metal poisoning

MetalsMetals

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.

toxic metals 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”. 

Distinguishing Physical Distinguishing Physical CharacteristicsCharacteristics

1. Ability to conduct electricity◦ Diminishes with increasing temperature

2. Excellent conductivity of heat3. High reflectivity of light from a polished

surface commonly known as metallic luster

4. Malleable ◦ Deform rather than shatter on impact or

under pressure

Cont…Cont…

5. Metal oxides reacts with water forming basic solutions – basic anhydrides or basic oxides

6. 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 strength

ARSENICARSENIC

ARSENICARSENIC

Widely distributed in soilUsed 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.

Mechanism of ToxicityMechanism of Toxicity

Irritants: skin, mucous membranes, respiratory and gastrointestinal tract

Once absorbed, arsenic disrupts cellular metabolism by binding to sulfhydryl groups on variety of enzyme

B. Known CARCINOGENB. Known CARCINOGEN

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 toxic

ToxicityToxicity

5 – 10% is excreted in the feces90% is excreted in the urineLethal dose is 120 to 200mg (very toxic)

Clinical PresentationClinical Presentation

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 loss

Cont…Cont…

2. Chronic exposureIrritation 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 cancers

TreatmentTreatment

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 charcoal

MERCURYMERCURY

MERCURYMERCURY

Several forms:Metallic (elemental) mercury

Extraction of gold and silver from oreDental amalgams Technical equipments

Mercury salts Antiseptics and stool preservativesDiuretics

Organic mercuryFungicides and anticepticsMethyl mercury may accumulate in sea waters after

environmental contamination

Mechanism of toxicityMechanism of toxicity

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

Organomercurial compounds are toxic to the CNS and methyl mercury is teratogenic

Toxic doseToxic dose

Acute toxicity depends largely on the form and route of exposure (inhalation, ingestion or percutaneous)

Chronic exposureChronic exposure

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

placentaHalf-life is 60 days

Cont…Cont…

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 skinHalf-life is 40 days

Cont…Cont…

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 daysMinamata Disease – Japan where there is

methylation of mercury salt waste

Clinical PresentationClinical Presentation

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 occur

Cont…Cont…

Chronic inorganic mercury poisoning (vapor)◦Causes permanent CNS toxicity, including

irritability, memory loss, shyness, depression, insomnia and tremor (erythism)

◦Gingivitis, stomatitis and salivation are common

Cont…Cont…

Acute organic mercury poisoningCauses parethesias, ataxia, visual and

hearing disturbances

DiagnosisDiagnosis

CBC, electrolytes, glucose, BUN, creatinine, liver function tests and urinalysis

Specific levelsNormal whole blood mercury is usually

below 10 ug/dL and normal urine level is below 50ug/dL

TreatmentTreatment

Supportive measures◦Vapor – oxygen◦Ingestion – IV fluid replacement and

hemodialysis for 1 to 2 weeks◦Monitoring of patient

DrugsDimercaprol 3-5 mg/Kg IM every 6 hoursOral penicillamine

ANTIMONYANTIMONY

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

Stibine (antimony hydride)Stibine (antimony hydride)

Colorless gas; rotten egg odor Formed when antimony is contacted with

acids

Mechanism of toxicityMechanism of toxicity

Antimony Binds with sulfhydryl groups and causes

inactivation of enzymesStibineHemolysis and irritates the URT

Clinical PresentationClinical Presentation

Acute ingestion◦Nausea, vomiting and diarrhea (often bloody)◦Hepatitis and renal insufficiency occur

Acute stibine inhalation◦Acute hemolysis anemia and jaundice,

hemoglobinuria and renal failureChronic exposure to dust and fumes

◦Headache, anorexia and dermatitis (antimony spots)

TreatmentTreatment

Antimony ◦IV fluid replacement

Stibine ◦May require blood transfusion

Drugs◦BAL and penicillamine

BISMUTHBISMUTH

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

Industrial usesIndustrial uses

Anti-syphilitic drugs and a component in cosmetic powders

Added in aluminum alloys, steels and other alloys

Toxicity Toxicity

Foul breathBlack line ate the alveolar marginsBlack spots seen in the mouth and throatStomatitisChronic: malaise, albuminuria, diarrhea

and dermatitishepatitis

LEADLEAD

Found in all animalsBatteriesPaints Pots and ceramicsLeaded gasoline

Under steady conditions 95% of lead is found in the red blood cells

In adults, 90% are stored in the bonesHalf-life is 24 to 40 days

Mechanism of toxicityMechanism of toxicity

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 system

THALLIUMTHALLIUM

Soft metal that quickly oxidizes upon exposure to air

Used in optical lenses, photoelectric cells Also used as rodenticides

Mechanism of toxicityMechanism of toxicity

Affects the mitochondria and a variety of enzymes resulting to cellular toxicity

Inhibit potassium flux across the membrane

Toxic dose is 12-15mg/KgMore soluble (thallous acetate and thallic

chloride) slightly more toxic than insoluble thallium (Thallic oxide and thallous iodide)

Clinical PresentationClinical Presentation

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 weeks

Chelating agentsChelating agents

Dimercaprol (BAL) ◦Diffuses into the erythrocytes and enhances

fecal and urinary excretionEDETATE (EDTA)

◦Administered through IV or IMSUCCIMER (dimercapto-succinic acid)

◦Water soluble orally administeredPENICILLAMINE

◦Only commercially available oral chelating agent