Coal Worker's Pneumoconiosis 

Updated: Dec 16, 2015
Author: Farhan J Khan, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP 



Coal worker's pneumoconiosis (CWP) can be defined as the accumulation of coal dust in the lungs and the tissue's reaction to its presence.[1] The disease is divided into 2 categories: simple coal worker’s pneumoconiosis (SCWP) and complicated coal worker’s pneumoconiosis (CCWP), or progressive massive fibrosis (PMF),[2] depending on the extent of the disease. Also see Silicosis and Coal Worker Pneumoconiosis. Note the images below.

Gross specimen demonstrating simple coal worker's Gross specimen demonstrating simple coal worker's pneumoconiosis.
Gross specimen demonstrating progressive massive f Gross specimen demonstrating progressive massive fibrosis in a coal miner.


Anthracosis is the asymptomatic accumulation of carbon without a consequent cellular reaction. Such accumulation can be found in varying degrees among most urban dwellers and in tobacco smokers. Inhaled coal dust becomes a problem when the body's natural mechanisms for defending against and processing the dust becomes overwhelmed and, subsequently, overreactive.

Inhaled coal dust reaches the terminal bronchioles, and the carbon is engulfed by alveolar and interstitial macrophages. Phagocytosed coal particles are transported by macrophages up the mucociliary elevator and are expelled in the mucus or through the lymphatic system.

When this system becomes overwhelmed, the dust-laden macrophages accumulate in the alveoli and may trigger an immune response. (The lungs must be exposed for a significant amount of time to dust particles 2-5 µm in diameter in order for the dust to be retained in the alveoli.) Fibroblasts involved in this response secrete reticulin, which entraps the macrophages. If the macrophages lyse, the fibroblastic response is augmented and more reticulin is laid down in the area.

Coal that contains silica lyses macrophages faster and stimulates the fibroblasts to add more collagen to the network. The lymphatic tree is contained in the pulmonary interstitium, along with arterial and venous vessels. If these macrophages have partially migrated up the lymphatic vessels, arterioles can become strangulated from the resultant interstitial fibrosis. As more and more dying macrophages, fibroblasts, reticulin, and collagen are deposited along the vascular tree, the vessels become compromised, and ischemic necrosis ensues.

Areas of focal deposition of coal dust and pigment-laden macrophages are known as coal macules and are the histologic hallmark of coal worker’s pneumoconiosis. As these macules extend, they join other macules in the vicinity, forming discrete areas of interstitial fibrosis. This growing collagen network causes distention of the respiratory bronchioles, forming focal areas of emphysema. Widespread areas of focal emphysema can accrue without significant respiratory impairment.

A study of autopsied coal miners and non-miners conducted by Kuempel et al showed that inhalation of respirable coal dust is a highly significant predictor of emphysema severity beyond other contributory factors, including cigarette smoking, race, and age at death.[3, 4]

Depending on factors that are still not fully understood, the macules may arrest or may continue to enlarge and form nodules that produce progressive massive fibrosis when they coalesce. This process can be exacerbated by tuberculosis or rheumatoid factor, which accelerates the rate of progression of focal ischemic necrosis and fibrosis.

Progressive massive fibrosis in association with rheumatoid arthritis is known as Caplan syndrome. Caplan first described this condition in 1953. He noticed that miners with rheumatoid arthritis had changes on chest radiographs similar to those of progressive massive fibrosis, although the distribution in the lungs was different. Unlike lesions caused by progressive massive fibrosis, which congregate in the upper lobes, these new lesions (subsequently known as Caplan lesions) tend to coalesce in the peripheral lung fields.

