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FILE NAME: Engineering (ENG) DATE: 1936 May DOC#: ENG025 DOCUMENT DESCRIPTION: Published Conference Presentation - Pneumoconiosis
PNEUMOCONIOSIS
ROBERT B. HUNT, M. D.
'
Boston, Mass.
Address delivered to International Association of Industrial Accident Boards and Contmissions9 AshevillG9 t*
SINCE the middle of the 16th century, it has been observed that men who have worked in a dusty occupation have been more prone to contract dis eases of the lungs than those in any other occupation. Down through the following years has come the everincreasing knowledge that men who have worked where dust is great and the exposure long, showed a consid erable prevalence to respiratory infection. We note va rious terms which have been coined in the different types of industry referring to diseases of the lungs, such
as grinder's rot and miner's asthma. Whenever the incidence of tuberculosis rises sharply
above the normal average in any community, there usually follows an investigation as to the cause.^ The British government experienced that condition in the gold mines of South Africa and Australia. A general survey of the areas showed a marked increase in tuber culosis, and following the report of the survey intensive study was made of the working conditions. When the report of that work was published, it stimulated a con siderable amount of interest in the United States and investigations revealed that our miners were affected in a similar manner. Incidentally, it stimulated scientific
and experimental work as to the cause and effect o
various types of dust upon lung tissue. During the early part of the last depression, thou
sands of men lost employment through no fault of their own. All workmen have a right to live and when fi nances were gone and men were confronted with want and starvation, they quite obviously turned to every factor which might provide them with sufficient funds to support themselves and their families. A genera depression does not affect one class but all classes, and it might have been expected that many of the unem ployed aided and abetted by the legal profession, would eventually find their way to their physician's office, and that is exactly what happened in this country. The outcropping of thousands of claims for silicosis sud denly burst upon the unsuspecting world, and industry and labor were confronted with a serious economic and social problem. With this increase in the number of claims, there also arose a certain amount of hysteria
amon- all of the factions more or less concerned with such claims. Those of a pessimistic nature might con sider the outcropping as an emergency; but industry has met and conquered emergencies of greater moment
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` in the past, and I have every reason to believe that the
solution of this problem will terminate to the mutual
satisfaction of all concerned. .
.. .
What is this condition called pneumoconiosis? To
clarify and remove any reasonable doubt <ts to the ter
minology used in this discussion, let me explain the
meaning of several words:
Pneumoconiosis, refers to the presence of dust within
the lungs whether that dust is harmful or harmless, or
ganic or inorganic.. It is a general term to denote the
cause and location of the disease but is so broad in its
scope and so non-specific that we try as far as possible
to use a term more applicable to the individual case. It
is not a diagnosis but merely a symptom.
Silicon is an element which never occurs in the free
state, so we are not particularly concerned with that
name.
-
Silicon dioxide, bearing the chemical formula SiC>2
and represented by quartz, causes a form of pneumoco
niosis. When silicon dioxide combines with other
elements, such as iron, aluminum, etc., it forms a
silicate.
The lungs are equipped with a method of drainage
which we call the lymphatic system. It is composed of
a network of fine, connected tubes throughout the lung
structure, following, in general, the course of the
arteries, veins and bronchi and terminating in the gland
ular tissue of the mid chest. Another branch of the
same system follows the outer contour of the lungs and
pleura and ends in the mediastinal glands. The func
tion of this drainage system is to rid the lungs of for
eign material, whether it be bacteria, the result of in
fection, dust? or any other foreign body which has
entered the lungs.
Such a system would be of no practical value without
a means to convey the extraneous material into the
tubes, and the body has provided such an agency in the
white cells of the blood. Each white cell, called a
phagocyte or scavenger, is a mobile unit capable of
ingesting foreign material and transporting it from the
lungs to within the lymphatic system.
When dust enters the upper respiratory tract through
the nose or mouth, it becomes immediately wetted, and,
by far, the largest proportion enters the gastro-intestinal
tract by the act of swallowing, and becomes inert. A
portion of the dust accumulates on the mucous mem
branes of the nose and it is removed by the elimination
of the nasal secretions and expectoration. The ex
tremely small amount of dust that finds its way into the
larynx meets considerable opposition in its downward
progress from the cilia, or hair-like structures of the
cells lining the bronchi. It is their particular function
to retard the advance of foreign material.
Some of this dust is removed by coughing. Having
evaded all of the protective agencies of the respiratory
tract and arriving within the air spaces of the lungs,
the dust particles are ingested by the white cells, or
phagocytes, carried through the wall of the lymphatic
system, and are eventually deposited within the glandu
lar tissue. The smaller the size of the dust particles,
the greater seems to be the activity of the blood cells,
_and conversely, the larger the particles, the more slug
gish they become. .
-
The unit of dust measurement is the micron, 1/25
thousandth of an inch. Experimentation has proven
that dust greater than 10 microns in diameter is prac
tically harmless as far as the lungs are concerned, but
from dust averaging between 2 and 5 microns may be
expected the maximum amount of lung pathology. Such
microscopic dust is invisible to the naked eye.
The transportation and storage of dust continues until the lymphatic system has been filled to saturation. Other depositories must then be utilized. In that event, the phagocytes move out through the walls of the lym phatics and deposit their dust load in the partitions be tween the air spaces of the lungs. That process always occurs in both lungs and is never unilateral. It starts from the hilus area, extends outward toward the pe riphery and eventually may involve all lobes. The en trance of a foreign body within the lung structures stim ulates the protective devices to greater action and soon the blood stream lays down cells about the dust deposits, in the endeavor to encircle the mass with a wall of thick fibrous tissue, in the hope that the progress and harm ful effects might be checked or reduced to the mini
mum.
