No abstract

The quantitative extraction of asbestos fibres from asbestotic lung by alkali digestion has been refined by maceration of the tissue without prior drying, the minimum use of centrifugation, and the adoption of phase contrast microscopy. Preliminary experiments suggested that, using this technique, asbestos fibre counts were accurate to within at least ± 20% and in most instances to within ± 10%.The method was used to assess asbestos concentrations in lung tissue showing various degrees and forms of fibrosis. The results, as determined by light microscopy, indicated that uncoated fibres generally outnumbered coated fibres. In mild and moderate asbestosis there was a progressive increase in concentration of asbestos fibres, both coated and uncoated, with increasing severity of fibrosis, whereas in severe asbestosis no correlation existed between the fibre concentration and the form or the extent of the pathological reaction. It is suggested that the severe fibrosis results from the supervention of non-specific inflammatory processes.Asbestos fibre diameter distributions, gauged by electron microscopy, were fairly constant irrespective of the degree of fibrosis. Optically visible fibres constituted between 12 and 30% of the total, so that an optical count may be said to give an approximate indication of the total asbestos concentration and, so far as asbestosis is concerned, may well serve for comparative purposes. The relation between asbestos and neoplasia will, however, require identification and quantitation of particular types of the mineral by microanalytical techniques.

No abstract

If genetically resistant and susceptible rabbits inhale a certain number of human type tubercle bacilli, no tuberculosis in the lungs of the resistant animals is seen, as a rule several months after infection, while there is a variable and often extensive disease in the susceptible rabbits. The analogy to the presence or absence of active tuberculosis in man infected with the tubercle bacillus is evident. The inhaled tubercle bacilli multiply for but a short time in the resistant rabbits and are usually rapidly and completely destroyed. In the susceptible rabbits, the bacilli multiply profusely for a much longer time and persist in large numbers even months after inhalation. Whatever be the cause of the more rapid destruction of tubercle bacilli in the resistant animal, the resulting more rapid release of the contained antigens enhances the development of allergic sensitivity and antibodies in these animals. The development of an acquired resistance against tubercle bacilli of the human type is sufficiently rapid to affect the genesis of the initial gross primary pulmonary foci that result from the inhalation of a given number of bacilli. The greater the genetic resistance, the fewer the initial primary foci. Variations in genetic resistance are essentially variations in the rate of development of acquired resistance. It is suggested that variations in genetic resistance to inhaled human type tubercle bacilli may affect the prevalence of alveolar phagocytes capable of acquiring adequate resistance to the growth of the bacilli in their cytoplasm. The prevalence of such cells is subject to hormonal and immunological influences.