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1. Metals

2.  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.

3.  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.

4.  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

5. 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.

6. 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”.

7. 1. Ability to conduct electricity
◦ Diminishes with increasing temperature
1. Excellent conductivity of heat
2. High reflectivity of light from a polished
surface commonly known as metallic
luster
3. Malleable
◦ Deform rather than shatter on impact or
under pressure
Distinguishing Physical
Characteristics

8. 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
Cont…

9. AR

10. 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

11. Irritants:skin, mucous membranes,
respiratory and gastrointestinal tract
Once absorbed, arsenic disrupts cellular
metabolism by binding to sulfhydryl
groups on variety of enzyme
Mechanism of Toxicity

12. 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
B. Known CARCINOGEN

13. 5 – 10% is excreted in the feces
90% is excreted in the urine
Lethal dose is 120 to 200mg (very toxic)
Toxicity

14. 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
Clinical Presentation

15. 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 cancers
Cont…

16. 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
Treatment

17. MERCURY

18. 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 contamination
MERCURY

19. 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 teratogenic
Mechanism of toxicity

20. Acute toxicity depends largely on the form
and route of exposure (inhalation,
ingestion or percutaneous)
Toxic dose

21. 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 days
Chronic exposure

22. 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 days
Cont…

23. 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 waste
Cont…

24. 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
Clinical Presentation

25. 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…

26. Acute organic mercury poisoning
Causes parethesias, ataxia, visual and
hearing disturbances
Cont…

27. CBC, electrolytes, glucose, BUN,
creatinine, liver function tests and
urinalysis
Specific levels
Normal whole blood mercury is usually
below 10 ug/dL and normal urine level is
below 50ug/dL
Diagnosis

28. 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 penicillamine
Treatment

29. ANTIMONY

30. 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

31. Colorless
gas; rotten egg odor
Formed when antimony is contacted with
acids
Stibine (antimony hydride)

32. Antimony
Binds with sulfhydryl groups and causes
inactivation of enzymes
Stibine
Hemolysis and irritates the URT
Mechanism of toxicity

33. 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

34. Antimony
◦ IV fluid replacement
Stibine
◦ May require blood transfusion
Drugs
◦ BAL and penicillamine
Treatment

35. BISMUTH

36. 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

37. Anti-syphilitic
drugs and a component in
cosmetic powders
Added in aluminum alloys, steels and
other alloys
Industrial uses

38. Foul breath
Black line ate the alveolar margins
Black spots seen in the mouth and throat
Stomatitis
Chronic: malaise, albuminuria, diarrhea
and dermatitis
hepatitis
Toxicity

39. LEAD

40. Found in all animals
Batteries
Paints
Pots and ceramics
Leaded gasoline

41. 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

42. 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
Mechanism of toxicity

43. THALLIUM

44. Soft metal that quickly oxidizes upon
exposure to air
Used in optical lenses, photoelectric cells
Also used as rodenticides

45. Affects the mitochondria and a variety of
enzymes resulting to cellular toxicity
Inhibit potassium flux across the
membrane
Mechanism of toxicity

46. Toxic dose is 12-15mg/Kg
More soluble (thallous acetate and thallic
chloride) slightly more toxic than insoluble
thallium (Thallic oxide and thallous iodide)

47. 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
Clinical Presentation

48. 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
agent
Chelating agents