Document 4aR3z479g8VG5yZVwL9jbvwbG

FILE NAME: Talc (TALC) DATE: 1951 Feb DOC#: TALC100 DOCUMENT DESCRIPTION: NY Dept of Labor Monthly Review Dust Inhalation in Relation to Pulmonary Disease The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright' NewYork State Department o f Labor MONTHLY REVIEW Division o fIndustrialHygiene S afety Standards Voi. 30 February, 1951 No. 2 DUST INHALATION IN RELATION TO PULMONARY DISEASE John E. Silson, M.D. Medical Unit Everyone is inhaling some dust with almost every breath taken, but the results of this dust upon the lungs is considered part of the natural process of aging when it occurs outside of his oc cupation. The relationship of dust inhalation to pulmonary disease is therefore usually considered only from the point of view of industrial exposure. Observations on the effect of dusts in industry have consequently been limited largely to those pathological processes which can be clearly dif ferentiated from pulmonary diseases of non-oc cupational origin. To these characteristic changes in the lungs produced by dust, the term pneumo coniosis has been applied. Diagnostic Factors in Pneumoconiosis In order to establish the diagnosis of pneumo coniosis, two factors m us| be present: 1.'pulmon ary pathology which might have been produced by exposure to a particular dust, and 2. an occu pational history of exposure to that dust. The chest physician is generally in a good position to evaluate the first factor, through the medium of signs, symptoms, x-rays and laboratory tests. In determining the second factor, he is often handi capped by his paucity of knowledge of the nature of his patient's work and the materials handled. Most physicians are aware that a rock miner or stone cutter may be exposed to free silica in am ounts capable of causing silicosis. They may not be aware, however, that a worker in a soap factory, which includes in its products scouring powders, may be handling large amounts of silex, which is almost pure pulverized silica. In other instances, the etiology of the pulmonary pathology may not be so readily recognized because the physician is unaware of the more obscure effects upon the lungs of a material such as talc or bagasse. Another factor which makes it difficult to recog nize the importance of an industrial dust exposure in the pathogenesis of a pulmonary disease is the close resemblance which frequently exists between Presented at the Annual Meeting of the New York State Chapter, Amer ican College of Chest Physicians, February 16th, 1950--New York City. that disease and some other pulmonary pathology of non-industrial etiology. When the x-ray pic ture is characteristic, as in an obvious case of nod ular silicosis, the physician is apt to inquire very carefully into the worker's occupation, and to en list the aid of industrial hygienists or other ex perts in an effort to establish a dust etiology. When the clinical and sometimes even the pathological findings are almost identical with some non-oc cupational disease of the lungs, however, he is not so likely to seek far afield for an occupational exposure. It was not until the unusual incidence of workers dying from what was presumed to be Boeck's sarcoid in a plant manufacturing fluor escent lamps was noted, that the toxicity of one of the materials which they were handling was even suspected, and that the identity of chronic pulmonary granulomatosis due to beryllium was established.1 Recognition of the dust etiology is even more difficult when the pathology is identical with that of a non-occupational disease, as for in stance the primary lung carcinoma seen with increased frequency in chromate workers.2 Another way in which dust inhalation may affect pulmonary disease is by aggravation of a pre or co existing non-occupational disease. Today, the fact that silicosis predisposes a worker to tuberculosis, and renders that tuberculosis much more severe, is well established. We are just becoming aware, however, that some of the more innocuous dusts may adversely affect the course of tuberculosis and other pulmonary infections.3 It is no longer considered good practice for an individual with arrested tuberculosis to return to work in any dusty environment. We all too frequently, how ever, see workers with chronic bronchitis, pulmon ary emphysema or even bronchiectasis who are permitted to work in an extremely dusty atmos phere. Even the increased coughing induced by a dust which is ^ig h t^m fitsn t-^o the upper res piratory passage, or wk(R&f3Yto Uteqr these pas sages of the^ccumuiatecL p tid e s , may be suffi cient to aggravate ^ t & t e f l l ^ U i ^ n a r