Document gOJ82YqDjLD2eKJDZNJ16ENa

_,#" c Ti-:t; ,-,-.:..it" YORK TIMES, TUZSDAY: MAY 2, 19/8 ---- ----~------------ I. vvarning to Y//orkers Seen as Start of U.S. Effort to Put Focus on Asbestos B~ JANE ' E BRODY i. . who will servicing ~e old, exposed in the f~ture asbestos-lined ships. while -~ aucsreods.sTwfroomwertehemeBr~i;woohkol:linveNd aovrywoYrakredd. may _be possible ol eure, to increase the chances ex_pAel~tthsoI~tg, hwams the .eyes of too httle and some health too late, the warnmg w01:kers rIsespureedsenWtsedaneFsed~aeyralto asbestos eff_ort to . The warning issued last week by JoEeph A: Califano Jr., Secretary of Health, EducatiOn and Welfare, was undoubtedly prompted _in large part by the growing Four cases of mesothe~t?ma have 6ccurred among the families of rormer Paterson asbestos workers. Asbestos-.Coated Clotl\es ~c. maTohuu&n~tchcoaafnnccaeesrboeifsstdo<eslvireeml.cotplt~inn-egrebaolndayat,s'b.be~J,s~tttohs1.et ' I . . . . .begm to foc_us more P?bhc attentwn on a longstandmg and Widespread occupationa! health hazard. Eight to 11 million Ameri- number of lawsuits filed against Federal ~gencies for Illness. and death causea !>y Job-related asbestos exposure, . I n Q. umcy, ~ass., .a 35-year-old. woman awsrbthestmoses~oothre~heorm\Ja:'hios the daughter of an died of mesothello- ItSakneottoknporwonduhceowdiJsiettalsee.asTbehsrtoousghlt.mduasyt co-ntrol and better work practices ashes- tos workers tOday are far better protect .., News cans have been exposed Thus far, the . cot~rts have held that rna, as d1d his w1fe. The young woman ed than those of decades past;., But is Analysis to this persistent mineral once ~he Gover~ment Jt~~ws 9f a haz~rd .recalls .her moth,er's practice of shakin_g current pr_otection good enough? : through their work, however resultm~ from rts activities, rt must. ~n- ?ut _her husbands asbestos.coated cloth :In addition, virtually all city-dwellers brief, in asbestos plants, form tho~e who have. be~n put ~t !n- mg m the Y~rd where the children played. and many other Americans harbol' ashes I Ishipyard~, co.nstruction and elsewhere. These workers, especially those ex- creased nsk. If there ts an opportumty for redress, the Government sho':lld also Wfat goo~ can. come of Secretary Ca_Iifz.no s warnmg, si~ce asbestos-caused diS- f!JS particles tissues, the irllesthuelti.ro1tunagisrbaonrdnoe t hpearr tl)ioed!y~ . posed years ago when asbestos dust was '. say that ~hose ~ar~ed ar_e ent1t;!ed to eases ar.e !a-rgely mcur~ble? The chances that wear off brake linings. buildings ana 1 rampant in the work environment, face compensation. . . of devel?pmg asbestos-mduce~ lung can- air-condWoning systems. Surveillance of - greatly elevated risks of developing and Worker's Right to Sue . cer, wh1ch causes one In five deaths present and former ash_ estos work$'$ may 1. dying of a wide range of cancers, espe- cially lung cancer and an otherwise rare and, thus far . invariably fatal cancer According to Dr Sidney Wolfe head of the Heal~. Rese~ rch Group, a w' at~- msam~lok?1Jnft~g;~egaswrbeoedrsuktcoeesrs dwtohoeesrk.nDes:rOkst,.smaTrohekroepu:rgQahcutletaitircnl~yf help to delineate the hazards of low-level expOsure and th& tos .may play Jn rcoalue~iinfgancy,:ntcheart ,asbes- itt, the .. called mesothehoma, as well as the lung dog agenc_Y m Washmgton, D.C., Mr. Cab- detection of asbestos-caused cancers. it general populatiOn.. _. .o ; disease, asbestosis. As little as a month's fano failed to tell workers. of their right _ occupational exposure to asbestos has in- to sue the Government. He noted that 1duced_ cance: decades later. some 500 asbe.rtos workers had already The warnmg comes late because these collected $20 million in damages inclu_d- . dangers have been known for decades. The first report of asbestosis among . mg $5 .. m1lhon from the Federal ~ovem- . - - " "J American asbestos workers was made in 1930.. In 1961, Dr. Mount Sinai Medical Icrveinn~ rJi.n selikoff of New York. ment Dr. should W~!osolfehasvaei.!d?rtghaam~zethdea Gsuo~veeirl?lmanecnet a leading researcher into the effects of asbestos, first revealed the grave cancer pmreo~graGmo,vecomnmt~acttmwgoarknedrsextaomdmemtegrmfm~re risk faced by tHose who worked. in a wh1ch one~ mrght hav~ b~n exposed to dusty asbestos plant in Paterson, N. J. asbestos Without knowrng 1t. Hazards to Insulation Workers As Dr. Selikoff has found, lt sometimes takes detailed s-earching through the job In 1963, insulation workers who han- histories of mesothelioma patients to find dled asbestos products were shown to the time, perhaps only weeks long, when be facing similar hazards. In 1971 Dr. relatively large doses of asbestos were SeHkoff warned the United States Nary undoub~dly inhaled. Nearly all the ship- that shipyard workers, eyen those who yard workers who have develope4 me- worked only a month or two during the sothelioma never worked directly with war and did not -directly handle asbestos, the mineral, but ever.y workday they in ., risked developing mesothelioiT)a 30 or 40 haled asbestos-llulen atr. s: 'years later. Asbestos was the favored in The Secretary also did not address I~ sulation material in ships; as well as "in himself to the fa<:t the mesothelioma has . homes, factories and office buildings . begun to show up in people who never 0 .1 The Navy stopped using asbestos a few worked with or near asbestos; rather, Ce1nl 1vears ago but that does little to help these cancer victims lived .with asbestos 'the millions already exposed or those workers or near where asbestos was C1l ~ ._,.,.~ ,,. ftn.,3~ -.-. ~~., '"'' -~ 4C-10 FLEET OWNER ' BI-MONTHLY 74,100 JAN 1978 Bds: fleet praised for fighting asbestos hazard For its "excellent performance in protecting district mechanics from a cancer-causing substance, asbestos in fiber form," California's Health Dept. has commended the Golden Gate Bridge, Highway and Transportation District. Golden Gate Transit, operating a fleet of 248 buses, was praised for protecting the 42 district mechanics who work with asbestos lining while performing brake and clutch maintenance and repairs on buses. California is the first state to require employers to report workplace use of asbestos. Asbestos is the most widely used of 18 cancercausing chemicals and substances regulated in California as part of a comprehensive program to prevent job-related cancer. Excessive exposure to asbestos fibers can cause lung cancer, a rarer form of cancer known as mesothelioma, and a lung ailment called asbestosis. State Health Director Jerome A. Lackner, M.D., said, "State industrial hygienists are discovering in inspections that asbestos in bus, truck and auto brake-repair shops is a significant potential health hazard to California workers, but one which safe work practices can control. "An estimated 74,000 mechanics and other workers in 22,000 autoand brake-repair shops serving the public are potentially exposed to asbestos through brake-repair work. Several thousand more workers doing brake repairs for transit systems, truck and bus lines and utility-vehicle fleets potentially risk similar expo- sure. Several citations for unsafe use of asbestos have been issued. "So it is encouragingly good news when we learn that a large fleet operator such as Golden Gate Transit is effectively protecting its mechanics against exposure to abestos fibers. "The district's San Rafael braI~e..... repair facility is an outstanding example of safe asbestos use. It is well equipped to minimize dust. The district mechanics are using safe work practices." The district mechanics are mem- bers of the International Association of Machinists & Aerospace Workers (lAM), Marin County lodge No. 238. The Machinists union was represented, along with employer, gov- ernment, and science representatives, on the State Health Dept. advisory committee, which early this y~ar drafted the asbestos regulation now in effect. Dr. Fred Ottoboni, Ph.D., head of the department's Occupational Cancer Control Unit, said the transit district followed these key procedures to maximize worker protection ag~inst asbestos fibers: o New brake linings are "arced" (shaped to fit) with a low-speed lathe rather than a power sanding ma- chine that could produce airborne fibers. 0 Arcing is done in a room separate from other workers so that asbestos waste is isolated from other workers. o The small amount of dust generated by this process is collected by an exhaust system. . 0 Waste material is put in labelled containers and disposed of in plastic bags. 0 Cleanup of brakes prior to repair is done with a damp rag rather than with compressed air, thus elimi- nating a serious source of dust. - / FMSI 05655 / Wanted: 'reasonable' cancer plan The American Industrial Health Council, an ad hoc industry group formed to oppose the policy proposed by the Occupational Safety and Health Administration for defming and regulating carcinogens, launched its attack last week at OSHA's lengthy hearings in Washington, D.C. (CW, May 24, p. 14). Paul Oreffice, president of Dow Chemical and AIHC chairman, stressed that the OSHA proposal needs "substantial modification" but the AIHC is taking a "positive and open stance" and is "seeking dialogue and cooperation." In laying the foundation for AI HC's 17 scientific witnesses who followed, Oreffice emphasized the "need for control and regulation of carcinogens in the \vorkplace." He said OSHA's categorization plan-separating suspect chemicals according to the likelihood that they will cause cancer-can be made "practical and workable" if it is designed along the lines of AIHC's proposed vers.ion rather than OSHA's. Robert E. Olson, a St. Louis University professor of medicine, criticized OSHA's policy for leaning "too heavily" on data from laboratory mice and for ignoring human evidence that shows no risk of cancer when animal tests indicate otherwise. When there is "vast human exposure to given chemicals without a detectable increase in cancer incidence," Olson said, "this evidence should be weighed heavily in interpreting mouse or rat test results." He also took exception to the implication in OSHA's policy that there is an "epidemic of cancer." Olson claimed that tobacco, alcohol and rich diets are responsible for 75-79% of total cancer mortalities, and that the number of cases caused industrial carcinogens is "much less than !