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The nonfibrogenic (benign) pneumoconioses
The Nonfibrogenic
(Benign)
Pneumoconioses
By 0. A. SANDER, M.D.
TERM “benign” was first applied to the nonfibrogenic pneumoconioses by Pendergrass and Leopold’ in 1945, denoting “a retention of in1 ert dust in the lungs which can be visualized by x-ray when the material is radiopaque.” This inert dust deposition does not result in fibrosis, bronchial irritation, allergy, impairment of lung function, or increased susceptibility to tuberculosis or any other infection. If any reaction does occur, the resulting lung changes are no longer referred to as “benign.”
mHI-3
CARBON AND COAL
Everyone living in cities has inhaled varying amounts of inert carbon dust through the years, many to such a degree that their lungs show extensive black pigmentation at autopsy. It happens that this writer interned in Pittsburgh before smoke control went into effect and saw at autopsy many lungs of city residents just as black as those of coal miners. Yet their lungs looked entirely normal on chest roentgenograms except for occasional prominence of the bronchovascular markings. Even though carbon or soot particles in the lungs do not result in small nodular shadows on the roentgenogram as do metal particles, anthracotic pigmentation still represents a pneumoconiosis in the strict definition o’f the term. Actually, then, everyone has some pneumob coniosis because we all have retained particulate matter in lymphatic foci o’r lymph nodes in our lungs, whether or not it can be seen on chest films. It should be mentioned here that the pathological changes in the lungs of some old coal miners seem to differ somewhat from this benign picture. Coal is a rather complex substance containing numerous minerals and hydrocarbons, along with free silica ( SiO,) in crystalline fo3r-m.The latter varies considerably in amount depending on the mine and the type of coal being mined. All anthracite miners and many soft coal miners have had considerable silica dust exposure along ‘with the coal dust, so when they have roentgen changes in their lungs, these are not due to benign anthracotic pigmentation, but often are a combination of silicosis and focal emphysema. Such pathological changes are generally found in the older coal miners who had heavy coal dust exposure for many years. IRON OXIDE ( SIDEROSIS)
Another dust which has been shown to be inert in the lungs is iron oxide or metallic iron, the resulting roentgen nodulation being known as siderosis. This condition was first recognized pathologically in an electric arc welder in 0. A. SANDER, M.D.: Clinical Professor of Occupational and Environmental Medicine, Marquette University ’ School of Medicine; Consulting Staff: Milwaukee County General Hospital, Columbia Hospital and St. Luke’s Hospital, Milwaukee, Wise. 312
NONFIBROGENIC,
BENIGN,
PNEUMOCONIOSES
313
a report published by Enzer and the writer in 1938.2 This welder had had heavy exposure for ten years to concentrated welding fumes while working inside steel tanks. The particulate matter of such fumes is iron oxide in extremely fine dispersion. Grossly, the lungs were black and looked like they were involved with extensive anthracotic pigmentation. When the microscopic sections were stained for iron with potassium ferrocyanide stain, all the pigment gave the characteristic Prussian blue reaction. All the iron particles lay within phagocytes, which were grouped together in the perivascular and peribronchial lymphatics. There was complete absence of fibrous tissue reaction and bronchial irritation. Because iron is opaqe to x-rays, these collections were visualized on the chest roentgenogram as a nodular pattern simulating silicosis. Since this original report, there has been increasing pathological proof of the inertness of iron in the lungs from studies of other occupations which expose the workers to iron dust and fumes. 