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3.        Organizzazione mondiale della Sanità (OMS) su mercurio e amalgama  -  vedi: Materiali Dentari e denti tossici
(documento W.H.O., 1991) W.H.O. 1991  - Environmental Health Criteria for inorganic mercury

The general population is primarily exposed to mercury from dental amalgam and the diet.
Table 2 indicates the average daily intake and retention of total mercury and mercury compounds in the general population not occupationally exposed to mercury.

Table 2

exposition source (mg/ day)

mercury vapour

inorganic mercury compounds

methylmercury

air

0.03 (0.024)

0.002 (0.001)

0.008 (0.0064)

food: fish

0

0.6 (0.042)

2.4 (2.3)

food: no-fish

0

3.6 (0.25)

0

drinking water

0

0.050 (0.0035)

0

dental amalgam

3.8–21 (3–17)

0

0

total

3.83–21 (3.1–17)

4.3 (0.3)

2.41 (2.31)

Human studies  
The release of mercury vapour from dental amalgam fillings has been known for a very long time (Stock, 1939). The next major contribution to this field was that of Frykholm (1957). Using a radioactive mercury tracer, he showed that the insertion of amalgam in both humans and dogs resulted in significant concentrations of mercury in urine and faeces. In humans the concentrations of urinary mercury increased during a 5-day period following the insertion of 4-5 small occlusal fillings. A new higher peak occurred a couple of days after removal of these fillings. Faecal elimination showed a similar pattern, appearing on the second day after amalgam insertion. Another maximum appeared 1-2 days after amalgam removal. Frykholm (1957) also measured the concentration of mercury in the oral cavity during amalgam placement in teeth. Recently, concern over amalgam usage has been revived by the pubblication of a number of experimental studies showing that, among other elements, inorganic mercury is released from amalgam in vitro (Brune 1981, Brune & Evje 1985). More importantly, mercury vapour released in the mouth in vivo leads to an increased uptake of mercury in body tissues (Gay 1979, Svare 1981, Abraham 1984, Ott 1984, Patterson 1985, Vimy & Lorscheider 1985a,b, Vimy 1986, Langworth 1988, Nylander 1987, 1989, Berglund 1988, Aronsson 1989). Vimy and Lorscheider (1985b) showed that the release rate of mercury vapour increases dramatically when the amalgam is stimulated by continuous chewing, reaching a plateau within 10 min. After the cessation of chewing, it takes approximately 90 min for the mercury release rate to decline to the basal pre-chewing value. (Fig.1) A confirmatory study has recently been published by Aronsson (1989) who also made daily dose estimates.
Critical reviews have been made of published information on mercury release and exposure from amalgam (Enwonwu 1987, Friberg & Nylander 1987, Langan 1987, Mackert 1987, Olsson Bergman 1987, Clarkson 1988a). Several studies have correlated the number of dental amalgam fillings or amalgam surfaces with the mercury content in brain and kidney tissue from human autopsy. Subjects with no dental amalgam had a mean mercury level of 6.7 ng/ g in the occipital cortex; whereas subjects with amalgams had a mean level of 12.3 ng/g (Friberg & Nylander 1987; Nylander 1987). Amalgam free subjects had a mean mercury level in kidneys of 49 ng/g, whereas subjects with amalgam fillings had a corresponding level of 433 ng/g. In a similar investigation, Eggleston & Nylanber (1987) showed mean mercury levels of 6.7 ng/g and 3.8 ng/g in grey and white brain matter, respectively, in subjects with no amalgam fillings. In subjects with amalgam fillings, mercury levels were 15.2 ng/g and 11.2 ng/g for grey and white matter, respectively. In a more recent extensive study, Schiele (1988) showed a mean brain occipital mercury concentration of 10 ng/g for 44 subjects with an average of 14 amalgam surfaces each. Kidneys from the same subjects showed a sex difference in the mercury concentrations, mean values being 484 ng/g for the 16 females and 263 for the 28 males.
