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Occupational health

Occupational health: Promotion & Maintenance of the highest degree of physical, mental & social wellbeing of workers in all occupations (WHO & ILO, 1950 & revised in 1995).
Occupational medicine: A branch of preventive medicine with some therapeutic function (Royal College of Physicians, 1978).

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Occupational health

  1. 1. Dr. Dalia El-Shafei Assist.Prof., Community Medicine Department, Zagazig University http://www.slideshare.net/daliaelshafei
  2. 2. 1) To define occupational health, occupational medicine, occupational disease, and work-related disease. 2) To demonstrate the difference between occupational medicine and clinical medicine. 3) To demonstrate occupational health services and the duties of occupational health professionals. 4) To enumerate and identify occupational hazards. 5) To recognize and diagnose different occupational diseases.
  3. 3. Promotion & Maintenance of the highest degree of physical, mental & social wellbeing of workers in all occupations (WHO & ILO, 1950 & revised in 1995).
  4. 4. A branch of preventive medicine with some therapeutic function (Royal College of Physicians, 1978). Industrial Medicine Occupational Medicine Occupational & Environmental Medicine
  5. 5. Health promotion for workers & proper prevention & ttt. Work environment & its adverse effects on workers’ health Health problems of workers at any workplace
  6. 6. More than 2,000,000 people die from work-related accidents or disease every year, equivalent to 1 death every 15 seconds. Progress in bringing occupational health to the industrializing countries is painfully slow. In the poorest countries, there has been no progress at all.
  7. 7. It is a disease arising out of or during the course of employment and its cause present in the occupation (e.g. silicosis). Worker has the right to receive medical care at the expense of the employer. Worker has the right for paid sick leave. If disability occurs, the worker has the right for compensation. Why its diagnosis is very critical?
  8. 8. Some diseases are not specially caused by exposures on job, but they are aggravated by occupational stressors. so it can be found in the general population (e.g. HPN). Work-related disease
  9. 9. Occupational health is concerned with physical, mental & social conditions of a worker in relation to his/her work & working environment as well as his/her adjustment to work & the adjustment of work to the worker.
  10. 10. Physician Hygienist Ergonomist Nurse Safety Engineer Epidemiologist
  11. 11. Occupational physician Designs & implements OH program Conducts medical exam. & biological monitoring Provides 1st aid & emergency ttt. Supervises the rehabilitative program for disabled workers Team leader
  12. 12. Assists the physician in providing medical services Assists in supervising the work environment Educates workers Keeps medical records
  13. 13. Occupational Health Program
  14. 14. Health Promotion Improvement of the health & working capacity of workers Improvement of work environment Hazard Prevention Medical Engineering Hygienic Hazard Control Medical examinations “pre-placement & periodic” ttt 1st aid Rehabilitation & Compensation
  15. 15. Adequate nutrition • Nutrition education & support • Prevention & control of parasitic diseases. Socioeconomic development • Improving workers' income • Proper expending of this income. Social welfare • Management of family problems. • Making good social relations at work. • Encouragement of sport activities. Health education & keeping good medical records
  16. 16. Good design of the machines Suitable housekeeping Proper lighting & ventilation Good control for physical hazards Washing facilities & suitable transportation means
  17. 17. Pre-employment medical exam. “PEME” Pre-placement exam. Periodic medical exam. “PME” Health education Immunization & chemoprophylaxis • Choose suitable worker. • Put the suitable worker in the suitable process. • Early detection of any health hazards arises from workplace. • Early symptoms & signs of occup. diseases • To combat any infectious disease.
  18. 18. Law specifies the periodicity of the PME for workers in each work or job “48 Occupational diseases”. It is either every 6 Ms or every 2 Ys depending on duration of exposure needed to develop the occupational disease. Workers may be temporally or permanently removed from further exposure or may be advised to continue work.
