Pneumoconiosis

Pneumoconiosis- dust with size and different types of occupational pneumoconic diseases, clinical features, diagnosis and prevention of pneumoconiosis.

1. PNEUMOCONIOSIS Dr. Sravani Assistant Professor

2. Definitions The term pneumoconiosis derives its meaning from the Greek words: pneuma = air and konis = dust The International Labour Organization defines pneumoconiosis as “the accumulation of dust in the lungs and the tissue reactions to its presence”. Not included in the definition of pneumoconiosis are conditions such as asthma , chronic obstructive pulmonary disease (COPD), and hypersensitivity pneumonitis , in which there is no requirement for dust to accumulate in the lungs in the long term.

3. Dust within the size range of 0.5mm to 3 micron, is health hazard producing, after a variable period of exposure, a lung disease known as PNEUMOCONIOSIS, which may gradually cripple a man by reducing his working capacity due to lung fibrosis and other complications.

4. INHALATION : Dust is finely divided solid particles Dust ranges from 0.5 – 150 microns Released into atmosphere during crushing, grinding, abrading, loading and unloading. > 10 microns – settle down <5 microns – inhaled Ogranic & inorganic Soluble & insoluble

5. The hazardous effects of dusts on the lungs depend upon a number of factors such as: Chemical composition Fineness Concentration of dust in the air Period of exposure Health status of the person exposed.

6. Definitions In other words – Pneumoconiosis can be defined as the non-neoplastic reaction of lungs to inhaled minerals or organic dust and the resultant alteration in their structure excluding asthma, bronchitis and emphysema. – Textbook of Pulmonary Medicine , D Behera

7. Pathogenesis For clinical p n eu m oco n iosis to deve l o p , 3 e s s e nti a l fa c tors a re required: Exposure to specific substance : coal, appear relatively inert and may accumulate in considerable amounts with minimal tissue response; while silica and asbestos, have potent biologic effects. Particles of appropriate size to be retained in lung (1-5μm) Exposure for a sufficient length of time (usually around 10 years)

8. Pathogenesis From an occupational health point of view, dust is classified by size into following categories: Inhalable Dust : is the one which enters the body, but is trapped in the nose, throat, and upper respiratory tract. Particle size is usually 6-25μm . Respirable Dust : particles that are small enough to penetrate the nose and upper respiratory system beyond the body's natural clearance mechanisms of cilia and mucous and are more likely to be retained in the lungs. Particle size is usually 1-5μm . Particles of <1 μm are exhaled out.

9. Pathogenesis

10. Pathogenesis

11. FIBROSIS Pulmonary Fibrosis is a chronic lung disease that causes inflammation, scarring, thickening and stiffening of the lung’s tissues .

12. T y p es Silicosis – from silica dust Asbestosis – from asbestos dust Coal work e rs pneu m oconio s is (a n t h ra c o s i s ) – from coal dust Byssinosis – from cotton dust Bagassosis – from sugarcane dust Far m e r ' s lung - from hay other agricultural products. Berylliosis – from beryllium dust or m old spor es or

13. T ypes Siderosis – from iron oxide Tanosis – from tin oxide Talcosis – from talc (hydrated magnesium silicate) Bauxite fibrosis – from bauxite dust Mixed dust pneumoconiosis – from a mixture of dusts Hard m et a l pneu m oconio s is – f r om ce r tain m et a ls li k e cobalt . In addition, others dust such as aluminum , barium, antimony, graphite and mica can also cause pneumoconiosis

14. T y p es Pneumoconiosis is usually divided into three groups: – Major pneumoconiosis Minor pneumoconiosis Benign pneumoconiosis “ Fibrotic Pneumoconiosis”

15. T y p es Major Pneumoconiosis: Inhalation of some dusts results in “ major fibrosis ” of the lungs, which results in interference of lung architecture or lung function tests. Examples are: Silica  silicosis Asbestos  asbestosis Coal  anthracosis Healthy lung Silicotic lung

16. T y p es Minor Pne u m oconiosi s : Inhal a t i on o f s o m e d u sts resu l ts in “ minor fibrosis ” of the lungs There is minimal fibrosis of the lungs without interference of lung architecture or lung function tests . These dusts include: Mica pneumoconiosis Koalin (china clay) pneumoconiosis

17. T y pes Benign Pneumoconiosis : There isn't any reaction in the lungs, but dust deposition casts a shadow in x-ray of the lung. There is no fibrosis and no disturbance of lung functions . It can result from the inhalation of: Iron dust  siderosis Tin dust  T annosis Calcium dust  chalcosis They are characterized by the presence of small rounded dense opacities on a chest film due to perivascular collections of dusts. The deposits in the lung disappear when exposure is discontinued.

