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Neurological and Immune Reactive Conditions Affecting Kids
 
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Neurological and Immune Reactive Conditions Affecting Kids


Neurological and Immune Reactive Conditions Affecting Kids:
The mercury connection to neurological pervasive developmental disorders
(autism, schizophrenia, dyslexia, ADD,
childhood depression, learning disabilities, OCD
, etc.)
and developmental immune conditions (eczema, asthma, and allergies)
Bernard Windham- Chemical Engineer

http://www.home.earthlink.net/~berniew1/kidshg.html

The incidence of neurotoxic, allergic, and immune reactive conditions such as autism, schizophrenia, ADD, dyslexia, allergies, asthma, eczema, psoriasis, childhood diabetes, etc. have been increasing rapidly in recent years(1,2,3,5,23,50,52,75,82,86). A recent report by the National Research Council found that 50% of all pregnancies in the U.S. are now resulting in prenatal or postnatal mortality, significant birth defects, developmental disabilities or otherwise chronically unhealthy babies(3). There has been a similar sharp increase in developmental disabilities in Canadian children over the last 2 decades(71), including learning disabilities and behavioral problems, asthma and allergies, and childhood cancer. Exposure to toxic chemicals or environmental factors appear to be a major factor in much of the developmental problems of the 4 million U.S. children born each year(3,1,2), with at least 1 in 6 having one of the neurological conditions previously listed(1-3).

U.S. EPA has estimated that over 3 million of these are related to lead or mercury toxicity, with at least 25% of U.S. kids getting mercury exposure at dangerous levels (1,81). The U.S. Dept. Of Education indicates that over 5 million children attending school have neurological related disabilities reported by state agencies, other than ADD(2a). According to the American Academy of Pediatrics between 4 to 12 % of all school age children are affected by ADHD(4) and a similar number have some degree of dyslexia(1). However large surveys of elementary level student records finds much higher levels- with over 20% of elementary school boys in some areas being treated for ADD(75). Studies have found that long term use of stimulent drugs commonly causes significant adverse neurological and health effects(76), and options are available to deal with such conditions without such adverse effects including dealing with the underlying causes. Estimates of the percentage of children with mood or anxiety orders are as much as 20%. Studies indicate that over 60,000 children are born each year with neurodevelopmental impairments due to prenatal exposure to methyl mercury (45,46), and two other sources of mercury exposure appear more common and at higher levels than this, mercury from vaccines and amalgam dental fillings(22,50,81).

A study at the U.S. CDC found "statistically significant associations" between neurologic developmental disorders such as autism, attention deficit disorder(ADD) and speech disorders with exposure to mercury from thiomersal-containing vaccines before the age of 6 months (62,80). An analysis of the U.S. CDC VAERS database for adverse reactions from vaccines regarding effects of the diptheria-tetanus-pertusis vaccine found that those receiving DTaP and DTucP vaccines with thimerosal had significantly higher rates of autism, speech disorders, and heart arrest than those receiving DtaP vaccine without thimerosal, and that the rate of these increase exponentially with dose(81). An analysis of the U.S. Dept. of Education report on the prevalence of various childhood conditions among school children found that the rate of autism and speech disorders increased with increasing levels of thimerosal exposure from vaccines(81).

Changes in birth proceedures in hospitals such as immediate cord clamping has also been found to be a factor in the increase in neurological developmental problems(83).

Also according to the U.S. FDA, at least 26 million have allergies, at least 17 million have asthma, 15 million have systemic eczema, and childhood diabetes is increasing rapidly(82). Although Russian and U.S. studies from the 1980s found that thimerosal was highly toxic and recommended thats its use as a medical preservative should be discountinued(70,79) , its use was not discontinued. One study(60a) found 5 times higher rate of allergy among a group vaccinated with pertussis vaccine(DPT) as opposed to an unvaccinated group, and 2 other studies(60bc) found increased asthma, allergies, and eczema among the vaccinated group. Over the last 20 years the percent of diabetes cases below 20 years old has increased from 2% to over 30%, and there was a 70% in cases under 40 years of age between 1990 and 1998(50,52,59). Studies in the U.S. and Sweden have confirmed vaccinations to be a major factor in the increased diabetes cases(52). Currently approx. 16 million have diabetes. DPT vaccinations have also been linked to sudden enfant death syndrome(SIDS)(61). DPT vaccines are mostly given at 2, 4, and 6 months of age and 85% of SIDS cases occur during this age span. One study found babies die at a rate 8 times the normal rate within 3 days of DPT shots(60a), while another found that among SIDS victims 61% had DPT within the 2 previous weeks and 13% within 24 hours of DPT vaccination(60c). A monitoring study of infant breathing patterns after DPT vaccinations showed large increases in breathing difficulties including episodes of ceased breathing, which continued for months after DPT in some cases(61b). Some cases of seizures after DPT were also observed. Another study found significantly higher rates of heart arrest in those getting DpaT vaccines with mercury thimerosal compared to those without(81). Prenatal exposure to mercury has also been found to predispose animals and infants to seizures and epilepsy(85).

Mercury has been found to cause an increase in inflammatory Th2 cytokines(58). In the pancreas, the cells responsible for insulin production can be damaged or destroyed by the chronic high levels of cytokines, with the potential of inducing type II diabetes - even in otherwise healthy individuals with no other risk factors for diabetes(52). Mercury inhibits production of insulin and is a factor in diabetes and hypoglycemia, with significant reductions in insulin need after replacement of amalgam filings and normalizing of blood sugar(52,22). In addition to this mechanism, other links between vaccines and diabetes have also been found and there is evidence vaccines are the number one cause of Type I diabetes in young children(52).

The largest increase in neurological and immune conditions has been in infants (1,2,5-7,23,4,50,81), with an increase in autism cases to over 500,000 (1,2,23,22,86), an over 900% increase to a level of approx. 1 per 500 infants in the last decade(2ab), making it the 3rd most common chronic childhood condition. For 1999 through 2002, the number of professionally diagnosed in California with full syndrome autism has doubled(2e,86). There have been similar increases in ADD and dyslexia to over 10 million, similar large numbers(over 10%) with childhood depression or anxiety, and over 10 % of infants- approximately 15 million in the U.S. with systemic eczema(1,2,82). Studies researching the reason for these rapid increases in infant reactive conditions seem to implicate earlier and higher usage of vaccines containing mercury(thimerisol) as a likely connection (2cd,23,30,40,80,81). A recent study comparing pre- and post-vaccination mercury levels, found a significant increase in both preterm and term infants after vaccination(42), with post-vaccination mercury levels approximately 3 times higher in the preterm infants as compared with term infants. The study found mercury blood levels up to 23.6 ug/L and received an average dose of 16.7 ug/kg. Just this one vaccination gave an exposure to mercury that is many times the U.S. ATSDR adult minimum risk level(MRL) for mercury of .3/ug/kg body weight per day(41,81).

