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3. How can dental patients and workers be exposed to mercury from amalgams?

    The SCENIHR opinion states:

    3.3.2. Exposure to Mercury

    Mercury is a metallic element that occurs naturally and also in the form of several types of ore, the mercury burden of the environment being derived predominantly from natural sources. Input into the earth’s atmosphere occurs regularly through emissions from volcanoes, soil erosion and the combustion of fossil fuels. Widespread utilisation of mercury and its compounds in a number of industries over the last several centuries has resulted in the release of large amounts of mercury into the atmosphere, increasing the total amount in the ecosphere. Of special importance has been the accumulation of some mercury compounds in the aquatic food chain and the use of mercury compounds in a variety of medical and cosmetic products including dental amalgam. It is clear that exposure to mercury by individuals will be controlled by several factors, including ambient mercury levels (determined by geographical location and life-style choices), the diet, especially in relation to fish consumption, the possibility of occupational exposure for those who work in mercury-related industries and practices, and the use of mercury containing medical or cosmetic products, including amalgam. The exposure of individuals with amalgam restorations and dental personnel has to be considered in the context of this broader exposure scenario.

    3.3.2.1. Major Forms of Mercury

    It is also important to note that there are several different forms of mercury. First there is elemental mercury itself, a volatile form of the liquid metal, referred to as Hg0. Secondly, mercury is stable in two other oxidation states (Hg1+ and Hg2+) and is able to form inorganic compounds, of either monovalent or divalent form, including mercuric chloride (HgCl2), mercurous chloride (Hg2Cl2), mercuric sulphide (HgS), and mercuric selenide (HgSe). Thirdly, mercury is able to form a variety of organic compounds, including methylmercury. There is a clear connectivity between these forms with respect to the global cycle of mercury (Nielsen et al. 2006). Elemental mercury may be converted to soluble inorganic forms, which may be methylated in water, especially by microorganisms, which enter the food-chain and accumulate in the tissues of large predatory fish. The ratio of methylmercury in these fish to the mercury concentration in the water can be as high as 105.

    Each form of mercury has its own toxicological profile, although, in general terms, the toxicity of these forms is highest with the organic mercury compounds, followed by elemental mercury and inorganic mercury compounds. This is important when considering different exposure routes to these forms.

    3.3.2.2. Evidence of exposure to mercury from dental amalgam restorations

    Exposure to Mercury in Adults

    Exposure to mercury is difficult to measure. The indications for mercury exposure are therefore normally obtained by measuring mercury levels in urine and blood of individuals. Autopsy/post-mortem studies give an indication of the overall exposure of individuals during their whole lifetime due to all kinds of mercury sources, including dental amalgam. As such, these studies suffer certain unquantifiable limitations. Therefore, data dealing with blood and urine mercury determination were considered more relevant as they reflect actual exposure.

    Mercury is distributed ubiquitously in the environment and can therefore be taken up by the general population via food, water and air, potential sources of exposure including the inhalation of mercury vapors in ambient air, the ingestion of drinking water and food, and exposure to mercury through dental and medical treatments. Dietary intake is the most important source of non-occupational exposure to methylmercury, with fish and other seafood products being the dominant source of this highly absorbable form in the diet. Intake of elemental mercury from dental amalgams is another source contributing to the total mercury burden in humans in the general population (WHO 1990, WHO 1991). Tolerable limits for methylmercury content of fish and human consumption have been set by various organisations. In the USA, the Environmental Protection Agency set a limit, the so-called Tissue Residue Criterion, of 0.3 mg methylmercury / kg fish (EPA 2001). In Europe, the 2005 Opinion of the Scientific Panel of the EFSA on contaminants in the food chain (EFSA 2005) contained detailed reference to methylmercury in fish. In practice, levels range from under 0.1 mg/kg fish up to 0.5 mg/kg. The provisional tolerable weekly intake (PTWI) has been established at 1.6 µg/kg body weight, implying that a high consumption of a predatory fish such as bluefin tuna, which may have a methylmercury level around 0.5 mg/kg, gives up to twice the recommended intake. Because the two major sources of mercury body burden include dietary intake of methylmercury and intake of elemental mercury from dental amalgams, mercury is inevitably present at low concentrations in human tissues. Mercury has been detected in blood, urine, human milk, and hair in individuals in the general population. The mercury concentrations in whole blood of individuals with or without amalgam fillings are usually below 5 µg/l blood, but these concentrations do depend on dietary habits and the number of amalgam fillings (ATSDR 1999, BAT 1997).

