Coal Worker’s Pneumoconiosis

Coal Worker’s Pneumoconiosis

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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.

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.

Morgan WK, Seaton A. Occupational Lung Diseases. Philadelphia, Pa: WB Saunders; 1975. 149-210.

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Farhan J Khan, MD Fellow in Pulmonary Disease, University of Tennessee Medical Center

Farhan J Khan, MD is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women’s Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba Faculty of Medicine; Site Director, Respiratory Medicine, St Boniface General Hospital, Canada

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, World Medical Association

Disclosure: Nothing to disclose.

Amit Dhingra, MD Fellow in Pulmonary Disease, University of Tennessee Medical Center at Knoxville

Disclosure: Nothing to disclose.

Richard A Obenour, MD (Retired) Professor and Vice-Chair, Department of Medicine, University of Tennessee Graduate School of Medicine

Disclosure: Nothing to disclose.

Julia Richards van Zyl, MD Staff Physician, Knoxville Inpatient Physicians, Department of Internal Medicine/Hospitalist, University of Tennessee Medical Center

Julia E Richards is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine and American Medical Association

Disclosure: Nothing to disclose.

Coal Worker’s Pneumoconiosis

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