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

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Presentation on theme: "Environmental and Occupational Lung Diseases Dr. Yeşim YASİN Fall-2013."— 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 2

3 Ramazzini He published De Morbis Artificum Diatriba in 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 environment that leads to acute or chronic respiratory ailments. 4

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 5

6 Major classification 1.Diseases due to physical agents: a. Heat b.Cold c. Light d. Pressure e. Noise f. Radiation 2.Diseases due to chemical agents: a. Gases: Gas poisoning b. Pneumoconiosis c. Metals and their compounds: Chemicals & solvents 3.Diseases due to biological agents: Leptospirozis, anthrax, actinomycosis, tetanus 4.Occupational cancers: Cancer of skin, lungs, bladder 5.Occupational dermatosis: Dermatitis, eczema 6.Diseases of psychological origin: Industrial neurosis, hypertension, peptic ulcer, etc. 6

7 Major Type of Exposure Associated with Clinical Disease Gases Corrosive substances (acids, alkalis) Dyes and stains Dusts and powders Asbestos and other fibers Infectious agents Insecticides and pesticides Metal and metal fumes Organic dusts (cotton, wood, biologic matter) Plastics Solvents Petrochemicals (coal, petroleum distillates) Physical factors (noise, lifting, thermal stress, vibration, repetitive motion) Emotional factors (stress) Radiation (electromagnetic fields, X-ray radiation,ultraviolet radiation)

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 9

10 AgentExamples of agentsDisease/response Inorganic dustsCrystalline silicaSilicosis AsbestosAsbestosis, lung cancer, mesothelioma Coal dustCoal workers’ pneumoconiosis Organic and metallic dusts Cotton, flax, hempByssinosis Proteins, metallic salts, antibiotics, chemicals Occupational asthma Moldy hay, grain, sugar cane, contaminated humidifiers Hypersensitivity pneumonitis Gases and fumesNitrogen, CO2, CO, methane, ozone Asphyxiation, irritation, pulmonary edema Viable aerosolsBacteria, virusesBrucellosis, psitticosis, anthrax FungiHistoplasmosis, aspergillosis Respiratory carcinogensArsenic, asbestos, chromium, nickel Lung cancer 10

11 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

12 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

13 Causal exposure/industries ExposureIndustry/uses IsocyanatesCar body shops Platinum saltsPlatinum industry Acid anhydridesManufacturing use of epoxy resins Rosin fluxElectronics (soldering) Proteolytic enzymesManufacturing of biological washing powders Animal proteins (urine/dander)Laboratory animal research Grain dust, flourBakeries, agriculture Antibiotics, cimettidine, isphagulaPharmaceutical manufacturing Glutaraldehyde, natural rubber latexHealth care Wood dustConstruction, forestry, carpentry Persulphate salts or hennaHairdressing Fish proteins, soya bean, tea dustFish preparation, food industry Reactive dyesCosmetic and rubber manufacture Metal working fluidsManufacturing 13

14 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. 14

15 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. 15

16 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 16

17 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 17

18 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. 18

19 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).

20 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 20

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

22 ILO radiologic classification Rounded opacities: p ( 3 mm) Irregular opacities: s, t, or u Profusion: 12 point scale (0/0 thru 3/3) Grading of pleural thickening

23 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 ) 23

24 Asbestos related diseases Asbestosis Pleural disorders Mesothelioma Diffuse pleural thickening Benign pleural effusion Pleural plagues Lung cancer Laryngeal cancer 24

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

26 Asbestosis Diffuse fibrosis caused by a persistent alveolar inflammation Irregular opacities predominately in the lung bases Rales invariably present Clubbing is common 26

27 27 Asbestos-Related Pleural Abnormalities DiseaseDescriptionTypical Symptoms Asbestos- related pleural abnormalities Occurs when asbestos fibers reach the lining of the lungs; pleura. Presence of asbestos fibers can cause various reactions in the lung linings, many which are pretty mild.

28 28 Asbestos-related Lung Cancer DiseaseDescription Typical Symptoms Lung cancer The same type of cancer caused by smoking and other factors None (until late stage) Sometimes: Cough, wheezing, and difficulty breathing

29 29 Asbestos-related Laryngeal Cancer DiseaseDescription Typical Symptoms Laryngeal cancer The same type of cancer caused by smoking and other factors Persistent hoarseness, chronic sore throat, painful swallowing, pain in the ear, lump in the neck

30 30 Mesothelioma DiseaseDescription Typical Symptoms Mesothelioma A type of cancer that affects the lining of the lungs or the lining of the abdomen None (until late stage) Sometimes: Cough, chest pain, and difficulty breathing

31 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.

32 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. 32

33 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. 33

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

35 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. 35

36 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 36

37 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

38 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.

39 Common denominator through which all occupational lung diseases aggravate: Tobacco smoking! 39

40 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

41 THANK YOU! 41

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