Document mq38LjZ3vwvMXnxzGvL6Z7wDd

PLAINTIFF'S EXHIBIT DOW-269 Portonao. v*. J. 04*6), 42. 413. PATHOLOGICAL K- a Y/z ~ ( Ia<,\ CIS OF ASBESTOSIS C/T --t o o 0.0'B. Hocnihaw. M.D.. M.C.Path., D.C.PX ScM of WmMUUD recognition of nheuoth dam from the vkofk of Merewrther and Price in 1930. They imcstipaied 343 asbestos workers and concluded that there was a pneumoconiosis resulting from ashc*ios inhalation, that this condition siiortcncd bfc. and that measures to diminish the atmospheric cimcvntraiion of asbestos dust mould reduce the incidence of the disease. In 1911 asbestos* was accepted as a compcnsalable disease in Great Bnum and steps were taken to reduce the risk in .the aslvsios industry. IN years later Wyers <I949| Astral *liat the aer at death m this disorder had increased and that tingcr-clubhing had become more common. I Ic suggested that these changes were due to a more chronic form of the disease resulting from imprmed dust ctmirul m the industry following the legislation of 1931. Currently homeser. the number of new cases of asbestosts in Great Britain is incirmn*. ihor frequency suegesting an incidence rate of at least foe per thousand of those occupation. Jly exposed iMcVune. I945. Though earlier reports indicated that tuberculosis was common in asbestosts I Wyers, 1949; Gkiyne. 1951; Drawer, FouMs and Swsin. |9$M it aptwars to be a rare complication at the present time (Buchanan. 194$). Within the past few years it has become increav ndy apparent that exposure to asbestos is aswviated with a further hazard. This is the dexetnpment of malignant disease in the lung and serosal mem branes and possiNy the gastrointestinal tract. These nenptestie complications base gisen rise to much concern in new of the widespread use of asbestos #<s industry, its almost uhwiuitous distniMion m the iikdan urban community and the fan that current information does not permit the defimtion of safe levels of exposure. Paihotog*c*J studies have made an important crattnNition to knowledge of the etfects of asbestos espowre and are reviewed in this paper. Fwlttlau f AdoMdt The main pathological characteristics of ashestosis have been described m a senes of papers by Gkoyne `Wood and Gloyne. 1930; Gloyne. 1932 1J; Wood and Gloyne. 19)4; Gloyne. 1931). Our own espencncc it baaed upon pathological matcnal from CPJ. _ w. T. E. McCauonkt, M.D.. CtUtgr, DM* y ... . fw#, * W. & ro o Fa I--Cut surface of lung showing modcraltty wwne rthrovrx. Confluence of hbrotc (m m lower right has gw* rite io an arcs of ineorvdtaal flbrmn. 4 cases who had been found to base dinieai ashesious m the London Hospital. Details of each patient are accessible (Itounhanc. 1945aL The lung from an uncomplicated fully-developed case of ashestosis is typically small and firm with a dry cut surface. A Ane nodular librosis can oflcn be appreciated (l:ig. I k usually most vexere in the lower pans of the lung and suhpituraUy where the tibmnc noduloa may become confluent. l-ess frequently oHd arm of Abraau titty develop tn other pans of the tunc (Gough, IMS). Cystic changes may be found in the air spaces batworn flbrotic areas pvmg rise to sorfelkd "honeycomb lung.** hut this is rarely extensive. Bronchiectasis may also occur, and right ventricular cardiac hypertrophy is a common finding at nacrapay. DOU 06032 14 FOS1CRADL'Al I. MEDICAL JOURNAL Oftohrr S T 0 0 I1821 fI Vi 1' *4 * ,1 Ir r - * t. - * ,' .. "' >[. ,, V~--* ',*1 : v:-. * .; *.. fV * *. Fui. 2-- PeribciwhWar fibrosis estcndinf into slscot* from a caw of ashcsuwts. II. A E. * 120. Fio. J--A central damp of intraeeftolBr h pertly surrounded by Mmm "" M. At x 4M, *v* _ f .S'* 'rV e^.-sr- * *7 NW . `'v'.J.sV *t #;,f| . )J.I,* ,0 x,< -vV ,^ > * . / # :V4*V/ . * v " ; .> f y * * '**** "'V' > '7 f* -< i. Tj 4 Ir. ';\V.r'^.vF y/' < 4/* r***. * i 1 Fio. 4--?