1. Ocupational Poisoning By : Dr ASLANI OCCUPATIONAL MEDICINE SPECIALIST 1

2. Content 2 DefinitionDefinition EtiologyEtiology Types of ToxicityTypes of Toxicity Lead Mercury

3. Introduction 3

4. Introduction 4

5. HEAVY METALS 5

6. CHEMICAL PESTICIDES 6

7. ORGANIC SOLVENTS 7

8. Gases and vapors 8

9. Types of Toxicity Acute toxicity Chronic toxicity Irritation and corrosivity Sensitization Carcinogenicity Reproductive toxicity

10. Types of toxicity continues Mechanisms of toxicity: Direct local toxicity to tissues first in contact with the substance Systemic effects due to the absorption of the substance

11. Occupational toxicity deals with the chemicals found in the place of work. Persons working in various industries may be exposed to various agents during the synthesis, or through their use during the occupation. 11

12. Lead 12

13. 13 Lead metal Soft Malleable Corrosion resistance Low melting point 13

14. Some Sources of Lead Exposure 14

15. Battery manufacturing Chemical industry Gasoline additives production Foundry workers Welders Jewelers Lead miners Pigment manufacturing Plastics industry Pottery workers Radiator repair Soldering of lead Rubber industry products Occupational exposure 15

16. Lead in the Environment Varies from place to place Soil near roadways Elevated in soil, water, or air near lead mining or smelting facilities Near smaller businesses and industries that involve lead

17. Routes of Entry Lead gets into the body by the following routes of entry: Inhalation (breathing) Ingestion (swallowing) Skin absorption 17

18. 18 Inhalation Inhalation is the primary route of entry for lead. – Occurs when lead dust or fume is released into the air and inhaled. welding on steel coated with lead-based paint Approximately 40 to 50 percent of the lead that is inhaled is absorbed into the body

19. Ingestion Lead-based paint was banned from residential because of lead poisoning in children. 19

20. Skin absorption Certain lead compounds can be absorbed through the skin (TEL). 20

21. Toxicology Absorption  Respiratory (30 to 40 % ):  Gastrointestinal systems: (10 to 15% ) adults < children  Cutaneous 21

22. Toxicology Increased Absorption: Deficient in calcium Iron Phosphorus zinc 22

23. Neurological Effects Health effects of lead Gastrointestinal Effects Heme Synthesis Renal Effects Reproductive Effects Other 23

24. Acute Inorganic Lead Toxicity 24 Acute Inorganic Lead Toxicity: Excessive exposure in brief period Acute lead poisoning syndrome. Classic clinical findings : Abdominal colic Constipation Fatigue hemolytic anemia CNS dysfunction. in profound case: Acute encephalopathy with Coma Convulsions papill edema In milder exposures : headaches personality changes

25. Acute Inorganic Lead Toxicity 25 Acute Inorganic Lead Toxicity: Abdominal colic (lead colic) it has sometimes been misdiagnosed as  appendicitis,  peptic ulcer,  biliary colic,  pancreatitis,  pelvic inflammatory disease

26. Chronic Inorganic Lead Toxicity Late effects : Chronic renal failure Hypertension Gout Chronic encephalopathy Classic abdominal colic of acute lead poisoning is absent. Symptoms: Arthralgias Headache Weakness Depression Loss of libido Impotence Sperm count dec. 26

27. Physical Exam 27 Lead line

28. 28 Heath Effects vs Symptomology Some workers may experience symptoms at lower blood lead levels while others may tolerate very high levels without showing symptoms

29. Organs and Systems Affected by Lead 29

30. Hematologic toxicity Anemia induced by lead : 30

31. Effects on the Nervous System Damage to the brain may also result in behavioral problems, i.e., Poor memory Reduced intelligence Instability of mood(40-70µg/dl) Visual disturbances Confusion Encephalopathy (a degenerative brain disease) may occur. 31

32. Effects on the Nervous System Peripheral neuropathy: – Weakness and/or paralysis of the hands or legs can cause "wrist drop" or "foot drop". – Motor-sensory neuropathy – Asymmetry  NEW Months to years of high dose lead exposure (eg, blood lead concentrations >80 μg/dL) may be associated with a predominantly motor peripheral neuropathy 32

33. Effects on the Kidneys Often damage is not detected until it’s too late Increase BUN and Cr. until 50-70%of the nephron destroyed. 33  NEW Months to years of high dose lead exposure (eg, blood lead concentrations >80 μg/dL) may be associated with a predominantly nephropathy characterized by interstitial fibrosis and nephrosclerosis.

34. Lead and hypertension Increase mortality heart disease and stroke 34

35. Effects on the Reproductive System Female Reproductive Health and Pregnancy: – Reduces fertility – Spontaneous abortion 35

36. Organic lead skin absorption Acute or sub acute CNS symptoms and signs (TEL): Early symptoms: insomnia, anorexia, muscle irritability severe poisoning: Agitated encephalopathy, delirium tremens, cerebellar signs( tremor, ataxia), increased DTR. CSF examination usually is normal. 36

37. LAB FINDING Whole blood lead concentration: is the most common and useful laboratory test to confirm exposure Noninvasive K x-ray fluorescence measurement of lead in bone: a biomarker of long-term cumulative lead exposure, is used predominantly as a research tool. Measurement of lead in urine following a dose of a chelating agent (chelation challenge testing): correlates satisfactorily in most cases with blood lead test results, and is seldom indicated in clinical practice. 37

