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DOW 05861
ST0ZU V U A
Vol. 280 No. 9
ABDOMINAL SURGERY-WELCH
487
207. Brawley, R. K.. Cameron. J. L.. and Zuidema. G. D. Severe
upper abdominal injuries (reated byl pancreaticoduodenectomy. Surg.. Gynee. A Obsl. 126:516-522.' 1968.
208. Trapnell. J. E . and Anderson. M. C. Role of early laparotomy in acute pancreatitis. Ann. Surg. 163:49-55. 1967.
209. Peterson. L. M,, Collins, J. J.. Jr., and Wilson. R. E. Acute pan creatitis occurring after operation. Surg.. Gvnec. A Obsl. 127:23-
28. 1968.
210. Mallet-Guy. P. Place of sphincterotomy in treatment of diseases of pancreas. J. Rov. Coll. Surgeons Edinburgh 12:318-325.
1967.
211. Warren. K. W.. Poulantzas, J. K,, and Kune. G. A. Life after
total pancreatectomy for chronic pancreatitis: clinical study of
eight cases. Ann. Surg. 164:830-834. 1966.
212. Cameron. J. L., Anderson. R. P.. and Zuidema. G. D. Pan
creatic ascites. Surg.. Gvnec. A Obsl. 123:328-332. 1967. 213. Howard. J. M. Pancreatico-duodenectomy: forty-one consecutive
Whipple resections without operative mortality. Data presented
at meeting of American Surgical Association. Boston. Massa chusetts. April 17-19, 1968.
214. Warren. K. W. Discussion of Howard.1'3
215. Park. C. D.. Mackie. J. A., and Rhoads. R. E. Pancreaticogastrostomy. Am. J. Surg. 113:85-90, 1967.
216. Waddell, W. R.. and Loughry, R. W. Gastric acid secretion after pancreaticoduodenectomy. Arch. Surg. 96:574-585. 1968.
217. Warren. K. W.. Veidenheimer, M. C.. and Pratt. H. S. Pancreati
coduodenectomy for periampullary cancer. S. Clin. North Ameri
ca 47:639-645, 1967.
218. Laroche. G. P., Ferris. D. O . Priestley. J. T.. Scholl. D. A., and Dockerty, M. B. Hyperinsulinism: surgical results and manage
ment of occult functioning islet cell tumor: review of 154 cases.
Arch. Surg. 98:763-772. 1968. 219. Mengolt, L.. and Le Quesne. L. P. Blind pancreatic resection for
suspected insulinoma: review of problem. Brit. J. Surg. 54:749-
756.1967.
220. Papaioannou. A. N. Collective review: tumors other than insuli nomas associated with hypoglycemia. Surg., Gynec. A Obsl.
123:1093-1109. 1966.
221. Zollinger. R. M.. Tompkins. R. K.. Moore. F. T.. and Amer^ son. J. R. Identification of diarrheogenic hormone associated with
non-beta islet cell tumors of pancreas. Presented at meeting'of American Surgical Association. Boston, Massachusetts. April 17-
19.1968.
222. Lillehei. R. C , et al. Transplantation of stomach, inteslfne. and
pancreas: experimental and clinical observations. Surgery 62: 721-741. 1967.
223. Reemtsma. K.. Giraldo. N.. and Depp. D. A. Islet cell trans
plantation. Data presented at meeting of American Surgical As
sociation. Boston. Massachusetts, April 17-19. {968.
224. LeVeen. H. H.. Diaz. C. A., Piccone, V. A/. Jr., and Falk. G.
Surgical approach to diabetes mellitus. Data.presented at meeting for Society for Surgery of the Alimentary 'Tract, San Francisco,
California. June 15 and 16. 1968.
/
225. Norman. J. C.. Covelli. V. H., and SjSe. H. S. Transplantation
of spleen: experimental cure of tiertiophilia. Surgery 64:1-16.
1968.
/
225a. Peacock. E. E.. Jr. Discussion of Ndrman, Covelli and Sise."*
225b. Darling. R. C. Peripheral arterial surgery. New Eng. J. Med.
260:141-146.1969.
