Document o92JMkorkzwkvn77L9w64vMK8

CM.iMl NCV. JI7 PU) E. I. du Pont oe Nemours S Company Wilmington. Delaware 19898 EMPLOYEE RELATIONS DEPARTMENT CC: Departmental Occupa Environmental Coo PSIRD Managers Plant Managers EQC Members EXHIBIT DUP-2130 June 25, 1980 COMPANY PHYSICIANS ASBESTOS-RELATED CHANGES The attached article by Sargent provides pertinent information regarding pleural plaques and the association with asbestos exposure and may be helpful to you. MEDICAL DIVISION BWK:ceb Bruce W. Karrh, M.D. Director DUP 0 9 3 7 3 6 9 SETTER THINOS TOR SETTER UVINO . . . TwROUOW ;' DU 038339 Pleural Plaques: A Signpost of Asbestos Dust Inhalation E. Nicholas Sargtnt. M.Q., Georg* Jacobson. M.O.. and Jay S. Gordonson. M.O. The general contamination of the urban at mosphere by asbestos dust has become a have been implicated, but the highest rate of association occurs with anthophyllite.* matter of public concern. Industrial exposure of In addition, other factors such as the site and workers to this dust is also widespread. The nature of the geologic deposit of the asbestos radiologist and other physicians should be fa may be Important. For example, in the miliar with the occupations in which asbestos chrysoiile mining areas of Quebec, tbe occur dust exposure occurs and should be aware that rence of pleural plaques in miners Is common in asbestos is used in more than 3000 commercial some mines, rare in others, and absent in one of items. The major cause for failure of public the largest mines not too distant from tbe health agencies to coatroi asbestosis is the long others." In nonoccupationaily exposed popula latent period (often 20 years or more) between tions, particularly in Finland, the prevalence of the beginning of work exposure and the ap pearance of overt disease. The disease now be pleural plaques relates to the proximity of resdenct to certain mining areas, and the air ing discovered was initiated by industrial ex is so polluted that even cattle are con posure during or before World War II. Before taminated.1"*11 Similarly, plaques have been the 1950s, few precautions were taken to observed in some agrieuitural'pcpuiadons" and protect workers from this noxious dust. Thus it in cattle" in areas in which the soil is contam follows that to prevent asbestos dust disease in inated with asbestiform materials, the year 2000 we must recognize its charac teristic radiographic appearance now and take PATHOGENESIS ANO PATHOLOGY .appropriate measures to reduce exposure To date, no totally satisfactory explanation wherever evidence of the disease is found. . has been developed to explain how the pleural t~Although asbestos dust inhalation is not thel reaction that results in plaques develops in I sole cause of pleural plaques, it is certainly thej response to the inhalation of asbestos fibers and / most common. The association between pleural particles. Asbestos bodies have rarely been plaques and occupational or nonoeeupational asbestos dust exposure has been amply con found in plaques," but asbestos fibers may be present. However, the lack of asbestos fibers in firmed by population studies-'TSteprevaienceof pleural changes seen on radiographs has been plaques mentioned by previous investigators has largely been due to inadequate techniques." 3y shown to increase in relation to the estimated means of recently developed techniques of dose of asbestos, the age of the patient, and the transmission electron microscopy, selective length of time after initial exposure to us- area electron diffraction, and microchemical bestos.**"*51*1' This is further confirmed by a analysis of particles, many small submicro- fairly strong correlation between pleural scopic asbestos fibers in pleural plaques have plaques found on postmortem studies11 and a been identified unequivocally by morphologic, history of previous exposure to commercial structural, and chemical studies."