British Medical Journal

Our medical research library holds 33 studies published in British Medical Journal (1924–1978). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 8 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it. For 9 studies PubMed has no abstract for, we give the abstract printed in the article or, where there is none, a summary we wrote from it, each labeled as such.

About the journal

• Publisher: British Medical Association
• Published: 1857–1980, England
• Language: English
• ISSN: 0007-1447 (print)
• Its record in the NLM Catalog

1970s

• Malignant mesothelioma and gas-mask assemblers. D.B. Jefferys, J.A. Vale. 1978;2(6137):607. Case report PubMed · Publisher · Free full text

• Risks of environmental exposure to asbestos. 1978;1(6121):1164-5. Editorial PubMed · Publisher · Free full text

• Frequency of HLA antigen in asbestos workers with and without pulmonary fibrosis. C.C. Evans, H.C. Lewinsöhn, J.M. Evans. 1977;1(6061):603-5. PubMed · Publisher · Free full text

  Abstract

  HLA antigens were determined in 37 patients with asbestosis and 37 matched controls with equivalent asbestos exposure but no pulmonary fibrosis. All had worked in the same textile factory. No significant differences in the prevalence of antigens were found between the two groups or between either group and controls who had not been exposed to asbestos. When the data were combined with findings from other pilot studies the previously suggested association between asbestosis and HLA-B27 was not confirmed. Subjects who were positive for HLA-B12 tended also to have advanced radiographic fibrosis. Asbestos workers without pulmonary fibrosis had an unexpectedly high frequency of HLA-BW5, which might indicate that this antigen protects against the development of pulmonary fibrosis.

• Unsuspected exposure to asbestos and bronchogenic carcinoma. K.M. Martischnig, D.J. Newell, W.C. Barnsley, et al. 1977;1(6063):746-9. Case report PubMed · Publisher · Free full text

  Abstract

  Two hundred and fifty men admitted to a thoracic surgical centre and matched controls were questioned in detail about their occupations after leaving school and their smoking habits. Of 201 men with confirmed bronchial carcinoma 58 gave a history of occupational exposure to asbestos, whereas only 29 out of 201 men matched for age and residential area who were admitted with other diseases gave such a history. This difference was statistically highly significant. The usual association of bronchial carcinoma with heavy smoking was observed, but asbestos exposure increased the risk of carcinoma whatever the level of smoking. These results are consistent with the hypothesis that asbestos exposure and the level of smoking act independently in causing bronchial carcinoma. The patients with carcinoma who had been exposed to asbestos presented on average three years earlier than those who had not been exposed. Asbestos regulations have eliminated the risk of exposure to workers in scheduled industries, so asbestos-induced diseases will probably be increasingly found among the many workers who have had incidental exposure to asbestos. It is therefore important to take a full occupational history.

• Editorial: Exposure to asbestos dust. 1976;1(6022):1361-2. PubMed · Free full text

• Letter: Exposure to asbestos dust. D.C. Britton. 1976;2(6028):175. Case report PubMed · Publisher · Free full text

• The HL-A system in asbestos workers. J.A. Merchant, P.T. Klouda, C.A. Soutar, et al. 1975;1(5951):189-91. PubMed · Publisher · Free full text

  Abstract

  In a study of the HL-A system in 56 selected asbestos workers referred to the Pneumoconiosis Medical Panel with definite or suspected asbestosis, the W 27 antigen was found more often than among a control population. Six of the 10 asbestos workers with the W 27 antigen had definite radiographic evidence of asbestosis compared to 13 out of 46 without the W 27 antigen. These observations, if confirmed, suggest that the W 27 antigen may provide a useful marker of an enhanced susceptibility to the tissue-damaging effects of asbestos dust.

