Document ga8rLg8nR1g71bmM84w34Ra4J
FILE NAME: Saranac 7th Symposium (SSY) DATE: 1952 DOC#: SSY058
DOCUMENT DESCRIPTION: Transcript of Presentation by Dr. Vorwald - The Inhalation of Certain Substances
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tio n should be a t r i-p a r t members o f th is group, with Doc-
i to r E i lle r and Doctor Peterson to formulate a d efh itio n
under the aegis of in d iv id u a ls, s p e c ific a lly concerned with : the use o f terns* Then I place that re sp o n sib ility upon
Doctor Seward E i l l e r , Doctor Peterson, hoping they can ar
range th is committee*
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(Adjournment o f morning session 12:20 P .N .)
SUBJECT: TEE INHALATION OF CERTAIN INDUSTRIAL SUBSTANCES
Chairman: Theodore F . Hatch .
Kondev, Sep t. 22. 2:00 - 5 0 0 P. K.
B r ie f Reviews
S ilic a
Thomas K. Durkan
Asbestos
Arthur J . Vorvald, K. D.
Beryllium
Harriet L . Hardy, K. D.
Bauxite
C. C. Shaver, K.D. and
Donald Solandt, K. D.
Discussion.
New Synethetic S i l i c a
P h ilip C. P r a tt, K. D*
The Fate of Inhaled P a rticu la te s
K e rril Eisenbud
Discussion, le d by
Theodore ? . Hatch.
BY DOCTOR VORWALD
lin y PROM PAGE* '
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By DOCTOR VOEtfALD:
Zt's not aasy to cover the topic cf asbestos and asbestosis In the abort tine which we m et, and I shall only try, and eh*n try to be very brief*
is you perhaps know, the disease asbestosis was first described about 1900 in England and since that tine, there have been many, nany reports concerning asbestos and notably those reports by Doctor Merevether in England, Doctor Lanza and. McConnell and Fennel of the United - of the Metropolitan Life Insurance Cozpany; by Doctor lynch and others, and again by Doctor Lanza in the Monograph, published by the Oxford University Medical Publications, entitled "Silicosis and isbestosis".
And, following these reports, i t was thought that
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BY MR. PDRKAlf;
Kr* Chairman, Members of the Symposium:
(Doctor Durkan read M s prepared paper, which is on f i l e at the Laboratory)*
BY DOCTOR BATCH: In view of the f a c t that our several subjects in
th is topic are expressed in several papers, i t would be b e st to perhaps lim it discussion and comments to the end o f the presentation, so I c a ll next on Doctor Vorwald who w ill duscuss the findings in reference to asbestos*
BY DOCTOR VORWALD:
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It* s not easy to cover the topic of asbestos and
asbestosis in the short time which we must, end I sh a ll
only tr y , and sh a ll try to be- very b rie f*
Is you perhaps know, the disease asbestosis was
f i r s t described about 1900 in England and since that time,
there have been many, many reports concerning asbestos ar.d
notably those reports by Doctor Merewether in England,
Doctor Lanza and McConnell and Fennel of. the United - of the
Metropolitan L ife Insurance Company; by Doctor Lynchnand
o th ers, and again by Doctor Lanza in the Monograph, p u b lish
ed by the Oxford University Medical Publications', e n title d
" S ilic o s is and Asbestosis"*
And, follow ing these rep o rts, i t was thought that
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we knew e l l about asbestos i s ,
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th a t could be known. However, I don' t believe that that
view i s substantiated and, c e r ta in ly , a l l o f T^s recognize
th a t there are s t i l l many, many problems concerning the disease a sb esto sis, problems which are very complex end
problems which must s t i l l be considered. Therefore, in my remarks, I ce rta in ly do not
wish to appear dogmatic in any way. I w ill merely try to point out some o f the things which are established and seem to be estab lish ed , and other things which appear to be v a lid in accordance with our present knowledge.
