1. FIOH / Tampere Pneumoconiosis Tööga seotud kopsuhaigused Tartu 8.-9. oktoober 2003 PNEUMOCONIOSES Panu Oksa Soome Töötervishoiu Instituut Tampere, Soome Finnish Institute of Occupational Health Tampere, Finland

2. FIOH / Tampere Pneumoconiosis Pneumoconiosis pneumon = lung konis = dust Pneumoconiosis = accumulation of inorganic dust in lungs, following non-neoplastic tissue reaction.

3. FIOH / Tampere Pneumoconiosis Falling of dust Particle size (  m) 100 50 10 5 1 0.2 0.1 Falling speed 100 cm/s 20 - " - 0.8 cm/s=48 cm/min 0.18 cm/s=48 cm/min 3.5 cm/h 1.1 - " - 0.8 - " - Mineral dust  = 2.6 g/m 3, no wind

4. FIOH / Tampere Pneumoconiosis

6. diffusioncollision falling on surface Dust in airways, effect of particle size Accumulation in airways 100 80 60 40 20 0,010,1 % 1,010100 mm Alveoli Upper airways Nose

7. FIOH / Tampere Pneumoconiosis During rest 0,5 l x 20 min = 4800 l/8 t During heavy work 2 l x 40 min = 38400 l/8 t If there are 0.5 fibers/cm 3 in the breathing zone, a worker in heavy work will inhale 1 920 000 fibers in 8 hours. Fibers thinner than 10 µm can reach the terminal bronchioles and alveoli. Breathing

8. FIOH / Tampere Pneumoconiosis nose: blowing, wiping, sneezing ciliated airways from trachea to terminal bronchioles: mucociliary clearance terminal bronchioles and alveoli: alveolar clearance with pneumocytes, macrophages, via lymphatic vessels Clearing of airways

9. FIOH / Tampere Pneumoconiosis If there is a large number of fibers in the airways, clearance mechanisms may be insufficient, especially in the alveolar region. Fibers cause an inflammatory reaction and finally: normal lung tissue will be replaced with fibrosis Lung fibrosis 1/2

10. FIOH / Tampere Pneumoconiosis number, size, shape and solubility of fibers individual features of person ( immunological mechanism ) Lung fibrosis factors affecting the fibrosing process 2/2

11. FIOH / Tampere Pneumoconiosis asbestosis silicosis hard metal disease aluminum fibrosis, Shaver's disease berylliosis talcosis kaolin pneumoconiosis. coal workers' pneumoconiosis Fibrogenic pneumoconioses "true pneumoconioses"

12. FIOH / Tampere Pneumoconiosis Causes: antimony barium boric acid manganese iron tin titanium bismuth Non-fibrogenic pneumoconioses benign pneumoconioses

13. FIOH / Tampere Pneumoconiosis Pneumoconiosis caused by crystalline silicon dioxide (quartz (silica), tridymite, cristobalite) Exposure Most common mineral in earth: in granite, sand, ore, kaolin etc. in most rocks. Finnish TLV 0.2 mg/m 3 does not protect from possibility to develop silicosis. Latency period is long, median 19 years. 5 % of diseases develop in 10 years. Silicosis 1/5

14. FIOH / Tampere Pneumoconiosis Pathogenesis Unknown. Silicon dioxide is toxic for macrophages. Collagen fibers develop and are hyalinized. Clinical forms of silicosis, symptoms Typical and most common is the chronic nodular form. Rheumatoid silicosis and silicoproteinosis seldom occur. First symptom is shortness of breath in exercise. Silicosis 2/5

15. FIOH / Tampere Pneumoconiosis Findings X-ray: 1 - 2 mm round nodules at first only in upper parts of the lungs, will spread to lower parts, grow and melt together. Lung functions react later: reduction of lung volumes, VC, FVC decreas first, and finally also TLC, RV and FRC Silicosis 3/5

16. FIOH / Tampere Pneumoconiosis Diagnosis Typical radiographic changes and sufficient exposure to silica. Differential diagnosis: tuberculosis, sarcoidosis, siderosis, histoplasmosis, alveolar microlitiasis, complication of measles. Silicosis 4/5

