Document zQgwgdve8Ggp1138wqVjOXD63

--COLLEN 285 Comment it is likely that every com0 or more will have affiliats larger medical centers an test laboratory, which will nbulatory patients for periinations, health evaluations :oses (occupational, insursickness consultations and s; and which will be availpatients for admission and druinations. These multitest undoubtedly be afRIiafprf - ' omputer center which will ocessing services through lone lines. 1 multitest laboratories will ncreasingly utilized by in general and occupational is. MS, compiled the statistics in. ., and Eads, W.S.: Experience : Breast Carcinoma, Cancer 1966. t al: Automated Multiphasic 'osis, Amer J Public Health i. '.bin, L., and Davis, L.: "Comc Screening," in Stacy, RW. Computers in Biomedical Reademic Press, Inc., 1965, vol 1. of the nervous system, inated rapidly without duly ask his patient to cructure of the nervous :he old patterns cannot areful to select out the his skill to seeing that ms.--Stead, E.A., Jr.: >37 (Dec) 1966. * , St } / *< American Academy of Occupational Medicine I PLAINTIFF'S i EXHIBIT % Asbestos as a Hazard to Health - Fact and Speculation W. Clark Cooper, MD, Berkeley, Calif Cr A RESURGENCE of interest in the as bestos minerals as environmental hazards to ' health has arisen because of increasing world production of asbestos, successive in dications of associations between asbestos * and pulmonary fibrosis and various malig nancies, and, more recently, the demonstra: tion of asbestos or asbestoid bodies in pre sumably nonexposed populations. The major asbestos minerals of commerce " are chrysotile, crocidolite, amosite, and an- thophyllite, with tremolite and actinolite being of considerably less importance. The properties of these various fibrous minerals have led to an extraordinary variety of uses, so that world production has increased from V a few thousand tons in 1900, to 1.3 million ' tons in 1950, to over 3.5 million tons in 1965. Over 90% of this is chrysotile. The United States uses about one fourth of world pro duction, practically all imported from Canada^er-Africa.1 Asbestosis The first facts to be discussed will be those relating to asbestos pneumoconiosis, the disease that has come to be known as as- ' Submitted for publication June 19, 1967; accepted June 28. From the School of Public Health, University of California, Berkeley. _ Read before the 19th anting? meeting of the Amerlean Academy' of Occupational Medicine, San Francisco, Feb 8, 1967. Reprint requests to School of Public Health, Earl ' Warren Hall, University of California, Berkeley 94720 (Dr. Cooper). bestosis. No one disputes a cause-and-effect relationship here; but we are still deficient in our knowledge of pathogenesis. Are all forms of asbestos equally hazard ous? The evidence is against this. Chryso tile disappears more readily from the lungs than other forms and in animals seems to be less fibrogenic. The prominence of pleural calcification varies from area to area and type to type. For example, in Finland, Raunio2 has recently reported a review of 600,000 chest x-ray films which show that in communes where anthophyllite mines are located, up to 9% of films showed pleural calcifications, whereas in other parts of East Finland not bordering on producing com munes the prevalence was only 0.5% per thousand. Nothing comparable to this has been reported in other asbestos-mining areas. A second question regarding asbestosis relates to its prevention by industrial hy giene. Is it true that all that is needed is the application of currently recommended standards for dust control? Most people who have looked into the basis for the present threshold limit value of 5 million particles per cubic foot for asbestos, which has been recommended by the American Conference of Governmental Industrial Hy gienists (ACGIH) since 1946, realize that it rests on shakier evidence than most. Midget impinger sampling used in determining dust concentrations include all dusts; and the asbestos-containing dust that is counted is mainly grains, although, rarely, some fibers are included. A large proportion of asbestos 236 ASBEST0S1S--COOPER fibers have diameters below the resolving power of the light microscope and are not counted at all. Nevertheless, most industrial hygienists have felt that the impinger count is a good indirect measure of dust control and that dust counts averaging 5 million particles per cubic foot (mppcf) should con trol asbestosis. Evidence is beginning to develop that this is not