Hertz-Picciotto’s blood mercury autism study: what the researchers omitted

Hertz-Picciotto’s blood mercury autism study: what the researchers omitted

Teresa Binstock
Researcher in Developmental & Behavioral Neuroanatomy
October 21, 2009

Irva Hertz-Picciotto & colleagues have published results of a study comparing mercury (Hg) levels in children with and without autism (1). The study does not report findings about total body burden of Hg in children, nor does the study evaluate levels of Hg in the brain or other specific organs in autistic and non-autistic children.

Indeed, the researchers who did the blood-Hg study state: “As only 5% of body burdens of Hg are estimated to be in circulation, (Burbacher et al. 2005; Stinson et al. 1989) reliable conclusions about distribution are not possible from one-time observational measurements in blood.” (1) Since various forms of mercury can enter the brain and remain there (17), and since different tissues of humans and other species retain mercury at various rates (16), the larger context of Hertz-Picciotto et al’s findings need be considered.

Relevant questions include: What do Hg levels in blood signify? Alternatively, what don’t they signify? And what does intra-body and intra-brain mercury mean for children with weak alleles in glutathione-related pathways or born to mothers with weak alleles in glutathione-related pathways?

Although the new study purports to offer a review of autism genetics, Hertz-Picciotto et al (1) omit an important category of citations related to mercury, glutathione, methylation, and autism (eg, 2-14).

Furthermore, the researchers cite two studies of in vivo thimerosal levels (Pichichero et al 2002, 2008) while omitting consideration of Waly et al 2004, who investigated thimerosal levels lower than those described by Pichichero et al 2002 in human infants, found that methionine synthase was inhibited, and concluded that “The potent inhibition of this pathway by ethanol, lead, mercury, aluminum and thimerosal suggests that it may be an important target of neurodevelopmental toxins.” (15)

Why were these important findings omitted? Weren’t the reviewers aware of cites 1-15 hereinbelow?

In seeking to understand intra-body and intra-brain Hg, Lorscheider et al provide important insights.

In a study available free online, data reviewed by Lorscheider et al (16) indicate that Hg exposure does not lead to equivalent concentration in all tissues. For instance, from chronic exposure via amalgam vapors, some tissues accumulate more Hg than do other tissues (16).

Caveat: ingesting one’s own amalgam vapors probably includes olfactory exposure as well as oral/gastrointestinal exposure and therefore is not perfectly akin to ingesting Hg by eating fish. Nonetheless, Hg distribution findings due to amalgams may be instructive.

“The degree to which body tissues can sequester amalgam Hg after exposure has been demonstrated in a variety of human and animal experiments… The brain/CSF Hg ratio had increased threefold by 4 wk after amalgam fillings had been installed…” (16)

“Repeated observations in adult sheep… demonstrate that after placement of amalgam fillings the blood Hg levels remain relatively low even though the surrounding body tissue concentrations of Hg become many fold higher than blood. This suggests that tissues rapidly sequester amalgam Hg at a rate equivalent to its initial appearance in the circulation. Such a phenomenon may explain why monitoring blood levels of Hg in humans is a poor indicator of the actual tissue body burden directly attributable to continuous low-dose Hg exposure from amalgam.” (16)

Lorscheider et al (16) summarize another important point:

“Both intracellular Hg2 and Hg are ultimately bound covalently to glutathione (GSH) and protein cysteine groups. Hg2 is the toxic product responsible for the adverse effects of inhaled Hg0. Body tissues have various retention half-lives for Hg and Hg2 ranging from days to years… ”

Implications ensue from the Hg/GSH genetics findings in autism and from the Hg-distribution studies reviewed in Lorscheider et al:
a) Tissue levels of Hg are are likely differ from and to be greater than Hg levels found in blood.
b) Subgroups of children who have developed autism are known to have one or more problems in pathways related to glutathione and methylation (eg, 2-14) may detoxify Hg and related compounds poorly and thus may sequester Hg and related compounds disadvantegeously.
c) Blood levels of Hg in autistic children (1) tell us little about Hg in their brain and other tissues.

As Hertz-Picciotto et al mention, several studies have found associations between autism rates and environmental mercury (18-20), and these findings conjoin with the often ignored fact that thimerosal in early life vaccines increases risk for autism and for developmental disabilities requiring special education (21-22).

Be aware: some brands of H1N1 (“swine”) flu vaccine and non-H1N1 influenza vaccines contain substantial amounts of thimerosal (eg, 23).

