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488 THE NEW ENGLAND JOURNAL OF MEDICINE
MEDICAL INTELLIGENCE
-Jio* Hto
Feb. ^7. I96y
CURRENT CONCEPTS Asbestos or Ferruginous
Bodies*
Edward A. Gaensler, M.D., and Whitney W. Addington, M.D.
T HE health hazards of asbestos have been rec-
lerns of asbestos pneumoconiosis (asbestosis) and asbestos-related neoplasms ha\ e increased alarming ly despite much improved dust control.1 Th;., is because of a rapidly rising use of asbestos and because ot an ever larger variety of asbestos-containimi products, which are often used without aware ness of their composition and under poor supervi sion.' In our laboratory in New England some 35 different occupations ranging from cigarette-filter manufacturing to wire braiding base been incrimi nated. Community "asbestos air pollution" is being recognized only now. and its importance is uncer tain. Increasingly, practicing physicians are being confronted by these problems and then, almost in variably, the consequences of "asbestos bodies" are discussed. A review of current concepts concerning these structures is timelv.
Morphology
In 1906 Marchand1 first noted "peculiar pigment crystals" in lungs. His description of what came to be known as "asbestos bodies" is still apt: within the alveoli were masses of peculiar, rod-shaped structures with clubbed ends. They were light yel low to reddish brown, 30 to 200 p. long and 1 to 6 p. thick. Striking was the segmentation of the bodies into disk-shaped structures that remained intercon nected by colorless threads (Fig. 1). Because they turned black near areas of putrefaction, Marchand suspected that the yellow pigment contained iron; this he confirmed by intense blue coloring with potassium ferrocyanate. In proximity to the "crys tals" he noted masses of "epithelial cells," which contained yellow granular material and which
'From the Thoracic Services, departments of Medicine and Surgery. Boston University School of Medicine (address reprint requests to Dr. Gaensler at Boston University School of Medicine. SO E. Concord St., Boston. Mass. 02 I 18).
Supported in part by a research grant iHE-05933). a research ca reer award (5-K6-H E-1 1 'Ll l and a [raining grant (HTS-S5621 from the National Heart Instilule. National Institutes of Health. United States Public Health Service, and bs a grant from the Massachusetts Tuber culosis and Health League. Incorporated.
Figure L I-ang Biopsy of a 42-Year-Old Rubber Shredder with Diffuse Pulmonary Infiltration* tPerle's Blue Stain. Ougtnal
Magnification X1300) Talc crystals were identified throughout the specimen as well n.s m the atmosphere at his place of work. Here shown is a "psrudoa-.br.tos body" undoubtedly due to asbestos amphiboles present m commer
cial talc
looked like heart-failure cells. Because neither of his two autopsied patients gave other evidence of chronic passive congestion, and because some gran ules looked like segments of the "crystals," he de duced that this material was debris and not hemo siderin. Finally, the appearance of the unusual bodies led him to inquire about the occupation of the patients, but asbestos was not then incriminated.
Terminology
Cooke,5 unaware of Marchand's paper, 20 years later described "curious bodies" throughout the lungs of an asbestos worker and thought that these were of vegetable origin. Stewart* first recognized such "brown bodies" as the result of inhaled asbes tos, concluded that they were diagnostic of asbesto sis and introduced the term "asbestosis bodies Soon thereafter, such bodies were found in the lungs of asbestos workers without associated fibrosis, and therefore the name was shortened to "asbestos body." Subsequently, morphologically indistinguishable structures were noted in talcworkers7 and designated "pseudoasbestos bodies" (Fig. 1). During the last years a number of other
l
Vol. 280 No. 9
ABDOMINAL SURGERY-WELCH
487
I
207. Brawley, R. K.. Cameron, J L., a\id Zuidema. G D Severe upper abdominal injuries treated byl pancreaticoduodenectomy
ascites by retnfusion of unmodified autogenous ascitic fluid An' een 62 248-254. 1967
Surg.. Gynec. <4 Obu. 126 5 16-522J 1968.
