After reading the following you may want to have a read of my plea to dentists

The Effects of Mercury on Dental Personnel

Why do dentists have such a high suicide rate?

A common refrain from the dental associations is that if mercury from amalgam is so dangerous for the patients, than why aren’t the dentists sick, as they are exposed to levels on a daily basis, far higher than most patients.  It’s an interesting proposition, which if it were true would be fair enough to ask. 

The results published by the IAOMT show that;

When cutting amalgam with a high speed drill, the levels of mercury vapour 18 inches from the mouth, can exceed 4,000mcg/m3

When the nurse opens a freshly mixed amalgam capsule the level of mercury vapour she (and the rest of the surgery) will be exposed to is 1,000 mcg/m3. This is 200 times above OSHA standards and 50,000   above the ATSDR levels.

These figures are beyond comprehension, especially when our very own dental associations claim that they are safe.  A reminder to all dentists and dental associations:

In 1991 (criteria 118) the World Health Organization stated clearly that the No Observable Effects Level (NOEL) for mercury vapour is ZERO. 

Are the dental associations really looking after their member's interests by recomending that they expose themselves and their staff to these sorts of levels of mercury vapour?

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From 1975 till 1983 the American Dental Association conducted a survey of the dentists who participated in the Health Assessment Programs they conducted.  This study looked at urinary mercury levels of 4,272 Dentists in the USA.  They measured straight urine/mercury levels.  We could expect that if a DMPS Challenge test had been employed, the figures would be at least five times higher.

These 4,272 dentists had a mean mercury urine level of 14.2mcg/l (micrograms per litre). What was then considered to be the maximum normal level as stated by the American Dental Association was 20mcg/l.  The observed ranges of urine mercury levels was 0 to 556 mcg/l.

The study showed that;

1. 19.1% are over the maximum normal measurement of 20 ugHg/L
2. 10.9% are over the C.D.C. maximum acceptable level of 30 ugHg/L
3. 4.9% are over 50 ugHg/L, the level found to cause induced tremors
4. 1.3% are over 100 ugHg/L, the level found to cause tremors

This study was used for many years to show how well dentists were!  Note that the reference levels used were 20 micrograms of mercury per litre of urine.  The new German guidelines for urine mercury levels since 2006 have dropped significantly. The new reference level for urinary mercury is now 0.7 mcg/l.  This would suggest that dentists with a level of 20 mcg/l would show significant physical and psychological disturbances.

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A study from 2001 explored the mercury levels in dental students and dental teachers over a one year period.  This study is published in the British Dental Journal!  (Tezel H  Ertas OS  Erakin C  Kayali A   Blood mercury levels of dental students and dentists at a dental   school. Br Dent J (2001 Oct 27) 191(8):449-52)

“There were statistically significant increases  in plasma mercury concentration between measurements in all groups at the end of the academic year. Red cell mercury levels were also consistently elevated. Although the highest levels of mercury were recorded in persons working with amalgam, increased levels were also found in subjects working in the teaching classrooms but not with amalgam (controls and first year students).”

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“Our results indicate that the urinary mercury levels of the tested dental professionals were significantly higher than those of the control group”

“This study showed that there may be a mercury health hazard in some dental environments.”

“…it is apparent that exposure to mercury during the preparation of silver amalgam definitely presents an additional occupational hazard as an allergen in the dentist.”

“The results showed that mercury levels in the urine and head hair of dental personnel were significantly higher than in the controls
The highest urine mercury level was found in the group of dental assistants.
The amounts of urine mercury from dental assistants, dentists and dental students were 81.0%, 38.2% and 43.5% higher than the threshold limit value respectively.”

“General dentists were found to have more than twice the level of mercury in toenails than non-dental health professionals  … and 60 percent higher than dental specialists …”

“Of the 298 dentists evaluated, 28% had greater than 20 micrograms/g of mercury in the head.”

“The urinary concentrations of mercury of the dentists who used amalgam in their work were statistically highly significantly   elevated.”

Another study from 1991 concluded;  “In the group of dental personnel, the effect of their own amalgam fillings on Hg concentrations....was as important as their occupational exposure to Hg”.

