Occupational Lung Disorders (Diseases)

Definition:- Damage to lungs caused by Dusts, Fumes, Noxious Substances inhaled by workers in certain Specific occupations are known as Occupational Lung Diseases. Mercury is also LOD as it is haled & causes Systemic Symptoms. Causes:1) Dust:- Organic, Inorganic, Respirable, Non-Respirable 2) Gases & Vapours:- Asphyxiants, Irritants & Poisons 3) Fumes:- e.g. Welding 4) Mist:- e.g. Instecticide spray 5) Smoke Effects of Noxious Substances in Lungs 1) Mechanical:Due to reaction of Gas Exchange Unit 2) Irritation:- Chlorine, Ammonia 3) Toxicity:- Mercury Vapours 4) Fibrosing:- Silica, Asbestosis 5) Allergic:- DizoMethane 6) Granulomatous Changes:- e.g. Beryllium, 7) Nasal Septal Perforation:- Arsenic, Chromium Dust:- Lung reaction depends upon:- 1) Nature & Property of the Dust 2) The mount os dust retained:- e.g. Coal Dust 3) Duration of Exposure 4) Individual Susceptibility 5) Immunological Reactivity of the subject 6) Shielding Effect:- Coal Deposited layer by Layer Behaviour of Dust Properties in Lungs:1) Gravimetric Settlement:- Fibres less than 3 Microns enters into smaller airways through this process. 2) Impaction:- Particles or fibres less than 10 Micron & More than 3 Micron size follow this process. The partices are impacted in the nose or at bifurcation of big airways. 3) Interception:- Long fibres of smaller diameter are intercepted by collision at the wall of terminal & Respiratory Bronchioles 4) Deposition:Fine particles follow this process at Lower Halves of Upper Lobes, and Upper Halves of Lower & Middle Lobes. Inhalable Dust is of less than 100 Microns Thoracic Dust is Below 10 Microns TLV is 5 Mg/Cu MM Respirable Dust:- 0.5 to 5 Microns Defence Mechanism:- Brownian Movement

Pneumoconiosis:ILO Definition:- Lung Diseases caused by inhalation of fine dusty particles & the reaction of the lungs to the dust. Text Book Definition:- Pneumoconiosis is defined as Non Neoplastic reaction of lungs to inhaled Minerals or Organic Dust in various occupations & the resultant alternations in their structure EXCLUDING Asthma, Bronchitis & Emphysema. Types of Pneumoconiosis:1) Dust which cause Small Rounded Opacities alone e.g. Siderosis, Stannosis, Barritosis (Barium) 2) Dust which cause Small Rounded Opacities which may be complicated by Massive Lesions e.g. Coal Workers Pneumoconiosis, Silicosis, Mixed Dust fibrosis 3) Dust which cause SmallIrregular Opacities e.g. Asbestosis, Talk Pneumoconiosis 4) Dust which cause Small Rounded Opacities, which may progress to Upper Lobe Fibrosis e.g. Extrinsic Allergic Alveolitis, Bagassosis, Chronic Berrylium Disease Diagnosis:Silicosis:- Silicosis is a fibrotic Disease of the lungs caused by inhalation of & Retension of with Pulmonary Reaction to Crystalline Silica SiO2). Crystallins Silica when it is freshly fractured is more active due to active radicles present with fresh Crystalline Silica. Types of Silica:- 1) Quartz 2) Tidimites:_ When Quartz is heated to 600C 3) Cristobalite:- When Quartz is heated to 1,200C Occupations Involved:- Cleaners of Furnace Lining, Brick Workers, Pottery (Brick:- H2S, Silica & Heat) Types of Silicosis:- 1) Acute Silicosis 2) Accelerated Silicosis 3) Chronic Silicosis 4) Progressive Massive Fibrosis Pathogenesis:Difference Between Silicosis & TB 1) Moist Shadows Soft Cotton Type seen in TB 2) Silicosis is Symmetrical, while TB is Asymmetrical 3) Axial Appearance:- Hilar Lymph Nodes are Calcified in Silicosis

4) Pleural Effusion in TB, while Pleural Plaques in Silicosis 5) Cavitation seen in TB & not in Silicosis. Within the cavity if Fungal Infection (Aspergilosis) occurs, the cavity may show fungus Ball in X-Ray. 6) Primary Complex is present in TB. Asbestosis:- Caused by Biopersistant Durable mineral fibers, most commonly Chrysolite, Amosite or Crosidolyte Asbestos. Mainly Chrysolite & Amphibole Group:- Amorite (Brown) & Crosidolite (Blue) Properties:- 1) Interaction is more if if sharpness is more 2) Asbestos is retained in the body for long time. Macrophages try to engulf the fibres but fail to do so. Then the Asbestos Bodies are formed.

These Asbestos bodies can be seen under Phase Microscope of sputum examination. Presence of Asbestos Bodies does not confirm Asbestosis. It only confirms the Exposure. Crysidolite or Blue Asbestos DO NOT Form Asbestos Bodies. Their surface is not suitable for deposition of Ferro Hematic Substances. Dust production is more in Amphibols, as they are brittle. Corrugated Asbestos Sheets & Pipes:- When the Asbestos is Compact & Enclosed into the Cement it is much safer, but it breaks it is dangerous. When water is passing through the Asbestos Pipes some Asbestos fibers are released due to friction. It was also used as an Insulating Material and now the Disposal has became a problem. Put the figure here Asbestos Serpentine Fibres

Amphiboles

India is a large producer of Asbestos since many years & has many Asbestos Mines. But the need is so much that it is importing also from Canada & Russia. In India they have Manual Method of handling of Asbestos like a mud. Ship Breaking Units:- They release Asbestos in plenty. In ship it is used as an insulator & Fire Protector.