y Wsease.4 MAR 20 195] L I 3 R<AA R Y 1 The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S Copyright law. MONTHLY REVIEW of the DIVISION OF INDUSTRIAL HYGIENE AND SAFETY STANDARDS NEW YORK STATE DEPARTMENT OF LABOR 80 CENTRE STREET NEW YORK 13, N. Y. Industrial Commissioner EDWARD CORSI 1st Deputy Industrial Commissioner THOMAS F. MOORE, Jr. Deputy Industrial Commissioner in Charge EDWARD A. NYEGAARD 8 The Division LEONARD GREENBURG, M.D Director MAY R MAYERS M.D., Medical U nitr J. BURKE, Chemical Unit ^YDRGE P. KEOGH, Code Unit ARTHUR C. STERN, Engineering Unit LEONARD A. PERRIN, E n g i n e S ^ Unit1^ " * Building Plans ,, P ^ er and aYe a11 of these specific aspects i; the generai effect of dust on the aging processei m! ?aldd<eg bhy^,Dn r3'- tEJdgaUrl(LMhakyeer,toinquaontearatnicoleb5sehrevaptiuobr J d a few years ago: " ----- Respiratory infee pnrrmovfooVkendpuYlm`on' agreynecFhaalngdeuss.t Tehxeproesuerxeistevoennltyuadlliyf ferences m degree, not in kind, between the so- m0Unt of P l e n a r y fibrosis so ?evJri fihrotlothe generat .population and those f.Ey^re fibrotic processes which destroy the lungs of workers m industries wherein exposures exist to Ssammef acgf0enncftsntprraetseedntainnd gcroenattienrudoiulsutieofnfecint tohfe tahte mosphere of industrial centers." / ' Dust Characteristics f 4 Pre-requisite to the understanding of the efledee off thpV nhal? i0n Upon the lungs is a knowhhaavve? c hhosient +topeco0fvemr amtentahlisunpdaeprerdisacllusfsoiormn.sWoef in d u s f r in n 1 umattt r generated in the course of thhee?irr ^effects are similar or evinen80idmenatniycasl.taFnibceerss c ln d S f1^ 3S WeU 3S dusts have therefore been in exact meanTnt n f un+certai?ty exists as to the fxfQaCJi,mi?ailm? of these terms in industrial hygiene i w SbaU st,art Wlth a few definitions. The term haannedmlinngg,PccuuHttifnngr, cthruesh^inligd, Pgarirntidcilnegs porrodnmucmerdiinbcyr LS eTwc1'ocof?i11,inf<>0r0gdr >iScram, etc. F2ibers* are5 the 5par ticles similarly produced from organic or inorgan ic matenal composed of thread-like or slender e^ SDesotos,SaannddChaarraePSa;lsott0cnre'aTted5m s"uc.ht oapereaetidoonrrs aast lfmrt*edtto0 tthhe fsShd panardti.c^leeasvcinrega-teFdTMbey cisonadetenrsma tion from a gaseous state, generally after volatili nation from molten metals', ?nd often accompanied 6 by a chemical reaction such as oxidation. Con trary to general usage, it does not refer to con densations to a liquid droplet form, which are Cu mists, or to a uniform gaseous dispersion, whether visible or invisible, which is referred to as a vapor or gas. . ^he common denominator of all these materials is thus the fact that they are present in the atmosphere as solid particles. An important characteristic of these particles is their size.6 It has been shown both theoretically and experiment ally that on inhalation those which are too large do not reach the lung but are filtered out in the upper respiratory passages. Particles which are too small, on the other hand, do not settle out, and are therefore theoretically not retained in the alveoli but are re-exhaled. The question of the in nocuousness of these sub-microscopic particles has recently been open to question. It is a generally accepted principle, however, that the particles ex ert their greatest deleterious effect upon the lungs when they are between 0.5 and 3 microns in di ameter. The other important factor determining the re action of a dust upon the lungs is its composition, ;bat is, its chemical and physical characteristics 7 Where it is a mixture of several different com pounds, such as the dust created in a granite quarry, the percentage of the most active ingred ient (in this instance free silica) is of the utmost importance. Even where the mixture is man-made and not a natural product, its composition has to be taken into consideration. For example, the sand used m an iron foundry may consist of almost pure ?. a>.but the dust released in a shake-out opera tion will have a much lower silical content because a large part of it comes from the iron oxide par ticles separated from the surface of the casting Ihe partide structure also appears to play a role crystalline silica has long been considered a far more active substance than the amorphous form. Tumes from a melting operation are frequently much more reactive than the same material creat ed as a dust by grinding or crushing. In some in stances even the shape of the particles has signif icance, particularly when their effects are depen- ritation 3 krg6 6Xtent upon local mechanical ir- Protective Mechanisms There are a number of mechanisms by which l 