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The publication in 1985, of a huge study of 9,241 people has hardly raised an eyebrow.   A study of this size has great statistical significance yet has not made it into the dental association information.  This group was comprised of 3,454 male dentists,  1,125 female dentists, 4,662 female dental nurses.  It showed that the rate of a particular type of brain cancer called a Glioblastoma was twice as high in this group of dental personnel compared to the rest of the population.
 
Another study of 298 dentists revealed that 30% of the high mercury group had polyneuropathies.  No polyneuropathies were detected in the control group. 

The high mercury group had mild visuographic dysfunction; they also had more symptom-distress than did the control group.
These findings suggest that the use of mercury as a restorative material is a health risk for dentists.

A different study of 66 dentists;
“with a sample of 37 (56%), 22 dentists (59.5%, 19 male, 3 female) and 15 dental assistants (40.5%, all female).
Most frequent symptoms referred by dentists were: irritability   (54.5%), cephalalgia (45.4%), arthralgias (40.9%), and the ones more   referred by assistants were arthralgias (53.3%), irritability (46.7%)   and cephalalgia (46.7%).”

Female Dental Personnel

A study published in the Journal of the American Dental Association states that for female dental personnel;

“rates of spontaneous abortion or non-congenital abnormalities  in children during this period, were higher in respondents exposed to high levels of mercury in the dental environment than those exposed to low levels.”

In fact the rate of infertility, miscarriage, stillbirths, and congenital deformities is up to twice the rate of the rest of the population.  The incidence of menstrual problems increases with length of exposure. ,

The US Environmental Protection Agency have stated that;
“Women chronically exposed to mercury vapour experienced increased frequencies of menstrual disturbances and spontaneous abortions.”
“A high mortality rate was observed among infants born to women who displayed symptoms of mercury poisoning.”

These   findings indicate that dental work could be another occupational hazard with respect to reproductive processes.

The probability of falling pregnant at each menstrual cycle for women who prepared 30 or more amalgam fillings per week is only 63% of that for unexposed women. 

As long ago as 1981 it was shown that female dentists had a higher rate of spontaneous abortions then a control of female medical personnel or the rest of the population.  The Peri-Natal Mortality Rate for the female dentists was significantly higher than for the rest of the population 19.5 / 1000 as compared to 7.5 / 1000  - twice the rate of the controls.

Female dental personnel are perhaps the most sensitive of the dental fraternity exposed to mercury.  Many girls start a career in dental nursing in their early teens.  They continue often into their 30’s and some longer.  This is the prime reproductive age. 

Psychological Effects

Psychological studies of dentists show some really scary results.   One such by Professor Joel Butler, Professor of Psychology at the University of North Texas, and entitled “Neuropsychological Dysfunctioning Associated with the Dental Office Environment" has the following results.
Fifty-one dentists and dental personnel were studied on standardised tests, which revealed there were a significant number who measured in the abnormal range;
Some motor tremor – 90%
Some psychomotor dysfunction – 41%
Severe psychomotor dysfunction – 16%
Impaired immediate recall – 58%
Impaired auditory memory - 84%
Visual memory reduced – 52%
Vigilance attention concentration and cognitive comprehension – 52%
Work and lives felt to be pointless -36%
Tactile sensory dysfunction/inability to locate finger position – 52%
Logical thinking and story recall impaired – 79%
Spatial and visual memory impaired – 68%
History of unsatisfying interpersonal relationships – 27%
Out of normal range on emotional stability scale – 72%
Suicidal depression / disgust with life / despondency and despair – 27%
Increased state of agitation – 30%
Increased scores on psychopathic scale – 42%

This study concludes that as a group, dentists are, after a number of years, at least one standard deviation below the rest of the population in IQ levels.  Considering that a dentist must be at least one standard deviation above the rest of the population to have passed dental school, this represents an enormous and significant drop!

Another study from 1995 stated;
… analysis showed that the coefficient of urinary mercury was statistically and adversely associated with complex attention (switching task), the perceptual motor task (symbol-digit   substitution), symptoms and mood.

In the same year other research by Echeverria et al came up with a similar conclusion. “Significant urinary Hg dose-effects were found for poor mental concentration, emotional lability, somatosensory irritation, and mood   scores.”  There was Evidence of subtle pre-clinical changes in behaviour associated with Hg exposure. Urine mercury Levels Directly related to; Reduced Concentration and Emotional Instability and Fine Motor Function was seriously effected.  