3-5 One such report by McLaughlin et al.G was that of a silver polisher who had used rouge (iron oxide) as an abrasive. The chest roentgenogram and the microscopic sections in this case resembled in every detail those described by us in our report on the welder. A combined report published by Hamlin et al. and Vorwald et a1.5 confirmed these findings experimentally, utilizing animal inhalation of dust collected from the grinding of steel castings. Petrographic, x-ray diffraction, and chemical analyses of the dust showed it to contain from 3 to 6 per cent quartz and up to 70 per cent iron oxide. After three years of exposure to this dust, the animals showed fine nodular stippling on chest roentgenograms. Postmortem examination of their lungs showed focal collections of iron pigment but no nodules of the silicotic type. Also, in another group of animals exposed to this dust, the course of tuberculous infection did not appear to be affected in any way. I should like to report here several additional cases, some of which I have been able to observe over a period of 20 to 30 years. Case I. P.L., age 80. Grinder in foundries for 14 years before 1933, when we found him to have a fine nodulation in both lungs and advised him to discontinue foundry work because we believed him to have well-developed, second degree silicosis (Fig. 1A). Thereafter he was awarded $3,000 compensation for a 50 per cent permanent disability due to silicosis. From 1934 to 1941 he had numerous out-of-door jobs. He returned to us in 1941 and wanted his old job back. When we saw that no progression of the Erie nodulation had occurred since 1933 (Fig. lB), we realized that in all probability the condition was largely siderosis with a negligible amount of silicosis. We allowed him to return to grinding, and he continued this job on clean castings in an essentially nonsilica area until he retired in 1960 at age 73. Since then we have seen him every 2 or 3 years and have found that, allowing for the differences in roentgen techniques, the nodulation has increased very little in the past 33 years. He now has evidence of hypertension and early left heart insufficiency. It still is my opinion that the nodulation is largely iron oxide retention (Fig. lG), with only an insignificant degree of silicotic nodular fibrosis.
Besides grinding and welding, the cutting or burning of steel or iron with a gas (oxyacetylene) flame may cause the same iron oxide fume exposure. In fact, the cutting or burning fumes may be considerably more concentrated than welding fumes, as illustrated by the next case.
IDER
Fig . I.-(Case 1). In 1933, he had been a grinder in several steel foundries for 14 years. A. 1933. Nodular silicosis was diagnosed from this film. There were no chest sy;wtoms. B. 1942. No change since 1933.
NONFIBROGENIC,
BENIGN,
Fig. 1 (Case I-Cont’d.). nodulation, which is now
PNEUMOCONIOSES
C. 1966. At age 80, very little further believed to be largely iron retention.
315
change in the roentgen
Case 2. M.H., age 34, was a steel cutter or burner for the past 13 years and a chipper and grinder with respirator worn for 3 years before that. Slight iron retention started after 3 years of “burning” without a respirator (Fig. 2A). In spite of regular use of a respirator after that and better smoke control, iron continued to accumulate in the lungs. At no time, however, were there chest symptoms. A roentgenogram in 1966 showed severe iron retention (Fig. 2B ). Lung function studies in November, 1966 showed only slightly reduced lung volume, normal spirometry, diffusing capacity, and resting arterial blood gases. This man was transferred to a new “heat treat” department in July, 1966, where there is no dust or iron smoke exposure. We plan to continue taking chest films yearly, hoping to see a gradual reduction in the evidence of iron retention in these lungs.
As the British observers, Doig and McLaughlin, have shown,? the fine nodulations of welders have disappeared roentgenographically after a period in which no further iron oxide fume inhalation occurred. It appears that most of the iron-laden phagocytes remain mobile and are constantly being eliminated from the lungs by way of the lymphatic circulation. We, too, have now seen several similar cases. Case 3. L.P., age 53. There had been no fume or dust exposure until December, 1933, when ho started work in a steel foundry cleaning room as a gas (oxyacetylene) flame cutter. After about 10 years of rather heavy iron fume exposure on this job, which involved very little silica dust, his chest film in June, 1943, showed a definite fine nodular pattern (Fig. 3A). The hilar shadows showed no change in size or density. This appearance suggested iron retention. In December, 1943, he was promoted to another job which entailed no further dust or iron fume exposure. During the next 20 years, there was a gradual lessening of the fine nodulation, with complete disappearance by March, 1966 (Fig. 3B). He has never had pulmonary symptoms.
