced no elevated risk, while those with small opacities (1/0 or higher) had substantially elevated risk (SMR > 400). Exposures in these two groups had been similar. These results suggest that asbestosis may be a necessary precursor for asbestos-induced lung cancer; if so, then the no-threshold model for lung cancer risk is inappropriate since there is general agreement that very low exposures will not result in radiologically detectable lung fibrosis. Further data on this potential link are needed. As in other industries, mesothelioma risk was strongly related to amphibole exposure, especially to crocidolite in asbestos-cement pipe manufacture. A cluster of cases has recently been reported in a family amosite-cement business. Among New Orleans workers, risk of asbestosis was related to cumulative exposure but there was little evidence of risk below 30 f ml-1-years. Progression of asbestosis in these workers was slow, related to past cumulative exposure and not related to lung function decline. Asbestosis risk is therefore not likely to develop in workers under current controlled exposure conditions.

Asbestos↗
PubMed1986

Asbestos content of lung tissue in asbestos associated diseases: a study of 110 cases.

Diseases associated with asbestos exposure include asbestosis, malignant mesothelioma, carcinoma of the lung, and parietal pleural plaques. In this study the asbestos content of lung tissue was examined in groups of cases representing each of these diseases and in several cases with non-occupational idiopathic pulmonary fibrosis. Asbestos bodies (AB), which are the hallmark of asbestos exposure, were present in the lungs of virtually everyone in the general population and present at increased levels in individuals with asbestos associated diseases. The highest numbers of AB occurred in individuals with asbestosis, all of whom had levels greater than or equal to 2000 ABs/g wet lung tissue. Every case with a content of 100,000 ABs/g or higher had asbestosis. Intermediate levels occurred in individuals with malignant mesothelioma and the lowest levels in patients with parietal pleural plaques. There was no overlap between the asbestos content of lung tissue from patients with asbestosis and those with idiopathic pulmonary fibrosis. Lung cancer was present in half the patients with asbestosis, and the distribution of histological patterns did not differ from that in patients with lung cancer without asbestosis. The asbestos body content in patients with lung cancer was highly variable. Control cases had values within our previously established normal range (0-20 ABs/g). There was a significant correlation (p less than 0.001) between AB counted by light microscope and AB and uncoated fibres counted by scanning electron microscopy. The previous observation that the vast majority of asbestos bodies isolated from human tissues have an amphibole core was confirmed.

Aged↗
PubMed1988

Correlation between fibre content of the lung and disease in east London asbestos factory workers.

The lungs from 36 past workers at an east London asbestos factory who had died from asbestos related disease were compared with lung tissue from 56 matched control patients being operated on in east London for carcinoma of the lung, correlating the severity of asbestosis and the presence of pulmonary carcinoma or mesothelioma of the pleura or peritoneum with an asbestos exposure index and type and amount of mineral fibre in the lungs. Asbestosis was associated with far heavier fibre burdens than mesothelioma. There was also a striking difference in the degree of asbestosis between the subjects with mesothelioma and those with carcinoma of the lung, the asbestosis being more severe in the latter. A further finding was that crocidolite and amosite were strongly associated with asbestosis, carcinoma of the lung complicating asbestosis, and mesothelioma, whereas no such correlation was evident with chrysotile or mullite. It is suggested that more emphasis should be placed on the biological differences between amphibole and serpentine asbestos fibre.

Asbestosis↗
PubMed2005

Asbestos in the non-mining industry on the Witwatersrand, South Africa.

