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Various Types of Pneumoconiosis

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Various Types of Pneumoconiosis Pneumoconiosis MEANING Pneumoconiosis is a chronic lung disease caused due to the inhalation of various forms of dust particles, particularly in industrial workplaces, for an extended period of time. Hence it is also said to be an occupational lung disease, which are a particular subdivision of occupational related diseases that are related primarily to being exposed to harmful substances, whether they are gas or dusts, in the work place, and the pulmonary disorders that may result from it. The severity and type of pneumoconiosis depends on what the dust particles comprise of; for example, small amounts of certain substances, such as asbestos and silica, can lead to serious reactions, while others may not be as harmfulCoalworker's pneumoconiosis Various Types of Pneumoconiosis • The most common types of pneumoconiosis are: • coal workers’ pneumoconiosis, silicosis, • asbestosis. As is evident by their names, these pneumoconioses are caused due to the inhalation of coal mine dust, silica dust, and asbestos fibers. Usually, it takes several years for these pneumoconioses to develop and manifest themselves. However, sometimes, particularly with silicosis, it can develop quite rapidly, within a short period of being exposed to large amounts of silica dust. In their severe form, pneumoconioses often result in the impairment of the lungs, disability, and even untimely death. Asbestosis: This is caused due to the inhalation of fibrous minerals that asbestos is made of. The exposure begins with the baggers, who handle the asbestos by collecting them and packaging them, to workers that make products out of them such as insulation material, cement, and tiles, and people working in the shipbuilding industry, and construction workers. It usually takes about 20 years, or more, for the symptoms of asbestos pneumoconiosis to manifest itself. Silicosis: This type of pneumoconiosis occurs in people who handle silica, generally as quartz, which is found in sandstone, sand, granite, slate, certain types of clays, and so on. The people who have the most amount of exposure to silica are those who make glass and ceramic products, quarry workers, foundry workers, silica millers, tunnel builders, miners, and sandblasters. Silicosis leads to fibrosis within the lungs, which increases progressively, and impairs the functioning of the lungs. It is further exacerbated in people who smoke cigarettes. Apart from the above mentioned pneumoconioses, there are also other kinds such as: berylliosis, due to inhaling beryllium dust; bauxite fibrosis, because of inhaling bauxite dust; siderosis, due to inhaling iron dust; byssinosis, due to inhaling cotton dust. Some of the other types of dusts that cause pneumoconiosis are: aluminum, barium, antimony, graphite, kaolin, talc, mica, and so on. There is also a type known as mixed-dust pneumoconiosis. As far as public health is concerned, pneumoconiosis is completely a man-made disease, which can be prevented with adequate dust control and protective gear in the work place Coal workers' pneumoconiosis (CWP), colloquially referred to as Black Lung Disease, is caused by long exposure to coal dust. It is a common affliction of coal miners and others who work with coal, similar to both silicosis from inhaling silica dust, and to the long- term effects of tobacco smoking. Inhaled coal dust progressively builds up in the lungs and is unable to be removed by the body; that leads to inflammation, fibrosis, and in the worst case, necrosis. Coal workers' pneumoconiosis, severe state, develops after the initial, milder form of the disease known as anthracosis (anthrac - coal, carbon). This is often asymptomatic and is found to at least some extent in all urban dwellers[1] due to air pollution. Prolonged exposure to large amounts of coal dust can result in more serious forms of the disease, simple coal workers' pneumoconiosis and complicated coal workers' pneumoconiosis (or Progressive massive fibrosis, or PMF). More commonly, workers exposed to coal dust develop industrial bronchitis[2], clinically defined as chronic bronchitis (i.e. productive cough for 3 months per year for at least 2 years) associated with workplace dust exposure. The incidence of industrial bronchitis varies with age, job, exposure, and smoking. In nonsmokers (who are less prone to develop bronchitis than smokers), studies of coal miners have shown a 16%[3] to 17%[4] incidence of industrial bronchitis. Pathogenesis Coal dust is not as fibrogenic as is silica dust. Coal dust that enters the lungs can neither be destroyed nor removed by the body. The particles are engulfed by resident alveolar or interstitial macrophages and remain in the lungs, residing in the connective tissue or pulmonary lymph nodes. Coal dust provides a sufficient stimulus for the macrophage to release various products, including enzymes, cytokines, oxygen radicals, and fibroblast growth factors[10], which are important in the inflammation