Alzheimer etc: mercury and APOe4 and autism

[Guest guest]

Cite 11 is free online and may be useful. Cites 12 and 13 link

environmental Hg and autism, along with other environmental factors.

Reducing levels of pollutants in the environment seems like a sensible

goal, but effectively moving towards that goal requires major changes in

our lifeways, in The Economy, in the products we buy and use. And, since

increased rates of pathologies enhance pharma revenue streams, pharma

and its servants in the US govt have major financial incentives to

resist change.

Late last spring I became an environmental refugee. I fled the

increasing and often severe pollution in Estes Park and nearby Rocky

Mountain National Park and journeyed to Montana. Much to my surprise, I

had traded Front Range air pollution for wildfire pollution, which too

is full of toxins (eg, 14). An article posted a few minutes ago

describes the many brain pathologies that appear in elderly humans. As

cites herein make clear, mercury and other metals are implicated in

autism and in Alzheimer's. I've visited a number of cities in the US.

Each city has pollution that injures. Seemingly pristine locales like

National Parks are recipients of pollutants from agriculture (eg,

15-18), at least some of which are associated with autism (D'Amelio et

al 2005; Winham et al 2007).

My early years were spent in the toxic air of industry-cities s.e. of

Chicago. My vision of a healthful future does not include sinking with a

pollutional Titanic (19-22).

- - - -

*1: *Fortschr Neurol Psychiatr. <javascript:AL_get(this, 'jour',

'Fortschr Neurol Psychiatr.');> 2007 Sep;75(9):528-38. Epub 2007 Jul 12.

Related Articles

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ame=pubmed_pubmed & LinkReadableName=Related%20Articles & IdsFromResult=17628833 & ord\

inalpos=1 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstra\

ct>,

Links <javascript:PopUpMenu2_Set(Menu17628833);>

Click here to read

<http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3400 & itool=Abstract-def\

& uid=17628833 & db=pubmed & url=http://www.thieme-connect.com/DOI/DOI?10.1055/s-2007\

-959237>

*[Mercury and Alzheimer's disease]*

[Article in German]

*Mutter J*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Mutter%20\

J%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstract>,

*Naumann J*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Naumann%2\

0J%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_\

RVAbstract>,

*Schneider R*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Schneider\

%20R%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubme\

d_RVAbstract>,

*Walach H*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Walach%20\

H%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstract>.

Institut für Umweltmedizin und Krankenhaushygiene,

Universitätsklinik Freiburg (Franz Daschner), Breidacher Strasse

115b, 79106 Freiburg i. Brsg. joachim.mutter@...

Higher mercury concentrations were found in brain regions and blood

of some patients with Alzheimer's disease (AD). Low levels of

inorganic mercury were able to cause AD- typical nerve cell

deteriorations in vitro and in animal experiments. Other metals like

zinc, aluminum, copper, cadmium, manganese, iron, and chrome are not

able to elicit all of these deteriorations in low levels, yet they

aggravate the toxic effects of mercury (Hg). Main human sources for

mercury are fish consumption (Methyl-Hg) and dental amalgam (Hg

vapour). Regular fish consumption reduces the risk of development of

AD. Amalgam consists of approx. 50 % of elementary mercury which is

constantly being vaporized and absorbed by the organism. Mercury

levels in brain tissues are 2 - 10 fold higher in individuals with

dental amalgam. Persons showing a genetically determined subgroup of

transportation protein for fats (apolipoprotein E4) have an

increased AD risk. Apoliprotein E (APO E) is found in high

concentrations in the central nervous system. The increased AD risk

through APO E4 might be caused by its reduced ability to bind heavy

metals. Latest therapeutic approaches to the treatment of Alzheimer

disease embrace pharmaceuticals which remove or bind metals from the

brain. Preliminary success has been documented with chelation of

synergistic toxic metals (Fe, Al, Zn, Cu) and therefore also Hg. The

available data does not answer the question, whether mercury is a

relevant risk factor in AD distinctively. In sum, the findings from

epidemiological and demographical studies, the frequency of amalgam

application in industrialized countries, clinical studies,

experimental studies and the dental state of Alzheimer patients in

comparison to controls suggest a decisive role for inorganic mercury

in the etiology of Alzheimer's disease. Other factors currently

discussed as causes (e. g. other metals, inflammations, dietetic

factors, vitamin deficiency, oxidative distress, and metabolic

impairments) may act as co-factors.

Publication Types:

* English Abstract <javascript:AL_get(this, 'ptyp', 'English

Abstract');>

* Review <javascript:AL_get(this, 'ptyp', 'Review');>

PMID: 17628833 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

*2: *Rev Environ Health. <javascript:AL_get(this, 'jour', 'Rev Environ

Health.');> 2006 Apr-Jun;21(2):105-17.

