Here are some relatively recent abstracts on amalgam and Hg toxicity.
Perhaps some actual data can shed some light on the debate.
J Dent 1999 May;27(4):249-56
Reproductive toxicity of occupational mercury. A review of the literature.
Schuurs AH
Department of Cariology, Endodontology and Pedodontology, Academic Centre
for Dentistry Amsterdam (ACTA), The Netherlands.
OBJECTIVES: This paper aims to give the dental practitioner insight into
the potential reproductive effects of handling dental silver amalgam, c.q.
mercury. DATA SOURCES: Experimental studies on animals, case reports and
epidemiologic studies. STUDY SELECTION: Experimental animal studies show
high doses/concentrations of mercury to increase the risk of reproductive
disorders, e.g. infertility, spontaneous abortion, stillbirth and
congenital malformations. Some case reports suggest an association between
the disorders in humans and high levels of mercury. Therefore, the present
article reviews epidemiological studies on the relationship between
occupational exposure to mercury, mainly as vapour in the dental practice,
and females' procreative ability. Studies concerning the reproductive
effects of males' occupational mercury body burden are scarce. The
reproductive risk of patients' mercury uptake from silver amalgam fillings
is assessed. CONCLUSIONS: It seems warranted to conclude that negative
reproductive effects from exposure to mercury in the dental office are
unproven, but safe levels have not been established. Seemingly problems are
unlikely to occur, unless a poor hygiene causes the mercury concentration
in the air to exceed females' time-weighted long-term Threshold Limit Value
(TLV). Consequently, in view of the in general low amounts of mercury
stemming from dental amalgam fillings, the population at large is at even
less risk than dental staff. The effects of occupational elemental mercury
concentrations lower than the TLV on the menstrual cycle, conception, male
fertility and children's behaviour need, however, more research.
J Am Dent Assoc 1999 Feb;130(2):191-9
Alzheimer's disease, dental amalgam and mercury.
Saxe SR, Wekstein MW, Kryscio RJ, Henry RG, Cornett CR, Snowdon DA, Grant
FT, Schmitt FA, Donegan SJ, Wekstein DR, Ehmann WD, Markesbery WR
Geriatric Oral Health Program, College of Dentistry, University of
Kentucky, Lexington, USA.
BACKGROUND: Mercury, or Hg, is a neurotoxin that has been speculated to
play a role in the pathogenesis of Alzheimer's disease, or AD. Dental
amalgam releases low levels of Hg vapor and is a potential source of Hg for
a large segment of the adult population. METHODS: The authors studied 68
subjects with AD and 33 control subjects without AD to determine Hg levels
in multiple brain regions at autopsy and to ascertain the subjects' dental
amalgam status and history. The subjects were from central Kentucky and Elm
Grove, Wis. The authors conducted dental amalgam assessments during the
lives of the majority of subjects and in some subjects at the time of
autopsy only. The authors also determined three dental amalgam index
scores--Event (placement, repair or removal of amalgam), Location and Time
In Mouth--in addition to the numbers of and surface area of occlusal
amalgam restorations. The authors determined Hg levels in multiple brain
regions and performed full neuropathologic evaluations to confirm the
normal status of the brain or the presence of AD. RESULTS: The authors
found no significant association of AD with the number, surface area or
history of having dental amalgam restorations. They also found no
statistically significant differences in brain Hg level between subjects
with AD and control subjects. CONCLUSIONS: Hg in dental amalgam
restorations does not appear to be a neurotoxic factor in the pathogenesis
of AD. The authors found that brain Hg levels are not associated with
dental amalgam, either from existing amalgam restorations or according to
subjects' dental amalgam restoration history. CLINICAL IMPLICATIONS: Dental
amalgam restorations, regardless of number, occlusal surface area or time,
do not relate to brain Hg levels.
Wien Klin Wochenschr 1998 Jul 31;110(13-14):467-72
Published erratum appears in Wien Klin Wochenschr 1998 Sep 4;110(16):585
Effects of dental amalgam and its components of histamine release from
human basophils and tissue mast cells.
Schedle A, Samorapoompichit P, Ghannadan M, Franz A, Sperr WR, Sperr W, Valent P
School of Dentistry, Department of Internal Medicine I, University of
Vienna, Austria.