232. Hyde. G. L.. and Eiseman. B. Peritoneal atrial shunt for intract
208 Trapnell. J. E.. and Anderson. \1 C Role of early laparotomy in
able ascites Arch. Surg. 95 369-373. 1967.
acute pancreatitis. Ann. Surg 165:49-55. 1967
233 Vasko. J. S.. and Tapper. R I Surgical significance of chvlous
209 Peterson, L. VI . Collins. J J . Jr., and Wilson. R E Acute pan
ascites. Arch. Surg. 95:355-368. 1967.
creatitis occurring after operation Surg . Gxnec <4 Obsi 127 23-
234 Dudnck. S. J., Wilmore. D. W.. Vars. H. M ..and Rhoads. J E
28. 1968.
Long-term parenteral nutrition with growth/ development, and
210 Maliet-Guy. P Place of sphincterotomy in treatment of diseases
positive nitrogen balance. Surgery 64 134-142. 1968.
of pancreas. J Rax Call. Surgeons Edinburgh 12:318-325.
235 Wilmore. D W.. and Dudnck. S J Grovuth and development of
1967,
infant receiving all nutrients exclusively-fey vein. JA Vf.4 203
211 Warren. K. W.. Poulantzas. J K.. and Kune. G A. Life after
860-864. 1968
total pancreatectomy for chronic pancreatitis clinical study of 236 Schwartz. F D., Kallmeyer. J . Dunea. G . and Kark. R M
eight cases. Ann. Surg. 164-830-834. 1966
Prevention of infection during peritoneal dialysis JAMA. 199"
212. Cameron, J. L.. Anderson, R. P.. and Zuidema. G D Pan
79-81. 1967.
creatic ascites. Sun*. Gxnec AObst 125:328-332. 1967
237. Noon. G. P . Beall. A. C.. Jr. J6rdan. G L . Jr., Riggs. S . and
213. Howard, J. M. Pancreatico-duodenectomy forty-one consecutive
De Bakey. M. E. Clinical evaluation of peritoneal irrigation with
Whipple resections without operative mortality. Data presented
antibiotic solution. Surgerx 82:73-78, 1967.
at meeting of American Surgical Association. Boston. Massa 238. Laver. M. Personal communication.
chusetts. April 17-19. 1968
239. Roberts. S. S.. et al. Prognostic significance of cancer cells in
214. Warren, K. W. Discussion of Howard-"
circulating blood ten yar evaluation. Am J Surg. 113 *,5~-"62.
215 Park. C. D.. Mackie. J A., and Rhoads, R. E. Pancreatico-
1967
gastrostomy. Am. J Sur*. 1 13.85-90. 1967.
240. Localio. S. A . Francis. K. C.. and Rossano, P G. Abdominosa-
216. Waddell, W. R., and Loughrv. R. W Gastric acid secretion after pancreaticoduodenectomy. Arch. Surg. 96.574-585. 1968
cral resection of sacrococcygeal chordoma. Ann. Surg 166 394402. 1967
217. Warren. K W.. Veidenheimer, M. C . and Pratt. H S Pancreati
24| Goldsmith. H. S . De los Santos, R.. and Beattie. E. J . Jr. Re
coduodenectomy for periampullary cancer S. Clin Xorth Ameri
lief of chropic lymphedema by omental transposition Ann Sw,,
ca 47.639-645. 1967
166:573-^85. 1967.
2 18 Laroche. G. P.. Ferns. D O.. Pnestley. J. T.. Scholz. D. A., and 242. Higgins* C C. Ureteral injuries during surgery: review of 8"
SToii.h 7(,t,A
Dockerty, M. B. Hypennsulinism surgical results and manage
cases. JAMA. 199.82-88. 1967
ment of occult functioning islet ceil tumor, review- of 154 cases.
