****** LEAD
*******
The major source of lead exposure in
modern times is the lead–based paint. Lead is used in type metals, storage
batteries, paints, toys and in gasoline industry.
Sources of exposure
1. Industrial
workers are exposed to lead fumes and dusts in smelting plants to lead salts in
the pigments and storage batteries as well as to lead silicate in potter
industry.
2. Inhalation
represents the most serious made to exposure
3. Children
are exposed to lead containing paints.
Symptoms
1. Loss
of appetite, headache, irritability, neurological symptoms and intermittent
vomiting.
2. Finally
encephalopathy with cranial nerve paralysis, delirium and coma may occur.
3. Basophilic
stippling of red cells in peripheral blood.
4. X–ray
evidence of dense band at the epiphysis of the long bones of children
represents additional evidence of lead poisoning.
5. More
evident sign of plumbism are lead lines in the gums, emaciation, anemia and
increase CNS symptoms. Since lead is secreted very slowly, it accumulates in
the tissues to toxic concentrations.
6. Increased
urinary excretion of porphyrin. Porphyrinuria is usually earlier found and more
frequent than erythrocytic stippling.
Mechanism of toxicity
The toxic effects of lead are due its
ability to non–competitively inhibit many enzyme systems. The effects of lead
on heme synthesis and the resultant anemia are directly related to methods of
clinical laboratory diagnosis. Lead inhibits the activity of several enzymes in
the biosynthetic pathway for heme, including delta– aminolevulinic acid (ALA)
dehydrase and ferrochelatase. The substrates of these enzymes, ALA and
protophorphyrin IX, accumulate in red blood cells. When ferrochelatase is
inhibited or when iron is not available, excess protoporphyrin IX combines with
zinc in the erythrocyte produces zinc protoporphyrin (ZPP).
Methods of determination:
1. Tompsett
colorimetric analysis
2. Hematofluorometry
3. Flameless
Atomic Absorption Spectrophotometry
4. Anodic
Stripping Voltammetry
****** THALLIUM
******
Thallium is being used as rodenticides
by professional exterminators. The principal compound responsible for poisoning
is thallium sulfate and thallium acetate. The thallium salts are absorbed from
the skin as well as from the digestive tract.
Toxic dose:
1. 0.12
– 60 g – for adults
2. 8.5
mg / kg body weight – for children
3. 8
– 10 mg – will cause epilation
Etiology of poisoning
1. Accidental
ingestion of poisoned grained intended for rodent extermination.
2. Suicidal
3. Homicidal
4. Medication
or cosmetic to depilate the skin
Symptoms and actions
1. Acute
poisoning from a single dose, nausea and vomiting may occur early, but
oftentimes the symptoms occur several hours after.
2. Metallic
taste, nausea and vomiting
3. Dryness
of the mouth, soreness of gums
4. Rhinorrhea
and conjunctivitis
5. Puffiness
of eyes and face
6. Insomnia,
deafness and scrotomas
7. Tingling
pains on the feet and hands as well as muscle sores.
8. In
a few days, severe stomatitis and paralysis of one or more muscles may occur.
9. Loss
of hairs occurs within three weeks, leaving only a fringe of hair along the
forehead, the eyebrows and the pubic hair are characteristically retained.
10. Eight
weeks after poisoning, white strips across the nails are seen.
11. Mental
and neurological symptoms occur
12. A
gingival line is sometimes seen
13. Delirium,
convulsion and coma are terminal symptoms.
Fate and excretion
Thallium is a cumulative poison and is
found in the liver, kidney, bone, muscle and in highest concentration in
epididymis.
Pathology
Inflammation of the gastro–intestinal mucosa and parenchymatous degeneration of the liver and kidneys are
seen in acute poisoning. Marked loss of hair and severe anemia may be noted.
Eosinophilia has been reported. Permanent organic changes in the brain may
occur.
Methods of quantitation
1. Fluorescence
test
Dilute 1 ml of
the solution with 9 volume of saturated NaCl in a small beaker. Expose to the
ultraviolet light of a mineralized ultraviolet lamp. A bright blue fluorescence
is given by a quantity of thallium as small as 1 mg.
2. Microscopic
test
a. To
a drop of solution on a glass slide and a drop of dilute HCl, these forms a
precipitate of white irregular crosses and clusters of radiating crystals.
b. Uranyl
acetate yields a precipitate of needles and prisms with albumin.
3. Action
of bromine on Thallium
Thallium is
converted to its oxidized form by the action of bromine water. After
destruction of excess bromine, the thallic ion is complexed with methyl violet
to form a blue to violet compound of unknown structure that is soluble in
benzene
Procedure
a. Into
a glass–stoppered tube, place 1 ml of urine and 3 drops of concentrated HCl.
Mix.
b. Add
5 drops of bromine water. Mix thoroughly.
c. Add
5 drops of 20% sulfosalicylic acid to decolorize the bromine.
d. Add
1 drop of methyl violet solution and mix.
e. Add
1 ml of benzene, stopper the tube and shake thoroughly. After separation of the
layer, decant or aspirate of the benzene and observe its color if any.
Interpretation
A colorless
benzene layer rules out the presence of 0.3 ug or more of thallium
A positive
test imparts a blue violet color to the benzene
No
interference is seen with levels up to 1 mg of borate, oxalate, chlorate,
nitrate, phosphate, sulfate, chlorides, bromide, perchlorate or EDTA.
Color
formation is inhibited by 1 mg quantities of nitrite, sulfite, sulfides,
thiosulfates and thiocyanate. The only metal that gives a false positive is 0.1
mg of mercury.
