Pneumoconiosis

1. Pneumoconiosis

3. Pnemoconiosis • Pulmonary diseases caused due to inhalation of inorganic or organic dust in occupational environment Chronic Interstitial lung disease Chronic Restrictive lung disease

4. Pnemoconiosis Factors determining damage Size and shape of particles Solubility and physiochemical composition Amount of dust retained The additional factors - smoking Host factors and immune status

5. The most dangerous particles range from 1-5µ in diameter because they may reach the terminal small airways and air sacs and settle in their linings

6. Inorganic dusts

9. Organic dust

10. Mouldy hay – Farmers lungs • Bagasse- Bagassosis • Cotton - Bysinosis • Bird droppings – Bird fanciers lung • Mushroom compost dust – Mushroom workers lung • Malt dust –Malt workers lung • Mouldy maple bark – Maple bark diseases

11. Associated disorders • Tuberculosis • Caplan’s syndrome ( Rheumatoid arthritis)

12. Complications • Pulmonary hypertension • Cor- pulmonale • Malignancies

13. Clinical features • Chronic cough with expectoration • Progressively increasing dyspnoea • Recurrent bacterial infections • Respiratory failure • Pulmonary hypertension • Right heart failure Chest x ray- Diffuse ground glass opacities in the lung field suggesting interstitial lung disease

16. Coal-workers pneumoconiosis

17. Coal-workers pnemoconiosis • Coal miners handling coal for 20-30yrs • Anthracosis • Simple coal workers pnemoconiosis - mild initial form • Progressive massive fibrosis- ( complex lesions )

19. Simple coal workers-pneumoconiosis • Coal macules (1-2mm in diameter) • Carbon laden macrophages • Coal nodules • Carbon laden macrophages + small amounts of collagen fibres. • Upper lobes and upper zones of lower lobes more involved. • Centrilobular emphysema

21. Complicated CWP • Progressive massive fibrosis • Many years to develop • Intensely blackened scars 2-10cms diameter • Usually multiple These may break centrally forming cavities containing blackish fluid . The pleura and regional lymphnodes are also blackened and fibrotic

23. CAPLANS SYNDROME Rheumatoid arthritis in few cases of coal workers pneumoconiosis , silicosis and asbestosis ( rheumatoid pneumoconiosis ) • Grossly- lungs have firm rounded nodules with central area of necrosis , cavitations or calcification • Microscopy – lung lesions show central zone of dust laden macrophages and fibrinoid necrosis enclosed by palisading fibroblasts and mononuclear cells . • Rheumatoid factor and antinuclear antibodies are positive

24. Silicosis • Knife grinders lung ,miners , workers( granite, sand stone, slate,coal ,tunnelers , grinders , ceramic workers etc • Inhalation of silicon di oxide • Infrequent acute silicosis • Common chronic form

25. Pathogenesis • Silica particles < 5micrometer on reaching the alveoli are taken up by macrophages which undergo necrosis ,debris engulfed by other macrophages . • Some of these reach respiratory bronchioles, alveoli and interstitial tissue causing inflammatory cell infiltration • Silica is fibrogenic specially quartz elicits fibroblastic response

26. Macrophage derived growth factors (IL-1) favors fibroblast proliferation and collagen deposition • There is also activation of T and B lymphocytes with increase in IgG,IgM antinuclear antibodies , rheumatoid factor

27. Pathologic changes • Grossly- hard fibrotic nodules 1-5mm scattered through out lung ,common in upperzones simultaneous deposition of coal dust and calcification is seen .pleura is thickened and show fibrotic nodules and also regional lymph node .

29. Nodules consists of central hyalinized material with scanty cellularity and dust ,surrounded by concentric laminations of collagen,surrounded by more cellular connective tissue and chronic inflammatory cells . • Severe form with coalesce of adjacent nodules cause complicated silicosis • Intervening lung parenchyma may show emphysematous changes .