38. LAB FINDING An elevation in erythrocyte protoporphyrin (often measured as zinc protoporphyrin or ZPP): reflects lead-induced inhibition of heme synthesis. Because there is a time lag of several weeks associated with lead-induced elevation in ZPP, the finding of a blood lead of ≥30 μg/dL with no concurrent increase in ZPP suggests that the lead exposure was of recent onset. 38

39. OSHA standard o whole BLL : o 1.every 6 months if BLL <40 µg/dl o 2.every 2 months If BLL>40 µg/dl until 2times BLL <40 µg/dl o 3.monthly during removal o Removal from exposure: o 1. worker BLL>60 µg/dl o 2. worker average BLL >50 µg/dl o 3. worker at risk of health impairment 39

40. OSHA standard  NEW Current OSHA lead standards that require medical removal from elevated workplace lead exposure when blood lead levels exceed 50 or 60 μg/dL were enacted several decades ago and offer insufficient protection 40

41. OSHA standard  NEW An expert panel in 2007 recommended that removal be initiated for a single blood lead level greater than 30 μg/dL, or when two successive blood lead levels measured over a 4-week interval are ≥20 μg/dL. The longer-term goal should be for workers to maintain blood lead levels <10 μg/ dL 41

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43. Primary Prevention of Lead Poisoning Engineering controls Substitution of less hazardous material Isolation via containment structure Ventilation via local exhaust system Personal protective equipment Respirator utilization Work practices Personal hygiene practices Periodic inspection/maintenance of control equipment 43

44. Mercury

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46. Exposure elemental mercury:is a liquid at room temperature with a substantial vapor pressure Inorganic mercury salts:(mercuric sulphide (HgS), mercuric oxide (HgO) and mercuric chloride (HgCl2)) organic mercury:  short-chain alkyl: methyl mercury salts  long-chain alkyl  non-alkyl organic compounds: phenyl mercury 46

47. General consideration Toxicity: Specific form and compounds Route of exposure Dose Age Bind to sulfhydryl groups and interfere with numerous cellular enzyme systems.

48. Elemental mercury Heavy shiny silver-white metal liquid or vapor at room temperature

49. Elemental mercury Occupational exposure: Extraction of mercury & silver & gold Burning fossil fuels (high- sulfur coal) Maintenance work on furnaces, flues Chloralkali production plants ( use of mercury in the electrolysis of salt) Dentist & dental technicians

50. Elemental mercury Absorption: Inhalation is major route of exposure (pulmonary retention is more than 80%) Skin and gastrointestinal absorption are poor (0.1%) Heating increase absorption Elimination : - urine

51. Elemental mercury Acute effect: Primarily affects the respiratory system ( MFF, bronchial irritation, chemical pneumonitis ) Gingivitis & stomatitis few weeks after recovery Residual restrictive impairment & ↓ DLCO ACD (rare)

52. Elemental mercury Chronic effects: Elemental mercury concentrated in CNS & kidneys Classic mercurialism :Primary target organs are Nervous system, Oral cavity and Kidneys

53. Elemental mercury Classic mercurialism (neuropsychiatry): Fine intention tremor of the extremities, tongue and lips (early sign of neurotoxicity) Erythrism :psychological disturbances, Irritability, Shyness, Memory loss, Hallucination Peripheral polyneuropathy (sensor motor axonopathy) with distal paresthesias DD x : Gilan- Barre

54. Exposure to Amalgam  Dental amalgam consists of ( by weight ): 50% mercury, 35% silver, 9% tin, 6% copper and a trace amount of zinc  Occupational exposure of dental personnel has been well documented.  Patients exposure to amalgam are small

55. Inorganic mercury More commonly found in nature Sulphide, oxide, chloride

56. Inorganic mercury Occupational exposure: Paint & dyes Tannery worker Wood preservative Taxidermy Medicine (antiseptic, diuretic)

57. Inorganic mercury  Absorption : skin & GI tract (10%)  Acute clinical effects : GI: Ingestion of mercuric chloride (HgCl2) May be lethal (suicide).Direct GI irritation with fluid loss and shock. Kidney: ARF, ATN

58. Organic mercury Non alkyl compounds (phenyl) Long-chain alkyl compounds Short-chain alkyl compounds ( methyl and dimethyl mercury )

59. Organic mercury Occupational exposure: Fungicides Bactericides Insecticides Farmer Wood preservatives

60. Organic mercury Absorption Alkyl Mercury Compounds: Readily absorbed through all routes skin, gastrointestinal (95%), inhalation concentrated in RBC & CNS SCA cross the placenta

61. Organic mercury Acute overdose: Paresthesias Ataxia Generalized weakness Visual & hearing impairment Tremor Muscle spasticity Coma Death

62. Renal effect The kidneys contain the highest concentration of mercury following exposure to inorganic salts of mercury and mercury vapor organic mercury has a greater affinity for the brain.

63. Biologic monitoring Exposure to elemental, inorganic or non S-C-A mercury compounds: Periodic measurement of mercury in 24-hour urine specimens. Exposure to S-C-A mercury compounds: Periodic assessment of mercury in whole blood.

64. Air exposureUrine LevelAction >50 µg/m³>100 µg/g cr  Remove from exposure until <50  Medical examination if over 150 or if two consecutive levels exceed 100  Repeat measurement weekly 50 µg/m³75-100 µg/g cr  Monitor weekly  Perform hygiene assessment to limit exposure 25-50 µg/m³50-75 µg/g crMonitor monthly 25 µg/m³35-50 µg/g crMonitor quarterly <25 µg/m³<35 µg/g crMonitor semiannually

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