1|CC2 LEC 13

TRACE ELEMENTS DIFFERENT TRACE ELEMENT

→ Compound in the body which are found in a very small ESSENTIAL→ Trace elements which has specific health
amount, that is why it is called as such. It could either be effect in terms of deficiency, so if it is deficiency and
classified as ESSENTIAL OR NON-ESSENTIAL toxicity, it means that this is an essential trace element

→ ESSENTIAL – whenever they are needed for the NON-ESSENTIAL – just pure toxicity
different processes in the body, → One basic
ALUMINUM → NON-ESSENTIAL TRACE ELEMENTS
characteristic of an element to be considered as essential
is that essential trace elements cause DEFICIENCY → it • Crystalline silver white ductile metal
results to deficiency if you have low intake of this • Most abundant metal in the earth’s crust
particular trace element, it means that deficiency of this
particular element would impair several biochemical and → usually, aluminum is bind to oxygen, silicon, and
functional processes in the body and the means to fluorine (antacids)
alleviate deficiency would be through replacement of the
• Oxygen, silicon & fluorine
element
• Obtain in Aluminum containing (materials)
→ NON-ESSENTIAL – not really required by the different minerals
cells in the body so this are considered to be of no → Characteristics:
medical significance and considered to be TOXIC.
• Good conductivity of heat & Electricity
→ ESSENTIAL: CLINICALLY IMPORTANT o Could be used in welding because it
TRACE ELEMENTS
could be easily welded it has tensile
→ HEALTH EFFECTS, TOXICITY AND
strength and lightweight, and it is used
DEFICIENCY → Seen if clinically important or as a coating because it provides a
if the element is essential but for the corrosion resistant oxide coat
→ NON-ESSENTIAL: is the toxic one, which is
primarily we will only be focusing on the health → USED: mostly the utilization of our aluminum is more
effects and the toxicity. There is no deficiency on the industrial and household use
corresponding to those or considered to be non-
essential → aluminum would be seen in soda cans, beverage cans,
pots and pans in our homes and the roofing of the
→ LABORATORY METHODS AND
INSTRUMENTATION houses, it can also be seen and use in the utilization such
o Iron, copper and zinc – mg/L/ppm as being used as an alum metal or aluminum water
o Ultra-trace – selenium, chromium, treatment, alumina abrasive
manganese – ug/L / ppb
→ In terms of clinical used: aluminum is a significant
METHODS AND INSTRUMENTATION composition of antacids as well astringents and buffered
aspirin and also in some other cosmetics and in anti-
• Atomic Absorption Spectrometer (AAS) perspirants
• Atomic Emission Spectrometer (AES)
• Flame Atomic Absorption Spectroscopy → In terms of how we absorb aluminum in the body:
(FAAS)
• through ingestion or through inhalation but for
• Graphite Furnace Atomic Absorption
aluminum there is no indication dermal
Spectroscopy [GFAAS])
absorption is applicable
• Inductively Coupled Plasma Atomic Emission
Spectroscopy (ICP-AES) → Absorption efficiency of aluminum in our body is
• Inductively Coupled Plasma Mass dependent on the chemical form (transferrin) if what type
Spectrometry (ICP-MS) of aluminum we are exposed to, the particle size if we are
looking for the inhalation which is the reason or route
administration and as well as the concurrent dietary
exposure
2|CC2 LEC 13
• chelators→ these are compounds which binds → Signs and symptoms of aluminum toxicity would be
with a particular substance, some chelator which including:
connected to aluminum would be the citric acid
• Encephalopathy → evidence by stuttering, there
and lactic acid (bone and lung tissues)
would be gait disturbance myoclonic jerks,
→ Once there is an entry of aluminum inside the body if it seizures, coma, and there would be an abnormal
is through ingestion, it would really be taken by our EEG pattern),
intestinal cells and eventually reach our blood circulation • Osteomalacia or aplastic bone disease → in
which the patient would be experiencing painful
• once that the aluminum is in the blood
spontaneous fractures, and also, they can have
circulation, the transport becomes slower and
hypercalcemia and tumorous calcinosis,
usually in the plasma aluminum is bound to a
• There would be also a Proximal myopathy, and
carrier protein → carrier protein where
the patient is at risk of infection
aluminum could bind is transferrin → aside from
transferrin it could also bind into the different → Under the microscope, the blood picture which shows
ligands in the blood and this may cause the microcytic anemia, and then in the cardiac muscles
distribution of aluminum in the different organs specifically the heart itself there would be an increase
• Accumulation: usually the one which accumulate left ventricular mass and there would be a decrease
the higher concentration of aluminum would be myocardial function.
the bone, and lung tissues
• Correlation with age group: when the age of the → Toxicity could also be seen in a group of individuals
patient increases the accumulation of aluminum who are suffering from renal insufficiency specifically
is also increases those who are treated with:
• Excretion: through urine. Almost 95% of ➢ DIALYSIS → those who is treated in dialysis may
aluminum is excreted in urine and the remaining
accumulate large amounts of aluminum causing
percentage could be eliminated in the bile
aluminum toxicity whenever they are being
A. HEALTH EFFECTS & TOXICITY treated with aluminum coat contaminated
solution or oral agents which may be containing
→ ALUMINUM IS CONSIDERED TO BE NON-ESSENTIAL aluminum
TRACE ELEMENTS o INDICATOR THAT THEY HAVE
ALUMINUM TOXICITY: → presence of
→ As of the moment its toxicity is not yet understood but
anemia, bone disease, progressive
in terms of its effects it is known to interfere with variety
dementia, and impaired neurologic
of enzymatic processes inside the body
development
→ In terms of exposure specifically ingestion of
aluminum which may be found in over-the-counter oral • Toxicity is not well understood
products, it is of clinical significance if it is taken above • Encephalopathy
the recommended dose • Osteomalacia or aplastic bone disease
• Proximal myopathy
→ A very high dose, some adverse effect maybe • Increased risk of infection
observed specifically those whose using it for a long • Microcytic anemia
period of time • Increased left ventricular mass & decreased
→ In terms of the industrial exposure, worker whose myocardial function
inhaling large amounts of aluminum could have several • Renal insufficiencies
lung problems, which may initially present as a • Anemia
continuous coughing, and possible changes which may • Bone disease
eventually show up in chest x-ray • Progressive dementia
• Impaired neurologic Development
3|CC2 LEC 13
B. LABORATORY: A. HEALTH EFFECTS & TOXICITY

→ Aluminum is primarily measured using ICP MS or Sign and symptoms: would depend on the duration and
GFAAS so the measurement of aluminum could be the extent of the exposure to the type of arsenic might be
complicated if there is a possible risk of having a sample the inorganic (organic) or the methylated species of
which is contaminated with industrial or environmental arsenic, together with the effect of it to the patient if
sources of aluminum there are any underlying condition that the patient have.