true. In 1965, Wells3 reported briefly on his observations over 30 years in asbestos textiles. His view was that multiplying average counts by years of ex posure provided a good rough guide and that after 50- to 60-mppcf years workers began to show evidence of asbestosis. At the threshold limit value (TVL), this would be reached in 10 to 12 years. In 1966, Ferris examined insulating workers in a New England ship yard that had been surveyed by Fleischer et al4 20 years earlier. His preliminary results indicate that conditions and counts now ap pear comparable to those of 20 years ago and average near 5 mppcf (B.G. Ferris, oral communication, Dec 8, 1966). Nevertheless, a large proportion of workers had radio graphic asbestosis, which had begun to ap pear as early as 10 to 12 years before. Marr's counts5 in shipyards, in 1964, did not indi cate weighted averages above 5 mppcf; and current studies of insulating workers in San Francisco bear this out (J.L. Balzer and W.C. Cooper, unpublished data, 1967). Nev ertheless, asbestosis appears, which suggests that a time-weighted average of 5 mppcf may be too high. This is consistent with actual practices in the better controlled as bestos industries. Mitchell,8 reporting in 1961 on improved conditions in North Caro lina textile mills, cited counts ranging from 0.4 to 4.6 mppcf. English industries under Asbestos Industry Regulations have never operated with a numerical standard, instead depending upon enclosure, ventilation, and masks to keep exposures as near zero as possible. There are numerous other questions that one can ask relative to asbestos pneumo coniosis. Have we been too complacent in assuming that the expectoration of large numbers of asbestos bodies is the expected response of an asbestos worker, or is this in the new employee really an indicator that we are tolerating too much exposure? I do not think we know the answer. There are also fundamental questions on pathogenesis, on the nature of the pulmonary vascular im pairment, and the factors determining sus ceptibility. Malignancies Asbestos would not be in the headlines if asbestosis, affecting a few hundred miners, millers, and insulating workers, were the only problem. It is the more recently demon strated association between asbestos and malignancies that has created an entirely new series of facts, fantasies, fallacies, and fancies. Let us first look at the evidence. That there is an increased incidence of lung cancer in many groups of workers ex posed to asbestos is a fact. The cumulative evidence from epidemiologic studies (Table 1) that began with Merewether's analysis7 of causes of death in certified cases of asbes tos in the United Kingdom from 1924 to 1947 is now overwhelming. The evidence is not convincing as to the relative importance of different types of asbestos. Chrysotile seems less certainly im plicated; and one looks forward with inter est to an up-dating of the experience of Que bec chrysotile miners who, several years ago, when analyzed by Braun and Truan11 ap peared to have no excess risk. It is of inter est that Jacob and Anspach15 who a few years ago could demonstrate no increased risk in Dresden asbestos workers now find twice the expected number of cases of lung cancer in men and ten times the expected number in women. Their exposures were mixed, and we do not have the answer to whether the association is truly less for chrysotile than it is for crocidolite and amo* site. The next question, and this will apply to other malignancies to be mentioned later, is whether or not asbestos minerals per se are carcinogenic. A promising area of current research is aimed at determining the role of the asbestos fibers and fibrils as carriers of trace metals or of carcinogenic chemicals, such as the polycyclic hydrocarbons, to vul nerable sites. The idea of a fibril that can migrate and then become a semipermanent implant is an intriguing one. This falls into the area of speculation, or fancy if you wish to call it that, but one that may prove pro ductive. Arch Environ Health--Vol 35, Sept 3967 Table 1.--Epide Place United Kingdom7 United Kingdom* United Kingdom9 United Kingdom1 Quebec11 Pennsylvania12 New York & New Jersey13 California14 Pi Reported dea Cases of asos autopsies w Asoestos text areas. 