<tero<ic sestet in shewotic lung. Asbestos bodin arc indistinct below and 10 the left, and haenwiosyphitic collagen is present in metal pens of the Arid. II. A E. > 200. J>fe.M. I J* a-jT4,' Flo. 5--Dark granulet in the wall of a wnal 1 H. A E. x 20Q. Hhtoloficafly. the bos< lesion is a peribronchiolar fibrosis which obliterates surrounding alveoli a< it eatends outwards from the bronchirle trig. 2). In wno of aolid ftbroth laminated collagen replacet the entire parenchyma I Fig. J). Alveolar cell hyperplasia may be prominent in rones of tevere ftbroth, and the vessels in tuch area* are frequently adcrotie (I ig. 4). The fibrout tissue within asbcstotic lungt may how an unusual hnematosypii'ia (I'igs. .1 and 4), end dark granulet may eurround the luntina of mall blued vessels in fibmtie treat (Tig. 5). Thit materiat doet not ttain at DNA nr calcium, but it reaert weakly for iron, and yitet infente rcacliont for neutral and acid mucopuly^accli-iridct. Atbettot fihret and bodict are generally pretent in large numhert and the bodict are readily detectable i vwfinnt frig. J). They may wur tingly or In dumpa and may bt associated with a 1--wo phage or giancft rtoction, ctpcciaRy when thm hat been recent taposutt to asbestos. They may lie fV*e In the air tpnees or may be buried in and partly obteurad by tear thsue. Asbestos fibres are usually numerous In cnees of lucent (6 12 months) exposure but are difficult to tea without special tachniqgev Tha hmgs often contain much carbon, and short asbestos fibres appear to be especially numerous within carbon aggregates, being made visible by Incineration which drives off the obwuring carbon (llourihane, 106$ bh The impression has been gained that long ftbres (>20|i) become converted into asbestos bodies and tend to remain in the vicinity of the bronchiole, whereat short fibres (S 20p) are transported In local lympUud agga** gates where they remain at fibres, largely masked from view by carbon pigment. DOUI 06033 pcl.j*rr 19fA HOL RIMAM tsn McCAUGHEY: httkMgf of Athete*it | S T 0 0 I1822 j'liV:T'T r-S * I' ll i: Mji! ;i|t,|;iii( I *.. h Typical hyaline plaque on diaphragmatic pleura. The tmall projccth*nt at l*cr kfi and the trmtnh cartilagmout appearance at uprer right are both common feature*. 7 Cl| 9i i.o i;i Flu. 7--CToie-up tin* of a vnal! plaque of parietal . pleura. The combination of "knobbly" pro jecturn and wooexh turface* it apm cV*r1> tllOMfl. Ia Radiograph i f tpcvmten lumn in l ie. h tlnntt dittnbution of caktiiin within the plaque. Mrttrat Changrt The pleura m a cate of atNftnitit it nearly alwayt abnormal. Terminally, a primary dilTutc pleural neoplatnt may dctclop. Itee below > or rarely, (here may be difTute fthrotit of both 1a>ert obliterating the pleural cavity but without hittological evidence of neoplatia. However, hyalin- plaquet arc the com* monett pleural Wtiont found, and were noted by one of into. O'B. H.) in all of 16 caret m which they were apcrtAcelty toupht. Hyaline pleural plaquet occur at tliphtN elevated, firm, glistening treat of thiclenjng. preferentially affecting tlic parietal pleura in itt lower halve*. trig* . 6 and 7). Plaquet vary from 10 cm to I cm in diameter, and are generally of alnunt cattriapnou* consistency. focal calcification may occur wtth*n the laminated, hyaline, acellular collagen of which they are composed. (fig. Si and tuch calcification may be visible radiological!). il?". of pljqiu* detected at nccropty had Nxn teen in radiograph* during life). . The** plaquet anr not neoplastic and may tepeeeiit reactive fihrotit to`contained aKttot fihrc (Hourihane, l.rttnf and Richard*ori. l*ve.i Ucmu.il tcaiom occur in the abtcnce of asKttosit althou^'i evidence of athctiot evptttunr can generally tv found, and experience suggests that their incidence in a population prohibit reflects the extent to hicb a commimity It exposed to aslvsto* tkoiluoto I960; llounhane and otherv IlNhi, D0UJ 06034 * 6U POSTGRADUATE MEDICAL JOURNAL S T 0 0 I1823 th.. 9-AvhcMm K>J> in fluid v|-.