Related Articles

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & DbFrom=pubmed & Cmd=Link & LinkN\

ame=pubmed_pubmed & LinkReadableName=Related%20Articles & IdsFromResult=16898674 & ord\

inalpos=2 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstra\

ct>,

Links <javascript:PopUpMenu2_Set(Menu16898674);>

*Involvement of environmental mercury and lead in the etiology of

neurodegenerative diseases.*

*Monnet-Tschudi F*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Monnet-Ts\

chudi%20F%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.\

Pubmed_RVAbstract>,

*Zurich MG*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Zurich%20\

MG%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_\

RVAbstract>,

*Boschat C*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Boschat%2\

0C%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_\

RVAbstract>,

*Corbaz A*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Corbaz%20\

A%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstract>,

*Honegger P*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Honegger%\

20P%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed\

_RVAbstract>.

Department of Physiology, University of Lausanne, Switzerland.

Florianne.Tschudi-Monnet@...

The incidence of neurodegenerative disease like Parkinson's disease

and Alzheimer's disease (AD) increases dramatically with age; only a

small percentage is directly related to familial forms. The etiology

of the most abundant, sporadic forms is complex and multifactorial,

involving both genetic and environmental factors. Several

environmental pollutants have been associated with neurodegenerative

disorders. The present article focuses on results obtained in

experimental neurotoxicology studies that indicate a potential

pathogenic role of lead and mercury in the development of

neurodegenerative diseases. Both heavy metals have been shown to

interfere with a multitude of intracellular targets, thereby

contributing to several pathogenic processes typical of

neurodegenerative disorders, including mitochondrial dysfunction,

oxidative stress, deregulation of protein turnover, and brain

inflammation. Exposure to heavy metals early in development can

precondition the brain for developing a neurodegenerative disease

later in life. Alternatively, heavy metals can exert their adverse

effects through acute neurotoxicity or through slow accumulation

during prolonged periods of life. The pro-oxidant effects of heavy

metals can exacerbate the age-related increase in oxidative stress

that is related to the decline of the antioxidant defense systems.

Brain inflammatory reactions also generate oxidative stress. Chronic

inflammation can contribute to the formation of the senile plaques

that are typical for AD. In accord with this view, nonsteroidal

anti-inflammatory drugs and antioxidants suppress early pathogenic

processes leading to Alzheimer's disease, thus decreasing the risk

of developing the disease. The effects of lead and mercury were also

tested in aggregating brain-cell cultures of fetal rat

telencephalon, a three-dimensional brain-cell culture system. The

continuous application for 10 to 50 days of non-cytotoxic

concentrations of heavy metals resulted in their accumulation in

brain cells and the occurrence of delayed toxic effects. When

applied at non-toxic concentrations, methylmercury, the most common

environmental form of mercury, becomes neurotoxic under pro-oxidant

conditions. Furthermore, lead and mercury induce glial cell

reactivity, a hallmark of brain inflammation. Both mercury and lead

increase the expression of the amyloid precursor protein; mercury

also stimulates the formation of insoluble beta-amyloid, which plays

a crucial role in the pathogenesis of AD and causes oxidative stress

and neurotoxicity in vitro. Taken together, a considerable body of

evidence suggests that the heavy metals lead and mercury contribute

to the etiology of neurodegenerative diseases and emphasizes the

importance of taking preventive measures in this regard.

Publication Types:

* Review <javascript:AL_get(this, 'ptyp', 'Review');>

PMID: 16898674 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

*3: *Neuro Endocrinol Lett. <javascript:AL_get(this, 'jour', 'Neuro

Endocrinol Lett.');> 2004 Oct;25(5):331-9.

Related Articles

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & DbFrom=pubmed & Cmd=Link & LinkN\

ame=pubmed_pubmed & LinkReadableName=Related%20Articles & IdsFromResult=15580166 & ord\

inalpos=3 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstra\

ct>,

Links <javascript:PopUpMenu2_Set(Menu15580166);>

*Alzheimer disease: mercury as pathogenetic factor and

apolipoprotein E as a moderator.*

*Mutter J*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Mutter%20\

J%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstract>,

*Naumann J*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Naumann%2\

0J%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_\

RVAbstract>,

*Sadaghiani C*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Sadaghian\

i%20C%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubm\

ed_RVAbstract>,

*Schneider R*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Schneider\

%20R%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubme\

d_RVAbstract>,

*Walach H*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Walach%20\

H%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstract>.

Institute for Environmental Medicine and Hospital Epidemiology,

University Hospital Freiburg, Germany. jmutter@...