20 yi Reported dea Chrysotile mi with over 5 Workers in as plant, aged of 1938-35 Insulatrng wc? since jonmj Insulating woi in trade, ag- Dresden19 United States16 United Kingdom12 All asbestos t: exposures Asbestos texti in 1948-51. Reported dea" ' Includes cases reported by M i includes cases reported by M* Within the past five year increasing evidence of an tween asbestos and diffuse ; toneal mesotheliomata. Sin< onstration of a major series Wagner, Sleggs, and Me have been over 25 reports . In many of them there hav associations with asbestos, e tional history or demonstrat bodies in lung tissue section; mesotheliomata were regarde ly rare tumors until recently, of even two or three in a se. workers becomes statistical Separating fact and fancy bit more difficult. First, he our diagnoses of diffuse i There is no question but th to exclude primary turnon necessary inasmuch as the h teristics of undifferentiated mors of the pleura and per: always distinctive. Close sc series of diagnosed cases resu don of many of them. Nev rigid criteria have been ap> cases studied by Hourihani. Arch ASBESTOSIS--COOPER 287 il questions on pathogenesis, the pulmonary vascular im* he factors determining sua- Malignancies .id not be in the headlines if ting a few hundred miners, :sulating workers, were the : is the more recently demon* don between asbestos and' lat has created an entirely icts, fantasies, fallacies, and irst look at the evidence. s an increased incidence of many groups of workers ex* >s is a fact. The cumulative ipidemiologic studies (Table with Merewether's analysis7 th in certified cases of asbes ted Kingdom from 1924 to erwhelming. * is not convincing as to the ance of different types of otile seems less certainly im- ne looks forward with inter* ing of the experience of Qufi- :liners who, several years ago, by Braun and Truan11 ap* no excess risk. It is of inter* and Anspach15 who a few ; 1 demonstrate no increased t t asbestos workers now find ted number of cases of lung - and ten times the expected i men. Their exposures were do not have the answer to ssodation is truly less for it is for crocidolite and amo* .`Stion, and this will apply to cies to be mentioned later, is asbestos minprala per se promising area of current 2d at determining the role of ers and fibrils as carriers cf r of carcinogenic chemicals, ycyclic hydrocarbons, to vul* Tie idea of a fibril that can en become a semipermanent itriguing one. This falls into .ulation, or fancy if you wish., but one that may prove pr* Table 1.--Epidemiologic Studies of Asbestos Exposures and Lung Cancer ` Place United 7*" Kingdom7 ; United Kingdom* * United Kingdom' United Kingdom* Quebec*1 j Pennsylvania12 S.:'v *' New York & New Jersey13 California14 vW*-* Population Studied Reported deaths from asbestos No. 235 Cases of asbestosis in 1247 autopsies with pneumoconiosis 121 Asbestos textile workers, dusty 113 areas. 20 yrs or more exposure Reported deaths from asoestosis 365 Chrysotile miners <1 mill workers, with over 5 yrs employment Workers in asbestos products plant, aged 25-64, employed as of 1938-39 Insulating workers, over 20 yrs since joining union Insulating workers mixed, 15 yrs in trade, age 3S-64 5,958 1.495 632 529 +r* States1* Kingdom17 All asbestos trades mixed exposures Asbestos textile workers, employed in 1948-51. age 13-64 Reported deaths from asbestosis * |nC[uaes cases reported by Merewether 1949. 2.636 2.833 584 Years Followed 1924-1947 1922-1953 1924.1955 -1950-1955 1940-1960 1932 1962 1S34-1957 to 1962 av. 7.1 yrs 1924-1963 1951-1963 1924-1963 No. With Lung Cancer 31/235 (13.1%) 17/121 (14.1%) 11/39 deaths 65/365' (17.8%) 9/187 deaths 19/186 deaths Comparison Silicotics Silicotics 0.8 6-f 5.61 expected 45/255 deaths 10/41 deaths 6.6 2.8 expected 34/250 deaths 24/286 12.9 11.9 146/584f- (2b%) ------------------------- s-? Within the past five years, there has been . increasing evidence of an association be tween asbestos and diffuse pleural and peri toneal mesotheliomata. Since the first dem- "onstration of a major series of cases, that of Wagner, Sleggs, and Marchand,18 there have been over 25 reports in the literature. In many of them there have been suggested aotiations with asbestos, either by occupa tional history or demonstration of asbestos ^bodies in lung tissue sections. Inasmuch as otheliomata were regarded as excessive ly tare tumors until recently, the occurrence London Hospital, the association with asbes tos has been strengthened, not weakened. A second question regarding these tumors is whether or not their incidence in the popula tion as a whole is increasing. The impres sion one gets is that they are. Third, if there is an association, is it more evident with one form of asbestos than