  19. 19. Mechanization of heavy work process to lighten the physical strain. Enclosure & segregation of hazardous process. Good ventilation, lighting & control of other physical hazards at workplace.
  20. 20. Providing good sanitary facilities as washing, changing clothes Supplying PPE as respirators, protective clothes, and ear muffs or plugs Work environment monitoring for detection & evaluation of environmental pollutants Ensuring that work legislations are applied & investigation of workers' absenteeism
  21. 21. Provides base line data about workers' health status Detection of any deviation from these data on subsequent PME.
  22. 22. OD can be identified in its early stage to prevent progression of the abnormal physiologic condition It includes: Survey “history of exposure & any abnormal symptoms or complains”. Clinical examination. Laboratory investigations Biologic monitoring for early detection of any disturbed physiologic function
  23. 23. Early ttt of diagnosed occupational diseases. 1st aid ttt of any occupational injuries.
  24. 24. Minimize or prevent the disability. Retraining the disabled worker for a new job suitable for his new physical & mental capacities. Compensation of disabled workers after evaluation of the disability resulted from occupational disease or accident & giving him some privileges.
  25. 25. To diagnose an OD, the nature of the worker's occupation & the cause of it must present in the occupation. So, if a worker in a factory of batteries suffered from exposure to lead toxicity (OD), but he works as driver away from exposure to lead, he will not be diagnosed as having an OD as John Stone reported in his book on occupational health. 48 ODs in the Egyptian law.
  26. 26. Occupational hazards Physical Chemical MechanicalBiological Psycho- social
  27. 27. Physical Temperature Radiation Noise Vibration Atmospheric pressure Electricity Chemical Metals Solvents Dusts & fumes Gases Pesticides Biological Bacteria Viruses Parasites Rickettsia Psychosocial Stress & PTSD Violence Long working hours Mechanical Wrong lifting Wrong movements Wrong postures Slippery floor or stairs
  28. 28. Systemic Heat cramps Heat exhaustion Heat stroke Skin Rash Burn Psychoneurotic Chronic heat fatigue Eye Cataract “U.V rays”
  29. 29. Excessive sweating & water intake without salt replacement causing hyponatremia. C/P: ttt: - Prevention by adequate salt intake - Supplementation with salts “oral or I.V. infusion”. - Control of hot environment to eliminate or minimize heat hazards. Severe painful cramps in muscles of limbs during work. Severe spasm at intestinal smooth muscles Headache, dizziness Body temperature “normal or slightly ↑”.
  30. 30. Excessive sweating, salt & water depletion without replacement causing heamo- concentration & hypovolemia & circulatory failure. C/P: ttt: - Removal of the patient to cool place. - Water & salt replacement. - ttt of shock. Headache, weakness, fatigue. Anorexia, vomiting. ↑ body temperature (<40 °C) & excessive sweating. Peripheral circulatory failure (Pallor, Cold moist skin, HPN, Weak rapid pulse).
  31. 31. Disturbance of heat regulating center at brain → heat retention → hyperpyrexia. C/P: ttt: - Rapid cooling of body by all possible means. - Removal of patient from the hot environment. - Symptomatic “sedatives or stimulants, I.V. saline, O2 inhalation, bed rest” Abrupt ↑ of body temperature (≥40°C). Flushed hot dry skin. Delirium, convulsion Coma & death
  32. 32. Blocking of sweat gland ducts → sweat retention & inflammatory reactions. C/P: ttt: - Removal to cooler environment. - Skin cleanliness to prevent infections. - Cool showers. - Mild drying & soothing lotions. Raised red vesicles on the affected skin. Prickling & itchy sensation on exposure to heat.
  33. 33. Noise is any unwanted or undesirable sound. Auditory field lies between 20-20000 hertz (Hz) or cycles/second. If noise is below the lower level of normal hearing (<20Hz) it is called infra sound but if the noise above the upper limit of normal hearing (>20kHz) it is called ultrasound.
