Environmental Engineering Reference
In-Depth Information
human studies have focused on neurologic health effects
(IPCS, 1991). The whole body half-life of inhaled mercury
vapor is about 60 days (Clarkson and Magos, 2006). Once
mercury vapor enters the bloodstream, it can also cross
the placenta. The presence of amalgam restorations is posi-
tively associated with inorganic mercury levels in maternal
and umbilical-cord blood (Palkovicova et al., 2008). Brain,
blood, and urine mercury levels have also been correlated
with the number of amalgam restorations in a person's
mouth (Nylander et al., 1987; Akesson et al. 1991; Vahter
et al., 2000; Guzzi et al., 2006). Urine mercury concentra-
tion increases approximately 1 to 1.8 µg/L for every 10 cov-
ered surfaces (Kingman et al., 1998; Dye et al., 2005), but
people who chew gum regularly or grind their teeth tend
to have higher levels (Barregard et al., 1995; Sallsten et al.,
1996). Removing amalgam fi llings may also result in tran-
siently higher levels (Molin et al., 1990).
It has been hypothesized that exposure to mercury from
dental amalgams may play an etiologic role in neurologic
disorders such as Alzheimer's disease, chronic fatigue syn-
drome, and multiple sclerosis (IPCS, 1991; Siblerud et al.,
1994; Mutter et al., 2004; Brownawell et al., 2005; Bates,
2006; Aminzadeh and Etminan, 2007). However, the esti-
mated average daily dose of mercury vapor inhaled from
amalgam restorations is low (urine levels typically under
2.0 µg/g creatinine) as compared with levels of occupa-
tional exposure, which have been associated with kidney
damage and neurologic symptoms (urine levels typically
over 50 µg/g creatinine) (IPCS, 1991; Kingman et al., 1998;
Clarkson and Magos, 2006). Rigorous scientifi c studies
have failed to provide evidence for neurologic or neurode-
velopmental risks associated with the mercury exposure
from dental amalgams (Clarkson et al., 2003; Karol et al.,
2004; Kingman et al., 2005; SCENIHR, 2008). They have
also failed to identify reproductive risks associated with
the placement of amalgams during pregnancy (Daniels et
al., 2007; Hujoel et al., 2005). One explanation for previous
reports of associations is confounding by sociodemographic
factors that are related to both the presence of amalgams
and poorer neurocognitive outcomes (Lygre et al., 2010).
There continues to be interest in this topic.
Research to address the question of whether there are
adverse effects from exposure to mercury amalgams has
focused on children because of their heightened sensitivity
to mercury toxicity. The New England Children's Amalgam
Trial has been following 534 children 6 to 11 years of age
at enrollment for renal and neuropsychological end points
(Bellinger et al., 2006). Children were randomly assigned
to receive either amalgam fi llings or composite resin. After
5 years of follow-up, no adverse effects of mercury amal-
gams on neuropsychological measures have been detected
(Bellinger et al., 2006). Similarly, another trial conducted
in Portugal on 507 children found no evidence for adverse
neurobehavioral effects after 7 years of follow-up (DeRouen
et al., 2006; Lauterbach et al., 2008; Mackert, 2010). The
New England Children's Amalgam Trial reported an
association between amalgam placement and an increased
prevalence of microalbuminuria, which is one marker of
renal function, but the fi nding was not corroborated in
the Portuguese study (Barregard et al., 2008; Woods et al.,
2008). Other markers of renal dysfunction were not associ-
ated with the placement of amalgams.
Mercury in Teething Powders, Laxatives, and
“Traditional Medicine Products”
Mercury has been used in home remedies and traditional
medicine products for centuries. India and China still use
inorganic mercury compounds (in addition to other met-
als) as part of medical systems that date back thousands
of years (Saper et al., 2004, 2008; Liu et al., 2008). A 2004
survey of 193 medicines from the Indian Ayurvedic tra-
dition, purchased over the Internet and manufactured
in either India or the United States, found that 4% con-
tained mercury (median concentration, 104 ppm) (Saper
et al., 2008), and 6 of 70 Ayurvedic medicines produced in
South Asia and purchased from stores in Boston in 2003
contained a median mercury concentration of 20,000 ppm
(Saper et al., 2004). Until the mid-20th century, calomel
(mercurous chloride) was an ingredient of teething pow-
ders and deworming products sold in the United States,
Europe, and other parts of the world. In some areas, these
products were used by as much as 40-50% of the popula-
tion (Warkany and Hubbard, 1953). Calomel has also been
used in laxative preparations, as has elemental mercury
(Goldwater, 1972).
Gastrointestinal absorption of inorganic mercury com-
pounds varies from less than 0.2% for mercury sulfi de
(cinnabar) to 7-15% for mercuric chloride [corrosive subli-
mate] (Liu et al., 2008). Absorption in young children may
be higher (Clarkson and Magos, 2006). Only a fraction of
exposure to inorganic compounds crosses the blood-brain
barrier. The kidney is most sensitive to the toxic effects of
inorganic compounds, but the central nervous system may
also be affected by long-term exposure. Central nervous
system damage, and death due to renal failure, occurred in
several instances of long-term ingestion of a calomel laxa-
tive (Clarkson and Magos, 2006). In contrast, elemental
mercury is not absorbed by the gastrointestinal tract in any
signifi cant amount (IPCS, 1991).
By the 1950s, it became known that mercury com-
pounds used in teething powders and other products could
cause acrodynia—or Pink disease—in children (Warkany,
1966). It took years to establish mercury as the cause,
because the disease occurred in only one of several hun-
dred exposed children. Acrodynia manifests with a vari-
ety of cardiovascular, dermal, and neurologic symptoms.
Sensitive individuals may suffer from elevated blood pres-
sure, tachycardia, pink palms and soles—sometimes with
peeling skin, gingivitis and loosening of the teeth, profuse
sweating and salivation, irritability, insomnia. and photo-
phobia (Warkany and Hubbard, 1953). Despite efforts to
