Most of the patients with this disease may remain asymptomatic for quite some time. As the disease progresses, symptoms that are common to most form of pneumoconiosis may develop. These include

• Cough 
• Shortness of breath
• Difficulty in breathing
• Chest pain
• Wheezing
• Swelling of feet

Chronic forms are characterized by anorexia, night sweats, severe form of dyspnea, and cur pulmonale. The disease course may be vary with the type of pneumoconiosis

• Silicosis – accumulation of protein fluid is observed in patients exposed to freshly fractured silica dust. Patients may present with weight loss, fatigue, and also develop respiratory failure. Heavy exposure to silica may result in accelerated silicosis which is characterized by the presence of granulomas in lungs. This may lead to pulmonary massive fibrosis. Chronic form is characterized by fibrous nodules in the lungs that get calcified. Patients may also present with chronic bronchitis and respiratory failure. 
• Coal worker’s pneumoconiosis – it is categorized into simple and complicated. Simple coal worker’s pneumoconiosis may remain asymptomatic, but lung function tests may be abnormal. Complicated form of coal worker’s pneumoconiosis presents with chronic bronchitis, emphysema and COPD. Fibrous nodules develop in the lungs that later join together to form pulmonary massive fibrosis. Lungs may then develop cavities. 
• Asbestosis – Cough, chest pain, clubbing of fingers, and decrease in lung function tests are the common symptoms of this condition. Lungs or pleura may develop thickening. Later stages are characterized by pulmonary massive fibrosis. 

The key diagnostic factor of any type of pneumoconiosis is the presence of risk factors as revealed from the medical history of the individual. Exposure to silica, coal or beryllium, with sufficient latency, is one of the major risk factors associated with the development of pneumoconiosis [6]. Physical examination generally remains normal early in pneumoconiosis. Chest percussion may show areas of dullness pulmonary massive fibrosis is present. Patients may be cyanotic, and develop a barrel chest. With increased severity, clubbing of fingers and toes may be noted.
The main diagnostic tool used for pneumoconiosis is radiographs. Chest X-ray is more specific than pulmonary function testing. It reveals the presence of lung opacities in silicosis and coal worker’s pneumoconiosis. Pulmonary function tests like spirometry, lung volume and diffusing capacity are suggested in all patients who have radiographic changes, significant exposure to irritants and symptoms of shortness of breath. Spirometry is used to determine the severity of disease and is also useful in planning the treatment modality. It is usually recommended for all patients who have radiographic changes suggestive of pneumoconiosis. Obstructive changes are shown in patients with a history of exposure to mineral dust and smoking [7]. If chronic beryllium disease is suspected, beryllium lymphocyte proliferation test is useful.
High resolution CT scan of the chest is a sensitive imaging technique to identify interstitial fibrosis. It also aids in identifying the progression of the disease [8]. It is usually recommended in patients with shortness of breath, but without any significant changes in radiography or pulmonary function tests. Open lung biopsy is used only when lung cancer is suspected.

Treatment modality is similar to that of other chronic lung diseases. Oxygen therapy, pulmonary rehabilitation, and bronchodilator therapy are suggested depending on the severity of symptoms. Oral corticosteroids are recommended for chronic beryllium disease. One of the first step in the treatment is the removal of patients from further exposure. Those presenting with exertional dyspnea may need pulmonary rehabilitation. This helps to reduce dyspnea, and improve the quality of life. One of the most common complications of pneumoconiosis is COPD, and bronchodilator therapy is suggested for the same. Lung transplantation is suggested in case of end-stage respiratory failure who do not respond to standard medical therapy [9]. Lung lavage is suggested for acute silicosis [10].

Early identification and cessation of exposure to irritant gives a good prognosis for pneumoconiosis. Chronic exposure to the mineral dust result in increased morbidity. Mortality rate of people who have a history of respiratory failure is about 40%. There is six times increased risk of lung cancer in people with asbestosis. In some cases, pulmonary hypertension and cor pulmonale may result as complications of pneumoconiosis.

Pneumoconiosis is an occupational disease caused by chronic inhalation of organic and inorganic dusts. The most common causes of this disease are inhalation of asbestos, silica and coal mine dust. Exposure to silica dust occur in a number of occupations like mining, quarrying, sand blasting, and pottery making. Silicosis results even with exposure to small quantities in the range of 5-6 grams. Prolonged exposure to asbestos leads to asbestosis [2]. Exposure to large amounts for a short period cause severe form of pneumoconiosis. Coal dust exposure leads to coal dust pneumoconiosis or black lung disease [3]. Graphite, tin, barium, chromate, clay, and iron are also known to cause pneumoconiosis. Beryllium dust is yet another inorganic substance causing this disease.
Allergic response to organic irritants including molds from hay, malt, sugarcane, mushroom, and barley cause this disease after prolonged exposure. Fibers of cotton, hemp, and flax produce brown lung disease, also known as byssinosis. A number of chemical irritants are also implicated in the development of pneumoconiosis. This include Sulphur dioxide, nitrogen dioxide, ammonia acid, and chloride. These chemical irritants are absorbed into the lining of lungs quickly.
Some of the less common pneumoconioses are talcosis, kaolin pneumoconiosis, aluminum pneumoconiosis, Flock worker’s lung, and pneumoconioses caused by miscellaneous dust. Kaolin or china clay is used in the manufacture of paints, paper and cement. Exposure to aluminum oxide dust and fumes causes pulmonary fibrosis. Workers of nylon flock plants are reported to have interstitial lung disease characteristic of pneumoconiosis. Exposure to dusts of iron, barium, tin, antimony, and titanium is also known to cause accumulation in the lungs, but without much impairment to the function of the organ. Talc exposure occurs during mining of soapstone, manufacture of ceramics and roofing materials.