The etiology of most cases of Alzheimer's disease (AD) is as yet

unknown. Epidemiological studies suggest that environmental factors

may be involved beside genetic risk factors. Some studies have shown

higher mercury concentrations in brains of deceased and in blood of

living patients with Alzheimer's disease. Experimental studies have

found that even smallest amounts of mercury but no other metals in

low concentrations were able to cause all nerve cell changes, which

are typical for Alzheimer's disease. The most important genetic risk

factor for sporadic Alzheimer's disease is the presence of the

apolipoprotein Ee4 allele whereas the apolipoprotein Ee2 allele

reduces the risk of developing Alzheimer's disease. Some

investigators have suggested that apolipoprotein Ee4 has a reduced

ability to bind metals like mercury and therefore explain the higher

risk for Alzheimer's disease. Therapeutic approaches embrace

pharmaceuticals which bind metals in the brain of patients with

Alzheimer's disease. In sum, both the findings from epidemiological

and demographical studies, the frequency of amalgam application in

industrialized countries, clinical studies, experimental studies and

the dental state of AD patients in comparison to controls suggest a

decisive role for inorganic mercury in the etiology of AD.

Publication Types:

* Research Support, Non-U.S. Gov't <javascript:AL_get(this,

'ptyp', 'Research Support, Non-U.S. Gov\'t');>

* Review <javascript:AL_get(this, 'ptyp', 'Review');>

PMID: 15580166 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

*4: *J Alzheimers Dis. <javascript:AL_get(this, 'jour', 'J Alzheimers

Dis.');> 2003 Jun;5(3):189-95.

Related Articles

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & DbFrom=pubmed & Cmd=Link & LinkN\

ame=pubmed_pubmed & LinkReadableName=Related%20Articles & IdsFromResult=12897404 & ord\

inalpos=4 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstra\

ct>,

Links <javascript:PopUpMenu2_Set(Menu12897404);>

Click here to read

<http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3314 & itool=Abstract-def\

& uid=12897404 & db=pubmed & url=http://iospress.metapress.com/openurl.asp?genre=arti\

cle & issn=1387-2877 & volume=5 & issue=3 & spage=189>

*Apolipoprotein E genotyping as a potential biomarker for mercury

neurotoxicity.*

*Godfrey ME*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Godfrey%2\

0ME%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed\

_RVAbstract>,

*Wojcik DP*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Wojcik%20\

DP%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_\

RVAbstract>,

*Krone CA*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Krone%20C\

A%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstract>.

Bay of Plenty Environmental Health Clinic, Tauranga, New Zealand.

godfrey@...

Apolipoprotein-E (apo-E) genotyping has been investigated as an

indicator of susceptibility to heavy metal (i.e., lead)

neurotoxicity. Moreover, the apo-E epsilon (epsilon)4 allele is a

major risk factor for neurodegenerative conditions, including

Alzheimer's disease (AD). A theoretical biochemical basis for this

risk factor is discussed herein, supported by data from 400 patients

with presumptive mercury-related neuro-psychiatric symptoms and in

whom apo-E determinations were made. A statistically relevant shift

toward the at-risk apo-E epsilon4 groups was found in the patients

p<0.001). The patients possessed a mean of 13.7 dental amalgam

fillings and 31.5 amalgam surfaces. This far exceeds the number

capable of producing the maximum identified tolerable daily intake

of mercury from amalgam. The clinical diagnosis and proof of chronic

low-level mercury toxicity has been difficult due to the

non-specific nature of the symptoms and signs. Dental amalgam is the

greatest source of mercury in the general population and brain,

blood and urine mercury levels increase correspondingly with the

number of amalgams and amalgam surfaces in the mouth. Confirmation

of an elevated body burden of mercury can be made by measuring

urinary mercury, after provocation with 2,3,-dimercapto-propane

sulfonate (DMPS) and this was measured in 150 patients. Apo-E

genotyping warrants investigation as a clinically useful biomarker

for those at increased risk of neuropathology, including AD, when

subjected to long-term mercury exposures. Additionally, when

clinical findings suggest adverse effects of chronic mercury

exposure, a DMPS urine mercury challenge appears to be a simple,

inexpensive procedure that provides objective confirmatory evidence.

An opportunity could now exist for primary health practitioners to

help identify those at greater risk and possibly forestall

subsequent neurological deterioration.

PMID: 12897404 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

*5: *Bull Environ Contam Toxicol. <javascript:AL_get(this, 'jour', 'Bull

Environ Contam Toxicol.');> 2001 Dec;67(6):800-6.

