The Clinical Manifestation of Black Lung Disease – Respiratory System Example

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"The Clinical Manifestation of Black Lung Disease" is a great example of a paper on the respiratory system.   Black lung disease is also called as Coal Worker's Pneumoconiosis (CWP) or Anthrosilicosis (“ Coal worker's pneumoconiosis” , 2013). It is a lung disease that is caused by the inhalation of coal or graphite dust over a long time. The name of this disease is derived from the fact that the lungs of patients suffering from this disease appear black rather than pink. The term black lung disease currently encompasses a variety of respiratory impairments in coal miners subjected to coal dust for a long period of time and does not specifically refer to CWP (Schwarz, 2010).

Coal dust includes a mixture of coal, silica, mica, and kaolin (Paul and Williams, 2009). History The disease was first referred to as phthisis melanotic by British physicians in the 1820s, which is a Greek term that means ‘ black wasting away’ (Greenberg, 2003). Although it was definite that the disease was caused by coal, it was unclear as to whether the disease resulted from swallowing or inhaling coal. By 1949, the condition was first recognized as a disease by Great Britain, while it was not until 1969 that the United States recognized it as a disease.

The moniker ‘ black lung’ was however already in use among coal workers prior to the recognition of the condition as a disease. Collis in his paper published in 1928 provided the first report on the disease, recognizing it as being different from silicosis and identifying that that it is caused due to long term exposure to coal (Greenberg, 2003). Pathophysiology and Clinical Manifestation of Black Lung Disease The disease is an occupational one, resulting from exposure to coal dust among coal miners.

The coal dust deposited in the respiratory bronchioles and alveoli due to inhalation by coal miners is engulfed by macrophages through phagocytosis. These are then transported to terminal bronchioles and are eliminated via mucociliary action. However, due to overexposures for a long time, the elimination mechanism fails to effectively clear the dust load. Dust particles of 1-10 micrometers cannot be cleared from the lungs (Greenberg, 2003). Due to this, there is an aggregation of macrophages in the bronchioles and alveoli, following which a reticulin network develops around the dust-laden macrophages upon the formation of fibroblasts.

Consequently, the alveoli and bronchioles are clogged with dying macrophages, coal dust, and fibroblasts that result in the development of coal macules (primary lesions). These are black dots that form on the lungs. As the macules grow in size, the bronchioles are weakened. Dilation of these bronchioles results in localized emphysema. The disease is not localized. It forms in the upper lobes and subsequently spreads to the lower lobes of the lungs.

Initial symptoms of the disease include the production of sputum, shortness of breath, and chronic cough followed by dyspnea at later stages. Patients cough up black fluid in large amounts. The disease ultimately results in pulmonary heart disease and respiratory failure (Paul and Williams, 2009; Greenberg, 2003). Risk Factors and Disease Contraction Black lung disease is acquired due to the inhalation of coal dust over a long period of time. It is of two kinds: simple and complicated. The complicated form of the disease is also called PMF (progressive massive fibrosis).

Inhalation of coal dust can occur during coal trimming, mining, milling, or manufacturing stages. Disease severity is dependent upon the kind of coal dust inhaled, the time period of exposure, and the dust load in the air. The risk of acquiring the disease depends on the period of exposure to coal dust. The disease is more commonly seen in coal miners over 50 years of age. The risk of acquiring this disease is not increased by smoking, although the practice may append the harm on the lungs (“ Coal worker's pneumoconiosis” , 2013).

The disease incidence is not influenced by racial factors, ethnicity, or cultural factors. Disease Diagnosis Diagnosis of the disease is performed through physical examination of the lungs and stethoscopy. Lung function tests and chest CT scans and x-rays are also performed (“ Coal worker's pneumoconiosis” , 2013). The diagnosis of this disease is not straightforward. For a proper diagnosis, workers should have been exposed to coal for a long time, at least for a period of ten years. In the early stages, the disease is asymptomatic. The results of physical examinations are also non-specific.