18. S i l i c os i s Develops w i th repe a ted and usua ll y long - te r m exposure to crystalline silica (silica dust) The sil i ca dust caus e s i r r i ta t ion and i n fla m m a t i o n of t h e airways and lung tissue. Scar tissue fo r m s when the in f la m m at i on h e a ls, re s u lting in fibrosis that gradually overtakes healthy lung tissue. The fibrosis continues extending through the lungs even after exposure ends.

19. si l i c os i s Occupations with exposure to silica dust Mining Tunnelling Quarrying Sandbla st ing Ceramics Brick-making Silica flour manufacture Slate Pencil Industry Agate Industry Quartz Grinding

20. si l i c os i s Brick-making Sand blasting

21. si l i c os i s Exposure: Incubation period vary from few months to 6 years of exposure.

22. S i l i c os i s CLINICAL FEATURES: Chronic cough Dyspnea (shortness of breath) that worsens with exertion. Fatigue Loss of appetite Chest pain Acute silicosis patie n ts may also h a ve fever and ex p erience rapid, unintended weight loss .

23. Phagocytes Ingest dust Accumulate block LC Pathologically, Dense “nodular” fibrosis. Nodules: 3 – 4 mm in diameter. Advanced cases, Impairement of TLC. X-ray Findings show: ‘Snow-storm’ appearance.

24. Silico -tuberculosis Pul m o na ry t u b er c ul o sis o c c urs in abo u t 25 % of patients with acute or classic silicosis. "E g gs h ell " c alcifi c atio n , when pres e nt,is stron g l y suggestive of silicosis On histopathology, the hallmark of silicosis is the silicotic nodule

25. si l i c os i s Chest radiography showing Eggshell calcification Polarized light microscopy showing Crystals of silica

26. Prevention Dust Control Measures: Substitution, Complete enclosure, Isolation, H ydroblasting , G ood house-keeping, PPE or measures Regular physical examination

27. ASBESTOSIS Asbestosis is diffuse interstitial pulmonary fibrosis that occurs secondary to the inhalation of asbestos fibers. It is considered separately from other asbestos-related diseases, such as benign pleural effusion , plaques , malignant mesothelioma, and bronchogenic carcinoma.

28. They are silicates of varying composition. Silica combined with bases of magnesium, Fe, C a , Na and Al.

29. Serpentine (93% of commercial use) Amphibole (7% of commercial use) Chrysolite Amosite , Crocidolite, ASBESTOSIS Anthophyllite,

30. Serpentine- Hydrated magnesium silicate Asbestos fibres are 20 – 500 microns in length and 0.5 – 50 microns in diameter .

31. ASBESTOSIS Significant occupational exposure to asbestos occurs mainly in Asbestos cement factories Asbestos textile industry and Asbestos mining and milling. Asbestos cement factories Asbestos textile industry Asbestos mining

32. ASBESTOSIS Symptoms Average latency period is 20-30 years Dyspnoea Cough Chest pain In advanced cases, clubbing of fingers , cardiac distress and cyanosis. At histopathologic a na lys i s, asbestos bod i es, which m ay consist of a single asbestos fiber surrounded by a segmented protein-iron coat, can be identified in intraalveolar macrophages.

