Document G66qzN0LyNpydR2QG96enrL7x

FILE NAME: RT Vanderbilt (RTV) DATE: 1960 DOC#: RTV230 DOCUMENT DESCRIPTION: Book Excerpt - Occupational Chest Diseases Modern Occupational Medicine Modern Occupational Medicine Editors A- I- FLEMNC, M.Sc., M.D., F.A.C.P. S h -d u d D u n tn r. E. I. ,lu Po, ,/ , .Vcm,,u,, c , AND c . A. D'ALONZO, M.D., F A C P ** . , f aM ;le ^ mj - ^ Associate Editor * - J- A. ZAPP, Ph.D. ' au TM n< dc Semours 6- Cnmimnu me . A Illustrations. / Co/or Second Edition--Thoroughly Revised PHILADELPHIA Lea & Febiger Chapter 33 Occupational Chest Diseases (*. XV. IF. Schept'is, D.Se., M.l). I'u .xio.vaiix disability resulting from occupational factors always lias been ami still remains an important problem in industrial medicine. In the l niter I States alone more than 4 million industrial workers are ex posed to potentially hazardous substances. The current bibliography on the subject exceeds S.iXiO references, and it is obviously possible"to review hem only those occupational chest ailments which are of Greatest topical importiyjce. At the same time, emphasis will be placed on basic prim maples afitl pragmatic issues. I. SILICOSIS Urcause of the predominance of silica in the earth s crust, it is natural that silicosis should constitute an important occupational chest disease. Of the more than 3.IXX) known minerals, more than 500 are compounds of silica. It is indeed fortunate that many of these naturally occurring varieties of silica, as well as the clement silica, are biologically inert. It should, however, be cautioned that epidemiologic surveys and experi mental inquiry have concerned themselves with fewer than 10 per cent of these substances. In recent years, numerous synthetic siliceous sub stances have been introduced. Many theories of the biological action of SiO^ have been suggested, eg., (n) the mechanical injury concept, which presumed that angnfar .-quartz particles can lacerate vital cell com|)onents: (In the solubility theory, silicic acid being presumed to Ik*the pathogen: (<) the polymer ization theory, the slow formation of polysilicic acid being invoked to explain the retarded development of silicotic nodules: (ill the piezoelec tric theory, based on the assumption that the well-known piezoelectric ^ c h a r a c t e r i s t i c 0f quartz may cause local tissue njurv: (cl the -jhhiu^plKcd valency theory, which postulates the existence of a laver of htggy reactive SiO molecules at the fracture angles of quart*/. Prti S f (f) the colloidal silica theory, which is based on the concept that the crystalline quartz particle is covered with a film of toxic colloidal -- silica: (<i) the protein denaturing theory, which postulates that the phvsical h v l^ it the surface of the quartz particle induces organic chemical 4(56 Occupational Chest Diseases .Asbestos is provoked wherever cynosures to asbestos dust occurs. However, in textile industries there appears to be a renter prevalence* of severe disease. In contrast with silicosis, the asbestotie reaction in the lung is excited not by minute particles but bv relatively long fibers. Thus if asbestos be pulverized to particles no longer than 3 microns, very little disease develops and the process advances much more slowlv than when the aerosol contains a predominance of fibers of 10 to 50 microns. Again, if the fibers are introduced into the Inns: in a high caliber form (e.g. conjoined multiple fibrils), less disease results than when the individual fibers are split into their component fibrils of sub micron caliber. Asbestosis is essentially an interstitial pulmonary lesion in which all component tissues arc involved with focal emphasis of the process. The lesions range in severity from mere alveolar mural cellular infiltration of a microscopic nature, not detectable by radiography or even on gross anatomical examination, to massive consolidation with associated vascu lar occlusion, bronchiectasis, and carcinomatosis. The interstitial lesions result after fine short fibers have been ingested by phagocytes and transferred into the lymphatic channels of the alveo lar septa. Here fibroevtes proliferate, new capillaries form and rcticulin, collagen and new clastic fibers are laid down. This type of lesion cannot readily be distinguished from other interstitial pneumonitides unless the asbestos fibrils arc detected hv oil immersion or electron microscopy. Rarely, some of these fibrils wiil be rendered obvious by conversion into an asbestos body through proteinaceous encapsulation and ferrous pig mentation. If the disease remains limited to this stage, disability may remain limited living merely due to increased work of breathing/ With extension of the process three major complications arise. Thenmay be progressive invasion of venous adventitia with perivascular fibrosis, intimal hyperplasia, and ultimately occlusion of the vascular lumen. Relatively large venous channels mav liecomo involved but arteries tend to escape early damage. This obstruction to the venous channels leads to progressive elevation of pulmonary tension and marked cor pulmonale. Heart failure is the usual cause of death in these cases. Tlie asbestotie origin of the venous obstruction is readily proven bv demonstrating the asbestos fibers in the fieri- and endovascular granula tion tissue. Peris stain often is sufficient for this purpose as it will demon strate the presence of iron deposits in the protein sheaths around the