That protective cellular element is called connective tissue, and when found in the lungs is known as fibrosis. The formation of fibrosis is not peculiar to the presence of dust, but is present in its defensive role in practically all diseases of the lungs, whether it be tuberculosis, pneumonia, bronchitis, asthma, or the results of in flammation. It is rare indeed to find an X-ray of the lungs in which fibrosis cannot be demonstrated.
Connective tissue is non-elastic. It is quite obvious that the constant replacement of normal lung tissue by tough, non-elastic fibres, will in time produce embarrass ment of respiration. It happens in tuberculosis, in asthma, in silicosis and in the absorption of other dusts.
The description of the lungs physiology in the pres ence of a foreign substance which has just been de scribed is applicable to the absorption of many dusts, whether of a silicotic nature or silica-free. When sili con-dioxide is the prevailing dust, whether in the form of quartz, granite, sandstone, or flint, we become in volved in a further process characteristic of silica alone. When the white cells group together and deposit their load of silicon-dioxide at a common point, the connec tive tissue cells encircle the mass, and we have formed the so-called silicotic tubercle. This is the first tangible evidence of silicosis. Tubercles and connective tissue may increase, which simply denotes that the process has advanced. We attempt to divide the silicotic proc ess into three stages of development, but as there is no sharp line of demarcation between them, opinions will be as numerous as the number of persons who examine the films. It is quite suffiicent, however, for all prac tical purposes to simply note the presence of fibrosis
(Continued on page 237)
(Continued from i'age IJ4-J fie:. , Modulation when examining the films, riil-' When quartz is present, a chemical action is noted ?^"wiiich is apparently characteristic of silicon-dioxide and t'not f0und in the presence of other types of dust, with the exception of asbestos which will be described later. Silicon-dioxide is soluble in the weak body alkalies, ;'r and such reaction produces a toxin or poison. That poisonous chemical reagent so alters the immediate sur rounding tissue that it loses its resistance and becomes incapable of protecting itself against the invasion of foreign bacteria. Pneumonia occurs not infrequently in silicotics, probably due to the frequency of the organ 'ism of that disease in the upper respiratory tract and the inability of the lung tissue to offer any defense. The disease in which we are particularly interested, how ever, is tuberculosis whether pre-existing or super
imposed upon a silicotic process. It is estimated that 75 per cent of all tuberculosis is
acquired before the age of 15. If a person is compara tively young, say around 30 years of age and sometime during his life has contracted tuberculosis which has be come non-active and walled off by the connective tissue barrier, the silicotic poison formed, exerting its in ' fluence on the outer wall and the action of the bacilli from within, often succeed in breaking through that de fense. The tubercle bacilli are then liberated within the lung tissue and meeting little or no resistance spread rapidly and usually cause a fatal ending. If that pro tective barrier of connective tissue was sufficiently strong and tough to resist the action of the toxin, no particular harm would result.
Basing our conclusions upon the actual facts of medi cal and experimental knowledge to date, I think it is safe to say that the non-siliceous dusts, represented by coal, cement, lime and marble and the silicates of iron, aluminum, clay and many others, are essentially harrrlless when introduced within the lungs, but silicon dioxide in the form of "quartz, sandstone, granite or flint are particularly hazardous in the presence of in fection..
'> Gardner divides the action of the dusts in the lungs into three classes: namely, the linear fibrosis caused by '/most inert material, the nodular type which is confined to silica and the diffuse as represented by asbestos.
Asbestos is a magnesium silicate containing about 42 cent of silicon dioxide. Its entrance into the lung
[eauses a diffuse fibrosis which is characteristic only of that substance. The exact cause of the reaction is not
known, but one theory advanced relates to the loose combination between the silica and the magnesium re sulting in enough irritation to cause areas of diffuse tfibrosis., It may advance to a degree sufficient to cause ^incapacity and may terminate fatally without the inter-
of infection.
gteKe-non-siliceous dusts and many of the silicates may gy^Rraucj varying amounts of fibrosis and may occlude
_ ny of the lung's air spaces. The former condition, ff-carried to excess, may influence the respiration to a
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certain extent. The lungs are composed of millions of air spaces and the obliteration of thousands would hard ly be noticed. Tuberculosis, or operations upon the lungs, have wiped out entire lobes and yet produced no discomforts, so why need we become alarmed at the loss function of small areas due to dust obliteration?
It was formerly thought that the pathology within the lung created by the presence of silica was due to the mechanical action of the dust particles. The sharp edges and corners of the dust were supposed to so muti late the tissue that it could not withstand attacks of in fection. That theory could not account for the action of many of the dusts, such as aluminum oxide or dia mond dust whose edges are sharper than those of quartz and yet were unable to aggravate tuberculosis into activity. That theory has been given up in favor of the chemical reactions. It was then thought that a colloid might be formed, but again that theory could not account for the variations in the reactions of dusts. At present, the chemical theory with the formation of definite poisons has been accepted. It at least gives us a fair explanation of the action of silica and the harm less dusts.
We may be obliged to change our opinions later con cerning the actions of certain dusts in the light of ad vancing knowledge. Our present knowledge concern ing the actions of some of the silicates is rather vague and not entirely satisfactory.
(Continued in the June issue)
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