Document JRkD4nwrgV1MEaRYRG9mgX62

FILE NAME Talc TALC DATE 1960 DOC TALC495 DOCUMENT DESCRIPTION Book Excerpt - Occupational Chest Diseases Modern Occupational Medicine Occupational Medicine Editors A. J. FLEMING M.Sc. M.D. F.A.C.P. Medical Director E. 1. du Pont de Nemours & Company AND ; C. A. D'ALONZO M.D. F.A.C.P. istant istant Medical Director Medical Division E. 1. du Pont de Nemours & Company = + Associate Editor Director Haskell E. J. A. ZAPP Ph.D. Laboratory for Toxicology and Industrial 1. du Pont de Nemours & Company Medicine 6666 Illustrations 1 Color Plate Second Thoroughly Revised =% ; PHILADELPHIA Lea & Febiger Chapter 33 Occupational Chest Diseases G. W. Schepers D.Sc. M.D. PULMONARY disability resulting from occupational factors always has been and still remains an important problem in industrial medicine In the United States alone more than 4 million industrial workers are ex- posed to potentially hazardous substances The current bibliography on _ the subject exceeds 000 references and it is obviously possible to review here only those occupational chest ailments which are of greatest topical importance At the same time emphasis will be placed on basic prin ciples and pragmatic issues * I. SILICOSIS Because 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 3,000 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 element 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 N of these substances In recent years numerous synthetic siliceous sub- stances have been introduced _ Fs sete Many theories of the biological action of SiO have been suggested eg a the mechanical injury concept which presumed that angular quartz particles can lacerate vital cell components b the solubility theory silicic acid being presumed to be the pathogen c the polymerization theory the slow formation of polysilicic acid being invoked to explain the retarded development of silicotic nodules d the piezoelec trie theory based on the assumption that the known piezoelectric forces characteristic of quartz may cause local tissue injury e the sated valency theory which postulates the existence of a layer reactive SiO molecules at the fracture angles of quartz partic ; f the colloidal silica theory which is based on the concept that the crystalline quartz particle is covered with a film of toxic colloidal field s^>licag the protein denaturing theory which postulates that the physi- cal the surface of the quartz particle induces organic chemical 44 406 Occupational Chest Diseases Asbestosis is provoked wherever _ exposures However in textile industries there appears to be a greater prevalence of severe disease In contrast with silicosis the asbestotic reaction in the lung is excited not by minute particles but by 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 slowly than when the aerosol contains a predominance of fibers of 10 to 50 microns Again if the fibers are introduced into the lung 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 are 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 fibrocytes proliferate new capillaries form and reticulin collagen and new elastic fibers are laid down This type of lesion cannot readily be distinguished from other interstitial pneumonitides unless the asbestos fibrils are detected by oil immersion or electron microscopy Rarely some of these fibrils will 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 being merely due to increased work of breathing With extension of the process three major complications arise There may be progressive invasion of venous adventitia with perivascular fibrosis intimal hyperplasia and ultimately occlusion of the vascular lumen Relatively large venous channels may become 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 The asbestotic origin of the venous obstruction is readily proven by demonstrating the asbestos fibers in the peri- and endovascular granula- tion tissue Perl's stain often is sufficient for this purpose as it will demon strate the presence of iron deposits in the protein sheaths around the asbestos fibers Another tale feature consists of the deposition of abundant perivascular elastic laminae and fibers While the stage of the alveolar mural invasion is not radiographically- radiographicalydetectable except for blurring of lesser pulmonary markings the stage of perivenous fibrosis is characterized on the ray by the development of a coarse web and the effacement of the normal vascular pattern The Occupational Chest Diseases 407 extent of the latter damage is often underestimated until angiography are resorted to tomography or Massive fibrosis tends to which are in constant develop mainly in the parts of the lung agitation such as the lung apex the matic zone of the basal lobes and the supradiaphrag consolidation is effected cardiac components The by progressive interstitial invasion atelectasis trapping of fibers within alveolar them and spaces where phagocytes surround on both organization sides of the takes place and by abundant pleural thickening lamina elastica In these zones so complete that all semblance of carnification