1. The lesions produced by the different dusts employed in these experiments, and the conclusions to be derived thereform, have already been discussed in Section 6 of this paper (see p. 455, et seq.).
2. Plaque formation has been discussed. Evidence has been produced to show that the large plaques which tend to be formed in the parenchyma represent permanent pulmonary lesions. Small plaques, on the other hand, may be formed within the pulmonary lymphatics, in which case they may disintegrate in course of time. Such plaques have been termed “intralymphatic plaques.”
3. Evidence has been brought forward against the view that the degree of harmfulness of a dust is proportionate to the degree of angularity and sharpness of its consituent particles. Nor has the supposition that the dusts which stimulated phagocytosis were those which contained organic matter been confirmed experimentally. Although silica may be regarded as a cellpoison and that this may account for the inability of the phagocytes to remove it, there are probably other factors than this, since shale—universally admitted to be one of the least harmful dusts—contains from 55 per cent. to 60 per cent. of silica. As to why one dust is harmful, and another not, is a problem as yet unsolved.
4. The origin of the dust-cells has been studied. Reasons have been given to justify the belief that dust-cells are frequently derived from the alveolar epithelium. This, however, does not exclude the possibility of some participation of leucocytes or endothelial cells in the phagocytosis of dust particles.
5. The chief modes of elimination of dust from the lungs have been discussed. It has been shown that the dusts which stimulate phagocytosis tend to be eliminated from the lung by both bronchi and lymphatics, while such elimination as occurs of the dusts which elicit but a feeble phagocytic response is through the lymphatics rather than the bronchi.