Pneumoconiosis

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These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university

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Pneumoconiosis

  1. 1. Pneumoconiosis Hamdi Turkey- Pulmonologist
  2. 2. Definition •Non neoplastic lung reaction to inhalation of mineral dusts encountered in the workplace. •Also includes diseases induced by organic, inorganic particulates and chemical fumes and vapors. •Important to diagnose as they are “occupational lung diseases.”e.g. silica, coal, asbestos •Some dusts e.g. tin, iron are innocuous
  3. 3. Normal protective mechanisms •Mucociliary apparatus >10 μm diameter, deposit in bronchi & bronchioles and removed in the mucociliary escalator. •Intra-alveolar macrophages-phagocytosis of particles & expectorated. Some go through interstitium into lymphatics. •Very Small particles behave like gas & exhaled
  4. 4. •Nose & trachea traps all particles >10 μm & 50% of 3μm •Mucociliary blanket 2-10 μm removed in the mucociliary escalator. •Alveolar macrophages <2 μm removed •Very small particles are not phagocytosed,but exhaled. Normal protective mechanisms
  5. 5. •Amount of dust retained in the lung (concentration, duration, clearence mechanisms) •Size, shape and bouyancy of particles (aerodynamic diameter) (1-5μ size dangerous sized particles reach the periphery : bronchioles & alveoli) •Additional effects of other irritants (smoking) • Solubility & physiochemical • reactivity Factors affecting fibrogenic potential
  6. 6. Solubility & cytotoxicity of particles •Small particles dissolve in pulmonary fluids→ acute toxicity •Larger,non soluble persist in lung parenchyma •Some dusts directly penetrate the epithelial cells into the interstitium. Physiochemical reactivity •Direct injury to tissue (free radicals )e.g. Quartz Fibrosing pneumoconiosis (eg silicosis) Factors affecting fibrogenic potential
  7. 7. Pathogenesis • Ingested dusts trigger macrophages to release chemical mediators that trigger fibrosis (TNF, IL 1,PDGF). • Persistent release of factors causes fibrosis • Migrating macrophages to lymphatics trigger immune reaction • Fibrosis (nodular-silica, interstitial – asbestos ??)
  8. 8. • Inhalation • Escape removal by defence apparatus • Particles penetrate epithelium → direct injury • Fibrosis • Engulfment by alveolar & interstitial macrophages → lymphatics → lymph node (modify immune response ) Pathogenesis
  9. 9. • Associated with coal mining industry • Carbon + silica (anthracosilicosis) Classification • Asymptomatic anthracosis (anthracite –coal) • Simple CWP- no dysfunction • Complicated CWP- (progressive massive fibrosis PMF) Coal workers pneumoconiosis (CWP)
  10. 10. •Gross Streaks of anthracotic pigment in lymphatics and draining hilar lymph nodes Microscopy •Carbon pigment in alveolar and interstitial macrophages,in connective tissue and lymphatics and lung hilus. Anthracosis (urban dwellers)
 morphology
  11. 11. Gross :Coal macules (1-2mm) & Coal nodules >upper lobes and upper zones of lower lobes Microscopy: Carbon laden macrophages & delicate collagen fibres. Adjacent to respiratory bronchioles initially (where dust settles), later interstium & alveoli. Dilatation of respiratory bronchioles –focal dust emphysema Simple CWP
  12. 12. Gross •Multiple.,>2 cm ,v dark scars Microscopy: •Dense collagen and carbon pigment. •Central necrosis (+/-) Complicated CWP
  13. 13. • Usually asymptomatic with little decrease of lung function • PMF pulmonary dysfunction (restrictive) • Pulmonary hypertension, cor pulmonale • Progressive even if further exposure to dust is prevented • ↑ chronic bronchitis and emphysema • No association with TB or carcinoma Clinical course
  14. 14. • 1st described in coal workers, may be seen in other pneumoconiosis • ?? Immunopathologic mechanism • Rheumatoid arthritis (RA) + Rheumatoid nodules (Caplan nodules) in the lung • Rheumatoid arthritis + pneumoconioses • Caplans nodule = necrosis surrounded by fibroblasts,monocytes and collagen • s/s RA > lung symptoms Caplans syndrome
  15. 15. Silicosis •Silicosis-nodular fibrosing disease after 20-40 yrs exposure to silica •Sand blasters,mine workers,stone cutting, polishing of metals,ceramic manufacturing etc. •(Acute silicosis following massive exposure –alveolar lipoproteinosis like. Rapidly progressive disease. )
