Document LJM7ajLJBp40gr3KLqvvx16rq

AS3ESTJS CONFERENCE ATTENDEES June 2, 1972 Biochenicals J. B. Young - Belle Plant Central Research D. J. Beatty - Experimental Station I*. A. Wharry - Experimental Station S. R. Willis - Experimental Station Elastomer Chemicals S. Wenzel - Louisville Plant w. T. .Muncaster - Wilmington A. F. Myers - Wilmington Emolovea Relations C. W. Eddy - Haskell Laboratory J. R. Haden - Safety & fire O. G. Windsor - Safety & Eire Engineering J. R. Allen - Louviers Building ?. H. Fuller - Louviers Building H. A. Moak - Louviers Building E. A. Palmer - Louviers Building J. L. Parsons - Louviers Building w. M. Ohrich - Construction - Louviers Building I. Zeise - Construction - Louviers Building Fabrics & Finishes J. C. Pang - Marshall Laboratory - Philadelphia G. A. Johnsen - Marshall Laboratory T. J. Nelson - Marshall Laboratory A. J. Geib - Wilmington G. R. McClure - Wilmington E. E. Swain - Wilmington -----,==r. PLAINTIFF'S EXHIBIT JD-U.P-99 jP,it ' ILq'T'\~GG ^r;'jsJEEH '.ronounNi 3 TOwnoii i-:c. CV.il i/lEDiriORJHJ;W) reporter: 0930493 ou? i I mi Film C. Franklin - Clinton Plant A. E. Barton - Spruance Plant R. Misak - Tecuraasen Plant W. 2. Neff - Wilr.ir.gtrn Industrial Chemicals G. R. Amery - Niagara Falls Plant G. F. Reichwein, M.D. - Reoauno Works J. A. Robbe - Reoauno Works J. G. Haverty - Wilmington Organic Chemicals W. L. Sprout, M.D. - Chambers Works J. C. Warner - Chambers Works W. E. Acquard - Corpus Christi Plant C. I*. Hobbs - Jackson Lascratcry Photo Products F. Reig - Brevard Plant Pigments J. T. Cavanaugh - Edgemoor Plant R. M. Luekring - Edgemoor Plant Piaeties Y. L. Power, M.D. - Carney's Point E. O. Randolph - Carney's Point A. Schelling - Carney's Point <7. B. Annitage - Experimental Station H. H. Gibbs - Experimental Station S. Hatrman - Sabine River Works Polvmer Intermediates J. P. Hooten - Cape Fear Plant D. Zippier - Savannah River Plant DUP 0930494 Tax e Fibers J. W. Chroray - Chestnut Run J. M. Martin - Chattanooga Plant P. V. Nolan, M.D. - Chattanooga Plant W. S. McMahon - Kinston Plant B. R. Bolton - Martinsville Plant S. J. Bright - May Plant W. 0. Cotty - May Plant C. F. Higgins, M.D. - May Plant E. C. Shepherd - Old Hickory C. M. Gardner - Seaford Plant F. S. Klein - Seaford Plant R. P. Coon - Waynesboro Plant W. J. Gatzek, M.D. - Waynesboro Plant P. F. Philyaw - Waynesboro Plant R. E. Sayre - Waynesboro Plant J. G. Bernard - Wilmington M. L Bradley - Wilmington S. Danby, Jr. - Wilmington R. E. Ferrari - Wilmington R. B. Hayden - Wilmington J. A. Sigman - Wilmington H. E. Swink - Wilmington 0OP 0930495 MHiiatiittij iaiiifwiiiiir ASES5TCS SEMINAR June 2, 1972 8:45 a.a. ' ~ Introduction 8:50 a. a. Types end Uses of Asbestos 9:05 a.a. Health Effects of Exposure to Asbestos 9:30 a.a. Changing Requireaents under CSKA 10:00 a.a. C0FTEE 3HSAK _____10:30 a. a. Medical Surveillance of Asbestos Workers 11:00 a.a. Surveillance of Working Envixonaent 11:45 a.a. LUNCH 1:00 p.a. Means of Lust Control 1:45 p.a. Potential Substitution of Asbestos in Insulation 2:00 p.a. Liscussion of Topics 3:30 p.a. Adjoumaent R. J. Hubiak C. T. Reinhardt, M.0 J. F. Morgan - H. J. Trochiao:.*icz R. J. Hubiak Coa. S. 3arboo, USN G. E. Lang, III DUP 0930496 Jil.ki.ai m-A&m ; 6-iAgaii \ - ..XszJSAis^uiEzmi, mmmam. Most introduction by Jena A. Zapp, Jr. Lee at say a feu vorda about vhy va're having chit particular Conference on Atbescot. If I were to rank thote chemicals made and used by Du Pont in order of concern to me, I would not put asbestos at the top of the list. But, it has the spotlight on it at the present time for other reasons. There art enough workers throughout the U.S. who are exposed to asbestos and there are enough cases of occupational disease resulting from this exposure to have caused labor unions and the Federal Government to give this problem of asbescosis, and associated lung cancer, the first, and primary attention, under the Occupational Safety and Health Act of 1970. This attention occurred two ways. First of all, asbestos is the first chemical substance to have been made the subject of an emergency standard. This was on the motion- of the labor unions chat insisted that the current level of exposure as permitted under the Occupational Safety and Health Act of 12 fibers/ml was too high, and therefore, they put pressure on the Department of Labor to sac a lower emergency standard. This was set at the current reesatnended. level by the American Conference of Governmental Industrial Hygienists at 5 fibers/ml. This number five is noe as low as the labor unions would have liked, so chat pressure has con tinued on the Department of Labor to establish a permanent standard lower than 5 fibers/ml. The mechanism for getting at a permanent standard chat affects health, is for the Department of Labor to request the National Institute of Occupational Safety and Health to prepare a criteria document DUP 0930497 ...iMijgKln.