*11 It is of types of asbestos.1**1' All varieties of asbestos interest that these are more concentrated in the calcified rones than in the fibrous rones." As bestos fibers are also commonly observed in the lung tissues of patients with plaques.r*" E. MicMae Su|. M.Ou Frefasaar a/ Raiieletf. LaC'USC Mtdlad Couer, Lea Anjtia. Calif. Course lacetaee. M.Dj Frafaaaar #/ Railoiatf. LAC,USC SfaScat Cottar. La* Aayalaa. Calif Jay S. Cotdonaaa. M.Du Ataistamt Frafaaaar af Radlalagy. LAC'USC Hrdieal Cauar. Las Anytiaa. Cdlf Rtprint rtpuata thaaU So addrtstrd ta E. tOaMm Sarjnu. IAS.. Sex 477. Dtpartmant af Radielefy. LAC' USC Sftdiad Ctntar. 1200 N. State Strati. Lot Anttiaa. Calif 9C01J. S 1977 by Grunt A Stratton, Ike. ISSfd.'COJ7-l9IX. Inhaled fibers longer than those that can be phsgocytosed by histiocytes or giant cells move downward and outward in the lungs. This type of gravitational movement (so unusual in other pneumoconioses) is influenced by the coinci dence of three variables: the presence of thin, sharp asbestos fibers; the soft, easily punctured pulmonary structure; and tile constant motion of the lung." Stm/'nsr* tn Aoi/itf Vol. XII N4 4 (OctMfi 1 #77 217 DUP 0 9 3 7 3 7 0 DU 038340 attiiagrj r Baii-r-i fa a.. L l- Lfii&iiiii nw olio : Ffl i to eavi aior m. iss i ,c!e her: :s, t ion < loca peci be 3 si n t] ver lib. ant a3 ` Oil* ill ! tor i e pi dis invc * (if t vryir a is mr n rt td t erh: ire aris- ). 1 lical celli colli >ara. tact ith i ecu )t i jr e esot ara' sa he p Thu ibea l pie - a' Pleural Plaques: A Signpost of Asbestos Dust Inhalation E. Nicholas Serpent. M.D.. George Jacobson. M.O., and Jay S. Gordoncon. M.O. The general contamination of the urban at have been implicated, but the highest rate of mosphere by asbestos dust has become a association occurs with antbophyllite.1 matter of public concern. Industrial exposureof In addition, other factors such as the site and workers to this dust is also widespread. The nature of the geologic deposit of the asbestos radiologist and other physicians should be fa may be important. For example, in the miliar with the occupations in which asbestos chrysoiile mining areas of Quebec, tbe occur dust exposure occurs and should be aware that rence of pleural plaques in miners is common in asbestos is used in more than 3000 commercial some mines, rare in others, and absent in one of items. The major cause for failure of public the largest mines not too distant from the health agencies to cootrol asbestosis is the long others.1* In nonoccupationaily exposed popula latent period (often 20 years or more) between tions, particularly in Finland, the prevalence of the beginning of work exposure and the ap- pleural plaques relates to the proximity of pearance of overt disease The disease now be residence to certain mining areas, and the air ing discovered waj initiated by industrial ex is so polluted that even cattle are con posure during or before World War II. Before taminated.1 lfcu Similarly, plaques have been the I9$0s, few precautions were taken to observed in some agricultural populations'* and protect workers from this noxious dust. Thus it in cattle'* in areas in which the soil is contam follows that to prevent asbestos dust disease in inated with asbestiform materials. the year 2000 we must recognize its charac teristic radiographic appearance now and tike PATHOGENESIS ANO PATHOLOGY .appropriate measures to reduce exposure To date, no totally satisfactory explanation wherever evidence of the disease is found. ,__ has been developed to explain how the pleural f Although asbestos dust inhalation is not the reaction that results in plaques develops in f sole cause of pleural plaques, it is certainly th_, response to the inhalation of asbestos fibers and most common. The association between pleural particles. Asbestos bodies have rarely been "plaque* and occupational or nonoceupattonaJ asbestos dust exposure has been amply con- found in plaques.11 but asbestos fibers may be present. However, the lack of asbestos fibers in Srmed by population studies.1 The prevalence of pleural changes seen on radiographs has been shown to increase in relation to tbe estimated plaques mentioned by previous investigators has largely been due to inadequate techniques.1* By means of recently developed techniques of dose of asbestos, tbe age of the patient, and the transmission electron microscopy, selective length of time after initial exposure to us* area electron diffraction, and microchemical besto*.