It has been estimated that if all of the vaccines recommended by the American Assoc. of Pediatrics are given and contain thimerisol, then by age 6 months an infant would have received 187 micrograms of ethyl mercury which is more than the EPA/ATSDR health standard for organic mercury(33,41,81) and by age 3 the typical child has received over 235 micrograms of mercury thimerisol from vaccinations which is considerably more than Federal mercury safety guidelines(41,81), in addition to significant levels from other sources for many(23). Infants during this period have undeveloped blood brain barriers and much of the mercury goes to the brain, resulting in significant adverse neurological effects in those that are most susceptible (43,3). The bioaccumulation in the brain and toxic effects of ethyl mercury are comparable to that of methyl, with mercury accumulation in the brain and physical effects actually being more extensive(79).

Because of the evidence the FDA has completed a study and written a letter to vaccine manufacturers asking that mercury be removed from vaccines. The updated letter stated, "The Center for Biologics Evaluation and Research (CBER) has completed its evaluation of the use of thimerisol in vaccines.. Our review concluded that reducing or eliminating thimerisol from

vaccines is merited(44). The letter pointed to a joint statement by the American Academy of Pediatrics and the United States Public Health Service in 1999, which "called for the

removal of thimerisol from vaccines as soon as possible." A Congressional Committee after holding a hearing has also called for elimination of mercury in vaccines as soon as possible.

Many thousands of parents have reported that their child got such conditions after vaccination, and tests have confirmed high levels of mercury in Many of those tested, along with other toxic exposures. An additional source of thimerisol to the fetus of women who are RH negative is the 30 micrograms in the RhoGAM shot they receive, which has been found to be a significant factor in autism incidence(86). Underweight infants that get the same dose of thimerisol as other infants have also been found to be at special risk. Many of those diagnosed with high mercury levels have also been found to have significant improvement after mercury detoxification(23,30,40,11,35,51). Thimerisol had been previously removed from similar preservative uses in eye drops and eye medications after evidence of a connection to chronic degenerative eye conditions. After over 15,000 law suits were filed in France over adverse effects of the Hepatitis B vaccine, the French Minister of Health ended the mandatory hepatitis B vaccination program for all school children. Adverse effects included neurological disorders and autoimmune disorders such as multiple sclerosis and lupus. Some hospitals in the U.S. also quit recommending certain vaccinations.

Although vaccinations appear to be the largest source of mercury in infants, mercury has been found to be transmitted from the mother to the fetus through the placenta and accumulate in the fetus to higher levels than in the mother's blood(22). Infants of mothers who had dental work involving amalgam during pregnancy had significantly higher levels of mercury in hair tests(78,86). Breast milk of women who have amalgam fillings is the 2nd largest source of mercury in infants and young children(22,69), but eating a lot of fish has also been found to be a significant source(45). Milk increases the bioavailability and retention of mercury by as much as double(22,68,69) and mercury is often stored in breast milk and the fetus at much higher levels than that in the mother's tissues (22,69). Mercury is transferred mainly by binding to cassein(68,24). The level of mercury in breast milk was found to be significantly correlated with the number of amalgam fillings(69), with milk from mothers with 7 or more fillings having levels in milk approx. 10 times that of amalgam-free mothers. The mercury in milk sampled ranged from 0.2 to 6.9 ug/L. Prenatal mercury exposure can also developmentally damage the metals detox system of the liver which can lead to accumulation and toxicity of later metals exposure(22).

A recent study found that prenatal mercury exposures and susceptability factors such as ability to excrete mercury appear to be a major factors in those with chronic neurological conditions like autism(86). Infants whose mothers received prenatal Rho D immunoglbulin injections containing mercury thimerosal or whose mother's had high levels of amalgam fillings had a much higher incidence of autism. While the hair test levels of mercury of infants without chronic health conditions like autism were positively correlated with the number of the mother's amalgam fillings, vaccination thimerosal exposure, and mercury from fish, the hair test levels of those with chronic neurological conditions such as autism were much lower than the levels of controls and those with the most severe effects had the lowest hair test levels, even though they had high body mercury levels. This is consistent with past experience of those treating children with autism and other chronic neurological conditions(23). Very low levels of exposure have been found to seriously affect relatively large groups of individuals who are immune sensitive to toxic metals(11,35), or have an inability to detoxify metals due to such as deficient sulfoxidation or metallothionein function(18,36,51) or other inhibited enzymatic processes related to detoxification(15-24,30) or excretion of metals(87). Those with the genetic allele ApoE4 protein in the blood have been found to detox metals poorly and to be much more susceptable to chronic neurological conditions than those with types ApoE2 or E3(87).

A direct mechanism involving mercury's inhibition of cellular enzymatic processes by binding with the hydroxyl radical(SH) in amino acids appears to be a major part of the connection to these allergic/immune reactive conditions(15-23,36,47,51). For example mercury has been found to strongly inhibit the activity of xanthine oxidase and dipeptyl peptidase (DPP IV) which are required in the digestion of the milk protein casein(15,16,17,19,20,22), and the same protein that is cluster differentiation antigen 26 (CD26) which helps T lymphocyte activation. CD26 or DPPIV is a cell surface glycoprotein that is very susceptible to inactivation by mercury binding to its cysteinyl domain.

Mercury and other toxic metals also inhibit binding of opioid receptor agonists to opioid receptors, while magnesium stimulates binding to opioid receptors(15). Studies involving a large sample of patients with autism, schizophrenia, or mania found that over 90 % of those tested had high levels of the milk protein beta-casomorphine-7 in their blood and urine and defective enzymatic processes for digesting milk protein(24,25,27), and similarly for the corresponding enzyme needed to digest wheat gluten(24,26).The studies found high levels of Ig A antigen specific antibodies for casein, lactalbumin and beta-lactoglobulin and IgG and IgM for casein. Beta-casomorphine-7 is a morphine like compound that results in neural disfunction (24,25), as well as being a direct histamine releaser in humans and inducing skin reactions (14,21,25c). Similarly many also had a corresponding form of gluten protein(26). Elimination of milk and wheat products and sulfur foods from the diet has been found to improve the condition. A double blind study using a potent opiate antagonist, naltrexone(NAL), produced significant reduction in autistic symptomology among the 56% most responsive to opioid effects(28). The behavioral improvements was accompanied by alterations in the distribution of the major lymphocyte subsets, with a significant increase in the T-helper-inducers and a significant reduction of the T-cytotoxic-suppressors and a normalization of the CD4/CD8 ratio.

