Document xdyZvwRjnRywn3RQ12BqyGoLm

t FMSI 05654 W arning to W orkers Seen as Start of U.S. E ffo rt to P ut Focus on Asbestos 4C-10 FLEET OWNER BI-MONTHLY 74,100 JAN 1978 'CUPPEOay'l [BACONS] Bus fleet praised for fighting asbestos repair facility is an outstanding exam ple of safe asbestos use. It is well equipped to minimize dust. The hazard district mechanics are using safe work practices." ; For its "excellent performance in The district mechanics are mem- protecting district mechanics bers of the International Association from a cancer-causing substance, of Machinists & Aerospace Workers | ; asbestos in fiber form," California's (1AM), Marin County Lodge No. 238. Health Dept, has commended the The Machinists union was repre Golden Gate Bridge, Highway and sented, along with employer, gov Transportation District. ernment, and science representa Golden Gate Transit, operating a tives, on the State Health Dept, advi fleet of 248 buses, was praised for sory committee, which early this protecting the 42 district mechanics year drafted the asbestos regulation who work with asbestos lining while now in effect. performing brake and clutch mainte Dr. Fred Ottoboni, Ph.D., head of nance and repairs on buses. the department's Occupational Can California is the first state to cer Control Unit, said the transit j require employers to report work district followed these key proce- : place use of asbestos. Asbestos is dures to maximize worker protec the most widely used of 18 cancer- tion against asbestos fibers: causing chemicals and substances - New brake linings are "arced" regulated in California as part of a (shaped to fit) with a low-speed lathe comprehensive program to prevent rather than a power sanding ma job-related cancer. chine that could produce airborne Excessive exposure to asbestos fibers. j fibers can cause lung cancer, a rarer Arcing is done in a room sepa form of cancer known as mesothe rate from other workers so that lioma, and a lung ailment called asbestos waste is isolated from other asbestosis. workers. State Health Director Jerome A. The small amount of dust Lackner, M.D., said, "State industrial generated by this process is col hygienists are discovering in inspec lected by an exhaust system. tions that asbestos in bus, truck and Waste material is put in labelled auto brake-repair shops is a signifi containers and disposed of in plastic cant potential health hazard to Cali bags. fornia workers, but one which safe Cleanup of brakes prior to work practices can control. repair is done with a damp rag rather "An estimated 74,000 mechanics than with compressed air, thus elimi and other workers in 22,000 autoand brake-repair shops serving the nating a serious source of dust. JjHP , S' public are potentially exposed to asbestos through brake-repair work. Several thousand more workers do ing 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 abes- tos fibers. "The district's San Rafael braise /v' FMSI 05655 t I " . V* , , Wanted: `reasonable' cancer plan The American Industrial Health Coun cil, an ad hoc industry group formed to oppose the policy proposed by the Occupa tional Safety and Health Administration for defining and regulating carcinogens, launched its attack last week at OSHA's lengthy hearings in Washington, D.C. (CIV, May 24, p. 14). Paul Orcffice, president of Dow Chemi cal and A1HC chairman, stressed that the OSHA proposal needs "substantial modi fication" but the AIHC is taking a "posi tive and open stance" and is "seeking dialogue and cooperation." In laying the foundation for AIHC's 17 scientific witnesses who followed, Oreffice empha sized the "need for control and regulation of carcinogens in the workplace." He said OSHA's categorization plan --separating suspect chemicals according to the likeli hood that they will cause cancer--can be made "practical and workable" if it is designed along the lines of AIHC's proposed version 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 other wise. 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 implica tion in OSHA's policy that there is an "epidemic of cancer." Olson claimed that tobacco, alcohol and rich diets are respon sible for 75-79% of total cancer mortali ties, and that the number of cases caused industrial carcinogens is "much less than 1%." George Claus, a toxicologist with Rut gers 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 consul tant, disputed OSHA's position that there is "no safe level" for humans for material that causes cancer in animals. He empha sized 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 in dustry'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 irre sponsible firms had a competitive advan tage. "That's why we support reasonable regulation," Oreffice replied. He likened it to the "reasonable" 55-mph. speed limit rather than a "unreasonable but undenia ble 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 Wash ington, where he led off industry's testimo ny 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 re search 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 regu lation-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 (CIV, June 7, p. 22). Unless Dow can reach an agreement with the Environmental Protection Agen cy over emissions from coal-fired power plants at Midland, Mich., it will tempo rarily shift some operations to other loca tions 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 millirems/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 reebrds. 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 1,100 tons of Niger 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 f i CURRICULUM VITAE Hans Weill, M. D. Education Tulane University, 1951-54, B.A., June, 1955 Tulane University School of Medicine, 1954-58, M.D. , June, 1953 Post-Graduate Medical Training . Intern, Mt. Sinai Hospital, New York City, 1958-59 Resident, Charity Hospital of Louisiana, New Orleans, Tulane Medical Unit, . 1959-60 Research Fellow, Department of Medicine, and Pulmonary Laboratory, 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 Associate 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 Appointments Visiting Physician, Charity Hospital of Louisiana at New Orleans, Tulane Unit Chief, Pulmonary Function Laboratory, Veterans Administration Hospital, ` New Orleans, 1963-present Consultant in Pulmonary Diseases and Medicine, USPHS Hospital. New Orleans, 1964-present I I FMSI 05657 Hans Weill, M. D. - CV cont'd Honors and Societies Phi Beta Kappa, 1955 Alpha Omega Alpha, 1958 American Thoracic Society, 1962 , Orleans Parish Medical Society, 1963 Diplomats, American Board of Internal Medicine, 1965 _ Fellow, American College of Chest Physicians, 1965j Governor for Da. , 1970 Fellow, American College of Physicians, I9&? ' Certified in Puimona , 'w L 5 ? cl 3 ,. "lean Boa.rd of Internal Medicine, 1966 American Federation for Clinical Research, 1967 Southern Society for Clinical Investigation, 1969 - Chairman, Post-Graduate Course, Pulmonary Fu.nctioit.ini Health, and Disease, 1970-72 . Fellow, Royal Society of Medicine, 1971 New York Academy of Sciences, 1971 ' Society for Occupational and Environmental Health, 1972 Councilor-at-large, American Thoracic Society, 1973 - President-elect, American Thoracic Society, 1975 - Consultant and Committee Assignments : Member, Task Force on Environmental Lung Diseases, National Heart and Dung Institute, NIH, 1972 _* Consultant, National Institute of Occupational Safety and Health, TDI Criteria Document, 1973, Phosgene Criteria Document, 1975 Planning Committee, Occupational Dupg Disease post-graduate course, * Annual Meeting of American Thoracic Society, 1973 Program Committee, American Dung Association,. 1973 - Faculty Advisory Committee, Tulame University School of Medicine, 1973 - Secretary-Treasurer, New Orleans Academy at Internal.Medicine, 1973 - FMSI 05658 ASBESTOS INFORMATION ASSOCIATION NORTH AMERICA 1660 L Street, N.W. / Washington, D C. 20036 / (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. R. H. Mereness Executive Director cc: Stanford Christian, Bendix Corp. Jim Armstrong, Bendix Corp. Ike Weaver, Raybestos-Manhattan, Inc. 1/^d Drislane, FMSI . Enclosures RHM:vld V FMSI 05659 Is brake lining dust harmful ? information Association .. North America ' 1660 L Street, N. W. Washington, D.C. 20036 --asbestos L information Lz: committee 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 con ventional 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 ? 