Ce diaporama a bien été signalé.
Nous utilisons votre profil LinkedIn et vos données d’activité pour vous proposer des publicités personnalisées et pertinentes. Vous pouvez changer vos préférences de publicités à tout moment.

Occupational heart diseases

Two important facets of cardiac disease as it relates to health at work. Agents used in the workplace may produce toxic effects manifested as heart disease or dysfunction. Possibly more important, however, is the effect that heart disease (common in Western society) has on the ability to work.

  • Soyez le premier à commenter

Occupational heart diseases

  1. 1. OCCUPATIONAL HEART DISEASES Dr. Dalia Abdallah El-Shafei Lecturer, Community medicine department, Zagazig University
  2. 2. OCCUPATIONAL HEALTH & THE HEART  Primary causes of disease  Exacerbations of underlying disease  Attribution & workers’ compensation  Work capacity & abilities  Workplace as focus for prevention efforts Workplace exposures & their effects on the heart Cardiovascular health & its effects on work 1-3% of CVD deaths are work-related.
  3. 3. PROBLEMS IN IDENTIFICATION OF OCCUPATIONAL ETIOLOGIES OF CVD  Common in our society: Increased risks superimposed on high baseline  Multifactorial etiology: Work contributions difficult to tease out  Long latency  No accurate noninvasive tests for early disease  Similar Clinical expressions with non- occupational cause
  4. 4. AGENT & WORK EFFECTS ON THE HEART Angina CO + Nitrates+ Temp Atherogenesis CS2 Dysrhythmias Solvents Cardiomyopathy Co + As Hypertension Pb + CS2 + Noise
  5. 5. • Extremes of Temperature • Noise - Vibration. • Radiation - Electricity. Physical • CO - CS2 • Nitrates - Solvents - OPC+Carbamates • Heavy metals (As, Pb, An, Co, Cd) Chemical Biological • Psychological Stress + Shift Work • Sedentary Work Psychologic al • Brucellosis (Subacute bacterial endocarditis)
  6. 6. When you smell an odorless gas, it is probably carbon monoxide.
  7. 7. Sources of incomplete combustion: • Furnaces, boilers • Internal combustion engine (warehouses, auto plants) Hazards increased in COLD weather with closed doors & windows
  8. 8. AT RISK OCCUPATIONS  Fire fighters  Garage mechanics  Aircraft refuelers  Truck Drivers  Kiln & furnace operators  Forklift operators  Janitorial staff  Disaster relief workers  Miners  Parking garage attendants  Agricultural workers
  9. 9. Chronic exposure to CO associated with cardiovascular mortality: NYC bridge & tunnel officers ??? Atherosclerosis
  10. 10. DIHALOMETHANES ”“METHYLENE CHLORIDE & BROMIDE
  11. 11.  Solvent: degreasing, paint stripping  Absorption through respiratory route or through skin  Metabolized in bloodstream to …… CO METHYLENE CHLORIDE (CH2CL2)
  12. 12. May elevate COHb to 10% or more especially in poorly ventilated space Probably not significant to healthy person; may become mildly symptomatic Cigarette smokers, those with angina or current CHD a concern: excess CO may trigger symptoms METHYLENE CHLORIDE
  13. 13. Methylene Chloride OSHA Standard: 25 ppm/ TWA8: STEL 125 ppm NIOSH: As low as can be achieved (carcinogen) Because of metabolic conversion to CO, the biological life of COHb from methylene chloride is longer than that from direct CO exposure !
  14. 14. CO HALF LIFE Ambient air 5 hs. 100% O2 1 h. Hyperbaric O2 15-30 min.
  15. 15. % COHb = % CO in air X Time X K At Rest 3 Light physical work 5 Heavy physical work 11
  16. 16. CARBON MONOXIDE  CARBOXYHEMOGLOBIN  Binds to Hb more avidly than O2 (200x)  Shifts oxygen dissociation curve to “left”: Tissue anoxia  Binds mitochondrial enzymes & myoglobin (50x)  Increases platelet stickiness  Deceases arrhythmia threshold
  17. 17. CARDIOVASCULAR PHYSIOLOGICAL CHANGES ↓COP + Threshold for VF. ↑Myocardial LDH
  18. 18.  2-4%→↓exercise tolerance esp. in COPD.  6%→↑ Multiple vent. Premature cont. after exercise + arrhythmias in MI.
  19. 19. Carbon monoxide: Exposure limits NIOSH REL: 35 ppm for 10-hour TWA Equivalent to 5% COHgb level OSHA PEL: 50 ppm /TWA8 ACGIH: TLV® : 25 ppm/ TWA8 .
  20. 20. NITRATES
  21. 21. Explosive industry: - Ammonium - Na nitrate - Ethylene glycol dinitrate - Nitroglycerine. - Di- & Tri-nitrotoluene
  22. 22. Acute effects in workers noted in early 1960s: Sudden death: 24-96 hours after exposure ceased (weekends/holidays) “Monday Morning Angina”: Relieved by RTW, nitrate meds: coronary spasm in absence of CAD 3 -fold increase in acute deaths in younger men from IHD
  23. 23.  Potent VD → Throbbing headache ("NG head" or "bang head“ or “ Powder head”) + Tachycardia + Palpitation → Tolerance → Withdrawal (Weekend, vacations) → Rebound VS → Monday Morning Angina + Monday Morning death.  Family members (Take home exposure)  MetHb → IHD  PN
  24. 24. CARBON DISULFIDE (CS2)
