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Question. Give the jury some idea of the extent to which you have done that.

Answer. Well, previously it was the custom to run these lungs through in the pathological laboratory and make a microscopic examination to determine the nature of the diseased process that was there, so that that has been going on in my experience for at least 25 years. More recently that is done less, and in the last 10 years we have given much more attention to the X-ray pictures. In fact, the gross pathology that one sees when the chest is opened and the lungs are looked at by the naked eye, is now in most cases practically as good as a microscopic examination.

Question. Can you tell the jury, Doctor, about how many cases of silicosis you have actually seen in your practice and experience?

Answer. About 500 that I felt were positively diagnosed as such. Of course, you will remember we all have the experience of having many cases referred that we do not eventually consider are silicosis.

Question. How many actual cases of silicosis have you diagnosed in your own practice?

Answer. About 325 in my own practice.
Question. Are you at the present time in the consulting practice on silicosis?
Answer. I am.
Question. For the State of Ohio?
Answer. Yes, sir.

Question. How many cases of silicosis have you had in your practice, say, in the last year?

Answer. About 20. Question. Do you know when the last case of silicosis was referred to you? Answer. Well, prior to my coming here, week before last, a case from Toledo, Ohio.

Question. In what industries and occupations did these silicosis cases occur that you have examined ?

Answer. Well, they have occurred over quite a range. For instance, the pottery, porcelain, vitrolite, enamel industries, iron and steel foundries, stone cutters, so-called marble cutters, monument workers, even cement, stucco, basic slag, asbestos, glass, coal miners, porcelain enameling—perhaps that is a duplication. Well, that is a representative source of them. Oh, sandstone quarries and quarry workers. I forgot that.

Question. Doctor, is there any classification of dust?

Answer. Why, there are many possible, depending upon the object in view. Usually, though, for practical purposes we divide dust into the harmless and the harmful, and then we take the harmful and divide it into that which is poisonous and that which is harmful but not poisonous.

Question. What have you to say about silica dust in that respect, as to its classification?

Answer. I agree with the prevailing view at the present time and the evidences that have been submitted that silica dust is a poisonous dust.

Question. Tell the jury whether or not silica dust is an industrial hazard.
Answer. Silica dust is an industrial hazard; yes, sir.
Question. How long has it been known as such?

Answer. Well, it has been known as such almost since silica has been identified by the chemists. That is over a hundred years. But long before silica was identified, its effects were known. In the ancient days of the skilled trades the craftsmen-in fact, silicosis is probably the oldest occupational disease. There is reason to believe that it existed before written history, in connection with the making of arrowheads, and spearheads, and so forth, by ancient warriors.

Question. How long has it been known and considered as an industrial hazard in the United States?

Answer. About 30 years. Twenty-five-about 30 years, I should judge. It has been identified as such in the United States since 1915.

Question. Tell the jury what you mean by silicosis. Describe it, if you will.

Answer. Silicosis is a disease which results from silica dust in the air being inhaled into the lungs, where it sets up a gradual scar tissue formation in a peculiar way. It does not do it in a broad sheetlike manner, but in spots, or nodules, as they are called, and those gradually increase in size until they block up the drainage from the lungs, and eventually they block the blood supply, and then they block the air passageways. While this is going on the person suffers certain symptoms, such as increasing shortness of breath, and can't take a deep breath. He gets pains around through his chest, and he notices that he can't work as vigorously as before. He is very apt to develop tuberculosis, much more susceptible as the result of this silica in his lungs and otherwise

Question. What do you say about pneumonia in that respect?

Answer. Very much more susceptible to pneumonia, particularly in the first two-thirds of the course of the disease. After that he is more susceptible to tuberculosis, and

Question. Pardon me, Doctor, just wait there, I don't quite catch that. Read that last statement and let me get that.

(The answer of the witness was read by the official reporter.)

Question. Pardon me, Doctor, you were saying something else. I did not quite catch that. I want to understand it.

Answer. The X-ray pictures finally are the most accurate means of telling, before the man has passed away, what he has got.

Question. The testimony in this case, Doctor, is that in excavating this tunnel in project no. 1, there was sandstone which contained, I believe, 98 or 99 percent of pure silica. I will ask you to tell the jury whether or not that silica, when breathed, would be harmful to a person's lung?

Mr. Couch. We object.
The COURT. Read that question.
(The question was read by the official reporter.)
The Court. I suppose you refer to the dust of this silica.
Mr. BACON. Yes the dust arising from that rock.
The COURT. The objection is overruled. The witness will answer.