316
0. A. UNDER
Fig< , 2.-Siderosis. (Case 2). A. 1953. Normal chest roentgenogram before any exElosure to ironn fumes. B. 1966. Nodulation with no chest symptoms and no impairment of lung functic 3n.
NONFIBROGENIC,
BENIGN,
PNEUMOCONIOSES
Fig. 3.4iderosis. (Case 3). A. Flame burner or cutter of steel for 10 years in founf cleaning room, with clear-cut evidence of slight siderosis. No chest symptoms. B. After further exposure to iron fumes for over 20 years, there has been complete disappeara of the fine nodulation.
no
rice
318
0. A. SANDER
If iron dust retention in the lungs is so truly benign and causes no symptoms, no lung fibrosis and no lung impairment, a natural question follows: Why should there be any discussion at all of such a bland condition in any report on the dust diseases of the lungs? The answer is simply that roentgenographitally iron retention looks so much like silicosis that it is usually mistaken for it. Workers with no more than minimal iron retention are being told that they have silicosis and that it will progress. They are being advised to quit their jobs as welders, burners, or grinders, which they often do quite unnecessarily. The author has in his files, among many other similar ones, the case of a welder who had a bare minimal amount of siderosis, but developed a cough after a cold. He was a two-pack-a-day cigarette smoker. The chest roentgenogram was reported by the radiologist, who did not know of the work history, as “pneumoconiosis.” To the average general physician, a diagnosis of pneumoconiosis still means a progressive fibrotic disease of the lungs which, if not disabling now, soon will be if he does not stop working at his dusty job. The welder, at age 37, did quit his job, stayed at home as a baby-sitter while his wife worked, worried about his lung condition and continued smoking heavily. He developed a rather advanced degree of hyperventilation syndrome and died suddenly a year later of a heart attack. At autopsy, a myocardial infarction was found, which undoubtedly was the cause of death. The lung sections showed only focal retention of iron, with no evidence of fibrosis or emphysema. It is such cases which make it apparent that radiologists should try to state the specific type of pneumoconiosis (which is not always possible), and for doctors generally to understand that the term pneumoconiosis means only that dust is retained in the lungs and does not denote the type of dust or the reaction to it. It no longer can be considered sound to consider all dusts as harmful to the respiratory system. OTHER INERT DUSTS
There are two other metallic dusts which are readily visualized roentgenographically when retained in the lungs in sufficient concentration: tin oxide and barium sulfate. Because of their greater density than iron (atomic weights: Fe 56, Sn 119, Ba 137), they cause more sharply defined and denser nodular shadows than does iron. For this reason, they actually are less easily confused with silicosis. Both are considered entirely inert and do not cause lung fibrosis or other reaction or alteration of lung function (Figs. 4 and 5). There are other dusts which clearly fall in the inert group, aluminum being an outstanding example. In some high silica industries in which quartz rock dust or sand dust is difficult to control adequately, workers have been deliberately exposed to aluminum dust daily to neutralize the silica reaction. Experimentally in laboratory animals, a modifying effect has definitely been demonstrated, although there has been disagreement as to the results in man. Because of marked engineering improvement in silica dust control in most industries, added aluminum dust exposure no longer is being utilized as a preventive measure against silicosis. Be that as it may, aluminum dust is considered inert
NONFIBROGENIC,
BENIGN,
PNEUMOCONIOSES
319
Fig. 4.-Stannosis. Heavy retention of tin oxide dust in a worker exposed for over 15 years to tin oxide powder in a bagging operation. There were no chest symptoms and lung function studies were normal. (Courtesy of Dr. J. B. Stocklen, Cleveland, Ohio.)
