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Biomedical subjects

A W Musk

Publications and source records attributed to A W Musk.

At least 127 records · Page 7Linked to original sources
PubMed1988

Increased pulmonary gamma interferon production in asbestosis.

In order to determine if disordered cellular immune processes are present in the lungs of persons with asbestosis, we performed bronchoalveolar lavage (BAL) on 26 patients with either crocidolite- or chrysotile-induced pulmonary asbestosis and measured the spontaneous release of gamma interferon (IFN gamma), a marker of increased cellular immune activity. For comparison, 18 control subjects and 7 patients with active pulmonary sarcoidosis were also studied. Recovered BAL cells were cultured for 24 h (5 x 10(6)/ml), and the supernatant was assayed for interferon by determining inhibition of cytopathic effect on encephalomyocarditis virus-induced lysis of WISH cells and characterized by monoclonal anti-IFN gamma antibody inhibition. Nine (35%) patients with asbestosis released increased amounts of IFN gamma, up to 320 units/ml, the levels seen in the sarcoidosis patients. All control subjects released less than or equal to 10 units/ml. All interferon released was IFN gamma. In asbestosis patients, IFN gamma production was not related to a history of cigarette smoking, there was no significant difference in the ratio of helper/inducer (Leu-3) to suppressor/cytotoxic (Leu-2) cells in IFN gamma producers compared to non-IFN gamma producers (p greater than 0.05), and IFN gamma production correlated significantly with serum IgG levels (p less than 0.001) but not with the levels of IgM, IgA, antinuclear factor, or rheumatoid factor. These data suggest that active cellular immune processes are present in the lungs of a proportion of patients with asbestosis.

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↗
PubMed1987

Mortality from asthma in Western Australia.

From a cohort of all 5760 male and 4979 female patients who were admitted to WA hospitals and were discharged with a diagnosis of asthma between 1976 and 1980, 265 deaths in men and 189 deaths in women were identified by the end of 1982. The standardized mortality ratio (SMR) for all causes of death for this cohort was 1.6 for men (P less than 0.001) and 1.7 for women (P less than 0.001). Both sexes showed a significant increase in deaths that were attributable to asthma (SMR, 57.9), chronic airflow obstruction (SMR, 9.3) and ischaemic heart disease (SMR, 1.3). The excess death rates for asthma were observed in all age groups, but those for chronic airflow obstruction and ischaemic heart disease were present in older age groups only. These findings indicate that asthma remains a potentially fatal disease in the Australian community. The excess mortality ratios for chronic airflow obstruction that were observed in patients who were admitted to hospital with asthma also suggest that asthma may result in irreversible airflow obstruction.

Adolescent↗
PubMed1986

Morphology of bronchogenic carcinoma in workers formerly exposed to crocidolite at Wittenoom Gorge in Western Australia.

Cytology and histology material from 46 bronchogenic carcinomas occurring in ex-workers from the Wittenoom crocidolite mine and mill in Western Australia and a matched random sample of 234 other bronchogenic carcinomas occurring in Western Australia over the same period were reviewed by a single histopathologist without knowledge of asbestos exposure status. Squamous-cell carcinomas formed 45.7% of the cancers in the asbestos-exposed group but only 32.5% of the cancers in the comparison group. This difference could not be explained by differences in smoking history between the two groups of lung cancer patients or in the type of histopathological material available for review. The excess of squamous-cell cancers was observed in subjects both with and without parenchymal asbestosis.

Adult↗
PubMed1986

Associations between asthma history, atopy, and non-specific bronchial responsiveness in young adults.

In 105 subjects taken from a student population and aged between 15 and 30 there was a strong positive association between the presence of the atopic state, defined by skin tests, and a high level of non-specific bronchial responsiveness to methacholine (chi 2 = 10.5, d.f. = 2, P = 0.01). Regression analysis showed a history of asthma, and the symptom of wheeze, to be predominantly predicted by the degree of bronchial responsiveness (R2 = 31%), with only a minor independent contribution from the degree of atopy (R2 a further 5%). The genetic or other reasons for the association between bronchial responsiveness and atopy may have importance in understanding the aetiology of allergic asthma.

Adolescent↗
PubMed1986

Atopy, non-allergic bronchial reactivity, and past history as determinants of work related symptoms in seasonal grain handlers.

One hundred and five young subjects with little or no previous exposure to grain dust were studied before and after a seven week period of grain handling work to determine if there was an association between symptoms experienced at work and pre-employment respiratory symptoms, allergy skin test responses, and non-allergic bronchial reactivity. The incidence of work related symptoms was cough 18%, wheeze 13%, and dyspnoea 14%. The results showed that pre-employment history of respiratory symptoms, positive allergy skin test responses, and a high level of non-allergic bronchial reactivity were significantly associated with these symptoms. These measurements may be useful to predict symptoms associated with exposure to grain dust in new employees and the results suggest that these work related symptoms may be due to allergen induced asthma.

Adolescent↗
PubMed1986

Prevalence of radiographic asbestosis in crocidolite miners and millers at Wittenoom, Western Australia.

