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Pneumoconiosis
This document summarizes pneumoconiosis, which are non-cancerous lung diseases caused by inhaling mineral or metallic dusts. It discusses the definition, types based on causative agents like silica and coal, normal lung protective mechanisms, factors affecting disease development, pathogenesis, clinical features of specific types like coal workers' pneumoconiosis and silicosis, and prevention. Pneumoconiosis are important to diagnose as occupational lung diseases.
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Pneumoconiosis
- 1. PneumoconiosisPneumoconiosis Man B PaudyalManB Paudyal IOMIOM
- 2. Definition • Non neoplasticlung 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. Nomenclature • According tothe causative agent – silicosis • Occupation eg knife grinders lung=silicosis
- 5. Normal protective mechanisms • Mucociliaryapparatus >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
- 6. Normal protective mechanisms • 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.
- 7. Factors affecting fibrogenic potential •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
- 8. Factors affecting (cont…) •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)
- 9. Pathogenesis of fibrosis •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 ??)
- 10. Pathogenesis • Inhalation • Escaperemoval by defence apparatus • Particles penetrate epithelium → direct injury • Fibrosis • Engulfment by alveolar & interstitial macrophages lymphatics lymph node→ → (modify immune response )
- 11. Coal workers pneumoconiosis (CWP) •Associated with coal mining industry • Carbon + silica (anthracosilicosis) • Classification • Asymptomatic anthracosis (anthracite –coal) • Simple CWP- no dysfunction • Complicated CWP- (progressive massive fibrosis PMF)
- 12. Anthracosis (urban dwellers) morphology • GrossStreaks 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.
- 13. Simple CWP Gross :Coalmacules (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
- 14. Complicated CWP • Gross •Multiple.,>2 cm ,v dark scars • Microscopy: • Dense collagen and carbon pigment. • Central necrosis (+/-)
- 15. Clinical course • Usuallyasymptomatic 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
- 20. Caplans syndrome • 1st describedin 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
- 21. Silicosis • Silicosis-nodular fibrosingdisease 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. )
- 22. Pathogenesis • Fibrogenic activitydepends 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
- 23. Gross Morphology • Discretepale 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
- 24. Microscopy • Concentric hyalinizedcollagen surrounded by condensed collagen,fibroblasts & lymphocytes. • Birefringent silica particles (polarized light) • Nodules incorporate normal lung tissue into themselves.
- 26. Clinical features • 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 ??
- 27. Prevention • Air handlingequipment in work place • Use of face masks.
- 28. Asbestos related diseases • Fibrousplaques-focal/diffuse • Pleural effusion • Parenchymal interstitial fibrosis (asbestosis-diffuse interstitial process) • Lung carcinoma • Malignant Mesothelioma • Extrapulmonary malignancies- larynx,?colon
- 29. Asbestos related disease •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
- 30. Forms of asbestos 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
- 31. Pathogenesis Fibrogenic potential likeother 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
- 32. Morphology • Diffuse pulmonaryinterstitial fibrosis • Begins in the lower lobes & subpleurally (silica &CWP >upper) • Honeycomb lung • Pleural plaques
- 33. Microscopy • Interstitial fibrosisaround 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
- 38. Clinical course • Dypsnoea •Cough with sputum • May progress to respiratory failure , cor pulmonale • Cancer
- 42. Idiopathic pulmonary fibrosis •This is characterised by diffuse interstitial inflammation and fibrosis resulting in severe hypoxemia and cyanosis in the late stage • Synonyms:-- • Chronic interstitial pneumonitis • Hamman-Rich Syndrome • Cryptogenic fibrosing alveolitis
- 43. Pathogenesis • Sequence ofevents:-- • Injury to alveolar wall • Interstitial oedema • Accumulation of inflammatory cells(alveolitis) • Type 1 pneumocytes injured • Hyperplasia of type2 pneumocyte • Proliferation of fibroblasts
- 44. Pathogenesis(contd.) • Fibrosis ofalveolar walls and alveolar exudate • Loss of architecture of lung • Cause:-?immune mechanism
- 46. Morphology(contd..) • END-STAGE:- • Spaceslined by cuboidal /columnar epithelium separated by inflammatory fibrous tissue(Honey- comb lung) • (end stage lung same in all conditions)