Pathologically, the nodule exhibits a central area of coal dust and necrotic collagenous tissue lying in concentric rings. Surrounding these rings is an area of neutrophils with palisading fibroblasts. Caplan nodules tend to progress faster than lesions associated with progressive massive fibrosis and may precede the onset of rheumatoid lesions. Sixty-two percent of miners with peripheral nodules have positive serology findings for rheumatoid factor.[5]

Research is currently underway to further understand the inciting factors in the inflammatory process. Boitelle et al[6] have suggested that chemokines released to attract alveolar macrophages may be a plausible target for further pharmaceutical intervention to arrest the inflammatory process, which leads to destruction and fibrosis. Levels of monocyte chemoattractant protein-1 have been found to be increased in bronchoalveolar lavage specimens taken from patients with simple coal worker’s pneumoconiosis or progressive massive fibrosis compared with controls. This chemokine, which attracts and activates monocytes, is responsible for the domino effect of respiratory burst, further cell recruitment, and release of lysosomal enzymes. This chemokine may be a key factor in the chronic inflammation of the macrophage, which is central to the pathophysiology of coal worker’s pneumoconiosis.[6]

Other interesting areas that may become promising are the antioxidants selenium and glutathione peroxidase. Both substances have been found to be at lower concentrations in patients who have been exposed to coal-mine dust and tobacco smoke compared with control subjects. This suggests a consumptive process and a weakened defense against reactive oxygen species, which cause cellular damage and potentiate coal worker’s pneumoconiosis and progressive massive fibrosis.[7]

In a 2005 study by Huang et al,[8] a correlation has been found between bioavailable iron (BAI), pyrite concentration, and the regional progression of lung disease. BAI is iron that dissolves in 10 mmol/L phosphate solution at pH 4.5, which mimics the interior of lysosomes. Huang et al[8] found an increased prevalence of coal worker’s pneumoconiosis and progressive massive fibrosis at Pennsylvania mines, where BAI values are higher, compared with Utah mines, where BAI levels are lower. They also demonstrated that pyrite-containing coal contributed to the higher prevalence of progression to coal worker’s pneumoconiosis and progressive massive fibrosis in Pennsylvania. McCunney et al have suggested that iron, not quartz, is the active agent in coal responsible for coal worker’s pneumoconiosis.[9]

When mixed with water, pyrite produces hydrogen peroxide[10, 11] and hydroxyl radicals.[12, 13] These reactive agents have been shown to degrade yeast RNA, ribosomal RNA, and DNA.[11] Cohn et al[14] demonstrated that these pyrite-induced reactive oxygen species can be implicated as the cause of the cellular damage and chronic inflammation that lead to chronic disease in the lungs of coal miners. In order to proceed to RNA degradation, the concentration of sulfur (pyrite) in the coal necessary to produce hydrogen peroxide and hydroxyl radicals must exceed 1%.[14] These findings suggest that personnel at individual mines can measure the amount of sulfur in its coal and implement proper measures to ensure that miners in these high-risk areas either have improved protective gear or decreased long-term exposure to coals with increased BAI.

A case control study by Wang et al in China found that polymorphism in the E-selectin (an adhesion molecule participating in multiple inflammatory processes) gene (SELE) and smoking increased vulnerability to coal worker's pneumoconiosis.[15]



United States

The prevalence of coal worker’s pneumoconiosis is related to the length and the type of exposure to coal dust and is therefore more prevalent in people exposed to higher concentrations.[16, 17] In the United States, most coal is mined in eastern Pennsylvania, western Maryland, West Virginia, Virginia, and Kentucky. Disease prevalence varies in different areas of the country and from mine to mine because coal content varies by region. In the 1960s, the Interagency Study determined the overall prevalence of coal worker’s pneumoconiosis to be 30% and the overall prevalence of progressive massive fibrosis to be 2.5%.[1] Sixteen percent of coal miners in the United States can progress to interstitial fibrosis.[18]

A 2004 study[19] reviewed death certificates from 1968-1982 and 1982-2000 with coal worker’s pneumoconiosis as the cause of death. A 36% decrease was noted in the reporting of male deaths due to coal worker’s pneumoconiosis from 1982-2000 compared with from 1968-1982. This overall decline is likely multifactorial, due to the decline of the coal-mining workforce in general and the institution of the Federal Coal Mine Health Safety Act. Despite these national findings, regions of the country have demonstrated an increase in the progression to coal worker’s pneumoconiosis and progressive massive fibrosis in Kentucky and Virginia.[20, 21] This has prompted studies researching the toxic content of coal in isolated mines, which may be contributing to a regional variation in the progression of lung diseases.[22, 23]