Asbestos Lung Injuries

1) Benign Pleural Disease:a) Pleural Effusion b) Pleural Fibrosis or Hyaline Fibrous Plaques c) Rounded Atelectasis that mimic Cancer 2) Benign Asbestos Induced Parenchymal lesion of Lung Disease:a) Lung Fibrosis b) Small Airways Disease (Still Controversial) 3) Malignant Disorder:- Ca Lung, Malignant Mesothelioma, Oesophegeal & other GIT Cancers, Ca Larynx 4) Skin Disease:- Asbestos Wort or Corn in the skin. Pleural Plaques:- Grossly:- White or Yellow lesions Mostly parietal lesions. Typically Lower Zone of the Posterior Parietal Pleura. The can be extensively calcified. Microscopically:-Typical plaqus are acellular, Collagin, sharply demarcated from the underlying adipose tissue of chest wall. Pleural Plaques and Pleural thickening is very difficult to diagnose. Few differentiating Points are:Pleural plaques are at Parietal Pleura Diffuse Pleural Thickening is at Visceral Pleura In Diffuse Pleural Thickening CostoPhrenic angle is obliterated followed by elongated thickening. Phase I:- Plaques in the centre Phase II:- Goes to lateral side It initiates from lower side & from Periphery Honey Comb Type I, Type II, & Type III Carcinoma:- Mesothelima of Pleura produce localized bulging of chest wall. It is undifferentiated. Carcinoma of Lung. Substitute for Asbestos:- PVA Fibres, Cellulose Fibres, or Glass Fibres. PPEs:- Use Respirator

Classification of Pneumoconiosis according to the Type of Dust

Type of Dust 1) Mineral Inorganic

Reaction A) a) No Fibrosis b) Some Interaction c) Accumulation of local Macrophages d) Mild Reticulosis Fibrosis B) Granuloma Formation a) Sarcoid Type

Disease A) a) Siderosis b) Stanosis c) Barritosis d) Soot (Carbon) Anthracosis

2) Organic (Non Mineral)

B) a) Beryllium Disease (Due to Hard Light Metal) b) Foreign Body Granuloma b)Talk Pneumoconiosis Type Magnesium Silicate C) Collagen Fibrosis a) Nodular (Massive) a) Silicosis, Anthrocosis, Late Stage PMF b) Diffuse Interstitial b) Asbestosis, Talk Fibrosis Pneumoconiosis, Chronic Beryllium Disease A) No fibrosis only Reaction a) Translucent Interstitial Pneumonia (Acute Allergic Reaction) b) Sarcoid Type of Reaction B) Collagen Fibrosis C) Cotton Dust a) e.g. When Massive Dust is Inhaled b) Extrinsic Allergic Alveolitis (EAA) B) Mushroom & Bagassosis C) Byssinosis

Coal Workers Pneumoconiosis

First Coal Bronchitis & then converts into Coal Workers Pneumoconiasis, & then gets converted into Progressive Massive Fibrosis. Coughing of Black Sputum (Jet Black Sputum) known as Melanoptysis. Focal Emphysema is also seen in Coal Workers Pneumoconiasis. ___________________________________________________________________ Common Pneumoconisis (Definition in ILO 4th International Conference 1971) Disease Cause Main Source 1) Barritosis (Barium) Barium Sulphate Mines of Barium Salts 2) Sidrosis Iron Oxide Welding 3) Stannosis Tin Oxide Smelting 4) Kaolinosis Hydrated Aluminium China Clay Silicate 5) Aluminosis (Shivers Disease) Stampede Aluminium Paint 6) Coal Workers Coal Dust Mining Pneumoconisis (Anthracosis) 7) Talcosis Hydrated Magnesium Rubber Silicate 8) Berylliosis (Chronic Beryllium Compound Atomic Reactor Beryllium Disease) Asbestosis Asbestos Fibres Mining Occupational Asthma 1) Allergens:- Feather, Grain Dust 2) Plant & Vegetable Material:- Mustard Powder, Saw Dust, Cotton Dust 3) Antibiotics:- Penicillin 5) Chemicals:- Insecticides, Aluminium Flax, Platinum Salts. 6) Agents used in Plastics, Paints & Adhesives:- Isocynates, Phthallic Anhydride 7) Proteolytic Enzymes:- Alcalase & Muxatase:- Both are formed by Baccilus Subtiis

Extrinsic Allergic Alvelolitis (EAA)

EAA is the term applied in some conditions in which the inhalation of organic dust results in hypersensitivity reaction of Alveolar Wall, associated with the production of Precipitants. Two main forms of Allergic responses may occur in the lungs following inhalation of Organic Dust.

1)

2)

In Atopic individuals the bronchi may be affected , giving Asthmatic Symptoms, Mediated by Non Precipitant, Liagenic antibodies called as Type I Allergy Second form of Pulmonary Allergic Condition, which affects Non Atopic Persons after repeated exposure to antigens concerned & is mediated by Precipitant called as Type III Allergy. It gives predominantly Alveolar Reaction.

