Lead is the #2 "CERCLA" toxin in the US (www.atsdr.cdc.gov/clist.html). This means you are very likely to be exposed in everyday life. About 75% of lead is excreted in the urine, 15% in the bile, with the remainder deposited mostly into the sweat, hair, and nails, aorta, kidneys, liver, adrenals and thyroid. Lead levels in the urine fluctuate depending on diet and physiological factors but a provoked heavy metal challenge with EDTA or DMSA is thought to reflect "total body burden". The typical amount of time lead stays in the blood (half life) is several months and the half life in bones is decades. The most important thing to do with a person with lead toxicity is to remove the source of exposure. Up to 90% of lead is stored in bone and is not released until later in life, when bone breakdown exceeds bone building. This generally occurs between ages 40-65 years old. Other medical conditions can cause early release, including stress, steroids, lack of hormones, and hyperthyroidism, and pregnancy.

In March 2003, The Journal of the American Medical Association (JAMA) published an article proving that high blood pressure that started between ages 40-65 was statistically related to lead blood levels as low as 1 microgram/dl and that the lead source was from bone turnover, not current outside exposure. In 2003, The New England Journal of Medicine (NEJM) published multiple articles on lead in children demonstrating significant health risks at levels below 10 micrograms/dl. The ATSDR states on their website that despite blood levels of lead still being quoted as the standard, that total body burden is much more accurate. NO LEVEL IS SAFE ACCORDING TO THE ATSDR. The January 2003 article in NEJM demonstrated that thirty IV EDTA treatments in "high normal" urine lead patients returned impaired kidney function back to baseline and reduced all health care costs 95% over the following three years. These results were statistically related to total body burden per urine testing and NOT blood serum levels.

Lead binds to sulfhydryl membrane groups as well as hydroxyl, phosphate, and amino acid sites on proteins. It interferes with heme synthesis, iron transport, red blood cell lifespan and many of the liver detoxification (Cytochrome P450) metabolic pathways. Other health effects include reduced Vitamin D synthesis, slowed nerve conduction, neuropathy, hypertension, loss of mental function and lower IQ. Anemia, encephalopathy and neuropathy are end stage conditions of lead excess. Porphyrias with abdominal pain, skin lesions and mental disorders can also result. Inflammatory vascular disease, starting with hypertension, is thought to progress to atherosclerotic disease. Heavy metal ions such as lead are implicated in this process.

In adults, early lead toxicity is typically overlooked or misdiagnosed. Neurological complaints such as peripheral neuropathy or carpal tunnel syndrome can be early signs of lead related health problems. Surgery has resulted from incorrectly diagnosed abdominal pains. Moderate lead toxicity can result in concentration problems, headaches, tremor or general fatigue. Muscular exhaustion, diffuse abdominal pain, constipation, weight loss or vomiting can also be seen at this level. Severe lead toxicity results in paresis or paralysis, lead lines on gingival tissue, encephalopathy, seizures, coma, and severe colic/abdominal pain. In children, early lead symptoms are frequently neurobehavioral changes, poor classroom performance and impaired interaction responses with others.

Sources of lead in adults come from release of lead from aging bone as well as occupational exposure from work with lead. Other sources include joints in old water mains, batteries, bullets, fishing sinkers, contaminated food and candy (Mexico), old paints and ceramic glazes, sewage sludge, and old building materials. Children are at increased risk due to increased absorption and have demonstrable IQ drops with lead levels below even 10ug/dl. It should also be noted that heavy metals can be passed from mother to child in both pregnancy and by breastfeeding.

Occupational Standards ( These are compromised political numbers not related to medical symptoms -see NPR Morning edition, Apr 19, 2004 ): NIOSH .1mg/mg/m3 air so that worker's blood level remains .060mg/gm whole blood; OSHA PEL .05mg/m3 (8 hr day-40 hr/week; CDC : 10 micrograms/dl is considered poisoned ATSDR : Minimal Risk Level (MRL): There is NO safe threshold for lead's most sensitive effects especially nerves.



