Dr Alireza Safaeian Occupational Medicine Specialist Occupational lung
- Slides: 89
Dr. Alireza Safaeian Occupational Medicine Specialist
Occupational lung diseases • Occupational lung diseases are a broad group of diagnoses caused by the inhalation of dusts, chemicals, or proteins • The severity of the disease is related to the material inhaled and the intensity and duration of the exposure. • Even individuals who do not work in the industry can develop occupational disease through indirect exposure. • These diseases have been documented as far back as ancient Greece and Rome
Occupational lung diseases • • • Pneumoconiosis Occupational Asthma COPD H. P. (Hypersensitivity pneumonitis) Occupational Respiratory Infections Occupational lung cancers
Pneumoconiosis • A group of interstitial lung diseases caused by the inhalation of certain dusts and the lung tissue’s reaction to the dust. • There is a long delay (up to ten years or more) between exposure and onset of disease,
Pneumoconiosis The main types: • Asbestosis • Silicosis • coal workers’ pneumoconiosis Other forms pneumoconioses • • • can be caused by inhaling dusts containing : Aluminum Antimony Barium Graphite Iron Kaolin Mica Talc mixed-dust pneumoconiosis Byssinosis: exposure to cotton dust
ASBESTOSIS
Introduction (Asbestos) • Naturally occurring material • Hydrate silicate with variable magnesium content • Fibrous structure: length to width more than 3/1
Types of Asbestos Serpentine Amphibole (93% of commercial use) (7% of commercial use) Chrysotile Actinolite, Amosite, Anthophyllite, Crocidolite, Richterite, Tremolite
Types of Asbestos The most common commercial forms: • Chrysotile - “White asbestos” • Amosite - “Brown asbestos” Others: • Tremolite (sometimes found in vermiculite) • Actinolite • Anthophyllite • Crocidolite - “Blue asbestos” All types of asbestos have been associated with all of the malignant and non-malignant conditions,
Properties of Asbestos • Naturally occurring fibrous minerals • Good tensile strength • Flexible • Heat resistant • Electrical resistance Asbestos ore • Good insulation • Chemical resistant – Resistant to breakdown by acid, alkali, water, heat, and flame Asbestos fibers Because of these unique properties, asbestos was used extensively in variety of products.
Uses of Asbestos in industry Asbestos has been used for centuries, but greatly increased during and after World War II in ship insulation. • • • Insulation Textiles Cements Friction materials (brake linings, Clutch casings) Construction mining & milling, shipyard sheet metal worker plumbers & pipefitters Steamfitter • • • plasterboard worker transport Acoustic products Automobile undercoating Floor tiles Fire-fighting suits Fireproof paints Roofing materials Ropes Steam pipe material
Examples of Uses of Asbestos Sheet vinyl containing asbestos Sprayed-on fireproofing material These products may be found in homes and buildings constructed before 1981. Vinyl asbestos flooring
Damaged asbestos pipe insulation This damaged pipe insulation is a health hazard to persons working around it, handling it or removing it. Asbestos fibers are visible on the torn edges.
Asbestos Roofing Material
Cement-asbestos pipe (Transite) Cement-asbestos pipe, sometimes called Transite, was used underground above ground in years past and may show up in pipe replacement jobs, building demolition jobs or excavations.
Asbestos Ceiling Tile close-up
Asbestos shingles and siding Removal done correctly Found in older houses – not to be confused with newer asbestos-free cement siding. There is little hazard unless disturbed. The top right hand picture shows a siding replacement job with broken green asbestos shingles which would have released dust and fibers into the air if done incorrectly.
