Pneumoconiosis

Definitions
Pathogenesis
Types
Silicosis
Asbestosis
Anthracosis
Byssinosis
Preventive measures

1. pneumoconiosis DR. RAGHAVENDRA HUCHCHANNAVAR Junior Resident, Deptt . of Community Medicine, PGIMS, Rohtak

2. contents History Definitions Pathogenesis Types Individual diseases Silicosis Asbestosis Anthracosis Byssinosis Preventive measures Recent updates

3. History It is likely that humans have suffered from occupational lung disease since the change from hunting to agriculture as a means of providing food. In Roman times it was recorded that mining was a dangerous trade, fit only for convicts and slaves. The first recorded mention of breathlessness among handlers of grain was done by Ramazzini , the father of occupational medicine , in 1713. Bernardino Ramazzini (1633 - 1714 )

4. History In the eighteenth and early nineteenth centuries, it was thought that the symptoms from black lung disease were asthma-related. The term "black lung" was coined when medical professionals discovered the blackening of miners' lungs in post-mortem. The first documented case of an asbestos-related death was reported in 1906 when the autopsy of an asbestos worker revealed lung  fibrosis. In the early twentieth century, it was observed that many asbestos workers were dying unnaturally young.

5. History In 1924, Nellie Kershaw , an English textile worker was the   first case of asbestosis to be described in medical literature . Dr William Edmund Cooke testified in Kershaw's inquest that "mineral particles in the lungs originated from asbestos and were, beyond reasonable doubt, the primary cause of the fibrosis of the lungs and therefore of death" Berylliosis was described first in Germany in 1933 and in the USA in 1943. Nellie Kershaw (1891 –1924 ) 

6. Definitions As per International Labour Organization (ILO) The term “occupational disease” covers any disease contracted as a result of an exposure to risk factors arising from work activity . Two main elements are present in the definition of an occupational disease: The causal relationship between exposure in a specific working environment or work activity and a specific disease; and The fact that the disease occurs among a group of exposed persons with a frequency above the average morbidity of the rest of the population .

7. 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.

8. 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

9. Pathogenesis For clinical pneumoconiosis to develop, 3 essential factors are 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 ( 1-5 μ m) Exposure for a sufficient length of time (usually around 10 years)

10. 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 6-25 μ m . 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 1-5 μ m . Particles of <1 μ m are exhaled out.

11. Pathogenesis

12. Pathogenesis

13. types Silicosis – from silica dust Asbestosis – from asbestos dust Coal workers pneumoconiosis ( anthracosis ) – from coal dust Byssinosis – from cotton dust Bagassosis – from sugarcane dust  Farmer's lung - from   hay dust or  mold  spores or other  agricultural products . Berylliosis – from beryllium

14. types 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 metal pneumoconiosis – from certain metals like cobalt In addition, others dust such as aluminum , barium, antimony, graphite, kaolin and mica can also cause pneumoconiosis.

15. types Pneumoconiosis is usually divided into three groups: Major pneumoconiosis Minor pneumoconiosis Benign pneumoconiosis “ Fibrotic Pneumoconiosis”

16. types 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

17. types Minor Pneumoconiosis: Inhalation of some dusts results 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

18. types 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 stannosis 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.

19. silicosis Develops with repeated and usually long-term exposure to crystalline silica (silica dust ) The silica dust causes irritation and inflammation of the airways and lung tissue. Scar tissue forms when the inflammation heals, resulting in fibrosis that gradually overtakes healthy lung tissue. The fibrosis continues extending through the lungs even after exposure ends.

20. silicosis Occupations with exposure to silica dust Mining Tunnelling Quarrying Sandblasting Ceramics Brick-making Silica flour manufacture Slate Pencil Industry  Agate Industry  Quartz Grinding 

21. silicosis Brick-making Sand blasting

22. silicosis Three forms of silicosis: Acute silicosis : occurs with exposure to fine dust with high quartz content; very heavy exposure for months, shows symptoms within weeks to months of exposure, Accelerated silicosis : shows rapidly progressive symptoms after 5 to 10 years of high exposure to fine dust of high silica content. Chronic silicosis : the most common form, results from long-term exposure (10 to 20 years or longer ) to dust containing less than 30% silica content.

