THE PULMONARY RESPONSE TO COAL DUST

THE PULMONARY RESPONSE TO COAL DUST

Paul Gross, Daniel C. Braun, and Robert T. P. deTreville

Department of Pathology, Medical University of South Carolina Charleston, South Carolina 29401

and The Industriol Health Foundation Pittsburgh, Pennsylvania 15232

The term “coal dust” is often used to categorize the dust to which coal miners are exposed. This characterization is, of course, incorrect. The correct designation is coal mine dust. The latter includes dusts from pulverized rocks associated with the coal and from traction sand. Some of these dusts may be fibrogenic, such as those containing crystalline silica or certain silicates or both. It can therefore be anticipated that the tissue reaction to coal mine dust will vary according to its composition. The character and the amount of the coal mine dust inhaled may not, however, be the only determinants of the nature and severity of the tissue reaction evoked by its presence. The status of the host tissues may profoundly alter their response to coal mine dust deposits in the lungs. Because of these variables, the tissue response to coal mine dust may logically be categorized according to the immunological status of the host tissues and also according to the presence of significant amounts of fibrogenic dusts.

RESPONSE OF NORMAL PULMONARY AND LYMPH NODAL TISSUES

Response to Coal Dust Alone

The tissue reaction to pulverized coal has been studied in animals that inhaled the dust or were injected intratracheally with it. The dusts of both bituminous coal and lignite were readily phagocytosed by macrophages that then “silted” up alveoli, beginning with those in the respiratory bronchioles and extending to the more peripherally situated air spaces as the dust inhala- tions continued. The effects of lignite dust have been studied on rats, mice, guinea pigs, and monkeys; whereas the effects of bituminous coal dust have been studied on rats, guinea pigs, rabbits, ponies, and hamsters.?, The results have been similar in all animal species: there was no significant difference between the reaction to lignite dust and that caused by bituminous coal.

Many air spaces packed with dust-filled macrophages, not only alveoli and alveolar sacs, but also alveolar ducts, become atelectatic; that is, the alveolar walls become tightly apposed to the dust masses, and the septal cells appear more prominent and more numerous. These findings suggest that alveolar cells have been damaged, causing diminution or cessation of surfactant secretion, which, in turn, causes atelectasis. The tight envelopment of the dust masses by the septal walls effectively sequesters the dust (FIGURE 1).

Because of the density and opacity of coal dust, it is usually not feasible to study the stromal reaction to the dust. Where the dust-filled macrophages are loosely arranged, however, it is often possible to demonstrate a few argentophilic (reticulin) fibers coursing between and around some of the dust cells

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156 Annals New York Academy of Sciences

FIGURE 1. Portion of a coal dust macule in the lung of a normal guinea pig injected intratracheally with bituminous coal dust and killed two months later. The m a d e is composed of dense dust masses of various sizes and shapes. The absence of demon- strable air space between the dust masses and the alveolar walls is indicative of close apposition of these walls to the agglomerated dust and suggests atelectasis. The apparent increase in the number of cells is in agreement with this concept. Hema- toxylin and eosin. x 100.

(FIGURE 2) . Such fibers may also be observed in human lungs in which edema fluid has caused the separation of cells and tissue elements of dust depots (FIGURE 3 ) .

A so-called biologically inert dust, better termed a nonfibrogenic dust, has been defined as one which evokes a tissue reaction having three attributes: (1) It leaves the alveolar architecture intact. (2) The stromal reaction is scanty and consists of reticulin fibers that do not collagenize. (3) The reaction is potentially reversible. The dusts of lignite and bituminous coal evoke reactions that have all of these attributes and are therefore properly classified as nonfibrogenic.1 The satellite lymph nodes of lungs containing coal dust alone are blackened by foci composed of packed dust-filled macrophages but without collagenous stromal reaction.

Response to Coal Mine Dust

The pulmonary reaction to coal mine dust that contains significant amounts of fibrogenic mineral particles may differ from that caused by coal dust alone by the presence of a greater amount of stroma, the amount of stroma being roughly in proportion to the amount and fibrogenicity of the mineral dust present. With increasing amounts of crystalline silica mixed with the inhaled

Gross et al.: Pulmonary Response to Coal Dust 157

coal dust, it is not uncommon to find thickened septa1 walls and collagenous fibers in the coal dust deposits. It has been stated that when the percentage of crystalline silica in coal mine dust exceeds 18%, the tissue reaction evoked by it is recognizable as si l ic~sis.~ In contrast to the rounded, concentrically arranged nodules seen after the inhalation of relatively pure quartz dust, however, those found in the lungs of silicotic coal miners are stellate and lack the concentric arrangement of collagen fibers.$ More commonly, relatively little free silica and, hence, little collagen are associated with the dust deposits in coal miners’ lungs. The localization about a respiratory bronchiole of alveoli “silted” with coal mine dust forms a grossly visible black macule that, as it increases in size by “silting” the more peripherally situated air spaces, may fuse with adjacent macules, thus diminishing the amount of functioning lung tissue. The respiratory bronchiole, the alveoli of which are occluded by dust, often undergoes considerable enlargement so as to become grossly visible as a hole surrounded by dense black material. This enlargement, which is not associated with alveolar destruction, is known as focal emphysema.* These coal dust macules, generally evenly distributed throughout the lungs, constitute the “simple” pneumoconiosis of coal workers, and they are responsible for the appearance of poorly circumscribed small opacities (from a few millimeters to less than 1 cm in diameter) seen in the chest x-ray of about 10% of working coal miners.’