Studies have found mercury causes increased levels of the CD8 T-cytotoxic-suppressors(29). As noted previously, such populations of patients have also been found to have high levels of mercury and to recover after mercury detox(23,11,22,30,40). As mercury levels are reduced the protein binding is reduced and improvement in the enzymatic process occurs(22,11).

Studies have also found heavy metals to deplete glutathione and bind to 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(39,43,45-47, 63-65,22). In addition to forming strong bonds with SH and other groups like OH,NH2, and Cl in amino acids which interfere with basic enzymatic processes, toxic metals exert part of their toxic effects by replacing essential metals such as zinc at their sites in enzymes.

An example of this is mercury's disabling of the metallothionein protein, which is necessary for the transport and detoxification of metals. Mercury inhibits sulfur ligands in MT and in the case of intestinal cell membranes inactivates MT that normally bind cuprous ions(66), thus allowing buildup of copper to toxic levels in many and malfunction of the Zn/Cu SOD function. Another large study(51) found a high percentage of autistic and PDD children are especially susceptible to metals due to the improper functioning of their metallothionein detoxification process, and that with proper treatment most recover. Mercury has also been found to play a part in neuronal problems through blockage of the P-450 enzymatic process(67). Mercury induced reactive oxygen species and lipid peroxidation has been found to be a major factor in mercury's neurotoxicity, along with leading to decreased levels of glutathione peroxidation and superoxide dismustase(SOD) (63). 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(63,22) , as well as chronic autoimmune conditions and diseases(35)

Additional cellular level enzymatic effects of mercury's binding with proteins include blockage of sulfur oxidation processes such as cysteine dioxygenase, gamma- glutamyltranspeptidase(GGT), and sulfite oxydase, along with neurotransmitter amino acids which have been found to be significant factors in many autistics(18,36,47,17), plus enzymatic processes involving vitamins B6 and B12, with effects on the cytochrome-C energy processes as well. For example, the Vitamin B6 activating enzyme, B6-kenase, is totally inhibited in the intestine at extremely low(nanamolar) concentrations(56). Epson salts(magnesium sulfate)baths, supplementation with the p5p form of Vit B6 and vit B12 shots are methods of dealing with these enzymatic blockages that have been found effective by those treating such conditions. Mercury has also been found to have adverse effects on cellular mineral levels of calcium, magnesium, zinc, and lithium(39,22,47,50). Supplementing with these minerals has also been found to be effective in the majority of cases(39,50), and lithium has even been found to cause regeneration of neurons in damaged areas of the brain such as the hippocampus. Another of the results of these toxic exposures and enzymatic blockages is the effect on the liver and disfunction of the liver detoxification processes which autistic children have been found to have(30,36,51,22). All of the autistic cases tested were found to have high toxic exposures/effects and liver detoxification profiles outside of normal(30a).

Another aspect of gastrointestinal dysfunction that is found in the majority of autism cases are intestinal inflammation, enterocolalitis, lymphondular hyperplsia, abnormal intestinal permeability, or malabsorption(17,53). Such damage to the intestines and gastrointestinal processes are known from animal studies to be caused by mercury(54). Inorganic mercury is the predominant excretionary form in the intestines,whatever the source form. All forms are absorbed by the intestines and inorganic mercury accumulates in intestinal tissues, especially in young animals or infants(55), which are known to have poor biliary excretion of mercury. As noted previously children in the U.S. are exposed to high levels of mercury thimerisol, a highly toxic organic form of mercury. Organic mercury in primate studies is found to cause paneth cells in the intestines to be enlarged and packed with secretionary granules(57). This is also common in autistic children(17c).

Along with these blockages of cellular enzymatic processes, mercury has been found to cause additional neurological and immune system effects in many through immune/autoimmune reactions(11,12,35). Mercury(22) as well as thimerisol(31,32) and other toxic metals(50) also have direct neurotoxic effects on brain nucleoid binding proteins through their effect on Ca2+ATPase and Na+/K+ATPase activity. But the effects on the neurological and immune systems of exposure to various toxic substances such as toxic metals and environmental pollutants has also been found to have additive or synergistic effects and to be a factor in increasing eczema, allergies, asthma, delayed food allergies, and sensitivity to other lesser allergens(14-22,35,50). Most of the children tested for toxic exposures have found high or reactive levels of other toxic metals, and organochlorine compounds (30,40,11,12,35,48). Other than the organochlorines or toxic metals which are discussed later, three common pollutants that have been documented to have effects on such conditions are traffic and industrial pollutants nitrogen oxide, power plant residual oil fly ash, and organochlorine pollutants(48).

Mercury has also been found to cause reduced acetylycholine levels(77) and to be a factor in autism. When the author succeeded in removing excessive metal deposits using cilantro and upregulation techniques, he found Acetylcholine suddenly increased towards a normal level, short-term memory, the ability to concentrate and think clearly improved significantly; and often those who had abnormal or anti-social and irritable behavior returned to more acceptable behavior.

Another effect of mercury and toxic metals is a reduction in B- lymphocytes (37,38,50,22). One of these studies(37a) dealing with autistic patients and further work with such patients has found this causes a tendency to be more seriously affected by viruses and to develop intestinal disorders including leaky gut, lymphoid modular hyperplasia, and a high incidence of parasites. Metals by binding to SH radicals in proteins and other such groups can cause autoimmunity by modifying proteins which via T-cells activate B-cells that target the altered proteins inducing autoimmunity as well as causing aberrant MHC II expression on altered target cells(72). Studies have also found mercury and lead cause autoantibodies to neuronal proteins, neurofilaments, and myelin basic protein (73,74). While zinc binding with MBP stabilizes the association with brain myelin, mercury and cadmium have been found to intefere with zinc binding to MBP and thus cause disfunction and autoimmunities(74). Dr. Stejskal(11) recently began testing children with autism. Her preliminary results on 18 autistic children and 11 controls, found that 5 of 18 autistic children had a positive proliferative ("allergic") response on MELISA to Thimerosal, vs. 1/11 controls. Similar results were recently found for methyl mercury (6/10 autistics vs 0/11 controls) and inorganic mercury (6/18 autistics, vs 0/11 controls). Most importantly, 13/16 autistics tested positive for reactivity to the mercury-MBP vs. only 3/10 controls. The mercury-MBP reactivity is presumed to be caused by the mercury reconfiguring the three-dimensional MBP, to which the body generates the allergic (autoimmune) response.

Immune mechanisms are thus seen to be a major factor in neurotoxicity of metals seen in conditions such as autism and ADD(37b,63,72-74).

