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 & Poisons3) Fumes:- e.g. Welding4) Mist:- e.g. Instecticide spray5) Smoke

Effects of Noxious Substances in Lungs1) Mechanical:- Due to reaction of Gas Exchange Unit2) Irritation:- Chlorine, Ammonia3) Toxicity:- Mercury Vapours4) Fibrosing:- Silica, Asbestosis5) Allergic:- DizoMethane6) Granulomatous Changes:- e.g. Beryllium, 7) Nasal Septal Perforation:- Arsenic, ChromiumDust:-Lung reaction depends upon:- 1) Nature & Property of the Dust

2) The mount os dust retained:- e.g. Coal Dust3) Duration of Exposure4) Individual Susceptibility5) Immunological Reactivity of the subject6) 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 MicronsThoracic Dust is Below 10 MicronsTLV is 5 Mg/Cu MMRespirable Dust:- 0.5 to 5 MicronsDefence 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 Opacitiese.g. Asbestosis, Talk Pneumoconiosis

4) Dust which cause Small Rounded Opacities, which may progress to Upper Lobe Fibrosise.g. Extrinsic Allergic Alveolitis, Bagassosis,

Chronic Berrylium DiseaseDiagnosis:-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) Quartz2) Tidimites:_ When Quartz is heated to 600®C3) Cristobalite:- When Quartz is heated to 1,200®C

Occupations Involved:- Cleaners of Furnace Lining, Brick Workers, Pottery (Brick:- H2S, Silica & Heat)Types of Silicosis:- 1) Acute Silicosis

2) Accelerated Silicosis3) Chronic Silicosis4) Progressive Massive Fibrosis

Pathogenesis:- Difference Between Silicosis & TB1) Moist Shadows Soft Cotton Type seen in TB2) Silicosis is Symmetrical, while TB is Asymmetrical3) Axial Appearance:- Hilar Lymph Nodes are Calcified in

Silicosis

4) Pleural Effusion in TB, while Pleural Plaques in Silicosis5) 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 hereAsbestos

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 Effusionb) Pleural Fibrosis or Hyaline Fibrous

Plaquesc) Rounded Atelectasis that mimic

Cancer2) Benign Asbestos Induced Parenchymal lesion of Lung

Disease:- a) Lung Fibrosisb) 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 PleuraDiffuse Pleural Thickening is at Visceral PleuraIn Diffuse Pleural Thickening CostoPhrenic angle is obliterated followed by elongated thickening.Phase I:- Plaques in the centrePhase II:- Goes to lateral sideIt initiates from lower side & from PeripheryHoney 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 Reaction Disease1) Mineral Inorganic A) a) No Fibrosis A) a) Siderosis

b) Some Interaction b) Stanosis c) Accumulation of local Macrophages

c) Barritosis

d) Mild Reticulosis Fibrosis d) Soot (Carbon) Anthracosis

B) Granuloma Formation a) Sarcoid Type B) a) Beryllium Disease (Due to

Hard Light Metal) b) Foreign Body Granuloma Type

b)Talk Pneumoconiosis Magnesium Silicate

C) Collagen Fibrosis a) Nodular (Massive) a) Silicosis, Anthrocosis, Late

Stage PMF b) Diffuse Interstitial Fibrosis

b) Asbestosis, Talk Pneumoconiosis, Chronic Beryllium Disease

2) Organic (Non Mineral)

A) No fibrosis only Reaction

a) Translucent Interstitial Pneumonia (Acute Allergic Reaction)

a) e.g. When Massive Dust is Inhaled

b) Sarcoid Type of Reaction b) Extrinsic Allergic Alveolitis (EAA)

B) Collagen Fibrosis B) Mushroom & BagassosisC) Cotton Dust C) Byssinosis

Coal Worker’s PneumoconiosisFirst Coal Bronchitis & then converts into Coal Worker’s 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 Source1) Barritosis (Barium) Barium Sulphate Mines of Barium Salts2) Sidrosis Iron Oxide Welding3) Stannosis Tin Oxide Smelting4) Kaolinosis Hydrated Aluminium

SilicateChina Clay

5) Aluminosis (Shiver’s Disease)

Stampede Aluminium Paint

6) Coal Workers Pneumoconisis (Anthracosis)

Coal Dust Mining

7) Talcosis Hydrated Magnesium Silicate

Rubber

8) Berylliosis (Chronic Beryllium Disease)

