HEAVY METALS, DISEASE & TREATMENT
The U.S. Center for Disease Control ranks toxic metals as the number one environmental health threat to children, adversely affecting large numbers of children in the U.S. each year (1-4). According to an EPA/ATSDR assessment, the toxic metals lead, mercury, and arsenic are the top three toxic metals having the most adverse health effects on the public based on toxicity and current exposure levels in the U.S. (1), with cadmium, chromium and nickel also highly listed. Large numbers of people have been found to have allergic conditions and immune reactive autoimmune conditions due to the toxic metals, especially inorganic mercury and nickel (5, 6).
Heavy metal poisoning is so common these days that it is literally impossible to avoid it as even young newborns have been shown to have heavy metals as soon as they emerge from their mother’s womb, as well as receive mercury from breastfeeding (7 – 10). A recent report published by Reuters from the Environmental Working Group showed that blood samples of umbilical blood taken by the American Red Cross from ten babies showed an average of 287 contaminants in the blood, including mercury, fire retardants, pesticides and the Teflon chemical PFOA (11).
Interesting research has shown a positive correlation between the level of mercury in mother’s breast milk and the number of dental amalgams in their mouth. The mean levels of mercury in milk of amalgam-free mothers was < 0.2 microgram/L, while milk from mothers with 1-4 amalgam fillings contained 0.57 microgram/L, with 5-7 fillings 0.50 microgram/L and with more than 7 fillings 2.11 micrograms/L (12).
Many epidemiologists believe that this prenatal or postnatal exposure to toxic metals is probably responsible for over 50% of learning difficulties and cognitive disturbances in all U.S. children. Many studies are estimating that over 20% of the children in the U.S. have had their health or learning significantly adversely affected by toxic metals such as mercury, lead, and cadmium. Furthermore, toxic metals have been documented to be reproductive and developmental toxins, causing birth defects and damaging fetal development, as well as causing neurological effects, developmental delays, learning disabilities, depression, and behavioral abnormalities in many otherwise normal-appearing children (13–46). Such effects are also found in adults (46).
Sources of exposure to Toxic Metals
Heavy metals have been implicated in various research studies to cause as many as 20% of learning disabilities, 20% of all strokes and heart attacks, and in certain areas to be a factor in over 40% of all birth defects (46). The U.S. Center for Disease Control has found that primary exposure to lead is from paint chips, drinking water, fertilizer, food, auto and industrial emissions, and dust. High levels of cadmium are found in regions with high emissions from incinerators, coal plants, or cars (5), as well as in shellfish (47) and cigarette smoke (5). Other common sources include rural drinking water wells (5), processed food, fertilizer, and old paint. Common exposures to aluminium include aluminium cookware, antiperspirants, cheese and other processed food. Nickel, which is highly toxic and commonly causes immune reactions, is commonly seen in dental crowns and braces, along with jewellery, etc. (nickel and inorganic mercury commonly produce allergic type autoimmune problems, (6). Manganese and other metal exposure can come through welding or metal work. Cadmium, mercury, arsenic, chromium, silver, copper, and are other metals to which Floridians and others are commonly exposed in drinking water, food, or dental materials (47-49).
The most common significant exposure for most people is to mercury vapor from amalgam fillings (46). Dental amalgams usually emit 1-10 ug/day; the amount of mercury in the brain is strongly correlated with the number of dental fillings. Researchers have shown that chewing gum can double the mercury levels in the blood and treble the levels in urine for those that have amalgam fillings.
Seafood contaminated with mercury is another issue of concern – generally larger fish have most mercury, due to bioaccumulation in the food chain. The highest levels of mercury have been found in the following fish (mean mercury levels in parts per million (ppm); Tilefish 1.45; Swordfish, 1.00; Shark, 0.96; King Mackerel, 0.73 and Grouper (Mycteroperca) 0.43. Lowest levels have been found in the following fish – Tuna (fresh or frozen) 0.32; Lobster Northern (American) 0.31; Halibut 0.23; Tuna (canned) 0.17; Crab Blue 0.17; Scallop 0.05; Catfish 0.07; Salmon ND; Oysters ND; Shrimp ND (ND = not detectable). During the spring of 2001 the State Department of Health (DOH) issued a fish-consumption advisory for women of childbearing age and children under age six, due to high levels of mercury in certain breeds of carnivorous fish, such as shark, swordfish, tilefish, king mackerel, and tuna.