in both metallic and hydrous forms because it has resulted in no reaction in the lungs. Another dust which is entirely inert in the lungs is finished cement. As a matter of fact, it does not even result in a benign pneumoconiosis because it is SO rapidly absorbed that it never is visualized on the chest roentgenogram. It is only mentioned in this discussion, because it so often is considered a cause of disabling pneumoconiosis. This author re-surveyed roentgenographically a group of cement workers in 1958.e Clear lungs were seen in some 50 “baggers” of finished cement, a few of them having worked up to 40 years in extremely concentrated cement dust atmospheres. Cement is essentially calcium silicate and calcium oxide, which should present on chest films much as endogenous calcium. Because it is removed from the lungs so rapidly, however, there is no evidence of calcium (or cement) dust on chest films after inhalation. The same is true for gypsum, which is a calcium sulfate compound. There are other inert dusts which have sufficient density to be seen as fine nodulation on chest roentgenograms, but they are relatively few and unimportant. An example is graphite, which has two sources. Mined graphite may contain considerable free silica in crystalline form, but when this is the case, it probably is not the graphite which causes the roentgen shadows, but the reaction to the free silica. The other source of graphite is lampblack from
320
0. A. SANDER
Fig. 5.-Baritosis. Heavy exposure to fine barium dust in a worker exposed for many years to barium sulfate powder in a bagging operation. There were no symptoms referable to the chest. (Courtesy of Dr. E. P. Pendergrass, Philadelphia, Pa.)
petroleum. While its dust may cause anthracotic pigmentation of the lungs, the material is not dense enough to cast shadows on the chest roentgenogram. DISCUSSION The nonfibrogenic (or benign) pneumoconioses are of importance only because they must be differentiated from those which are fibrotic and which may cause impairment of lung function. This differential diagnosis is seldom easy, mainly because the roentgen resemblance to nodular silicosis is so close. The most detailed history-taking is therefore necessary in these cases, along with knowledge of the biological characteristics of the dust to which the worker has been exposed. In addition, the concentration and duration of the dust exposure must also be considered, as well as whether or not respiratory protection was provided. A particularly difficult diagnostic problem to resolve occurs when both inert and fibrogenic dust exposures have been mixed. The appearance of the hilar shadows is helpful in the differential diagnosis between siderosis and nodular silicosis. When the hilar shadows are normal both in size and density, siderosis is favored and, conversely, large, dense hila are evidence for silicosis, or for a combination of siderosis and silicosis. Detailed lung function studies are important, including blood gas studies and diffusing capacity, in recognizing
NONFIBROGENIC,
BENIGN,
321
PNEUMOCONIOSES
a silicosis component, since they are normal in siderosis and may be abnormal in nodular silicosis or combination pneumoconiosis. Differential diagnosis between silicosis and the inert dusts is especially important when there is associated pulmonary tuberculosis. Where there is no silicosis (i.e., when the nodular roentgen shadows are due only to iron retention), then the associated tuberculosis is an incidental disease and cannot be considered occupational under workmen’s compensation laws. Iron retention or siderosis clearly is not a predisposing factor for tuberculosis whereas silicosis is widely considered causally related. Microscopic study of resected lung often is necessary to resolve this problem. This opportunity is afforded when a tuberculous cavity must be resected surgically. Occasio8nally, however, a lung biopsy is necessary solely to determine if there is silieosis rather than inert pneumoconiosis. ACKNOWLEDGMENTS The author wishes to thank Dr. Ross Kory and Dr. Edith Hapke of the V.A. Hospital, Wood, Wisconsin, for their assistance in the preparation of the illustrations in this chapter.