is often pletely lost Major blood vessels pulmonary architectonics is com which reveal their elastic can only be identified by elastic stains skeletons Radiographically these consolidated zones spreading opacities along the present as diffuse and and on either side of the upper mediastinum above the diaphragm heart whose silhouette becomes blurred the called shaggy heart feature Calcification zones may occur in these dense tioSnymunplteosmsatthiecraellisy mtahrekseedpatients usually are merely dyspnoeic on exer- accompanying vascular obstruction In such cases pulmonale will be the usually small and immobile predominating lesion The thorax is while breath sounds vocal fremitus and resonance are markedly impaired over the affected and bronchiolitis are not zones Bronchitis common in asbestosis though some of these air passages may become involved in the granulomatous reaction cystic bronchiectasis Adanced distortion of the may develop as a result of the fibrotic some fluid lung At first there is mere bronchial distension and or mucus may become trapped in the dilated ducts infection supervenes with all the attendant Later ing chronic suppurative bronchiectasis Tihneflammatory processes lead- differ do not much from symptoms in these cases that conventional varieties of bronchiectasis hemoptysis is less common and cor except Tuberculosis may occur in asbestotic pulmonale develops early subjects but is not more among these than it is in the general population prevaThe lesions not any more severe than those are a the fibrous barriers caused by the uassubaelsltyossiesen and often are limited by relationship Pulmonary carcinoma has been observed with high frequency_in frequency_in employees asbestos industry that a causal relationship accepted by most authorities Indeed has been pensable as an pulmonary pulmonary carcinoma is com- Africa Most of tohcecupcaatricoinnaomlatdaisaeraese in England Germany and South mesort^'esiolomais also squamous cell epitheliomata Pleural Since the quite prevalent especially in crocidolite industries neoplasm lymphatic lymphatic system is not completely destroyed in asbestosis sive interstitimaal yfisbrporseiasd dTihfifsusdeloyesthnrootughout the lung in spite of exten- readily occur in silicosis 470 Occupational Chest Diseases In industries in which asbestos is handled extensively warts are not uncommonly experienced at points of cutaneous friction e.g. hands collar belt cuff zones Many of these acanthotic lesions are indistinguishable from benign warts but occasionally the tale causative asbestos fibers are 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 onset 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 country 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 Talcosis Two varieties of this condition occur The first is caused by tremolite tale and the disease is essentially asbestosis with the same range of severe lesions found after chrysotile amosite or crocidolite exposures Tale bodies similar to asbestos bodies also occur This con- dition should be carefully distinguished from the pulmonary reaction to other forms of commercial tale which may consist of pure magnesium silicate alpine tale or may be a mixture of the latter with antigorite chromite dolomite magnesite and spinell Most of these substances are relatively inert When breathed in excessive quantities and especially when there is some existing pulmonary lesion e.g. virus pneumo- nitis they may cause respiratory incapacitation usually transient through extensive alveolar mural cellular infiltration Because of the multiplicity of uses of tale such cases may occur in diverse industries where tale is used as a slipping agent e.g. paper mills rubber industry These pathogenic tales have no place as surgical or toiletry accessories Rock Wool is a syntheftibirocus silicate extruded from slag It is extensively used as an insulating material When its long fibers are inhaled repeatedly and in great quantity pulmonary 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 Occu or the pulmonary scars Glasswool is made fro as a textile as insulation and structural materials consist of relatively thick lung if inhaled Fatal a result of uncontrolled ex fibril varieties of glassw observed clinically and dust In the lesions isol asbestos bodies have be In recent years Fiberg as a medium for constru consists of a mixture of filler Shaping and bun factured from this subs a certain amount of skin have yielded conclusive ever experimental evide are readily produced i attended by no complica Micatosis Mica expc lomatosis with some fibr Within these reactive i These are analogous to ments of mica ensheathe derived from the bodie representative of pulmo regional condensations from apparent normality Slate Worker's Lung may follow exposures limited geographic distr in the hilar lymph nod fibrosis and periadenitis struction with bronchie segments may be prodi vascular fibrosis is a pro contrast vividly with the a single lobe not unco in which case a favorat vention Sillimanite is a less fibrous silicate it has th Similar remarks apply . vl-