Related Articles

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ame=pubmed_pubmed & LinkReadableName=Related%20Articles & IdsFromResult=11692193 & ord\

inalpos=5 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstra\

ct>,

Links <javascript:PopUpMenu2_Set(Menu11692193);>

Click here to read

<http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3055 & itool=Abstract-def\

& uid=11692193 & db=pubmed & url=http://link.springer-ny.com/link/service/journals/00\

128/bibs/1067006/10670800.html>

*Mercury induced Alzheimer's disease: accelerating incidence?*

*Ely JT*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Ely%20JT%\

22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVA\

bstract>.

Radiation Studies 351650, University of Washington, Seattle, WA

98195, USA.

Publication Types:

* Research Support, Non-U.S. Gov't <javascript:AL_get(this,

'ptyp', 'Research Support, Non-U.S. Gov\'t');>

PMID: 11692193 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

*6: *J Neurochem. <javascript:AL_get(this, 'jour', 'J Neurochem.');>

2000 Jan;74(1):231-6.

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<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & DbFrom=pubmed & Cmd=Link & LinkN\

ame=pubmed_pubmed & LinkReadableName=Related%20Articles & IdsFromResult=10617124 & ord\

inalpos=6 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstra\

ct>,

Links <javascript:PopUpMenu2_Set(Menu10617124);>

Click here to read

<http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3046 & itool=Abstract-def\

& uid=10617124 & db=pubmed & url=http://www.blackwell-synergy.com/openurl?genre=artic\

le & sid=nlm:pubmed & issn=0022-3042 & date=2000 & volume=74 & issue=1 & spage=231>

*Mercury induces cell cytotoxicity and oxidative stress and

increases beta-amyloid secretion and tau phosphorylation in SHSY5Y

neuroblastoma cells.*

*Olivieri G*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Olivieri%\

20G%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed\

_RVAbstract>,

*Brack C*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Brack%20C\

%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RV\

Abstract>,

*Müller-Spahn F*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22M%C3%BCll\

er-Spahn%20F%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPan\

el.Pubmed_RVAbstract>,

*Stähelin HB*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22St%C3%A4h\

elin%20HB%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.\

Pubmed_RVAbstract>,

*Herrmann M*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Herrmann%\

20M%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed\

_RVAbstract>,

*Renard P*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Renard%20\

P%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstract>,

*Brockhaus M*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Brockhaus\

%20M%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubme\

d_RVAbstract>,

*Hock C*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Hock%20C%\

22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVA\

bstract>.

Neurobiology Laboratory, Psychiatric University Hospital, Basel,

Switzerland. Olivieri@...

Concentrations of heavy metals, including mercury, have been shown

to be altered in the brain and body fluids of Alzheimer's disease

(AD) patients. To explore potential pathophysiological mechanisms we

used an in vitro model system (SHSY5Y neuroblastoma cells) and

investigated the effects of inorganic mercury (HgCl2) on oxidative

stress, cell cytotoxicity, beta-amyloid production, and tau

phosphorylation. We demonstrated that exposure of cells to 50

microg/L (180 nM) HgCl2 for 30 min induces a 30% reduction in

cellular glutathione (GSH) levels (n = 13, p<0.001). Preincubation

of cells for 30 min with 1 microM melatonin or premixing melatonin

and HgCl2 appeared to protect cells from the mercury-induced GSH

loss. Similarly,

3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)

cytotoxicity assays revealed that 50 microg/L HgCl2 for 24 h

produced a 50% inhibition of MTT reduction (n = 9, p<0.001). Again,

melatonin preincubation protected cells from the deleterious effects

of mercury, resulting in MTT reduction equaling control levels. The

release of beta-amyloid peptide (Abeta) 1-40 and 1-42 into cell

culture supernatants after exposure to HgCl2 was shown to be

different: Abeta 1-40 showed maximal (15.3 ng/ml) release after 4 h,

whereas Abeta 1-42 showed maximal (9.3 ng/ml) release after 6 h of

exposure to mercury compared with untreated controls (n = 9,

p<0.001). Preincubation of cells with melatonin resulted in an

attenuation of Abeta 1-40 and Abeta 1-42 release. Tau

phosphorylation was significantly increased in the presence of

mercury (n = 9, p<0.001), whereas melatonin preincubation reduced

the phosphorylation to control values. These results indicate that

mercury may play a role in pathophysiological mechanisms of AD.

Publication Types:

* Research Support, Non-U.S. Gov't <javascript:AL_get(this,

'ptyp', 'Research Support, Non-U.S. Gov\'t');>

PMID: 10617124 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

*7: *J Neural Transm. <javascript:AL_get(this, 'jour', 'J Neural

Transm.');> 1998;105(1):59-68.