Parathyroid Hypertensive Factor (PHF) is produced by the parathyroid gland and is measurable by the University of Alberta. Preliminary PHF determinations on over 100 patients through the Pfieffer Treatment Center have revealed very high levels for autistic patients . Heavy metals are known to block calcium L-channels at the cell membrane, whereas PHF is known to open calcium L-channels [84a] and stimulate phosphodiesterase [84b]. Calcium L-channels perform numerous functions, including initiation of transcriptional events which support learning, memory and endocrine secretion. Mercury inhibits L-channels at micromolar concentration [84c] in an irreversible manner in hippocampal neurons. Hypothetically, elevated PHF may serve to at least partially compensate Hg-inhibition of L-channels. Mercury is also a potent inhibitor of cAMP [84d], cellular levels of which presumably further decrease with PHF-stimulation of phosphodiesterase. Thus, in the context of mercury toxicity, PHF may play both adaptive and maladaptive roles. The very mechanism of mercury-induced auto-immune disease in mercury-sensitive rats is related to L-channel signaling. This process involves induction of interleukin-4 gene expression, which is mediated by protein kinase C-dependent calcium influx through L-channels [84e]. PHF hypothetically may affect the auto-immune response

In addition to large numbers of cases affecting infants, allergic contact eczema is the most frequent occupational disease(1,22,82); and the most common cause of contact eczema is exposure to toxic metals(1, 6-12,22). The metals most commonly causing allergic immune reactivity are nickel, mercury, chromium, cobalt, and palladium(1,6-14,22). The highest level of sensitization is to Infants, who are most reactive to thimerisol, a form of mercury that has been used as a preservative in vaccines and eye drops(6,7). Many with immune reactive conditions like eczema and psoriasis recover after tests and treatment for the cause of the immune reactivity(11,22 ).

There has been strong suggestive and clinical evidence for a connection between toxic metals and autism spectrum conditions(2bcd,15-40,50) and recent studies using government databases have confirmed the connection(80,91). There also appear to be subgroups of exposure and symptom patterns among the many different types of persuasive developmental disorders (PDD) including autism, Asperger's syndrome, obsessive compulsive disorder(OCD),

dyslexia, ADD/ADHD, learning disabilities, childhood depression, etc. Some of the apparent subgroups of autism include one group of general brain-related encephalies and/or immune effects of toxic exposures(23), the Singh subgroup of autoimmune reactions to brain myelin sheath(37b), the Wakefield/MMR subgroup with intestional leaky gut and involvement of measles virus(37a), and the Megson/DPT visual abnormality related group(49). Since most children have been been found to have high levels of toxic exposure, most of those affected appear to have symptoms related to both the first subgroup plus often one or more of the other exposures/subgroups. The Megson group are often helped significantly by treatment with Vitamin A from cod liver oil an urocholine. Thousands of autistic children are being treated for metals toxicity using chelation protocols after tests have documented high exposures to mercury and other toxic metals, and the majority have shown significant improvement(23,40,51).


References

(1) (a)Weiss B, Landrigan PJ. The developing brain and the Environment. Environmental Health Perspectives, Volume 107, Supp 3, June 2000; & EPA spokesman, U.S.News & World Report, "Kids at Risk"(cover story), 6-19-2000; & Frith CD et al, More Dyslexia in English Speaking Countries, Science, Mar 2001; & EPA spokesman, U.S.News & World Report, "In the Air that they Breathe", Science & News, 12-20-99; & U.S. EPA, Region I, 2001, http://www.epa.gov/region01/children/outdoors.html; & Dr. Fionta Stanley, Department of Paediatrics, the University of Western Australia "Before the bough breaks: 21st Centry kids in crisis" Zonta International Conference, Gothenburg Sweden, July 2, 2002 http://www.zonta.org/Member_Resource_Center/StanleySpeech.pdf

& (b) ATSDR/EPA Priority List for 2001: Top 20 Hazardous Substances, Agency for Toxic Substances and Disease Registry,U.S. Department of Health and Human Services, http://www.atsdr.cdc.gov/clist.html

(2) (a)The Center for Education Statistics, http://nces.ed.gov/ ; & Annual Report to Congress on the implementation of the Individuals with disabilities act. http://www.ed.gov/offices/OSERS/OSEP/ (1994 to 1998); & U.S. Dept. of Education, Office of Special Education Programs, Data Analysis Section, partB, Chapter1: 1990-1997; & (b) State government agency reports on autism incidence trends for the last decade for California, New Jersey, Maryland, Rhode Island, Illinois, Pennsylvania, Colorado, Washington, etc. in: Autism 99 : A National Emergency, http://www.garynull.com/documents/autism_99.htm; & © Gary Null, Second Opinion: Vaccinations, Gary Null and Associates, Inc. 2000, http://www.garynull.com/marketplace/documents.asp & (d) Bernard Rimland, Ph.D, Autism Research Institute, The Autism Epidemic Is Real, and Excessive Vaccinations Are the Cause, http://www.autismcanada.org/News/RimlandstatementJuly2003.htm face="Arial" size="-1"> (e) California Department of Developmental Services (DDS), "Autistic Spectrum Disorders, Changes in the California Caseload: 1999-2002". May 2003.

(3) National Academy of Sciences, National Research Council, Committee on Developmental Toxicology, Scientific Frontiers in Developmental Toxicology and Risk Assessment, June 1, 2000, 313 pages. & Press Release; Evaluating Chemical and Other Agent Exposures for Reproductive and Developmental Toxicity Subcommittee on Reproductive and Developmental Toxicity, Committee on Toxicology, Board on Environmental Studies and Toxicology, National Research Council National Academy Press, 262 pages, 6 x 9, 2001; & National Environmental Trust (NET), Physicians for Social Responsibility and the Learning Disabilities Association of America, "Polluting Our Future: Chemical Pollution in the U.S. that Affects Child Development and Learning" Sept 2000; http://www.safekidsinfo.org

(4) American Acadamy of Pediatrics, American J of Psychiatry, 2000, 157:1077-1083; & American Acadamy of Pediatrics, Report to Clinicians; http://www.aap.org/policy/autism.html; & James A Kaye, Maria del Mar

Melero-Montes, Hershel Jick; Boston Collaborative Drug Surveillance Program, Boston University School of Medicine, 11 Muzzey Street, Lexington, MA 02421, USA, 2000, National Vaccine Information Center

http://www.909shot.com

(5) American Academy of Dermatology, Press Release, February, 2000; & Silhan P, Arenberger P. Standard epicutaneous tests in ambulatory care of patients. Cas Lek Cesk 1999, 138(15):469-73..