Recent studies have shown that metal ions can be released from dental
amalgam or other dental materials, and can cause toxic effects on various
cells. In this study, the effects of amalgam-conditioned culture medium
(ACCM), components of amalgam (Ag+, Cu2+, Sn2+, Hg2+) and dental
composite-conditioned culture medium (CCCM) on histamine release from human
blood basophils (healthy subjects, n = 3) and tissue mast cells (n = 3)
were analyzed. ACCM and CCCM were prepared using either fresh or
6-weeks-aged specimens. Of the metal ions tested, Ag+, and Hg2+ were found
to induce histamine release from basophils (Ag+, 0.33 mM: 83 +/- 11% vs
Hg2+, 0.33 mM: 100% vs control medium: 5 +/- 5%) and mast cells (Ag+, 0.33
mM: 91 +/- 16% vs Hg2+, 0.33 mM: 99 +/- 1% vs control: 2 +/- 1%), whereas
no effects were seen with Cu2+ and Sn2+. Neither ACCM from freshly prepared
amalgam nor ACCM from 6-weeks aged amalgam, produced histamine release in
basophils or mast cells. Inductively coupled plasma atomic emission
spectrometry (ICP) revealed that the Ag(+)- and Hg(2+)-concentrations in
ACCM were below the range in which histamine release occurred. Similar to
ACCM, no effects on basophils or mast cells were observed with CCCM. In
summary, our data show that distinct metal ions present in dental amalgam,
can induce (toxic) histamine liberation from basophils and mast cells.
However, the amounts of metal ions released from amalgam apparently were
too low, to cause histamine release.
FASEB J 1998 Aug;12(11):971-80
Neurobehavioral effects from exposure to dental amalgam Hg(o): new
distinctions between recent exposure and Hg body burden.
Echeverria D, Aposhian HV, Woods JS, Heyer NJ, Aposhian MM, Bittner AC Jr,
Mahurin RK, Cianciola M
Battelle Centers for Public Health Research and Evaluation, Seattle,
Washington 98105, USA.
Potential toxicity from exposure to mercury vapor (Hg(o)) from dental
amalgam fillings is the subject of current public health debate in many
countries. We evaluated potential central nervous system (CNS) toxicity
associated with handling Hg-containing amalgam materials among dental
personnel with very low levels of Hg(o) exposure (i.e., urinary Hg <4
microg/l), applying a neurobehavioral test battery to evaluate CNS
functions in relation to both recent exposure and Hg body burden. New
distinctions between subtle preclinical effects on symptoms, mood, motor
function, and cognition were found associated with Hg body burden as
compared with those associated with recent exposure. The pattern of
results, comparable to findings previously reported among subjects with
urinary Hg >50 microg/l, presents convincing new evidence of adverse
behavioral effects associated with low Hg(o) exposures within the range of
that received by the general population.
J Dent Res 1998 Jun;77(6):1415-25
Activation of the immune system and systemic immune-complex deposits in
Brown Norway rats with dental amalgam restorations.
Hultman P, Lindh U, Horsted-Bindslev P
Department of Health and Environment, Linkoping University, Sweden.
Dental amalgam restorations are a significant source of mercury exposure in
the human population, but their potential to cause systemic health effects
is highly disputed. We examined effects on the immune system by giving
genetically mercury-susceptible Brown Norway (BN) rats and
mercury-resistant Lewis (LE) rats silver amalgam restorations in 4 molars
of the upper jaw, causing a body burden similar to that described in human
amalgam-bearers (from 250 to 375 mg amalgam/kg body weight). BN rats with
amalgam restorations, compared with control rats given composite resinous
restorations, developed a rapid activation of the immune system, with a
maximum 12-fold increase of the plasma IgE concentration after 3 wks (p <
0.001; Mann-Whitney's test). LE rats receiving amalgam restorations showed
no significant increase of plasma IgE (p > 0.05). After 12 wks, BN rats
with amalgam restorations showed significantly increased (p < 0.05) titers
of immune-complex (IC) deposits in the renal glomeruli and in the vessel
walls of internal organs. These rats also showed a significant (p < 0.05),
from six- to 130-fold, increase in tissue mercury concentration in the
concentration order kidney > spleen > cerebrum occipital lobe > cerebellum
> liver > thymus, and the tissue silver concentration was significantly (p
< 0.05) increased from three- to 11-fold. Amalgam-implanted BN rats showed
a significant (p < 0.05) increase in copper concentration in the kidney and
spleen, and in kidney selenium concentration. We conclude that dental
amalgam restorations release substantial amounts of their elements, which
accumulate in the organs and which, in genetically susceptible rats, give
rise to activation of the immune system and systemic IC deposits.
