Metal poisoning
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Metal poisoning






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Metal poisoning Metal poisoning Presentation Transcript

  • Metals
  •  Toxic metals are metals that form poisonous soluble compounds and have no biological role, or are in the wrong form[ Toxic metals comprise a group of minerals that have no known function in the body and, in fact, are harmful. Today mankind is exposed to the highest levels of these metals in recorded history. This is due to their industrial use, the unrestricted burning of coal, natural gas and petroleum, and incineration of waste materials worldwide. Toxic metals are now everywhere and affect everyone on planet earth. They have become a major cause of illness, aging and even genetic defects.
  •  toxicmetals sometimes imitate the action of an essential element in the body, interfering with the metabolic process to cause illness. Toxicity is a function of solubility. Insoluble compounds as well as the metallic forms often exhibit negligible toxicity. In some cases, organometallic forms, such as dimethyl mercury and tetraethyl lead, can be extremely toxic. Decontamination for toxic metals is different from organic toxins: because toxic metals are elements, they cannot be destroyed. Toxic metals may be made insoluble or collected, possibly by the aid of chelating agents.
  •  Minerals are the building blocks of our bodies. They are required for body structure, fluid balance, protein structures and to produce hormones. They act as co-factors, catalysts or inhibitors of all enzymes in the body. Copper and iron, for example, along with other minerals are required for the electron transport system, and thus needed for all cellular energy production.Minerals are classified into four groups:The macrominerals, or those needed in large quantity, ◦ calcium, magnesium, sodium, potassium, phosphorus, sulfur, iron, copper and zinc. Required trace minerals ◦ manganese, chromium, selenium, boron, bromine, silicon, iodine, vanadium, lithium, molybdenum, cobalt, germanium
  • Possibly required trace minerals ◦ fluorine, arsenic, rubidium, tin, niobium, strontium, gold, silver and nickel.Toxic metals ◦ beryllium, mercury, lead, cadmium, aluminum, antimony, bismuth, barium, uranium and others.Minerals needed in lesser quantities are usually toxic in greater amounts. ◦ Examples are copper, iron, manganese, selenium and vanadium.Even calcium and sodium are quite toxic in excess.
  • Today mankind is exposed to the highest levels in recorded history of lead, mercury, arsenic, aluminum, copper, nickel, tin, antimony, bromine, bismuth and vanadium.Dr. Henry Schroeder, MD ◦ “Most organic substances are degradable by natural processes. However, no metal is degradable…they are here to stay for a long time”.
  • 1. Ability to conduct electricity ◦ Diminishes with increasing temperature1. Excellent conductivity of heat2. High reflectivity of light from a polished surface commonly known as metallic luster3. Malleable ◦ Deform rather than shatter on impact or under pressureDistinguishing PhysicalCharacteristics
  • 5. Metal oxides reacts with water forming basic solutions – basic anhydrides or basic oxides6. Metals combine with non-metal to form ionic compounds ◦ Metals can be fused with other metals to form new metallic compounds called ALLOYS  hard, tough, resistance to corrosion and with mechanical strengthCont…
  • AR
  • Widely distributed in soilUsed as weed killers, wood preservatives, pesticides, rodenticides and hardening agentsExposure may be during production of pigments, glass and silicon chips and smelting of copper ores.ARSENIC
  • Irritants:skin, mucous membranes, respiratory and gastrointestinal tractOnce absorbed, arsenic disrupts cellular metabolism by binding to sulfhydryl groups on variety of enzymeMechanism of Toxicity
  • A. Arsenic compounds may be organic or inorganic Pentavalent (arsenate) ◦ Ubiquitous in nature, rapidly excreted by the kidneys Trivalent (arsenite) ◦ Absorbed more readily and are found in concentration in the leukocytes ◦ Crosses the placenta but not the blood brain barrier ◦ Highly toxicB. Known CARCINOGEN
  • 5 – 10% is excreted in the feces90% is excreted in the urineLethal dose is 120 to 200mg (very toxic)Toxicity
  • 1. Acute exposure ◦ Symptoms occur rapidly after ingestion (throat and abdominal pain) ◦ Vomiting and profuse diarrhea: profound fluid and electrolyte loss may cause death within 24 hours ◦ Delirium and coma have been reported ◦ Survivors may develop peripheral sensory neuropathy, exfoliative dermatitis and hair lossClinical Presentation
  • 2. Chronic exposureIrritation of the skin and mucous membrane and respiratory tract with occasionally perforation of the nasal septumSystemic effects: weakness, anorexia, nausea, vomiting, diarrhea, hepatitis, peripheral sensory neuropathy and alopeciaSkin hyperpigmentation and transverse white lines on the nails (MEES LINES)Associated to lung and skin cancersCont…
  • BAL or Dimercaprol is administer 3- 5mg//Kg intramuscularly every 4 to 6 hoursOral chelation therapy may be given with penicillamine after patient has been stabilizedDecontamination by ◦ inducing emesis or performing gastric lavage ◦ Administration of activated charcoalTreatment
