Coal Workers’ Pneumoconiosis

Coal workers’ pneumoconiosis (CWP) is defined as the nonneoplastic reaction of the lung to inhaled coal-mine dust. It is characterized by nodular and/or coalescent opacities on chest X-ray. Symptoms are usually limited to dyspnea in advanced stages of the disease. Computed tomography better defines radiological abnormalities.

Simple coal workers’ pneumoconiosis has no significant effect on spirometric measures, whereas lung function in the more advanced stages of progressive massive fibrosis (PMF) shows an obstructive and restrictive pattern. Pathologically, simple CWP is associated with the macular and nodular lesions, whereas complicated CWP is associated with PMF (opacity lesion of 1 cm in diameter or more) and the lesions of rheumatoid pneumoconiosis.

No specific treatment affects the course of coal workers’ pneumoconiosis, though treatment options are available for complications such as tuberculosis and chronic hypoxemia. Supportive care includes bronchodilators in patients with obstructive syndrome, routine vaccination, antibiotics for exacerbations, and pulmonary rehabilitation.


Pneumoconiosis is defined as the accumulation of dust in the lungs and the reaction of tissues to its presence. The prolonged inhalation of coal-mine dust may result in the development of coal workers’ pneumoconiosis (CWP), silicosis, and industrial chronic bronchitis and emphysema, either singly or in various combinations. CWP is the term generally applied to interstitial disease of the lung resulting from chronic exposure to coal dust, whereas silicosis is due to inhalation of dust containing silica. The pneumoconioses differ in a number of ways from the acute allergic and toxic interstitial diseases that are associated with exposure to organic dusts, principally because of the long latency period (usually 10– 20 years or more) between exposure and recognition of the disease.

Coal workers’ pneumoconiosis was first recognized in Scottish miners in 1830. In recent decades, the incidence of CWP has been declining in industrial countries due to improved dust controls, though increased mechanization in the mid-1960s led to a temporary increase in dust levels in some countries. Over the period 1950–80, the annual UK rate for the recognition of CWP for state compensation in working and retired miners decreased from about 7% to 1–2%. The overall prevalence of CWP in US coal miners declined from about 12.7% to 3.9% between 1969 and 1988, but there were substantial regional differences. The overall prevalence of simple CWP is 2.8%; the highest rate of 14% occurs in workers with 30 years or more of mining experience. Similar regional differences and similar declines have been noted in the US and other countries.


Coal dust is not a mineral of fixed composition and comprises coal and quartz in various proportions. Coal is graded by rank, the rank reflecting its carbon content and thus coal quality and combustibility; anthracite is the highest ranked coal, with a carbon content of around 98%. Lower-ranked coals have carbon contents of around 90–95% carbon. The rank of coal has an influence on the risk of disease (higher-rank coals entail higher risk than lower-rank coals) and the progression of pneumoconiosis. Exposure to coal dust with a quartz concentration greater than 15% is associated with a high risk of a rapidly progressive form of pneumoconiosis that has the characteristics of silicosis. In open mines, dust levels rarely approach those of underground mines.

Coal is currently actively mined in the US, UK, Western and Eastern Europe, India, China, South America, Australia, and Africa. There are three groups of factors that are known to influence the character and severity of lung tissue reaction to the mineral dusts. The risk of pneumoconiosis is related to the intensity and years of exposure. However, among a group of workers exposed to the same dust, only a fraction develop pneumoconiosis, because of an individual susceptibility. The nature and properties of each specific dust constitute the third factor under consideration; for each mineral, geometric and aerodynamic properties, chemistry, and surface properties have to be considered. In order to cause pneumoconiosis, particles must be small enough (0.5–5 mm) to reach the respiratory bronchioles and be deposited there.


The lesions of coal workers’ pneumoconiosis are focal in nature. Simple CWP is associated with the macular and nodular lesions, whereas complicated CWP is associated with progressive massive fibrosis (PMF, opacity lesion of 1 cm in diameter or more) and the lesions of rheumatoid pneumoconiosis (Caplan’s syndrome). On gross examination the pleural surfaces in patients with coal dust exposure show an irregular pattern of bluish black pigmentation, often outlining the pleural lymphatics when dust exposure is fairly mild, but sometimes completely blackening the pleura when exposure has been heavy. Peribronchial, hilar, and paratracheal lymph nodes are enlarged, black, and firm. Microscopically, the lymph nodes show large numbers of pigmented histiocytes and a variable degree of fibrosis.