  25. 25. • Cellulose-derived materials • Rayon • Cellophane • Solvent for rubber, oils • Pesticides • Fumigant for grain, books • Microelectronics industry
  26. 26. Wood Flakes Raw Cellulose Cellulose Xanthate Viscose Filtering “Ripening” SpinningRayon Filaments Zn++ H2SO4 CS2 CS2Lye CS2 H + Solution Viscose process for Rayon manufacture
  27. 27. Cellulose flakes after lye treatment Viscose emerging from spinneret. CS2 is given off when viscose cross- links to form rayon
  28. 28. RR of 2 to 5x for death from CAD Direct role in atherogenesis in blood vessels ↑ LDL Enzyme inhibition by metabolites of CS2 {Dithiocarbamates & carbonyl sulfate (COS)}. • React with amino acids to form dithiocarbamates: these chelate trace metals & react with enzyme cofactors • Interfere to ↑ elastase activity, disrupting Bl.vessel walls • ↓ fibrinolytic activity & enhance thrombosis CARBON DISULFIDE & ATHEROGENESIS
  29. 29. Japanese CS2 workers Retinal hemorrhages Retinal microaneurysms
  30. 30. CARBON DISULFIDE OSHA Standard: 20 ppm TWA8 ????? NIOSH REL: 1 ppm TWA10 STEL: 15 ppm/15 minutes
  31. 31. NOISE Bulldozer: 85dBA Quite Room: 30 dBA Normal Conversation: 50 dBA Normal City Noises: 65 dBA Artillery/Good Rock Band: 120 dBA
  32. 32. ↑EPINEPHERINE + HYPERLIPEDAEMI A
  33. 33. Each ↑5 dB → ↑ 0.5 mmHg in systolic Bl.pr
  34. 34. 42 Moderate vibration High vibration  impact wrenches  carpet strippers  chain saws  percussive tools  jack hammers  scalers  riveting or chipping hammers • grinders • sanders • jig saws HAND ARM VIBRATION SYNDROME “HAVS”
  35. 35. 43 HAV SYMPTONS  Attacks of whitening (Blanching) of one or more fingers when exposed to cold/wet  Tingling & Numbness in the fingers  Loss of light touch  Pain & cold sensations between periodic white finger attacks  Loss of grip strength  Bone cysts in fingers and wrists
  36. 36. PERIPHERAL VASCULAR DISEASE  Amplification of response of α2- adrenoreceptors, norepinepherine constriction receptors on vascular smooth muscle cells in hand blood vessels.  Chronic PN.  ↑ Blood viscosity.
  37. 37. HVlab
  38. 38. EXTREMES OF TEMPERATURE  Acute coronary artery disease → IHD → Angina + MI  Exacerbate heart problems.  Atherosclerosis  Idiopathic dilated cardiomyopathy.  Cold → Slow myocardial repolarization + VF
  39. 39. CFC & SOLVENTS & PESTICIDES  Chlorofluorocarbons (Freon® etc) • Refrigeration, air conditioning, propellants. • ↑ Myocardial sensitiivity to catecholamines effects (↑ with Noise) • Direct myotoxic action • Occasional deaths (excess physical activity near leaking refrigerants).
  40. 40.  Other solvents implicated in sudden death (first noted in solvent abusers & glue sniffers):  Trichloroethylene, Trichloromethan, Perchloroethylene, Toluene, Benzene, Xylene, Gasoline.  Halogenated derivatives of aliphatic hydrocarbons are more active than corresponding hydrocarbons (Tetrachloroethan more active than Ethan)
  41. 41. Arrhythmias Sinus brady- or - tachycardia HB Vent. Tachycardia (torsade de pointes) Prolonged Q-T segment
  42. 42. ↓ FEV1 Hypoxic effect on heart Co- inflammation in Coronary artery Atherosclerosis Pre- existing HF Cigarette smoking Obesity Sedentary life
  43. 43. Asbestosis (3-fold ↑ for IHD risk), mainly with calcified plaques.
  44. 44. COBALT  Cobalt: used to stabilize beer foam (1960’s: Canada, Belgium)  Cardiomyopathy reported in beer drinkers several months afterward (Quebecois beer drinkers)
  45. 45. Dose-related: seen in heavy drinkers greatest risk in those drinking >10L/day (!) 22 - 50% mortality in some series Why this group????? CM not seen in cobalt therapy for anemia Probable synergistic effect with Alcohol & Poor Diet
  46. 46. ARSENIC  Cardiomyopathy (beer drinkers of As contaminated beer “2-4 ppm”) → congestive HF  Peripheral vascular disease: - 0.8-1.8 ppm As contamination of drinking water in Chile & Taiwan “Normal <0.01” → Black foot syndrome “Arteriosclerosis + Thrombangitis obliterans + Hyperpigmentations + Keratosis + Gangrene”  HTN  IHD “2-3 fold ↑”  Vasospastic “Raynaud” disease.  Arrhythmias “ Torsade de pointes”
  47. 47. ANTIMONY&CADMIUM&LEAD Lead:  HTN, probable mechanism is via renal injury  May also increase vascular tone and resistance Chelation may improve HTN in acute intoxication, but not reverse with longstanding renal damage Cadmium  HTN; occur at levels below nephrotoxic dose Antimony
  48. 48. JOB STRAIN Main associations are with exposure to high psychological demands and low control over job
  49. 49.  10% of CVD.  HTN “ Bus drivers”
  50. 50. Shift work
  51. 51. SEDENTARY WORK Physical Activity Work- time (Anaerobic) ↑CAD Leisure-time (Aerobic) ↓CAD
  52. 52. SOCIAL CLASS & CVD Increased CHD mortality related to social status. Unskilled manual workers (Class V) have considerably increased risk when compared with professionals (Class I) 50 70 90 110 130 150 170 190 I II III IV VSTANDARDIZEDMORTALITYRATIO

×