• Editorial: Asbestos hazard. 1973;4(5888):312-3. PubMed · Free full text

• Study of the secular trend in asbestos bodies in lungs in London 1936-66. C.H. Um. 1971;2(5756):248-51. PubMed · Publisher · Free full text

  Abstract

  Thick sections (30mu unstained) cut from blocks of lung tissue from 100 consecutive necropsies for the years 1936, 1946, 1956, and 1966 at the Archway Hospital, London, have been searched for asbestos bodies. The incidence rose progressively-0, 3, 14, and 20% respectively. The rise was not explained by the increasing age of death in the later years or by the likely effects of changes in the areas within London in which the deaths occurred. There was no similar increase in the incidence of other bodies in the lungs which might be mistaken for asbestos bodies. The rising incidence is shown to fit reasonably with a model based on the hypothesis that the risk of inhaling asbestos increases in relation to the cumulative total of asbestos imported into the country from 1910 onwards. The rising incidence does not fit a model in which the risk depends simply on the current level of asbestos imports.

• Circulating rheumatoid and antinuclear factors in asbestos workers. M. Turner-Warwick, W.R. Parkes. 1970;3(5721):492-5. PubMed · Publisher · Free full text

  Abstract

  In an unselected series of 80 patients with asbestos exposure referred to the London Pneumoconiosis Medical Panel, antinuclear and rheumatoid factors were found in 28 and 27% respectively. This probably represents at least a fourfold increase over their incidence in random populations. The presence of these autoantibodies was not related to the duration of exposure, but was related to the extent of radiographic abnormality.

• Mesothelioma in Scotland. J. McEwen, A. Finlayson, A. Mair, et al. 1970;4(5735):575-8. PubMed · Publisher · Free full text

  Abstract

  In a retrospective study of the incidence of mesothelioma in Scotland for 1950-67 80 cases were traced from pathological reports and biopsy material of malignant tumours invading the pleura and peritoneum. These cases were matched with two sets of controls. Detailed histories of residence, occupation, and degree of exposure to asbestos confirmed that the incidence of mesothelioma in Scotland is similar to that in other parts of Britain.

• Occupational cancer of the lung and smoking. 1970;2(5705):313. PubMed · Free full text

1960s

• Correlation between lung asbestos count at necropsy and radiological appearances. P. Macpherson, J.K. Davidson. 1969;1(5640):355-7. PubMed · Publisher · Free full text

  Abstract

  In the first 100 of a series of 600 consecutive necropsies for which a chest x-ray film had been taken within a year of death the features of asbestosis were observed in eight of the nine cases where the asbestos count at subsequent necropsy exceeded 40. In only one of these cases had the diagnosis of asbestosis been suggested during life. The higher the asbestos count the greater the likelihood of radiographic abnormalities, particularly calcified and non-calcified pleural plaques on the chest wall and diaphragm.

• Asbestos bodies in routine necropsies on Tyneside: a pathological and social study. T. Ashcroft. 1968;1(5592):614-8. PubMed · Publisher · Free full text

  Abstract

  Smears were prepared from the base of the right lung in 311 routine necropsies of patients over 15 years of age. Asbestos bodies were found in 20.3 % of cases (25.5% of 196 males and 11.3% of 115 females). The majority of smears contained scanty bodies, but in 17 cases they were numerous. In cases with positive smears histological sections failed to reveal asbestos bodies in over 50%. Histological evidence of minimal asbestosis was found in 10 cases. There were no cases of classical asbestosis. The series includes one case of mesothelioma of pleura. There was no significant excess of positive smears in patients dying from gastrointestinal or lung carcinoma. The incidence was higher in patients living in urban areas (25.6%) than in those from rural areas (3.5%). Twenty-nine patients definitely or probably were exposed to asbestos dust at work and two further patients had non-occupational exposure. Neighbourhood contamination with asbestos dust is probably not important in this series. When compared with a series of 23 cases of mesothelioma of pleura or peritoneum, 21 (91%) of which showed asbestos bodies in histological sections of lung, the greater incidence of asbestos bodies in the cases of mesothelioma is statistically highly significant.

  PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

• Asbestos bodies. H.C. Lewinsohn. 1968;2(5597):120. PubMed · Publisher · Free full text

• Asbestos bodies. T. Ashcroft. 1968;2(5606):696-7. PubMed · Publisher · Free full text

• Cancer and asbestos. 1968;3(5616):448-9. PubMed · Free full text

• Cancer and asbestos. J. Beattie. 1968;4(5623):123-4. PubMed · Publisher · Free full text

• Effects of asbestos in dockyard workers. G. Sheers, A.R. Templeton. 1968;3(5618):574-9. PubMed · Publisher · Free full text

  Abstract

  The prevalence of pleural and pulmonary abnormalities attributed to asbestos among 15,000 workers in a naval dockyard has been studied by means of a one-in-ten sample. Ninety-four per cent. of the men in the sample were examined. Of these, 3% had experienced continuous occupational exposure to asbestos and half of the remainder (representing approximately 6,800 men) had been exposed intermittently. The prevalence of pleural fibrosis ranged from 28% in continuously exposed workers to 1.9% in those with least exposure.Most cases of pulmonary fibrosis occurred in laggers and sprayers who had been continuously exposed for between 15 and 20 years. Pulmonary fibrosis was also seen in a variety of intermittently exposed trades, and had been preceded by extensive pleural thickening in some cases. Ten cases of pleural mesothelioma have occurred in the last three years and a large number of men appear to be potentially at risk.

• Hyaline and calcified pleural plaques as an index of exposure to asbestos. D.O. Hourihane, L. Lessof, P.C. Richardson. 1966;1(5495):1069-74. PubMed · Publisher · Free full text

  Abstract

  A close association between exposure to asbestos and the development of pleural plaques has been shown. A cause-and-effect relationship is probable. The most extensive lesions are radiologically detectable, and the disease asbestosis is then also present, despite the absence of any other radiological abnormality. The sources of asbestos are considered and evidence is presented to suggest that there is a widespread non-industrial community exposure. Mesotheliomata are common in patients with pleural plaques, and it is suggested that there is a dose-response relationship between the asbestos and the development of these neoplasms. The question of a relationship between lung cancer and asbestos is left open, but the value of radiological surveys for pleural plaques is emphasized in any study of this problem. Asbestos is not the sole cause of pleural plaques, but it is certainly the most common.

  PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

• Diffuse mesothelioma of the pleura and asbestos. P.C. Elmes, W.T. McCaughey, O.L. Wade. 1965;1(5431):350-3. PubMed · Publisher · Free full text

• Asbestos and malignancy. Z. Cope. 1964;2(5403):202. Historical article PubMed · Publisher · Free full text

  Summary

  This leading article reviewed the published evidence linking asbestos exposure with malignant disease. It noted that since Lynch and Smith described a case of lung cancer with asbestosis, evidence connecting the two had increased. Gloyne found bronchial carcinoma in 14% of a series of asbestosis cases. Doll calculated a lung cancer risk ten times that of the general population in workers exposed for 20 years or more. Braun and Truan, in Canada, failed to show an association. Enticknap and Smither described eleven peritoneal tumours in asbestos workers, all with histological evidence of asbestosis and at least twenty years after first exposure. Selikoff and colleagues followed 632 insulation workers for 20 years and found lung cancer seven times, and cancer of the stomach, colon and rectum three times, more often than expected, plus three pleural and one peritoneal mesothelioma. Wagner and co-workers described 47 patients with diffuse pleural mesothelioma, all but one probably exposed to crocidolite, only eight with confirmed asbestosis. The article also discussed difficulties in diagnosing diffuse mesothelial tumours, asbestos bodies in patients' lungs, fibre types, possible mechanisms and limited animal work. It concluded that until these questions were answered all exposure to asbestos dust should be considered hazardous, and that supervision should be extended to insulation workers in ships, factories and domestic buildings.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Diffuse mesothelioma and exposure to asbestos dust in the Merseyside area. W.G. Owen. 1964;2(5403):214-8. PubMed · Publisher · Free full text

• Exposure to asbestos and mesothelioma of the pleura. P.B. Fowler, J.C. Sloper, E.C. Warner. 1964;2(5403):211-3. PubMed · Publisher · Free full text

  Abstract

  Two cases of mesothelioma of the pleura are reported. Despite the absence of severe pulmonary fibrosis, the lungs in both contained "asbestos bodies"; in both, too, there was an occupational history of exposure to asbestos, although in the second this was obtained with difficulty and after death. The association between mesothelioma of the pleura and exposure to asbestos is unlikely to be fortuitous ; but to establish this point all cases of mesothelioma, whatever their occupational history, should be studied with this possibility in mind; for evidence is now accumulating that this disease is an industrial hazard.

  PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

• Exposure to asbestos dust and diffuse pleural mesotheliomas. J.G. Thomson. 1963;1(5323):123. PubMed · Publisher · Free full text

  Summary

  In this letter, the author, writing from the Department of Pathology at the University of Capetown Medical School, responded to earlier correspondence by Smithers and colleagues and by McCaughey and colleagues on the association between malignant pleural mesothelioma and exposure to asbestos dust. He summarised a recent article in which he had described a condition he called basal, or limited, asbestosis. In this condition the lesion was largely confined to the lung bases, produced no signs or symptoms, and was usually overlooked at necropsy unless sections from the lung bases were examined. He suggested that the lesion might locally reach a carcinogenic concentration and, because it did not shorten life, might later prove to produce more malignant tumours than classical asbestosis. In three years in the necropsy service of a teaching hospital he had encountered six malignant mesotheliomas, three pleural and three peritoneal, and basal asbestosis was demonstrated in five. In 1961, at four centres in the United States, he found basal asbestosis in nine of 15 pleural and peritoneal mesotheliomas with adequate lung for study, and it had been overlooked in all but two. He noted that world asbestos consumption had risen from 500,000 tons in 1942 to 2,400,000 tons in 1961. He cited necropsy evidence that a large and increasing percentage of the population inhaled asbestos fibres, and wondered whether in 20 years asbestos-induced mesothelioma might be as common as lung cancer.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

1950s

• Talc pneumoconiosis in the textile industry. B. Mann, J.B. Deasy. 1954;2(4902):1460-1. PubMed · Publisher · Free full text

1920s

• Asbestos dust and the curious bodies found in pulmonary asbestosis. W.E. Cooke. 1929;2(3586):578-80. PubMed · Publisher · Free full text

  Summary

  This paper, read at the 1929 Annual Meeting of the British Medical Association in Manchester, described the findings behind the 1924 diagnosis of pulmonary asbestosis and further work on the "curious bodies" found in asbestotic lungs. The author recalled an unpublished 1899–1900 case of a man who had worked ten years in an asbestos factory, and noted that the first published case was in 1924. Chrysotile asbestos and factory dust were analysed. The iron content, as ferrous oxide, was 2.81 per cent in chrysotile, 0.1 per cent in the finished article and 18.4 per cent in carding-room dust. Lung sections and trypsin digests showed abundant fine black granular dust, an almost complete absence of the very fine spicules that made up most factory dust, and large fragments of 10 to 360 microns that closely matched particles in asbestos dust. The curious bodies, found in every necropsy in pulmonary asbestosis, measured 20 to 100 microns or more, were golden brown, did not stain with aniline dyes and gave the Prussian blue reaction for iron. The author proposed that the bodies formed when fine asbestos spicules became coated with colloidal aggregates derived from plasma proteins. Because no other mineral dust is fibrous, he concluded that the bodies, if found in any numbers, are pathognomonic of pulmonary asbestosis.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Clinical aspects of pulmonary asbestosis. A.C. Haddow. 1929;2(3586):580-1. PubMed · Publisher · Free full text