Development of pneumoconiosis is related to length and intensity of exposure to the irritants. It may develop in any age group, gender, and race. Thus, people who have prolonged exposure to any of the irritants have any increased risk of developing this disease.
About 1.7 million people in US are exposed to silica dust, of which 10% are at high risk of developing silicosis. The number of deaths reported from silicosis in this country is about 160 per year. Approximately 700 deaths are reported due to coal worker’s pneumoconiosis. But the number of coal miners have decreased considerably in the last two decades in US. About 1.3 million people are exposed to asbestos dust in different occupations. In Europe, about 7200 cases of pneumoconiosis are reported in one year. The overall mortality rates due to the three primary pneumoconioses have reduced in the last few years. There has been an increase in the number of cases of berylliosis reported due to better diagnostic measures [4].

In general, pneumoconiosis is an interstitial fibrosus lung disease. Fibrosis, either diffuse or nodular in nature, is initiated by activation of fibroblast cells and the production and metabolism of a number of connective tissue components including collagen, elastin and glycosaminoglycans. Pathogenesis of pneumoconiosis happens with a cascade of events. The sequence of events include alveolar macrophage alveolitis, signaling by inflammatory cytokine, oxidative damage, proliferation and activation of fibroblasts, and metabolism of collagen and elastin.
Accumulation of mineral dusts in the lungs releases an increased number of activated macrophages. This triggers the release of excessive quantities of mediators including oxidants, chemotaxins, fibroblasts growth factors and protease. Neutrophils and macrophages are attracted to the site and this leads to the release of oxidants that damage the interstitial epithelium. This provides access to the fibroblast growth factors into the interstitium. Fibroblasts replicate within this tissue and also increase the production of collagen.
The cascade of events starts with the first encounter of irritant in the lungs. Each type of pneumoconiosis is characterized by a primary lesion. The fundamental lesion in asbestosis is the fibrosing alveolitis around airways. Small particles of silica ingested by the macrophages trigger the cytolysis of macrophages. The site of deposition of dust shows an inflammatory response. This generates fibrogenic proteins and growth factors. Freshly fractured coal contain more free radicals that increase the release of inflammatory cytokines. Pathophysiology of beryllium is different from that of other minerals. Increased duration of exposure causes more severe form of disease. After initial exposure, T cells bind to the mineral and this makes them react differently when presented with antigen [5].

As this is a disease caused by exposure to mineral dusts, reduction or cessation of exposure is the best preventive measure. Exposure to dust at workplace should be limited and workers should have protective gears. Smoking worsens the symptoms and hence quitting smoking is equally important in preventing complications.

Pneumoconiosis refers to a group of interstitial lung disease caused by the accumulation of organic and inorganic dust in the lungs [1]. The type and severity of this disease depend on the composition of irritant. Some irritants like silica and asbestos produce severe reactions even when present in small quantities, while milder irritants produce notable reactions only when exposed to large amounts. Different types of pneumoconiosis include

• Asbestosis
• Silicosis
• Coal worker’s pneumoconiosis
• Berylliosis
• Byssinosis
• Kaolin pneumoconiosis
• Siderosis

The primary ones among them are asbestosis, silicosis and coal workers pneumoconiosis. In general, the onset of the diseases occur after several years of exposure to the irritant. Some forms like silicosis may manifest in a progressive form even in a short period, but with intense exposure. Pneumoconiosis is characterized by lung fibrosis and may lead to lung impairment and premature death.

Pneumoconiosis refers to the group of respiratory diseases caused by chronic inhalation of mineral dusts. Different types of pneumoconiosis include asbestosis, silicosis, berylliosis, and coal worker’s pneumoconiosis. As name indicates, asbestosis is caused by inhalation of asbestos dust, while silicosis is caused by prolonged inhalation of silica dust. Berylliosis and coal worker’s pneumoconiosis is caused by exposure to beryllium and coal dust, respectively. These diseases may develop in any age group in both genders. Those who work in environments with increased exposure to the mineral dust have a high risk of developing this disease.

The exact pathology of the disease varies with the duration of exposure and the type of irritant.
Exposure to the dust causes inflammation of the lung tissue which becomes swollen. The inflammation and damage to tissue may continue with chronic exposure to the substance. Permanent tissue damage occurs in the form of fibrosis of the lung. Smoking, size of the irritant, intensity of exposure and age at the time of first exposure, all affects the severity of symptoms.

Most of the patients remain asymptomatic for a long time. Signs and symptoms arise as the disease progresses. Some of the common symptoms of the disease include cough, shortness of breath, and chest pain. As the disease progresses, it may lead to weight loss, fatigue, fever, night sweats, and difficulty in breathing.

Diagnosis of pneumoconiosis is based on physical examination, history of exposure to mineral dust and radiography. Physical examination may not show any specific signs unless the disease is advanced. Clubbing of fingers and crackles in lungs are noted in asbestosis. Pulmonary function tests reveal reduced lung capacity. CT scan helps to reveal the damage to lung tissue. Bronchoscopy is suggested if cancer is suspected.

Early diagnosis and cessation of exposure to the mineral dust is the most effective treatment for any form of pneumoconiosis. In most of the cases symptomatic treatment is suggested. Corticosteroids are used to reduce inflammation while bronchodilators are used to open up the airways. When breathing becomes more and more difficult, oxygen therapy is recommended. Prognosis of any type of pneumoconiosis is good if it is detected early and exposure is stopped. But occasionally, chronic exposure may result in disabling lungs.

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