Another major exposure source to infants is from thimerosal, a water-soluble, cream-colored crystalline powder used as a preservative in vaccines that contain 49.6% mercury by weight and is present in over 30 licensed vaccines in the US in concentrations of 0.003% to 0.01%. In the human body, thimerosal is metabolised to ethylmercury and thiosalicylate (67, 68).
The EPA safe limit for mercury exposure is 0.1 mcg/kg; that is one tenth of a microgram. It is common for most children to be vaccinated on the day of birth with the hepatitis B vaccine which contains 12 mcg of mercury (30 times the safe level); at 4 months with the DtaP and HiB vaccine on the same day which provides a further 50 mcg of mercury (60 times the safe level); at 6 months they receive the Hep B, Polio with a further 62.5 mcg of mercury (78 times the safe level). These figures are calculated for an infant’s average weight in kilograms for each age. By age two, American children have received 237 micrograms of mercury through vaccines alone, which is thousands of times more than the EPA safe limit (52).
It is known that the mercury in the thimerosal preservative in vaccines is 50 times more toxic than liquid mercury. This is because injected mercury is far more toxic than ingested mercury and converts to ethylmercury, which has a natural affinity for brain cells and nerves. The fact that babies do not have a blood-brain barrier makes penetration easier. Moreover, infants have difficulty excreting mercury, as they do not produce bile, which is required for proper excretion (51, 67, 68). If the nurse giving the injection did not shake the vial according to directions before drawing out the vaccine dose, there is a chance that the child receiving the last dose could get as much as 10 times the usual amount in one dose.
Harmful Effects of Heavy Metals
Studies have found that heavy metals such as mercury, cadmium, lead, and tin affect chemical synaptic transmission in the brain and the peripheral and central nervous system (32a, 40-43, 46, 50). They also have been found to disrupt brain and cellular calcium levels that significantly affect many body functions: such as (a) calcium levels in the brain affecting cognitive development and degenerative CNS diseases (5, 13, 28, 46, 52) (b) calcium-dependent neurotransmitter release which results in depressed levels of serotonin, norepinephrine, and acetylcholine (5,13, 51-55, 46) – related to mood and motivation; (c) cellular calcium-sodium ATP pump processes affecting cellular nutrition and energy production processes (5,13, 46); (d) calcium levels in bones causing skeletal osteodystery (13, 56) . Toxic metals have also been found to affect cellular transfer and levels of other important minerals and nutrients that have significant neurological and health effects such as magnesium, lithium, zinc, iron, Vitamins B-6 & B1-12 (21, 49, 54, 56, 57). Based on thousands of hair tests, at least 20 % of Americans are deficient in magnesium and lithium (13, 58, 59), with zinc deficiencies also common. The resulting deficiency of such essential nutrients has been shown to increase toxic metal neurological damage (13, 46, 51, 56).
Studies have also found heavy metals to deplete glutathione and protein-bound sulfhydryl SH groups, resulting in inhibiting SH-containing enzymes and production of reactive oxygen species such as superoxide ion, hydrogen peroxide, and hydroxyl radical (42, 46, 53-55). This has been found to be a major factor in neurological and immune damage caused by the heavy metals, including damage to mitochondria and DNA(40-43, 46), as well as chronic autoimmune conditions and diseases (6).
High lead levels have been found to be associated with Attention deficit hyperactivity disorder (ADHD), impulsivity, and inability to inhibit inappropriate responding (28a). High aluminium levels are related to encephalopathies and dementia (60). Some individuals have been found to be more sensitive to toxic metals depending on genetic sensitivity and past exposure to toxic substances (5, 6). Nickel exposure is common and nickel exposure has been found to be significantly related to perinatal unthriftiness and mortality in animal studies and large numbers of people affected by allergic conditions such as eczema and psoriasis vulgaris (61) and serious autoimmune conditions such as lupus and CFS (5).