• ICP MS acute arsenic poisoning → the patient would be

• GFAAS exhibiting signs and symptoms such as:

→ In terms with analyte, urine and serum could be used, • Gastrointestinal: Nausea, emesis, abdominal
there are useful in determining toxic exposure, pain, rice water diarrhea
monitoring exposure overtime, and monitoring of • Bone marrow: Pancytopenia, anemia, &
chelation therapy basophilic stippling
• Cardiovascular effect: they will be having an
• Urine and serum levels are useful in abnormalities in the ECG patterns/ changes
determining toxic exposures, monitoring
• Central nervous system: Encephalopathy &
exposure overtime, and monitoring chelation
neuropathy
therapy
• Kidney: Renal insufficiency & renal failure
ARSENIC → toxic or NON-ESSENTIAL TRACE • Liver: Hepatic systems/ hepatitis
ELEMENTS,
→ If the condition is chronic or the exposure is already
→ It is a ubiquitous element displaying metallic and chronic, the patient would be experiencing or the signs
nonmetallic property and symptoms would be including the presence of:

➢ Garlic and metallic taste ➢ MEES LINES → line we can see in the nails
➢ Metallic & nonmetallic properties which would be significantly seen in patients
➢ Earth’s crust (1.5- 2.0 mg/kg) with arsenic poisoning
➢ In terms with humans and arsenic: Food (25- ➢ HYPERKERATOSIS, HYPERPIGMENTATION,
50 ug/day) largest source of arsenic exposure ALOPECIA → these are the dermatologic effect
→ In term with other sources: of chronic exposure
➢ HEPATIC → patient might experience cirrhosis
➢ Anthropogenic sources and hepatomegaly
o This would be pertaining to the other ➢ CARDIOVASCULAR SYSTEM → the patient might
sources such as arsenic as a byproduct have hypertension as well as peripheral vascular
of production of metals, burning of coil, disease (PVD)
fossil fuels, and as well as it’s used in
terms with agriculture • Mees Lines”, hyperkeratosis,
o The source of arsenic could be coming • hyperpigmentation, & alopecia
to the anthropogenic sources • Cirrhosis & hepatomegaly
• Hypertension & PVD
→ In terms of used: this is considered as toxic or NON-
o in the cardiovascular system, the
ESSENTIAL TRACE ELEMENTS, so therefore most of its
patient might have hypertension as well
utilization would be primarily in the industrial purposes, it
as peripheral vascular disease
is used as a composition of pesticide.
• CNS neuropathy & tremor
➢ primary component of rat poisons, but since it o CNS effects such as socks and gloves
was identified to be used mostly for poisoning, neuropathy, and possible tremors
so the component of pesticide has now been
→ chronic exposure would also eventually lead to
reformulated.
malignancies involving squamous cell, liver, skin,
➢ Aside from pesticide, it has also been used as a
bladder, or lung and renal type of carcinoma
pigments or ammunition for semiconductor
processing as well as for assay content of poison
gases
4|CC2 LEC 13
• Squamous cell, hepatocellular, skin, → In the year 2000, the US-FDA also approved the use
• bladder, lung, & renal carcinomas of:
• “Black foot disease
• chronic and arsenic exposure has been • arsenic trioxide that can be used as a treatment
known to cause as the black foot of acute promyelocytic leukemia (APL) → so this
disease is the arsenic composition of medicine
• advance stage of peripheral vascular o but then again, the level of arsenic
disease (PVD) so this is the severe form would not be that much high in a way
of PVD that it can be fatal for the pace of
• it is called as black foot disease course this is prepared in a way that
because this result to gangrenous would be beneficial for the patient.
changes in the extremities o Arsenic can also be used as a
composition for medications.
→ Arsenic is used before as a common poison because ▪ Cannot be accessed without a
arsenic is known to be odorless and tasteless which prescription from a physician
means it can easily be mix in the food without the victim
knowing that the food have an arsenic laden, so B. LABORATORY: Absorption, transport, and
sometimes it is used for slowly killing an individual and excretion of arsenic
before when it is not yet identify that this is a common • Ingestion – primary route of exposure
cause of poisoning, it is not easily identified and o Arsenic could be found in some food
diagnosed that there is arsenic poisoning but rather they sources, arsenic-laden water, and
correlate it with other condition beverages (e.g., contaminated water
→ Household that uses rat poison and contaminated beverages)
• Inhalation
→ Rat poison – direct access to arsenic o Both sources and routes of exposure are
complex on means on how the amount
→ Accidental poisoning
of arsenic would generally be toxic
When can it become toxic to individual? depending on the route of exposure.

• the little dose is roughly about 0.12- 0.3 grams • FORMS OF ARSENIC:
although there is some person who have a high o Inorganic – toxic form of arsenic
tolerance in terms of arsenic poisoning so it is ▪ the ones which are obtained
dependent on the current health condition of the from industrial sources seen in
patient rocks, soil, and groundwater.
▪ Highly toxic
Treatment: Lavage (commonly used) and use of
▪ Seen in synthetic products
activated charcoal and followed by chelating agents
such as pesticides, poisons,
• Common treatment → used of chelators (those and other industrial processes.
that binds in a particular compound in order to o Organic – such as the arsenobetaine
render that compound to be readily excretable) and arsenocholine (CONSIDERED TO BE
• Chelating agent used for arsenic: NON-TOXIC) are the types of arsenic
o DIMERCAPROL which may be present in fish and other
o PENICILLAMINE (common chelator for seafood. Non-toxic for the human body.
other trace elements) ▪ It is readily cleared from the
o SUCCIMER body and excreted through
urination immediately after 1-2
days.
o Methylated (such as the MMA and BMA)
– intermediate toxicity
▪ Toxic but higher dose is
needed before it can
5|CC2 LEC 13
elicit/cause signs and • Gastrointestinal (from dietary sources) would
symptoms for the patient. roughly be about 5%.
▪ Same with the organic form, it • Mostly of the exposure would be through
is readily excretable. inhalation. Ingestion is less.
Elimination could last for 1 • Smokers– the cadmium present in tobacco
week up to 3 weeks. products or absorption of cadmium in cigarettes
would also be about 10-50%.
• ICP MS → (Inductively coupled plasma mass o There is a high possibility that cadmium
spectrophotometry) can be obtained simply through
• GFAAS cigarette or smoking of tobacco
• HG AAS products.
• Arsenic speciation is desired, a separation o It is known that smokers have higher
method is employed either online or offline amount of cadmium as compared to
prior to metal analysis non-smokers.
o Non-smokers would mostly be through
SAMPLE USED:
inhalation or ingestion.
• Urine sample is typically used. (BEST SAMPLE) • Cadmium, in terms of its accumulation, it
• In terms of sample, when arsenic speciation is accumulates more in female patients, primarily
desired, typically urine sample is used. If you because of higher iron stores because it has
need to identify a particular type of arsenic, a affinity to iron molecules.
separation technique should be employed. A o Cadmium accumulates more in females
separation technique is done initially to identify as compared to male patients.
the particular form of arsenic a patient has. • Kidney – primary organ where it will mostly
accumulate and could eventually cause
CADMIUM → non-essential trace element. proteinuria.
• Soft, bluish white metal which is easily cut o Proteinuria – distinct characteristic of
with a knife smokers who also have renal
o Chemically: it could easily be cut with a conditions. Correlates with high
knife. cadmium concentration in the blood
o UTILIZATION: one of the primary circulation.
industrial uses of cadmium is for the A. TOXICITY
manufacturing of pigments and
batteries. • Cadmium is considered to be a non-essential
▪ Battery have the biggest trace element.
consumption of cadmium • Cadmium has no known role in the normal
content) → Ensure that if you human physiology. It is a toxic trace element.
have batteries that are no • Toxicity is believed to be a result of “Protein
longer used/ leaked batteries, Cd” (protein cadmium) adducts → causing
you have to immediately denaturation of the associated proteins which
dispose it properly. results to the loss of function of organ (kidney is
▪ Leakage could cause cadmium the primary organ affected)
poisoning in children. • Severe nausea, vomiting, and abdominal
• Burning of fossil fuels such as coal and oil & pain → ingestion of high amount
incineration of municipal waste materials →
primary source of cadmium are the ones which Renal dysfunction → most common presentations of
are airborne. chronic exposure

ABSORPTION AND EXCRETION OF CADMIUM: o Slow-onset proteinuria

• INHALATION : Nasal epithelial damage and
• In terms of absorption, it would mostly come lung damage similar to emphysema
from airborne type of cadmium. o The breathing of cadmium vapors could
• About 10-50% of came from inhaled/airborne result to nasal epithelial damage and
cadmium. lung damage similar to emphysema.
6|CC2 LEC 13
o Acute effects of inhalation of fumes A. HEALTH EFFECTS:
which may be containing cadmium may
• Hexavalent chromium is considered to be better
eventually result to respiratory distress
absorbed but more toxic than trivalent
due to chemical pneumonitis and
chromium.
edema and may eventually lead to death
• In terms of absorption and transport mechanism,
of the patient.
chromium requires carrier proteins such as
Cadmium could accumulate in the different organs in the transferrin and albumin to allow its circulation in
body. the vascular network or vascular system.
• Transferrin binds the newly absorbed chromium
• Cadmium exposure could affect the liver, bone, at site B while albumin access a transporter of
immune system, blood, and nervous system. chromium.
• If in case, all the transferrin sites are saturated
• TREATMENT: “EDTA can be used as a
• Other plasma proteins as well as beta-globulin,
chelating agent in cadmium poisoning
some of the beta-globulins and gamma-globulins
B. LABORATORY: are also capable of binding with chromium.

