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Definition :

Definition Occupational lung disorder has been defined as diseases arising out of or in the course of employment . The Encyclopedia of Occupational Health and Safety of the International Labour Organization (ILO) [1] defines pneumoconiosis as “the accumulation of dust in the lungs and the tissue reactions to its presence”

Classification of Occupational Lung Disorder:

Classification of Occupational Lung Disorder MAJOR DISEASE CATEGORY CAUSATIVE AGENT Upper respiratory tract irritation - Irritant gases, fumes, dusts Airway disorders Occupational asthma Sensitization Low molecular weight - Diisocyanates , anhydrides, wood dusts High molecular weight - Animal-derived allergens, latex Irritant-induced, RADS - Irritant gases, smoke Byssinosis - Cotton dust Grain dust effects - Grain Chronic bronchitis/COPD - Mineral dusts, coal, fumes, dusts

Cont… :

Cont… MAJOR DISEASE CATEGORY CAUSATIVE AGENT Acute inhalation injury Toxic pneumonitis Irritant gases, metals Metal fume fever Metal oxides: zinc, copper Polymer fume fever Plastics Smoke inhalation Combustion products Hypersensitivity pneumonitis Bacteria, fungi, animal proteins Infectious disorders Tuberculosis, viruses, bacteria Pneumoconioses Asbestos, silica, coal, beryllium, cobalt Malignancies Sinonasal cancer Wood dust Lung cancer Asbestos, radon Mesothelioma Asbestos

Chest Imaging(ILO) :

Chest Imaging(ILO) Small opacities in the parenchyma are classified by shape and size: p , q , or r for rounded opacities (diameter, <1.5 mm, 1.5-3 mm, or >3 mm, respectively) and s , t , or u for irregular opacities (width, <1.5 mm, 1.5-3 mm, or >3 mm, respectively). Profusion category (or concentration) is read on a 12-point scale (0/–, 0/0, 0/1, up to 3/2, 3/3, and 3/+) in comparison with the standard radiographs Large opacities are classified as category A ( for one or more such opacities with a diameter of 1 cm but not exceeding a combined diameter of 5 cm ), category B (one or more opacities > 10 cm in diameter and whose combined area does not exceed one upper zone), and category C (>B) Provision is made to grade pleural thickening for width ( a ≤ 5 mm, b > 5 mm but < 10 mm, and c ≥ 10 mm) and extent ( 1 = up to one quarter, 2 = one quarter to one half, and 3 = over one half of the lateral chest wall). The extent of pleural calcification also is graded


ASBESTOSIS Asbestos is a fibrous hydrated magnesium silicate with more than 3000 commercial uses due to its indestructible nature,fire resistance. Types- 1. Chrysolite -m.c used (serpentine) 2. Amphibole ( amosite )-straight fibre 3. Crocidolite -needle shaped long fibre Initially, asbestos - used in fireproof textiles and later as insulation for boilers and pipes. More recently, asbestos has been used in cement pipes for potable water, and roofing and floor products.

Types of exposure :

Types of exposure Primary exposures - miners and millers. Secondary exposures-manufacturing plants using asbestos in the production of textiles, friction materials, tiles,and insulation material The most significant exposures seen in the construction trades . 1. Asbestos insulators , who mixed asbestos cement on site to insulate joints and elbows on pipes; 2. Boilermakers and sheet-metal workers, who worked adjacent to the asbestos workers; 3. Electricians, carpenters, plumbers, and others who worked in the vicinity of work requiring asbestos exposure. These exposures mainly to chrysotile asbestos

Nonmalignant pleural manifestation:

Nonmalignant pleural manifestation Pleural disease – M.C manifestation of asbestos exposure 1.circumscribed pleural plaques 2.diffuse pleural thickening 3.rounded atelectasis 4. pleural effusions

Pleural Plaques :

Pleural Plaques 1. M.C manifestation 2. Focal, irregular, raised white lesions- on the parietal and, rarely, the visceral pleura 3. May be small or extensive 4. Commonly - in the lateral and posterior mid lung zones, where they may follow rib contours and the diaphragm 5. Enter lobar fissures and can invade the mediastinum or pericardium; rarely invade the apices / costophrenic sulci 6. Histologically -extensive collagen fibrils arranged in a basket-weave pattern, and a thin covering of mesothelial cells. 7. The two pleural surfaces - free of adhesions 8. Pleural calcifications frequently 9. On average, the latency time for the appearance of plaques - 30 years, but the time can vary greatly

Clinical and Physiological Features:

Clinical and Physiological Features In absence of concomitant asbestosis or obliteration of the CP angle, pleural plaques are usually asymptomatic. Most often they are incidental findings on chest radiographs. They do not cause significant abnormalities such as pleural rubs, rales , or rhonchi on auscultation of the chest. Decrease in FVC & FEV1-more in smokers

Radiographic Features :

Radiographic Features The radiograph shows bilateral calcified pleural plaques en face and on top of the diaphragm. The pleura is diffusely thickened bilaterally and the costophrenic angles are blunted. Mediastinal pleural calcification is present on the right .

Cont… :

Cont… The CT scan can recognize plaques at a much earlier and less well-defined state than the conventional chest radiograph. The CT scan is particularly useful for perivertebral and pericardiac plaques, and high-resolution CT scanning (HRCT) helps to establish the presence of diaphragmatic lesions. In all cases, the CT scan can help to differentiate plaques from extrapleural fat pads and can detect concomitant parenchymal abnormalities.

Diagnosis & Treatment :

Diagnosis & Treatment Pleural plaques due to asbestos exposure are usually bilateral (80 percent of the time), whereas unilateral pleural plaques d/t trauma, previous TB, or, rarely, other causes,like CVD The lesions are usually stable and remain the same size for months. This helps to differentiate plaques from pleural tumors . No specific treatment required for asbestos pleural plaques. Periodic chest radiographs, is recommended .