*c/ed from lung vurfxT. Ihn Mrwlim ho Hie cla'dcal segmentation of its shaft. and (hr bulbous terminations. Unstained 1000. The /4t\'srm /Mr The asbestos body was first accurately described by MacDonald <1927) who also demonstrated its iron content. Citoync (1932) studied the nature of the bodies and concluded that they were composed of an cn\ elope of iron and protein surrounding a central asKrstos fibre, and that their presence in King merely indicated a previous esposurv to asbestos and did not necessarily mean that the disease asbcsto*is uas present. Simson and Strachan 09)1) had already shown that 90*; of asbestos workers had such bodies in sputum and that they might be present after as little as 4 months employment. Asbestos bodies typically are elongated structures of yellowish-bro*n or golden.yetiow colour which gist a posifivr tor* reaction for iron. They may hast a smooth outline, but commonly show tegmentation and bulbous estremeties (Fig. 9). As illustrated by Gloyne (1932) many different shapes may be found. Their resistance to acid (Gloyne. 1932) and heat (Hourihane, I965h) suggest an inorganic composition. The fibres lose their intrinsic bircfrigence when cotted, but the presence of a central asbestos fibre can be readily seen using phase-contrast microscopy (Fig. 10). The absence of a visible fibre within some bodies suggests that the fibre silicate may be utilised in the formation of the body envelope, perhaps to form iron silicate. Gardner and Cummings (1931) after producing structures similar to asbestos bodies !m tltro postulated that the coating of the fibre contained silicate. Davrs (1964a) has studied the formation of asbestos bodies in guinea pip. Using electron microscopy bodies were seen tn begin as an aggre* gation of dark granules (possibly ferritin) around phagneytosed fibres, while a formed body showed simitar granules ocmuonntly alternating with pale layers (possibly protein). The whole was occasion ally enclosed by an outer membrane (possibly coftagen or fibrous ferritin). Human asbestos bodies re similar (Davis, 1964 bJL Asbestos bodies usually represent only a fraction of the total asbestos in a lung, and there is experi mental evidenoe to support the concept that fibres and not bodies are the fibrogcnic agent (Gardner and Cummings, 1931; Gardner, 1942; Voruatd. Durtaa and Pratt, 1991). However, the suggestion of Knox tod beanie (1954 b) that bodies may fragment within lung and that the resulting small particles may be the fibro- genie agent should be borne in mind. It is possible that the type of segmentation shown in Fig. 9 might be the initial stags In fragmentation, and ft is cer tainly the ease that dny pantekt derived IVonr asbestos bodies would be indistinguishable (bom hecmosidcrin with light microscopy and that haemotidcrin-Uke granules arc common within Imra-eKeolar macrophages and in sew tissue in asbestoslk In easts of substantial or heavy asbestos exposure, typical bodies may be present within hilar lymph nodes In addition to thorn in the lung. A case has dqwi www in imcboi Doy w iwww in the spleen (Stewart, Bueher and Coleman. 1931), and probable asbestos fibres have been found within pleural and peritoneal mesotheliomas (Hourihane. 1965 bh Their appearance in the (alter site could be due to penetration of gut by swallowed fibres in sputum, as ll has been shown that such penetration may occur In ran (Westlake, Spjut end Smith, 1965). The specificity of the asbestos body has been questioned but most reports of confusion with other particulate matter may be readily dh*iel. Rouleaux of erythrocytes and graphite particles DoUJ 06035 HOLKIIIAM. ami MrCAL'GIII.Y: Path>d,,g} of AihrUom S T 0 0 I1824 . ; .-o , F*.. 11 - Thick vquat bkxlicx in (be lung of cof laic pncumoconimn. The re^mNance it ahe>(m bodws it do'c. but is kidenable a* a resemb lance. Ocn%Mi*ult>. structures indistingviishable from clasMcal asbestos bodies may be found in the tunes of a talc worker. H. A F. < 400. should, never lead to error with an experienced m*cTseoptM. However. similar (Tig. II) or even identical bodies may be seen in the lungs of talc workers, but in such cases, examination with crossed Nieotv will usually demonstrate large numbers of talc fragments (I ig. 12k far greater in number and of different sltapc from tlie fibres found in asbestos workers. With