• GFAAS & ICP MS • The trivalent chromium Cr (+3) is the ones which
• ICP AES is considered to be significant.
• Urinary excretion is about 70% in the RBC o It is considered as the essential dietary
→ it has a high affinity to iron molecules, the element and primarily its responsibility
cadmium in the blood reflects the average is to maintain normal metabolism of
uptake during the past few months because it is glucose, fat, and cholesterol.
slowly eliminated from the blood circulation.
o It is not immediately identified in the • Enhances insulin action → for emergency cases
blood circulation because of prolonged of hypoglycemia in diabetic patients, when given
exposure. insulin it also contains chromium to further
• URINARY EXCRETION: 0.001% & 0.01% of enhance the activity or action of insulin.
the body burden per 24 hours.
o At low exposure, urine is used as a
• HEALTH EFFECTS: chromium deficiency is
sample.
uncommon. The ones involved are the persons
▪ Urine cadmium reflects the
with specific situation such as total parenteral
total accumulation of cadmium.
nutrition, diabetes, and malnutrition.
CHROMIUM → ESSENTIAL o Deficiency = no direct sources, no food
source resulting to malnutrition,
• Greek word “CHROMA” which means dependent, parenteral nutrition (gastric
“color” tubes which food passes through/
• Chromium is an element which makes prepared food)
rubis red & emeralds green • CHROMIUM DEFICIENCY – characterized by
• 21st most abundant element in the glucose intolerance, glycosuria,
• earth’s crust hypercholesterolemia, decreased longevity,
• Used for the manufacturing of stainless decreased sperm count, and may cause
steel impairment in fertility.
• Occupational exposure to chromium:
o would be coming from industrial • Hexavalent chromium Cr (+6) – considered
sources such as those involved as the toxic one and a powerful oxidizing agent.
on wood treatment, stainless steel
o The hexavalent chromium could cause
welding, chrome plating, and
production of free radicals and it would
leather tanning industry.
eventually lead to oxidation of DNA
which potentially induce cell death.
• Chromium exists in 2 valency state:
o Those individuals who are exposed to
o Trivalent chromium = Cr (+3)
o Hexavalent chromium = Cr (+6) hexavalent chromium salt may have
severe dermatitis and skin ulcer.
7|CC2 LEC 13
• SKIN CONTACT → Workers (cement workers, • Cr (3+) - protein complex
metal workers, painters, and leather gunners) • Airway irritant, airway obstruction, & possibly
from industrial sources can have contact lung cancer
dermatitis, allergic dermatitis with eczema. • Lung, kidneys, liver, skin, & immune system
• INHALATION → hexavalent chromium is • Transient renal effects
considered to be a respiratory tract irritant which • Elevated urinary B 2 Microglobulin (an
may cause airway irritation, airway obstruction. indicator of renal tubular damage)
o For chronic/prolonged exposure → lung
D. LABORATORY:
carcinoma
o Lungs – target organ if route of • GFAAS → (Graphite Furnace Atomic
exposure is through inhalation. Absorption Spectrometry)
o Other organs may also be affected and • NAA
accumulate since it could be carried by • ICP MS → (Inductively coupled plasma
our protein. It can also accumulate in mass spectrometry)
the kidney, liver, and immune system. • Plasma, serum, and urine do not indicate
the total body status of the individual,
• For individuals exposed at low doses of whereas
chromium in industrial sources it can cause an o urine levels may be useful for
impact to: metabolic studies
o Kidney → cause an elevation of beta-2 • Chromium determination is used for those who
microglobulin. have undergone MOM (metal on metal hip
replacement) – failed implant devices
• Exposure = exposed in industrial places such COPPER → ESSENTIAL TRACE ELEMENT
as chrome plater
• Age group = younger patients • 3rd most abundant
• Kidney – causes renal tubular damage. • Relatively soft yet tough metal with a good
o The indicator of renal tubular conducting property for both electricity
damage is the presence of beta 2 and heat.
– microglobulin. • Widely distributed in elemental forms and
• Metabolism of glucose, fat, & cholesterol compounds.
• Adequate daily intake of chromium (50 • Electrical & heat conducting
200ug/d) → (nutritional/dietary requirement • Forms alloys w/ zinc, tin, & nickel
for chromium) • Copper is an essential trace element which is
found in 4 oxidation sites:
B. DEFICIENCY:
o Cu (0), Cu (1+), Cu (2+), Cu (3+)
• Insulin resistance o the cuprous iron Cu (2+), is the
• Impaired glucose tolerance most stable.
• Hyperlipidemia CLINICAL USE:
• Glucose intolerance, glycosuria,
hypercholesterolemia, decreased longevity, • Cofactor of several metalloenzymes
decrease in sperm counts, and impaired • Heme synthesis
fertility • Cellular respiration
• Collagen synthesis
C. TOXICITY:
A. HEALTH EFFECTS:
• Cr(6+) Powerful oxidizing agent
• CrO4 • The human body contains about 50-120mg of
• 2+ At physiological pH copper
• It similarity to essential phosphate & sulfate o typically seen in adults and is being
anions distributed in the different organs of the
• Skin ulcer, renal & hepatic necrosis body but the highest concentration
• Severe dermatitis & skin ulcers would be found in the liver, brain,
• Allergic dermatitis with eczema heart, and kidneys.
8|CC2 LEC 13
• Osteoporosis & various bone and joint
• Aside from the primary organs, copper could abnormalities → reflection of copper deficient
also be found in the cornea, spleen, intestines, cross-linking of the bone, collagen, and
and lungs. connective tissue
o Majority of the ones found in the • Decreased pigmentation of the skin and
intestines are those which are derived general pallor
from ingested copper. • Hypotonia, apnea, and psychomotor → latter
o The average daily intake is about 10 mg stages, neurologic abnormalities
or more for adults. • Retardation
o For those copper-containing food • Coronary heart disease
intake, copper, once absorbed by the
GIT will be transported to the liver “Menkes Disease” → extreme form of copper
deficiency
bound to an albumin molecule,
transcuprein, and other low molecular → This invariably fatal, progressive brain,
weight components in the portal disease characterized by peculiar hair, also
system. called kinky or steely, and retardation of
• LIVER → copper is incorporated into the growth.
ceruloplasmin which is responsible for the → Clinical signs: Progressive mental
distribution of copper all throughout the body. deterioration, coarse feces, disturbance of
o Ceruloplasmin – alpha 2 type of globulin muscle tone, seizures, and episodes of
under the proteins and contains 6 atoms severe hypothermia
of copper. → Signs and symptoms:
• In a normal physiological state, about 98% of o appear at the age of 3 months after birth
copper is excreted through the bile and the rest and do not survive for long.
is through urine and sweat. o 5 years of age – longest age they
• CLINICAL SIGNIFICANCE → copper is a could attain.
component of different metalloenzymes in the
C. HEALTH EFFECTS & TOXICITY:
body such as:
o Ceruloplasmin, cytochrome C • Copper toxicity is associated mostly with those
oxidase, superoxide dismutase, in copper-producing facilities such as mining
tyrosinase, metallothionein, industries, industrial activity.
dopamine hydroxylase, lysyl oxidase, o Water passing through water pipes
clotting factor V and unknown
o Cooking with copper line vessels
enzyme that cross links keratin in
o Exposure to algaecides, surfacide,
hair
paratechnique, ceramic glazes,
B. DEFICIENCY: CONDITIONS INVOLVING electrical wiring or welding supplies.
DEFICIENCY OF COPPER • Copper has redox potential
• Interferes with absorption of iron and zinc.
• Premature infants
• Copper is an irritant to epithelia & mucus
• IMPAIRMENT OF COPPER ABSORPTION: membranes.
o Severe diffuse diseases of small
• Hepatic & renal damage with hemolysis.
bowel, lymphosarcoma, &
• Copper induced emesis has characteristic
scleroderma
“blue green color” → vomit
• COPPER DEFICIENCY IS RELATED TO
THE FF: “Wilson’s Disease”
o Malnutrition, malabsorption, chronic
diarrhea, hyperalimentation, & → Genetically determined copper accumulation
prolonged feeding with low copper, disease that usually presents between ages
total milk diets of 6 and 40 years
• SIGNS OF COPPER DEFICIENCY: → Neurological disorders, liver dysfunction, and
o Neutropenia & hypochromic anemia Kayser Fleischer (green-brown discoloration)
in early stages rings in the cornea caused by copper
deposition
9|CC2 LEC 13
→ Green-brown discoloration = evidence of IRON → ESSENTIAL
copper accumulation/disposition in the cornea.
• 4th most abundant element in the earth’s crust
→ TREATMENT:
o Use of zinc acetate as chelating agent • Most abundant transition metals
or any other chelators that can be used → Methods on extracting iron, these are used even
for chelation therapy. before because it is one of the most easily identified as
→ DIAGNOSTICS: an element used for different industrial purposes
o KEY DIAGNOSTIC: Measurement
of serum ceruloplasmin level and → The physical properties of iron alloys can be varied
the direct measurement of free over enormous range of alloy and heat-treating methods,
copper
• so this allows iron to be molded
INTERPRETATION OF COPPER TESTING depending on strength, hardness,
RESULTS (SERUM COPPER) (URINE COPPER) toughness, and corrosion resistant. It
Nutritional deficiency, menkens syndrome, acute also has magnetic properties and has
copper toxicity, chronic copper toxicity, Wilson;s an ability to take and hold a sharp edge
disease, smoking inflammatory conditions, estrogen, THESE ARE ALL FOR INDUSTRIAL PURPOSES
pregnancy, N, normal
→ SIGNIFICANCE IN THE BODY - it is significantly known
Interpretation Of Copper Testing Results
serum copper urine copper as a trace element meaning it is found in trace amount in
Nutritional decreased decreased the blood circulation
deficiency
Menke’s syndrome decreased Increased → Iron ion can be able to participate in redox reactions
Acute copper Increased or Increased
toxicity significantly inside the body both in its a ferrous and ferric stage
increased (Fe+2 and Fe+3) → this is the variety of iron ion which we
Chronic copper Increased Increased can be found in the blood circulation
toxicity
Wilson’s disease Normal or Increased OR
decreased significantly → It allows iron to fill numerous various biochemical
increased roles as carrier of other biochemically active substance
Smoking, Increased or Normal
such as oxygen. Irons high activity is a double edge word
inflammatory significantly
conditions increased and free iron would be participating in destructive
Estrogen, Increased or Normal chemistry specifically in catalyzing formation of toxic and
pregnancy significantly
increased free radicals, that is due to its capability or characteristic
to be involved in redox as well as in electron transfer
reactions

