1. OCCUPATIONAL LUNG DISEASES
Dr. M. SOFI
MD; FRCP (London); FRCPEdin; FRCSEdin

2. Occupational lung diseases: are a broad group of pulmonary disorders that develop from inhalation of specific particles.
Although each disease has a slightly unique presentation, they all lead to progressive deterioration in lung function that can cause severe respiratory compromise if appropriate measures are not undertaken.
Asbestosis an occupational lung disease caused by inhalation of asbestos fibers, and shows extensive pleural plaques and diffuse interstitial fibrotic disease of the lungs.

3. OCCUPATIONAL LUNG DISEASES
HYPERSENSITIVTY
PNEUMONITIS
PNEUMOCONIOSIS
Farmers lung
Asbestosis
Bagassosis
Berylliosis
Humidifier/Air-conditioner lung
Silicosis
Bird breeder’s lung
Coal worker’s lung
Cheese worker’s lung
Byssinosis
Malt worker’s lung
Baritosis
Paprika splitter's lung
Chalicosis
Mollusk shell hypersensitivity
Chemical worker’s lung
Wheat Weevil

4. DISEASE SOURCE OF EXPOSURE MAJOR ANTIGEN Farmer’s lung Moldy hey
Saccharopolyspora rectivirgula
Bagassosis
Moldy sugar cane fiber
Thermoactinomyces sacchari
Grain handler’s lung
Moldy grain
S rectivirgula, T vulgaris
Humidifier/Air-conditioner lung
Contaminated forced-air system, heated water reservoir
Bird breeder’s lung
Pigeons, Parakeets, fowl, rodents
Avian or animal protein
Cheese worker’s lung
Cheese mold
Penicillium casei
Malt worker’s lung
Moldy malt
Aspergillus clavatus
Paprika splitter's lung
Paprika dust
Mucor stolonifer
Wheat weevil
Infested wheat
Sitophilus granarius
Mollusk shell hypersensitivity
Shell dust
Sea nail shell

5. Pathophysiology
The pathophysiology of HP is based on IgG antibodies to inhaled antigens induces a cell-mediated immune response that causes extensive inflammation and fibrosis.
The 3 forms of hypersensitivity (HP) pneumonitis include:
acute, subacute, and chronic.
Acute: Non-caseating peribronchial granulomas
Sub-acute: Bronchiolitis, interstitial fibrosis, and possibly organizing pneumonia.
Chronic: Progressive interstitial fibrosis and honeycombing

6. HYPERSENSITIVTY PNEUMONITIS
Diagnosis of HP:
History
Physical examination
Radiographic findings.
Symptoms include fever, chills, malaise, cough, dyspnea, and headaches
4-6 hours after heavy exposure to an inciting agent in acute HP.
Sub-acute and chronic forms are characterized by cough, progressive dyspnea, fatigue, anorexia, and weight loss.
Physical signs include fever, tachypnea, diffuse fine basilar crackles; with muscle wasting, clubbing, and RDS in severe cases.
CXR may show micronodular or reticular opacities

7. HYPERSENSITIVTY PNEUMONITIS
Inhalation challenges:
BAL
PFT Adjunctive
Lung biopsy
Treatment:
Antigen avoidance
Corticosteroids
Long-term prognosis is not affected.
Most will recover the majority of lung function, but it may take several years.
Patients with significant fibrosis have a poorer prognosis.
HRCT will show:
Acute disease : Ground-glass opacities
Subacute phase: Diffuse micronodules lesions
Chronic phase: Extensive fibrosis honeycombing and air trapping

8. Scanning electron micrograph asbestos fibers
Asbestosis
Asbestosis is a fibrotic lung disease caused by inhalation of asbestos fibers.
Asbestos fibers are long, thin fibers of silicon that come in 1 of 2 major varieties.
The curved fibers are serpentine and the straight fibers are amphiboles.
Due to their heat-resistant properties they were extensively used to insulate heating and cooling units in World War II ships and buildings
Scanning electron micrograph asbestos fibers

9. Asbestosis
Asbestosis is a risk factor bronchogenic carcinoma and malignant mesothelioma.
Mesotheliomas may have latency period up to 50 years.
Tumor growth occurs along the lower part of the chest.
Extends into the parenchyma, brachial plexus, and SVC.
Treatment combinations of chemotherapy, radiation, and surgery has limited success.
Median survival is only 11 months and the disease is almost always fatal.
The CT scan of mesothelioma with extensive pleural thickening, effusion, and lung volume reduction in the affected hemithorax.

10. Asbestosis: Treatment
Removal of any ongoing asbestos exposure.
Quit smoking.
Prompt treatment of any subsequent respiratory infections and
Immunizations against pneumococcal pneumonia and influenza.
Patients may require home oxygen therapy.
Corticosteroids and immunosuppressive drugs do not alter the course of the disease.
HRCT scan at the lower lobes shows “reticular pattern” subpleural traction bronchiolectasis and bronchiectasis, honeycombing. The calcified subpleural and diaphragmatic pleural plaques (white and black arrows) gives a definitive clue for the diagnosis of asbestosis

11. Silicosis
A fibronodular lung disease caused by inhalation of dust crystalline silica.
Crystalline silica, most commonly quartz, is found in granite, slate, sandstone, and other common building materials.
Individuals who work in mining, sandblasting, manufacturing of cement, masonry, construction, or grinding are at risk of developing disease.
Silicotic nodule composed of concentric layers of collagen. There is no central necrosis. Polarized light reveals birefringent silica crystals.
Silicotic nodule

12. Silicosis
Small silicon particles are inhaled into the distal alveoli generate silicon-based free radicals that damage cell membranes.
Alveolar macrophages ingest the particles and release inflammatory mediators.
The result is inflammation that damages cells and the extracellular matrix leading to fibrosis.
Silica particles outlive the alveolar macrophages, thus continuing the cycle of injury.
Egg shell calcification

13. Common Silicosis Symptoms:
Shortness of breath following physical exertion.
Severe cough.
Fatigue.
Loss of appetite.
Chest pains.
Fever.
Cyanosis (bluish skin)
Chest X-ray, demonstrating silicosis with progressive massive fibrosis.

