Occupational lung diseases radiology

coal worker pnemoconiosis,silicosis

1. OCCUPATIONAL LUNG DISEASES

2. Dust Deposition and Lymphatic Clearance: deposition of particles 1–5 µm in diameter in and around the respiratory bronchioles- centrilobular location Perilymphatic disease subpleural,peribronchovascular or along lobular septae . Posterosuperior segment predilection of dust retention.

3. PNEUMOCONIOSIS CLASSIFICATION ACCORDING TO ILO (INTERNATIONAL LABOUR OFFICE) TYPE OF OPACITIES Silicosis, coal worker's pneumoconiosis nodular opacities: p = <1.5 mm q = 1.5-3 mm r = 3-10 mm Asbestosis linear opacities: s = fine t = medium u = coarse/blotchy PROFUSION/SEVERITY 0 = normal 1 = slight 2 = moderate 3 = advanced

4. Induction Periods Short: Asthma Infections Allergic alveolitis Toxic poisonings Long: Pneumoconioses Neoplasms

5. acute reactions chronic reactions inflammation and edema fibrosis or granuloma 1.Upper Respiratory Tract Irritation Occupational Rhinitis 2.Airway Disorders Occupational Asthma Reactive Airways Dysfunction ( Byssinosis ) 3.Inhalation injury Hypersensitivity Pneumonitis 4.Pleural Disease Pleural effusions and pleuritis (Asbestos) 1.Interstitial Fibrosing Diseases Asbestosis (non-malignant pulmonary disease) Silicosis Coal Workers ’ Pneumoconioses Berylliosis Chronic Bronchitis and Chronic Airways Disease 2.Malignancies Malignant Mesothelioma Lung Cancer Laryngeal Cancer Sinonasal Cancer

6. CLASSIFIED fibrotic ( focal nodular ,diffuse fibrosis ) nonfibrotic (particle-laden macrophages, no fibrosis ) 1.silicosis - Nodular fibrosis 2.coal worker pneumoconiosis- Macule formation with focal emphysema 3.asbestosis -- Diffuse fibrosis 4.berylliosis- Granulomatous reaction 5.talcosis 1.siderosis 2.stannosis 3.baritosis

7. Silicosis principal sources- free silica in mining, quarrying, and tunneling . fine crystalline silicon dioxide Inhalation Silica particles- breakdown of macrophage releases enzymes –progressive fibrogenic response even after cessation of dust exposure.

8. Silicosis small, well-circumscribed nodules that are 2–5 mm in dia , mainly inv upper & posterior lung zones. GGO 20% calcify centrally Lymphadenopathy is common Eggshell calcification of hilar nodes (5%) DDx : Sarcoidosis

9. SILICOSIS 2 clinical forms:  Acute silicosis ( alveolar silicoproteinosis )  classic silicosis ( chr interstitial reticulonodular disease) simple complicated OBSTRUCTIVE LUNG DISEASE LUNG CANCER Silicotuberculosis

10. Acute Silicosis Rare heavy exposure to free silica-in closed spaces for 6–8 months. rapidly progressive, with death caused by respiratory failure. HRCT - "crazy paving" pattern No silicotic nodules. DD-Alveolar proteinosis ( silicoproteinosis )

11. bilateral consolidation , GGO in perihilar region “ central bat-wing consolidation .”

12. CHRONIC SIMPLE SILICOSIS 10--20 years of dust exposure Rt upper lobes--posterior lung zones nodules are in perilymphatic distribution centered along the bronchovascular bundles, centriacinar portion of the lobule, & in the subpleural lung, where the nodules form these pseudoplaques .

13. 1-10mm well defined rounded opacities  centrilobular & peribronchial ; nodules surrounded by focal emphysema (focal dust emphysema) calcify hilar + mediastinal lymphadenopathy , may calcify in 5% (eggshell pattern)

14. Simple silicosis pseudoplaques diffuse nodular opacities with relative sparing of the basal lung zones HRCT shows numerous small nodules

15. Complicated Silicosis ( PROGRESSIVE MASSIVE FIBROSIS) large opacities >1 cm in diameter mid zone /periphery of upper lung migrating toward hila Relatively bilateral symmetric + nonsegmental conglomerate sausage-shaped masses with ill-defined margins (in advanced stages) compensatory emphysema in unaffected portion between mass + pleura slow change over years may calcify + cavitate (ischemic necrosis/TB)

16. CXR-large b/l opacities in the upper zones of the lung, as well as upward elevation of both hila . CT-shows bilateral conglomerate masses with calcifications, findings that represent PMF in the upper zone of both lungs.