  • Several forms: Metallic (elemental) mercury  Extraction of gold and silver from ore  Dental amalgams  Technical equipments Mercury salts  Antiseptics and stool preservatives  Diuretics Organic mercury  Fungicides and anticeptics  Methyl mercury may accumulate in sea waters after environmental contaminationMERCURY
  • Mercury reacts with sulfhydryl groups – binding to proteins and causes to inactivate enzymesMetallic mercury vapor is well absorbed by the CNS ◦ Irritates the lungsInorganic mercuric salts are highly corrosives to the skin, eyes and GIT ◦ NephrotoxicOrganomercurialcompounds are toxic to the CNS and methyl mercury is teratogenicMechanism of toxicity
  • Acute toxicity depends largely on the form and route of exposure (inhalation, ingestion or percutaneous)Toxic dose
  • Metallic mercuryvapor ◦ PEL is 0.05 mg/cu.m as an 8 hour time weighed average ◦ IDLH is 28 mg/cu.mCrosses the blood brain barrier BBB and placentaHalf-life is 60 daysChronic exposure
  • Inorganic mercuric salts ◦ LD of mercuric chloride is 1mg ◦ Accumulates primarily in the kidneys ◦ Distributed in the liver, red blood cells, bone marrow, spleen, lungs, intestines and skinHalf-life is 40 daysCont…
  • Organic mercury compounds ◦ Highly lipid soluble and freely passes through the placenta and blood brain barrier and enters the breast milkHalf-life is 70 daysMinamata Disease – Japan where there is methylation of mercury salt wasteCont…
  • Acute inhalation of high concentration of metallic mercury vapor may cause severe chemical pneumonias and noncardiogenic pulmonary edemaAcute ingestion of inorganic mercuric salts causes vomiting, diarrhea (often bloody) and shock ◦ Renal failure occurs within 24 hours (proteinuria and hematuria ◦ Hepatitis may occurClinical Presentation
  • Chronic inorganic mercury poisoning (vapor) ◦ Causes permanent CNS toxicity, including irritability, memory loss, shyness, depression, insomnia and tremor (erythism) ◦ Gingivitis, stomatitis and salivation are commonCont…
  • Acute organic mercury poisoningCauses parethesias, ataxia, visual and hearing disturbancesCont…
  • CBC, electrolytes, glucose, BUN, creatinine, liver function tests and urinalysisSpecific levelsNormal whole blood mercury is usually below 10 ug/dL and normal urine level is below 50ug/dLDiagnosis
  • Supportive measures ◦ Vapor – oxygen ◦ Ingestion – IV fluid replacement and hemodialysis for 1 to 2 weeks ◦ Monitoring of patientDrugsDimercaprol 3-5 mg/Kg IM every 6 hoursOral penicillamineTreatment
  • Widely used as hardening agent in soft metal alloysColoring agents in dyes, varnishes, paints and glassesOrganic antimony compounds are used as antiparasitic drugs
  • Colorless gas; rotten egg odorFormed when antimony is contacted with acidsStibine (antimony hydride)
  • AntimonyBinds with sulfhydryl groups and causes inactivation of enzymesStibineHemolysis and irritates the URTMechanism of toxicity
  • Acute ingestion ◦ Nausea, vomiting and diarrhea (often bloody) ◦ Hepatitis and renal insufficiency occurAcute stibine inhalation ◦ Acute hemolysis  anemia and jaundice, hemoglobinuria and renal failureChronic exposure to dust and fumes ◦ Headache, anorexia and dermatitis (antimony spots)Clinical Presentation
  • Antimony ◦ IV fluid replacementStibine ◦ May require blood transfusionDrugs ◦ BAL and penicillamineTreatment
  • Hard brittle, lustrous pinkish silver-white metal which is usually covered with a film of bismuth oxideGood conductor of electricity but a poor conductor of heatTrioxides are present in areas as an impurity in manufacturing lead and copper
  • Anti-syphilitic drugs and a component in cosmetic powdersAdded in aluminum alloys, steels and other alloysIndustrial uses
  • Foul breathBlack line ate the alveolar marginsBlack spots seen in the mouth and throatStomatitisChronic: malaise, albuminuria, diarrhea and dermatitishepatitisToxicity
  • LEAD
  • Found in all animalsBatteriesPaintsPots and ceramicsLeaded gasoline
  • Under steady conditions 95% of lead is found in the red blood cellsIn adults, 90% are stored in the bonesHalf-life is 24 to 40 days
  • Lead displaces other metals such as iron, zinc and copper from normal binding sites to produce some of its biochemical effectBinds to sulfhydryl groups and disrupt cellular metabolismPrimary organs affected are CNS and kidneys and the reproductive and hematopoietic systemMechanism of toxicity
  • Soft metal that quickly oxidizes upon exposure to airUsed in optical lenses, photoelectric cellsAlso used as rodenticides
  • Affects the mitochondria and a variety of enzymes resulting to cellular toxicityInhibit potassium flux across the membraneMechanism of toxicity
  • Toxic dose is 12-15mg/KgMore soluble (thallous acetate and thallic chloride) slightly more toxic than insoluble thallium (Thallic oxide and thallous iodide)
  • Acute: abdominal pain, vomiting and diarrhea  shockChronic: muscle weakness and atrophy; hair loss and nail dystrophy (MEES lines) may appear in 2 to 4 weeksClinical Presentation
  • Dimercaprol (BAL) ◦ Diffuses into the erythrocytes and enhances fecal and urinary excretionEDETATE (EDTA) ◦ Administered through IV or IMSUCCIMER (dimercapto-succinic acid) ◦ Water soluble orally administeredPENICILLAMINE ◦ Only commercially available oral chelating agentChelating agents