• Classified as a trace element

• Oxygen transport
• Participates in redox chemistry
• Agent in redox & electron transfer reactions

HEALTH EFFECTS AND CLINICAL SIGNIFICANCE

D. LABORATORY: OF IRON:

• Flame AAS, ICP MS, ICP AES, AND ASV How do we absorb iron from dietary sources?
• Serum copper & urine copper → used for
→ Absorption of iron would primarily the means of
monitoring nutritional adequacy as well as
regulating amount of iron in the body. Majority of iron in
determination of subacute management of
the blood circulation are those which are derived from
copper toxicity.
dietary intake from intestinal absorption
• Direct measurement of free copper & Serum
ceruloplasmin → for determination of Wilson’s → ABSORPTION OF IRON - our body could only absorb
disease iron in its ferrous state (Fe+2) we can’t absorb directly
ferrous iron molecules
10 | C C 2 L E C 1 3
• for that matter because iron is in different form → In terms of iron loss, iron is loss primarily by
and usually ferric ions is their predominant form disclamation of red cell loss to urine and stool
• it is important to reduce first the iron into its
→ In female patients, for each menstrual cycle women
ferrous state (ferric to ferrous state).
lose about 20-40 ml of iron that is why it is also crucial to
o Usually, it is only allowed to use the
supplement iron for those who take ferrous sulfate or
reducing agents such as VITAMIN C or
other derivatives which is containing iron in order to
our own INTESTINE/ BODY → it is
supply or support the loss which happen on a monthly
because usually there is a moment
basis.
where majority or predominant of the
iron we can get in the dietary intake → In terms of iron distribution of 3-5 grams of iron in the
would be in its ferric state, so therefore body approximately large portion of it
our body is also capable and that is
done by releasing ferric reductase by ➢ about 2-2.5 gram of iron is found in the
the intestine which are also capable of hemoglobin, and this hemoglobin is mostly
doing the same mechanism as with found in the RBC’s as well as in another red cell
VITAMIN C precursor.
• that is also the reason why we are given ferrous ➢ Aside from hemoglobin moderate amount of iron
sulfate supplement usually with vitamin C and it could also be seen in myoglobin the oxygen
is important to take it at the same time because carrying protein of muscle.
that is the purpose of it to reduce the ferric ions ➢ Iron can also be bound to different enzymes and
if in case it is not totally in the form of, although this enzyme would require iron for it to be able to
usually the ferrous sulfate is already in ferrous perform it activity or function.
sulfate form but the vitamin C would actually be → Who’s in need of iron? Peroxidase, cytochromes, as
enhancing the absorption of the supplements well as other krebs cycle enzyme
with iron content
→ STORAGE:
→ Once absorb, the iron molecules could be bound by
ferritin for storage and it may be eliminated after • it is stored as ferritin and hemosiderin, so it is
sloughing off or be exported on different side of the body, the storage form of iron.
the basal lateral side o Ferritin and hemosiderin are stored in
the bone marrow, spleen, and liver
→ Iron is absorbed in its ferrous form (Fe+2) which is the o about 3-5 ml of iron would be found in
initial who pass through towards the blood circulation the blood circulation and most of it are
and then eventually it then oxidizes again to convert it associated or bound to transferrin,
into ferric ion molecule which would now be bind in albumin, and pre-hemoglobin
APOTRANSFERRIN → for its transportation all throughout
the vascular network of the body. CONDITIONS OR HEALTH EFFECT IN TERMS OF
SERUM IRON
→ ABSORPTION BY THE GASTROINTESTINAL TRACT:
Increased in serum Iron:
➢ there is a peptide hormone which is known as
HEPCIDIN → which is responsible for regulating a) Condition of increased erythrocyte
the iron absorption by the upper GIT, and at the destruction (hemolytic anemia)
same time it also helps in modulating the export b) Decreased blood formation (lead
poisoning, pyridoxine deficiency)
of iron from cells by the FERROPORTIN.
c) Increased release of iron from the body of
→ Iron in our blood circulation, primarily as the stores (release of ferritin in acute hepatic
composition of RBC, this iron would be degraded after cell necrosis)
120 days by the spleen, liver and macrophages which d) Defective iron storage (pernicious
would be intern liberate iron for reused. anemia)
e) Increased rate of absorption
→ Absorption and transporting capacity can be increase (hemochromatosis and transfusion
in conditions such as if there is iron deficiency, anemia, siderosis)
or hypoxia
11 | C C 2 L E C 1 3
o Tissue accumulation of iron, affects
liver function, hyperpigmentation of
skin
Decreased in serum Iron:
→ Condition that can be associated with
a. Generalized iron deficiency (lack of hemochromatosis:
sufficient dietary iron)
✓ Diabetes mellitus, arthritis, cardiac arrythmia,
b. Inadequate absorption of iron
cirrhosis, hypothyroidism, impotence, liver
c. Chronic loss of iron as a result of bleeding or
cancer
nephrosis → (loss in the urine)
d. Impared releases of iron from the TREATMENT:
reticuloendothelial system (infection)
e. Malignant ✓ use of therapeutic phlebotomy
f. Rheumatoid arthritis ✓ Chelators → such as deferoxamine
✓ Absence of transferrin: We can also provide
Increase in TIBC: → Total iron binding capacity transferrin → condition involving
a. Iron deficiency atransferrinemia
b. Late pregnancy → Secondary iron overload (which means there is a
c. Oral contraceptives
primary condition) this could be because of too much
d. Viral Hepatitis
uptake of iron which can be due to diet, medicine, or
Decreased in TIBC: transfusional iron intake, and can be due to metabolic
dysfunction
a. Chronic infections
b. Malignancy → Hemosiderosis → there is an iron overload in which
c. Iron poisoning there is an increase in total serum iron, also increase in
d. Nephrosis total iron binding capacity (TIBC), plus the transferrin
e. Kwashiorkor level but with the absence of tissue damage
f. Thalassemia
LABORATORY
DEFICIENCY AND THE OVERLOAD OF IRON
→ disorders of iron metabolism are evaluated based on
Iron Deficiency different parameters such as the:
✓ High Risk – Pregnant Women, Young • packed cell volume
children, adolescents, women of reproductive
• hemoglobin
age
• RBC indices
Causes: • RBC count,
• total iron level and the total iron binding
✓ Increased blood loss, decreased dietary capacity.
intake, decrease release from ferritin
• Aside from that we also measure the percent
saturation transferrin and ferritin