243 Gardner. W J.. and Storer, J. Use of G suit in control of intra-
Arch. Surg. 96:763-772. 1968.
abdominal bleeding. Surg.. Gynec. <Sc Obst. 123 792-798. 1966
219 Mengoli, L., and Le Quesne, L P Blind pancreatic resection for
244 Postoperative wound infections influence of ultraviolet irradia
suspected insulinoma review of problem. Brit. J. Surg. 54 749-
tion of operating room and of various other factors: report of Ad
756, 1967.
Hoc Committee of Committee on Trauma. Division of Medical
220 Papaioannou, A. N Collective review tumors other than insuli
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nomas associated with hypoglycemia. Surg.. Gxnec & Obst.
Council Ann. Surg. iSupp.) 160.1-192. 1964
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245. Hart. D . Postlethwait, R. W.. Brown. 1. W.. Jr.. Smith. W. W .
221 Zollinger. R. M. Tompkins. R. K. Vloore. F T. and Amer-
and Johnson. P A. Postoperative wound infections- further report
son. J. R. Identification of diarrheogenic hormone associated wi^h
on ultraviolet irradiation with comments on recent < 1964) National
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Research Council Cooperative Study report. Ann. Surg 167
American Surgical Association. Boston, Massachusetts. AprW 17-
728-743. 1968
19. 1968.
246. Altemeier, W. Discussion of Hart, Postlethwait. Brown. Smith,
222 Lillehei. R. C . et al. Transplantation of stomach, intestine, and
and Johnson.*45
pancreas: experimental and clinical observations. Surgerx 62:
247. McVay. C. B. Inguinal hemioplasty common mistakes and pit
I 721 -741, 1967.
falls. S: Clin. Xorth America 46:1089-1100. 1966.
223 Reemtsma. K., Giraldo. N.. and Depp. D. A Islet cell trans
248. Erskinc. J. M. Hernia through foramen of Winslow Surg.. Gxnec.
plantation. Data presented at meeting of American Surgical As
A Obst. 125:1093-1109, 1967.
sociation. Boston. Massachusetts. April 17-19. 1968
249 Freeark. R. J., Shoemaker. W. C . and Baker, R. J. Aortography
224 LeVeen, H H . Diaz, C A.. Piccone. V A*1, Jr., and Falk. G
in blunt abdominal trauma Arch Surg. 96 705-711. 1968.
Surgical approach to diabetes mellitus. Data-presented at meeting
250. Boijsen. E.. Ekman, C.-A., and Lundh. G. Selective splanchnic
for Society for Surgery of the Alimentary 'Tract, San Francisco,
angiography. Advances tn Surg. 3:13-73. 1968.
California. June 15 and 16. 1968.
,
251. Little, J. M., McRae, J.. Smitananda. N.. and Morris. J G Ra
225 Norman, J. C.. Covelli, V H.. and S$e. H S. Transplantation
dioisotope scanning of liver and spleen in upper abdominal trau
of spleen: experimental cure of hemophilia. Surgery 641-16.
ma. Surg.. Gvnec. <5l Obst. 125.725-729, 1967.
1968.
/
252. LeMire, J. R.. Earley, D. E., and Hawley. C. Intra-abdominal
225a. Peacock, E. E.. Jr. Discussion of Ndrman, Covelli and Sise.115
injuries caused by automobile seat belts. JA VIA 201:735-737.
225b.Darling. R. C. Peripheral arterial surgery.
Eng J Med.
1967.
280141-146. 1969
253. Witte, C. L. Mesentery and bowel injury from automotive seat
226 Donovan. T J . and Bucknam. C A. Aorto-enteric fistula Arch
belts. Ann Surg. 167:486-492. 1968.
Surg 95 810-820. 1967 '
254. Sube, J., Pizerman. H. Ha and Mclver. W J. Seat belt trauma
227 Szilagyi. D E.. Elliott. J. P . and Berguer. R. Coincidental malig
to abdomen. Am. J. Surg. 1 13 346-350. 1967
nancy and abdominal a/>rtic aneurysm problems of management.
