Search

The 1930 International Labour Office Conference on silicosis in Johannesburg was a turning point in the history of silicosis and in the recognition of the associated pathologic patterns. Since 1930, pneumoconioses such as silicosis have become much rarer in developed countries and can now be diagnosed at an early stage based on clinical and radiologic criteria. However, in spite of these advances, pathologists must remember to look for silica in tissues, particularly when clinical and radiologic findings are more uncertain. Furthermore, nowadays pathologists essentially observe silicotic lesions as incidental findings adjacent to lung cancers. In addition to identifying the characteristic lesions, pathologists must also try to identify their causative agent, in the case of crystalline silica firstly by using polarized light examination, followed as appropriate by more sophisticated devices. Finally, pathologists and clinicians must always keep in mind the various implications of exposure to silica compounds in a wide range of diseases.

We present a case of complicated silicotuberculosis in a former gold miner with a sufficiently heavy silica dust exposure to cause International Labor Organization grade 2/2 silicosis after a cumulative exposure duration of 11 years. We describe a cascade of complications-active pulmonary tuberculosis despite recent isoniazid prophylactic therapy, non-tuberculous mycobacterial disease, chronic airways obstruction, and spontaneous pneumothorax-and the difficulties, which arose, in diagnosis and management of such combined disease. We highlight three implications of such cases: the need to understand the interaction of silicosis and tuberculosis in this setting, the importance of maintaining continuity of care in the management of these conditions in miners and former miners, and control of silica dust exposure as a primary form of prevention of tuberculosis.

Through the concept of "thought collectives" in particular, Ludwik Fleck was a pioneer in demonstrating how much scientific knowledge is inherently made up of social and historical material. In this article, I propose to follow a Fleckian path by comparing the proceedings of the 1930 International Labour Office Conference on silicosis in Johannesburg on the one hand, and on the other the content of the debates that took place in France in the 2000s to revise the "tables" of occupational diseases which define the compensation rules for salaried workers in the French general (as well as the farm) health insurance scheme. The text offers an analysis of the striking similarities between these two distant sources, pointing out particularly the repetitiveness of ignorance and knowledge, and the nature of what can be admitted as a body of "evidence" in medico-legal issues such as the definition and compensation of occupational diseases.

The 1930 International Labour Office Conference on silicosis in Johannesburg was a turning point in the history of silicosis and in the recognition of the associated pathologic patterns. Since 1930, pneumoconioses such as silicosis have become much rarer in developed countries and can now be diagnosed at an early stage based on clinical and radiologic criteria. However, in spite of these advances, pathologists must remember to look for silica in tissues, particularly when clinical and radiologic findings are more uncertain. Furthermore, nowadays pathologists essentially observe silicotic lesions as incidental findings adjacent to lung cancers. In addition to identifying the characteristic lesions, pathologists must also try to identify their causative agent, in the case of crystalline silica firstly by using polarized light examination, followed as appropriate by more sophisticated devices. Finally, pathologists and clinicians must always keep in mind the various implications of exposure to silica compounds in a wide range of diseases.

Scholarly understanding of the nature of the science around silicosis has been strongly influenced, in recent years, by the idea that the mine doctors were responsible for hiding an epidemic, on the mines and in the countryside. In this paper, I try to show that the opposite was in fact the case, and that the science and government institutions for the regulation of silicosis and tuberculosis in white and black male workers were distinctively elaborated, and very largely successful in tracking and controlling the disease. This singular visibility, funded by the mines, stands in marked contrast with disease in general in South Africa, and forms a major part of the explanation for the very strong association of silicosis with mine work.

Very rapidly progressive "acute silicosis" was observed prior to the 1930 International Labour Office Conference on silicosis, but its clinical significance and pathologic relationship to classic silica caused pneumoconiosis were not settled.Textual analysis of the 1930 Conference proceedings identified data relevant to rapidly progressive silicosis. Standard bibliographic searches identified relevant biomedical literature dating from before and after the Conference.The 1930 Johannesburg Conference contained descriptions of acute silicosis, especially in the abrasive powders industry, but acute silica-related lung disease did not conform to a three-stage disease model in which tuberculosis supra-infection caused advanced disease, a model accepted at the Conference. Over following decades, additional reports appeared of rapidly progressive silicosis, unrelated to tuberculosis. Pulmonary alveolar proteinosis was identified only in 1958.Adoption by the 1930 Johannesburg Conference of a classification scheme into which acute rapidly progressive disease unrelated to tuberculosis fitted poorly may have impeded the understanding of acute silicosis and its importance.