    In a study on the influence of fish consumption and number of amalgam fillings, (Schweinsberg 1994), blood mercury concentrations in individuals without fish consumption and dental amalgams were in the range of 0.2 - 0.4 µg/l. Blood mercury concentrations were raised the least in individuals without fish consumption but with more than 6 amalgam fillings, followed by high fish consumers with no amalgam restorations, and highest in high fish consumers with more than six fillings, at 1.5 to 4 µg/l. Average blood mercury levels below 3 µg/l in individuals with amalgam fillings are also reported in several other studies. Barany et al. (2003) studies 245 17-year-old Swedish individuals and found a geometric mean level of 1.1 µg/l in their blood, which were positively correlated with fish consumption and serum mercury was influenced by the number of fillings as well as fish consumption. Dye et al. (2005) found that the average urinary mercury level in women of childbearing age was 1.34 µg/l and it was estimated that an increase of 1.8 µg/l would be seen in the urinary levels for each ten dental surfaces restored with amalgam. Zimmer et al. (2002) reported median mercury levels in blood of 2.35 µg/l in 40 females who had claimed to suffer from serious health damage due to amalgam fillings and 2.40 µg/l in a series of 43 control female subjects. The mercury concentrations in the urine of persons not occupationally exposed to mercury are usually below 5 µg/l. Again, the urinary excretion may vary considerably depending on non-occupational sources of mercury, such as fish consumption and amalgam fillings. In one study with 380 Italians without occupational exposure to mercury, a mean value of 3.5 µg/l urine was observed, with a range from 0.1 to 6.9 µg/l (BAT 1997). Median values between 1.5 and 1.8 µg/l urine have been reported (Zimmer et al. 2002). In a study of 1127 healthy males, Kingman et al. (1998) found an average total mercury urinary concentration of 2.55 µg/l with a significant correlation between this level and amalgam exposure equivalent to an increase of 1 µg/l of urine for each 10 amalgam surfaces.

    As discussed by Barregard (2005) and Barregard et al. (2006) values of urinary mercury expressed in relation to creatinine vary between countries, especially with reference to different food habits and national health care systems. Median levels in subjects with dental amalgams were 1.2 µg/g creatinine in Italy but 0.6 µg/g creatinine in Sweden, corresponding figures for those without amalgams being 0.9 and 0.2 µg/g creatinine respectively. Elevated levels, approximately five times higher than controls are found in individuals who regularly use nicotine chewing gums as a smoking replacement therapy (Sallsten et al. 1996).

    In a population of 245 German children, mercury concentrations in urine ranged between <0.1 and 5.3 µg/l, with a mean of 0.25 µg/g creatinine, with some correlation with the number of teeth with amalgam fillings and also the number of defective amalgam fillings (Pesch et al. 2002). Differences were noted between mercury in plasma and erythrocytes by Halbach et al. (2000, 2007). The authors conclude that the integrated daily mercury dose of 7.4 µg for a high amalgam load is well below the tolerable dose of 30 µg (WHO 2003, ATSDR 1999). A recent paper indicated that there may be difference in mercury excretion between boys and girls 8-18 years of age, treated with dental amalgam (Woods 2007).

    Exposure during pregnancy and breast-feeding

    Mercury is normally present in amniotic fluid. In one study of 72 pregnant women, (Luglie et al. 2005) there was an overall mean mercury concentration in amniotic fluid of 0.37 +/- 0.49 ng/ml. The women were divided into those with a low concentration of less than 0.08 ng/ml (26.4% of the subjects) and those with a high concentration of greater than 0.08 ng/ml, mean 0.49 +/- 0.52 ng/ml (73.6% of subjects). The amniotic fluid concentration was dependent of the number of amalgam fillings and fish consumption; the low concentration group having an average of 2.26 amalgam fillings and the high concentration group having an average of 5.32 fillings. However, no adverse effects were observed throughout pregnancies and in the newborn. Only a small fraction of divalent inorganic mercury is transferred to the fetus, whereas placental transfer of methyl mercury and elemental mercury occurs easily.

