The 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.
Arsines 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.
Sources 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 wood preservative.
70% 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.
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:
DIAGNOSTIC TESTING TO ASSESS ARSENIC STATUS
|Age Group (yrs)||<ppm||<mg/24 hr||<ug/hr|
If 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.
Symptoms 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 hematuria.
ARSENIC DETOXIFICATION THERAPY DETOXICATION OF ARSENIC
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.
Therapy should be continued until urinary arsenic levels are consistently below those stated above
REFERENCES ON ARSENIC:
Bibliography of texts dealing with arsenic exposure, toxokinetics, laboratory findings and treatments: