Coal Workers' Pneumoconiosis (Black Lung Disease)

Updated: Dec 19, 2019
Author: Fatima J Wong, DO; Chief Editor: Zab Mosenifar, MD, FACP, FCCP 


Practice Essentials

Worldwide, coal remains one of the largest sources for energy, contributing to approximately one fourth of the global energy supply and over one third of the fuel that is used to produce electricity.[1]  It has been projected that coal will be used to produce approximately 40% of the electricity worldwide and 34% in the United States until 2040.[2]

Coal dust particles are created during the process of coal production. Excessive exposures to coal dust can overwhelm the lungs’ mechanism to clear these particulates, causing them to accumulate over time.[3]  Because of modern technological advancements, significant volumes of coal can be mined per shift.[4]  Through constant exposure and inhalation of coal dust particles, coal miners are at an increased risk for developing respiratory illnesses categorized as coal mine dust lung disease (CMDLD). These pulmonary conditions can range from airflow limitation or obstruction to causing interstitial lung diseases.

When these particles are introduced into the respiratory tract, they can cause a reactive process in the lung tissue known as pneumoconiosis.[5]  Coal workers’ pneumoconiosis (CWP) is also known as “black lung disease,” one of the most common conditions that belong in the category of CMDLD, along with silicosis, mixed-dust pneumoconiosis with coexistent silica exposure, chronic bronchitis, emphysema, and dust-related diffuse fibrosis.[1, 4]

CWP is divided into two categories: simple CWP (SCWP) and complicated CWP (CCWP), or progressive massive fibrosis (PMF),[3, 4]  depending on the extent and severity of the disease. Also see Silicosis and Coal Worker Pneumoconiosis. Note the images below. 

Coal workers' pneumoconiosis (black lung disease). Coal workers' pneumoconiosis (black lung disease). Gross specimen demonstrating simple coal worker's pneumoconiosis.
Coal workers' pneumoconiosis (black lung disease). Coal workers' pneumoconiosis (black lung disease). Gross specimen demonstrating progressive massive fibrosis in a coal miner.

No cure for CWP currently exists. Treatment for both SCWP and CCWP is symptomatic, and prevention is the key to management of this condition. Lung transplantation has been used in the setting of end-stage pulmonary disease.


Anthracosis has previously been used synonymously for coal workers’ pneumoconiosis (CWP) (black lung disease) or for describing the process of detecting a substantial amount of pulmonary carbon deposits on autopsies secondary to recurrent exposure to several factors, such as air pollution, smoke inhalation, or coal dust fragments.[6, 7]  Dust particles as small as five microns can enter the lungs and infiltrate the peripheral bronchioles and alveoli. The presence of these particles can obstruct the airways and lead to primary lesions composed of coal dust, macrophages, and fibroblasts.[5]  Accumulation of these particulate matter in the lung tissues can be the stimulus to the development of several pathologic conditions described as harmless pulmonary anthracosis, emphysema, and/or lung fibrosis.[4]

The exact mechanism for how pneumoconiosis develops is still unclear; however, several theories have been proposed to help explain its pathogenesis, including oxidative stress theory, immunology, cytokine network theory, and single nucleotide polymorphisms.[8]  Mossman described that lung tissue as a common organ affected by inhaled pollutants such as metals, mineral dust, particulates, and reactive gases.[9]  Vanhee and coworkers reported three phenomena that occur after the pulmonary tissues are exposed to coal dust: (1) Inflammatory cells accumulate and activate inflammatory cells in the lower respiratory tract; (2) fibroblast proliferation; and (3) augmented formation of extracellular matrix components.[10]  It has also been suggested that macrophages play a significant role in the development of pneumoconiosis.[8, 9, 10, 11, 12, 13]  Zhang and colleagues indicated that the presence of dust causes the alveolar macrophages to induce an immune response that may ultimately lead to fibrosis.[8]  

