Dr. Lokesh Lalwani Silicosis presentation.pptx

silicosis is a major problem in india

1. Pathogenesis, Clinical Evaluation and Management of Silicosis DR. Lokesh Kumar Lalwani Assistant Professor Department of Respiratory Medicine ESIC Medical College & Hospital, Alwar

2. History Mining and metal work goes back to ancient times Rock cutting and stone carving to build temples also present since a long time in India Emerged with increasing industrialization C. Krishnaswami Rao was first to confirm cases of Silicosis in India in 1934* *Current Science, Page No. 283- 284 “Incidence of Silicosis in Kolar Gold Fields, Mysore”

3. Silicosis Most prevalent chronic occupational lung disease* Irreversible and chronic fibrotic disease caused by inhalation, retention and pulmonary reaction to large amounts of silica dust (SiO2)

4. Source of Silica Crystalline silica is found in materials such as soil, sand, concrete, mortar, granite, and other minerals Industries such as construction, mining, oil and gas extraction, stone countertop and foundries. Other form of silica is Amorphous. “R espirable crystalline silica" (RCS) are less than 5 μm in diameter . https://www.lung.org/lung-health-diseases/lung-disease-lookup/silicosis/learn-about-silicos .

5. New sources of silicosis

6. Prevalence of Silicosis Prevalence varies widely among various industries Rupani Journal of Occupational Medicine and Toxicology

7. Estimated workers in India According to a report, in FY 2017-18, there were 229,522 persons are employment in the quarries in Rajasthan It excludes workers from MSMEs, traders, exporters or transport Sandstone mining industry in India employs nearly 1.3 million people on a seasonal basis. 8.5 million more work in construction related activities Silicosis and silicotuberculosis in India, WHO bulletin, Sharma N et al.

8. Pathogenesis

9. Clinical Course – 3 forms

10. Chronic Silicosis Develops following low-to- moderate level exposure to silica dust for >20 yrs . 1 st  Silica laden macrophages accumulate Later  Silicotic nodules form as a result of host response to the foreign body . Calcified LN maybe seen

11. Silicotic nodule Central area organised with concentric whorl-like collagen fibres with inflammation in periphery Also called histological tornadoes

12. Simple Chronic Silicosis Also Called Nodular silicosis Small rounded opacities – from pinhead sized to 1 cm 1 st upper zones  then all over lung fields Pathology: Silicotic Nodule is characteristic lesion Egg shell calcification of lymph nodes may be seen

13. Simple Chronic Silicosis (Nodular Silicosis)

14. PMF (Complicated Silicosis) When one or more nodules attain a size of > 1 cm MC in posterior segments of upper lobes or superior segments of lower lobes Asymmetrical Development influenced by: Mycobacterial infection Immunologic response

15. Complicated Chronic Silicosis

16. Accelerated Silicosis Heavy silica exposure in 5 to 10 years Progresses faster than chronic silicosis Sometimes associated with CTD

17. Acute silicosis Very High concentration of silica exposure over weeks to months – eg. Sandblasters, rock drilling, etc B/l alveolar opacities without silicotic nodules Hypertrophic Type II pneumocytes  produce excess surfactant  Resembles PAP

18. Clinical evaluation Strong history of exposure Acute Silicosis- Rapid progression of dyspnoea, weight loss, and fatigue with diffuse bilateral crackles. Hypoxemia and respiratory failure is common. Chronic Silicosis- May be Asymptomatic Many patients develop progressive dyspnoea and cough Pulmonary consolidation, pulmonary hypertension, and Respiratory failure with/without Right Heart Failure may develop.

19. Radiology

20. Radiology

21. ILO classification of Radiograph

22. Chest X- ray Schedule Duration Age X- ray schedule <10 years All age Every 5 years >10 years <30 years Every 5 years >10 years 35- 44 years Every 2 years >10 years >45 years Every year (Donaldson k et al. Ann Occ Hyg 1998;42)

23. Pulmonary function testing Restrictive pattern Decreased FeV 1 Decreased FVC Reduced diffusion capacity and gaseous exchange

24. Other diagnostics Auto immune serology such as antinuclear antibodies and rheumatoid factor used to rule out CTD. Sputum culture and cytology and bronchoscopy can be used for other diagnosis like tuberculosis, cancer or ILD.