31. Polarised light – Birefringent particles of silica

32. ASBESTOSIS

33. Family of crystalline hydrated silicates that form fibres Types of asbestos • Serpentine • Chrysotile (White asbestos) • Amphibole • Amosite (Brown asbestos) • Crocidolite (Blue asbestos)

34. Serpentine chrysotile – most commonly used • Flexible curled structure • Impacted in the upper respiratory passages and removed by mucociliary elevator. • Amphiboles, though less prevalent, are more pathogenic than chrysotiles, particularly with respect to induction of malignant mesothelioma. • Straight stiff fibres align themselves in the airstream & delivered deep into the lungs • Penetrate epithelial cells & reach interstitium.

35. Localised fibrous plaques or rarely, diffuse pleural fibrosis • Pleural effusions • Parenchymal asbestosis / interstitial fibrosis • Lung carcinoma • Mesothelioma • Extrapulmonaryneoplasms

36. PLEURAL PLAQUES • Most common • Well-circumscribed plaques of dense collagen often containing calcium • Anterior and Posterolateral aspects of parietal pleura • Domes of diaphragm • Size and number do not correlate with degree of exposure • No asbestos bodies

37. MORPHOLOGY • Diffuse pulmonary interstitial fibrosis • Presence of multiple asbestos bodies • Begins as fibrosis around respiratory bronchioles and alveolar ducts and extends to involve adjacent alveolar sacs and alveoli. • Fibrous tissue distorts the architecture enlarged air spaces enclosed within thick fibrous walls Honeycomb lung

38. Begins in the lower lobes and subpleurally • Middle and upper lobes become affected as fibrosis progresses • Scarring traps and narrow pulmonary arteries Pulmonary hypertension Corpulmonale

39. Asbestos bodies • Golden brown, fusiform or beaded rods • Transluscent centre • Asbestos fibres coated with iron-containing proteinaceous material • Arise when macrophages attempt to phagocytose asbestos fibres • Iron from phagocyte ferritin

40. HONEYCOMB LUNG • Fibrous tissue distorts the architecture, creating enlarged air spaces enclosed within thick fibrous walls

41. MALIGNANT MESOTHELIOMA • Increased incidence among people with heavy exposure to asbestos • Life time risk in heavily exposed asbestos workers is 7-10% • Long latent period 25-45 years

42. Berylliosis • Heavy exposure to dust or fumes of metallic beryllium used in nuclear and aerospace medicines , atomic reactors industrial ceramics . Types – acute chronic

43. Acute berylliosis • Occurs in unsually sensitive heavily exposed individuals for 2-3 weeks • Pulmonary chemical pneumonitis ,alveoli filled with proteinaceous fluid with formation of hyaline membrane • Present with sudden dyspnoea, hyperpnoea and substernal pain • Patients recover completely

44. Chronic berylliosis • Occurs after 20yrs of exposure • Lesions are due to cell-mediated hypersensitivity • Lesions are multiple non caseating granulomas distributed along pleura, septae and bronchovascular bundles, progression leading to end stage fibrosis

45. Giant cells contain–birefringent crystals Concentrically laminated haematoxyphilic schaumanbodies (small calcifications with lamellar structure) Acidophil star shaped crystals –asteroid bodies

46. Organic dusts

47. HYPERSENSITIVITY PNEUMONITIS • Hypersensitivity pneumonitis is a cell-mediated immune reaction to inhaled antigens in susceptible persons.

48. Antigens derived from bacteria, mould, fungi or other proteins • Patients must be sensitized by an initial exposure, with subsequent re-exposure leading to acute hypersensitivity pneumonitis or chronic hypersensitivity pneumonitis. • Patients with acute hypersensitivity pneumonitis usually present with sudden shortness of breath, chest pain, fever, chills, malaise, and a cough that may be productive of purulent sputum

49. Patients who are chronically exposed to low levels of inhaled antigens can develop subtle interstitial inflammatory reactions in the lung that do not result in noticeable symptoms for months to years • these patients present with severe, impairing disease, which can be very difficult to distinguish from IPF.

50. . • Involves primarily alveoli hence allergic alveolitis. • Loosely formed interstitial granulomas and chronic inflammation