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Plain chest radiographs from a one in six random sample of the workforce of the asbestos industry at Wittenoom, Western Australia between 1943 and 1966 have been classified for degree of profusion and pleural thickening by two independent observers according to the 1980 UICC-ILO Classification of Radiographs for the pneumoconioses to clarify the effect of degree of radiological abnormality on survival. A total of 1106 subjects were selected. Each subject's age, cumulative exposure to crocidolite, and time since first exposure were determined from employment records, the results of a survey of airborne concentrations of fibres > 5 mu in length conducted in 1966, and an exposure rating by an industrial hygienist and an ex-manager of the mine and mill at Wittenoom. By the end of 1986 193 subjects had died. Conditional logistic regression was used to model the relative risk of death in five separate case-control analyses in which the outcomes were deaths from: (1) all causes, (2) malignant mesothelioma, (3) lung cancer, (4) asbestosis, and (5) other causes excluding cancer and asbestosis. Up to 20 controls per case were randomly chosen from all men of the same age who were not known to have died before the date of death of the index case. After adjustment for exposure and time since first exposure, there were significant and independent effects of radiographic profusion and pleural thickening on all cause mortality. The effect of profusion was largely a result of the effect on mortality from malignant mesothelioma and asbestosis but not lung cancer. The effect of pleural thickening was greatest on mortality from other causes, mainly ischaemic heart disease. This study has shown that degree of radiographic abnormality has an independent effect on mortality from malignant mesothelioma, asbestosis, and all causes even after allowing for the effects of age, degree of exposure, and time since first exposure.

Thirty three pairs of chest radiographs taken up to 10 years apart were obtained for 33 subjects suffering from asbestosis who had applied for compensation to the Pneumoconiosis Medical Board of Western Australia. Multiple films from the period before the first radiograph in each pair, from the intervening period between the two, and from the period subsequent to the second radiograph were also available and all films were read by two independent readers according to the 1980 ILO classification of pneumoconiosis. Films were read twice as side by side pairs ten years apart, twice as two separate randomly ordered films ten years apart, and once as part of the full series of all available chest radiographs on each subject to assess which method provided the best consistency (between reader variation) and repeatability (within reader variation). Judging by consistency, the full series method performed as well as either of the other methods when assessing radiographic changes and significantly better when assessing the level of profusion of small opacities. There was little to choose between the other two methods either judging by consistency or repeatability, which could not be estimated for the full series method. Use of all available films for a subject is recommended for assessing single films, as in a prevalence study, as well as for documenting change in a longitudinal study.

Serial plain chest radiographs taken between 1943 and 1982 for 280 claimants for compensation for asbestosis and 32 claimants for malignant pleural mesothelioma from the Wittenoom asbestos industry were reviewed by two observers to identify diffuse pleural thickening and pleural effusion. A pleural effusion which appeared and resolved within two years without radiographic or clinical evidence of underlying malignancy, infection or cardiac failure was seen in 15 cases by reader 1 and 24 cases by reader 2. Eighteen cases of effusion, determined from clinical records to be caused by malignant pleural mesothelioma, were seen by reader 1 and 20 by reader 2. The latent periods between commencing work and the first radiograph showing effusion were much shorter for subjects with benign asbestos pleural effusion than for subjects with effusion due to malignant pleural mesothelioma, although there was considerable overlap in the range. The longest latent period for benign asbestos pleural effusion was 22 years and the shortest period for effusion due to malignant pleural mesothelioma was 12 years. The latent period for benign asbestos pleural effusion was inversely related to total cumulative exposure, whereas that for effusion due to malignant pleural mesothelioma was significantly shorter for subjects who had worked in the mill than for those who had worked in the mine. A long latent period and a history of working in the mill were significant discriminators for a malignant as opposed to a benign basis for an effusion. The appearance of a benign asbestos pleural effusion appeared to be a risk factor for the severity of subsequent diffuse pleural thickening.(ABSTRACT TRUNCATED AT 250 WORDS)