BACKGROUND AND INTRODUCTION: For many decades, and until fairly recently, asbestos was commonly found in most sectors of South African industry. Consequently there is a large but indeterminate pool of formerly exposed workers, some of whom will present to medical practitioners for evaluation of possible asbestosis, the pneumoconiosis caused by the fibre. Fundamental to the diagnosis of asbestosis is a history of asbestos exposure sufficient to cause the disease. Attending practitioners need to be aware of the common asbestosis-inducing industries and jobs and the duration of exposure reported by patients if we are to obtain and interpret their exposures. This paper describes asbestos exposure in 141 cases of asbestosis. METHODS: Cases were identified from patient records at the Occupational Medicine Clinic of the National Institute for Occupational Health (NIOH, formerly NCOH), for the years 1980-2000. Patients were only included in the series if they had no asbestos exposure in mining, if they had been certified with asbestosis by a compensation panel, and if on re-reading of the chest radiograph a radiologist reported irregular opacities (profusion 1/0 or greater on the International Labour Organisation (ILO) scale). Asbestos exposure was taken from the patient's records. RESULTS: Only one patient was exposed in an industry where asbestos was incidental to the enterprise's operation, while 54% of cases arose from exposure in primary asbestos industries, i.e. companies selling, distributing, refining, milling or using raw asbestos to manufacture products. The mean reported duration of exposure was 17.5 years. Surprisingly, 21 cases (15%) reported less than 5 years' exposure. Unexpectedly, 7 cases had a latency period from first exposure to diagnosis of less than 6 years. CONCLUSION: The data presented should assist practitioners in the purposeful exploration of asbestos exposure and in interpretation of its significance with regard to asbestosis.

Adult↗
PubMed1989

Fibre content of lung in amphibole- and chrysotile-induced mesothelioma: implications for environmental exposure.

Using 9 pairs of exposure-period-matched shipyard and insulation workers (amphibole exposure) and chrysotile-industry workers (chrysotile exposure) with mesothelioma, and an additional 9 pairs of workers with asbestosis, we found that the chrysotile workers with mesothelioma had 400 times the median lung fibre burden of the shipyard and insulation workers with mesothelioma. Mesothelioma in the chrysotile workers was associated with a 3 times greater median fibre burden than asbestosis, whereas in the shipyard and insulation workers mesothelioma was associated with only 1/35 the median amphibole burden seen in cases of asbestosis. In the chrysotile workers, the tremolite:chrysotile ratio and the mean fibre sizes were the same for both mesothelioma and asbestosis cases. These data suggest that total fibre load is crucial to the induction of mesothelioma by chrysotile, and that this phenomenon requires, on average, as high a fibre burden as induction of asbestosis by chrysotile. By contrast, for amphibole exposure, mesothelioma appears at a much lower fibre burden than asbestosis. The fibre types appear to differ by at least two orders of magnitude in their potential for inducing mesothelioma. Estimates of risk from environmental exposure must take these differences into account.

Aged↗
PubMed1989

Pulmonary functional impairment from years of arc welding.

PURPOSE: The adverse effects of arc welding on pulmonary function have been previously documented. However, in many of these studies, the effects of welding exposure and smoking were not separated. Also, some studies did not adjust for or ignored the effects of asbestosis on pulmonary function. We assessed the long-term effects of welding on pulmonary function in welders who had no evidence of asbestosis on chest radiographs, and adjusted each individual value for height, age, and years of cigarette smoking. PATIENTS AND METHODS: The study consisted of 226 male construction welders who had never worked in shipyards. Forced vital capacity (FVC) and flows were measured by spirometry, chest radiographs were obtained and examined for evidence of asbestosis using International Labor Office (ILO) criteria, and thoracic gas volume (TGV) was determined by planimetry. The subjects were also administered an occupational and respiratory questionnaire. Data on workers with asbestosis (ILO profusion 1/0 or greater) and pleural abnormalities were excluded. The mean age for the 226 subjects without asbestosis was 45 years, mean height was 175.7 cm, and mean duration of welding was 21.3 years. Pulmonary function measurements are presented as mean percentage of predicted (pop) and adjusted for height, age, and years of smoking. RESULTS: In 151 current cigarette smokers, mean midflows and terminal flows were decreased, FEF25-75 to 93.2 pop and FEF75-85 to 91.2 pop, but FVC, forced expiratory volume in one second (FEV1) and TGV were normal. The 43 nonsmokers also had reductions in flows but normal FVC and TGV. Flows in both groups were significantly (p less than 0.05) below those of the referent group. The regression coefficient was -0.0031 for years of welding and FVC pop, -0.0035 for FEV1 pop, and -0.0080 for midflow pop (FEF25-75) (all significant at p less than 0.05), but the coefficient for FEF75-85 pop was not significant. As calculated from regression equations, 40 years of welding would reduce FVC to 95.2 pop, FEV1 to 92.2 pop, midflow to 79.2 pop, and FEF75-85 to 81.7 pop. CONCLUSION: Long-term exposure to welding gases and fumes reduced flows in small airways of welders without asbestosis.