    Bjornberg et al. (2005) report that infant blood inorganic mercury is similar to maternal blood mercury at delivery but decreases until 13 weeks of age. In breast milk inorganic mercury decreased from day 4 to 6 weeks after delivery, and remained unchanged thereafter. Total mercury in breast-milk was associated with maternal but not infant inorganic mercury. The exposure to both methylmercury and inorganic mercury was low, being higher before birth than during the breast-feeding period. Methylmercury contributes more than inorganic mercury to infant exposure post-natal via breast milk. The median value for methylmercury in maternal blood at delivery is 0.99µg/l, decreasing to 0.38 µg/l by 13 weeks after birth. The median for inorganic mercury concentration was 0.09µg/l in maternal blood at delivery and 13 weeks. The same values were found in infant blood at delivery, reducing to 0.05µg/l at 13 weeks. The child’s exposure to methylmercury and inorganic mercury is much greater before birth than during breast-feeding. In breast milk, the mercury level correlated significantly to maternal blood inorganic mercury (0.29µg/l). Gundacker et al. (2002) indicate that the mean concentration of total mercury in human breast milk is 1.59µg/l, which they considered to pose no risk to infants.

    Intake estimates for mercury from dental amalgams

    Mercury vapour is released from silver amalgam restorations during chewing, tooth brushing, and parafunctional activities including bruxism. The parameters of this release of mercury vapour by amalgam depends of the number of fillings, the filling size and placement, chewing habits, food texture, grinding and brushing teeth, nose-mouth breathing ration, inhalation-absorption, ingestion and body weight, and the surface, composition and age of the amalgam restorations. Therefore, there are large variations in the estimation of daily mercury absorption and release.

    Mercury released from dental amalgam distributes in the oral cavity as inhalable mercury vapour, or is dissolved in saliva after oxidation or suspended in it as amalgam particles. There is no evidence that biotransformation of amalgam-derived mercury takes place intra-orally in association with bacterial activity. With respect to systemic exposure assessment, only the inhaled fraction is relevant since elemental mercury and inorganic mercury are poorly absorbed from the GI-tract and therefore have only a very minor contribution to systemic exposure. The daily uptake of mercury from amalgam fillings is estimated to be up to 27 µg/day in individuals with large numbers of fillings. One study shows an intake from 1 to 5 µg/day from dental amalgam for people with 7-10 fillings. The World Health Organization reported a consensus average estimate of 10 µg/day of amalgam derived mercury (range: 3-17 µg/day) (WHO 1991). Weiner and Nylander (1995) estimated the average uptake of mercury from amalgam fillings in Swedish subjects to be within the range of 4-19 µg/day. Skare and Engqvist (1994) estimated that the systemic uptake of mercury from amalgams in middle - aged Swedish individuals with a moderate amalgam load (30 surfaces) was, on average, 12 µg/day.

    3.3.2.3. Exposure to mercury in dental personnel

    The mercury body burden of dental personnel is normally higher than in the general population. The mean urine mercury levels in dental personnel has been variously reported to range from 3 µg/l to 22 µg/l, compared to 1-5 µg/l as the normal range for non-occupational groups (Hörsted-Bindslev 2004). This increased body burden is attributed to dental personnel mixing and applying dental amalgam and removing amalgam restorations; Ritchie et al. (2004) showed that dentists had, on average, urinary mercury levels over 4 times that of control subjects although all but one dentist had urinary mercury below the UK Health and Safety Executive health guidance value. Dentists were significantly more likely than control subjects to have suffered from disorders of the kidney but these symptoms were not significantly associated with their level of mercury exposure as measured in urine. Over 67% of the 180 surgeries visited had environmental mercury measurements in one or more areas above the Occupational Exposure Standard (OES) set by that Executive. In the majority of these surgeries the high levels of mercury were found at the skirting and around the base of the dental chair. In 45 surgeries (25%) the personal dosimetry measurement (i.e. in the breathing zone of dental staff) was above the OES.