  Summary

  This paper, read at the 1929 Annual Meeting of the British Medical Association in Manchester, described asbestos workers seen in a general practice in Leeds. In 1926 the author and a colleague noticed that several patients with chest complaints were asbestos workers. They examined every asbestos worker who came their way, about fifteen in all, and had most of them radiographed. Four workers had died: three women and one man. Their average age at death was 41, and they had spent on average under twenty years in the factory, mostly in asbestos mattress-making. The man's death was certified as bronchopneumonia secondary to chronic asbestos poisoning causing pulmonary fibrosis, which led to a coroner's inquest and official recognition of the disease. Tubercle bacilli were found in the sputum of only one of the four. The author also described four advanced cases under treatment. All were women from the mattress department, with an average age of 35 and an average of fourteen years in the factory. They had breathlessness on exertion, cough, anorexia, reduced chest expansion and signs at the lung bases. Radiographs showed infiltration in the lower zones, particularly on the right. Asbestosis bodies were found by lung puncture in two of the four and in the sputum of three. The author concluded that inhaled asbestos dust produces fibrosis that is mainly basal and peripheral. He found that the disease is usually not complicated by tuberculosis and is first recognized after more than five years' exposure. He reported that it worsens in winter, and that sputum examination and radiography are useful in diagnosis.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• A case of pneumoconiosis: result of the inhalation of asbestos dust. H.E. Seiler. 1928;2(3543):982-980.1. PubMed · Publisher · Free full text

• Clinical Aspects of Pulmonary Asbestosis. T. Oliver. 1927;2(3491):1026-7. PubMed · Publisher · Free full text

• Histology of Pulmonary Asbestosis. S. McDonald. 1927;2(3491):1025-6. PubMed · Publisher · Free full text

• Pulmonary Asbestosis. W.E. Cooke. 1927;2(3491):1024-5. PubMed · Publisher · Free full text

  Summary

  This paper, read at the Annual Meeting of the British Medical Association in Edinburgh in 1927, described the case of a woman who died after working in an asbestos factory. The author had published a short note on her in 1924. He reviewed the only similar case he knew of: a man aged 33 who had worked for ten years in the carding room of an asbestos factory and died at Charing Cross Hospital in 1900. The paper also covered the history, composition and manufacture of asbestos, and the iron content of asbestos dust. Analyses showed iron, as ferrous oxide, at 0.1% in the finished article, 2.81% in crude raw material and 18.4% in carding-room dust. The woman began work at 13 in a factory with no dust extraction. She developed a cough soon after starting, had ill health from 1917, stopped work in July 1922, and died on 14 March 1924, aged 33. X-ray showed extensive fibrosis, worse in the right lung. Post-mortem examination found pleural thickening, lung fibrosis, cavities, caseation and calcified tuberculous glands. Lung sections contained abundant fine granular pigment and large angular particles 3 to 360 microns long. The author concluded that these particles were heavy, brittle, iron-containing fragments of asbestos fibre. He explained the greater involvement of the right lung by the more vertical right bronchus.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Fibrosis of the lungs due to the inhalation of asbestos dust. W.E. Cooke. 1924;2(3317):147-140.2. PubMed · Publisher · Free full text

  Summary

  The author, pathologist at Wigan Infirmary, reported a fatal case of lung fibrosis that he described as the first in English medical literature to be definitely proved as due to asbestos dust. He noted that doctors in asbestos-manufacturing areas had long suspected the dust of causing chronic bronchitis and fibrosis, and that Professor J. M. Beattie had shown the dust causes fibrosis in guinea-pigs. The patient was a woman aged 33 who had worked in asbestos factories from the age of 13. Her attendance had been intermittent for five years before she stopped work in July 1922, and she died on March 15th, 1924. The Rochdale coroner sent her lungs for further examination. An x-ray plate showed extensive fibrosis, more marked in the right lung, and calcareous glands at the root of the left lung. At examination, both lungs had thickened pleura with adhesions. The right lung was small, firm, fibrosed and largely airless, with a large apical cavity, areas of caseation and dilated bronchi. The left lung showed similar but less marked changes, with calcified tuberculous glands and a walnut-sized cavity. Under the microscope there was extensive fibrosis, caseous foci and giant cells, and tubercle bacilli were present. Mineral particles, mostly sharp-angled and measuring 393.6 to 3 microns in length, were seen in both caseous and fibrotic areas. The author compared these with photomicrographs of asbestos dust.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

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