(6) Brasch J, Geier J, Schnuch A. Differentiated contact allergy lists serve in quality improvement. Hautarzt 1998; 49(3): 184-0

(7) Manzini BM, Ferdani G, Simonetti V, Donini M, Sedernari S. Contact sensitization in children. Pediatr Dermatol 1998; 15(1): 12-17; & Romaguera C, Vilaplana J. Contact dermatitis in children: 6 years experience. Contact Dermatitis 1998; 39(6): 277-80.

(8) Sun CC. Allergic contact dermatitis of the face from contact with nickel and ammoniated mercury. Contact Dermatitis 1987, 17(5):306-9.

(9) Xue C, He Z, Zhang H, Li S. Study on the contact allergen in patients with dermatitis and eczema. Wei Sheng Yen Chiu 1997, 26(5): 296-8.

(10) Aberer W, Holub H, Strohal R, Slavicek R. Palladium in dental alloys- the dermatologists responsibility to warn? Contact Dermatitis 1993. 28(3): 163-5.

(11) V.D.M.Stejskal, Dept. Of Clinical Chemistry, Karolinska Institute, Stockholm, Sweden LYMPHOCYTE IMMUNO-STIMULATION ASSAY -MELISA" & "Mercury-specific Lymphocytes: an indication of mercury allergy in man", J. Of Clinical Immunology, 1996, Vol 16(1);31-40; see: http://www.melisa.org

(12) Sterzl I, Prochazkova J, Stejaskal VDM et al, Mercury and nickel allergy: risk factors in fatigue and autoimmunity. Neuroendocrinology Letters 1999; 20:221-228; & V.Stejskal, "MELISA: A New Technology for Diagnosing and Monitoring of Metal Sensitivity", Proceedings: 33rd Annual Meeting of American Academy of Environmental Medicine, Nov. 1998, Baltimore, Maryland.

(13) Redhe O, Pleva J. Recovery from asthma, allergies,ALS after removal of dental amalgam fillings. Int J of Risk & Safety in Medicine 1994; 4:229-236.

(14) Kurek M, Przybilla B, Hermann K, Ring J. An opioid peptide from cows milk, beta-casomorphine-7, is a direct histamine releaser in man. Int Arch Allergy immunol 1992; 97(2): 115-20.

(15) Tejwani GA, Hanissian SH. Modulation of mu, delta, and kappa opioid receptors in rat brain by metal ions and histidine. Neuropharmology 1990; 29(5): 445-52.

(16) Mondal MS, Mitra S. Inhibition of bovine xanthine oxidase activity by Hg2+ and other metal ions. J Inorg Biochem 1996; 62(4): 271-9.

(17) Sastry KV, Gupta PK. In vitro inhibition of digestive enzymes by heavy metals and their reversal by chelating agents: Part 1, mercuric chloride intoxication. Bull Environ Contam Toxicol 1978; 20(6): 729-35; & W.Y.Boadi et al, Dept. Of Food Engineering and Biotechnology, T-I Inst of Tech., Haifa, Israel, "In vitro effect of mercury on enzyme activities", Environ Res, 1992, 57(1):96-106; & Horvath K, Papadimitriou JC, Rabsztyn A, Drachenberg C, Tildon JT; Gastrointestinal abnormalities in children with autistic disorder. J Pediatr 1999, 135:559-63.

(18) Mc Fadden SA, Phenotypic variation in xenobiotic metabolism and adverse environmental response: focus on sulfur-dependent detoxification pathways. Toxicology, 1996, 111(1-3):43-65; & Markovich et al, "Heavy metals (Hg,Cd) inhibit the activity of the liver and kidney sulfate transporter Sat-1", Toxicol Appl Pharmacol, 1999,154(2):181-7; & Matts RL, Schatz JR, Hurst R, Kagen R. Toxic heavy metal ions inhibit reduction of disulfide bonds. J Biol Chem 1991; 266(19): 12695-702; & T.L. Perry et al, "Hallevorden-Spatz Disease: cysteine accumulation and cysteine dioxygenase defieciency", Ann Neural, 1985, 18(4):482-489; & Ceaurriz et al, Role of gamma- glutamyltraspeptidase(GGC) and extracellular glutathione in disposition of inorganic mercury",J Appl Toxicol,1994, 14(3): 201-

(19) Shibuya-Saruta H, Kasahara Y, Hashimoto Y. Human serum dipeptidyl peptidase IV (DPPIV) and its unique properties. J Clin Lab Anal. 1996;10(6):435-40; & Blais A, Morvan-Baleynaud J, Friedlander G, Le Grimellec C. Primary culture of rabbit proximal tubules as a cellular model to study nephrotoxicity of xenobiotics. Kidney Int. 1993 Jul;44(1):13-8; & Puschel G, Mentlein R, Heymann E, 'Isolation and characterization of dipeptidyl peptidase IV from human placenta', Eur J Biochem 1982 Aug;126(2):359-65; & Kar NC, Pearson CM. Dipeptyl Peptidases in human muscle disease. Clin Chim Acta 1978; 82(1-2): 185-92; & Seroussi K, Autism and Pervasive Developmental Disorders , 1998, p174,etc., http://www.autismndi.com/

(20) Stefanovic V. et al, Kidney ectopeptidases in mercuric chloride-induced renal failure. Cell Physiol Biochem 1998; 8(5): 278-84.

(21) Crinnion WJ. Environmental toxins and their common health effects. Altern Med Rev 2000, 5(1):52-63.

(22) Windham, B. Annotated Bibliography: Adverse health effects related to mercury and amalgam fillings and

clinically documented recoveries after amalgam replacement. (over 1500 peer-reviewed references);

www.home.earthlink.net/~berniew1/amalg6.html & (b) U.S. EPA,

http://www.epa.gov/grtlakes/seahome/mercury/src/ways.htm

(23) Bernard S, Enayati A, Redwood L, Roger H, Binstock T. Autism: a novel form of mercury poisoning. Med Hypotheses 2001 Apr;56(4):462-71 http://www.autism.com/ari/mercurylong.html; &(b)Dr. A Holmes, Autism Treatment Center,Baton Rouge, La, http://healing-arts.org/children/holmes.htm; &(c) Jaquelyn McCandless, M.D., Autism Spectrum Treatment Center, Woodland Hills, CA,

& Jaquelyn McCandless, M.D, Children with Starving Brains, A Medical Treatment Guide for Autism Spectrum Disorder, 2003 http://www.autism-rxguidebook.com/DesktopDefault.aspx?tabindex=11&tabid=15; & (d)L.Redwood, Mercury and Autism, Vitamin Research News, May 2001, 15(5):1-12; &(e) Andrew H. Cutler, PhD, PE; Amalgam Illness:Diagnosis and Treatment; 1996 , http://www.noamalgam.com/