Diffuse Pleural Thickening :

Diffuse Pleural Thickening Pleural fibrosis- localized or diffuse and either U/L or B/L The lesions- vary in thickness from a whitish discoloration of the lung surface to a thick white peel that can encase pulmonary str. Diffuse pulmonary thickening-most often seen as a continuous sheet that is 5 to 10 cm in length & in 90% of patients it affects the CP> Interlobar and interlobular fissures- commonly involved Disease of the visceral pleura

Pathogenesis :

Pathogenesis Three mechanism- 1. Confluence of large pleural plaques-10-20% 2. Extension of subpleural fibrosis to the visceral pleura(10-30%) 3. Fibrotic resolution of a benign pleural effusion-M.C

Clinical and Physiological Manifestations:

Clinical and Physiological Manifestations Mild, diffuse pulmonary fibrosis- asympto and discovered as an incidental finding on a chest radiograph . Diffuse nature of the lesion- leads to pulmonary symptoms, including dyspnea on exertion, chronic dry cough, and chest pain. Restrictive physiological abnormality. Rarely, in patients with severe B/L disease, respiratory insufficiency and death have occurred.

Radiographic Features :

Radiographic Features Continuous pleural opacity extending over more than 25 % of the pleural surface of a lung, often blunting the costophrenic angle. U/L or B/L and seen in the presence or absence of concomitant asbestosis and pleural calcifications. Rarely, the pleural fibrosis will produce a fibrotic pseudotumor with a pleural basis (rounded atelectasis ).

Diagnosis & Treatment :

Diagnosis & Treatment Based on the clinical presentation and chest radiograph. Diffuse pleural fibrosis - not unique to asbestos-exposed persons and can represent old inflammatory reactions from tuberculosis, thoracic surgery, hemorrhagic chest trauma, or drug reactions. Bilateral interstitial changes in the lower lung zones in association with pleural plaques or calcifications strongly support a diagnosis of asbestos exposure. No specific therapies Pleurectomy in severe cases

Rounded Atelectasis :

Rounded Atelectasis Caused by scarring of the visceral and parietal pleura and the adjacent lung, with the pleural reaction folding over on itself. The pleural surfaces then fuse to one another, trapping the underlying lung and leading to atelectasis . As a result of this alteration, a mass lesion that mimics lung cancer can be seen on the PA chest radiograph This lesion is most easily appreciated to be a pseudotumor with use of CT scanning. HRCT can noninvasively demonstrate continuity to areas of diffuse pleural thickening, evidence of volume loss in the adjacent lung, or a characteristic comet tail of vessels and bronchi sweeping into wedge-shaped mass . HRCT scans localized most cases of rounded atelectasis to the lower, posterior portion of the lung (right).

PowerPoint Presentation:

The chest radiograph shows left-sided pleural effusion, bilateral pleural thickening, greater on the left than on the right, and a mass in the left midlung field. HRCT demonstrates the mass to be rounded atelectasis , with bronchovascular structures entering the trapped lung. It also reveals the pleural effusion, bilateral pleural thickening .

Acute Benign Pleural Effusions:

Acute Benign Pleural Effusions 20 - 40 years Latency period for these effusions-shorter(12-15y after exposure) Small to moderate in size Asymptomatic- 50% cases Symptomatic cases-the manifestations may be those of a pleurisy (chest pain, chest tightness, dyspnea , cough, and fever) The effusions are exudative and often bloody; glucose concentrations are normal.Mesothelial cells are found in 50% of patients. In about 25% of patients, the fluid is eosinophilic . The collections may persist for 6 months or more. They frequently clear spontaneously, only to recur on the C/L side. Tharacocentesis & pleural biopsy –essential Diagnosis of a benign pleural effusion cannot be fully established until a tumor -free interval of 3 years has elapsed- long F/U necessary.

Asbestosis (Pulmonary Parenchymal Fibrosis):

Asbestosis (Pulmonary Parenchymal Fibrosis) Pathology and Pathogenesis- Prominent in the lower lobes and in the subpleural areas The lungs are small, streaks of fibrosis outline lobar and interlobar septa, and the visceral pleura is invariably thickened in advanced stage Honeycombing - prominent subpleurally & in the lower lobes Distinguishable from advanced fibrosis d/t any other cause - by the presence of asbestos bodies or uncoated asbestos fibers Mild asbestosis - scattered and usually consist of foci of peribronchiolar fibrosis with local chronic interstitial inflammation, accumulation of macrophages in the air spaces, and proliferation of type II pneumocytes . Second- and third-order bronchioles and alveolar ducts - involved as the disease progresses and the fibrosis spreads to involve the alveolar interstitium

PowerPoint Presentation:

Lung tissue from a 64-year-old asbestos insulator illustrates peribronchiolar fibrosis, interstitial chronic inflammation,accumulation of macrophages in the airspaces, and proliferation of type II pneumocyte .

PowerPoint Presentation:

Lung slice showing lower zone fibrosis of asbestosis. Two areas of relatively normal lung, to left and right, are separated by coarse irregular fibrosis.

PowerPoint Presentation:

Low-power view of early asbestosis showing peribronchiolar fibrosis

Cont… :

Cont… Alveolitis - resolve if the fiber burden is low and the fibers are cleared Nonprogressive distal airway lesion, mineral dust-induced peripheral airway disease- fiber load is low but retained Dust load retained - high and phagocytosis of fibers by alveolar & interstitial macrophages– incomplete fibronectin & free oxygen rad realesed recruit fibroblast collagen dep chronic interstitial lung fibrosis.