It is interesting to note that although the lungs of some coal miners may show no evidence of silicosis, the satellite lymph nodes may be involved by

FIGURE 2. This field is the same as in FIGURE I but after silver impregnation. Com- parison of the dust masses suggests that they contained some material-probably of endogenous origin-that dissolved out during the silver impregnation. The reticulin fibers are delicate but show a slightly increased nrborescence. Gordon and Sweets. x 100.


FIGURE 3. This is a silver impregnation of a coal dust deposit in a coal miner’s lung. It presents an unusual appearance insofar as the deposit is in the process of being broken up by edema fluid-the dust is being mobilized. The septa1 walls are thickened by a plexiform meshwork of coarse fibers that has extended into the air- space and apparently has served to “anchor” some of the dust-filled cells. One such cell (above and to the right of center) is still attached by a short fiber to the meshwork, whereas another cell above and slightly to the right of the attached cell is detached, but still has a short reticulin fiber projecting radially from its periphery. Note that with this technique, cells are not visualized except insofar as they contain opaque dust particles. Also of interest are scattered extracellular dust particles, apparently suspended in the edema fluid. Gordon and Sweets. x 350.

diffuse, dense collagenous fibrosis and may contain discrete silicotic nodules. This finding is probably related to the facility with which inhaled silica dust is transported to satellite lymph nodes.G+

RESPONSE OF IMMUNOLOGICALLY ALTERED HOST TISSUES

The response to coal mine dust of pulmonary and lymph nodal tissues that have been altered by certain systemic diseases such as tuberculosis, rheumatoid arthritis, and perhaps other as yet unrecognized entities, results in much more serious disease than that of simple pneumoconiosis. This pulmonary involve- ment, formerly called “infective” pneumoconiosis, now known as “compli- cated” pneumoconiosis and also as progressive massive fibrosis of the lungs or PMF affects about 30% of those working miners who have pneumoconiosis, or 3% of all working miners.*

As the term PMF indicates, the deposition of dust is associated with exten- sive collagenous fibrosis, resulting in the permanent obliteration of air spaces


and the development of opacities in the chest x-ray, which measure 1 cm or larger in diameter. The parenchymatous fibrosis may become so severe as to leave insufficient functioning lung tissue to sustain life. Secondary severe sclerosis of pulmonary vessels may develop, associated with hypertrophy and dilatation of the right heart (COT pulrnonale) .

The extent to which the tissue response to coal dust may be modified by an associated immunological challenge can be seen from the results of a recent experiment.\ Guinea pigs vaccinated with BCG were injected intratracheally with coal dust with and without PPD tuberculin. Another group was injected intratracheally with tuberculin alone. One half of the animals given coal dust plus tuberculin were also given subcutaneous injections of a steroid (prednisolone). The others were not so treated.

The lungs of animals injected with coal dust alone showed coal macules with minimal stromal and cellular proliferations (FIGURES 1 and 2) . The effect of tuberculin alone in sensitized guinea pigs, two months after the challenge, was the persistence of foci of chronic pneumonitis characterized by cellular septa1 thickening and mild stromal proliferations (FIGURES 4 and 5 ) .

Animals injected intratracheally with coal dust plus PPD tuberculin showed diffuse proliferation of cells and reticulin fibers when killed two months after the intratracheal injection (FIGURE 6 ) . Surprisingly, treatment with steroid resulted in maximal fibrosis, obliteration of air spaces, and production of scattered granulomatous foci in lungs and satellite lymph nodes (FIGURES 7-1 2) . Search for acid-fast bacteria in the granulomas revealed no organisms.

FIGURE 4. From a guinea pig sensitized to tuberculin and injected with PPD tuberculin intratracheally. It was killed two months later. This field shows a remnant of the pneumonitis that constitutes the pulmonary tuberculin reaction. There is a somewhat stellate, intensely cellular thickening of sepal walls centered about several alveolar ducts and gradually attenuating toward the periphery. The cells are mono- nucleated and cannot be further categorized. Hematoxylin and eosin. x 100.


FIGURE 5. The same field as in FIGURE 4 after silver impregnation demonstrates that parallel to the cellular proliferation, there is an associated meshwork of fine argentophilic fibers. The interstices formed by the fibers are unusually small. Gordon and Sweets. x 100.


