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INDUSTRIAL DUST
Hygienic Significance, Measurement and Control
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BY
PHILIP DRINKER, S.B., Ch.E.
Professor of Industrial Kyffinw, Harvard School of Public Health
AND
THEODORE HATCH, B.S., S.M.
Instructor in Industrial Sanitation, Harvard School of Public Health and Harvard
..-------- .. Graduate School of Engineering
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AU rights reserved. This book, or partsthereof, may not he reproduced in any form \rithout permission of':
the publishers.
abT le 4.-- N umber o r D eatiir Expected from Specified Causer and N umber W hich A ctually Occurred amono P ersons
E noaoed in C ertain Occupations E xpohed to Silic a D ust1
EFFECTS OF DUSTS AND FUMES UPON MAN
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fully that, if ho has silioosis, he got it in Cunndu and Canada
will take care of him.
In the ease of a first-stngo silicotic without tubercular infection,
thore is no method, as yet, for determining his lessened efficiency. The lung-change, if'any, caused by his du6t inhalation is too
small to measure.
:
McCann and Hurtado (177) have estimated disability from
lung fibroses of various origins but have not yet succeeded in
developing a method that is simple enough for routine use-by -
compensation boards, insurance examiners, and the like. Their
procedures involve various simple measurements of respiratory
function but they have not established any methods of detecting
fibrosis which are more sensitive than : the present X-ray
examination.
Of course, industry would welcome a diagnostic routine for
detecting early harm from dust or, better, for forecasting harm. \
No such method is available and it seems fruitless to expect '^.;
such help. The pneumoconioses are not diagnosed until harm :
~is demonstrable byr X-ray.
.,
Cbllis(42) has stressed the difference-between the age group-
mgs in pulmonary' tuberculosis and in silicosis, with or without ~ -
tubercular infection superimposed. Tuberculosis is most preva
lent between the ages sixteen to twenty-four, while silicosis rarely
becomes disabling until later in life. Inasmuch as a good many
y'ears of dust exposure are required before the average ca.-.- of
silicosis (or asbestosis) becomes evident, it is obvious that is
not likely to be acquired early' in life. However, there is an
epidemiological side to the question which is of groat importance
and it is that which Collis especially emphnsized. The average
healthy individual has acquired a fairly effective immunity
or resistance to tuberculosis. His chest X-ray is likely to show
t-one "or more healed scars or fibrosed nrcas from tuberculosis.
S Such an individual, Cummings emphasizes (211), is a 1)01100"
silicosis risk than the man who shows no evidence of past exposure
to pulmonary tuberculosis. Consequently it is wise to select
for dusty jobs men who are past the age of forty' and not y'oung
; men just taking up a trade.
^ Asbestosis. The X-ray picture of the typical asbestotic chest
is confusing to the layman. The effect is described as a diffuse
. fibrosis... Characteristic silicotic nodules Bre. absent and even
EFFECTS OF DUSTS AND FUMES UPON MAN
33
the expert roentgenologist withholds his diagnosis until the case history is complete.
The pathology produced by asbestos is not like that of silicosis. The asbestos fibers group about the neck of an alveolus and shut it off, causing what is known as atelectasis. There is no definite migration or transportation of the dust particles to the lymph nodes and no formation of the fibrous nodules as shown in Fig. 13. As the atelectatic areas increase, the reduction in lung
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area causes serious dyspnea or labored breathing. Lanza (158) suggests that the enlarged hearts noted frequently in his cases of second-stage asbestosis may be the result of the increased work of the heart resulting from this condition; it takes more work to pump blood through the atelectatic than through the normal lung.
In Bilicosis it seems TT be a general rule that, after a certain point, the victim's condition grows worse even if his dust exposure has ceased. But Wood and Gloyne (258) state that they have Been patients with asbestosis "whose condition appears to have
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34 INDVSTHiAL DUST
remained stationary since stopping work in the factory, IluT they advise definitely that the ushestot ic individual l>e removed from his dusty job. Mercwcther (1 S3) and Lanza are less certain on this point.
Asbcslosis Bodies. In the lungs of patients who died after prolonged exposure to asbestos dust and in the sputum of,men with considerable asbestos-dust exposure are found what first were called curious bodies and later asbcslosis bodies (Fig. 15) (75). While somewhat similar bodies occur in the lungs of coni workers ... and even of normal persons, it is admitted that asbestosis bodies in sputum are characteristic of asbestosis. Stewart (223) gives considerable diagnostic weight to their presence.