REFERENCES 1. Pendergrass, E. P., and Leopold, S. S.: Benign pneumoconiosis. J.A.M.A. 127: 701703, 1945. 2. Enzer, N., and Sander, 0. A.: Chronic lung chauges in electric arc welders. J. Indust. Hyg. & Toxicol. 20: 333-350, 1938. 3. Fawcitt, R.: Radiological evidence in haematite iron-ore workers. Brit. J. Radiol. 16: 323-330, 1943. 4. Sander, 0. A.: Benign pneumoconiosis due to metal fumes and dust. Amer. J. Roentgen. 58: 277-282, 1947. 5. Hamlin, L. E., and Weber, H. J.: Siderosis. A benign pneumoconiosis due to the inhalation of iron dust; and Vorwald, A. J., Pratt, P. C., Durkan, T. M., Delahant,
A. B., and Bailey, D. A.: An experimental study of the pulmonary reaction following inhalation of dust generated by foundry cleaning room operations. Indust. Med. & Surg. 19: 151-180, 1950. 6. McLaughlin, A. I. G., Grout, J. L. A., Earrie, H. J., and Harding, H. E.: Iron oxide and the lungs of silver polishers. Lancet 1: 337-341, 1945. 7. Doig, A. T., and hlcLaughlin, A. I. G.: Clearing of x-ray shadows in welders’ siderosis. Lancet 1: 789-791, 1948. 8. Sander, 0. A.: Rcentgen resurvey of cement workers. A.hl.A. Archives of Indust. Health 17: 96-103, 1958.
(Benign)
Pneumoconioses
By 0. A. SANDER, M.D.
TERM “benign” was first applied to the nonfibrogenic pneumoconioses by Pendergrass and Leopold’ in 1945, denoting “a retention of in1 ert dust in the lungs which can be visualized by x-ray when the material is radiopaque.” This inert dust deposition does not result in fibrosis, bronchial irritation, allergy, impairment of lung function, or increased susceptibility to tuberculosis or any other infection. If any reaction does occur, the resulting lung changes are no longer referred to as “benign.”
mHI-3
CARBON AND COAL
Everyone living in cities has inhaled varying amounts of inert carbon dust through the years, many to such a degree that their lungs show extensive black pigmentation at autopsy. It happens that this writer interned in Pittsburgh before smoke control went into effect and saw at autopsy many lungs of city residents just as black as those of coal miners. Yet their lungs looked entirely normal on chest roentgenograms except for occasional prominence of the bronchovascular markings. Even though carbon or soot particles in the lungs do not result in small nodular shadows on the roentgenogram as do metal particles, anthracotic pigmentation still represents a pneumoconiosis in the strict definition o’f the term. Actually, then, everyone has some pneumob coniosis because we all have retained particulate matter in lymphatic foci o’r lymph nodes in our lungs, whether or not it can be seen on chest films. It should be mentioned here that the pathological changes in the lungs of some old coal miners seem to differ somewhat from this benign picture. Coal is a rather complex substance containing numerous minerals and hydrocarbons, along with free silica ( SiO,) in crystalline fo3r-m.The latter varies considerably in amount depending on the mine and the type of coal being mined. All anthracite miners and many soft coal miners have had considerable silica dust exposure along ‘with the coal dust, so when they have roentgen changes in their lungs, these are not due to benign anthracotic pigmentation, but often are a combination of silicosis and focal emphysema. Such pathological changes are generally found in the older coal miners who had heavy coal dust exposure for many years. IRON OXIDE ( SIDEROSIS)
Another dust which has been shown to be inert in the lungs is iron oxide or metallic iron, the resulting roentgen nodulation being known as siderosis. This condition was first recognized pathologically in an electric arc welder in 0. A. SANDER, M.D.: Clinical Professor of Occupational and Environmental Medicine, Marquette University ’ School of Medicine; Consulting Staff: Milwaukee County General Hospital, Columbia Hospital and St. Luke’s Hospital, Milwaukee, Wise. 312
NONFIBROGENIC,
BENIGN,
PNEUMOCONIOSES
313