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 tem peratures 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 cent1 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 1 -65 per cent to 0-03 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 0-22 per cent to 0-003 per cent2. Experiments with disc brakes have shown that, in their case, the free asbestos fibre is an even lower fraction FMS1 05661 of the total products of wear. In tests carried out by research staff of the Ford Motor Company. Detroit, on a produc tion disc brake3, less than 0-02 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 de signed 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 in 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 situa tions. 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 occupa tional. 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 continuous machining and maintenance FMSI 05662 work is carried out. Such work, how ever, 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 explain ing 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. 2. Brake and Clutch Emissions generated during Vehicle Operation, M G Jacko, R T DuCharme and J H Somers, Proceedings of Auto mobile Engineering Meeting of the Society of Automotive Engineers, May 14th to 18th 1973. 3. Asbestos Emissions from Brake Dynamometer Tests by A E Ander son, R L Gealer, R C McCune and J W Sprys, Proceedings of Auto mobile 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 Re search Council, P.O. Box 18, Cleckheaton, West Yorkshire. BD19 3UJ. The Asbestos Information Committee 2 Old Burlington Street London. W1X 2LH Telephone: 01 -734 0081 November, 1975 Staube und Gase am Arbeitsplatz International Conference Dust and Gases in the Work-Place ( Colloque International Poussidres et Gaz au Poste de Travail 18. - 2o.6.1975 Bonn - Bad Godesberg Stadthalle Zusammenfassungen Abstracts Resumes S t n v.b forr.ci)uncjsInsti tut A :r. Hauptverbandes der verblichen Berufsgenossenschaften e,V. Bonn FMSI 05664 15- G. Kunnen, G. Heidermanns, A. Schiitz, Bonn und . R. Prochazka, Mtinehen (BRD) Dusfc Concentration During Production of Friction Linings and their Treatment in Garages 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 treatment) as well as in the brake service of garages. The aim of these technical investigations which were made within 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 chrysotile, at the brake services above the TRK value, however, for short ex position times only. During blowing out of brake drums a short termed high dust concentration occurs, however, asbestos was not proved to be evident.. Laboratory and test stand experiments issued that asb estos is transformed morphologically by the temperatures nr educed v; Ittii n t h a friction area . Under extreme condit : one. FMSI 05665 . . ./ .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 for 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 of 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-vitroclinical, 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 syndrome groups had to be reduced to 5 types of diagnoses with defined degrees of diagnosed security: Type i Type II Type III Type IV Type V AIF eventually AIF possible AIF not presumable AIF competible diagnosis AIF normal diagnosis FMSI 05666 !0 2 the transformation into Forsterit has been proven. The trans formation, probably, succeeds via an amorphe phase. Due to these results, besides dust protection, we regard prophy lactic 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 blow out or brush out brake drums 0,0 % resp. 5,6/5 The considerations in respect of occupational health resulting from this will be discussed according to the specific risks of operating methods. FMSI 05668 iWS AND COMMENT DEC 0 1 1977 ranted by the scientific evidence and that the lower standard is technically impos Occupational Cancer: Government Challenged in Beryllium Proceeding sible. It seems that in the early 1970's few people paid much attention 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 (pub The beryllium industry and the gov cause the animal data are negative for lished in 1971 and 1972) examined large ernment have been locked for months in beryllium copper, the form to which cohorts of beryllium workers at several an intense struggle over the question of some 70 percent of all the industry's plants and found no unusual incidence of whether beryllium should be declared a workers are exposed. The government's lung cancer. But at some point, Bayliss carcinogen. At issue are not only the case, based only on animal data, there and Wagoner decided to restudy the life merits of an epidemiological study con fore looks iffy. histories of workers at a single plant. ducted by the chief government agency But Bayliss III. claiming on epidemio They picked one at Reading, owned by involved, the National Institute for Oc logical grounds that human beings ex Kawecki Berylco Industries, Inc. (KBl). cupational Safety and Health (NIOSH), posed to beryllium incur a lung cancer In early 1977. OSHA scheduled a hear but questions of fair play in government risk, has strengthened the government's ing on the proposed new standard; the regulation. Even the conduct of the di case. If the study is considered accept two major producers of beryllium, KBI rector of NIOSH, John F. Finklea, a re able, it will increase the likelihood that and Brush Wellman. Inc., who knew of spected but controversial federal official, the Administrator of OSHA, which is the existence of a new study partly be has come under question, because he en part of the Department of Labor, will ap cause it had been reported in a Cleve gaged in a telephone conversation that prove a new, stricter standard and that land, Ohio, newspaper, began asking industry says was a naked threat to in the courts would uphold a subsequent NIOSH for the data it was examining. In timidate industry witnesses. appeal. But by the same token the study March, Brush hired a Washington con The focus of the controversy is a study has caused the industry great alarm. sulting firm. Equitable Environmental done by NIOSH which concludes that, Aside from the questions of scientific Health Corp., to handle the human epi among the beryllium workers employed merit and fair play, the NIOSH beryl demiological issues relating to the pro since the 1940's at a plant in Reading, lium controversy also involves the issue posed standard. Pennsylvania, the incidence of fatal lung of when animal data alone can be the At this time, there began a series of cancer was unusually high. Industry has basis of federal standard setting, and events through which each side has be accused NIOSH of "gerrymandering" what level of human epidemiological evi come embittered, with each accusing the its data to produce this result. Joseph K. dence should serve as allowable in feder other of harassment, obstructionism, Wagoner, who is a principal author of al regulation. These questions are all the and bad faith. The entire controversy, the study and is now a special assistant more important now because the and many of the associated emotions, to the director of the Occupational OSHA's new director, Eula Bingham, is were aired on the public record in Au , Safety and Health Administration a former cancer scientist, who has an gust and September during the hearing. I (OSHA), which must decide on beryl nounced a new, gel-tough stance on reg The industry charges, first, that. lium's carcinogenicity, defends the ulating carcinogens in the workplace NIOSH did not make a good faith effort study, saying the deficiencies are due to (Science, 21 October). to turn over its data on the more than industry's poor records. "There is absolutely no doubt in my Toxicity of Beryllium 3000 Reading workers it was using as the basis of Bayliss III. so that industry mind that beryllium is a human carcino- The beryllium industry came of age in could check NIOSH's calculations and 1 gen," Wagoner told Science. But the 