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Environmental and Occupational Lung Diseases

Environmental and Occupational Lung Diseases. Dr. Yeşim YASİN Fall-2013. Outline. Description of occupational lung diseases Basic classifications Major occupational lung diseases Prevention Occupational history. Ramazzini.

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Environmental and Occupational Lung Diseases

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  1. Environmental and Occupational Lung Diseases Dr. Yeşim YASİN Fall-2013

  2. Outline • Description of occupational lung diseases • Basic classifications • Major occupational lung diseases • Prevention • Occupational history

  3. Ramazzini • He published De MorbisArtificumDiatribain 1700 (Treatise on the Diseases of Workers). He described: • Dyspnea and metal poisoning in miners • Bronchitis from irritant fumes • Lung fibrosis in potters • Asthma from exposure to corn &flour • Silicosis in stonemasons

  4. Description Occupational lung diseases are a group of diseases that are caused by either repeated, extended exposure or a single, severe exposure to irritating or toxic substances present in the work environmentthat leads to acute or chronic respiratory ailments.

  5. Main difference: • Occupational diseases: Diseases related to a specific occupation, such as asbestosis, coal worker’s pneumoconiosis (black lung), beryllosis (brown lung), silicosis • Work-related diseases: Diseases that are not occupation-specific, but are aggravated at work, such as occupational asthma, industrial bronchitis

  6. Major classification • Diseases due to physical agents: a. Heat b.Cold c. Light d. Pressure e. Noise f. Radiation • Diseases due to chemical agents: a. Gases: Gas poisoning b. Pneumoconiosis c. Metals and their compounds: Chemicals & solvents • Diseases due to biological agents: Leptospirozis, anthrax, actinomycosis, tetanus • Occupational cancers: Cancer of skin, lungs, bladder • Occupational dermatosis: Dermatitis, eczema • Diseases of psychological origin: Industrial neurosis, hypertension, peptic ulcer, etc.

  7. MajorType of ExposureAssociatedwithClinicalDisease • Gases • Corrosivesubstances (acids, alkalis) • Dyesandstains • Dustsandpowders • Asbestosandotherfibers • Infectiousagents • Insecticidesandpesticides • Metal and metal fumes • Organicdusts (cotton, wood, biologicmatter) • Plastics • Solvents • Petrochemicals (coal, petroleumdistillates) • Physicalfactors (noise, lifting, thermalstress, vibration, repetitivemotion) • Emotionalfactors (stress) • Radiation (electromagneticfields, X-ray radiation,ultravioletradiation)

  8. Induction Periods • Short: • Asthma • Infections • Allergic alveolitis • Toxic poisonings • Long: • Pneumoconioses • Neoplasms

  9. Classification of OLD • Inflammation of airways • Inflammation of lining of respiratory system • Obstructive lung disease • Reversible: Occupational asthma, Byssinosis • Irreversible: Industrial bronchitis, Emphysema • Restrictive lung disease • Pneumoconiosis: Silicosis, Asbestosis • EAA: Farmer’s lung

  10. Inflammation/irritation of airways • Main substances • Soluble in water • Can produce inflammatory effect • The site of the effect depends on the degree of solubility • Highly soluble  Upper respiratory tract • Moderately soluble  middle respiratory tract • Sparingly soluble lower respiratory tract

  11. Occupational asthma and rhinitis • Caused by immunological sensitization to agents in the workplace • Approx. 10% of adult onset of asthma is occupational. • Asthma symptoms: wheeze, chest tightness and dyspnea. Classically, symptoms are worse at work or soon after work, and better during weekends and holidays. • Rhinitis and conjunctivitis symptoms: rhinorrhea, nasal stuffiness and itching of the eye/nose, sneezing; often associated by asthma and may precede chest symptoms. • When sensitized, symptoms can be precipitated by non-specific irritation (e.g smoking or cols air)

  12. Asthma and rhinitis-prognosis • Symptoms usually resolve after removal from exposure, but the practical constraints of exposure control can be a real threat to employment. • Where exposure cannot be controlled completely, individuals are sometimes allowed to continue to work wearing PPE. However, they must be informed about risk, and have a frequent health surveillance.

  13. Byssinosis • Associated with the exposure to cotton dust. • Symptoms: wheezing and chest tightness. Typically worse after a break from work (Mondays!), improving with return to exposure (better towards the end of the working week). Temporal relationship can be obscured after prolonged exposure. • Textile and rope making industries • Development of disease is rare if the exposure is < 10 years; in general 20 years or more • Prevention: exposure controls include enclosure of carding operations, and steaming of raw cotton to reduce particle formation.

  14. Hypersensitivity pneumonitis (HP) • Also known extrinsic allergic alveolitis (EAA) • Inflammatory disorder of the lower RS results from an immunological reaction to specific allergens in moldy organic material. • The most prevalent form is Farmer’s hypersensitivity pneumonitis (FHP) or Farmer’s lung. • Clinical Features • Acute form: Fever, chills, cough, dyspnea, myalgia, headache; Onset 4-8 hours after exposure to antigen; Resolution after 1-3 days • Subacute/chronic form: Gradual onset of dyspnea over months or years; Recurrent acute attacks; Chronic productive cough

  15. HP (Cont.) • Causal exposures/industries: • Agricultural workers, Forestry workers, Mushroom workers, Bird handlers, Sugar cane producers, Distillery workers • Prevention: • Reduction of exposure to moldy organic material • PPE for high exposure activities

  16. COPD • Characterized by generally irreversible airflow limitation, with impairment of lung function and debility in severe cases. • Causal exposures/industries: • Mineral dusts; i.e. coal mining, construction, cement, silica • Organic dusts; i.e. farming, cotton textile work, wood. • Chemicals; i.e. cadmium, welding fumes, isocyanates • Prevention: exposure controls, ventilation, dust reduction measures, and use of PPE.