(24) J.R. Cade et al, Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism, Mar 1999. http://www.hsc.ufl.edu/post/post0399/post03_19/1.html; & Application of the Exorphin Hypothesis to Attention Deficit Hyperactivity Disorder: A Theoretical Framework by Ronald Hoggan A Thesis Submitted To The Faculty Of Graduate Studies In Partial Fulfilment Of The Requirements For The Degree Of Master Of Arts, Graduate Division Of Educational Research,Calgary, April, 1998 University of Calgary

(25) Reichelt KL. Biochemistry and psycholphisiology of autistic syndromes. Tidsskr Nor Laegeforen 1994, 114(12):1432-4; & Reichelt KL et al, Biologically active peptide-containing fractions in schizophrenia and childhood autism. Adv Biochem Psychopharmocol 1981; 28: 627-43; Lucarelli S, Cardi E, et al, Food allergy and infantile autism. Panminerva Med 1995; 37(3):137-41; & Shel L, Autistic disorder and the endogenous opioid system. Med Hypotheses 1997, 48(5): 413-4.

(26) Huebner FR, Lieberman KW, Rubino RP, Wall JS. Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates. Peptides 1984; 5(6):1139-47.

(27) Willemsen-Swinkels SH, Buitelaar JK, Weijnen FG, Thisjssen JH, Van Engeland H. Plasma beta-endorphin concentrations in people with learning disability and self-injurious and/or autistic behavior. Br J Psychiary 1996; 168(1): 105-9; & Leboyer M, Launay JM et al. Difference between plasma N- and C-terminally directed beta-endorphin immunoreactivity in infantile autism. Am J Psychiatry 1994; 151(12): 1797-1801.

(28) Scifo R, Marchetti B, et al. Opioid-immune interactions in autism: behavioral and immunological assessment during a double-blind treatment with naltexone. Ann Ist Super Sanita 1996; 32(3): 351-9.

(29) Eedy DJ, Burrows D, Dlifford T, Fay A. Elevated T cell subpopulations in dental students. J prosthet Dent 1990; 63(5):593-6; & & Yonk LJ et al, CD+4 helper T-cell depression in autism. Immunol Lett, 1990, 25(4):341-5.

(30) Edelson SB, Cantor DS. Autism: xenobiotic influences. Toxicol Ind Health 1998; 14(4): 553-63; &

Liska, DJ. The detoxification enzyme systems. Altern Med Rev 1998. 3(3):187-98; & © HRI-Pfeiffer Center Autism Study; paper presented to Dan Conference, Jan 2001; http://www.hriptc.ort/Publish0900/index.html.

(31) Sayers LG; Brown GR; Michell RH; Michelangeli F. The effects of thimerisol on calcium uptake and inositol1,4,5-trisphosphate-induced calcium release in cerebellar microsomes. Biochem J 1993 Feb 1;289

( Pt 3):883-7; & Elferink JG. Thimerisol: a versatile sulfhydryl reagent, calcium mobilizer, and cell function-modulating agent. Gen Pharmacol 1999 Jul;33(1):1-6

(32) Lewis RN; Bowler K. Rat brain (Na+-K+)ATPase: modulation of its ouabain-sensitive K+-PNPPase activity by thimerisol. Int J Biochem 1983;15(1):5-7; & Anner BM, Moosmayer M. Mercury inhibits Na-K-ATPase primarily at the cytoplasmic side. Am J Physiol 1992; 262(5 Pt2):F84308.

(33) Halsey, NA. Limiting Infant Exposure to Thimerisol in vaccines. J. of the Amer. Medical Assoc., 282: 1763-66.

(34) 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.

(35) 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; & V.D.M.Stejskal et al, "Mercury-specific Lymphocytes: an indication of mercury allergy in man", J. Of Clinical Immunology, 1996, Vol 16(1);31-40, & V.Stejskal, "MELISA: A New Technology for Diagnosing and Monitoring of Metal Sensitivity", Proceedings: 33rd Annual Meeting of American Academy of Environmental Medicine, Nov. 1998, Baltimore, Maryland. See http://www.melisa.org

(36) Alberti A, Pirrone P, Elia M, Waring RH, Romano C. Sulphation deficit in "low-functioning" autistic children.

Biol Psychiatry 1999, 46(3):420-4.

(37) (a)Wakefield A et al, Ileal-lymphoid-nodular hyperplasia and pervasive developmental disorder in children.

Lancet 1998, 351(9103):637-41; & Kawashima H, Mori T, Kashiwagi Y, Takekuma K, Hoshika A, Wakefield A. Detection and sequencing of measles virus from peripheral mononuclear cells from patinets with inflamatory bowel and autism. Dig Dis Sci 2000 45(4):723-9; & Wakefield A et al, Inflammatory bowel disease syndrome and autism, Lancet, Feb 27, 2000; & (b)Singh VK; Lin SX; Yang VC. Serological association of measles virus and human herpesvirus-6 with brain autoantibodies in autism. Clin Immunol Immunopathol 1998 Oct;89(1):105-8; & G. Bell, Sterling Univ., Evidence of Toxic Metals/MMR connection in Autism, Autism Research Trust, 2002

(38) B.J.Shenker et al,"Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in B-cell function and viability" Immunopharmacol Immunotoxicol, 1993, 15(1):87-112; & J.R.Daum,"Immunotoxicology of mercury and cadmium on B-lymphocytes", Int J Immunopharmacol, 1993, 15(3):383-94.

(39) Pfieffer SI; Norton J; Nelson L; Shott S. Efficacy of vitamin B6 and magnesium in the treatment of autism. J Autism Dev Disord 1995 Oct;25(5):481-93; & Chuang D. Et al, National Institute of Mental Health, Science News, Nov 11, 2000, 158:309; & Lithium Protects Against Neuron Damage by Glutamate, Science News, 3-14-98, p164; & Moore G.J.et al, Lancet Oct 7, 2000; & Science News, 10-31-98, p276.

(40) Autism-Mercury@egroups.com, web group of parents with autistic kids and autism doctors and researchers; &(b)Dr. SB Edelson, http://www.edelsoncenter.com ; & © Eppright TD, Sanfacon JA, Horwitz EA. ADHD, infantile autism, and elevated blood-lead: a possible relationship. (case study) Mo Med 1996; 93(3):136-8.

(41) Agency for Toxic Substances and Disease Registry, U.S. Public Health Service, Apr 19,1999 Media Advisory, New MRLs for toxic substances, MRL: methy mercury/ oral/acute; & http://www.atsdr.cdc.gov/mrls.html.

(42) Stajich GV, Lopez GP, Harry SW, Sexson WR, Iatrogenic exposure to mercury after hepatitis B vaccination in preterm infants. Journal of Pediatrics, May 2000, 136(5):679-81.

