This document discusses various types of pneumoconiosis, including anthracosis, silicosis, and asbestosis. It defines pneumoconiosis as non-neoplastic lung disease caused by inhaling mineral dusts in the workplace. The key causes are inhaled coal dust, crystalline silica, and asbestos fibers. The pathogenesis involves particle retention in the lungs, uptake by macrophages, and activation of inflammatory responses. Specific diseases are discussed, including their morphology, clinical features, and relationships to lung function impairment and cancer risks.

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!