Pneumoconiosis

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 5-10 μ m are unlikely to reach the distal airways Smaller than 0.5 μ m move in and out of the alveoli without substantial deposition and injury 1-5 μ m 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; Coal workers pneumoconiosis (CWP) - Coal dust Silicosis - Silica Asbestosis – Asbestos Berylliosis – Beryllium Siderosis – Iron oxide Alluminosis – Alluminium 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; Simple CWP; a milder form of the disease 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

10. 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

11. 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

12. 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]

13. 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

14. 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.

15. 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.

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

17. 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

18. TREATMENT AND PREVENTION Palliative Withdrawal from exposure Limitation of exposure

19. 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

20. REFERENCES Harsh Mohan, MD, MNAMS, FICPath , FUICC (2010), Textbook of Pathology, 6 th edition, Jaypee Brothers Medical Publishers (P) Ltd, pp 487-493. ISBN: 978-81-8448-702-2 Kumar et al (2013), Robbins Basic Pathology, 10th Edition. Philadelphia, Pennsylvania: Elsevier Saunders. pp. 508–512. ISBN 978-0-323-35317-5. 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

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