Mercury is the #3 "CERCLA" toxin in the US (www.atsdr.cdc.gov/clist.html). This means you are very likely to be exposed in everyday life. Mercury comes in various chemical forms and each form binds to different tissues, has different half lives, and is excreted differently. There are three forms of mercury: inorganic, organic and elemental. Inorganic mercury is found in the salt form, is in cleansers such as Ajax and Comet, Dove and Ivory soaps. It is minimally absorbed from the skin (2-3%) and minimally absorbed in the GI tract (7-15%) but can be changed into a very toxic form if candida or other bowel dysbiosis is present. Inorganic mercury does not cross into the brain. Elemental mercury is found in dental amalgams, electrical switches, thermometers, fossil fuel plants, and latex paints prior to 1992, and is able to cross into the brain, where it can stay for twenty years. The amount of time it can stay in the blood is forty-five days. It is primarily excreted in the bile, although urinary excretion will increase as the toxic burden increases. Organic mercury is extremely toxic and stays fifty to eighty days in the blood and twenty years in the brain. It is converted from inorganic mercury by microorganisms and then taken up by plants and fish, working its way up the food chain to humans. Fish meal fed to poultry has high concentrations of mercury. Coal burned to produce energy (common in the Midwest ) emits over 30% of the mercury in the environment, another 19% comes from municipal incinerators, and the remainder comes from miscellaneous sources. Surveyed lands show an increase in topsoil mercury of 300% since 1850. One in ten women of child bearing age have amounts of mercury in their body considered toxic to developing fetuses. The main exposure in the US today is from fish. Mercury in the organic form is absorbed 90% from the gut. This absorption can be reduced by eating foods high in sulfamethyl glutathione at the same time as exposure such as egg whites, milk and red meat. DMSA is an oral chelator that is much more specific for mercury than EDTA, although DMPS has an even higher affinity.


Mercury can be a severe neurotoxin, cause immune dysfunction including autoimmune conditions, and lead to hormone disruption. Chronic mercury exposure produces excitability and tremor, memory loss, insomnia, anorexia and weight loss, gingivitis and stomatitis. "Pink" disease in children features acrodynia, rash, photophobia, increased perspiration and salivation. Acute vapor exposure inflames the bronchial tubes and causes pneumonitis. Irreversible neurological damage is common. Organic mercury has a high affinity for the posterior cortex of the brain while inorganic mercury concentrates mostly in the kidneys. Hypertension, especially in young children, skin peeling, excessive sweating, cardiovascular problems, renal tubular disease, nausea and diarrhea and elevated liver function tests are also medical conditions seen with excessive mercury.



Cadmium is the #7 "CERCLA" toxin in the US (www.atsdr.cdc.gov/clist.html). It is a very toxic substance and carcinogenic at any level. The half life in the human body is ten to forty years and urine is the preferred method of measuring body burden. While over 500,000 people are potentially exposed at their occupational environment (jewelers, metal plating, cadmium batteries, soldering, smelting, zinc and lead mining, production of plastics), contaminated topsoil is the most likely mechanism of human exposure through edible produce and tobacco. Leafy greens and potatoes have the most cadmium, but grains, fruits and vegetables are also contaminated through fertilizers made of sewage sludge and zinc tailings. Organ meats and shellfish have very high reported concentrations. The current EPA Minimal Risk Level (MRL) for cadmium is 2 micrograms/kg/day (14 micrograms for the average person) and the WHO reported that the average intake in non-polluted areas is 40-100 micrograms/day and as much as 200+ micrograms/day in polluted areas. Only 5% is absorbed orally in the GI tract but smokers absorb 1-2 micrograms per pack. Inhaled cadmium is absorbed 10-50%. Low intake of protein, low levels of minerals including zinc, iron, or copper, and increased alcohol intake causes increased cadmium absorption. Iron deficiency anemia increases absorption 5-20% and patients with a serum ferritin below 12 micrograms/dl are considered to be high risk for cadmium induced renal lesions.

Cadmium binds metallothionein (a protein that is 33% cysteine) in the liver preventing it from depleting glutathione and thereby causing damage. In the kidney, this complex is then filtered and can cause nephrotoxicity with proteinuria, excessive excretion of amino acids, damage to kidney tubules, and poor metabolism of Vitamin D with resulting osteomalacia. Besides impairment of renal tissue, cadmium binds to sulfhydral, hydroxyl, carboxyl and phosphatidyl sites and can cause dysfunction of cellular energy production. Cadmium also absorbs in the bone, pancreas, adrenal glands, and placenta although over 50% is concentrated in the liver and kidneys.

Oral cadmium can cause GI distress, and vapor can cause pulmonary edema or emphysema. Iron deficiency anemia can result from absorbed cadmium and neuropsychiatric disorders are reported. Synergistic toxicity occurs in combination with lead and mercury. Acute exposures can result in the symptoms of painful urination, frequent urination, shortness of breath, chest pain, irritability, headache, and dizziness. Chronic exposures result in damage to genes, inflammation, vascular damage, cancer, osteoporosis and renal lesions.

Removal of cadmium from the body and reduction of toxicity is the main goal. Zinc has been shown to increase metallothionein and protect organs against damage. Lipoic acid, selenium, and melatonin help mitigate oxidant damage. NAC, methionine, cysteine and zinc, when combined with chelation agents like DMPS or DMSA raise metallothionein levels and remove intracellular cadmium stores.