Exposure history • Onset & latency -more than 20 years for fibrosis & plaque -several years for pleural thickening • Duration -more than 6 months for fibrosis & plaque -shorter for pleural thickening
Exposure history • Intensity 1) direct exposure : insulator 2) bystander exposure : sheet-metal worker 3) indirect exposure : family members
Exposure limit • OSHA (PEL) : 0. 1 fiber /cm 3 (TWA) Short time exposure : 1 fiber / cm 3 • Reducing in asbestos usage from 1970 in USA • Asbestos ban from 1989 by EPA
Asbestos-related disease Non-malignant Malignant • Parenchymal Asbestosis • Asbestos-Related Pleural Abnormalities • Lung Carcinoma • mesothelioma
Parenchymal Asbestosis • Diffuse interstitial fibrosis with: – Restrictive pattern of disease on pulmonary function testing (but can see mixed pattern) – Impaired gas exchange – Progressive exertional dyspnea • Radiographic changes: >10 years • Latency period: more than 20 years
Chest Radiograph Findings: Parenchymal Asbestosis • Small, irregular oval opacities • Interstitial fibrosis • “Shaggy heart sign” List of certified B Readers: http: //www. cdc. gov/niosh/pamphlet. html
Asbestos-Related Pleural Abnormalities • Four types of abnormalities: – – Pleural plaques Benign asbestos pleural effusions Diffuse pleural thickening Rounded atelectasis • Mostly asymptomatic, though some can cause dyspnea or cough • Latency periods: 10 -30 years (shorter latency is for pleural effusion)
Chest Radiograph Findings: Asbestos-Related Pleural Abnormalities • Pleural plaques – Areas of pleural thickening – Sometimes with calcification • Pleural effusions • Diffuse pleural thickening – Lobulated prominence of pleura adjacent to thoracic margin (over ¼ of chest wall) – Interlobar tissue thickening • Rounded atelectasis – Rounded pleural mass – Bands of lung tissue radiating outwards
Lung Carcinoma • Risk depends on: – – – Level, frequency, and duration of exposure Time elapsed since exposure Age at time of exposure Smoking history (synergistic) Individual susceptibility factors (under investigation) • Latency period: 20 -40 years
Chest Radiograph Findings: Mesothelioma • Pleural effusions • Pleural mass • Diffuse pleural thickening
Clinical Presentation Disease Signs and Symptoms Parenchymal Asbestosis • Insidious onset of dyspnea on exertion Asbestos-Related • Usually: None Pleural Abnormalities • Sometimes: Progressive dyspnea and intermittent chest pain (depending on the type of pleural abnormality) Lung Cancer • Usually: None (until later stages) • Fatigue • Sometimes: Fatigue, weight loss, or chest pain Mesothelioma • Usually: None (until later stages) • Sometimes: Dyspnea, chest pain, and fatigue
Physical Examination • Focus on lungs, heart, digits, and extremities • Pulmonary auscultation to detect bibasilar inspiratory rales (not always present) • Observation of other signs, such as clubbing of the fingers and cyanosis
HRCT Indication: Equivocal CXR , significant symptom with unremarkable CXR , pleural obscuring abnormalities -Prone views for assess basilar, posterior and subpleural regions • Septal thickening : intra lobular or interlobular • Subpleural lines and opacities • Parenchymal bands • Ground-glass • honeycombing
Diagnosis Based on : Exposure + Clinic + CXR + PFT • Exposure : sufficient intensity , 6 months duration , 20 years latency • ILO classification: 1/0 or greater on CXR • PFT : restrictive or mixed • HRCT • Biopsy : exclusion of malignancy
Management • Unfavorable response to corticosteroids and immunosupressive agents : case-by-case in progressive alveolitis • Therapy is supportive : -bronchodilator , ipratropium , inhaled steroid -oxygen -treatment of infections
Management -stopping of exposure -Influenza and pneumococcal vaccines -Smoking cessation
Medical surveillance • No clear evidence for the benefit • Spiral CT : early detection against risk and cost of evaluating false positive
Medical surveillance • Exposed worker with normal CXR & PFT : CXR and PFT every 2 to 5 years (based on the latency period) • ILO 1 or sign or symptom : annual CXR and full PFT every 2 years • Isolated pleural thickening : CXR and PFT biannually (more frequently if presence of increasing symptoms or pleural involvement)
SILICOSIS
Introduction: Most common pneumoconiosis in world (occupational exposure to crystalline silica) *quartz, cristobalite, tridymite, … OSHA(PEL) : 100 μg/m 3
High risk trade for Crystalline Silica Exposures • • Tunneling Hard-rock mining Sandblasting Quarrying Stonecutting Foundry work Ceramics work • • • Abrasive work Brick making Paint making Polishing Stone drilling Well drilling
Crystalline Silica Exposures
Silica-induced diseases • • • Chronic bronchitis Emphysema Silicosis Tuberculosis Lung cancer Collagen vascular diseases
Silicosis Depends on exposure intensity and quartz content of dust • Chronic simple ( classic ) silicosis • Chronic complicated ( PMF ) silicosis • Accelerated silicosis • Acute silicosis
Simple silicosis: • No symptoms or Breathlessness Dyspnea(initially with exercise), Cough with or without sputum • P/E: often normal but may rales or decreased breath sound. • CXR: Rounded opacities(1 -10 mm) *Eggshell calcification • PFT: often normal but may restrictive(mainly) obstructive or mixed pattern.
