1. 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 coal dust Silica Silica Asbestos Asbestos Berillium Berillium

3. Mineral dust Disease Examples of exposure Coal dust I.Simple pneumoconiosis II.Progressive massive Fibrosis III.Caplan's syndrome Coal mining, especially hard coal Silica I. SilicosisFoundry work, sandblasting, stone cutting,hard rock mining Asbestos I. Asbestosis II. Benign asbestos- related pleural disease III. Mesothelioma IV. Lung cancer Mining, milling, and fabrication. Installation and removal of insulation Beryllim I. Acute berylliosis II. Beryllium granulomatosis Mining, fabrication of electrical and electronic equipment, workers in nuclear and aerospace industry.

4. Iron oxideSiderosisWelding Barium sulphate BaritosisMining Tin oxideStannosisMining AluminiumLike silicosis (bauxite worker's lung, Shaver's disease) Mining, firework, painting, and armament manufacture

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 lymphatic system be cleared via the airway be cleared via the airway or remain in the alveolus 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 Simple pneumoconiosis which can progress to Complicated pneumoconiosis - also known as progressive massive fibrosis (PMF) 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 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 cavitation and necrosis areas of calcification 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 c o r p u l m o n a l e 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 c o r p u l m o n a l e

26. CXR In simple pneumoconiosis nodular shadowing of varying size- up to 10 mm in the upper and middle zones nodular shadowing of varying size- up to 10 mm in the upper and middle zones graded according to the number of different sized nodules graded according to the number of different sized nodules p = < 1.5 mm p = < 1.5 mm q = 1.5-3 mm q = 1.5-3 mm r = 3-10 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 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 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 FEV1 and FVC are normal TLCO may be slightly decreased TLCO may be slightly decreasedPMF: Mixed feature airway obstruction due to emphysema airway obstruction due to emphysema restriction due to loss of lung volumes restriction due to loss of lung volumes TLCO is reduced TLCO is reduced

31. Management Minimization of dust exposure with Minimization of dust exposure with improved mine ventilation improved mine ventilation respirator provision respirator provision monitoring of dust levels 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 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 occur on a background of simple pneumo coniosis and with a relatively low coal dust exposure multiple and may cavitate multiple and may cavitate Cause no significant functional impairment and have no malignant potential Cause no significant functional impairment and have no malignant potential Has to be considered in the D/D of T.B. malignency etc Has to be considered in the D/D of T.B. malignency etc

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 dry cough shortness of breath shortness of breath feeling of tightness on breathing deeply Rapid deterioration over a few weeks feeling of tightness on breathing deeply Rapid deterioration over a few weeks Fine crepitations over the lower zones bilaterally Fine crepitations over the lower zones bilaterally Leads to respiratory failure Leads to respiratory failure CXR Patchy bilateral lower air space consolidation, which may look like pulmonary oedema 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 Chronic silicosis occurs with lower dust concentrations

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

51. Management Prevention by monitoring and minimizing dust levels with adequate ventilation by monitoring and minimizing dust levels with adequate ventilation Masks useful for short-term use Masks useful for short-term use Stop smoking Stop smoking

53. I. I. Acute berylliosis II. II. Beryllium granulomatosis Subacute and chronic berylliosis) ( Subacute and chronic berylliosis)

54. Acute Berylliosis A cute alveolitis due to the direct effects of high-dose inhaled beryllium fumes widespread airway and pulmonary oedema causes widespread airway and pulmonary oedema causes Dyspnoea Dyspnoea Cyanosis Cyanosis widespread inspiratory crepitations widespread inspiratory crepitations CXR shows pulmonary oedema CXR shows pulmonary oedema

55. self-limiting if mild self-limiting if mild severe is usually fatal severe is usually fatal Corticosteroids may prevent progression, but the patient is often left with residual pulmonary impairment Corticosteroids may prevent progression, but the patient is often left with residual pulmonary impairment

56. Subacute and chronic berylliosis  hypersensitivity-type disease that occurs long time after beryllium exposure in a minority of individuals  clinically indistinguishable from sarcoidosis  seen in wives of beryllium workers wives of beryllium workers who live near beryllium refineries who live near beryllium refineries

57. cell-mediated immune response, with production of numerous inflammatory cytokines granulomatous inflammation. cell-mediated immune response, with production of numerous inflammatory cytokines granulomatous inflammation. Following a long latent period up to 10 years + after exposure, non-caseating granulomatous tissue reactions occur in Following a long latent period up to 10 years + after exposure, non-caseating granulomatous tissue reactions occur in lungs or lungs or on the skin Similar to on the skin Similar to

58. granuloma – ball-like collection of immune cells which forms when the immune system attempts to wall off substances that it perceives as foreign but is unable to eliminate granuloma – ball-like collection of immune cells which forms when the immune system attempts to wall off substances that it perceives as foreign but is unable to eliminate granuloma is a special type of inflammatory reaction that can occur in a wide variety of diseases, both infectious and non-infectious granuloma is a special type of inflammatory reaction that can occur in a wide variety of diseases, both infectious and non-infectious Such substances include Such substances include –infectious organisms bacteria & fungi as well as –other materials such as mineral dust keratin suture fragments and vegetable particles

60. Clinical features Symptoms Cough Cough dyspnoea dyspnoea Macular skin lesions, which do not resolve Macular skin lesions, which do not resolveSigns clubbing & crepitations with established fibrosis clubbing & crepitations with established fibrosis Hepato/splenomegaly and macular skin lesions Hepato/splenomegaly and macular skin lesions

61. Skin lesions in berryliosis

63. CXR Fine reticulonodular appearance throughout both lungs. Finer nodules than sarcoidosis. Fine reticulonodular appearance throughout both lungs. Finer nodules than sarcoidosis. Progression to irregular interstitial fibrosis, with irregular linear opacities seen in the lung bases. Progression to irregular interstitial fibrosis, with irregular linear opacities seen in the lung bases. Hilar lymphadenopathy can occur, but always in association with interstitial lung disease Hilar lymphadenopathy can occur, but always in association with interstitial lung disease

65. BAL- High levels of T-lymphocytes PFTs Restrictive defect, with decreased KCO No single test to distinguish berylliosis from sarcoidosis

66. Management Corticosteroids prevent disease progression. Continue indefinitely as few patients gain complete resolution of symptoms Annual screening of beryllium-exposed workers with CXR breathlessness or skin rashes- an indication to start oral steroids to delay progression to interstitial fibrosis

67. Prognosis with very low exposure who develop CXR changes may resolve Granulomata do not spontaneously resolve Granulomata do not spontaneously resolve can be excised if causing problems, such as troublesome lesions on the skin can be excised if causing problems, such as troublesome lesions on the skin  Interstitial fibrosis occurs in the lungs- progressive and leads to cyanosis and death. complications include  Pneumothorax  Hypercalcaemia & hypercalciuria  Nephrocalcinosis