New distinctions between subtle preclinical effects on symptoms, mood, motor function, and cognition were found associated with Hg body burden as compared with those associated with recent   exposure. … presents convincing new evidence of adverse behavioral effects associated with low Hg(o) exposures within the range of that received by the general population.

In neurobehavioural tests measuring motor speed (finger tapping),   visual scanning (trail making), visuomotor coordination and   concentration (digit symbol), verbal memory (digit span, logical   memory delayed recall), visual memory (visual reproduction, immediate   and delayed recall), and visuomotor coordination speed (bender-gestalt time), the performance of the dentists was significantly worse than that of the controls.
In trail making, digit span, logical memory delayed recall, visual reproduction delayed recall, and bender-gestalt time test scores were more than 10% poorer. … the performance decreased as the exposed dose increased. These results raise the question as to whether the current threshold limit value of 0.050 mg/m3 (TWA) provides adequate protection against adverse effects of mercury.

Another study was performed “to find out if the first "professional" contact of dental students with amalgam resulted in an increased mercury excretion.”
The study was conclusive.  The longer the students were exposed to mercury in the clinic, the greater was their body burden of mercury. 

The levels of Hg in the urine samples of the dentists was about three times higher than the control subjects. …

30% of the 23 high mercury dentists had polyneuropathies. No   polyneuropathies were detected in the control group. The high mercury group had mild visuographic dysfunction; they also had more symptom- distress than did the control group. These findings suggest that the use of mercury as a restorative material is a health risk for dentists.

Dentists were significantly more likely than control subjects to have had disorders of the kidney and memory disturbance.

The older dentists showed significantly better performance on the simple reaction time test and significantly poorer performance in the   immediate word recall and delayed word recall tests.

In light of new research, which shows that over time there is a reduction in kidney filtration and a reduction in urine mercury levels due to the inability to excrete, these statements become even more terrifying.

After reading the above you may want to have a read of my plea to dentists

Studies demonstrating increased mercury levels and serious health effects in Dentists.

Just to give you an idea that there is more than one interesting study out there demonstrating serious health effects on dentists and dental personnel, I offer the following:

1. Molin M  Marklund SL  Bergman B  Nilsson B   Mercury, selenium, and glutathione peroxidase in dental personnel.  Acta Odontol Scand (1989 Dec) 47(6):383-90

2. Morton J  Mason HJ  Ritchie KA  White M   Comparison of hair, nails and urine for biological monitoring of low   level inorganic mercury exposure in dental workers. Biomarkers (2004 Jan-Feb) 9(1):47-55

3. Ritchie KA  Burke FJ  Gilmour WH  Macdonald EB  Dale IM  Hamilton RM     McGowan DA  Binnie V  Collington D  Hammersley R   Mercury vapour levels in dental practices and body mercury levels of   dentists and controls. Br Dent J (2004 Nov 27) 197(10):625-32;

4. Brown D   A study of the mercury levels in Scottish dentists. Br Dent J (2004 Nov 27) 197(10):621

5. Tezel H  Ertas OS  Erakin C  Kayali A   Blood mercury levels of dental students and dentists at a dental   school. Br Dent J (2001 Oct 27) 191(8):449-52

6. Ngim CH  Foo SC  Boey KW  Jeyaratnam J   Chronic neurobehavioural effects of elemental mercury in dentists. Br J Ind Med (1992 Nov) 49(11):782-90

7. Verschoor MA  Herber RF  Zielhuis RL   Urinary mercury levels and early changes in kidney function in   dentists and dental assistants.
8. Community Dent Oral Epidemiol (1988 Jun)

9. Moszczynski P  Moszczynski P   [Health damage due to exposure to mercury vapour (Hg)] Szkody zdrowotne wywolane narazeniem na pary rteci (Hg). Czas Stomatol (1989 Apr) 42(4):233-8

10. Visser H  Pieper K  Isemann M  Stalder K   [A prospective study on the incidence of mercury levels in dental   students. 2. Correlation analysis] Eine prospektive Untersuchung uber die Quecksilberbelastung von   Zahnmedizinstudenten. 2. Korrelationsanalysen. Dtsch Zahnarztl Z (1991 Aug) 46(8):555-7

11. Ott KH  Grimmeisen J  Alt F  Messerschmidt J  Tolg G   [Mercury in the hair of dentists and dental personnel]Quecksilber im Haar von zahnarztlichem Personal.  Dtsch Zahnarztl Z (1991 Feb) 46(2):154-8