Adult↗
PubMed1988

Lobe of origin in the attribution of lung cancer to asbestos.

Lung cancer originates most commonly in the upper lobes in the general population but among workers with asbestosis it is most common in the lower lobes. Published data on lobar distribution were used to estimate the probabilities that lung cancer among asbestos workers is attributable to exposure to asbestos. This attribution varies directly with the relative risk. Critical values of the relative risk at which attribution of lung cancer to asbestos equalled its attribution to other causes, mainly smoking, were calculated. At a relative risk above 2.81 upper lobe cancers were more likely to be due to asbestos than not. For middle and lower lobe cancers, the critical relative risk was 1.55. These critical values were compared with published standardised mortality ratios reported for cohorts of workers with asbestosis. Since the ratios ranged from 6.3 to 9.1, the probability that lung cancer in such cases is due to asbestos is high regardless of lobe of origin. In many cohorts unstratified by the presence or absence of asbestosis the risk ratios are below one or both of these critical values. Since risk ratios are so high among workers with asbestosis, the ratios must be lower for workers without asbestosis than the overall ratios for unstratified cohorts. Therefore, the critical values may be useful in workers without asbestosis among such cohorts to estimate the upper limit of the probability that lung cancer in a given lobe is due to exposure to asbestos.

Asbestos↗
PubMed2006

24 years of pneumoconiosis mortality surveillance in Australia.

Asbestosis, silicosis and Coal Worker's Pneumoconiosis (CWP) represent three of the most important occupationally-related dust diseases in Australia. To gain a clear picture of pneumoconiosis trends over time, a 24-yr retrospective analysis of national mortality data was performed for the period 1979 to 2002. Over 1,000 pneumoconiosis-related fatalities occurred during this time, 56% of which were caused by asbestosis, 38% by silicosis and 6% by CWP. Between 1979 and 1981, silicosis accounted for 60% of all pneumoconiosis-related fatalities in Australia, followed by asbestosis (31%). By 2002 however, asbestosis was causing 78% of all fatalities, while silicosis accounted for only 19%. Asbestos-related mortality increased three-fold between 1979 and 2002, with a clear excess risk demonstrated among males. On the other hand, mortality rates for silicosis and CWP declined significantly during the same time period. Overall, this study suggests that pneumoconiosis, particularly asbestosis, continues to be an important occupational disease in Australia. Although progress has been made in reducing deaths due to occupational silicosis and CWP, asbestosis rates continue to rise, reflecting the long latency between dust exposure and clinical disease. Countries which continue to use asbestos products in the workplace should note the tragic legacy of this material within contemporary Australia.

Asbestos↗
PubMed2000

The prevalence of pleural plaques and/or pulmonary changes among construction workers in Okayama, Japan.

