Asbestos related lung disease

Asbestos-related diseases include non-malignant disorders such as asbestosis, diffuse pleural thickening, pleural plaques, pleural effusion, rounded atelectasis and malignancies such as lung cancer and malignant mesothelioma.

1. Asbestos-Related Lung Disease Dr Kamal Bharathi. S Post Graduate, Department of Pulmonary Medicine, Sri Manakula Vinayagar Medical college and Hospital.

2. Asbestos Asbestos is a fibrous hydrated magnesium silicate. Derives Greek meaning unquenchable or inextinguishable. Long, thin fibers with a length to width ratio of 3:1. Properties are  sound absorption , average  tensile strength , affordability, and  resistance to fire , heat, and electricity.

3. Commercial forms of Asbestos Serpentine form Chrysotile- wavy and long Amphibole s Crocidolite - needle-shaped with many long fibers Amosite - thicker Anthophyllite Actinolite Tremolite

4. TYPES OF EXPOSURE Primary exposures- miners and millers. Secondary exposures- manufacturing plants using asbestos in the production of textiles, friction materials, tiles, and insulation materials.

5. Direct Exposure- sheet metal work, plumbing, pipefitting, insulation, railroad and utility work, and school or building custodians. Indirect exposures- household contact. Bystander exposures- working near asbestos workers

6. Asbestos Bodies Asbestos fibers accumulate in the interstitium of the lung and are coated by iron and hemosiderin in a beaded, clubbed fashion referred to as ferruginous or asbestos bodies.

7. NON-MALIGNANT PLEURAL MANIFESTATIONS Pleural plaques Diffuse pleural thickening Rounded atelectasis Acute pleural effusion

8. PLEURAL PLAQUES Most common manifestation Pathogenesis : 1) Asbestos fibers – transported by subpleural lymphatics to the pleural space- inflammation, and eventually fibrosis. 2) Mesothelial cells- internalize asbestos fibers via an integrin receptor that recognizes vitronectin ; & pleural mesothelial cells also can synthesize collagens (types I, III, and IV), elastin, laminin , and fibronectin .

9. Macroscopically - appear as grey-white regions of pleural thickening, often thickest at the margins, giving rise to the  holly leaf appearance  

10. Histologically - Extensive collagen fibrils arranged in a basket-weave pattern, and a thin covering of mesothelial cells. The parietal pleura is uniformly involved, with minimal thickening of the visceral pleura.

11. Clinical Features- usually asymptomatic Incidental findings on CXR, usually bilateral. Radiographic Features commonly in the lateral and posterior midlung zones. rolled or holly-leaf pattern, especially if calcified. CT- increases plaque detection Treatment- No specific, Medical surveillance.

12. DIFFUSE PLEURAL THICKENING The fibrotic responses can be localized or diffuse and either unilateral or bilateral. Appears whitish discoloration of the lung surface to a thick white peel 90% of patients it affects the costophrenic angle. Most commonly affects visceral pleura & subadjacent interstitium .

13. Pathogenesis- fibrotic resolution of a benign pleural effusion. Clinical features- asymptomatic dyspnea on exertion, chronic dry cough, chest pain.

14. Radiographic Features- continuous pleural opacity. blunting the costophrenic angle. unilateral or bilateral. Treatment- no specific therapies Medical surveillance

15. ROUNDED ATELECTASIS  or Blesovsky syndrome Rare complication. Caused by scarring of the both the pleura & the adjacent lung, with the pleural reaction folding over on itself- trapping the underlying lung- atelectasis. Pseudotumor HRCT- diffuse pleural thickening, characteristic comet tail (produced by the pulling of bronchovascular bundles giving the shape) & bronchi sweeping into a wedge-shaped mass

16. ACUTE BENIGN PLEURAL EFFUSIONS Common 20 to 40 years of age. Latency period is shorter. Effusions are exudative and often bloody, glucose concentrations are normal. Mesothelial cells in effusions are found in about 50% of patients.