14. Beryllium causes 2 pulmonary syndromes:
Berylliosis
Beryllium causes 2 pulmonary syndromes:
Acute chemical pneumonitis
Chronic granulomatous lung disease.
It is often confused with sarcoidosis as they have very similar chest radiographs.
In acute beryllium disease, the metal acts as a direct chemical irritant causing an inflammatory reaction.
Occurs after exposure to beryllium dust or fumes found in products:
computers
automotive electronics
nuclear reactors
aircraft components
The pathogenesis is delayed-type hypersensitivity reaction stimulating proliferation of T cells leading to inflammatory, fibrosis, and granuloma formation.

15. Physical signs uncommon other than inspiratory crackles.
Berylliosis
Patients may present with cough, chest pain, arthralgias, fatigue, and weight loss.
Physical signs uncommon other than inspiratory crackles.
Diagnosis is made by beryllium lymphocyte proliferation test from blood or bronchoalveolar lavage.
Treatment focuses on exposure avoidance and corticosteroid therapy for 4-6 weeks.
Prognosis is highly variable and ranges from complete recovery to lung transplantation.
Peribronchial and subpleural nodules  identical to sarcoid
Non-necrotizing granulomas on lung biopsy on H-E stain.

16. Coal worker's lung
Focal areas of coal deposition produce coal macules, hallmark or coal worker's pneumoconiosis, extend into one another leading to focal emphysematous changes.
Coal dust in the alveoli ingested by macrophages which expel the particles through mucus or via the lymphatic system.
Overwhelmed accumulation of the macrophages triggers an immune response leading to inflammation and fibrosis
Periarterial fibrosis can lead to strangulated vessels and ischemic necrosis.
Coal worker's lung

17. Coal worker's lung
The degree of fibrosis is related to the duration of exposure, age at first exposure, and the quantity of inhaled silica within the coal dust.
Patients with early disease are typically asymptomatic but may eventually report productive cough and dyspnea.
Diagnosis is based on history, physical examination findings, and evidence of fibrosis on radiographic imaging.
Treatment is largely supportive and preventative.
Mortality is related to the degree of fibrosis and oxygen requirement.

18. Bird fancier's lung
Bird fancier's lung, also called bird-breederds lung is a type of hypersensitivity pneumonitis caused by bird droppings.
The lungs become inflamed with granuloma formation.
Exposure to avian proteins present in the dry dust of the droppings and sometimes in the feathers of a variety of birds.
Birds such as pigeons, Parakeets, Parrots, turtle , doves, turkeys and chickens have been implicated.

19. Within hours following significant exposure
Bird fancier's lung
Acute HP:
Flulike syndrome of fever, chills, malaise, cough, chest tightness, dyspnea
Within hours following significant exposure
Symptoms resolve gradually within 12 hours to several days following exposure removal
Recur following re-exposure
Sub-acute HP:
Insidious productive cough, dyspnea, fatigue over weeks to months
Progression to persistent cough and dyspnea
May occur with frequent acute reactions
Anorexia and/or weight loss
Chronic HP:
Insidious onset of progressive dyspnea, cough, fatigue, malaise, and/or weight loss
May have had unrecognized or untreated acute/subacute disease

20. Bird fancier's lung
This disease is inflammation of the alveoli in the lungs.
In bird fanciers lung medical tests will show a normal range of results and it will be identified by X-ray or CT scans showing a ground glass appearance.
In the chronic form there is usually anorexia, weight loss, tiredness and progressive interstitial fibrosis. 
Condition is occasionally fatal.

21. Farmer’s lung
Immune response are by exposure to thermophilic actinomycetes which generates IgG-type antibodies.
Subsequent exposure, IgG antibodies combine with the inhaled allergen to form immune complexes in the walls of the alveoli in lungs.
This causes fluid, protein, and cells to accumulate in the alveolar wall which slows blood-gas interchange and compromises the function of the lung.
Is a HP induced by the inhalation of biologic dusts coming from hay dust or mold spores or other agricultural products. 
Results in a type III hyper-sensitivity inflammatory response and can progress to a chronic condition, potentially dangerous.
Inhaled allergens provoke IgE antibodies that circulate in the bloodstream

22. FARMER’S LUNG A B
Radiological characteristics in farmer's lung disease. (A) Chest HRCT in a patient with acute farmer's lung. Ground glass infiltrates and centrilobular nodules can be observed. (B) Chest HRCT in a patient with chronic farmer's lung. Note the reticular pattern in middle fields with low-grade ground glass infiltrate.

23. Laboratory Studies
No single laboratory test is specific to the diagnosis of farmer's lung.
The most important diagnostic tool is a detailed environmental history.
Leukocytosis with neutrophilia (but not eosinophilia) and elevated ESR, CRP level, quantitative immunoglobulin level are noted.
Precipitating IgG antibodies confirms past exposure but does not indicate active disease.
Laboratories must select antigens based on knowledge of local climate and agricultural practices rather than reliance on commercially available antigen panels.

24. THANK YOU