Pathologic Diagnosis in Occupational Lung Diseases

1. Pathologic Diagnosis in Occupational Lung Diseases Dr.E.Handan Zeren Çukurova University

2. Occupational lung disease ≠ Pneumoconiosis • Pneumoconiosis = Retention of and pathologic effects from the inhalation of dust particles • Many of the diseases named occupational lung disease do not match with this definition

3. In most cases, the diagnoses is made without tissue examination…. • History of the patient • Clinical findings • Radiologic features • Epidemiologic features

4. Properties of inhaled dust particles… • Size (Particles <10μm and more likely <5μm reach the lung parenchyma) • Fibers, esp. asbest can reach the parenchyma when larger than 10 μm.Width is an important factor • Chemical properties • Mineralogic properties all affect the potency of a dust particle to cause lung injury

5. Pathologic reaction patterns • Fibrogenic particles (asbestos, silica) • Nodular fibrosis • Intersititial fibrosis • Both • Non-Fibrogenic particles (carbon)

6. Centriacinar emphysema • Centriacinar dust macules • Mineral dust airway disease • Dust-laden macrophages along lymphatic routes- bronchovascular bundles, pleura, interlobular septa • Noduler fibrosis • Diffuse interstitial fibrosis- UIP • Massive fibrosis • Other reactions- granulomatous reaction, alveolar proteinosis, hipersensitivity pneumonitis etc.

7. Hyaline pleural plaques • Pleuritis and pleural fibrosis

8. Coal Worker’s Pneumoconiosis(CWP) • The most significant factor in the development of CWP is the cumulative exposure to coal dust • Simple CWP- Macules of coal dust and focal emphysema (centriacinar- similar to smoker’s emphysema)

9. CWP: Different pathologic patterns Coal nodules Rheumatoid pneumoconiosis Progressive massive fibrosis

10. Silicosis • Nodular fibrosis • < 10 mm- simple silicosis • >1 cm- complicated silicosis • At least a latent period of 20 years • Accelerated silicosis- A latent period of 3-10 years

11. Dr.Andrew Churg- Van Couver, Canada

12. Acute Silicoproteinosis • Same morphology with alveolar proteinosis • Heavy silica inhalation • Symptomatic within 3 years, fatal in most cases

13. Early Silicosis

14. Formation of the silicotic nodule

16. PMF (Progressive massive fibrosis) in silicosis • If necrosis is present, TB must be roled out

17. Mixed dust pneumoconiosis

18. İsolated pleural silicosis ZEREN EH, COLBY TV, ROGGLI VL. SILICA-INDUCED PLEURAL DISEASE: AN UNUSUAL CASE MIMICKING MALIGNANT MESOTHELIOMA. CHEST (1997)112:1436-8

19. Diseasesassociated with Asbestos exposure • Asbestosis • Asbestosairway disease • Non-neoplastic pleuralpatologic conditions • Benign asbestos effusion • Visseral pleural fibrosis • Hyaline pleral plaque • Lung cancer • Malignant mesothelioma

20. Asbestos bodies Ghio AJ, Churg A, Roggli VL; Toxicologic Pathology (2004)32:643-649

22. Asbestosis • Heavy exposure, latent period ↓ • Pleural involvement- an important clue • Involvement of the lower lobes

23. Pulmonary Siderosis • Deposition of iron and iron oxides following the exposure- not very uncommon • No clinically apparent disease unless mixed with other fibrogenic dusts • Small airway dysfunction and emphysema if inhaled in large amounts Asbestosis + Siderosis

24. Berilliosis-chronic berillium disease • Metal working, ceramic, electronic, computer industry, space industry, dental laboratories using berillium alloys, florescent lamp manufacturing • Multisystemic disease • Similar clinic and pathologic features with sarcoidosis

25. Hard metal (Cobalt) lung disease • As hard as dimond- ideal for ctting of metal tools • Formerly, categorized as “Giant cell intersititial pneumonia” in Leibow’s classification

26. Occupational hipersensitivity pneumonia (HP) (extrinsic allergic alveolitis) • Organic antigens or simple inorganic chemical compounds • The exposure is obvious in most cases (e.g: Farmer’s lung); whereas it can be difficult to identify in some others (e.g: Contamination of ventilation system) • Hot-tub disease- Water supplies contaminated by M.Avium

27. HP • Type 3 (immune complex) ve Type 4 (T-cell mediated, delayed type hypersensitivity ) immune reactions • Acute- 4-6 hours • Subacute- days-weeks • Chronic- long lasting, low amounts of antigen exposure. Irreversible respiratory function disability and fibrosis can occur

28. Chronic bronchiolitis + peribronchiolar interstitial pneumonia Lyphocytic + histiocytic inflammation, rare eosinophils and plasma cells Loose granulomas in 2/3 of cases HP-Histology

29. HP • Fibroblastic plugs filling the alveol lumens (Masson bodies) • In old cases, irreversible changes such as UIP features and end stage lung- difficult to diagnose

30. Differential diagnosis-HP • Collagen vascular diseases, drug reactions, infections, NSIP • DETAILED CLINICAL INFORMATION + SPECIAL STAINS FOR MICROORGANISMS +IDENTIFICATION OF THE RESPONSIBLE ANTIGEN

31. Organic dust toxic syndrome • Acute, systemic illness following massive exposure to organic dusts containing microorganisms or their endotoxins • Farmers exposed to grains or moldy hay contaminated with fungi • Not a real immune reaction as it occurs without prior history of sensitization • Intraalveolar space- neutrophils and histiocytes • Acute bronchiolitis

32. Gases and Fumes • ARDS • Chronic bronchitis • Necrotizing bronchiolitis • Asthma • Bronchiectasis • Organizing pneumonia

33. Conclusions • The diagnosis of occupational and environmental diseases is made by combining the clinical, epidemiological, radiologic, and pathologic features with the patient’s occupational and environmental status

34. In the diagnosis, these questions are important: • Is there a clear evidence of exposure to a known agent that is associated with the findings identified? • How strong is this association and chance of developing the disease? • What is the temporal sequence ofthe exposure, and the onset of the disease? • Can the pathologic findings be explained only by the exposure? • Is the exposure related to a single disease?

35. THANK YOU…