Answer. If he breathes enough of it over a sufficient length of time, and the dust is sufficiently fine, it will be harmful to his lungs.

Question. State whether or not it would be dangerous to life.
Answer. It would be dangerous to life; yes, sir.

Question. What is it about the silica dust that makes it harmful and dangerous to human life when breathed ?

Answer. Well, the dust is not irritative immediately, so that the lungs and the respiratory passageways do not tend to throw it out as it comes in, which is true of most other dusts. As a result, it very subtly gets into the tissues of the lungs. Once in it begins to undergo a very slow dissolving, and when it gets in a dissolved state it is poisonous, and as the result of that poisoning nature in the lungs, tries to wall it up, and scar tissue begins to form around the particles of the dust, even one particle, a little mass of particles, and that scar tissue is what we see in the X-rays as these nodules all over the plates. They are scattered uniformly over the plates. Do you want me to go on and describe that?

Question. Yes; I wish you would, without further questions, go on and explain what takes place.

Answer. Before these nodules form, these cells that have picked up the dust have been allowed to travel through the drainage system of the lungs toward the outlet portals near the lymph glands or lymph nodes. First they block those up, because those won't let them through. They come too fast. When those lymph glands, which are supposed to throw out dust, and do with ordinary dust, are blocked up, then the passageways—we call them lymph ducts leading to them with the fluid in that begins to block up, and that blocking causes these cells to localize then behind this area all over the lungs, and where they stop this scar tissue begins to form, and it enlarges, gets big enough to be seen, to be felt if you have the lungs out where you can feel them, and to be diagnosed, because this is the only kind of dust that does this. As the condition goes over, these nodules get so thick that they conglomerate, they run together, and they push aside the normal breathing tissue, the tissue that has the air cells in it which supply the blood with air, and they finally push them against each other and crowd them shut, so that gradually the breathing area of the lungs is reduced, the blood vessels are squeezed shut, and masses of these hard nodular scar tissues occur. Those scar tissues and the slow poison in there invite tuberculosis. The tuberculosis germ in the system perhaps already—you know perhaps 80 or 90 percent of us have tuberculosis germs in our systems anyhow, playing around more or less intimately in the blood-manage to get into those nodules, and once in they start things going. They begin to be broken down from the tubercular infection, and from then on the man has usually a rapidly developing case of consumption. Sometimes in the midst of that he gets a cold, gets a flu attack, pneumonia lights up, because he is very susceptible, he has less breathing space, his blood supply is poor, his resistance is down, and he passes out with pneumonia.

Question. Now, Doctor, you speak of scar tissue forming in the lungs. Is that the same thing as fibrosis that has been referred to?

Answer. That is what I mean by scar tissue. The technical name is fibrosis.

Question. You said, I believe, when the silica-dust particles enter the lung in great quantities, that the reaction is not sufficient to throw off the dust, I believe. Is that true of coal dust, for example?

Answer. It is truer of practically all dust than silica dust. Some of the silica dust is thrown off. It is collected up in the mucus, it is raised up and we spit it out. But coal dust has sufficiently irritating qualities that we get a little catarrh and it is brought up readily. Some of it' gets in, and when it gets into the lungs it is picked up by these same sort of cells, but it is not poisonous, and the cells just transport it through these lymph channels down to the portals or exit, and it is dumped out there, spread out, to get out of the body, or else it is spotted around in different parts of the lungs where it lies innocently for man's lifetime. It is not poisonous, does not produce nodular scars. It may form a little scar tissue around it, not anything to be seen or felt.

Question. I will ask you to tell the jury, Doctor, whether or not

Answer (continuing). That is to be seen with the naked eye, I should say.

Question. Tell the jury whether or not a person who has inhaled bituminous coal dust is more susceptible to silicosis.

Answer. If he has inhaled coal dust priorly for a few years, he is more apt to develop silicosis; that is, the silicosis affects him more readily and more quickly—not so much, but it increases it. It does not decrease it. It does not decrease silicosis. I would rather be a man who had not been a miner in coal if I had to go into silicosis work.

Question. Did anyone show you the lungs of Cecil Jones and also Walter Street?

Answer. Yes, sir.
Question. Who was that?
Answer. It was Dr. Harless.
Question. Did you make an examination of those sets of lungs?
Answer. I did.
Question. I wish you would tell the jury whether or not those lungs were

Judge LEE. We object.
The COURT. Objection overruled.
Answer. They were.