The initial lesions in the lung are the coal dust macules, which correspond macroscopically to focal areas of black pigmentation. Microscopically, the macule is composed of macrophages laden with coal dust within the walls of the respiratory bronchioles and adjacent alveoli. Focal emphysema around the coal dust macule is sufficiently common to be considered as an integral part of the lesion of simple coal workers’ pneumoconiosis. Focal emphysema is a form of centriacinar emphysema.

Nodules may be the only lesions in the lung, but are more commonly seen against a background of macules. They are not confined to the respiratory bronchioles, but are also seen in the subpleural and peribronchial connective tissues. Nodules have round or irregular borders and may be surrounded by enlarged airspaces. There is a tendency for nodules to cluster and eventually coalesce to produce PMF. Nodules may be calcified. Histologically, they consist of dust-laden macrophages in a fibrotic stroma composed of collagen and reticulin. Nodules centered on respiratory bronchioles probably develop through progressive enlargment and collagenization of pre-existing macules.

PMF almost invariably occurs against a background of severe simple CWP (usually of nodular type) and is usually bilateral. PMF lesions appear as black fibrotic masses that may be round, oval, or irregular in shape; they are well demarcated from the surrounding lung but are not encapsulated. Satellites nodules are usually found in the adjacent lung. The lung and bronchovascular rays become markedly distorted; a characteristic feature of PMF is the tendency of the lesion to transgress normal anatomic boundaries, with fissures, bronchi, and vessels becoming obliterated as the lesion progresses. Microscopically, the lesions are composed of bundles of haphazardly arranged hyalinized collagen fibers and/ or reticulin fibers and coal dust. Dust particles near the periphery of the lesion are mainly found within macrophages, whereas in the center, the dust tends to lie free in clefts and cavities. Areas of liquefactive necrosis containing fragments of degenerating collagen and cholesterol crystals are frequently observed. A giant cell reaction may be seen in association with necrosis cells and collagen degradation. Miners with PMF have more severe emphysema than do those with less severe categories of CWP. All types of emphysema may be observed.


The pathogenesis of pneumoconiosis is similar to that of all interstitial lung diseases. There is a chronic inflammatory state (alveolitis) in which inflammatory cells are activated and damage the pulmonary architecture. This produces fibrotic scarring. Inorganic particles are phagocytosed by alveolar macrophages, causing activation and the release of inflammatory mediators such as cytokines and arachidonic acid metabolites. The mediators in turn induce the recruitment of other inflammatory cells within the alveolar wall and on the alveolar epithelial surface. The alveolitis is dominated by alveolar macrophages. Toxic oxygen derivatives and proteolytic enzymes are released by the inflammatory cells, which cause cellular damage and disruption of the extracellular matrix.

The inflammatory phase is followed by a reparative phase in which growth factors stimulate the recruitment and proliferation of mesenchymal cells and regulate neovascularization and re-epithelialization of injured tissues. During this phase, abnormal or uncontrolled reparative mechanisms may result in the development of fibrosis. Tumor necrosis factor alpha (TNF-a) seems to play a key role in the recruitment of inflammatory cells induced by toxic dusts. In addition, neutrophils recruited in the area of inflammation may contribute to the alveolitis, and respiratory and endothelial cells may play a further role by releasing inflammatory mediators like MIP-2, IL-8, and ICAM-1. Several studies demonstrate a key role of transforming growth factor beta (TGF-b) in the pathogenesis of lung fibrosis, and elevated TGF expression has been observed in coal workers’ pneumoconiosis. Thus, increased levels of TNF-a and IL-1 have been observed in CWP. Several human studies demonstrated that alveolar macrophages of individuals with CWP spontaneously release significant amounts of growth factors such as platelet-derived growth factor (PDGF), insulin-like growth factor (IGF), and fibroblast growth factor (FGF). These mediators are involved in the proliferative response of type II epithelial cells that occurs in PMF. Lastly, recent studies have also demonstrated an association between apoptosis and inflammation supporting a potential role for IL-1bdependent nitric oxide-mediated apoptosis in the development of pneumoconiosis.