1940's, when there was increased de conclusions. Brush's Vice President, Wagoner and other officials stress that mand for the tough, lightweight, heat-re Martin B. Powers, testified that sound epidemiology is hard to do be sistant metal during the Second World "throughout 1976" the company made cause industry may be tampering with or War. Since then, beryllium has been both informal and formal Freedom of In destorying worker records. The beryl widely used in electronics and missile formation Act requests to obtain the lium companies deny doing any improp parts, and in other applications. But data. Although NIOSH kept giving the er meddling. They would like to see the from the start it was known that beryl industry other information and docu study redone, or another study made of a lium is toxic to humans; it causes a dis ments, it did not hand over the Bayliss II separate cohort of beryllium workers. ease known as berylliosis. Since the paper or accompanying backup until 1 Wagoner, however, says another study 1940's then, the industry has had to limit July 1977, shortly after officials met with "will mean more delay and increased exposures to 2 micrograms per cubic me OSHA's Bingham, and threatened to sue risk to the health of the American work ter for workers. if the material was not forthcoming. In er." ' Although animal data linking beryl deed. it seems that, throughout the hear The study, known as Bayliss III be lium to tumors in some animals have ing NIOSH continued to hand over infor cause it is the third study of beryllium been around for years, NIOSH only re mation at the last minute, and then only workers by NIOSH bench scientist Da cently (in 1972) issued a "criteria" docu in response to formal, freedom of infor vid L. Bayliss, is crucial to the determi ment laying out the case against the met mation act requests--in some instances nation of a new standard for beryllium. al as carcinogenic. In 1975, NIOSH pro 72 hours, or 48 hours, before industry NIOSH proposed a new standard on the posed that the 2 microgram per cubic was to present expert testimony on the basis of animal data in 1975. The indus meter standard be lowered to 0.5 micro material. try has argued that the animal data are an gram per cubic meter. Industry has re NIOSH's version of these events' is insufficient base for the new standard be- sponded that such a change is unwar that the repeated freedom of information 898 SCIENCE, VOL. 198 CA) FMSI 05669 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 bat tened down to the point where we couldn'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 1 July, and turned it over to Equitable, when anoth er incident occurred. Industry charges that Pinklea, through a telephone threat, caused Equitable to cease working with Brush and to prevent one of its scien tists, 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 al so working on Equitable's NIOSH con tracts 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 tan tamount to a threat of the loss of NIOSH business if Equitable did not stop work ing for the beryllium industry. Brush may sue Equitable for breach of con tract, while another Equitable official, a beryllium expert, who objected to Mal loy'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 Fed eral 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 atten tion." But Edward J. Baier, deputy director of NIOSH, 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 con cern known by a phone call to Utidjian's boss, instead of by a more conventional route. Industry is also charging foul play be cause NIOSH did not produce the princi pal 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 de liberately kept away because his testimo ny would have admitted the weaknesses in the case against beryllium. NIOSH's Wagoner, who was Bayliss' superior at the time, told Science, "Bay liss didn't want to testify. We asked him and he said he didn't want to come." Science located Bayliss in North Caro lina, 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 in vitation stands if I cared to testify. He indicated that Wagoner could handle the whole thing though, so 1 said 1 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 Bay liss 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 con clusion that beryllium workers have an increased risk of getting lung cancer. NIOSH counters that any errors that have been found in the paper are "in significant." Wagoner told Science that the Bayliss study, and another one pro duced 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 "irrefut able." Bayliss III examined the histories of 3070 workers, who worked at the Read ing 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 hin ged on the fact that the observed number of lung cancer deaths was larger, namely 46. At the hearing, Brush's statistical con sultant 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 ma jority 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 1 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, "1 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 III 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 coun ty in which the plant is located was be low 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 44-- numbers 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 can cer deaths became even more than those actually observed. Wagoner, interviewed about the spe cifics of the study, admitted that there were deficiencies in the information available on the cohort of workers. "We ' ( 1 ! j 2 DECEMBER 1977 899 FMSI 05670 had sjtme people whom we weren't sure whether they were alive or dead," he said, "so we assumed they were alive." He explained the shifting size of the co hort, which at different times numbered 3070, 3201, and 3035, was because NIOSH was trying to square its informa tion with that offered by Mancuso in his study, which included some Reading workers. Industry's position on the Man cuso study is that it should be stricken from the record, since the paper seems not to mention smoking at all, and since Mancuso has said he would give his backup data to the industry but has failed to do so. Interestingly, the authors of the Bayliss study differ on how strong a case their paper makes. Bayliss told Science, "I thought there was a pretty, reason ably strong case, but of course that's a judgmental matter." Wagoner, in a sepa rate interview, maintained that the evi dence was all "converging" and the case "irrefutable." Infante said: "The results and the interpretation don't change. We had to keep stating, defining, who the co hort was . . . We know what the meal is. but we have to go out and buy the meat and vegetables." The hearing ended in September, but the administrative judge before whom it was held, has allowed until mid-Decem ber for posthearing submissions. On the NIOSH side, these include a fourth Bay liss paper. Industry will submit the most comprehensive rebuttal yet to the Bay liss and Mancuso studies^ Warfare Continues But the warfare continues. Brush's vice president. Powers, questions whether the hearing record will make any difference, since Wagoner, one of the most ardent supporters of a new be ryllium standard, recently moved to OSHA to be Eula Bingham's special as sistant. Industry believes that Wagoner should not participate in Bingham's deci sion-making on beryllium, and is seeking a written reply from Bingham on Wagon er's role. Brian MacMahon, professor of epide miology at Harvard, has gone over the latest cohort tape which has 3055 work 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 treadmill, 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 ! the beryllium industry ultimately knuck- i les under to a new tighter, standard. It is more important as a precedent. for beryllium is among the first of many alleged carcinogens on which OSHA's Bingham j i i j will have to rule. j These decisions will have their politi- i cal element; that is. Bingham will want ! to not only protect American workers, I but to give the appearance of protecting j American workers. But she will also i have to judge whether the scientific evi- : dence in each case ultimately supports or j erodes those political decisions. ' --Deborah Shapley National Laboratories: Focused Goals and Field Work Hinted Under DOE Even before the federal energy agency underwent two face-liftings, people were saying that the national laboratories were declining in importance and were in need of new missions. Their old roles-- as practitioners of basic research, nucle ar reactor development and weapons de sign--proved to be embarrassingly nar row when the Energy Research and De velopment Administration (ERDA) in herited the labs from the Atomic Energy Commission in 1975. Although ERDA expanded the breadth of energy research at many of the individual laboratories, it never quite determined what should be the laboratories' role in the national en ergy program. In the 2 months since the Department of Energy inherited all of ERDA's former programs, officials of the new en ergy agency have been crisscrossing the airways to inspect some of their 25 labo ratories and research centers. The new undersecretary of the department has visited three laboratories in the west, 2 DECEMBER 1977 Sandia, Los Alamos, and Livermore. The man who had primary responsibility for getting the new department running, Tom Reed, has visited a number of east coast labs. The major laboratory direc tors have also met with the under secretary as a group. The message in these meetings has been that no abrupt changes will occur, but the past roles of the labs are being analyzed care fully and their future roles may gradually change. Soundings taken in Washington when the energy department was inaugurated in early fall raised a number of problems. The laboratories had accumulated a mul titude of new programs to spearhead ERDA's acceleration of energy research. Some critics said that the labs spend too much money on projects that are not put up for bids and that their expenditures would be more productive if brought un der zero-based budgeting. The various laboratories have enjoyed considerable autonomy during most of their history. On paper there are reasons for the lab oratories to worry about losing their in dependence. The reorganization that ac companied the formation of the energy department created two new vehicles for monitoring the work of the various labo ratories 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 administrator at the rank of assistant sec retary in the department. In addition, the laboratories will be regularly scrutinized by a newly created council composed of all the line administrators of the depart ment. The council will be chaired by the same man who has responsibility for day-to-day coordination of all the depart ment's energy research activities. Un dersecretary Dale D. Meyers, and that may be an indication of how closely the laboratories' efforts will eventually be in terwoven into the whole research and de velopment fabric. Whatever develops in the new depart ment's relations with the field, the possi bility that the changes pose a threat to the traditional independence of the labo ratories is taken seriously in some quar ters. Two weeks ago the House Science and Technology Committee called in the directors of eight major labs to testify in a hastily arranged hearing that had no ap parent routine purpose. Some observers thought that the committee, which has 901 FMSI 05671 3 M*& r f i tt y Jri.v IS, 1974 TUB MEDICAI, JOUKNAI, OF AUSTKAUA 45 Clinical Revimvs THE BIOLOGICAL EFFECTS OF ASBESTOS S. F. McCutj^agh, m.d., b.sc,(mbd.)* Sydney Med. J. Aiist., 1974, 2: 45-49. Recent developments are reviewed. The terms pulmonary asbestoses 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 described recently which may make this measurement practicable In the routine surveillance of an asbestos exposed work, force. Pleural asbestosis may mimic restrictive lung disease but only if the pleural 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 their physical rather than of their chemical structure. 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 cigarette smoking In the lung cancer of asbestos workers. Current standards of work* place hygiene are reviewed and conflicting opinions about methods of medical surveillance compared. In the general urban atmosphere, the amount of asbestos is between one hundred thousandth and one millionth of that held to be safe in the workplace. Motor-car brake linings release little, if any, asbestos in their normal road use. The amount of asbestos in water and beverages is likewise negligible. * Chiof Mcdiiai Officer. Janiea Hurdie & Coy Ply Limited. Address for rejwmts: Or K. I*\ McOidlngh. James Hardie fs Coy fly Limited, p.O. Uox *215, Granville, N'.S.'W. 2112. Titr. biological effects of asbestos are Increasingly engaging the interest of scientific workers, and the annual number of papers on the subject published each year con* timies to increase exponentially (Figure 1). NUMBER OF SCIENTIFIC PUBLICATIONS ON BIOLOGICAL EFFECTS OF ASBESTOS 1900-1971 IN IOEH FILES I'tocus l: Number of scientific publications on biological effects ol* asbestos to 1571. Recently a working group met at Lyons, in France, to review progress in this field. It is largely on the papers delivered at this meeting, and on subsequent work, that lho remarks in this paper are based. Earlier work is von i\s$oc\ation onenca oUeet, N. Vi- j;^Vun2,ton' DC- ' 7 (1^) FMSI 05672 THE MEDICAL JOUK.YAL OE AUSTRALIA .! l.r IS. l'.)74 referred to only in so far as it is relevant to recent developments. PULMONARY ASBESTOSIS Confusion is arising over this term (McCullagh, 1069), since to some the word "asbestosis" means pulmonary asbestosis, while to others it also includes the pleural reaction and the two do not necessarily go together. My 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-Massey has lately reported that emphysema was found in one-third of the asbestotics in the recent and most important Quebec study (M. R. Becklake, 1972, personal communication). Tho 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 Organisation in Geneva. One of the most important recent developments is the study reported by Jodoin et alii (1971). A group of 24 men was studied; alt had had normal chest radiographs but 13 had had a substantially greater exposure to chrysotile asbestos than the other 11. A battery of lung function tests was administered to them, and static pulmonary com pliance was outstandingly the most reliable of these in separating one group from the other (P< 0-005). The early detection of pulmonary response to asbestos exposure is of particular importance in the routine, periodical medical examination of asbestos-exposed workforces. Here tofore we have had to rely primarily on the chest radio graph but it now appears that a much more sensitive screening test may be available. The late Dr McKerrow and his colleagues (Sevan 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 quiet 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 asbestos-exposed workforce is currently being investigated by us in association with Professor Bryan Gandevia and his colleagues of the University of New South Wales. Diffusing capacity, incidentally, is of little value in the early diagnosis (Harries, 1971; Becklake et alii, 1972). PLEURAL ASBESTOSIS Since 1927, thickening of the pleura has been associated with exposure to asbestos (Cooke, 1927) and, more recently, several other substances (Smith, 1952). These changes have generally been held to be of no more con sequence than the cailusses on the hand of a smithy. At Lyons, Jones (1972) emphatically held to this view. On the other hand Harries (1971) has reported substantial decrements of lung function in men who had only pleural, and no pulmonary asbestosis. Recklake et alii (1970) have expressed the view that such decrements only occur with very extensive pleural thickening. Eisenstadt (19C5u and 1965b) has reported 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 meso thelioma. It seems improbable that pleural asbestosis, which is known to he parietal (Thomson. 