CLINICAL FEATURES Earliest, most consistently reported, and most distressing symptom is dyspnea . Persistent dry cough reported commonly, almost as frequently as dyspnea Chest tightness or pain, or both- not uncommon (pleural reaction) Basal crackles, an early and distinctive feature of asbestosis- often heard first over axillary and basal regions and then more generally as the disease advances Coarse crackles and rhonchi -may occur Clubbing of fingers & the toes Respiratory & circulatory failure and cancer-late manifeatation ( causes of death)

Radiographic Features :

Radiographic Features The ILO classification uses the term “small irregular opacities” to describe the irregular linear shadows that develop in the lung parenchyma and obscure the normal bronchovascular str. The parenchymal opacities - seen first in the lower lateral zones. Borders of the heart – obscured(advance stage) Early fibrotic changes - better visualized by HRCT for subpleural parenchymal changes Visceral pleural thickening of the interlobar fissures Presence of pleural plaques ( if b/l ) or of pleural thickening - additional evidence Hilar node enlargement - not a feature of asbestosis

Cont… :

Cont… Irregular rounded opacities found on PAchest radiographs -expressed them on a 12-point scale(according to size) Category 0 - defined as a (N) radiograph and category 1 as mild asbestosis Typically, a profusion of irregular opacities at the level of 1/0 is taken as the break point between normal and abnormal. Moderate asbestosis and advanced asbestosis - defined as category 2 and 3 chest radiographs, respectively. Five HRCT features of asbestosis have been identified: (1) curvilinear subpleural lines, (2) increased intralobular septa, (3) dependent opacities, (4) parenchymal bands and interlobular core structures, (5) honeycombing

PowerPoint Presentation:

HRCT scan with irregular opacities of the lung parenchyma and interlobar structure .


LUNG FUNCTION Restrictive lung function-established asbestos FVC and the D l CO – reduced Mixed or obstructive function profile-in a subset of patients FVC measurement-to assess evolution of ds


DIAGNOSIS Most published criteria consider HP as the best means of establishing the diagnosis In its absence, the following criteria proposed: (1) a reliable history of asbestos exposure; (2) an appropriate lag time between exposure and detection; (3) evidence of lung fibrosis on the chest radiograph or HRCT scan; (4) a restrictive pattern of lung function; (5) bilateral fixed inspiratory crackles; and (6) clubbing of the fingers or toes, or both Sputum analysis - useful for identifying asbestos bodies as an indication of lung dust burden but is far less sensitive than BAL The fewer the features, the less certain the diagnosis; the more trivial the exposure, the less likely that it is causal.

Cont… :

Cont… Biopsy material may be helpful in identifying the nature of the disease. Asbestos fibers exist in the lung in two forms: uncoated or bare fibers - visible only on electron microscopy, and coated fibers ( also called asbestos bodies )- visible by light microscopy Uncoated fibers –more common Presence of asbestos bodies or asbestos fibers - hallmark of exposure, past or current. Although asbestos bodies probably reflect exposure, their absence by no means excludes it Asbestos bodies can also be detected in BAL samples One asbestos body per ml of BAL fluid correlates with 1000 to 3000 asbestos bodies per gram of dry lung tissue .

PowerPoint Presentation:

Light microscopic appearance of an asbestos body in a cytocentrifuged preparation of alveolar macrophage lavaged from a nonsmoking asbestos insulator .

Complication & Treatment :

Complication & Treatment Lung cancer ( amphibole- crocidolite , amosite or tremolite , or mixed amphibole- chrysotile than only to chrysotile & with longer fibre) Mesothelioma Tuberculosis & rheumatoid pneumoconiosis -uncommon complications At present, there is no established treatment for this disorder. Because of the risk of lung cancer and mesothelioma , medical surveillance is recommended . Current permissible exposure limit-0.1 fibre/ml


SILICOSIS DEFINITION Silicosis is an occupational lung disease attributable to the inhalation of silicon dioxide, commonly known as silica, in crystalline forms, usually as quartz, but also as other important crystalline forms of silica(i.e., cristobalite and tridymite )(fibrotic ds of lung caused by inhalati on,retention,reaction to silica). Silica content in different rock formations, such as sandstone, granite, and slate, varies from 20% to100% Type of silica exposure-more in drilling or sandblasting, mining, quarrying, tunneling , abrasive blasting, construction

PowerPoint Presentation:

A typical roadside stonecrushing operation in India

Diseases associated :

Diseases associated SILICOSIS -- Chronic silicosis Accelerated silicosis Acute silicosis ( silicoproteinosis ) Progressive massive fibrosis CHRONIC OBSTRUCTIVE LUNG DISEASE -- Emphysema Chronic bronchitis Mineral dust–induced small airways disease LUNG CANCER MYCOBACTERIAL INFECTION -- Mycobacterium tuberculosis Nontuberculous mycobacteria IMMUNE-RELATED DISEASES -- Progressive systemic sclerosis Rheumatoid arthritis Chronic renal disease Systemic lupus erythematosus

Clinicopathological Desciption:

Clinicopathological Desciption CHRONIC (CLASSIC) SILICOSIS- 1. asymptomatic or result in insidiously progressive exertional dyspnea or cough 2. latency of 15 years or more 3. small (< 10 mm) rounded opacities predominantly in the upper lung zones 4. pathological hallmark- silicotic nodule ( cell-free central area of concentrically arranged, whorled hyalinized collagen fibers , surrounded by cellular connective tissue with reticulin fibers ) 5. polarized light, birefringent particles are typically seen most prominently in the periphery of the silicotic nodule 6. Silicotic nodules in the visceral pleura, regional lymph nodes 7. One or more groups of the small lung nodules of chronic silicosis may coalesce and result in larger shadows on the chest radiograph (> than 10mm) , heralding the onset of complicated or conglomerate silicosis (often referred to as progressive massive fibrosis) 8. occur even after exposure to silica-containing dust has ceased.

PowerPoint Presentation:

Low-power view of silicotic nodules showing onion-skin appearance & aggregation .

Cont… :

Cont… PROGRESSIVE MASSIVE FIBROSIS- 1. nodular opacities > 1 cm on the chest X-ray 2. diminished carbon monoxide diffusing capacity, reduced arterial oxygen tension at rest or with exercise, and a demonstrable restrictive pattern on spirometry and lung volume. 3. exertional dyspnea & productive cough 4. recurrent bacterial infection may occur 5. weight loss and cavitation of the large opacities - concern for TB or other mycobacterial infection. 6. pneumothorax - life-threatening complication 7. hypoxemic respiratory failure with cor pulmonale and congestive heart failure -common terminal findings

PowerPoint Presentation:

Complicated silicosis demonstrating progressive massive fibrosis.