1U7nfr perenfcpyma is protected from inhaled Sby thhne cMoaarsye hlai-rhse gpuaartridcilnegs tmheayenbetrafnilcteeretod tohuet nose, or trapped by the moist walls of the turbin ates. Particles deposited on the surface of the mu cous membranes of the trachea and bronchi are carried back towards the pharynx by the wave like vibrations of the cilia, and also by the cough branesllldUCed by the irritation to the lining mem- Particles which succeed in passing these barriers and gain entrance into the alveoli are ingested bv macrophages which arise from the alveolar walls ^ d ar commonly referred to as "dust cells." f- Phagocytes, laden with dust, may pass up into the bronchioles and eventually be car- The materia! on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyrights ried off in the sputum; the others pass through the walls and into the regional lymphatics. Some of the latter are arrested locally in the peribronch iolar tissue, hut the remainder pass onward into the peribronchial and perivascular lymphatics, and are finally trapped in the lymph nodes at the root of the lung. Types of P athology The type of pulmonary pathology which may be caused by the inhalation of a specific dust is de termined by the manner in which this lung cleans ing mechanism is disturbed, and by the type o reaction which results. Probably the best known is the fibrotic reaction produced by exposure to silica.8 This reaction represents a specific cellular response to the material. The particles engulfed by the dust cells stimulate the production oi fibroblasts in any area where they are congregated and these fibroblasts are eventually replaced by dense fibrous tissue. In the case of dusts other than silica, this fibrosis is usually fairly generalized but with silica, it tends to nodular formations along the lymphatics. In either case, the net effect is to make the lungs less elastic, increase their bulk while decreasing their capacity, and de? ^ f pulmonary circulation and aeration of the blood 1 Less characteristic is the action of those dusts which act as general irritants,9 particularly on the respiratory passages, but do not exhibit a specific fibrosing action. Included in this category are most of the organic dusts. Workers first exposed to them respond by sneezing and coughing, but usu ally quickly become acclimatized so that the ir ritant action is no longer found troublesome. Con tinued inhalation of these dusts, however, may re sult in chronic inflammatory changes m the mu cous membranes. . In addition to this generalized irritant action, certain dusts may elicit a specific inflammatory response.9 This may be of a chemical nature, as in the case of beryllium or Thomas slag, or may be infectious, due to bacteria or fungi carried in by the dust. In both instances, the pathology of the response depends upon the material producing it, and may be acute or chronic, reversible or per manently damaging. With some materials, for in stance beryllium, the pathology is quite character istic Even when the dust particles exert no irritant ' action whatsoever, there may be slight pulmonary changes due to their mechanical effects. Alter all, insoluble particles which are phagocytized and passed into the lymphatics may be permanent y retained in the lungs. It is not reasonable to expect that the lungs can become a physiological trap lor inordinate amounts of dust and yet retain all their elasticity. Prolonged exposure to excessive quan tities of even completely inert dusts, therefore, may eventually accumulate in such amounts as to impair function..Such impairment would be the result of a mechanical process: the physical pres ence of large amounts of inert foreign material. The term benign pneumoconiosis has been given to this type of pathology in order to contrast it with diseases resulting from the inhalation of ir ritant matter. Pulmonary allergy is a type of response observ ed with certain organic dusts, 12 particularly those of plant or animal origin. The picture is one of a typical asthma, and only the occupational history differentiates it from identical reactions so com monly seen from pollens or house dusts. The dis tinction often can only be made by patch testing or similar procedures, which will demonstrate that the responsible antigen is present in the man s occupational rather than non-occupational environ ment. Primary carcinoma of the lung has at one time or another been ascribed to a great many of the industrial dusts produced in industry. Provm gor disproving the carcinogenic properties of any par ticular material is often an extremely difficu procedure, because the pathology in no way