
If the question is, "does a can of tuna have more mercury than an average amalgam filling?", then the answer is a hands down no. A 5 oz can of tuna is estimated to contain roughly 28 ug of mercury (methylmercury). Whereas a single spill filling contains 300,000 ug (300 mg) of elemental mercury.
But amalgam fillings are mixed with various amount of copper, tin, zinc and silver which reduces the amount of mercury released. The estimates of mercury released from amalgams vary widely as determined by the number of fillings, how big the fillings are and where the fillings are placed. In addition how much copper the fillings contain, the friction or heat the fillings encounter and if they are placed next to dissimilar metals also induces a greater release of mercury. All of those factors effect not only how much mercury is released, but also how much mercury is absorbed into the body. Our numbers for amalgam mercury exposure are taken from the only amalgam risk assessment of the U.S. population, coordinated with the FDA and published in the peer reviewed journal Science of the Total Environment.
Since the argument pro-amalgamist use when trying to downplay the exposure to mercury from dental amalgam fillings is to say that, "there is more mercury exposure from a tuna fish sandwich compared to that from dental mercury fillings". Taking all of the above mentioned variables into consideration, the question should actually be framed as this...
"Does a single 2.5 oz tuna sandwich expose one to as much mercury from the average number of amalgam fillings in a person ?
So we decided to examine the merits of that argument by comparing mercury levels from a 5 oz. can of tuna to the many various exposure levels from that of dental amalgam.
For levels of mercury exposure from tuna, we used numbers taken from the report, In Harm's Way: Toxic Threats to Child Development, by Greater Boston Physicians for Social Responsibility Prepared for a Joint Project with Clean Water Fund (pages 62-63). To keep things simple we use a 5 oz. can of tuna for our reference. This amounts to 28 ug in one 5 oz. can of tuna fish (or 14 ug / per sandwich / per day). We acknowledge that some people eat more than 2.5 oz of tuna on their sandwiches and some may also eat more than one tuna sandwich a day ( thus raising the level of mercury they are exposed to).
This document is available as a download at the bottom of this article.
As soon as one starts to try and determine the exposure from dental amlgam, one quickly realizes there are a lot of variables. Luckily Mark Richardson, author of the study "Mercury exposure and risks from dental amalgam in the US population, post-2000" has already examined the CDC's NHANES data and broken down exposure in three different scenarios in his study. It is important to note that Mark consulted with the FDA in preparation for this risk assessment.
"Based on the information reviewed from NHANES data, it was decided to approach the assessment of exposure to Hg0 from amalgam in 3 different ways:"
1) Consistent with the assumption of Dye et al. (2005), all 5-surface fillings were assumed to be treated with crowns composed of materials other than amalgam, and were thereby omitted from analysis. All remaining filled surfaces (1 surface fillings to 4 surface fillings) were assumed to be composed of amalgam.
2) For scenario 2, in addition to the assumption for scenario 1, it was further assumed that, in each NHANES survey participant with restored tooth surfaces, only 50% of those filled tooth surfaces were composed of dental amalgam. This assumption was based on the reports of Kingman et al. (1998) and Rosenstiel et al. (2004) in which amalgam comprised approximately 50% of in-place restorations. In all cases where the total number of restored surfaces was an odd number ≥3, the assumed number of amalgam surfaces was rounded down to the nearest whole number (3÷2 was set to 1, for example). However, for persons with only 1 filled tooth surface, 50% were randomly ascribed to have 0 amalgam filled surfaces, and the other 50% ascribed to have 1 amalgam filled tooth surface.
3) Finally, for scenario 3, it was further assumed, in addition to the assumptions outlined for scenarios 1 and 2 above, that 30% of persons with restored tooth surfaces had all of those surfaces restored with a dental material other than amalgam. This assumption was made recognizing that approximately 30% of dentists in the US (Haj-Ali et al., 2005) reported being amalgam free, and the possibility that all of their patients might have all existing fillings placed/replaced with materials other than amalgam. This assumes that dental patients are distributed equally across all dentists in the US.
Table 5.
Summary of Hg doses estimated for the US population with amalgam fillings.

RESULTS:
All categories of population: Dose as ug Hg/day
So the answer to the question, Does a tuna fish sandwich expose one to more mercury than dental amalgam fillings? is both yes and no based upon various scenarios as indicated in the charts below.
Scenario 1.
5 surface fillings excluded, all others assumed to be amalgam.
Scenario 1 Results
Maximum: Only toddlers would get more mercury from a tuna sandwich. Whereas children, adolescents, adults and seniors would recieve a higher dose of mercury from their amalgam fillings compared to that of a tuna fish sandwich. This represents roughly ? million people (TBD).
Mean: Seniors and adults narrowly get more Hg from tuna, while adolescents, children and toddlers also get more mercury from a tuna fish sandwich.
Minimum: All groups, Seniors, Adults, Adolescents, Children and Toddlers all get more mercury from a tuna fish sandwich.
PERSPECTIVE:
So "most" people with the average amount of amalgam fillings would get more mercury from a single tuna fish sandwich in one day. But, considering most people do not eat a tuna sandwich every single day, it's important to look at how much more mercury someone recieves from their amalgam fillings per week and per year, assuming they eat 2 cans of 5 oz tuna (56 ug) a week (4 sandwiches), consistently for every week of the year (for a total of 2,912 ug).