1970a), should be the precursor of mesothelioma, which is believed to be a tumour of the visceral pleura (Thomson, 1970b). It is also to. be noted that while exposure to the asbestos anthophyllite commonly leads to pleural thickening (Raunio, 1906), it has never been known to lead to meso thelioma (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 more likely to be due to talc or mica, and indeed, in the formal report of the Lyons meeting it is recovded that "pleural plaques have been associated with past exposure to all commercial types of asbestos. But additional factors, other than asbestos itself, are involved" (International Agency for Research on Cancer, 1972). It has been suggested (Kiviluoto, 1965) that the inci dence of pleural asbestosis might be used as an epidemio logical 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 1S7 out of 3.SG0 routine Chest X-ray 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 unimpres sive 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 character istics (Stanton, 1972; Timbrell, 1972). We have all long wondered why the mesotheliomogenic potency of crocidolite should be so much greater than that of other asbestoses, among which is included the particular form of crocidolite found in the Transvaal (Sluls-Cremer, 1965). Timbrell and his colleagues (1971) have produced very good 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 crocidolites, much more than any other asbestoses, which give rise to mesothelioma. It is to be noted, how ever, 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 Roe, 1965; Gibbs, 1969) or to some associated trace metal or benzpyrene (Dixon et alii, 1970) is not now generally held, THE ROLE OF TOBACCO SMOKING The very important role of cigarette smoking in asbestosassociated lung cancers was first pointed out by SelikofI FMSI 05673 I 'i'JIK MEDICAL JOncXAL OK .UASTWALfA and liis colleagues (Selikoff ct alii. 19GS). In the con tinuing study both of Hammond and Selikoff's group of insulators in New York (Hammond and Selikoff, 1972) and by .Muriel Xewhouse and her colleagues (1972), 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 evidence that tobacco smoking plays any role in the development of mesotheliomata. RESPIRATORY CANCER This term is used here since the international classi fication 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 1970, a group of male asbestos textile workers first employed after the introduction of the British Asbestos Regulations of 1933, but before 19G4. These she divided into those who had experienced high, moderate and low exposures. She had earlier reported (Xewhouse, 19G9) an excess of respiratory cancer among those who had experienced a high exposure, but she has now reported (Xewhouse, 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 Selikoff's (1972) data would suggest. Among their 370 insulation workers, there have been 42 deaths from lung cancer, when only 4-75 were to be expected on the basis of age-specific male white United Stales 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 (AVagner et alii, 1971) that some S5% to 90% of mesotheliomata are attributable to asbestos exposure while, in the remaining 10% to 15%, the cause is unknown. Likewise, it is generally accepted (International Agency for Research oil Cancer, 1972) that all commercially used forms of asbestos, with the exception of anthophyllite, may give rise to meso thelioma, though tile overwhelming majority of cases of this still uncommon tumour are attributed to the finefibred crorido'iites. Throughout the world, the asbestos chrysotilc accounts for more than 90% of total usage. Davis (1972), of the Institute of Occupational Medicine in Edinburgh, has produced "mesotheliomata" in mice and rats using intraperitoneal emplacement of crociilolite and fibreglass. He has shown that, at least initially, the abnormal cell reproduction is sub-mesothelial and takes place under a continuous layer of undisturbed mesotbelium which only later disintegrates. This observation raises the interesting, if academic, question: "Are mesotheliomata really mesotheliomata or are they something else?" OTHER CANCERS Excessive numbers of cases of gastrointestinal cancer among those exposed to asbestos continue to be reported (McDonald, 1372; Meurman el alii, 1972; Xewhouse, 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 McGill, 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 centi metre (f./cnr1) (British Asbestos Regulations, 1969; (British) Department of Employment and Productivity, 1970); at the moment in the United States it is 5 f./cm', but will become 2 f./cm3 on July 1, 1974 ((United States of America) Department of Labour, 1972) though it is to be noted that the Threshold Limit Value Committee of the American Conference of Govern mental Industrial Hygienists stands firm in its view that the standard should remain at 5 f./cm1 (Stokinger, Chair man of the TLV Committee, 1972, personal communica tion). In Australia the standard, though it has at present no statutory authority, is a time weighted average of 4 f./cm' (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 ef alii, 1973) suggests that the standard should probably lie somewhere between 4 and 5 f./cm1. One cannot say that any of these standards has a sound scientific foundation, hut in the American study exposures appear to have been more accurately established. It is, I think, unanimously agreed that the most accurate method of measuring workplace asbestos-in-air levels is the counting of fibres on a membrane filter on which they have been collected from a known volume of air (a pro cedure which, however, entails much tedious microscopy). Recent provisions for the surveillance of workplace asbestos-in-air levels in the United States ((United States of America) Department of Labor, 1972), and iu Germany (Shultz, 1972, personal communication) impose such a burden by this tedious microscopy that in hoth countries (Holmes, 1972; Shultz, 1972, personal communications) there is an inclination to return to gravimetric sampling. However, the accuracy of this method leaves very much indeed to be desired. A happier solution would he the further development of a device known as the Quanlimet-72U which, it is hoped, will prove capable of automatically counting one complete membrane filter every four minutes. FMSl 05674 48 TUS AlKDICALi JOURNAL, OF AUSTRALIA Jt.t.Y 13. 1974 MEDICAL SURVEILLANCE OF THE WORKFORCE The usual practice, when a workforce is exposed 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) Department of Labor, 1972). No such provision is made in the British regulations. When these regulations were drawn up it was decided that it would be far better to study, with great care, the men working for the major employers, whose exposure levels were measured aud known and the progress of whose health could be watched by a factory doctor with special knowledge and understanding of the problem, with H.M. Factory Inspectorate supervising and coordinating the study. Proceeding thus it is to be expected that our know ledge and understanding of the biological effects of asbestos will progressively increase and that the adequacy of the hygiene standard will be more readily and promptly assessed.. 1 am in no doubt that this philosophy is the correct one and very much hope that any regulations that may be adopted in Australia will be so framed as 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 these differences and to establish iuterlaboratory 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 atmosphere are of the order of nanograms per cubic metre (10'* gm/nt3) and can only be measured by electron microscopy. In 16 such measurements in and about the town of Rochdale in England, the level in seven cases was of the order of 10-' grn/nP 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 Rochdale town centre. The British workplace hygiene standard of 2 t./cm! Is equivalent to 01 mg/m* or 10" gm/m- ((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 in the United Stales have reported levels of the order of 10" gm/nv. Even "in lower Manhattan about construction sites where exten sive spraying of asbestos containing fire proofing material was taking place", asbestos in air levels one-eighth to one-quarter oC a mile (some 200 to 400 metres) away averaged 60 x 10" gm/m', the highest count being 375 x 10" gm/m3 (Nicholson and Pundsack, 1972; Sclikoff el alii, 1972). There is no evidence to suggest that urban asbestosiu-air levels are anything other than harmless. Something should be said about the mucli-maligncd brake lining. Every application of the brake, it is widely believed, releases a shower of fibrous asbestos into the atmosphere. This was never a very promising hypothesis since it is most unlikely that any asbestos would survive the temperatures generated at the braking interface. Lyuch (19CS) of the United States Public Health Service. 