You a l l know what asbestos i s . Of course, the
name is not r e a lly one that re fe rs to a d e fin ite s p e c ific
m ineral, but i t rather i s a term which is applied to a v a rie ty of several d iffe r e n t substances occurring as - in the fibrous form, and one could mention cry s o tile ano var ious other types of asbestos in accordance witn a commer
c ia l term- which has been given to them. How, the to ta l number of persons engaged in the
asbestos industry probably does not exceed 1,500. The number of such, at le a s t in th is country. The numbers of
such workers inhaling asbestos dusts is not d e fin ite ly
However, in d u strial hygiene surveys and the frequency of pulmonary-changes in such workers would indicate that only
a few of the to ta l number of men exposed to s u ffic ie n t
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q u an tities of asbestos fib e rs develop asbestosis* Thus, the condition d iffe r s considerably from the condition r e s u ltin g from the present deposition of free cry sta llin e s ilic a * C e rta in ly , i t nay go d iffe r e n tly , the magnitude o f the problem in one is d iffe r e n t than in the other*
Nov, i t would appear th at in d u strial environments th a t e x is t today n ecessitate generally ten or more years of exposure to asbestos dust in concentrations exceeding one m illio n fib e rs longer than ten microns per cubic foot of a ir* I t appears that way* This is b a s ic a lly su b ject to c r itic is m and we know o f other le v e ls o f perm issible con centration that have been estab lish ed fo r asbestos, but from our studies and our in te rp re ta tio n , and I repeat, i t appears that in d u strial environments which e x ist today n ecessitate generally ten or more years of exposure to as bestos dust in concentrations exceeding one m illio n fib ers longer than ten microns per cubic foo t o f air*
Kov, of course, exceptions to th is occur* In su bjects exposed to concentrations above that tentative per m issib le lim it , and I r e c a ll to your mind, the statement brought out by Doctor Fletch er th is morning, namely, the concentration. After a l l , i f the concentration is high, w e ll, then we fin d w ithin the pulmonary tis s u e , many change so, too, with asbestos*
Now, an occasional c ase has come to us for study
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w ith m anifest pulmonary changes and profound symptoms, whose
occupational histo ry d isclo ses an exposure o f le s s than
fiv e years, but I again hasten to add in those instances,
to an extremely high atmospheric concentration of long
fib e r asbestos# In view o f the experimental stu d ies, the
pulmonary deposition o f long fib e rs of asbestos seems to
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be the agent responsible fo r changes in the lung which
are- id e n tifie d as asbestosis#
Rather than to c ite a l l the experimental evidence,
our evidence here at the Saranac Laboratory, and those by
Smith, Voodin and King in England, have fa ile d to show
evident pulmonary change with fib e r s le s s than ten microns
in length in our instance, and le s s than 2 .5 microns in
the instance of King and h is workers, co-workers in England,
and th a t, Vhereas long asbestos fib e r s , in our experience,
caused well-marked para-bronchiolar and in t e r s t i t i a l resem
blance, the condition, as we see i t in human subjects expos
ed to asbestos*
Now, as you a l l know, the pulreonery changes due
to the asbestos fib e r occur i n i t i a l l y as co lla rs of fibrous
tissu e about the respiratory b ro n ch ials, and the progres
sion o f that fib r o s is occurs and i t is characterized by ex-
tention into the adjoining alveolar w a lls, which d isto rts
those walls and d isto rts the formed alveolar space, giving
r is e often to what we Id e n tify as anatomical emphysema and
also to c lin ic a l manifestations of respiratory d iffic u lty due, perhaps, to that emphysema and perhaps due to a d iffu sion phenomena. I s h e ll not dwell upon th a t, because that i s going to be a su bject fo r discussion by Doctor Gregoire on Thursday.