Reduction of iron source: → Characteristic:

✓ Decrease RBC count, MCHC (mean “TOTAL IRON CONTENT”

corpuscular hemoglobin concentration),
→ Measurement which refers specifically to the iron,
microcytic RBC’s
which is bound to transferrin, so this is not the iron
Iron Overload → excessive iron circulating as free hemoglobin in a serum. The one
measuring here is the iron bound to transferrin
✓ Hemochromatosis → general term or
collective term for iron overload • Fe (3+) bound to transferrin
o condition which may lead to • Serum or heparinized plasma
abnormally high (iron) Fe absorption
which may culminate in iron overload → SPECIMEN:
12 | C C 2 L E C 1 3
• Serum → without anticoagulant → Increase: Chronic infection, malignancy, and
• Plasma → the anticoagulant used is heparin viral hepatitis
• Oxalate citrate and EDTA are
→ IRON DEFICIENCY: increase transferrin, decrease
UNACCEPTABLE ANTICOAGULANT
ferritin
o primarily because they bind with iron
molecules → IRON OVERLOAD AND HEMOCHROMATOSIS: decrease
• Early morning sample transferrin, increase ferritin
o because of the diurnal variation
• Specimen with visible hemolysis should be LABORATORY
avoided
• AAS
TIBC → Total iron binding capacity • ICP-ms
• Iron quantification in liver is not used for the
→ Theoretical amount of iron which would be bound if evaluation of acute iron toxicity.
transferrin and other iron binding proteins were saturated • Hepcidin testing has not yet been shown
→ 1/3 of the iron binding sites of transferrin are to be clinically useful.
considered to be saturated, this the measurement to → Hepcidin is a significant analyte specifically
know if how effective the iron binding protein is in its for the absorption of iron by the gastrointestinal
capability to binding and transporting iron across the tract
blood circulation. TABLE SHOWING THE SUMMARY OF THE
EXPECTED RESULT / LABORATORY MARKERS
→ Amount of iron that could be bound if
OF THE IRON STATUS IN SIGNIFICANT OR
transferrin amount of iron that could be
SEVERAL DISEASE STATE
bound if transferrin and other minor iron
binding proteins present in the serum or condition seru transfer ferritin percent tibc
plasma sample were saturated m ritin saturation
iron
“PERCENT SATURATION” → also called the Iron D I D D I
deficiency
transferrin (transferin) saturation Iron I D I I D
overdose
→ The percent saturation, also called the Hemochrom I Slightly I I D
transferrin saturation, is the ratio of serum atosis D
Malnutrition D D D Variable D
iron to TIBC. Chronic D D I D D
→ Approximately 20% to 50%, but it varies Infection
with the gender, age and sex of the Acute liver I variable I I Varia
disease ble
patient. Chronic D N or D N or I D N or
Anemia D
“TRANSFERIN”
→ Iron deficiency: serum iron, ferritin and percent
→ Measured by immunochemical methods saturation are decrease. REMEMBER: Iron deficiency,
such as nephelometry. transferrin and TIBC would be expected to be increase

→ increase in iron deficiency and decrease in iron → Iron overdose: serum iron is increase but the
overload and hemochromatosis transferrin as well as the TIBC would be decrease.
Opposite of iron deficiency, same characteristic of the
→ Iron deficiency hemochromatosis but the only difference would be the
→ Decrease if there is a → chronic infections & transferrin level is slightly decreased
malignancy
→ Iron overload & hemochromatosis → Malnutrition: difference with the deficiency is that in
malnutrition even the transferrin and TIBC would also
“FERRITIN” decrease
→ Measured using: Immunochemical methods → Chronic infection: serum ion would be decrease
→ Decrease: Iron deficiency anemia together with the transferrin, percent saturation and
→ Increase: Iron overload and & TIBC, but the ferritin level would be increase
hemochromatosis
13 | C C 2 L E C 1 3
→ Acute liver disease: the transferrin and TIBC would be → Lead could be obtain through respiration/ inhalation or
variable, but the serum iron, ferritin, and percent through ingestion (respiratory or gastrointestinal)
saturation are increase
✓ INHALATION → is more effective it accounts for
→ Chronic anemia: serum iron and percent saturation are 30-40 % absorption efficiency
decrease and the transferrin would be normal but in some ✓ INGESTION → lesser. In ingestion varies
cases it can also be decrease, ferritin would either be according to the status of the patient
normal or increase, TIBC would either be normal or o as to the nutritional status, as well as
decrease the age of the patient.
✓ The younger the age is, the GIT is more efficient
→ Since the TIBC (total iron binding capacity) is also the
in absorbing the lead which is not good because
measurement of iron binding capacity, you can see here
first and foremost they are the possible whose
that they are almost the same with the different
very much exposed to lead before there have
conditions, they have same characteristic with the
been a recall of Mattel toys, the one which are
transferrin. And then for serum iron, ferritin, and percent
producing/ creating barbie, so there are several
saturation they almost have the same but also it depends
lot numbers of barbie dolls that need to be pull
on the case but most of the time they have the same
out in the market because it is was found to be
effect on the concentration so we will be using it to
high in lead
correlate with the certain condition
o Take note that that toy is pricey so how
LEAD → NON-ESSENTIAL about the cheap one or low-price toys.