/
226. Donovan. T. J.. and Bucktvxm, C. A. Aorto-enleric fistula. Arch. Surg. 83:810-820. 1967. /
227. Szilagyi, D. E.. Elliott, J/P.. and Berguer. R. Coincidental malig nancy and abdominal nflrtic aneurysm: problems of management.
Arch. Surg. 83:402-412, 1967.
228. Marable, S. A.. Kaman. M. F.. Beman. F. M.. and Molnar, W.
Celiac compression syndrome. Am. J. Surg. 113:97-102.
1968.
/
229. Snyder. M. A./Maboney. E. B.. and Rob. C. G. Symptomatic
celiac artery ifenosis due to constriction by neurofibrous tissue of celiac gajlglion. Surgery 61.372-376. 1967.
230. Drapanas/T. Discussion of Marable. Kaplan, Beman. and Mol nar.** /
231. Pearlrpen. D. M.. and Duremdes. G. Treatment of intractable
ascites by reinfusion of unmodified autogenous ascitic fluid. Sur
gery 62:248-254. 1967.
232. Hyde. G. L.. and Eiseman, B. Peritoneal atrial shunt for intract
able ascites. Arch. Surg. 95:369-373. 1967.
/
233. Vasko. J. S.. and Tapper. R. I. Surgical significarice of chylous
ascites. Arch. Surg. 83:355-368. 1967.
/
234 Dudrick. S. J.. Wilmore. D. W.. Vars. H. M.yflnd Rhoads. J. E. Long-term parenteral nutrition with growth/development, and
positive nitrogen balance. Surgery 64:134-142, 1968.
235. Wilmore. D. W,, and Dudrick. S. J. Growth and development of
infant receiving all nutrients exclusively/fcy vein. JA MA 203
860-864. 1968.
/
236. Schwartz. F. D.. Kallmeyer. J.. Duitea. G.. and Kark. R. M.
Prevention of infection during perit/neal dialysis. JA MA 199:
79-81, 1967.
/
237. Noon. G. P.. Beall. A. C.. Jr.. Jbrdan. G. L.. Jr.. Riggs. S.. and
De Bakey. M. E. Clinical evaluation of peritoneal irrigation with
antibiotic solution. Surgery ^62:73-78, 1967.
238. Laver. M. Personal comtryonication.
239. Roberts. S. S.. et al. Prognostic significance of cancer cells in
circulating blood: ten year evaluation. Am. J. Surg. 113:757-762.
1967.
240. Localio, S. A.. Fraricis. K. C.. and Rossano. P. G. Abdominosa
cral resection of Sacrococcygeal chordoma. Ann. Surg. 166:394-
402. 1967. /
241. Goldsmith. H.'S.. De los Santos, R.. and Beattie. E. J.. Jr. Re
lief of chroptc lymphedema by omental transposition. Ann. Surg.
166:573-^85. 1967.
242. Higgins* C. C. Ureteral injuries during surgery: review of 87
cases, JA.MA. 199:82-88. 1967.
243. Gardner. W. J.. and Storer, J. Use of G suit in control of intra
abdominal bleeding. Surg.. Gynec. A Obsl. 123:792-798. 1966.
244. Postoperative wound infections: influence of ultraviolet irradia-
/ tion of operating room and of various other factors: report of Ad
/ Hoc Committee of Committee on Trauma, Division of Medical
/ Sciences. National Academy of Science-National Research
Council. Ann. Surg. (Supp.l 160:1-192. 1964.
245. Hart. D., Posilethwait. R. W., Brown. I. W.. Jr.. Smith. W. W..
and Johnson. P. A. Postoperative wound infections: further report
on ultraviolet irradiation with comments on recent (19641 National
Research Council Cooperative Study report. Ann. Surg. 167:
728-743. 1968.
246. Altcmeier. W. Discussion of Hart. Postlethwait. Brown. Smith,
and Johnson.**
247. McVay. C. B. Inguinal hemioplasty: common mistakes and pit-
falls. T: Clin. North America 46:1089-1100. 1966.