PowerPoint Presentation:

Chest film of hardrock miner showing eggshell calcification of hilar nodes and progressive massive fibrosis in right upper zone .

PowerPoint Presentation:

Silicotic lung showing grey fibrotic nodules that have coalesced in the upper and middle lobes to form massive fibrosis

Cont… :

Cont… ACCELERATED SILICOSIS- 1. shorter (5 to 10 years) duration than chronic form, while symptoms, radiographic findings, physiological measurements, and lung pathology are similar. 2. deterioration of lung function more rapid 3. develop superimposed mycobacterial infection 4. autoimmune diseases, including scleroderma, rheumatoid arthritis, or SLE, seen in association with silicosis, more often in the accelerated type.

PowerPoint Presentation:

Chest film of patient with accelerated silicosis showing irregular upper lobe fibrosis and lower zone emphysema .

Cont… :

Cont… ACUTE SILICOSIS- 1. within a few months up to about 5 years after a massive inhalation of silica 2. dramatic dyspnea , weakness, and weight loss - often presenting symptoms. 3. diffuse alveolar filling pattern, with a lower lung zone predominance-chest X-ray finding 4. histological findings similar to PAP 5. air bronchogram may be seen 6. renal and hepatic abnormalities-seen 7. severe hypoxemic ventilatory failure and death-rapid

PowerPoint Presentation:

Chest film of stonemason with 6 years of exposure to 1mg/m3 respirable quartz following 30 years of exposure to low concentrations showing diffuse finely nodular bilateral shadowing of acute silicosis shortly before his death


CLINICAL FEATURE The symptoms and signs of chronic silicosis may be minimal. The main symptom is breathlessness. Abnormal chest radiograph-only presentation Cough and sputum production common – (related to chronic bronchitis but may reflect the development of TB or lung cancer) Chest pain,fever,clubbing -not seen

Radiographic Patterns in Silicosis:

Radiographic Patterns in Silicosis Earliest radiographic signs of uncomplicated silicosis - small, rounded opacities(“q” and “r” type) Other patterns- linear or irregular shadows. Silicotic nodules - symmetrically distributed and tend to occur first in the upper zones Occasionally calcified- resembling microlithiasis Enlargement of the hilar nodes may precede the development of the parenchymal lesions Eggshell calcification- strongly suggestive, but not pathognomonic of silicosis Pleural abnormalities - not common CT scanning often documents localized pleural thickening, particularly in association with conglomerate lesions

Cont… :

Cont… PMF is characterized by the coalescence of small rounded opacities to form larger lesions; they are graded on the ILO scale according to size and extent (categories A-C) With time, the mass lesions contract, usually to the upper lobes, leaving hypertranslucent zones at their margins and often at the lung bases. Rapid development of several large lesions suggests rheumatoid silicosis New lesions, especially if cavitated -think of mycobacterial disease Radiographic distinction between PMF lesions and lung malignancies may be difficult- FDG-PET helpful Acute silicosis - characterized radiologically by diffuse changes that usually display an air space and interstitial pattern rather than the usual nodularity


LUNG FUNCTION Determined by the extent of silicosis as well as associated or concomitant airway and vascular changes Chronic silicosis- spirometric tests ( [FEV 1 ], FEV 1 /FVC ) usually reflect airflow limitation. Reduction in D l CO - generally apparent in more advanced cases Acute silicosis- restrictive defect and impairment of gas exchange, which leads to respiratory failure and death from intractable hypoxemia.

Diagnosis and Complications:

Diagnosis and Complications On basis of H/O exposure and the characteristic radiographic changes Detection of silica in BAL material may suggest the diagnosis. Lung biopsy - necessary to distinguish PMF or other atypical features from lung cancer, tuberculosis, and other diagnoses. Biopsy material should be submitted for microanalysis for dust, including silica.

Cont… :

Cont… Less common complications - cor pulmonale , spontaneous pneumothorax , and tracheobronchial obstruction from enlarged calcified hilar nodes The presence of cough, hemoptysis , weight loss, fever, or any new radiologic feature should be pursued with culture of sputum or BAL fluid or with culture and histologic examination of tissue for TB


MANAGEMENT & CONTROL Change in occupation to an environment free of silica-containing dust Lung lavage to remove silica from the lung T/t of all forms of silicosis should be directed toward control of mycobacterial disease. All subjects with silicosis should have a tuberculin skin test or an interferon-γ (IFN-γ) release assay smoking-cessation acute and accelerated silicosis - lung transplantation The most important aspect of the management of silicosis - prevention


COAL WORKERS PNEUMOCONIOSIS Definition and Occupations at Risk- Coal workers pneumoconiosis (CWP) is a distinct pathologic entity resulting from the deposition of coal dust in the lungs. The tissue reactions to deposits of dust include the coal macule and the coal nodule ( simple CWP ) and PMF ( complicated CWP )

Cont… :

Cont… The main occupation at risk for CWP - coal mining Coal mine dust contains a variable amount of quartz Coal miners also develop silicotic nodules Other occupations at risk - coal trimming , the mining and milling of graphite in carbon plants, the manufacture of carbon electrodes, and the manufacture and use of carbon black. Coal mining( even in the absence of CWP) - associated with chronic bronchitis, chronic airflow limitation, and emphysema.

PowerPoint Presentation:

Roof bolting in underground coal mine. A potentially high-risk operation for respiratory exposures to airborne silica .

Pathology :

Pathology The primary lesion - coal macule , ( not palpated) 1. macroscopic exam - small (≤4 mm) pigmented lesion, distributed initially in the upper lobes, although the lower lobes may subsequently become involved 2. microscopic exam- dust and dust-laden macrophages in the wall of a distal airway with reticulin and a few collagen fibers Focal emphysema, a form of centriacinar emphysema, occurs within and around the coal macule , and together they form the characteristic lesion of CWP

PowerPoint Presentation:

A coal macule , microscopic section .

