1) Asbestos is a fibrous mineral that was widely used in commercial applications for its desirable properties but is now known to cause several lung diseases. Exposure can occur through mining, manufacturing, or maintenance work. 2) Asbestos fibers accumulate in the lungs and cause non-malignant conditions like pleural plaques or diffuse pleural thickening. It can also cause the serious conditions of asbestosis or malignant mesothelioma. 3) Asbestosis is characterized by fibrosis of the lung tissue and is associated with dyspnea and reduced lung function. Malignant mesothelioma presents as tumors of the pleural lining and commonly affects older males with a history of asbestos exposure.

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
Amphiboles
• 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.

14. 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.

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

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

18. 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

20. 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.

21. 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.

22. 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.

23. • 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.

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

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

26. 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.

27. 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.

30. 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.

31. 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.

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

33. 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.

34. • 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.

35. 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.

36. 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).

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

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

41. 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.

42. Thank you…!!!