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Free radicals are considered to play an important role in the pathogenicity of a number of lung conditions including asbestos-related lung diseases (Donaldson et al., 1994). We have been investigating pro-oxidant characteristics of asbestos and other respirable fibres which cause cancer and fibrosis in humans or experimental animals and have demonstrated that asbestos has strong hydroxyl radical activity that is mediated by iron (Gilmour et al., 1996). An important role for iron has been demonstrated in the TNF response of macrophages exposed to asbestos and, indeed, the chelating of surface iron effectively abolished the TNF-stimulating activity of amphibole asbestos (Simeonova and Luster, 1995). Any particle, including fibres, that deposit in the lung first encounter the lung lining fluid which is a complex mixture of proteins and phospholipids. We have previously demonstrated that the biological activity of fibres can be modulated by coating them with immunoglobulin (Hill et al., 1996), but little is known of the modifying effect of lung lining fluid. The pH of the alveolar surface is close to neutrality, whilst the pH of the phagolysosome is 4-5 (Nyberg et al., 1992). Therefore the ability of any particle depositing in the lung to release iron will be an important factor in dictating its pathogenicity. Furthermore, the release of reductants such as H2O2 or superoxide from the macrophage respiratory burst could have important effects in causing redox cycling of iron with the generation of hydroxyl radical. These putative factors that contribute to oxidative stress in fibre-exposed lung are summarised in Fig. 1. As part of an HSE-funded study we are investigating a panel of respirable fibres of differing pathogenicity to determine which in vitro endpoints, related to the above sequence, correlate with pathogenicity, with a view to refining the shortterm assay approach for the prediction of fibre pathogenicity. We report here on:

annals of occupational hygiene

Effect of the pH and Biochemical Milieu of the Lung on Release of Iron from the Surface of Respirable Industrial Fibres and Ability to Cause a Respiratory Burst in Alveolar Macrophages