255 Pridgen. J. E.. et al. Penetranng wounds of abdomen analysis of
Arch. Surg. 95:402-412, 1967
776 operative cases Ann. Surg 165:901-907. 1967.
228 Marable, S. A., kajrtan. M F . Beman, F M., and Molnar. W,
256 Whelan. T. J.. Jr. Burkhalter. W E., and Gomez. A Manage
Celiac compression syndrome. Am. J Surg. 1 15:97-102,
1968
/
ment of war wounds. Advances */i Surg. 3:227-350. 1968. 257 Schmitt. H. J.. Patterson, L. T.. and Armstrong. R G Reopera-
229. Snyder. M A /Mahoney. E B. and Rob, C G Symptomatic
tive surgery of abdominal war wounds. Ann. Surg. 165 173-185.
celiac artery stenosis due to constriction by neurofibrous tissue
of celiac ganglion. Surgery 61.372-376. 1967. 230 Drapanas/T Discussion of Marable. Kaplan. Beman. and Mol
nar -* / 231 Pearlrpan. D M. and Duremdes. G. Treatment of intractable
1967
,
258 Schechter. D C Problems relevant to major surgical operations
in Jehovah's Witnesses. Am. J. Surg. 116-73-80. 1968
259 Konstam. P G Surgical problems in West Afnca. Am J Surg
1 12:864-868. 1966.
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Vol. 280 So. 9
MEDICAL INTELLIGENCE-GAENSLER AND ADDINGTON
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substances have been shown to cause asbestosbody-like structures, and therefore Gough" suggested the name "mineral fiber bodies," Perhaps the most suitable term, "ferruginous bodies," was coined by Gross8 to describe structures that have a coating containing iron demonstrable by the Prus sian blue reaction, that look like asbestos bodies and that ma> or may not have asbestos fibers as their core.
U LTRASTRUCTURE
The original descriptions have now been made more precise by electron microscopy. The core of the bodies is variable. Chrvsotile consists of hollow tubes 150 to 400 A in diameter that may be filled with crystal fragments.111 The amphibole group, which includes crocidolite, amosite and tremolite, has solid fibers that are much larger, the smallest being 8(H) A in diameter. Davis" has shown that the coating consists of ferritin granules approximately 60 A in diameter, and of amorphous material, proba bly protein. This coating may be very thin or as thick as 5 M Several fine needles of asbestos, 0.05 to 0 5 fj. in length, may be scattered throughout the body with their axes parallel to the surface. Ferritin may accumulate around very small dust particles and produce "asbestos bodies" of a size below the resolution of the light microscope. Although the deposition of the protein-iron complex was thought to be an extracellular process, electron microscopy now has shown that the formation is intracellular, probably within giant cells or macrophages.
bestos bodies" in random post-mortem material. At first, they were found in 26 per cent of autopsies in Capetown near mining operations, but later, surpris ingly enough, a similar percentage was demonstrated in Miami, Florida.1* Since then a still greater prev alence has been reported from other cities.18 Animals apparently are subject to the same air pollution because asbestos bodies can be found in don keys, field rats and baboons near mines.17 The method of sampling is important; on routine histo logic examination ferruginous bodies were found in only 2 per cent of lungs without fibrosis; this prev alence increased to 21 per cent if squeezed lung juice was used, and it rose to 48 per cent with scraping of the cut surface.18 The sampling site was also important, right basilar segments giving the highest yield. A distillation process has revealed a few asbestos bodies in 97 per cent of lungs.18 In none of these autopsy surveys was there a relation between the prevalence of asbestos bodies and pul monary fibrosis or cancer. The source of asbestos or other mineral fibers in the city atmosphere has been the subject of much speculation. Dust from automobile brake linings and clutch faces was soon suspected.13
Chemistry
The principal component of the asbestos body is organic, mainly protein with iron; usually there is less than 5 per cent asbestos. Early workers be lieved that the bodies were formed free within the alveoli and that the coating was derived from hemo globin released from vessels injured mechanically by the fibers. Another theory was that the coating is deposited by phagocytes.'* The finding of hydroxyproline led some to suggest that it contains collagen deposited by fibroblasts.1* Amino acid residues in the protein of asbestos bodies have been examined in the hope of differentiating collagen from other proteins. The analytical values for proline, hydroxyproline, leucine and glycine were all too low for collagen to be the main part of the protein enve lope.14 The protein resembles that of general lung proteins and is also similar to that of serum gamma globulin, globins and hemoglobins. This chemi cal evidence supports the finding, on electron mi croscopy, that the coating is formed by the cyto plasm of alveolar macrophages or giant cells. The iron may be derived from disintegrating erythro cytes also ingested by these cells.