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ame=pubmed_pubmed & LinkReadableName=Related%20Articles & IdsFromResult=9588761 & ordi\

nalpos=7 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstrac\

t>,

Links <javascript:PopUpMenu2_Set(Menu9588761);>

Click here to read

<http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3055 & itool=Abstract-def\

& uid=9588761 & db=pubmed & url=http://link.springer.de/link/service/journals/00702/b\

ibs/8105001/81050059.htm>

*Increased blood mercury levels in patients with Alzheimer's disease.*

*Hock C*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Hock%20C%\

22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVA\

bstract>,

*Drasch G*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Drasch%20\

G%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstract>,

*Golombowski S*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Golombows\

ki%20S%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pub\

med_RVAbstract>,

*Müller-Spahn F*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22M%C3%BCll\

er-Spahn%20F%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPan\

el.Pubmed_RVAbstract>,

*Willershausen-Zönnchen B*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Willersha\

usen-Z%C3%B6nnchen%20B%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_\

ResultsPanel.Pubmed_RVAbstract>,

*Schwarz P*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Schwarz%2\

0P%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_\

RVAbstract>,

*Hock U*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Hock%20U%\

22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVA\

bstract>,

*Growdon JH*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Growdon%2\

0JH%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed\

_RVAbstract>,

*Nitsch RM*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Nitsch%20\

RM%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_\

RVAbstract>.

Department of Psychiatry, University of Basel, Switzerland.

Alzheimer's disease (AD) is a common neurodegenerative disorder that

leads to dementia and death. In addition to several genetic

parameters, various environmental factors may influence the risk of

getting AD. In order to test whether blood levels of the heavy metal

mercury are increased in AD, we measured blood mercury

concentrations in AD patients (n = 33), and compared them to

age-matched control patients with major depression (MD) (n = 45), as

well as to an additional control group of patients with various

non-psychiatric disorders (n = 65). Blood mercury levels were more

than two-fold higher in AD patients as compared to both control

groups (p = 0.0005, and p = 0.0000, respectively). In early onset AD

patients (n = 13), blood mercury levels were almost three-fold

higher as compared to controls (p = 0.0002, and p = 0.0000,

respectively). These increases were unrelated to the patients'

dental status. Linear regression analysis of blood mercury

concentrations and CSF levels of amyloid beta-peptide (A beta)

revealed a significant correlation of these measures in AD patients

(n = 15, r = 0.7440, p = 0.0015, Pearson type of correlation). These

results demonstrate elevated blood levels of mercury in AD, and they

suggest that this increase of mercury levels is associated with high

CSF levels of A beta, whereas tau levels were unrelated. Possible

explanations of increased blood mercury levels in AD include yet

unidentified environmental sources or release from brain tissue with

the advance in neuronal death.

Publication Types:

* Comparative Study <javascript:AL_get(this, 'ptyp',

'Comparative Study');>

* Research Support, Non-U.S. Gov't <javascript:AL_get(this,

'ptyp', 'Research Support, Non-U.S. Gov\'t');>

PMID: 9588761 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

*8: *J Pineal Res. <javascript:AL_get(this, 'jour', 'J Pineal Res.');>

1998 Jan;24(1):15-21.

Related Articles

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & DbFrom=pubmed & Cmd=Link & LinkN\

ame=pubmed_pubmed & LinkReadableName=Related%20Articles & IdsFromResult=9468114 & ordi\

nalpos=8 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstrac\

t>,

Links <javascript:PopUpMenu2_Set(Menu9468114);>

*The interaction of melatonin and its precursors with aluminium,

cadmium, copper, iron, lead, and zinc: an adsorptive voltammetric

study.*

*Limson J*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Limson%20\

J%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstract>,

*Nyokong T*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Nyokong%2\

0T%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_\

RVAbstract>,

*Daya S*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Daya%20S%\

22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVA\

bstract>.

Department of Chemistry, University, Grahamstown, South Africa.

Melatonin, a pineal secretory product, and its precursors,

tryptophan and serotonin, were examined for their metal binding

affinities for both essential and toxic metals: aluminium, cadmium,

copper, iron, lead, and zinc. An electrochemical technique,

adsorptive stripping voltammetry, showed the varying abilities of

melatonin and its precursors to bind the metals in situ. The results

show that the following metal complexes were formed: aluminium with

melatonin, tryptophan, and serotonin; cadmium with melatonin and

tryptophan; copper with melatonin and serotonin; iron(III) with

melatonin and serotonin; lead with melatonin, tryptophan, and

serotonin; and zinc with melatonin and tryptophan. Iron(II) showed

the formation of an in situ complex with tryptophan only. These

studies suggest a further role for melatonin in the reduction of

free radical generation and metal detoxification, and they may

explain the accumulation of aluminium in Alzheimer's disease.

