Causes of death of workers employed in an asbestos factory

Causes of death of workers employed in an asbestos factory

II8 Stimulus BRITISH THORACIC‘ AND ‘TUBERCULOSIS ASSOC’IATTOh Host immediate negative) Mechanisms _- * - . __ Direct histamine Reflex bronc...

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II8 Stimulus

BRITISH

THORACIC‘

AND

‘TUBERCULOSIS

ASSOC’IATTOh

Host

immediate negative)

Mechanisms

_- * - . __

Direct histamine

Reflex bronchial constriction REFERENCES PEPYS, J. (1967).Journal of the Royal College of Physicians of London, 2,42. BROSTOFF, J., GREAVES, M. F., & ROITT,I. M. (1969). Lancet, 1, 803.

HAZARDSOF ISOCYANATES ANGUS ROBSON(High Wycombe)

Isocyanates are organic chemicals chiefly used for the production of flexible foams and polyurethane finishes. Their use is expanding very fast. Isocyanates may produce symptoms resembling coryza, bronchitis or asthma and the occupational cause may be overlooked. Onset of symptoms may be delayed for some time after exposure or may be insidious. Clinically the pattern of symptoms may resemble an allergic illness but no good immunological evidence of allergy has been demonstrated. Evidence is presented that workers in contact with isocyanates have a greater fall in the F.E.V. than would be expected and this fall is greater in patients with previous respiratory symptoms, It is suggested that such patients be excluded from contact and that all workers should have in-service checks. CAUSESOF DEATH OF WORKERSEMPLOYEDIN AN ASBESTOS FACTORY M. L. NEWHOUSE(London)

The factory where these men worked was founded in the East End of London in 1913 and was in continuous production for the following 55 years. Its chief products were asbestos textiles and insulation materials. All three types of asbestos, crocidolite, amosite and chrysotile were used. The personnel records of this firm include details of all who have worked in the factory at any time and were the source of the data used in this study. By tracing through the central registers of the Department of Health and Social Security and of the National Health Service it was possible to establish whether a past employee of the factory was alive or dead in May, 1964. The Registrar General supplied the causes of death. The subjects in the study were categorized by the jobs they had held in the factory and by their length of employment. Their mortality was compared with the national figures. No excess was found until at least 16 years had elapsed between first exposure in the factory and death, but among those who were followed for longer periods and who had had jobs with heavy exposure to asbestos dust there was a significant excess of deaths both from lung and other cancers.

BRITISH THORACIC

AND

TUBERCULOSIS

ASSOCIATION

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Only men with records of long periods of employment showed an excess mortality from respiratory diseases. Where possible postmortem reports and histological material were obtained from the Pneumoconiosis Panels and hospitals where the patients had died and were reviewed by Dr. J. C. Wagner. Carcinoma of bronchus had not been seriously under-recorded on the death certificates. A mesothelial tumour had only been recorded as a cause of death on five death certificates but after review of the available histological material a further five pleural and 11 peritoneal mesotheliomas were identified; seven of the latter had been registered as deaths due to cancer of the gastrointestinal tract. A STUDY OF SOMEIMMUNOLOGICALFACTORSASSOCIATEDWITH ASBESTOSIS W. RAYMOND PARKES(London)

This preliminary study (done in collaboration with Dr. M. Turner-Warwick) of tissue antibodies -antinulear factors (ANF) and rheumatoid factors (RF)-was undertaken for two reasons:(1) The clinical syndrome of asbestosis is similar to that of the ‘mural’ type of cryptogenic fibrosing alveolitis (or diffuse interstitial fibrosis) in which an increased prevalence of these antibodies has been found. (2) RF is present in some cases of coal pneumoconiosis with or without arthritis. Chest radiographs were correlated with ANF and RF (DAT and latex fixation) in 77 unselected persons with a history of past asbestos exposure who were referred to the Pneumoconiosis Medical Panel in London. Radiographic appearances were graded quite simply as ‘round’ or ‘linear and irregular’, and according to size and coarseness and their extent in the conventional lung zones. The presence or absence of ‘honeycombing’ was noted and so was pleural thickening in lung zones. Only unequivocal changes were recorded and referred to as ‘obvious changes’. ANF and RF were found singly or together in 39 of the 77 cases-about 50 per cent ‘obvious lung changes’ occurred in 57 cases, pleural changes alone in 8 cases, and ‘normal’ radiographs in 12 cases. ANF and RF were present in 29 cases with ‘obvious changes’. Only weak positive latex tests were present in four cases. Antibodies were absent in 24 cases. That is, antibodies were present in 55 per cent of the cases. By contrast, ANF and RF are each found in approximately five per cent of the general population. There appeared to be a trend suggesting that coarse opacities are more likely to be associated with antibodies than fine opacities. All four subjects who had unusual, small, round shadows had antibody. ‘Honeycombing’ was not apparently associated more or less with the presence of antibodies. Of 19 subjects followed for five years six of 10 with progressive disease had antibodies, whereas antibodies were detected in the form of a doubtful positive latex reaction in only one out of nine with non-progressive disease. The possible significance of these findings was discussed. It was suggested that asbestos-provoked lung fibrosis tends to select out the five per cent of the general population with enhanced tissue antibody production though the antibodies themselves may not play any part in pathogenesis.

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It was thought that certain cases of respiratory illness among workers in a factory using a dry powder containing proteolytic enzyme derived from Bacillus subtilis were due to inhalation of the