Prevalence
In recent years a search has been made for "as
Figure 2. Section of the Lung of a 56-Year-Old Shipyard Pipe Coverer Who Died of Squamous-Cell Bronchogenic Carcinoma with Brain Metastases (Hematoxyttn and Eosin Stain, Original Mag
nification X32).
He urn at our laboratories nine years earlier because of asbestoses. The section shows at the top diffuse interstitial fibrosis with hnnevcombmg. In the lefL lower field the carcinoma is surrounded hs
masses of asbestos bodies.
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THE NEW ENGLAND JOURNAL OF MEDICINE
Feb. J7. Uti9
formation that may provide the ideal environment tor coating. Rats do not form bodies, perhaps because asbestos dust causes early fibrosis.2* Only a tiny fraction, probably less than 1 per cent of all the fibers in the lung, become coated (Fig. 4). Whether a special environment is required for the coating is being investigated by means of pleural injection Preliminary results suggest that acid mucopolysac charides and colloidal iron both must be present.-1"-'1 In tissue cultures, even the smallest dust particles are taken up by macrophages and fibroblasts, but no ty pical asbestos bodies develop.25
Nonasbestos Ferruginous Bodies
Today, respirable fibers are legion. Diatomaceous earth, graphite and carborundum already have been identified as the core of typical "asbestos bodies" in man.26 Substances believed to be biologically inert, including fibrous aluminum silicate (Fig 5), fibrous glass (Fig. 6), silicon carbide ana forsterite have caused ferruginous bodies in hamsters and guinea pigs.9,20 Even fragments of the lung's own elastictissue may produce "elastosis bodies" that look sim-
ST0566768
FiGL'RE 3. Section oj Pleura of a 6!`Year-Old Man Who Had Been an Asbestos-Sheet Slacker for 22 Years (Hematoxylin and Eostn
Stain, Original Magnification X600)
Seven years earlier asbestosis was recognized at our laboratory. He died three months after the onset of dyspnea, weight low, chest pain and recurrent serosangumeous pleural effusion}1 At the bottom (here is a nest oj asbestos bodies within a mesothelioma In the upper tight area theie are several smaller bodies and fine crystals with early beading.
The chrysotile imbedded by heat in the plastic of these linings becomes anhydrous forsterite. Animal experi ments have now shown that forsterite indeed can produce ferruginous bodies but that, unlike asbes tos, it is nonfibrogenic.*
Sputum of asbestos workers frequently contains asbestos bodies, the frequency increasing with time of exposure (22 per cent under one year and 38 per cent over five years) and increasing with higher dust concentration.21 However, asbestos bodies in sputum are not necessarily indicative of asbestosis. They have also been found in feces, presumably from swallowed sputum, and in the spleen, tonsils and lymph nodes of exposed persons. Neoplasms, particularly bronchogenic carcinoma and pleural and peritoneal mesothelioma, may contain asbestos bodies within and around them (Fig. 2 and 3).