Exposure • Moderate exposure • at least 10 yr exposure • less than 30% quartz
Progressive massive fibrosis: • Cough / exertional dyspnea to respiratory failure. • P/E: decrease respiratory sounds. • CXR: Rounded opacities(>10 mm) • Pulmonary impairment
Accelerated silicosis: • Time from exposure to X-Ray & PFT change is much shorter. • Moderate-high exposure to silica with 40 -80% quartz. • Latent period: 2 -5 yr ( from exposure to presentation) • Rapid progression to progressive massive fibrosis.
Acute silicosis (silicoproteinosis) • Short duration and high concentration. (Tunneling, abrasive blasting, …) • Latent period: few months-3 yrs after exposure • Symptoms: rapidly progressive dyspnea. Respiratory failure to death. • P/E: crackles (alveolar & airway fluid) • CXR: – Diffuse perihilar alveolar filling( consolidation, A type of alveolar proteinosis. ) – Ground-glass opacities • PFT: Progressive restrictive impairment • Fatal 1 -2 yrs after initiation of symptoms
Diagnosis 1)History of silica exposure that sufficient to cause this illness. 2)Chest radiograph features consistent with silicosis. 3)Absence of other illness that mimic silicosis.
WHO recommendation: • CXR Ø at baseline Ø after 2 -3 years of exposure Ø then every 2 -5 years. • Spirometry & questionnaire Ø at baseline Ø then annually or at the same frequency as CXR.
Associated illnesses: • Mycobacterial infections (20 -fold increased risk in silicosis , 3 -fold increased risk in silica exposure without silicosis) • • PPD + / Isoniazid /at least 1 year Lung cancer : group 1 IARC Connective tissue disease (Caplan’s syndrome) Renal disease: Glomerulonephritis, nephrotic syndrome, ESRD Silicotic Lesions (liver, spleen, BM, lymph nodes)
Prevention: Engineering intervention Administrative controls Respiratory protective devices
Example of a Combination of Controls Source: What Dental Technicians Need to Know About Silicosis. NJDHSS.
Respiratory protective devices • if other methods are not sufficient Use Proper Respiratory Protection
Example of a Combination of Controls Source: NIOSH Publication No. 2002 -105: Silicosis in Sandblasters: A Case Study for Use in U. S. High Schools
Treatment • Corticosteroid with Isoniazid (acute silicosis, CTD) • Lung lavage • Lung transplant
Occupational Asthma
Asthma Overview • Asthma is an inflammatory disorder of the airways. • When an asthma attack occurs, the muscles surrounding the airways become tight and the lining of the air passages swell. • This reduces the amount of air that can pass by, and can lead to wheezing sounds. • Variable airflow obstruction and/or airway hyperresponsiveness (Reversible obstruction(+/- treatment)
Asthma Symptoms • Asthma symptoms vary from person to person 1. Wheezing (The most common symptom) 2. Shortness of breath 3. Chest tightness or pain 4. Chronic coughing 5. Trouble sleeping due to coughing or wheezing
Asthma attack • Most people with asthma have wheezing attacks separated by symptom free periods • Asthma attacks can last minutes to days and can become dangerous if the airflow becomes severely restricted.
Asthma attacks caused by: • Allergies and exposure to allergens such as pet dander, dust mites, pollen or mold. • Non-allergic triggers include smoke, pollution or cold air or changes in weather.