Serial plain chest radiographs of 384 men who worked at the Wittenoom crocidolite mine and mill between 1943 and 1966 and who applied for pneumoconiosis compensation between 1948 and 1982 have been examined independently by two trained observers for pleural disease using the 1980 ILO-UICC classification of radiographs to record width and extent of pleural disease. Radiographs covering follow up periods of from two to 38 years were examined (median number of films per subject was nine). The degree of crocidolite exposure was estimated from employment records and a survey of airborne fibre concentrations performed in 1966. Agreement between the observers on the presence and degree of pleural disease in the final film for each subject was moderately close (Kendall's tau B = 0.62) and was least for subjects with thickening less than 5 mm in width. Diffuse pleural thickening extending for greater than 50% of the lateral chest wall was the most common type recorded by both observers. Minor pleural thickening frequently progressed in extent along the lateral chest wall but progression beyond 5 mm in thickness was less common. Pleural plaques were not seen to progress beyond their initial thickness or extent. The rate of onset of thickening in this population increased continually from the time of first exposure and also increased slightly with age. There was evidence that the level of total cumulative exposure to crocidolite increased the rate of onset of pleural thickening in the period between five and 15 years after first exposure. Rate of progression of established thickening was greatest in subjects who first developed thickening early after first exposure. The relative rate of progression decreased slowly with time from first signs of thickening and there was no evidence of any progression more than 15 years after onset.

This study compares the relationship between lung function and radiological abnormality in 46 subjects with asbestosis and 38 subjects with cryptogenic fibrosing alveolitis. Radiographs were graded separately by two observers according to the 1980 International Labour Organisation criteria for classification of the pneumoconioses. The correlation between the transfer factor of the lungs and the radiographic profusion of small parenchymal opacities was found to be greater in subjects with asbestosis than in subjects with cryptogenic fibrosing alveolitis. At any level of radiological profusion transfer factor was higher in cases with asbestosis than in cases with fibrosing alveolitis. As pleural thickening is seen commonly in asbestosis and may influence lung volumes and the ratio of transfer factor to effective alveolar volume, the results of these measurements were compared only in the cases showing absent or minimal pleural thickening. Both of these variables were higher in the subjects with asbestosis. The results indicate that despite pathological, functional and radiographic similarities, lung function for a given degree of radiographic parenchymal abnormality is better in subjects with asbestosis than in subjects with cryptogenic fibrosing alveolitis, and that changes in the plain chest x-ray appearances in asbestosis correlate more closely with the results of lung function tests.

During a retrospective survey of patients with pulmonary shadows and blood eosinophilia between the years 1965 and 1980, 42 patients were found with allergic bronchopulmonary fungal disease. Eleven of these had no clinical evidence of asthma. Three of these 11 had hypersensitivity to fungi other than Aspergillus sp. In the absence of asthma there was some difficulty in making a diagnosis, particularly where collapse of the upper lobe occurred in middle-aged or elderly patients and bronchogenic carcinoma was presumed responsible. We suggest that the term allergic bronchopulmonary aspergillosis be replaced by allergic bronchopulmonary fungal disease, the diagnosis be considered in patients with lung disease and blood eosinophilia even in the absence of asthma, and a wider range of fungal allergens be used for skin and precipitin tests.

The survival of 354 claimants for compensation for pulmonary asbestosis among former workers of the Wittenoom crocidolite mine and mill in Western Australia has been examined. There were 118 deaths up to December 1982. The median time between start of work and claim for compensation was 17 years. The standardised mortality ratio (SMR) for deaths from all causes was 2.65 (p less than 0.0001). The SMR for pneumoconiosis was 177.2 (p less than 0.0001), bronchitis and emphysema 2.6 (p = 0.04), tuberculosis 44.6 (p less than 0.0001), respiratory cancer (including five deaths from malignant pleural mesothelioma) 6.4 (p less than 0.0001), gastrointestinal cancer 1.6 (p = 0.22), all other cancers 1.6 (p = 0.17), heart disease 1.4 (p = 0.07), and all other causes 2.18 (p = 0.004). Plain chest radiographs taken within two years of claiming compensation were found for 238 subjects and were categorised independently by two observers according to the International Labour Organisation criteria without knowledge of exposure or compensation details. Profusion of radiographic opacities, age at claiming compensation, work in the Wittenoom mill, and degree of disability awarded by the pneumoconiosis medical board were significant predictors of survival, but total estimated exposure to asbestos was not. Radiographic profusion and degree of disability were, however, predictable by total exposure. The median survival from claim for compensation was 17 years in subjects with ILO category 1 pneumoconiosis, 12 years in category 2, and three years in category 3.

