Just received the results, I am not surprised in terms of mercury since I had many amalgam fillings most of my life, I am especially surprised at the high level of Cesium as this is quite rare, according to information provided from the lab it is not so clinical significant. I am guessing this is post Chernobil effect. Also what is surprising is relatively low level of Iodine after I have been taking 5 mg for almost a month before this test. The level of lead is highly concerning.
Also high level of copper came as a surprise. I do wear copper/silver ring but I am not sure if this could be the culprit. Lab information says that most common source is the drinking water.
I am guessing high levels of lead are probably due to high concentration of cars per square meter where I live.
Its not mentioned how to detoxify Nickel, so I have to do some research on this. If anyone has any information it would be much appreciated.
So here are my elevated values with explanation:
Copper 100.009 mcg/g Creatine ( norm 1.45-60)
COPPER (Cu) HIGH:
This trace element is an important metallo-enzyme, essential in hemoglobin synthesis. Adults absorb approximately 56% of
dietary Cu, with < 50mcg/day excreted in the urine under normal and unprovoked conditions. The adult body contains
approximately 80mg copper, one third in muscle and the reminder in other tissue and body fluids. In the divalent state copper
has the capacity to readily complex with many amino acids and proteins, such as metallothionin , which facilitate Cu-absorption
from the stomach and the duodenum. In a large number of cuproproteins, Cu is a fixed proportion of the molecular structure,
and these metalloproteins form an important group of oxidase enzymes, including ceruloplasmin (ferroxidase), SOD
(superoxide dismutase), cytochrome oxidase, lysyl oxidase, dopamine beta-hydroxylase, tyrosinase, uricase, spermine
oxidase, benzylamin oxidase, diamine oxidase, and tryptophan-2,3 dioxygenase (tryptophan pyrrolase).
LABORATORY AND TESTING INFORMATION:
Urine analysis of unprovoked urine is not an adequate measure to assess copper stores or copper metabolism. Blood copper
levels, SOD levels and serum ceruloplasmin are other, often more indicative measurements for copper status. Increased
urinary copper levels can be caused by nutritional supplementation with copper or be the result of a high dietary intake due to
copper-containing drinking water. Supplements containing high molybdenum may stimulate an increase in copper excretion,
because Cu and Mo are mutually antagonistic in terms of body retention.
CLINICAL SIGNS AND SYMPTOMS:
•Bacterial or other infection may cause hypercupremia, and published studies such as Vivoli, Sci Total Eniviron, 66p 55-64,
1987 have correlated increased urinary copper levels with increased blood pressure in hypertensives. Biliary obstruction or
insufficiency can decrease normal excretion of copper via the bile while increasing blood and urine levels.
•Hyperaminoacidurias, including histidinuria can result in copper wasting since histidine is a powerful chelator of copper.
Hyperaminoacidurias can be of various origins including genetic factors, chemical or elemental toxicities (high urinary copper is
often seen with high mercury levels) infectious agents, hyperthyroidism, sugar intolerances, nephrotic symptoms, etc.
•In Wilson's disease, urinary copper levels may increase to above 100mcg/24hrs without provocation or chelation.
Cesium 12.931 mcg (norm <11)
CESIUM (Cs):
We tested Cs-133, which is a nonessential rare earth element. We did not test for the radioactive Cs-137 which received much
attention after the Chernobyl nuclear disaster. Of the known 39 Cesium isotopes, only Cs-133 is stable. Due to its biological
half-life, the human body will excrete it within approximately 110 days.
Cs-133 is in close physiological relationship to potassium and their extracellular ionic concentration influences nerve and
muscle function, including ECGs. Studies indicate that the cesium content of injured tissue of myocardial infected heart is
reduced. There are no clinical indications that cesium is toxic; however it is suggested that overexposure may have similar
effects than excess potassium.
Cesium is used in the electronic industry for the manufacture of photoelectric cells, cesium lamps and photomultiplier tubes.
LABORATORY INFORMATION: Red blood cells contain 6x the amount as found in serum or plasma. And whole blood can be
used for the diagnosis of an immediate or acute exposure. Research indicates that hair contains relatively high levels of
cesium; thus hair can be used to evaluate long-term cesium exposure.
Mercury 13.721mcg ( norm <1)
MERCURY (Hg):
Mercury compounds readily react covalently with sulfhydryl groups in proteins, resulting in inhibition of functional activity. Both
organic and inorganic mercury are potent toxic compounds.
TOXICITY:
• Excretion levels of 100 mcg/g creatinine in random urine prior to chelation are representative of acute exposure, reflecting
toxicity. Values equal to the Hg-Orientation Range indicate a mild exposure, values above that range and below the excretion
level of 100mcg/g creatinine are representive of a past or present intoxication. Early Symptoms of Chronic overexposure may
occur at much lower levels including Insomnia, dizziness, fatigue, drowsiness, weakness, depression, tremors loss of appetite,
loss of memory, nervousness, headache, dermatitis, numbness, and tingling of lips and feet, emotional instability and kidney
damage.
SOURCES: Overexposure may stem from paints, bleaches, explosives, electrical apparatus, batteries, mercurial diuretics,
fungicides, fluorescent lamps, cosmetics, hair dyes, amalgams in dentistry, contaminated seafood, and petroleum products.
Vaccines such as tetanus toxoid contain thimerosal, which is a mercury compound. Improper disposal of broken mercury
thermometers and other apparatuses that use mercury including button cells and tube lights are additional sources of mercury
exposure.
TREATMENT: Consider chelation treatment with DMPS or DMSA.