^Laii;!MgMii;yiiHgaaai:jai^wiMigiMMwwiagsi4lj!isiaii!fiw -2 and reeoTMnd a standard. So we have another first. This was the firs; criteria document recommending a permanent standard to be prepared by the National Institute of Occupational Safety and Health and to which they have complied with the requests of the Secretary of Labor by isauir.g a criteria document, entitled Criteria for a Recommended Standard Occupa tional Exposure to Asbestos. A criteria document is not a standard. A criteria document simply describes the effects observed at different levels of exposure. Based upon the criteria document however, one can recommend a standard. Criteria documents are descriptive. They describe. Standards are prescriptive. They say what you can do and what you can't do. This particular document contains a reeosmended standard and the criteria on which that recommended standard is based. However, it should be pointed out that this document itself does not necessarily reflect the final standard that will be adopted by the Department of Labor. And, I might just quota Dr. Marcus Key, Director of the National Institute of Occupational Safety and Health, in a talk ha gave in February where he said, "Please remember, under the Occupational Safety and Health Act, HEW'a reconnendacions are not standards. The Department of Labor vill review our recomendations and thoaa of ad hoc review committees and hold public hearings, if naeassary, and will promulgate the final atandard." Nov the publie bearings on asbestos have already bear. held. They lasted about two weeks, and I understand that it accumulated quite a stack of testimony. Now, the next phase of the current phase is the digestion of this testimony by the Department of Labor. Out of that vill come their recommendation for a final standard that vill be published DUP 0930498 *J - in Che Federal Register co cake effete or. a cereals cine after puaiicacic We have not yet reached chat point. But because this document is cut, because it recommends a low standard of 2 fibers/r.l, this standard itself has achieved maximum exposure conditions. It has excited mere of a discussion and a lot of questions vere being asked by people who sight have to deal with this problem. As a result of this attention foeused on asbestos, plus the intended standard which we don't raally know coo much about yet, that has caused us to feel that the time wes right for another Seminar on Asbestos. Whet we're going to cry to do today is co give you some of the dimensions of the problem, but again I caution you. The final standard has sot yet been promulgated so don't go beck end say you have co do this right away, X: may well be chat the Department of Labor will not adept all the recotmnendations of NIOSH after they have considered all of the testimony before them, ell cccoents of experts, professional societies, indusery, and labor. Xe may ba for political riuoni ehsy will adopt it. We don't know. So chat part is still an unknown. But, X hope that you will leave here today with a beccar understanding of aone of the reasona for the recommendations of the National Institute of Occupational Safety and Health or NTOSE, as you will hear ie referred co, and, perhape a better understanding ef what you may have to do when the final standard is adopted. RJH/neh/jtd June 23, 1972 DUP 0930499 S CF IXFCSUES TO AS2ESTCS by Charles F. P.einiardt, M. E. The diseases shown on the first slide are the ones which nay be associated with exposure to asbestos. First, is the primary one which is asbestosis--a fora of fibrosis of the lung. Then there are at least two types, and possibly more, of cancer. There is bronchogenic cancer-- a cancer of the branchial tubes of the lung. This is the coznen type of cancer associated with closure to asbestos. Then there is mesothelioma, a rare fora of cancer. It is cancer of the pleura and peritoneum. The pleura is the thin aetibrsne which covers the surface of the lung and lines the thoracic cavity. The peritonea is the sane type membrane which lines the abdominal cavity and covers the surface of the organs within the abdomen. In addition, although not listed here, there