Anthracosilicosis


Anthracosilicosis

Description, Causes and Risk Factors:

Pneumonoconiosis from accumulation of carbon and silica in the lungs from inhaled coal dust; the silica content produces fibrous nodules.

Anthracosilicosis 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.

Anthracosilicosis

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.

Anthracosilicosis occurs in two forms:

    Simple anthracosilicosis: Simple pneumoconiosis is the disease in its early form and is characterised by the presence of nodular aggregations within the lungs that occur at the site at which the coal dust has aggregated. A chest x-ray will determine the extent and severity of the disease. This form of the disease is asymptomatic and a fairly mild form. Many urban dwellers will unwittingly be sufferers due to poor air quality issues in some large cities.

  • Progressive anthracosilicosis: The simple form of the disease can develop into progressive massive fibrosis if prolonged exposure to the source of dust is continued over time. PMF sufferers will develop large masses of dense fibrosis in the lungs which will lead to a decrease in lung function. It has been known for people suffering from PMF to be more susceptible to autoimmune conditions such as rheumatoid arthritis and scleroderma.

Your risk of getting anthracosilicosis depends on how long you have been around coal dust. Most people with this disease are older than 50. Smoking does not increase your risk of developing this disease, but it may have an additional harmful effect on the lungs.

If anthracosilicosis occurs with rheumatoid arthritis, it is called Caplan syndrome.

Symptoms:

Symptoms may include:

    Shortness of breath.

  • Chronic cough (with increased risk of chronic bronchitis).

  • Shortness of breath.

  • Chronic cough.

  • Black sputum.

  • Lung dysfunction.

  • Pulmonary hypertension.

  • Heart problems.

Diagnosis:

There are three basic criteria for the diagnosis of anthracosilicosis:

    Chest radiography consistent with anthracosilicosis.

  • An exposure history to coal dust (typically underground coal mining) of sufficient amount and latency.

  • Exclusion of alternative diagnoses.

Symptoms and pulmonary function testing relate to the degree of respiratory impairment, but are not part of the diagnostic criteria. As noted above, the chest X-ray appearance for Anthracosilicosis can be virtually indistinguishable from silicosis. Chest CT, particularly high-resolution scanning (HRCT), are more sensitive than plain X-ray for detecting the small round opacities.

Treatment:

Treatment for both simple anthracosilicosis and progressive anthracosilicosis is symptomatic. Use oxygen as hypoxemia demands.

No evidence supports the hypothesis that removing the miner from the mining environment arrests the disease once progression to progressive massive fibrosis has begun. Therefore, serially monitoring the chest radiographs of miners in order to prevent the development of complicated anthracosilicosis is prudent. Advise workers who develop evidence of simple anthracosilicosis to transfer to jobs with low dust exposure.

Since smoking has an additive effect on anthracosilicosis, smoking cessation should be strongly recommended.

All patients should receive immunizations for influenzae and pneumococci.

One should strongly consider the possibility of superimposed mycobacterial infection in any patient with unexplained weight loss, chronic cough, fever, or night sweats.

NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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