248. Enkine. J. M. Hernia through foramen of Winslow. Surg.. Gynec.
A Obsl. 126:1093-1109. 1967.
249. Freeark. R. J., Shoemaker, W. C.. and Baker, R. J. Aortography
in blunt abdominal trauma. Arch. Surg. 96:705-711. 1968.
250. Boijsen. E.. Ekman. C.-A.. and Lundh. G. Selective splanchnic
angiography. Advances in Surg. 3:13-73. 1968.
251. Little. J. M,, McRae, J.. Smitananda. N.. and Morris. J. G. Ra
dioisotope scanning of liver and spleen in upper abdominal trau
ma. Surg., Gynec. A Obsl. 126:725-729. 1967.
252. LeMire, J. R.. Earley. D. E.. and Hawley. C. Intra-abdominal
injuries caused by automobile seal belts. JA.MA. 201:735-737.
1967.
253. Witte, C. L. Mesentery and bowel injury from automotive seat
belts. Ann. Surg. 167:486-492. 1968.
254. Sube. J., Pizerman, H. H.v and Mclver. W. J. Seat belt trauma
to abdomen. Am. J. Surg. 163:346-350. 1967.
255. Pridgen, J. E.. et aL Penetrating wounds of abdomen: analysis of
776 operative cases. Ann. Suh. 168:901-907. 1967.
256. Whelan. T. J., Jr.. Burkhalter. W. E., and Gomez. A. Manage
ment of war wounds. Advances in Surg. 3:227-350, 1968.
257. Schmitt. H. J.. Patterson. L. T.. and Armstrong. R. G. Reopera
tive surgery of abdominal war wounds. Ann. Surg. 166:173-185.
1967.
\
258. Schechter. D. C. Problems relevant th major surgical operations
in Jehovah's Witnesses. Am. J. Surg. 616:73-80, 1968.
259. Konstam, P. G. Surgical problems in West Africa. Am. J. Surg.
112:864-868. 1966.
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DOU 05862
s T & it
Vol. 280 No. 9
ABDOMINAL SURGERY-WELCH
487
207. Brawlcy. R. K.. Cameron. J. L.. and Zuidema. G D. Severe
upper abdominal injuries treated byl pancreaticoduodenectomy. Surg.. Cynec. A Obst. 126:5 16-522.'1968.
208. Trapnell. J. E.. and Anderson. M. C. Role of early laparotomy in acute pancreatitis. Ann. Surg. 165:49-55. 1967.
209. Peterson. L. M.. Collins. J. J.. Jr., and Wilson. R. E. Acute pan creatitis occurring after operation. Surg.. Gvnec. 41 Obst. 127:2328. 1968.
210. Mallet-Guy. P. Place of sphincterotomy in treatment of diseases of pancreas. J. Rov. Coll. Surgeons Edinburgh 12:3 IB-325. 1967.
211. Warren. K. W.. Poulantzas. J. K., and Kune. G. A. Life after
total pancreatectomy for chronic pancreatitis: clinical study of
eight cases. Ann. Surg. 164:830-834. 1966.
212. Cameron. J. L.. Anderson. R. P.. and Zuidema. G. D. Pan
creatic ascites. Surg.. Cynec. A Obsi. 125:328-332. 1967.
213. Howard. J. M. Pancreatico-duodenectomy: forty-one consecutive Whipple resections without operative mortality. Data presented
at meeting of American Surgical Association. Boston. Massa chusetts. April 17-19, 1968.
214. Warren, K. W. Discussion of Howard.*13
215. Park. C. D.. Mackie. J. A., and Rhoads. R. E. Pancreaticogastrostomy. Am. J. Surg. 113:85-90, 1967.
216. Waddell. W. R., and Loughry. R. W. Gastric acid secretion after pancreaticoduodenectomy. Arch. Surg. 96:574-585. 1968.
217. Warren. K. W.. Veidenheimer. M. C., and Pratt. H. S. Pancreati coduodenectomy for periampullary cancer. S. Clin. North Ameri
ca 47:639-645. 1967.
