1 / 41

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.

corin
Download Presentation

Environmental and Occupational Lung Diseases

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  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!

More Related