1. Occupational Lung Diseases Internal Medicine Curriculum Presbyterian Hospital of Dallas October 2003

2. A Brief History of Occupational Medicine Ancient Times The Middle Ages Ramazzini (1633-1714) The Industrial Revolution The Modern Era

3. Ancient Times Major economic activities included agriculture, mining for metals, and quarrying. Pliny the Elder (AD 23-79) recorded the danger to miners from inhalation of fumes and vapors Because mining was so dangerous, it was considered suitable only for slaves and as punishment for criminals.

4. The Middle Ages The Erz Mountains in Bohemia was an important area for the mining and refining of useful and precious metals. A physician named Agricola became the town physician of Joachimsthal. He recognized that mining activities could lead to conditions that caused chronic shortness of breath. Agricola was probably observing silicosis and tuberculosis

5. Ramazzini He published De Morbis Artificum Diatriba in 1700 (Treatise on the Diseases of Workers). He describes: Dyspnea and metal poisoning in miners Bronchitis from irritant fumes Lung fibrosis in potters Asthma from exposure to corn &flour Silicosis in stonemasons

6. Ramazzini “When a doctor visits a working class home he should be content to sit on a three-legged stool, if there isn’t a guilded chair, and he should take time for his examination; and to the questions recommended by Hippocrates, he should add one more – what is your occupation?”

7. Ramazzini “Medicine, like jurisprudence, should make a contribution to the well-being of workers, and see to it that, so far as possible, they should exercise their callings without harm. So I for my part have done what I could and have not thought it unbecoming to make my way into the lowliest workshops and study the mysteries of the mechanic arts.”

8. The Industrial Revolution Production of steel on an industrial scale. Increased coal mining to make coke Fabrics are made in factories from cotton and wool thanks to new machinery. Charles Turner Thackrah, a town doctor, reported his observations on lung disease in miners and metal grinders and described a new method of measuring lung volume.

9. The Industrial Revolution Continued Britain institutes Workmen’s Compensation Acts. As of 1897, injured workers had rights to compensation from compensation from contributions paid by employers. Silicosis (1919) and Asbestosis (1931) were later recognized and covered.

10. The Modern Era E.R.A. Merewether (1892-1970) established the danger of asbestos and promoted the first legislation to control it. Late 19 th century, occupational lung cancers are described in miners. Allergic alveolitis is described in 1932 Berylliosis is described in Germany in 1933 1970, Congress passes OSHA legislation.

11. Principles of Occupational Lung Disease Industrial processes change and become increasingly complex. We should anticipate the appearance of a wider range of potentially toxic substances in the air. It is unlikely that the lung will develop many new ways to react to inhaled substances. We’ll see old lung diseases with new causes

12. Induction Periods Short: –Asthma –Infections –Allergic alveolitis –Toxic poisonings Long: –Pneumoconioses –Neoplasms

13. The Occupational History All jobs held in their lifetime and the duration. Do symptoms improve with weekends and vacations? The longer they have had symptoms from occupational asthma, the less clear the connection between symptoms and work What they did, not their title: –“brusher” drills into hard rock –“caulker” uses electric arc equipment to gouge and fuse metal plates

14. The Occupational History Toxic exposures can produce airway symptoms or an alveolitis. If everyone in the workplace is affected in a dose-dependent manner, the etiology is likely to be toxic rather than immunologic. Toxic reactions can occur on the first exposure. Immunologically-mediated diseases require re-exposure

15. Toxic Gases and Fumes Asphyxiating gases displace oxygen in the alveolus, on the hemoglobin molecule, or prevent oxygen utilization by the cytochrome Irritants are noticed quickly by the patients and create symptoms proximally to distally. (chlorine and ammonia) Toxins that attack the alveolar membrane (phosgene and nitrogen dioxide)

16. Occupational Asthma Symptoms usually begin several weeks after exposure begins. Early in the syndrome, the patient may just notice a dry cough. Patient may not be continuously exposed to provoking antigen. A portable peak-flow meter and a diary is very helpful in determining if a work-place antigen is responsible

17. Industrial Bronchitis Identical symptoms to chronic bronchitis seen with cigarette smoking Coal workers Grain Workers Most non-smokers do not have a decrement in FEV 1.0

18. Hypersensitivity Pneumonitis An inflammatory, immunologically mediated response at the alveolar and bronchiolar level to organic particles or gases. Acute, persistent, and subacute-recurrent forms of the disease.

