Document Z82qdr2M7d7EBpB1Jq6LO5pq8
FILE NAME: Talc (TALC)
DATE: 1946 Apr
DOC#: TALC115
DOCUMENT DESCRIPTION: Medical Journal Article - Pathology of Talc Pneumoconiosis with Report of an Autopsy
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NORTHERN NEW YORK MEDICAL JOURNAL
21!
Pathology of Talc Pneumoconiosis with Report of an Autopsy
P. W. P orro, M.D., Watertown, N.Y. and N. M. Levine, M.D., Ogdensburg, N.Y.
PNEUMOCONIOSIS is the general term applied co the effects of inhaled dust on th e lungs. Only in recent years have most of the known important facts about this group of conditions been established by observations and experimental work. Some form s of pneumoconiosis such as anthracosis, due to the inhalation of coal dust, and siderosis, due to the inhalation of iron ore dust, are generally considered to be relatively harmless. Silicosis, from the inhalation of du3t containing much un combined silicon dioxide ("free silica"), and asbestosis, due to the inhalation of dust from the fibrous silicate, asbestos are. gen erally recognized ns serious forma of pneu moconiosis capable of causing pulmonary fibrosis and consequent disability. Silicosis was established us n disease entity about the beginning of this century and asbetwain ra th e r more recently in 1024 by CooUg(1 ). The various aspects of silicosis and aabestoais have considered in detail by Lfttr/,ii, et. nl. (8 ). A brief eons deration is given by G ardner(6).
Among other types of dust that have received recent attention in connection with the production of pneumoconiosis is talc, which in mined and milled in St. Law rence County, N.Y., as well as several o th er p arts of the United States. Reports of the w orking condition and effects m this area have been made by Dreecn(2) and by Sie.gal, Smith and G reenbuigCll). Porro, P atton, and Hobbs (10) Imve re ported clinical und roeritgcmogniphic find ings on fourteen cases of pneumoconiosis in talc w orkers including autopsy findings on five of the eases. In addition observa tion on the talc industry in Cieorpiia have been reported by Drecsen and DallaVallc
(3 ). Ail of these observers have found cases with increased pulmonary densities and w ith disability in advanced cases,
The pathologic findings in the lungs of talc w orkers consist grossly of <i Ken^1`l fibrous stiffening of the lungs and oiten
old fibrous pleural adhesions. Microscopi cally there lire found nsbestoais bodies and pigment laden macrophages in the alveoli and respiratory bronciolcs. In addition there is thickening in many alveolar walls and septa with the reaction consisting of histiocytes, fibroblasts, loosely arranged collagen fibers, scar tissue and a few lymphocytes as well as some amorphous pigment. There is hyperplasia of the lymph nodules along the septa. In thu alveoli poorly formed giant cells are some time present. There are also varying de grees of atalectasis, compensatory emphy sema and sometimes metaplusk1of alveola! epithelium into a layer of cuboid! cells in fihrotie areas. In addition there is aotartimea complicating silicosis, luhcrculosia, or other pulmonary disease. These finding are similar in nature to those described in asbeatosis by Gloyne (7) and othms.
The aabestoais bodies are the most spefie finding. These are brown, headed and umbe.ll ahaped rod, in length, usually sev,-al times the diameter of a leukocyte, hey have, been shown to be composed of thin silicate filler which is covered bv rown pigment which contains iron, wob
bly hemosiderin. They were originally otod in the lungs of asbestos workers and im-e first observed in the lungs of a tale ,orkcr by Gnrdncv<5) from a case ob eyved clinically by Patton (9) and aulo,.ted by F re e (4 ). Tale is made Tram aevnd silicates of similar chemical conrpomon to asbestos and some of winch are brous- although not an much so as lhe ninerals from which asbestos is made, t'hese. bodies have been found in no other
onditiona.
The following ease with autopsy m the
irst available in a talc worker nine* previously reported(10) and is of m tu e . .
iue Lo the sim ilar pulmonary finding-''--" H istory: J. R., ago 40, male, white, a U< minor*for 14 year. He entered the A. Barton Hepburn Hospital, Ogdenaburfi.
24
NORTHERN NEW YORK MEDICAL JOURNAL
General View of Lung X300 showing rod shaped asbestosis bodies and macrophages in the air spaces and a fibrocellular reaction in the interstitial tissue.
N.Y., Sept. 7, 1945 under the care of
Dr. J. K. Patton, He hnd been unable to
work fo r three years because of difficulty in breathing, Two weeks before, he started to expectorate bloody sputum and complain of pain in the left aide of the chest. X-ray findings revealed th e left lung field below the level of the first interspace to be com pletely obscured and in the rig h t lung field, a dense reticulation. The dyspnea con tinued to be severe and the patient expired
on Oct. 30, 1945.
Gross Autopsy Findings: The body is th at of a white, fairly well nourished, well developed male, 46 years of age, There is cyanosis of the finger tips and slight hypo static lividity and fully developed rigor mortis. The legs a rc edematous up to the
mid-portion.
The abdominal panniculus adiposus is yellow and moderate in amount. The peri
toneal cavity contains a considerable amount of serous fluid. The liver is three fingers below the costal margin and on section shows a pronounced nutmeg appear ance. The spleen is large and soft with prominent Malphigian corpuscles. The pancreas and gastrointestinal tract contain no gross lesions. The kidneys are con gested and the medulla of the adrenals is soft from autolysis. The bladder and prostate arc normal.
Both pleural cavities are partially ob literated by fibrous and fibrinous adhesions. A small amount of cloudy fluid is present on the left side. The pericardial sac con tains a small amount of serous fluid.