(43) Rodier P.M. Developing brain as a target of toxicity. Environ Health Perspect 1995; 103(Supp 6): 73-76; &

Rice DC, Barone S, Critical Periods of Vulnerability for the Developing Nervous System: Evidence from human and animal models. Environ Health Persect 2000, 108(supp 3):511-533.

(44) The Center for Biologics Evaluation and Research (CBER), The US Food and Drug Administration(FDA), Jul 4, 2000.

(45) Grandjean P; Jurgensen PJ; Weihe P. Milk as a Source of Methylmercury Exposure in Infants.

Milk as a Source of Methylmercury Exposure in Infants. Environ Health Perspect 1994 Jan;102(1):74-7.

(46) (a)Science News, Methylmercury's toxic toll. July 29, 2000, Vol 158, No.5, p77; & National Research Council, Toxicological Effects of Methylmercury, National Acadamy Press, Wash, DC, 2000; & U.S. CDC,

Second National Report on Human Exposure to Environmental Chemicals, http://www.cdc.gov/exposurereport/

& U.S. Centers for Disease Control, Mar 2001, Blood and Hair Mercury Levels in Young Children and Women of Childbearing Age --- United States, 1999 http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5008a2.htm;

& (b)Grandjean P, 2000, Health effects of seafood contamination with methylmercury and PCBs in the Faroes.

Atlantic Coast Contaminants Workshop, June 22-25, 2000, Bar Harbor Maine; & Environ Res, 1998; 77: 165-72

(47) Moreno-Fuenmayor H, Borjas L, Arrieta A, Valera V, Plasma excitatory amino acids in autism. Invest Clin 1996, 37(2):113-28; & Rolf LH, Haarman FY, Grotemeyer KH, Kehrer H. Serotonin and amino acid content in platelets of autistic children. Acta Psychiatr Scand 1993, 87(5): 312-6; & Naruse H, Hayashi T, Takesada M, Yamazaki K. Metabolic changes in aromatic amino acids and monoamines in infantile autism and a new related treatment, No To Hattatsu, 1989, 21(2):181-9; & Carlsson ML. Is infantile autsim a hypoglutamatergic disorer? J Neural Transm 1998, 105(4-5): 525-35.

(48) Reichrtova E et al, "Cord Serum Immunoglobulin E Related to Environmental Contamination of Human Placentas with Oganochlorine Compounds", Envir Health Perspec, 1999, 107(11):895-99; & Gavett SH et al. Residual Oil Fly Ash Amplifies Allergic Cytokines, Airway Responsiveness, and Inflammation in Mice. Am J Respir Crit Care Med, 1999, 160(6):1897-1904; & Kramer U et al, Traffic-related air pollution is associated with atopy in children living in urban areas Epidemiology 2000, 11(1): 64-70.

(49) Megson MN, Is Autism A G-Alpha Protein Defect Reversible with Natural Vitamin A? http://www.megson.com;

(50) B. Windham, Cognitive and Behavioral Effects of Toxic Metals, (over 100 medical study references) http://www.home.earthlink.net/~berniew1/tmlbn.html

(51) Walsh, WJ, Health Research Institute, Autism and Metal Metabolism,www.hriptc.org/autism.htm, Oct 20, 2000; & Walsh WJ, Pfeiffer Treatment Center, Metal-Metabolism and Human Functioning, 2000,http://www.hriptc.org/mhfres.htm;

& HRI-Pfeiffer Center Autism Study; paper presented to Dan Conference, Jan 2001;

(52) Dr. Gerald Bernstein, Beth Israel Medical Center, NY, past Pres., Amer. Diabetes Association; & U.S. Centers for Disease Control, 2001, http://www.mercola.com/2000/sept/17/diabetes_epidemic.htm; & Dr. Anthony Iacopino. Conference Paper, American Academy of Periodontology ; & Dr. Bart Classen, Vaccines are the largest cause of insulin-dependent diabetes in young children, paper given at American College for Advancement in Medicine., Nashville, Tenn., May 14, 2001 ; Harris Coulter, Childhood Vaccinations and Juvenile-Onset (Type-1) Diabetes, Testimony before the Congress of the United States, House of Representatives, Committee on Appropriations, subcommittee on Labor, Health and Human Services, Education, and Related Agencies, April 16, 1997, http://www.909shot.com/hcdiabetes.htm & Classen B. ,Autoimmunity August 2002 Vol. 35 (4), pp. 247-253 & Swedish researchers, Ann. N.Y. Acad Sci. 958: 293-296, 2002

(53) Furlano RI, Anthony A, Day R, Murch SH, et al, Colonic CD8 and gamma delta T-cell infiltration with epithelial damage in children with autism. J Pediatr 138:366-72, 2001; & D'Eufemia P, Celli M, Giardini O, et al, Abnormal intestinal permeability in children with autism. Acta Paediatr 85:1076-9, 1996; & Goodwin MS, Cowen MA, Goodwin TC. Malabsorption and cerebral dysfunction: a multivariate and comparative sutudy of autistic children. J Austism Child Schizophr 1:48-52, 1971.

(54) Bamerjee S, Bhattacharya S. Histopathological changes induced by chronic nonlethal levels of mercury and ammonia in the small intestine of channa puntatus. Ecol Environ Safety 31:62-8 (1995); & Bohme M, Diener M, Mestres P, Rummel W. Direct and indirect actions of HgCl2 and methyl mercury chloride on permeability and chloride secretion across the rat colonic mucosa. Toxicol Appl Pharmacol 114:285-94 (1992); & Andres P. IgA-IgG disease in the intestine of Brown-Norway rats ingesting mercuric

chloride. Clin Immunol and Immunopath 30:488-494 (1984).

(55) Sasser LB, Jarboe GE, Walter BK, Kelman BJ. Absorption of mercury from ligated

segments of the rat gastrointestinal tract. Proc Soc Exp Biol Med 157:57-60 (1978).; & Kostial K, Kargacin B, Landeka M. Gut retention of metals in rats. Biol Trace Elem Res 21:213-218 (1989).

(56).Srikantaiah MV, Radhakrishnan AN. Studies on the metabolism of vitamin B6 in the

small intestine: Part III--purification and properties of monkey intestinal pyridoxal

kinase. Indian J of Biochem 7:151-156 (1970).

(57) Chen W, Body RL, Mottet NK. Biochemical and morphological studies of monkeys

chronically exposed to methylmercury. J Toxicol Environ Hlth 12:407-416 (1983).