**"-lw* This is further confirmed by a analysis of particles, many small submicro- fairly strong correlation between pleural scopic asbestos fibers in~pleural plaques have plaques found on postmortem studies11 and a been identified unequivocally by morphologic, history of previous exposure to commercial structural, and chemical studies.'*-31 It is of types of asbestos.1151 All varieties of asbestos interest that these are more concentrated in the calcified zones than in the fibrous zones.11 As bestos fibers are also commonly observed in the lung tissues of patients with plaques.1-11 L KfeMaa Saf|M. M.Ou Profttior af Kadiatofj. LAC-USC Mrttral Cmmt. Lot Artfrla. Calif. Oerjs Jacabaaa, M.Ou Proftuor of Kadlolofj. HC-USC MoStd Cotur. Lot Atgtim. Calif. Jay S. GortSonsca. M.Du Aultmm Proftuor of Kodioiofy. LAC-USC MtdStd Ctnttr. Lot Atyda Cdif Rifrial rttattu tbotdd bo oddrntri la tCehoim Strfou. MS. lot 177, Otytrtmtot of Rodieloyy. LaC USC Mtdktl Conor. 1200 ft. Stott Strut. Lot Anuta. Cdif. non. S H77 by Grunt 4 Stratton, lot. ISSy.'0037-l94X Inhaled fibers longer than those chat can be phngocytosad by histiocytes or giant cells move downward and outward in the lungs. This type of gravitational movement (so unusual in other pneumoconioses) is influenced by the coinci dence of three variables: the presence of thin, sharp asbestos fibers; the soft, easily punctured pulmonary stricture; and the constant motion of the lung.11 m Vol. XU Nfl. 4 (Ocroocft. I *77 217 DUP 0 9 3 7 3 7 1 bV 03834l i fiKaiigjgl ^::l:i,. :aaaa. f A proposed theory of pathogenesis of pleural plaques is as follows: Fibers, particularly the long ones, lend to move toward the lung pe riphery, some leaving the lung and reaching the parietal pleura along the chest wall, diaphragm, and pericardium. Most of the emergent as bestos fibers pass through the soft tissue of the intercostal muscles and muscular portion of the diaphragm. Others are blockaded by the hard tissue of the ribs, the dense fibrous tissue of the tendinous portion of the diaphragm, or the peri cardium. The localization of pleural plaques at these sites, especially posteriorly and laterally, is also said to be enhanced by the recumbent position during sleep./Tbe plaques are almost exclusively on the parietal pleura and are practically never encountered in the apices of the lung, below the 1 Itb rib, in the region of the' costophrenie angles, or anteriorly near the costal cartfiagesTlThus the plaques result from mechanical or other reaction to the asbestos fi bers. Individual sensitivity is probably also aa important factor in their formation. Grossly, the pleural plaque is characterized .by byalinized discrete elevated gray-white or ( pearly areas involving the parietal pleura (Fig. 1). Despite varying sizes and shapes, the pattern of the plaques is repetitive. There is a flat or slightly uneven surface, with steep edges rising abruptly from the surrounding normal pleura, and here and there rounded mounds, with * somewhat overhanging edges.1* The thick pleu ral plaques are typical in appearance, and the classic comparison is to frosting or sugar icing (Zuckerfvts), as is seen on serous mem branes.1* Microscopically the plaques consist mainly of avascular, acellular, hyalinized, laminated, in termingling collagenous fibers, usually with an orientation parallel to the surface. Elastic