→ Considered to be a toxic trace elements so its NON- → Gut absorption could also be affected by several
EESENTIAL TRACE ELEMENTS compound.

→ Characteristically metallic lead is a soft bluish white, → There is some compound which can decrease lead
highly malleable, and ductile compound absorption:

• Soft, bluish white, highly malleable and ✓ Iron

ductile ✓ Calcium
• Poor conductor of electricity & heat and ✓ Magnesium
resistant to corrosion ✓ Alcohol
✓ Fat
→ majority of its used and purpose would be for
industrial purpose.

→ tetraethyl lead → used before as an additive in the This can weaken the lead absorption
gasoline in the petroleum industry because of its ability
→ Compound which can increase or enhance lead
to increase the fuel octane rating
absorption:
✓ Significant reason why we do still have lead in
✓ Zinc
the environment because it is a composition
✓ Vitamin C
before of our petroleum product
✓ Citric acid
✓ It is a composition also of paint
✓ Lead based house paint is used before (1970s) → LEAD IS CONSIDERED NON-ESSENTIAL AND
they start banning it but unfortunately there are CONSIDERED TO BE TOXIC
still some old buildings in some other country
which may be having the same old paint → 99% of absorbed lead are typically taken up by the
✓ There are some recall few year ago in terms of RBC in which it would affect the hemesynthesis in RBC
toy simply because they found that it is → Aside from binding or being taken up by the RBC, lead
contaminated by lead may also accumulate in some tissues such as:
✓ This make the color of paint more pleasing to the
eyes ✓ Liver
✓ Kidneys
A. TOXICITY: ✓ Brain
How do we absorbed or how we are exposed to lead?
14 | C C 2 L E C 1 3
o Organs containing tissues where
lead can also accumulate

B. LABORATORY
→ ELIMINATION
METHOD USED FOR TESTING
➢ Majority of lead that absorbed by the body is
readily being excreted ✓ ICP-MS
✓ ICP-AES & GFAAS
➢ URINE → Majority is excreted through urine
about 70% and above.
• The most common specimen type is
➢ While some is excreted through feces/stool.
whole venous blood, the result of which is
➢ Then the rest which is the smaller percentage
commonly referred to as the BLL → blood
about less than 10% is excreted through the
lead level
hair, sweat, nails and other body fluids
o most preferred compare to plasma and
When is it considered toxic? serum sample, since large amount of
absorb lead would be incorporated or
→ It is considered toxic when it goes above certain level will bind with the RBC
• 60 μg/dL→ upper threshold → above 60, there • Elevated lead levels in capillary blood
is already a significance signs and symptoms specimens should be confirmed with a
and there is already a clinical presentation venous specimen → in order to avoid the
possible reason of contamination due to the
→ Once it goes above 45 micrograms (lower limit) external causes

• 45 μg/dL → toxicity in children, threshold for → We can also use urine as sample, but this is used
acute intervention primarily for detecting recent or current exposure,
and also for monitoring chelation therapy
→ Children is more potent and causes IQ declines even
in a particular level for about 10 ug/dL → Other testing, we can used would be:

• IQ declines are seen in children with blood ✓ Measurement of aminolaevulinic acid

lead levels of 10 μg/dL or more specifically the plasma ALA
• Other Symptoms: Clumsiness, gait ✓ Measurement of zinc protoporphyrin
abnormalities, headache, behavioral ✓ Measurement of free RBC or erythrocyte
changes, seizures, & severe cognitive and protoporphyrin
behavioral problems.
• GASTROINTESTINAL TYPE OF SYMPTOMS: This can be used for determination or screening purposes
Abdominal pain, constipation, and colic in of lead which could be due to occupational sources
children.
→ Non-invasive technique would be involving the use of:
→ In some cases, they may have acute nephropathy →
✓ Radiographic method
damage involving the kidneys, and anemia
TREATMENT
FOR ADULTS:
→ Chelation therapy
→ The symptoms which are being observed are:
• This would be significant for patient who
✓ Peripheral neuropathies
exposed to industrial sources
✓ Motor weakness
✓ Kidney condition → kidney insufficiency MERCURY → NON- ESSENTIAL
✓ Renal insufficiency
✓ Hypertension • ALSO KNOWN AS “Quicksilver” → Name as
✓ Anemia such primarily because it exhibits being liquid at
a room temperature and pressure together with
bromine
15 | C C 2 L E C 1 3
o In their group of elements, only mercury o Inhaled mercury vapor retains in
and bromine will be liquid at a room the lungs for quite some time
temperature and pressure 2. Ingestion → mercury containing food (e.g., Fish
• Heavy, silvery metal species with mercury content like the shark fin,
• Liquid at room temp. & pressure fish who do not have scales, tuna) but it
• 3 oxidation state: Hg (0), Hg(1+), and Hg(2+). depends on the omega-3 content of the fish
• Organic mercury → the one which is bound to a. the higher the omega-3 is the less
a carbon atom absorption is
3. Cutaneous absorption → there is a particular
→ In terms of our exposure to mercury, it came from
form of mercury which would penetrate the latex
several sources:
glove, so usually we have a methyl mercury that
✓ Mercury which is naturally occurring in our can pass through the latex gloves
earth’s atmosphere because it is a product 4. Injection of mercury → mercury containing
of the natural degassing of rocks tattoo pigments
✓ It could be also in exposure because of a 5. Dental amalgams
mercury containing compound such as
→ Inhaled mercury vapors retain in lungs for quite some
dental amalgams which used silver or gold
time about 80%
aside from pasta, and for it to bind to our
teeth sometimes a mercury is being used. → while the liquid mercury which you can possibly get
o 3 pieces of amalgams with mercury from GIT it is relatively unabsorbed
is considered to be ACCEPTABLE.
✓ Seen industrially in the production of ➢ then the one from ingestion depends on the form
electrical switches, germicide, fungicide, of mercury but our small intestine is not that
fluorescent light bulbs potent or effective in absorption of mercury

→ Mercury is used before as a typical composition of → Mercury enters the food chain primarily through
medication, because it is considered before as having an sources such as coal combustion, or mining which is a
antibacterial effect, portion of it contains mercury.

➢ it is put for the production of some topical → One of the potent or common source here in the
antiseptic, or can be seen in ointments, diaper Philippines because there is some small mining company
rash, as well as eyedrops and nasal sprays. here, they use amalgams to bind the gold they get, so
• Some mascara also contains small amount of they use droplets of mercury. In the mining process, it
mercury exposes our bodies of water on the mercury which can
contaminate the water that is common in the mining
We have so much exposure when it comes to mercury, industries
mostly before it has several uses such as:
→ Dietary intake – if we are eating mercury containing
✓ Thermometer → before the digital products, which might be absorb from several resources.
mercury thermometer
✓ Sphygmomanometer → used for blood → Kidney – one of the major storage organs - this organ
pressure is one of the primary affected if there has been a mercury
exposure
→ There is a law that implement to stop using mercury
because of its toxic effect → Brain – mercury can also be absorbed or accumulate in
the brain
A. HEALTH EFFECTS & TOXICITY
Forms of mercury that can absorbed by our body
→ NON-ESSENTIAL OR A TOXIC ELEMENT
✓ Elemental mercury
HOW DO WE EXPOSED TO MERCURY? ✓ Inorganic mercury
✓ Methyl mercury – commonly ingested which is
→ we have different route of exposure
from our food intake
1. Inhalation → we can inhale an elemental o The movement of methyl mercury
mercury vapor, anddimethyl mercury across the brain barrier would be
16 | C C 2 L E C 1 3
dependent on the protein which is
known as cysteine
MANGANESE → ESSENTIAL
✓ Aside from kidney and brain the mercury can
also be absorbed in the liver, spleen, pancreas, • 12th most abundant element in the earth’s
thyroid gland, and reproductive organs crust
• Found in over 250 minerals → in which 15
ELIMINATION → the elimination is quite slow depending
or half is commercially important.
on the route of exposure, usually it take 60 days before
• Constituent of metalloenzymes and as an
our body can excrete the mercury, but it depends if the
enzyme activator
one we obtain is the organic form of mercury this would
• Manganism – a toxic trate causing
accumulate more in the brain and it takes years before
hallucinations and violence
our own body can actually process or eliminate the
mercury → We do use manganese for industrial purposes such as