  34. 34. Weaving Hammering of metals Military exposure due to explosions & shooting Building & construction Aviation & submarines
  35. 35. Duration of exposure Intensity of the sound Frequency of sound waves Type of noise “continuous or impact which is more dangerous” Personal susceptibility
  36. 36. NIHL Auditory effect • HR: ↑ or ↓ “type of noise”. • RR: often ↑. • Performance of psycho-motor tasks “↓or ↑”. • ↑ community mental illness. Non-auditory effects
  37. 37. Reduction of noise at source. Limit exposure with or without ear protectors. Routine monitoring of the place for noise level & the population at work for hearing ability “PME”.
  38. 38. Radiation is the straight line transport of energy through space or matter Electromagnetic or particulate radiation capable of producing ions, directly or indirectly when passing through matter. Ionizing radiation “IR” Electromagnetic radiation with a wave length not sufficient for ionization. Non ionizing radiation “NIR”
  39. 39. Mechanism of action: a) Ionization: is to ripe electrons away from atoms & molecules. b) Excitation of molecules. Electromagnetic radiation “EMR” • X- ray • Gama “γ”ray Corpuscular radiation • Alpha “α” particles “low power of penetration & great power of ionization”. • Beta “β” particles “greater power of penetration”. • Neutrons • Protons • Electrons.
  40. 40.  or X-rayNeutron
  41. 41. OH . (hydroxyl radical) H . Radiation Damage Water molecule -ray 2 OH .  H2O2 What happens when the water molecule is struck by the gamma ray?
  42. 42. Alpha Particles Stopped by a sheet of paper Beta Particles Stopped by a layer of clothing or less than an inch of a substance (e.g. plastic) Gamma Rays Stopped by inches to feet of concrete or less than an inch of lead Radiation Source Neutrons Stopped by a few feet of concrete:: 1:100:10,000
  43. 43. Uranium miners & atomic millers Nuclear reactors & atomic energy plant Radiologist Scientists using radioactive materials
  44. 44. Whole body irradiation Exposure to doses > 1Gy → acute radiation syndrome “Prodromal symptoms (nausea, vomiting) & bone marrow depression (leukaemia, anaemia, thrombocytopenia)”. Local irradiation Skin reactions according to the dose “mild erythema → tissue necrosis & ulceration”.
  45. 45. Chronic radiation sickness. Chronic radio- dermatitis: disturbed sensation, focal hyperkeratosis, congestive hyperaemia, painful cracks & ulceration with malignant changes. Eye cataract: starts at posterior pole of lens capsule. Carcinogenic & hereditary harm. Chronic effect
  46. 46. Working in compressed air that is too rapidly decompressed (Caisson disease). Divers who surface too rapidly from depths >10 m. Crew or paratroopers in aircraft who ascend too rapidly from sea level to heights >5487 m.
  47. 47. Manifestations of DSI are due to formation of nitrogen bubbles in body fluids & tissues. Site in which bubbles are formed • Site of symptoms Size & Rate of growth of bubbles • Severity of symptoms
  48. 48. Type I • Mild or severe limb pain. • Skin mottling or skin irritation. Type II • Paralysis or weakness, Tingling or numbness of the limbs, • Vertigo, Headache, coma • Dyspnea, chest pain, Hypotension.
  49. 49. Aseptic necrosis of the bones “dysbaric osteonecrosis”. Neurological or psychological symptoms.
  50. 50. Gradual decompression according to the well known standards Use of pressurized airplanes. Inhalation of helium/oxygen mixture instead of air by divers to avoid nitrogen narcosis. PEME: “exclude chronic sinusitis, otitis media, lung cysts or emphysema”. PME
  51. 51. ttt: recompressing the patient & reducing pressure in accordance with a protocol laid down in set of tables.
  52. 52. Pneumoconiosis or dusty lung = dust collection in the lung & the lung reaction to its presence.
