Environmental Lung Diseases

1. Environmental Lung Diseases Dr. E. Sevda Özdoğan

2. Environmental lung diseases are caused by harmful particles, mists, vapors, or gases that are inhaled (usually while people work ) • Where? within the airways or lungs an inhaled substance ends up and what type of lung disease develops depend on the size and kind of particlesinhaled.

3. Size of the particle • Aerodynamic diameter: The diameter of a dust particle floating in the air • Inhalable particles are < 10 micron (they can pass through the nose and reach the peripheral airways • Respirabl particles: 0,5-5 micron ((they can reach the lung paranchym

4. Other factors • Chemicalandphysicalproperties of thedust (Inertdustlikeferrum do not cause a reaction in thetissue, simplyaccumulate but silicadustcause a progressivetissuereaction) • Theamount of dust in theair • Theperiod of exposure • Theeffectivity of respiratorydefencemechanisms of theperson (Normalyclears 98-99% of thedust)

5. Many different kinds of particles can harm the lungs. Some are organic, meaning that they are made of materials that contain carbon and are part of living organisms (such as grain dusts, cotton dust, or animal dander). • Some are inorganic, meaning that they usually come from nonliving sources, such as metals or minerals.

6. Pneumoconiosis • Pneumoconiosis is the disease caused by the accumulation of inorganic dust and tissue reaction in the lungs that ends up with fibrosis • Pneumoconiosis is mostly an occupational disease

7. Repeated and long term exposure to certain irritants on the job can lead to lung diseases called occupational lungdiseases • Occupational lung diseases are the number one cause of work-related illness. • Most occupational lung diseases are caused by repeated, long-term exposure, but even a severe, single exposure to a hazardous agent can damage the lungs. • Occupational lung diseases are preventable. • Smoking can increase both the severity of an occupational lung disease and the risk of lung cancer.

8. Common Types of Pneumoconiosis • Silicosis • Coal Workers Pneumoconiosis • Asbestosis

9. Clinical Evaluation and Diagnosis in pneumoconiosis • The patient with risk factor (job) can be asympthomatic (regular check up) • Symptoms from chronic cough, mild to severe dyspnea and respiratory failure can be seen • Occupational history (detailed) including the period of exposure to toxic material is important • Diagnosis: • History of exposure • Convenient radiology • Differential diagnosis

11. Workers in high risk areas should be examined regularly but the most important point is prevention • Prevention: • Ventilation • Vacuum techniques • Wet cleaning • Personal precautions (mask, respirator) • Alternative material use

12. Differential diagnosis of pneumoconiosis includes diseases that cause milier interstitial radiologic changes • Tuberculosis • Sarcoidosis • Fungal infections • Interstitial lung diseases

13. Silicosis • Silicon dioxide (SiO2)(free silica) is the mineral most frequently found on earth surface (25%)

14. Early diagnosis of Silicosis is important because the disease is progressive even after the cessation of exposure • Clinical Forms • Acute Silicosis • Subacute Accelerated Silicosis • Chronic Silicosis

15. Acute Silicosis (Silicoproteinosis, alveoloproteinosis) • Exposure to high concentrations of cristaloid silica, symptoms occur in a few months time • Cough, weight loss, fatique • Diffuse crackles • Lower zone asiner infiltrations on chest x ray • Progression to fulminan respiratory failure over several months • Survival after the onset of symptoms<2years

16. Subacute Accelerated Silicosis • Initial exposure to the onset of the disease is 7-10 years • Clinicaly identical to classical forms • High levels of silica exposure • Shortened life span

17. Chronic Silicosis • Initial exposure to the onset of the disease is >15 years • No symptoms in the beginning • Dispnea and nonproductive cough is the main symptoms and when it is syptomatic it is usually in the form of PMF(PMF: Progressive massive fibrosis)

18. Radiology is the most important diagnostic method for silicosis • Mainly upper and middle zone 3-10 mm noduler opacities (silicotic nodules) • ILO clasification p,q,r • Hiler calcification (Egg shell calcification) PMF: • Coalescence of radiologic opacities (conglomeration • Nodules>10 mm • ILO clasification A,B,C • Honey combing can be seen in end stage disease

19. Silicosis is a risk factor for tuberculosis • Fever, hemopthysis, weight loss should be alarming for tuberculosis • Silico-tuberculosis is frequent and difficult to diagnose Pulmonary Function Tests: • Usually normal or mild decrease in lung volumes in simple silicosis • Progressive decrease in lung volumes and diffusion in PMF (Ends up with fulminan respiratory failure)

22. Simple CWP 5-10 years old coal dust exposure Small rounded opacities, first in the upper zones but as the disease advances mid and lower zones can become involved Small emphsemateus changes around the nodule (coal macule) Usually normal lung function unless associated with smoking Asymptomatic in the early stages PMF Severe progressive shortened ventilatory capacity and life span (reason?) Progressive dyspnea Large opacities sometimes may necrose and cavitate Mixed type respiratory function decrease Black sputum: melanoptisis Poor prognosis Coal Workers Pneumoconiosis • The respiratory condition that results from the inhalation and deposition of coal dust and tissue reaction (in miners or exposure outside)

23. CWP does not progress after the worker has ceased mining (cessation of exposure) • Mixed dust pneumoconiosis can be seen in miners (together with silicosis) • Caplans Syndrome: Multipl pulmonary nodules+ Rheumatoid artritis in a coal miner • There is no specific treatment for pneumoconiosis • Early diagnosis • Cessation of exposure • Supportive treatment

