Thank you, Linda.  I was aware of that.  Now, would all those who said I
imagined my mercury poisoning care to apologize?

However, the web site has lies on it, as in no harm to kids, low doses, etc,
blah, blah blah.

http://www.health.gov/environment/amalgam1/appendixIII.htm

Of course some of the web sites below may have disappeared.
I have *many* in my mercury files.

http://www.holisticmed.com/dental/amalgam

===

http://www.y2khealthanddetox.c­om/mercuryinfo.html

14. Both Health Canada (1996) and world Health Organization (1991) consider
dental amalgams to be the single largest source of mercury exposure for the
general public, with amalgam potentially contributing up to 84% (WHO, 1991)
or
total daily intake of all forms of mercury from all sources,

http://www.valleyadvocate.com/­articles/dental.html

Autopsy studies in Sweden, Germany and the United States have also
established
that people with amalgams have significantly more mercury in their brains
and
kidneys than those without, and the mercury concentration increases with the
number of amalgams. Furthermore, the World Health Organization has stated
that
amalgam fillings constitute the majority of mercury exposure for people with
amalgams -- more than every other mercury source combined. This finding has
been independently verified by the national insurance program Health Canada
and
by the National Institutes of Dental Research.

===

http://www.icnr.com/uam/hgcourse/M4/SciLit5.html

The mercury vapor from dental amalgam alone is a bigger source than all

1: Ned Tijdschr Tandheelkd. 1993 Apr;100(4):179-82.Related Articles, Links

[Amalgam. IV. Metabolism of mercury]

[Article in Dutch]

Gladys S, van Meerbeek B, Vanherle G, Lambrechts P.

Afdeling Conserverende Tandheelkunde en Tandheelkundige Materialen, School
voor Tandheelkunde, Mondziekten en Kaakchirurgie, Katholieke Universiteit te
Leuven, Belgie.

After absorption in the body by four ways, each type of mercury undergoes a
specific metabolism. Elementary mercury as mercury vapour becomes rapidly
oxidized to Hg2+ and, afterwards, is metabolized as an inorganic mercurial
compound. From the blood circulation mercury reaches target organs like the
kidneys, the central nervous system, the liver and the hypophysis, in which
mercury accumulates. The retention time varies by organ and is longest in
the brain. Mercury is mainly eliminated with urine and faeces, to a lesser
degree with transpiration and mother's milk and sometimes by respiration.

Publication Types:
Review
Review, Tutorial

PMID: 11822127 [PubMed - indexed for MEDLINE]

http://www.greenfacts.org/mercury/l-2/mercury-2.htm#2

.2 How are we exposed to mercury?
The main source of elemental mercury vapour is dental amalgam (a tooth
filling).
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=11799732
1: Bull Group Int Rech Sci Stomatol Odontol. 2000
May-Dec;42(2-3):88-93.Related Articles, Links

Salivary mercury levels in healthy donors with and without amalgam fillings.

Pizzichini M, Fonzi M, Gasparoni A, Fonzi L.

Department of Biomedical Science, University of Siena, Siena, Italy.

Dental amalgam (AMG) is the most diffused dental filling material. Since it
is constituted for at least 40-45% of Hg, many questions have raised about
its safe use. Hg particles from dental amalgam dissolve in saliva and, being
ingested, they reach the blood stream through the intestinal mucosa. It has
been demonstrated that amalgam fillings continuously release Hg vapour and
that there is detectable Hg in expired and inspired air of amalgam owners.
It is not yet fully accepted that AMG fillings represent the principal
source of Hg for man and the aim of this study was to evaluate if the
mercury level in saliva: 1) was higher within people bearing dental amalgam
restorations than in people with no restorations; 2) was different between
males or females; 3) increased in relation to the surface of amalgam
restorations. The results showed a correlation between number of fillings
and salivary Hg, between amalgam surface and salivary Hg. The Authors could
finally assert that AMG fillings represented the principal source of
salivary Hg in the subjects studied.

PMID: 11799732 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=14651282

1: J Endod. 2003 Nov;29(11):743-6.Related Articles, Links

In vitro neurotoxic evaluation of root-end-filling materials.

Asrari M, Lobner D.