By Mr. BACON: Question. What evidence did you find in the lungs themselves of that condition?

Answer. The naked-eye appearance of the lungs was enough to establish that (liagnosis. They had black pigmented areas on the surface of the lungs almost any place you looked in the cross section of the lungs, and those areas were palpable—that is, they were able to be felt. They stuck up above the surfaces. They were, therefore, nodular. They were scar tissue. Ordinary coal-dust pigmentation would not do that. You would have the black areas everywhere, but they would lie flat. You couldn't feel them. If your eyes were shut, you would not know they were there. But with these lungs, the outside feel of them, even after they had been in formalin, 10 percent, I believe he saidthat would be a 4-percent formaldehyde it was very plainly discernible, both by sight and by feeling, that these lungs had scar-tissue nodulation. The only substance that we know that will produce that in a uniform manner—that is, scattered all over the lungs—is silica dust. I further examined them microscopically.

Question. What did you observe as to the elasticity of these two lungs compared to the normal lung? Just describe that feature of it, will you?

Answer. Well, of course, I recognized that these lungs had been in formalin, and that would reduce their elasticity. It would tend to stiffen and harden somewhat, as it does in all tissue preserved in that manner, but as compared with normal lungs you can compress them practically shut, like you do a wet sponge, and they spring out again to their normal size and shape, but these lungs you couldn't compress them; hardly any impression could you make. We expect some of that in any preserved tissue. Perhaps you can take an ordinary lung, preserved in formaldehyde, as I understand those were, maybe 6 or 8 months, and compress them half of the way, or two-thirds of the way, but you couldn't compress these lungs one-fifth of the way.

Question. Tell the jury just why they could not be compressed?

Answer. They were so full of scar-tissue nodules that you couldn't squeeze you can't squeeze a rock together, that is the size of it.

Question. What caused that?

Answer. That was the effect of silicosis of the lungs. There was less, of course, of the normal elasticity in those lungs, elastic fibers.

Question. Is that due to silica dust?
Answer. That is the secondary effect.
Question. How do you determine whether a man has silicosis?

Answer. By his history of exposure, the nature of that exposure, by his symptoms that he tells us about, by the physical examination, by the X-ray especially, and post mortem after he has gone, by examining his lungs.

Question. Is the diagnosis of silicosis easly made or not?
Answer. It is one of the most easily diagnosed occupational diseases there is.
Question. Is there more than one stage of silicosis?
Answer. Well, arbitrarily we have devised three stages.

Question. You may name those stages and describe the difference, if there is any difference in the three stages.

Answer. In the average case of silicosis, the first stage when silicosis can be recognized, will show an increase in the general scar tissue in the lungs, and with that increase, which is particularly in the central or root regions of the lungs, but extending evenly bilaterally, somewhat lateralward, there will be found little fine nodules by the X-ray or post mortem, even by the naked eye, if the lungs can be seen directly. It requires in this classification nodulation before silicosis can be diagnosed. If you can't find nodules you can't be sure there is any silicosis there. In all cases of doubt in the first stage in which alleged cases of silicosis are brought to us, everything points to silicosis but we can't find nodulation, we just say, “Well, let's wait awhile if this is silicosis give us 6 months, maybe 3 months, take another picture." By that time, some time in that vicinity, these nodules begin to appear. As quick as they appear we know we have first stage silicosis. They must agree to certain rules. They must be spread on both sides of the lungs—both lungs, that is. They must be of sharp-cut character, not fuzzy looking. They must be of pretty small size. If it is first stage they should not be larger than small split peas. From that we begin then to talk about a second stage. The second stage is simply a stage in which these nodules have gotten larger. They are more numerous. They are thicker as you get outward—that is, they are thickest along the central portions of the lungs, but you notice they are getr ting thicker all around the outskirts of the lungs, and these larger nodules get to be the size of a large-sized pea in the X-ray, and if you feel them in the lung they are about that size perhaps a little less than that as you feel, because, you remember, the X-ray picture is a shadowgraph picture, and therefore things are enlarged slightly as you see them on the plates. That will depend though, upon the technique of taking them. Well, we call that second stage when they are plainly visible, plenty of them, they look alike, and there are no evidences of complications. That is second stage silicosis. That may be complicated by a bronchial pneumonia with tuberculosis, several other things at that time, but I am describing the true case. In the third stage we find these nodules in clumps. They have gotten so thick that they have conglomerated and are in chunks, so to speak, around through the lungs. Three or four of those conglomerations we call that an early third stage. If there is a dozen of them and perhaps with some excess of scar tissue running from one to the other like a band, adhesions or fibrous lay-outs, we would call that á model third stage. If the lung has large solid like areas in it, that is an advanced or massive third stage of silicosis.

