On December 14 and 15, 2010, the FDA convened a scientific panel to re-examine the issue of mercury exposure from amalgam dental fillings. Two private foundations, assisted by IAOMT, have commissioned G. Mark Richardson, PhD, formerly of Health Canada, to provide the scientific panel and FDA regulators with a formal risk assessment using the latest information from the scientific literature (CDC’s NHANES dataset).
We got to interview Mark Richardson PhD about the results of the final study, Mercury exposure and risks from dental amalgam in the US population, post-2000, which was published in the journal “Science of the Total Environment”. The amalgam risk assessment study reveals 120+ million exposed to unsafe levels of mercury from fillings.
Based on the least conservative of the scenarios evaluated, it was estimated that some 67.2million Americans would exceed the Hg dose associated with the reference exposure level (REL) of 0.3 ug/m3 established by the US Environmental Protection Agency; and 122.3million Americans would exceed the dose associated with the REL of 0.03 ug/m3 established by the California Environmental Protection Agency.
Mercury exposure and risks from dental amalgam in the US population, post-2000
G.M. Richardson, R. Wilson, D. Allard, C. Purtill, S. Douma, J. Gravière
Dental amalgam is 50% metallic mercury (Hg) by weight and Hg vapour continuously evolves from in-place dental amalgam, causing increased Hg content with increasing amalgam load in urine, faeces, exhaled breath, saliva, blood, and various organs and tissues including the kidney, pituitary gland, liver, and brain. The Hg content also increases with maternal amalgam load in amniotic fluid, placenta, cord blood, meconium, various foetal tissues including liver, kidney and brain, in colostrum and breast milk.
Based on 2001 to 2004 population statistics, 181.1 million Americans carry a grand total of 1.46 billion restored teeth. Children as young as 26 months were recorded as having restored teeth. Past dental practice and recently available data indicate that the majority of these restorations are composed of dental amalgam. Employing recent US population-based statistics on body weight and the frequency of dentally restored tooth surfaces, and recent research on the incremental increase in urinary Hg concentration per amalgam-filled tooth surface, estimates of Hg exposure from amalgam fillings were determined for 5 age groups of the US population. Three specific exposure scenarios were considered, each scenario incrementally reducing the number of tooth surfaces assumed to be restored with amalgam. Based on the least conservative of the scenarios evaluated, it was estimated that some 67.2 million Americans would exceed the Hg dose associated with the reference exposure level (REL) of 0.3 μg/m3 established by the US Environmental Protection Agency; and 122.3 million Americans would exceed the dose associated with the REL of 0.03μg/m3 established by the California Environmental Protection Agency.
Exposure estimates are consistent with previous estimates presented by Health Canada in 1995, and amount to 0.2 to 0.4 μg/day per amalgam-filled tooth surface, or 0.5 to 1 μg/day/amalgam-filled tooth, depending on age and other factors.
Mercury (Hg) is globally recognized as a toxic substance with numerous national and international efforts to phase out its use, the most recent being the initiative of the United Nations Environment Programme on a global phase out strategy (UNEP, 2009), for which negotiations began in June 2010. The one lingering exception to this phase out is dental amalgam.
Although now banned in Sweden and Norway (Norway Ministry of Environment, 2007; Sweden Ministry of Environment, 2009), dental amalgam is still a restorative material of choice for the majority of US general dentists for repair of dental caries (cavities) (ADA, 2008a).
It is a solid emulsion composed of a mixture of metals comprising approximately 50% metallic mercury (Hg0) byweight. Formulations vary in their Hg content, ranging from 43 to 50.5% Hg by weight, mixed with a powder of other metals typically containing silver (40 to 70%), tin (12 to 30%), copper (12 to 30%), indium (0 to 4%), palladium (0.5%) and zinc (0 to 1%) (Berry et al., 1994).
Dental amalgam has been used in North American dentistry for perhaps 150 years or more (Clarkson and Magos, 2006) and during that time has been the subject of repeated controversy, often referred to as the Amalgam Wars (Clarkson and Magos, 2006). A brief historical account of its introduction, use and controversy is provided by Molin (1992). Scientific articles regarding amalgam’s potential toxicity date back at least to 1885 (Talbot, 1885). These wars or debates have been due to the recurring concern for the potential health risks posed by exposure to the Hg used in the manufacture of dental amalgam.
It is now accepted that dental amalgam continuously releases Hg0 which results in exposure in those persons possessing fillings composed of this material (USFDA, 2009).