Chest radiography, bronchoscopic lung biopsy, and lung washings are also employed in the diagnosis of the disease. In order to standardize the diagnosis of the disease, a classification system given by the International Labour Office is adopted to score chest radiographs. According to this classification system, nodular opacities observed in chest radiographs are rated on the basis of their number and size. Spirometry testing has not found much utility in the diagnosis of this disease because the results of such tests in coal miners suffering from the disease appear normal or close to normal.

Coal miners suffering from the disease in the early stages do not show any symptoms. Simple CWP is expected to be present if round small opacities of 10mm or less than 10mm diameter are found in chest radiographs. In the early stages of disease progression, these opacities are found in the upper fields of the lungs. As the disease progresses, such opacities are found in the middle and lower fields as well. Examination of lung mechanics, pulmonary artery pressures, blood flow rates, and diffusing capacity show the limited influence of simple CWP.

In the complicated form of the disease (PMF), opacities observed in chest radiographs are greater than 10mm diameter (Greenberg, 2003). Disease Treatment and Management There is no specific treatment for black lung disease and further progression of the disease can only be averted by avoiding further exposure to coal dust (“ Coal worker's pneumoconiosis” , 2013). Lung transplantation could be a solution. However, it has not been very successful, unlike other organ transplantations (Greenberg, 2003). Because of the lack of effective treatment options, prevention is the only solution to the disease.

Early diagnosis followed by the management of complications is the only kind of medical management possible (Paul and Williams, 2009). The condition can be prevented from worsening by ceasing smoking and dust exposure. In some cases, oxygen therapy is given in the presence of severe dyspnea (Timby and Smith, 2005). Prevention and Prognosis The disease can be effectively prevented by using a protective mask or well-fitted respirators while working around coal, carbon, and graphite. It is preferable to avoid smoking (“ Coal worker's pneumoconiosis” , 2013). The disease is rarely fatal. Epidemiology The prevalence of the disease in the United States in the 1970s was reportedly between 4-46% of miners (Greenberg, 2003).

Regulations were implemented in the United States from 1969 onwards to lower the exposure of workers to coal dust. As a result of these regulations, the disease risk was significantly reduced (Hendryx et al. , 2013).   A study reported in 2011 showed that before the regulatory measures, the prevalence of PMF in autopsies was 10.3% for coal miners who worked prior to 1969 and 1.2% among those who worked after the regulations were implemented (1971 to 1996).   After showing a decline in incidence, the disease incidence is reportedly undergoing an upsurge.

Reports by Laney and Attfield (cited in Hendryx et al. , 2013) have shown that in the early 2000s, there was an increase in the incidence of the disease. The prevalence of CWP was 6.5% in the 1970s, which decreased to 2.1% in the 1990s and then increased to 3.2% by 2000. While the cause of this increase in incidence is yet unknown, certain evidence suggests that failure to comply with safety regulations is the cause.

References

“Coal worker's pneumoconiosis”. (2013, May 30). A.D.A.M. Medical Encyclopedia. Retrieved from http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001187/.

Greenberg, M. I. (Ed.). (2003). Occupational, Industrial, and Environmental Toxicology. Pennsylvania: Elsevier Health Sciences.

Hendryx, M., Persily, C., Conley, J., & Fedorko, E. (2013). Rates of Black Lung Disease in Relationship to Black Lung Treatment Centers. Retrieved from http://publichealth.hsc.wvu.edu/wvrhrc/2013/08/Black%20Lung%20Clinics%20final%20report%20final%20073013.pdf.

Paul, P., & Williams, B. (2009). Brunner & Suddarth's Textbook of Canadian Medical-surgical Nursing. Philadelphia: Lippincott Williams & Wilkins.

Schwarz, M. I. (2010). Interstitial Lung Disease. Connecticut: People’s Medical Publishing House.

Timby, B. K., & Smith, N. E. (2005). Essentials of Nursing: Care of Adults and Children. Philadelphia: Lippincott Williams & Wilkins.

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