this possible exception, asbestos bodies would appear to be specific for asbestos esposure. Much less reliance can he placed upon the recognition of asbestos fibres by traditional light microscopy, although X-ray diffraction and possibly electron microscopy permit accurate identification. Ineldener of /lArtfet Rodin In Population Sanrjrs Necropsy studies of the prevalence of asbestos bodies in the lungs of urhen dwellers have shown that they may occur with remarkable frequency. Thomson, Kaschula and McDonald (1963) reported that about one quarter of the adult necropsy population in Cape Town showed asbestos bodies in lung fluid, and similar results base been obtained from surveys Hi Miami, Florida (Thomson. 1965k Pittsburgh. Rmnsylvania (Cauna, Totten and Gross, 1965) and Hi London, (tlourifune. 1965 a). In the majority of cases, fibrosis is absent, and ashestosis is therefore not present (3 out of 137 cases showed ashestosis in the London series.) The bodies may be found in fluid tqihv/ed from the cut-surface of the lungs or in routine histological preparations. The yield of eases with asbestos bodies rises when unstaineil. histological sections of 20 - JO |i thickness are substituted for the routine, stained sections of 5 m thickness 127", of 127 eases showed brxfics In 50 |i unstained preparations Fm. 12- Same field as previews Pig. The enormous number of bi icfrijtm plates of talc arc dearly shown. It. A f. * 4*8. Crossed Steals. compared with IT; of 100 case* in trained 9 p preparations Hi the London Hospital Series. It has been stated (Thomson and others, 1963) that the lung bases contain the largest number of asbestos bodies and Abrek This finding would terse to explain why fibrosis mot* acsert Hi this area in cases of asbestotis, and the particular tendency for lung cancer to occur in the lower lobes in this disease. The most widely used type of asbestos it chrysolite and there it experimental evidence that it may disappear from lung and subcutaneous tissue (Gardner, 1942: Wagner and Skidmore. 1965k It is therefore possible that surveys of hmg tissue (or asbestos may underestimate the incidence of ex posure to this type of dust. Widespread asbestos contamination of urbane communities mey be reflected in high incidence of- hyaline pleural plaques Hi the same population; four and eleven per cent of the consecutive necropey subjects showing such plaques Ht 2 separate aeries In London (Hourihane and others. 1966k ft is likely that radiological surveys to assess the incidence ' of plaques would he tneflil adjunct to post-morsent studies, ht epidemiological investigations of aibeesoi^ esposure. >- Most reports tinting with tag ameer and asbestos exposure have been concerned with the incidence of cancer at necropsy Hi wbjects with severe (compcnsataNe) ashestosis. In such cases the incidence of lung cancer has ranged between 13 and 17.3 per cent (Mcrewether. 1955: Wyen. 1949; Oloyne. 1951; Bonser and othera. 1955k Dolt 11955) found the incidence of lung comer in persons with tangomtinued heavy exposure to asbestos to he in the region rf ten times the expected rate, ttuctanan (1965) has'observed (hat currently over 50 (kr cent of mates dying with asbestosH in the United DOW 06036 S T 0 0 I1825 41* Caw V. lit l* 127 >:* n 1)2 142 145 155 t Caw No. IIS 114 124 12* 1)0 1)7 l 141 149 150 151 114542 154 IS* 14) 125 FOSTGRAfH'ATi: MEDICAL JOURNAL TAMXIV C*<n oe Lurwf* Aaurrwa FiHuithinMn Set Aft ClftfDay Hhlniitfiril Type F 43 Adam F 4) F 44 F 70 F sa F 50 F 4) Fn F 54 F 44 Mem age t rtm cam 54.4 yean. 7 of 9 tumour* iraw in fewer lows f77.7%) 4 of I tumour* aro*r * ngfe tunc 4444%) Of a tout 74 nmwi In Mi mn 45J% wiflaMf within kmn Mn (compart tdi 244% of M4 cam pmetwed by Bryvon and Spensar (I93IIL r> TABLE 2 Cano* or Li**o h Aa Mau Patout* 'A VC* . Sex A*e Cto/Day HMogicBl Typo M 44 M 54 M 40 M 47 M 44 M 4) M 4) M 5) M 55 M 71 M 49 M 57 M 57 M M 5) 40 M 44 M 50 40 0 5 20 to to 30 0 5 20 30 10 10 0 30 0 0at<e9 Umliffuintfeiad Mtan aft of thaw cam 51.2 jean. of It in knar lobe* (52.4%) II of 17 in right king (44.7%) Kingdom alvo have an intrathoeacic ncoplavm. lit alro note* that **tha incidence appear* tn he increav ing and that thn. if true. i* a dinurhing itatt of affair* cvpcctalfy a* there ha* been in operation for upward* of JO yean *trin|tnt *v*cm of vtafulory nr athe4to%:' Alto tigniftcant in relation to modem (ndiruriat and occupational condition* it the (indint that taiMint imutailon worker* in New Yort have an incidence of lung cancer 4*7 time* the expected rate. Tfme worker* were conddcted to have hod relatively light intermittent exposure to avbetto* (Seiikoff. Churg and Hammond. 