Beryllium Compound Atomic Reactor

Asbestosis Asbestos Fibres Mining

Occupational Asthma1) Allergens:- Feather, Grain Dust2) Plant & Vegetable Material:- Mustard Powder, Saw Dust, Cotton Dust3) Antibiotics:- Penicillin5) Chemicals:- Insecticides, Aluminium Flax, Platinum Salts.6) Agents used in Plastics, Paints & Adhesives:- Isocynates, Phthallic Anhydride7) 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) In Atopic individuals the bronchi may be affected , giving Asthmatic Symptoms, Mediated by Non Precipitant, Liagenic antibodies called as Type I Allergy

2) 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) Source of Antigen Precipitant Present Against

1) Farmer’s Lung Mouldy Hay Micropolispods Feani2) Bagassosis Mouldy Overheated Sugar Cane T Vulgaris, Thermo

Actinomyces Bulgaris3) Mushroom Worker’s Lung

Mushroom Compost M. Feani & T. Vulgaris

4) Maple Bark (stripper’s Lung)

Mouldy Maple Bark Cryptostroma

5)Malt Worker’s Lung Mouldy Barley, Malt Dust Aspergillis Cleavagas6) Bird Fencer’s Lung Pigeon, Budgenger, Hem,

Parrot’s droppingsSr. Proteins from droppings

7) Pituitary Snuff Taker’s Lung

Heterologus Pituitary Powder Serum Proteins, Pituitary Antigens

8) Wheat Weegil’s Disease Infected wheat flour Sitophylus Granarius9) Sequoiosis Mouldy red wood Saw Dust Audio Basidum PallutansCheese worker’s Lung Cheese Mould PenicillinCorn Flour’s Lung12) Suberosis Mouldy Oak Bark or Cork Dust Mouldy Cork Dust13) New Guinea Lung Mouldy Thatch Dust Thatch of Huts14) Humidifier’s Lung Humidifying Hot Air System M. Feani15) Animal Food Worker’s Lung

Fish Meal ??

16) Furrier’s Lung Fox Fur ??17) Smallpox handler’s Lung

Casts from Small Pox lesions ??

18) Coffee Worker’s Lung Coffee Bean Extract ??19) Black Fat Tobacco Smoker’s lung

Black fat Tobacco ??

20) Paprica Splitter’s Lung Paprica Dust ??

Difference between Extrinsic Allergic Alviolitis (EAA) & Occupational Asthma

Occupational Asthma EAA1) Individual Predisposition

Important Unimportant

2) History Edema & Eosinoplills Infiltration of Bronchial wall

Cellular infiltration of Alveoli & Interstitium or Epithelial Granules

3) Site Bronchi Alveoli & Interstitium4) Onset Rapid after exposure to

allergens causing Asthma5-6 hours after exposure to relevant antigens

5) Systemic Upset Slight Marked6) Signs Rhonchi Crepitations7) X-Ray Findings Hyperinflation only Milliary Mottling in Acute Stage8) Serology No Precipitants Precipitants to relevant

Antigens9) Eosinophilia Common Absent10) Skin Test Immediate Type

HypersensitivityArthus Type Response

Physiology Obstructive Pattern of Ventilatory Abnormalities

Restrictive Pattern of Ventilatory Abnormality with Marked Diffusion Defects

Difference Between Obstructive & Restrictive Pattern

Obstruction Restriction1) TLC2) RV3) VC/FVC4) FEV1/FVC Or Normal5) RV/TLC Ratio Normal6) Resistance Normal7) Compliance8) Diffusion Normal9) Arterial pO210) Arterial pCO211) Arterial pH Normal or

Diagnosis of Occupational Lung Disease (OLD)A) History 1) Occupational History:- Hist. To be taken in chronological orders

Material Handling Brick Field Activities2) Para Occupational History

3) Environmental History:- Pt. Residing outside the company may suffer

4) Domestic HistoryB) Exclusively given to smoking habits:-1) Asbestos 2) Uraniumc) Clinical Features:- 1) Dyspnoea:- e.g. Mild Dyspnoea due to simple Coal

Worker’s 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 Fever6) Irritation of Upper & Lower respiratory Tract:- Ammonia,