Clinical Features


The diagnosis of coal workers’ pneumoconiosis can be made using radiologic as well as pathologic criteria. CWP is usually first recognized from the plain chest radiograph, which is critical also in evaluating disease progression. Requirements for the diagnosis include a history of significant exposure, radiographic features consistent with these illnesses, and the absence of illnesses that may mimic these diseases (primarily infections with a predominantly miliary radiographic pattern, such as tuberculosis, fungal infections, or sarcoidosis). The radiographic appearances are most usefully described by the coding system devised for standard films of pneumoconiosis under the auspices of the International Labour Organization (ILO). In clinical practice, simple CWP is characterized by small rounded opacities (nodules) rather than small irregular opacities, though the latter may be seen in much lesser profusion. Surgical biopsy is very rarely required in the investigation of CWP. However, biopsy material (whether surgical, transbronchial, or from percutaneous fine needle aspiration) may be needed in special circumstances; for example, when there is uncertainty over the nature of conglomerate lesions in PMF or the nodular lesions in simple CWP (is lung cancer present?).

Symptoms and Signs

Simple coal workers’ pneumoconiosis and category A complicated CWP are not associated with respiratory symptoms. Breathlessness and cough in coal miners are usually a consequence of cigarette smoking. However, coalmine dust may itself cause chronic bronchitis and chronic obstructive pulmonary disease (COPD). By contrast, complicated pneumoconiosis (PMF) at categories B and C may present with undue breathlessness and productive cough. Melanoptysis is the result of necrosis within the conglomerate, coal-containing lesions that characterize PMF. Progressive undue exertional dyspnea is usually the dominant symptom, but rarely there may be breathlessness at rest.

There are no specific abnormal physical signs in coal workers’ pneumoconiosis, but when complicated CWP is very advanced the signs of emphysema or fibrotic lobar shrinkage may be detected. Finger-clubbing and fine inspiratory crackles are not features of the disease and if these are present, another explanation should be sought (especially hypersensitivity pneumonitis, idiopathic-like pulmonary fibrosisy Only in a small proportion of severe cases of complicated disease does coal workers’ pneumoconiosis evolve to produce chronic respiratory failure and cor pulmonale. When this does occur, extensive and multifocal conglomerate lesions are to be expected, generally with emphysema and concomitant disabling chronic airway obstruction.

Associated Disorders

Emphysema and bronchitis

There is a clear relationship between coal-mine dust and the development of emphysema. A further association with complicated CWP, if manifested by bullous emphysema, is spontaneous pneumothorax, though this is not likely to occur excessively in simple pneumoconiosis. The advanced stages of complicated CWP are additionally associated with recurrent episodes of acute and subacute bronchitis, as well as a regular productive cough. Persistent productive cough, shortness of breath, and wheezing are also common in coal miners in the absence of CWP; a significant dose–response relationship between coal-mine dust exposure and chronic bronchitis has been observed.

Autoimmune diseases

The autoimmune disorders rheumatoid disease and progressive systemic sclerosis may be associated with coal workers’ pneumoconiosis. The latter, however, is more clearly associated with silicosis, and it is not clear whether it occurs with greater incidence than expected when there is occupational exposure to coal alone. The association of rheumatoid disease with CWP is known as Caplan’s syndrome. The diagnosis is suggested by the association of coal dust exposure, rheumatoid arthritis, and multiple well-defined, large, rounded opacities (nodules with diameter 10 mm) on the chest radiograph. Spontaneous disappearance is common, with or without initial cavitation, and new nodules commonly emerge in different locations. If the nodules become superimposed, suggesting conglomerate masses, PMF may be simulated, but often the radiological appearances of simple CWP are absent and there is a need to consider the possibility of primary lung tumor. There is no evident relationship between the severity of the rheumatoid disease and the extent of Caplan’s syndrome. Pathologically, the Caplan nodule is generally bigger than the nodule of complicated CWP, smoother in outline, and distributed at random within the lung fields. Caplan nodules histologically show a necrotic center with a peripheral palisade of histiocytes and giant cells. The Caplan nodule is indistinguishable pathologically from necrobiotic nodules of rheumatoid disease unassociated with coal dust exposure; it is more likely to cavitate, thereby producing a concentric ring pattern, and so is also known as a necrobiotic nodule.


