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Mr. YANT. Yes; I am connected with the experimental station at Pittsburgh.

Mr. Dunn of Pennsylvania. Do you not think it is necessary to furnish those who work in mines and tunnels with information issued by your Department, so that they may know what to do? Do you not think the managers and owners of these mines and tunnels should have that information and circulate it among their employees?

Mr. YANT. Yes.

Mr. Dunn of Pennsylvania. Does your Bureau have sufficient funds that are appropriated by the Federal Government to carry on the important work that should be carried on in this connection?

Mr. YANT. That is a matter about which I am not permitted to express an opinion for the Bureau of Mines. You gentlemen would have to get that information, if it is available, from Dr. Finch.

The Bureau of Mines has been a pioneer in the work devoted to industrial hygiene, the prevention of accidents and diseases in situations of these kinds, and we look at such conditions somewhat more broadly than simply conditions of dust formations. We have done much work in connection with all angles of this important problem.

For example, from the beginning our work has dealt with the toxicity and dangers of mine gases, not only those formed of natural origin but also those formed by the use of explosives.

Our researches have found ways and means for taking care of all situations either by the use of less-harmful procedures or by preventive measures. We carry on a broad educational program in which in normal

years we train as many as 100 miners in first aid and hundreds of executives in accident prevention. It would be very easy to incorporate in these educational programs a course that would teach the miners to avoid dusty operations. Also, it would be advisable and possible to carry this educational program to the mining industry in general. The amount of this work that can be done is entirely limited by funds received from the Congress.

Mr. GRISWOLD. It is time now to go to the House, and if there are no further questions, the subcommittee will adjourn, to meet next Tuesday morning at 10:30 a. m.

(Thereupon, at 12:30 p. m., Wednesday, Jan. 29, 1936, the subcommittee adjourned, to meet at 10:30 a. m., Tuesday, Feb. 4, 1936.)

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Washington, D. C. The subcommittee this day met at 10:50 a. m., Hon. Glenn Griswold presiding.

Mr. GRISWOLD. The subcommittee will please be in order. Our witness this morning is Dr. Leonard J. Goldwater, chief of the occupational-disease clinic of the New York University College of Medicine, 477 First Avenue, New York City.

I presume, Doctor, that you have a prepared statement or some sort of general statement embodying your testimony, and if you will proceed with that general statement the committee will afterward question you on matters where it desires further understanding.

Dr. GOLDWATER. Mr. Chairman and gentlemen of the committee, I think it would be well to start with a general discussion of just what most people understand by the term silicosis. I might preface these remarks by saying that the disease has been known for several thousand years, but it has only been within the past 20 years or so that any serious attention has been paid to it by the medical profession; and, actually, it is only within the last 5 years or so that any concerted effort has been made in research concerning the subject.

For this reason there are a number of points in connection with silicosis which are still a matter of controversy. There are a few things which are generally accepted by all those who have studied the subject. There are other things upon which there are widely divergent views, and anybody who is familiar with medical science understands that this is not an unusual situation, that many things in medicine, many sets of facts, may be subject to various interpretations by different individuals.

In giving a summary of silicosis I will try to point out those things which are generally accepted, and in some cases I shall mention those matters which are subject to various views and interpretation.

As for a definition of silicosis, most persons agree that silicosis is primarily a disease of the lungs which is caused by the inhalation of dust containing particles of silica, the chemical SiO2, of which quartz is probably the most familiar example.

The disease is characterized pathologically by certain definite changes in the lungs involving the deposition or formation of fibrous tissue in certain areas of the lungs. It is difficult for me to express



myself accurately in lay language, because I am accustomed to technical terminology, which would be out of place here, of course.

These changes in the lungs are associated with certain characteristic X-ray pictures and also with certain clinical signs and symptoms.

Most people who describe silicosis divide the disease into several stages, depending upon the progress which the abnormal changes in the lungs have made. The American writers usually speak of first-, second-, and third-stage silicosis, although some follow the English or South African classification of ante-primary, primary, and secondary. Actually, they are speaking of about the same thing.

There are a number of factors which enter into the development of silicosis. These factors may be divided into two main groups, namely, those involving the individual and those involving the environment of the individual. So far as the individual is concerned, the important things are, first, the efficiency of the nasal filter. We all know that different people have different types of noses, and one of the functions of the nose is to filter dust which we inhale. In some persons the efficiency of this filtering mechanism is much greater than it is in others.

Along the same line there is also the efficiency of the layers of cells: which line the bronchial tubes. These cells have little hairs which are constantly in action and the function of these hairs is to propel dust that has been inhaled into the lungs outward so that the dust may be expectorated. Different individuals differ very decidedly in the efficiency with which these mechanisms work. Careful experimental work bears out this view.

Another factor in connection with the individual is the state of the lungs themselves. It is generally accepted that persons who have had numerous infections of the lungs, whether these be tuberculous or otherwise, are more likely to develop silicosis than persons who have not had infections of the lungs. Conversely, people exposed to silica dust—this is diverging a little—are more likely to develop pulmonary infections.

A third important factor in relation to the individual is the manner in which the individual works and breathes. Those who have studied this subject have observed that some workers labor in a rather slow, orderly, rhythmic fashion. Their pace is quite even. On the other hand, other workers will labor very vigorously for a few minutes or more and then tend to relax. Such differences in the method of work are also associated with differences in the speed and depth of respiration incident to breathing. The even, orderly workers breathe more regularly an even amount of air. The air reaches a certain depth in the lung and then it is expired. On the other hand, those who work vigorously, in fits and starts, we might say, are more likely at times to breathe very deeply and inhale air or particles of dust more deeply into the lower portion of the lung or more remote portions.