23. silicosis Clinical features: C hronic cough Dyspnea (shortness of breath) that worsens with exertion. Fatigue Loss of appetite Chest pains Acute silicosis patients may also have fever and experience rapid, unintended weight loss. Silicotuberculosis : Pulmonary tuberculosis occurs in about 25 % of patients with acute or classic silicosis " Eggshell" calcification, when present, is strongly suggestive of silicosis On histopathology the hallmark of silicosis is the silicotic nodule

24. silicosis Chest radiography showing Eggshell calcification Polarized light microscopy showing Crystals of silica

25. silicosis According to NIOH (National Institute of Occupational Health, New Delhi ) about 3 million people are occupationally exposed to free silica dust and are at potential risk of developing silicosis. The various studies carried out by NIOH Slate Pencil Industry  Agate Industry  Quartz Grinding  Stone quarries Source: www.nioh.org

26. silicosis Slate Pencil Industry: Study done in Mandsaur , Madhya Pradesh revealed that The air borne free silica dust levels were several times higher than the limits prescribed under the Factories Act. Radiological evidence of silicosis was observed in 54.6% slate pencil workers. About 50% of the workers suffering from silicosis were below 25 years of age and had worked for less than 7 years. Source: www.nioh.org

27. silicosis Follow up examination of these workers after an interval of sixteen months revealed rapid progression of the disease. 4 % of the subjects who had  participated in the initial survey died during the intervening  period. Their mean age at the time of death was 34.7 (18‑55)  years and the mean duration of work was 11.75 (3‑20) years. Source: www.nioh.org

28. silicosis Agate Industry: Prevalence of   silicosis – Male 39.8% Female 34.2%   Developed silicosis within five years: male 19% , female 22% The overall prevalence of tuberculosis: male 37.4 % female 40.3% Pulmonary function abnormalities were found in about 51% grinders.  Stone Quarries: Silicosis in 22.4% workers, most of them had worked for >10 years. About 32% workers showed evidence of tuberculosis. Source: www.nioh.org

29. silicosis Treatment: There is no specific treatment for the silicosis , There is no known method of intervention to prevent the condition's progression. Silica exposure has to be stopped to prevent further damage to the lungs, Smokers should quit smoking. Tuberculosis positive patients need to be put on anti-tuberculosis treatment The course of progression often extends over decades even after cessation of exposure. Prevention remains the most effective therapeutic approach.

30. 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 and plaques, malignant mesothelioma, and bronchogenic carcinoma.  Asbestos  is classified into two groups: serpentine and amphibole.

31. Serpentine (93% of commercial use) Amphibole (7% of commercial use) Chrysolite Actinolite, Amosite, Anthophyllite, Crocidolite, Richterite, Tremolite ASBESTOSIS

32. 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

33. ASBESTOSIS NIOH (National Institute of Occupational Health, New Delhi) has carried out studies in Indian Asbestos industries. Its observations were Asbestos Cement Industry : Study carried out in 4 (Ahmedabad , Hyderabad, Coimbatore and Mumbai) of the total 18 asbestos cement factories in India. The prevalence of asbestosis in these factories varied from 3% to 5%. The levels of asbestos fibres were found to be higher than the permissible levels of 2 fibres/ml in two of the factories. Source: www.nioh.org

34. ASBESTOSIS Asbestos Textile Industry : The average levels of air borne asbestos fibres varied from 216 to 418 fibres / ml. The permissible level is 2 fibres/ml. The prevalence of asbestosis was 9%. This relatively low prevalence of asbestosis despite high environmental levels was attributed to high labour turn over. Cases of asbestosis were observed in workers having less than 10 years exposure in contrast to the reported average duration of over 20 years. Source: www.nioh.org