Coal workers’ pneumoconiosis has also been linked with a number of specific infections, the most prominent of which historically has been tuberculosis. The association observed with coal mining (and hence CWP) in some countries appears to have been a consequence only of close contact during long hours of work in the confined mine environment. Nontuberculous mycobacteria, on the other hand, may infect lungs damaged by CWP with greater than usual frequency, and so CWP does appear to increase the risk for infection with opportunistic organisms. The development of mycobacterial infection in a patient with CWP may be symptomless, at least in its early course, and it may be difficult or impossible to distinguish it radiographically from PMF lesions since both characteristically begin in the apices. Similarly, it may be difficult to attribute changes in the radiographic appearances to advancing infection or progressive PMF. Other opportunistic infections have been reported in association with CWP, and Aspergillus species have been noted to colonize cavities in conglomerate lesions of complicated coal workers’ pneumoconiosis.

Lung cancer

There is no evidence of a causal relationship between coal workers’ pneumoconiosis and carcinoma of the lung, though there is strengthening evidence linking silica exposure with lung cancer. In 1996 International Agency for Research on Cancer (IARC) reclassified crystalline silica as a group I carcinogen stating that: ‘‘sufficient evidence of carcinogenicity indicates that there is a causal relationship between the exposure and human cancer.’’

Chest Radiology

The radiographic pattern of simple coal workers’ pneumoconiosis is typically one of small rounded opacities, which appear first in the upper zones. The middle and lower zones become involved as the number of opacities increases. The nodules increase in profusion with increasing dust exposure; a change in profusion after dust exposure has ceased is very unusual. Calcification of the nodules may occur (10–20% of cases). Complicated pneumoconiosis is defined as a lesion of 1 cm or greater in longest diameter. The large opacities are usually predominant in the upper lobes, may be uni- or bilateral, and are symmetrically or asymmetrically distributed. The pattern of change in size is variable and unpredictable. Most PMF occurs on a background of simple pneumoconiosis, but this is not invariably so, and it may occur after dust exposure has ceased. Cavitation can develop within a PMF lesion, and occasionally there is a dense peripheral arc or rim at its lower pole, which represents calcification. Dense calcification with the lesion is also sometimes seen. PMF is often associated with bullous emphysema and fibrotic scarring leading to distortion of the lung, and shift of the trachea and mediastinum to the affected side. Irregular, mainly basal, opacities may also be seen on standard radiographs. Large nodular opacities can be rheumatoid nodules of Caplan’s syndrome, and lung cancer must be kept in mind. Eggshell calcification as well as pleural effusion are uncommon in CWP. 

Computed tomography (CT) scans can show parenchymal lesions, which are not visible on normal chest radiographs. CT scans have greater sensitivity than plain radiographs in detecting simple CWP, but there is less obvious benefit for the detection of complicated pneumoconiosis. There is a posterior and right-sided predominance in the upper zones. Nodules are usually observed against a background of parenchymal micronodules and are generally associated with subpleural micronodules. Coalescence of subpleural micronodules produces ‘pseudoplaques’. Two categories of lesions can be observed in PMF: lesions with irregular borders that are associated with disruption of the pulmonary parenchyma and lead to typical scar emphysema; and lesions with regular borders that are not associated with scar emphysema. When the lesions are larger than 4 cm in diameter, irregular areas of aseptic necrosis can be observed with or without cavitation.