Examples of Extrinsic Allergic Alveolitis (EAA)

Disease (Condition) 1) Farmers Lung 2) Bagassosis 3) Mushroom Workers Lung 4) Maple Bark (strippers Lung) 5)Malt Workers Lung 6) Bird Fencers Lung 7) Pituitary Snuff Takers Lung 8) Wheat Weegils Disease 9) Sequoiosis Cheese workers Lung Corn Flours Lung 12) Suberosis 13) New Guinea Lung 14) Humidifiers Lung 15) Animal Food Workers Lung 16) Furriers Lung 17) Smallpox handlers Lung 18) Coffee Workers Lung 19) Black Fat Tobacco Smokers lung 20) Paprica Splitters Lung Source of Antigen Mouldy Hay Mouldy Overheated Sugar Cane Mushroom Compost Mouldy Maple Bark Mouldy Barley, Malt Dust Pigeon, Budgenger, Hem, Parrots droppings Heterologus Pituitary Powder Infected wheat flour Mouldy red wood Saw Dust Cheese Mould Mouldy Oak Bark or Cork Dust Mouldy Thatch Dust Humidifying Hot Air System Fish Meal Fox Fur Casts from Small Pox lesions Coffee Bean Extract Black fat Tobacco Paprica Dust Precipitant Present Against Micropolispods Feani T Vulgaris, Thermo Actinomyces Bulgaris M. Feani & T. Vulgaris Cryptostroma Aspergillis Cleavagas Sr. Proteins from droppings Serum Proteins, Pituitary Antigens Sitophylus Granarius Audio Basidum Pallutans Penicillin Mouldy Cork Dust Thatch of Huts M. Feani ?? ?? ?? ?? ?? ??

Difference between Extrinsic Allergic Alviolitis (EAA) & Occupational Asthma Occupational Asthma Important Edema & Eosinoplills Infiltration of Bronchial wall Bronchi Rapid after exposure to allergens causing Asthma Slight Rhonchi Hyperinflation only No Precipitants Common Immediate Type Hypersensitivity Obstructive Pattern of Ventilatory Abnormalities EAA Unimportant Cellular infiltration of Alveoli & Interstitium or Epithelial Granules Alveoli & Interstitium 5-6 hours after exposure to relevant antigens Marked Crepitations Milliary Mottling in Acute Stage Precipitants to relevant Antigens Absent Arthus Type Response Restrictive Pattern of Ventilatory Abnormality with Marked Diffusion Defects

1) Individual Predisposition 2) History

3) Site 4) Onset 5) Systemic Upset 6) Signs 7) X-Ray Findings 8) Serology 9) Eosinophilia 10) Skin Test Physiology

Difference Between Obstructive & Restrictive Pattern Obstruction 1) TLC 2) RV 3) VC/FVC 4) FEV1/FVC 5) RV/TLC Ratio 6) Resistance 7) Compliance 8) Diffusion 9) Arterial pO2 10) Arterial pCO2 11) Arterial pH Restriction

Or Normal Normal Normal Normal

Normal or

Diagnosis of Occupational Lung Disease (OLD) A) History 1) Occupational History:- Hist. To be taken in chronological orders Material Handling Brick Field Activities 2) Para Occupational History 3) Environmental History:- Pt. Residing outside the company may suffer 4) Domestic History B) Exclusively given to smoking habits:-1) Asbestos 2) Uranium c) Clinical Features:1) Dyspnoea:- e.g. Mild Dyspnoea due to simple Coal Workers Pneumoconiosis - Continuous in Progressive Massive Fibrosis (PMF) & at Rest 2) Cough:- May be dry or Mucoid or may be Blood Stained e.g. Silico-TB, Black in PMF 3) Chronic Pain:- Usually not in Silicosis but common in PMF due to Pleural Involvement 4) Wheeze or Rhonchi:5) Fever:- Metal Fume Fever 6) Irritation of Upper & Lower respiratory Tract:- Ammonia, Phosgene 7) Clubbing:- Due to Asbestosis or Lung Ca. 8) Some Non respiratory Symptoms:e.g. Benzene Vapours go to System D) Physical Signs:- 1) Fine to medium crepitations during inspiration 2) Mild Expiratory Crepts, mainly at the base 3) Mid Inspiratory Crepts along mid-axillary line at the base E) Investigations:- PFT:-Nonspecific X-Ray:- How to detect Residual Volume on X-Ray PA & Lateral View Procedure:- 1) Area of each lung field in PA Film, Excluding the mediastinum by Planimeter 2) Area in the lateral film including the heart is measured Calculation:- 1) Multiply the area of Right Lung field by Laterial area 2) Multiply the area of lateral Lung field by lateral area 3) Calculate the 4th root of each value 1 & 2 & thus to obtain X-Ray Volume of each Chest. 4) Add Tow volumes to obtain total X-Ray volume Total Lung Capacity = (0.567 % of X-Ray Chest Volume) + 320

