eMedicine Specialties > Pulmonology > Occupational Lung Diseases

Coal Worker's Pneumoconiosis

Author: Julia Richards van Zyl, MD, Staff Physician, Knoxville Inpatient Physicians, Department of Internal Medicine/Hospitalist, University of Tennessee Medical Center
Coauthor(s): Richard A Obenour, MD, Professor and Vice-Chair, Department of Medicine, University of Tennessee Graduate School of Medicine
Contributor Information and Disclosures

Updated: Nov 20, 2009

Introduction

Background

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 pulmonary massive fibrosis (PMF), depending on the extent of the disease. Also see Silicosis and Coal Worker Pneumoconiosis.

Pathophysiology

Anthracosis is the asymptomatic accumulation of coal pigment without 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 defense and processing of the dust becomes overwhelmed and, subsequently, overreactive.

Inhaled coal dust enters the terminal bronchioles, and the carbon pigment 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 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.

Depending on factors that are still not fully understood, the macules may arrest or may continue to enlarge and form nodules that produce pulmonary 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.

Pulmonary 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 pulmonary massive fibrosis, although the distribution in the lungs was different. Unlike lesions caused by pulmonary 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 necrotic collagen and coal dust 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 pulmonary 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.²

Research is currently underway to further understand the inciting factors in the inflammatory process. Boitelle et al³ 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 pulmonary 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.³

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 pulmonary massive fibrosis.⁴

In a 2005 study by Huang et al,⁵ 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 al⁵ found an increased prevalence of coal worker's pneumoconiosis and pulmonary 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 pulmonary 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,⁶

When mixed with water, pyrite produces hydrogen peroxide^7,8 and hydroxyl radicals.^9,10 These reactive agents have been shown to degrade yeast RNA, ribosomal RNA, and DNA.⁸ Cohn et al¹¹ 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%.¹¹ 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.

Frequency

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. 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 pulmonary massive fibrosis to be 2.5%.¹ Sixteen percent of coal miners in the United States can progress to interstitial fibrosis.¹²

A 2004 study¹³ 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 pulmonary massive fibrosis in Kentucky and Virginia.¹⁴ This has prompted studies researching the caustic content of coal in isolated mines, which may be contributing to a regional variation in the progression of lung diseases.^15,16

International

In Great Britain, most coal is mined in Wales. As in the United States, 16% of miners can progress to interstitial fibrosis.¹²

Mortality/Morbidity

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.²

A recent 41-month retrospective study performed by Shen et al¹⁷ 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 pulmonary 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.

Race

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

Sex

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

Age

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.

Clinical

History

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 determine exposure to respirable coal dust. The length of time spent underground and the age at first exposure are important in determining the risk of progressing to pulmonary 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 pulmonary massive fibrosis, suggest changing to a job within the mine that requires less exposure to respirable dust.

Physical

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.¹² 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.¹²

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.

Causes

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 follows² :
  • 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 exposure¹ :
  • 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.

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