17. OBSTRUCTIVE LUNG DISEASE AND LUNG CANCER chronic bronchitis, & Emphysema . Tobacco smoking may cause an additive effect. Silicotuberculosis synergistic relationship between silicosis + tuberculosis

18. Coal miners are exposed to dusts that contain a mixture of coal, mica and silica in varying proportions . COAL WORKER PNEUMOCONIOSIS

19. CWP Simple CWP- asymptomatic & is often a radiographic diagnosis. Progressive massive fibrosis (PMF) can occur more frequently with exposure to silica. CXR- small nodules predominantly in upper & posterior zone. Hilar lymph node enlargement is not uncommon eggshell calcification does not generally occur. usually bilateral, progressive, and may cavitate or become calcified. DD--tumors, tuberculosis scars, or Caplan’s nodules

20. 22 CAPLANS SYNDROME coal workers with rheumatoid disease may develop nodules even after relatively low exposures to dust. The lesions are typically subpleural . The lesions may grow rapidly,appear in crops(in contrast to silicotic /CWP nodules that appears over a period of time) cavitate and produce a pneumothorax

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22. 24 Differentiate PMF from lung cancer Clinically and radiologically important bilateral occurrence : DDx with tumors or tuberculosis Unilateral masses occur : DDx is difficult Chest PA  Shape of mass  Calcification  Satellite Nodules  Course of PMF

23. 25 Differentiate from lung cancer Shape of mass  typically in periphery of lung  smooth, sharp, elongated lateral border parallel rib cage  projected 1~3 cm from lateral costal margin  medial border : ill-defined vs. lateral : sharp  tends to be thin, carcinomas tend to be spherical Calcification  thick eggshells -> exclude primary lung cancer central dot calcification,  Linear calcifications ; not in cancer

24. 26 Differentiate from lung cancer Satellite Nodules  multiple small nodules near a lung mass in pneumoconiosis or infection  rare in carcinoma Course of PMF  mass formed by coalescence of nodule, rather than by growth of a single nodule  mass has decreased in size

25. 27 Differentiate from lung cancer # MR imaging : useful ★ lung cancer vs PMF High SI on T2WI vs low SI T1WI, T2WI Low SI on T2WI MR images -> PMF # PET Intensive uptake of FDG in PMF Observation of resultant mass enhancement on images -> confusion of PMF with lung cancer  Histopathologic analysis should be performed

26. Progressive massive fibrosis (a)HR CT scans --irregularly marginated 20–30mm nodules accompanied by smaller satellite nodules and surrounding reticulation in the upper lobe of both lungs. (b) T1-w image - slightly hyperintense lesions in both upper lobes. (c) T2-w image -absence of signal at the lesion sites and a small pleural effusion in the rt lung. (d) PET-CT scan -increased uptake of FDG in both nodules and in a right paratracheal LN.

27. Lung cancer and coal worker pneumoconiosis (a) HRCT- welldefined 2-cm-diameter nodule in an upper segment of the lower lobe of the left lung, a finding that represents a combined neuroendocrine large cell carcinoma and adenocarcinoma , as well as multiple smaller nodules (b) T2-weighted -high-signal-intensity nodule in the lower lobe. (c) (PET)-CT scan - a high uptake of FDG in the nodule, suggestive of malignancy. (d) gross specimen- left lower lobectomy shows the cancer (arrow) and multiple black-pigmented nodules (arrowheads)In the lung parechyma and pleural surface

28. refers to pulmonary fibrosis secondary to asbestos exp. Risk factors: Longer ( approx. 20 years) exposure to the amphibole fiber type. not associated with smoking Two large groups: serpentines (Chrysotile)and amphiboles( crocidolite ). Asbestosis

29. 2 major sources of asbestos dust : ( a ) the primary occupations in asbestos mining. ( b ) secondary occupations --insulation manufacturing, textile manufacturing, construction, shipbuilding, and the manufacture and repair of gaskets and brake linings. Asymptomatic until 20 years after initial exposure. Long asbestos fiber (up to 100 µm in length), penetrates deeply into the lung and pleura, and has a fibrogenic effect on respiratory bronchioles, alveoli, and pleura.