asliestos fillers. Another tell-tale feature consists of the deposition of abundant perivascular elastic laminae and fibers. While the stage ol the alveolar mural iuvitsiou is not radiographically **' detectable, except lor blurring of lesser pulmonary markings, the stage of perivenous fibrosis is characterized on the sr-rav by the development of a coarse web and the cffacement of the normal vascular pattern. The uccupntional Chest Diseases 4C7 18f" n un.,I tomography or w l^ i, T P zone of the basal h b ', ' " d 1 consolidation is effected b v n r n ^ v trapping of fibers within -ilveofir4F " " * * * <* 'u - 8 ' S T ' "* Para*card ilc components. The . inter^titia* invasion, atelectasis, them ami organization takes p i r a -in tu ii l>baS'K'>'te! surround un both side, of the l a m S ' S in t f c , . ^ T 1. ,h,ckTMin5 so complete that all semblance of s I zones camification is often pletely lost. . \ |,, L l 2 | * Lh i t ^ T "?i "rchitectonra is eon,. svhich reveal t h e T e S ^ ""'y ^ '*m U M * al la * < sp r2 ih ,g r*opae2s i l o n g 2 2 ,SH^t,UtW^,.z<,nt's P'uwnt as diffuse, and Olid on t h J Z h e , 7 Pi,r ul-ve the diaphragm JW-c-allcd - s h a g ^ L r t - f e t 2 '* a m " bl"" 2 * > zone,. ' k M m - Cal * " "u" may .r a n , in these dense eases,to r ,,8uallv " * m" e'ovb`' VTM5p"*o,*'i.c -In s|lt-|, usually small and immobile w " ,h<'ras " uance are markedly ila b m l o ^ h e T ' lTM ai ^trer t st re= : t r F ~ ...... fluid or mu i may l 2 l , 7 ' " 7 " ' ,rntbial " ' infection s o p e r v r m T w X a ^ r ,, i ' Pr . 'C <Wuto' <U,CK' ^ ,te;::r t e i ing tradironic suppurative bronch'lolm *" T h e 'T ''? " ' `'" 'T "" fa,d- do n<#rdifFor much from . M s>mIn<)ms m these eases .ha, m .r a .i s le, a m o n ^ l ^ i i r t 8" " *",'*'" '** b" f prvva- , m ore^veraih,, t h j l . f u `'" ''" ' f 0"' The le!i" " re H'ufihmn, b a c i t i ; i,! :X 'X " ;r n `",l1 U,,en b> aiaaiL!l^!ino!ffi> I' bpm observed ml,I, .....i, .... . p ii ' s t e tk'iis'iliin ' inisiithki i 7 , 7 7 IB S ' causai reh..,Jnslp U t SL. rrrL.'i r iu *W - a ; '" indeed, pulmonary caronorniTlTTSSr c.iretnom,da are squamous ee epitlieliomata PL,,r.,l "7 7 * a ms,plasm may spread 'diffusely th r o 7 S u .'\t.`hmg''m<1,,m >'ve interstitial fibrosis. This dm, no, L l i l / t ^ d E , ; ' ' 470 Occupational Chest Diseases In industries in which asbestos is handled extensively, warts are not uncommonly experienced at point* of cutaneous friction, eg.. hands, collar, belt, cuff zones. Many of these acanthotic lesions arc indistinguish able from benign warts, but occasionally the tell-tale causative asbestos fibers arc identifiable. Later these warts, if left untreated, have a strong tendency to progress to malignant anaplasia. They should, therefore, be radically extirpated as soon as they are identified. Important features in all cases of asbestosis are the existence of a lag period before the oaset of the symptoms and the inexorable progression of the disease despite cessation of dust exposure. There is evidence to support the view that the first few years of exposure to asbestos fibers are as important determinants of the final outcome as are most of the remaining years of exposure. Thus, in one verified case, a single month of exposure to asbestos dust in a textile plant in one country was followed thirty years later in another oountry by fulminating fatal asbestosis. The intervening period was one of good health and no further asbestos dust exposures had occurred. Continued exposure will, of course, aggravate the process. The severity of the asbestosis is thus a function of the duration of the exposure multiplied by the period which has intervened between the inception of exposure and the onset of the disease. This principle at the same time accounts for the progression of asbestosis after exposure has been discontinued. Cases are currently cropping up in men and women who had worked as pipe insulators on liberty ships during the second world war without since having had any further asbestos exposure. Tleoste: Two varieties of this condition occur. The first is caused by tiemolfte talc and the disease is essentially asbestosis with the same range of severe lesions found after chrysotile, amosite or crocidolite exposures. Talc bodies similar to asbestos bodies also occur. This con dition should be carefully distinguished from the pulmonary reaction to other forms of commercial talc which may consist of pure magnesium silicate (alpine talc) or may be a mixture of the latter with antigorite, chromite, dolomite, magnesite, and spincll. Most of these substances are relatively inert. When breathed in excessive quantities, and especial ly when there is some pre-existing pulmonary lesion {e.g. vims pneumonitis), they may cause respirator)- incapacitation, usually transient, through extensive alveolar mural cellular infiltration. Because of the multiplicity of uses of talc, such cases may occur in diverse industries where talc is used as a slipping agent ( e.g. paper mills, rubber industry). These pathogenic talcs have no place as surgical or toiletry accessories. Rock Wool is a synthetic fibrous silicate extruded from slag. It is extensively used as an insulating material. When its long fibers arc inhaled repeatedly and in great quantity, pulmonar)' lesions closely similar to those seen in asbestosis may result. Once more, the clue to diagnosis is the discovery of "rock wool bodies" in the granulation tissue