The Topographic Distribution of Mineral Dusts in Some Pneumoconiotic Lungs

¹ Research Pathologist Industrial Hygiene Foundation Mellon Institute.
² Medical Director Johns-Manville Corporation.

By means of a photographic method it has been possible to study the topographic distribution of otherwise occult mineral dust deposits in the lungs. The more important features of mineral dust distribution in several types of silicosis as well as of asbestosis are described and illustrated.

The progressive character of silicosis is explained on the basis of the transport of silica from the site of deposition to new locations where fresh inflammatory reactions are initiated. Such transport is demonstrated in ancient hyaline nodules which exhibit a peripheral "reactive" zone of younger, cellular inflammatory tissue in which mineral dust particles are heavily concentrated. Another striking indication of how the transport of mineral dust may lead to the development of new inflammatory foci is seen in the demonstration of heavy mineral dust infiltrations into uninvolved parenchyma adjacent to silica nodules.

The non-progressive character of asbestosis is explained by the paucity of demonstrable mineral in asbestotic scar tissue and by the difficulty of mobilizing and transporting asbestos fibers through the impeding lattice work of stromal fibrils.

The significance of rounded versus stellate, and of laminated versus nonlaminated silicotic nodules is discussed in the light of the present observations and demonstrations.

Areas of tuberculous inflammation, particularly of caseous necrosis, though occurring in the midst of silicotic tissue are shown to be free of demonstrable mineral dust particles.

An example of the cristobalite type of silicosis is shown to possess a fulminating progressiveness 17 years after the last exposure to this dust. An interesting side light to this disease is the demonstration of mineral dust infiltrating vessel walls.