30. Asbestos-related diseases B enign Pleural diseases 1.plaques 2.diffuse pleural thickening 3.effusion 4.calcification Parenchymal diseases 1.Asbestosis [ parenchymal fibrosis caused by asbestos inhalation] 2.Rounded atelectasis 3.Benign fibrotic masses 4.Transpulmonary bands Malignancy 1.M alignant mesothelioma 2.Bronchogenic carcinoma

31. FOCAL PLEURAL PLAQUES (65%): Incidence: most common manifestation of exposure Location: bilateral + multifocal; following rib contours; Site: parietal pleura (visceral pleura typically spared ) Plaques are often holly leafed shaped Apices + costophrenic angles typically spared.

32. DIFFUSE PLEURAL THICKENING : smooth uninterrupted diffuse thickening of parietal pleura extending over at least 1/4 of chest wall ( visceral pleura involved in 90%, but difficult to demonstrate) smooth; difficult to assess when viewed en face Usually involves the costophrenic angles May be associated with rounded atelectasis DDx : pleural thickening from parapneumonic effusion, hemothorax , connective tissue disease

33. pleural plaques right side∕ rounded atelectasis diffuse pleural thickening Diaphragmatic pleural plaques

34. visceral pleural plaque in the right major fissure & curvilinear bands of hyperattenuation in the posterior subpleural area. calcified pleural plaques hallmark of asbestos exposure.

35. 37 PLEURAL CALCIFICATION: HALLMARK of asbestos exposure! detected by radiography in 25%, by CT in 60% Histo: calcification starts in parietal pleura; calcium deposits may form within center of plaques Dense lines paralleling the chest wall, mediastinum, pericardium, diaphragm Bilateral diaphragmatic calcifications with clear costophrenic angles are PATHOGNOMONIC advanced calcifications are leaflike with thick-rolled edges DDx: talc exposure, hemothorax, empyema, therapeutic pneumothorax for TB (often unilateral, extensive sheet like on visceral pleura)

36. Pleural effusion earliest manifestation - within 10 years of exposure, usually transient but requires close follow-up .

37. Asbestosis Parenchymal fibrosis begins in and around the respiratory bronchioles in the lower lobes adjacent to the visceral pleura progress to diffuse interstitial fibrosis and "honeycombing ," with complete destruction of the alveolar architecture. Asbestos bodies- observed microscopically in bronchoalveolar lavage fluid or tissue section . It may remain static or progress over time.

38. Radiologic changes consist of small, irregular opacities or linear hyperattenuating areas fine reticulations coarse linear pattern with honeycombing. most severe in the posterior subpleural lower lungs.

39. RETICULAR INFILTRATES

40. HONEYCOMB LUNG

41. Prone HRCT scan – b/l subpleural reticular hyperattenuating areas, small cysts, traction bronchiectasis , & GGO.

42. 44 ASBESTOSIS VS IPF FAVORS ASBESTOSIS Pleural plaques Subpleural branching opacities Subpleural curvilinear lines Parenchymal bands Homogeneous subpleural opacities

43. Pleural plaques Sub pleural curvilinear lines Parenchymal bands Traction bronchectasis Bronchiloectasis honeycombing ASBESTOSIS IPF

44. ATELECTATIC ASBESTOS PSEUDOTUMOR/ ROUND ATELECTASIS/ FOLDED LUNG In folding of redundant pleura + segmental/ subsegmental atelectasis b/l posterobasal , 2.5-8 cm focal subpleural mass abutting a region of thickened pleura CT: rounded/ lentiform shaped peripheral mass abutting pleura pleural thickening ± calcification curving of pulmonary vessels and bronchioles into edge of lesion ( vacuum cleaner/comet tail sign ) volume loss of affected lobe crow's feet = linear bands radiating from mass into lung