1044). DOW 06037 i STOOI 1826 Or/i^T I ^ HOURIIIANr. aso McCAUQIlEY.* Pm*ut*y *f A+n*%ix The distribution of lung cancer iKiiKd with y - ashextosix is unusual in that the lower lobe h tOOTC^t frequently involved than the upper lobe (Aohlf Jacob. 17* and our own cxf*nciKc confirms rtda*'-- -' (lahtcs I and 2). There i* no clear indication m to whether ashcsim exposure predisposes to Mljr particubr type of lung cancer. Our impression haed on personal experience and informal div evtsuon with others is that adenocarcinoma occurs with unexpected frequency. Recently evidence has been rapidly accumulating that asbestos may he a major factor in the aetiology of diffuse mesothelioma, an uncommon tumour which is believed to arise from the lining cells (mesothelium) of the serosal cavities. These tumours show a striking tendency to spread extensively oxer the affected serr-at membrane PM. 13--Hcaral (Fig. 13k They infiltrate adjacent tissues and fre quently metastasis* to regional ly mph nodes and less a frequently to more distant sites. Accurate diagnosis of this tumour during life must usually be based on biopsy and the criteria have recently been reviewed (Hourihane, 1963b; McCaughcy. 1965k Differenti of tha shorter exposure time fat women aai (heir ation from metastatic carcinoma may be difficult. cocfPpoww(7 imper wwii wm These tumours are often associated with an effusion mown opowf 10 onuii mo omnwy imimi and cyioloyical examination of the fluid by an one of Knox and Beattie's (1954 a) similar obserwa- experienced observer may permit confidant tion with regard o Actors influencing the degree of identification of the tumour. The presence of pulmonary flbroda in patterns with atbetmtrs. It hyaluronic acid in the fluid may also be a helpful may weft be that once a critical lesd of asbestos hat pointer to likely cases. been inhaled, the uma of subsequent flbrosh or Groxips of diffuse mesotheliomax of the pleura nenplaiia Is reiatisefy flaed. and is prtdesermined and peritoneum axxociatcd with axhextos expoxure many years in advance. haw now been reported from South Africa (Wagner, However, at lower leseb of asbenos exposure Steggx and Marchand. I960), Germany (Kenig, there is evidence of a dose-response retationship I960}, the United Kingdom (Hourihane. 1964; batwaan (ha aneouat of asbestos inhaled and the Owen. 1964; Elmct, McCaughry and Wade. 1965) preportion of ewbeequiwt amutheleraae, In the and the United Stases (Seltkoff, Chuff and London Hospital general necropsy pepMetiea the Hammond. 1963k In many of these cases exposure incidence of tffltoe mmothdionm is and has been light and frequently not associated with most subjects with thh tumour have smal amounts pulmonary fibrosis. Although diffuse mesothelioma of asbestos in tha lung, with no more than 10*; has accounted for only a small proportion of having any knowledge of absestos espoeare (diet recorded imruthoraeic neoplasms in cases of nondndustrialk In datiical asbestos*. with huge asbestosls the experience of one of us tD. 0*11 H.) amounts ef asbestos in huvs and a history of at the London Hospital would sugeest that it may be common. Thus among 4} drathx in male asbestos** industrial exposure. tha proportion of Nscta who develop diffuse mesothchorns* Met to 37*. patients 17 had diffuse mesotheliomas (g pleural. Subject* with pleura! plaques at necropsy and with, 9 peritoneal), as opposed to 17 with lung cancer; out denial asbestos!