Cont… :

Cont… Coal nodule (palpable lesion)- dust and dust-laden macrophages and dense, irregular depositions of collagen. 1. result from exposure to coal dust admixed with silica 2. silicotic nodule-dust contains > 18% quartz Other features - subpleural dust deposits, enlargement of hilar and mediastinal nodes, and on occasion, tattooing of the parietal pleural lymphatic channels by coal dust.

Cont… :

Cont… PMF (complicated CWP) is defined as a fibrotic pneumoconiotic lesion 1 cm or greater in diameter (typically bilateral) 1. bulky, often irregular, well-defined, heavily pigmented rubbery black tissue masses 2.usually occur in a background of severe simple CWP. 3. posterior segment of the upper lobes or apical segments of the lower lobes Diffuse interstitial fibrosis has also been reported in coal miners.

PowerPoint Presentation:

Section of coal-miner’s lung showing progressive massive fibrosis, diffuse centriacinar emphysema and relatively sparse coal macules

Cont… :

Cont… Rheumatoid pneumoconiosis- 1.One variant of which is called Caplan's syndrome 2.Form of CWP associated with rheumatoid arthritis . 3.Nodules are larger than coal nodules (≤5 cm in diameter) and have smoother borders. 4.Pigmentation is arranged in concentric laminations, and relative to PMF lesions, they contain little dust. 5.These lesions may cavitate or calcify. 6. Active areas in the nodules - dust-laden macrophages, lymphocytes, polymorphonuclear leukocytes, and plasma cells. 7.Vasculitis is seen in vessels within and surrounding these lesions 8. Active arthritis or circulating rheumatoid factor commonly associated

Pathogenesis :

Pathogenesis CWP increases with the intensity & duration of exposure to coal dust (Anthracite - highest , lignite - lowest ) Lung burden of dust increases alveolar macrophages activated reactive oxygen species released release of cytokines, including interleukins and TNF inflammation & fibrogenesis Exact pathogenic mechanisms of PMF –unknown Total dust burden - most important factor

Role of silica :

Role of silica Silica does not play a primary role in the causation of CWP but coal miners, especially those mining anthracite, may develop the lesions of silicosis. Combined exposure to silica and coal dust may produce less silicosis than would a similar pure exposure to silica.

Other association :

Other association Airflow obstruction and chronic bronchitis commonly seen d/t-mucus hypersecretion & bronchial hyperresponsiveness . Tuberculosis and cancer- 1.Mycobacterial infection,not more common in association with CWP in the absence of silicosis. 2.Most evidence suggests that the occupation of coal mining is not associated with lung cancer. An increased risk of stomach cancer although seen.


CLINICAL FEATURES Simple CWP - disease state without symptoms or physical signs. The diagnosis is based on the radiologic features. The symptoms of cough and sputum reported by most coal miners - consequence of dust-induced chronic bronchitis. Breathlessness on effort - caused by associated chronic airflow limitation / by the development of PMF. Respiratory impairment and disability develop as PMF progresses

Cont… :

Cont… Lesions of PMF that impinge on airways may cause abnormal breath sounds. Large or bilateral PMF lesions may be associated with hypoxemia and right heart failure. The presence of new lung lesions with rheumatoid arthritis, subcutaneous rheumatoid nodules, or positive rheumatoid factor raises the possibility of rheumatoid pneumoconiosis. The lung lesions may or may not develop concomitantly with joint disease

Chest Radiography :

Chest Radiography The hallmark of simple CWP on the chest radiograph - presence of small rounded opacities in the lung parenchyma. Coal macules - usually associated with small (<1.5 mm) p nodules(large amt of coal dust) on the chest radiograph. Radiograph may show no nodularity with mild to moderate grades of CWP. When the larger q and r nodules are visible radiologically - presence of coal nodules CT useful when chest X-ray insensitive Small rounded opacities - seen first in the upper zones All lung zones are unlikely to be involved unless profusion category 3 is present Small rounded opacities probably never regress but the presence of emphysema appears to reduce the reading of profusion on the chest radiograph. Some enlargement of hilar nodes is usual

PowerPoint Presentation:

Simple coal-workers’ pneumoconiosis: (a) type p, pinpoint opacities; (b) type q, micronodular opacities; (c) type r, nodular opacities typically associated with quartz exposure

Cont… :

Cont… ILO system-simple pneumoconiosis is divided into major categories 1, 2, and 3 according to the profusion of small opacities in the lung fields. Each major category, including 0, is subdivided into 3 subcategories, providing a full range of 12 categories of simple CWP. A reading of category 1/0 indicates the definite presence of opacities consistent with pneumoconiosis Complicated pneumoconiosis (PMF) is divided into categories A, B, and C, based on the size of the large opacities.

Cont… :

Cont… PMF - diagnosed radiologically when the parenchymal opacities > 1 cm in diameter 1/3 cases diagnosed as PMF on the radiograph at autopsy- represent other lesions including tumors , rheumatoid nodules, or tuberculosis scars PMF lesions - more common in the upper lobes, posterior Advance cases- the lesions nearly always B/L They may take bizarre shapes, cavitate , or calcify. As the lesions shrink toward the hilum or to the apex, bullous lesions may be seen in the surrounding lung

PowerPoint Presentation:

Coal-workers’ pneumoconiosis: extensive (category 3) simple pneumoconiosis with early massive fibrosis (stage A) in right upper zone

Cont… :

Cont… Rheumatoid pneumoconiosis - similar to those of PMF but usually multiple & peripherally located. The lesions( 0.5 to 5.0 cm)- may appear within weeks Lesions generally appear in the presence of lesser degrees of nodule profusion In some cases, the lesions disappear, often completely, but may be followed at a later date by a fresh crop of lesions Cavitate & calcify

PowerPoint Presentation:

Multiple rounded lesions of Caplan’s syndrome in coal-miner with rheumatoid disease .