a report published by Enzer and the writer in 1938.2 This welder had had heavy exposure for ten years to concentrated welding fumes while working inside steel tanks. The particulate matter of such fumes is iron oxide in extremely fine dispersion. Grossly, the lungs were black and looked like they were involved with extensive anthracotic pigmentation. When the microscopic sections were stained for iron with potassium ferrocyanide stain, all the pigment gave the characteristic Prussian blue reaction. All the iron particles lay within phagocytes, which were grouped together in the perivascular and peribronchial lymphatics. There was complete absence of fibrous tissue reaction and bronchial irritation. Because iron is opaqe to x-rays, these collections were visualized on the chest roentgenogram as a nodular pattern simulating silicosis. Since this original report, there has been increasing pathological proof of the inertness of iron in the lungs from studies of other occupations which expose the workers to iron dust and fumes. 3-5 One such report by McLaughlin et al.G was that of a silver polisher who had used rouge (iron oxide) as an abrasive. The chest roentgenogram and the microscopic sections in this case resembled in every detail those described by us in our report on the welder. A combined report published by Hamlin et al. and Vorwald et a1.5 confirmed these findings experimentally, utilizing animal inhalation of dust collected from the grinding of steel castings. Petrographic, x-ray diffraction, and chemical analyses of the dust showed it to contain from 3 to 6 per cent quartz and up to 70 per cent iron oxide. After three years of exposure to this dust, the animals showed fine nodular stippling on chest roentgenograms. Postmortem examination of their lungs showed focal collections of iron pigment but no nodules of the silicotic type. Also, in another group of animals exposed to this dust, the course of tuberculous infection did not appear to be affected in any way. I should like to report here several additional cases, some of which I have been able to observe over a period of 20 to 30 years. Case I. P.L., age 80. Grinder in foundries for 14 years before 1933, when we found him to have a fine nodulation in both lungs and advised him to discontinue foundry work because we believed him to have well-developed, second degree silicosis (Fig. 1A). Thereafter he was awarded $3,000 compensation for a 50 per cent permanent disability due to silicosis. From 1934 to 1941 he had numerous out-of-door jobs. He returned to us in 1941 and wanted his old job back. When we saw that no progression of the Erie nodulation had occurred since 1933 (Fig. lB), we realized that in all probability the condition was largely siderosis with a negligible amount of silicosis. We allowed him to return to grinding, and he continued this job on clean castings in an essentially nonsilica area until he retired in 1960 at age 73. Since then we have seen him every 2 or 3 years and have found that, allowing for the differences in roentgen techniques, the nodulation has increased very little in the past 33 years. He now has evidence of hypertension and early left heart insufficiency. It still is my opinion that the nodulation is largely iron oxide retention (Fig. lG), with only an insignificant degree of silicotic nodular fibrosis.
Besides grinding and welding, the cutting or burning of steel or iron with a gas (oxyacetylene) flame may cause the same iron oxide fume exposure. In fact, the cutting or burning fumes may be considerably more concentrated than welding fumes, as illustrated by the next case.
IDER
Fig . I.-(Case 1). In 1933, he had been a grinder in several steel foundries for 14 years. A. 1933. Nodular silicosis was diagnosed from this film. There were no chest sy;wtoms. B. 1942. No change since 1933.
NONFIBROGENIC,
BENIGN,
Fig. 1 (Case I-Cont’d.). nodulation, which is now
PNEUMOCONIOSES
C. 1966. At age 80, very little further believed to be largely iron retention.
315
change in the roentgen
Case 2. M.H., age 34, was a steel cutter or burner for the past 13 years and a chipper and grinder with respirator worn for 3 years before that. Slight iron retention started after 3 years of “burning” without a respirator (Fig. 2A). In spite of regular use of a respirator after that and better smoke control, iron continued to accumulate in the lungs. At no time, however, were there chest symptoms. A roentgenogram in 1966 showed severe iron retention (Fig. 2B ). Lung function studies in November, 1966 showed only slightly reduced lung volume, normal spirometry, diffusing capacity, and resting arterial blood gases. This man was transferred to a new “heat treat” department in July, 1966, where there is no dust or iron smoke exposure. We plan to continue taking chest films yearly, hoping to see a gradual reduction in the evidence of iron retention in these lungs.