For those in scenario 1, with the average number of fillings, this would amount to someone having to eat 131.42 cans of tuna per year, to equal the amount of mercury exposure to adults with the average number of amalgam fillings.
Since the number of Americans with the average number of amalgam fillings is roughly ??? million. It stands to reason this number is much higher than the percentage of people who eat 131 cans of tuna in a year (although unknown).
Something to consider which the charts above do not address: Standard risk assessment would present doses in units of ug Hg/kg of body weight/day. Assuming that a child and an adult would eat the same amount of tuna in a sandwich, the child would have a greater dose per unit of body weight because they weigh less.
TOXICITY:
When considering the toxicity of both methylmercury (from tuna) and mercury vapor (Hg0) / inorganic mercury (Hg++) as from dental amalgam, one must take into account that most of the methylmercury in fish is bound to selenium. Multiple scientific studies (as indicated below) have shown that the mercury bound to selenium (as found in fish) reduces the toxicity of methylmercury. So while one may be exposed to more methylmercury from fish, it is not as toxic as the mercury from dental amalgams.
Another aspect to consider when trying to determine the comparable toxicity of metehylmercury versus elemental mercury (vapor) and inorganic mercury is that of established government safety levels. The form of mercury with the lowest safety level should be considered more toxic. Mercury Vapor has a lower safety level than methylmercury. (Need to provide references)
Below is information about the toxicokinetics of elemental mercury, From EPA's 1997 Mercury Study Report to Congress.
TOXICOKINETICS: (i.e., absorption, distribution, metabolism, and excretion) of mercury is highly dependent on the form of mercury to which a receptor has been exposed.
The absorption of elemental mercury vapor occurs rapidly through the lungs, but it is poorly absorbed from the gastrointestinal tract. Oral absorption of inorganic mercury involves absorption through the gastrointestinal tract; absorption information for the inhalation route is limited. Methylmercury (unbound to Selenium) is rapidly and extensively absorbed through the gastrointestinal tract.
Once absorbed, elemental mercury is readily distributed throughout the body; it crosses both placental and blood-brain barriers. Elemental mercury is oxidized to inorganic divalent mercury by the hydrogen peroxidase-catalase pathway, which is present in most tissues. The oxidation of elemental mercury to the inorganic mercuric cation in the brain can result in retention in the brain. Inorganic mercury has poor lipophilicity and a reduced capacity for penetrating the blood-brain or placental barriers. Once elemental mercury crosses the placental or blood-brain barriers and is oxidized to the mercuric ion, return to the general circulation is impeded, and mercury can retained in brain tissue.
Distribution of Elemental Mercury
Because of its lipophilicity, absorbed elemental mercury vapor readily distributes throughout the body, crossing the blood-brain barrier in humans (Hursh et al., 1976; Nordberg and Serenius, 1969) and the placenta in rats and mice (Clarkson et al., 1972). The distribution of absorbed elemental mercury is limited primarily by the oxidation of elemental mercury to the mercuric ion and reduced ability of the mercuric ion to cross membrane barriers. The oxidation is sufficiently slow, however, to allow distribution to all tissues and organs. Once it is oxidized to the mercuric ion, it is indistinguishable from Hg2+ from inorganic sources (i.e., the highest levels of mercury accumulate in the kidneys) (Hursh et al.1980; Rothstein and Hayes 1964). Based on an in vitro study by Hursh et al. (1988), oxidation of mercury in the blood is slow and, therefore, inhaled mercury reaches the brain primarily unoxidized (i.e., as dissolved vapor) and is available for rapid penetration into brain cells. Once in the brain, oxidation of elemental mercury to mercuric mercury in the brain enhances for the accumulation of mercury in these tissues (Hursh et al. 1988; Takahata et al. 1970).
For example, ten years after termination of exposure, miners exposed to elemental mercury vapor had high concentrations of mercury (120 ppm) in the brain (Takahata et al. 1970). A similar effect occurs when elemental mercury reaches the fetus and (after oxidation) accumulates in the tissues as inorganic mercury (Dencker et al.1983).
In the blood, elemental mercury initially distributes predominantly to the red blood cells; at 20 minutes, 98% of the mercury in the blood is found in the red blood cells. Several hours following parenteral, oral or inhalation exposure, however, a stable ratio of red blood cell mercury to plasma mercury of approximately 1:1 is established (Gerstner and Huff, 1977; Clarkson, 1972; Cherian et al., 1978). The rise in plasma mercury levels was suggested to be due to binding to protein sulfhydryl groups by mercuric mercury formed when the elemental mercury was oxidized.
Late 2009, while Mark Richardson was still at Health Canada he was contacted by Michael Adjodha of the Food and Drug Administration (FDA) who was seeking some clarifications about his 1995 Risk Assessment for Health Canada and about his recently (at that time) published article on mercury vapour and setting the reference exposure levels (REL) for mercury. During those phone conversations with Adjodha, Mark answered various questions about his research and publications; the details of which he admits are vague at this point.