Phosgene7) Clubbing:- Due to Asbestosis or Lung Ca.8) Some Non respiratory Symptoms:-

e.g. Benzene Vapours go to SystemD) Physical Signs:- 1) Fine to medium crepitations during inspiration

2) Mild Expiratory Crepts, mainly at the base3) Mid Inspiratory Crepts along mid-axillary line at the base

E) Investigations:- PFT:-NonspecificX-Ray:- How to detect Residual Volume on X-Ray – PA & Lateral

ViewProcedure:- 1) Area of each lung field in PA Film, Excluding the

mediastinum by Planimeter2) Area in the lateral film including the heart is measuredCalculation:- 1) Multiply the area of Right Lung field by

Laterial area2) Multiply the area of lateral Lung field by lateral

area3) 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 – FVCPredicted 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= AgeFEV1 = 0.396 H – 0.0212 A – 3.130PEFR = 4.236 H – 2.0981 A – 109.5

For Females:- FVC = 0.0370 H – 0.0070 A – 3.187PEFR = 3.310 H – 1.865 A – 81.0FEV1 = 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 trappedFunctions measured by 1) Fluroscopy:- Measures movements of diaphragm &

Mediastinum2) Radio isotope technique3) 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 Asthma5) To study the type of hypersensivity Reaction Type I or Type III6) Serological Examination:- e.g. IgE is increased in Occupational

Asthma, Precipitants are increased in EAA7) Biological Monitoring:- If he is inhaling lead fumes, urine lead

estimation.8) Lung Biopsy:- e.g. for As, Si9) CT, HRCT Scan 10) Perfusion Cintography11) Computerised tomography mainly for peripheral lesions12) Bronchofluroscopy13) Pulmonary Lavage14) Legman P Test15) Methacholine Test

Safety Measures:- Medical MeasuresStatutory Measures

Engineering Measures1) Substitution of hazardous material innocuous material or a modification of the process designed to render the substance innocuous.2) The complete enclosure of the process3) 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 Services7) Environmental Monitoring8) Statical Monitoring9) ResearchSafety Measures:- 1) Substitution

2) Enclosure of Machine3) Enclosure of the person4) Isolation of the person.5) Use of PPEs6) Ventilation7) load Ventilation8) Hydro blasting9) Statutory Methods

Statutory:- Factory Act 1948Mines Act 1952Workman’s Safety ActPollution Control ActDock Worker’s Safety Act

Environmental Protection Act.ESISPlantation Act

Maternity ActHazardous Chemical Storage & Transportation ActWorkman’s Compensation ActEP Acts & Rules

Administrative controls:- Diagnosis at the level of NITTSAcclimatization

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SilicosisQuartz, Tidimites & CrisolyteIndustries Involved:- Mining, Quarrying, Drilling, Tunnelling

FoundryRefractoryPottery

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 AsteroidsFreshly 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) Complicated2) 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 Dyspnoea3) Nodular Opacities more than 10 mm size4) Reduced CO Diffusion Capacity5) Decreased pO2 (Arterial) at Rest6) Both Obstructive & Restrictive Defects.7) Distortion of Bronchial Tree8) Recurrent Bacterial Infection9) Weight Loss & Cavitations of large Opacities concern

for TB10) 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 rapid4) More susceptible to TB5) 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 Failure7) It is most prone for TB known as Silico Tuberculosis.

Treatment:- 1) No specific Therapy2) Therapeutic measures are similar those used in the management of

any a) Airway Obstruction b) Infection c) Pneumothorax

d) Hypoxemia c) Respiratory Failure3) 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 TransplantDifferential Diagnosis:- 1) Pulmonary TB

2) Eosinophilia3) Sarcoidosis4) Pulmonary Alveolar Mico Lithiosis5) Calcified lung lesions as a sequele of Chicken Pox6) Histoplasmosis:-a) Lacking Upper Zone Predominance

b) Homogenous calcified lymph nodes in histoplasmosis

Other Forms of Investigations:- 1) Branchography2) CT & HRCT3) Bronchial Arterio Angiography4) Lung Biopsy5) Sputum Culture for TB6) Test for Rheumatoid & Anti Nuclear Antibodies7) ECG for Corpulmonale8) Serum Angiotensin Converting Enzyme increases in

