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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.

Gross specimen demonstrating simple coal worker's pneumoconiosis.

Gross specimen demonstrating progressive massive fibrosis in a coal miner.

PathophysiologyAnthracosis 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]

Source 2:Coal worker’s pneumoconiosis (CWP) also known as (black lung

disease) is classified as an industrial disease that is the result of breathing in dust from coal, graphite or manmade carbon over a period of years. The dust is inhaled into the body and resides in the lungs where it progressively builds up over time if the individual is subject to prolonged exposure because the lungs are unable to excrete the dust from the lungs. This can lead to inflammation, fibrosis and in the worst cases, necrosis. The condition is associated with the mining (coal) industry and in the United States alone approximately $44 billion in benefits has been distributed by the government to the afflicted miners or their widows.

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Understanding PneumoconiosisWhat is Pneumoconiosis?

Pneumoconiosis, also known as Black Lung Disease, is an occupational lung disease caused by inhaling coal dust. There are two types of pneumoconiosis— simple, known as coal workers' pneumoconiosis (CWP) and complicated, known as progressive massive fibrosis (PMF). Pneumoconiosis is a type of interstitial lung disease. In this type of disease: the lung is damaged (in this case, by coal dust); the walls of the air sacs are inflamed; and the lung stiffens from scarring of the tissue between the air sacs.

There is no known treatment for pneumoconiosis, but doctors treat the symptoms and complications of the disease.

Who Gets Pneumoconiosis?

People who work in jobs where they are exposed to coal dust get pneumoconiosis. This includes working in a coal mine or loading coal for storage, working in a graphite mine or mill, and manufacturing carbon electrodes and carbon black. Carbon electrodes are used in some large furnaces, and carbon black is used in tires and other rubber goods, as well as many other products.

What does Pneumoconiosis do to Your Body?

People who inhale coal dust may not have any symptoms for many years. Over time, however, as the coal dust has settled deep in the lung, it eventually causes the lung to harden. As the lung hardens, breathing becomes more difficult and gets worse over time.

Possible complications of pneumoconiosis include:

Cor pulmonale (failure of the right side of the heart)

Lung cancer

Pulmonary tuberculosis

Respiratory failureHow Serious is Pneumoconiosis?

Pneumoconiosis is not treatable or curable. How severe each person's disease becomes is the result of the conditions of his or her work during exposure to coal dust.  

Symptoms, Diagnosis and TreatmentsWhat are the Symptoms of Pneumoconiosis?

Chronic cough

Shortness of breathHow is Pneumoconiosis Diagnosed?

Chest X-rays

Occupational history

Pulmonary function testsHow is Pneumoconiosis Treated?

There is no known treatment for pneumoconiosis. Doctors treat the symptoms and complications of the disease to lessen breathing difficulties.  

Preventing PneumoconiosisCan Pneumoconiosis be Prevented?

The only way to prevent pneumoconiosis is by not inhaling coal dust.

The Occupational Safety & Health Administration (OSHA) (part of the U.S. Department of Labor) sets standards for workers. Those standards include protective requirements for anyone who works around coal, graphite, or man-made carbon. Workers should wear a mask to help prevent pneumoconiosis and follow other personal safety procedures. And companies are required by law to enforce maximum dust levels that surround workers.

If you are exposed to coal dust follow these procedures to help protect yourself:  

If coal dust contacts the skin, workers should wash the affected areas with soap and water.

If your clothing is contaminated with coal dust, remove it immediately. Your employer should have a place and a system for the safe removal of the dust from your clothing. People who launder the clothes should also know about the dangers of coal dust so that they can protect themselves.

If you handle coal dust, thoroughly wash your hands, forearms, and face with soap and water before eating, using toilet facilities, applying cosmetics, taking medication, using tobacco products, etc.

Do not eat, drink, use tobacco products, apply cosmetics, or take medication in areas where coal dust is handled, processed, or stored.