Myth #9: Mercury from dental amalgam can be dangerous to dentists; therefore, it is hazardous to patients.

Michael J. Wahl, D.D.S.
November 1, 2002

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Amalgam — Resurrection and Redemption Part 2:

The Medical Mythology of Anti-Amalgam

Michael J. Wahl, D.D.S.

Myth #9: Mercury from dental amalgam can be dangerous
to dentists; therefore, it is hazardous to patients.

Fact #9: Dentists and dental assistants have higher body levels
of mercury than those not in the dental profession, but dentists
and dental assistants with good mercury hygiene have not exhibited
systemic health or reproductive problems from working with amalgam.

Some anti-amalgamists assert that mercury from working with dental amalgam is dangerous to dentists and therefore is also harmful to patients who have amalgam restorations [1]. They claim that the American Dental Association is hypocritical when it advises dentists to use precautions when handling amalgam in their offices, but asserts that amalgam is safe and effective as a filling material. Domb called it a “logical disconnect” that amalgam is considered hazardous when handled or disposed of as scrap, but considered safe in people’s mouths as restorations [1].

Mean urinary mercury levels for dentists have been declining in the United States. Mean urinary mercury levels in dentists screened at ADA meetings have decreased from 5.8 ug/l in 1985 and 7.6 ug/l in 1986 [2] to 4.9 ug/l in 1991 [12]. In dentists with low exposure, the number of amalgams in their own mouth is probably a more significant contributor to urinary mercury level [3]. Dentists with poor mercury hygiene (e.g., mercury spills, the use of squeeze cloths, office-prepared capsules, not using water spray and high vacuum suction during amalgam removal, and older triturators with mercury dispensers) generally have higher urinary mercury levels than dentists who use disposable precapsulated amalgam without squeeze cloths and modern triturators [3].

A 1982 study showed that dentists with more than 20 mg/g “tissue mercury levels” had mild visuographic dysfunction and more symptom-distress than a control group of dentists with no detectable exposure [4]. These mercury levels were in the top 20% of 298 dentists tested, so they must have been extraordinarily high although urinary mercury levels (usually more accurate) were not determined, only head and wrist mercury levels by X-ray fluorescence.

A 1992 study reported compared a group of 98 dentists in Singapore occupationally exposed to mercury vapor versus a group of 54 unexposed dentist controls [5]. The exposed dentists performed significantly worse on various neurobehavioural tests than the control group. This study has been criticized by Mackert for several reasons [6]. The study was not double-blind: the investigators knew the exposure status of the subjects being tested. The authors measured a single day’s mercury exposure in each office to estimate average exposure, but further testing of several offices showed there were wide variations in high and low mercury air levels in some of the offices in the test group, differing by as much as a factor of 2 in one week. The authors did not report how they corrected for confounders, including the prevalent use of mercury-containing traditional medicine in the population.

The levels of mercury vapor in the air in many of the practices in this study were probably not representative of the mercury levels in dental offices in the United States. Many of the practices in the study did not use disposable capsules or modern triturators when the study was done. Most importantly, the control group was inappropriate for this study. According to the authors, the practicing dentists with occupational exposure to mercury typically worked 10 hours per day, 6 days per week. Such long hours could adversely affect their performance on neurobehavioral tests. It is unlikely the control group of university staff worked such long hours. Echeverria et al stated, “The use of university staff as referents rather than unexposed dentists increased the risk of confounding due to factors such as the use of vibrating tools such as dental drills (which affect fine motor manual dexterity), socioeconomic status, and test-taking training.”

Of 1706 dentists screened at an ADA meeting in 1991, only 29 (2%) had urinary mercury levels exceeding 19 mg/l. [7] Echeverria et al compared 19 of these “exposed” dentists with high levels of urinary mercury with 20 dentists with undetectable urinary mercury levels Based on the results of vocabulary, symptom, mood, and behavior tests, the investigators determined that the dentists in the exposed group had “some evidence of adverse preclinical effects at mercury doses averaging 36 mg/l urine.” [7] It should be noted that the mercury exposure in these dentists was correlated with poor mercury hygiene (the use of squeeze cloths).

In 1998, Echeverria et al studied a group of 47 dentists and dental assistants with very low levels of mercury exposure given DMPS chelation therapy. The chelation therapy was shown to be effective in raising urinary excretion of mercury. There was a significant improvement on the post-chelation over the pre-chelation tests for mood, motor function, and congnition. The authors concluded that this study “presents convincing new evidence of adverse behavioral effects associated with low Hgo exposures within the range of that received by the general population” and raised concerns that equally low levels of mercury from amalgam fillings may also have neurobehavioral effects [8]. This study does not provide convincing evidence for this assertion. Although the test administrators were blinded as to the subjects’ urinary mercury levels, they were apparently not blinded to pre- or post-chelation status of the subjects. In addition, there was no placebo group to serve as controls. Similar studies involving symptoms associated with mercury exposure have shown no difference in improvements when subjects were given placebo versus chelation therapy [9,10]. Studies on dentists and dental assistants have also failed to show signs of renal [11,12] or immune [12] dysfunction.