The quantity of Hg0 released from amalgamis often referred to as ‘minute’ (ADA, 2008b; CDA, 2005) or ‘very small’ (AGD, 2007). However, it is not the dose itself that determines safety, it is how that dose compares to levels considered ‘safe’ or without anticipated harm that determines whether or not the dose is significant with respect to health concern. Irrespective of quantity, aminute dose can present a risk if the substance is sufficiently toxic and received in sufficient dose to exceed a reference level considered ‘safe’.
Dental amalgam has been identified as the largest single source of continuous Hg exposure for members of the general population who possess amalgam fillings (WHO, 1991; Heath Canada, 1996). Previous assessments of dental amalgam have demonstrated that the dose of Hg received as a result of this dental material exceeds what is considered to be a safe or reference dose (see Health Canada, 1995; Richardson and Allan, 1996).
A series of recent studies have reported urinary Hg concentrations (variably corrected or uncorrected for urine creatinine content) as a function of amalgam filling load (Barregard et al., 2008; Dunn et al., 2008; Melchart et al., 2008; Woods et al., 2007; Bellinger et al., 2006; Dye et al., 2005; Factor-Litvak et al., 2003; Pesch et al., 2002; Kingman et al., 1998). In these and in earlier studies (reviewed by Richardson and Allan, 1996; Health Canada, 1995), the average urine Hg content is consistently greater in groups with amalgam fillings than in those without, and urine Hg content consistently increases as amalgam load increases.
Numerous other studies have also demonstrated that the Hg exposure or concentration increases with increasing amalgam load in the following tissues and situations:
- Due to chewing, brushing and bruxism (Hansen et al., 2004; Ganss et al., 2000; Isacsson et al., 1997; Sallsten et al., 1996; Berdouses et al., 1995; Bjorkman and Lind, 1992; Forsten, 1989; Vimy and Lorscheider, 1985a, b; Berglund, 1990; Svare et al., 1981; Gay et al., 1979);
- In exhaled or intra-oral air of persons with amalgam fillings (Halbach andWelzl, 2004; Skare and Engqvist, 1994; Gay et al., 1979; Svare et al., 1981; Patterson et al., 1985; Vimy and Lorscheider, 1985a,b; Berglund et al., 1988; Jokstad et al., 1992);
- In saliva of persons with amalgam fillings (Fakour et al., 2010; Melchart et al., 2008; Zimmer et al., 2002; Ganss et al., 2000; Pizzichini et al., 2000; Bjorkman et al., 1997; Berglund, 1990);
- In blood of persons with amalgam fillings (Gerhardsson and Lundh, 2010; Halbach et al., 2008;Melchart et al., 2008; Lindberg et al., 2004; Pizzichini et al., 2003; Ganss et al., 2000; Vahter et al., 2000; Kingman et al., 1998; Oskarsson et al., 1996; Skare and Engqvist, 1994; Akesson et al., 1991; Abrahamet al., 1984; Snapp et al., 1989;Molin et al., 1990; Jokstad et al., 1992; Svensson et al., 1992; Herrstrom et al., 1994);
- In various organs and tissues of amalgam bearers, including the kidney, pituitary gland, liver, and brain or parts thereof, (Barregard et al., 1999, 2010; Björkman et al., 2007; Guzzi et al., 2006; Weiner and Nylander, 1993; Nylander et al., 1987, 1989; Eggleston and Nylander, 1987);
- In faeces of amalgam bearers (Engqvist et al., 1998; Bjorkman et al., 1997; Skare and Engqvist, 1994);
- In amniotic fluid, cord blood, placenta, and various foetal tissues including liver, kidney and brain, in association with maternal amalgam load (Palkovicova et al., 2008; Ursinyova et al., 2006; Luglie et al., 2005; Ask-Björnberg et al., 2003; Lindow et al., 2003; Ask et al., 2002; Vahter et al., 2000; Lutz et al., 1996; Drasch et al., 1994);
- In colostrum and breast milk in association with maternal amalgam load (Ursinyova et al., 2006; Ask-Bjornberg et al., 2005; Da Costa et al., 2005; Drexler and Schaller, 1998; Drasch et al., 1998; Oskarsson et al., 1996).
- Amalgam fillings are sufficiently significant to personal Hg exposure that the influence of amalgam load on blood and urine Hg concentration can be detected despite moderate occupational Hg exposure, occupational exposure that results in up to about 10 μg Hg/L urine (Skare et al., 1990; Martin et al., 1995; Soleo et al., 1998a; Jokstad, 1990).