may be other typee of tumors aeaocieted with exposure to asbestoe since there is an increased incidence-of cancer of the gastrointestinal tract in asbestos worsens. (Next Slide) Asbestosis was first described about the turn cf this century in London at a post-mortem examination by Dr. Montague Murray. After that, for the nert 20 years dr so, there were few deaths attributed to asbestoaia. However, in the 1930's, asbestos was shown to be a major cause of disability in workers in the asbestos textile industry in England and in the United States. The latent period for this disease is 10 to 20 years. This is the period of time which elapses between the first DUP 0930508 exposure am the onset of the disease. This is an average which is shown here am it say he shorter or it nay be longer, it could he as short as 5 year* under very dusty conditions. Now to neve on the synptcss am signs of asbestosis. First, let re mention that the onaet of this disease is incideous, that is, it may creep tp on is individual am he may he unavare that It Is present. Cc cause of this is that the early synptcss, that is, shortness of breath and chest pain, art rather cononnn types of synptoms that are not particularly characteristic of this disease am therefore, diagn.ois at this stage is somewhat uncertain. However, later in the disease, certain signs will occur which are more diagnostic. The first of these is basal rales. This is a physical finding of the lungs which is due to a collection of fluid in tbs base of the lungs am is detected tpon examination of the lungs. There may be clubbing of the fingers, which means an enlargement of the ends of the fingers. Clubbing may also involve the toes. There ere usually characteristic x-ray changes of the lungs; typically, there would be a ground-glass appearance. This is due to the diffuse interstitial fibrosis which is characteristic of asbestosis. This type of fibrosis is in contrast to the nodular type seen in silicosis. There may be pleural thickening which may be detected on the chest x-ray. ether findings may include abnormal lung function. I vill not describe what each of these is in detail because they are somewhat technical in nature. However, in general, there is a restrictive functional pattern. In asbestosis, ths lungs bscoms stiff and lose their elasticity or ecapliance. Cue of the characteristic findings is impaired diffusion. This refers to diffusion of gases serosa the alveolar-capillary msmbrsne in the lungs. DUP 0930509 .L . Lungs fran urban areas contain typical asbestos bodies ir. wv! numbers, depending on whose figures you read, asbestos bodies nay be found in from 50 percent to 100 percent of the lungs which are examined. Cne eorplieating factor here is that other mineral fibers can become coated in the sane Banner and aaybe this is wly the tern ferruginous bodies is prafarred by some. (Haxt Slide) I thought you Bight be interested in soae of the theories of the pathogenesis of asbestos is, i. e. bow it occurs or why it occurs. Originally there was the theory of physical irritation and this aeans simply what it says. That is, the presence of asbestos fibers in the terminal air spaces causes irritation and damage to the walls of the alveoli of the lungs leading to fibrosis. However, th-i theory is not generally accepted today. Then there is the solubility theory which says that fibrosis is due to the effects of the silie acid and metal ions leaching out from the asbestos fibers. Again this is not a widely accepted theory on the pathogenesis of asbestosis. Then there is the autoissiune theory. There are two concepts here. First, the presence of asbestos in lungs and its reaction with phagocyxes or fibroblasts produces or localizes abnormal globulin leading to fibrosis. Phagocytes end fibroblasts are hinds of cells which nay be found in the lungs. Phagocytes are of particular interest because they are the cells that engulf or scavenge foreign materials that enter the lungs. The second concept under the autoimmune theory is that there is lysis of trapped phagocytes. They would be phagocytes which have picked up asbestos fibers and they release a substance that is not accepted by the DUP 0930511 I|i 11 iiiii ~i ............................. -? - tissue os self. That is, it is a foreign material in the lungs and therefore the body resets to it by producing fibrosis. Again, these two theories, the auto insure theories, are not widely accepted. However, the fourth theory, the stagnation of phagocytes, which is soaewhat siaiiar to the