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Occupational Lung Disease Respiratory Block: 2016 Sunita Mulpuru MD FRCPC & Steven T. Bencze MD FRCPC Respiratory Medicine Disclosure You may only access and use this PowerPoint presentation for educational purposes. You may not post this presentation online or distribute it without the permission of the author. Session Objectives List common occupational exposures that lead to occupational asthma Describe key causes, symptoms and types of occupational lung disease Occupational Lung Disease Key Features • Respiratory illness caused by the work environment • May occur years after the exposure (decades) • Exposures can affect: – Airways (bronchi/alveoli) – Lung Interstitium (area around the airspaces) – Pleura Lung Structure Bernardino Ramazzini (1633 - 1714): De Morbis Artificum, 1713 Occupational Asthma: Definition “Disease characterized by variable airflow obstruction and/or airway hyper-responsiveness due to causes and conditions attributable to a particular work environment and not to stimuli encountered outside the workplace” • It is usually new-onset asthma, but can occur in people with pre-existing asthma • Pathophysiology: – Immunologically mediated (via IgE antibodies to HMW of LMW agents) – Induced by respiratory irritant at work (less common) Can Respir J Vol 5 No 4 1998 Occupational Asthma: Breakdown Occupational Asthma: Mechanisms 1 • Sensitization to a High or Low molecular weight agent occurs, with a latency period of weeks to years – Re exposure can cause an asthmatic response • Sensitization by an immunologic mechanism occurs for many agents (latex proteins, flour, animal allergens) Occupational Asthma: Mechanisms 2 • Alternatively, OA can be caused by high level irritant exposure at work – Starts within 24 hrs, no latency period, no sensitization, re-exposure will usually not trigger asthma OA: HIGH MOLECULAR WEIGHT antigens Sensitizers Occupation Animal, insect Animal handlers, Health Care Workers Food , animal protein, bacteria, fungi Food processing Latex Health Care Workers Flour Bakers Vegetable gums Printers OA: Low MOLECULAR WEIGHT Antigens Sensitizers Occupation Isocyanates Painters , autobody, glues Wood dust Carpenters, forestry Dyes Textile workers Epoxy Auto industry Persulfate Hairdresser Fluxes Electronics Metal dust Welders Occupational Asthma: Clinical History • Must have a high index of suspicion • Occupational history – exposure to a known asthma inducing agent (get the material safety data sheets) – Symptoms started after employment – Improvement of symptoms during weekends and holidays – Worsening of symptoms on returning to work • History alone is insufficient, so objective testing is needed Occupational Asthma: Objective Testing • Demonstrate the presence of asthma objectively – Spirometry pre and post bronchodilator (Beta 2 agonist) with 24 hrs of work place exposure or during symptoms – Methacholine challenge test (if spirometry normal) • Use Objective tests to assess the relationship with work – – – – Immunological tests (identify specific IgE antibodies to a work place allergen) Serial PEF measurements both on and off work On and off work methacholine challenge tests Specific inhalation challenges or occupational type of exposure tests - "gold standard" OA Diagnosis: Monitoring of PEF - How to do it ? • At least 2 weeks at work and off work – At least 4 times daily, preferably every 2 hours • Medication allowed: 1. Keep it constant and at minimum dose 2. Short acting Beta-2 agonist as needed 3. Continue asthma controllers 4. Avoid, if possible, long-acting beta-2-agonist • False positive – Subject not exposed during monitoring – Poor compliance False negative – Change in medication (inhaled steroids) – Malingering (falsification of results) • PEF Monitoring: Example American Thoracic Society: Occupational Asthma Occupational Asthma: Methacholine Challenge Testing • Have patient on / off work for 2 week periods • Complete methacholine challenge testing while working, then at the end of a 2-4 week period off work • If improvement in the PC20 level (concentration of MCT at which FEV1 falls improves while off work: highly supportive of OA 20%) – Looking for a 3-4 fold increase in the concentration of methacholine that produces a drop in FEV1 Reactive Airways Dysfunction: Diagnosis • Generally not confirmed by objective tests – Depends on history – Objective confirmation of asthma – Onset within 24 hrs of large exposure – Symptom duration of at least 3 months • Reactive Airways Dysfunction Syndrome (RADS) among Rescue and Recovery Workers in the World Trade Center Health Registry (WTCHR) – (Am J Respir Crit Care Med 179;2009:A5853) RADS: Diagnostic Criteria ACCP: Diagnosis and Management of Work-Related Asthma RADS: Some Causative Agents Sensitizers Smoke Chlorine Sulphur dioxide Cleaning agents Isocyanates (paints) Diesel exhaust Other Occupational Lung Diseases 1) Hypersensitivity Pneumonitis – Hypersensitivity (allergic) reaction to inhalation of antigenic organic particles/fumes 2) Pneumoconioses – Airway and Interstitial pulmonary disease resultant from inhalation of inorganic and organic dusts Hypersensitivity Pneumonitis (HP) • First recognized in 1713, in wheat reapers • 5 -15% prevalence in population exposed to known inciting antigens • Presents along a spectrum of acute, subacute, and chronic • May hear about HP as “Farmer’s Lung” or “Bird Fancier’s Lung” depending on the exposure that caused it – > 200 different organic antigens associated with HP • More common among non-smokers Hypersensitivity Pneumonitis: Clinical Presentation and Diagnosis • Acute form: – occurs several hours after exposure – subside within a few days • Subacute form: – can occur with gradual onset of dyspnea over weeks and months, chronic productive cough • Chronic form: – Long standing exposure to the offending antigen can lead to irreversible fibrotic changes in the lung • Diagnosis: – Compatible History of exposure to known causative agent – Classic Radiology patterns – Resolution with removal of the offending exposure Hypersensitivity Pneumonitis: Known Inciting Antigens Hypersensitivity Pneumonitis: Factors in Pathogenesis Host factors Agents Genetic background antigens Smoking history Non-antigenic elements HP Viral infection(s) Hypersensitivity Pneumonitis: Management • Avoidance of the antigen is the key – May continue farming without development of irreversible fibrosis • Precautions – Dust masks with filters – Appropriate ventilation – Mechanisation feeding process – Close monitoring • Despite avoidance of antigen – Chronic form may fail to improve (development of fibrosis) • For severe cases – Prednisone 40-60 mg/day x 7-14 days – Tapering dose over 4-6 weeks • Not recommended to continue steroid therapy past 6 months Pneumoconioses: Inhalation of Inorganic/Organic Dusts Compounds • Definition: – Lung disease (non-neoplastic) resulting from inhalation of inorganic and organic dusts – Examples: Silicosis, Asbestosis, Coal Worker’s Pneumoconiosis, Talc-related lung disease, Bauxite Pneumoconiosis • Sources of exposures: – Coal: Coal miners – Silica: Sandblasters, Miners, Foundry workers, Potters, Dental Workers, Construction, Glass workers, Stone cutters (sandstone, granite) – Asbestos: Mining, Shipyard workers, Plumbers, Electricians, Construction • Factors that determine severity of lung reaction to these materials – Intensity and duration of exposure – Individual sysceptibility – Nature and properties of the dust (size, toxicity, etc.) Coal Workers Pneumoconiosis (Coal Workers Lung) • Coal Worker’s Pneumoconiosis: – Small particles are inhaled, causes an inflammatory state, pulmonary architecture is damaged – Pulmonary nodules and progressive massive fibrosis can result (usually stops when exposure stops) – Years – Decades to develop – Symptoms: Chronic cough, sputum production (melanoptysis), dyspnea – PFT: Progressive airflow limitation (obstruction) • Exposure to coal dust can also result in chronic bronchitis and chronic obstructive pulmonary disease “industrial bronchitis” Imaging Examples: Coal Worker’s Pneumoconiosis Progressive Massive Fibrosis Silicosis • Silicosis – Silica is silicon dioxide (SiO2) which comprises large part of granite, sandstone and slate – Silicosis is lung disease caused by inhalation of fine silica dust (acute or chronic) and subsequent inflammatory reaction (continues even without exposure) – Acute Silicosis: alveolar filling with inflammatory infiltrates (rare) – Chronic Silicosis: nodules, and progressive massive fibrosis (coalescing of the nodules), 20-30 years after exposure – Symptoms: Cough, dyspnea • Patients are susceptible to Mycobacterial infections (like M.Tuberculosis) Imaging Examples: Silicosis Silicosis (Nodular Disease) Silicosis (progressive, massive fibrosis) Asbestos Related Lung Disease Asbestos Related Lung Disease • Naturally occurring fibre used widely in the construction and insulation industries (high tensile strength) • Two Types of Asbestos Fibres – Serpentine Fibres (Chrysotile, 90% of commercial use, less toxic) – Amphibole Fibres (crocidolite, amosite, tremolite ) • Cause clinical respiratory disease by direct toxic effects on pulmonary cells, and subsequent release of cytokines, reactive oxygen species Asbestos Related Lung Disease: Occupation & Clinical Manifestations • Some Occupations Associated with Exposure: – Plumbers, Pipefitters, Electricians, Insulation Workers, Carpenters, Boilermakers, Welders, Work with Brakes (linings), Shipyard workers, Textile workers (making fireproof clothing and blankets) – Other forms of exposure: living near asbestos mines, residential remodelling • Clinical Manifestations: – Pleural effusion (benign) – Pleural plaques – Diffuse pleural thickening, rounded atelectasis – Asbestosis (interstitial lung fibrosis) – Malignant mesothelioma (cancer of the pleura) – Bronchogenic carcinoma Asbestos Related Lung Disease: Effusion • Benign Asbestos-Related Pleural Effusion (BAPE) – Usually seen within 15 years of exposure (much before appearance of interstitial lung disease) – Usually unilateral – Often “exudative” in nature – May recur, persist, or leave pleural thickening Asbestos Related Lung Disease: Pleural Plaques • Pleural Plaques - Benign – Calcifications usually involving the parietal pleura, usually asymptomatic – Occur in approximately 50% of asbestos-exposed individuals (significant exposure) – Most common manifestation of previous asbestos exposure – 20-40 year latency (at time of detection) Asbestos Related Lung Disease: Asbestosis (ILD) Asbestosis: Fibrotic lung disease secondary to asbestos exposure: - Usually 20-30 yr latency period, inversely proportional to exposure intensity - CT example of lung fibrosis caused by Asbestos Exposure: “Honeycomb Cysts” Asbestos Related Lung Disease: Malignant Mesothelioma • Mesothelioma is a cancer of the mesothelial surfaces of the pleura or periotoneum • 10% lifetime risk of developing mesothelioma in asbestos workers (high estimate) • Dose-response relationship between exposure and mesothelioma • Latency period of 30-40 years • Not known to be independently associated with smoking – Asbestos exposure and smoking act synergistically to increase the risk of lung cancer to 60x’s that of a non-smoker, non-asbestos exposed person Asbestos Related Lung Disease: Malignant Mesothelioma Clinical Presentation: • More common in men, presenting age 5070 • Most common to present with pleural effusion • Symptoms: breathlessness, pleuritic chest pain, constitutional symptoms (with disease progression) • X ray may show pleural effusion, or pleural thickening, CT can show diffuse circumfrential nodular pleural thickening 1. Diagnosis: • Pleural biopsy • CT Guided • Thoracoscopy 1. Drug Discovery Today:Disease Mechanisms Vol 4, No.2, 2007 Pneumoconioses: Summary American Thoracic Society, Occupational Lung Diseases Occupational Lung Disease Key Features • Obtain an Occupational history (this is key) • Type of work, setting, duration, exposures • Seek objective evidence of cause and effect relationship • Reduction of exposure is the key to prevention • Advise Patients about Workplace Safety and Insurance Board (WSIB) and compensation (if warranted) Occupational Lung Disease: Summary • Many lung disorders can be caused or exacerbated by occupational or non-occupational factors and exposures • Some occupational exposures can cause several different lung disorders • Multiple different exposures (including cigarette smoke) may be important for development of clinical disease • Exposure dose matters • Individual differences in susceptibility are important • Some disorders take a long time to develop • Occupational & exposure history is crucial!! Occupational Lung Disease Summary Occupational Asthma Hypersensitivity Pneumonitis Pneumoconioses Mechanism Immune or Irritant Immune / Allergic Immune / Chronic Inflammation Onset Weeks-Months Immediate (RADS) Months-Years Long Latency Diagnosis - Methacholine Testing - Compatible History - Compatible History - Radiographic Findings - Improves with removal of antigen - Compatible history (workplace) - Radiographic Findings (Asbestos/Coal/ Silica) Any Questions?