Other agents including mercury are known to accumulate in endocrine system organs such as the pituitary gland, thyroid, and hypothalamus and to alter hormone levels and endocrine system development during crucial periods of development (27, 39, 40, 46). Such effects are usually permanent and affect the individual throughout their life. Some of the documented effects of exposure to toxic metals include significant learning and behavioural disabilities, mental retardation, autism, etc. But even some of the relatively subtle effects that have been found to occur such as small decreases in IQ, attention span, and connections to delinquency and violence, if they occur in relatively large numbers over a lifetime can have potentially serious consequences for individuals as well as for society (34, 40, 44, 45). The incidence of neurological conditions in children such as autism has increased over 200% in the last decade (62), and mercury has been found to be a factor in most of those tested (63).
Treating Heavy Metal Toxicity
Many health practitioners use synthetic chelating agents such as DMPS, DMSA, EDTA and others to mobilize and eliminate heavy metals from the body. There are advantages and disadvantages to using these. One advantage is the power of their mobilizing activity – they are quick to mobilize and eliminate certain metals in the body, but this may place a huge burden on the body’s detoxification system. DMSA, for example, can create tissue redistribution of mercury as decreasing mercury levels in the kidney (the organ accumulating mercury most abundantly) increase mercury concentrations in the blood, brain, lung, heart, muscle and liver (Gregus et al).
34. Smith DR, et al: Succimer and the urinary excretion of essential elements in a primate model of childhood lead exposure, Toxicological Sciences 2000 Apr;54(2):473-80.
35. Ding GS, Liang YY: Antidotal effects of dimercaptosuccinic acid, Journal of Applied Toxicology, 1991 Feb; 11(1):7-14.
Natural medical physicians throughout the US have reported MS symptoms in adults and intractable seizures in paediatric patients with high dose and extended use of DMSA (2, 3-dimercaptosuccinic acid), Chemet or Succimer.
Other Problems with DMSA
Extended use of DMSA can cause mild to moderate neutropenia with increased SGOT, SGPT, Platelet count, Cholesterol, Alkaline Phosphatase and Blood Urea Nitrogen (BUN). Adverse reactions to DMSA include ataxia, convulsions, rash, nausea, diarrhea, anorexia, headache, dizziness, sensorimotor neuropathy, decreased urination, arrhythmia, infection. Zinc excretion doubles during the administration of DMSA. Patients must be kept hydrated as renal function can be compromised.
For the above-described reasons in all good conscious we cannot recommend the use of DMSA for the treatment of mercury toxic pediatric patients.
Approaching the fragile brain architecture of young children with autism, PDD and seizure disorders brings about tremendous responsibility in protecting the children from invasive interventions that risk alteration in brain function.
Talk about HMD ……………………………………
1) ATSDR/EPA Priority List for 1997: Top 20 Hazardous Substances, Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services, 1998, http://www.atsdr.cdc.gov/cxcx3.html & EPA targets 17 toxics, Science News, February 16,1991; & 9-13-86, p164.
2) U.S. Environmental Protection Agency, Hazardous Air Pollutant Hazard Summary Fact Sheets, EPA: In Risk Information System, 1995; & U.S. Environmental Protection Agency (EPA), 1996, Integrated Risk Information System, National Center for Environmental Assessment, Cincinnati, Ohio (& webpage);
3) Nriagu, J.O. Global Metal Pollution – Poisoning the Biosphere, Environment, Vol 32, No. 7, Sept. 1990; & Shukla GS, Singhal RL. The present status of biological effects of toxic metals in the environment: lead, cadmium, and manganese. Can J Physiol Pharmacol 1984; Aug; 62(8):1015-31; & Science News, Nov 6, 1986, P327-.
4) Agency for Toxic Substances and Disease Registry, U.S. Public Health Service.
5) Stewart-Pinkham, S M. The effect of ambient cadmium air pollution on the hair mineral content of children. The Science of the Total Environment 1989; 78: 289-96. (28).
6) Stejskal VDM, Danersund A, Lindvall A, Hudecek R, Nordman V, Yaqob A et al, Metal-specific memory lymphocytes: biomarkers of sensitivity in man. Neuroendocrinology Letters, 1999; & Tibbling, L., Stejskal VDM, et al, Immunological and brain MRI changes in patients with suspected metal intoxication, Int J Occup Med Toxicol 1995; 4(2):285-294. (29).