(58) P.W. Mathieson, "Mercury: god of TH2 cells",1995, Clinical Exp Immunol

(59) Asthma, mercury, and vaccines. http://www.whaleto.freeserve.co.uk/vaccines/asthma.html

(60) Odent MR, Culpin EE, Kimmel T; Pertussis vaccination and asthma: is there a link? JAMA, 1994, 272:592-30; & (b) Dr. Julian Hopkn, Churchill Hospitial, Oxford, Asthma & allergy risk increased by vaccination, paper at meeting of British Thoriac Society, Dec 1997; & (c) Pertusiss vaccine associated with increased asthma and allergies, Archives of Pediatrics and Adoloescent Medicine, 1998; 152:734-738.

(61) Fine JM, Chen LC; "Confounding in studies of adverse reaction s to vaccines", Amer J Epidemiology, 1992, 136:

121-35; & (b) Dr. Vera Scheibner, Leif Karlsson; "Association between DPT injections and Cot Death", 2nd Immuniztion Conference, Canberra, Australia, May 27, 1991; & Torch WC, DPT Immunization: a potential cause of sudden enfant death syndrome(SIDS), Amer Acad of Neurology, 34th Annual Meeting, Apr 25, 1982; Neurology, 32(4), pt 2.

(62) Dr Thomas Verstraeten, US Centres for Disease Control and Prevention, Summary Results: Vaccine Safety Datalink Project - a database of 400,000 children , May 2000.

(63) P.Bulat, "Activity of Gpx and SOD in workers occupationally exposed to mercury", Arch Occup Environ Health, 1998, Sept, 71 Suppl:S37-9; & Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med 1995; 18(2): 321-36.

(64) Spivey-Fox MR. Nutritional influences on metal toxicity. Environ Health Perspect 1979; 29: 95-104; & Pfeiffer SI et al, Efficacy of vitamin B6 and magnesium in the treatment of autism. J Autism Dev Disord 1995, 25(5):481-93.

(65) Hernberg S; & Moore MR. in Lead Toxicity, R.Singhal & J.Thomas(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.

(66) Lars Landner and Lennart Lindestrom. Swedish Environmental Research Group(MFG), Copper in society and the Environment, 2nd revised edition. 1999.

(67) J.C.Veltman et al, "Alterations of heme, cytochrome P-450, and steroid metabolism by mercury in rat adrenal gland", Arch Biochem Biophys,1986, 248(2):467-78; & A.G.Riedl et al, Neurodegenerative Disease Research

Center, King's College,UK, "P450 and hemeoxygenase enzymes in the basal ganglia and their role's in Parkinson's disease", Adv Neurol, 1999; 80:271-86

(68) Mata L, Sanchez L, Calvo M, Interaction of mercury with human and bovine milk proteins. Biosci Biotechnol Biochem 1997 Oct;61(10):1641-5; & Kostial K, Rabar I, Ciganovic M, Simonovic I, Effect of milk on mercury absorption and gut retention in rats. Bull Environ Contam Toxicol 1979, Nov;23(4-5) :566-7; & Rowland IR, Robinson RD, Doherty RA, Effects of diet on mercury metabolism and excretion in mice given methylmercury: role of gut flora, Arch Environ Health 1984 Nov-Dec;39(6):401-8

(69) E.Lutz et al, "Concentrations of mercury in brain and kidney of fetuses and infants", Journal of Trace Elements in Medicine and Biology, 1996,10:61-67; & G.Drasch et al, "Mercury Burden of Human Fetal and Infant Tissues", Eur J Pediatr 153:607-610,1994; & A.Oskarsson et al, "Mercury in breast milk in relation to fish consumption and amalgam", Arch environ Health, 1996,51(3):234-41; & Drasch et al, "Mercury in human colostrum and early breast milk", J.Trace Elem. Med.Biol., 1998,12:23-27

(70) Kravchenko AT, Dzagurov SG, Chervonskaia GP. III. The detection of toxic properties in medical biological preparations by the degree of cell damage in the L132 continuous cell line. Zh Mikrobiol Epidemiol Immunobiol 1983 Mar;(3):87-92 [Article in Russian]

(71) The Health of Canada's Children--A Canadian Institute of Child Health (CICH), Profile: 3rd Edition, 2000, 325 pages; http://oncology.medscape.com/26856.rhtml

(72) (a) HultmanP, Johansson U, Turley SJ; Adverse immunological effects and autoimmunity induced by dental amalgam in mice. FASEB J 1994; 8: 1183-90; &.(b) Pollard KM, Lee DK, Casiano CA; The autoimmunity-inducing xenobiotic mercury interacts with the autoantigen fibrillarin and modifies its molecular structure ad antigenic properties. J Immunol 1997; 158: 3421-8; &(c) P.L.Bigazzi, "Autoimmunity induced by metals", in Chang, L., Toxicology of Metals, Lewis Publishers, CRC Press Inc. 1996., p835-52; & (d) Hu H; Moller G; Abedi-Valugerdi M. Major histocompatibility complex class II antigens are required for both cytokine production and proliferation induced by mercuric chloride in vitro. J Autoimmun 1997 Oct;10(5):441-6;

(73) (a)C.J.G.Robinson et al, "Mercuric chloride induced anitnuclear antibodies In mice", Toxic Appl Pharmacology, 1986, 86:159-169. & (b) El-Fawai HA, Waterman SJ, De Feo A, Shamy MY. Neuroimmunotoxicology: Humoral Assessment of Neurotoxicity and Autoimmune Mechanisms. Contact Dermatitis 1999; 41(1): 60-1;

& (c) Hu H; Moller G; Abedi-Valugerdi M. Mechanism of mercury-induced autoimmunity: both T helper 1- and T helper 2-type responses are involved. Immunology 1999 Mar;96(3):348-57;

(74) Earl C, Chantry A, Mohammad N. Zinc ions stabilize the association of basic protein with brain myelin membranes. J Neurochem 1988; 51:718-24; & Ricco P, Giovanneli S, Bobba A. Specificity of zinc binding to myelin basic protein. Neurochem Res 1995; 20:1107-13.

(75) The extent of drug therapy for attention deficit-hyperactivity disorder among children in public schools. (American Journal of Public Health. 1999; 89(9):1359-64); & http://www.niehs.hih.gov/oc/news.adhd.htm

(76) Adverse health effects of Ritalin and other stimulant drugs: http://users.cybercity.dk/~bbb9582/ritalin.htm; & http://www.healthysource.com/ritalin.html; & http://www.breggin.com/RitalinNIHSPEECH.html; &

www.healthoptions.com/ritalin.html; & http://lifefellowship.org/-Updatables/Articles/40.html face="Arial" size="-1">;

Michael R. Lyon, Healing the Hyperactive Brain th

 

 
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