Main elimination route is the same with other trace • first yield production
elements: • production of battery
• composition of fertilizer.
✓ Urine
✓ Feces/ stool → But aside from an element use for industrial sources,
→ MERCURY IS CONSIDERED TO BE TOXIC AND NON- ➢ manganese is also use by our body to act as
ESSENTIAL, so mercury has no particular function in the metalloenzyme, so it acts an activator.
human body
→ Majority of our manganese is obtaining through
→ The effect may cause: ingestion
• Cause or trigger autism in children → acts ➢ manganese can be absorbed in the small
on a due to most of all the anti-vaccine groups, intestine
because before there are some which we called
thimerosal → composition of vaccine but at this → THESE WOULD AFFECT THE INGESTION OF
moment it is already been banned and not use, MANGANESE IN THE BODY
or if there is some it is very small or limited ✓ Iron
amount only ✓ Calcium
→ most target is the central nervous system as well as ✓ Phosphate
the peripheral nervous system and may cause: ✓ Fiber

• Headache, tremor, impaired coordination, → Manganese absorption can also be age dependent in
abdominal cramps, diarrhea, dermatitis, which infant has high retainment compared to adults
polyneuropathy, proteinuria, and hepatic
→ MANGANESE IS CONSIDERED TO BE ESSENTIAL, so
dysfunction
normally it can be seen inside the different tissues in the
B. LABORATORY body

METHOD: ➢ its highest accumulation would be in the fat

tissues as well as in the bone.
• ICP-MS
• Cold vapor AAS ELIMINATION: manganese is eliminated in the body
• Mercury is usually determined as total through BILE → use for elimination of excess manganese
mercury levels in blood and urine without
regard to chemical form. → either it is
elemental, methyl or inorganic.
17 | C C 2 L E C 1 3
mask-like faces. → common cause would be
from industrial sources such as too much inhaled
A. HEALTH EFFECTS
manganese due to mining industry.
→ Manganese is considered to be an essential trace • Locuramanganica- manganese madness
element. → individuals who have manganese toxic
sometimes go crazy or have compulsive urge to
➢ Used by the body to act as the metalloenzyme to either laugh or cry.
help in the activity of the enzymes.
D. LABORATORY
MANGANESE CONTAINING ENZYME:
• ICP-MS
➢ Arginase, pyruvate carboxylase, and • GFAAS
manganese superoxide dismutase of the • Urine manganese is used in conjunction with
mitochondria. serum manganese to evaluate possible
toxicity or deficiency
MANGANESE ACTIVATED ENZYMES:
MOLYBDENUM → ESSENTIAL
➢ Hydrolases, kinases, decarboxylases, and
transferases • Hard, silvery white metal
o Manganese is not the sole • Occurs naturally as Molybdenite, wulfenite,
metalloenzyme that will act as an & powellite
activator for the stated enzymes. • Industrial uses → production of alloys, flame
o Not fully dependent on manganese, retardants, smoke depressants, and pigments
there are other metal ions which could
readily take part if in case of → Molybdenum is also considered to be an essential
manganese deficiency trace element because it would have a significant
• Many of these activations are not specific to function inside the body.
manganese and other metal ions How do we obtain molybdenum?
(magnesium, iron, or copper)
o Low manganese = replaced with ➢ Molybdenum is obtained from means of
magnesium iron and copper (masking exposure through dietary intake and ingestion.
manganese deficiency) Typically absorbed by the small intestine and the
absorbed molybdenum could either be stored in
B. DEFICIENCY
the liver, bone, and kidney.
• Manganese depletion effects/ total depletion →
Blood clotting defects, hypocholesterolemia, • Blood circulation → molybdenum is extensively
dermatitis, and elevated serum calcium, bound to alpha-2-macroglobulin and
phosphorus, and alkaline phosphatase molybdenum can possibly be seen as bound to
activity (ALP) RBC membrane.
• Low level of manganese/ signs and symptoms → • Molybdenum can readily cross the placenta, too
Epilepsy, hip abnormalities, joint disease, much molybdenum coming from the diet of the
congenital malformation, heart and bone mother would cause accumulation of
problems, and stunted growth in children molybdenum in the liver of the neonate.
C. TOXICITY A. HEALTH EFFECTS
• too much manganese, but does not come from → Molybdenum is vital to the human health because of
dietary sources its inclusion in 3 significant enzymes namely: Xanthine
• derived from industrial sources such as oxidase, aldehyde oxidase, and sulfite oxidase
manganese elements from mining industries.
• Nausea, vomiting, headache, disorientation, • Xanthine oxidase, aldehyde oxidase, and
memory loss, anxiety, and compulsive sulfite oxidase
laughing or crying. • “Molybdopterin” → active site of the enzymes
• Signs and symptoms: resemble Parkinson’s binds with the molybdenum in the form of
disease with akinesia, rigidity, tremors, cofactor molybdopterin.
18 | C C 2 L E C 1 3
o Also significant in the activity of the • Also used for industrial purposes, electronics
enzymes stated. industry, and composition for pesticides and
• Dietary molybdenum deficiency is rare rubber.
o Usually seen in secondary to another • Selenium together with zinc may also be found in
condition. anti-dandruff shampoos and fungicides.
o There had been cases of dietary
A. HEALTH EFFECTS
molybdenum in a patient with Crohn’s
disease. • Selenium is well absorbed in the small intestine
• Molybdenum cofactor deficiency is a through ingestion.
recessively inherited error of metabolism • Majority of selenium exposure would mostly be
o Cause seizures, anterior lens the ones which are ingested.
dislocation, decreased brain weight in • Aside from food containing selenium, drinking
neonates, and very low possibility to water can also contain selenium.
survive. They can die prior to age of one o Water may either contain inorganic
(1). sodium selenate, or it may also contain
▪ 1 year of age sodium selenite.
o Molybdenum is very uncommon but not • Selenium homeostasis is achieved through its
rare → caused by dietary and excretion in excess through urine and stool.
occupational exposures • Our body could also reduce selenium in excess
• Elevated uric acid in blood and an increased through other means such as sweat and very
incidence of gout high intakes through exhalation of volatile forms
o Since it is involved with the enzyme, of selenium.
xanthine oxidase, it is involved in uric
acid. SIGNIFICANCE:
o Too much molybdenum can cause
• Before, selenium is considered as a toxic
elevation in the uric acid concentration
element and even as a carcinogen.
in the blood and increasing the
possibility of gouty arthritis or simply
• Glutathione peroxidase (in the form of
gout.
selenocysteine) → – a part of the protective
o Molybdenum is rapidly eliminated both
in the urine as well as in the bile. compound in the body to act as an antioxidant
o Excretion would be through urine. defense system.
o Not used solely for whitening purposes.
B. LABORATORY o Glutathione on its own has protective
function of avoiding possible damages
• ICP-Ms
to your cell as your cell is undergoing
• GFAAS
different metabolic processes
• Blood levels are less than 60 μg/L
specifically, the possible damaging
SELENIUM → ESSENTIAL effect of free radicals.
• Deiodinaseenzymes and thioredoxin
• Naturally occurring metalloid reductase
• Similar to sulfur (chemical & physical) o Selenium is also responsible/involved in
• Essential trace elements the metabolism of some thyroid
• Major constituent of 40 minerals & minor hormones, those involving the
constituent of 37 others Deiodinase enzymes and thioredoxin
• Vitamin E reductase