7) Tsuchiya, H; Mitani K; Kodama K; Nakata, T. Placental transfer of heavy metals in normal pregnant Japanese women, Arch Environ Health, 1984 Jan, 39:1, 11-7.
8) Ong, CN; Chia, SE; Foo, SC; Ong, HY; Tsakok, M; Liouw, P. Concentrations of heavy metals in maternal and umbilical cord blood, Biometals, 1993 Spr, 6:1, 61-6.
9) Truska, P, Rosival, L, Balazova, G, Hinst, J, Rippel, A, Palusova, O, Grunt, J. Blood and placental concentrations of cadmium, lead, and mercury in mothers and their newborns. J Hyg Epidemiol Microbiol Immunol. 1989;33(2):141-7.
10) Yang J, Jiang Z, Wang Y, Qureshi IA, Wu XD. Maternal-fetal transfer of metallic mercury via the placenta and milk. Ann Clin Lab Sci. 1997 Mar-Apr; 27(2):135-41.
11) Maggie Fox, Unborn Babies Soaked in Chemicals, Survey Finds, Reuters, July 14, 2005.
12) Drasch G, Aigner S, Roider G, Staiger F, Lipowsky G. J. Mercury in human colostrum and early breast milk. Its dependence on dental amalgam and other factors. Trace Elem Med Biol. 1998 Mar; 12(1):23-7.
13) Goyer RA, National Institute of Environmental Health Sciences. Toxic and essential metal interactions. Annu Rev Nutr 1997; 17:37-50; & Nutrition and metal toxicity. Am J Clin Nutr 1995; 61(Suppl 3): 646S-650S. (5)
14) Marlowe M, Cossairt A, Moon C. Errera J. Main and Interactive Effects of Metallic Toxins on Classroom Behavior, Journal of Abnormal Child Psychology 1985; 13(2): 185-98. (6)
15) Pihl, RO, Parkes, M. Hair element content in learning disabled children. Science 1977 Oct 14;198(4313):204-6. (7)
16) Moon, C, Marlowe, M Stellem, J, Errera, J. Main and Interactive Effects of Metallic Pollutants on Cognitive Functioning, Journal of Learning Disabilities 1985; 18(4):217-221. (8)
17) Lewis, M, Worobey, J, Ramsay, DS, McCormack, MK. Prenatal exposure to heavy metals: effect on childhood cognitive skills and health status. Pediatrics 1992;89(6 Pt 1):1010-15. (9)
18) Capel, ID, Pinnock, MH, Dorrell, HM, Williams, DC, Grant, EC. Comparison of concentrations of some trace, bulk, and toxic metals in the hair of normal and dyslexic children. Clin Chem 1981 Jun;27(6):879-81. (10)
19) Marlowe, M, Errera, J, Jacobs, J. Increased lead and cadmium burdens among mentally retarded children and children with borderline intelligence. Am J Ment Defic 1983 Mar; 87(5):477-83; & Journal of Special Education 1982; 16:87-99. (11)
20) Thatcher, RW, Lester, ML, McAlaster, R, Horst, R. Effects of low levels of cadmium and lead on cognitive functioning in children. Arch Environ Health 1982 May-Jun;37(3):159- 66. (12)
21) Marlowe, M, Errera, J, Cossairt, A, Welch, K. Hair mineral content as a predictor of learning disabilites. Journal of Learning Disabilites 1985. (13)
22) Marlowe, M, Errera, J, Jacobs, J. Increased lead and mercury levels in emotionally disturbed children. Journal of Orthomolecular Psychiatry 1983; 12: 260-267; & Journal of Abnormal Psychology 1983; 93:386-9. 14
23) Marlowe, M, Moon, C, Errera, J, Jacobs, J. Levels and combinations of metallic toxins and measures of behavioral disturbance. In: Rutherford RB(Ed.), Monographs in Behavior Disorders, Vol 5, p76-85; Council for Children and Behavior Disorders, Reston Va. 15
24) Wecker, L, Miller, SB, Cochran, SR, Dugger, DL, Johnson, WD. Trace element concentrations in hair from autistic children. Defic Res 1985; 29(Pt 1): 15-22. 16
25) Rimland B, Larson GE. Hair mineral analysis and behavior: An analysis of 51 studies. Journal of Learning Disabilities 1983; 16: 279-85. 17