%." George Claus, a toxicologist with Rutgers Medical School, challenged much of the government's cancer plan. Specifically, it ignores the significance of the various routes of administering chemicals tested, permits use of only a single test species, and ignores negative findings in cases where a carcinogen has been tested on two or more species, he says. Bernard L. Oser, a toxicological consultant, disputed OSHA's position that there is "no safe level" for humans for material that causes cancer in animals. He emphasized that "there is a wide judgmental gap between the findings in a group of animals and the conclusion that the substance is a potential carcinogen" to humans. Dept. of Labor attorney Edward Klein and labor representatives questioned industry's policies rather than the scientific issues. Klein .asked Oreffice whether companies differed in the degree of responsibility with which they treat their employees and, if so, whether more irresponsible firms had a competitive advantage. "That's why we support reasonable regulation," Oreffice replied. He likened it to the "reasonable" 55-mph. speed limit rather than a "unreasonable but undeniable safer" 10-mph. limit. Oreffice concluded by saying that industry wants government to understand that "we are not trying to injure or kill people, we are trying to protect people as best we can." No time to sit back "The days when business people can sit back in the bushes and not participate in the public decision-making process are over," Dow Chemical President Paul Oreffice said last week in a wide-ranging interview with McGraw-Hill editors. That will be a key to developing a "rational" approach to government regulation of industry, he said. Oreffice had just returned from Washington, where he led off industry's testimony on the Occupational Safety and Health Administration's proposed cancer policy as a chairman of the American Industrial Health Council (see story, left). "Regulation is the single most inflation. ary thing" affecting Dow, he said. The company's health and environmental research has been growing at a rate of 20-30%/year and now amounts to about 15% of the over-all R&D budget. Calling it "defensive" research, he explained that the company is considering splitting regulation-inspired research into a separate category to assure that emphasis on basic product and process R&D is not diluted. The company will spend $230 million on R&D this year, a gain of 12% over the $205 million spent in 1977. Oreffice said he is dedicated to keeping "offensive" R&D going "up and up and up." Touching on other areas, he said: The company will soon announce an on-site co-generation project at Freeport, Tex. It recently withdrew from a project to supply lignite to Houston Lighting & Power (CW, June 7, p. 22). Unless Dow can reach an agreement with the Environmental Protection Agency over emissions from coal-fired power plants at Midland, Mich., it will tempo~ rariJy shift SOf!1e operations to Other locations until the Consumer's Power nuclear plant comes on-line in 1982. Dow now buys "a lot of naphtha" from Russia, and company executives have met With soviet Chemical Minister Leonid Kostandov to discuss possible future deals. Thorium traces in pit The Nuclear Regulatory Commission is reviewing AMAX's plans for cleaning up a thorium-contaminated pit at the Par- kersburg, W.Va., plant formerly owned by the company. NRC says the highest levels of radioactivity found at the site- 2 milli- rems/hour, measured aboveground -do not pose a short-term health problem to workers, but are unacceptable long-term levels. But cleanup efforts, normally a simple procedure, are being slowed by the presence of highly combustible zirconium also in the soil. The problem arose when L.B Foster (Pittsburgh), which bought the plant last year from AMAX Specialty Metals Corp., was installing equipment for its planned $2-million piping plant. While digging a hole inside a building, the zirconium caused an explosion. In a later incident there, the tracks of a bulldozer were reportedly melted off during grading work. Subsequent analysis of the soil showed traces of the highly combustible zircon- ium, and also of the thorium. NRC notes the thorium was contained in Nigerian zircon sand used to manufacture zircon- ium alloy rods, and 'that thorium was not used in the process itself. NRC says the 20-30-ft.-deep pit also contains discarded machinery and as- sorted acids. NRC says the agency never gave any authority for thorium burials there, but it adds that agency provisions allow up to 12 burials/year of small amounts under certain conditions, includ- ing keeping records of burials. NRC is reviewing such records. AMAX Speciality Metals says it did not bury any radioactive materials there at any time. It did speculate that there may have been some undetected spillage when the company removed I, I00 tons of N igcr- ian sands to a disposal site approved by the former nuclear agency-the Atomic Ener- gy Commission-after AMAX bought Carborundum's half of the venture in 1967. It adds, however, that AEC inspected the operation at the time and was satisfied about the operation. Carbo- rundum also denies any dumping of radioactive materials. June 28, 1978 CHEMICAL WEEK 17 FMSI 05656 i I ! l r CURRICULUM VITAE Hans Weill, M.D. Education Tulane University, 1951-54, B.A., June, 1955 Tulane University School of lV(edicine, 1954-581 M.D. 1 June, 1958 Post-Graduate Medical Training 1 Intern, Mt. Sinai Hospital, New Yor~ City. 1958-59 Resident, Charity Hospital of Louisiana, New Orleans. Tulane Medical Unit, 1959-60 Research Fellow Department of Medicine. and Pulmonary Laboratory, 1 Tulane University School of Medicine, 1960-61 Chief Resident, Charity Hospital of Louisiana, New Orleans, Tulane Medical Unit, 1961-62 Teaching and Research Appointments Instructor in Medicine, Pulmonary Diseases Section and Pulmonary Laboratory, Tulane University School of Medicine., 1962-64 Assistant Professor cf Medicine, Tulane University School of Medicine, 1964-67 Asso~iate Professor of Medicine, Tulane University School of Medicine, 1967-71 Professor of Medicine, Tulane University School of Medicine. 1971-present Director, Specialized Center of Research (SCOR) in Occupational Respiratory Disease, NHLI, 1972- Hospital Ap2ointments Visiting Physician, Charity Hospital of Louisiana at New Orleans, Tulane Unit Chief, Pulmonary Function Laboratory, Veterans Administration Hospi to.l, New Orleans, 1963-present Consultant in Pulmonary Diseases and Medicine, USPHS Hospi. tal, New Or-leans, 1964- present ' FMSI 05657 . H:ans Weill, M;D. - CV cont'd ' .. .J Honors and Societies Phi Beta Kappa, 1955 Alpha Omega Alpha, 1958 American Thoracic Society, 1962 Orleans Parish Medical Society, 1963 Diplomate, American Board o-f Internal Medicine# 1965 Fellow, American College of Chest Physicians~ 1965; Governor for La. 1970 Fellow, Atnedcan College of Physicians, 1967 Cc-:tLEi .-~d in Pul-~-,_o~J;:/ 'C>~s 2a.s a~ .....~~r:~1~~ u::;::an.. Boa~d o Internal!',..{~Jt~i:le,. 1~6& American Federation for Cli:1ica.i. Research,. 1967 Southern Society fo1' Clinical Investigation, 1969 Chairman, Post-Graduate Course,. Pulmonary Fu.nction.Ju Health aD.d Disease, 1970-72 Fellow, Royal Society o! Medicine, 1971 Ney;r York Academy o:f Sciences, 1971 Society for Occupational and Envi'ronmental Hea.l!:b.., 1972. Co{mcilo:r-at-la.rge, American Tnoracic Society,.. 1973 Pres:i.dent-ele.ct1 Ame.d.ca.n Thor<i?.c.:ic S?~iety,. 1975 1-Jlember, Task Force on Environmental Lung Diseases,. Nati.ona1 Heart and Lung Institute, NIH, 1972 Gonsultant3 :National Institu:~e ot Occupational. Safety and Health. TDI Criteria Document, 1973~ Phosgene Crit~da Document,. 1975 Planning Committee, Occupational i.il~}tg Di,sease paot-gra.duate course. - Annual Meeting o: American Th.a:racic:: Society,. 1973 Program Corr...rnittee, A.-neric:a.n Lung Associa.ti~. 1973 Faculty Advisory Committee. Tuli:'..ne University Scllool o:fMedicine,. 1973 Secretary-Treasurer, New Orleans Acacle.rny of I'nte:~:nal Medicin&, 1973 - FMSI 05658 ', T ~~ASBESTOS INFORMATION ASSOCIATION NORTH AMERICA 1660 L Street. N.W. I Washington. D.C. 20036 1 (202) 223-4885 17 November 1975 Memorandum For: John Marsh, Raybestos-Manhattan John Riopelle, Bendix Corporation E. H. Feierabend, Abex Corporation Subject: Materials of interest concering friction materials The enclosed material is forwarded as a matter of interest: 1. "Is Brake Lining Dust Harmful?" pamphlet, Nov., 1975 Asbestos Information Committee, U.K. 2. Extracts from two papers presented at International Conference, Dust and Gases in the Work-Place, June 18-20, 1975, Bonn, Germany As you are aware the Association proposes to rewrite the pamphlet, "Asbestos and Brake Linings" (also enclosed). Your recommendations will be appreciated. fJtt._ R. H. Mereness Executive Director cc: Stanford Christian, Bendix Corp. Jim Armstrong, Bendix Corp. Ike Weaver, Raybestos-Manhattan, Inc. ~d Drislane, FMSI Enclosures RHM:vld --------- FMSI 05659 Is brake lining dust harmful? *,f., ~CD asbestos information committee FMSI 05660 Is brake lining dust harmful? The brake linings on which drivers of motor vehicles depend to bring them to a safe stop incorporate asbestos fibre. However. writers on this subject occasionally express the view that the braking of millions of vehicles emits particles of asbestos into the urban atmosphere in such quantities as to create a risk to the health of the general population. What are the facts? This dust consists almost entirely of degraded resin. fillers and other brake lining additives. and products of wear from the metal brake drum or disc. Although the asbestos content of conventional brake linings may vary from 25-65 per cent by weight it is almost entirely converted by the considerable heat generated by the action of braking into other materials. What happens in braking 1 Any examination of this theory must start with what happens when the brakes of a vehicle are applied. Vehicle brakes operate by converting the energy of the moving vehicle into heat which is then dissipated into the air. In drum brakes a friction lining is applied to a brake drum; in disc brakes friction pads grip a rotating disc on the wheel hub. Asbestos is an essential ingredient in friction linings and pads primarily because it acts as a reinforcing agent which maintains its strength and stability through a wide range of temperatures and pressures. For technical reasons only chrysotile (white) asbestos is employed in friction materials. Little dust liberated The friction between lining and drum or between pad and disc creates wear products. which look like a fine dust. Experiments carried out by various Government and industrial laboratories throughout the world have shown that the free asbestos fibre in the small amount of dust liberated from brake linings rarely exceeds 1 per cent 1 of the total products of wear. The Environmental Protection Agency of the US Government commissioned the Bendix Corporation to set up a test programme to measure brake and clutch emissions during actual vehicle operation. The asbestos content of the brake emissions ranged in two sets of tests from 165 per cent to 003 per cent; only in 3 out of 90 analyses was it over 1 per cent. In a third group of tests the range was from 022 per cent to 0003 per cent 2 . Expenments with disc brakes have shown that. in their case. the free asbestos f1bre is an even lower fraction ----- FMS\ 05661 of the total products of wear. In tests carried out by research staff of the Ford Motor Company. Detroit. on a production disc brake3 less than 002 per cent of the lining wear was released as asbestos fibres. Amount not harmful Asbestosis is a disease associated with the inhalation of high concentrations of asbestos fibres over many years. The British Occupational Hygiene Society has published a Hygiene Standard for Chrysotile Asbestos Dust which is designed to virtually eliminate the risk of developing the earliest recognisable clinical signs of asbestosis. This standard is the basis of those which apply under the Asbestos Regulations 1969. to work with asbestos and asbestos products. The minimisation of asbestosis has. at the same time. minimised any associated risk of lung cancer. Tests made 1n the urban atmosphere have recorded the presence of asbestos in amounts at least 1.000 times below those regarded as the standard for chrysotile dust in occupational situations. There is no evidence that this trace amount of asbestos in the urban environment can cause damage to the lungs of the general public Thus the risk of contracting asbestosis or lung cancer through the application of brakes on motor vehicles is negligible for the general public. The risk of contracting mesothelioma (a rare tumour which has been mainly associated with crocidolite (blue) asbestos) can be virtually discounted as this type of asbestos is not used in the manufacture of brake linings. It is recognised that chrysotile asbestos is less likely to produce mesothelioma and where it has done so the dust levels to which the cases were exposed were greater than could occur in the urban air as the result of vehicles applying their brakes. "Asbestos bodies" may be found in the lungs of people in random series of autopsies. The presence of asbestos bodies does not necessarily imply a connection with asbestos-associated disease nor is it an indication of it. Where large numbers of asbestos bodies have been found they have invariably been the result of occupational. not general environmental exposure. Occupational exposure The only possibility of a risk to health from brake and clutch linings arises in their manufacture and where regular or contmuous machining and maintenance FMSI 05662 work is carried out. Such work, however. is controlled by the 1969 Asbestos Regulations to ensure that those employed on such operations are not exposed to excessive amounts of dust likely to impair their health. The Environmental Control Committee of the Asbestosis Research Council has produced a Control and Safety Guide and a simple illustrated leaflet explaining the precautions which may be necessary for workers involved in these activities. REFERENCES 1. Brake Lining Decomposition Pro- ducts. by Jeremiah R Lynch, National Centre for Urban and Industrial Health, Journal of the Air Pollution Control Association, Vol. 18, No. 12. pp 824-826. Exposure to Asbestos during Brake Maintenance by D E Hickish and K L Knight. Annals of Occupational Hygiene. Vol. 13. No. 1 ; January 1970. pp 17-21. 