G. Chiappino

Translocation pathways for inhaled asbestos fibers

We discuss the translocation of inhaled asbestos fibers based on pulmonary and pleuro-pulmonary interstitial fluid dynamics. Fibers can pass the alveolar barrier and reach the lung interstitium via the paracellular route down a mass water flow due to combined osmotic (active Na+ absorption) and hydraulic (interstitial pressure is subatmospheric) pressure gradient. Fibers can be dragged from the lung interstitium by pulmonary lymph flow (primary translocation) wherefrom they can reach the blood stream and subsequently distribute to the whole body (secondary translocation). Primary translocation across the visceral pleura and towards pulmonary capillaries may also occur if the asbestos-induced lung inflammation increases pulmonary interstitial pressure so as to reverse the trans-mesothelial and trans-endothelial pressure gradients. Secondary translocation to the pleural space may occur via the physiological route of pleural fluid formation across the parietal pleura; fibers accumulation in parietal pleura stomata (black spots) reflects the role of parietal lymphatics in draining pleural fluid. Asbestos fibers are found in all organs of subjects either occupationally exposed or not exposed to asbestos. Fibers concentration correlates with specific conditions of interstitial fluid dynamics, in line with the notion that in all organs microvascular filtration occurs from capillaries to the extravascular spaces. Concentration is high in the kidney (reflecting high perfusion pressure and flow) and in the liver (reflecting high microvascular permeability) while it is relatively low in the brain (due to low permeability of blood-brain barrier). Ultrafine fibers (length < 5 μm, diameter < 0.25 μm) can travel larger distances due to low steric hindrance (in mesothelioma about 90% of fibers are ultrafine). Fibers translocation is a slow process developing over decades of life: it is aided by high biopersistence, by inflammation-induced increase in permeability, by low steric hindrance and by fibers motion pattern at low Reynolds numbers; it is hindered by fibrosis that increases interstitial flow resistances.

Hard metal disease: clinical aspects

On the basis of the data available in the literature and of our experience, the clinical patterns of respiratory troubles which can be observed in workers exposed to inhalation of hard metal dusts can be schematized as follows: Irritation forms, mild and transient, or severe up to pulmonary oedema, dose-correlated, which occur in all subjects exposed to sufficiently high atmospheric concentrations; Asthmatic forms, either reversible after cessation of exposure or persistent after stopping the exposure, which occur in a relatively low percentage of exposed subjects and also apply to the states quoted below; Dyspnoic patterns due to alveolitis (lymphocytic alveolitis with inverted helper/suppressor ratio, or giant cell-eosinophilic alveolitis, with or without fibrotic changes of pulmonary interstitium); Interstitial sclerotic lung disease, associated with or without an alveolitic component. The present diagnostic potentialities, particularly bronchoalveolar lavage (BAL), have helped in defining the clinical patterns and have confirmed the fundamental role of individual susceptibility in the occurrence of clinical manifestations (with the exception of the irritation forms), but so far have not yet enabled us to clarify whether the different clinical patterns are the results of a single pathogenetic mechanism or constitute pathogenetically distinct entities.

Bronchoalveolar Lavage Cells in Occupational Exposure to Mineral Fibers

In the last decade, the possibility of obtaining informations on the cellular, biochemical and mineralogical content of the deep lung by studying bronchoalveolar lavage (BAL) fluid has largely increased our knowledge on the pulmonary reactions to inhalation of dusts. The lung effects of asbestos exposure are among the most extensively studied, but several problems remain open. In our institution, workers occupationally exposed to mineral fibers represent approximately one third of over 300 subjects investigated by BAL since 1983.

Talc Pneumoconiosis in Italy

Since the reports published in the United States on contamination of commercial talc with asbestiform fibres (Cralley et al, 1968; Dement et al, 1972; Snider et al, 1972; Rohl et al, 1976), much attention has been focused on the possible risks for exposed subjects. A recent survey by the National Health Institute in Italy (Istituto Superiore di Sanita, Rome) has reported that a large number of cosmetic talc products contaminated with chrysotile or, more often, with amphiboles are still on the Italian market; most of these contaminating fibres are ultramicroscopic in size (Paoletti et al, 1984). It has been demonstrated that contaminating fibres are also present in industrial talc (Marconi et al, 1986).

Evaluation of Alveolar Burden of Mineral Fibres in Cases of Occupational and Non Occupational Exposure to Asbestos

Counts of fibres from lung tissue are of increasing importance in medicolegal cases in Germany. For this purpose, different fibrerecovery techniques have been developed and different microscopic methods and instruments have been employed. Besides the examination of dust samples from lung tissue few data have been presented on the fibre content in broncho alveolar lavage (BAL) samples. This study was designed to determine the fibre concentration, size distribution and composition of fibres in BAL-samples from individuals with different occupational exposure.