another? Here, there is no question but that crocidolite, and especially Cape blue crocidolite, is the type where evidence is strongest. In this country, reported series have involved mixed even two or three in a series of asbestos porkers becomes statistically significant. Separating fact and fancy here becomes a bit more difficult. First, how accurate are exposures, usually including amosite. Claims have been made that because amosite was not used in the United States to any extent before 1935 and since mesothelioma diagnoses of diffuse mesotheliomata? is no question but that rigid criteria exclude primary tumors elsewhere are P**ssary inasmuch as the histologic charac- characteristically have very long latent peri ods from first exposure to diagnosis, we are either seeing responses to chrysotile or are seeing only the first cases in an epidemic of of undifferentiated spreading tuttots of the pleura and peritoneum are not ways distinctive. Close scrutiny of most f diagnosed cases results in the excluof many of them. Nevertheless, where criteria have been applied, as in the taseg studied by Hourihane,20 in 1964, in effects from amosite. That anthophyllite is not a problem in this respect is strongly sug gested by a recent report by Raunio2 in which the very high prevalences of pleural calcification in anthophyllite mining areas of Finland was not associated with any in creased frequency of cancer of the lung or of 67 Arch Environ Health--Vol 16, Sept 1967 288 ASBEST0S1S--COOPER malignant pleural or peritoneal tumors. We are left with a strong body of evidence that individuals with light, moderate, and heavy exposures to crocidolite, amosite, or mix tures of amosite and chrysotile show tumors of a type that is much less common in the general population. Studies in animals in 1962 by Wagner20 in Wales and in 1965 by Smith21 and others in New Jersey have led to production of mesothelial tumors in hamsters in which various types of asbestos were introduced intropleurally. The difficulty in preventing cross contamination in laboratories has com plicated some of these animal studies, so that differences in response to different types of asbestos and co-factors remain un clear. Nevertheless, the carcinogenic poten tial of asbestos minerals appears to have been confirmed, although the role of co-fac tors has not been settled. Ferruginous Bodies The final question is, is it true that from a fourth to a half of the general population harbors asbestos fibers in its lungs? The ba sis for such a statement is the fact that a number of studies of routine consecutive au topsy specimens in recent years have dem onstrated "asbestos bodies," or as Gough22 would prefer to call them, "mineral-fibrebodies," or Gross, "ferruginous bodies." As far back as 1928, Stewart24 had shown that smears of the cut surface of the fresh lung at autopsy would reveal large numbers of as bestos bodies in the asbestotic. If anyone tried this in a supposedly unexposed popula tion before studies done in South Africa in the 1960's, it was not published. In 1963, Thomson et al25 showed 26.4% in 500 con secutive autopsies in Cape Town and later, in 1966,28 27.2% in 400 autopsies in Miami. These and other studies are summarized in Table 2. The facts that have emerged from these are as follows: 1. Morphologically and in staining prop erties, these meet all criteria for asbestos bodies. 2. In no studies, so far published, have there been supporting data to indicate whether all, most, or some of the bodies were asbestos. 3. In most series, about 80% to 90% of Table 2.--Ferruginous Bodies in Human Lungs in Autopsy Series* Place Year Percent Positive Cape Town25 Miami*5 Pittsburgh2* Johannesburg2* Finland2* Montreal30 San Franciscot 2 963 1965 1965 1965 1966 1966 1966 27.2 41 39.2 57.5 48 42 Based on lung smears except series from Finland where thick sections were examined. n"` t W. C. Cooper and I. R. Tabershaw, uno0blih data. 1966. the positive reports were on the basis of rel. atively few asbestos bodies per case. 4. In those with many bodies, there wet* often but not invariably occupational or res. idential clues as to a source of asbestos and they were most commonly in males. 5. In none of the series, all small, whet* correlations were attempted with diagnosis was theFe any apparent association with malignancies or other specific cause death. 