  17. Pneumoconiosis • The term is currently defined by the International Labor Organization (ILO) as the accumulation of dust in the lungs and the tissue reactions to its presence. • Tissue reaction may be non-collagenous (minimal stromal reaction) or collagenous (when scarring is permanent).

  18. Pneumoconiosis (Cont.) Etiologic Determinants: • Size of inhaled particle • 1 to 5 μm reach the alveoli • Chemical nature of the particle • Concentration of the particle • Length of exposure • Individual’s susceptibility

  19. Pneumoconiosis (Cont.) • Asbestosis • Silicosis • Coal Worker’s pneumoconiosis • Berylliosis

  20. ILO radiologic classification • Rounded opacities: p (<1.5mm), q, and r (>3 mm) • Irregular opacities: s, t, or u • Profusion: 12 point scale (0/0 thru 3/3) • Grading of pleural thickening

  21. Asbestos and related diseases • Asbestos is a generic term for a group of six mineral silicates • Asbestos fibers are: • Very strong • Highly flexible • Resistant to breakdown by acid, alkali, water, heat, and flame • Non-biodegradable • Environmentally persistent SERPENTINE (93% commercial use) AMPHIBOLE (7% commercial use)

  22. Asbestos related diseases • Asbestosis • Pleural disorders • Mesothelioma • Diffuse pleural thickening • Benign pleural effusion • Pleural plagues • Lung cancer • Laryngeal cancer

  23. Acoustic products Automobile undercoating Brake lining Cements Clutch casings Dockyards Floor tiles Fire-fighting suits Fireproof paints Insulation Roofing materials Ropes Steam pipe material Asbestosis-industry/uses

  24. Asbestosis • Diffuse fibrosis caused by a persistent alveolar inflammation • Irregular opacities predominately in the lung bases • Rales invariably present • Clubbing is common

  25. Asbestos-Related PleuralAbnormalities

  26. Asbestos-related Lung Cancer

  27. Asbestos-related Laryngeal Cancer

  28. Mesothelioma

  29. Coal Worker’s Pneumoconiosis (CWP) • Coal dust is inert and not particularly fibrogenic. • Can cause industrial bronchitis, emphysema, and progressive massive fibrosis. • Xray looks worse than patient • Many symptomatic coal miners have silicosis or tobacco induced COPD • The onset of CWP normally occurs after 10 years, and son incidence and mortality reflects past exposures.

  30. CWP (Cont.) • Mortality is declining in developed countries • Cases are still common in China, and there is low but significant incidence in India. • Two forms: Simple CWP (often asymptomatic with minor impairment in pulmonary capacity); Complicated CWP (Progressive Massive Fibrosis-PMF, development of large or confluent solid fibrotic nodules in the lung parenchyma, dyspnea and productive cough. • Prevention: exposure controls in the mining industry including ventilation, dust reduction measures, and use of PPE.

  31. Silicosis • A type of pneumoconiosis associated with the exposure to respirable crystalline silica. • Clinical forms: • Acute: early onset of dyspnea and dry cough within a few months of heavy exposure to fine dusts (i.e. Sandblasting) • Subacute: graduate onset of dyspnea and dry cough over years after moderate exposure. • Chronic: slow development of nodules on CXR over many years after lower exposure. • Prevention: Control of exposure through substitution of low-silica sand for molding and sandblasting, dust control measures (ventilation, suppression) and use of PPE.

  32. Tunneling Hard-rock mining Sandblasting Quarrying Stonecutting Foundry work Ceramics work Abrasive work Brick making Paint making Polishing Stone drilling Well drilling Silicosis-Industry/uses

  33. Prevention • Primary prevention is concerned with preventing the initiation of disease by controlling the exposure to its causes. • control of the source, • control at the transmission path, • control at the level of the worker. • Secondary prevention is concerned with preventing disease complications early in its natural history by early diagnosis and intervention • Tertiary prevention is concerned with preventing and compensating permanent disability.

  34. A few examples • Pre-employment screening • Atopy • Genetic factors • Cigarette smoking • Education • Engineering measures • Indoor air quality control • Reduce exposure • If doable, replace the substance • Medical monitoring/surveillance • Screen for potential respiratory sensitizers

  35. The Occupational History • All jobs held in their lifetime and the duration • Do symptoms improve with weekends and vacations? • What they did, not their title: • “brusher” drills into hard rock • “rodeo sander” Sandblasts jeans through compressed-air

  36. The Occupational History (Cont.) • Toxic exposures can produce airway symptoms or an alveolitis. • If everyone in the workplace is affected in a dose-dependent manner, the etiology is likely to be toxic rather than immunologic. • Toxic reactions can occur on the first exposure. Immunologically-mediated diseases require re-exposure.

  37. Common denominator through which all occupational lung diseases aggravate: Tobacco smoking!

  38. Summary • Awareness of occupational exposure as a cause of disease is important • Occupational history is crucial • To establish a work relationship, objective evidence of exposure and occurrence of symptoms or changes in lung function is necessary • Reduction of exposure is the key to prevention • Engineering measures as well as medical monitoring • Prohibition of smoking in the workplace is necessary • Education/awareness raising

  39. THANK YOU!

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