In a retrospective chart review of 138 West Virginian coal miners from 2000-2009, Wade et al found an increased number of cases of rapidly progressive pneumoconiosis and progressive massive fibrosis in young coal miner's after 2001. This caused increased morbidity and mortality. These coal miners developed progressive massive fibrosis at a mean age of 52.6 years, after an average of 30 years of exposure and after an average of 12 years from the last normal chest radiography finding. This report asserts the need for close surveillance for this disease and a need for improvements in preventive measures.[2, 24]

The changing epidemiological patterns of coal workers pneumoconiosis in the Appalachian region of the United States attributes the increased exposure to respirable silica, as suggested by radiographic abnormalities consistent with silicosis.[2, 25]


In Great Britain, most coal is mined in Wales. As in the United States, 16% of miners can progress to interstitial fibrosis.[18]


Mortality and morbidity are strictly related to the type of coal dust and the length of exposure. Disease severity increases as coal rank increases and in miners who have greater exposure to respirable dust. As a result, coal worker’s pneumoconiosis is rarely observed in coal miners younger than 50 years.[5]

A 41-month retrospective study performed by Shen et al[26] describes a prognostic relationship between coal worker’s pneumoconiosis and the first episode of respiratory failure requiring mechanical ventilation. The investigators found that radiographic evidence of progressive massive fibrosis was not associated with increased ICU mortality. No mortality difference was delineated between patients with simple coal worker’s pneumoconiosis and patients with complicated coal worker’s pneumoconiosis. The following 3 independent variables predicted outcomes:

  • Hypercapnia (PaCO2 >45 mm Hg) at the time of intubation exhibited a protective effect, suggesting a less severe acute illness as the cause of the respiratory failure compared with normocapnic individuals.

  • An Acute Physiology and Chronic Health Evaluation II (APACHE II) score greater than 25 at the time of intubation was associated with a worse mortality rate.

  • A ratio of PaO2 to fraction of inspired oxygen (FiO2) of less than 200 mm Hg at the time of intubation was associated with a worse mortality rate.

The ICU mortality rate for patients with coal worker’s pneumoconiosis with their first episode of respiratory failure requiring mechanical ventilation was 40%, and the in-hospital mortality rate was 43%.


Coal worker’s pneumoconiosis has no predilection for any racial or ethnic group.


Coal worker’s pneumoconiosis has no predilection for either sex.


The onset of coal worker’s pneumoconiosis does not occur at any specific age. The onset of disease depends on the length and severity of exposure to coal dust and thus depends on when the coal miner began working in the mines and the specific nature of his or her exposure.




Taking a good history is perhaps the most important step in evaluating for coal worker’s pneumoconiosis. Ask patients what their specific job entails in order to estimate dust levels. The length of time spent underground and the age at first exposure are important in determining the risk of progressing to progressive massive fibrosis. Determine the type of coal mined, its rank, and, if possible, its silica content.

Obtain a smoking history because miners who smoke have more symptoms than miners who do not smoke.

Treatment for coal worker’s pneumoconiosis is palliative and preventive. Most miners are not receptive to recommendations to change career. If their respiratory status worsens, or if they are at risk for progression to progressive massive fibrosis, suggest changing to a job within the mine that requires less exposure to respirable dust.


Miners with simple coal worker’s pneumoconiosis are usually asymptomatic. They may report cough or sputum production, but this is generally secondary to industrial bronchitis or smoking and not to the body's reaction to coal.[18] Complicated coal worker’s pneumoconiosis produces cough, dyspnea, and lung function impairment. If the disease is advanced, cor pulmonale may be found with associated right ventricular heave, large A waves, hepatomegaly, and peripheral edema. These late physical findings are rare in the United States.[18]

Coal worker’s pneumoconiosis results from mechanical and architectural destruction of the lungs. Fever, night sweats, and other constitutional symptoms suggest a secondary infective process.