The oxidative stress theory is one of the possible mechanisms to help describe the pathogenesis of pneumoconiosis. This theory suggests that exposure to dust particulates in the lung tissues provokes an inflammatory response, which then leads to the formation of reactive oxygen and nitrogen species (ROS/RNS) by alveolar and interstitial macrophages, along with polymorphonuclear cells.[9]  Mossman describes alveolar and interstitial macrophages as playing a role in oxidative stress through an oxidative burst response that produces ROS/RNS. However, other cells, such as epithelial cells, can also generate a similar reaction.[9]  Therefore, the reactive process by macrophages and epithelial cells may be the stimulus for an immune response and functional changes that occur in surrounding cells, including fibroblasts, which can lead to the development of fibrosis. In addition, Pinho and coworkers described the production of ROS leading to other changes in the lungs, such as inactivation of antiproteases, disturbances in the basal membrane, and injury to the alveolar cells.[11]

 Another possible mechanism to explain the occurrence of pneumoconiosis is the production of cytokines. Besides the production of ROS,[10, 12, 13, 14]  macrophages are also thought to release mediators (eicosanoid metabolites, destructive proteolytic enzymes, and inflammatory growth and differentiation factors),[10]  and cytokines have been implicated in the development of pneumoconiosis. These cytokines have been described as signaling proteins that influence inflammatory and fibrotic reactions. Several proinflammatory cytokines have been identified with the development of this condition including interleukin (IL)-6, tumor necrosis factor-α (TNF-α), and IL-1β.[14]

An investigative study by Ulker and colleagues evaluated the serum and bronchoalveolar lavage (BAL) inflammatory cytokine levels in a total of 85 subjects with simple pneumoconiosis (SP) and progressive massive fibrosis (PMF).[12]  Active and retired miners served as control subjects. The study results demonstrated that subjects with SP and PMF had higher levels of IL-1β, IL-6, and TNF-α in serum and BAL.[12]

Single nucleotide polymorphisms (SNPs) are another suggested mechanism for the pathogenesis of CWP, entailing the notion that certain individuals may be at increased risk for developing CWP because of their genetics. There have been discussions regarding the concept of allelic variations with SNPs being more frequently identified, and that there are certain functional variants that may be conducive to potentiating an increased risk for certain disease states.[15, 16]  Previous studies investigating an association between gene polymorphisms involving TNFα and CWP in Belgian and Japanese coal miners demonstrated that those with CWP had a higher rate of TNFα-308 variant compared to those without the lung disease.[16]  In a case control study, Wang and coworkers evaluated the association between three functional SNPs in the SELE gene (T1880C/rs5335, T1559C/rs5368, and A16089G/rs4786) with the risk for developing CWP in the Han Chinese population.[15] Their results demonstrated that there may be an association between SELE rs5368 and an increased risk for CWP.[15]


The distinguishing feature of coal workers’ pneumoconiosis (CWP) (black lung disease) is the primary lesion, coal macule, characterized as a small (≤ 4 mm) pigmented lesion “...of dust particles, collagen, fibrin, and dust laden macrophages”[17]  located around the respiratory bronchioles.[18]  Reticulin fibers develop in the vicinity of the coal macule, leading to airspace dilatation and giving the appearance of focal emphysema, considered a form of centriacinar emphysema. With these focal emphysema, bullae do not project from the lung surface and are thought to be due to a mechanical disturbance within the secondary lobules of the lung.[19]  

In contrast, coal nodules are lesions that contain dust larger than those found in macules ( >4 mm in size), with increased fibrosis and collagen arranged in a random arrangement. Unlike coal macules, these nodules are not restricted to the bronchioles but may be found throughout the lung parenchyma, including subpleural sites in the interlobular septa.[20]  Coal nodules have a tendency to develop when there has been exposure to coal dust containing silica.[18]

Once the process of fibrosis has developed with pneumoconiosis, it is deemed irreversible even if exposure to the offending agent has ceased. The causes of these fibrotic changes remain unknown; however, one hypothesis is that persistent damage to the alveolar epithelial cells along with increased extracellular matrix are linked to the development of fibrosis. An investigative study by Zhang and coworkers on rats demonstrated that DNA methylation (defined as epigenetic modification of DNA) affecting gene expression may be a factor in pulmonary fibrosis.[8] They also observed that treatment with a DNA methylation inhibitor, 5-aza-dC, decreases the fibrotic changes. 