Dentists who place and/or remove amalgam fillings are exposed to higher levels of mercury than most patients. Rather than hypocritical, it is only sensible to use simple methods of mercury hygiene for dentists and staff. Mean urinary levels of mercury in dentists have been decreasing partly because of better mercury hygiene and partly because fewer amalgams are placed today than in the past. The few dentists with very high urinary mercury levels generally are the ones who have poor mercury hygiene.

There are many examples of substances that are beneficial in small doses, but can be harmful in large doses. In small doses, chlorine’s antibacterial effect makes water safe to drink; in higher doses, chlorine can be deadly. The anticoagulant warfarin sodium (Coumadin) prevents stroke and thromboemobolisms in patients with a variety of medical conditions, but is used as rat poison in higher doses. In small doses, fluoride has a beneficial anticaries effect; in somewhat higher doses, it can cause fluorosis. In still higher doses, fluoride is poisonous. In small doses, botulinum toxin is an effective treatment for a variety of neurological disorders [13], even including severe bruxism [14]. In high doses, the toxin is deadly. Even water itself, necessary for life in small doses, can cause drowning in large doses.

Few anti-amalgamists would condemn the proper use of x-rays or curing lights, but there are similar recommendations for exposing radiographs and using curing lights. The taking of many daily radiographs can lead to much higher levels of radiation exposure in dentists and dentists and/or dental staff who stand in the room than periodic x rays do as part of a patient’s dental treatment. Similarly, using a curing light without a proper light shield can theoretically harm the operator’s eyes. Although there is a possible risk of harm to the dentist or dental staff without proper precautions, there is virtually no risk to patients.


  1. Domb B. Give Dr. Dickerson credit. [Letter.] Dent Econ 1999;89(7):17.
  2. Naleway C, Chou H-N, Muller T, et al. On-site screening for urinary Hg concentrations and correlation with glomerular and renal tubular function. J Pub Health Dent 1991;51:12-17.
  3. Martin MD, Naleway C, Chou H-N. Factors contributing to mercury exposure in dentists. JADA 1995;126:1502-11.
  4. Shapiro IM, Cornblath DR, Sumner AJ, et al. Neurophysiological and neuropsychological function in mercury-exposed dentists. Lancet 1982;1:1147-50.
  5. Ngim CH, Foo SC, Boey KW, Jeyaratnam J. Chronic neurobehavioural effects of elemental mercury in dentists. Br J Ind Med 1992;49:782-90.
  6. Mackert JR, Berglund A. Mercury exposure from dental amalgam fillings: absorbed dose and the potential for adverse health effects. Crit Rev Oral Biol Med 1997;8:410-36.
  7. Eley BM. The future of dental amalgam: a review of the literature. Part 2: Mercury exposure in dental practice. Br Dent J 1997;182:293-7.
  8. Echeverria D, Heyer NJ, Martin MD, et al. Behavioral effects of low-level exposure to Hg among dentists. Neurotoxicol Teratol 1995;17:161-8.
  9. Echeverria D, Aposhian HV, Woods, JS, et al. Neurobehavioral effects from exposure to dental amalgam Hg: new distinctions between recent exposure and Hg body burden. FASEB J 1998;12:971-80.
  10. Grandjean P, Guldager B, Larsen IB. Placebo response in environmental disease: chelation therapy of patients with symptoms attributed to amalgam fillings. J Occup Environ Med 1997;39:707-14.
  11. Sandborgh Englund G, Dahlqvist R, Lindelöf B. DMSA administration to patients with alleged mercury poisoning from dental amalgams: a placebo-controlled study. J Dent Res 1994;73:620-8.
  12. Langworth S, Sällsten, Barregård L, et al. Exposure to mercury vapor and impact on health in the dental profession in Sweden. J Dent Res 1997;76:1397-1404.
  13. Jankovic J, Brin M. Therapeutic uses of botulinum toxin. N Engl J Med 1991;324:1186-94.
  14. Tan E-K, Jankovic J. Treating severe bruxism with botulinum toxin. JADA 2000;131:211-6.

Dr. Wahl practices dentistry in Wilmington, Delaware. This article was originally published in Quintessence International 32:696-710, 2001, and is reproduced here with the kind permission permission of Quintessence Publishing Co. The author thanks Drs. J. Rodway Mackert, Ivar A. Mjör, and Fred Eichmiller for reading the manuscript and offering several helpful suggestions.

Part 1:
Intro |||
1 |||
2 |||
3 |||
4, 5, 6, 7 |||
8, 9 |||
10, Conclusion

Part 2:
Intro |||
1 |||
2 |||
3 |||
4 |||
5 |||
6 |||
7 |||
8 |||
9 |||
10, Conclusion

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This page was posted on November 1, 2002.