Pneumoconiosis Research Paper spring 2014

Topics: Pulmonology, Asthma, Pneumonia Pages: 6 (1193 words) Published: April 19, 2015

Jorge Cantu
RSPT 2310 Mr. Ramos

Pneumoconiosis can be interpreted as the accumulation of dust in the lungs and the tissue’s reaction to its habitation. It is considered to be an occupational lung disease caused by the long-term exposure to dust. There are several interstitial lung diseases caused by the inhalation of certain dusts. The primary cause of the pneumoconioses is work-place exposure; environmental exposures rarely give rise to these diseases. Pneumoconiosis refers to a range of diseases that are caused by the inhalation of a range of organic and non-organic dusts which are then retained in the lungs. The main types of pneumoconiosis are: Asbestosis, Berylliosis , Byssinosis, Coal Worker’s Pneumoconiosis (also known as “black lung”), Kaolin Pneumoconiosis, Siderosis, and Silicosis. The most common type of pneumoconiosis is Coal Worker’s Pneumoconiosis (CWP). The Black lung is actually a set of conditions and it wasn’t till the 1950s that its dangers were not well understood. There are currently about 130,000 underground coal miners that are currently working in the United States. Mining and the production of coal is a large part of the economy in several developed countries therefore, leaving thousands of American miners dead from CWP. Even though this disease is preventable by using the appropriate safety equipment, there are still many miners that end up developing advanced and severe cases of the disease.

The coal dust itself is not as fibrogenic as silica dust is. Once the coal dust enters the lungs it can neither be destroyed nor removed by the body. When the coal dust is inhaled it reaches the terminal bronchioles, then is engulfed by alveolar and interstitial macrophages. The phagocytosed coal particles are then transported by the macrophages up the mucociliary elevator and are expelled with mucus or even through the lymphatic system. Once this system becomes overwhelmed, the dust-laden macrophages accumulate in the alveoli triggering an immune response to the foreign particles. The lungs must be exposed for a long period of time to dust particles 2-5 micrometers in size in order for the dust to be retained in the alveoli.

CWP involves two clinical forms of pneumoconiosis: there is the simple and complicated Coal worker’s pneumoconiosis. Usually, simple CWP does not show many symptoms. It is mostly identified by a history of underground exposure of more than 10 years. In the contrary, complicated CWP is characterized with symptoms and a noticeable impairment of lung function. These symptoms include dyspnea or (shortness of breath), cough and sputum production, tightness of the chest, cough, breathlessness, cyanosis, bronchitis, chronic cough, and even emphysema. If the patient is an advanced disease state then cor pulmonale may be seen with associated right ventricular heave, large A waves, hepatomegaly, and peripheral edema. Other symptoms that suggest a secondary infective process are fever and night sweats. The presence of the substance in the lung can cause an inflammatory reaction that can turn the normal elastic lung wall into fibrous scar tissue which, in turn, can cause the lung to loose elasticity and impair the function of the lungs in the patient. It can take several years to develop and the severity is dependent on several factors including: age at first exposure, length of time spent underground, smoking, and size particles.

There are three basic criteria for the diagnosis of CWP. The first one is upon describing the symptoms you are currently suffering, your physician should take a full occupational history from you going back plenty of years or from the date since you started working in that line of work, including any hobby or pasttimes that you may have that are relevant to the disease. Once the physician has taken your history he should order lung function and CXR tests accompanied by CT scan to properly diagnose and correctly be able...

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