RV = TLC FVC Predicted Values means according to height & weight. It is required for Restrictive Index = (FEV1 X FVC ) X 100 Predicted values of PFT according to Kamat S.R. For Males:- FVC = 0.0503 H 0.0136 A 4.488 H = Height A= Age FEV1 = 0.396 H 0.0212 A 3.130 PEFR = 4.236 H 2.0981 A 109.5 For Females:FVC = 0.0370 H 0.0070 A 3.187 PEFR = 3.310 H 1.865 A 81.0 FEV1 = 0.0274 H 0.0103 A 1.995 Trapping Index:- VC FVC Less than 5% is not significant, Increase by 75 % in Asthma because in Asthmatics the air is trapped Functions measured by 1) Fluroscopy:- Measures movements of diaphragm & Mediastinum 2) Radio isotope technique 3) Broncho spiromerty Other Tests:1) X-Ray Chest PA View which will be matching with ILO Radiograph 2) Sputum Examination for AFB or Eosionophils, Asbestos bodies, Melanoptysis or Haemoptysis 3) Skin Tests:a) To identify atopic individual. 4) Patch Test:- To identify the offending agent asin case of occupational Asthma 5) To study the type of hypersensivity Reaction Type I or Type III 6) Serological Examination:- e.g. IgE is increased in Occupational Asthma, Precipitants are increased in EAA 7) Biological Monitoring:- If he is inhaling lead fumes, urine lead estimation. 8) Lung Biopsy:- e.g. for As, Si 9) CT, HRCT Scan 10) Perfusion Cintography 11) Computerised tomography mainly for peripheral lesions 12) Bronchofluroscopy 13) Pulmonary Lavage 14) Legman P Test 15) Methacholine Test Safety Measures:- Medical Measures Statutory Measures

Engineering Measures 1) Substitution of hazardous material innocuous material or a modification of the process designed to render the substance innocuous. 2) The complete enclosure of the process 3) Partial enclosure of the process with Exhaust Ventilation applied locally. 4) High velocity Exhaust Ventilation in case of Fumes & Dust applied at source. 5) Suppression of dust by Wet Process (Hydro blasting) 6) Use of Protective Clothing & Respirators. 7) Maintain good House Keeping. 8) Efficient Storage & Transport of Dangerous Substances. 9) Controlled Disposal of Potentially Dangerous Waste Substances. Preventive Medical Measures:1) Medical Examination:Pre-Employment and Periodic Medical Examination Pre-Placement, Pre-Retirement Medical Exam. Special Medical examination. 2) Notification of Notifiable Diseases. 3) To provide First Aid boxes. 4) OHS Centre (Statutory Requirement) within the campus. 5) Provision of a Hospital. 6) OHS Occupational Services 7) Environmental Monitoring 8) Statical Monitoring 9) Research Safety Measures:- 1) Substitution 2) Enclosure of Machine 3) Enclosure of the person 4) Isolation of the person. 5) Use of PPEs 6) Ventilation 7) load Ventilation 8) Hydro blasting 9) Statutory Methods Statutory:- Factory Act 1948 Mines Act 1952 Workmans Safety Act Pollution Control Act Dock Workers Safety Act Environmental Protection Act. ESIS Plantation Act

Maternity Act Hazardous Chemical Storage & Transportation Act Workmans Compensation Act EP Acts & Rules Administrative controls:Diagnosis at the level of NITTS Acclimatization
-----------------------------------------------------------------------------------------------------------------------------

Silicosis
Quartz, Tidimites & Crisolyte Industries Involved:Mining, Quarrying, Drilling, Tunnelling Foundry Refractory Pottery Mechanism:The surface property of silica particles activate macrophases. These cells then release mediators that results in further cellular response by polymorphonuclear leucocytes, lymphocytes & additional macrophages. Fibroblast stimulating factors are released that promote hyalinization & collagen deposition. The resulting pathologic silicotic lesions in the form of Silcotic Nodules. These Nodules contain:-1) A central acellular zone 2) With extracellular Silica surrounded by whorls of collagen & fibroblasts. 3) And an Active Zone comprising Macrophages, Fibroblasts, Plasma Cells, & Additional Extra Cellular Silica. Impaired Macrophages function also play a role in susceptibility to infectious organisms like Mycobacterium Tuberculosis & Nocardia Asteroids Freshly fractured Silica is more toxic than Aged Silica. Perhaps related to presence of Reactive Radical groups on the cleavage plane of freshly fractured Silica. Types of Silicosis:- 1) Ordinary Silicosis:- A) Simple & B) Complicated 2) Acute Silicosis Detailed Classification:A) Chronic Silicosis:1) It is usually Asymptomatic 2) Exposure Time is more than 15 years. 3) Radiological Abnormalities found are Small Rounded Opacities(less than 10 mm) predominantly in the upper zone. 4) PFT are normal but may be mild restrictive Type