→ FUNCTION: used by the body for several processes B. DEFICIENCY – low selenium concentration
one of which would be through its activity as
• Cardiomyopathy, skeletal muscle weakness,
selenocysteine, which helps in glutathione in the
and osteoarthritis
protection of the cell against free radical damage
• Selenium intakes and the rate of cancer of
the large intestine, rectum, prostate, breast,
19 | C C 2 L E C 1 3
ovary, and lungs and leukemia. → (significant • ICP-MS
negative correlation) - anticarcinogen • GFAAS
• Determination of urinary and blood selenium
is a useful measure of selenium status.
o For toxicity and deficiency status

“Keshan disease” ZINC → ESSENTIAL

→ An endemic cardiomyopathy that affects • 2nd most important after iron / 2nd most
mostly children and women in childbearing abundant trace element
age • Bound to RBCs
→ SYMPTOMS: dizziness, malaise, loss of • Bluish-white lustrous metal.
appetite, nausea, chills, abnormal • Stable in dry air and becomes cover with a
electrocardiograms, cardiogenic shock, white coating when exposed to moisture.
cardiac enlargements, and congestive heart • Preparation of Alloys, especially brass (with
failure copper), in galvanizing steel, in die casting, in
→ documented in China paints, in skin lotion.
→ readily alleviated through selenium o Also, in anti-dandruff shampoos
supplementation • Treatment for “Wilson’s disease” (copper
toxicity) → for medical purposes
“Kashin-beck disease”
o Copper toxicity – have antagonistic
→ an endemic osteoarthritis that occurs effect
during adolescent and preadolescent years. • Zinc is also considered to be an essential trace
→ Linked with low selenium status in China but element. Its deficiency might be common for
also seen in North Korea as well individuals who are not ingesting meat or who
→ as in Siberia. are not eating any alternative to meat in terms of
zinc content.
C. TOXICITY → high exposure to selenium • We obtain zinc through ingestion.
• Acute oral exposure (gastrointestinal symptoms) • Majority of the zinc will be present/ distributed
into the muscles and bones.
→ Nausea, vomiting, and diarrhea
o 60% in muscles
• Tachycardia (increased heart rate) →
o 30% in bones
cardiovascular symptoms
o Remaining 10% would be in other
• Chronic exposure → Nails and skin and hair tissues in the body (eyes, prostate,
loss, as well as neurologic problems such as hair)
unsteady gait or paralysis
• Zinc from dietary sources are absorbed in the
• Selenium sulfide – consider as carcinogen
small intestine, specifically in the jejunum of the
• anti-carcinogen - Selenium coming from our diet small intestine.
or the natural ones but have particular form
• in terms of absorption, animal proteins in the
which is carcinogen in nature.
diets and amino acids in meals help in the
DIFFERENCE: They do have physical and chemical absorption of zinc.
characteristic as those with selenium found in fruits. • Factors decreasing absorption:
o intake of iron
• Since selenium may also be found in water o taking zinc on an empty stomach
sources, there have been several cases of o presence of copper at high levels.
selenium poisoning and have chronic selenosis. • In the blood circulation, zinc is found among the
= can cause loss of hair and nails, dermal effects plasma concentration, but the bulk is seen in
such as skin lesions, tooth decay, and RBCs. About 3% are seen in the WBCs.
abnormalities of the central nervous system. • In terms of eliminating excess zinc in the body,
• Happened in Hubei, China we eliminate excess through its incorporation in
the stool.
D. LABORATORY
20 | C C 2 L E C 1 3
A. HEALTH EFFECTS → Slow growth or weight loss, altered taste,
delayed puberty, dwarfism, impaired dark
• It comes second after iron in terms of its adaptation, alopecia, emotional instability
importance in the processes in the body. and tremors.
Specifically, same as with other trace elements → Lymphopenia and death → severe cases
it is significant for metabolic processes to act as
due to an overwhelming problem of zinc
a cofactor in enzymes, so it is very significant in
deficiency
the activity of enzymes under:
o Oxidoreductases, transferases,
hydrolases, leases, isomerases, and
lipases. C. TOXICITY
o Zinc is responsible/significant in the • Initially, zinc is relatively non-toxic but repetitive
structure regulation and catalytic high dosage so too much zinc for several months
activity of enzyme may lead to gastrointestinal symptoms.
• Synthesis and metabolism of DNA & RNA • Gastrointestinal symptoms
o Indirectly involved
• Decrease in heme synthesis → because
• Synthesis and metabolism of proteins
copper is significant in heme synthesis.
• Metabolism of glucose and cholesterol,
Increased zinc (copper is not absorbed
membrane structure maintenance, insulin
optimally)
function, and growth factor affect
• Hyperglycemia
o To avoid damage to the cell by
maintaining the membrane structure of “Zinc fume fever” → zinc derived from industrial
a particular cell. sources which are inhaled and accumulates in the lung
o Has effects on growth factor. tissues.
• Chronic oral zinc supplementation might
interfere with copper absorption. → SYMPTOMS: Chemically induced
• Too much zinc could cause copper deficiency pneumonia, severe pulmonary inflammation,
because it prevents absorption of copper. fever, hyperpnea, coughing, pains in legs
and chest, and vomiting
B. DEFICIENCY
D. LABORATORY
• Mostly due to malnutrition or cereal based
diets • FAAS, ICP-AES, ICP-MS
• Growth retardation, slows skeletal • Low urine zinc levels in the presence of low
maturation, causes testicular atrophy, and serum zinc levels usually confirm zinc
reduces taste perception. deficiency.
• Old age, pregnancy, lactation, and • Serum zinc cannot be interpreted as
alcoholism evidence of normal zinc stores
o Decrease/capability of the body to • Zinc concentration in RBCs is
effectively absorb zinc from the approximately 10 times that in serum.
gastrointestinal tract. o In terms of concentration of zinc, many
o Low dietary intake or sources of zinc. are found in the RBC (about 10 times)
as compared to zinc present in the
“Acrodermatitis enteropathica” → zinc plasma.
malabsorption • Copper status should be monitored in
patients undergoing long-term zinc therapy
→ First develop a characteristic facial and o Antagonistic.
diaper rash o Suppresses absorption of copper.
→ If left untreated it would eventually cause: o Patients undergoing long-term zinc
Growth retardation, diarrhea, impaired T-cell therapy – their copper level must always
immunity, insufficient wound healing,
be checked because it may cause
infections, delayed testicular development in
copper deficiency if the amount of zinc
adolescence, and early death
is in excess.
“adolescent”
COBALT
21 | C C 2 L E C 1 3
• Hemoglobin synthesis; component of vitamin
B12
• Anemia, growth depression
• Heart failure, hypothyroidism

FLUORINE

• Prevents dental caries

MANGANESE

• Bone and connective tissue functions

• Skeletal defects
• Psychiatric disorders, Parkinson’s disease

MOLYBDENUM

• DNA metabolism
• Growth depression, cretinism, goiter
• Anemia, thyrotoxicosis

ZINC

• Protein synthesis
• Acrodermatitis, enteropathica, growth
retardation, immune deficiency, infertility,
delayed wound healing, osteoporosis
• Gastrointestinal irritation