slant ing shows intact lamellae beneath the plaque, in continuity with the surrounding normal parietal pleural connective tissue. The pleural plaque is, in fact, not a pleural plaque at all. but subpleural or extrapleural. Early in its forma tion, the mesotheiiai eeQ lining of the normal parietal pleura takes no pan in the process, but merely acts as a passive .covering,U-M The growth of the plaque is slow and is of nonexud ative type. Thus adhesions between the visceral and parietal pleurae are virtually absent. Plaque SAflGWT. JACOtSOH. ANO COnoONSON rf 1. Pwgunvftim gpcfmn wttft* hyinnLv4 pl*u *1 th MriraJ pwri, $m*4 pftquaft rtm ainwra f #> wHh t yipv rib*. Larfr n4vt ana tf>* inttrsMon vr tf io*r rib* p*rt*rirtr. n<m4 pt*r* t* pswnl hirwwt viH w4>marfriit4 b*rdn / tfu plgqwib formation on the visceral pleura is rare and then only minimaL Caleium deposition is present microscopically m a high proportion of plaques. It is ofthe dys trophic type, appearing as granules along the course of the acellular and degenerated collagen fibers and ceasing abruptly where the abnormal connective tissue ebanges into normal pleural tissue. RAOIOGRAPHIC ASPECTS The radiographic changes in the pleura following asbestos inhalation result from two types of parietal pleural reaction. Mott frequent is the localized, limited, plateaulike smooth or nodular area of pleural thickening that corresponds to the pathologically observed pleural plaque. Much less eommoniys a non specific extensive difftise pleural thickening may be found. DUP 0 9 3 7 3 7 ? DU 038342 n.rJAU PLAQUCS -gaaaat: "Awf-itiiriiiifrli iiiiiBi jg^^Bfggyggg^ 11) DUI> 0 9 3 7 3 7 3 Rf, 2. A**ranc4 Itiff tl ^awtl Uqu tomctfwi muin| intMiral wiifc Hta tM Wir margta (**) nk. wfcr Vi e(*qus r Man in mem* tturoo?fi i Mftpvia. Tormf *1 * nwfifia auftOTffirfy m4 inlartertv it nritant. parqeultrtf n * rifta. Imb0m4 wdMr<0M4 piaqut* altar via aamaar f via IWt herfMtftephrtfm tfttf la a laasar aaant rifht (wMtt arraw haadai. Nonealeifitd Pleural Plaques Noncalcified hyalingcd pleural pi aqua are not visualized radiographically until the fibrous tissue is sufficiently thick: thus they often go un detected, sad their prevalence during life is underestimated. Only t small percentage of early plaques identified at postmortem exami nation bare been detected on routine Pa ra diographs,' In this projection a well-developed pleural plaque results in either a profile presentation or in n face presentation. The plaque in profile appears as a sharply marginated white band of water density, roughly paralleling the inner margin of the lateral thoracic wail, it is usually not obscured by che overlying scapular shadow (Fig. 2). The very early plaque will show only a thin white line of increased density adjacent to the rib that has been likened to a flange.1 Thus the profile line of early plaque formation is easily overlooked and often detected only in retro spect (Fig. particularly when it resembles the normal inner rib surface. As it enlarges, it becomes somewhat oval and moderately protuberant, with tapering superior and inferior margins typical of an extrapleural lesion (Fig. 4). A plaque rarely extends vertically more than DU 038343 S^CtKT. J^COMOM. AKO OOAOOKSOH l ISO V \ *t. ; - * X Minim*! p!*vr4 piaqtj# (smill *rrwrL liw **Hy oJedfcrUp* in cfc rgon of right di**hr*g plwr (Urg* */rowrk * *. O'*1[!>* o'TM-**. ( ln. Not. * DUP 0 9 3 7 3 7 4 ( r+. JA DU 038344 utiMlaU;; t .stiiaiii PLV*AL PLAQUES 251 DUP 0 9 5 7 3 7 5 ( F"!f.. I. hntm f (> AHiiffMM ^mral l4w {MaA imml, Mwi< ftrtaricHU4l m ftCM, (A) FA Aim. Th* fu *<* iMdfln iIm Aif <(< t#r r *>* A fw tmil 0tqv r >**t (a pro*** Mm <*). vw. T>i * /a Kt r|--irt p*atridf * * n^ftt *t*4 tntOMMiy * *> (aft (moil. IC1 Lift ibtitwi '. Thi *** ( *<#*, TJ# DU 038345 292 four interspaces.The thickness of the plaques varies from I mm to more than 10 mm. but it is usually in the range of 1-5 mm. Plaques are usually bilateril and often symmetric. Most commonly they lie adjacent to the 5th, 6th, 7th7~ and 8th ribs and interspaces.