26) Jiang HM, Han GA, He ZL. Clinical significance of hair cadmium content in the diagnosis of mental retardation of children. Chin Med J (Engl) 1990 Apr; 103(4): 331-4. 18
27) Chisolm, J. Toxicity from heavy metal interactions and behavioral effects. Pediatrics 1974; 53:841-43. 19
28) Bonithon-Kopp, C, Huel, G, Moreau, T, Wendling, R. Prenatal exposure to lead and cadmium and psychomotor development of the child at 6 years. Neurolbehav Toxicol Teratol 1986; 8(3): 307-10. 20
29) Needleman, HL, Leviton, A, Reed, R. Deficits in Psychological and classroom performance of children with elevated dentine lead levels. New Eng J of Med 1979; 300: 689-95 21
30) Winneke, G, Kramer, U, et al. Neuropsychological studies in children with elevated tooth lead. International Archives of Occupational Environmental Health, 1983; 51:231-252. 22
31) Burde de la, B, Dhoate, M. Early asymptomatic lead exposure and development at school age. Journal of Pediatrics 1975; 87: 638-642. 23
32) Albert, RE, Shore, RE, Sayers, AJ, et al. Environmental Health Perspectives 1974; 7:33-40. 24
33) Needleman, HL. Behavioral Toxicology. Environ Health Perspect 1995; 103(Supp6): 77-79. 25
34) Abadin, HG, Hibbs, BF, Pohl, HR, U.S. Department of Health, Division of Toxicology, Agency for Toxic Substances and Disease Registry. Breast-feeding exposure of infants to cadmium, lead, and mercury: a public health viewpoint. Toxicol Ind Health 1997; 13(4): 495-517. 26
35) Boadi, WY, Urbach, J, Branes, JM, Yannai, S. In vitro exposure to mercury and cadmium alters term human placental membrane fluidity, Pharmacol 1992; 116(1): 17-23. 27
36) Clarkson, T.W. et al, Reproductive and Developmental Toxicity of Metals, Scandinavian J. of Work & Environmental Health, 1985; 11:145-154. 30
37) Lutz, E, Lind, B, Herin, P, Krakau, I, Bui, TH, Vahter, M. Concentrations of mercury, cadmium, and lead in brain and kidney of second trimester fetuses and Infants. Journal of Trace Elements in Medicine and Biology 199;10:61-67. 31
38) Drasch, G. et al, Mercury Burden of Human Fetal and Infant Tissues, Eur J Pediatr 153:607- 610,1994; 32
39) Colburn, T. et al, Developmental Effects of Endocrine-Disrupting Chemicals in Wildlife and Humans, Environmental Health Perspectives, Vol 101(5), Oct 93; & Mercury Found in Dead Florida Bay Cormorants, Tallahassee Democrat, 1-15-95; & Are Environmental Hormones Emasculting Wildlife, Science News 1994;145: 25-27; & Facemire, C.F. et al, Reproductive impairment in the Florida Panther, Health Perspect,1995, 103 (Supp4):79-86; & Gerhard, I. et al, The limits of hormone substitution in pollutant exposure and fertility disorders, Zentralbl Gynakol, 1992, 114, 593-602. 33
40) Casdorph, H.R., Toxic Metal Syndrome, Avery Publishing Group, 1995 & S.E. Levick, Yale Univ. School of Medicine, New England Journal of Medicine; July 17, 1980. 37
41) Atchison, WD. Effects of neurotoxicants on synaptic transmission: lessons learned from electrophysiological studies. Neurotoxicol Teratol 1988 Sep-Oct;10(5):393-416. 38
42) Stohs, SJ, Bagchi, D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med 1995 Feb;18(2):321-36. 39
43) Lopez-Ortal, P, Souza, V, Bucio, L, Gonzalez, E, Gutierrez-Ruiz, M. DNA damage produced by cadmium in human fetal hepatic cell line. Mutat Res 1999 Feb 19;439(2):301-6. 40
44) Rodier, P.M. Developing brain as a target of toxicity. Environ Health Perspect 1995; 103(Supp 6): 73-76. 41