differs from that of a lung cancer of unknown etiology. Merely demonstrating th co-existence of cancer and some other pulmonary disease such as silico sis, is not sufficient, since there is no reason why the incidence of malignancy in silicotics should be any lower than it is in non-silicotics. The only sat isfactory proof of such carcinogenicity is the un equivocal demonstration of an incidence of cancer in workers exposed to a particular dust which is sufficiently higher than that of a comparable group of non-exposed workers to have statistical signifi cance. Great care must be taken m selecting the control group to insure that all extraneous factors, such as age distribution, sex and non-industrial environment are identical. The high incidence of lung cancer in the uranium mines of Schneeberg and Joachimatal has been known for sometime. More recently, an increased incidence of pulmon ary malignancy has been demonstrated in workers exposed to chromate dusts,2 although the statis tical significance of the data which have been col lected on this material is still being investigated. Asbestos has on occasion been indicated as predis posing to lung cancer. P ulmonary Disease Due to Silica Having presented the general types of Pulmon ary pathology which may be produced by dusts ! would like to devote the remaining time to a brief description of the specific pulmonary effects producedPby certain materials. As has been previously pointed out, undoubtedly the most ?,f these is silica. This is the oxide of the element sil icon and is widely distributed, both free and com bined in the earth's crust. Crystalline silica occurs pure as quartz and as beach sand, and is also scat tered iq varying percentages throughout many forms of rock, such as granite, marble and sand stone. Dusts containing free silica can be created industrially in a multitude of ways, such as dnlhng and blasting operations m the courseofm im ngand ouarrving cutting and shaping of stone, rocK crushing sand blasting or any o th er. operations in which auartz sand or silica-containmg rock is TM s s e d qThedisease* is characterized anatomic ally by generalized fibrotic changes and the (level opment of miliary nodulation throughout the lu g fields, and clinically by cough and progressive shortness of breath. Chest x-rays show at first an 7 I; g; 1, ?;!! 1 K' v- exaggeration of the lung markings and lymph node enlargement, which is followed by nodulation, and finally by coalescence and conglomeration. Tuber culosis may be super-imposed at any stage, and is believed by some to be present in all areas where coalescence has taken place. As a rule, there is no fever or weight loss in simple silicosis, and these signs may be indicative of a complicating tuber culosis. The patient tends to go downhill very rapidly with the development of an active tuber culosis lesion. Many observers have been of the opinion that silicosis could be caused only by the crystalline form of silica, but evidence is accumulating to the effect that the amorphous form as well is capable of producing pulmonary damage. Observations upon the effects of amorphous silica15 have been made largely on workers exposed to diatomaceous earth, which is a light fluffy material formed by the accumulation of skeletons or shells of diatoms. It has a wide use in industry as filters, fillers and absorbents. In contrast to crystalline silica, it pro duces fibrosis of the lungs without discrete nodu lation. The fibrosis is much more marked when the exposure is to calcined material, during which pro cess microcrystals of chrystobalite may be formed. Another possible example of pulmonary damage due to non-crystalline form of silica occurs in work ers fusing bauxite in electric furnaces in the man ufacture of alumina abrasives.1 The fumes given off in this operation consist17 of 25% to 40% sil icon dioxide and 40% to 60% aluminum oxide, together with small amounts of iron oxide and numerous other impurities. Under the electron mi croscope they are revealed as fused particles varya1u s^ze ^rom 1/100 to Vz micron in diameter. A high percentage of the workers exposed to these fumes have developed cough with expectoration weight loss, anorexia, tightness in the chest, and dyspnea on exertion. X-ray examinations show a lace-like or granular increase in the lung markings beginning at the apices. These gradually extend to involve the entire lung fields, and may be ac companied by pleural adhesions causing distor tion of the thoracic contents. Spontaneous pneu mothorax is a common complication. While the al uminum oxide has generally been advanced as the etiological agent