For the people like us

1. PNEUMOCONIOSIS
DR. SAPANA SEDHAIN
MD PATHOLOGY

2. OBJECTIVES
• Definition & Classification
• Pathogenesis
• Anthracosis
• Silicosis
• Asbestosis

3. INTRODUCTION
DEFINITION:
• Pneumoconiosis, originally coined to describe the non-neoplastic lung
reaction to inhalation of mineral dusts encountered in the workplace
• Now also includes disease induced by chemical fumes and vapors.

4. CLASSIFICATION

5. PATHOGENESIS
1. Dust retention, which is determined by
- dust concentration in ambient air,
- duration of exposure, and
- effectiveness of clearance mechanisms.
2. Particle size:1 to 5 μm in diameter, most dangerous.
3. Particle solubility and cytotoxicity:
-Small particle-highly soluble-rapid injury
-Large particle-less soluble-chronic injury
Depends upon:

6. PATHOGENESIS
4. Particle uptake by epithelial cells:
-allows direct interactions with fibroblasts and
interstitial macrophages.
5. Activation of the inflammasome,
-occurs following the phagocytosis of certain particles
by macrophages.
-This innate immune response amplifies the intensity
and the duration of the local reaction.
6. Tobacco smoking,
-worsens the effects of all inhaled mineral dusts,
-hampers mucociliary clearance

7. COAL WORKER
PNEUMOCONIOSIS
(ANTHRACOSIS)

8. COAL WORKER PNEUMOCONIOSIS
• lung disease caused by inhalation of coal particles and other admixed forms of
dust.
• The spectrum of lung findings in coal workers:
-Anthracosis: Asymptomatic
-Simple coal workers’ pneumoconiosis: little to no pulmonary dysfunction,
-Complicated coal workers’ pneumoconiosis/progressive massive fibrosis
(PMF): lung function is compromised.
• Coal workers may also develop emphysema and chronic bronchitis independent of
smoking.

9. PATHOGENESIS
• Common in Coal miners and Tobacco smokers
• Inhaled carbon pigment
• engulfed by alveolar/interstitial macrophages
• accumulate in connective tissue along the lymphatics or in
lymphoid tissue.
ANTHRACOSIS

10. MORPHOLOGY
- Anthracosis: tiny black pigmentation scattered throughout.
- Simple coal workers’ pneumoconiosis: Palpable or non-palpable
darkly pigmented foci . Coal macule: (1-2 mm) ,Coal nodule
- Complicated coal workers’ pneumoconiosis, or progressive
massive fibrosis(PMF): heavily pigmented, destructive fibrous
nodules.

11. Anthracosis
Simple coal
workers’
pneumoconiosis
Complicated coal
workers’
pneumoconiosis,or PMF)

12. MORPHOLOGY
Microscopy:
• Antracosis- Pigment laden interstitial macrophages
• Simple CWP- Deposition of black pigment, with associated fibrosis within and
around the walls of respiratory bronchioles and alveolar duct. Rarely small fibrotic
nodules.
-Coal macule: (1-2 mm) consists of carbon-laden macrophages
-Coal nodule: carbon laden macrophages & collagen fibers
• Complicated CWP or Progressive massive fibrosis (PMF)- Coarse collagen
bundles arranged in a haphazard manner. Interspersed with black pigment.

14. CLINICAL FEATURES
• usually benign, little decrement in lung function.
• majority - do not affect lung function
• 10% progressive massive fibrosis develops - increasing pulmonary
dysfunction, pulmonaryhypertension, and cor pulmonale.
• Caplan's syndrome -When coal miners develop rheumatoid arthritis,
they tend to develop large rheumatoid nodules in the lung

15. SILICOSIS

16. SILICOSIS
• Most prevalent chronic occupational disease in the world
• usually presents after decades of exposure
• as a slowly progressing, nodular, fibrosing pneumoconiosis

17. SILICOSIS
• Cause: inhalation of proinflammatory crystalline silicon dioxide (silica).
• Forms of Silica:
- Crystalline
- Amorphous
• Crystalline forms (quartz, cristobalite, and tridymite): more fibrogenic and
more important in pathogenesis.

18. SILICOSIS
Risk:
- individuals involved with the
repair, rehabilitation, or
demolition of concrete structures
- sandblasting, stone carvers,
and jewelers using chalk molds

19. PATHOGENESIS
• Inhalation of silica crystal
• Phagocytosis by macrophages and activation of the inflammasome and
• Release of inflammatory mediators particularly IL-1 and IL-8.
• Recruitment of additional inflammatory cells and activates interstitial
fibroblasts,
• leading to collagen deposition.

