OCCUPATIONAL LUNG DISEASE

1. OCCUPATIONAL LUNG DISEASE ALOK SINHA Department of Medicine Manipal College of Medical Sciences Pokhara, Nepal

2. Occupational lung disease (Pneumoconiosis)permanent alteration of lung structure caused by inhalation of a mineral dust and the reaction of the lung tissue to this dust • Substances known to cause lung disease • coal dust • Silica • Asbestos • Berillium

5. Pneumoconioses • non-neoplastic pulmonary diseases caused by the reaction of the lung to the inhalation of mainly mineral • Inhaled particles of dust size < 5 µm reach the terminal airways and alveoli and settle on the epithelial lining • slowly cleared by macrophages or alveolar cells. They may pass into the • lymphatic system • be cleared via the airway • or remain in the alveolus

6. lead to an inflammatory reaction within the lung, depending on their physical and chemical properties • causes characteristic alterations in pulmonary structure and radiological abnormalities

7. barium, tin, and iron – no fibrosis • silica - nodular fibrosis • asbestos - diffuse fibrosis • coal dust - Macule formation with focal emphysema • beryllium- systemic response and induce a granulomatous reaction in the lungs Pneumoconioses can appear and progress after the exposure has ceased

8. Coal-workers' pneumoconiosis

13. Open cast mines

14. deposition of coal dust within the lung and its associated inflammatory reaction Coal workers pneumoconiosis is of two types- • Simple pneumoconiosis which can progress to • Complicated pneumoconiosis - also known as progressive massive fibrosis (PMF) • Related to degree of exposure to coal dust

15. Healthy lung

17. progressive massive fibrosis

18. Simple pneumoconiosis • Coal dust inhaled into the alveolus & engulfed by macrophages • form a black stellate lesion - the coal macule

19. coal macule Dilated terminal bronchiole with Peribronchiolar Coal ladened macrophages

20. coal macules are found throughout the lung, especially in the upper zones of the upper and lower lobes • associated with surrounding bronchiolar dilatation • leading to focal emphysema

21. cytokine release and subsequent inflammatory cell recruitment, leading to fibroblast activation Progression of the disease

22. P.M.F. • PMF occurs on this background • with aggregation of the fibrotic nodules to form larger lesions – 2 to10 cm diameter • central area of nodules- necrotic • outer rim - firm and collagenous

23. distort the adjacent lung and cause emphysma • lesions continue to progress out of the work environment • Larger lesions may have • cavitation and necrosis • areas of calcification

24. Clinical features Simple pneumoconiosis • asymptomatic with no associated clinical signs Progressive massive fibrosis • Cough with mucoid or blackened sputum • breathlessness on exertion • may lead to the development of c o r p u l m o n a l e

25. Investigations

26. CXR In simple pneumoconiosis nodular shadowing of varying size- up to 10 mm in the upper and middle zones • graded according to the number of different sized nodules p = < 1.5 mm q = 1.5-3 mm r = 3-10 mm

27. PMF • diagnosed when one or more opacities of > 1 cm diameter are present, on the background of simple pneumoconiosis • located in the upper lobes and enlarge, becoming increasingly radio dense and clearly demarcated

28. simple pneumoconiosis

29. PMF

30. PFTs • Simple pneumoconiosis: • FEV1 and FVC are normal • TLCO may be slightly decreased PMF: • Mixed feature • airway obstruction due to emphysema • restriction due to loss of lung volumes • TLCO is reduced

31. Management • Minimization of dust exposure with • improved mine ventilation • respirator provision • monitoring of dust levels • Periodic CXR every 4 years • moved to less dusty work if they show signs of pneumoconiosis, to prevent development of PMF • Miners with signs of coal workers' pneumoconiosis are entitled to industrial injury benefits

32. Caplan's syndrome • Miners with seropositive rheumatoid arthritis can develop large well-defined nodules • occur on a background of simple pneumo coniosis and with a relatively low coal dust exposure • multiple and may cavitate • Cause no significant functional impairment and have no malignant potential • Has to be considered in the D/D of T.B. malignency etc

34. Silicosis

36. chronic nodular densely fibrosing pneumoconiosis, caused by the prolonged inhalation of silica particles. • Long lag time of decades between exposure and clinical disease • Insidious onset & progressive • Larger radiological opacities than those seen in coal-workers' pneumoconiosis, and more rapid progression • The pattern of disease depends on the level and duration of the silicone dust exposure

37. quartz

38. Silica is present as crystalline quartz • mined and quarried • used in industries • ceramics, brick-making, and stone masonry

39. Pathology • Dust particles in the alveoli are phagocytosed by macrophages • removed to the lymphatics • cause diffuse inflammatory change • Layers of collagen are deposited around the dust particle. Nodules are found within the secondary pulmonary lobule

40. types of silicosis • Acute silicosis • Subacute silicosis & chronic silicosis • Silicotuberculosis

41. Acute silicosis • intense exposure to fine dusts produced by sand blasting • apparent in workers within a few months to a year of starting work • Rapid deterioration over 1- 2 years, with treatment being ineffective.

42. Clinically • dry cough • shortness of breath • feeling of tightness on breathing deeply Rapid deterioration over a few weeks • Fine crepitations over the lower zones bilaterally • Leads to respiratory failure • CXR Patchy bilateral lower air space consolidation, which may look like pulmonary oedema

43. Subacute silicosis • Dry cough • gradual onset of s o b Chronic silicosis • occurs with lower dust concentrations

44. PFTs- Slow decline • mild restrictive pattern • obstructive or • mixed picture (Due to emphysema)

45. Silicotuberculosis • Increased likelihood of active TB infection in people with silicosis, most likely due to the reactivation of quiescent lesions. • tuberculosis is three times greater than that of age-matched controls. Those with acute and accelerated silicosis have the highest incidence of mycobacterial disease.

46. individuals with silicosis or long-term exposure to crystalline silica should receive a tuberculin skin test. If the reaction is 10 mm or greater tuberculosis chemoprophylaxis should be administered even in absence of evidence of active tuberculosis • T.B. suspected when • Cavitation • Haemoptysis • fever • new soft CXR opacities

47. CXR • A few upper and mid-zone nodules occur, which become calcified after 10 years or so. no associated parenchymal distortion • may be associated hilarlymphadenopathy with egg shell calcification • disease may progress on further silica exposure with coalescence of nodules

48. widespread nodules measuring 2-5 mm in diameter, with a predominance in the middle and upper lung zones.