Experimental Production
Asbestos bodies can be produced in animals with out necessarily causing fibrosis or tumor Indeed, they have been found after only seven days of expo sure.-'2 Some animals produce them readily, most notably guinea pigs Thev respond b> granuloma
Figure 4. Section of the Lung of a 55-Year-Old Man Who Had Been an Asbestos Sheet Planer for Sine Years tPartialis Polarised.
Hematoxylin and Eosm Stain. Original Magnification \H() i
A left upper lobectomy was performed because of a large nodule, which proved to be an asbestoma. There are numerous free asbestos pbers throughout the section. Many macrophages are plied with yel low granular debris. There is one well preserved segmented asbesi,.. bods at the top (upper arrow} and several broken-off. sound beads
of bodies at the bottom (lower arrow).
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MEDICAL INTELLIGENCE-GAENSLER AND ADDINGTON
491
of asbestos used in the United States is of this type, it was concluded that the vast majority of ferruginous bodies found at random autopsies are not from asbestos.20
Figcre 5. Smear of Sediment of Saline Washing oj Hamster Lung Sine Months after Endotracheal Injection with Ceramic Aluminum
Silicate tPerle's Blue and Eostn Stain X800). A ferruginous bods has macrophages attached at each end. I This material was kindly supplied by Dr, Paul Cross, director of the In
dustrial Hygiene Foundation Laboratories, Pittsburgh, Pa )
ilar.M Technics are now available for analysis of the core fibers. They include electron beam and x-ray diffraction, laser microprobes, ultrasonic disintegration and mass spectroscopy. The electronbeam diffraction patterns of ferruginous bodies trom 22 lungs of '`unexposed" persons did not coincide with that of chrysotile. Since 95 per cent
Biologic Importance
Obviously, the diagnosis of asbestosis, based on the finding of ferruginous bodies in an apparently unexposed person, must be made with caution. However, one must be equally cautious in making a diagnosis of "nonspecific interstitial pneumonitis" in a person with known exposure because there is no relation between the number of bodies and the severity of asbestos pneumoconiosis. On the contra ry, we and others have noted an inverse relation.'* " In persons with prolonged but distant exposure, of ten retired because of respiratory impairment, the lungs frequently show severe fibrosis with only rare asbestos bodies whereas in patients with more re cent exposure, lung biopsy reveals alveoli filled with bodies and debris-laden macrophages but little or no fibrosis.
This paradox can be explained m a number of wavs. The small number of asbestos bodies in work ers with fibrosis who were exposed long ago may be the result of clearing of the intra-alveolar materi al. This clearing occurs most rapidly in areas of supple alveolar walls whereas it is delayed in the more noncompliant regions near the thickened pleura and around larger vessels and bronchi. Therefore, the distribution of asbestos bodies is uneven, and their number in any section need not be representative.20,24 The relation between the number of visible asbestos bodies and the degree of fibrosis is also poor because only a very small and variable fraction of fibers become coated (Fig. 4) Probably the tiniest, uncoated particles, which are invisible by light microscopy, are most fibrogenic because they have the largest aggregate surface area. This is important because at some stage a chemical reaction must initiate the process of fibrosis. The visible asbestos bodies, therefore, are best considered as markers, rather than as important causative agents
Figure 6. Section oj Hamster l ung 16 Months after Endotracheal lulection with Fibrous Class Dust tHematoxylin and Eosin Stain.
Original Uagnipcation X600}
Well developed ferruginous hollies are seen tn the upper left and lower light pelds < Material jiom Dr. Paul Cross l
Conclusions
In 1929 Cooke said that "curious bodies have been found in every necropsy in pulmonary asbes tosis, and the problems we have to decide are, first, what the bodies are, and second, whether they are diagnostic of asbestosis." Although at first answers seemed deceptively simple, new information in creasingly has raised new questions. That asbestos bodies may contain asbestos is clear. It is equally clear that structures apparently indistinguishable from asbestos bodies may have as their core other materials. Unfortunately, the methods of identifi cation are exceedingly complex, and, even m the best hands, results remain tentative. Neverthe less, recent animal exposure and analytical work suggests that, until asbestos has been identified as
CO / nr.
c r
49 2
THE NEW ENGLAND JOURNAL OF MEDICINE
Feb '27. 1"H9
the core of an "asbestos body,' it is best to use the
more general term "ferruginous bod>."
