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Minisymposium 8

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Silica related health effects


J. C. McDonald.National Heart and Lung Institute, Imperial College London, London, UK

Epidemiological evidence will be reviewed for and against the evaluation, made in 1996 by an IARC Working Group, that crystalline silica in the form of quartz or cristobalite from occupational sources is carcinogenic to humans (Group 1). The Working Group had considerable difficulty in reaching this decision, did not do so unanimously, and might not have done so at all, had it not been emphasised that it was concerned with hazard identification, not risk. Of the many studies examined by the Working Group, 10 were identified as providing the least confounded evidence of risk: five including one of registered silicotics were considered positive, and five others negative or equivocal. Since 1997, there has been comparatively little further epidemiological evidence on the lung cancer issue, apart from two somewhat overlapping studies of North American industrial sand workers. Significant relationships between exposure and mortality from lung cancer and silicosis were found in both these studies and, in one, after allowance for smoking. The latter of these two studies, and another of British pottery workers (included among the five considered positive the IARC Working Group), have been recently updated, with results awaiting publication. Since 1977, however, there have been a small number of attempts to relate the scanty available data on exposure–response relationships for lung cancer to that for silicosis and non-malignant respiratory disease. Although limited, the data thus available on risk in relation to estimated exposure now allows a rational consideration of environmental control limits, including the pressing question of whether silica related lung cancer can be eliminated by the effective prevention of silicosis.


D. Heederik.Institute for Risk Assessment Sciences, Division of Environmental and Occupational Health, Utrecht University, Utrecht, Netherlands

Occupational exposures to dust, fumes and gases are known risk factors for chronic obstructive pulmonary disease (COPD). Silica dust is among the better described toxic occupational respiratory agents. An important question is whether silica can cause COPD. This question can be found back in the literature since the late seventies, when it was considered in a broader context and when the scientific interest in COPD was emerging, just after World War II. In many editorials and reviews of that time, airflow limitations resulting from an occupational (dust) exposure were considered of minor degree and not sufficient to impair lung function and disable the worker unless he was a smoker also. Others disagreed strongly and argued that lifetime exposure to mineral dusts could result into respiratory impairment measured by spirometry, and lead to changes in lung function in the same order of magnitude as the effect of smoking. This discussion should be considered against the background of the absence of longitudinal studies and methodological limitations (poor endpoint definition, exposure assessment and statistical analysis). More recent reviews have shown that COPD is also related to occupational mineral dust exposure, independent of smoking with evidence from different study designs, for different endpoints. Although the discussion on COPD ended, the answer to this question for silica dust specifically is not straightforward. Again, the epidemiological evidence available needs to be interpreted carefully because of the omnipresent role of smoking. Moreover, silica causes other respiratory diseases, among which silicosis, which can be accompanied by respiratory function changes as well. The presence of silicosis can complicate the interpretation of lung function studies. However, evidence from various sources; toxicological, epidemiological and pathological studies all indicate that crystalline silica dust exposure can lead to COPD, independent from smoking and in the absence of silicosis. The available evidence suggests that chronic exposure to (crystalline) silica dust, even below levels associated with silicosis, may cause COPD. Amorphous silica seems less toxic and is not clearly related to COPD.


N. Cherry.Department of Public Health Sciences, University of Alberta, Edmonton, Alberta, Canada

Reports of a relation between silica exposure and autoimmune disease have been published for close to a century, with an excess of scleroderma, rheumatoid arthritis and chronic renal disease being found in some exposed cohorts. The 1997 IARC monograph comments on renal dysfunction and scleroderma-like disorders. Since 1997 interest has focused particularly on immunological changes following experimental exposure and on renal outcomes. Both direct effects and an autoimmune response have been postulated as mechanisms for silica related renal disease. The strength of the evidence for an excess of chronic non-malignant renal disease will be reviewed. The interpretation of silicosis - as a marker of high exposure or of susceptibility - is uncertain but if an excess of autoimmune disease occurs without fibrosis on chest radiographs this would imply that restricting exposures to levels sufficient to prevent silicosis might not protect against autoimmune disease.


Y. X. Liang, G. B. Xiao, Q. Y. Xiang.Department of Occupational Health, Fudan University School of Public Health, China

The number of workers exposed to silica-containing dust in China is estimated to be as high as 12 million. Pneumoconiosis has long been ranked at the top of the 10 leading causes of occupational diseases in China and it contributes the major part of statutory occupational lung diseases. Between 1949 and 2002, 581 377 confirmed pneumoconiosis cases were reported, of whom 139 77 (24%) had died. There are 12 000–15 000 new cases reported annually, representing 70–80% of the total reported cases of occupational diseases in recent years. In addition, at least 500 000 workers (living) are suspected of having pneumoconiosis. The highest occurrence of pneumoconiosis has been found in coal-mining industries. This is known as anthracosilicosis, accounting for 52.7% of the total reported cases. Manufacture of construction materials accounts for 11.8% of cases, the metallurgical industry 9.9%, the non-ferrous metallurgical industry 6.1%, and the machinery industries 4.3%, representing the five industries with the highest potential for causing pneumoconiosis. It has been estimated that the direct and indirect costs of pneumoconiosis are ¥25 billion, which is 0.4% of the total GDP (¥6000 billion, in 1999), representing an unacceptably high economic burden. A study in a Shanghai foundry found that dust controls are effective in reducing both the number of pneumoconiosis cases and the associated economic burden, with the ratio of benefit to cost estimated to be 13.7. However, dust control is always a challenge, particularly in industrialising countries, such as China. In the 1960s, a control strategy, known as “Eight Guiding Principles” emphasising “Prevention First” was successfully instituted. Unfortunately, these principles have not always been effectively implemented, especially during the rapid development of the national economy. The recent passage of the Occupational Diseases Prevention and Control Act of 2002 (ODPCAct) in China and the introduction of new occupational exposure limits are signs of the Chinese government’s commitment to improving the workplace environment and to achieving the WHO/ILO global goal of the “Elimination of Silicosis”.

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