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 significant release of free fibre occurred only under conditions extreme enough to produce brake failure". There have been several other studies but none that I know of has led to a contrary conclusion. Sellkoft (1970) summed the matter up: "Brake linings do not constitute a hazard". Since asbestos occurs commonly in nature, though only infrequently in commercially worthwhile amounts, it has no doubt been preseat in many of the world's drinking waters since time immemorial. Its presence in North American waters (Cunningham and Pontefract, 1971; Nicholson and Pundsack. 1972) and in British beer (Biles and Emerson, 196S) has lately been reported. It has been estimated by the Asbestos Information Committee in London that the total annual British output of beer, of over one thousand million gallons, contains only two thousandths of an ounce of asbestos, or some 10" gm/m3. CONCLUSION 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 properties and its use in brake linings, asbestos has saved far more lives than 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 express my thanks . to Dr P. V. Pelnar of the Institute of Occupational and Environmental Health in Montreal, who provided me with Figure 1 of this paper. REFERENCES Becklake, M. r,, Focknier-Mamsky, C.. McDonald. J. c.. et alii (1970). Lung function in relation to chest radio graphic changes in Quebec asbestos workers: 1. Methods, results and conclusions, Bnil. Physio-pathiologique Peapiratoire, 6: G37. Becklake, M. R.. Fol-rsier-Massey, G., Rossiter, C. E., and McDonald, J. C. (1972), Lung function in chrysothe asbestos mine and mill workers, .Arch, enrironm. Jllth, 24: 401. Bevan, C., McKerrow. E. M., and Morgan, K. J. (1971), A method of measuring pulmonary compliance without an oesophageal tube, J. Physiol. 217: lliF. Biles, B., and Emerson, T. R. (196S), Examination of fibres in beer, Nature, 219: 93. Bohlig, h., Bristol, L. J.. Cabtikb, r. IT., ct alii (1970). t'HJC/Cincrnnali elassilication of the radiographic appear ances of pneumoconioses. Chest, 5$ : 57. (British) dkpautmknt of Employment and Productivity (U>7o). Standards for Asbestos Dust Concentrations for Use with Asbestos Regulations of 1969, H.M. Factory Inspectorate, Technical Data Note 13. Burns ic Occupational. Hygiene Sociktt (196$), Hygiene standards for chrysotile asbestos dust, ,,lnn. occnp, lly/f., 11 : 47. Cookk. \V, K. (1927), Pulmonary nsbostosis, Itrit. mcd. J.$ 3 191 : 1024. CoTTRRi.f., K., and Holt, P. 1*\ (1972), An examination of crocidolites from North West Cape and Transvaal mines, Apjd. Ktirth Xci.. St : 13109. Cunningham, H. M,, and Pontefract, R (1971), Asbestos fibres in beverages ami drinking water, Suture, 232: 332. Davis. J. M. G. (1972), Proceedings of the Worfcm// Croup to licrutr thr Jiiolof/irtil Efieri.* of .V.vh* al.yonx, France, Ovtofar, JiH 2, discussion (in the press). Dixon. J. It.. Lowe. I). R. Hrui/.wms, ]>. R. ct alii (1970), The role of trace metals in the chemical careiliogonesls: Asbestos cancers. Cancer lies., 30: 1UGS. FMSI 05675 July 13, 1974 THE MEDICAL JOURNAL OF AUSTRALIA 13 Eijienstadt, H. D. vied. AsS., 192: 419. Benign asbestos pleurisy, /. Amer. Eisenstaot, H. B. (19651)), Ann. N.Y. Acad. Sci., 132: 596 (discussion). Ginns. G. W. (1969), Some problems associated with the storage of asbestos in polyethylene bags, Amer*. industr. Uyg. AsS. J., 30: 458. Gilson*. J. C. (1969), Asbestos health hazards, recent observa tions in the United Kingdom, Proceedings of the International Conference on Pneumoconiosis, Johannesburg, Oxford University Press, London: 173. Hammond, E. C-, and Selikoff, I. J. (1972), Relation of cigarette smoking to risk of death of asbestos-associated disease among insulation workers in the United States, in Proceedings of the Working Group to Review the Bio logical Effects of Asbestos, Lyons, France, October, 1012 (in the press). Harries, P. G. (1971), The effect and control of diseases asso ciated with exposure to asbestos in Devonport Dockyard, thesis, The University of London. Harrinctox, J. S., and Roe, F. J_ C. (1965), Studies of carcino genesis of asbestos fibres and their natural oils, Ann. N.Y. Acad. Set, 132: 439. Holmes, S. (1973), Asbestos cancer of head and neck (Letter), Lancet: 339. International Agency for Research on Cancer (1973), Report of the Advisory Committee on Asbestos Cancers, Ann. Occup. ffyg., 16: 9. International Labour Office (1972), Report of Meeting of Experts on the Control and Prevention of Occupational Cancer, Geneva, Jan. 10-17, 1972: 6, paragraph 24. JooorN, G., Gibbs, G. W., Macklem, P. T., et alii (1971), Early effects of asbestos exposure on lung function, Amer. Rev. Rcsp. Dis., 104 : 525. Jones, J. S. P. (1972)), Pleural plaques, In Proceedings of the Working Group to Review the Biological Effects of Asbestos, Lyons, France, October, 1072 (in the press). Kiviluoto, R. (1965), Pleural plaques and asbestos: further observations of endemic and other non-occupational asbestosis, Ann. N.Y. Acad. Sci., 132: 235. Lynch, J. B. (196S), Brake lining decomposition products, J. Air Pollution Control Ass., 13: 324. McClxlagh, S. F. (19G9), Fifteen cases of pleural mesothelioma associated with occupational exposure to asbestos in Victoria (letter), Med. J. Aust., 2: 1029. McDonald, J. C. (1972), Cancer in ehrysotile mines and mills, in Proceedings of the Working Group to Rcvictv the Bio logical Effects of Asbestos, Lyons, France, October, 1972 (in the press). Meurman, L. O., Kiviluoto, R., and Hakama, M. (1972), Mor tality and morbidity of employees of authophyllite asbestos mines in Finland, in Proceedings of the Worfciitp Group to Review the Biological Effects of Asbestos, Lyons, France, October, 1972 (in the press). National Health and Medical Research Council (1970), Afmosphct'ic Contaminants, Hygienic Standards for Con taminants of the Air of the Workplace, Commonwealth Government Printing Office, Canberra. Newhouse, M. L. (1969), A study of the mortality of workers In an asbestos factory, Brit. J. industr. Med., 2C: 294. Newhouse. M. L. (1972), Cancer among asbestos workers In the asbestos textile Industry, in Proceedings of the Work ing Group to Review the Biological Effects of Asbestos, Lyons, France, October, 1972 (in the' press). 1 Nicholson, W. J., and Pundsacic, F, L. (1972). Asbestos In the environment, in Proceedings of the Working Group to Review the Biological Effects of Asbestos, Lyons, France, October, 1912 (in the press). Raunio, V. (1966), Occurrence of unusual pleural calcification in Finland, studies on atmospheric pollution caused by asbestos, Ann. Med. intern. Fenn., 55, Supplement: 47. Rossxter, C. E. (1972), Initial repeatability trials of the UICC/ Cincinnati classification of the radiographic appearances of the pneumoconioses, Brit. J. industr. Med., 29: 407. Selikoff, I. J., Hammond, E. C., and Churg, J. (1968), Asbestos exposure, smoking and neoplasia, j. Amer. mcd. Ass., 204: 106. Selikoff. I. J. (1970), in Proceedings of the International Conference on Pneumoconiosis, Johannesburg, Oxford Uni versity Press, London: 51 (discussion). Selikoff, I. J., and Hammond, E. C. (1972), Cancer risk of Insulation workers in the United States, in Proceedings of the Working Group to Review the Biological Effects of Asbestos, Lyons, France, October, 1972 (In the press). Selikoff, I. J., Nicholson, W. J., and Lancer, A. M. (1972). Asbestos air pollution, Arch. ewflronwt. tilth, 25: 1. Sluis-Cremer. G. K. (1965), Asbestosis in South Africa--certain geographical and environmental considerations, Ann. N.Y. Acad. Sci., 132: 215. Smith, A. B. (1952), Pleural calcification resulting from exposure to certain dusts. Amer. J. Roentgenol, 67: 375. Stanton, M. F. (1972). Some etiologic considerations of fibre carcinogenesis, In Proceedings of the Working Group to Review the Biological Effects of