CT, particularly high-resolution images, may additionally distinguish other pathological processes whether they are related to CWP or not. Focal lung emphysema indicates distension of the bronchioles within macules and is considered an integral part of the lesions of CWP. On the other hand, two major forms of emphysema occurring in coal workers can be detected on CT: bullous changes around PMF lesions referred to as paracicatricial or scar emphysema; and nonbullous emphysematous lesions defined as centrilobular emphysema. Lesions of diffuse pulmonary fibrosis can be detected on high-resolution CT as honeycombing or areas of ground-glass attenuation. Two specific etiologies of fibrosis of coal miners should be considered: a direct effect of deposited coal or silica particles; or an indirect effect due to an association with scleroderma.

Lung Function Testing

Simple coal workers’ pneumoconiosis does not have a significant effect on spirometric measures, when prior dust exposure is taken into account and when smoking habits are also considered. Studies of lung function in the more advanced stages of PMF have shown an obstructive and restrictive pattern, compliance is usually somewhat decreased, diffusing capacity is usually reduced, and a slight reduction in arterial oxygen tension on effort may be observed. Oxygen desaturation is not present at rest or on moderate effort in the nonconglomerate stages of disease but cardiopulmonary exercise testing can add significant information in patients with early disease and mild impairment on resting studies. As in the case of radiographic progression, the changes in pulmonary function are more likely to occur in workers who have had intense exposure to dust. In addition it must be pointed out that miners who did not have coal workers’ pneumoconiosis on chest radiography may exhibit lower FEV1 than controls, suggesting that coal dust may induce chronic obstructive pulmonary disease. In PMF, lung function depends on the extent of the lesions and associated emphysema. Ultimately, hypoxemic acute respiratory failure may occur; their long-term prognosis is poor.

Biological Tests

There are no specific biological features for pneumoconiosis. However, immunological abnormalities are now well described due to the presence of positive circulating antinuclear antibodies and rheumatoid factor. Serum immunoglobulins IgA and IgG have significantly raised levels in miners with pneumoconiosis, compared to non-miners. Finally, increased serum angiotensin-converting enzyme levels were observed in 45% of pneumoconiotic coal miners, whatever the radiological classification of pneumoconiosis. Bronchoalveolar lavage usually demonstrated an increase in cell numbers without change in differential cell count, in contrast to a number of other interstitial disorders of the lung.


Simple coal workers’ pneumoconiosis is not associated with premature mortality; approximately 4% of deaths in coal miners are directly due to complicated pneumoconiosis, especially in miners and ex-miners with category B or C complicated coal workers’ pneumoconiosis. The rate of progression to PMF appears to be influenced chiefly by the age at which the miner begins to show radiographic changes of coal workers’ pneumoconiosis reflecting individual susceptibility and the level of cumulative exposure. 

Management and Current Therapy

No specific treatment affects the course of coal workers’ pneumoconiosis, though treatment options are available for complications such as tuberculosis and chronic hypoxemia. Supportive care includes bronchodilators in patients with obstructive syndrome, routine vaccination, antibiotics for exacerbations, and pulmonary rehabilitation. When a miner is found to have CWP, further dust exposure should be excluded. Simple pneumoconiosis does not necessarily require complete exclusion from mining, especially in older subjects; however, if PMF is detected, further exposure to coal dust should be avoided. Pulmonary function tests give additional information since the development of an obstructive ventilatory defect (due to dust exposure) may occur in the absence of coal workers’ pneumoconiosis. In all patients who smoke, advice and support in smoking cessation should be given. If a physician concludes there is disablement from CWP, the patient should then be given advice on how to seek compensation.


The prevention of pneumoconiosis depends on keeping exposure to concentrations of ambient dust at levels known to be associated with minimal and acceptable risk. Dust control is achieved primarily by ventilation, though water sprayed at points of dust generation is a useful technique for dust suppression. When each process is limited by practical constraints in unusual situations, the miner can be provided with respiratory protection equipment or the duration of exposure can be limited. The effectiveness of such measures should be monitored by regular assessment of dust concentrations, and regular clinical and radiological surveillance of the workforce. Static samplers are commonly used at the coalface and other potential sites of exposure to monitor exposure levels, the respirable particles of 1–7 mm diameter being collected by size-selective, gravimetric elutriators. Personal samplers worn by individual miners can also be used when necessary.

