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
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
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
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
Implications ensue from the Hg/GSH genetics findings in
autism and from the Hg-distribution studies reviewed in Lorscheider et
) Tissue levels of Hg are are likely differ from and to be greater
than Hg levels found in blood.
) 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.
) 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
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: Müller 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
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.
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
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.
"The odds of receiving EIS were approximately nine times as great for
vaccinated boys... as for unvaccinated boys..., after adjustment for
23. H1N1 Vaccines Approved: What's In It For You?
By Jackie Lombardo
Contact Teresa Binstock by email