Publication Types:

* Comparative Study <javascript:AL_get(this, 'ptyp',

'Comparative Study');>

* Research Support, Non-U.S. Gov't <javascript:AL_get(this,

'ptyp', 'Research Support, Non-U.S. Gov\'t');>

PMID: 9468114 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

*9: *Neurotoxicology. <javascript:AL_get(this, 'jour',

'Neurotoxicology.');> 1997;18(2):315-24.

Related Articles

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & DbFrom=pubmed & Cmd=Link & LinkN\

ame=pubmed_pubmed & LinkReadableName=Related%20Articles & IdsFromResult=9291481 & ordi\

nalpos=9 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstrac\

t>,

Links <javascript:PopUpMenu2_Set(Menu9291481);>

*Mercury vapor inhalation inhibits binding of GTP to tubulin in rat

brain: similarity to a molecular lesion in Alzheimer diseased brain.*

*Pendergrass JC*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Pendergra\

ss%20JC%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu\

bmed_RVAbstract>,

*Haley BE*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Haley%20B\

E%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstract>,

*Vimy MJ*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Vimy%20MJ\

%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RV\

Abstract>,

*Winfield SA*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Winfield%\

20SA%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubme\

d_RVAbstract>,

*Lorscheider FL*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Lorscheid\

er%20FL%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu\

bmed_RVAbstract>.

College of Pharmacy, University of Kentucky, Lexington 40536, USA.

Hg2+ interacts with brain tubulin and disassembles microtubules that

maintain neurite structure. Since it is well known that Hg vapor

(Hg0) is continuously released from " silver " amalgam tooth fillings

and is absorbed into brain, rats were exposed to Hg0 4h/day for 0,

2, 7, 14 and 28 d at 250 or 300 micrograms Hg/m3 air, concentrations

present in mouth air of some humans with many amalgam fillings.

Average rat brain Hg concentrations increased significantly (11-47

fold) with duration of Hg0 exposure. By 14 d Hg0 exposure,

photoaffinity labelling on the beta-subunit of the tubulin dimer

with [alpha 32P] 8N3 GTP in brain homogenates was decreased 41-74%,

upon analysis of SDS-PAGE autoradiograms. The identical

neurochemical lesion of similar or greater magnitude is evident in

Alzheimer brain homogenates from approximately 80% of patients, when

compared to human age-matched neurological controls. Total tubulin

protein levels remained relatively unchanged between Hg0 exposed rat

brains and controls, and between Alzheimer brains and controls.

Since the rate of tubulin polymerization is dependent upon binding

of GTP to tubulin dimers, we conclude that chronic inhalation of

low-level Hg0 can inhibit polymerization of brain tubulin essential

for formation of microtubules.

Publication Types:

* Research Support, Non-U.S. Gov't <javascript:AL_get(this,

'ptyp', 'Research Support, Non-U.S. Gov\'t');>

* Research Support, U.S. Gov't, P.H.S. <javascript:AL_get(this,

'ptyp', 'Research Support, U.S. Gov\'t, P.H.S.');>

PMID: 9291481 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

*10: *Met Ions Biol Syst. <javascript:AL_get(this, 'jour', 'Met Ions

Biol Syst.');> 1997;34:461-78.

Related Articles

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & DbFrom=pubmed & Cmd=Link & LinkN\

ame=pubmed_pubmed & LinkReadableName=Related%20Articles & IdsFromResult=9046580 & ordi\

nalpos=10 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstra\

ct>,

Links <javascript:PopUpMenu2_Set(Menu9046580);>

*Inhibition of brain tubulin-guanosine 5'-triphosphate interactions

by mercury: similarity to observations in Alzheimer's diseased brain.*

*Pendergrass JC*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Pendergra\

ss%20JC%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu\

bmed_RVAbstract>,

*Haley BE*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Haley%20B\

E%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstract>.

College of Pharmacy, Division of Medicinal Chemistry and

Pharmaceutics, University of Kentucky Medical Center, Lexington

40536-0082, USA.

Publication Types:

* Research Support, Non-U.S. Gov't <javascript:AL_get(this,

'ptyp', 'Research Support, Non-U.S. Gov\'t');>

* Research Support, U.S. Gov't, P.H.S. <javascript:AL_get(this,

'ptyp', 'Research Support, U.S. Gov\'t, P.H.S.');>

* Review <javascript:AL_get(this, 'ptyp', 'Review');>

PMID: 9046580 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

*11: *Adv Dent Res. <javascript:AL_get(this, 'jour', 'Adv Dent Res.');>

1992 Sep;6:110-3.

Related Articles

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & DbFrom=pubmed & Cmd=Link & LinkN\

ame=pubmed_pubmed & LinkReadableName=Related%20Articles & IdsFromResult=1292449 & ordi\

nalpos=11 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstra\

ct>,

Links <javascript:PopUpMenu2_Set(Menu1292449);>

Click here to read

<http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3051 & itool=Abstract-def\

& uid=1292449 & db=pubmed & url=http://adr.iadrjournals.org/cgi/pmidlookup?view=long & \

pmid=1292449>

*Side-effects: mercury contribution to body burden from dental amalgam.*

*Reinhardt JW*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Reinhardt\

%20JW%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubm\

ed_RVAbstract>.