3. Asbestos Emissions from Brake Dynamometer Tests by A E Anderson. R L Gealer. R C McCune and J W Sprys. Proceedings of Automobile Engineering Meeting of the Society of Automotive Engineers, May 14th to 18th 1973. 4. Report of the Advisory Committee on Asbestos Cancers to the Director of the International Agency for Research on Cancer (World Health Organisation). Lyon, October 1972. 5. Control & Safety Guide No. 8. Asbestos-based Friction Materials and Asbestos-reinforced Resinous Moulded Materials; Environmental Control Committee. Asbestosis Research Council. P.0. Box 18. Cleckheaton. West Yorkshire. BD19 3UJ. 2. Brake and Clutch Emissions generated during Vehicle Operation, M G Jacko. R T DuCharme and J H Somers. Proceedings of Automobile Engineering Meeting of the Society of Automotive Engineers. May 14th to 18th 1973. The Asbestos Information Committee 2 Old Burlington Street London. W1X 2LH Telephone: 01-734 0081 November. 1975 .'" .. . ,,~ FMSI 05663 Staube und Gase am Arbeitsplatz International Conference Dust and Gases in the Work-Place ( Colloque -International Poussieres et Gaz au Poste de Travail 18. - 2o.6.197S :aonn - Bad Godesberg Stadthalle zusa~~enfassungen Abstracts RCsum2s FMSI 05664 --""--'-"_________________________________ 15. G. KU.hnen~ G. Heidermanns, A. Schiltz, Bonn und R. Prochazka, MU.nchen (BHD) Dust Concentration During Production of Friction Linings and their Treatment in Gara~.2. In connection with the Accident Preventing Regulations i.e. ''Protection against Hazardous Mineral Dusts" (VBG 119) measure- ments on dust concentration and of the asbestos content were taken during the production of friction linings (final treat~ent) as well as in the brake service of garages. 'l'he aim of these technical investigations \:hich were made vrithin a research plan of the "Employer's Liability Insurance" together with medical investigations, was the identification of eventual hazards to health of the employees occupied with these labours. Friction linings contain 20 to 60 % of chrysotile asbestos depending on the utilization purpose. These values have been figured out during measurements of the dust concentration at working sites during mechanical treatment of friction linings as well as during manufacturing and at the brake service. The evident dust concentration depends on the way and extent of preventive dust protection actions. During manufacturing the concentration is about the TRK value for chrysotilc, at the broke services above the TfiK value, however, for short ex- position times only. Juring blov:inp: out of brake drums a short termed high dust co:--t~entrat "'Lon occurs, ho'.-;cver, asbe~;tos \;as not proved to be eviCcnt. Laboratory nnd test stand cxperimen~s issued tha~ .J.::.t~ st_.o~~ i~'. t:r;J.nsform'~d r:10rpholop;i cally by the tern11~r<1tu~:-::; FMSI 05665 ... I 2 . 16. Woitowitz, H.-J. und Valentin, H. Erlangen (BRD) Occupational Medicine Investigations on Hazards to Health by Dusts Containing Asbestos In Germany in 1973 extensive regulations or the protection of asbestos exposed persons became effective (VBG 119). Hereby, the question arose whether workmen exposed to dusts of brake linings containing asbestos can be generally considered as endangered in respect of fibrogenic effects via inhalation. In regard to this operating method problem there has been per- formed on a selective universe a casual cross section study with retrospective onset. 210 male and female workers with at least ten years brake lining dust exposition and o three operating methods out of about 50 different plants were involved. The data for each person comprised 200 details together more than 40.000 i.e. concerning the anamnesis, under special consideration of profession and working site, and the diagnosis. The thorough examinations were led by occupational physicians and internists who applied physical, in-vitro- clinical, electro-cardiographic, radiological and latest lung functional analysis procedures. The occupational medical evaluation of diagnoses of an asbestos exposed worker, nowadays has to be multidimensional, principally. The extensive data, therefore, after formation of syndrmtie groups had to be reduced to 5 types of diagnoses with defined de~rees of diagnosed security: 'l'yp~ I 'l'ype II Type III 1';/ ~~ e IV v'"~y~l'__: AIF eventually AU' possible A1F not presumable AIF competible diagnosis AIF normal diagnosis FMSI 05666 I? - 2- ' the transformation into Forstcrit has been provP~. The transformation, probably, succeeds via an amorphe phase. Due to these result~ besides dust protectio~we regard prophylactic examinations in respect to occupational health of all employees in the final manufacturing as necessary. At the brake services all employees occupied with the mechanical treatment of friction linings should be controlled by the occupational physicians in case the weekly exposition time to asbestos dusts exceeds 3 hours. The employees occupied with blowing out do not have to be controlled unless the result of the medical examination does make it necessary. FMSl 05667 . '. - 2 - The judgement of risks is mainly based on diagnoses in respect to eventual AIF (Type I). Suspected diagnoses in respect to a beginning AIF (Type II) were not disregarded. The prevalent diagnoses of type I and II amounted to: a) 51 males who produced brake linings or handled unused brake linings 5,9 % resp. 15,7 % 43 females of the same operating method 0,0% resp. 7,0% b) 63 males in the truck service who treat unused brake linings and blow out brake drums 1,5 %resp. 14,5 % c) 53 males in the car brake service who blovr out or brush out brake drums 0,0 %resp. 5,6 % The considerations in respect of occupational health resulting from this will be discussed according to the specific risks of operating methods. FMSI 05668 IIJ" ,.. y I I I l _ . WS AND COMMENT DEC 011977 Occupational Cancer: Government Challenged in Beryllium Proceeding The beryllium industry and the government have been locked for months in an intense struggle over the question of whether beryllium should be declared a carcinogen. At issue are not only the merits of an epidemiological study conducted by the chief government agency involved, the National Institute for Occupational Safety and Health (NIOSH), but questions of fair play in government regulation. Even the conduct of the director of NIOSH. John F. Finklea, arespected but controversial federal official, has come under question, because he engaged in a telephone conversation that industry says was a naked threat to intimidate industry witnesses. The focus of the controversy is a study done by NIOSH which concludes that, among the beryllium workers employed since the 1940's at a plant in Reading, Pennsylvania, the incidence of fatal lung cancer was unusually high. Industry has accused NIOSH of "gerrymandering" its data to produce this result. Joseph K. Wagoner, who is a principai author of the study and is now a special assistant to the director of the Occupational Safety and Health Administration (OSHA). which must decide on beryllium's carcinogemctty, defends the study, saying the deficiencies are due to industry's poor records. "There is absolutely no doubt in my mind that beryllium is a human carcinogen," Wagoner told Science. But Wagoner and other officials stress that sound epidemiology is hard to do because industry may be tampering with or destorying worker records. The beryllium companies deny doing any improper meddling. They would like to see the study redone. or another study made of a separate cohort of beryllium workers. Wagoner. however, says another study "will mean more delay and increased risk to the health of the American work- er." The study. known as Bayliss III because it is the third study of beryllium workers by NIOSH bench scientist David L. Bayliss, is crucial to the determination of a new standard for beryllium. NJOSH proposed a new standard on the basis of animal data in 1975. The industry has argued that the animal data are an insufficient base for the new standard be- 898 cause the animal data are negative for beryllium copper. the form to which some 70 percent of all the industry's workers are exposed. The government's case. based only on animal data, therefore looks iffy. But Bayliss III. claiming on epidemiological grounds that human beings exposed to beryllium incur a lung cancer risk. has strengthened the government's case. If the study is considered acceptable, it will increase the likelihood that the Administrator of OSHA, which is part of the Department of Labor, will approve a new, stricter standard and that the courts would uphold a subsequent appeal. But by the same token the study has caused the industry great alarm. Aside from the questions of scientific merit and fair play, the NIOSH beryllium controversy also involves the issue of when animal data alone can be the basis of federal standard setting, and what level of human epidemiological evidence should serve as allowable in federal regulation. These questions are all the more important now because the OSHA's new director, Eula Bingham, is a former cancer scientist, who has announced~ new, get-tough stance on regulating carcinogens in the workplace (Science, 21 October). Toxicity of Beryllium The beryllium industry came of age in the 1940's, when there was increased demand for the tough, lightweight, heat-resistant metal during the Second World War. Since then. beryllium has been widely used in electronics and missile parts, and in other applications. But from the start it was known that beryllium is toxic to humans: it causes a disease known as berylliosis. Since the 1940's then, the industry has had to limit exposures to 2 micrograms per cubic meter for workers. Although animal data linking beryllium to tumors in some animals have been around for years. NIOSH only recently (in 1972) issued a "criteria" document laying out the case against the metal as carcinogenic. In 1975, NIOSH proposed that the 2 microgram per cubic meter standard be lowered to 0.5 microgram per cubic meter. Industry has responded that such a change is unwar- ranted by the scientific evidence and that the lower standard is technically impossible. It seems that in the early 1970's few people paid much attentiQn to the pos sible carcinogenic potential of beryllium to humans. particularly since the only two well-known studies of the subject, known as Bayliss I and Bayliss II (Published in 1971 and 1972) examined large cohorts of beryllium workers at several plants and found no unusual incidence of lung cancer. But at some point, Bayliss and Wagoner decided to restudy the life histories of workers at a single plant. They picked one at Reading, owned by Kawecki Berylco Industries, Inc. (KBI). In