The lungs are firmer than normal, yel lowish as in chronic passive congestion, and have areas of firm triangular bluish dis coloration. On section these are hem orrhagic and the lung cuts more firmly than
normal. Old infai nre present.
The left auricl trophied and th en of the left ventru shows some sclerc is marked stenosis
perm its n small f slight arleriosc.lt valve.
Microscopic Fii
of the myocarchur are present.
In the liver the lar congestion ant
One section ol b e n io n h ag ic in fa many alveoli coni and macrophage:
Some of the bodies. Localize tasis is presen t septa and some ened by a fibroce histiocytes, .scat blasts, collagen f pigm ent. No lu arc found.
P athologic Di carditis and end' sis; pneumocom i chronic passive hem orrhagic in passive congest! and lower extre:
L
I
T he l u n g find
of a moderately
osis sim ila r to
such cases corm
there are many
i are the same as
in pneumoconio
| bora here, in pi
I pneumoconiosis
A pbotograp
reaction and a
spaces is shown
The fibrosis
sidered to be i
1 faction, especi:
! greatly increas
but th e re is n
pulmonary' o'.fi
)
* ' i V.
- ' % 1
(] macrophages
a considerable The liver is three
margin and on cl nutmeg' appearje and soft with corpuscles. The inal tract contain kidneys are conf the adrenals is 'he bladder and
ire partially obrinous adhesions. ' fluid is present card ial sac conrous fluid, han normal, yele congestion, and juiar bluish dis these are hemmore fmnlv than
NORTH ERN NEW YORK MEDICAL JOURNAL
25
normal, Old infarctions up to 5 cm across are present.
The left auricle is dilated and hyper trophied and there is a similar hypertrophy of the left ventricle. Section of the heart shows some sclerosis of the vessels. There, a mnrked stenosis of the m itral valve which permits a small linger to enter. There is slight arteriosclerosis about the aortic valve,
Microscopic Findings: There is scarring of the myocardium and some Aschoff bodies re present.
In th e liver there is marked central lobu lar congestion and necrosis.
One section of lung consists largely of hemorrhagic infarct. Other sections reveal many alveoli containing fluid, erythrocytes, and macrophages containing hemosiderin, Some of the alveoli contain asbestos bodies. Localized emphysema and atalectasis is present. Many of the interlobular septa and some alveolar walla are thick ened by a fibrocelluar reaction consisting of histiocytes, scattered lymphocytes, fibro blasts, collagen fibers and amorhous brown pigment. No tubercles or silicotic nodules are found.
Pathologic Diagnosis: Rheumatic myo carditis and endocarditis with mitral steno sis; pneumoconiosis (tale) with fibrosis; chronic passive congestion of the lungs; hemorrhagic infarcts of lungs; chronic passive congestion of lungs, liver, viscera and lower extrem ities; ascites.
DISCUSSION
The lung findings in this ease are those of a moderately advanced tale pneumoconi osis sim ilar to the findings in all previous such cases coming to autopsy. In addition there are many heart failure cells. These are the same a a the dust laden macrophages in pneumoconiosis but are in greater num bers h ere in proportion to the amount of pneumoconiosis.
A photograph showing the fibrocellular reaction and asbestosis bodies in the air
spaces is shown. The fibrosis present in this case is con
sidered to be due to pneumoconiosis. In fection, especially tuberculosis, may cause greatly increased fibrosis in pneumoconiosis but th ere is no evidence of this or other pulmonary infection in ibis case,
The heart disease is the principal dis
ease. However in pneumuconiosis with fibrosis (Usability may occur from the fibrous alone with the principal symptom being dyspnea which is caused by the de struction of lung tissue and perivascular fibrosis.
SUMMARY
1. The general aspects of pneumoconiosis Rnd the pathology of talc pneumoconiosis are considered,
2. A case report including autopsy find ings in talc pneumoconiosis is reported,
3. The findings in this case are similar
in genera! nature to those previously re
ported and are. similar to those reported in
asbestosis.
,
REFERENCES
1. Cooke, W. E. Fibrosis of the lungs due to the inhalation of asbestos dust., Brit.
M. J., 1924, 2, 147.
2. Dreesen, W. C., Effects of certain sili cate dusts on the lung., J. Indust. Hyg., 1933, 15, 66-78.
3. Dreesen, W. C. and DalhiValle, J. M., Effects of the exposure to dust in two Georgia talc mills and mines., Pub. Health Rep., 1935, 50, 131-143.
4. Free, J. E. Personal Communication.
6. Gardner, L. U. Personal Communica tion,
6. Gardner, L. U., The pathology and roentgenographic manifestations of pneumoconiosis., J. A. M. A,, Feb, 17,
1940, 114, 535. 7. Gloyne, S, R. in Lanza, et al. Silicosis
and Asbestosis, Oxford University Press, New York, 1938.
8. Lanza, A. J., Editor, Silicosis and As bestosis, Oxford University Press, New
York, 1938. 9. Patton, ,f. R,, Personal Communication.
10. Porro, F. \V,, Patton, J. R., and Hoi bs,
A. A. Jr., Pneumoconiosis in the talc
industry. Am, J, Roentgenol, & Rad.
w,, Therapy, 1942, 47, 507-524.
11. Siegal,
smith, A. R., and Green
' burg, 1., The dust hazard in temoiitw
talc "mining including roengenologieal
findings in tide workers. Am. J. Itoen-
genol, & Rnd. Therapy, 1943, 49, 11-29.