Pneomoconiosis

Dust induced respiratory diseases

1. pneumoconiosis By-Anubhav Agrawal,514

2. Contents Introduction Pathogenesis Classification Silicosis Diagnosis

3. Introduction Pneumoconiosis is an occupational lung disease and a restrictive lung disease caused by the inhalation of dust, often in mines and from agriculture. In 2013, it resulted in 260,000 deaths, up from 251,000 deaths in 1990. Of these deaths, 46,000 were due to silicosis, 24,000 due to asbestosis and 25,000 due to coal workers pneumoconiosis. The first recorded mention of breathlessness among handlers of grain was done by Ramazzini , the father of occupational medicine, in 1713.

4. The term "black lung" was coined when medical professionals discovered the blackening of miners' lungs in post-mortem. The first documented case of an asbestos-related death was reported in 1906 when the autopsy of an asbestos worker revealed lung fibrosis.

5. Pathogenesis For clinical pneumoconiosis to develop, 3 essential factors are required: Exposure to specific substance: coal, appear relatively inert and may accumulate in considerable amounts with minimal tissue response; while silica and asbestos, have potent biologic effects. Particles of appropriate size to be retained in lung (1-5μm) Exposure for a sufficient length of time (usually around 10 years)

6. Classification Depending upon the type of dust, the disease is given different names: Coal worker's pneumoconiosis (also known as miner's lung, black lung or anthracosis ) — coal, carbon Asbestosis — asbestos Silicosis— crystalline silica dust Bauxite fibrosis — bauxite Berylliosis — beryllium Siderosis — iron Byssinosis — cotton Silicosiderosis — mixed dust containing silica and iron Labrador lung (found in miners in Labrador, Canada) — mixed dust containing iron, silica and anthophyllite, a type of asbestos

7. Silicosis Silicosis (previously miner's phthisis, grinder's asthma, potter's rot and other occupation-related names) is a form of occupational lung disease caused by inhalation of crystalline silica dust, and is marked by inflammation and scarring in the form of nodular lesions in the upper lobes of the lungs. It is a type of pneumoconiosis. Silicosis resulted in 46,000 deaths globally in 2013 down from 55,000 deaths in 1990.

8. Classification Three forms of silicosis: Acute silicosis: occurs with exposure to fine dust with high quartz content; very heavy exposure for months, shows symptoms within weeks to months of exposure, Accelerated silicosis: shows rapidly progressive symptoms after 5 to 10 years of high exposure to fine dust of high silica content. Chronic silicosis: the most common form, results from long-term exposure (10 to 20 years or longer) to dust containing less than 30% silica content.

9. Clinical features Chronic cough Dyspnea (shortness of breath) that worsens with exertion. Fatigue Loss of appetite Chest pains Acute silicosis patients may also have fever and experience rapid, unintended weight loss. Silicotuberculosis : Pulmonary tuberculosis occurs in about 25% of patients with acute or classic silicosis

10. Diagnosis Positive indications on patient assessment: Shortness of breath Chest X-ray may show a characteristic patchy, subpleural , bibasilar interstitial infiltrates or small cystic radiolucencies called honeycombing. Pneumoconiosis in combination with multiple pulmonary rheumatoid nodules in rheumatoid arthritis patients is known as Caplan's syndrome.

11. For uncomplicated silicosis, chest x-ray will confirm the presence of small (< 10 mm) nodules in the lungs, especially in the upper lung zones. Using the ILO classification system, these are of profusion 1/0 or greater and shape/size "p", "q", or "r". Lung zone involvement and profusion increases with disease progression. In advanced cases of silicosis, large opacity (> 1 cm) occurs from coalescence of small opacities, particularly in the upper lung zones. With retraction of the lung tissue, there is compensatory emphysema. Enlargement of the hilum is common with chronic and accelerated silicosis. In about 5-10% of cases, the nodes will calcify circumferentially, producing so-called "eggshell" calcification. This finding is not pathognomonic (diagnostic) of silicosis. In some cases, the pulmonary nodules may also become calcified.

12. PA chest radiograph of an 80-year-old man who was a miner decades ago shows multiple large opacities (arrows, large opacity = parenchymal opacity greater than 1 cm) and several tiny rounded opacities in the right lower and left mid/lower lung zones. With the history of exposure, adequate lag time and chest radiographic findings, the patient has findings consistent with coal worker pneumoconiosis.

13. Image shows small nodules predominantly in the middle-to-upper lung zones, several of which are calcified. Eggshell calcification is present in the bilateral hilar lymph nodes. The large mass in the infrahilar region of the right lung is consistent with progressive massive fibrosis.

14. Silicosis with progressive massive fibrosis. Image shows large, conglomerate nodules in both the middle and upper lung zones. Peripheral hyperlucency represents emphysematous lung tissue secondary to central migration of the large nodules. Bilateral upper lobe volume loss is also noted.