45) Rice, D.C., Issues in developmental neurotoxicology: interpretation and implications of the data. Can J Public Health 1998; 89(Supp1): S31-40. 42
46) Windham, B. Annotated Bibliography: Health Effects Related to Mercury from Amalgam Fillings and Documented Clinical Results of Replacement of Amalgam Fillings 1999. (over 600 references) 43
47) Florida Dept. of Environmental Protection, Florida Coastal Sediment Contaminants Atlas: A Summary of Coastal Sediment Quality Surveys, 1994; & Mac Donald Environmental Sciences Ltd., Development of an Approach to the Assessment of Sediment Quality in Florida Coastal Waters,FDEP,January 1993; & Trefry, J.H. et al, Marine & Environmental Chemistry Laboratories, Fla. Institue of Technology, Toxic Substances Survey for the Indian River Lagoon System, Volume I: Trace Metals in the Indian River Lagoon, SJWMD, Feb 1993; & D.C.Heil, Fla. Dept. of Natural Resources, Division of Marine Resources, Evaluation of Trace Metal Monitoring in Florida Shellfish, March 1986; & U.S. EPA, Environmental Monitoring and Assessment Program, Estuaries: Louisianian Province-1992 & 1991. (36)
48) U.S. Fish & Wildlife Service, Cadmium Hazards to Fish, Wildlife, and Invertebrates, Contamination Hazard Biological Report 85(1.2), 1987; & Mercury bioaccumulation in lake ecosystems, Electric Power Research Institute, EPRI Journal, December, 1994, p5. 34
49) Birth Defects Prevention News, March 1986, p3. 35
50) Boadi, WY, Urbach, J, Branes, JM, Yannai, S. In vitro exposure to mercury and cadmium alters term human placental membrane fluidity, Pharmacol 1992; 116(1): 17-23. 27
51) Petit, TL, et al, Early lead exposure and the hippocampus. Neurotoxicology 1983; 4(1): 74-79. 57
52) Smith, JB; Dwyer, SD; Smith, L. Cadmium evokes inositol polyphosphate formation and calcium mobilization. Evidence for a cell surface receptor that cadmium stimulates and zinc antagonizes. J Biol Chem 1989 May 5;264(13):7115-8. 74
53) Webb, M. Cadmium. Br Med Bull 1975, 31: 246-50; & Singhal, RL, Merali, Z. Aspects of the biochemical toxicity of cadmium. Biochem Aspec Toxic Agents 1979, 35: 75-80; & Underwood, EJ. Trace Elements in Nutrition. 1977, Academic Press, NY, NY. 44
54) Spivey-Fox, MR. Nutritional influences on metal toxicity. Environ Health Perspect 1979; 29: 95-104. 46
55) Hernberg, S; & Moore, MR. in Lead Toxicity, Singhal, R. & Thomas, J. (eds), Urban & Schwarzenberg, Inc. Baltimore, 1980; & Govani, S, Memo, M. Chronic lead treatment differentially affects dopamine synthesis, Toxicology 1979, 12:343-49; & Scheuhammer, AM, Cherian, MG. Effects of heavy metal cations and sulfhydyl reagents on striatal D2 dopamine receptors. Biochem Pharmacol 1985, 34(19): 3405-13. 47
56) Nonaka, S. et al, Nat. Inst. of Mental Health, Bethesda Md., Lithium treatment protects neurons in CNS from glutamate induced excitibility and calcium influx, Neurobiology, Vol 95(5):2642-2647, Mar 3, 1998. 75
57) Huel, G, et al, Cadmium and lead content of maternal and newborn hair: relationship to parity, birth, and hypertension. Arch Environ Health 1981; 36(5): 221-7; & Huel, G, et al, Increased hair cadmium in hair of newborns of women occupationally exposed to heavy metals. Environ Res 1984; 35(1): 115-21. 54
58) Starobrat-Hermelin, B. The effect of deficiency of selected bioelements on hyperactvity in children with certain specified mental disorders. Ann Acad Med Stetin 1998; 44:297-314. [article in Polish] 68