* occupy M intermediate while in 26 deaths in female axhrstosi* patients. 9 had diffuse mesothelioma* (I pleural, 8 peritonealk position (Hourihane and othrn, 1966k A similar consideration of Nog cancer is of and 10 had lung cancer. The Interval between Ihe flrxt exposure to esbesto* and the development of mesothelioma had usually tvm at least JO. .10 years. Table 3 gives the details of astvxio* exposure In those cases in a total series of 76 patients with txhcxtpvix where data were available. It can h? seen (Merest. Lung cancer occurs in aNxit 40*. of patients with classical asbestos*. and in 12*. of un*cletted necropsy subject* m the same ho-pual It is possible that a d*e-rc*[vm*` rvUtiwi;might exist here also, as Knox, IV4I ami IhM t im**. has shown a decreasing rate iff King cancer witl that the time from first known exposure to death is imprmed shot <v.urol. fairly constant around Xf years, for each sex and Although csHknce from South Africa wouV for each major diagnosis. This i surprising in view suggest that Hue asbestostcrsvidolitci ts panicuiath DOW 06038 <00 Cause of Death Msift Lung fiixn MoithrlMni Heen faitwoe Fiuu.it Lung Cancer Mesothelioma Heart Failure Roth Stxit Alive and Welt Heart Failure 5T0011827 POSTGRADUATE MEDICAL JOURNAL OrtaArr IK TABLE ) ffctuit n Atatira EtfnMin m SumvM. n Aaoum Avtwiov Tvpsurc lAveuft in >earvi Last f.tpnwne to (Vath (Average m yearti First Etpmure w Death 1 Average m years) : C14 cawl 19.3 (Dnmi -- IJD (12 cates) fftiT " 14.9 0 caves) 12.5 (Hemes) 26.9 (12 ernes) 26J () ernes) 4.2 (9eawvt 1.1 (4 casesl -- 26.5 (9 cateti IU (4 cates) VP (4 cates) 29J (9 cases) 24jg (4 ernes) 36J (6 cases) 425 (5 caves) 5.5 (It caves) 23.1 (4 cates) 21.0 (7 cases) 22J (5 ernes) 30J f9 caves) Age at Death (Averagn 992 (17 ernes) SIA (IT ernes) (TOM) 3X1 (fOcmea Stl (9 ernes). ttS #6 ernes) JTJ Deeses) 54J (13 ernes) likely to produce diffuse mesothelioma (Wagner and industry in particular thit virtually Mestraeti others, I960), not enough evidence it available on material hat become widely distributed. Ahho *orM'Widc both to assess the relative carcinogenicity some of the haardt of occupational exposure of the main typct of asbestos in thit rctpcct or in the asbestos have been apparent for many yean ; production of lung cancer. Experimental evidence active measures have been taken to reduce Indutt (Wagner. 1965) however, would suggest that mcvo> thetial tumoun can be readily induced hy intra* pleural inoculation of any of the three main typct of exposure it is dear that in spite oTa few mcourat reports (Knox and ethers, I96S) the measures ta in general have been (hr horn effective in ehrmnai asbestos (CVyvMlte. croddolitc or amoiiteX sbesrosis or hmg cancer. The report of the Mini Harlngton (1965) and llarington and Roe (1965) have reviewed the ehentittry of atbcttoa and the possible meehaniwm of carcinogenesis. The aunty of limitation workers by SellkolF and othen (1964) hat produced evidence of poeaible of tomtom and National tnsanwca ter the > 1964 in teat shows that the number of new cate * pvnwn ipnipvnwwn jwi thing. Tha record!ton of a daae ameeia between asbestos exposure and diffuse mesothd* connection between pstrodntcstinal malignancy and aipoeure to asbestos duvt. of the plctira and peritoneum and the teet the many cases of this tumour exposure has been sli emphasises that even low levels of exposure car tNueid-- be considered safe, tn this light it h disturbing I The prevent century hav witnessed an enormout etpantlon in the uve of avhettov by induttry for a wide range of produetv. Current world production it ettimated at over 3 million torn, (Hendry. 