    Dental personnel may now be exposed to much less mercury than in the past, in view of the increased use of encapsulated dental amalgam, improvements in amalgam capsule design, the heightened awareness and practice of appropriate dental mercury hygiene measures, and the increasing use of alternative, non-mercury-containing materials (ADA 2003, Hörsted-Bindslev 2004). However, despite trends to reduce exposure to mercury, large, highly statistically significant differences (P<0.0001) may be found between dental personnel (in particular dentists) and controls, with respect of mean urinary, hair (head and pubic) and nail (finger and toe) mercury levels, with the reasons for such differences being considered to be multifactorial (Morton et al. 2004)

    Since most dental chairside personnel do not touch dental amalgam during mixing and placement, it is considered that the main sources of mercury exposure are aerosols, created in the immediate working environment during and in particular, the removal of restorations of dental amalgam, and the exhaust air from dental vacuum systems. These mercury vapour releases can be substantial and well in excess of human exposure limits (Stone et al. 2007). Immediate working environment aerosols and exhaust air from dental vacuum systems will be inhaled despite the wearing of face masks, which may provide little, if any, barrier to mercury vapour entering the lungs and being absorbed. Correlations have been found amongst dentists between urinary mercury levels and the number of hours worked in the surgery (r=0.22, P=0.006) and the number of amalgam restorations placed (r=0.38, P<0.001) and removed (r=0.29, P<0.001) in a week, with urine mercury levels in dentists ranging from 0.02 to 20.90 (mean 2.58) nmol mercury per nmol creatinine. A confounding factor in such investigations is the number of amalgam surfaces dentists have in their own mouths (Ritchie et al. 2002, Ritchie et al. 2004).

    3.3.2.4. Metrology

    While the analytical instruments for the determination of mercury concentrations in biological samples are well developed and sufficiently sensitive, a number of problems with sampling, the determination of mercury speciation, and the interpretation of results are evident. For the determination of total mercury in occupation exposures, the German BAT-commission (which sets limit values for occupational exposures to chemicals and develops and validates analytical methodology) recommended a specific sampling procedure and analytical methods to determine mercury in blood or urine. Sampling procedures for mercury determination are also described by the “Humanbiomonitoring Kommission” of the German UBA (Umweltbundesamt, Federal Environment Agency, Dessau-Rosslau, Germany). These authorities also concluded that the often proclaimed exposure assessment for mercury release from dental amalgams, “dimercaptopropane sulfonate (DMPS) mobilisation test” for mercury, does not provide additional important information. This mobilisation test uses DMPS to chelate mercury, which results in an increased elimination of mercury with urine for a short time after DMPS-application (BAT 1997, UBA 1999).

    Rapid and reliable detection of mercury in blood and urine resulting from environmental and occupational exposure may be carried out in most analytical laboratories, using, for example, atomic fluorescence spectrophotometry (Berglund et al. 2005). Measurements of total mercury in the urine tend to reflect inorganic mercury exposure and total mercury levels in whole blood are more indicative of methylmercury exposure. However other fluids, such as saliva, hairs or nails or faeces have been proposed and used. Total mercury in red blood cells may be a suitable proxy for methylmercury exposure. The mercury concentration in saliva and scalp hair is more controversial. According to Pesch et al. (2002), hairs reflect fish consumption, the age of a child and the smoking habits of parents, with a low correlation between the hair and urine mercury content. Mercury content in saliva ranged between 0.32 and 4.5 µg/l and below the limit of quantification for more than 70% of the samples. Pesch et al. (2002) concluded that saliva does not seem to be a suitable tool to monitor the mercury burden. Although in general no correlation was found between elemental concentration in hairs and internal organs (Yoshinaga et al. 1990) a hair-organ relationship was found by Suzuki et al. (1993) for mercury concentration. More recently, the total mercury levels in hair, toenail and urine were shown to result from fish consumption, but the method was applicable neither to occupational exposure nor to dental filling mercury release (Ohno et al. 2007).

    Mercury levels in saliva determined by cold vapour atomic absorption spectrometry did not correlate with the concentration in blood and urine, and therefore is not recommended for a biological monitoring (Zimmer et al. 2002). Faeces reflect the elimination of metallic mercury by abrasion and therefore do not present any usefulness in the context of a potential burden. Generally blood and urine are preferred for the assessment of mercury exposure.

    Source & ©: SCENIHR,  The safety of dental amalgam and alternative dental restoration materials for patients and users (2008) 3.3.2 Exposure to Mercury, p.16


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