25. Complications Tuberculosis Cor pulmonale Spontaneous pneumothorax Tracheobronchial obstruction Lung cancer Hypoxemic ventilatory failure

26. Silico-tuberculosis The association of Silicosis and TB has been suspected several hundred years In 1902 JS Holdene committee reported that “Stone dust predisposes enormously to TB in the lung” Exposure to silica causes a renewed multiplication of bacilli in the healing TB lesions

27. Incedence In India silicotuberculosis incidence - 28.6% (Sikand BK, Pamra SP Proceedings of Seventh TB workers conference, 1949) 10.7% in stone cutters, 22.5 % in Slate Pencil Workers (Tiwari RR et al,NIOH ) 23% in stone quarries of Rajasthan (P K Sishodiya et al, NIMH 2012) 12% with silicosis had Sputum Positive PTB (Keerthivasan et al, 2013) TB is 3 to 7 times higher in Indians with silicosis . (Gupta SP et al. India J Med Res 1972)

28. Interaction of S ilicosis with TB Exposure of silica has an unfavourable influence on the course of induced TB There is more fibrosis produced by combination . Synergistic effect of silicosis and TB  Rapid fibrosis It may develop PMF with cavitation Poor response to ATT  Longer duration needed

29. Iron Hypothesis Mycobacteria are dependent on iron for growth and produce the iron chelator – mycobactin Silica particles absorbed body iron and act as a reservoir of iron Silicato- iron complexes may activate dormant tubercle bacilli

30. Diagnostic dilemma Symptoms of silicosis and silicoTB are misleading . Interpretation of the Chest X ray flim of the silicotic is difficult The recovery of AFB in the sputum of patients suffering from silicotuberculosis is difficult. Most patients are sputum negative because of walling in of the tubercle foci by silicotic fibrosis which prevents the discharge of tubercle bacilli in the sputum

31. Pointers to TB Clinical - Fever, Expectoration, Hemoptysis, LoA, LoW In miliary TB patient is toxaemic – compared to simple chronic silicosis Poorly demarcated “soft” infiltrates of variable size that do not cross the lung fissures s/o TB Presence of a cavity in a nodule

32. Pointers to TB The nodules in miliary tuberculosis are smaller than those in silicosis . Associated pleural/pericardial effusion . Rapid worsening in radiology .

33. A nti T ubercular T reatment Prolongation of the continuation phase from 4 to 6 months decreased the rate of relapse from 22 to 7 % (Blumberg et al. Am J Resp & crit care Med Feb 15- 2003)

34. Treatment of Silicosis No specific therapy for silicosis Prevent further exposure to silica dust .

35. Experimental treatments Cytokines inhibitors against IL-1, TNF- α Antioxidant therapy e.g. N-acetyl cysteine Intratracheal administration of bone marrow derived mononuclear cells Polyvinyl pyridine N-oxide (PVNO) Inhalation of aluminium Not proven useful

36. Role of Antifibrotics Conclusion - Role of antifibrotics is described in animal model but human studies are still pending….

37. Issues to be addressed in India Lack of awareness among workers, employers and doctors Inadequate infrastructure for diagnosis and management Small scale and unorganized sector not covered by legislation Poor quality or absence of health surveillance programme in industry Cases notified reflect only tip of Iceberg – most cases not recognised/reported Misdiagnosis and treatment of silicosis as tuberculosis Lack of coordination among stake holders for elimination of silicosis

38. Take home message. Silicosis remains an important and under-recognized occupational lung disease. Chronic silicosis is the most common form. Diagnosis is based on a history of exposure and consistent imaging findings. Silicosis is associated with increased risk of tuberculosis, COPD, lung cancer, and rheumatic disease. Treatment is largely supportive.

39. A way forward….