Silicosis9) 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:- CorPulmonale3) Bronchitis4) Emphysema5) Spontaneous PneumoThorax6) Segmental & middle lobe collapse7) Rheumatoid Syndrome8) Systemic Sclerosis9) 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 Compression12) Nephropathy:- a) Thickening of glomerular Capillaries loop

& Desment Membrane.b) Increase number of Mesengeal &

Endothelial Cellsc) PeriGlobular Fibrosis

All these three lead to a) Proteinurea & b) Systemic Hypertension

Lung Function Abnormalities in Silicosis:- 1) Decreased Vital Capacity2) Decreased TLC3) Decreased Residual Volume4) Decreased FRC5) Decreased FEV16) Decreased FVC

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Mixed Dust FibrosisIf 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/m³/ % of free Silica + 2e.g. 10 / say 78 + 2 = 10/80 = 1.04 mg/m³

Iron Dust = SidrosisInert 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 Consolidation3) Bronchogenic Ca.

WHO Silicosis Compensation CalculationEstimation:- 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 mortalityYLD:- 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 yearsReduction 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 22,000Thus YLD = 12.2 X 22,000

YLL = 21.82 X 22,000DALY = YLL + YLD = (12.2 X 22,000) + (21.82 X 22,000)

= 34 X 22,000So Years loss per person = 34 X 22,000/22,000

= 34Suppose 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 675®C. 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) Tremolitee) Actinolite

Occupations Involved:- 1) Asbestos Cement & its products2) Water & Drain Pipes3) Corrugated Roofing Material4) Insulating Material5) Fire Fighting Material6) Sound Proofing Material7) 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 rest2) Chest Tightness3) Inability to Deep Breathing4) 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 cases7) Central Cyanosis in advanced cases8) Cor Pulmonale

Investigations:- 1) Sputum Examination for Asbestos Bodies2) Broncho-Alveolar Lavage for Asbestos Bodies3) 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 Asbestosis5) 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 & HRCTRadiology:- 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 Pleura2) Benign Pleural Effusion3) Diffuse Pleural Thickening4) Diffuse Malignant Misothelioma of Pleura & Peritoneum.5) Lung Cancer6) Laryngeal Cancer7) GIT Cancers8) LymphoProliferative disease like Lymphatic Malignancies9) Skin Corn10) 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 MesotheliomasMulticystic Mesotheliomas (Low Grade)Benign Papillary Mesothelioma.

Ca Lung:- Types:- Squamous Cell Ca.AdenocarcinomaLarge 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 TissueAnother Count:-

2 Fold Increase of Risk = 5,000 to 15,000 Asbestos Bodies per Millilitre of BronchoVascular Lavage Fluid.

ByssinosisDefinition:- 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 responsibleIt 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 worker’s 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 ½ of the shift, called as “Monday Morning Fever”Grading:- See Roach & Schiling ClassificationWHO ClassificationClassification SymptomsGr 0 No SymptomsGr B1 Chest Tightness & Short of Breathing on most of the days on back

to workGr B2 Chest Tightness &/Or Short of Breath on the first & also other days

of working week Classification according to Respiratory Tract IrritationClassification SymptomsGr RTI1 Cough associated with Dust ExposureGr RTI2 Resistant phlegm on most of the days during 3 months of a year,

initiated or exacerbated by dust exposureGr 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 FunctionsClassification SymptomsAcute 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 shiftChronic 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 changes2) Smoking & Byssinosis has Potentiating Effect (One can Potentiate the other’s effect)

Case Fatality Rate is 40 %

Coal Worker’s 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 CoalCoal 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 Bronchitis2) Coal Worker’s Pneumoconiosis

a) Simple CWPb) Complicated (Pulmonary Massive Fibrosis PMF)c) Capalan’s 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 Worker’s Pneumoconiosis (CWP):- CWP can be described as inhalation & deposition of coal dust into the lung & Lung’s Reaction to it’s 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 volumec) Elevation oh Hilad) Basilar Emphysemae) 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

Coplan’s 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 Tests3) Chest X-Ray4) HRCT5) Pulmonary Lavage6) 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/mᶟ for the narrow base mines2) 7 mg/ mᶟ for the narrow base mines3) 3 mg/ mᶟ 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 :- Corpulmonale2) Rheumatoid Pneumoconiosis3) Systemic Sclerosis4) Ischemic Heart Disease5) Chronic Bronchitis6) Susceptible for infection of lungs 7) ? Ca Lung