Coal Worker's Pneumoconiosis
Coal worker's pneumoconiosis is a progressive, nodular pulmonary disease. It's also known as black lung, coal miner's disease, miner's asthma, anthracosis, and anthracosilicosis. The disease occurs in two forms: simple and complicated. With the simple form, the patient has characteristically limited lung capacity. In this patient, complicated coal worker's pneumoconiosis (also known as progressive massive fibrosis) may develop. In the complicated form, fibrous tissue masses form in the lungs.
A person's risk for coal worker's pneumoconiosis depends on various factors, including how long he has been exposed to coal dust (usually at least 15 years), the intensity of his exposure (dust count and size of inhaled particles), his proximity to the mine site, the silica content of the coal (anthracite has the highest silica content), and his susceptibility. The highest incidence of this disease is among anthracite miners in the eastern United States.
Causes and pathophysiology
Inhalation and prolonged retention of respirable coal dust particles (less than 5 microns wide) cause coal worker's pneumoconiosis. In the simple form, macules (coal dust -laden macrophages) form around terminal and respiratory bronchioles and are surrounded by a halo of dilated alveoli. At the same time, supporting tissues atrophy and harden, causing permanent small-airway dilation (focal emphysema). Simple coal worker's pneumoconiosis may progress to the complicated form - most likely if the disease begins after a relatively short exposure.
Complicated coal worker's pneumonoconiosis may involve one or both lungs. Fibrous tissue masses enlarge and coalesce, grossly distorting pulmonary structures as the disease progressively destroys vessels, alveoli, and airways.
Signs and Symptoms
CWP does not usually cause symptoms. Most chronic pulmonary symptoms in coal miners are caused by other conditions, such as industrial bronchitis from coal dust or coincident emphysema from smoking. Cough can be chronic and problematic in patients even after they leave the workplace, even in those who do not smoke.
PMF causes progressive dyspnea. Black sputum (melanoptysis) is rare and is caused by rupture of PMF lesions into the airways. PMF often progresses to pulmonary hypertension with right ventricular and respiratory failure.
Chest X-rays in simple coal worker's pneumonoconiosis show small opacities (less than 10 mm in diameter). These opacities may inhabit all lung zones but appear more prominent in the upper lung zones. In complicated coal worker's pneumoconiosis, X-rays may show one or more large opacities (1 to 5 cm in diameter). Some may exhibit cavitation.
Pulmonary function studies indicate a vital capacity that is normal in simple coal worker's pneumoconiosis but decreased in the complicated form; decreased forced expiratory volume in 1 second (FEV1 ) in the complicated form; and a normal ratio of FEV1 to forced vital capacity. The ratio of residual volume to total lung capacity is normal in the simple form but decreased in the complicated form. Diffusing capacity for carbon monoxide - significantly below normal in the complicated form - reflects alveolar septal destruction and pulmonary capillary obliteration.
Arterial blood gas analysis typically shows normal partial pressure of arterial oxygen (Pao2) in simple coal worker's pneumoconiosis but decreased Pao2 in complicated disease. Partial pressure of arterial carbon dioxide is normal in the simple form (possibly decreasing in hyperventilation) but may increase if the patient is hypoxic and has severely impaired alveolar ventilation.
The goal of treatment is to relieve respiratory symptoms, manage hypoxia and cor pulmonale, and avoid respiratory tract irritants and infections. Treatment also includes observation for developing tuberculosis.
Respiratory signs and symptoms may be relieved by bronchodilator therapy with theophylline or aminophylline (if bronchospasm is reversible), oral or inhaled sympathomimetics (such as metaproterenol), corticosteroids (such as oral prednisone or aerosolized beclomethasone), or inhalable cromolyn sodium. Chest physiotherapy may be used to mobilize and remove secretions.
Other measures include increased fluid intake (at least 3 L [3.2 qt] daily) and respiratory therapy with aerosolized preparations, inhaled mucolytics, and intermittent positive-pressure breathing or incentive spirometry. Diuretic agents, digitalis glycoside preparations, and sodium restriction may be ordered to treat cor pulmonale.
In serious illness, oxygen may be administered by cannula or mask (usually 1 to 2 L/minute) if the patient has chronic hypoxia, or by mechanical ventilation if Pao2 falls below 40 mm Hg.
Respiratory tract infections require prompt administration of antibiotics.
Enforcement of maximum permitted dust levels in occupational settings and the use of protective masks are preventive measures used to minimize occupational exposure to coal dust.
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