12. Pieper K  Visser H  Isemann M  Stalder K   [Prospective study on the mercury uptake of dental students. Part 1:   Increase in mercury excretion during simulated training]  Eine prospektive Untersuchungen uber die

13. Quecksilberbelastung von   Zahnmedizinstudenten. Teil 1: Anstieg der Hg-Ausscheidung im Verlauf   des Phantomkurses.  Dtsch Zahnarztl Z (1989 Sep) 44(9):714-6

14. Kroncke A  Ott K  Petschelt A  Schaller KH  Szecsi M  Valentin H   [Mercury concentrations in blood and urine in persons with and   without amalgam fillings]  Uber die Quecksilberkonzentrationen in Blut und Urin von Personen mit   und ohne Amalgamfullungen.  Dtsch Zahnarztl Z (1980 Aug) 35(8):803-8

15. Kessel R  Bencze K  Hamm M  Sonnabend E   [Mercury concentrations in the air, in the blood and urine of   dentists in dental clinics and free practice]  Untersuchungen uber die Quecksilber-Konzentrationen in der Raumluft,   im Blut und im Urin bei zahnarztlicher Tatigkeit in Klinik und freier   Praxis.  Dtsch Zahnarztl Z (1980 Apr) 35(4):457-61

16. Mayer R   [Work-hygienic studies connected with the manipulation of silver-tin-   mercury alloys at the dentists working place]  Arbeitshygienische Untersuchungen bei der Verarbeitung von Silber-   Zinn-Quecksilberlegierungen am zahnarztlichen Arbeitsplatz Dtsch Zahnarztl Z (1975 Mar) 30(3):181-8

17. Urban P  Lukas E  Nerudova J  Cabelkova Z  Cikrt M   Neurological and electrophysiological examinations on three groups of   workers with different levels of exposure to mercury vapors. Eur J Neurol (1999 Sep) 6(5):571-7

18. Arenholt-Bindslev D   Environmental aspects of dental filling materials.  Eur J Oral Sci (1998 Apr) 106(2 Pt 2):713-20

19. Echeverria D  Aposhian HV  Woods JS  Heyer NJ  Aposhian MM  Bittner AC     Mahurin RK  Cianciola M  Bittner AC Jr   Neurobehavioral effects from exposure to dental amalgam Hg(o): new   distinctions between recent exposure and Hg body burden.  FASEB J (1998 Aug) 12(11):971-80

20. Nadorfy-Lopez E  Torres SH  Finol H  Mendez M  Bello B   Skeletal muscle abnormalities associated with occupational exposure   to mercury vapours. Histol Histopathol (2000 Jul) 15(3):673-82

21. Karahalil B  Rahravi H  Ertas N   Examination of urinary mercury levels in dentists in Turkey. Hum Exp Toxicol (2005 Aug) 24(8):383-8

22. Sikorski R  Juszkiewicz T  Paszkowski T  Szprengier-Juszkiewicz T   Women in dental surgeries: reproductive hazards in occupational   exposure to metallic mercury.  Int Arch Occup Environ Health (1987)

23. Fan PL  Arenholt-Bindslev D  Schmalz G  Halbach S  Berendsen H   Environmental issues in dentistry--mercury. FDI Commission.  Int Dent J (1997 Apr) 47(2):105-9

24. Newman SM   The relationship of metals to the general health of the patient, the   dentist and office staff.  Int Dent J (1986 Mar) 36(1):35-40

25. Steinberg D  Grauer F  Niv Y  Perlyte M  Kopolovic K   Mercury levels among dental personnel in Israel: a preliminary study.  Isr J Med Sci (1995 Jul) 31(7):428-32

26. Vandenberge J  Moodie AS  Keller RE  Keller RE Jr   Blood serum mercury test report.  J Am Dent Assoc (1977 Jun) 94(6):1155-7

27. White RR  Brandt RL   Development of mercury hypersensitivity among dental students.  J Am Dent Assoc (1976 Jun) 92(6):1204-7

28. Chang SB  Siew C  Gruninger SE   Examination of blood levels of mercurials in practicing dentists   using cold-vapor atomic absorption spectrometry.  J Anal Toxicol (1987 Jul-Aug) 11(4):149-53