Lead 14.75mmcg ( norm <5)
LEAD (Pb) HIGH:
Occupational and environmental exposure are common causes of high urinary concentrations. A lead concentration above the
baseline reference range and below the Orientation Range reflects a mild exposure; a concentration equal to or higher than
the Orientation Range may reflect a chronic or acute exposure in need of detoxification treatment. Consult a physician
knowledgeable in clinical metal toxicology.
Common Sources:
Leaded gasoline, canned goods, lead paint, newsprint, tobacco smoke, air pollution, and contaminated water.
Biochemical basis of toxicity:
Only 8 to 12% of the orally ingested lead is absorbed by the small intestine, but toxic effects are severe. Lead can react with
sulfhydryl groups in enzymes, thereby inactivating important enzymes such as the aminolevulinic acid dehydratase (ALA) and
ALA synthetase, leading to haematological manifestations. Lead reduces the body's ability to utilize calcium, magnesium, zinc,
iron and other important nutrients. Lead is easily absorbed by children.
Clinical Signs:
The pathological effects of Pb have been recognized for centuries. Lead affects all physiological systems including renal,
nervous, reproductive, endocrine, immune, and hemopoietic. Exposure to lead, either chronic or acute, presents a variety of
signs, symptoms, and chemical evidence. The exposed person may be asymptomatic or symptomatic.
• Mild Symptoms include tiredness, lack of energy, constipation, slight abdominal pain and discomfort, anorexia, altered sleep,
irritability, anemia, hair loss, pallor, and less frequently diarrhea and nausea. Formation and precipitation of lead sulfide may be
evidenced as a blue-black ‘lead line’ near the gingival margin of the teeth.
• Severe symptoms include colic, reduction of muscle power, muscle tenderness, parethesia, and symptoms of neuropathy
and encephalopathy.
• Frequent Symptoms in children as reported by the Center for Disease control are irritability, vomiting, abdominal pain, ataxia,
anorexia, behavioral changes, speech disturbances, seizures, intercurrent fever, and dehydration. Other symptoms reported
are ataxia and stupor.
Treatment:
Chelating agents such as EDTA, Dimercaprol (BAL) and penicillamine have been medically recommended. The use of oral
DMSA was approved by the FDA for the detoxification of children. Micro Trace Minerals / Trace Minerals International data
evaluation indicates that DMPS, ZnDTPA and CaDTPA are highly effective chelating agents with a binding capacity that equals
or is greater than BAL and penicillamine. This data also indicates that the combination treatment of EDTA + DMSA has a great
lead binding capacity and significantly increases the lead excretion. Vitamin C and cysteine have a good lead binding capacity
and may be used as supportive measures during chelation therapy.
Laboratory Analysis:
Two classes of persons must be considered:
1.) The occupationally exposed:
• A case of occupational lead overexposure is defined as an adult (15 years of age or older) with a BLL greater than or equal to
25 mcg/dL or 250 mcg/L.
• Childhood lead poisoning is defined by the Centers for Disease Control and Prevention as a blood lead level of 10 ug/dL or
above. Long-term effects may include slow development, reduced Intelligence Quotient (IQ), learning disabilities, hearing loss,
reduced height and hyperactivity. Most lead intoxicated children do not have any symptoms. Appearing symptoms are often
confused with other childhood illnesses. Very severe lead exposure (levels greater than 80 ug/dL) can cause coma,
convulsions and even death.
2.) Low level chronic exposure:
• Blood levels may or may not be significant, depending on the immediate exposure.
• Long-term exposed individuals typically show elevated hair lead.
Blood lead and urine concentrations have been reported to be about 10 to 20% higher in males than females, both in children
and adults.
Nickel 3.863mcg (norm <3)
NICKEL (Ni) HIGH:
Smoke, cigarette smoking and food are major sources of nickel exposure. A equal or above the Reference Range indicates a
mild exposure; a value between the Baseline Reference Range and the Orientation Range represents a moderate exposure.
When the urine concentration levels is higher than the Orientation Range, a chronic or acute case of intoxication might be
present. A physician experienced in metal toxicology should be consulted.
Environmental/Occupational Sources:
• Ni is found in ambient air at very low levels, as a result of releases from manufacturing facilities, oil and coal combustion,
sewage sludge incineration, and other sources.
• Exposure may be through contact with everyday items such as nickel-containing jewelry, cooking utensils, stainless steel
kitchens, and clothing fasteners.
Toxicity and Symptoms:
• Nickel carbonyl is the most acutely toxic nickel compound, also found in cigarette smoke. Symptoms include headache,
vertigo, nausea, vomiting, insomnia, and irritability, followed by chest pains, dry coughing, cyanosis, gastrointestinal symptoms,
sweating, visual disturbances, and severe weakness.
• Lung and kidney appear to be the target organs for acute nickel carbonyl toxicity in humans and animals, with pulmonary
fibrosis and renal edema reported.
• EPA's Office of Air Quality Planning and Standards, for a hazard ranking under Section 112(g) of the Clean Air Act
Amendments, considers nickel carbonyl to be a "high concern" pollutant based on severe acute toxicity.
Chronic Effects (Non-cancer):
• Contact dermatitis is the most common effect in humans from nickel exposure, and have been reported following
occupational and non-occupational exposure, with symptoms of itching of the fingers, wrists, and forearms.
• Chronic exposure to nickel in humans also results in respiratory effects, including asthma due to primary irritation or an
allergic response, and an increased risk of chronic respiratory tract infections.
Cancer Risk:
• Human studies have reported an increased risk of lung and nasal cancers among nickel refinery workers exposed to nickel
refinery dust. Nickel refinery dust is a mixture of many nickel compounds, including nickel subsulfide. EPA has classified nickel
refinery dust and nickel subsulfide as carcinogens.
• Nickel carbonyl has been reported to produce lung tumors in rats exposed via inhalation.
