Document kQO0wp9Lrabbw86wzKo8zQ1B

Barry Castleman's DuPont File ^CD-ROM Document # DP ^ DATE /?o Type of Document - published report from journal - published report from conference - published abstract from conference - unpublished report - unpublished presentation - meeting agenda minutes report - letter - memo - government report - industry warning information L boo, oxcorp, - legal deposition of_________ - notes of BC on Modern Occupational Medicine Editors J A. J. FLEMING, M.Sc., M.D.. F.A.C.P. Medical Director, E. I. tin Pont tie Scmours i* C'oiti/iion/ AND - C. A. D'ALONZO, M.D., F.A.C.P. jf/fistant Medical Director, Medical Division, E. I. tin Pont tic Scnwurs ir Company Associate Editor . J. A. ZAPP, Ph.D. Director. Haskell Laboratory for Toticology and Industrial Medicine . E. I. du Pont tic Semours O Cam/tany fifi Illustrations. / Color Plate Second Edition--Thoroughly Revised = Lea & Febiger PHILADELPHIA Occupational Chest Diseases O. \V. IF. Scllepers, D.Se., M.l). I'l l.mosaic disability resulting from occupational factors alwavs lias been ami still remains an important problem in industrial modieine. In tin1 t inted States alone more than 4 million industrial workers are ex posed to potentially hazardous substances. The current bibliographx on the subject exceeds S,(X)0 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 attil 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,(XX) known minerals, more than 5(X) 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 IU 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, e.g.. (ti) the mechanical injure concept, which presumed that angnhir .-quart/, particles can lacerate vital cell components: (It) the solubility theory, silicic acid being presumed to Ik* the pathogen: (v) the polymer ization theory, the slow formation of polysilieic acid being invoked to explain the retarded development of silicotic nodules; (<li the piezoelec tric theory, based on the assumption that the xvell-known piezoelectric forces characteristic of quartz may cause local tissue injury: If) the 4ps;Jp%cd valency theory, xvhieh postulates the existence of a layer of hftjjsy reactive SiO molecules at the fracture angles of quartz partipj (f) the colloidal silica theory, which is based on the concept that the crystalline quartz particle is covered with a him of toxic colloidal silica: fg) the protein denaturing theory, which postulates that the physi cal fieliLjit the surface of the quartz particle induces organic chemical < 44:1. m Occupational Chest Diseases .Asbesto.sis is provoked wherever exposures to asbestos dust occurs. However, in textile Industries there appears to be a greater prevalence of severe disease. In contrast with silicosis, the ashestotic 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 (eg. 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 fibroevtos proliferate, new capillaries form and rcticulin, collagen and new clastic fibers are laid down. This type of lesion cannot readily he distinguished from other interstitial pneumonitides unless the asbestos fibrils arc detected bv oil immersion or electron microscopy. Rarely, some of these fibrils will he 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. 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 liecomc involved hut 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 aslicstos fillers. Another tell-tale feature consists of the deposition of abundant perivascular elastic laminae and fibers. While the stage of the alveolar mural iuvitsiou is not radiographically t detectable, except for blurring of lesser pulmonary markings, the stage of perivenous fibrosis is characterized on the x-ray by the development of a course web and the cffacement of the normal vascular pattern. 1 he Occupational Chest Diseases 4G7 extent of the latter damage is often underestimated until tomography or angiography are resorted to. Massive fibrosis tends to develop mainly in the parts of the lung which are in constant agitation, such as the lung ape.v, the supradiaphrag matic zone of the basal lobes, and the para-cardiac components. The consolidation is effected bv progressive interstitial invasion, atelectasis, trapping of fibers within alveolar spaces where phagocytes surround them and organization takes place, and by abundant pleural thickening on both sides of the lamina elastica. In these zones ramification is often so complete that all semblance of pulmonary architectonics is com pletely lost. Major blood vessels can only be identified by elastic- stains which reveal their elastic skeletons. Radiographically, these consolidated zones present as diffuse and spreading opacities along the upper mediastinum, alwwe the diaphragm and on either side of the heart, whose silhouette becomes blurred: the jo-rallcd "shaggy heart" feature. Calcification may occur in these dense zones. Symptomatically, these patients usually are merely dvspnoeic on exer tion unless there is marked accompanying vascular obstruction. In such easex_4t)r pulmonale will be the predominating lesion. The thorax is usually small and immobile while breath sounds, vocal fremitus and resonance are markedly impaired over the affected zones. Bronchitis and bronchiolitis are not common in asln-stosis, though some of these air passages may become involved in the fibro-gramilomatous reaction. Acteuiced cystic bronchiectasis may develop as a result of the fibrotie distortion of the lung. At first there is mere bronchial distension and some fluid or mucus may become trapped in the dilated ducts. Later infection supervenes with all the attendant inflammatory processes lead ing tutchronic suppurative bronchiectasis. The symptoms in these eases do iu?rdiffcr much from conventional varieties of- bronchiectasis except that hemoptysis is less common and cor pulmonale develops early. Tulwrculosis may occur in aslrestotic subjects, but is not more prevalent_among these than it is in the general population. The lesions are not any more severe than those usually seen and often are limited by the fibrous barriers caused by the usbestosis. Pulmonary carcinoma has been observed UMllLjuich-high fremtenev in emplovewoTtfie**asbestos industry that a causal relationskip~nas T?een accepted by most authorities. Indeetl, pulmonary carcinoma is com* pciisuhh* as an occupational disease in England, Germany and South Africa. Most of die carcinomata are squamous cell epitheliomata. ]eunil ijn^oth^j^li^lIliiJ^-abo quite prevalent, especially in crocidolite industries. Since IhelMnplutncs^Icmis'TorTxnnpletely destroyed in usbestosis, a neoplasm may spread diffusely throughout the lung in spite of exten sive interstitial fibrosis. This docs not readily occur in silicosis.