(Phthisis with Melanosis,) "Anthracosis,"-and diseases described under the name "Rag-pickers' or Wool-carders' asthma, Garbage-gatherers' phthisis," are evidently of similar origin.

The disease has been variously described as a chronic bronchitis due to irritation; as asthma, induced by peripheral irritation; as phthisis, and as a distinct type of fibroid phthisis or chronic pheumonia (Bristow.)

There is little doubt but that these terms have all been applied to cases of one and the same disease, having as a common origin the presence of large quantities of dust in the lungs, with, perhaps, as a single exception, the spurious asthma originating in peripheral excitation of the nerves by small filiments of cotton or woolen fiber.

I shall endeavor to show that the disease is in reality a distinct variety of Fibroid Phthisis, known also by the names Fibroid Consumption and Chronic Pheumonia, and that it is a true cirrhosis or hardening of the lung; that it is in no respect an asthmatic affection; that it is melanic in certain cases only, and in these the melanic character is spurious . e., accidental; and that it is not bronchial, although bronchitis is often a concomitant complication.

The symptoms developed in those subjected to the inhalation of air loaded with large quantities of dust are naturally in divisions dependent upon the character of the matter inhaled; thus this material may be

1. Sharp, granular, and irritating.

2. Smooth, non-irritating material.

3. Fibrous.

Fibrous materials may possibly produce a very different train of symptoms from those caused by grains of dust, these symptoms need not be considered here.

The inhalation of dust composed of minute grains of mineral matter must necessarily produce symptoms, the severity of which is governed by the character of the dust, -this has been shown by Hirt, (quoted by Buck,) although contra-stated by other writers,-who found that among needle polishers, file cutters, and flint workers more than sixty per cent. of those sick were suffering from lung dis

ease; among grinders, grindstone makers, and stone cutters this percentage ranged from thirty to forty, while among masons and coal miners it was much less.

It seems certain that a material like quartz or corundum which pulverizes in sharp angular grains must always produce symptoms of greater severity than coal or slate dust.

This is shown by the well-demonstrated fact that pulmonary disease runs a much more rapid course among axe and knife grinders than among (school) slate workers.

The experiments of Fournié, Knauff, and Rosenthal have shown that dirt inhaled in large quantities is partially deposited in the nose and pharynx, but that the remainder passes down into the bronchi and much finds its way into the pulmonary (lung) tissue.

On entering an anthracite coal breaker where the dust is so dense that lamps were used at mid-day, the deposition of dust is mainly confined to the nose for the first two or three minutes, then, as a sense of dryness is perceived in the nostrils, the deposit extends downwards and the pharynx becomes streaked and the larynx somewhat irritated. The amount of dust retained in the upper passages probably depends upon the amount of mucous secretion. In those suffering from a copious catarrhal discharge nearly all of the dust would probably be caught in these upper passages.

When the quantity passing to the bronchi and bronchioles is small, it may possibly be removed by the ciliary action of the mucous membrane, and ejected in the sputa, but when the quantity of dust is large enough to overload this action the surplus must accumulate in the lungs. Traube sug gests that the bronchial disorders induced by irritation may derange the ciliary action and incapacitate it from perform ing its proper work.

The experiments of Knauff, Greenhow, and Rosenthal show that matter in a finely divided state readily finds its way into the air-cells, into the ciliated epithelium, the lymphatics, bronchial glands and may even pass to the pleura. The results of these experiments are confirmed by post mortem examinations made by many observers, notably by

those of Peacock and Greenhow in which exhaustive chemical tests were made to determine the identity of the interstitial deposits with the matter inhaled.

Lung tissue infiltrated with foreign substances is variously described as brownish, black, or grayish, according to the character of the inhaled matter, and is sometimes additionally darkened by the apparent presence of a species of local melanic degeneration. It is traversed by bands of nearly white fibroid material which may obliterate all signs of true lung tissue; its specific gravity is increased (Zenker) and it is much harder and more dense than normal lung tissue (Greenhow.) Hard, apparently encysted, nodules from the size of a bird-shot to that of a pea, and composed largely of the inhaled substance, are not uncommon in welldeveloped cases.