early 1977. OSHA scheduled a hearing on the proposed new standard; the two major producers of beryllium, KBI and Brush Wellman. Inc.. who knew of the existence of a new study partly be cause it had been reported in a Cleveland, Ohio. newspaper, began asking NIOSH for the data it was examining. In March, Brush hired a Washington consulting firm, Equitable Environmental Health Corp.. to handle the human epidemiological issues relating to the proposed standard. At this time, there began a series of events through which each side has become embittered, with each accusing the other of harassment, obstructionism, and bad faith. The entire controversy, and many of the associated emotions, were aired on the public record in August and September during the hearing. The industry charges, first, that. NIOSH did not make a good faith effort to turn over its data on the more than 3000 Reading workers it was using as the basis of Bayliss III. so that industry could check NIOSH's calculations and conclusions. Brush's Vice President, Martin B. Powers, testified that "throughout 1976" the company made both informal and formal Freeqom of Information Act requests to obtain the data. Although NIOSH kept giving the industry other information and documents, it did not hand over the Bayliss II paper or accompanying backup until 1 July 1977, shortly after officials met with OSHA's Bingham, and threatened to sue if the material was not forthcoming. Indeed. it seems that, throughout the hearing NIOSH continued to hand over information at the last minute, and then only in response to formal, freedom of information act requests-in some instances 72 hours. or 48 hours, before industry was to present expert testimony on the material. NIOSH's version of these events is that the repeated freedom of information APt ~3<? SCIENCE, VOL. 1118 ( 3J FMSI 05669 t'? requests were intended to paralyze NIOSH's attempts to get its beryllium study finished for the hearing. Said Peter Infante of the NIOSH Cincinnati staff, where he and Bayliss were working on it, "They strap you down with all those requests. They had the whole staff battened down to the point where we cpuldn't get our own work done ... We could have met the [hearing] deadline easily if we hadn't had those requests." In any event, industry received a copy of the Bayliss III paper-which turned out to be a first version, a second was submitted at the hearing-on I July, and turned it over to Equitable, when another incident occurred. Industry charges that Finklea, through a telephone threat, caused Equitable to cease working with Brush and to prevent one of its scientists, Michael Utidjian, from testifying on the deficiencies in the NIOSH study. According to the hearing transcript, on 12 August, 4 days before the hearing was to begin, Finklea telephoned William Malloy, the executive vice president of Equitable, and "suggested that there might be a conflict of interest on Dr. Utidjian's part if he participated in the hearing on Brush's behalf." Finklea was referring to the fact that Utidjian was also working on Equitable's NIOSH contracts to prepare criteria documents on other substances. The following day Malloy ordered Utidjian off the Brush contract and told Brush that Equitable would not participate further. Brush officials say the call was tantamount to a threat of the loss of NIOSH business if Equitable did not stop working for the beryllium industry. Brush may sue Equitable for breach of contract, while another Equitable official, a beryllium expert, who objected to Malloy's decision is leaving the company. Finklea was abroad for several weeks and could not be reached for comment on this incident. Both Wagoner and Howard Walderman, a lawyer who works on NIOSH matters, declined to comment on Finklea's actions and what he really intended to accomplish. At the hearing, Finklea defended himself by saying that he wanted "Mr. Malloy to look at the contract he had with the Federal government, which had a clause in which people were seeking to avoid the appearance as well as any actual conflict of interest. I expressed concern about that and ... just called that to his aitention." But Edward J. Baier. deputy director ofNIOSH, told Science that Finklea had been under the impression that Utidjian was working full time on NIOSH work, and became alarmed when he saw Utid- jian's name on the industry witness list. But in Finklea's absence, Baier declined comment on why Finklea made his concern known by a phone call to Utidjian's boss. instead of by a more conventional route. Industry is also charging foul play because NIOSH did not produce the principal author of the paper, Bayliss, at the hearing. By all accounts, on 16 August when the hearing began, Bayliss was on leave from his NIOSH job in Cincinnati and was registering as a doctoral student in the department of epidemiology at the University of North Carolina. Industry believes that Bayliss was deliberately kept away because his testimony would have admitted the weaknesses in the case against beryllium. NIOSH's Wagoner, who was Bayliss' superior at the time, told Science, "Bayliss didn't want to testify. We asked him and he said he didn't want to come." Science located Bayliss in North Carolina, where he gave his version of these events. Bayliss says he received a phone call from his boss's boss, Finklea, the Friday before he was to register. "He said he wanted it to be known that an invitation stands if I cared to testify. He indicated that Wagoner could handle the whole thing though, so I said I didn't see any need for me to go." He says NIOSH has barely contacted him since, and that he learned of the "Where's Bayliss" controversy through "a third party who had access to an OSHA newsletter." Study Under Fire Besides the fair play issues, the Bayliss II study has become the major focus of the controversy. Brush's president and chief executive officer, Robert W. Biggs, claims that the study is "slanted" and that the cohort of workers has been "gerrymandered" to come to the conclusion that beryllium workers have an increased risk of getting lung cancer. NIOSH counters that any errors that have been found in the paper are "insignificant." Wagoner told Science that the Bayliss study, and another one produced by Thomas Mancuso on the first day of the hearings showing an increased risk, "converges" with the animal data presenting a total case that is "irrefutable." Bayliss Ill examined the histories of 3070 workers, who worked at the Reading KBI plant, between January 1942 and December, 1967. The study calculated the expected number of deaths from lung cancer for the group at 33. The conclusion that beryllium is linked to lung cancer hinged on the fact that the observed number of lung cancer deaths was larger, namely 46. At the hearing, Brush's statistical consultant H. Daniel Roth, testified that the results were impossible to verify because the tables that he received in July on 3070 individuals showed no birth dates for 70 percent of the cohort, or everyone listed as alive. Since the ages of the majority of the cohort were unknown, it was impossible to replicate NIOSH's life table analysis or verify its expected lung cancer death rates. The NIOSH paper presented blocks showing that the largest number of lung cancer deaths occurred among workers employed at the Reading plant 5 years or less. But examining the 46 cases of lung cancer death, name by name, Roth found that 4 who had been classified as being there for approximately 20 years actually worked there a year or less. Moreover, Roth found of the 46, some 30 had been there fewer than I year, 24 had worked there fewer than 6 months, and 17 had worked there fewer than 3 months. Both Roth and other expert witnesses testified they knew of no theory of cancer where the risk increased as the length of time of exposure shortened. (In an interview, Wagoner admitted he knew that a large number of the deaths were among people who had been employed less than a year. Asked why this fact was not mentioned in the paper, Wagoner replied, "I don't know what it would have meant.") Roth claimed that the "excess" of 46 lung cancer deaths as compared to the expected 33 is explained by correcting for smoking and the plant's location. The Bayliss lii paper used the assumption that smoking habits of the cohort were similar to those of U.S. males in 1964. Although the paper acknowledged that a 1968 plant survey showed smoking at the plant to be higher than this figure, it was discounted on the grounds that the county in which the plant is located was below national average. Factoring in the actual 1968 smoking data instead of assumed 1964 data, Roth calculated the expected lung cancer deaths among the cohort to be 38 to 44numbers which eliminate the statistical significance of the observed value of 46. But Roth pointed out that the lung can- cer death rate in Reading itself-an old industrial town-was much higher than both the surrounding county and the U.S. as a whole. In fact, applying the Reading rate to the KBI plant population. Roth says. the expected lung cancer deaths became even more than those actually observed. Wagoner, interviewed about the specifics of the study, admitted that there were deficiencies in the information available on the cohort of workers. "We 1 1 ; 1, 2 DECEMBER 19n 899 FMSI 05670 ~ tme people whom we weren't sure but we have to go out and buy the meat whether they were alive or dead," he and vegetables." said, "so we assumed they were alive." The hearing ended in September. but He explained the shifting size of the co- the administrative judge before whom it hort, which at difl"erent times numbered was held, has allowed until mid-Decem- 3070, 3201, and 3055, was because ber for posthearing submissions. On the NIOSH was trying to square its informa- NIOSH side, these include a fourth Bay- tion with that offered by Mancuso in his liss paper. Industry will submit the most study, which included some Reading comprehensive rebuttal yet to the Bay- workers. Industry's position on the Man- liss and Mancuso studies~ cuso study is that it should be stricken from the record, since the paper seems Warfare Continues not to mention smoking at all, and .since But the warfare continues. Brush's Mancuso has said he would give his vice president, Powers, questions backup data to the industry but has failed whether the hearing record will make to do so. any difference. since Wagoner, one of Interestingly, the authors of the Bay- the most ardent supporters of a new be- liss study differ on how strong a case ryllium standard, recently moved to their paper makes. Bayliss told Science, OSHA to be Eula Bingham's special as- "I thought there was a pretty, reason- sistant. Industry believes that Wagoner ably strong case, but of course that's a - should not participate in Bingham's deci- judgmental matter." Wagoner, in a sepa- sion-making on beryllium. and is seeking rate interview, maintained that the evi- a written reply from Bingham on Wagon- dence was all "converging" and the case er's role. "irrefutable." Infante said: "The results Brian MacMahon, professor of epide- and the interpretation don't change. We miology at Harvard, has gone over the had to keep stating, defining, who the co- latest cohort tape which has 3055 work- hort was ... We know what the meal is, ers and 47 lung cancer deaths. The added lung cancer death is that of a man who was hired and terminated on the same day. Science asked Wagoner whether he knew of the man's brief employment. "I guess we didn't have that information" he replied. So the parties to the controversy seem locked in an epidemiological treaqmill. with NIOSH blaming the problems in its cohort data on industry, and industry blaming the "slanted'' data on NIOSH. In the long run, the controversy's im- portance lies not so much in whatever ths:: beryllium industry