8. How serious are the risks of indirect exposure to mercury from disposal dental amalgams?
The SCENIHR opinion states:
3.2 Question 2
Mercury is distributed ubiquitously in the environment from many sources and can therefore be taken up by the general population via food, water and air.
Potential sources of exposure to mercury include inhalation of mercury vapours in ambient air, ingestion of drinking water and food contaminated with mercury, and exposure to mercury through dental treatments.
Dietary intake is the most important source of non-occupational exposure to mercury, with fish and other seafood products being the dominant source of mercury in the diet. Most of the mercury consumed in fish or other seafood is methylmercury (WHO 1990, 1991) (Table 1).
Taking these considerations on exposure into account, for indirect intake of mercury from the environment due to the uses of dental amalgams, the toxicology of inorganic mercury and methylmercury are relevant for risk assessment.
Oral ingestion of elemental mercury results only in a very limited absorption (< 0.01 % of dose). Dermal absorption of liquid elemental mercury is also very limited. In contrast, approximately 80 % of the inhaled elemental mercury is absorbed in the lungs. Due to the high lipid solubility, elemental mercury rapidly penetrates alveolar membranes and is then distributed to all tissues of the body. Elemental mercury is slowly oxidized in the blood.
After consumption of inorganic mercury (Hg2+), only a small part of the dose ingested is absorbed from the gastrointestinal tract. Hg2+ absorbed or formed by oxidation of elemental Hg may be eliminated by excretion with urine and/or faeces. The elimination of elemental mercury or Hg2+ follows complex kinetics with half-lives in the range of 20 to 90 days.
In contrast to inorganic mercury, most of an oral dose of methylmercury is absorbed from the gastrointestinal tract. Absorbed methylmercury is rapidly and evenly distributed in the organism. The biological half-life of methylmercury blood is around 70 days. The faeces are the most important route of excretion for mercury after short-term or long- term absorption of methylmercury (approximately. 90 % of a single oral dose).
The major target organ for the toxicity of inorganic mercury is the kidney. Ingestion of high doses of Hg2+ results in kidney damage characterized by proximal tubular injury. In contrast, long term oral administration of Hg2+ to rodents causes glomerulonephritis as the most sensitive endpoint. Higher doses of inorganic mercury also cause neurotoxicity.
Methylmercury is highly toxic. Human exposures following high dose poisonings resulted in effects that included mental retardation, and sensory and motor impairment. Long term, low dose prenatal exposures to methylmercury due to maternal fish consumption has been associated with more subtle endpoints of neurotoxicity. Results from animal studies also show effects on cognitive, motor and sensory functions indicative of neurotoxicity.
Legal limits for human exposures to both Hg2+ and methylmercury have been established by several organisations (Table 2).
Tolerable limits for methylmercury content of fish have also been set by different organisations. The US EPA, in a detailed analysis of studies on effects of methylmercury in humans and average fish consumption in the US, has developed a fish tissue residue criterion (concentration in fish that should not be exceeded) of 0.3 mg methylmercury/kg fish (regarding human consumption) which is similar to a maximum tolerable content of 0.5 mg methylmercury for many fish species set by EU. For a group of fish including tuna, sword fish, and halibut a limit value of 1 mg/kg is established (EC, 2006b). Therefore, the predicted indirect exposures of humans to methylmercury resulting from emissions due to dental amalgams are much lower than these tolerable limits indicating a low risk for serious health effects.
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