Question. Can these various stages be distinguished by X-ray pictures of the chest?

Answer. Fairly easily. My experience is that when four or five persons who know silicosis assemble at a symposium they agree almost 100 percent on the stages of silicosis. Sometimes there will be some argument about a beginning silicosis-shall we call it “a true silicosis” or “a preliminary fibrosis”?-not after the disease is established. It is pretty easy to agree. For instance, I might call the case "a late second”, you might call it "early third." There are no sharply marked stages, you understand, between these stages.

Question. Does silicosis cause death?
Answer. Yes, sir.
Question. In what stage?

Answer. Silicosis by itself will cause death if the exposure is excessive and the process is rapid. It does that through, to put it in simple terms, plain suffocation. If it is slower, the death is most apt to be associated with tuberculosis. About three-fourths of the cases of medium progress, rate of progress, die of tuberculosis ; 15 to 18 percent of them die of pneumonia. The others die of enlarged hearts. The heart has constantly an increasing job in trying to force blood through these hardening lungs. Others die with high-blood pressure, and there are several other possibilities.

Question. Is there any cure for silicosis? Answer. No satisfactory treatment is known. The disease if it becomes fixed and in progress—then it will take care of itself from then on. The man will have those symptoms, perhaps, the rest of his life at that stage, but if it is constantly proceeding then there is no prospect; and there is no treatment other than what we would advise any man who is incapacitated—quit work, rest up, read, get his mind off his trouble, don't overexercise, don't eat indigestible things, and so on.

Question. What causes death in pure silicosis, when there is no complication ?

Answer. Lack of enough air in the blood, oxygen in the blood, to supply the demands of the cells for life.

Question. Doctor, does the period of exposure vary in silicosis cases?

Answer. It varies greatly, yes, sir; that is, sometimes the disease comes on very rapidly, depending upon circumstances, and sometimes it is years and years before there is evidence.

Question. Upon what does that depend as to the time of exposure necessary to contract silicosis?

Answer. Well, looking at the individual first, the man who is delicate, predisposed to lung diseases, particularly to tuberculosis, is a bad risk. The man who has to work more than his normal capacity, at a higher rate, greater speed, who has to increase the depth of his respiration in order to keep up to his job, that becomes a much greater risk. In fact, it is well known that if a man has worked in a dust that is even poisonous and is permitted to breathe very lightly, he may escape poisoning entirely, because that dust is caught in the upper air passageways and removed before it gets down into the lungs. It has been found experimentally that on deep inspirations and full physical exercise a man may inhale into the ultimate air cells in his lungs 40 or 50 percent of the dust that passes through his glottis, the opening of his windpipe here; if he is permitted to breathe very little over an hour or two of the time, as little as 2 percent only may get into his lungs, so the depth of respiration is a tremendous factor. If we look at the dust itself, the richer the dust is in silica, the more hazardous in percent of silica. You understand many of these dusts are combined with other mineral matters. It is a very pure silica that runs over 90 percent of silica—very pure dust. If the dust is fine, and it usually is in any kind of pulverizing process, the hazard becomes much greater. As an illustration of that, for instance, we, walking about, inhale silica dust. The most of the dust that we inhale is of pretty good-sized particles. It gets into our lungs. It can be readily found on post mortem by chemical analysis. But the dust that a person gets in any kind of an abrasive silica process becomes extraordinarily fine. It becomes so fine that it can't be seen by the finest microscope. It becomes so fine that it is known as colloidal, and that kind of dust is dust that is carried the farthest. It practically obeys the laws of gases. It hardly settles at all. For instance, a dust 1 micron in size will take 24 hours in a quiet atmosphere to settle 1 foot, and that dust is about a thousand to a hundred thousand times larger than the dust that comes from fine abrasive processes.

Mr. Couch. Read that last answer.
(The annswer was read by the official reporter.)

By Mr. BACON : Question. Tell the jury the size of the dust particles that do the damage to the lung when breathed.

Answer. Well, the particles are less than five.

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