Surveillance allows early recognition of workers with simple pneumoconiosis, who are likely to be those with greatest susceptibility, so that ongoing exposure can be restricted (perhaps by transfer to jobs with lower exposure) and the risk of future disablement from PMF reduced. Permissible levels of respirable dust vary among countries, though they are often based on the same epidemiologic studies. The following standards are currently in use:

  • US: 1mgm3
  • UK: 3.8 mgm3
  • Australia: 3 mgm3
  • Germany: 4 mgm3

Variability in individual susceptibility is likely to be an important determinant for coal workers’ pneumoconiosis, as is the case for most occupational disorders, and a number of predictive factors may be useful in identifying miners with higher than average risk: initially expiratory wheezes, an obstructive pattern of lung function, and many micronodules on CT scans, suggesting a predictive value for the initial CT abnormalities, and for these early symptoms and lung function abnormalities. An alternative approach for the future might involve genetic screening, which may provide markers of undue individual susceptibility. TNF-a is known to be important in the development of fibrosis due to silica exposure, and is probably relevant to the development of PMF in coal miners. A recent study showed a polymorphism in the promoter of the TNF-a gene in coal miners with a predominance of the genotype A308 in miners with PMF, compared to simple pneumoconiosis. A further study has shown an increased plasma level of soluble TNF-a receptor in coal miners with pneumoconiosis. 

In any event, control of exposure levels alone is likely to prevent most cases of disabling PMF, and it has been predicted that an exposure concentration over 35 working years that does not exceed an average of 4.3 mgm3 is associated with a probability for the development of category 2 or more coal workers’ pneumoconiosis of no more than 3.4%. This represents a dramatic reduction in risk over the last 50 years. 

Further Reading

Begin R, Cantin A, and Masse´ S (1989) Recent advances in the pathogenesis and clinical assessment of mineral dust pneumoconioses: asbestosis, silicosis and coal pneumoconiosis. European Respiratory Journal 2: 988–1001.

Brichet A, Salez F, Lamblin C, and Wallaert B (1999) Coal workers’ pneumoconiosis and silicosis. Occupational Lung Disorders, Monograph 11. European Respiratory Monograph 4: 136–157.

Coggon D and Newmann-Taylor A (1998) Coal mining and chronic obstructive pulmonary disease: a review of the evidence. Thorax 53: 398–407.

Green FHY (1998) Coal workers’ pneumoconiosis and pneumoconiosis due to other carbonaceous dusts. In: Churg A and Green FHY (eds.) Pathology of Occupational Lung Disease, 2nd edn., pp. 129–208. Williams and Wilkins.

International Agency for Research on Cancer (1996) Silica, Some Silicates, Coal Dust and Para-amid Fibrils. Lyon: IARC.

Morgan WKC and Lapp NL (1976) Respiratory disease in coal miners. State of the art. American Review of Respiratory Diseases 113: 531.

National Institute for Occupational Safety and Health (1995) Criteria for a recommended standard: occupational exposure to respirable coal mine dust. National Institute for Occupational Safety and Health Publication 95–106: 1–336.

Parkes WR (1994) Pneumoconiosis associated with coal and other carbonaceous materials. In: Parkes WR (ed.) Occupational Lung Disorders, 3rd edn., pp. 366–368. London: Butterworths.

Remy-Jardin M, Remy J, Farre I, and Marquette CH (1992) Computed tomography evaluation of silicosis and coal workers’ pneumoconiosis. Radiologic Clinics of North America 30: 1155–1176.

Rom WM and Crystal RG (1991) Consequences of chronic inorganic dust exposure. In: Crystal RG, West JB, et al. (eds.) The Lung: Scientific Foundations. New York: Raven Press.

Schins RPF and Borm PJ (1999) Mechanisms and mediators in coal dust induced toxicity: a review. Annals of Occupational Hygiene 43: 7–33.

Seaton A (1995) Coal workers’ pneumoconiosis. In: Morgan WK and Seaton A (eds.) Occupational Lung Diseases, 3rd edn., pp. 374–406. London: Saunders.

Vanhee D, Gosset P, Boitelle A, Wallaert B, and Tonnel AB (1995) Cytokines and cytokine network in silicosis and coal workers’ pneumoconiosis. European Respiratory Journal 8: 1–9.