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.

Adult↗
PubMed1986

Symptoms and longitudinal changes in lung function in young seasonal grain handlers.

A total of 119 seasonal grain handlers (mean age 23) were assessed before and towards the end (mean work period 18 days) of the 1983 Western Australian grain harvest to determine if respiratory symptoms that occur with exposure to grain dust are associated with changes in ventilatory capacity or non-specific bronchial reactivity to methacholine. Eighteen per cent of subjects had wheeze, breathlessness, or chest tightness and 18% had cough or sputum production at work. Subjects complaining of wheeze, chest tightness, or breathlessness at work had a significantly greater decline in FEV1 than subjects who did not experience these symptoms (p less than 0.05). Symptoms were not associated with changes in bronchial reactivity. In young grain handlers who develop respiratory symptoms on short term exposure to grain dust changes in FEV1 but not in non-specific bronchial reactivity have been demonstrated.

Adolescent↗
PubMed1986

The natural history of asbestosis in former crocidolite workers of Wittenoom Gorge.

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.

Adult↗
PubMed1986

Genetic studies in familial fibrosing alveolitis. Possible linkage with immunoglobulin allotypes (Gm).

A family containing 12 subjects spanning three generations and including six cases with clinical evidence of definite or probable fibrosing alveolitis has been investigated. Histologic confirmation was available for three cases. The subjects were between 15 and 54 years of age at diagnosis. Although the size of the sample is small, the mode of inheritance of fibrosing alveolitis within this family appeared to be dominant with incomplete penetrance. HLA typing showed that at least one of the affected siblings did not share any HLA haplotypes with other affected siblings in the third generation. This makes it unlikely that a disease gene would be in association with HLA genes on chromosome 6. In contrast, all affected siblings, as well as two as yet unaffected siblings, carried the immunoglobulin haplotype Gm 1. These studies indicate that familial fibrosing alveolitis in this family may be inherited by a dominantly inherited gene located on chromosome 14 close to the loci encoding for Gm.

Adolescent↗
PubMed1986

Alveolitis of pulmonary asbestosis. Bronchoalveolar lavage studies in crocidolite- and chrysotile-exposed individuals.

Bronchoalveolar lavage (BAL) findings in 27 individuals with crocidolite- or chrysotile-induced asbestosis were compared to BAL findings in 29 unexposed control subjects. Alveolitis, defined as an increase in the proportions and/or absolute numbers of inflammatory cells present in BAL fluid compared to values in control subjects, was present in 26 (96 percent) subjects with asbestosis. Most exhibited a neutrophil-eosinophil alveolitis, with neutrophil proportions increased to 7.4 +/- 0.7 percent and eosinophil proportions increased to 2.2 +/- 0.4 percent, compared to 2 +/- 0.5 percent and 0.4 +/- 0.01 percent, respectively, in control subjects (p less than 0.01 for both neutrophils and eosinophils). An increase in the total number of neutrophils and eosinophils per ml of lavage fluid was also seen (neutrophils 23 +/- 5 and eosinophils 13 +/- 4 per ml; p less than 0.05 compared to control subjects). Severity of the alveolitis, defined by the neutrophil or eosinophil proportions, was independent of a history of exposure to cigarette smoke. The pattern and severity of alveolitis in crocidolite- and chrysotile-induced asbestosis were similar. There was a significant correlation between duration of exposure to asbestos and neutrophil proportions (p less than 0.01). No significant difference in the severity of the alveolitis was observed between individuals with radiologic and physiologic evidence of asbestosis compared to those with asbestos exposure and crackles alone, suggesting that, in asbestosis as in other chronic interstitial lung diseases, radiologic and physiologic parameters do not reflect the severity of the alveolitis. This study demonstrates that a neutrophil-eosinophil alveolitis is present in individuals with crocidolite- and chrysotile-induced asbestosis, that this alveolitis is independent of cigarette smoking, and that the severity of the BAL changes is not reflected in radiologic and physiologic changes.

Asbestos↗
PubMed1985

Trends in mortality from malignant mesothelioma of the pleura, and production and use of asbestos in Australia.

Annual mortality from malignant mesothelioma of the pleura (MMP) in Australia (as represented by ICD8 codes 163.0 and 212.4, and ICD9 codes 163 and 212.4) increased in men aged 30 years and older from about 0.5/100 000 in 1968-1970 to 2.1/100 000 in 1983. Corresponding rates in women varied from 0.1/100 000 to 0.2/100 000 between 1968 and 1980, then rose to 0.3/100 000 in 1983. The rise in MMP mortality in men probably corresponds to the increasing use of asbestos, particularly amosite, in Australia during and after World War II. That production and importation of amosite and crocidolite in Australia reached a peak in 1958 may mean that peak mortality from MMP will not be reached until the 1990s (allowing a 35-year lag period). Substantial increases in importation and later production, of chrysotile in the 1950s, 1960s and 1970s may lead to increases in the incidence of other asbestos-related cancers, not reflected in trends in the incidence of MMP.

Adult↗