The following factors increase the risk of coal worker’s pneumoconiosis:

  • Type of dust: More silica increases the risk of fibrosis. Coal rankings are as follows[5] :

    • High: This coal is older and has the least amount of volatile matter (eg, anthracite coal [hard and shiny]).

    • Medium: This coal is of moderate age and has a greater amount of volatile matter (eg, bituminous coal).

    • Low: This coal is younger and has the greatest amount of volatile matter (eg, lignite coal [brown and crumbly]).

  • Age at first exposure

  • Length of time spent underground

  • Smoking

  • Size of dust particles

  • Type of job: Certain jobs require more exposure to respirable dust. Most dust is found at the coal face; therefore, individuals who work directly on the cutting of the coal have the highest exposure. The following list details dust exposure related to job title, beginning with the highest exposure[1] :

    • Cutting-machine operator: This worker cuts coal directly at the face. Respirable dust levels are highest here.

    • Roof bolters: These individuals drill through rock and thus are also exposed to silica. The continuous mine operator, loading machine operator, and shot firer are also exposed to higher amounts of respirable dust.

    • Train operators: They drop sand onto the tracks for traction and may therefore develop silicosis.

    • Motormen, brakemen, drivers, and shuttle car operators: These individuals have less dust exposure because the coal has already been cut by the time they work with it, thus decreasing their exposure to respirable dust.

    • Mechanics, electricians, and maintenance personnel: They have the least amount of dust exposure.





Laboratory Studies

Obtain a CBC count and perform a sputum culture (as needed) to exclude infective processes.

Imaging Studies

Historically, radiographs remain the main diagnostic tool. The International Labor Organization developed a 12-point classification for standardizing the diagnosis of coal worker’s pneumoconiosis. A standard set of radiographs reflecting the amount of coal retained in the lungs is used for comparison. The scale represents a continuum of dust accumulation with nodule formation from category 0/0 to 3/4. Generally, complicated coal worker’s pneumoconiosis appears on a background of category 3 or 4 simple coal worker’s pneumoconiosis.

Simple coal worker’s pneumoconiosis usually develops as small, rounded opacities first observed mostly in the upper lobes. These densities can be classified as follows:

  • P - Up to 1.5 mm in diameter

  • Q - 1.5-3 mm in diameter

  • R - 3-10 mm in diameter

The lung zones are identified as follows:

  • RUZ and LUZ - Right upper zone and left upper zone, respectively

  • RMZ and LMZ - Right mid zone and left mid zone, respectively

  • RLZ and LLZ - Right lower zone and left lower zone, respectively

Any nodular opacity greater than 1 cm in diameter on radiographs is considered complicated coal worker’s pneumoconiosis or progressive massive fibrosis. Subcategories for this group are as follows:

  • A - Any opacity 1-5 cm in diameter

  • B - Any opacity with a diameter of 5 cm that occupies less than a third of the lung

  • C - One or more opacities whose diameter exceeds a third of the total area of the lung

Of note, in a small study by Reichert and Bensadoun, positron emission tomography (PET) with F-18-fluorodeoxyglucose proved to be of limited value in the evaluation of coal worker’s pneumoconiosis and associated malignancy, yielding a high rate of false-positive results.[27]

Other Tests

On pulmonary function test results, persons with simple coal worker’s pneumoconiosis do not show significant impairment of lung function or a decrease ventilatory capacity. A slight decrease in the alveolar-arterial pressure gradient can be observed, along with a minor reduction in diffusing capacity (P category) and minimal hypoxemia observed in categories 2 and 3 (secondary to physiological shunting). If present, focal emphysema can result in a slight increase in compliance of the lung and an increase in residual volume.[18]

With regard to pulmonary function tests in persons with complicated coal worker’s pneumoconiosis, abnormalities are detected in stages B and C. Ventilatory capacity is reduced in proportion to the size of the conglomerate mass.[18] Diffusing capacity is also decreased. If the mass is large enough to destroy significant vascularity, pulmonary hypertension ensues. Additionally, hypoxemia develops earlier and more frequently in miners who smoke.

