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It is no longer reasonable to maintain that all kinds of dust are equally dangerous to the lungs. A very convincing array of clinical, statistical and experimental observations has demonstrated that dusts composed, in whole or in part, of silica are capable of exciting a characteristic, progressive, nodular fibrosis of the lungs and that at the same time these organs become abnormally. susceptible to the tubercle bacillus. All the other types of dust that have thus far been investigated can apparently be inhaled almost with impunity for long periods of time.It was originally claimed that only uncombined or "free" silica in the form of quartz was capable of producing this effect, but in recent years there has been a growing tendency to look with suspicion on some of the silicates (combinations of silica with bases). One of them, asbestos, a silicate of magnesium, is now a well recognized cause

To the pathologists who coined it, the term pneumoconiosis was useful to describe all pulmonary reactions due to the inhalation of dust. Under the impetus of compensation laws this group of conditions has received so much attention that today pneumoconiosis is almost a household word. But too few are aware of its original significance and even some medical writers use it interchangeably with the specific term silicosis. As a pathologist I prefer to retain the original meaning and use pneumoconiosis as a generic term to describe all forms of pulmonary reactions to inhaled dust, with no implication as to character, severity or effect on function. The two clinically important forms of pneumoconiosis that are known as silicosis and asbestosis are respectively due to inhaled free silica and asbestos dusts. Other forms have been given special names to indicate the kind of mineral that produces them, but such terms have little

Although the term pneumoconiosis was not introduced until the nineteenth century, clinical symptoms were naturally enough associated with the inhalation of dust in occupation by the earliest medical writers. In the Renaissance both physicians and mining engineers were well aware of the fact that the metal miner suffered from shortness of breath and died prematurely, and anatomists had described "heaps of sand" in the lungs of stone cutters which grated on their knives. They called the condition phthisis, their term for any chronic disease of the lungs which was associated with emaciation and expectoration. While most of the various conditions originally known by this name were differentiated and fully described in the eighteenth and nineteenth centuries, it was not until 1902 that the role of inhaled dust began to be understood. In that year an English departmental committee, of which Dr. J. S. Haldane was the outstanding member, pointed out

Possibly no other television broadcasting system has so developed along lines familiar to American broadcasters than the Japanese. Both the general outlines of Japanese television and specific programs would fit readily into familiar patterns, as visitors to Japan have remarked. This article is intended to present quantitative information on the similarities and differences between the two systems, based upon analysis of the published program schedules in Tokyo and Minneapolis-St. Paul.

Anatomic and roentgenologic studies of the lungs of persons exposed to various types of industrial dusts have demonstrated that inhaled foreign substances do not all produce the same kind of pathologic reaction. Present knowledge is limited by the lack of a sufficient amount of autopsy material to illustrate the evolution of all types of pneumonoconiosis, but the forms produced by pure chemical substances tend to fall into one of three categories. Such disease is predominantly either linear, nodular or diffuse in character. A linear pattern characterizes the general type of response to most inhaled inert foreign materials; nodular lesions are apparently confined to silicosis, while diffuse reaction is exemplified in asbestosis. Mixed patterns are produced by dusts such as granite, which is composed of several different elements. The stages in the reaction to these well known dusts will be analyzed in an attempt to explain the variations in the resultant

In carrying out studies on the cellular reactions provoked in the guinea pigs’ peritoneal cavity by the injection of tubercle bacilli, differential cell counts were made upon a series of peritoneal fluids previous to the inoculations. This has furnished such a large number of counts upon the normal peritoneal fluid that it has seemed worth while to collect and report the figures, particularly since there is no general uniformity in the results published by other writers,1, 2, 3, 4, 5, 6Peritoneal fluids from 237 apparently healthy guinea pigs have been examined, and as no effort was made to select a particular type of animal, this group probably represents a fair average of any laboratory stock. The observations have been carried on over a period of several years during both winter and summer months. Therefore any effects attributable to seasonal or dietary conditions may be assumed to have been comprehended. The majority of the animals were purchased from 4 different sources; a few were raised in the laboratory. They were of both sexes, of many colors, and they varied in age from a few days to several years.Without previous injection of salt solution or other liquid, samples of peritoneal fluid were withdrawn through sterile capillary pipettes and supravital preparations with neutral red or neutral red-Janus green were made. Differential cell counts were done on 200 living cells after 5 or 10 minutes’ incubation in the warm box. At first as many as 1,000 cells were counted, but this was found to be unnecessary as the distribution of cells in the fluid from the normal peritoneum is very uniform if the preparations are properly made. The serosal cells were not tabulated as their occurrence is probably more or less accidental.

The method to be described is a modification of that used by McJunkin1which proved to be inapplicable for use on lung tissue. After our technique had been perfected Cash2reported a similar method, but ours, we believe, offers certain advantages. Two pathways are employed for injection of the vital stain, either the intratracheal, the intravenous or a combination of the two. In using the former the animal is first killed by air embolism. For the latter method the dye is injected into a vein 10 minutes before its death. In rabbits intravenous injections are made into the ear vein; in guinea pigs, the jugular veins are exposed under local anesthesia with 3 per cent cocaine. Ether cannot be used, as it destroys the capacity of the pulmonary cells to react specifically to the dye.Supravital Staining—(a) Intratracheal injection: 30 to 40 cc. of a warm 1:1500 solution of neutral red made up in physiological salt solution is injected into the guinea pig's trachea, which is then tied off. The whole animal is incubated at 37° C. for 5 to 30 minutes. After this interval the dye ceases to react specifically and stains the nuclei. (b) Intravenous injection: 60 to 80 cc. of the same solution are slowly injected into the jugular vein or carotid artery of a guinea pig. If the animal survives it is allowed to live 10 minutes before being killed by air embolism. Occasionally it dies and the whole body is incubated as just described.Fixation—This is accomplished by dropping the lungs and heart into alkaline Zenker-iormol solution. After intravenous staining the lungs are distended with air. To prepare this fixative add sufficient solid NaOH to U. S. P. formaldehyde solution to give a pH value of 7.6.

TO THE EDITOR:— An editorial in The Journal, September 23, entitled "Exit Talcum from the Surgical Scene" has provoked considerable comment among industrial hygienists. There you make the statement that "These lesions [the talc granulomas] are permanent because the body does not have adequate reparative power against talcum, which is essentially a silicate and which therefore induces a silicosis."I would question the validity of the assumption that a silicate can cause silicosis, and several people have already written me to protest against your generalization. All experimental evidence derived from study of pure silicates indicates that as a class these minerals do not dissolve within the body to liberate their component silica with resultant fibrosis. In fact, most of the silicates are inert materials and only a few of them, like asbestos and possibly mica, may be irritating because of peculiar physical properties. These experimental results, based on the study