I should like to put these factors on the blackboard so that we may refer to them and elucidate matters a little better.

There is a fourth and very important but, unfortunately completely unknown, factor in regard to the individual, and that is the mysterious something known as individual susceptibility. I am sure that we have all heard that phrase. We use it glibly without knowing its real meaning. Actually what it means is that one individual working side by side with another, exposed to the same conditions, may develop a disease or some abnormal state and his fellow worker may not do so. That we call individual susceptibility; and we don't know very much of what that really means.

As for the influences external to the individual which may alter the development of silicosis, there are also several. In the first place there is the matter of time of exposure. This means time noti only in point of months or years worked in an atmosphere of dust, but also the number of hours worked.

There is, secondarily, the matter of concentration of dust in the atmosphere breathed. On this point, in the writings on the subject, there is considerable confusion because different observers are in the habit of using different terminologies. For example, some people will describe dust concentration in number of particles per cubic foot of air, others will describe the dust counts in terms of cubic meters of air, which is approximately 30 times as great a volume as a cubic foot; some will speak of the number of particles per cubic centimeter, and still others will speak of dust content in terms of weight of dust contained in a given volume of air. This lack of uniformity in terminology is a source of some considerable confusion.

To go back, we were speaking of the concentration of dust in the air, which is an important factor in determining the development of silicosis. A third factor is the matter of size of the particles, and this is extremely important. The original investigators who worked in silicosis thought that the particles must be smaller than 10 mi

A micron is one-thousandth of a millimeter. In other words, it is impossible to see it with the naked eye. Later, further work tended to show that it was particles even smaller

Mr. GRISWOLD. If I may interrupt you?
Dr. GOLDWATER. Certainly.

Mr. GRISWOLD. Does the microscopic dust only affect in silicosis or does other dust also affect?

Dr. GOLDWATER. It is principally the very, very small microscopic particles that are important. I shall enlarge on that presently:

The present view is that the particles even smaller than a micron or as small as a micron, which cannot be seen with the ordinary microscope without a special attachment to get a certain type of dark field illumination, are important. So that the size of the particle is extremely important. Most observers agree that it is the small ultra-microscopic particles which are the dangerous ones and which produce greatest damage to the lung.

The fourth factor in connection with these others is the content or percentage, or proportion of silica present in the dust. There, too, there is still a matter of controversy among the different authors. Some persons feel that it is only the free silica which has the Sio, formula that is important in producing silicosis. Quartz is the most familiar example of pure silica. It is practically pure silica as is most sand. Still others believe that it is also some of the silicates or salts, others chemical combinations of silica which are apt to produce silicosis. That is a controversial point; but all agree that the percentage of silica or silicate in a dust is an extremely important factor in the development of silicosis.


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Just to get those two things on the board, I will put them down hastily, so that we may refer back to them if necessary. [The witness is now writing on a blackboard.]

First are the factors involving the individual. Under that we have the nasal filter and as a subhead of that the efficiency of the cilia. Next is the length of time of exposure; next is the nature of the working habits of the workers; next are previous infections of the lungs; next are individual susceptibilities.

Under another heading, called B, there are external causes. First is the length of time of exposure; second, the dust concentration; third, the size of particles; fourth, the silica content.

Those are the eight most important factors which influence the development of silicosis.

Possibly you would like to hear a few words about changes in the lungs and also something about the clinical pictures.

I mentioned briefly in the introduction that this disease is characterized by certain typical changes in the lungs, caused by the deposition of these silica particles. I think it would be just as well if I did not bore you with a typical description using pathological terms. It is hard to describe these things otherwise. It is sufficient to say that these particles as they enter the lungs, these small particles, tend to become dissolved in the normal juices present in all human tissue. Here is a matter of controversy, but the weight of evidence is in favor of the view that silica particles do not act as an irritant but as a poison in the lungs. That is why the small particles are more important than the large particles. We all know that any substance which is finely divided is more likely to go into solution than a substance which is in a large chunk. That is a familiar fact to all, of course. So it is with silica, although quartz is relatively a very insoluble substance.

These very minute particles are in a state whereby they probably can be dissolved in the tissue juices of the lung. If they go into solution, they form a poisonous substance. That matter is still one of controversy, but the weight of evidence now favors the view that silica does not act as an irritant like sandpaper or any other hard particle but acts as a poison if it is dissolved in the tissue juice of the lung. The changes which the silica produce are in the form of a deposition of fibrous tissue which encroaches upon the normal lung tissue and interfere with the proper circulation of blood and lymph through the lung.

The pathological changes are associated with more or less typical X-ray film appearances and also with certain fairly well defined clinical symptoms. It is unfortunate that we have not been able to have a projection lantern here, because I have some slides which would indicate the changes when silicosis is present as they appear in the X-ray film of the lung. I could describe those changes, but that would be a poor second to actual demonstration of them by film. In the early stages the X-ray appearance is that of an increased density along the course of the blood vessels and the air tubes in the lung. I can give you a rough idea of that by a sketch. If we take this sindicating] to show a lung, we have the lines radiating from the center here [indicating] where the air tubes come down from the mouth, trachea, and bronchi. We have these fine lines representing the shadows cast by the air tubes and blood vessels. In the early

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