** As stated earlier, involvement of the apices or costophrenie angles is extremely rare. Early, the plaque may be solitary, but later several dis tinct nonconfluent plaques are often found. Less than 25% of patients with plaques have evidence of accompanying interstitial lung disease.1* Diffuse pleural thickening is infrequent and is characterized by uniform homogeneous density, by a lack of nodularity of contour, and particu larly by accompanying costophrenie angle obliteration. Pleural effusion is quite rare. Plaques in profile are found less commonly on the diaphragm and rarely on the pericardial sur face, where they appear as one or more lo calized elevations on the normal convex surface of these structures. These are usually accom panied by additional plaques along the lateral thoracic wall: they are seldom isolated lesions. On the diaphragm they are found at some distance from the angles, i.e., dose to the central tendon. When uncalcifiod, they must be differentiated from normal (scalloping) or ab normal variations in diaphragmatic contour (Figs. 2 and 7). The second type of radiographic presentation, the en face projection, is that of a faint, ill-de fined veillike opacity or shadow.1 These also oc cur most commonly in the region of the 5th to 8th ribs (Fig. 5A-C). They are rarely detected when in the medial half of a thorax, but they arc often obvious when they overlie the lateral aspect, where they are more oblique to the xray beam and hence absorb more radiation. The en fact plaque rarely appears uniformly rounded; it shows a peripheral irregularity of contour that has been likened to the fringe of a map or hoDy leaf. Because of the faintness in outline, it is often dismissed as an artifact on a single radiograph; persistence on repeat exami nation will prevent this error. Because it is flat, it is less raiflopaque than an mtrapulmonary nodule of the same diameter. Careful observa tion shows that the en/aee shadow is often less dense centrally, unlike the more uniform homo geneous density of the round or oval in* trapulmonary nodule. When multiple, the indi S*.*GEKT, JAC09S0H. 1H0 GOKOONSON vidual en face plaques are often separated by a band of normal radioluccnt lung. The use of oblique views is strongly recom* mended, not only for confirmation oI suspects! pleural plaque formation but also for detection of additional plaques or pleural thiclcemn? unsuspected in the l*A projection (Tig. SA-Cl With these views, the en face plaque will often present a profile appearance. The use of fluo roscopy and spot filming to determine the proper obliquity for demonstrating a plaque in profile is of great value. Oblique views have confirmed the fact that plaques spare the apices and the costophrenie angles and are most frequently found along the posterior reflection of the costal pleura. They may extend laieralty and anteriorly as far as the costal cartilage junction, but they rarely overlie the rib cartilages. Pneumothorax has confirmed the parietal location of a plaque and has demonstrated the absence of adhesions between the vijeeral and parietal pleura. Adhesions, if present, do not occur in areas of plaque forma tion. Tomography is of little assistance in demonstrating noncalcified plaques, as the com posite shadows of adjacent ribs tend to blur out the ill-defined shadows of the plaques. Com puterized axial tomography has demonstrated the plaques.11 Ultrasonic examination baa been offered as a more sensitive modality for detec tion of pleural plaques. It has been suggested that plaques less than 2-3 mm thick, wbich are missed by radiographie examination, can be de tected by ultrasound." Plaques versus normal anatomic shadow. The combined thickness of the tissue] compris ing the visceral and parietal pleural layers that surround