As mentioned previously, CWP is divided into two categories: simple CWP (SCWP) and complicated CWP (CCWP), or progressive massive fibrosis (PMF).[3, 4] With SCWP, the coal macules are surrounded by fibrosis smaller than 10 mm, often located in the upper lung regions, with a latency period of at least 10 years.[1, 4, 5, 14]  In addition, SCWP tends to affect older miners with fewer, less severe symptoms, such as dyspnea or cough; individuals with SCWP may not have any symptoms at all. 

The early development of SCWP is the most important risk factor for the development of complicated pneumoconiosis. which is closely linked to the intensity and duration of respirable dust exposure. PMF is distinguished from CWP by the presence of scars in the lungs larger than 10 mm. Lesions with PMF are often located in the “posterior segments of the upper lobes or apical segments of the lobes” and frequently bilateral.[18]  Younger miners have been observed to have increased diagnoses of PMF in relatively recent years.[3] Symptoms are usually more severe than those of SCWP such as black sputum, chronic cough, and frequent pneumonia.[5]

Several factors have been identified that raise an individual’s risk for developing CWP, such as the concentration of respirable coal dust, the size and composition of the dust particles, quartz or free silica content, as well as the duration of exposure, individual’s age, the work environment, and work practices.[21]  However, the composition of respirable dust, coal rank, and duration of exposure are deemed the most significant factors. Respirable dust has been defined as “the fraction of airborne particulates that can be deposited anywhere in the lung gas-exchange regions.”[22]  Coal rank is dependent on the age and carbon content of coal, and there appears to be a direct relationship between an increased risk for CWP and higher carbon content in the coal.[21]

Huang and colleagues found a correlation between bioavailable iron (BAI), pyrite concentration, and the regional progression of lung disease.[23]  BAI is iron that dissolves in 10 mmol/L of phosphate solution at a pH 4.5, which mimics the interior of lysosomes. They observed an increased prevalence of CWP and PMF at Pennsylvania mines, where BAI values are higher, compared to Utah mines, where BAI levels are lower.[23]  The investigators also demonstrated that pyrite-containing coal contributed to the higher prevalence of progression to CWP and PMF in Pennsylvania. In addition, McCunney and coworkers have suggested that iron, not quartz, is the active agent in coal responsible for CWP.[24]

When mixed with water, pyrite produces hydrogen peroxide[25, 26]  and hydroxyl radicals.[27, 28]  These reactive agents have been shown to degrade yeast RNA, ribosomal RNA, and DNA.[26] Cohn and colleagues 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.[29]  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%.[29]  These findings suggest that personnel at individual mines can measure the amount of sulfur in the 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 coal with increased BAI.

Exposure to coal mine dust is determined by the mining methods used as well as a miner’s job duties. It has been widely accepted that miners who work underground have higher exposure levels compared to surface coal miners. In addition, transportation of coal out of the mines can cause further dispersal of dust. For surface miners, considerations must take into account whether or not miners are exposed to dust in open or enclosed cabs, as well as the amount of time spent outside cutting, drilling or blasting rock.[2, 4]


In 2017, the three top coal-producing countries were China, the United States, and Australia.[5] The prevalence of coal workers’ pneumoconiosis (CWP) (black lung disease) was higher in China compared to the other two countries because of China's earlier focus on occupational health. There was an average of 21,719 new cases of occupational diseases reported each year in the 14-year period between 2003 and 2016, with 44.83% of these cases being lung diseases due to coal dust in China. In the United States, there were 37,965 cases of CWP reported from 1968 to 2015; approximately 75,000 deaths of coal miners were reported to either be the underlying or contributing cause. Australia has the lowest prevalence of CWP among these three countries, with over 1000-related deaths in Australia between 1979 to 2002.[5]

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. Following decades of decline, the prevalence of CWP among active US underground coal miners has been increasing since the late 1990s.[30, 31, 32]  In addition, an increase in the progression to CWP and progressive massive fibrosis (PMF) has been seen in Kentucky and Virginia.[33, 34]

