THE early detection and correct classification of pneumoconiosis is still one of the difficult problems in diagnostic roentgenology. It may, therefore, be of interest to summarize recent observations concerning the diagnosis and differential diagnosis of the disease, and to discuss its classification from the point of view of the clinical radiologist. Pneumoconiosis has been defined as the series of injurious changes, fibrotic and usually progressive in character, produced in the lungs by the inhalation of unusual quantities of certain dusts. While dust containing particles of silica is the chief offender, it is now known that certain silicates, coal dust, and other dusts also produce changes. Some workers believe that sericite, hydrous aluminum silicate, rather than silica, SiO2, is the principal noxious agent, but agreement is far from complete on this point; Cummins (1) recently observed that “silicosis” may yet be found to be “silicatosis.” The majority favor silica as the cause and believe that it produces specific changes in the cells of the lung either on account of its colloidal properties or by acting as a protoplasmic poison (16). In spite of modern preventive methods in industry, it is alleged that the incidence of pneumoconiosis is increasing. It is quite certain that the industrial production of fine silica powder, now an important constituent of many chemical compounds in daily use, is on the increase. Lanza and Vane (7) estimate that over half a million workers in the United States are exposed to the silica-dust hazard (and that the mortality from tuberculosis is appreciably affected by such). Technic of Roentgen Examination The diagnosis of pneumoconiosis is based on (1) the history, (2) the clinical findings, and (3) the roentgen findings. The weakest link in the chain is the clinical examination and the strongest the roentgen evidence. The diagnosis requires the intelligent correlation of all three types of data, and, since it constitutes the strongest link, the most thorough type of roentgen examination. This examination should include (a) a careful fluoroscopic examination, to aid in the detection of complicating emphysema, pleural adhesions, cavities, and right-sided cardiac enlargement, and (b) clear sharp teleroentgenograms made in 1∕20 of a second or less. The latter should consist of stereoscopic anterior and plain lateral films, as a minimum procedure; the importance of intensifying screens with good contact cannot be over-emphasized. Re-examination at the end of four weeks is frequently necessary to exclude the existence of complicating acute inflammatory processes which may exaggerate a mild fibrosis at the initial examination.