  16. 16. A 35-year old stonemason was referred to hospital following routine health surveillance at his work. He reported no respiratory symptoms. Lung function tests had shown an FEV1 of 5.0L (114% predicted) when he was aged 25 and, although remaining within normal limits, had fallen over the intervening 10 years to 3.3L (85% predicted). A chest X-ray showed a profusion of small nodules in the upper and mid zones consistent with silicosis (Figure 2). He had smoked 20 cigarettes per day from his late teens. Clinical scenario
  17. 17. Pathogenesis • Fibrogenic activity depends on physical form, association with other minerals. • Crystalline silica (quartz) more toxic. • (Amorphous forms talc, mica less toxic) • Size 0.2-2μm more dangerous • Silica particles ingested by alveolar macrophages, kill them and release fibrogenic factors. Released silica ingested again. • Recruitment of lymphocytes and macrophages • Fibrotic silicotic nodule
  18. 18. • Discrete pale to black nodules <1cm dia. • Upper zone of lungs • Hard collagenous scars-central softening • Fibrosis in hilar lymph nodes and pleura • Enlarged fibrotic LN with peripheral (eggshell) calcification • PMF nodules >2 cm dia+ silicosis Gross morphology
  19. 19. • Concentric hyalinized collagen surrounded by condensed collagen,fibroblasts & lymphocytes. • Birefringent silica particles (polarized light) • Nodules incorporate normal lung tissue into themselves. Microscopy
  20. 20. • Asymptomatic, Dry cough, SOB • Early :X Ray fine nodularity in upper zones of lungs. Eggshell calcification in hilar LN • PFT normal/moderately affected initially • PMF: Progressive disease even after exposure stopped. • X ray nodules >2 cm dia. • PFT markedly ↓ • Associated tuberculosis (↓CMI) • Carcinogenic ?? Clinical features
  21. 21. Prevention • Air handling equipment in work place • Use of face masks.
  22. 22. • Asbestos = unquenchable • Asbsetos is resistant to physical and chemical destruction and is therefore used for fire proofing, insulation, brake lining etc. • Construction material • Ship demolition industry Asbestos
  23. 23. Clinical scenario A man of 78 reports gradually worsening breathlessness; he has no relevant medical history of note and has never been a regular smoker. His spirometry reveals that both his FEV1 and FVC are about 50% of their predicted values; the machine interprets this as a ‘restrictive’ picture. In his 20’s-30’s he spent about 15 years working in the boiler rooms of a power station. A chest X-ray reveals several pleural plaques, some calcified, but no other abnormalities. Because of his symptoms and pulmonary function abnormality (neither of which could be explained by pleural plaques alone – see Box 1) he was referred for further investigation. A thoracic CT scan identified a limited degree of bilateral, lower zone fibrosis. The combination of these findings with his history of occupational exposure was considered sufficient for a diagnosis of asbestosis.
  24. 24. • Fibrous plaques-focal/diffuse • Pleural effusion • Parenchymal interstitial fibrosis (asbestosis-diffuse interstitial process) • Lung carcinoma • Malignant Mesothelioma • Extrapulmonary malignancies- larynx,?colon Asbestos related lung diseases
  25. 25. Serpentine • Curly,more used in industry e.g.chrysotile. • less pathogenic • Breaks into fragments • Fibrogenic • Impacts in upper airways & removed by mucociliary apparatus & more soluble- leached out • Not associated with mesothelioma Amphibole • straight & stiff • e.g. crocidolite • more pathogenic • Resists breaking into fragments • Fibrogenic • Align in airstream & go deep ,penetrate epithelium,enter interstitium • <0.5 μm thick,>8 μm long more fibrogenic • Associated with mesothelioma Forms of asbestos
  26. 26. Fibrogenic potential like other inorganic dusts Tumour initiator and promoter Asbestos fibers localized in distal airways (close to mesothelium) release reactive free radicals Absorption of carcinogens on asbestos fibres e.g. smoking Pathogenesis
  27. 27. • Diffuse pulmonary interstitial fibrosis • Begins in the lower lobes & subpleurally (silica &CWP >upper) • Honeycomb lung • Pleural plaques
  28. 28. • Interstitial fibrosis around respiratory bronchioles and alveolar ducts, involves adjacent alveoli • Asbestos bodies –golden brown fusiform or beaded rods with a tranluscent centre (asbestos fibre coated by iron containing proteinaceous material) • Trapping & narrowing of pulmonary arteries Microscopy
  29. 29. Clinical course • Dypsnoea • Cough with sputum • May progress to respiratory failure , cor pulmonale • Cancer

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