As the British observers, Doig and McLaughlin, have shown,? the fine nodulations of welders have disappeared roentgenographically after a period in which no further iron oxide fume inhalation occurred. It appears that most of the iron-laden phagocytes remain mobile and are constantly being eliminated from the lungs by way of the lymphatic circulation. We, too, have now seen several similar cases. Case 3. L.P., age 53. There had been no fume or dust exposure until December, 1933, when ho started work in a steel foundry cleaning room as a gas (oxyacetylene) flame cutter. After about 10 years of rather heavy iron fume exposure on this job, which involved very little silica dust, his chest film in June, 1943, showed a definite fine nodular pattern (Fig. 3A). The hilar shadows showed no change in size or density. This appearance suggested iron retention. In December, 1943, he was promoted to another job which entailed no further dust or iron fume exposure. During the next 20 years, there was a gradual lessening of the fine nodulation, with complete disappearance by March, 1966 (Fig. 3B). He has never had pulmonary symptoms.
316
0. A. UNDER
Fig< , 2.-Siderosis. (Case 2). A. 1953. Normal chest roentgenogram before any exElosure to ironn fumes. B. 1966. Nodulation with no chest symptoms and no impairment of lung functic 3n.
NONFIBROGENIC,
BENIGN,
PNEUMOCONIOSES
Fig. 3.4iderosis. (Case 3). A. Flame burner or cutter of steel for 10 years in founf cleaning room, with clear-cut evidence of slight siderosis. No chest symptoms. B. After further exposure to iron fumes for over 20 years, there has been complete disappeara of the fine nodulation.
no
rice
318
0. A. SANDER
If iron dust retention in the lungs is so truly benign and causes no symptoms, no lung fibrosis and no lung impairment, a natural question follows: Why should there be any discussion at all of such a bland condition in any report on the dust diseases of the lungs? The answer is simply that roentgenographitally iron retention looks so much like silicosis that it is usually mistaken for it. Workers with no more than minimal iron retention are being told that they have silicosis and that it will progress. They are being advised to quit their jobs as welders, burners, or grinders, which they often do quite unnecessarily. The author has in his files, among many other similar ones, the case of a welder who had a bare minimal amount of siderosis, but developed a cough after a cold. He was a two-pack-a-day cigarette smoker. The chest roentgenogram was reported by the radiologist, who did not know of the work history, as “pneumoconiosis.” To the average general physician, a diagnosis of pneumoconiosis still means a progressive fibrotic disease of the lungs which, if not disabling now, soon will be if he does not stop working at his dusty job. The welder, at age 37, did quit his job, stayed at home as a baby-sitter while his wife worked, worried about his lung condition and continued smoking heavily. He developed a rather advanced degree of hyperventilation syndrome and died suddenly a year later of a heart attack. At autopsy, a myocardial infarction was found, which undoubtedly was the cause of death. The lung sections showed only focal retention of iron, with no evidence of fibrosis or emphysema. It is such cases which make it apparent that radiologists should try to state the specific type of pneumoconiosis (which is not always possible), and for doctors generally to understand that the term pneumoconiosis means only that dust is retained in the lungs and does not denote the type of dust or the reaction to it. It no longer can be considered sound to consider all dusts as harmful to the respiratory system. OTHER INERT DUSTS
There are two other metallic dusts which are readily visualized roentgenographically when retained in the lungs in sufficient concentration: tin oxide and barium sulfate. Because of their greater density than iron (atomic weights: Fe 56, Sn 119, Ba 137), they cause more sharply defined and denser nodular shadows than does iron. For this reason, they actually are less easily confused with silicosis. Both are considered entirely inert and do not cause lung fibrosis or other reaction or alteration of lung function (Figs. 4 and 5). There are other dusts which clearly fall in the inert group, aluminum being an outstanding example. In some high silica industries in which quartz rock dust or sand dust is difficult to control adequately, workers have been deliberately exposed to aluminum dust daily to neutralize the silica reaction. Experimentally in laboratory animals, a modifying effect has definitely been demonstrated, although there has been disagreement as to the results in man. Because of marked engineering improvement in silica dust control in most industries, added aluminum dust exposure no longer is being utilized as a preventive measure against silicosis. Be that as it may, aluminum dust is considered inert
NONFIBROGENIC,
BENIGN,
PNEUMOCONIOSES
319
Fig. 4.-Stannosis. Heavy retention of tin oxide dust in a worker exposed for over 15 years to tin oxide powder in a bagging operation. There were no chest symptoms and lung function studies were normal. (Courtesy of Dr. J. B. Stocklen, Cleveland, Ohio.)