35. ASBESTOSIS Asbestos Mining and Milling : Done in Cuddapah (Andhra Pradesh) and Devgarh (Rajasthan ). In asbestos mines at both locations, the air borne fibre levels were within permissible limits. The average fibre levels in milling units varied from 45 fibres/ml to 244 fibres/ml of air. The overall prevalence of asbestosis in mining and milling units was 3% and 21% respectively. Source: www.nioh.org

36. ASBESTOSIS Symptoms Average latency period is 20-30 years Dyspnoea Cough Chest pain In advanced cases, clubbing of fingers At histopathologic analysis, asbestos bodies, which may consist of a single asbestos fiber surrounded by a segmented protein-iron coat, can be identified in intraalveolar macrophages.

37. 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 ”

38. 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

39. Anthracosis Anthracosis / Coal Worker's Pneumoconiosis ( CWP) / Black lung disease: Accumulation of coal dust in the lungs and the tissue'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 CWP and Complicated CWP or Progressive Massive Fibrosis (PMF).

40. 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

41. Anthracosis Complicated Coal Worker's Pneumoconiosis Is diagnosed when large opacity of 1cm or more 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 large lesions may cavitate as a result of ischemic necrosis or infection (T.B ). PFT (Pulmonary function test) reveals decreased FVC, FEV1/FVC and increased residual volume.

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

43. Anthracosis In a study conducted by National Institute of Occupational Health  in collaboration with the International Development Research Centre (IDRC), Canada,  (5777 underground coal miners and 1236 surface coal miners) revealed that the prevalence of pneumoconiosis (category 1/1 and more) in underground coal miners was 2.84% and in the surface coal workers it was 2.10 %. The overall prevalence of functional abnormalities of lung in underground coal miners and surface coal workers was 45.4% and 42.2% respectively. Source: www.nioh.org

44. 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

45. 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)

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

47. Preventive measures Preventive measures: Medical measures Engineering measures Other measures

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: Washing hands and face before eating, drinking, going to the toilet, smoking. Do not eat, drink, smoke, or apply cosmetics in areas where silica is being used . Wear protective clothes and respiratory protection (Respirators must fit tightly .) Before leaving work , shower and change into clean clothes. Leave dusty clothes at work . Preventive measures

50. Engineering measures Design of building Conduct air monitoring to measure the workers’ exposure to crystalline silica . Minimize exposures by controlling the creation of airborne particles, for example, use wet drilling, local exhaust ventilation. Personal Protective Equipments : Provide workers with protective clothes, respiratory protection, and facilities for washing (showers) and changing. Enclosure / isolation Environmental monitoring Preventive measures

51. Prohibit Dry Cutting Promote wet Cutting Preventive measures

52. Personal Protective Equipments 52 PPT-002-01 Tyvek suit Gloves Goggles Boots Respirator Preventive measures

53. Fume extractor system Labeling of products Preventive measures

54. Other measures: Legal measures: Measures to minimize dust emissions and exposure to dust. Law compliance mechanisms, including effective workplace inspection systems Cooperation between management and workers and their representatives A mechanism for the collection and analysis of data on occupational diseases Collaboration with social security schemes covering occupational injuries and diseases Preventive measures

55. 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.

56. Recent updates 63 rd National Conference of Indian Association of Occupational Health was held in Bengaluru, 22 nd – 25 th January, 2013. “An International meet on climate, the workplace and the lungs” 6 th -8 th December 2012. Main topics discussed were Integration of occupational health with primary health care Imaging for occupational and environmental respiratory disorders Study of Pneumoconiosis in Thermal Power Station Workers, K. D. Garkal , Shete Anjali N. in International Journal of Recent Trends in Science And Technology , Beed district, Maharashtra 2012.

57. WORLD HEALTH DAY THEME 2013 – HIGH BLOOD PRESSURE Thank you