  53. 53. Collagenous Non-collagenous (benign pneumoconiosis) • Fibrosis. • Permanent destruction of normal alveolar architecture • Silicosis • Asbestosis • Coal workers pneumoconiosis • Talcosis • Minimal reticular reaction. • Alveolar architecture intact. • Iron oxide: siderosis • Tin: stannosis • Barium: baritosis • Titanium: titanosis Types of pneumoconiosis
  54. 54. Investigations X-ray PFTs Autopsy & Biopsy C/P Symptoms ”D” Signs “3C” Occupational History
  55. 55. 1- Occupational history. 2- Clinical picture: a- Symptoms: -The most important is progressive dyspnea. -Melanoptysis in CWP. b- Signs: Cyanosis Clubbing Crepitations
  56. 56. (a) Chest X- ray: shows lung opacities, ILO classification of lung opacities include: * Small opacities: < 1cm Rounded Irregular P Q R Up to 1.5mm From 1.5 – 3mm From 3- 10mm S T U Fine opacities Medium sized opacities Coarse opacities
  57. 57. * Large opacities > 1cm A: area of opacity from 1-5 cm2 B: combined area of opacity < area of Rt. upper lobe. C: combined area of opacity > area of Rt. upper lobe. (b) Pulmonary function: restrictive or obstructive or mixed pattern. (c) Autopsy or biopsy: - Nature of the dust. - The pathological reaction in the lung.
  58. 58. Fibrotic lung disease due to inhalation of dust containing crystalline silicon dioxide (free silica) Miners or workers in tunnels Sand blasters Quarry workers Glass workers Ceramic workers
  59. 59. • Repeated exposure of low level of silica for >20 years. • Lung: Discrete fibrotic nodules of 2-3mm, mainly in upper lobes with whorled pattern. These nodules may coalesce together → Progressive massive fibrosis “PMF” → central ischemic necrosis with cavitation. • Pleura: thickening, fixed, hard with fibrotic nodules. Chronic classic silicosis • As classic but progress more rapidly. Accelerated silicosis • Inhaled high level of recently fractured quartz → immediate damage of the alveoli → acute alveolitis → fibrosis. Acute silicosis
  60. 60. • It needs 20 years to develop: • Early stages asymptomatic discovered accidentally by chest X-ray. • Progressive dyspnea. • Cough & sputum due to bronchitis. Chronic or Classic silicosis • As chronic silicosis but progress within shorter period. Accelerated • It is fatal. It develops in few weeks & progress in 1-3 years only. • Progressive dyspnea. • Massive proteinuria with renal failure. • Respiratory failure & death. Acute silicosis
  61. 61. History C/P X-ray PFTs
  62. 62. X- ray is the clue diagnostic tool. Pulmonary function tests: (restrictive pattern). • Small rounded opacities in the upper lung zones. • In massive fibrosis: bilateral opacities “cavitation if TB infection occurred”. • Egg shell calcification: Hilar & mediastinal LNs are enlarged & calcified. • Bilateral pleural thickening adjacent to pulmonary fibrotic nodules. Chronic silicosis • As chronic silicosis but progress more rapidly. Accelerated • Ground glass appearance. Acute silicosis
  63. 63. Complications Management TB “silicotuberculosis” Respiratory failure Emphysema Bronchitis Removal from exposure Corticosteroid Anti-TB drugs ttt of complications
  64. 64. Medical measures • PEME & PME. Engineering measures •Substitution of silica by safer material. •Enclosure of dusty processes. •Proper ventilation of the work place. Hygienic measures • Work place monitoring for keeping dust level ˂ threshold limit value (TLV). • Use of respiratory protective devices. • Avoid smoking.