Department of Operative Dentistry, University of Iowa College of

Dentistry, Iowa City 52242.

The purpose of this paper is to examine and report on studies that

relate mercury levels in human tissues to the presence of dental

amalgams, giving special attention to autopsy studies. Until

recently, there have been few published studies examining the

relationship between dental amalgams and tissue mercury levels.

Improved and highly sensitive tissue analysis techniques have made

it possible to measure elements in the concentration range of parts

per billion. The fact that mercury can be absorbed and reach toxic

levels in human tissues makes any and all exposure to that element

of scientific interest. Dental amalgams have long been believed to

be of little significance as contributors to the overall body burden

of mercury, because the elemental form of mercury is rapidly

consumed in the setting reaction of the restoration. Studies showing

measurable elemental mercury vapor release from dental amalgams have

raised renewed concern about amalgam safety. Mercury vapor

absorption occurs through the lungs, with about 80% of the inhaled

vapor being absorbed by the lungs and rapidly entering the

bloodstream. Following distribution by blood circulation, mercury

can enter and remain in certain tissues for longer periods of time,

since the half-life of excretion is prolonged. Two of the primary

target organs of concern are the central nervous system and kidneys.

Publication Types:

* Review <javascript:AL_get(this, 'ptyp', 'Review');>

PMID: 1292449

*12: *Environ Health Perspect. <javascript:AL_get(this, 'jour', 'Environ

Health Perspect.');> 2006 Sep;114(9):1438-44.

Related Articles

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & DbFrom=pubmed & Cmd=Link & LinkN\

ame=pubmed_pubmed & LinkReadableName=Related%20Articles & IdsFromResult=16966102 & ord\

inalpos=1 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstra\

ct>,

Links <javascript:PopUpMenu2_Set(Menu16966102);>

Click here to read

<http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3040 & itool=Abstract-def\

& uid=16966102 & db=pubmed & url=http://www.ehponline.org/members/2006/9120/9120.html\

>

Click here to read

<http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3494 & itool=Abstract-non\

def & uid=16966102 & db=pubmed & url=http://www.pubmedcentral.nih.gov/articlerender.fc\

gi?tool=pubmed & pubmedid=16966102>

*Autism spectrum disorders in relation to distribution of hazardous

air pollutants in the san francisco bay area.*

*Windham GC*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Windham%2\

0GC%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed\

_RVAbstract>,

*Zhang L*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Zhang%20L\

%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RV\

Abstract>,

*Gunier R*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Gunier%20\

R%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstract>,

*Croen LA*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Croen%20L\

A%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstract>,

*Grether JK*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Grether%2\

0JK%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed\

_RVAbstract>.

Division of Environmental and Occupational Disease Control,

California Department of Health Services, Richmond, California, USA.

gwindham@...

OBJECTIVE: To explore possible associations between autism spectrum

disorders (ASD) and environmental exposures, we linked the

California autism surveillance system to estimated hazardous air

pollutant (HAP) concentrations compiled by the U.S. Environmental

Protection Agency. METHODS: Subjects included 284 children with ASD

and 657 controls, born in 1994 in the San Francisco Bay area. We

assigned exposure level by census tract of birth residence for 19

chemicals we identified as potential neurotoxicants, developmental

toxicants, and/or endocrine disruptors from the 1996 HAPs database.

Because concentrations of many of these were highly correlated, we

combined the chemicals into mechanistic and structural groups,

calculating summary index scores. We calculated ASD risk in the

upper quartiles of these group scores or individual chemical

concentrations compared with below the median, adjusting for

demographic factors. RESULTS: The adjusted odds ratios (AORs) were

elevated by 50% in the top quartile of chlorinated solvents and

heavy metals [95% confidence intervals (CIs) , 1.1-2.1], but not for

aromatic solvents. Adjusting for these three groups simultaneously

led to decreased risks for the solvents and increased risk for

metals (AORs for metals: fourth quartile = 1.7 ; 95% CI, 1.0-3.0 ;

third quartile = 1.95 ; 95% CI, 1.2-3.1) . The individual compounds

that contributed most to these associations included mercury,

cadmium, nickel, trichloroethylene, and vinyl chloride. CONCLUSIONS:

Our results suggest a potential association between autism and

estimated metal concentrations, and possibly solvents, in ambient

air around the birth residence, requiring confirmation and more

refined exposure assessment in future studies.