LUNG FUCTION Controversy regarding the association between simple CWP and abnormal lung function has persisted because coal dust has been shown to cause both obstructive lung disease & pneumoconiosis Complicated CWP – 1. reduction in FVC and FEV 1 2. increased TLC and RV 3. decreased D l CO Pulmonary hypertension – advance PMF

Diagnosis & Management :

Diagnosis & Management A history of occupational exposure to coal and a chest radiograph are the fundamental elements in the diagnosis of CWP.( CT when chest X-ray insensitive) Treatment of latent tuberculosis infection should be considered for coal workers who are thought to have had significant silica dust exposure or who have evidence of silicosis Younger subjects with radiologic disease of profusion category 1 or greater -advised to change their occupation Smoking-cessation counseling Management of chronic bronchitis and emphysema


BYSSINOSIS In 1831, Kay described chest tightness and fever that commonly occurred on Monday after workers had been off work over the weekend. It was because of this observation that the term Monday morning fever was coined Certain jobs in the textile mill are associated with a higher risk for development of bronchitis. Ginning, opening, or carding work carry a higher degree of risk. Strippers and grinders,who maintain the carding machinery that cleans and aligns the cotton, are particularly at risk for development of symptoms. Indeed, in the past, byssinosis was called “strippers’ asthma .”

Clinical Features & Risk Factors:

Clinical Features & Risk Factors Shortness of breath often occurs on the day back to work at the textile mill after several days off, as on a Monday after being off over the weekend. Workers with a higher grade of symptoms tend to have a more rapid decline in pulmonary function. Risk factors include (1) length of employment in a cotton mill and (2) level of dust exposure. Tobacco smoking has been shown to be synergistic with exposure to cotton dust in producing chronic bronchitis.

Grading of Byssinosis(Schilling):

Grading of Byssinosis (Schilling ) Grade 0 - No symptoms on first day of work Grade ½ - Occasional chest tightness or irritation of respiratory tract on the first workday of week Grade 1 - Chest tightness on every first day of workweek Grade 2- Chest tightness on first and other days of workweek Grade 3- Chest tightness on first and other days of workweek and physiological evidence of permanent disability

PFT-Abnormality :

PFT-Abnormality Characteristically, byssinosis is associated with a reduction in the forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) on the day of return to work after an absence. The degree of reduction in these parameters increases over the workday. This change is generally more severe on the 1st day of work after an absence than on subsequent days.

Pathology & Pathogenesis :

Pathology & Pathogenesis The histopathology of byssinosis is similar to that of the bronchitis that is induced by tobacco smoke—with hyperplasia of mucous glands and infiltration of the bronchi with polymorphonuclear neutrophils . Cotton dust also stimulate mast cells and macrophages, to release molecules that attract neutrophils . New evidence points to a lipopolysaccharide ( endotoxin ) produced by bacterial contaminants of cotton as the causative agent of byssinosis . Byssinosis have elevated serum histamine levels.

Evidence of Endotoxin :

Evidence of Endotoxin 1. Measurable levels of endotoxin can be detected in cotton dust. 2. Inhaled endotoxin can cause airway inflammation in animals and humans. 3. In a controlled setting, ambient levels of endotoxin correlate with degree of airflow reduction occurring in a simulated carding room. 4. Repeated inhalation of endotoxin results in an attenuation of the airway response similar to that noted in patients with byssinosis . 5. Measures that reduce levels of ambient endotoxin reduce the incidence of byssinosis .

Treatment and Prevention:

Treatment and Prevention The most important treatment - removal of the individual from the offending work environment. Screening pulmonary function testing at the workplace is important to identify susceptible individuals who exhibit airflow abnormalities. Measures have been taken in developed countries to control cotton dust levels in textile mills( eg . steam-clean cotton while it is still in the bale)


OCCUPATIONAL ASTHMA Definition- Occupational asthma is characterized by variable airway obstruction resulting from exposure to ambient dusts, vapors , gases, or fumes incidentally present at a workplace. Bronchial hyperresponsiveness to nonspecific agents, such as methacholine or histamine- present in these patients. Here, asthma may be caused de novo by the offending agent, as in the case of isocyanate -induced asthma, or underlying asthma may be exacerbated by the offending agent.

ACCP Definition :

ACCP Definition A. Physician diagnosis of asthma B. Onset of asthma after entering workplace C. Association between symptoms of asthma and work D. One of the following: 1. Workplace exposure to agent known to cause occupational asthma 2. Work-related changes in FEV1 or PEF 3. Work-related changes in bronchial responsiveness 4. Positive response to specific inhalation challenge test 5. Onset of asthma with a clear association with a symptomatic exposure to an inhaled irritant agent in the workplace Definite occupational asthma requires A, B, C, and D(2) or D(3) or D(4) or D(5) Likely occupational asthma requires A, B, C, and D(1)

Cont… :

Cont… Agents that have been associated with induction of occupational asthma can be conveniently grouped into categories of high- and low-MW compounds . All of these agents tend to sensitize the individual, so that low ambient concentrations of the substance can ultimately cause significant bronchoconstriction . High MW compound- animalproduct,seafood,insects,plants,latex,gum Low MW compound- diisocyanates,anhydrides,wood dust,fixatives

Risk Factor :

Risk Factor Atopy (family/personal )-high MW compound Smoking (increased IgE )-platinum & anhydride compound 3. Genetic- MHC class II important for development of occupational asthma due to acid anhydrides, diisocyanates , western red cedar, platinum salts, latex, and animal proteins.

Clinical Presentations:

Clinical Presentations Occupational asthma presents in a similar manner as other forms of asthma Most commonly patients develop symptoms after a period of exposure to the inciting agent ( occupational asthma with latency) Less commonly they develop immediate symptoms with exposure to the agent ( occupational asthma without latency or irritant induced asthma ). In general, the former is associated with a true allergic reaction to the offending agent while the latter is generally mediated nonimmunologically .