  65. 65. Asbestos ore Asbestos fibers Naturally occurring fibrous minerals Good tensile strength Flexible Good insulation Heat resistant Electrical resistance Chemical resistant
  66. 66. - Chrysotile - “White asbestos” - Amosite - “Brown asbestos” - Crocidolite - “Blue asbestos” Most commonly used
  67. 67. Greatly ↑ during & after World War II in ship insulation. Use has greatly declined since the late 1970’s Pipe insulation Surfacing insulating materials Reinforcement of materials Fireproofing Acoustic & decorative plaster Textiles
  68. 68. Asbestosis Hyaline plaques in parietal pleura Asbestos warts Cancer: Pleura “Malignant mesothelioma”, Lung, larynx
  69. 69. Definition: diffuse interstitial pulmonary fibrosis which is usually accompanied by pleural fibrosis & thickening. Pathogenesis:
  70. 70. Clinical picture: Symptoms: progressive Dyspnea. Signs: Diagnosis: 1- History of exposure. 2- Clinical picture. Clubbing Cyanosis Crepitations “Bilateral basal” Limitation of the movement of the lower chest wall
  71. 71. Chest X-ray of a patient with asbestosis.
  72. 72. Complications Treatment Cancer lung Respiratory failure PH+ & core pulmonale Corticosteroid “relieve dyspnea” ttt of respiratory failure Stop smoking
  73. 73. Developed after 10 years. Non-malignant Bilateral yellowish well demarcated raised areas of hyaline fibrosis. X-ray: bilateral linear opacities parallel to ribs.
  74. 74. Latent period about 40 years. Most commonly affecting pleura > peritoneum Crocidolite “most involved type”.
  75. 75. Dose dependent Smoking is risk factor Long thin fibers (crocidolite) Adenocarcinoma type
  76. 76. Lung cancer causes the largest number of deaths from asbestos exposure. The risk greatly increases in workers who smoke.
  77. 77. Engineering Hygienic Medical • Substitution • Enclosure • Ventilation • Keeping asbestos dust concentration in work place below TLV. • PPE & Avoid smoking. • PEME & PME.
  78. 78. Chronic respiratory disease affecting proportion of workers involved in the manufacture of Cotton Flax Hemp Jute Sisal
  79. 79. Mechanical irritation • Short cotton fibers →Mechanic al irritation of airway epithelial surface → BC. Pharmacolog ical agents • Histamine in Cotton → BC. • Cotton dust inhalation→ liberate histamine. • Release of BC mediators from PNL “Slow reacting substance of anaphylaxis, Leukotriene, Platelet activation factors”. Immunologic mechanism “Massoud & Taylor” • Type III immune complex hypersensiti vity reaction. Chemotactic • Chemotaxis of P.N.L. Endotoxin activity Fungus enzymes
  80. 80. No specific abnormalities in lung & bronchi.
  81. 81. - Byssinosis usually requires 20-25 years to develop. - Symptoms appear on the 1st day back to work by chest tightness & breathlessness.
  82. 82. 1- History of exposure to cotton, flax, hemp. 2- Typical manifestations. 3- PFTs “Obstructive”: Forced vital capacity in 1st sec. (FEV1) Forced vital capacity (FVC). Forced expiratory flow (FEF) 25-75%. Peak expiratory flow rate (PEFR). FEV1/FVC%
  83. 83. Continuous dust conc. measurements PEME & PME: PFTs Cotton ttt before processing (washing, steaming, ttt with alkali)
  84. 84. Simple asphyxiants Nitrogen Methane CO2 Chemical ashyxiants Carbon monoxide (Co) Hydrogen cyanide (HCN) Hydrogen sulphide (H2S) Systemically active gases Arsine (Powerful hemolytic agent). Stibene (Hemolytic agent). Phosphine (Respiratory irritant & neurotoxic). Irritant gases Upper respiratory irritants: Highly soluble in water → dissolved in URT → irritation ”Ammonia (NH3) & SO2” Lung tissue irritants: Less soluble in water → penetrate deep to lung tissue “Chlorine – Phosgene - Fluorine - NOx- O3
  85. 85. Sources of incomplete combustion: • Furnaces, boilers • Internal combustion engine (warehouses, auto plants) Hazards increased in COLD weather with closed doors & windows.