FIGURE 6. From a guinea pig sensitized to tuberculin and injected intratracheally with coal dust and PPD tuberculin. It was killed two months after the intratracheal injection. There is focal widespread atelectasis with increased cellularity of the tissue associated with dust deposits. The individual dust masses are small, suggesting that the alveolar lumens were already diminutive when the dust arrived in these spaces. Although not shown here, the reticulin stroma consisted of much coarsened fibers, forming a plexiform meshwork with much larger interstices than seen in FIGURE 5 . Hematoxylin and eosin. x 100.

FIGURE 7. From a guinea pig treated like the one in FIGURE 6 but also given prednisolone subcutaneously. In general, this picture resembles that of FIGURE 6, although the dust masses are somewhat larger. Many of them are elongated and thin. The impression of greatly increased cellularity is also suggested. Hematoxylin and eosin. x loo.

FIGURE 8. The same field as in FIGURE 7 but after silver impregnation. The stroma shows severe arborization to form a tight plexiform meshwork of argentophilic fibers that are often coarse. Some air spaces are nearly obliterated. Gordon and Sweets. x 100.

FIGURE 9. From a guinea pig treated in the same manner as the animal in FIGURE 7. There are occasional granulomatous nodules in the lung in addition to the foci pictured in FIGURES 7 and 8 . These nodules, found only in animals treated with prednisolone, are composed of concentrically arranged fibers between which abundant histiocytic cells are interspersed. The center contains a cluster of leuko- cytes in various stages of degeneration. Dust masses are found only on the periphery of the nodule. No acid-fast organisms could be found. Hematoxylin and eosin. ~ 2 0 0 .

FIGURE 10. After silver impregnation, the same field as in FIGURE 9 demonstrates stroma composed of a concentrically arranged plexiform collagenous meshwork. Only the center is composed of argentophilic fibers. Gordon and Sweets. ~ 2 0 0 .


FIGURE 1 1 . This is a portion of a granulomatous nodule in an enlarged satellite lymph node from an animal treated like the one in FIGURE 7. The nodule is composed of an irregularly arranged, cellular, collagenous tissue containing many giant cells. No acid-fast organisms were found. Hematoxylin and eosin. ~ 2 0 0 .

FIGURE 12. Silver impregnation of the tissue in the above field reveals that the nodule is easily identified by the condensation of a plexiform collagenous tissue at its periphery. Elsewhere in the nodule, the collagen fibers form a looser network. Gordon and Sweets. x 200.


SUMMARY

Although coal dust itself can be categorized as a nonfibrogenic dust, coal mine dust-the dust inhaled by coal miners-may also contain varying amounts of fibrogenic mineral dust. The character of the tissue reaction to coal mine dust depends to some extent upon its fibrogenic silica and silicate content but, more importantly, on the presence of a n altered immunological status of the pulmonary tissue caused by tuberculosis, rheumatoid arthritis, and other, as yet, unidentified entities. Whereas, short of the development of silicosis by a free silica content of 18% or more, coal mine dust in otherwise normal tissue will produce simple pneumoconiosis, in immunologically altered tissue, the same dust may cause the production of progressive massive fibrosis of the lungs or PMF.

REFERENCES

1. GROSS, P. & C. A. NAU. 1967. Lignite and the derived steam-activated carbon: the pulmonary response to their dusts. Arch. Environ. Health 1 4 450-460.

2. HEPPLESTON, A. G. 1954. Pathogenesis of simple pneumoconiosis in coal workers. J. Path. Bact. 67: 51-63.

3. GROSS, P., R. T. P. DETREVILLE, M. A. BABYAK, M. KASCHAK & E. B. TOLKER. 1968. Experimental emphysema: effect of chronic nitrogen dioxide exposure and papain on normal and pneumoconiotic lungs. Arch. Environ. Health 1 6

4. INTERNATIONAL CONFERENCE ON CWP. Sept. 10-12, 1969. Synopsis of the work session proceedings. Spindletop Research, Inc. Lexington, Ky.

5. DrBusi, W. 1954. Bemerkungen zu einigen Punkten aus der pathologischen Anatomie der Silikose. I n Die Staublungenerkrankungen. K. W. Jotten, W. Klosterkotter & G. Pfefferkorn, Eds. : 25. Steinkopf. Darmstadt, West Germany.

6. KLOSTERK~TTER, W. & H. J. EINBRODT. 1965. Quantitative tierexperimentelle Untersuchungen iiber den Abtransport von Staub aus den Lungen in die regionalen Lymphknoten. Arch. Hyg. Bakt. 149: 367-384.

7. GROSS, P. & T. HATCH. 1962. Pneumoconiosis: the requirements for lymphatic dust transport. Intern. Arch. Gewerbepath. Gewerbehyg. 19: 660-666.

8. GROSS, P. & R. T. P. DETREVILLE. 1971. Unpublished.

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THE PULMONARY RESPONSE TO COAL DUST