ultimately knuckles under to a new tighter, standard. It is i ! I \ more important as a precedent. for beryl- lium is among the first of many alleged carcinogens on which OSHA's Bingham will have to rule. These decisions will have their politi- cal element; that is, Bingham will want to not only protect American workers . but to give the appearance of protecting American workers. But she will also have to judge whether the scientific evi- dence in each case ultimately supports or erodes those political decisions. -DEBORAH SHAPLEY I I. ! ; On paper there are reasons for the lab- oratories to worry about losing their in- dependence. The reorganization that ac- National Laboratories: Focused Goals companied the formation of the energy department created two new vehicles for and Field Work Hinted Under DOE - monitoring the work of the various laboratories at the highest levels of the agen- cy. For their institutional needs, the lab- oratories will no longer report to regional operations offices but will report to an Even before the federal energy agency Sandia, Los Alamos, and Livermore. administrator at the rank of assistant sec- underwent two face-liftings, people were The man who had primary responsibility retary in the department. In addition, the saying that the national laboratories for getting the new department running, laboratories will be regularly ~.::rutinized were declining in importance and were in Tom Reed, has visited a number of east by a newly created council composed of -need of new missions. Their old roles- coast labs. The major laboratory direc- all the line administrators of the depart- as practitioners of basic research, nucle- tors have also met with the under- ment. The council will be chaired by the ar reactor development and weapons de- secretary as a group. The message in same man who has responsibility for sign-proved to be embarrassingly nar- these meetings has been that no abrupt day-to-day coordination of all the depart- row when the Energy Research and De- changes will occur. but the past roles ment's energy research activities, Un- velopment Administration (ERDA) in- of the labs are being analyzed care- dersecretary Dale D. Meyers, and that herited the labs from the Atomic Energy fully and their future roles may gradually may be an indication of how closely the Commission in 1975. Although ERDA change. laboratories' efforts will eventually be in- expanded the breadth or energy research Soundings taken in Washington when terwoven into the whole research and de- at many of the individual laboratories, it the energy department was inaugurated velopment fabric. never quite determined what should be in early fall raised a number of problems. Whatever develops in the new depart- the laboratories' role in the national en- The laboratories had accumulated a mul- ment's relations with the field, the possi- ergy program. titude of new programs to spearhead bility that the changes pose a threat to In the 2 months since the Department ERDA's acceleration of energy research. the traditional independence of the labo- of Energy inherited all of ERDA's Some critics said that the labs spend too ratories is taken seriously in some quar- former programs, officials of the new en- much money on projects that are not put ters. Two weeks ago the House Science ergy agency have been crisscrossing the up for bids and that their expenditures and Technology Committee called in the airways to inspect some of their 25 labo- would be more productive if brought un- directors of eight major labs to testify in ratories and research centers. The new der zero-based budgeting. The various a hastily arranged hearing that had no ap- undersecretary or the department has laboratories have enjoyed considerable parent routine purpose. Some observers visited three laboratories in the west, autonomy during most of their history. thought that the committee, which has 2 DECEMBER J9n 901 FMSI 05671 Jn.Y 1:1, 1974 TIIJ<; llEOICAI, .JOtm~UI, OF AUSTlL\LL\ 45 Clinical Revietvs THE BIOLOGICAL EFFECTS OF ASBESTOS S. F. McCur.LAGH1 M.D., s.sc.{uED.) Sydney ,Yed. J. A1lst~ 197~. ll: 45-49. Recent development!!! are reviewed. The terms pulmonary asbestosis and pleural asbestosis should be Introduced to avoid confusion between the two. Pulmonary compliance is the single most valuable test of lung function in the detection of pulmonary asbestosis, and a method has been desc.-ibed recently which may make this measurement practicable in the routine surveillance of an asbestos exposed workforce. Pleural "asbestosis may mimic restrictive lung disease but only If the pleu.al changes are very extensive. There is little evidence linking these essentially benign changes with mesothelioma. It is now thought that the carcinogenicity of asbestos and of other fibres is a function of th!!lr physical rather than of their chemical structurl!. Lung cancer in an asbestos worker can be attributed to asbestos exposure only if there is also evidence, albeit perhaps only histological, of pulmonary asbestosis. Accumulating evidence continues to emphasize the importance of cigarett:o smoking in the lung cancer of a~bestos workers. Current standards of work place hygil!ne are reviewed and conflicting opinions about methods of medical surveillance compared. In the general urban atmosphere, the amount of asbestos is between one hundrl!d thousandth and one millionth of that held to be safe in the workplace. Motor-.:ar brake linings release little, If any. asbestos in their normal road use. The amount of asbestos in water and beverages is likewise negligible. .. Chi<( ~(t,Hta.i omn.r. JaUI~.S Hardie & Cuy Ply Limitt"tl. Arldrf:-;:-:. for nprint~: Dr }i. F. ).lcC'ull;lt;"h. Janu-~ Har,lie & Coy f'ty Llullttol, 1'.0. Box 219, Gmn,illt, :'\.S.,\. 21-1~. Tm; biological effects of asbestos are: fncreaslngly engaging the interest of scientific worlten, and the annual number of papers on the subjeel published each :rear continues to increase exponentially (Figure- 1). NUMEIER OF SCIENTIFIC PU~LICioTIONS ON BIOI..OGICAL EFFECTS 01' ASBES10S 1900-1971 IN IOEN FILES TOTAL 1532 U.S.A. 26/o UK 21/o GrR~ANY 11/o ltJOO 900 800 100 1>00 500 .coo 300 200 100 i>IOL"ItC 1: Number oC scientific publlcallons on blologlc::tl ~ff"<:ts oC a:.-;hts\u::t 1900 to l~';'l. Recently a working grou1 met at Lyons, in France, to review pro~:ress In this field. It is laq::ely on the p:l.pers delhf'red at this meeting, and on subsequent work, that lhf' remarks in this l>:ll>er are based. Earlier work is I \ 1 '1\ ~! FMSI 05672 - ' Hi referred to only In so far as it is relevant to recent dev'lopments. PULMONARY ASBESTOSIS Confusion is arising over this term (:\lcCullagh, 1!l69), since to some the word "asbestosis" means pulmonary asbestosis, while to others it also includes the pleuml reaction and the two do not necessarily go together. l\ly opinion is that the specific term "pulmonary asbestosis" should be adopted. In the 1960s it was generally held that emphysema was not a feature of pulmonary asbestosis. This view has, in recent years, been losing ground, and Fournier-:\!assey has lately reported that emphysema was found in one-third of the asbestotics in the recent and most important Quebec study (l\1. R. Becklake, 1972, personal communication). The former ILO radiographic classification of the pneumoconioses has been reviewed and a new classifi cation, more suited to the radiographic changes of asbestosis, has been prepared ( Bohlig et alii, 1970) and validated (Rossiter, 1972). Standard films illustrating this classification may now be obtained from the International Labour Organi~ation in Geneva. One of the most important recent developments Is the study reported by Jodoin et alH {1971). A group of 24 men was studied; all had had normal chest radiographs but 13 had had a substantially greater exposure to chrysotile asbestos than the other 11. A battery of lung !unction tests was administered to them, and static pulmonnrr compliance was outstandingly the most reliable of these in <separating one group from the other (P 0005). The early detection of pulmonary response to asbestos exposure Is of particular importance in the routine, periodical medical examination of asbestos-exposed workforces. Heretofore we have had to rely primarily on the chest radiograph but It now appears that a much more sensitive screening test may be available. The late Dr McKerrow and his colleagues (Devan et alii, 1971) have devised a technique which eliminates the need for the balloon; they report that, except in the grossly obese and those whose respiratory disability necessitates the use of their sternomastoid muscles in qttict breathing, "early results suggest a good correlation with the inspiratory static compliance using the oesophageal balloon in normal subjects and in patients with pulmonary fibrosis and emphysema". The suitability of this method for the medical surveillance of an asbestosexposed workforce is currently being investigated by us in association with Professor Bryan Gandevia and his colleagues of the University of New South Wales. Ditrusing capacity, incidentally, Is of little value in the early diagnosis (Harries, l!l71; Becklake et alii, 1972). PLEURAL ASBESTOSIS Since 1927, thickening of the pleura has been associated with exposure to asbestos (Cooke, 1927) and, more recently, s.everal other substances (Smith, 1952). These changes have generall] been held to be of no more con sequence than the callusses on tbe hand of a smithy. At Lyons, Jones (1972) emphatically held to this view. On the other han<l Harries ( 1971) has ft!IJOrted sub~tanti::\1 dccreincnls of Iun!: function in men who had only pleural, and no llUlmonary asbe~tosis. Recklake d alii (1!!70) have expn~ssed the view that such decn~ments only occur with very extenshe pleural thickening. Eisenstadt (1965u and 19G~b) has reJ!ortcd four cases of mesothelioma following apparently benign pleurisy with effusion. Some clinicians have inferred, unjustly I think, that the changes we have referred to here as pleural asbestosis may on occasion give rise to pleural mesothelioma. It seems Improbable that pleural asbestosis, which is known to be parietal (Thomson. 19i0a), should be the precursor of mesothelioma, which is believed to be a tumour of the visceral pleura (Thomson, 197011). It Is also to . be noted that while exposure to the asbestos anthophyllite commonly leads to pleural thickening (Raunio, 1966), it has never been known to lead to mesothelioma (Raunio, 1966; International Agency for Research on Cancer, 1972). In Canada, G. W. Gibbs (1972, personal communication) has expressed the view that "pleural asbestosis" is mOTe likely to be due to talc or mica, and indeed, in the formal report of the Lyons meeting it is recorded that "pleural plaques have been associated with past exposure to all commercial types of asbestos. But additional factors, other than asbestos itselt, are inYo\ved" (International Agency for Research on Cancer, 1972). It has been suggested (Kiviluoto, 1965) that the Incidence of pleural asbestosis might be used as an epidemiological tool. In the study of those known to be substantially exposed to asbestos this may be so, but in the general urban community it Is not so. Gilson (1969) found pleural thickening in 187 out of 3,SGO routine chest Xr:!.y films taken in the Midlands. The asbestos exposure of 113 of these subjects was compared with that of 113 age and sex matched controls. He found only "a slight but unimpressive excess of positive histories of exposure to asbestos among the cases". THE CARCINOGENICITY OF FIBRES Evidence is Increasingly accumulating to show that the carcinogenicity of asbestos is a function of its physical, not its chemical, characteristics and that this ability Is shared by other fibres having similar physical characteristics (Stanton, 1972; Timbre\1, 1972). We have all long wondered why the mesotheliomogenic potency of croci dolite should be so much greater than that of other asbestoses, among which Is Included the particular form of crocidolite found In the Transvaal (Siuis-Cremer, 1965). Tlmbrell and his colleagues (1971) have produced nry gooQ, evidence to show that it is the fine straight fibre of most crocidolites, including that formerly mined at Wittenoom in Western Australia, which enables them to be more readily and deeply inhaled and thus it is these fine crocido\ites, much more than any other asbestoses, which give rise to mesothelioma. It is to be noted, however, that Cottrell and Holt (1972) have failed to confirm this work; the matter Is thus sub judice. The view that lung cancer associated with asbestos exposure is, in fact, due not to asbestos but to carcinogenic oils (Harrington and noe, 1!l65; Gibbs, 1969) or to some associated trace metal or benZJ!yrene (Dixon et alii, 1970) is not now generally held. THE ROLE OF TOBACCO SMOKING The very important role of cir:aretle smoking in asbestosassociated lung cancers was first pointed out by Selikotr FMSI 05673 "' J f ... and hi:; coll<'agues ( Selikoff ct alii. I!JGS ). In the con tinuing study both of Hammond and SclikoiT's group of insulators in New York (Hammond and Sclikoff, 1972) and by .