In a retrospective (2000-2009) chart review of 138 West Virginian coal miners, Wade and colleagues found an increased number of cases of rapidly progressive pneumoconiosis and PMF in young coal miners after 2001, resulting in increased morbidity and mortality.[3]  These coal miners developed PMF 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 radiographic finding. This report asserts the need for close surveillance for this disease and a need for improvements in preventive measures.[3, 14]  

The changing epidemiologic patterns of CWP in the Appalachian region of the United States has led to an increased exposure to respirable silica, as suggested by radiographic abnormalities consistent with silicosis.[3, 35]  

The onset of CWP does not occur at any specific age but depends on the length and severity of exposure to coal dust and, thus,s on when the coal miner began working in the mines and the specific nature of their exposure.


Prognosis is poor once the patient with coal workers’ pneumoconiosis (CWP) (black lung disease) has been determined to have progressive massive fibrosis (PMF). Treatment is mainly palliative. 

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 with greater exposure to respirable dust. Over the past two decades, there has been a rapidly progressive form of pneumoconiosis observed in some US coal miners, which is associated with significant respiratory compromise and premature death.[20] This severe lung disease is seen in younger miners.[20]

In a 41-month retrospective study (1998-2002), Shen and coworkers described a prognostic relationship between CWP and the first episode of respiratory failure requiring mechanical ventilation.[36] The investigators found that radiographic evidence of PMF was not associated with increased intensive care unit (ICU) mortality. No mortality difference was delineated between patients with simple CWP (SCWP) and those with complicated CWP (CCWP). The following three independent variables predicted outcomes[36] :

  • Hypercapnia (partial pressure of carbon dioxide [PaCO2] >45 mmHg) at the time of intubation exhibited a protective effect, suggesting a less severe acute illness as the cause of the respiratory failure relative to 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. 

  • A ratio of partial pressure of oxygen (PaO2) to the fraction of inspired oxygen in the air (FiO2) of less than 200 mmHg at the time of intubation was associated with an increased mortality. 

There was a 40% ICU mortality for patients with CWP with their first episode of respiratory failure requiring mechanical ventilation, and a 43% in-hospital mortality.[36]


Complications of CWP include the following:

  • Airflow obstruction 
  • Chronic bronchitis 
  • Respiratory tract infections 
  • Respiratory failure 
  • Hypoxemia 
  • Cor pulmonale 
  • Arrhythmias 
  • Pneumothorax 

Complications such as airflow obstruction, respiratory tract infection, respiratory failure/ hypoxemia, cor pulmonale, arrhythmias, and pneumothorax may occur. If there has been significant crystalline silica exposure, Mycobacterial infection is a possible complication. Diffuse interstitial fibrosis is a potent accelerator of peripheral squamous cell carcinoma (SCC).[37]  

First described in 1953 in Welsh miners, Caplan syndrome is a condition with combined features of rheumatoid arthritis (RA) and pneumoconiosis. There are several well-defined, rounded pulmonary nodules often located in the lung periphery of patients with RA and concurrent inorganic dust exposure. These nodules may eventually cavitate or calcify.[1]  The pathogenesis and a causal relationship between pneumoconiosis, RA, and pulmonary changes in Caplan syndrome are still unclear. Questions remain regarding whether coal dust exposure or the presence of an autoimmune disease predispose the other condition to occur or develop. For the majority of patients, the nodules with Caplan syndrome are asymptomatic do not cause any significant changes to pulmonary function testing. Approximately 70% of affected patients will have a positive rheumatoid factor (RF).[38]




Taking a detailed history is perhaps the most important step in evaluating patients for coal workers' pneumoconiosis (CWP) (black lung disease). Ask patients what their specific job entails to estimate dust levels. The length of time spent underground and the age at first exposure are important in determining the risk of progression to progressive massive fibrosis (PMF). 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 CWP is palliative and preventive. Many miners are not receptive to recommendations to changing their career. Thus, if their respiratory status worsens, or if they are at risk for progression to PMF, it may be helpful to suggest they change to a job within the mine that requires less exposure to respirable dust.

