order of decreasing toxicity (most to least) for arsenic is: arsines, inorganic
arsenites, organic arsenoxides, inorganic arsenates, arsenorganics with As valence of +5, and metallic As.
can penetrate rubber and are well absorbed through the skin which will become vesicated and blistered during the exposure. Arsines
combine with hemoglobin in RBCs, cause hemolysis and cell destruction. Chronic
exposures to arsines can result in anemia. Myocardial failure due to oxygen
deprivation can occur in severe cases.
of arsenic include: contaminated foods
(especially seafoods), water or medications.
Industrial sources are: ore smelting/refining/processing plants, galvanizing,
etching and plating processes. Tailings from or river bottoms near gold mining
areas (past or present) may contain arsenic. Insecticides, rodenticides and
fungicides (Na-, K- arsenites, arsenates, also oxides are commercially
available). Commercial arsenic products include: sodium arsenite, calcium
arsenate, lead arsenate and "Paris green" (cupric acetoarsenite) a
of commercial chickens raised for meat in the U.S. are fed Roxarsone, a benzene
arsenic compound, according to Science News.
There is concern that this deposits in the meat that humans consume and
has become a source of arsenic.
effects are multiple and complex in terms of
biochemistry. The mitochondria of cells accumulate the element. The pyruvate
dehydrogenase complex (catalyzes formation of acetyl coenzyme A from
mitochondrial pyruvic acid) is inhibited by As+++. Pyruvic acidosis
may result; citric acid cycle function and formation of ATP are slowed. The citric acid cycle itself is impaired at
the alpha-ketoglutaric acid dehydrogenase step; formation of succinyl coenzyme
A is impaired. Both of these enzymatic
steps require the active thiol, lipoic acid.
Arsenic readily combines with sulfhydryl (-SH) groups.
Lipoic acid is
Depending upon transport in various
tissues, arsenic may react with any of the enzymes in the body that have
sulfhydryl groups. Monoamine oxidase, which has eight cysteinyl residues with
–SH groups is an example. Monoamine
Oxidase inhibitors are used for severe depression. Other effects of arsenic include irritation
of the skin and mucous membranes, chromosomal damage in lymphocytes and
erythroblasts in bone marrow with leukopenia, and myocardial capillary damage.
Symptoms of arsenic exposure include:
Slight exposure may clear skin
lesions such as acne.
Garlic-like breath occurs with
fatigue, malaise, and nausea. Skin and
mucus membrane lesions may develop with eczema or allergic-type dermatitis,
raindrop areas of lost skin color (hypopigmentation), hair loss, white marks on
fingernails, thickening of the skin of the palms and soles (hyperkeratosis),
“melanosis” of the eyelids, areolae of nipples, and
neck), conjunctivitis, bronchitis, and gingivitis.
Excessive salivation, stomatitis,
Jaundice, peripheral neuropathy,
polyneuritis, hemolysis, anemia, leukopenia, cyanosis of the fingers, Raynoud’s
Syndrome. Chronic arsenic exposure has
been associated with basal cel1 carcinomas (Harrison's Principles, llth ed, p. 850.)
Long term arsenic exposure may lead
to the progression or acceleration of carotid artery atherosclerotic
TESTING TO ASSESS ARSENIC STATUS
1. Blood chemistry analysis, CBC with cell
differential. Red cell arsenic levels
are part of the several red cell mineral panels. Blood plasma or serum levels
of arsenic do not correlate well with exposure or with cellular levels capable
of causing disturbed physiology or pathologies.
2. Hair element analysis. Arsenic exceeding 7 ppm in hair
is cause for concern.
3. Urinary arsenic in unchelated,
non-glutathione-dosed individuals is expected to be below the levels tabulated
below for optimal physiological functioning of -SH bearing enzymes and
Age Group (yrs)
high urinary As is found it is recommended that the test
be repeated for confirmation with a new urine collection 4 to 5 days later.
This is because urine As levels can and commonly do
vary by a factor of 5 from day to day depending on diet. Seafoods and some canned foods may contain
variable and high As levels.
A reduced L-glutathione (GSH) provocation can be done using 300 mg of GSH
orally, fid. A 24-hour urine collection skipping the first am urination and
collecting for the next 24 hours including the first urination of the next am
provides the urine specimen. Levels of
concern are the same as in the above table.
consistent with arsenic excess include (garlic breath, dermatitis) together
with elevated hair As provide strong evidence of
toxicity. With symptoms and two urine analyses showing high arsenic, the
evidence is irrefutable. Other confirming laboratory results would be: elevated pyruvic acid in serum or plasma,
elevated alpha-ketoglutaric acid in a plasma organic acid analysis, and
DETOXIFICATION THERAPY DETOXICATION OF ARSENIC
must be methylated using methyl donors such as SAMe,
trimethylglycine, dimethylglycine, methionine, etc. Some arsenic is bound to sulfur groups
such as glutathione and excreted in the urine or bile.
- Remove the individual from sources
of arsenic. Treat for anemia if indicated.
- Give sulfurated methyl groups
and foods rich in sulfurated amino acids (garlic, eggs, beans)
- Nutrients protective against the
effects of arsenic include selenium, iodine, calcium, zinc, and vitamin
C. Supportive therapy with
magnesium, B-vitamins, vitamin C, vitamin E, selenomethionine, lipoic acid
- Drink adequate water (an adult's
urine volume should be > 2 liters/day).
- Do not give cysteine. Although
it will readily combine with As, it will also
move it around in body tissues and will not necessarily clear it from the
- Aggressive therapy for excess
arsenic can employ sulfhydryl-group type conjugating agents.
Therapy should be continued until
urinary arsenic levels are consistently below those stated above
of texts dealing with arsenic exposure, toxokinetics,
laboratory findings and treatments:
- Carson B.L., H.V. Ellis and J.L. McCann Toxicology and
Biological Monitoring of Metals in Humans, Lewis Publishers, Chelsea,
MI, 1987, p. 27-33.
- Tsalev D.L. and Z.K. Zaprianov
Atomic Absorption Spectrometry in Occupational and Environmental Health
Practice, Vol. I, CRC Press, Boca Raton,
FL 1983, p. 87-93.
- Clarkson T.W., et al., Eds. Biological
Monitoring of Toxic Metals. Plenum Press, New York
NY 1988, p. 309-315.
Principles of Internal Medicine,
various editions, McGraw
Hill, New York, NY.
- Science News, April 6, 2002; p 214