Occupational Asthma with Latency:

Occupational Asthma with Latency High- and low-MW molecules-responsible Individuals exposed to the agent for weeks to months before developing symptoms. With the appearance of symptoms, nonspecific airway hyperreactivity , determined by methacholine or histamine challenge, is present. Also with appearance of symptoms, the individual develops hypersensitivity to low ambient concentrations of the offending agent. Exposure to very low concentrations of the material in the workplace precipitates severe bronchoconstriction in these patients.

Irritant-Induced Asthma:

Irritant-Induced Asthma Less common. Symptoms develop within hours of exposure. Pathological changes are generally similar to those occurring in the syndrome of occupational asthma with latency, although epithelial changes such as desquamation and subepithelial fibrosis may be more prominent. Agents that commonly cause this syndrome are irritant gases or fumes such as chlorine or ammonia. In addition, certain agents such as acid anhydrides and isocyanates can cause occupational asthma with and without latency

Mechanisms and Pathology:

Mechanisms and Pathology High-Molecular-Weight Compounds induce asthma through IgE dependent classic immediate hypersensitivity reactions. skin tests using extracts of the substance show positive results. atopic individuals more at risk latent period for developing the reaction – long 5. pathologically- bronchial infiltration of lymphocytes and eosinophils , indistinguishable from other forms of allergic asthma

Cont… :

Cont… Low-Molecular-Weight Compound 1. Cause IgE -dependent bronchoconstriction . 2. In contrast to higher-MW agents, specific IgE or IgG antibodies produced in these individuals are directed at the low-MW compound coupled to a protein within the serum. 3.There is also some evidence that low-MW compounds induce asthma through IgE -independent mechanisms, possibly by affectingT lymphocytes directly, as shown for cobalt and nickel salts as well as isocyanates . 4. The bronchial pathology is similar whether or not the response is an IgE -dependent reaction.


DIAGNOSIS 1. HISTORY - the current and previous occupational history documentation of specific jobs of the individual at the specific workplace as well as potential exposures during performance of those jobs. clinical history that suggests occupation-related asthma includes symptoms that occur at work and improve when the patient is away from work for a period of time, as during vacations. The duration of symptoms prior to removal from the offending environment is important for predicting prognosis. history of tobacco use important. A past history or family history of asthma may suggest that the patient’s symptoms are not occupation-related

Cont… :

Cont… 2. Physical Examination- Signs of atopy should be assessed Pulmonary examination may be entirely normal when the patient is seen outside of the workplace. However, wheezing, either during quiet respiration or on a forced maneuver , suggests airflow obstruction. Signs of dermatitis may support the diagnosis

Cont… :

Cont… 3. SKIN & IMMUNOLOGIC TESTING- routine skin testing, using a panel of allergens, for wheal-and-flare reactions can be useful extracts from flour, animal by products, coffee, and other sources have been used for skin testing in various studies. specific IgE antibodies to extracts-detected by RAST & ELISA positive results in all of these tests do not necessarily indicate that disease is due to the specific agent; they simply suggest sensitization

Cont…. :

Cont… . 4. Pulmonary Function Tests- (N) pulmonary function tests when away from the inciting agent. Peak-flow measurements -at least four times per day: on awakening, at the beginning &end of work, and before bed. Timed measurements should also be performed on days that the subject is off work. Measurements should be performed each day over at least 4 weeks Supplemental portable spirometer - measure FVC and FEV1 at hourly intervals during work .

Cont… :

Cont… 5. Bronchial Provocation Tests- Bronchial hyperreactivity to methacholine and histamine. An arbitrary cutoff of a provocative concentration producing a 20% decline in FEV1 Challenge also be used to choose the concentration of specific allergen that should be employed in a specific bronchial provocation test Exposure levels should start low and gradually increase The two most common patterns are an immediate reaction, occurring within a few minutes of challenge and peaking at 10 to 15 min after challenge, and a late reaction, occurring several hours after challenge and peaking at 5 to 8 h.

Management :

Management Once determined that an individual has developed asthma due to exposure in the workplace, he or she should be removed from the offending environment. Use of a protective mask to prevent airway exposure to the offending agent. Pulmonary function tests - done frequently to rule out progressive physiological impairment. Appropriate compensation for disability


BERYLLIUM LUNG DISEASE Individuals potentially exposed in the following industries: aerospace, electronics, ceramics, metal, including refining of scrap metal, nuclear (reactors, weapons), telecommunications, tool and die, and welding. Acute beryllium disease - attributed to toxic, dose-related lung injury characterized by acute inflammatory reactions in the upper airways, bronchiolitis , pulmonary edema , and chemical pneumonitis (recovery common,17% to CBD) CBD is a multisystem disorder characterized by noncaseating granulomas that occur throughout the body, although their primary manifestation is in the lung.

Pathology & Pathogenesis:

Pathology & Pathogenesis Beryllium enters the body by inhalation and, occasionally, via the skin acts as a specific antigen proliferation of specific CD4 lymphocytes release of lymphokines granuloma formation Evidence for delayed hypersensitivity to beryllium - assessed by the in vitro BeLPT on lymphocytes from blood or BAL CBD -characterized by the presence of a lymphocytic (helper/inducer T cells) alveolitis & noncaseating epithelioid granulomas indistinguishable from sarcoidosis Granulomatous lesions may be found - thoracic and abdominal LN, spleen, liver, kidneys, and adrenal glands Beryllium is now considered to be a human carcinogen

PowerPoint Presentation:

Sarcoid -like granuloma in the lung of patient with berylliosis

Sarcoidosis vs CBD :

Sarcoidosis vs CBD MANIFESTATION SARCOIDOSIS CBD Erythema Nodosum 10-20% Absent Hilar Adenopathy 50-75% <50% Hypercalcemia Occasional Rare Bone Changes In chronic ds Absent Parotid Involvement Occasional Absent Posterior Uveitis Occasional Absent Hepatic Involvement Common Frequent Splenomegaly Rare Rare CNS Involvement Occasional Absent Response to steroid Only active ds Only active ds

Clinical Features :

Clinical Features Acute beryllium disease - cough, chest pain, blood-tinged sputum, crackles, and patchy airspace disease on the chest radiograph. High exposure to beryllium- irritation and inflammation of the upper respiratory tract and conjunctivitis ( resolution within a year,death -10%). CBD - similar pulmonary sarcoidosis , hilar and mediastinal lymphadenopathy and splenomegaly not commonly observed. Symptoms - dyspnea , cough, chest pain, weight loss, fatigue, and arthralgias . Physical signs may include crackles, but signs of lung disease are often absent.