last one I mentioned, says that the phagocytes disintegrate in situ or in place in the lungs and in doing so release sclerosing agents which are probably lipids or lipoproteins. This is the theory which is currently favored as esplaining the development of asbestosis. (Next Slide) Moving on from asbestosis, we ccme to bronchogenic cancer. This is the type of cancer of the lung which one normally refers to when speaking of lung cancer; that is, the same type of cancer that occurs in cigarette smokers. It is cancer of the bronchial tubes. In the 1930's, an association was discovered between asbestosis and bronchial cancer. This was especially true in asbestos textile workers la whom an excess risk was firmly established in the 1950's. I mention this because this groip of workers apparently has a high exposure to asbestos dust. In other groips of workers this relationship has not been found to be as strong. The association appears to be with asbestosis rather than simply exposure to the asbestos dust. Cigarette smoking is an Important additional and possible synergistic factor. In fact, 2r. Selikoff estimates an increased risk factor.of $0. That is, the risk of developing cancer in an asbestos worker who smokes would be 90 times greater than an asbestos worker who doesn't smoke. This is quite something and I think it emphasizes the importance that if one is an asbestos worker, he should not smoke. The latent period here is 20 to 30 years; if you remember, this contrast with 10 to 20 years for the onset of asbestosis. 0930512 DUP .......a-^#-iHHiiii -o- (Next Slide) Mesothelioma, which as I mentioned os the first slide, is a rare tppe of cancer. It is a diffuse cancer spreading over the surface of the lungs and pleura and abdominal organs and peritoneum Cr.e of the interesting things regarding mesothelioma of the abdominal cavity is hew the asbestos fibers reach the peritoneal surface. In fact they have been found sot only on the peritoneal surface but in other organs in the abdominal cavity. Ho one is sure how they get there. Perhaps they migrate. The first large group of cases of mesothelioma was reported in South Africa in the late 1950's and it waa found that this form of cancer is associated particularly with ejposure to crocidolite fibers. However, apparently it is not limited to this type of asbestos. In the case of mesothelioma, asbestosis is often absent as contrasted to bronchogenic cancer. The latent period here is do years and you can see that the latent period is stretching out for each one of these conditions. It is rarely less than 20 years for mesothelioma, has not been shown to be a contributory factor as in the ease of the bronchogenic cancer. Exposures are not always occupational. Several eases have been found in persons living near a source of asbestos and even in members cf families of asbestos workers. That is, the workers come home with contaminated clothing and apparently there Is enough asbestos on this clothing to cause this type of disease in members of the family. (Next Slide) What are the possible mechanisms for the carcinogenic behavior of asbestos? Several theories have been put forward. The first of these suggests that metal conplexes found in asbestos naturally, or they can get there from processing the fibers miy be responsible. Such DUP 0930513 neuals as iron, chronics, or nickel nay be involved. particularly latter two, in certain ferns, are known to be carcinogenic. Second, oils associated with asbestos nay be a factor. These say be naturally occurlag or they nay be picked up from sacks or they nay occur la esulsions added for processing. It has beea fouad that these oils coatala beazapyrea aad related polycyclic areoatic compounds which are Jmovn to be carcinogen! Another theory is that asbestos nay act as a eo-careinogec, that is, by itself it nay not be a carcinogen but in the presence of other materials, it nay produce cancer. Lastly there is the prolonged residence in the tissue of a chenically inert naterial which is incapable of being removed by phagocytosis. This is referred to as the Cgpenheiner effect, but it is generally not thought of significance in this case because it seens to apply to larger inert bodies which have bean placed in tissues. Also, asbestos cannot be regarded as a chenically inert substance. In summary, asbestos may produce several type* of disease,.naaely, the characteristic asbestosls or fibrosis of the lungs and certain ferns of cancer--the bronchogenic cancer or a rare type of cancer, nesothellcna. DUP 093051