An estimate has been made of the prevalence of unrecognised pneumoconiosis in former crocidolite workers from Wittenoom, Western Australia. All plain chest radiographs relating to a one in six random sample (1025 men) of all former Wittenoom workers who had never entered a compensation claim to the Pneumoconiosis Medical Board of Western Australia were sought from Perth teaching hospitals and from the Perth Chest Clinic where compulsory examination of all workers in the mining industry takes place. Radiographs were recovered for 83% of the men and read independently by two observers. By means of logistic regression analysis a current prevalence of parenchymal abnormality (defined as a radiographic profusion of small opacities of category 1/0 or greater on the ILO classification) of nearly 20% was calculated after adjustment for age, time since first exposure, and cumulative exposure level. One hundred men randomly selected from those known to be alive in the sample were invited to attend for a new radiographic examination. Seventy four men attended and the predicted prevalence was confirmed. It is estimated from these data that there were between 450 and 900 former Wittenoom workers in Australia at the end of 1980 who had radiographic abnormality consistent with pneumoconiosis but had not claimed compensation or had asbestosis diagnosed. The data are consistent with there being no threshold dose of crocidolite exposure for the development of radiographic abnormality in this group.

Sixty eight impotent men underwent corpora cavernosography and corpora cavernosal pressure measurements during saline infusion. Nineteen of the men had internal pudendal arteriograms. Correlation between the cavernosograms and saline infusion induced pressure measurements was "good" in 56/66(84%), "approximate" in 5/66(8%) and there was no correlation in 5/66(8%). Two patients were excluded for technical reasons. The spread of results and the good correlation of the two tests speaks for the accuracy of the method. It was of value in diagnosis and will be of paramount importance if veno occlusive surgery becomes a reliable method of treatment.

The course of pulmonary asbestosis and its determinants have been examined in 280 applicants for compensation among former workers of the crocidolite mine and mill at Wittenoom Gorge, Western Australia. Serial chest radiographs accrued over more than 3 decades were graded for parenchymal disease separately by two observers according to the 1980 ILO Classification of Radiographs for Pneumoconioses and without knowledge of exposure histories or compensation details. In 136 subjects whose median duration of exposure was 37 months, radiographic asbestosis appeared between 1 and 34 yr after initial exposure and then progressed continuously. Total exposure to asbestos and time from first exposure to the appearance of definite radiographic asbestosis were significant determinants of the rate of progression of profusion of radiographic abnormality. Asbestosis should be considered to be an active disease even 3 decades after exposure has ended.

Anomalies in the ratio of transfer factor to effective alveolar volume as an indicator of pulmonary gas exchange in cases of asbestosis may be related to diffuse pleural thickening. To examine the effect of pleural disease on gas transfer the plain chest radiographs of patients with asbestosis were assessed by two observers for profusion of parenchymal opacities and extent of pleural disease and the results were related to lung function. In 30 cases of category 1 profusion of parenchymal abnormality (according to the ILO international classification of radiographs for pneumoconiosis) transfer factor was independent of the degree of pleural thickening. The ratio of transfer factor to effective alveolar volume correlated directly with the degree of pleural thickening as alveolar volume fell with increasing severity of pleural disease. The results indicate that correcting transfer factor for alveolar volume does not provide an accurate reflection of severity of diffuse parenchymal fibrosis in patients with asbestosis and even minor pleural disease.