1965) and beeauve of the widespread uve by the building low grade environmental exposure appears tc common ht several pant of the world. It must alto be renumbered in relation to neoplastic complications of asbestos esposure the interval between first exposure and the dew DOW 06039 k 1 I*K>. MCH KIHNM mi \t<CAlTilirV. rirffcdif; 1/ STOOI1828 ment of lung or pteiml cancer is usually at least 2U scars and especially in ttc of diffuse ntrw iScto<oa may tv as much a* 40.r ycais The tifntiwaoce of present levels of exposure may not twcomr apparent therefore for at least several The question of compensation in ease* mith the nropi.viN; sequelae of ashestosis taises a difficult problem. The l*neunwmm% Medical Panel* in (teat Britain accept lung cancer a* a sequela of ashesi***** and therefore compenxataMc What however can he retarded a\ a significant degree of asbestos* in this respect ? Both of 11* have seen many a<o of bronchogenic earemrena with asHystox bodies in the lung. In some of there there mat no ohsioux pulmonary fibrosis, in others only slight fihrosi* nhich might not ncccssanty hase been due to asbestos. The question is complicated not only by the high incidence of bronchogenic carcinoma m the community generally but by the existence of othcT acuotogical factors, notably smelting, (n tie* of the high (oser h>',| incidence of asbestos exposure in cases of diffuse mesothelioma and the relame rarity of these tumours there is clearly a much stronger case for regarding slight asbestos contamination of the lung as significant hen associ ated mith this tumour in either the pleura or peri toneum. It ix worth emphasising that some subjects mith mcxothcl'oma and asN*,ios bodies give no history of industrial exposure to asbestos, and appear to have contracted a fatal disease through residence in an urban community. It has been suggested in this paper that the incidence of mesotheliomas and possibly lung cancer also, is affected by the dos< of asbestos introduced to the body, and consequently that a "safe" level of exposure might he achieves!. What this level is one cannot say. hut it is clear that information on this point is urgently required, both from industrial and epkkmioUigtcal pom-* of view. The mcvlanism or mechanisms m hereby asbestos damages tissues base not yet been clearly established. Mechanical and chemical factors have hren impli cated in the production of fibrosis Neoplasia in the lung and possibly also in tlic serosal membranes could be a direct complication of this fibrosis. However. l has been shown that carcinogen* occur n asbestos. These include natural and contaminat ing oils, iron. nickel and chromium illanngton and Roc, l%$l. f urther imcoif.iiion of this subject combines! mith siuvfies of ca*Hvr rates asxtKiatcd muh pure espiroue to individtul types of advstos are obsu-usly of rnat uupoii.utce in devising effective safety rejMil.in<*ns foi the treatment ami hanvlfing of this imton.il RJ KJtKV.t.% bMi, II.. and Itna. fi. Noe r,rsO*vi*di uher den I wngmlrchs der Avhesiarheitcr. 0wA. mrd. Heb.. If. 211. bmu, (iueiasi M. firitn. f. V and Vtm*t. M. t. t|Mi IkvnfiusiMl C anr <4 1% t rmf> Tract in l)fViiffs Operalv and id tbe l ung m Ath.Mm Tetfdr Workers and Iron-ire Miners. Amet. J. rite. #W*.. . 12%. Bavuis.C.C..and Vsso*. N IH$ti: Carcinoma ofthe Bronchus. A (Iwwal and Pathnh-rscal Virvey of *A Cases Qmmt. /. Mr*. t 1*1 Itnusss W. O. llMdl: Ashesim* and denary Imrethmacm b aupbums Mm. N. I. Wf Sr*. IB, Csuss. O.. Toros, fi. S.. al Cam P. lli: Atkntotfinlnnl<MaUnp* Aatspy./.dwr. nnW. Xu, ML 771. Osvts. j. M. G. 1 ISM ai: The UbMneiM d Adeem Undwftwmfwnofn Uwp. bit. /. rtf. Mi. AS, %U. Osvis J. M. G. MW bl: The Ifikrasiructurc rf Stbrtet Bodies from lloman Lang. M. ML Oxi. R. ttb$5>: Mmsabty ffem Lung Cancer in Asbestos Workers Mr. J. Mbme. tW. IL *1. Elms P. C,, McCuner. W. T. E, and w, O. L. liMli: Defuse Mem*Maw of the fiwn and Asbestos Mr. mod./.. L Iff. Gskosan. L U. IM42>: CVysotd* Asbestos a* an Indicator of Subtle Differences m Ammnl Them, Amee, Iter. 7bnr. 45, Tli Gsaosta. L U,, and Cixrwiwoa. D. E. fll: Stodhs on Experimental PneumokomoovVI Inhalation of Asbestos Dust: its Effect upon Primary Tvbncwkmn Infection. / Amfctrr. it*?.. 15. %$ A *i. Gt nvst, S. B. tMI2t: The Asbestos Body. Dmf. L I Ml. Gimrv. S. B. <MJ2 Ml: The Morbid Anatoms and Hntokvgy of Asbestos TMvtf/r ifJMX 14. 44$. J and 5JB. GimrM. S. B. lMi: "Silicosis A Ashestous.