Pneumoconiosis

1. PNEUMOCONIOSIS
DAUDA MAGAJI KATUKA

2. OUTLINE
 Introduction
 Epidemiology
 Types
– Pathogenesis
– Clinical features
– Complications
– Morphological features
 Treatment
 Conclusion
 References

3. INTRODUCTION
 Pneumoconiosis also called ‘dust diseases’ or ‘occupational lung diseases’
refers to lung diseases caused by inhalation of dust, mostly at work. [1]
 Broadened to include diseases induced by organic and inorganic
particulates. [2]
 The reaction of the lung to dusts depends on the size of the particles
– Particles greater than 5-10μm are unlikely to reach the distal airways
– Smaller than 0.5μm move in and out of the alveoli without substantial
deposition and injury
– 1-5μm in diameter are the most dangerous.[2]

4. EPIDEMIOLOGY
 In 2013, pneumoconiosis resulted in 260,000 deaths up from 251,000
deaths in 1990.
 46,000 were due to silicosis
 24,000 due to asbestosis
 25,000 due to coal workers pneumoconiosis. [3].
 No sex, race or age predilection
 The current most prevalent is silicosis

5. TYPES [1]
Based on the type of dust inhaled, they include;
1. Coal workers pneumoconiosis (CWP) - Coal dust
2. Silicosis - Silica
3. Asbestosis – Asbestos
4. Berylliosis – Beryllium
5. Siderosis – Iron oxide
6. Alluminosis – Alluminium
7. Stannosis – Tin. etc

6. COAL WORKERS’ PNEUMOCONIOSIS
(CWP)
 Defined as lung disease resulting from inhalation of coal dust particles
 Has an incubation period of 20-30 years. [1]
 It exist in 2 forms;
1. Simple CWP; a milder form of the disease
2. Progressive Massive Fibrosis (Complicated CWP); the advanced form
 Anthracosis; pigment deposits without a perceptible cellular reaction
 About 2-8% of simple CWP progress to Complicated CWP. [1]

7. PATHOGENESIS [1][2]
• Stages in the evolution of fully formed coal-workers’ pneumoconiosis
include
Anthracosis Simple CWP PMF
 Entry of dust particles into the lungs
 Engulfment by alveolar macrophages
 Activation of inflammasome
 Production of pro-inflammatory and fibrogenic cytokines
 Inflammatory response leading to fibroblast proliferation and collagen
deposition
 Healing by fibrosis

8. CLINICAL FEATURES [1][2]
 Chronic cough with black expectoration
 Progressive dyspnoea
COMPLICATIONS
 Pulmonary hypertension
 Cor pulmonale

9. MORPHOLOGIC FEATURES [1]
SIMPLE CWP
 Grossly; Coal macules and nodules,
 Histologically; Dust-laden macrophages in the alveoli, bronchiolar and
alveolar walls.
PROGRESSIVE MASSIVE FIBROSIS
 Grossly;
 Multiple,dark black areas measuring >2cm,
 Fibrotic regional and hilar lymph nodes,
 Histologically;
 Fibrous lesion composed of dense collagen and carbon pigment
 Thickened walls of respiratory bronchioles and pulmonary vessels
 Scanty lymphocytes and plasma cells around the areas of massive fibrosis

11. SILICOSIS
 The most prevalent chronic occupational lung disease. [2]
 Caused by prolonged inhalation of silica
 Individuals at risk include silica miners, sandblasters, ceramic workers, and
quarry workers

12. PATHOGENESIS
 Inhalation of silica particles
 Engulfment by macrophages
 Activation of inflammasome
 Release of inflammatory mediators by macrophages
 Silica dust is cytotoxic, kills microphage that engulf it

13. CLINICAL FEATURES[1][2]
 May be symptomless
 Irritant cough
 Dyspnoea
COMPLICATIONS [1]
 Pulmonary hypertension
 Pulmonary tuberculosis
 Cor pulmonale
CHEST X-RAY
 Nodular lesions detected as egg-shelled shadows[1]

14. MORPHOLOGY
Macroscopically
 Well-circumscribed, hard, fibrotic nodules (1-5mm in diameter)
 Located in upper zones of the lung
Microscopically
 Silicotic nodules located in region of respiratory bronchioles, regional
lymph nodes, pleura
 “Whorled” appearance of collagen fibres
 Coalescence of adjacent nodules in severe progressive foam

16. ASBESTOSIS
 Lung condition caused by chronic inhalation of asbestos dust
 Has an incubation period of about 10 years
 Individuals at risk include miners, car components manufacturers,
plumbers, construction workers.

17. PATHOGENESIS [2]
 Macrophages phagocytose asbestos fibres
 Activation of inflammasome
 Damage of phagolysosomal membranes
 Release of pro-inflammatory factors and fibrogenic mediators
 Asbestos also functions as tumor initiator and promoter
 Leading to lung cancer and mesothelioma
• Smoking greatly increases the risk for lung cancer.

18. CLINICAL FEATURES
 Progressive dyspnoea
 Cough with sputum production
 Weight loss in cancer
COMPLICATIONS
 Cor pulmonale
 Congestive cardiac failure

19. MORPHOLOGY [2]
Macroscopically
 Affected lungs are small, firm, and thickened.
 Fibrosis, especially in subpleural areas and bases of lungs, in contrast with
CWP, and silicosis.
Microscopically
 Presence of asbestos bodies in involved areas
 Interstitial fibrosis
 Hilar lymph node involvement, but not as significant as in silicosis

21. TREATMENT AND PREVENTION
 Palliative
 Withdrawal from exposure
 Limitation of exposure

22. CONCLUSION
 Pneumoconiosis refers to lung diseases caused by inhalation of dust, mostly
at work.
 There are various types, but the 3 most common include; Coal workers
pneumoconiosis, Silicosis, and Asbestosis
 No definitive treatment
 Withdrawal from exposure and prevention are very important

23. REFERENCES
1. Harsh Mohan, MD, MNAMS, FICPath, FUICC (2010), Textbook of
Pathology, 6th edition, Jaypee Brothers Medical Publishers (P) Ltd, pp
487-493. ISBN: 978-81-8448-702-2
2. Kumar et al (2013), Robbins Basic Pathology, 10th Edition. Philadelphia,
Pennsylvania: Elsevier Saunders. pp. 508–512. ISBN 978-0-323-35317-5.
3. GBD 2013 Mortality and Causes of Death, Collaborators (17 December
2014)".Global, regional, and national age-sex specific all-cause and cause-
specific mortality for 240 causes of death, 1990-2013: a systematic
analysis for the Global Burden of Disease Study 2013"
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340604). Lancet. 385:
117–171

24. THANK YOU