5) In rare cases Mild Obstruction or reduced diffusion capacity. 6) It does not progress to more advanced disease or Pulmonary Massive Fibrosis (PMF) 7) It is less susceptible for TB. B) Complicated Silicosis:- 1) It is called as Progressive Massive Fibrosis (PMF) 2) Exertional Dyspnoea 3) Nodular Opacities more than 10 mm size 4) Reduced CO Diffusion Capacity 5) Decreased pO2 (Arterial) at Rest 6) Both Obstructive & Restrictive Defects. 7) Distortion of Bronchial Tree 8) Recurrent Bacterial Infection 9) Weight Loss & Cavitations of large Opacities concern for TB 10) Pneumothorax due to fibrolytic lung may be difficult to respond. 11) Hypoxemic Respiratory Failure with CorPulmonale is a common Terminal Event. C) Accelerated Silicosis:-1) It may appear after more intense exposure of short duration usually 5 to 10 years. 2) Symptoms, X-Ray findings are same as complicated form. 3) Deterioration of lung function is more rapid 4) More susceptible to TB 5) Auto immune Diseases like Scleroderma & Rheumatoid Arthritis are seen, if so X-Ray abnormalities & PFT Impairment are rapid. D) Acute Silicosis:- 1) It may develop within 6 months to 2 years of massive Silica Exposure. 2) Dramatic Dyspnoea, Weakness & Weight loss are often presenting symptoms. 3) X-Ray chest shows Ground Glass appearance with Coarse, Linear & Rounded Opacities throughout the lung fields. 4) Histological findings show Pulmonary Alveolar Proteinosis. 5) There may be extra pulmonary symptoms like Renal & Hepatic Abnormalities. 6) Severe Hypoxemic Ventilatory Failure 7) It is most prone for TB known as Silico Tuberculosis. Treatment:- 1) No specific Therapy 2) Therapeutic measures are similar those used in the management of any a) Airway Obstruction b) Infection c) Pneumothorax

d) Hypoxemia c) Respiratory Failure 3) If Fibrinolytic drugs are given give INH & Refempicin. If already have TB then give 4 drug regime. 4) Positive Tuberculin Test:- If Tuberculin Test is positive treat with INH of Rifampicin as a preventive measure for 6 months to 1 year. 5) Silicosis patients receiving Gluco Corticoids should also be given INH & Rifampicin as a Preventive Measure. 6) Active TB:- INH, Rifampicin, Pyrazinamide, Ethambutol for 6 to 9 months. 7) Fibrolytic Agents:-1) Steroids 2) Poly Vinyl Pyridine-N-Oxide (PVPNO) 3) Beta- Amino Proprio Nytrile (BAPN) 4) N-Oxide-Poly-1,2-Ethylene (NO-PE) 8) Treatment of Hypoxemia:- To be treated a) To prevent the development of Polycythemia b) To delay or prevent Pulmonary Hypertension & c) Corpulmonale d) To improve exercise tolerance. Main Goal of Oxygen Therapy is To elevate pO2 above 60 mm of hg. This can be achieved by Oxygen by nasal canula (2-4 Lit) 9) Airway Secretions causing Copious Tenacious Sputum for which adequate Hydration, Humidification & Postural Drainage is required. 10) In Acute Silicosis which may cause Severe Hypoxemia & Respiratory Failure:a) Aggressive therapy like Whole Lung Lavage under G.A. to improve gas exchange & Remove Alveolar Debris. b) Steroids:- 40-60 mg/day for 1 to 2 months & then Taper off to 15-20 mg/day for 6 months to 1 year. c) INH & Rifampicin to be given if Steroids are given. 11) In young patients with end stage Lung or Heart Lung Transplant Differential Diagnosis:- 1) Pulmonary TB 2) Eosinophilia 3) Sarcoidosis 4) Pulmonary Alveolar Mico Lithiosis 5) Calcified lung lesions as a sequele of Chicken Pox 6) Histoplasmosis:-a) Lacking Upper Zone Predominance

b) Homogenous calcified lymph nodes in histoplasmosis Other Forms of Investigations:1) Branchography 2) CT & HRCT 3) Bronchial Arterio Angiography 4) Lung Biopsy 5) Sputum Culture for TB 6) Test for Rheumatoid & Anti Nuclear Antibodies 7) ECG for Corpulmonale 8) Serum Angiotensin Converting Enzyme increases in Silicosis 9) Sitographic Scanning done after administration of Gallium 67. Silicosis Associated with Rheumatoid Disease:X-Ray:- Typical appearance of X-Ray Known as Coplan Type:- Necrobiotic Nodules, occasionally large ill-defined opacities develop rapidly, which develop peculiar behaviour over few years known as Valiant Behaviour & sometimes associated with recurrent transient Pleural effusion or with high titre of Circulating Rheumatoid Factor without overt Arthropathy. Complications:- 1) TB & Other Infections 2) Pulmonary Heart Disease:- CorPulmonale 3) Bronchitis 4) Emphysema 5) Spontaneous PneumoThorax 6) Segmental & middle lobe collapse 7) Rheumatoid Syndrome 8) Systemic Sclerosis 9) Carcinoma Lung:- As per IARC there is sufficient evidence in experimental animals but limited evidence in man. So yet it is not a confirmed Carcinogen. 10) Neurological:- Irreversible abductor paralysis of the left vocal cord due to involvement of left recurrent laryngeal nerve. 11) Oesophageal Compression 12) Nephropathy:- a) Thickening of glomerular Capillaries loop & Desment Membrane. b) Increase number of Mesengeal & Endothelial Cells c) PeriGlobular Fibrosis All these three lead to a) Proteinurea & b) Systemic Hypertension

Lung Function Abnormalities in Silicosis:- 1) Decreased Vital Capacity 2) Decreased TLC 3) Decreased Residual Volume 4) Decreased FRC 5) Decreased FEV1 6) Decreased FVC --------------------------------------------------------------------------------------------------------------