59) Schrauzer, GN, Shrestha, KP, Flores-Arce, MF. Lithium in scalp hair of adults, students, and violent criminals. Effects of supplementation and evidence for interactions of lithium with vitamin B12 and with other trace elements. Biol Trace Elem Res 1992 Aug;34(2):161-76. 76
60) Bowdler, NC, Beasley, DS. Behavioral effects of aluminum ingestion. Pharmacol Biochem Behav 1979; 10: 505-512; & Trapp GA, Miner GD. Aluminum levels in brain in Alzheimer’s Disease. Biol Psychiatry 1978; 13: 709-718. 49
61) Nielsen, FH, et al, Nickel deficiency in rats. J Nutr 1975; 105(12):1620-30; & Smith, SA, et al, Elevated serum nickel concentration in psoriasis vulgaris. In J Dermatol 1994. 33(11): 783-5. 59
62) California Health and Human Services Agency, Dept. Of Developmental Services, 1999; & Autism Research Center (http://www.autism.com/ari) and National Vaccine Information Center (http://www.909shot.com). 80
63) Autism: a unique form of mercury poisoning. http://www.canfoundation.org/newcansite/sciwatch/invest.html 81
64) Marlowe, M Stellern, J, Errera, J, Moon, C. Main and interaction effects of metal pollutants on visual-motor performance. Arch Environ Health 1985; 40(4):221-5. (6a).
65) David, OJ, Hoffman, SP, Sverd, J, Clark, K. Am J Psychiatry 1976; 133: 1155; & Perino, J, Ernhart, CB. Proc Annu Conv Am Psychol Assoc 1973; 81:719; & Leviton, A, Bellinger, D, Allred, EN. Pre- and postnatal low-level lead exposure and children’s disfunction in school. Environ Res 1993; 60(1): 30-43; & Eppright, TD, Samfacon, JA, and Horwitz, EA. ADHD, infantile autism, and elevated blood level: a possible relationship. Mo Med 1996; 93(3): 136-8; & Brockel, BJ, Cory-Slechta, DA. Lead, attention, and impulsive behavior. Pharmacol Biochem Behav 1998; 60(2):545-52. 20a
66) Annau Z, Cuomo V. Mechanisms of neurotoxicity and their relationship to behavioral changes. Toxicology 1988; 49(2-3): 219-25. 24a
67) Halsey, N. Limiting infant exposure to thimerosal in vaccines. JAMA 1999;282: 1763.
68) Pichichero, M.E., Cernichiari, E., Lopreiato, J., Treanor, J. Mercury concentrations and metabolism in infants receiving vaccines containing thimerosal: a descriptive study, The Lancet. November 30, 2002.
(48) Pfeiffer CC, Iliev V. A study of copper excess and zinc deficiency in schizophrenia. in: International Review of Neurobiology, Supplement 1, Academic Press, NY,NY, 1972, p141-164;& Alexander PE, Van Kammen DP. Serum magnesium and calcium levels in schizophrenia. Arch Gen Psychiatry 1979; 36: 1372-77.
Dietrich KN, Berger OG, Succop PA. The developmental consequences of low to moderate postnatal lead exposure. Neurotoxicol Teratol 1993; 15(1): 37-44.
(51) Tong S, Baghurst P, McMichael A, Sawyer M. Lifetime exposure to lead and children’s intelligence at 11-13 years: Port Pirie cohort study. BMJ 1996; 312(7046): 1569-75.
(52) Moon J, et al. Science of the Total Environment 1986; 54: 107-25.
(53) Frery N, et al, Validity of Hair Cadmium in detescting chronic cadmium exposure in general populations. Bulletin of Environ Contamination 1993; 501:736-43; & Frery N, et al, Environmental exposure to cadmium and human birthweight. Toxicology 1993; 79(2): 109-18.
(55) Bergomi M, et al, Blood, teeth, and hair: evaluation of exposure to lead and cadmium in children living in an industrial zone. Ann Ig 1989; 1(5): 1185-96; & Vivoli G, et al, Cadmium in blood, urine, and hair related to human hypertension. J Trace Elem Electrolytes Health Dis 1989;3(3):139-45.