19. Acute HP Fever, muscular aches, and malaise 4-8 hours after exposure to the antigen. May be associated with dry cough or chest tightness. Shortness of breath is a feature of a severe attack. Symptoms peak 8-12 hours after exposure and improve over the next 12-24 hours.

20. Persistent HP (acute) An atypical pneumonia picture with bilateral infiltrates on CXR, hypoxemia, and rales. May return to hospital within days after “improving” on antibiotics.

21. Recurrent HP Malaise, dry cough, shortness of breath Often mistakenly receive multiple courses of antibiotics or psychiatric referral. Some may progress to pulmonary fibrosis. In severe cases, CXR, pulmonary functions, and lung biopsy may be indistinguishable from end-stage idipathic pulmonary fibrosis

22. RADS: the Reactive Airways Dysfunction Syndrome The onset of an asthma like syndrome after a single severe exposure to a respiratory irritant. Not immunologically mediated Positive methacholine challenge test Symptoms of asthma may persist for more than one year after the event.

23. Pneumoconiosis The term is currently defined by the International Labour Organisation (ILO) as the accumulation of dust in the lungs and the tissue reactions to its presence; tissue reaction may be non-collagenous (minimal stromal reaction) or collagenous (when scarring is permanent.

24. The Pneumoconioses Asbestosis Silicosis Coal Worker’s pneumoconiosis Berylliosis

25. ILO radiologic classification Rounded opacities: p ( 3 mm) Irregular opacities: s, t, or u Profusion: 12 point scale (0/0 thru 3/3) Grading of pleural thickening

26. Asbestos A very fibrogenic dust, that causes pulmonary fibrosis pleural plaques, benign pleural effusions Mesothelioma, carcinoma of the lung

27. Pleural Reaction - Asbestos

28. Asbestosis Diffuse fibrosis caused by a persistent alveolar inflammation Irregular opacities predominately in the lung bases Rales invariably present Clubbing is common

29. Asbestos-related pleural plaques

30. Asbestos plaques

31. Gross appearance of Plaque

32. Silicosis Simple Silicosis: small nodules, predominately upper lobes; patient often asymptomatic Complicated Silicosis (Progressive Massive Fibrosis): coalescence into large nodules or masses with retraction of upper lobes Tuberculosis is a common complication

34. Coal Worker’s Pneumoconiosis (CWP) Coal dust is inert and not particularly fibrogenic. Can cause industrial bronchitis, emphysema, and progressive massive fibrosis. Xray looks worse than patient Many symptomatic coal miners have silicosis or tobacco induced COPD

36. Simple CWP An asymptomatic patient with normal pulmonary functions. CXR shows small rounded opacities predominately in the upper lobes.

37. Complications of CWP Tuberculosis PMF Caplan’s Syndrome: a syndrome with rheumatoid arthritis features, PMF, and, usually (>70%), a ppositive rheumatoid factor.

38. Hard Metal Disease Cobalt is the offending agent Used in metal cutting or grinding tools and in jet engine turbine blades Pulmonary fibrosis – probably due to fibrogenic properties of metal Asthma and hypersensitivity pneumonitis due to metals ability to provoke an immune response (?hapten)

39. Dung Lung Don’t ask

40. Sick Building Syndrome Reports began to appear about the time that new, “tighter”, more energy efficient office buildings were built. Hundreds of organic compounds have been identified in indoor air. Formaldehyde is an ubiquitous indoor organic that is a mucosal irritant.

41. Multiple Chemical Sensitivity Mucosal complaints Asthma like symptoms Neuro-cognitive complaints

42. Occupational Lung Cancers Asbestos Arsenic Bischloromethyl ether Coke oven fumes Insoluble Hexavalent chromium cmpds Soluble nickel Mustard gas Radon daughters

43. Mesothelioma

45. Small Cell Carcinoma of the Lung Bischloromethyl ether (BCME) – used as industrial intermediate for organic synthesis, organic solvents, bactericides, fungicides, and cross-linking agents. Radon Daughters – Radon-222 a decay product of U-238 is a gas and an alpha particle emitter as are its’ decay products: polonium-218,-214, and -210. Present in some metal mines.

46. Legal Aspects of Industrial Disease “I was never ruined but twice, once when I lost a lawsuit and once when I won.” »Voltaire