D/D of CBD :

D/D of CBD Sarcoidosis Hypersensitivity pneumonitis Tuberculosis Histoplasmosis Silicosis Talc granulomatosis Eosinophilic granuloma Idiopathic pulmonary fibrosis

Cont… :

Cont… Radiographic changes - ill-defined nodular or irregular opacities; hilar adenopathy is seen in approximately 40% of cases but is usually mild. In the later stages of the disease, patchy fibrosis occurs with adjacent hyperinflation or distortion and extensive honeycombing. CBD-pulmonary function shows a restrictive defect in advanced disease, but features including obstruction in mild to moderate cases The clinical course of CBD - variable.

PowerPoint Presentation:

Chest radiograph demonstrating nodular interstitial disease with adenopathy . . Chest CT mediastinal window demonstrating calcified bilateral hilar and mediastinal lymph nodes. C . Chest CT lung window demonstrating a diffuse, fine-nodular pattern of interstitial lung disease - most prominent in the mid and upper lung zones .

Diagnosis and Management :

Diagnosis and Management The diagnosis of CBD - based on documented exposure to beryllium, evidence of lung disease compatible with the diagnosis, and a positive BeLPT performed on blood or BAL fluid. Three categories of beryllium-associated disorders : beryllium sensitization ( positive blood or BAL BeLPT but negative biopsy ), subclinical beryllium disease (positive BeLPT and biopsy but no clinical or radiologic features of the disease), and chronic berylliosis (positive BeLPT and biopsy with clinical and radiologic features of disease). Most important step - complete cessation of further exposure to beryllium Corticosteroid therapy has been recommended in CBD, and long-term steroid therapy is believed to alter the course of the disease favorably .

Others… :

Others… Metal fume fever is a condition characterized by a metallic taste followed by rigors, high fever, muscle aches and headache following a few hours after acute exposure to metal fumes, particularly Zn,Cu and Mg and settles spontaneously, without sequelae,in 24 h (occurs in welding, smelting and galvanizing) Humidifier fever (Monday morning feeling)- in people working or living in buildings with humidifiers and air conditioners; episodes of malaise, fever and sometimes breathlessness, often associated with non-specific aches, occurring predominantly on the 1st day of the working week(chest X-ray often normal)

Cont… :

Cont… Pneumoconiosis can also occur with Al,Antimony,Barium,Carbon,PVC,Tin,Cobalt,Talc,Kaolin,Iron A number of toxic gas and fumes like vinayl cyanide,CO2,CO,HCN,H2S,N2,Methane,NH3,Cadmium,chlorine,Formaldehyde,N2O,Phosgene etc can cause lung disorder in workplaces .

PowerPoint Presentation:


Introduction :

Introduction Hypersensitivity pneumonitis (HP), also known as EAA, is defined as granulomatous , interstitial, bronchiolar, and alveolar-filling lung diseases resulting from repeated inhalation of and sensitization to a wide variety of organic aerosols and low-molecular-weight chemical antigens. Characterized by a lymphocytic alveolitis and granulomatous pneumonitis on pathologic examination. HP - treatable and preventable if exposure is recognized and antigen abatement done .

Etiology :

Etiology MICROBIAL AGENTS- 1. Bacteria- Thermophilics actinomyce (FLD, Bagassosis , Mushroom worker lung, Humidifier lung) , Bacillus subtilis ( conta wood dust ), Klebsiella (humidifiers), Epicoccum nigrum (moisture from base ment shower),NTM(metalworking fluid aerosol,indoor swimming pool &hot tub- Lifeguard lung). 2. Fungi- Aspergillus , Penicillium , Cladosporium , Trichosporon , Alternaria,Aureobasidium,Cephalosporium species ( spores, mycelial fragments, metabolites and partially degraded substrates, and toxins).

Cont… :

Cont… Animal Proteins- Bird proteins(bird fancier lung) from feathers , droppings, and serum of turkeys, chickens, geese, ducks, parakeets, parrots, budgerigars, pigeons, doves, love birds( IgA and IgG , are secreted from and coat birds’ feathers, creating a fine dust called bloom), rat urine, wheat weevil ( Sitophilus granarius - miller's lung), mollusk shell ( buttons ), silkworm larvae . CHEMICAL SENSITIZERS- Isocyanates , acid anhydrides, pyrethrum.

Epidemiology :

Epidemiology The worldwide prevalence of HP is unknown Environmental risk factors—including antigen concentration, exposure duration, frequency and intermittency, particle size, antigen solubility, use of respiratory protection, and variability in work practices—influence disease prevalence, latency, and severity. M ost common forms of HP show both seasonal and geographic variation- FLD is most common in late winter , and in regions with heavy rainfall and harsh winter conditions & pigeon breeder's disease in late summer.

Host factors :

Host factors Susceptibility or protection from HP may be explained in part by genetic polymorphisms. Polymorphisms in the MHC and (TNF-α) -associated with the development of HP. Overexpression of GATA-3-(regulator of Th2 differentiation)-decrease disease ( correcting the Th1 immune response). Variants in the tissue inhibitor of MMP-3 - protective against bird fancier's lung. HP - more in nonsmokers than in smokers(nicotine decrease T-dependant and T-independent response to inhaled antigens).Smokers have more recurrances & poor prognosis. HP can occur in infants & children (Avian proteins- M.C,subacute or chronic form with lymphocyte predominance )



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