The point to be made, however, i s t h i s , that as bestos m anifests i t s e l f in an e n tir e ly d iffe re n t way than does asbestosis m anifest i t s e l f in an e n tire ly d iffere n t way than does s i l i c o s i s . Asbestosis is a d iffuse pulmonary involvement, giving ris e to the ground glass appearance in the lower lu ng, often involving the lower lung, manifested Hoentgenographically. One cond ition, in our b e li e f , is accompanied in many instances by respiratory d i f f ic u l t y , whereas the other con d ition , simple nodular s i l i c o s i s , is often free of respiratory d iffic u lty .
The action o f in h alin g asbestos fib e r s , I think, the concensus o f opinion today i s , that i t is a mechanical actio n , that the fib e r being fle x ib le , is inhaled into the rep iratory bronchials and because o f i t s f l e x i b i l i t y , i t can be taken up by a c e ll and i t can be carried into the alveolar w all where i t is deposited and produces it s damage Our experimental evidence seems to prove th at since fib ers which are b r it t le and ju st as lo n g, glass w o o l-fib ers, whic can be broken very r e a d ily , f a i l to produce th is type of rea ctio n which we see characterizes the pulmonary response
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to the asbestos fib e r* Thus we b elieve that the f l e x i b i l i t y o f the fib e r is an important fa c to r in thecapacity of the asbestos fib e r to produce damage in the lung*
There are some, however, who b elieve that the chemical a ctio n s, that hsbestos produces i t s e ffe c t by chemical action* Supposing that the minerlogical coat ing of mineral substances is removed, leavin g bare the as bestos fib e r or s p ic u le , allow ing s i l i c a - s i l i c i c acid to be lib e ra te d and thus producing damage* I think that tr.at needs proof* I don' t - I do not believe that s i l i c i c acid produces the damage. Ve have been unable to reproduce the experimental e ffe c t , or reproduce i t experimentally*
The bsbestos bodies -- sometimes I lik e to refer to i t as commonly c a lle d , body - asbestcsis bodies, as the asbestos body* Why? Because these bodies appear anywhere in the lu n g. They often l i e free in the alveolar space. The body is coated with a layer of substance which gives a p o sitiv e reaction to iro n , which we and others believe is derived from tissue f lu i d s . I lik e to look upon the as bestos body as a - a body which has been removed or is in capable o f producing damage. This has been c ite d by other workers, notably, Colus, Lynch and others, and I lik e tc re fe r to i t as the asbestos body rather than the asbestcsis body, because the presence of th is body does not rceer. thst
asbestotic fib r o s is is present in the lu ng.
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Ve have sees a sb e sto sis, asbestos bodies appear i s the sputum, without evident change in the pulmonary tissu e* Therefore, the asbestos body i s the sputum is not diagnostic for the disease asbestosis* I t merely means that the individual has inhaled an asbestos fib e r , and that the body has reacted thereto by coating i t with iro n .
I have seen asbestos bodies ly in g free in the a l veolar space, without evident pulmonary change in the a l veolar w alls which form that space. I have seen asbestos bodies in the alveolar w all without evident fib r o s is . So, th erefo re, I lik e to look upon the asbestos body as a body which i s incapable of producing damage, that th e ir pres ence means merely th a t the fib e r has been deposited in the lu ng, and that - and that th e ir presence in the sputum has no reference whatsoever to the degree or extent of fib r o s is in the pulmonary area.
Asbestosis is productive of pulmonary disfunction and t h is , too, sh a ll be a topic fo r discussion en Thursday. S u ffic e i t to say fo r the present time that the symptomatol ogy o f asbestosis established as bestosis as dominated by phthismia and ir r it a t in g cough. The complications of as b e sto s, inh alation of the asbestos dust, does not apparently a lte r s ig n ific a n tly , the f in a l outcome of tuberculosis, e ith er experimentally or c l i n i c a l l y .