Occupational Standards: NIOSH Carcinogen at any level-reduce exposure to lowest level possible OSHA PEL: 5 micrograms/m3 (8 hour day/40 hour week) ATSDR: .0002 micrograms/kg/day (ingestion more than 350 days IDLH: 50mg/m3-dust; 9 mg/m3 fumes.



Arsenic is the #1 "CERCLA" toxin in the US (www.atsdr.cdc.gov/clist.html) meaning you have a very high chance of encountering it on a daily basis. It is a known environmental carcinogen causing 1 in 100 cancers in people exposed to water containing 50 micrograms/dl or more per day and 1 in 200 cancers with water at 20 micrograms/dl. Normal water concentrations allowed for other substances do not allow any substance with 1 in 10,000 chance of causing cancer. The half life in the body depends on which tissue it is deposited in and ranges from two hours to two hundred eighty days in lungs, skin, kidney, liver, spleen, bones and muscle. Increased urinary arsenic indicates exposure, but does not necessarily imply total body accumulation. A single fish meal can increase the arsenic level in urine fifty to one hundred times. Arsenic can be excreted in larger concentrations in the urine after ingestion of sulfhydryl detoxifying agents such as DMPS, DMSA, SAMe, and D-penicillamine. Arsenic can have various forms and oxidation states. Arsenic can be e liminated via the bile with glutathione, selenium and SAMe complexes in two to four weeks.

Acute symptoms of excessive arsenic ingestion include nausea, diarrhea, abdominal cramping, extreme sensations or pain in extremities, abnormal reflexes and abnormal EKG rhythms. These symptoms usually occur at levels of 50 micrograms/kg/day or higher. Chronic exposure causes leucopenia, anemia, peripheral neuropathy, elevated liver function tests, peripheral vascular disease, hypertension, headaches, fatigue, irritation of mucous membranes, white streaking of nails, thickening of the pads of feet and hands, hair loss, skin cancers (especially in non-sun exposed areas), cirrhosis of the liver and liver cancers. Characteristic brown skin lesions with teardrop shaped whitening in the middle are seen with chronic arsenic poisoning.

90% of all arsenic produced today is used as a preservative for wood. Copper arsenate (CCA) treated wood was phased out of production in 2004, however, existing treated wood, dust from such treated wood, and remodeling of structures built with treated wood creates a potentially dangerous level of exposure (as little as 2.5 ounces is dangerous to a child). While 60-90% of inhaled arsenic is absorbed, very low dermal absorption occurs. A child playing on treated wood playground equipment may ingest a large amount if food is ingested before washing hands. While inorganic arsenic compounds can no longer be used in agriculture in the US , organic arsenic is still used in large amounts. The greatest use of arsenic in alloys is in lead-acid auto batteries, semiconductors, photo-emitting diodes (blinking lights and lasers), bronzing, ceramics, fireworks (intense blue and white), leather tanning and taxidermy. Pesticides and herbicides contain arsenic compounds . EPA Minimum Risk Level (MLR) = .7-5.6 micrograms/adult. Twice this level results in chronic arsenosis. The total amount of arsenic from air, water and food daily is generally about 50 micrograms each day. The level of inorganic arsenic (the form of most concern) from these sources is generally about 3.5 micrograms/day. Those living near industrial exposure may have exposures up to 12 micrograms/kg/day!! Cigarettes have 1.4 micrograms arsenic per cigarette, 28 micrograms per pack!

Occupational: NIOSH: carcinogen at any exposure; NIOSH REL: .002mg/m3 (ceiling exposure of 15 min); OSHA PEL : .010 mg/m3; NOAEL: Up to .01 micrograms/kg/day ingestion; IDLH 100mg/m3

Special thanks to Lyn Patrick , ND for her article: Toxic Metals and Antioxidants: Part II. The Role of Antioxidants in Arsenic and Cadmium Toxicity. Alternative Medicine Review Vol 8, No 2, 2003

The ideas and advice contained on these pages based upon an extensive review of the scientific literature. However, this is definitely not intended to be a substitute for careful medical evaluation and treatment by a competent, licensed personal health care professional. Oaktree Wellness Center does not recommend changing any current medications or adding any new therapies without personally consulting a fully qualified physician. Oaktree Wellness Center and its staff specifically disclaim any liability arising directly or indirectly from information contained on these pages. Varying and even conflicting views are held by other segments of the medical profession. The information presented on these pages is intended to be educational in nature and is not intended as a bias for diagnosis or treatment. This information is current at the time and is published and distributed as a courtesy to the public.