29. Saengsirinavin C  Pringsulaka P   [Mercury levels in urine and head hair of dental personnel]  J Dent Assoc Thai (1988 Jul-Aug) 38(4):170-9

30. Langworth S  Sallsten G  Barregard L  Cynkier I  Lind ML  Soderman E   Exposure to mercury vapor and impact on health in the dental   profession in Sweden.  J Dent Res (1997 Jul) 76(7):1397-404

31. Chang SB  Siew C  Gruninger SE   Factors affecting blood mercury concentrations in practicing   dentists.  J Dent Res (1992 Jan) 71(1):66-74

32. Sutow EJ  Hall GC  MacLean CA   Effectiveness of wet and dry mercury vapour suppressant systems in a   faculty of dentistry clinic. J Oral Rehabil (2004 Aug) 31(8):822-6

33. Gonzalez-Ramirez D  Maiorino RM  Zuniga-Charles M  Xu Z  Hurlbut KM     Junco-Munoz P  Aposhian MM  Dart RC  Diaz Gama JH  Echeverria D     et al   Sodium 2,3-dimercaptopropane-1-sulfonate challenge test for mercury   in humans: II. Urinary mercury, porphyrins and neurobehavioral   changes of dental workers in Monterrey, Mexico. J Pharmacol Exp Ther (1995 Jan) 272(1):264-74

34. Eedy DJ  Burrows D  Clifford T  Fay A   Elevated T cell subpopulations in dental students.  J Prosthet Dent (1990 May) 63(5):593-6

35. Nimmo A  Werley MS  Martin JS  Tansy MF   Particulate inhalation during the removal of amalgam restorations.  J Prosthet Dent (1990 Feb) 63(2):228-33

36. Sinclair PM  Turner PR  Johns RB   Mercury levels in dental students and faculty measured by neutron   activation analysis.  J Prosthet Dent (1980 May) 43(5):581-5

37. Joshi A  Douglass CW  Kim HD  Joshipura KJ  Park MC  Rimm EB  Carino MJ     Garcia RI  Morris JS  Willett WC   The relationship between amalgam restorations and mercury levels in   male dentists and nondental health professionals.  J Public Health Dent (2003 Winter) 63(1):

38. Naleway C  Chou HN  Muller T  Dabney J  Roxe D  Siddiqui F   On-site screening for urinary Hg concentrations and correlation with   glomerular and renal tubular function.  J Public Health Dent (1991 Winter) 51(1):12-7

39. Cianciola ME  Echeverria D  Martin MD  Aposian HV  Woods JS   Epidemiologic assessment of measures used to indicate low-level   exposure to mercury vapor (Hg).  J Toxicol Environ Health (1997 Sep) 52(1):19-33

40. Woods JS  Martin MD  Naleway CA  Echeverria D   Urinary porphyrin profiles as a biomarker of mercury exposure:   studies on dentists with occupational exposure to mercury vapor.  J Toxicol Environ Health (1993 Oct-Nov) 40(2-3):235-46

41. Scarlett JM  Gutenmann WH  Lisk DJ   A study of mercury in the hair of dentists and dental-related   professionals in 1985 and subcohort comparison of 1972 and 1985   mercury hair levels.  J Toxicol Environ Health (1988) 25(3):373-81

42. Francis PC  Birge WJ  Roberts BL  Black JA   Mercury content of human hair: a survey of dental personnel.  J Toxicol Environ Health (1982 Oct-Nov) 10(4-5):667-72

43. Nylander M   Mercury in pituitary glands of dentists.  Lancet (1986 Feb 22) 1(8478):442

44. Shapiro IM  Cornblath DR  Sumner AJ  Uzzell B  Spitz LK  Ship II     Bloch P   Neurophysiological and neuropsychological function in mercury-exposed   dentists.  Lancet (1982 May 22) 1(8282):1147-50

45. Bloch P  Shapiro IM   An x-ray fluorescence technique to measure the mercury burden of   dentists in vivo.  Med Phys (1981 May-Jun) 8(3):308-11

46. Echeverria D  Heyer NJ  Martin MD  Naleway CA  Woods JS  Bittner AC     Bittner AC Jr   Behavioral effects of low-level exposure to elemental Hg among   dentists.  Neurotoxicol Teratol (1995 Mar-Apr)