and fibrosis of CWP. Aggregations of carbon-laden macrophages can be visualised under a microscope as granular, black areas. In serious cases, the lung may grossly appear black. These aggregations can cause inflammation and fibrosis, as well as the formation of nodular lesions within the lungs. The centres of dense lesions may become necrotic due to ischemia, leading to large cavities within the lung. Appearance The coal macule is the basic pathological feature of CWP, and has a surrounding area of enlargement of the airspace, known as focal emphysema. Continued exposure to coal dust following the development of simple CWP may progress to complicated CWP with progressive massive fibrosis (PMF), wherein large masses of dense fibrosis develop, usually in the upper lung zones, measuring greater than 1 cm in diameter, with accompanying decreased lung function. These cases generally require a number of years to develop. Grossly, the lung itself appears blackened. Pathologically, these consist of fibrosis with haphazardly-arranged collagen and many pigment-laden macrophages and abundant free pigment. Radiographically, CWP can appear strikingly similar to silicosis. In simple CWP, small rounded nodules (see ILO Classification) predominate, tending to first appear in the upper lung zones. The nodules may coalesce and form large opacities (>1 cm), characterizing complicated CWP, or PMF. Symptoms Both CWP and mild complicated CWP are often asymptomatic or only affect lung function slightly. When symptoms do occur, shortness of breath and chronic cough are the most common. Progression to PMF is marked by lung dysfunction, pulmonary hypertension, and cor pulmonale. Unlike silicosis, patients with CWP do not appear to have a substantial increased risk for tuberculosis, but coal miners may experience significant silica dust exposure, and therefore the accompanying risks. CWP is associated with a variety of autoimmune abnormalities, including rheumatoid arthritis (see Caplan's syndrome below) and scleroderma[12]. Diagnosis There are three basic criteria for the diagnosis of CWP: 1. Chest radiography consistent with CWP 2. An exposure history to coal dust (typically underground coal mining) of sufficient amount and latency 3. Exclusion of alternative diagnoses (mimics of CWP) 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 CWP 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. Symptoms of Pneumoconiosis In its milder forms, pneumoconiosis may not have any symptoms. However, when the symptoms do develop, they may be: * Shortness of breath, particularly on exertion * Wheezing * Chronic coughing, which may or may not be accompanied by mucus If there is severe fibrosis of the lungs, it can become extremely difficult to breathe, and when this occurs, it may lead to the fingernails and lips getting a bluish tinge. In the advanced form of pneumoconiosis, there may also be swelling in the legs due to excessive strain on the heart. TREATMENT avoid being exposed to the dust causing the pneumoconiosis. Medications that need to be inhaled will also be prescribed in order to reduce the inflammation of the air passages and to open up the bronchial tubes. In case the level of oxygen in the blood goes below 90 percent, you will have to make arrangements at home for additional oxygen, which you will have to breathe in according to the directions given. Also, immunization with pneumococcal and flu vaccines will also be recommended as a protective measure against infections of the lungs. If a lung infection does develop, antibiotics will most probably be prescribed. SURGICAL MANAGEMENT In case the breathing problems are extreme, the only cure is a lung transplant. How can Pneumoconiosis be Prevented? A protective mask should be worn when working with any of the above-mentioned material, such as coal, asbestos, silica, and so on. Also, governments should ensure that companies comply with the permitted levels of dust regulations. Pleurisy Pleurisy (also known as pleuritis) is an inflammation of the pleura,[1] the lining of the pleural cavity surrounding the lungs. Among other things, infections are the most common cause of pleurisy. The inflamed pleural layers rub against each other every time the lungs expand to breathe in air. This can cause sharp pain with inhalation (also called pleuritic chest pain). Symptoms The main symptom of pleurisy is a sharp or stabbing pain in the chest that gets worse with deep breathing, coughing or sneezing. The pain may stay in one place, or it may spread to the shoulder or back. Sometimes it becomes a fairly constant dull ache. Depending on what's causing the pleurisy, one may have other symptoms: * Shortness of breath * Cough * Fever and chills * Rapid, shallow breathing * Unexplained weight loss * Sore throat followed by pain and swelling in the joints [edit] Causes Pulmonary Two-thirds of pleural infections arise from underlying lung infections or penetrating thoracic trauma. Other sources of pleural infections are vascular dissemination or extension from an intra- abdominal source.
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