These lumps or nodules may originate

1. From an interstitial segregating action; or 2. By a pulmonary cell or lobule becoming thoroughly filled, occluded, and transformed into a cyst; or 3. By an ulcerative action within such a cell or lobule allowing its contents to pass bodily into the lung tissue.

The changes produced in the lung by prolonged inhalation of dust may be summarized thus:

1. A gradual infiltration of foreign matter into the lung tissue and the formation of interstitial fibroid deposits from the mechanical irritation thus produced, sometimes augmented by severe inflammation of the bronchioles.

2. Increased infiltration and condensation with concom itant diminution of the ærating surfaces. Some portions of the inhaled matter may become encysted (?) or segregated and form hardened nodules.

3. When nodules are present they may cause suppuration; the resulting abscesses then discharge into the bronchi or bronchioles followed by contraction and condensation of the pulmonary tissue with augmented fibrinous deposition. The abscesses may discharge in other directions occasioning serious complications.

That this disease is not asthma is evident, and that it simulates asthma only in its dyspnoic symptoms is equally

true. The dyspnoea seems to be directly dependent upon the reduced area of ærating surface and the diminished respiratory capacity.

The mucous membrane of the air passages is exceedingly tolerant of ordinary non-fibrous dust and only in a few cases does the inhalation of such material produce severe bronchial symptoms.

When such symptoms are induced, the presence of fibroid degeneration is often not recognized, and this is probably the reason why many writers attribute the symptoms wholly to the bronchitis of irritation.

Again, others while recognizing the fibrinous deposits, consider them wholly secondary to the existing bronchial affection, and believe the fibrine is deposited around the irritated bronchioles and air cells,-but it is not uncommon to find this disease far advanced with no commensurate bronchial lesions, and as it has been shown that inhaled material easily passes to the lung tissue it seems more rational, while not denying a possible bronchial origin,—to attribute the disease to this cause.

Symptoms.

In its early stages this disease is marked by no prominent symptoms. It is so essentially chronic, its progress is so slow (except in axe-grinders, etc.,) and the physical signs so slight, that the miner may not be conscious of any ailment until the lungs are largely infiltrated and the respiratory capacity greatly decreased by cirrhotic changes.

A slight dyspnoea, noticeable only after violent muscular exertion usually accompanied or preceded by a cough, with some chronic bronchitis and more or less expectoration colored with the material inhaled, are the first symptoms. The pulse and temperature are normal and there are no signs of emaciation or general debility, the appetite is not affected and the patient appears to be in good health; but on examination it is found that the percussion note lacks resonance, and there is a general increased sense of resist ance, while by auscultation ràles may sometimes be detected,

and the respiration is decidedly enfeebled with prolonged expiration.

As the disease progresses, the dyspnoea becomes more marked, the cough may become troublesome, but this is rare, and hemorrhage may occur. Among grinders hemorrhage is common at this stage of the disease, but among coal miners and slate workers it is rather uncommon.

As the disease advances, all the symptoms increase in severity; the dyspnoea is now troublesome after the slightest exertion, (mounting a flight of steps, etc.,) the temperature may be subject to temporary elevation, the appetite may fail, and vomiting occasionally occur. Hypertrophy of the right heart, with its concomitant complications, may occur if the patient is engaged at hard labor of any kind, otherwise it is rare, except in the final stage of the disease.

Severe pains from pleurisy or abscess are not uncommon. When an abscess breaks, expectoration of muco-purulent sputa containing lumps of the foreign matter may be expected.

These lumps are sometimes eliminated from the lung tissue many years after the dusty occupation has been abandoned. Coal miners freqently cough up such lumps many years after they have abandoned the occupation, and it is to this feature we owe the favorable prognosis it is almost always safe to make.

If the occupation be discarded for work in a pure atmosphere before the disease has progressed to the final stage, the symptoms rapidly disappear, and recovery may be almost entire.

If work be continued, all the symptoms continue with increased severity; hemorrhage may frequently occur, but the amount of blood lost is usually small; abscesses form by the breaking down of those tissues in which the pathological changes have been greatest, and these may discharge into the bronchi and bronchioles, followed by contraction and cicatrization, with propable concomitant retraction of the chest walls.

Dyspnoea is now extreme upon the slightest exertion; the temperature may be elevated either temporarily or con