6. There is ample evidence in the litera ture that so-called asbestos bodies can be found in workers with exposures other than asbestos, eg, graphite workers, soft coal min. ers, diatomaceous earth workers, etc. 7. Ferruginous bodies can be produced experimentally in guinea pigs with other dusts. Presumably, they represent a nonspa. cific response to any relatively insoluble fibrous material in the lungs. ^ Speaking of this, Cooke31 said, there is no reason why any fine spicule of mineral should not have colloidal matter deposited around it and become moulded into a curious body. But as no other mineral dust is fibrous, this occurrence must be rare as to be negligible from a diagnostic point of view." The question now, is Cooke's statement of 40 years ago true today? Or, are we adding fibers of many kinds to our environment, giving a confusing picture of our human samplers? If, as is probable, many of the bodies thai? are being seen are really asbestos mineral* there is need to determine their significant* It is unwarranted to draw the condusicl from what we now know that they necessari ly presage an epidemic of neoplasms. It il Arch Environ Health--Vol 15, Sept 1967 quite warranted to spec however. It is important positively these ferrugu to quantitate them b known exposures to va als. If those with small f of asbestos bodies sho' creased risk of disease, more secure about those are scant in number. It is also important t< these fibrous minerals lungs. The view that a indestructible is not c relative term only, am that the millions of toi tually enter our phvsi< ever. Many are bound i ucts that do not release released are subject to acids, and other instilertheless, it is importan of our asbestos balan Sumrr In summary, with tb indispensability of asb has come realization oi ards that must be bet trolled. Present standi do not appear adequat sis over a working life ments of industry aggn. problem have already t orous standards. The asbestos minerals and lungs, pleura, and peri: increasingly convincin must be directed towar: the importance of type importance of co-factc gested that asbestos fil carcinogenic metals oi vulnerable sites. The ruginous bodies in froi half of the lungs autopsies in a number world points to an urg tive identification of t are responsible. If the\ we do not know what response curve is rej ASBESTOSIS--COOPER 289' >,--ferruginous Bodies in Lungs in Autopsy Series* Year Percent Positive 1963 1965 1965 1965 1966 1966 1966 26.4 27.2 41 39.2 57.6 48 42 ig smears exceot series from Finland, ons were examined. ir and I. R. Tabershaw, unpublished jports were on the basis of rel:sbestos bodies per case. ... with many bodies, there were invariably occupational or resas to a source of asbestos and ost commonly in males, of the series, all small, where vere attempted with diagnosis, ny apparent association with or other specific causes of quite warranted to speculate on the matter, however. It is important not only to identify , positively these ferruginous bodies but also to quantitate them in populations with known exposures to various fibrous miner als. If those with small or moderate numbers of asbestos bodies show no detectable in creased risk of disease, then one could feel more secure about those in whom the bodies are scant in number. It is also important to learn the sources of these fibrous minerals that are found in lungs. The view that asbestos minerals are - indestructible is not quite true; this is a _ relative term only, and we cannot assume that the millions of tons used annually acv tually enter our physical environment for:ever. Many are bound indefinitely into prod_ ucts that do not release them; those that are V. released are subject to the effects of heat, jy- acids, and other insults to minerals. Nev' ' ertheless, it is important to get a better idea of our asbestos balance, so to speak. ample evidence in the litera- Summary called asbestos bodies can be kers with exposures other than > a- In summary, with the increasing use and graphite workers, soft coal min- " vc indispensability of asbestos minerals, there ceous earth workers, etc. has come realization of some very real haz- ious bodies can be produced - --ards that must be better defined and con in guinea pigs with other ably, they represent a nonspe* e to any relatively insoluble rial in the lungs, of this, Cooke31 said, ". eason why any fine spicule of . ild not have colloidal matter trolled. Present standards for dust control do not appear adequate to prevent asbestosis over a working lifetime, and many seg ments of industry aggressively attacking the problem have already been using more rig orous standards. The