in both metallic and hydrous forms because it has resulted in no reaction in the lungs. Another dust which is entirely inert in the lungs is finished cement. As a matter of fact, it does not even result in a benign pneumoconiosis because it is SO rapidly absorbed that it never is visualized on the chest roentgenogram. It is only mentioned in this discussion, because it so often is considered a cause of disabling pneumoconiosis. This author re-surveyed roentgenographically a group of cement workers in 1958.e Clear lungs were seen in some 50 “baggers” of finished cement, a few of them having worked up to 40 years in extremely concentrated cement dust atmospheres. Cement is essentially calcium silicate and calcium oxide, which should present on chest films much as endogenous calcium. Because it is removed from the lungs so rapidly, however, there is no evidence of calcium (or cement) dust on chest films after inhalation. The same is true for gypsum, which is a calcium sulfate compound. There are other inert dusts which have sufficient density to be seen as fine nodulation on chest roentgenograms, but they are relatively few and unimportant. An example is graphite, which has two sources. Mined graphite may contain considerable free silica in crystalline form, but when this is the case, it probably is not the graphite which causes the roentgen shadows, but the reaction to the free silica. The other source of graphite is lampblack from
320
0. A. SANDER
Fig. 5.-Baritosis. Heavy exposure to fine barium dust in a worker exposed for many years to barium sulfate powder in a bagging operation. There were no symptoms referable to the chest. (Courtesy of Dr. E. P. Pendergrass, Philadelphia, Pa.)
petroleum. While its dust may cause anthracotic pigmentation of the lungs, the material is not dense enough to cast shadows on the chest roentgenogram. DISCUSSION The nonfibrogenic (or benign) pneumoconioses are of importance only because they must be differentiated from those which are fibrotic and which may cause impairment of lung function. This differential diagnosis is seldom easy, mainly because the roentgen resemblance to nodular silicosis is so close. The most detailed history-taking is therefore necessary in these cases, along with knowledge of the biological characteristics of the dust to which the worker has been exposed. In addition, the concentration and duration of the dust exposure must also be considered, as well as whether or not respiratory protection was provided. A particularly difficult diagnostic problem to resolve occurs when both inert and fibrogenic dust exposures have been mixed. The appearance of the hilar shadows is helpful in the differential diagnosis between siderosis and nodular silicosis. When the hilar shadows are normal both in size and density, siderosis is favored and, conversely, large, dense hila are evidence for silicosis, or for a combination of siderosis and silicosis. Detailed lung function studies are important, including blood gas studies and diffusing capacity, in recognizing
NONFIBROGENIC,
BENIGN,
321
PNEUMOCONIOSES
a silicosis component, since they are normal in siderosis and may be abnormal in nodular silicosis or combination pneumoconiosis. Differential diagnosis between silicosis and the inert dusts is especially important when there is associated pulmonary tuberculosis. Where there is no silicosis (i.e., when the nodular roentgen shadows are due only to iron retention), then the associated tuberculosis is an incidental disease and cannot be considered occupational under workmen’s compensation laws. Iron retention or siderosis clearly is not a predisposing factor for tuberculosis whereas silicosis is widely considered causally related. Microscopic study of resected lung often is necessary to resolve this problem. This opportunity is afforded when a tuberculous cavity must be resected surgically. Occasio8nally, however, a lung biopsy is necessary solely to determine if there is silieosis rather than inert pneumoconiosis. ACKNOWLEDGMENTS The author wishes to thank Dr. Ross Kory and Dr. Edith Hapke of the V.A. Hospital, Wood, Wisconsin, for their assistance in the preparation of the illustrations in this chapter.
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