****** ARSENIC AND ARSINE ******
Arsenic is used in ant poison,
insecticide, weed killers, paint, wall paper, ceramics and glass. The action of
acids on metals in the presence of arsenic forms arsine gas. Alloys such as
ferrosilicon may release arsine upon contact with water since the ferrosilicon
may be contaminated with arsenic.
The fatal dose of arsenic trioxide is
about 120 mg. The allowable food residue is limited by federal law to 1.4 mg
/kg. The exposure limit for arsine is 0.05 ppm; for arsenic acid, arsenates,
arsenites and other compounds or arsenic is 0.5 mg/m3.
Arsenic presumably causes toxicity by
combining with sulfhydryl (–SH) enzymes and interfering with cellular
metabolism.
Clinical findings
The principal
manifestations of arsine poisoning are hemolysis.
1.
Acute
poisoning
a. Ingestion
– violent gastroenteritis, burning esophageal pain, vomiting, bloody diarrhea.
b. Inhalation
may cause pulmonary edema, restlessness, dyspnea, cyanosis, cough with foamy
sputum.
c. Exposure
causes burning and stinging of the face, tightness of chest, nausea, dysphagia,
hemolysis, hemoglobinuria, bronzing of the skin, enlargement and tenderness of
the liver and spleen
2.
Chronic
poisoning
a. CNS
– polyneuritis, optic neuritis, anesthesias and parasthesias.
b. Skin
– bronzing, alopecia, localized edema and dermatitis
c. Gastrointestinal
tract – cirrhosis of the liver, nausea, vomiting, abdominal cramps, salivation
d. General
effects – anemia, weight loss, aplastic anemia
e. Cardiovascular
system and kidneys – chronic nephritis, cardiac failure, dependent edema.
f.
Visual impairment and optic
atrophy
g. Arsenic
and its compound are carcinogenic
Detection of arsenic
The test commonly used as referred to
as the Reinsch test. It depends on the fact that metallic copper
in the presence of acid will reduce arsenic to the elemental form. The arsenic deposits
on the copper has a visible dark film.
3Cu
+ 2As
------------------> 3Cu2+ +
As
The oxidized form of antimony,
bismuth, mercury and selenium can also be reduced by metallic copper under this
condition.
Rieder’s modification
Reagents:
1. Concentrated
HCl
2. Copper
spiral – wind bright, clean copper wire around 3mm glass rod, about 8 – 10
times to make a tight spiral.
Procedure
1. Place
100 ml of urine in a shallow dish
2. Add
10 ml of concentrated HCl.
3. Boil
the solution until the volume is reduced to about 20 ml.
4. Remove
the copper, rinse gently with distilled water, examine and note any color
change.
Interpretation:
If copper is still bright red,
arsenic, mercury and selenium are ruled out
Arsenic, selenium gray to black
Mercury light gray to silvery and become
shiny on rubbing
Other substances that may produce a
gray to black color are: some Sulphur compounds, antimony, bismuth, tellurium
In the case of a positive result, the
nature of the deposit on the copper must be verified by further test.
Arsenic can be quantitated after wet
digestion of another specimen by colorimetric method.
Recently, the technique of atomic
absorption spectroscopy has been used.
Normal arsenic levels in urine are
less than 50 ug / ml.
Chronic poisoning – arsenic levels
will rise to 100 ug / l
Acute poisoning – 1 mg / l or more
Since arsenic is readily bound by
sulfhydryl groups in proteins, considerable arsenic is bound by keratin and
subsequently deposited in hairs and nails.
Minimum requirement – 1 gram of clean
hair clipped close to scalp should be submitted.
****** TEST FOR HEAVY METAL ******
Procedure:
1. 10
ml of macerated liver or kidney or urine or gastric contents is placed in a
small Erlenmayer Flask. Set up a positive and negative control.
2. Ad
2 ml of concentrated HCl and small copper sheath (5x10 mm). The copper must be
shiny clean to show clearly a contrast of a deposition of a heavy metal if
positive. A copper wire spiral may be used instead of the copper sheet.
3. Cover
the flask with a watch glass and heat gently for about 1 hour, avoid boiling to
prevent rapid evaporation. If large amount is present, deposits may occur in
less than 1 hour. After 1 hour, note the appearance of the deposits.
Mercury shiny silver deposits 0.50 mg / 10 ml
Arsenic dull back deposits 0.010 mg / 10 ml
Bismuth shiny black deposits 0.020 mg / 10 ml
Antimony dark purple sheen 0.020
mg / 10 ml
The amount should be reported as
negative, small, moderate or large to differentiate the dark deposit from each
other.
Mercury – dull black – place a copper
in a small amount test tube and add 15 drops of 10% potassium cyanide. The dark
deposits due to arsenic will dissolve. If large amount of arsenic deposits is
present, more cyanide is required to dissolve it. This test for arsenic is very
sensitive. Antimony or bismuth deposits are not dissolved.
Bismuth – shiny black – place the
copper and deposit into a small test tube and add about 15 drops of 15% sodium
sulfite and 1 ml of 15% nitric acid. The deposits due to bismuth dissolves
while that of arsenic or antimony will not. To the dissolved bismuth solution,
add 1 ml of water and 1 ml of bismuth test reagent – orange turbidity. Bismuth
test reagent consist of 1 gram of quinine sulfate dissolve in 100 ml of 0.5%
HNO3; then dissolve in 2 grams potassium iodide into solution. This
test is specific and sensitive to 20 ug of bismuth.
Antimony – purple shiny and unchanged
by both treatment.
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