the normal lung is not ordinarily measurable on the radiograph. The normal pleural tissue consists of a single layer of mesothelial cells covering the surface of a small amount of Sbroareoiar tissue measuring 10-S0ps in thickness. On the routine PA projection a vertical line of water density may be seen, sometimes paralleling the medial surface of the first three or four ribs along the lateral thoracic wall. This vertical line has variously been called the companion shadow, the pleural shadow, the pleural line, the pleural margin, and the pleural stripe. It is contributed to by a combination of muscles (subcostal and intercostal), the areolar tissue of the endothoracic fascia, and, to a 0937376 a DU 038346 rt-EUAAt. ruAQuts greater or lesser extent, deposition of fat. The sharp medial margin of the shadow is best seen when the x-ray beam in tangential to the surface of the tissu e causing this shadow. This normal pleural shadow Increases in width as it is traced superiorly toward the first rib; it usually taper* rapidly inferiorly, becoming imperceptible below the level of the 4th intercostal space. In the PA projection the thickness of the shadow is never greater than 5 mm; however, in the oblique projection this normal pleural shadow is wider, varying from 0 to 10 mm in the men and somewhat less in women." Occasionally, a very thin, barely perceptible line may be seen medial to the lower half of che lateral thoracic wall; I mm has arbitrarily been designated as the maximum acceptable thickness of this normal pleural shadow below the level of the 4th inter costal interspace. The costal slips of origin of the serratus an terior and external abdominal oblique muscles have a characteristic radiographic pattern: a rhythmic sequence of shadows betweea suc cessive intercostal spaces (Fig. They art most commonly visible over the 3th rib. but tbt 7th rib is also affected, and occasionally all of the ribs from the 5th to the 9th are involved. They appear as one or two distinct triangular shadows or a combination of two opacities su perimposed. They should not be mistaken for multifocal plaques, which may also show a series of shadows. Multiple plaques are more likely to differ from each other in size and shape, unlike muscle shadows, which are usually more uniform in size. The muscle shadow usually has one sharply defined border and elsewhere fades into the surrounding soft tissues. A slightly oblique projection will often resolve this difficult problem. A plaque that is well defined in profile becomes 31 defined when rotated to an en fact position. Additional plaques are often seen on the rotated film. Plaques may become more distinct as rotation moves the overlying muscle shadows, whereas musels shadows will alter their shape or disap pear. Pleural thickening should not be confused with extrapleural deposits of fat. The oblique view is again helpful, the fat producing a wavy margin most prominent on the posterolateral surface of the ribs, usually sparing the anterior and paravertebral areas." Tomography may be i W*mg| earal sOpa grffwt Mmrui airrtrw ***** tMsminsl mMUiu* rmisdva tv*m arm ttUtaraf irffiffiiani nmt m -vrm p(urai Th* Th tftjrp miffing fgtfg infmr^rty. od(>u v*ww helpful in revealing fat density in contrast to the water density of pleural thickening. Calcified Pleurd Plaques Pleural calcification usually occurs 20 years or more following exposure to asbestos, l he in cidence increases with the tune interval." The exposure to asbestos does not have to be prolonged; it can be on the order of only a few weeks or months, depending on the concentra tion of the dust. However, calcification in pleural plaques is a relatively uncommon ra diographic finding. It is much more common histologically, occurring in approximately 37% of plaques." Radiographically demonstrable evidence of interstitial pulmonary oisease has been reported in only one-third of patients with pleural olaoue calcification, but conversely more than 50% of patients with extensive DUP 0 9 3 7 3 7 / DU 038347 2 SAACcVT. JACOtSON. ANO SOAOOnSON pulmonary 6brosis eventually end up with pleural calcifications.