Asbestos, Lyons, France, October, 1972 (in the press). STbll, P. M., and McGill, T. (1973), Asbestos and laryngeal carcinoma. Lancet, 2: 416. Thomson, J. G. (1970a), pathogenesis of pleural plaques, in Proceedings of the International Conference on Pneumo coniosis, Johannesburg, Oxford University Press, London: 138. Thomson, J. G. (1970b), The pathological diagnosis of malig nant mesothelioma of pleura and peritoneum, in Proceed ings of the International Conference on Pneumoconiosis, Johannesburg, Oxford University Press, London: 150. Timbrell, V., Griffiths, D. M., and Pooley, F. D. (1971), Possible biological importance of fibre diameters of South African amphiboles, Nature, 232: 55. Timbrell V. (1972), Physical factors as etiological mechan isms, in Proceedings of the Working Group to Review the Biological Effects of Asbestos, Lyons, France, October, 1972 (in the press). (United States of America) Department of Labor (1972), Occupational Safety and Health Standards--Standard for exposure to asbestos dust, Federal Register, 37: 11318. Wagner. J. C., Gilson, J. C., Berry, G., and Timbrell. V. (1971), Epidemiology of asbestos cancers, Brit. med. Bull., 27: 71. Weill, H.f Wagcf.nspack, C., Bailey, W., et alii (1973), Radiographic and physiologic patterns among workers engaged in manufacture of asbestos cement products, J. occup. Med., 15 : 248. Wright, G. W. (1969), Asbestos and health in 1969, Amer. Rev. rcsp. Dis., 100 : 467. FMSl 0! -4 In the Forum m am uejs:- Is Short-Fibered Asbestos Dust a Biological Hazard? Paul Gross, MD, Charleston, SC ' Contrary to the detomibutton that tha Inasmuch as asbestos fibers smaller finor tha quartz' dual, tha greater Ha than 5/i tend to remain airborne pathogenicity; the pathogenicity of die longer than the larger ones, they have finest asbestos dust has been shown to a greater chance of being inhaled. be negligible. It has been the finding of research labo ratories in Germany, England, South Af rica, and the United States that short-ffbered asbestos, dust, la, less than 5p in length. Is Incapable of causing fibrosis or cancer. This finding. In conjunction with the failure of different laboratories In the Furthermore, although the anatomy of the respiratory tract tends to pre vent the intrusion into the airspaces of all but a few of the larger sus pended partides, this deterrence does not extend to the smallest partides. The latter very readily enter the air United Kingdom and in tola country to dis spaces with the inspired air. Some of cern abnormalities following prolonged the short asbestos fibers may settle asbestos feeding to rats, should lead to on the alveolar surface by sedimenta the abandonment of the present concept that maintains that mesotheliomas and gastrointestinal cancers arise from the In gestion of asbestos duet cleared from the lungs. These negative results should also al lay the alarm that has been raised as a re sult of tha finding of ultramicroscopic mineral fibers In certain beverages and tion, whereas the smallest fibers, behaving almost like gas molecules, contact the alveolar membrane by diffusion. ' What is the potential of these ex tremely fine submicronie fibers to produce disease? Is their potential greater than that of optically visible drinking water. ' fibers? Is the behavior of submicronie asbestos fibers as opposed to that of larger fibers similar to that of the fi- brogenic effect of very fine quartz By short-fibered asbestos dust is dust as compared with that of the meant that which has a fiber same weight of coarser quartz parlength of less than 5p. Although fiticles?1-* bers of this size usually constitute a These questions take on added im very small fraction of the weight of a portance in view of the commonly dust cloud, their numerical prepon held hypothesis that mesotheliomas derance over the larger fibers may be of the pleura and peritoneum arise by manifold. the transmigration of fibers to the pleura and peritoneum, respectively. In the case of abdominal mesothe Submitted for publication Sept 19, 1973; ac cepted 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. Gross). - liomas, it is assumed that the as bestos 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 trans migrate 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 cer- . tain beverages and city water, in ambient community air, and in the lungs of city dwellers.1-* Con sequently, the relevance of the above question must now extend to entire urban populations. However, lest un due alarm be raised by the last state ment, it should be pointed out that in city dwellers no disease has been found that could be attributed to the ' presence of submicronie asbestos fi bers in the pulmonary tissues. Nei- . ther has there been documentation of an increase in abdominal cancers 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, KlosterkOtter* found that both chrysotile and crocidolite, ground to an average fi ber length of less than 5g when in jected intratracheally or intraabdominally, produced no fibrosis. The Arch Environ Health/Vol 29, Aug 1974 Short-Fibered Asbestos Oust/Gross 115 FMSI 05677 pulro.-ury respond consisted only of a macrophage reaction. In contrast, longer fibers of the same asbestos re suited in fibrosis in both regions. At the same conference Timbrell and Skidmore' reported the results ob tained. in rats and guinea pigs ex posed to equal concentrations (by weight) of short-fibered amosite (90% of the fibers <4g long) and long-fibered asbestos (45% of the fibers >4ji long). They concluded, "minimal reac tion has been observed to short fibres but a marked reaction has been ob served to the longer fibres." In the following year, Webster reported . that monkeys inhaling finely ground crocidolite (fiber length <5a) also showed merely a macrophage reac tion in the lungs. In 1970, Hilscher et . al5 showed the chrysotile or croeidolite, when ground to a fiber length of - <3fi with a microtome and injected intraabdominally, produced no fi brous adhesions; whereas the same asbestos with greater fiber length did cause dense fibrous adhesions. In 1971, the Johns-Manville Re^ search Laboratory prepared for us chrysotile asbestos ground to a fiber length of <5p. 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 (unpub lished study). In 1973 Smith et al* re ported that hamsters injected in trapleurally with chrysotile ground to a fiber length of <l/i developed no pleural cancer, whereas hamsters in jected intrapleurally with longer chrysotile fibers did develop such can cers. Recently Wright (private com munication) disclosed that in his labo ratory short-fibered asbestos injected intratracheally also failed to elicit a fibrotic reaction. Maroudas et al10 have concluded that, "Particles (min eral fibers) smaller than 20p 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 <5p is de%'oid of pathogenic poten tial. This included not only the fibrogenic potential' "-'" but also the cancerogenie potential."1,1 It may be argued that when as- bestos is ground to a very small fiber 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" as bestos 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 al* was found to have maintained its fibrous structure after the grinding process. 