Tissue reaction following a second exposure to amosite asbestos.

An inherently long latency period exists between the time of asbestos exposure and the development of asbestos related clinical signs in man. By this stage the events reflect the cumulative responses and offer little with regard to characterizing the acute inflammatory reactions. Similarly, studies of asbestos-induced diseases employing animal models have often emphasized the investigation of chronic events, particularly the development of fibrosis and/or cancer. However, short-lived neutrophils, which exhibit a substantial potential to produce tissue damage through the generation of superoxide radicals and elastase, have been shown to constitute a component of the acute response to asbestos in this animal model. Repetitious exposures to asbestos could logically simulate extensions of this acute response and thus be an important contributor to the development of fibrosis. In order to assess this concept, animals received two exposures to asbestos. The parenchyma exhibited both 'established' lesions consisting primarily of foci of closely-packed, fibre-laden macrophages within alveoli, and 'new' lesions consisting of a mixed cell inflammatory response (including neutrophils and macrophages) as well as considerable alveolar exudate. Repeated infiltration of neutrophils to the site of renewed lung injury following a second exposure to asbestos may correspond to events occurring in human lungs exposed similarly to repeated exposures of the dust.