** A* i rule, cilcjaed plaques ire more obvious and more striking thin uncalcified plaques on the roentgenogram. When the x-ray beam strikes a plaque margin ungemiaily, the calci fication in the plaqu' :s seen as a dense white line, usually somew,._, discontinuous, parallel ing the chest wall, diaphragm, or cardiac border. Since the calcium is deposited near the center of the typical subpleural hyalinized plaque, it is separated from the inner surface of the rib by a line of water density produced by the surrounding pleural thickening. The calcifi cations are often small and (especially in films of low contrast) easily overlooked unless sys tematically sought after (Figs. 3 and 7). They are rare in the upper zones. If the x-ray beam strikes the surface of a calcified plaque.e/i/are. it presents an irregular and unevenly dense pattern, again often likened to the fringe of a holly leaf or map. Oblique views are extremely helpful in delecting calcifi cations that may be unsuspected in the PA pro jection, in confirming tn fact calcifications by bringing them into profile, in localizing calcifica tions in the region of the diaphragmatic pleura or the pericardium, and in excluding costal cartdige calcification (Fig. t). When calcified plaques are small or when they are superimposed on the relative denser ribs or diaphragm, but particularly when the film is underexposed or poorly processed, they are often overlooked. They are well seen on grid films. Unlike the uncalcified plaque, the calci fied plaque may be better outlined and better lo calized by tomography. Pneumothorax has demonstrated that the calcified plaque is in the parietal pleura and is not associated with vis ceral pleural involvement. The location of these plaques in the parietal pleura can also be con firmed during life by fiuoroseopy or cinera* . diography, which reveals that on respiration the lung moves independently of the plaque and the plaque moves synchronously with the chest wall.* ff9* 7. ! wial w4 dUtowtfmttfc btoural pi#qv (mwii C*<t4m4*. bfirwlnf i 1975. to wo* m<*Ju4 to 1971, Th ry uriy pUqo tornutai to 1997 wt nri>iiito m4 fet**4 rtwf<eto<<v. Qlttoftfiw#to> (Hvurto piaqua* fattoy Hour wiMut 44ttM0ia< ***# to* 9i rifc^ DIFFERENTIAL DIAGNOSIS The rare basilar pleural effusion of asbestosis resolves slowly and may leave signs of residual diffuse pleural thickening, particularly in the costophrenic angles. Pleural plaques may also DUP 0 9 3 7 3 7 8 DU 038348 fiaiiim. rmauo ft. i fcjSsrassM , -. -> i- . V.n_SS . '... '' >r&ffieSs r Wf. t CMIN pfwaral Itomii (A) *A fttrti III /* s^atfcaonrn rifbB Samt In **! in mWU**Al iw4*m4mn # pitnni m riflit w4 in piair<kf#n an left (fMnvM wr-rwflri; ftnanr uitlfluNM in vnM pvtfln in !ft 4Upftr*tmatfn pUwra. (I! Lnft *Mnwn BIm. A tV#*r piautnl e^afluiM t !#* In prartJ* in # *<*< mnwit at tfct r|M h#ni4inrnm (irmri Tha an i'ie piinvan l (A) nnw ppnr In pm<tf rtni ibtaar aaterffetoona Ivnw tfic*nt amarinr riPau 5 y*"v.y-/ * / ? 6^ * 6 o DV 038349 2)1 SAJJGENT. JACOBSON. ANO GOSOONSON be associated with bilateral obliteration of the costophrenic angles, but only uncommonly. Pleural thickening secondary to hemorrhage or infection usually involves the visceral pleura as well, particularly extending into the costo phrenic angles. Calcification of the pleura secondary to hem orrhage or infection is usually unilateral and often extensive and sheeilikc. Fluoroscopy of the chest or cineradiography may be of value in demonstrating chat the calcification is not con fined to the parietal pleura. The calcification does not move synchronously with the chest wall as does a calcified pleural plaque. Pneumothorax will show adhesions between the visceral and parietal pleurae along the area of calcification. Localized pleural thickening and callus. Simu latint asbestotic plaques, may occur from rib* fracture. These are generally unilateral, and the overlying rib deformity is helpful in differential diarnosis. Other rare causes ol plaquelike pleural calcifications include radiation, scleroderma.17 and chronic mineral oil aspira tion.