References
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2 Brodeur. P Magic mineral The Nmi Yorker (October I2i. 1968 Pp. I 17-165
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4 Graham. W G B . and Gaensler. E A Talco-sihcosis m rubber worker Wed. thoruc 22 590-604. 1965
5 Cooke. W, E. Fibrosis of lungs due to inhalation of asbestos dust Bru W J 2:147, 1924
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9 Gross. P. deTreville. R T P. Cralley. 1. J. and Daws. J M G Pulmonarv ferruginous bodies development m response to filamentous dusts and method of isolation and concentration ArOi Path 85'539-s46. 1968
10 Gaze. R Physical and molecular structure of asbestos .-f*/i Sf* > ark -it ad Si 1 32 23-30. |9f.5
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14 Blount, vl.. Holt. P, F.. and Leach. A A Protein coating ot asbestos Irodies. Biochem. J. 101'204-2CT. 1966
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20 Gross. P Studies of pathogenicity of synthetic and natural asbes tos and brake drum dust. Presented at Fibrous Dust Seminar. Mellon Institute, Pittsburgh. Pennsylvania. November 22. 1968.
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ST0566770
BY THE LONDON POST
for assistant lecturers, who would receiv e^-fnETeases
Rewards of Teaching and Research
in salary ranging from 10 to 17 per cent with much smaller increases for senior lecturers and professors.
|>H4\ Lister, M I). X
More controversial, however, t)tfn the reduction in the total claim was the comjrfent in the report that the present salaries and/tfareer structures of univer
THE recurring econoSuc problems of Britain have had an intensely depressing effect upon
sity teachers are biased toward research rather than teaching and ppamotion tends to depend on the
the whole nation, and one of the-.principles that hasnumber of mi&fications a teacher has made. To cor
become generally accepted as a means of stabilizing rect thk/bias the Board proposed that bonuses
the economy is the need lor everyon^ to accept amojHffing to 4 per cent of a university's total salary
some discipline in the matter of mcomeV-Jt is not
should be given up to half the teaching staff
surprising, however, that the principle is readily^ below the grade of professor so long as they had
acceptable in general but hard to accept in paptKu- passed a four-year or five-year period of probation.
lar. No section of the community is likely tyefie conV This system should be designed to reward a teach
tent to receive what it considers to be atfiidverse or er's hours of teaching, the quality of his teaching
unfair decision of the Prices and fndome Board, to aiX sometimes his load of administrative work.
which the majority of pay dairpsare now referred. AparfNfjmm obvious statistics of teaching work load
A major dispute has recendy'arisen from the report it was suggested that a teacher's merit should he
of the Board1 on the p.iy^m university teaching staff. assessed bXstudents through a carefully drafted
The Association oj/Tniversity Teachers had asked questionnaire oKbv the examination performance of
for a 15 per ceiHXalary rise, based on a comparison his students. Simifluyawards would be made to pro
with salaries^ffi industry and the civil service, hut fessors who had shovfco outstanding merit, particu
the BoardXroPosed only an average rise of 4.9 per larly in the setting up ahd administration of teach
cent arra emphasized the fact that the endless chain ing departments.
N^
ijfdncreases made because similar groups had re
Justifying his proposal to uNistudent opinion m
ceived increases must be broken. To recruit teach assessing the merit of their teachers M r. Aubrey
ers of quality the lamest rises were recoinmen ded Jones, the chairman of the Prices and Income
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