associations between '- asbestos minerals and malignancies of the ound it and become moulded lungs, pleura, and peritoneum have become s body. But as no other mineral increasingly convincing. Current efforts us, this occurrence must be so must be directed toward better definition of e negligible from a diagnostic the importance of type, size of fiber and the .v." : importance of co-factors. It has been sug on now, is Cooke's statement of g Rested that asbestos fibers act as carriers of true today? Or, are we adding __ *-> carcinogenic metals or other substances to ny kinds to our environment, ... - vulnerable sites. The demonstration of fer nfusing picture of our human ruginous bodies in from one-quarter to one- half of the lungs examined in consecutive obable, many of the bodies that y in are really asbestos minerals, r to determine their significance ranted to draw the conclusion , e now know that they necessary ;n epidemic of neoplasms. It13 .; autopsies in a number of cities around the ' r world points to an urgent need for the posi. *ive identification of the mineral fibers that ; are responsible. If they prove to be asbestos, we do hot know what point on the dosage . response curve is represented and conse quently are not now in a position to estimate their significance in terms of human health. Conclusions ' I have one final set of conclusions. I think you will notice that I have not conformed to the usual pattern of talks with titles such as the one I was assigned, lining up on the one hand a list of the things we really know and then decrying unwarranted and mischievous extrapolations. Actually, that could have been done here, as I do think misleading statements have been made with respect to asbestos. The more fundamental problem is one that is a major affliction of occupational health. We often try to emphasize that part of the challenge of the field is that it is at the forefront of medicine and technology, where environmental hazards can first be detected, in view of the relative levels of ex posure and the opportunities to study popu lations at risk. But when relationships are actually suspected and then gradually estab lished, very real and practical consequences become apparent. So the speculations, call them fancies if you will, that are part of the normal process of developing new knowl edge in other fields become menacing and are misused and misunderstood. Polariza tion of views and severance of communica tion is the rule, not the exception. I think that this has been the case history of much occupational disease research in the United States, and I cannot say I know how it could be eliminated. I do believe, however, that scientific progress requires both fact and fancy. References 1. May, T.: "Asbestos," in Mineral Facts and Problems, US Department of the Interior Bulletin No. 630, 1965. 2. Raunio, V.: Occurrence of Unusual Pleural Calcification in Finland: Study on Atmospheric Pol lution Caused by Asbestos, Supplement 47 to vol 55, Ann Med Intern Fenniae, Helsinki, 1966. 3. Wells, J.: in discussion Wills, D.W.: Economics ' of Dust Control, Ann NY Acad Sci 132:335-336 (Dec 31) 1965. 4 Fleischer, W.E., et al: A Health Survey of Pipe-Covering Operations in Constructing Naval Vessels, J Industr Hyg Tos 28:9-16, 1946. 5. Marr, W.T.: Asbestos Exposure During Naval Vessel Overhaul, Amer Industr Hyg Assoc J 25:264 268, 1964 6. Mitchell, J.: Health Progress in an Asbestos Textile Works, Arch Environ Health 3:37-41, 1961. 1967 Arch Environ Health--Vol 15, Sept 1967 290 ASBESTOSIS--COOPER I. Merewetber, E.R.A.: Annual Report of the Chief Inspector of Factories for the Year 1947, Lon don: Her Majesty's Stationery Office, pp 79-87, 1949. 8. Gloyne, S.R.: Pneumoconiosis: A Histological Survey of Necropsy Material in 1205 Cases, Lancet 1:810-814 (April 14) 1951. 9. Doll, R.: Mortality From Lung Cancer in As bestos Workers, Brit J Industr Med 12:81-86, (April) 1955. 10. Merewetber, E.R.A.: Annual Report of the Chief Inspector of Factories for the Year 1955, Lon don: Her Majesty's Stationery Office, 1955, p 206. II. Braun, D.C., and Truan, TJD.: An Epidemio logical Study of Lung Cancer in Asbestos Miners, Arch Industr Health 17:634-853, 1958. 12. Mancuso, T.F., and Coulter, E.J.: Methodolo gy in Industrial Health Studies, Arch Environ Health 6:515-524, 1963. 13. Seiikoff, I.J.; Churg, J.; and Hammond, E.C.: Asbestos Exposure and Neoplasia, JAMA 188:22-26, 1964. 14. Dunn, J.E., and Weir, JM.: Cancer Experi ence of Several Occupational Groups Followed Pro spectively, Amer J Public Health 55:1367-1375, (Sept) 1965. 