1. Blood Mercury Concentrations in CHARGE Study Children with and without Autism
Irva Hertz-Picciotto et al.

2: James SJ et al. Cellular and mitochondrial glutathione redox imbalance in lymphoblastoid cells derived from children with autism. FASEB J. 2009 Aug;23(8):2374-83.

3: James SJ et al. Efficacy of methylcobalamin and folinic acid treatment on glutathione redox status in children with autism. Am J Clin Nutr. 2009 Jan;89(1):425-30.

4: James SJ et al. Abnormal transmethylation/transsulfuration metabolism and DNA hypomethylation among parents of children with autism. J Autism Dev Disord. 2008 Nov;38(10):1966-75.

5: James SJ et al. Metabolic endophenotype and related genotypes are associated with oxidative stress in children with autism. Am J Med Genet B Neuropsychiatr Genet. 2006 Dec 5;141B(8):947-56.

6: James SJ et al. Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism. Am J Clin Nutr. 2004 Dec;80(6):1611-7.

7: Deth R et al. How environmental and genetic factors combine to cause autism: A redox/methylation hypothesis. Neurotoxicology. 2008 Jan;29(1):190-201.

8: Westphal GA et al. Homozygous gene deletions of the glutathione S-transferases M1 and T1 are associated with thimerosal sensitization. Int Arch Occup Environ Health. 2000 Aug;73(6):384-8.

9: M?ller M et al. Inhibition of the human erythrocytic glutathione-S-transferase T1 (GST T1) by thimerosal. Int J Hyg Environ Health. 2001 Jul;203(5-6):479-81.

10. Williams TA et al. Risk of autistic disorder in affected offspring of mothers with a glutathione S-transferase P1 haplotype. Arch Pediatr Adolesc Med. 2007 Apr;161(4):356-61

11. Geier DA et al. Biomarkers of environmental toxicity and susceptibility in autism. J Neurol Sci. 2009 May 15;280(1-2):101-8.

12. Ming X et al. Genetic variant of glutathione peroxidase 1 in autism. Brain Dev. 2009 Feb 3. [Epub ahead of print]

13. Al-Gadani Y et al. Metabolic biomarkers related to oxidative stress and antioxidant status in Saudi autistic children. Clin Biochem. 2009 Jul;42(10-11):1032-40.

14. Pasca SP et al. One Carbon Metabolism Disturbances and the C667T MTHFR Gene Polymorphism in Children with Autism Spectrum Disorders. J Cell Mol Med. 2008 Aug 9.

15. Waly M et al. Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal. Mol Psychiatry. 2004 Apr;9(4):358-70.

16. Lorscheider FL et al. Mercury exposure from “silver” tooth fillings: emerging evidence questions a traditional dental paradigm. FASEB J. 1995 Apr;9(7):504-8.

17. Burbacher TM et al. Comparison of blood and brain mercury levels in infant monkeys exposed to methylmercury or vaccines containing thimerosal. Environ Health Perspect. 2005 Aug;113(8):1015-21.

18. Palmer RF et al. Environmental mercury release, special education rates, and autism disorder: an ecological study of Texas. Health Place. 2006 Jun;12(2):203-9.

19.Windham GC et al. Autism spectrum disorders in relation to distribution of hazardous air pollutants in the san francisco bay area. Environ Health Perspect. 2006 Sep;114(9):1438-44.

20. Palmer RF et al. Proximity to point sources of environmental mercury release as a predictor of autism prevalence. Health Place. 2009 Mar;15(1):18-24.

21. Hepatitis B vaccination of male neonates and autism
[conference abstract as published]
CM Gallagher, MS Goodman, Graduate Program in Public
Health, Stony Brook University Medical Center, Stony Brook, NY
Annals of Epidemiology, p659
Vol. 19, No. 9 Abstracts (ACE) September 2009: 651?680
[triple the rate of autism among boys vaccinated with thimerosal versus boys not so vaccinated]

22. Hepatitis B triple series vaccine and developmental disability in US children aged 1-9 years
Gallagher C, Goodman M. Toxicol Environ Chem 2008 90(5):997-1008.
{free online}

“The odds of receiving EIS were approximately nine times as great for vaccinated boys… as for unvaccinated boys…, after adjustment for confounders.

23. H1N1 Vaccines Approved: What’s In It For You?
By Jackie Lombardo

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