218. Laroche. G. P . Ferris. D. O , Priestley, J. T . Scholz. D. A., and
Dockerty, M. B. Hyperinsulinism: surgical results and manage
ment of occult functioning islet cell tumor: review of 154 cases.
Arch. Surg. 96:763-772. 1968. 219. Mengoli. L.. and Le Quesne. L. P. Blind pancreatic resection for
suspected insulinoma: review of problem. Brit. J. Surg. 54:749-
756. 1967.
220. Papaioannou. A. N. Collective review: tumors other than insuli nomas associated with hypoglycemia. Surg.. Cynec. A Obst.
123:1093-1109. 1966.
221. Zollinger. R. M . Tompkins. R. K.. Moore. F. T.. and Amer-^
son, J. R. Identification of diarrheogenic hormone associated wijh
non-beta islet cell tumors of pancreas. Presented at meeting'of American Surgical Association, Boston, Massachusetts, April 17-
19.1968.
222. Lillehei. R. C , et al. Transplantation of stomach, inlesifne. and pancreas: experimental and clinical observations. Surgery 82:
721-741, 1967.
223. Reemtsma. K.. Giraldo. N., and Depp. D. A. Islet cell trans
plantation. Data presented at meeting of American Surgical As
sociation. Boston. Massachusetts. April 17-19. 1968.
224. LeVeen. H. H.. Diaz. C. A.. Picconc. V. A., Jr., and Falk. G.
Surgical approach to diabetes mellitus. Data presented al meeting
for Society for Surgery of the Alimentary/Tract, San Francisco.
California. June 15 and 16. 1968.
/
225. Norman. J. C . Covelli. V. H.. and Sjse. H. S. Transplantation
of spleen: experimental cure of hpriiophilia. Surgery 64:1-16.
1968.
/
225a. Peacock, E. E .Jr Discussion ofNdrman. Covelli and Sise m
225b. Darling. R. C. Peripheral arterial surgery. New Eng. J. Med.
280:141-146, 1969.
/
226. Donovan. T. J.. and Buckram. C. A. Aorto-enteric fistula. Arch. Surg. 95:810-820. 1967. /
227. Szilagyi, D. E. Elliott, j/P.. and Berguer, R. Coincidental malig
nancy and abdominal %6rtic aneurysm: problems of management. Arch. Surg. 95:402-41$, 1967.
228. Marable, S. A.. Kaplan. M. F. Beman. F. M, and Molnar. W.
Celiac compression syndrome. Am. J. Surg. 115:97-102.
1968.
/
229. Snyder. M. A./Mahoney. E. B., and Rob. C. G. Symptomatic celiac artery sfenosis due to constriction by neurofibrous tissue
of celiac ganglion. Surgery 61:372-376, 1967.
230. Drapanas/T. Discussion of Marable. Kaplan. Beman. and Mofnar.*" /
231. Pearlrpan. D. M.. and Duremdes. G. Treatment of intractable
ascites by reinfusion of unmodified autogenous ascitic fluid. Sur
gery 62:248-254. 1967.
232. Hyde. G. L.. and Eiseman. B. Peritoneal atrial shunt for intract
able ascites. Arch. Surg. 95:369-373. 1967.
/
233. Vasko. J. S . and Tapper. R. I. Surgical signific:yice of chylous
ascites. Arch. Surg. 95:355-368. 1967.
/
234. Dudrick. S. J.. Wilmore, D. W . Van. H. M.And Rhoads. J E.
Long-term parenteral nutrition with growth/development, and
positive nitrogen balance. Surgery 84:I34-|42. 1968.
235. Wilmore. D. W.. and Dudrick. S. J. Growth and development of
infant receiving all nutrients exclusively .$>y vein. JAMA 203:
860-864. 1968.
/
236. Schwartz. F. D.. Kallmeyer. J.. Duitea. G.. and Kark. R. M.
Prevention of infection during petWneal dialysis. JA MA 199:
79-81. 1967.
/
237. Noon, G. P.. Beall. A. C.. Jr.. J6rdan, iG L . Jr.. Riggs. S.. and
De Bakey. M. E. Clinical evakiation of peritoneal irrigation with
antibiotic solution. Surgery 92:73-78. 1967.