BACKGROUND: Since asbestos has been widely used in Japanese building materials since 1960s, a large number of Japanese construction workers may be exposed to asbestos occupationally. METHODS: Among 2951 construction workers in Okayama, Japan, the prevalence of asbestos-induced pleural or pulmonary changes was examined by screening chest x-rays; these findings were confirmed by computed tomography (CT) scanning of the chest. RESULTS: Among 2951 construction workers, 168 (5.7%) were found to have significant findings for pleural plaque or pulmonary changes on chest x-ray. Seventy-four had both pleural plaque and asbestosis, 85 pleural plaques alone, and 9 asbestosis alone. In 11 subjects, pleural plaques were suggested by chest x-ray, but neither pleural plaque nor asbestosis was demonstrated by chest CT. Honeycombing as one of the characteristic findings of asbestosis was found in 29 subjects. Others showed subpleural spots or curvilinear shadow, which suggested the early stage of asbestosis. The occupations of these workers were carpenters (64), plasterers (27), and concrete board cutters (14). About 30% of the workers with these findings were aware that they were handling asbestos in activities such as installation of asbestos boards, and/or asbestos spraying. CONCLUSIONS: As the incidence of malignant mesothelioma and primary lung cancer associated with asbestos exposure are high, screening by chest CT is necessary for detecting asbestos-induced pulmonary and/or pleural lesions. Education for protection such as telling about the presence of asbestos in building materials is also necessary.

Asbestosis↗
PubMed1987

Asbestos exposure, cigarette smoking, and airflow limitation in long-term Canadian chrysotile miners and millers.

To investigate further the relationships of asbestos exposure, cigarette smoking, and airflow limitation, we have obtained detailed pulmonary function tests (PFT) in 331 long-term Canadian chrysotile workers, 34 of whom were lifetime nonsmokers. Three disease categories were defined on the bases of standard diagnostic criteria, gallium-67 lung uptake, and the lung pressure-volume curve. Category A was composed of workers without changes suggestive of alveolitis or asbestosis. There were eight nonsmokers (ns), among whom we found a statistically significant 30% reduction in airflow conductance (Gus) at low lung volume, which is consistent with the concept of an asbestos airway lesion. The 85 smokers (sm) of category A had reduction of Gus at both high and low lung volumes. Category B was composed of workers without asbestosis but with evidence of asbestos alveolitis. In the six ns, Gus was significantly reduced to 50% normal at low lung volume. The 59 sm had reduction of Gus at both high and low lung volumes but less severely than sm in category A. Category C was composed of workers with asbestosis. The 20 ns had restrictive pattern of lung function, and Gus was decreased to 39% normal at 50% TLC. The 153 sm in C had airflow reduction comparable to sm in B. We concluded that asbestos exposure, which leads to asbestos airway disease, asbestos peribronchiolar alveolitis, and asbestosis, causes airflow limitation at low lung volume but does not reduce the expiratory flow rates on the flow-volume curve in lifetime nonsmokers. In the smoking asbestos workers with alveolitis or asbestosis, the major component of airflow limitation is a smoking effect. In these smoking workers, rigidity of the lung lessens airflow obstruction associated with smoking at the expense of increased work of breathing.

Adult↗
PubMed1990

Computer quantitation of gallium 67 lung uptake in crocidolite (blue asbestos) workers of Western Australia.

Pulmonary inflammation has been evaluated in 43 crocidolite-exposed asbestos (ASB) workers and 12 control subjects, using a quantitative index of gallium uptake (GI). The GI was compared with chest roentgenographs (CXRs) graded by the ILO classification. The ASB workers included 15 with asbestosis (CXR greater than or equal to 1/0), 19 with a normal CXR (CXR 0/0), and 9 with equivocal CXR changes (CXR 0/1). In individuals with asbestosis the GI was 3.6 +/- 0.3 (mean +/- SEM), P less than 0.01 compared with exposed patients without asbestosis. In exposed patients with equivocal CXR changes (0/1) the GI was 3.1 +/- 0.3, and in exposed patients with a normal CXR (0/0) the GI was 2.4 +/- 0.2. The GI for subjects without lung disease was 1.2 +/- 0.2, P less than 0.01 compared with exposed patients without asbestosis. The scans were scored independently by two observers, and the correlation coefficient of the two sets of GI was 0.95. These data demonstrate that subjects with crocidolite-induced asbestosis and exposed patients with equivocal CXR changes or a normal CXR have significantly increased GI.

Asbestos↗