Physical Examination

Miners with simple coal workers' pneumoconiosis (SCWP) (black lung disease) 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. Complicated CWP (CCWP) produces cough, dyspnea, and lung function impairment. In advanced disease states, cor pulmonale may be found, with an associated right ventricular heave, large a waves, hepatomegaly, and peripheral edema.

CWP results from mechanical and architectural destruction of the lungs. Fever, night sweats, and other constitutional symptoms suggest a secondary infective process.



Diagnostic Considerations

In patients with suspected coal workers’ pneumoconiosis (CWP) (black lung disease), it is important to rule out other causes for lung disease, especially if there has been less than 10 years of exposure to coal mine dust. The differential diagnosis includes mycobacterial infection, silica-associated granulomatosis with polyangiitis, and other interstitial pneumonias.[1]

Differential Diagnoses



Imaging Studies


Chest radiography (CXR) remains the criterion standard for diagnosis of coal workers’ pneumoconiosis (CWP) (black lung disease) on the basis of the International Labour Organization (ILO) classification that describes the abnormalities and ranges of severity.[39, 40] 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 which describes the profusion or concentration of small opacities in affected lung zones.[41] The chest radiographs are interpreted by at least two physicians who have received training or exhibited the ability to utilize the ILO pneumoconiosis classification system through the B Reader Certification Program, which is administered through the National Institute for Occupational Safety and Health (NIOSH).[42]

Opacities for simple CWP (SCWP) fall into either one of two categories based on size and shape.[41] Small opacities are divided into two types, rounded or irregular. The small, rounded opacities fall into three different size ranges and denoted as below:

  • p: Up to 1.5 mm in diameter

  • q: 1.5 to 3 mm in diameter

  • r: 3 to 10 mm in diameter

Alternatively, irregular opacities are also distinguished based on width, as follows:

  • s: Up to 1.5 mm

  • t: 1.5 to 3 mm

  • u: 3 to 10 mm

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/p>

Any nodular opacity larger than 1 cm in diameter on radiographs is considered complicated CWP (CCWP) or progressive massive fibrosis (PMF). Subcategories for this group according to the ILO classification are as follows[41] :

  • A: One large opacity with the longest dimension up to 50 mm, or several large opacities with the sum of their longest dimensions not exceeding about 50 mm

  • B: One large opacity having the longest dimension exceeding 50 mm but not exceeding the equivalent area of the RUZ, or several large opacities with the sum of their longest dimensions exceeding 50 mm but not exceeding the equivalent area of the RUZ

  • C: One large opacity which exceeds the equivalent area of the RUZ, or several large opacities which, when combined, exceed the equivalent area of the RUZ

Other imaging studies

The application of computed tomography (CT) scanning for the diagnosis of pneumoconiosis has received increasing attention and achieved a certain effectiveness as CXRs are not considered sensitive in early pneumoconiosis because of inter- and intrareader variabilities.[43]

In a study thatcompared findings on CXR and high-resolution CT (HRCT) scans between normal coal miners and those with early low-grade CWP, Savranlar et al demonstrated a high-discordance rate between the two imaging modalities,leading them to the conclusion that HRCT is more sensitive than CXR in evaluating coal workers with normal and early CWP.[43]

There have been several classification systems with attempts to use CT scans as a diagnostic modality for CWP. One such classification system is the Hosoda-Shida Classification,[44] which has been used mostly in Japan. This CT-based classification system displayed acceptable interreader agreement and compatibility with the ILO system. However, a drawback to this system was that the study participants included in the study were only those at risk for silicosis.[44]

Currently, both traditional radiography and CT scanning rely mainly on the lesion morphology and material density for diagnostic confirmation. Large shadows make distinguishing between pneumoconiosis and lung cancer tumors difficult. Magnetic resonance imaging (MRI) may improve the specificity and accuracy of diagnosis and reduce the false-positive rate according to a retrospective study of PMF in 25 CWP patients.[45]

In a small case series that evaluated the utility of positron emission tomography (PET) scanning with F-18-fluorodeoxyglucose (18F-FDG) in patients with CWP and suspected malignancy, Reichert and Bensadoun showed that even in patients with PMF without malignancy, the observed nodules were hypermetabolic on PET scan.[46] Therefore, the use of PET scans proved to be of limited value in the evaluation of CWP and associated malignancy, yielding a high rate of false-positive results.