Using pubblished experimental data (Svare 1981, Abraham 1984, Patterson 1985, Vimy & Lorscheider 1985b), the amalgam mercury release rate average daily mercury uptake, and its steady-state contribution to blood, urine, brain, and kidney were estimated by Clarkson (1988). These estimations gave brain, kidney and urine values that are similar to data reported from human studies (brain and kidney autopsy samples: Friberg 1986, Nylander 1987, Schiele 1988, urine: Nilsson & Nilsson 1986b, Olstad 1987, Langworth 1987). Estimates of daily dosages of mercury attributed to amalgam have also been reported by Mackert (1987) and Olsson & Bergman (1987), although they are somewhat lower than those of Clarkson et al. (1988).
Snapp (1989) studied the blood mercury level before and 18 weeks after the removal of amalgam fillings. After the removal, nine of the ten subjects examined exhibited a statistically significant mean decrease of 1.13 ng mercury/ml in the blood mercury level.
Recently Molin (1990) studied mercury concentrations in human plasma, erythrocytes and urine before and up 12 months after removal of amalgam fillings and replacementds with gold alloy restorations. They noted an initial increase in all recorded mercury levels after amalgam removal. About three months thereafter, plasma and erythrocyte levels decreased markedly. A continuous reduction in urine mercury levels took place, reaching a plateau of approximately 25% of the pre-removal mercury level within 9 months.
It is important to note that, in the studies cited, both the predicted mercury uptake from amalgam and the observed accumulation of mercury in the body are average values. It is also clear from the original reports that substantial individual variations exist.
Animal experiments - Frykholm (1957), using radioactive mercury in amalgam, studied the release and uptake of mercury in dogs and monkeys. He concluded that the mercury exposure from amalgam was essentially limited to the immediate placement procedures. This is in contrast to more recent studies that examined the disposition of radioactive mercury released from amalgam restorations in sheep (Hahn 1989, Vimy 1990).
Hahn (1989) demostrated by whole-body image scan that amalgam mercury could be readily visualized in the kidney, liver, jawbone, and gastrointestinal tract after only 29 days of chewing with amalgam. Vimy (1990a) demostraterd that the mercury levels in maternal blood, fetal blood, and amniotic fluid reached a peak within 48h after amalgam placement and remained at that level for the duration of the studies (140 days). Mercury levels of 4 ng/g in maternal blood and amniotic fluid and of 10 ng/g in fetal blood were found. The erythrocyte/plasma ratios of mercury from amalgam in both the ewe and the fetal lamb were less than unity. The maternal urine mercury concentration ranged from 1- 10 ng/g during a 16 day period. approximately 7.7 mg of mercury could be eliminated per day in faeces.
All tissues examined displayed mercury accumulation. By 29 days, kidney mercury levels rose to approximately 9000 ng/g, and these levels were mantained throughout the duration of the study. A similar pattern was observed in the liver, but the levels remained at approximately 1000 ng/g. The fetal kidney contained mercury levels of 10-14 ng/ g, whereas fetal liver had levels of 100-130 ng/g.
The maternal brain (cerebrum, occipital lobe, and thalamus) showed a mercury accumulation ranging from 3-13 ng/g. In the pituitary, thyroid and adrenal glands, concentrations ranged from approximately 10-1100 ng/g. In the fetal cerebrum, occipital cortex, and thalamus the highest levels were approximately 10 ng/g. the fetal pituitary gland had mercury concentrations of more than 100 ng/g, whereas the thyroid and adrenal glands contained less than 10 ng/g.
Milk obtained at lamb parturition or within several days following birth (25-41 days after amalgam placement) contained levels of mercury from dental amalgam that reached as high as 60 ng/g.
Other recent reports indicate that both kidney function (Vimy 1990b) and intestinal bacterial population (Summers 1990) may be affected when animals are exposed tio dental amalgam mercury.

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