47. Finkelstein Y  Vardi J  Kesten MM  Hod I   The enigma of parkinsonism in chronic borderline mercury   intoxication, resolved by challenge with penicillamine.  Neurotoxicology (1996 Spring) 17(1):291-5

48. Martin MD  Naleway C   The inhibition of mercury absorption by dietary ethanol in humans:   cross-sectional and case-control studies.  Occup Environ Med (2004 Feb) 61(2):e8

49. Ritchie KA  Gilmour WH  Macdonald EB  Burke FJ  McGowan DA  Dale IM     Hammersley R  Hamilton RM  Binnie V  Collington D   Health and neuropsychological functioning of dentists exposed to   mercury.  Occup Environ Med (2002 May) 59(5):287-93

50. Echeverria D   Mercury and dentists.  Occup Environ Med (2002 May) 59(5):285-6

51. Atesagaoglu A  Omurlu H  Ozcagli E  Sardas S  Ertas N   Mercury exposure in dental practice.  Oper Dent (2006 Nov-Dec) 31(6):666-9

52. Lehto T  Alanen P  Ronnemaa T  Helenius H  Kallio V   Urinary mercury concentrations in Finnish dentists.  Proc Finn Dent Soc (1989) 85(3):177-85
53. .
54. Brune D  Hensten-Pettersen A  Beltesbrekke H   Exposure to mercury and silver during removal of amalgam restorations. Scand J Dent Res (1980 Oct) 88(5):460-3

55. Skare I  Bergstrom T  Engqvist A  Weiner JA   Mercury exposure of different origins among dentists and dental   nurses. Scand J Work Environ Health (1990 Oct)

56. Nilsson B  Gerhardsson L  Nordberg GF   Urine mercury levels and associated symptoms in dental personnel.  Sci Total Environ (1990 May 15) 94(3):179-85

57. Skare I  Engqvist A   Urinary mercury clearance of dental personnel after a longterm   intermission in occupational exposure.  Swed Dent J (1990) 14(6):255-9

58. Nylander M  Friberg L  Eggleston D  Bjorkman L   Mercury accumulation in tissues from dental staff and controls in   relation to exposure.  Swed Dent J (1989) 13(6):235-43

59. Nilsson B  Nilsson B   Mercury in dental practice. II. Urinary mercury excretion in dental   personnel.  Swed Dent J (1986) 10(6):221-32

60. Kim DE  Song KB  Kim YJ   [Mercury contents in hair of dental personnel and evaluation of   various agents suppressing mercury vaporization]  Taehan Chikkwa Uisa Hyophoe Chi (1989 Jul)

61. Heyer NJ  Echeverria D  Bittner AC  Farin FM  Garabedian CC  Woods JS   Chronic low-level mercury exposure, BDNF polymorphism, and   associations with self-reported symptoms and mood.  Toxicol Sci (2004 Oct) 81(2):354-63

62. Zander D  Ewers U  Freier I  Brockhaus A   [Mercury exposure of the population. IV. Mercury exposure of male   dentists, female dentists and dental aides]  Untersuchungen zur Quecksilberbelastung der Bevolkerung. IV.   Quecksilberbelastung von Zahnarzten, Zahnarztinnen und   Zahnarzthelferinnen.   Zentralbl Hyg Umweltmed (1992 Dec) 193(4):318-28

63. Vimy MJ  Takahashi Y  Lorscheider FL Am J Physiol (1990 Apr) 258(4 Pt 2):R939-45

64. Hahn LJ  Kloiber R  Leininger RW  Vimy MJ  Lorscheider FL.   FASEB J (1990 Nov) 4(14):3256-60

65. Koos, Longo . Am J Obstet Gynecol., 1976: 126; 390-409

66. Koos, B.J. and Longo, L.D.: Mercury Toxicity in the Pregnant Woman, Fetus and Newborn Infant.   Am. J. Obstet. Gynecol. 12d, 390, 1970.

67. Warfvinge, K; Hua, J; Logdberg, B. Mercury distribution in Cortical Areas and Fiber Systems of the Neonatal and Maternal Adult Cerebrum After Exposure of Pregnant Squirrel Monkeys to Mercury Vapour. EnvironRes. 67(2):196-208,Nov 1994.