2. Smith et als prepared short-fi bered 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 path ogenicity.11 The latter has the same chemical and crystalline structure as the natural product. Therefore, the mere process of grinding with the as sociated heat production does not ac count for the lack of pathogenicity of the finely ground asbestos. However, by fitting together some newly de rived experimental findings, a theory has recently been formulated regard ing the locus of pathogenicity of as bestos dust that does offer a reason able explanation for this lack of pathogenicity.1* There is, however, one laboratory that reported that short-fibered as bestos is tumorigenic. Pott and Friedrichs13 and later, Pott et al14 maintained that 100 mg of chrysotile with a fiber length <3p injected into the abdomen of rats caused the devel opment of cancers. Nearly 80% of the tumors were sarcomas--mostly fibro sarcomas. The character of the tumors pro duced by this technique should have given the authors pause for reflec tion; not only because rats will pror duce fibrosarcomas secondary to in jected or imbedded materials known to be biologically inert, but also be cause subcutaneous fibrosarcomas are very common spontaneous tumors in aging rats. An indication of the ease and r.or.specificity of such tumor pro duction in rats is demonstrated in the first13 of the two above-mentioned pa pers when the authors list a better- than 60% tumor production with mag nesium hydroxide and a 55% tumor production with fibrous glass! In con trast, they reported only a 40% tumor production with ehrysotile. This lower tumor production was doubtlessly re lated to a high mortality caused, in turn, by the exceedingly high dosage of materials injected (100 mg). The employment of unrealistic dos age, of inappropriate routes of ad ministration, and of inappropriate animal species (all three "sins" were committed by the above- authors) to achieve positive results has recent ly been adequately discussed by Dr. H. E. Stokinger.13 When asbestos is ingested, it is the ultramicroscopically-sized asbestos fi bers that are assumed to be respon sible for the development of mesothe lioma by virtue of their alleged penetration and transmigration through the intact intestinal wall. The failure of short-fibered asbestos to induce mesotheliomas when in jected intrapleurally,-1 makes the above assumption highly question able. Unpublished data from differ ent laboratories (David B. Clayson, University of Leeds; L. M. Swin burne, St. James's Infirmary, Leeds, England; and John M. G. Davis, In stitute of Occupational Medicine, Edinburgh) in which rats were fed as bestos intimately mixed in their food, indicate complete failure to induce tu mors or any other kind of abnormal ity 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 experi mental rats had consumed on the pre vious day. This regimen was contin ued for 21 months. At the end of this time, the weight curve of the as bestos-fed animals was not signifi cantly different from that of the pair- 11S Arch Environ Health/Vol 29, Aug 1974 Short-Fibered Asbestos Dust/Gross FMSI 05678 iin mwr ~mmii i mi (ii ii 'i11ji i i <i ii n iliMiw 11lull wup lium ' r~i*t tr-'Tift-t" n-t ri' `"gflfiwTiti fmtirvt THjhfiUrnlilitDTtiii i t i> c f'.`d controls. The animals uere 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 le sion was observed.1* It is to be noted that in previous studies, the first asbestotic lung cancer death occurred 16 months after the initiation of the dust exposure11 and the first asbestotic pleural cancer death in rats oc curred 17 months after the intrapleu ral injection of asbestos dust.12 It is of interest in this connection that the dose of fibers in the intesti nal tract of the asbestos-fed rats was astronomical compared with the dose of fibers that is likely to be swallowed daily by a person occupationally ex posed to asbestos dust--and he, in turn, would have an astronomically 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 asbestos feeding results should cast some doubts on the tenability of the con cept that peritoneal mesotheliomas and an increased prevalence of gas trointestinal cancers arise in occupa tionally asbestos-exposed people from the ingestion of asbestos fibers cleared from their lungs. There must, of necessity, be some other explana tion! Although not an asbestos-feeding study, a recent report purports to demonstrate that the presence of as bestos in the intestinal lumen results in the penetration of asbestos fibers into the blood stream and organs throughout the body, inclusive of the brain.1'1 The writers injected the as bestos into the stomach by means of a syringe and needle, thereby ignoring the probable opening of vessels in the path of the needle track and the pres ence of injection! References 1. King EJ, et si: The action of different forms of pure silica on the lungs of rats. Br J Ind Med 10:9-17. 1953. 2. Hatch T, Kindsvatter VH: Lung retention of quartz dust smaller than one-half micron. J lnd Hyg Toxicol 29:342-346, 1947. 3. Gross P, et al: Mineral fiber content of hu man lungs: A comparison of the counts obtained from the lung3 of people of Pittsburgh, Pa, with those from the lungs of people of Charleston, South Carolina. Am Ind Hyg Assoc J 33:A162, 1972. 4. Gross P. et al: Lymphatic transport of fi brous dust from the lungs. J Occup Med 15:186 189, 1973. 5. Klosterkotter W: Experimentelle Unter- suchungen ilber die Bedeutung der FaserUnge fur die Asbestfibrose sowie L'ntersuchungen ilber die Beeinllussung der Fibrose durch Poly- vinylpyridin-N-Oxid, in Biologieehe Wirkungen dee Asbestes: Internationale Konferenz, 1968, Dresden. Berlin, Deutsches Zentralinstitot ftlr Arbeitsmedizin, pp 47-52. 6 Timbrel! V, Skidmore JW: Significance of fibre length in experimental aabestosia, in BMo- gieche Wirkungen dee Asbestes: Internationale Konferenz, 1968, Breeden, Berlin, Deutsches Zen- tralinstitut fur Arbeitsmedizin, pp 52-56. 7. Webster 1: The pathogenesis of asbestosis, in Shapiro HA (ed): Pneumoconiosis: Proceedings of the International Conference, Johannesburg, 1969. Cape Town, Oxford University Press, 1970, pp 117-119. 8. Hilscher W, et al: Zusammenhitage Zwi- schen Asbestose und FaaerUnge. Natunoissen- echaften 57:356-557,1970. 9. Smith WE, et al: Biologic differences in re sponse to long and short asbestos fibers. Am lnd Hyg Assoc J 33:A162, 1972 10. Maroudas NG, et al: Fibroblast anchorage in carcinogenesis by fibres. Lancet 1:807-809, 1973. 11. Gross P, Harley RA Jr The locua of patho genicity of asbestos dost: A theory. Arck Envi ron Health 27:240-242, 1973. 12 Gross P, Harley RA Jr Asbestos-induced intrathoracic tissue reactions. Arch Pathol 96:245-250, 1973. 12 Pott F, Friedrichs KH: Tumoren der Ratte nach Lp. Injektion faserformiger Staube. Natur- wissenschaflen 59:318,1972 . 14. Pott F, et al: Tumoren der Ratte nach i.p. Injektion von gemahlenen Chrysotil und Benzo (a) pyren. Zb Bakt Hyg I Abt Orig 155:463-469, 1972 15. Stokinger HE: Sanity in research and eval uation of environmental health: How to achieve a realistic evaluation (in seven commandments). Science 174:662-665, 1971. 12 Gross P, et al: Problems in the pathology of asbestosis, in Shapiro HA (ed): Pneu moconiosis: Proceedings ofthe International Con ference, Johannesburg, 1969. Cape Town; Oxford University Press, 1970, pp 126-132 17. Gross P, et al: Experimental asbestosis: The development of lung cancer in rats with pul monary deposits of chrysotile asbestos dust. Arch Environ Health 15:343-355, 1967. 12 Pontefract RD, Cunningham HM: Pene tration of asbestos through the digestive tract of rats. Nature 243:352553, 1973. Rebuttal In looking through "Biological Ef fects 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 re sult; one discussant, Ian Webster from South Africa agrees with it, and Gilson quotes it approvingly in his fi nal wrap-up. At least in 1965, ui- tramicroscopic asbestos particles were believed to have fibrogenic po tential for guinea pigs. . George W. Comstock, MD The Johns Hopkins University School of Hygiene and Public Health Hagerstown, Md I reply that Paul Holt used the same make hammermill to commi nute 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. Hav ing seen his set-up, I was impressed by the high density of the dust con centration (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 fi bers (those visible only with the elec tron microscope) must have been as tronomical. 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 at test to the plentiful dosage of long fi bers. 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 determinants) of asbestos tox icity is not known and I make no claim to such knowledge. However, in this article, I point to one aspect ofasbestos dust which is not associated with pathogenicity. By "submicronic" is meant some thing invisible with the light micro scope but visible 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 submi cronic, some would be thicker than 0.25p and therefore, optically visible. Perhaps, it would be best not to spec ify "submicroscopic" and speak only of "short" fibers as defined in the opening sentence of the report. Paul Gross Naples, Fla Arch Environ Health/Vol 29, Aug 1974 Short-Fibered Asbestos Dust/Gross 117 FMSI 05679