238. Laver. M. Personal communication.
239. Roberts. S. S,, et al. Prognostic significance of cancer cells in
circulating blood: ten year evaluation. Am J. Surg. 113:757-762.
1967.
240. Localio, S. A.. Francis. K. C.. and Rossano. P. G Abdominosa
cral resection of Sacrococcygeal chordoma. Ann. Surg. 166:394-
402. 1967. /
241. Goldsmith. Fj. S.. De los Santos. R.. and Beattie. E. J.. Jr. Re
lief of chronic lymphedema by omental transposition. Ann. Surg.
166:573-^85. 1967.
242. Higginv C. C. Ureteral injuries during surgery: review of 87
cases, JA MA 199:82-88. 1967.
243. Gardner. W. J., and Storer, J. Use of G suit in control of intra
abdominal bleeding. Surg.. Cynec. A Obst. 123:792-798. 1966.
244. Postoperative wound infections: influence of ultraviolet irradia-
, tion of operating room and of various other Actors: report of Ad
/ Hoc Committee of Committee on Trauma. Division of Medical
/ Sciences. National Academy of Science-National Research
Council. Ann. Surg. (Supp.) 160:1-192. 1964 -
245. Hart. D.. Postlethwait, R. W . Brown, I. W.. Jr.. Smith. W. W .
and Johnson, P. A. Postoperative wound infections: further report
on ultraviolet irradiation with comments on recent (1964) National
Research Council Cooperative Study report. Ann. Surg. 167:
728-743. 1968.
246. Altemeier, W. Discussion of Hart. Postlethwait. Brown. Smith,
and Johnson.**3
247. McVay, C. B. Inguinal hemioplasty: common mistakes and pit-
falls. J: Clin. North America 48:1089-1100. 1966.
248. Erskine. J. M. Hernia through foramen of Winslow. Surg.. Cvnec.
A Obst. 125:1093-1109. 1967.
249. Freeark, R. J., Shoemaker, W. C.. and Baker, R. J. Aortography
in blunt abdominal trauma. Arch. Surg. 96:705-711. 1968.
250. Boijsen. E. Ekman. C.-A.. and Lundh. G. Selective splanchnic
angiography. Advances in Surg. 3:13-73. 1968.
251. Little. J. M.. McRae, J., Smitananda. N., and Morris, J. G. Ra
dioisotope scanning of liver and spleen in upper abdominal trau
ma. Surg., Cynec. A Obst. 125:725-729. 1967.
252. LeMire. J. R.. Earley. D. E.. and Hawley. C. Intra-abdominal
injuries caused by automobile scat belts. JAMA. 201:735-737.
1967.
253. Witte. C. L. Mesentery and bowel injury from automotive scat
belts. Ann. Surg. 167:486-492. 1968.
254. Sube. J.. Pizerman, H. Ha and Mclvcr, W. J. Seat bell trauma
to abdomen. Am.J. Surg. 153:346-350. 1967.
255. Pridgen, J. E, et al. Penetrating wounds of abdomen: analysis of
776 operative cases. Ann. SuJg. 185:901-907. 1967.
256. Whelan. T. J.. Jr.. Burkhalter, W. E. and Gomez. A. Manage
ment of war wounds. Advances In Surg. 2:227-350. 1968.
257. Schmitt. H. J.. Patterson. L. T., and Armstrong. R. G. Reopera
tive surgery of abdominal war wounds. Ann. Surg. 195:173-185.
1967.
\
258. Schechter. D. C. Problems relevant m major surgical operations
in Jehovah's Witnesses. Am. J. Surg. 519:73-80, 1968.
259. Konstam. P. G. Surgical problems in Wyst Africa. Am. J. Surg.
112:864-868. 1966.
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DOW 05863
Vol. 280 No. 9
MEDICAL INTELLIGENCE--GAENSLER AND ADDINGTON
489
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 Gross* to describe structures that have a coating containing iron demonstrable by the Prus sian blue reaction, that look like asbestos bodies and that may or may not have asbestos fibers as their core.