* It should also be noted that residual barium in the peritoneal cavity from a ruptured viscus in the past can simulate diaphragmatic pleural calcification. Calcified or metallic pleural plaques occur in other pncumaconioiea. including those caused bv trcmolitc talc, mica, 3 ik elite, calcimine, tin, and barite.* Even more rarely, inhalation of silica and coal dust ha* been mentioned. However, more likely an un known exposure to asbestos dust is responsible, not necessarily in the mines but in other occupa tions associated with the mining process. Discrete, localized aoncalcioed pleural thickening in the pleura may occur with lo calized mesothelioma, metastatic disease, lym phoma, or myeloma. These are usually uni lateral and may mimic pleural plaques. Conversely, pleural thickening due to asbestosis may simulate multiple pulmonary nodules or even healing rib fractures. Differentiation between multiple nodular pleural plaques and pulmonary neoplasia can be made with oblique views, which confirm the pleural location of the plaques." Bilateral pleural plaques are signposts Indi- I eating pleural asbestosis. They will be detected I with greater frequency if1 p* a3rticularly looked for , on the radiograph. They should be considered to [ be caused By asbestos dust inhalation until 1 proven otherwise, and a careful lifetimeoccupa- tional history must be obtained. Epidemiologic studies have amply confirmed the association between asbestos dust exposure and bronchial carcinoma, and the risk is even greater if there is a history of heavy smoking. A recent study showed that bronchial carcinoma was 2.H times more frequent in men with pleural plaques.' In addition to its association with lung cancer, there is increasing evidence of an association between asbestos dust exposure and cancer of the larynx and cancer of the gas trointestinal tract. Furthermore, there is in increased incidence of primary malignant meso thelioma of the pleura, pericardium, and peritoneum. Since the occurrence of malig nancy is usually on the order of 24-32 years after the initial exposure to asbestos, any patient with bilateral pleural plaques should have lifetime surveillance. REFERENCES I. Aatai HC: Multiple pieuril plaques. Part IL Br J ti* dial 41J41-MB, IMS Z. Beeklakt Ml: Asbenes-rdated Aoia of the lung and ether ergtMt'lheir tpMceiolep sed implieaiioes far clinical practiatL Am Bar Basplr Dii 114:117.227,197* }. Edge JR Artem rdlled king diuiu in i British ship fcaMeg papebtite with particular regard te the iaddace at branchial eardnwaa ia act with plural plage*. A mortaficy iredy. Am Bee Bespir Die 113:211. 1977 (burial) 4. Fdaon B: Chad Boeatgcnelegy, Philadelphia. Wg Sauadcn. 197J. pp 49-493 3. Fletcher DE, Edge JRj The early radiological ehanga ia pulaioeary ead pleural asbestosis. Clia Radial 21JJJ-J4J, 1970 6. Harries FG, MeeKcnse FA. Sheen G. et alt Radio logical surrey of men expeted te ubestet in navel dockyardi. Br l led Med 2IJ74.Z79.1971 7. Hourihaae DO. Lcsaof L. Richardson PC; Hysliac and calcified pleural plaques a* ia index la ccposure la jibes as. A study of rsdielogical sad pathologies! features of IOO cases with a cansidcrauoo of epidemiology. Br Med J 1:1049-1074.I9M I. Jaacs JSP. Sheen 0: neural plaques. Biological effects of isbeetss. ia Bogeetki. F. GBsoe JC Timbrel! V. es al (edak Biological Effects of Asbestos. Proceedings of s Woikiag Conference. International Agency for Research oa Cancer (1972V Lyot. France. IARC Sdemillc PuHicauoa I.I97I.PP 24J-24I 9. 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