J Am Dent Assoc 1998 Apr;129(4):494-503
Dental amalgam: update on safety concerns. ADA council on Scientific Affairs.
This report of the Council on Scientific Affairs reviews and discusses
recent studies concerning the safety of dental amalgam, with an emphasis on
studies that have been published since the 1993 review of dental amalgam by
the U.S. Public Health Service Committee to Coordinate Environmental Health
and Related Programs. The Council concludes that, based on currently
available scientific information, amalgam continues to be a safe and
effective restorative material.
Scand J Work Environ Health 1997;23 Suppl 3:59-63
Symptoms and differential diagnosis of patients fearing mercury toxicity
from amalgam fillings.
Stenman S, Grans L
University of Helsinki, Department of Medicine, Finland.
Clinical signs, somatic symptoms reported by patients, and mercury
excretion in urine were studied for 348 patients selected by odontologists
or internists as amalgam-free referents, or as subjects with unexplained
clinical findings or who were self-selected due to their fear of mercury
intoxication from their amalgam fillings. Sixty patients were excluded
because other explanations could be given for their complaints. The age
distribution was bimodal, with peaks between 30 and 35 years and between 45
and 50 years. Mercury was determined in a morning urine sample and 30
minutes after the injection of 300 mg of 2,3 dimercapto-1-propane sulfonic
acid (DMPS), a mercury-chelating agent. The patients were followed for 1-3
years. Among the patients there were 26 who had had their amalgam fillings
removed and who, at the time of the follow-up, were subjectively cured.
When the patients were classified according to the excretion of mercury
after the DMPS challenge, those who belonged to the upper quartile had an
odds ratio of 7.2 (95% confidence interval 3.1-15.2) for becoming cured
after amalgam removal. The symptoms of the cured patients had been
predominantly mental. No consistent clinical picture could, however, be
found among the other patients, as various types of mental and physical
distress were reported.
Clin Exp Immunol 1997 Dec;110(3):418-22
In vitro effects of mercuric chloride (HgCl2) on human mononuclear cells.
Loftenius A, Ekstrand J, Moller E
Department of Basic Oral Sciences, Karolinska Institute, Huddinge, Sweden.
Due to the release of the toxic compounds of mercury from amalgam fillings,
dental amalgam has been questioned as an adequate restoration material for
tooth fillings. HgCl2 has been found to be mitogenic for human blood
lymphocytes in vitro. However, activation required much higher
concentrations than are ever found in vivo. This study has been initiated
to evaluate further the influence of HgCl2 on human immunocompetent cells
in vitro. It is found that HgCl2 in a narrow concentration range has the
ability to preferentially stimulate the CD4+ T cell subset to blast
transformation and DNA synthesis. The reaction, when monitored during days
2-6, is maximal at day 6, and most blasts express the IL-2 receptor
(IL-2R), indicating in vitro activation. The CD8+ T cell subset is not
affected to the same extent. In addition, HgCl2-induced lymphocyte
reactivity is dependent on accessory cells, i.e. CD14+ cells.
Neurotoxicology 1997;18(2):315-24
Mercury vapor inhalation inhibits binding of GTP to tubulin in rat brain:
similarity to a molecular lesion in Alzheimer diseased brain.
Pendergrass JC, Haley BE, Vimy MJ, Winfield SA, Lorscheider FL
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.
Crit Rev Clin Lab Sci 1997 Aug;34(4):369-403
The toxicology of mercury.
Clarkson TW
Department of Environmental Medicine, University of Rochester School of
Medicine, New York 14642, USA.
The major physical forms of mercury to which humans are exposed are mercury
vapor, Hg0, and methylmercury compounds, Ch3HgX. Mercury vapor emitted from
both natural and anthropogenic sources is globally distributed in the
atmosphere. It is returned as a water-soluble form in precipitation and
finds its way into bodies of fresh and ocean water. Land run-off also
accounts for further input into lakes and oceans. Inorganic mercury,
present in water sediments, is subject to bacterial conversion to
methylmercury compounds that are bioaccumulated in the aquatic food chain
to reach the highest concentration in predatory fish. Human exposure to
mercury vapor is from dental amalgam and industries using mercury.