68. Takahashi, Y; Tsuruta, S; Hasegawa, J; Kameyama, Y.: Number of Amalgam Fillings in Pregnant Rats and Mercury Concentration in Their Fetuses. J Dent Res. 71(SI):571. A-445. 1992.

69. Khera et al., Teratogenic and genetic effects of mercury toxicity. The biochemistry of Mercury in the environment. Nriagu, J.O.Ed Amsterdam Elsevier, 503-18,1979

70. Babich et al ., The mediation of mutagenicity and clastogenicity of heavy metals by physio chemical factors. Environ Res., 1985:37;253-286

71. Hansen K et al A survey of metal induced mutagenicity in vitro and in vivo J Amer Coll Toxicol ., 1984:3;381-430

72. Verchaeve L et al., Comparative in vitro cytogenetic studies in mercury exposed human lymphocytes Mutation Res., 1985:157;221-226.

73. PelletierL et al., In - vivo self reactivity of mononuclear cells to T cells and macrophages exposed to HgCl2 Eur. J Immune., 1985: 460-465

74. Veron et al Amalgam Dentaires et allergies J Biol Buccale., 1986 : 14; 83-100

75. NouyeM., Murao K., Kajiwara Y., Behavorial and neuropathological effects of prenatal methyl mercury exposure in mice. Neurobeahv.Toxicol Teratol. ,1985:7;227-232

 

 

[JADA  Vol. 122  August 1991  By Irwin Mandel DDS Assoc. Dean for Research School of Dental and Oral Surgery Colombia University New York]

[Nylander et al.Fourth international symposium Epidemiology  in Occupational Health.,Como Italy Sept 1985]

 

Mercury in the Environment

Many of us have over the years been caught up in a debate about the virtues of dental amalgam as a filing material.  Books have been written and many a fight has been had.  I too was caught up in this fantasy argument for many years, before realizing that dental amalgam is NOT the issue – mercury is. 

The total amount of mercury in dental amalgam sold in the U.S. during the calendar year 2001, as reported to the IMERC member states, was 61,409 pounds or 30.7 tons.

The issue is not the amalgam - The issue is the mercury in the amalgam.  Mercury is the single problem.  Mercury is banned everywhere except the mouth. 

Dental amalgam is considered to be toxic waste
except in the mouth
of a living human being.

In the Best Management Practices for Scrap Dental Amalgam 2001, set out by the Florida Department of Environmental Protection we are told:

“There are three sources of scrap amalgam from dental operations:

• Excess amalgam which is mixed, but not used; dam­aged capsules.
• Amalgam from the operatory. This can be unused mixed amalgam or amalgam retrieved from operatory drain traps. Amalgam from operatory drain traps can be handled as scrap amalgam as long as the traps contain little or no tissue.
• Amalgam contained in extracted teeth. Extracted teeth that have no amalgam would be regulated as medical waste and cannot be placed in the same container as extracted teeth with amalgam.”

The environmental impact of mercury contamination is well known.  
The disasters of mercury poisoning in Minamata Bay and Iraq are two examples.  From 1932 to 1968, Chisso Corporation, a company located in Kumamoto Japan, dumped an estimated 27 tons of mercury compounds into Minamata Bay. Kumamoto is a small town about 570 miles southwest of Tokyo.  The town consists of mostly farmers and fisherman.  When Chisso Corporation dumped this massive amount of mercury into the bay, thousands of people whose normal diet included fish from the bay, unexpectedly developed symptoms of methyl mercury poisoning.  The illness became known as the "Minamata Disease".  The mercury poisoning resulted from years of environmental destruction and neglect from Chisso Corporation.

“In the early 1970's a major methyl mercury-poisoning catastrophe occurred in which an estimated 10,000 people died and 100,000 were severely and permanently brain damaged. Saddam's regime was largely successful in suppressing information about the event.
The problem began in the late 1960's and early 1970's, when Iraq experienced a series of abysmal harvests. Since the "green revolution" was beginning, Iraq imported "wonder wheat" from Mexico. The risk was that the seed might grow moldy during the long, humid ocean transport to Iraq if it was not dressed with some fungicide. Methyl mercury became the most cost-effective fungicide, because it had recently been banned in Scandinavia and several American states due to environmental and toxicological risks. So the world market was flooded and prices dropped.

The crisis did provide doctors with some greater understanding of how to detect methyl mercury poisoning. "Quiet baby syndrome," for example, when mothers praise their babies for never crying, is now considered a warning sign for methyl mercury-induced brain damage in children.”

