The following dusts produce a fibrosis in the guinea-pig's lung, and are therefore to be classed as dusts whose inhalation in industry would be attended by risks of pneumoconiosis. The most deadly of all dusts examined was precipitated silica. Less dangerous, but all producing fibrosis, were the following, arranged in order of decreasing toxicity: flint, slate, aluminium hydroxide, precipitated chalk, magnesium carbonate and carborundum. In the concentrations used in the experiments calcspar and emery were border-line dusts, indicating that their inhalation in any considerable quantity would cause fibrosis. Wood charcoal inhaled in large amount produces a slight fibrosis, and must, therefore, be placed on the “dangerous” list. Colloidal coal, when inhaled in massive amounts, is potentially dangerous, while shale under similar conditions is rather more dangerous.Haematite, talc, and molecular mixtures of soluble silica with aluminium hydroxide and magnesium carbonate respectively were not found to cause any permanent lesions in the lung.The deductions to be drawn from this work are:1. All inhaled particles are rapidly ingested by certain individual cells belonging to the alveolar epithelium.2. These cells (dust cells or phagocytes) remain in the lung parenchyma until they have ingested an amount of dust constituting the cell's saturation load. This load varies with different dusts.3. A cell having attained its saturation load becomes sooner or later detached from the alveolar wall and either migrates into the lymphatics or becomes free in the alveolus. In the former case it passes into the pulmonary lymphoid tissue and thence to the bronchial lymph glands. In the latter case it passes up the bronchial tree to be either coughed out or swallowed.4. Dust cells which speedily leave the alveolar wall are principally eliminated by the bronchi.5. In the case of a dust cell being eliminated from the lung via the lymphatics, it may be arrested in the periatrial lymphatics on account of its bulk. The dam thus produced offers obstruction to the passage of other dust cells shed into the alveoli. Groups of free dust cells in the obstructed alveoli form plaques, which degenerate and liberate their dust. This is again ingested, and the irritation caused by such a process may lead to fibrosis.6. The continued presence of dust-laden cells in the lymphatics may set up a foreign body irritation, with resulting fibrosis.7. Most inhaled particles contain soluble matter to at least a very small extent. The solute may be either harmlessly active or toxic. If the former, the cell is stimulated to detach itself from the alveolar wall, and so remove the dust. If the latter, the solute effects the viability of the phagocyte, which becomes less able to detach itself. At the same time the solute diffuses into the neighbouring tissues, with irritation to them, and consequent fibrosis.8. The more soluble form of a substance causes greater pulmonary damage than the less soluble. The solute, therefore, plays a large part in the determination of damage.9. While many dusts cause pulmonary fibrosis, silica is the dust par excellence predisposing to tuberculosis. This is doubtless due to its influence in forming a medium suitable not only for the survival but the proliferation of the tubercle bacillus in the lung (Kettle, private communication). The harmful effects of soluble silica may be neutralised by simultaneous administration of basic dusts such as aluminium hydroxide or magnesium carbonate, though the latter are themselves harmful when inhaled alone. It is suggested that their respective solutes combine to form monosilicate. Monosilicates do not appear to have any harmful effect on the lung.10. Heavy inhalations of any dust are liable to cause pulmonary damage.11. The intensity of the initial pulmonary reaction to a dust is very generally in inverse ratio to the degree of eventual damage caused by the dust.
Analyzing the Carotenoid Composition of Melilot (Melilotus officinalis (L.) Pall.) Extracts and the Effects of Isolated (All-E)-lutein-5,6-epoxide on Primary Sensory Neurons and Macrophages