15. Jacob, G., and Anspach, M.: Pulmonary Neo plasia Among Dresden Asbestos Workers, Ann NY Acad Set 132:536-548 (Dec 31) 1965. 16. Eaterline, PJ3,: Mortality Among Asbestos Products Workers in the United States, Ann NY Acad Sci 132:156-165, 1965. 17. Buchanan, W.D.: Asbestosis and Primary Intrathoracic Neoplasms, Ann NY Acad Sci 132:507 518 (Dec 31) 1965. 18. Wagner, J.C.; Sleggs, C.A.; and Marchand, P.: Diffuse Pleural Mesothelioma and Asbestos Expo sure in the North-Western Cape Province, Brit J Industr Med 17:260-271, 1960. 19. Hourihane, D.O.: The Pathology of Mesothe- Iiomata and an Analysis of Their Association With Asbestos Exposure, Thorax 19:268-278, 1964. 20. Wagner, J.C.: Experimental Production of Mesothelial Tumors of the Pleura by Implantation of Dusts in Laboratory Animals, Nature 196:180, 1962. 21. Smith, W.E., et al: Mesotheliomas in Ham sters Following Intrapleural Injection of Asbestos, J Mt Sinai Hosp 32:1-8, 1965. 22. Gough, J.: Differential Diagnosis in the Pa thology of Asbestosis, Ann NY Acad Sci 132:368 372 (Dec 31) 1965. 23. Gross, P.: Today's Pressing Question--How Safe is Urban Ambient Air? Arch Path 86:195 (Aug) 1966. 24. Stewart, M.J.: The Immediate Diagnosis of Pulmonary Asbestosis at Necropsy, Brit Med J 2:509, (Sept 15) 1928. 25. Thomson, J.G.; Kaschula, R.O.C.; and Mc Donald, R.R.: Asbestosis as a Modem Urban Haz ard. S Afr Med J 37:77-81, 1963. 26. Thomson, J.G., and Graves, W.M. Jr.: Asbes tos as an Urban Air Contaminant, Arch Path 81:458-464 (May) 1966. 27. Cauna, D.; Totten. R.S.; and Gross, P.: Asbes tos Bodies in Human Lungs at Autopsy, JAMA 192:371-373 (May) 1965. 28. Webster, I., in discussion Thomson, S.F., Physiological Effects of D.O in Mammals. Ann NY Acad Sci 84:736-744, I960.' 29. Meurman, L,: Asbestos Bodies and Pleural Plaques in a Finnish Series of Autopsy Cases, Acta Path Microbiol Scand Suppl 181:107, 1966. 30. Anjilvel. L.. and Thurlbeck, W.: The Inci dence of Asbestos Bodies in the Lungs of Random Autopsies in Montreal, Canad Med Assoc J 95:1179 1182 (Dec 3) 1966. 31. Cooke, W.E.: Asbestos Dust and the Curious Bodies Found in Pulmonary Asbestosis, Brit Med J 2:578-580 (Sept) 1929. PUBLIC MEDICAL PROBLEMS We must stop this fragmentation in medicine as well as the fragmentation of our serv ices to the large indigent segment of our population. Our four public assistance medical programs should be one. And here I include prenatal, delivery and postpartum care, general hospital care for medical and surgical problems and the Head Start Project and school health program. Only in this way can we insure continuing supervision and con trol of disease. Consider the present situation in one of our larger cities. Families must visit, often simultaneously and also in another location, the health department for prenatal care, the county hospital for general medical services, the Head Start Project for their younger children, the school health program for those that are in school, the crippled children program if they have a crippled child, and the speech defect program for speech therapy. A typical pregnant indigent woman with four or five children must spend so much time and money for transportation to and from these nine separate so-called free services that it is no wonder she has no time or money to keep her family well, let alone happy.---Reis, R.A., MD: "Progress, Problems and Priorities," read before the AMA National Con ference on Infant Mortality in San Francisco (Aug 12, 13) 1966. Arch Environ Health--Vol 15, Sept 1957 American Academy oj ( Relat: Air] Phi F OR GOOD reason, dence, it is generally acc of cigarette smoking is manner with a risk of lu clear is the relationship the disease. Allied to th; how air pollution, or an> sociated with urban lit cigarette smoking: Is the of lung cancer explained separate effects, or is it i To begin with, it cam j air pollution hypothesis is true that carcinogens I^ ed air of cities, that lu: greater in urban than in some extent, greater in small cities. But the rela been modest, with excet and the characteristic measure exposure to air area of residence, or res ther of which may also b< ure of other things. Granted, a similar arg against the cigarette 1 smokers may differ from Submitted for publication April 12, 1967. From the California Cane gram, California State Depar Berkeley. _ Read before the 19th anmv ican Academy of Occupation cisco, Feb 9, 1967. Reprint requests to 2151 B Calif 94704 (Dr. Dunn).