17. FIOH / Tampere Pneumoconiosis

18. Complications, prognosis lower tolerance to mycobacteria, silicotuberculosis recurrent bronchitis, cor pulmonale lung cancer (IARC classification 2A, probably carcinogenic for humans) silicosis may progress even in the absence of further exposure Follow-up Thorax x-ray and lung function measurements in two (1 - 3) year intervals also after cessation of exposure Silicosis 5/5

19. FIOH / Tampere Pneumoconiosis Asthma is the most common disease caused by hard metal. Hard metal disease can be acute fibrosing alveolitis or the slow progressing symptomless form leading to chronic pneumoconiosis within years (rarely). Exposure hard metal always contains cobalt and wolfram carbide other agents, like titan, molybdenum and vanadin, may be needed, depending on technical demands. acute form can develop in a few years latency of chronic form is usually over 10 years Hard metal disease 1/4

20. FIOH / Tampere Pneumoconiosis Pathogenesis cause of hard metal disease is probably exposure to cobalt. repeated acute diseases lead to desquamative fibrosing alveolitis alveolar walls thicken and are infiltrated by plasma cells, lymphocytes and macro- phages. Later progressive fibrosing occurs between cells. Hard metal disease 2/4

21. FIOH / Tampere Pneumoconiosis Hard metal disease Clinical picture dry cough and shortness of breath lung auscultation: crepitation X-ray: irregular spotty shading, in chronic state irregular opacities in lower parts of lungs lung function: restriction and later also lower diffusion capacity BAL: typically multinuclear giant cells Prognosis Acute disease can be cured with steroids; chronic lung fibrosis is irreversible. 3/4

22. FIOH / Tampere Pneumoconiosis Exposure In 1977 - 1989 blade grinder in furniture factory, 3 x 5 m workroom in the beginning sharpened 10 disc saw blades in a day In 1980 new bigger workroom, same machines and filters. Wet grinding 15 blades/day and dry grinding 5 - 6 disc saw and drill blades In 1989: occupational hygienic measurements: cobalt 3 x TLV, wolfram 2 x TLV Exposure In 1977 - 1989 blade grinder in furniture factory, 3 x 5 m workroom in the beginning sharpened 10 disc saw blades in a day In 1980 new bigger workroom, same machines and filters. Wet grinding 15 blades/day and dry grinding 5 - 6 disc saw and drill blades In 1989: occupational hygienic measurements: cobalt 3 x TLV, wolfram 2 x TLV Disease Non-smoker who after 2 years of work in factory, developed dry cough Cooling agent "Kemso" suspected. In 1981 diffuse opacity in thorax x-ray, FEV 1 60%, VC 57%, DL 55%, DLVA 94%. No diagnosis. Did not come to re- examinations. In 1989 spotty infiltration in thorax X ray, cor pulmonale. VC 22%, FEV 1 25%, DL 18% and DL/VA 66%. Corticosteroids did not help. Oxygen enricher was used. Lung transplantation was suggested, Deceased 1991. PAD: dust in lungs, 80% wolfram, fibrosis. Occupational disease. Disease Non-smoker who after 2 years of work in factory, developed dry cough Cooling agent "Kemso" suspected. In 1981 diffuse opacity in thorax x-ray, FEV 1 60%, VC 57%, DL 55%, DLVA 94%. No diagnosis. Did not come to re- examinations. In 1989 spotty infiltration in thorax X ray, cor pulmonale. VC 22%, FEV 1 25%, DL 18% and DL/VA 66%. Corticosteroids did not help. Oxygen enricher was used. Lung transplantation was suggested, Deceased 1991. PAD: dust in lungs, 80% wolfram, fibrosis. Occupational disease. Hard metal disease 42-year-old blade grinder 4/4

23. FIOH / Tampere Pneumoconiosis Exposure levels: in production usually under 0.1 fibers/cm 3 also in "usual" work tasks. in using MMMF without adhesive medium over 10 fibers/cm 3 blowing MMMF about 1 fibers/cm 3 Man-made mineral fibers, MMMF 1/2

24. FIOH / Tampere Pneumoconiosis Dangers Animal studies: fibrosis and cancer Human experience and studies irritation of skin and mucous membrane, eczema, fibrosis?, cancer??? Man-made mineral fibers, MMMF 2/2