45. Comet tail sign

46. PARENCHYMAL BAND “CROWS FEET”

47. 49 LUNG CANCER In those with asbestosis, the cancer is more likely to arise in the lower lobes in contrast to general smokers. Associations with lung cancer and mesothelioma Asbestos-related lung cancer is usually either squamous cell or adenocarcinoma Bronchogenic carcinoma is almost always associated with cigarette smoking Mesotheliomas are not related to cigarette smoking       Mesotheliomas most often due to crocidolite particles 

48. 50 Mesothelioma Mesothelioma is a rare pleural malignancy seen with asbestos exposure. The majority have no plaques. Long thin fibers are more likely to induce mesothelioma, thus crocidolite is more neoplastic than chrysotile. The hemithorax is usually small, pleural effusion is nearly universal. Prognosis is poor, 12 month median survival.

49. Mesothelioma Rare. majority have no plaques. crocidolite is more neoplastic than chrysotile . small, pleural effusion poor Prognosis.

50. Malignant mesothelioma both parietal and visceral pleura mass.Local invasion is common CXR - Ipsilateral effusion to the pleural disease & contralateral pleural plaques diagnosed by Open biopsy .

51. Mesothelioma indicated by the central pleural effusion

52.   Byssinosis in a 56-year-old woman who had had frequent episodes of “Monday fever ” and dyspnea while working in a cotton factory over a 7-year period. (a) Chest radiograph shows diffuse, ill-defined haziness, predominantly in the lower lung zones. (b) High-resolution CT scan shows numerous ill-defined small nodules with ground-glass attenuation in both lungs .

53.   Mercury vapor poisoning in a 34-year-old woman worked for a mercurythermometer manufacturer for 30 months. presented with headache and dyspnea and suffered from chronicgingivitis.Chestxray showed perivascular haziness and fine reticular opacities in the parahilar area of both lungs. CT scan shows areas of ground-glass attenuation, poorly defined centrilobular nodules (arrows), and bronchial wall thickening. Note the relative sparing of the periphery of both lungs.

54. Occupational Lung Cancers Asbestos Arsenic Bischloromethyl ether Coke oven fumes Insoluble Hexavalent chromium cmpds Soluble nickel Mustard gas Radon daughters asbestosis lower lobes cancer is more likely- squamous cell or adenocarcinoma Bronchogenic carcinoma is almost always associated with cigarette smoking

55. SIDEROSIS inert iron oxide/metallic iron deposits diffuse fine reticulonodular opacities (may disappear after exposure discontinued) small round opacities (indistinguishable from silica/coal) NO secondary fibrosis + NO hilar adenopathy HRCT:--widespread poorly defined centrilobular micronodules branching linear structures extensive ground-glass attenuation without zonal predominance

56. BERYLLIUM-INDUCED LUNG DISEASE extremely light metal Beryllium with a high modulus of elasticity (stiffness). chronic beryllium disease (CBD or berylliosis )- delayed-type hypersensitivity reaction - granulomatous lung disease similar to sarcoidosis . Lung primarily affected. Other sites - extrapulmonary lymph nodes, skin, salivary glands, liver, spleen, kidney, bone, myocardium, and skeletal muscle. usually nonspecific Symptoms – later-- Dyspnea -mc symptom.

57. XRAY chest -50% patients normal . Abnormal findings - hilar adenopathy,increased interstitial markings. HRCT:GGO,parenchymal nodules,septal lines.

58. The diagnosis of CBD is based on the presence of: History of beryllium exposure positive blood or bronchoalveolar lavage beryllium-specific lymphocyte proliferation test presence of non-necrotizing granuloma on lung bx 25% may show negative results

59. CONCLUSION SILICOSIS-- multiple small rounded opacities in upper lobes 5% Eggshell calcification of hilar nodes. Asbestosis -- Pleural without parenchymal disease. B/l Parietal pleural plaques in the mid lung –mc. 50% Pleural calcification .

60. thank you