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FILE NAME: BF Goodrich (BFG) DATE: 1952 Apr DOC#: BFG046 DOCUMENT DESCRIPTION: Journal Article - Talc Pneumoconiosis
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1418 TALC PNEUMOCONIOSIS--FRIEDMAN ET AL.
TALC PNEUMOCONIOSIS Paul S. Friedman, M.D.
PLAINTIFF'S EXHIBIT
Milton A . Bell, M.D.
and
______
Leon Solis-Cohen, M.D., Philadelphia
There is increasing evidence that occupational inhala tion of pulmonary irritants is one of the major causes of pulmonary fibrosis. Free silica is a common etiologic agent. Talc, a hydrous magnesium silicate, is an unusual cause for such pneumoconiosis. The following case demonstrates the roentgen and clinical characteristics of talc pneumoconiosis.
REPORT OF A CASE
The patient, a 65-year-old white man, was referred' for roent gen study of the chest on June 19, 1950, because of a chronic cough which was intensified during the preceding week. He had a cough of many years' duration accompanied by production of frothy sputum. On June 9, 1950, sneezing, coryza, intensified cough, and purulent postnasal discharge and expectoration de veloped. There was accompanying onset of exertional dyspnea. Walking three blocks caused dyspnea.
For a period of 24 years since 1926, he had been employed in the handling and packaging of elastic cord (rubber thread) coated with talc powder. In the handling of this_rubber, he re moved rubber ribbons, heavily coated with talc, from their con taining box. He fed one end of the rubber into a reed that sep arated the strands; the rubber strands then passed onto a spindle which made skeins or cones of rubber lhread. From the moment the containing box was opened, the atmosphere of the working
J.A.M.A., April 19, 1
as well as areas of bronchial breathing were present through both lungs. No clubbing of the fingers was present. The pati was treated with bed rest. He received penicillin orally, in; muscularly, and by nose drops.
On June 13, he was clinically improved and returned to wc Temperature and pulse rate were normal. Cough was less pro nent, but dyspnea was still marked on walking four blocks uphill. There was minimal night cough when he was recumbt
Fi(. 1.--Chesi, poslcroanlerior projection. This demonstrates diffuse pulmonary fibrosis, pulmonary emphysema, pleural thickening, and talc plaque in right upper hemithorax.
area was cloudy with talc powder. No exhaust or ventilating fans Were present. In 1914 a right th o ra c o to m y f o r e m p y e m a was performed.
Physical examination on June 9 revealed a thin, white man with a temperature of 99.4 F, a pulse rate of 112, and blood pressure of 110/74. There was mucopurulent nasal secretion. There was a thoracotomy scar over the right lower posterior hemithorax. Chest expansion was restricted. Coarse moist rales
Fig. 2.--Chest, lateral projection. Note increased anteroposterior ameier accompanying the pulmonary emphysema, foci of pulmon calcificaiion.
There were momentary episodes of respiratory obstructs
Coarse moist rales were still heard over the lower lobe of .
right lung. Fluoroscopic and radiographic study of Ihe chest
June 19 revealed marked reduction in thoracic respiratory n
bility. There was reduced diaphragmatic excursion dun
respiration.
Lungs.--There was evidence of diffuse pulmonary empi
sema, characterized by low position of the diaphragm and
creased anteroposterior thoracic diameter. There was difL
linear intensification of the pulmonic markings owing to puln
nary fibrosis. This was most prominent in the right lung. Sta
foci of calcification due to previous tuberculous infection w<
visualized in the upper lobe and hilar region of the left lung (
1 and 2).
'
Pleura.--There was thickened pleura present, most promin
on the right, where it produced stragihtening of the right hei
diaphragm. A linear homogeneous opacity, 9 cm. in length 9 1 cm. in width, was demonstrated in the upper right hemithor.
Its axis was obliquely vertical, and it apparently representei
talc pleural plaque.
Heart and Mediastinal Structures.--There was no abnorr mobility during respiration. The heart was not measura'
enlarged. There was increased convexity of the left cardiac bor<
owing to prominence of the right ventricle. Elongation of ;
aorta due to arteriosclerosis was present. The sputum was ne five for tubercle bacilli.
A mixed catarrhal vaccine series was administered in an
tempt to improve immunity to respiratory pathogens. Penici
has been used periodically for acute episodes of tracheobr chitis with purulent secretions. The patient has been relativ comfortable though not entirely free of cough.
V<* 148, No. 16
\n electrocardiogram on Feb. 13, 1951, revealed low ampliiuje of the QRS component in the limb leads. It was otherwise
oaiural-
COMMENT
Talc pneumoconiosis has been described in talc miners
jnd millers. Since talc is used industrially as a filler, as a justing powder, and as an absorbent, the possibility of cXcessive exposure is not a limited one. Bethene. in 1935, xperimentally demonstrated its irritant characteristics
when pleural adhesions were caused in cats and dogs by
the intrapleural insufflation of talc powder. Since the free silica content of talc is 0.5% or less, its irritant char acteristics are apparently not a result of its free silica content.
Clinically, talc pneumoconiosis usually caused dysp
nea, chronic cough, chest pain, and fatigue. The dyspnea
is usually more intense than the roentgen manifestations
of fibrosis would suggest. Limited chest expansion is
invariably present. The patients are usually thin, mini
mally cachectic in appearance, and in 70% of cases exhibit curving nails or clubbed fingers. The patient de
scribed herein exhibited all of these changes except
dubbing of the fingers.
