3. PNEUMOCONIOSIS
•Non neoplastic lung reaction to inhalation
agents:
•Chemicals induced
•Vapor induced
•Organic and inorganic particulates
•Common minerals:
•Coal – coal worker pneumoconiosis
•Silica – silicosis
•Asbestos – asbestosis increased risk of
cancers
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4. PATHOGENESIS OF PNEUMOCONIOSIS
• Lung reaction will depend on:
• particle size – 0.5μm - 5μm
• Particle shape
• Particle solubility
• Particle reactivity –coal<silica, asbestos, beryllium
• Particle inhaled trapped in mucous blanket removed
from the lung thru’ cilia movement. This the normal
pathway
• Fate of the inhaled particle:
• Direct drainage into lymphatics
• Via alveolar macrophage into lymphatics
• Immune response to self proteins produced by the
particles
• Tobacco smoking worsens their effects -asbestos
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5. …
..Particles get impacted at alveolar duct bifurcation
engulfed by alveolar Macrophage inflammatory
immune response fibrosis and collagen deposition.
..Activation of alveolar macrophage leads release of
various mediators
i. Free radicals - reactive oxygen species which
damage the lung parenchyma.
ii. Chemotactic factors for various leucocytes
(leukotrienes, TNF, IL-8 and IL-6) resulting in
infiltration into pulmonary tissues by these
inflammatory cells which on activation cause
further damage.
iii. Fibrogenic cytokines such as IL-1, TNF and platelet
derived growth factor (PDGF) which stimulate
healing by fibrosis due to proliferation of fibroblasts
at the damaged tissue site
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7. COAL WORKERS PNEUMOCONIOSIS
• Pneumoconiosis due to coal dust inhalation
• Coal = carbon(mainly), crystalline silica, inorganic materials
(muscovite, kaolin), trace elements (arsenic, titanium and
beryllium)
• Types of coal – peat, lignite,(brown coal/immature coal)
sub-bituminous, bituminous(black)
anthracite(shiny/mature)
• Cola rank =ratio of carbon to the contaminating minerals
• The incidence and progression of CWP relates to
• the cumulative exposure of dust inspired,
• the coal rank, i.e. the amount of volatile matter within the
coal.
• The higher-ranked coals, containing the least amount of
volatile matter, have a higher incidence and severity of CWP
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8. MORPHOLOGY CWP
• Anthracosis simple CWP complicated CWP
(PMF)
• Anthracosis
• Asymptomatic
• Commonly seen in:
• urban dwellers
• Tobacco smokers
• Alveolar or interstitial macrophage engulf inhaled
carbon – macrophage accumulate :
• in the interstitial CT
• Along lymphatics –pleural and lymph nodes
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9. SIMPLE COAL WORKERS
PNEUMOCONIOSIS
• Gross:
• Mostly involve upper lobes or upper 2/3 of the lungs
• Lesions are scattered throughout the lungs
• Coal macules and sometimes nodules
• Histology:
• Macules – dust laden macrophages
• Nodules – small amounts of collagen array in a delicate
network
• Radiography - Simple” pneumoconiosis is
characterized by small, ill-defined, rounded opacities
in the outer thirds of the lung fields and the mid and
upper zones.
• Centrilobular ‘emphysema’ CAN OCCUR
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10. COMPLICATED COAL WORKERS
PNEUMOCONIOSIS
• Also known as the “black lung disease”
• A form of Progressive Massive Fibrosis (PMF)
• Occurs on a background of simple CWP Coalescence of
coal nodules
• Generally requires many years to develop and can progress
even if dust exposure ceases.
• Associated with increased incidence of clinical tuberculosis,
chronic bronchitis and emphysema
• Independent of smoking, PMF does not appear to increase
the risk of lung cancer
• Gross: Multiple intensely blackened scars - >2cm and up to
10cm
• Histology – dense collagen and carbon pigment
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12. CLINICAL FEATURES OF CWP
• Benign disease and hence produces little lung
dysfunction
• PMF
• increasing pulmonary dysfunction
Tightness in the chest
Dyspnea
Chronic Cough with black sputum
Cyanosis
• Pulmonary HTN
• “Cor pulmonale”
• No carcinoma in absence of smoking
• fever and night sweats -if a superimposed
mycobacterial infection is present
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13. PROGRESSIVE MASSIVE
FIBROSIS (PMF)
• Sometimes, these masses break down centrally due to
ischemic necrosis or due to tuberculosis forming cavities
filled with black semifluid resembling India ink.
• The pleura and the regional lymph nodes are also blackened
and fibrotic
• Factors determining PMF progression:
1. Older age of the miners.
2. Severity of coal dust burden engulfed by macrophages.
3. Prolonged exposure (20 to 30 years) to coal dust…Coal dust
exposure level
4. Concomitant tuberculosis.
5. Additional role of silica dust.
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14. CAPLAN’S/ KAPLAN’S SYNDROME
- 1st described in coal workers, may be seen in other
pneumoconiosis
- Results when PMF is associated with rheumatoid factor.
- ?? Immunopathologic mechanism
- RA + Rheumatoid nodules (Caplan nodules) in the lung OR
RA+ pneumoconioses
- Caplan’s nodule = necrosis surrounded by fibroblasts,
monocytes and collagen
- s/s RA > lung symptoms
- The Caplan nodules exhibit a central area of coal dust and
necrotic collagenous tissue lying in concentric rings and it is
surrounded by an area of neutrophils with palisading
fibroblasts
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15. DIAGNOSIS, TREATMENT, AND
MANAGEMENT.
• DX –
• Occupational history medical history Env’ history
• Chest radiographs
• Chest x-rays
• Computed tomography
• Bronchoscopy
• Spirometry
• CBC and Sputum Culture
• Arterial blood gases
• No treatment
• Lung transplant??
• Management – monitoring through chest radiographs
• Minimizing exposure to coal dust
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16. REFERENCES
• Robbins Basic Pathology 9th Edition by Vinay Kumar, Abul
K. Abbas, Jon C. Aster
• Towards Understanding Coal Workers Pneumoconiosis pdf
by Alice Maria Ciobanu SID: 3395606
• Harsh Mohan – Textbook of Pathology, 6th edition pdf
• Muirs Textbook of Pathology, 14th edition pdf
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