24. Asbest Related Diseases • Asbest is a family of naturally occuring flexible, fibrous sodium, magnesium, ferrum and silicates complex found in soil worldwide • Fibers are categorised as: • Serpentine (long and curly) • Amphybole (straight and rode like) • The most pathogenic form is amphybole (crocidolite) • Serpentine (Crysotile) is the most commercially used form (heat resistance, flexibility, friction resistance) • All commercial forms have been associated with both nonmalignant respiratory disorders and lung cancer and mesothelioma

25. Occupation with the risk of asbestos exposure • Construction industry • Roofing, pipes, cement, adhesive, wall covering • Ship building and repairing • Carpenters • Fireproof textile • Asphalt flooring, railway insulation • Friction materials, brake linings • Plastic and rubber manifacture

26. General exposure of asbest • Occupational exposure • Carry home asbest in hair and clothes of exposed workers • Found in normal levels in buildings under use (elevated exposures from remodelling) • Geographic areas (found in soil, air) • İç anadolu, Göller bölgesi (Nevşehir, Tuzköy, Karain), Diyarbakır (beyaz toprak), Eskişehir çevresi

27. Benign Asbestosis (DIF) Pleural plaques Benign pleural effusion Diffuse pleural fibrosis Malign Mesothelioma Lung Cancer Gastric, Over, breast cancer Asbest Related diseases

28. Asbestosis (Diffuse Interstitial Fibrosis) • Most patients asymptomatic 20-30 years after first exposure • Dyspnea with exertion-progression even in the absence of further asbestos exposure. • Bibasilar, fine end-inspiratory crackles • Corpulmonale may ensue in advanced cases • PFT: Reduced lung volumes, particularly the vital capacity and total lung capacity; diminished DLCO • Cigarette smoke may accelerate the progression of pulmonary fibrosis after asbestos exposure

31. Pleural Plaques • Hyalinised pleural plaques with sharp endings and calcification localised in parietal pleura • Usually first localized on diaphragmatic pleura and lower zone • Asymptomatic • 10-20 years after exposure

33. Benign pleural effusion Latent period 10-20 years Exudative Asymtomatic Diagnosis by excluding other causes and history of exposure Malign mesothelioma The lifetime risk of developing mesothelioma among asbestos workers is thought to be as high as 10 percent. There is a long latency of approximately 30 to 40 years from the time of asbestos exposure to the development of mesothelioma. Pleural effusion

34. Lung Cancer • Asbestos exposure in the absence of a smoking history is associated with a 6-fold relative risk of lung cancer • Combined exposure to asbestos and cigarette smoke appears to be multiplicative.

35. Malign Mesothelioma Environmental, nonoccupational exposure to asbestos and erionite (another fibrous zeolite) also can contribute to an increased risk of mesothelioma. In certain rural areas in Greece, Turkey (Erionite in Ürgüp, Göreme region), and Bulgaria, soil contains remarkably high levels of tremolite asbestos fibers, and many cases of mesothelioma in these regions

36. The most common clinical presentations are dyspnea, chest pain, unilateral decreased volume of the affected hemithorax (frozen chest) • Nodular thickening of the pleura, irregular thickening of the interlobar fissure, absence of mediastinal shift with massive pleural effusion (frozen chest) • Diagnosis by histologic examination • Treatment oncologic and surgical if possible, prognosis is poor

39. 2009

40. 2013

42. Organic Dust Exposure • Byssinosis • Seen in cotton workers due to cotton and flax dust (endotoxins, immunologic mechanisms?) • Divided into Acute and Chronic form • Acute Byssinosis: several degree of acute airway response (hyperreactivity) to cotton dust on first exposure (may cause an accelerated decline in lung function-COPD)

43. Chronic Byssinosis (Classical form) • Chest tightness and difficulty in breathing on the first day of work (Monday fever) • Latent period is around 5-6 years • Symptoms progress and becomes all week long by time ends with a COPD like disease • There is no specific chemical or radiologic sign • PFT (a decrease of 150-200 ml in FEV1 or FVC on the evening of mondays

44. Hypersensitivity Pneumonia(Extrinsic Allergic Alveolitis) • A disease that arises from hypersensitivity to inhaled organic dust and inflamatory response confined to lungs • Also known as farmers lung • Spectrum of the clinical illness varies which probably reflects factors specific to the individual, frequency and degree of exposure

45. Antigenes that cause hypersensitivity pneumonitis

46. Clinical features of EAA • Acute: shivering, fever, fatique, hedache, dyspnea, dry cough after 4-6 hours of high level of exposure • Repeated episodes of influensa like illness that subside spontaneously • Tachypnea, tachicardia, cyanosis, fine crackles on lung bases • Radiology: diffuse reticular pattern on the middle and lower zone • PFT: restrictive pattern occasionally obstructive

47. Subacute: similar to chronic bronchitis, • Cough, sputum, dyspnea on exercise, loss of appetite and weight • Symptoms subside slowly after cessation of the exposure • Chronic: İnsidious loss of exercise tolerance and increasing dyspnea • Upper zone diffuse fibrosis and honeycombing

48. Treatment • Avoid exposure • Prednisolone • Supportive care

49. Occupational Asthma • Irritation (Reactive Airway Disfunction Syndrome) • No history of airway disease • Acute large exposure to toxic agents • Dyspnea, cough starts in 24-72 hours • Symptoms continue at least 3 months • Nonspecific bronchial hyperreactivity • Diagnosis by excluding other diseases • Immunologic • Long term recurrent exposure to: Small or High molecular weight chemicals • Specific IgE synthesis and bronchial inflammation

50. Occupational Asthma • Small molecular weight chemicals: isocyanates, platinum salts,metals • High molecular weight: Complex plant and animal biological products. • Diagnosis requires • a defined occupational history, exposure to sentisizing agents, • absence of asthma symptoms before beginning employement, • A documented relationship between development of symptoms at the workplace and the reduction on withdrawal from the workplace