The roentgen changes resulting from talc pneumo coniosis are characterized by fibrosis, emphysema,
pleural thickening, pleural and subpleural plaques ( "talc plaques"), and a minimally increased incidence of tuber culous infection. The fibrosis is of a fine linear and granu
lar character, similar in type to that visualized in asbestosis. It tends to be most intense in the midportions of the lungs, extending into the basilar segments of the
lower lobes. A moderate degree of diffuse pulmonary
emphysema is present. Partially owing to the emphysema
and partially owing to the pulmonary fibrosis, there is
a prominence of hilar and intrapulmonic segments of the pulmonary arteries.
The pleura exhibits diffuse thickening and fibrosis. In addition, linear areas of pleural density, so-called talc plaques, occur. These were seen in 6.3% of all talc miners.1They occur in the peripheral and subpleural as pects of the visceral pleura. These may vary from single, linear, homogeneous, sharply marginated opacities, sev eral centimeters in length, to irregularly shaped, exten sive opacities of varying density. It is felt these occur secondary to accumulation of talc in peripheral lym phatics with lymphatic dilatation and stasis, associated with calcium localization.
There has been suggestive statistical evidence of in creased susceptibility to significant tuberculous infec tion.
SUMMARY
A case of talc pneumoconiosis is reported with typical clinical and roentgen characteristics. This report seemed indicated in order to direct attention to talc as an occu pational hazard and to the probable significance of other inhaled pulmonary irritants as causative agents in un explained pulmonary fibrosis.
1422 Chestnut St. (Dr. Friedman).
1. Greenburg, L.: The Dust Hazard in Tremolile Talc Mining. Yale J. Biol. & Med. 1 9 : 4$' . m .March) 1947.
BRONCHOGRAPHY--THEODOS 141
BRONCHOGRAPHY H i IODINE SENSITIVITY
Peter A. Theodos, M.D., Philadelphia
The instillation of iodized oil into the bronchial tree is widely used in the diagnosis of bronchiectasis, the de lineation of distorted or obstructed bronchi, and the de termination of communications between bronchi and the pleura, skin, or air cysts. All the radiopaque preparations commonly used in bronchography today contain iodine. Those most frequently used are lipiodol,* which contains 40% iodine in poppyseed oil, and iodochloral,' which contains 27% iodine and 7.5% chlorine in organic com bination with highly refined peanut oil. Bronchography with these agents is usually innocuous, but untoward re actions, such as iododerma and asthma-like reactions with fatal outcome in two cases, have been reported.1 It is imperative, therefore, that proper inquiry be made as to sensitivity to iodine prior to the use of any iodine-con taining contrast medium.
A patient with suspected bronchiectasis was recently admitted to the hospital for study. The presence of pro nounced iodine sensitivity made the use of iodized oil as a contrast medium for bronchography inadvisable and even hazardous. However, since the use of corticotropin (ACTH) had been reported in the treatment of sensitivity to iodine,* it was decided to carry out the iodized oil study after preliminary desensitization with corticotropin.. A satisfactory bronchogram with minimal reactions was obtained. Because of this favorable outcome, the follow ing report is considered of interest:
REPORT OF CASE
I. O., a 46-year-old white woman, was first seen in October, 1950, because of severe paroxysmal cough, copious foul ex pectoration, and pain in the left lower part of the chest posterior ly. A diagnosis of suspected bronchiectasis had previously-been made, in 1944, after an iodized oil study. At that time severe swelling of the submaxillary glands developed, along with "blotches all over the body resembling strawberry hives," which lasted 10 days after the bronchogram. Subsequent bronchograms, in 1945 and 1947, again produced reactions manifested by swell ing of the submaxillary glands, fever, and hives. Although these studies revealed equivocal evidence of bronchiectasis in the lowet lobe of the left lung, a segmented resection was done in 1947. Symptoms were then few, until November, 1948, when cough recurred. This had become progressively severer and was pro ductive of several cups of foul sputum daily at the time of the patient's admission to the hospital.
Physical examination disclosed nothing essentially abnormal except in the lungs, where there was impairment of percussion and distant breath sounds over the lower lobe of the left lung. No rales were heard.
Fluoroscopic and roentgenographic examinations revealed portions of the posterior segments of the 9th and 10th ribs to be missing. The left side of the diaphragm was slightly elevated
From the Barton Memorial Division and the Department of Medicine, Jefferson Medical College Hospital.
1. Belote. G. H,: Iododerma from Iodized Oil. J. A. M. A. 8 9 :8 8 2 . 1927. O'Donovon. W. J.; Intratracheal Injection of Lipiodol: Generalized Iodide ErupUon: Death. Brit. M. J. 2 : 35, 1927. Carmichael. D. A.: Iodine Poisoning and lodism from Lipiodol. Canad. M. A. J. 9 8 :3 1 9 , 1932. Scadding. J. G.: Acute lodism FoUowing Lipiodol Bronchography. Brit. M. J, 9 : 1147. 1934. Goldstein. D. W.: Fatal Iododerma FoUowing Injection of Iodized Oil for Pulmonary Diagnosis. J. A. M. A. 1 0 8 : I6S9, 193.
2. Ruh, A. R.: Hypersensitivity in Disease, with Special Reference to PeriarteriUs Nodosa. Rheumatic Fever. Disseminated Lupus Erythematosus and Rheumatoid Arthritis, Harvey Lect. 4 9 : 106. 1446-1947.