\luiel Xewhouse ant! hPr collea;;ues (1!1'i!l), of a group of asbestos textile workers in Britain, there has been no excess of lung cancer among asbestos workers who did not smoke cigarettes. There is no e\idence that tobacco smoking plays any role in the development or mesotheliomata. RESPIRATORY CANCER This term is used here since the international classification of causes of death, on which most records, and therefore most epidemiological studies, are based, does not distinguish between lung cancer and pleural mesothelioma. The only important recent development here is that reported by Xewhouse. She has followed, up to 1!>70, a group of male asbestos textile workers first employed after the Introduction of the British Asbestos R"gulations of 1933, but before 1%4. These she di<ided into those who had experienced high, moderate and low exposures. She had earlier reported (Newhouse, 1969) an excess of respiratory cancer among those who had experienced a high exposure, but she has now reported (1\ewhouse, 1972) that such an excess is beginning to appear among those whose exposures had been only low to moderate, though not if they had been exposed for less than two years. On the other hand things are perhaps not quite as grave as Hammond and Selikoft's (1972) data would suggest. Among their 370 insulation workers, there ha\e been 42 deaths from lung cancer, when only 475 were to be expected on the basis of age-specific male white United States death rates. The comparison would have been based better on local standardized mortality rates; but this objection does not substantially affect the conclusion to be drawn from the data. Lung cancer, attributable to asbestos exposure, "occurs, so far as is known, only in workers whose lungs show signs of pneumoconiosis" (International Labour Office, 1972). However, this does not necessarily imply clinical signs of pulmonary asbestosis; the evidence may lie in the parenchymal histological findings. MESOTHELIOMA It is now generally accepted (Wagner ct alii, 1971) that some 85% to 90'/c of mesotheliomata are attributable to asbestos exposure while, in the remaining 10'/o to 15'/c, the cause is unknown. Likewise, it is generally accepted (International Ag<'ncy for Research on Cancer, 1!>72) that nil commercially ueed forms of asbestos, with the exception of anthophyllite, may give rise to mesothelioma, though the overwhelminr; majority of cases of this ~till uncommon tumour are attrihuted to the finefihrrd crorido\ites. Throug-hout the world, the asbestos C'lu-ysotilc ll<"cuunts for more than 90% of total u~ap;e. Davis (1972), of the Institute of Occupational :'llcdicine in Edinburg-h, has produecd "uwsothcliomata" in mice and rats usinl': intraperitone;ll emplacement of crocitlolite and tihrcglass. lie has shown that, at least initially, the abnormal cell re11roduction is sub-mesothelial and takes place under a continuous layer of undisturbed mesothelium which only later di~integratcs. This observation raises the int(rcsting, if academic, question: "Are mesotheliomata really mesotheliomata or are they something else?" OTHER CANCERS Excessive nulllbers of cases of gastrointestinal cancer among those exposed to asbestos continue to be reported (McDonald, 1972; :\leunnan ct alii, 1972; Newhouse, 1972; Selikoff and Hammond, 1972) but in no case has the excess been statistically significant. A similar excess of cases of laryngeal carcinoma has been claimed (Stell and ;'l.lcGill, 1973), though the claim has been criticized (Holmes, 1973). The claim that exposure to asbestos was associated with ovarian tumours has not been supported by the first large mortality survey of women previously exposed to asbestos (International Agency for Research on Cancer, 1972). THE WORKPLACE HYGIENE STANDARD Briefly put, in the United Kingdom the standard is a time-weighted average of two fibres per cubic centimetre (f./em") (British Asbestos Regulations, 1969; (British) Department of Employment and Productivity, 1970); at the moment in the United States it is 5 f./em, but will become 2 r.;cm' on July 1, 1974 ((United States or America) Department of Labout, 1972) though it is to be noted that the Tiueshold Limit Value Committee- of the American Conference of Go\'ernmental Industrial Hygienists stands firm in its view that the standard should remain at 5 f./em (Stokinger, Chairman of the TLV Committee, 1972, personal communication). In Australia the standard, though it has at present no statutory authority, is a time weighted average of 4 f./em (National Health and Medical Research Council, 1970). The British Standard is based on the study of some 300 asbestos textile workers (British Occupational Hygiene Society, 1968). The recent study of 908 men in New Orleans who were employed in manufacturing asbestos cement products (Weill et alii, 1973) suggests that the standard should probably lie somewhere between 4 and 5 f./em'. One cannot say that any of these standards has a sound scientific foundation, but in the American study exposures appear to ha\e been more accurately established. It is, I think, unanimously agreed that the most accurate method of measuring workplace asbestos-in-ail" levels is the counting of fibres on a membrane filter on which they ha\e been collectl'd from a known volume of air (a procedure which, however, entails much tedious microscopy). Hecent prons10ns for the surveillance or workplace asbc~tos-in-air levels in the United States ((United States of America) Department of Labor, 1972). and in Germany (Shultz, 1972, pE'rFonal communication) impose such a burden by this tedious microscopy that in both countries (Holmes, 197:!; Shultz, 1972, personal communications) there is an inclination to return to gr:n-imctric sampling. ltowe;er, the accuracy of this method leaves very much illdt0d t" bt' de$ircd. A happiPI' solutiOn woultl be the rurther tll'\'l'inpment of a dPvice known as the Quanliml't-720 which, it is hoped, will pro\c capable of automatically counting one cOIIIl>lcte membrane filter every four minutes. FMSI 05674 ' n .+a.::z; = '\ :-.. TiiZ _I,L!<~DICAL JOGR~f AL OF AUST!ULI.\. MEDICAL SURVEILLANCE OF THE WORKFORCE 'l'he usual l>raclice, when a workforce i~ ext>osed to some substance known to be hazardous, is to require a periodical medical examination, as is now the case in America ((United States of America) De!'artment of Labor, 1972). No sueh provision is made in the Briti~h regulations. When these regulations were drawn up it was decided that it would be far better to study, with great care, the men wo1klng for the major em!'loyers, whose exposure levels were mensared and known and the progre11s o! whose health could be watched by a factory doctor with special "knowledge and understanding of the problem, with H.:.I.I. Factory Inspectorate sut>ervbing and coordinating the study. Proceeding thus it is to be expected tbat our know ledge and understandil1g of the biological effects of asbestos will progtesslvely increase and that tb.e adequacy of the hygiene standard will be more readily and promptly assessed., I am in no doubt that this philosophy is the correct one and very much l101le that any regulations that may be adopted in Australia. will be so framed a:; to enable this approach. I should add that the accurate counting of asbestos fibres on a membrane filter cannot be done by the Inexperienced, and two laboratories counting the same filters have been known to disagree by as much as a factor of 15 (Beckett, 1972, personal communication). Laboratories in the United Kingdom, the United States and Australia are now collaborating to reduce th~se differences and to establish lutclaboratory correlation. Unless they achieve these goals it will remain Impossible to measure the doseresponse relationship in man. THE GENERAL URBAN ENVIRONMENT Asbestos levels in the general atu1osphere are of the onler of nanograms per cubic metre (lo- gm/m") and can only be measured by electron micro>ICOI>Y In 16 such measurements In and about the town of Rochdale in England, the level in seven cases was of the order of to- gnt/nl' and in nine cases of the order of 10- gm;m. Unexpectedly the level on the moors was found to be higher than In the Roch~ale town centre. The British workplace hygiene standard of 2 f./em" Is equivalent to 01 mg;m' or 10 gmjm; ((British) Department of Employment and Productivity, 1970). Thus the level of asbestos in the urban air Is about one hundred thousandth to one millionth of the hygiene standard. Similar studies i11 the United States have reported levels of the ortler of 10 gm/m'. Even "in lower l\Ianhattan about construction sites where extensive stlraying of asbesto<~ containing fire-proofing material was taking place, asbestos in air levels one-eighth to one-quarter of a mile (some 200 to 400 metres) away averaged 60 x 1o gm/m', the highest count being 375 x 10 gm/m" (Nicholson and Pundsack, 1972; Sclikoff et alii, 1!172). There is no evidence to suggC'st that urban asbestos In-air levels are anything other than harmless. Something should he said about the mueh-maligned brake lining. Every application of the hrakc, it is widely hcliC\"<'d, releases a shower o( fibrOUS asbestos into the atmosphere. This was never a very promisitl!; hypothesis since It Is most unlikely that any asbestos would survive the t('mpenttures g!IH'rated at the brakin,:; interrace. Lyuclt (19GS) of the United State;; l'ublic Health Senice. having studied the matter, concluded that. "only a very small fraction of the asbestos escaped as free fibre while the remaining was transformed into some other non fibrous material. A si;nilicant release of rree fibre occurred only under conditions extreme enough to produce brake failure". There have been several other studies but none that I know of has Jed to a. co11trary conclusion. Seltkoff (1970) summed the matter up: "Brake linings do not constitute a hazard". Since asbestos occurs commonly In nature, though only infrequently in comuwrclally worthwhile amounts, It has no doubt been present. in many of the world's drinldng waters since time Immemorial. Its presence in- North American waters (Cunningham and Pontefract, 1911; NichoLson and Pundsack. 1972) and in British beer (Biles and Emerson, 196S) has lately been reported. It has been estimatlld by the Asbestos Information Committee In London that the total annual British. output ot beer, of over one thousand million gallons. contains only 1wo thousandths of an ounce ot asbestos, or some 10 gm/m'. CONCI.USION The industry is well aware of the hazards of asbestos, and having briefly reviewed these I think we should also remember that, if we consider no more than its fire retardant prollerties and its use in brake linings, asbestos has saved far more lhes thnn It has claimed. With the great improvement of standards of Industrial hygiene over the last decade this credit balance, if I may so call it, will increasingly grow more favourable. ACKNOWLEDGEMENT I would like to expr.,H.