responsible for this disease it seems quite possible that this may be a response to silica fume with a particle size far lower than that generally considered injurious. Silica, when present only in combined form as a silicate, has usually been regarded as relatively inert. Considerable evidence, however, has been accumulating against this concept. Probably the best known of the silicates producing severe pul monary damage is asbestos.1 This is a mineral sil icate occurring in the form of long fibers, which renders it capable of being carded, spun, and wovmfi+tonnb^ ui-ldi ^inegadsshi.aapneds.clIonthha>laotriobnonodfetdhewsiethficbeemrsenint the course of mining or processing asbestos has been shown to be responsible for the development Pu.lmo1nary fibrosis with diffuse thickening of the alveolar walls. The outstanding symptoms are dyspnea and a dry cough. Emphys ema, pulmonary infections, and secondary cardio vascular changes due to increased pulmonary re sistance are the most common sequelae. Chest xrays show a "ground glass" haziness, rather than the reticulation and nodulation of silicosis. Another combined silicate which has been shown to be not completely inert is talc, a hydrated mag nesium silicate used extensively in its powdered form as a dusting agent. It may contain variable percentages of free silica; and when these are high, the classical picture of silicosis has been ob served in workers mining, crushing, grinding or otherwise handling it. Even when it contains under 1% free silica, however, as is usually the case, the dust, when inhaled, is capable of producing a fine diffuse pulmonary fibrosis similar to asbestosis. It tends to be disabling, and is frequently accompanied by dyspnea, cough and fatigue. In addition, deposits of x-ray opaque material on the pleural surfaces in the form of plaques have been observed. :,. T suicaie snowing definite effects upon the lungs is mica, which is a double silicate of aluminum and either potassium or magnesium this mmera1, because it splits into thin sheets which are quite transparent, and have a high di electric constant, has innumerable uses in industry particularly in the manufacture of electrical equip ment. For some time, it had been believed that the chest pathology so prevalent where it is mined was due to the free silica present in the rocks in which mica deposits occur. Even among workers exposed solely to pure mica dust in grinding operations, however, there has been observed20 a high inci dence of increased pulmonary fibrosis, with cough X-rays show a fine granulation of uneven density with coalescence of the lesions in more advanced cases. In all these exposures, the common denominator has been silica, whether free or combined. Recent ly, however, carborundum, which is an almost pure silicon carbide containing less than 1% free silica has been suspected of being an agent capable of than usuailmnary changes indicatinS more fibrosis Pulmonary Diseases of N on-Silicotic Origin LA-- ,'"" 8" seen m coai miners nas long been attributed to the free silica content of the shale through which they had to dig to get at th,e. coal Recent large scale L d ie s in W aleshave indicated, however, that exposure to very heavy concentrations of coal dust with a negligible per centage of free silica, such as occurs among the coal trimmers on the docks, leads to a form of pneumoconiosis differing from the anthraco-sil- icosis of miners. There is a massive fibrosis of the lungs with nodular deposits of anthracotic pig ment scattered throughout. The principal symp- ^01j Si.?re due t marked secondary emphvsema and the cardiac changes produced by pulmonTiy c r S f S YSusceP TM y to tuberculosis is rraatthher lthhalnn nnod^ulatiio1Cnt,Urbuec1a3uosene ooff threeticluaclaktioonf opacity of the nodules. (Continued in the March, 1951 Issue.) - 8 - The material on this page was cop;ed from the collection of the National Library of Medicine by a third party and may be protectecffiy U.S. Copyright law. Castleman Asbestos File on TALC w/c = with cover letter or memo If DATE = 0, undated CD-ROM Document #: TALC for DATE = / .. - . r artjqle __leletteterr f.rforqmm mmeedical ,/ y u o L trade journal published presentation from conference -- published government report __ Fed Register notice __ government inspection results __ unpublished or internal report -- unpublished presentation from conference __ newspaper article letter memorandum __ industry warning labels __ industry sales literature __ industry recommended practices -- agenda ___ minutes ___ attendee list legal__deposition __ testimony of ________ __ medical records __ autopsy records