ULTRASTRUCTURE
The original descriptions have now been made more precise by electron microscopy. The core of the bodies is variable. Chrysotile consists of hollow tubes 150 to 400 A in diameter that may be filled with crystal fragments.10 The amphibole group, which includes crocidolite, amosite and tremolite, has solid fibers that are much larger, the smallest being SIX) 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 p. Several fine needles of asbestos, 0.05 to 0.5 ft 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.14 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.1* 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." 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."
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.1* The finding of hydroxyproline led some to suggest drat 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, hydroxypraline, leucine and glycine were all too low for collagen to be the main part of die 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
Fichu 2. Section of the Lung of a !6-Year-Old Shipyard Pipe Coverer Who Died of Squamous-CeU Bronchogenic Carcinoma with
Brain Metastases (Hematoxylin and Eosin Slam, Original Mag nification X32).
Hr was at our laboratories nine years earlier because of asbestosis. The section shows at the top diffuse interstitial fibrosis with honey combing. In the left lower field the carcinoma is surrounded by
masses of asbestos bodies.
DOW 0586*
490
THE NEW ENGLAND JOURNAL OF MEDICINE
Feb. 27, 1969
formation that may provide the ideal environment for coating. Rats do not form bodies, perhaps because asbestos dust causes early fibrosis.*4 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.J0,24 In tissue cultures, even the smallest dust particles are taken up by macrophages and fibroblasts, but no typical asbestos bodies develop."
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.** Substances believed to be biologically inert, including fibrous aluminum silicate (Fig. 3),- fibrous glass (Fig. 6), silicon carbide and forsterite have caused ferruginous bodies in hamsters and guinea pigs.*'" Even fragments of the lung's own elastic tissue may produce "elastosis bodies" that look sim-
ST0566768
Figure 3. Section of Pleura of a 61-Year-Otd Man Who Had
Been an Asbestos-Sheet Stacker for 22 Years (Hematoxylin and Eosin Stain, Original Magnification X600).
Seven years earlier asbestosis was recognized at our laboratory. He died three months after the onset of dyspnea, weight loss, chest pain and recurrent serosanguineous pleural effusion?1 At the bottom there is a nest of asbestos bodies within a mesothelioma. In the upper right area there 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.11 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. a Some animals produce them readily, most notably gu.inea pigs. They respond by granuloma
Ficuu 4. Section of the Lung of a 55-Year-Old Man Who Had Been an Asbestos Sheet Planer for \hu Years (Partially Polarized.
Hematoxylin and Eosin Slain, Original Magnification X800).
A left upper lobectomy was performed because of a large nodule, which proved to be an asbestoma. There are numerous free asbestos fibers throughout the section. Many macrophages are filled with yel low granular debris. There is one well preserved segmented asbestos body at the top (upper arrow) and several broken-off. round heads
of bodies at the bottom tlower arrow).
DOW 05865
Vol. 280 No. 9
MEDICAL INTELLIGENCE--GAENSLER AND ADDINGTON
491
: -
s-.' .t- "
Figure 5. Smear of Sediment of Saline Washing of Hamster Lung
Sine Months after Endotracheal Injection with Ceramic Aluminum Silicate tPerle's Blue and Eosin Stain X800).
A ferruginous body has macrophages attached at each end. (This material was kindly supplied by Dr. Paul Gross, director of the In
dustrial Hygiene Foundation Laboratories, Pittsburgh, Pa.)
iIar.H 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 from 22 lungs of "unexposed" persons did not coincide with that of chrysotile. Since 95 per cent
Figure 6. Section of Hamster Lung 16 Months after Endotracheal
lii/ectivn with Fibrous Class Dust (Hematoxylin and Eosin Stain, Original Magnification X600).
Well developed lentiginous bodies are seen in the upper left and lower right fields. (Material jrom Dr. Paul Cross.)
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.*
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.8,17 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 in a number of ways. 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.*'14 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.
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 in the best hands, results remain tentative. Neverthe less, recent animal exposure and analytical work suggests that, until asbestos has been identified as
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the core of an "asbestos body," it is best to use the more general term "ferruginous body."
References
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