  86. 86. Firefighters Kiln & furnace operators Garage mechanics Aircraft refuelers Truck Drivers Forklift operators Janitorial staff Disaster relief workers Miners Parking garage attendants Agricultural workers
  87. 87. Chronic exposure to CO NYC bridge & tunnel officers
  88. 88. Acute toxicity: depends on concentration of COHb in blood. Chronic toxicity: <10% No symptoms At 10% Headache 10-20% Headache, tinnitus, dyspnea 20-30% As above + nausea, vomiting 30-45% As above + confusion, coma > 50% Respiratory center depression & death Sleep disturbance, headache, memory loss. Arrhythmias Myocarditis Impaired ANS
  89. 89. Prevention & control Treatment Continuous environmental assessment PPE Smoking cessation program Removal from exposure O2 “100% or Hyperbaric” Blood transfusion Recommendation limits: TLV: CO in respirable air is 50 ppm & COHb in blood is 5g/100g Hb.
  90. 90. Uses: 1- Fumigant (rodenticide, insecticide). 2- Extraction of silver & gold. Mechanism of action: - HCN absorbed through the lung. - Excreted in urine & feces as thiocyanates. - It inhibits cytochrome oxidase enzymes.
  91. 91. Toxicity . Headache, Confusion, Nausea, Vomiting, Rapid weak respiration, Convulsions, Coma & Death. Acute Neurathenia Psychic alterations Allergic dermatosis Chronic
  92. 92. Treatment Removal from exposure Amyle or Na nitrite inhalation Na thiosulfate IV infusion Di cobalt EDTA (600 mg IV) & Na thiosulfate
  93. 93. Uses: - Manufacture pipes, sheet metals and foil. - In paints, enamels and glazes. Inlet to the body: Through inhalation of dust & fumes. Also, ingestion & absorption through the skin (by organic compounds) may occur.
  94. 94. A- Distribution in the body: - Bound to RBCs, membranes. - Precipitate in bone, teeth. - Exist in the plasma. B- Excretion: - Almost via the kidney. - Small amount excreted through bile. - Sweat & milk.
  95. 95. What are the Normal levels of lead??  Adults: <20 micrograms/dL of lead in the blood  Children: <5 micrograms/dL of lead in the blood
  96. 96. Vomiting, diarrhea. Abdominal colic. Constipation. G.I.T Headache. Psychiatric disturbances Tremors Mania, loss of weight. Nervous system Disturbance in haemosynthesis. Anemia is due to: -Direct effect on RBCs. -↓ life span of RBCs. Blood
  97. 97. Prevention: Engineering control measures Good industrial hygiene Regular clinical examination & investigation
  98. 98. Treatment of lead poisoning: Identification of source of lead poisoning. Removal from exposure Chelation therapy • Symptomatic patient with BLL >100 µg/dl. • Ca EDTA and/ or oral penicillamine.
  99. 99. The term "ergonomics" is derived from 2 Greek words: "ergo = work" & "nomi = natural laws”. Ergonomists study human capabilities in relationship to work demands. It is the application of knowledge as regards human abilities & limitations to the design of tools, machines, tasks etc.
  100. 100. All work activities should permit the worker to adopt several different, but equally healthy & safe postures. Where muscular force has to be exerted it should be done by the largest appropriate muscle groups available. Work activities should be performed with the joints at about mid-point of their range of movement. This applies particularly to the head, trunk, & upper limbs.
  101. 101. Repeated exertions Lack of balance between rest & activities Awkward & extreme postures Psychosocial stressors Mechanical stressors Extreme temperature
  102. 102. The following symptoms may be found: • These symptoms may not appear immediately because they develop over weeks, months, or years. By then, the damage may be serious. Tingling Joint swelling ↓ ability to move ↓ grip strength Pain from movement, pressure, or exposure to cold or vibration