Mixed Dust Fibrosis

If there is any inert dust it can develop into Sidrosis, Stannosis, etc. They are reversible by removing the person from the exposure. How to measure Free Silica:TLV for Free Silica :- Give personal sampler to the worker. Within 8 Hours the dust is collected on the filter. Within this inhaled dust free Silica % is measured & can be calculated. TLV = We follow OSHA = 10 mg/m/ % of free Silica + 2 e.g. 10 / say 78 + 2 = 10/80 = 1.04 mg/m Iron Dust = Sidrosis Inert property of inert dust is converted into irreversible fibrosis. Definition of Inert Dust Fibrosis:- It is due to the modification of the effects of small quantities of crystalline Silica (usually quartz) by the accompanying Non Fibrogenic Dust. The dust in hematite mines (Iron Ore) consists of Hematite, quartz & Mica, with the quartz contributing 4 to 6 % of total Dust. This proportion of quartz resembles but is rather more than Coal Pneumoconiosis. Clinical Features:- Symptoms, Physical Signs & PFTs are same as Silicosis. X-Ray:- When the lung lesions are small the opacities may be like discrete nodular just like Silicosis or CWP. When larger they are irregular opacities, usually in upper & middle zone, that is indistinguishable from Fibro Caseous TB. Calcification of the lesions & Axial appearance of hilar lymph nodes are not seen. Differential Diagnosis:- 1) Healed or Active TB 2) Collapse due to Consolidation 3) Bronchogenic Ca.

WHO Silicosis Compensation Calculation

Estimation:- When one person is exposed to Silica Dust, then the task is to find out how many people has Silicosis in the Mass Population Exposed. - Average Exposure Time - Mortality Rate - Life Expectancy, Average Life Then calculate Total Years Loss. Terms:DALY:- Disability Adjusted Life Year YLL:- Years of Life Lost, due to premature mortality YLD:- Years of Loss due to Disability DALY = YLL + YLD e.g. For example suppose in a particular area total exposure to silica dust is about 30 lakhs Onset of Silicosis at the age of 27 years (Average) Duration of Exposure 8 years (Average) Survival Time (Years) is calculated by Lou & Zhou 1989. Survival time is 12.2 years in India (Average Survival Rate) Average Age of Death is about 40 years. Life Expectancy at the age of 40 years in India is 31.5 years Reduction by 30% So the life expectancy is reduced to 21.82 years Prevalence of Silicosis in India is 12 to 55 %. The average comes to 32 %. Total people suffering in India due to Silicosis are 9.6 Lakh. Nakagawa Studies in 1985, the mortality rate in Silicosis is 2.3 %. Thus Means of Mortality = about 22,000 Thus YLD = 12.2 X 22,000 YLL = 21.82 X 22,000 DALY = YLL + YLD = (12.2 X 22,000) + (21.82 X 22,000) = 34 X 22,000 So Years loss per person = 34 X 22,000/22,000 = 34 Suppose Average income of the workers in Rs. 36,000 per year So Estimated Compensation = 36,000 X 34 = About 13 lakh

Asbestosis
Discovery of Asbestos was considered as Magic Cloth as it did not burn. Types of Asbestos Fibers:-1) Serpentine or Crysotile:- Soft & Silky fibers. It has high tensile strength, high flexibility & high resistance to alkalies. It undergoes decomposition above 675C. It is a curly fiber 2) Amphiboles:- It is straight & needle like fiber. It is more brittle & appear more dusty. It has greater resistance to heat & Acids. Types of Amphiboles:-a) Crocidolite (Blue) b) Amosite (Brown) c) Anthrophyllate (No colour) d) Tremolite e) Actinolite Occupations Involved:- 1) Asbestos Cement & its products 2) Water & Drain Pipes 3) Corrugated Roofing Material 4) Insulating Material 5) Fire Fighting Material 6) Sound Proofing Material 7) Ship Breaking Industry Clinical Features:Symptoms:- 1) Most important symptom is breathlessness on efforts, slight at first & then increasing in severity until it is present at rest 2) Chest Tightness 3) Inability to Deep Breathing 4) Cough:- It is absent in early stage & present in later stages. Usually it is dry cough or small quantity of viscid mucoid sputum. 5) Sputum:- Usually mucoid & tend to be increase in the first 2 hours after getting up in the morning (Morning Cough). 6) Haemoptysis:- It is not caused by Asbestosis but may be present due to Ca. Lung. Physical Signs:-1) Clubbing of fingers & Toes