Other Tests

On pulmonary function testing, persons with simple coal workers' pneumoconiosis (CWP) (SCWP) (black lung disease) do not always show significant impairment of lung function or decreased 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 noted in the Internation Labour Office (ILO) classification categories 2 and 3 (secondary to physiologic shunting). If present, focal emphysema can result in a slight increase in lung compliance and an increase in residual volume. 

However, in persons with complicated CWP (CCWP), abnormalities are detected in stages B and C. Ventilatory capacity is reduced in proportion to the size of the conglomerate mass. 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 determined that "worsening x-ray findings and pneumoconiosis were more often observed in coal miners with micronodules on CT [computed tomography] scans wheezing, low values of maximal midexpiratory flow (MMEF) and forced expiratory flow (FEF 25%-75%), and high dust exposure at first examination." These findings suggest 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 (PMF). CT scanning, therefore, may be a helpful screening tool to monitor progression to pneumoconiosis. 

Vallyathan et al found that "in miners without coal worker’s pneumoconiosis antioxidants, cytokine and growth factors are maintained at baseline levels present in control subjects."[47] In contrast, miners with SCWP exhibit markedly elevated bronchoalveolar lavage (BAL) 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 disease genesis. Increased levels of interleukins 1 and 6, tumor necrosis factor-alpha, transforming growth factors-beta1 and 2, alpha1-proteinase inhibitor, and fibronectin were found in the BAL fluid of miners with radiographically defined CWP. 

The simple 6-minute walk test (6MWT) can be performed as an ancillary test to help quantify possible impairment due to CWP. It can be used in addition to chest imaging and pulmonary function testing.[48]



Biopsy is not typically needed for the diagnosis of coal workers’ pneumoconiosis (CWP) (black lung disease). Bilateral symmetrical, elongated mass lesions in advanced CWP are rarely malignant. If there is concern about malignancy based on clinical symptoms or in the setting of a unilateral large opacity, a biopsy may be required to resolve diagnostic uncertainty.[1]



Approach Considerations

There is no cure for coal workers’ pneumoconiosis (CWP) (black lung disease). Treatment for both simple (SCWP) and complicated CWP (CCWP) is symptomatic. Supportive care also includes good general respiratory management. Patients should receive influenza and pneumococcal vaccinations. Encourage smoking cessation.

Medical Care

Supportive therapies include bronchodilators for airflow limitation, antibiotics for respiratory infections, and supplemental oxygen to manage hypoxemia.

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

The possibility of superimposed mycobacterial infection should be considered in any patient with unexplained weight loss, chronic cough, fever, or night sweats.


Surgical Care

Lung transplantation has increased as a treatment modality for individuals with end-stage coal workers’ pneumoconiosis (CWP) (black lung disease), with an estimated posttransplant survival of up to 4 years.[49]

A retrospective study (1999-2009) noted good clinical outcomes after lung transplantation in a small group of patients with CWP.[50] 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.[50]  In contrast, other investigators observed lower rates of survivability compared with transplants for chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and silicosis.[51]

Nevertheless, given the lack of other options for miners with CWP and end-stage lung disease, those caring for such miners who are appropriate candidates for transplantation should consider referring them for transplant evaluation.


Coal workers' pneumoconiosis (CWP) (black lung disease) is a completely preventable disease, with the key and primary goal of minimizing exposure to dust particles.[14]  Consequently, the Coal Mine Health and Safety Act of 1969 limited miners' exposure to respirable dust to below 1 mg/m3.[1]  In addition, undeground coal miners who have been diagnosed with pneumoconiosis have the legal right to request for transfer to a new position with lower dust job exposure, if available. Miners are encouraged to have an initial chest radiograph on the date of hire and at 5-year intervals thereafter.