Methylmercury compounds are found exclusively in seafood and freshwater
fish. The health effects of mercury vapor have been known since ancient
times. Severe exposure results in a triad of symptoms, erethism, tremor,
and gingivitis. Today, we are concerned with more subtle effects such as
preclinical changes in kidney function and behavioral and cognitive changes
associated with effects on the central nervous system. Methylmercury is a
neurological poison affecting primarily brain tissue. In adults, brain
damage is focal affecting the function of such areas as the cerebellum
(ataxia) and the visual cortex (constricted visual fields). Methylmercury
also at high doses can cause severe damage to the developing brain. Today
the chief concern is with the more subtle effects arising from prenatal
exposure such as delayed development and cognitive changes in children.
J Toxicol Environ Health 1996 Oct 25;49(3):221-70
Human exposure to mercury: a critical assessment of the evidence of adverse
health effects.
Ratcliffe HE, Swanson GM, Fischer LJ
Cancer Center at Michigan State University, East Lansing 48824-1316, USA.
The ubiquitous nature of mercury in the environment, its global atmospheric
cycling, and its toxicity to humans at levels that are uncomfortably close
to exposures experienced by a proportion of the population are some of the
current concerns associated with this pollutant. The purpose of this review
is to critically evaluate the scientific quality of published reports
involving human exposures to mercury and associated health outcomes as an
aid in the risk evaluation of this chemical. A comprehensive review of the
scientific literature involving human exposures to mercury was performed
and each publication evaluated using a defined set of criteria that are
considered standards in epidemiologic and toxicologic research. Severe,
sometimes fatal, effects of mercury exposure at high levels were primarily
reported as case studies. The disasters in Minamata, Japan, in the 1950s
and in Iraq in 1971-1972 clearly demonstrated neurologic effects associated
with ingestion of methylmercury both in adults and in infants exposed in
utero. The effects were convincingly associated with methylmercury
ingestion, despite limitations of the study design. Several well-conducted
studies have investigated the effects of methylmercury at levels below
those in the Iraq incident but have not provided clear evidence of an
effect. The lower end of the dose-response curve constructed from the Iraq
data therefore still needs to be confirmed. The studies of mercury exposure
in the workplace were mainly of elemental or inorganic mercury, and effects
that were observed at relatively low exposure levels were primarily
neurologic and renal. Several studies have investigated effects associated
with dental amalgam but have been rated as inconclusive because of
methodologic deficiencies. In our overall evaluation, 29 of 110
occupational studies and 20 of 54 studies where exposure occurred in the
natural environment provided at least suggestive evidence of an
exposure-related effect.
Am J Physiol 1996 Oct;271(4 Pt 2):R941-5
No evidence of renal toxicity from amalgam fillings.
Sandborgh-Englund G, Nygren AT, Ekstrand J, Elinder CG
Department of Dental Toxicology, Karolinska Institute, Huddinge, Sweden.
Dental amalgam continuously releases mercury. Studies of sheep [Boyd et
al., Am. J. Physiol. 261 (Regulatory Integrative Comp. Physiol. 30):
R1010-R1014, 1991] showed decreased renal function after placement of
amalgam fillings. In this study, renal function was investigated in 10
healthy volunteers before and after amalgam removal. The subjects had an
average of 18 tooth surfaces filled with amalgam, which was removed during
one dental session. One week before and sixty days after removal, the
glomerular filtration rate (GFR) was determined by 51Cr-EDTA clearance
technique. Blood and urine samples were collected for analysis of mercury,
creatinine, beta 2-microglobulin, N-acetyl-beta-glucosaminidase (NAG), and
albumin 1 wk before and 1, 2, and 60 days after amalgam removal. The plasma
mercury concentration increased significantly 1 day after removal. Sixty
days later, significantly lower mercury levels were found in blood, plasma,
and urine. The GFR values were similar before and after mercury exposure
(mean 94 and 94 ml/min per 1.73 m2, respectively). No detectable effects
occurred on excretion of NAG, beta 2-microglobulin, or albumin. It is
concluded that no signs of renal toxicity could be found in conjunction
with mercury released from amalgam fillings.