2) Chest Expansion:- Equilateral impairment of expansion of chest affecting mainly lower chest wall, is a characteristic of advanced disease. 3) Inspiratory Crackles (Crepts):- The most important physical sign, heard bilaterally only in the development of the disease. Patchily in the basal region of the lower lobe, usually posteriorly but often first in the lower axilla & sometimes in the middle lobe & in the lingular region. 4) Wheez & Rhonchi:- It is not the the feature of Asbestosis, but when it is present it is due to Bronchitis of some other cause. 5) Pleural Rub:6) Loss of Weight in advanced cases 7) Central Cyanosis in advanced cases 8) Cor Pulmonale Investigations:- 1) Sputum Examination for Asbestos Bodies 2) Broncho-Alveolar Lavage for Asbestos Bodies 3) Gallium 67 Scan:- This technique is used as an aid to diagnosis & increased Gallium Uptake has been demonstrated in established cases. 4) ESR:- raised in Asbestosis 5) Serology:Rheumatoid Factor Antinuclear Antibodies (ANA) 6) PFT:- A very early abnormality is the increase in Static Elastic Pressure, i.e. Decreased Compliance. The important PFTs show Restrictive type of changes. 7) Ct & HRCT Radiology:- a) PA View b) Suitable angle right or left anterior oblique views. A) Early Findings:- - It consists of more Fine Vessel Opacities. - Linear Opacities, which look like extension of vascular markings reaching to the periphery, often crossing each other to give a net like appearance. - Another early appearance is minute bead like opacities in the costophrenic angle. B) As Asbestosis Progresses:- Linear & Irregular opacities become thicker & Spread into the Middle Zone & Rarely in Upper Zone. - Costophrenic & CardioPhrenic Angles are obliterated. - With ill-defined haged in both Mid & Lower Zones due to Pleural Thickening.

C) Advanced of Difficult Case:- The lung fields are obscured due to Pleural Fibrosis. Complications:- 1) Hyaline Plaque of the Parietal Pleura 2) Benign Pleural Effusion 3) Diffuse Pleural Thickening 4) Diffuse Malignant Misothelioma of Pleura & Peritoneum. 5) Lung Cancer 6) Laryngeal Cancer 7) GIT Cancers 8) LymphoProliferative disease like Lymphatic Malignancies 9) Skin Corn 10) Pericardial Mesothelioma. Mechanism of Asbestosis:In the early stages Asbestos Fibres accumulate in those alveoli which open directly to the bronchioles. They penetrate the wall & Produce a Low Grade Inflammatory Response followed by Fibrosis. This causes Thickening & Narrowing of the Terminal Airways, which is picked up as a reduction of Gas Transfer & Compliance. These Fibres Migrate away from this CentriLobular area into Interstitium between the alveoli and Towards the Pleura, causing Extension of Low Grade Inflammatory Response & Interstitial Fibrosis. This interferes with Ventilation by making Lung Rigid & lead to Shrinkage of the affected area with HoneyComb Changes. This change affects only the Periphery of the lung & leaves the Central Part Undamaged. However, this normal lung has very little Functional Value, as it is held Immobile by the surrounding Damage & Fibrosis. Mesothelioma:- Malignant Mesothelioma due to exposure to Asbestos fibres affecting any Serosal Membrane (Sacs) , which is associated with Pleural Effusion, Dyspnoea & Chest Pain. It usually Produces:Pleural or Peritoneal Mesotheliomas Multicystic Mesotheliomas (Low Grade) Benign Papillary Mesothelioma. Ca Lung:- Types:Squamous Cell Ca. Adenocarcinoma Large Cell Ca. Small Cell Ca. Probability of Lung Ca to the Asbestos Exposure is assessed by Fibre Years. Fibre Years:- The fibre per Cu Cms/Year 1Fibre/Cu Cms/Year :- The chance of Ca Lung increases by 0.5 to 4 % i.e. Increased Estimated Risk. If it is 25 Fibre Year, then the increase in Risk is Two Fold i.e.200%.

Another Method of Estimation is 2 Fold Increase of Risk = 2 Million Amphibole Fibres = 5 Micron / Gm of Dry Lung Tissue Another Count:2 Fold Increase of Risk = 5,000 to 15,000 Asbestos Bodies per Millilitre of BronchoVascular Lavage Fluid.

Byssinosis
Definition:- Inhalation of cotton dust causes Byssinosis. Mechanism of Action & Pathogenesis:- All are Hypothesis 1) Immunological Mechanism:-a) A condensed polyphenol known as Leucocyanidine b) Some Fungus is responsible It is clear from studies that cotton dust is highly biologically active & capable of mediating an inflammatory response. 2) Bacterial Endotoxins are responsible. 3) The non immunological release of Histamine. 4) The Fungal Enzyme:- Cotton Dust has a Proteolytic Enzyme Activity originally from contaminating microorganisms. Clinical Features:- A) Acute Byssinosis:- Textile workers may experience Acute Symptoms known as Mill Fever on exposure to cotton dust characteristically occurs following the workers First Exposure to Cotton, Flax of Hemp Dust. It consists of Fever with Non Productive Cough, malaise & Sneezing, which usually last for few weeks, resolving despite continued exposure to dust. B) Chronic Byssinosis:- The development of Symptoms is rare in first 5 years & Requires 20 to 25 years of dust exposure. The symptoms consists of Chest Tightness & Breathlessness, characteristically developing on the first day of the working & over the second half of the working shift & experience most severely with the exertion & on returning home in the evening. Other workers described a very rapid onset of symptoms within 30 minutes of starting the work, which may be most severe over the first of the shift, called as Monday Morning Fever Grading:- See Roach & Schiling Classification WHO Classification Classification Symptoms Gr 0 No Symptoms Gr B1 Chest Tightness & Short of Breathing on most of the days on back to work Gr B2 Chest Tightness &/Or Short of Breath on the first & also other days of working week Classification according to Respiratory Tract Irritation Classification Symptoms Gr RTI1 Cough associated with Dust Exposure Gr RTI2 Resistant phlegm on most of the days during 3 months of a year, initiated or exacerbated by dust exposure Gr RTI 3 Persistent phlegm initiated or made worse by dust exposure, either with exacerbation of chest illness of persisting for 2 years, or more.

