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Products fabricated of man-made fibres, which are produced or processed in relatively large amounts in Austria, usually contain glass or rock wool. Regulations laid down limits for the exposure at the workplace to glass/rock wool dust. For this purpose, a gravimetric concentration threshold has been established for the assessment period "working year". A measuring procedure matched to the established threshold is employed to measure the concentration of airborne dust at the workplace.

The cancer risk can be reduced by replacing crocidolite and amosite by chrysotile asbestos, by replacing asbestos by man-made mineral fibres that produce less dust, and by nonfibrous materials. MMMF have been found to be carcinogenic in experiments in animals. All respirable mineral fibres that are retained in the lungs are suspected to increase the lung cancer risk, the fibre length and surface properties appearing to be the decisive factors. For most of these fibres, data so far collected in humans are still insufficient to permit definite conclusions to be drawn. There is a certain amount of evidence to suggest that rock/slag wool may be carcinogenic in humans: lung cancer in workers in the production area in the USA was found to be significantly increased (SMR 134%), and in the early phase of European production an SMR of 257% was observed. In the area of glass wool production, exposure to fibre and lung cancer rates were lower, but showed an increasing tendency with increasing time elapsed since the first exposure to respirable fibres. Methodological problems associated with published epidemiological studies are reviewed, and prevention strategies--which need to give consideration to the possibility that the carcinogenicity per fibre could be higher in the case of MMMF than in chrysotile asbestos--are discussed.

In principle, the fibrosing, preneoplastic and neoplastic morphological reactions to natural and man-made mineral fibres are relatively uniform, and are thus non-specific for the various different types of fibre. In order to establish a causal chain between the injurious "fibrous" agent and the morphologically and clinically manifest pathological lesion, close cooperation between epidemiologists, occupational physicians, pneumologists and pathologists is needed. On its own, the morphological contribution towards solving the problem is of only a limited nature. Light-microscopic, electron-microscopic and element-analytical studies, however, used in conjunction with the results obtained in animal experiments, in the individual case with consideration also being given to aspects of medical insurance, can lead to useful information for the clinical situation and for the generation of expertize.

The extent of the pulmonary reaction to intensive exposure to dust is influenced by a number of factors, in particular the nature of the fibre, morphometry, solubility, duration of dust exposure, dust concentration, and, finally, the manufacturing process of the MMMF product and its chemical composition. The biological effect of the fibres on the lung is manifest by enhanced infiltration by macrophages and an increase in the number of neutrophils. In agreement with numerous published results, our own investigations failed to reveal any signs of a fibrogenic effect of MMMF. The reason for this is presumably the lack of biostability, the tendency of the fibres to fracture crosswise, and the much lower concentration of fibres in the critical length-diameter range. In contrast, MMMF have been shown to induce an irritation of the mucosa and the upper airways. With respect to possible long-term damage produced by MMMF from our own production, we have had no such experience to date.