Department of Endodontics, Marquette University School of Dentistry,
Milwaukee, WI 53233, USA. masrari@wi.rr.com

Root-end-filling materials have been tested for toxicity on several cell
types, but their toxicity has not been tested on neurons. In this study we
evaluated the neurotoxicity in murine cerebral cortical cell cultures of
four commonly used root-end-filling materials: mineral trioxide aggregate,
amalgam, Super EBA, and Diaket. Standardized amounts of each material were
placed on culture-well inserts, allowing the material to be exposed to the
culture bathing media without causing physical disruption of the cells. Cell
death was quantified by assaying release of the cytosolic enzyme lactate
dehydrogenase. Exposure of cortical cultures to freshly mixed or 7-day-old
MTA did not cause significant neuronal death, whereas exposure to freshly
mixed or 7-day-old amalgam, Super EBA, and Diaket resulted in significant
neuronal death (p < .05). Thus, each material, except for mineral trioxide
aggregate, can induce neurotoxicity, even when allowed to set thoroughly.

PMID: 14651282 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=12752546

Community Dent Oral Epidemiol. 2003 Jun;31(3):200-6.Related Articles, Links

Reporting on adverse reactions to dental materials--intraoral observations
at a clinical follow-up.

Lygre GB, Gjerdet NR, Gronningsaeter AG, Bjorkman L.

Dental Biomaterials Adverse Reaction Unit, University of Bergen, Norway.
Gunvor.Lygre@odont.uib.no

OBJECTIVES: A national reporting system designed to monitor adverse
reactions to dental materials was established in Norway in 1993. The
activities have also included clinical examination of patients with
suspected reactions to dental materials. The ongoing activities are
coordinated by the Dental Biomaterials Adverse Reaction Unit at the
University of Bergen. The reporting procedure is based on voluntary
spontaneous reporting by dentists and physicians. The reports could be based
on subjective symptoms or objective findings, or both. The aim of the
present study was to compare reported objective intraoral findings with
those found during examination at the unit. METHODS: Reported reactions were
compared with clinical findings obtained following dental and medical
examination at the unit. From 1993 to 1999, a total of 899 reports were
received while 253 patients were referred and examined at the unit. RESULTS:
The reports on patients who were examined at the unit involved mainly
reactions related to amalgam fillings (84%), metals in fixed dentures (11%),
resin-based materials and cements (4%), materials used in removable dentures
(2%), and endodontic materials (2%). Edema, lichenoid reactions,
ulcers/vesicles, erythema, and atrophy were found in 80 patients during the
examination at the unit. For 35 of these patients, the intraoral findings at
the unit were also given in the reports. For another 45 patients, objective
intraoral signs of reactions were found upon examination at the unit, but
these findings had not been reported. CONCLUSION: A spontaneous reporting
system is a cost-effective method for monitoring intraoral reactions
associated with dental materials. Considering the increasing number and
complexity of these materials, there appears to be a need for continuous
validation of reports by a speciality unit. In order to receive more
accurate information about the adverse reactions, it would be advisable that
the reporting forms include more detailed guidance regarding signs of
reactions that practitioners should be on the look out for and consider.

PMID: 12752546 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=12018634

J Nephrol. 2002 Mar-Apr;15(2):171-6.Related Articles, Links

Mercury in dental restoration: is there a risk of nephrotoxicity?

Mortada WL, Sobh MA, El-Defrawy MM, Farahat SE.

Urology and Nephrology Center, Mansoura University, Faculty of Science,
Egypt.

BACKGROUND: Concern has been voiced about exposure to mercury (Hg) from
dental amalgam fillings, and there is a need to assess whether this leads to
signs of nephrotoxicity. METHODS: A total of 101 healthy adults (80 males
and 21 females) were included in this study. The population as grouped into
those having amalgam fillings (39 males and 10 females) and those without
(41 males and 11 females). Hg was determined in blood, urine, hair and nails
to assess exposure. Urinary excretion of beta2-microglobulin (beta2M),
N-acetyl-beta-D-glucosaminidase (NAG), gamma-glutamyltransferase (gammaGT)
and alkaline phosphatase (ALP) were determined as markers of tubular damage.
Albuminuria was assayed as an early indicator of glomerular dysfunction.
Serum creatinine, beta2M and blood urea nitrogen (BUN) were determined to
assess glomerular filtration. RESULTS: Hg levels in blood and urine were
significantly higher in persons with dental amalgam than those without; in
the dental amalgam group, blood and urine levels of Hg significantly
correlated with the number of amalgams. Urinary excretion of NAG, gammaGT
and albumin was significantly higher in persons with dental amalgam than
those without. In the amalgam group, urinary excretion of NAG and albumin
significantly correlated with the number of fillings. Albuminuria
significantly correlated with blood and urine Hg. CONCLUSION: From the
nephrotoxicity point of view, dental amalgam is an unsuitable filling
material, as it may give rise to Hg toxicity. Hg levels in blood and urine
are good markers of such toxicity. In these exposure conditions, renal
damage is possible and may be assessed by urinary excretions of albumin,
NAG, and gamma-GT.

PMID: 12018634 [PubMed - indexed for MEDLINE]