~ my thank.~ . to Dr P. V. Pelnar of the Institute at OccUtlntlonnl anti En\'ironrnental Health in :Montreal, who pro,ided me with Fh:ure 1 oC this Paller. REFERENCES BECKLAK>:, l(. R., FOUit:'<lERl!Ass>:Y, C., ltcDoN.\LO. J. C et alii (1970). 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Hyg., 16: 9. l~<n:n>:ATIO>:AL LABOUR OFFICE (1972), Re)IOrt of .lleeting of ~~~XJICTIB on the Contt'ol and Prevention of Occu1wtionol Cancer, Geneva, Jan. 10-17, 1972: 6, para~;raph H. .Jooor>t, G., GIBBS, G. w., lfACKLE)I, P. T., et alii (1971), Earb effects RcsJI. ot: Dis. asbesto , 104: sazeax. posur e on lung function, .tlmer. Rev. .JoNES, J. S. P. (19i2) ), Pleural J>laques, in ProccP<lings of tile lVorklng Gl'Olfp to Rcticu; the Biological Effects of Asbc:.to:r, I~yofls# Fr<wcc, October, 1!171 (In the pres.s). KIVILUOTO, R. (1965), Pleural plaques and asb~>stos: further observations of ~ndemk and other non-occupational asbestosis, Ann. N.Y. Acatl. Sci., 132: 235. LY>:CH, J. B. (1068), Brake llning decomposition products, J. Ail' Pollutlo" Contool Au., 18: 824. lllcCt:LLAGH, S. F. (1969), Fifteen cases of pleural mesothelioma associated with occupational exposure to asbestos in Victoria. (INter), liED. J. AUST., 2: 1029. lllcDo"ALD, J. C. (1972). Cancer In <'hrysotile mines and mi11s, In P3-ocrrtlhr.QII of tltr U!m4 kiuy G1oup to Rct:ic'lu tl~e Biological E/Jccts of Jlsbcstos, Lyons, F,ancc.. Octo[)cr, 19'72 (In the PN'SS). l\IErR~!AN, L. 0., KIVILUOTO, R., and HAKAMA, ){. on72), llortality and morbidity of emJ>loyees of anthoph)'llitc asbestos mines in Fintnnd. in P1occcclings of t11r. ll"atkiPig G't"OliiJ to Rct'iCiv the JJioloqicnl J.:ff,.cts oJ ..-1sbrstos, Lyons, Jt~rancc, Octo'bcr, 1973 (In ibe press). NATIONAl. HEALTH AND )[EDICAL HF'.sE.\RCH COL'NCIL (1970), AtmOSJJhctic ContlltniJtants, llYtJicuir. Stawlnnl!J for Contamiuants of the ..tir of tit~ lVotkplctcc, Commonwealth C.overnment Printing Onice, Canberra. NEWHOUSE, :\I. L. (1!Hi9) .\ sturly of the mortality of \vorlicrs In an asbestos factory, Brit. J. iltdr<str. .I!eel., 2.G: 2H. NEWHOl"Sf!~ ::\f. L. (l!li2). Caneer among asbestos workers In the a~bestos textile industry, In Proceedings of the Work- ing Group to Review the Biological Effect$ of .talteato, Lyons, fratzc~, Octob1.:r, 1!11 J (In the press.). N'rcnoLsON, \V. J., and Pu>:DSACK, F. L. (1912), Asbestos In the environment, in Proccetling. of 1/oc Working Group to Reuirw tla.e Biolnyical El/ecta of ,tsbcstos, Luons# Francs, October, 197J (In the press). RAU>:IO, V. (19G6), Occurrence of unusual pleural calcification In Finland. studies on atmospheric pollution caused by asbestos, Ann. 1/cd. ill tern. Fc>tn., 55, Supplement: 47. RossiTER, C. E. (1972), Initial repeatability trials of the UICC/ Cincinnati classification of the radiographic appearances of the pneumoconioses, Brit. J. illdn:ttr. Jltnl., 29 : 4{17. SELIKoFF, I. J., HA~UIOND, E. C., and CHuR.G, J. (1968 ), Asbestos exposure. srnoklng and neoplasia, J. Atue:r. tned.. Au., 20.: 106. SELIKOFT. I. J. (1970), In Proceedings of tile lt&ternatlonal Conference on P111:11mocolllosls, Johallne:tlmrg, Oxforcl University Press, London: 51 (discussion). SELIKOFF, I. J., and HA:nto~o, E. C. (1972), Cancer risk of Insulation workers In the United States, in Procecdlnna of the Workillg Group to Review the Biological BUcctll o[ Asbe&tos, Lyons, Ftauce, October,, 1912 (in the press). SELIKOFP', I. J., NICHOLSON, \V. J., and LA>:GF.R, A. )f. (19i2), Asbestos air pollution, .1rc1o. environm. Jllth, 25: 1- SLUls-Cn>:M~n. G. K. (19Ga), Asbestosis In South Africa-certain geographical and environmental considerations, .d.m1. N.Y. Acad. Sci., 132: 215. SMITH, A. R. (1952), Pleural calcification resulting from exposure to certain dusts, Allier; J. Roentgetlol., 67: 3 75. STANTON, :M. F_ (1972), Some etiologic considerations of fibre earcinogenes Review the ls. Bi In .Pro<"<e<lillga ()logical E/lt'ct,, o of f the lVookl>u Asbeatoa, Lyou sG, rForua1,n to ce, October, 1!171 (In the press). S"t&LL, P. ll., anti lfcGILL, T. (1973), Asbestos and laryngeal carcinoma, Lrn~t:et_,. 2: 416. THo~tso>:, J. G. (1970n), Pathogen<'sis of pleural pla<tues, In Proce!'diug.s of the lntcnuttional Confete~tce ou Pucum.o- couiosis, Johao111esburg, Oxford University Press, London: 138. THo~rso:oo, J. G. (19701>), The pathological diagnosis or malignant mesothelioma or Pl~>ura and J>erltoneum, in Procccd- inga of the IJ&ter"atlonol ConfeJencs on Pumotloconio.si8,. Johmuoesburg, Oxford University Press, London: lfiO. TUlBI:ELL, V., GRIFFITHS, D. l\1., and POOLEY, F, D. (1971), Possible biological Importance of fibre diameters of South African amphiboles, Nature, 232: 55. TnranELL V. ( 1972 l. Physi<'al factors as etiological mechan- isms, In Proccedi11gs of tile Working Grot<p to Review tle BlolotJical Bftccts of Asbestos, J,yous, Fallc.,, October, 191Z (In the press). (l'~ITED STATES OF AMERICA)' DEI'ARTMEl<T OF LABOR (1972), Oceupalional Safety and Health Standards-Standard for expo~ure to ashl!?'stos dust. J.~ctlrn1l R,-yi.9tf't, 3i: 11318. ''"AG~En. J. C., GJLSON, J. C., BERRY, G., and Tr3rBn:Er~L. V. (l!t7l ), Epidemiology of asbestos cancers, Btit. med. Bull., 27: 71. \VEtLL, H., \VA<:CF.N"PACK, C., BAII.EY, W., et alii (1973}, Radiographic and physiologic patterns among workers engaged in manufacture or asbestos cement products, J. occup...lied., 15: 248. WRIGIIT, G. \V. (19t;!J ), ,\shcstos nnd health In 1969, A titer. Rev. rrsp. Dis., 100: 467. fMS\ 05676 In the Forum Is Short-Fibered Asbestos Dust a Biological Hazard? Paul Gross, MD, Chariestoa. SC Conbary to U. deaetmiiU thet lhe finer the quartz' duet, the grMter Ita pathogenicity; the pelhogenlclty of the finest asbestoa dust 11M been llhOWI'I to be negligible. It has been the flndtng of ......-cit labo- ratories In Germeny, Englend. South Af.. rica, and the Unie.d Sbltee that st.rt-8- bered aabesaos, duet, Ia, leaa IbM s,. IR length, Is lncapallle of cauelftg llbroeia or cancer. Thla finding. In conjuncUoft with the failure ol dlu-nt labonltoriee In the United Kingdom and In lhla COUIMry 10 die- cern abnonnaiRIM following prolongelll asbeatoa feeding to rata. ahoukl IHd to the abandonment of ltle praM0t concepl that malntalna that masotheitOinea and gaatrolntaatlnal ca.-. arlee from the 1ft. geaUon of aabaalaa duM ct.Nd r - lhe tunp. These nagatlft,........ ~ .,_ llf- lay the alarm that hae been raiM aa a ,._ suit ol the llndlng of ultramlc:roacoplc mineral Iibera In certlllft bawara111 and drinking waler. By short-fibered asbestos dust is meant that which has a fiber length of less than S11- Although fibers of this ~ize usually constitute a very small fraction of the weight of a dust cloud, their numerical preponderance over the larger fibers may be manifold. Submitted for publicaUon Sept 19, 1973; accepted Jan 30, 1974. From the Department of Pathology, the Medi cal University of South Carolina. Charleston, SC. Reprint requests to the Department of Pathol ogy, Medical University of South Carolina, 80 Barre St, Charleston, SC 29401 (Dr. Groea). Inasmuch as asbestos fibers smaller than 51' tend to remain airborne longer than the larger ones, they have a greater chance of being inhaled. Furthermore, although the anatomy of the respiratory tract tends to prevent the intrusion into the airspaces of all but a few of the larger suspended particles, this deterrence does not extend to the smallest particles. The latter very readily enter the airspaces mth the inspired air. Some of the short asbestos fibers may settle on the alveolar surface by sedimentation, whereas the smallest fibers, behaving almost like gas molecules, contact the alveolar membrane by diffusion. What is the potential of these extremely fine submicronic fibers to produce disease? Is their potential greater than that of optically visible fibers? Is the behavior of submicronic asbestos fibers as opposed to that of larger fibers similar to that of the fibrogenic effect of very fine quartz dust as compared with that of the same weight of coarser quartz particles?'1 These questions take on added importance in view of the commonly held hypothesis that mesotheliomas of the pleura and peritoneum arise by the transmigration of fibers to the pleura and peritoneum, respectively. In the case of abdominal mesothe- liomas, it is assumed that the asbestos fibers cleared from the lungs are swallowed and then migrate through the intact intestinal wall to the peritoneum, there to initiate the development of mesotheliomas. So far as ability to penetrate into and t.ranamigrate across the intact intestinal wall is concerned, once again it would appear that the submicronie fibers would be better able to accomplish this feat than would the coarser fibers. Originally, the question ;Of the pathogenicity of the Short-fibered as- i bestos dust had relevance only to ..- people occupationally exposed to as- bestos; but more recently short as- bestos fibers have been found in ce!'tain beverages and city water, in ambient community air, and in the lungs of city dwellers... Con-' sequently, the relevance of the above question must now extend to entire .urban populations. However, lest undue alarm be raised by the last stat. ment, it should be pointed out that in city dwellers no disease has been ' found that could be attributed to the presence of submicronic asbestos fibers in the pulmonary tissues. Neither has there been documentation of an increase in abdominal cancel'l!l in . the general population, in spite of the fact that in many cities and smaller communities drinking water has been and is now transported in asbestos- . cement pipes. , At the International Conference on the Biological Effects of Asbestos held in Dresden in 1968, Klosterktltter> found that both chrysotile and crocidolite, ground to an average fiber length of less than 5)L when injected intratracheally or intraabdominally, produced no fibrosis. The Arch Environ Health/Vol 29, Aug 1974 Short-Fibered Asbeslos Dust/Gross 115 FMSI 05677 I.. u.::-:-"!, :~cy r::.:spon:;e cor:s!sted ~n1y of a macrophage reaction. In contrast, longer fibers of the same asbestos resulted in fibrosis in both regions. At the same conference Timbrell and Skidmore reported the results obtained in rats and guinea pigs ex- pos"ed to equal concentrations (by weight) of short-fibered amosite (90% of the fibers <41-' long) and long-fibered asbestos (45% of the fibers >4!1 14:lng). They concluded, "minimal reaction has been observed to short fibres but a marked reaction has been obsel'Ved to the longer fibres." In the following year, Webster' reported that monkeys inhaling finely ground crocidolite (fiber length <5~J-) also showed merely a macrophage reac- tion in the lungs. In 1970, Hilscher et al showed the ehrysotile or croeid~ lite, when ground to a fiber length of <SJ,L with a microtome and injected intraabdominally, produced no fibrous adhesions; whereas the same asbestos with greater fiber length did cause dense fibrous adhesions. ln 1971, the Johns-Manville Research Laboratory prepared for us 'chrysotile asbestos ground to a fiber length of<~ We injected this dust intratracheally into 10 rats and were able to confirm that such short~fi bered asbestos could induce no more than a macrophage reaction (unpublished study). In 1973 Smith et ai reported that hamsters injected intrapleurally with chrysotile ground to a fiber length of <11' developed no pleural cancer, whereas hamsters injected intrapleurally with longer chrysotile fibers did develop such cancers. Recently Wright (private communication) disclosed that in his laboratory short-fibered asbestos injected intratracheally also failed to elicit a fibrotic reaction. .Maroudas et al'" have concluded that, "Particles (mineral fibers) smaller than 201' in length induce neither growth in vitro nor mesothelioma in vivo." Thus, these reports from different laboratories are unanimous in finding asbestos that has an average length of <5Jl is devoid of pathogenic potential. This included not only the fibrogenic potential''''' but abo the cancerogenic potential."