(56) Hart RP, et al, Neuropsychological effects of occupational exposure to cadmium. J Clin Exp Neuropsychol 1989; 11(6):933-43.
(58) Raghunath R, et al, Retention times of Pb, Cd, and Zn in children’s blood. Sci Total Environ 1997; 207(2-3):133-9; & Zhuang GS; Wang YS; Tan MG; Zhi M; Pan WQ;Cheng YD. Preliminary study of the distribution of the toxic elements As, Cd, and Hg in human hair and tissues by NAA. Biol Trace Elem Res 1990 Jul-Dec;26-27:729-36.
(60) Hu H. Knowledge of diagnosis and reproductive history among survivors of childhood plumbism. Am J Public Health 1991; 81*8): 1070-2; & Lutz PM, et al, Elevated immunoglobulin E (IgE) levels in children with exposure to environmental lead. Toxicology 1999; 134(1): 63-78.
(61) Gottschalk LA, et al, Abnormalities in hair trace elements as indicatores of aberrant behavior. Compr Psychiatry 1991; 32(3): 229-37.
(62) Schauss A.G. Comparative hair mineral analysis in a randomly selected “normal” population and violent criminal offenders. Int J Biosocial Res 1981; 1:21-41.
(63) Cromwell P.F. et al, Hair mineral analysis: biochemical imbalances and violent criminal behavior. Psychol Rep 1989; 64:259-66.
(64) Fox MR, Jacobs Rm, Jones AO, Fry Be Jr, Stone CL. Effects of Citamin C and Iron on cadmium metabolism. Ann N Y Acad Sci 1980; 355: 249-61.
(65) Geertz R, Gulyas H Gercken G. Cytotoxicity of dust constituents to alveolar machrophages: interations of heavy metal compounds. Toxicoloty 1994; 86(1-2):13-27.
(66) Quig D. Cysteine metabolism and metal toxicity. Doctor’s Data, Inc., West Chicago, IL, USA. Inquiries@doctorsdata.com Altern Med Rev, 1998 Aug, 3:4, 262-70
(67) Kozielec T, Starobrat-Hermelin B. Assessment of magnesium levels in children with ADHD. Magnes Res 1997; 10(2):143-8.
(69) Starobrat-Hermelin B, Kozielec T. The effects of magnesium physiological supplementation on hyperactivity in children with ADHD: positive response to magnesium oral loading test. Magnes Res 1997. 10(2):149-56.
(70) Bekaroglu M, Aslan Y, Gedik Y, Karahan C. Relationships between serum free fatty acids and zinc with ADHD. J Child Psychol Psychiatry 1996; 37(2):225-7.
(71) Arnold LE, Votolato NA, Kleykamp D, Baker GB, Bornstein RA. Does hair zinc predict treatment improvement of ADHD? Int J Neurosci 1990; 50(1-2): 103-7.
(72) Haglund B, Ryckenberg K, Selinus O, Dahlquist G. Evidence of a relationship between childhood-onset diabtes and low groundwater concentration of zinc. Diabetes Care 1996; 19(8): 873-5.
(73) Shrestha KP; Oswaldo A. Trace elements in hair of epileptic and normal subjects.
Sci Total Environ 1987 Dec;67(2-3):215-25.
(77)Schrauzer GN, de Vroey E. Effects of nutritional lithium supplementation on mood. A
placebo-controlled study with former drug users. Biol Trace Elem Res 1994; 40(1):89-101.
(78) Schrauzer GN, Shrestha KP. Lithium in drinking water and the incidences of crimes, suicides, and arrests related to drug addictions. Biol Trace Elem Res 1990 May;25(2):105-13
(79) Sheard MH, Marini JL, Bridges CI, Wagner E. The effect of lithium on impulsive aggressive behavior in man. Am J Psychiatry 1976 Dec;133(12):1409-13
(82) Agocs MM, Etzel RA, Parrish RG, Hesse JL. Mercury exposure from interior latex paint. N Engl J Med 1990 Oct 18;323(16):1096-101.