* ed. by A. i. lanca. London: Oxford L'mseeuiy Press Gtotrsit. S. R. 1IBI1: Pncvmoconwwt*. A llntefegwal Survey of Necropsy Material in 120$ Case*. Larnt, L ilO. Gotr.M. J. 1 IMSi: Differential Diagnosis in the Pathoh-gy of Asbestos*. Am. S. Y. Atm/. Set.. I5L W. HsatxiTtis. i. S. tttttl: Cinal Studies of Asbestos. /W.. IJL }|. Hvusoins. i. i, and Bnt. P. J. C. <l%%5): Studies it Carcionerimi* of Asbestos ribres and their Natun>l . OiK fAnf- I5L 12. HtNnnv. N. W. tlM$: The Go>log>. Ocvurrcnees and Major Vscs of AsK-stm. /An/.. ML 12. IliuaiiisM. D. OB The Pathology of Mesothe<K*mata and an Analy** 'f *'*c,r Avwviav.w mith Ashcstcm Pxpv*sure. fiovi. M. 2W. HmatHSM. D. OTl. ilb! at: % Study of the Path ology of Diffuse Mesothehonvita and an \nab their Atmviattun mnh AJvxiin am* \shf*,K.. Thesis for National lUusersits InrMnd. Mm atitSM, O'R. tlbhlbi: \ l<T Senes of Vesothehvmnata. and Attempts * IJet'i> A*N'. . WHhm v.anr if the Tsnsirx Iw. V*. /*/ '* 152. M7. It<>iaiMssr. fi. tVA. liw. I., am* .............. . P. l\ Hanoi: Hyaline and rakitvd PW- i' *'-to as an Indrs if I'sismire to \S-i*s \ v.'.*- Radudiyriv'al and P.itlvit.igv,.il I ' M' * with a limuJeiatuin v-f I pHle'i'io'.-ev. ffo . j L loan. I, DOW 06040 It IN l* .K \; 11 Ml NUDUM Mil RNM I h t>4*rt I`I**. K* i< .. ii t.|(il'<. .1 * *1 \* / .. \.i\ a M f'>t iii*/ i \#* * h t. v . / "4 ' K v- % : 1 ..... In ' ... 1 .| i %>*.* l l 'i > I r I \|S'i ti- Vi S.ix-l.. |)ns| .< //.. w Imi, N*" ' * l . * ii II1 'nil m I)iliiliii;,..i iH V !.* 4.1*1 I il'tis ill tn' I i(In* rflli-f | S|S*s< 1 ll III \i|\ ilrl |1 l*t. I'l . I*fl/w'** //i|* |U. 41. K s I I . |V I . K. A . .mil III! l. I l> t I otaill i ill in li>tid.nit i'l IIiikkIimI ( at* i.iu'-.iia in a li'iliw \il'lii I Atmi, Inn. N.C, lull/ Si I . 1.12, 'ill Kunm.. .1 ii'kiii I tvi iliv VKmi'h'. 4uh. (Hiithri p.// i.< * /* <hj> , lb. l'`* Nlii \ii.nn, V\ I. I ii'ni'i i iiiv'iM fur Dmiimimi i'l lii:u*v Mi>nllik'ii4i 'miU'iiis. Inn, S'.Y. Arutl. .S*i,, M2 Mil \lii Hnnn. s < t*2V Iliiii'iii|*> n| INilimKury \MXVlHII, tit It, Mt/ /.. ii, m2' Mi Nii n. J I 1\stvstosis m (ircat lintatn, tn. A. ) l. ,U An.. M2. 12*. Nl. m wi inm. I . K V and |*m ,C. \V. I m l*l| r A Kcport in ihi- I iiivi *( -\vIvm<"i I>um nn the l.unc anti Dist Ni.ppri^MiHi in itte Asbestos industry. London. IIMMK Miimii iiita. I K. A. ||953: Annual Rrj**t of Chief lr.*p*vn*r I astories for the Year. I**55. p 20h. London II M.S.I). Oh in. W. O. tlYMi: OitTir< Mesothelioma and Ft* pKsure us Asbestos Dust in the Mcncysnk Amu B*ti. mrd. /. ii. 214. Stuaiwi. I. J,, Chi iu J.. and H*wrso, E. C. (|4Mi: Asbestos Kspouwt and Senpiaua, J. Amur. mrl. Au* in, 22. \l I l* H I . I ' I I <l< J . ..! t I I I < i I t i'll' . Ki ,,il>ii I t;i'*'ift Ii' S*ix in* ami Me'*-, : ...... . s.- /.*/ y /../. VI. U4t Nimvi*. I VS . a,i`l Si-in i.f- \ N \'.U* In . |l,.,1k. hi li.t S.'.il............. Afi. A *\uiMi% in . I iiii \\i'iti' *n an V's'ii*- Si, J t'nim Utml.. ,M I Si i vt ui, II I . Ill* ml*. I I .iiiil < in'll"., I I* i I*H| i AxIvnIik.ii Kcisai iH lni m, 4nk fat*. 12 IliuMviS, i (, K is ill i i, K. (i. an. I M* l>*si II M il'Milt UMm as a Mi.lettt I ihiii lia/aiil. A U* m d. J . .17. n (ihimvin, J. <i, *I'KA Axhest.iMi anti the I ihan I KtclVf. 4mm. .V 1. 4tmU. V<,, 111, 1% ViN*tsii, A. J. Dianas. I. M, anil IStir, P. f. ll*#Mi: Iperi<nrmai SiwIks of AiU'Ium*. 4"h ns/uitt. tt\r . .1. I. NVti.sia, J.C..St i*a,vC. A..and Mwinsu, P.tlSta*. llitliiH- itmrai MestNlviiiwiia and AsIvmi** l.spoawe *n titc Ninth West Cape Prosaue. H>m i. mJm*tr. M.d,. 17. 2. Wjm.nim. J. 1`. tl**ii5. Perainal < umm.ir<aaai. Wai.mm. J. t\. and StHiwei, 1. W, Axhra*s Dtixi DeptmtHin and Kctcnimn m Kat*. Amm. AM. 4uul. Sri.. M2, rr. Wimi . (i. h.. Srirt, II. J.. and Sum . Maanss N. iIh#*5i: fVnciratHin of Cohnw Mucni by Asbestos I'arivles. An Heelton Mkti*<o(c i't*dy Kats l ed Asbestos Oust. tmh. 14, 2017. Wi.ua. W. B.. and liunst. Si. R. il7J0 -. Ptdcnunao Atbntmi*. f*mtrt. L 44J. Wire*. W. Bl. and Gunsi. Si. R. (14341: Pdbnnnats AsbettM*. A Kmcrn of Owe Hundred Caaev 1444. 2 Wnu. H. (IMf): AatalQMN ^mmgmL mmiJm 23. *31 00 O O CD f\2 vo t 06041 It