-''' It may be argued that when as- bestos, i3 ground to a very smal! fi her size, either in a ball mill or a hammermill, much of the energy is converted into heat and the heat may change the chemical structure of the fibers. To continue this argument: since, strictly speaking, the fibers so altered may no longer be asbestos, the bio-logic "inertness" of such "altered" asbestos need not necessarily apply to fine asbestos dust that has not been heated to a high temperature. This argument is rendered void by the following facts: 1. The short-fibered asbestos of Hilscher et a! was found to have maintained its fibrous structure after the grinding process. 2. Smith et al prepared short-fibered asbestos as an aqueous slurry. This obviated excessive heat. 3. It has been concluded that the chemical structure of asbestos does not determine its pathogenicity since synthetic chrysotile is devoid of pathogenicity. 11 The latter has the same chemical and crystalline structure as the natural product. Therefore, the mere process of grinding with the associated heat production does not account for the lack of pathogenicity of the finely ground asbestos. However, by fitting together some newly derived experimental findings, a theory has recently been formulated regarding the locus of pathogenicity of asbestos dust that does offer a reasonable explanation for this lack of pathogenicity." There is, however, one laboratory that reported that short-fibered asbestos is tumorigenic. Pott and Friedrichs" and later, Pott et al" maintained that 100 mg of chrysotile with a fiber length <31' injected into the abdomen of rats caused the development of cancers. Nearly 80% of the tumors were sarcomas-mostly fibrosarcomas. The character of the tumors produced by this technique should have ghen the authors pause for reflection; not only because rats will pro-: duce fibrosarcomas secondary to injected or imbedded materials known to be biologically inert, but also b~ cause subcutaneous fibrosarcomas are very eommon spontaneous tumors in aging rats. An indication of the ease and nor.,;pecificity of such tur:wr :'r'>duction in rats is demonstrated in the first" of the two above-mentioned papers when the authors list a betterthan 60% tumor production with mag- nesium hydroxide and a 55% tumor production with fibrous glass! In contrast, they reported only a 40% tumor production with ehrysotile. This lower - tumor production was doubtlessly related to a high mortality a.used, in turn, by the exceedingly high dosage of materials injected (100 mg). The employment of unrealistic dosage, of inappropriate routes of administration, and of inappropriate animal species (all three "sins" were committed by the above- authors) to achieve positive results has recently been adequately discussed by Dr. H_ E. Stokinger." When asbestos is ingested, it is the ultramicroscopically-sized asbestos fibers that are assumed to be responsible for the development of mesothelioma. by virtue of their alleged penetration and transmigration through the intact intestinal wall. The failure of short-fibered asbestO$ to induce mesotheliomas when injected intrapleurally makes the above assumption highly questionable. Unpublished data from different laboratories (David B. Clayson, University of Leeds; L. M. Swinburne, St. James's Infirmary, Leeds, England; and John M. G. Davis, Institute of Occupational Medicine, Edinburgh) in which rats were fed asbestos intimately mixed in their food, indicate complete failure to induce tumors or any other kind of abnormality by these regimens. (A joint paper describing these investigations from the different laboratories is in prepa- ration.) As one example, the following ex- periment may be cited: ten weanling male rats were placed on a finely ground basal diet containing 5% by weight of chrysotile asbestos. Five litter mates were pair-fed with the same weight of food as the experimental rats had consumed on the previous day. This regimen was continued for 21 months. At the end of this time, the weight curve of the asbestos-fed animals was not significantly different from that of the pair- 116 Arch Environ Health!Vol 29, Aug 1974 Short-Fibered Asbestos OusttGross FMSI 05678 !5 .: j '~ I\' 'i !) l f" ,l~ ~ - .-. ..:;--- . fcd ,.,,n::o!:'>. The animal:; 11ere killed 21 months after the initiation of the feeding period. At autopsy, no gross abnormality was found in either group of animals and microscopically no tumor or other gastrointestinal lesion was obsened." It is to be noted that in previous studies, the first asbestotic lung cancer death occurred 16 months after the initiation of the dust exposure" and the first asbestotic pleural cancer death in rats occurred 17 months after the intrapleural injection of asbestos dust." It is of interest in this connection that the dose of fibers in the intestinal tract of the asbestos-fed rats was astronomical compared with the dose of fibers that is likely to be swallowed daily by a pel"Son occupationally exposed to asbestos dust-and he, in turn, would have an astrCinomically greater dose of fibers than the dose of fibers ingested daily by an urban dweller drinking a beverage or water containing mineral fibers. The uniformly negative asbestosfeeding results should cast some doubts on the tenability of the concept that peritoneal mesotheliomas and an increased prevalence of gastrointestinal cancers arise in occupationally asbestos-exposed people from the ingestion of asbestos fibers cleared from their lungs. There must, of necessity, be some other explanation! Although not an asbestos-feeding study, a recent report purports to demonstrate that the presence of asbestos in the intestinal lumen results in the penetration of asbestos fibers into the blood stream and organs throughout the body, inclusive of the brain." The writers injected the asbestos into the stomach by means of a sy-ringe and needle, thereby ignoring the probable opening of vessels in the path of the needle track and the presence of injection! References 1. King EJ, et al: The action of different forms of pure silica on the lungs of rats. Br J 1114 Med 10:9-17. 1953. 2. Hatch T, Kindsvatter VH: Lung retention of quartz dust smaller than one-half micron. J lnd Hyq Toricol 29:342-346, 1947. 3. Gr~ss P, et al: !llineral fiber content of human lungs: A comparison of the counts obtained from the lungg of JOopie of Pictsburgh, Pa. with thO<\& from the lungs of people of Charleton, South Carolina. Am lnd Hyg As80< J 33:A162, 1972. 4. Grou P. et al: Lymphatic transport of fi. brous dust from the lungs. J Ouup Mrd 15:1S~ 189, 1973. 5. Klosterkiitter W: Experimentelle Unter- suchungen ilber die Bedeutung der Faserlange fUr die Asbestfibrose sowie Untersuchungen ilber die Beeintlussung der Fibrose durch Poly \inylpyridin-N-Oxid, in Bio/ogiiK'M Wirku,... des Asbeslts: /nlernalitmale KtmfeTn~z, 19118, Drudrn. Berlin, Deut.sches Zentrallnstitut filr Arbeitsmedizin, pp 47-52. 6. Timbrel! V, Skidmore JW: Significance of fibre length in experimental aabesto.ia, in Bi<>lt>- giiK'he Wirku~rgtn dt Asbuts: Jnte'I'IIIJtiotoat. K01tjeruz. 19611. Dr..dtn. Berlin, Deutacbes Zen- tralinstitut fUr Arbeitsmedizin, pp 52-66. 7. Webster [: The pathogenesis of asbestosis, in Shapiro HA (ed): Pneumoronioa;.: f>roeeftli1tfll af tiM Jnten~atunu&l Canjrrrna. Jolta~tnuhl"!!. 1969. Cape Town, Oxlord University P~ 1970, pp 117-119. 8. Hibeher W, et a!: Zusammenblap Zwi- schen Asbestose und FaaerlliDge. Natu....n-. sclur.ftm 57:35tHi57, 1970. 9. Smith WE, et al: Biologic ditreNDCeS in re- sponse to long and short asbestDe fibere. A 111 1714 Hyg A...., J 33:A162, 1972. 10. Maroudas NG, et a!: Fibroblast aDchorage. in carcinogenesis by fibres. Lanc.t 1:807-809, 1973. 11. Gross P, Harley RA Jr: The locus of patho- genicity of asbestos dust: A theory. Artll Erwi. ron Health 27:240..242, 1973. 12. Grosa P, Harley RA Jr: Asbestoe-induced intrathoracie tissue reactioDL A...:.\ htlwl 96:245-250, 1973. 13. Pott F, Friedrichs KH: Tumoren der Ratte nach Lp. lnjektion faserformiger Staube. Nat1&7' tuisS~nsdtaften 59:318, 1972. . 14. Pott F, et al: Tumoren der Ratte nach i.p. Injektion von gemablenen Chrysotil und Benzo (a) pyren. Zb Bmkt Hyg I Alit Orig l55:463-469, 1972. 15. Stokinger HE: Sanity in resean:b and eval uation of environmental health: How to aehieve a realistic evaluation (in seven commandments). Scintu 174:662-665, 1971. 16. Gross P, et al: Problems in the pathology of asbestosis, in Shapiro HA (ed): Pneu """""'iosis: ProcetdiJI{Ia oftlu lntw!tat-w..al Coot f~ Joha11uaburg, 1969. Cape Town; Oxford University Press, 1970, pp 126-132. 17. Gross P," et al: Experimental asbesto8is: The development of lung cancer in rata ...-ith pul- monary deposita of duysot-ile asbestos dust. A1'Cil Em-irort Health 15:343-355, 1967. 18. Pontefract RD, Cunningham HM: Pene- tration of asbestos through the digestive tract of rats. Nature 243:352-3.53, 1973. RebuHal In looking through "Biological Effects of Asbestos" (Ann NY Acad Sci 136:87, 1965) i find one paper by Holt, Mills, and Young that says very small asbestos particles do cause fibrosis in the guinea pig lung. In the published discussion, no one challenges this result; one discussant, Ian Webster from South Africa agrees with it, and Gilson quotes it approvingly in his fi- nal wrap-up. At lea;;t in 19"i5, ultramicroscopic asbestos particles were believed to have fibrogenic potential for guinea pigs. w.GEORGE CO!IISTOCK, MD The Johns Hopkins University School of Hygiene and Public Health Hagerstown, Md I reply that Paul Holt used the same make hammermill to comminute his asbestos as I used. I fully agree with his statement that a high proportion of the particles to which he exposed his guinea pigs was too small to be seen by the light microscope. The more important aspect of Holt's statement is the long fibers were present in the dust cloud. Having seen his set-up, I was impressed by the high density of the dust concentration (unmeasured!) to which his guinea pigs were exposed. The dosage of long-fibered (optically visible) particles must have been enormous whereas the dosage of submicronic fibers (those visible only with the electron microscope) must have been astronomical. Holt's finding of many optically visible fibers in the lung sections of his animals as pictured in his illustra- tions and of many asbestos bodies attest to the plentiful dosage of long fibers. This undermines his claim that "Fine dust particles, too small to be seen under the light microscope, will produce asbestosis in the guinea pig." The determinant(s) of asbestos tox. icity is not known and I make no claim to such knowledge. However, in this article, I point to one aspect of asbestos dust which is not associated with pathogenicity. By "submicronic" is meant something invisible with the light microscope but 'liisible with the electron microscope. This generally means a . particle<0.25p. in thickness. Although the vast bulk of fibers that have been ground to a length <5p. are submicronic, some would be thicker than 0.25p. and therefore, optically visible. Perhaps, it would be best not to specify "submicroscopic" and speak only of "short" fibers as defined in the opening sentence of the report. PAUL GROSS Naples, Fla Arch Env~ron Health/Val 29, Aug 1974 Short-Fibered Asbestos Dust/Gross 117 FMSI 05679 I