I know that there ere those of you who w ill take
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exception to that statement* However, ur c lin ic study of c l i n ic a l p a tie n ts , our study o f experimental animals, in fe cte d with the tubercle b a c illu s , have f a ile d to demon strate that the asbestos fib e r deposited in the lung in creases the s u s c e p tib ility o f th a t tissu e to in fectio n by the tubercle b a c illu s , thus asbestosis is quite d iffere n t then or from s ilic o s is *
Inhalation of asbestos dust and carcinoma o f the lung is also a subject fo r discussion on Wednesday and I s h a ll not dwell upon th at a t th is moment. * There is often associated with asbestosis, w ell-established asoestosis, cardiac enlargement th at seems to r e s u lt from increased pulmonary tension*
B ronch iectasis, id e n tifie d as the dry type, is frequently associated as a com plication o f asb e sto sis, and i t i s lo g ic a l since the fib r o s is o f asbestosis gains about the respiratory bronchioles and about tue broncn.ia.LS, u..a* there is a degree of fib r o s is which in te rfe re s with the w all of the respiratory bronchiole and which w ill often cause a physiological d isfunction, thus retention of secre tio n s , thus also the appearance of bronchiectasis*
Experimental evidence with respect to asbestosis in d ic a te s, and also there is some c lin ic a l evidence, th a t on removal of the asb esto tic from the - from the atmosphere, th at there is appreciable clearin g of the asbestosis of the
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le sio n in the lu ng, th a t, thu s, I t also d iffe r s from s i l i c o s is . Remove a mac with s ilic o s is from h is - the atmos phere containing free c ry s ta llin e s i l i c a , that s ilic o s is v i l l progress fo r a short period of time and then i t w ill become s ta b iliz e d and indeed, i t may regress by reason of contraction of the fibrous tis s u e , but with the ash estotic, th a t in d iv id u a l, on removal from the dusty atmosphere, the disease in his lungs seems to s ta b iliz e very qu ickly, mucr. more quickly than that does to the free c r y s ta llin e s i li c a p a r tic le *
As fa r as therapy is concerned, studies by the Saranac Laboratory and also by Smith, Voooin and King, experimental studies with aluminum hydroxide, c o llo id a l aluminum hydroxide, showed no evident retention or re ta r dation of the development o f asbestosis in e:q?erimental anim als. Thus, again, i t d iffe r s from the reaction due to the free c ry sta llin e s i l i c a in the form of quartz.
Furthermore, th is asb esto sis, tn is aluminum hy droxide or aluminum, c o llo id a l aluminum hydroxide did net prevent the development of the reaction to the asbestos fib e rs deposited in the lu n g . I f anything, our experiment a l evidence, and that is also supported by the evidence fron King in England and his co-workers, is that aluminum hyd*ox ide augments the fib r o s is due to the asbestos fiber.
Cortisone? I know of no experimental or c lin ic a l
^ * c J't
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study where Cortisone has been used as a possible thera
peu tic agent against the pulmonary reactio n to asbestosis,
to asbestotic fib e r or for a sb e sto sis. I t seems to me, however, that Cortisone should be given a t r i a l . Ve have considered that fo r s i lic o s is , but by reason of the fa c t that the individual with free cry stallin e s ilic a in his lung i s more susceptible to tu b ercu lo sis, we have not fa v o r ed the use of Cortisone which also increases the suscepticil-
i t y of the lung to tu b e rcu lo sis. But that does not appear
to be the case in a sb e sto sis. Ve, therefore, consider giving Cortisone a t r ia l
in the a sb e sto tic . Thank you.
BY DOCTOR HATCH:
Im a l i t t l e curious to know why, in s e ttlin g the times for th is afternoon, Doctor Vorwald has a llo t t e e mere time for discussion of B eryllium . I thought Doctor Ear7 could't e l l us a l l about i t in fiv e minutes, but insteao of th a t, she is a llo tte d a l i t t l e longer tim e. I ` 11 ask Doctor
Hardy to ta lk on B eryllium .
B Y DOCTOR HAHDY:
professor Hatch and Members o f the Symposium: There has been in the past decade a tru ly impressive accum u la tio n of American and fo reign lite r a tu r e r e la tin g to the epidem iological, c lin ic a l and experimental aspects of exposure