20. MORPHOLOGY
Grossly:
• early stages - tiny, pale to blackened nodules in the hilar lymph nodes and upper zones
of the lungs.
• Progression >> coalesce into hard, collagenous scars.
• Superimposed tuberculosis or ischemia >> nodules may undergo central cavitation
• Calcification occur in the lymph nodes and are seen radiographically as eggshell
calcification (i.e., calcium surrounding a zone lacking calcification).
• Disease progress to produce progressive massive fibrosis (PMF).

21. MORPHOLOGY
Microscopy:
• characterized by a central area of whorled collagen fibers with a more
peripheral zone of dust-laden macrophages.

22. EGG SHELL
CALCIFICATION

23. • Advanced silicosis (transected lung).
• Scarring has contracted the upper lobe into a
small dark mass
• Several coalescent collagenous silicotic nodules
Silicotic nodule

24. CLINICAL FEATURES
• Pulmonary functions affected: when PMF develops
• Chest X-ray: Fine modularity in upper zone of the lung
• Silicosis >> decrease cell mediated immunity & decrease ability of
pulmonary macrophages to kill phagocytosed mycobacteria>>
• Increase susceptibility to TB

25. ASBESTOSIS

26. ASBESTOSIS
• Asbestos is a family of proinflammatory crystalline hydrated silicates
• Naturally occurring fibrous minerals- resistant to heat and corrosion.
• Insulation and fireproofing materials, automobile brakes, wall board
material, adhesives, metal fabrication etc)
• associated with pulmonary fibrosis and various forms of cancer

27. ASBESTOSIS
• Asbestos-related diseases include:
-Localized fibrous plaques or diffuse pleural fibrosis
-Pleural effusions
-Parenchymal Interstitial fibrosis (Asbestosis)
-Lung carcinoma
-Mesotheliomas
-Laryngeal & other Extrapulmonary Neoplasms (colon CA)

28. ASBESTOSIS
Serpentine:
• M/C (90%)
• Chrysotile
• More flexible and curved
• Likely to impacted in upper
respiratory passage
• Removed easily by
mucociliary apparatus
Amphibole:
• Less commonly used(more pathogenic)
• Amosite, Crocidolite,anthophyllite
• Stiff and short
• Likely to delivered deeper into the lungs
• Penetrate epithelial cells and reach
interstitial

29. ASBESTOSIS
• Length of the Amphibole fibers also play a role in the pathogenicity
• longer than 8µm & thinner than 0.5 µm are more injurious than shorter,
thicker ones.
• Complication: Mesothelioma (Amphibole).-tumor initiator & tumor
promoter.
• Risk of lung carcinoma: 5 folds when alone & 55 folds when combined with
smoking.

30. PATHOGENESIS
• Inhalation of Asbestos
• Interact with epithelial cells and macrophages and penetrate the alveoli and reach
interstitial
• Release of mediators
• Interstitial Fibrosis
Activation of inflammaosme in
macrophages
IL-1,Fibronectin, Lipid mediators,
oxygen derived free radicals and
fibrogenic cytokines
Also act as Tumor Initiator and Promotor ——— Carcinogenesis

31. MORPHOLOGY
• Diffuse pulmonary interstitial fibrosis
• Asbestos bodies: golden brown, fusiform or beaded rods>> consist of
asbestos fibers coated with an iron-containing protein
• Ferruginous bodies: other inorganic particulates coated with similar iron-
protein complexes
• Asbesteosis lower lobes and subpleurally

32. Asbestos body

33. MORPHOLOGY
Pleural plaques:
• Most common manifestation of asbestos exposure
• Well-circumscribed plaques of dense collagen containing Calcium
• Sites: parietal pleura, dome of diaphragm
• Do not contain asbestos bodies

34. Asbestos-related pleural plaques.
Large, discrete fibrocalcific plaques are seen on the
pleural surface of the diaphragm

35. CLINICAL FEATURES
• similar to other diffuse interstitial lung diseases
• rarely appear fewer than 10 years after first exposure
• more common after 20 to 30 years.
• Dyspnea is the first manifestation. Initially provoked by exertion, but later at
rest.
• The disease may remain static or progress to respiratory failure, cor-
pulmonale and death.

36. TAKE HOME MESSAGE
• Group of chronic fibrosing disease of the lung
• Exposure to organic and inorganic particulates, most commonly mineral dust.
• Alveolar macrophages -central role in Pathogenesis - Promote inflammation and
produce fibrogenic cytokines
• Coal dust -Asymptomatic anthracosis, Simple CWP, PMF- pulmonary
dysfunction,pulmonary hypertension and cor-pulmonale
• Silicosis-m/c. Crystalline silica (quartz). Disease progress even after exposure stops.
Asymptomatic silicotic nodules to dense fibrosis.Increased susceptibility to TB and
increased risk of Lung Cancer.
• Asbestos- 2 forms. Stiff Amphiboles- fibrogenic and carcinogenic

37. Thank you!