Background To assess the relationship between mixed dust fibrosis (MDF) and tuberculosis. Methods We performed a comparative analysis with MDF, silicosis, and macular pneumoconiosis (Mac), using autopsy records from 1975 to 1994. Results Prevalences of having tuberculosis among MDF, silicosis, and Mac were not significantly different, albeit a tendency of higher prevalence in silicosis. Cure rates of tuberculosis were, in order, silicosis MDF=Mac (P=0.911). With respect to the two types of association with tuberculosis, i.e., combined type (tuberculopneumoconiosis) and complicated one (pneumoconiosis with tuberculosis); the former was significantly dominant in silicosis, the latter was significantly dominant in Mac, and intermediate in MDF. As a whole, the complicated type had a tendency of a higher cure rate than the combined type (P=0.071). Although the differences of profiles between the combined and complicated types were not statistically significant, the combined type had a tendency to have longer duration of exposure to dusts, earlier registration for treatment, higher profusion score, and earlier death compared with the complicated type. Conclusions From our findings, MDF takes an intermediate position between silicosis and Mac regarding the relationship with tuberculosis. The type of association with tuberculosis rather than the kind of background pneumoconiosis seemed to be more important in light of responsiveness to the treatment. Am. J. Ind. Med. 37:260–264, 2000. © 2000 Wiley-Liss, Inc.

Silicotics have increased mortality from tuberculosis (TB) and from nonmalignant respiratory diseases (NMRD), including silicosis and silicotuberculosis. Since the publication of the International Agency for Research on Cancer monograph in 1987 indicating that silica was a probable human carcinogen, there has been an extensive debate about the cancer risks among silicotics. The authors identified 590 claims for silicosis among a registry of lung diseases compiled from California Workers' Compensation cases from 1945 to 1975. Using state vital records, we determined the mortality risks from 1946 to 1991. Our findings confirmed that these claimants had a significantly elevated risk for all causes of death with a standardized mortality ratio (SMR) of 1.30 (95% confidence interval [CI] = 1.18, 1.43); TB had a SMR of 56.35 (95% CI = 41.10, 75.40) and NMRD a SMR of 3.80 (95% CI = 3.11, 4.60). Cancers of the trachea, bronchus, and lung had a SMR of 1.90 (95% CI = 1.35, 2.60). For malignancies of the large intestine, there was a previously unreported SMR of 2.08 (95% CI = 1.14, 3.50). Mortality from all diseases of the heart was significantly less than expected with a SMR of 0.68 (95% CI = 0.55, 0.83); cancers of the prostate and lymphatic system were also significantly low with SMRs of 0.26 (95% CI = 0.03, 0.94) and 0.17 (95% CI = 0.04, 0.97), respectively. Workers with silicosis should be warned about these chronic disease risks, and prevention efforts to control occupational silica dust exposure should become a higher priority.

A comparison was made between the chief cause of death among 969 deceased white male granite workers in Vermont and the causes of death among other individuals not in that occupation. Tuberculosis deaths were ten times the number predicted, based on the U.S. white male experience. Of the 65 tuberculosis deaths, 48 were silicotuberculosis and 16 were pulmonary tuberculosis. A notable increase was found for deaths due to all respiratory diseases, with 28 deaths due to silicosis. Excluding deaths due to silicosis and tuberculosis left a small excess of emphysema-related deaths. For 25 men in the respiratory disease category whose cause of death was not listed as silicosis, ten had evidence of silicosis in their x-ray records suggesting some misdiagnoses may have occurred. An excess of lung cancer deaths was noted among sawyers and polishers, suggesting possible effects of abrasive exposures. No tuberculosis deaths were noted in men who started work in the post dust control period, after 1950. There was an excess of suicide deaths before 1970.

A cohort mortality study was carried out in Vermont granite workers who had been employed between the years 1950 and 1982. The cohort included men who had been exposed to high levels of granite dust prior to 1938-1940 (average cutters to 40 million parts/cubic foot), and those employed at dust levels after 1940, which on average were less than 10 million parts/cubic foot. Deaths were coded by a qualified nosologist and standardized mortality ratios were calculated. The results confirm previous studies that show that death rates from silicosis and tuberculosis, the major health threats in the years before 1940, were essentially eliminated after dust controls. However, we found excessive mortality rates from lung cancer in stone shed workers who had been employed prior to 1930, and hence had been exposed to high levels of granite dust. When information was available, 100% of those dying from lung cancer had been smokers.