Pneumoconiosis in Animals. Silicosis has been produced experimentally by quarts dusting guinea pigs, rabbits, mice, cats, and domestic fowl, thus emphasizing the specificity of quartz dust to biological tissue. In like manner asbestosis has been produced in experimental animals.
The Equidae, such as horses and mules,-apparently are not susceptible to ordinary pulmonary tuberculosis but there is no reason to believe they have any special immunity or resistance to silicosis. The normal silica content of horses' or mules' lungs is not known but it would seem wholly reasonable to use the lungs of animals which have worked 5 to 15 years underground in mines as physiological dust samples. A brief report on this subject was published by Haynes (121) but data such as one jmeds are singularly lacking.
TOXIC DUSTS
Poisoning from inhaling toxic, dusts is much more likely than poisoning from swallowing them. Dusts that reach the lungs may pass directly into the blood stream, thence, to the heart, and immediately be pumped all over the body. Distribution to all the body tissue is thus brought about rapidly and effeetively.. But dust taken in with the food goes to the stomach and the major part passes out in the feces. Some is picked up by the portal blood circulation and moves on to the liver. That portion which causes poisoning must first pass through the liver, which is an effective filter and detoxifier; only then can it enter the general circulation.
The practical significance of this physiological distinction between the two ports of entry of dust is considerable. Hamilton (103) states,
A great deal of money has been wasted by well-meaning employers who sought to protect lead furnacemen or oxide roasters or white lead grinders against poisoning, by providing baths and lunchrooms and clean overalls and mouth washes and such, instead of preventing the escape of lead into the air the men were obliged to breathe, and unfor tunately this has sometimes been done under a physician's advice. It must never be forgotten that the great majority of industrial poisons enter the body with the inspired air and that while a workman eats only three times a day he breathes sixteen times a minute during the eight or ten hours of his working day.
Goadby (8S) found thnt cats dusted with lead acquired lead poisoning more easily than did a control animal which was fed over ten times the total lead dosage for the dusted animals. Drinker and Shaw \51) showed how efficiently the liver removed foreign dust part: - s injected into the blood stream. Minot (18S) emphasized '.he much greater danger of lead poisoning from inhaled than from swallowed dusts. Blumgart (24) showed that the absorption of lead directly in the nasal passages was rapid and might be "of a magnitude far in excess of the minimal dose by mouth."
All this experimental evidence confirms the view so often expressed by the late Sir Thomas Lcgge (162), but which is only now beginning to be accepted, namely, that there is far more danger of being poisoned by inhaling toxic dusts than by ingesting them in food or drink.
Metal-fume Fever. Of interest in connection with the breath ing of dusts is metal-fume fever, a transient noncumulative malady that results from breathing rather heavy concentrations of metal fumes like zinc oxide, copper oxide, magnesium oxide, lead, probably lead oxide (227), and munganesc dioxide.
About 2 to 8 hr. after a heavy exposure to the well-dispersed metallic or metallic-oxide fumes, the victim experiences chills followed by fever like that of malaria or the protein reaction following a typhoid inoculation. The patient's fever may reuch uncomfortable heights (we have recorded 104F.) and the next day he feels debilitated but generally can go to work. With
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the fever goes nn increased whitc-blood-cell count oMcuc like that experienced in any infection. Uy the next morning the fever has abated but the Icucocytosis persists (Fig. 1G). Then the victim is fuirly immune; generally lie can take another inhalation without experiencing a second attack (70). In indus try it is a commonplace that attacks on successive dnys are
unlikely'. The cause of this peculiar malady' is probably the absorption
of protein material which results from the action of the inhaled
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Fig. ]C>.--A typical attack of motal-fume fever, showinj; increase in leucoc-.-ic
count, body temperature, and drop in vital rapacity. Note ihat fever abate* before the white count returns to normal. {After Slurpit rt of.; eourtr-iy J. lnd.
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fume particles upon the tissue of the respiratory passages. In our own experiments we found that the chills and fever were acquired far more easily' if one took a few dee;) breaths at a rate of say five breaths per minute than at the normal rate of twelve to fifteen breaths per minute. Slow, deep breathing insures penetration into the alveolar spaces.
Electric or acetylene welding in a confined spare may generate metal-fume concentrations in excess of those used by Lehmann or Drinker in studying metal-fume fever. At present there are no data on the effects of breathing dense concentrations for
615.65
Industrial dust. Hygienic significance, measurement and control
Drinker, Philip and Hatch, Theodore
Dust