In their 4-year longitudinal study, Bourgkard et al[28] determined that "worsening x-ray findings and pneumoconiosis were more often observed in coal miners with micronodules on CT scans, wheezing, low values of maximal midexpiratory flow (MMEF) and forced expiratory flow (FEF25-75%), and high dust exposure at first examination." This finding suggests that the presence of micronodules on CT scans, altered scores on pulmonary function tests, and wheezing signify a worse 4-year prognosis and increased risk of progression to progressive massive fibrosis. CT scanning, therefore, might be a helpful screening tool to monitor progression to pneumoconiosis.

Vallyathan et al[29] found that "in miners without coal worker’s pneumoconiosis antioxidants, cytokine and growth factors are maintained at baseline levels present in control subjects." In contrast, miners with simple coal worker’s pneumoconiosis exhibit markedly elevated bronchoalveolar lavage fluid concentrations of antioxidants, proinflammatory cytokines, and mediators, which increase fibroblast proliferation. The inability of the lungs to maintain a balance between oxidant burden and antioxidant defenses may play a crucial role in the genesis of the disease. Increased levels of interleukins 1 and 6, tumor necrosis factor-alpha, transforming growth factor-beta1, transforming growth factor-beta2, alpha1-proteinase inhibitor, and fibronectin were found in the bronchoalveolar lavage fluid of miners with radiographically defined coal worker’s pneumoconiosis.

The 6-minute walk test (6MWT), a simple to perform test can be done as an ancillary test to help quantify possible impairment due to CWP in addition to chest imaging and pulmonary function testing.[30]



Medical Care

Treatment for both simple coal worker’s pneumoconiosis and complicated coal worker’s pneumoconiosis is symptomatic. Use oxygen as hypoxemia demands.

No evidence supports the hypothesis that removing the miner from the mining environment arrests the disease once progression to progressive massive fibrosis has begun. Therefore, serially monitoring the chest radiographs of miners in order to prevent the development of complicated coal worker’s pneumoconiosis is prudent. Advise workers who develop evidence of simple coal worker’s pneumoconiosis to transfer to jobs with low dust exposure.

Since smoking has an additive effect on coal worker’s pneumoconiosis, smoking cessation should be strongly recommended.

Caplan syndrome is treated similarly to progressive massive fibrosis. Oxygen and bronchodilators are administered as needed. The rheumatoid component is treated separately, per rheumatological protocol.

All patients should receive immunizations for influenzae and pneumococci.

One should strongly consider the possibility of superimposed mycobacterial infection in any patient with unexplained weight loss, chronic cough, fever, or night sweats.

A retrospective study noted good clinical outcomes after lung transplantation in a small group of patients with coal worker's pneumoconiosis. Removal of native lungs was not problematic, and no complications were found during the perioperative and postoperative periods. Furthermore, no pulmonary complications due to the native lung in patients who underwent single lung transplantation were reported.[31]


Consultation with a pulmonary medicine specialist is required.



Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Respiratory agents

Class Summary

Are used to treat hypoxemia and include medications such as bronchodilators



Further Inpatient Care

Once a baseline radiograph has been established, patients should have follow-up radiographs every 5 years—more often if symptoms worsen.


Coal worker’s pneumoconiosis is a completely preventable disease. As such, the Coal Mine Health and Safety Act of 1969 limited miner's exposure to respirable dust to less than 1 mg/m3. Miners are encouraged to have an initial chest radiograph on the date of hire and at 5-year intervals thereafter.


Closely monitor patients who have developed diffuse interstitial fibrosis for progression to peripheral squamous cell carcinoma (SCC) because diffuse interstitial fibrosis is a potent accelerator of this type of cancer. Katabami et al[32] determined that a "positive causal relationship between pneumoconiosis and peripheral-type SCCs of the lung" exists.


Prognosis is poor once the patient has been determined to have progressive massive fibrosis. Treatment is palliative.