17. ASBESTOSIS Asbestosis is the interstitial pneumonitis and fibrosis caused by exposure to asbestos fibers. Characterized by discrete areas of fibrosis in the walls of respiratory bronchioles. Peribronchiolar cellular reaction that may narrow and obstruct the airway lumen.

18. PATHOGENESIS Asbestos fibers are deposited at respiratory bronchioles and alveoli- migrate into the interstitium - causes alveolar macrophages to accumulate- Alveolar macrophage alveolitis . Following most fibers are cleared If clearance is incomplete, fibrosis can ensue.

19. fibers induce apoptosis in the cells. coating of asbestos fibers to form asbestos bodies makes them less toxic. Most of fibers- remain uncoated Chrysotile- split longitudinally- generates additional fibers that can multiply the asbestos effect even after exposure has ceased.

20. Asbestos fibers stimulate macrophages to produce a variety of important cytokines & growth factors IL-8- recruits neutrophils to sites PDGF, IGF-1, IL-1 β , TNF- α - stimulate tissue fibrosis by fibroblast proliferation, chemotaxis and collagen biosynthesis.

21. BAL, CT scanning, and 67gallium scanning have demonstrated that inflammatory events occur well before the onset of clinical disease.

22. CLINICAL FEATURES: Dyspnea on exertion is the earliest symptom. Bibasilar rales are a distinctive feature. restrictive impairment with a reduction in lung volumes (especially FVC and total lung capacity), decreased lung diffusing capacity (DLCO), and arterial hypoxemia.

23. RADIOGRAPHIC FEATURES- no pathognomonic radiological features specific Bilateral diffuse reticulonodular opacities, predominantly in the lower lung zones. HRCT features: (1) Curvilinear subpleural lines, (2) increased intralobular septa, (3) dependent opacities, (4) parenchymal bands and interlobular core structures, (5) honeycombing.

24. TREATMENT no established treatment for this disorder. Because of the risk of lung cancer and mesothelioma, medical surveillance with CT scans (smoke >30 pack-years & age >55 years) annual basis is recommended.

25. MALIGNANT MESOTHELIOMA Appears as multiple, small, grayish nodules on the visceral and parietal pleura that evolve to coalesce and form larger masses of tumors. Invade by direct extension.

26. Three histological patterns: Epithelial- neoplastic cells are arranged in papillary, tubular, or solid nest configurations. Sarcomatous - has spindle-shaped cells. Mixed or biphasic

27. PATHOGENESIS Structural chromosomal abnormalities chromosomal gains (chromosome 22) and losses (chromosome 7) Deletions of the short arm of chromosome 3, the break point 1p11 to p22, chromosome 17, and structural and numeric changes in chromosome 7 described.

28. Upregulate the PDGF B-chain gene and, to a lesser extent, the PDGF A-chain gene. High levels of transforming growth factor and IGF-1 bioactivity have been reported.

29. CLINICAL FEATURES Common in males(3 and 4 to 1) 50 and 70 years of age Chest pain is the most common symptom. Effusion is an exudate, can be hemorrhagic. Paraneoplastic syndromes of inappropriate ADH secretion, clubbing, or hypoglycemia. Thrombocytosis is common.

30. RADIOGRAPHIC FEATURES- variety of radiographic abnormalities Include thick pleural peel along the lateral chest wall that can extend to the apex with an irregular nodular surface, multiple pleural nodules or masses, plaque-like opacities, and pleural effusion(s).

31. Pathological diagnosis of malignant mesothelioma may be difficult- IHC helpful.

32. Best negative markers are CEA, MOC-31, and B72.3 Thoracoscopy is the procedure of choice in establishing the diagnosis of mesothelioma.

33. TREATMENT Median survival time is app 8 to 12 months. Extrapleural pneumonectomy + radiation therapy, may result in improved survival. Chemotherapy with gemcitabine and carboplatin or pemetrexed and cisplatin . Immunotherapy with intrapleural or gene therapy with interferons has produced occasional complete or partial responses.

34. Thank you…!!!