Publication Types:

* Comparative Study <javascript:AL_get(this, 'ptyp',

'Comparative Study');>

PMID: 16966102 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

*13: *Health Place. <javascript:AL_get(this, 'jour', 'Health Place.');>

2006 Jun;12(2):203-9

Available at:

http://www.generationrescue.org/pdf/seed.pdf

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & DbFrom=pubmed & Cmd=Link & LinkN\

ame=pubmed_pubmed & LinkReadableName=Related%20Articles & IdsFromResult=16338635 & ord\

inalpos=2 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstra\

ct>

<javascript:PopUpMenu2_Set(Menu16338635);>

*Environmental mercury release, special education rates, and autism

disorder: an ecological study of Texas.*

*Palmer RF*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Palmer%20\

RF%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_\

RVAbstract>,

*Blanchard S*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Blanchard\

%20S%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubme\

d_RVAbstract>,

*Stein Z*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Stein%20Z\

%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RV\

Abstract>,

*Mandell D*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Mandell%2\

0D%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_\

RVAbstract>,

* C*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22%20\

C%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstract>.

University of Texas Health Science Center, San Department of

Family and Community Medicine, 7703 Floyd Curl Drive, San ,

Texas 78229-3900, USA. palmer@...

The association between environmentally released mercury, special

education and autism rates in Texas was investigated using data from

the Texas Education Department and the United States Environmental

Protection Agency. A Poisson regression analysis adjusted for school

district population size, economic and demographic factors was used.

There was a significant increase in the rates of special education

students and autism rates associated with increases in

environmentally released mercury. On average, for each 1,000 lb of

environmentally released mercury, there was a 43% increase in the

rate of special education services and a 61% increase in the rate of

autism. The association between environmentally released mercury and

special education rates were fully mediated by increased autism

rates. This ecological study suggests the need for further research

regarding the association between environmentally released mercury

and developmental disorders such as autism. These results have

implications for policy planning and cost analysis.

PMID: 16338635

*14.* December 19, 2007

*Wildfire ash can contain toxic mix*

The U.S. Geological Survey finds that soil runoff from residential

wildfires can harm aquatic species

http://pubs.usgs.gov/of/2007/1407/

A new U.S. Geological Survey (USGS) study of ash and soil samples from

the wildfires in Southern California last November suggests that metals

in the ash may create health and environmental problems. Ash samples

from 2 residential areas and 26 other sites within the burned areas

contained caustic alkali materials and may have elevated levels of

metals, such as arsenic, lead, zinc, and copper.

The study also shows that rainwater runoff from burned areas may

adversely affect ecosystems and surface drinking-water supplies.

Habitats critical for some aquatic species may be affected by spikes in

alkalinity as rainwater mixes with ash to form surface runoff, the

researchers note. The research was conducted as part of the USGS

Southern California Multi-Hazards Demonstration Project.

http://ca.water.usgs.gov/projects/hazards.html

*Report* PDF (2 MB)

<http://pubs.usgs.gov/of/2007/1407/pdf/OF07-1407_508.pdf>

Copyright © American Chemical Society

*15*. Tainted rainfall affecting parks

Agency's report finds more ammonia in Yellowstone, Glacier [etc]

By MIKE STARK

Of The Gazette Staff

http://www.billingsgazette.net/articles/2007/12/22/news/state/21-rainfall.txt

*16*. As beautiful as the mountains of Glacier National Park appear,

they have been polluted by airborne chemicals and pesticides brought in

from not just other ...

http://www.nationalparkstraveler.com/2007/10/glacier-national-park-not-pristine-\

it-appears

*17*. Summary of Nitrogen Deposition in Rocky Mountain National Park.

...... Rocky Mountain National Park (RMNP) is one of the crown jewels of

the National Park ...

http://www.cdphe.state.co.us/ap/rmnp/NDRPAugust07.pdf

*18*. Atmospheric deposition of nutrients, pesticides, and mercury in

Rocky Mountain National Park,. Colorado 2002. Water Resources

Investigations Report 03-4241, ...

http://www.cdphe.state.co.us/ap/rmnp/noxtech.pdf

*19*. Body burden is the amount of a harmful substance that is

permanently present in a person's body. It is usually expressed in mass

units, such as grams and ...

http://en.wikipedia.org/wiki/Body_burden

*20*. Human Toxome Project. What is the HTP? Through the Human Toxome

Project at the Environmental Working Group, scientists, engineers, ...

http://www.bodyburden.org/

*21*. Chemical body burden is the build-up of synthetic chemicals and

heavy metals in our bodies, which can have negative health effects as

discussed in this web ...

http://www.chemicalbodyburden.org/

*22*. The Pollution in Newborns

http://www.ewg.org/reports/bodyburden2

*eof*.