Occupational Asthma • Occupational factors account for approximately one in six cases of asthma in adults of working age, including new onset or recurrent disease. • (OSHA) reports : estimated 11 million workers in the USA are exposed to at least one of the more than 250 Asthmogen substances. • Occupational factors are associated with up to 15 percent of disabling asthma cases.
Work-related asthma Two distinct categories: • Occupational asthma: induced by exposure in the working environment to airborne dusts, vapors or fumes, in workers • Work-aggravated asthma: pre-existing or coincidental new-onset adult asthma, which is made by occupational exposure.
Occupational asthma 1) Sensitiser-induced occupational asthma: (approximately 90% of cases of occupational asthma) 2) Irritant-induced occupational asthma • For some agents, both immunological and nonimmunological mechanisms can be involved
Occupational asthma Irritant OA Sensitizer OA • Develops after a single, very high exposure to an irritant chemicals • Manifest asthma symptoms within 24 hours of the exposure • Improve over time and may go away entirely (3 months) • If symptoms persist beyond 6 months persistent problems are possible. • Sensitisation or becoming allergic to a specific chemical agent in the workplace over a Period of time • Latency period (several weeks or as long as several years) • The period of greatest risk is the first two years of exposure
workers who are at increased risk of developing occupational asthma • • • Bakers Detergent manufacturers Drug manufacturers Farmers Grain elevator workers Laboratory workers (especially those working with laboratory animals) Metal workers Millers Plastics workers Woodworkers
After sensitization • The smallest amounts of exposure will produce symptoms. • OEL does not protect the person already sensitized. • Symptoms can happen immediately after the worker starts working with the substance or soon afterwards. • The symptoms typically improve when the worker is away from the workplace on days off or holidays.
Respiratory sensitizers
Natural history of occupational asthma • If exposure to the causative agent ceases Completely: the condition will nearly always improve. 1. Within the first two years: complete recovery is usual 2. The longer the exposure continues: tendency for the condition to get worse, and less likely to be a complete recovery • a cessation of exposure is nearly always of benefit.
Prognosis • Generally, occupational asthma has a poor prognosis • approximately 2/3 of workers never achieving full symptomatic recovery • Approximately 3/4 having persistent nonspecific bronchial hyper-responsiveness. • Approximately 1/3 of workers with occupational asthma are unemployed up to six years after diagnosis
How is exposure prevented and controlled? • Engineering control (replace, segregate the work, enclose the process, partially enclose the process, local exhaust ventilation) • If after there is still exposure, provide suitable personal respiratory protection to workers
Pre Employment Medical assessment • Pre employment health questionnaire • Spirometry or Pulmonary function test (PFT) • Medical examination ü A previous history of asthma, significant atopy (or allergy) or an obstructive pattern on PFT may increase that individuals risk to getting more severe asthma.
Routine Health Surveillance • 3 months and 12 months after job commencement and annually thereafter. • The respiratory questionnaire should be completed again and results compared to pre employment ones. • Spirometry or Pulmonary function test (PFT) • Medical examination
occupational asthma evaluation The first step • confirmation of the diagnosis of asthma. 1. history and clinical examination 2. objective tests (serial peak flowmetry, spirometry and Bronchial Challenge tests Metacholine or Histamine) The next step • Determination of its potential to work • A history of symptoms being related to work is suggestive but not conclusive • Potential sensitisers in the workplace should be identified • objective tests (serial peak flowmetry, spirometry and Bronchial Challenge tests Metacholine or Histamine, blood tests and/or Prick tests) A specific Bronchial Challenge test is usually considered to be the Gold Standard in the diagnosis of occupational asthma.
Diagnosis • Spirometry (base and serial) for work related ↓ 10% of FEV 1 before and after. (across shift) • Methacholine or histamin challenge test after 1014 holydays associated with 3 time ↑Pc 20. • P. E. F serial (the best test for O. A). • Immunological tests(specific Ig. E→HMW &platinum) • Fe. NO, sputum induced analysis(4 -6 h and Eos) • C. X. R
What is a peak flow meter?
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