Black Lung Disease

 

Black Lung Disease / Coal Miners Pneumoconiosis

                          PKGhatak,MD

Coal dust was thought to be inert particles, but now it is well established that inhaled coal dust is responsible for black lung disease. The accumulation of coal dust in the lungs and the tissue reactions to its presence produce black lung disease.

Coal dust of 4 mu size or smaller can easily reach the alveoli, bypassing the mucociliary defense of airways. The small dust particles penetrate the alveolar membrane and travel via lymphatics to the local lymph nodes. Macrophages in the interstitial tissue of the lung engulf coal particles, but macrophages can not digest coal. Coal laden macrophages release cytokines. The cytokines cause inflammatory reactions. The accumulated macrophages form a small tiny flat collection of cells called macules. The macules are found in the upper lobes of the lungs. Later the macules coalesce to form nodules due to fibrosis. The fibrous tissues distort bronchioles and result in focal emphysema. Initially, the fibrosis may be localized but becomes diffuse when coal dust exposure continues.

The incidence of back lung disease is increasing in the USA due primarily to the relaxation of laws and regulations, over the years, limiting coal dust exposure to miners. Because of the wider use of coal in developing countries for electricity generation, global incidence is on the rise.

This is a major setback for those physicians, attorneys, social workers, researchers and others who worked so hard for so many years in hostile environments, created and financially supported by the management/investors, at the cost of the health and welfare of miners and their families.

In the USA the incidence of Black Lung Disease among coal miners is -

In 1975 - 32 cases / 1000 miners were diagnosed with black lung disease.

In 1980 - 13 cases / 1000.

In 1990 - 25 /1000.

In 2000 - 3.7 / 1000.

In 2010 - 19 /1000.

In 2015 - 51 / 1000.

Types of Coal and Black Lung Disease.

Anthracite coal is hard coal, it has 84 % of carbon and contains less volatile compounds. It is also the worse coal for the development of black lung disease. In Pennsylvania coal towns -Scranton and Wilkes Barre area where coal mines were the main employers, the incidence of black lung was 10 % in miners exposed to coal dust over 25 years. Since anthracite coal is exhausted from this area the mining companies switched to Bituminous coal mining. Bituminous coal is abundant in West Virginia, Kentucky and Pennsylvania. Bituminous coal is soft, and it is less harmful to the lungs.

Cigarette smoking does not directly exacerbate fibrosis but chronic bronchitis and emphysema secondary to smoking worsen the coal miners' symptoms.

The inhalation of coal dust is usually accompanied by the inhalation of silica dust. The coal seams are embedded in between the layers of hard rocks and had to be blasted off. That generates a cloud of dust in the underground mines due to poor ventilation. The silica and coal dust in large quantities are inhaled. At present, the practice of blasting off the top of mountains to reach the coal seams is also causing huge dust clouds. That is not only inhaled by miners but also by their children and other family members.

  

               Black lung.

Clinical presentation.

In early cases, the patients may have no symptoms but chest X-rays show multiple small lung nodules in the upper lobes of the lungs. In more advanced cases the apical portion of the middle lobe is also involved and the shows become more profuse. As the disease advances further the fibrosis becomes more diffuse. And lower lobes also show changes. In addition, pulmonary emphysema and cavities of different sizes may be present. This stage of the illness is called Progressive pulmonary Fibrosis.

In patients with Rheumatoid arthritis subpleural cavitary nodules are seen. This is known as Caplan syndrome

Symptoms.

There are no specific symptoms of back lung disease. Cough, and sputum production containing black dust may be present. Shortness of breath, exhaustion and weight loss and limitation of physical activities are usual and at this stage patients are disabled.

Disability Determination.

Federal and State laws developed over years, and their criteria are well described in publications. The criteria were developed based on

    1. Type and size of shadows in the x-rays.

    2. The percentage of lung area affected in relation to the whole lung.

3. The degree of pulmonary function test abnormality

4. Under saturation of Oxygen detected during a standard exercise. A detailed description of this subject can be obtained in the State Coal miners disability acts.

Complications.

Pulmonary hypertension and right heart failure and cardiac arrhythmia eventually develop. The lung cavities invite bacteria. Mycobacterial tuberculosis infections often coexist. Mycobacteria tuberculosis and atypical mycobacterial infections produce accelerated fibrosis.

Treatment.

Once the black lung disease is well established, the reversal of the disease is not possible. Treatment is directed toward controlling the secondary complications. The standard therapy for pulmonary emphysema and chronic bronchitis, heart failure and respiratory insufficiency are undertaken depending on the cases.

Prognosis.

In the USA 1,500 die each year from black lung disease and 25,000 globally.

Nomenclature.

Pneumoconiosis is a Greek word meaning dust disease of the lung. Pneuma= wind, kons= dust.

Black lung disease is known as Anthracosis in Greek / medical literature. Anthraco means coal.

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