Classification according to Pulmonary Functions Classification Symptoms Acute Changes a) No Effects Consistent decline in FEV1 of less than 5% or increase in FEV1 during the work shift. b) Mild effects A consistent decline of FEV1 between 5-10 % c) Moderate Effect A consistent decline of FEV1 by 10-20 % during the working Shift d) Severe Effect Decline of FEV1 more than 20 % during the shift Chronic Changes a) No Effect FEV1 is 80 % of predicted value b) Mild to Moderate FEV1 is 60 to 79 % of predicted value c) severe FEV1 is less than 60 % of predicated value Radiological Changes 1) There is no significant changes 2) Smoking & Byssinosis has Potentiating Effect (One can Potentiate the others effect) Case Fatality Rate is 40 %

Coal Workers Pneumoconisis

Coalification (How the coal is formed ?):- Coal is comprised of moisture, pure coal (Carbon), and Mineral matters ( Mainly Sulphur). The process of conversation is known as Coalification. Organic Matter follows a Transformation of Wood Peat Lianite Bituminous Coal Anthrocite Coal Coal may be of two types:- 1) Brown Coal & 2) Black Coal. Brown refers to the coal of low quality, while lack is of high quality. The rank depends upon:1) % of Carbon in the coal, 2) The completeness of Transformation from vegetation to coal, 3) The ecological age of the deposits with new deposits forming above old layer. 4) Bituminous variety contains 55% Carbon & 5) Anthracite variety contains 87 % Carbon. Health Hazards:1) Industrial Bronchitis 2) Coal Workers Pneumoconiosis a) Simple CWP b) Complicated (Pulmonary Massive Fibrosis PMF) c) Capalans Syndrome 1) Industrial Bronchitis:- It is commonly diagnosed amongst the workers exposed to dust (Coal Dust). It manifests a productive cough, which persists for at least 3 months per year; for at least 2 years, associated with work place dust exposure. It is due to inhalation of larger dust (Non Respirable), producing chronic burden to the Muco-Ciliary mechanism & act as a irritant to the airways. 2) Coal Workers Pneumoconiosis (CWP):CWP can be described as inhalation & deposition of coal dust into the lung & Lungs Reaction to its presence. Typically CWP is described as Simple or Pulmonary Massive Fibrosis (PMF). The radiograph of simple type shows small rounded opacities ranging from pinhead to

10 mm dimeter. First In the upper zone & then in the middle & lower zones. With prolonged excessive exposure these small opacities may coalesce & form larger opacities as PMF. PMF is characterized by one or more large opacities greater than 10 mm of diameter or bigger in the upper zone. PMF represents as a) Deviation of Trachea and major airways to the side of most prominent area of coalescence. B) Loss of upper zone lung volume c) Elevation oh Hila d) Basilar Emphysema e) Dyspnoea, cough & sputum production. Sometimes there may be Melenoptysis (Coughing out of Jet Black Sputum). (In Simple CWP there is no Melanoptysis) f) Pulmonary Arterial Hypertension Coplans Syndrome:A special case of Nodular Lung Reaction occurs in dust exposed individual, who either has Rheumatoid Arthritis or who develops Rheumatoid Arthritis, within the subsequent 5 10 years. This is due to the potential role of immunological factor. The nodular opacity varies from 5 50 mm in diameter & usually multiple. Diagnosis:- 1) Occupational History 2) Pulmonary Function Tests 3) Chest X-Ray 4) HRCT 5) Pulmonary Lavage 6) By excluding other diseases. Pathology:- This is a focal collection of coal dust in-pigment leaden macrophages, & round dilated Respiratory bronchioles known as Coal Macules, which is a characteristic lesion of CWP. Fine network of Reticulin within this collection of cells may be visible. There is a formation of Focal Emphysema. PMF is diagnosed when one or more nodules of size greater than 2 cms. In diameter, typically on a background of simple CWP. In PMF the lung reveals a solid, heavily pigmented with rubbery or hard texture. It is common in apical posterior portion of upper lobe, or superior segment of lower lobe. It tends to occur asymmetrically; first in one lung then to other; leading to suspicion of Malignancy. This lesion may also can cavitate & the workers may expectorate an Ink like fluid known as Melanoptysis. Mechanism:1) Direct cytotoxity of coal dust. 2) Release of oxidents (Hydrogen Peroxide, Hydroxyl Radicles) & leucotrine via break down of Arachinodic Acid which may lead to the beginning of process of inflammation & fibroblasts.

3) Stimulation of Cytokines released alveolar macrophases to recruit Effector Cells & stimulates Fibroblast proliferation & Collagin ynthesis in the area of coal dust deposition. Permissible limits of coal dust:1) 5 mg/m for the narrow base mines 2) 7 mg/ m for the narrow base mines 3) 3 mg/ m for the surface mines. Treatment:- No Treatment. Only Symptomatic treatment is given. Simple CWP is reversible. So our goal is to diagnosis at simple stage. Preventive Measures:Complications:1) Pulmonary Heart Disease :- Corpulmonale 2) Rheumatoid Pneumoconiosis 3) Systemic Sclerosis 4) Ischemic Heart Disease 5) Chronic Bronchitis 6) Susceptible for infection of lungs 7) ? Ca Lung