Long-Term Monitoring

No evidence supports the hypothesis that removing a miner with coal workers’ pneumoconiosis (CWP) (black lung disease) from the mining environment arrests the disease once progression to progressive massive fibrosis (PMF) has begun.[52]  Therefore, serially monitoring the chest radiographs of miners to prevent the development of complicated CWP (CCWP) is prudent. Once a baseline radiograph has been established, patients should have follow-up radiographs every 5 years—more often if symptoms worsen.

Advise workers who develop evidence of simple CWP (SCWP) to transfer to jobs with low dust exposure. Also, miners are encouraged to have repeat spirometry every 1-3 years to monitor any decline with their pulmonary function.[14]

Encourage smoking cessation to miners who smoke. 




Class Summary

These agents decrease muscle tone in both the small and large airways of the lungs, thereby increasing ventilation. This category includes beta-adrenergic agents, methylxanthines, and anticholinergics.

Albuterol (AccuNeb, ProAir Digihaler, Proair HFA)

Albuterol is a beta2 agonist that relaxes bronchial smooth muscle by action on beta2 receptors, with little effect on cardiac muscle contractility. Most patients (even those who have no measurable increase in expiratory flow) benefit from treatment. Inhaled beta-agonists initially are prescribed as needed. Frequency may be increased. Institute a regular schedule in patients on anticholinergic drugs who remain symptomatic. Albuterol is available as liquid for nebulizer, MDIs, and dry-powder inhalers.


Metaproterenol relaxes bronchial smooth muscle by action on beta2 receptors, with little effect on cardiac muscle contractility. Most patients (even those who have no measurable increase in expiratory flow) benefit from treatment. Inhaled beta-agonists initially are prescribed as needed. Frequency may be increased. Institute a regular schedule in patients on anticholinergic drugs who remain symptomatic. Metaproterenol is available as liquid for nebulizer, MDIs, and dry-powder inhalers.

Levalbuterol (Xopenex, Xopenex HFA)

Levalbuterol is used for the treatment or prevention of bronchospasm. It is a selective beta2-agonist agent. Albuterol is a racemic mixture, while levalbuterol contains only the active R-enantiomer of albuterol. The S-enantiomer does not bind to beta2-receptors, but it may be responsible for some adverse effects of racemic albuterol, including bronchial hyperreactivity and reduced pulmonary function during prolonged use.

Ipratropium (Atrovent, Atrovent HFA)

Ipratropium is chemically related to atropine. It has antisecretory properties, and, when applied locally, it inhibits secretions from serous and seromucous glands lining the nasal mucosa. Ipratropium is used on a fixed schedule with a beta-agonist.

Indacaterol, inhaled (Arcapta Neohaler)

Indacaterol is a long-acting beta2-agonist (LABA) indicated for long-term, once-daily maintenance bronchodilator treatment of airflow obstruction in patients with chronic obstructive pulmonary disease (COPD), including chronic bronchitis and/or emphysema. LABAs act locally in the lungs as bronchodilators. Indacaterol stimulates intracellular adenyl cyclase, causing conversion of ATP to cyclic AMP; increased cyclic AMP levels cause relaxation of bronchial smooth muscle. It is not for use as initial therapy in patients with acute deteriorating COPD.

Tiotropium (Spiriva HandiHaler, Spiriva Respimat)

Tiotropium is a quaternary ammonium compound. It elicits anticholinergic/antimuscarinic effects with inhibitory effects on M3 receptors on airway smooth muscles, leading to bronchodilation. It is available as a capsule dosage form containing a dry powder for oral inhalation via the HandiHaler inhalation device. It helps COPD patients by dilating narrowed airways and keeping them open for 24 hours.

Aclidinium (Tudorza Pressair)

Aclidinium is an M1-M3 muscarinic agonist (LAMA). It inhibits M3 receptors, leading to smooth muscle relaxation of bronchi; this leads to subsequent bronchodilation. Prevention of acetylcholine-induced bronchoconstriction effects were dose-dependent in in vitro and in vivo studies and lasted longer than 24 hours.