33. The fibrosis is due to mechanical irritation, peri - bronchial and diffuse in character. Basal in location. Sputum shows “ Asbestos bodies ”

34. ASBESTOSIS Translucent asbestos fiber (straight arrow) surrounded by a protein-iron coat and an alveolar macrophage (curved arrow) Chest x-ray showing Small, irregular oval opacities Interstitial fibrosis and “Shaggy heart sign”

35. ASBESTOSIS Treatment Strategy: Stopping additional exposure Careful monitoring to facilitate early diagnosis Smoking cessation Regular influenza and pneumococcal vaccines Disability assessment Pulmonary rehabilitation as needed Aggressive treatment of respiratory infections Health education to patient

36. Anthracosis Anthracosis/ Coal Worker's Pneumoconiosis (CWP) / Black lung disease: Accu m ulat i on of coal du st i n the lungs and the tis s ue's reaction to its presence. Associated with coal mining industry Takes one or two decades to cause symptoms The disease is divided into 2 categories: Simple Pneumoconiosis Progressive Massive Fibrosis (PMF).

37. Anthracosis Simple Coal Worker's Pneumoconiosis: Said to exist in the presence of radiological opacities < 1cm in diameter. Benign disease if no complications. Common symptoms: cough, expectoration (black in colour) and dyspnea. Slight decrease in FVC and FEV1/FVC

38. Anthracosis Complicated Coal Worker's Pneumoconiosis Is d i agnosed when la r ge op a city of 1cm o r m ore in diameter is observed in the CXR Pathologically it is characterized by large masses of black colored fibrous tissue. Symptoms are similar but more severe Recurrent pulmonary infection The la r ge lesions m ay cavi ta te as a re su l t o f is che m ic necrosis or infection (T.B). PF T (Pul m onary func t ion tes t ) reve a ls decr e ased F V C, FEV1/FVC and increased residual volume.

39. Anthracosis Cut section of lungs in anthracosis On histopathological examination

40. Byssinosis Byssinosis: Caused by inhalation of cotton fibre dust (textile and fibre industries) The chief symptoms are Chest tightness Shortness of breath Cough and Wheezing Typically occurring when patients return to work after a weekend or vacation. Smoking significantly exacerbates byssinosis

41. Byssinosis When detected in its early stages (acute byssinosis), byssinosis is reversible by eliminating exposure to the responsible irritant. When exposure continues the byssinosis can cause permanent damage to the lungs (chronic byssinosis)

42. Treatment: In the acute setting, patients are encouraged to consider alternative occupations or at least reduce the exposure in the work environment. Smokers should be encouraged to stop smoking. In the acute stages, treatment may include : Brochodilators for symptomatic relief Corticosteroids are best avoided for as long as possible, given only in severe cases

43. Chronic byssinosis : Supportive measures Nebulizer use Home oxygen therapy Physical activity and breathing exercises may help in the management .

44. Bagassosis Inhalation of bagasse or sugarcane dust. Sugar-cane earlier went to waste, now utilized in paper, cardboard and rayon manufacture. Due to thermophilic actinomycete - Thermoactinomyces sacchari Symptoms:Breathlessness , cough, haemoptysis and slight fever. Initially- acute diffuse broncolitis Skiagram – Mottling in lungs or shadow.

45. Pulmonary Impairment. If treated early, resolution of acute inflammatory condition of lung. Untreated, diffuse fibrosis, emphysema and bronchiectasis.

46. P revention Dust Control Personal Protection Medical Control Bagasse Control

47. Farmer’s Lung Inhalation of mouldy hay or grain dust. >30% moisture content – bacteria and fungi grow rapidly rise of temperature to 40-50 degree C Thermophilic actinomycetes ( Micropolyspora faeni )

48. Medical measures: Pre-placement examination Periodical examination Medical and health care services Notification Maintenance and analysis of records Health education and counselling Practicing good personal hygiene Preventive measures

49. Practicing good personal hygiene: W ashi n g hands and face bef o re eatin g , drinking, going t o the toilet, smoking. D o not e a t, dri n k, s m o k e, or apply c os m e t ics in ar e as whe r e silica is being used. Wear protective clothes and respiratory protection (Respirators must fit tightly.) Before leav i ng wor k , s h ower and c h an g e into c l ean clot h e s . Leave dusty clothes at work. Preventive measures

50. Prohibit Dry Cutting Promote wet Cutting Preventive measures

51. Personal Protective Equipments 52 Tyvek suit Gloves Goggles Boots Respirator Preventive measures

52. Fume extractor system Labeling of products Preventive measures

53. Preventive measures Other measures: – Training of health professionals in occupational diseases as majority of medical practitioners lack training in occupational health and consequently lack the skills to diagnose and prevent occupational diseases.

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