Some readers may remember the days of the good old mercury thermometers, which found their way into many of our body spaces.  Cases of people dying after thermometer breakages in the mouth are well documented.  If one of these thermometers were to break in an average sized hospital ward, the ward would have to be evacuated and decontaminated.  No wonder they were replaced with alcohol and electronic thermometers. 

At one stage mercury was added to wall paint to prevent the build up of fungus and mould.  They were soon taken off the market as it was found that they released levels of only 2 micrograms of mercury vapour per cubic meter.  Remember that the mouth will have levels of 30 – 150 mcg/m3.

Amalgam in the teeth of dead humans is considered toxic waste as the amalgam leaks mercury into the environment and crematoria chimneys spew out mercury at a rate of about 11 kg per chimney per year. , , ,  Do not live downwind from a crematorium.  Dead people are dangerous. 

In fact in July 2007 Reuters News agency reported;

Amalgam waste is the biggest source of mercury in EU waste water and dental use also leads to the widespread dispersal of mercury into the atmosphere from cremation.

In the UK dental amalgam and mercury from laboratory and medical devices, account for about 53 percent of total mercury emissions and annually 7.41 tons of mercury from amalgam are discharged to the sewer, atmosphere or land.

From the BBC – 10 January 2005 we read

“Strict rules for crematoria to limit mercury pollution caused when tooth fillings are vaporized have been announced by ministers.

The industry has been told mercury filtering equipment must be fitted at crematoria by 2012 to halve emissions.

Exposure to the metal is linked to damage to the brain, nervous system and fertility with crematoria responsible for 16% of the UK's mercury pollution.

…the government defended the new rules, saying that unless action was taken mercury emissions would rise by two-thirds by 2020.

… Environment Minister Larry Whitty said: "By 2020, crematoria will be by far the biggest single contributor to mercury emissions in this country.”

Mercury from dental amalgam in dead people’s mouths is vaporized during cremation and currently produces 16% of all mercury pollution in the UK.  This is toxic waste at its best.  When in a mouth that is attached to a living person it is a filling.  16% is an astronomical figure! 

To potentially be the single greatest source of mercury pollution in the English environment is beyond comprehension. 

The British Dental Journal makes the following comment;

Mercury emissions clampdown announced

Measures to cut by half the amount of toxic mercury which crematoria release into the atmosphere were announced by the government recently.
According to the Department for Environment, Food and Rural Affairs, crematoria are estimated to be responsible for up to 16 percent of all UK emissions of mercury, from fillings in teeth. Mercury emissions are predicted to rise by two-thirds by 2020 unless action is taken.
The new government statutory guidance means that all crematoria should install equipment to cut mercury emissions by 50 percent by 2012.
New crematoria should be fitted with mercury control equipment, but those conducting fewer than 750 cremations a year have until 2012 to meet the new requirements.
Other countries including Austria, Belgium, Germany, Holland, Norway, Sweden and Switzerland have taken steps to regulate mercury emissions from crematoria.
Britain has also signed up to an international treaty, the UN Heavy Metals Protocol, which aims to cut down on emissions of harmful metals, including mercury, and has already achieved one of its obligations by reducing emissions of mercury below 1990 levels, from 316 tonnes, to 8 tonnes in 2002.
Mercury, which accumulates in the air and in water, can harm the brain, kidneys, nervous system and unborn children.

It would be much cheaper just to ban the use of amalgam instead of promulgating the poisoning of the planet.  8 tonnes of mercury going into the atmosphere from Britain alone in just one year is inconceivable.  316 tonnes is simply rude.  The best way to stop polluting the earth is to stop polluting the earth.  If dental associations continue to ignore this issue than it must surely be time for governments to legislate.  We must stop polluting the environment that we live in and also the environment inside of us.

It is interesting to browse the world wide web on a search for “crematoria mercury”  - you will see the huge opposition to living close to crematoria.  Local citizen groups are up in arms, refusing to allow a crematorium to be built in Contra Costa County, reports the San Francisco Chronicle in 2006;

The Richmond neighbors say they've had enough industrial development. And they especially don't want a crematorium, which emits mercury from the dental fillings of burning bodies -- in this case, about 3 pounds of mercury a year from 3,000 to 4,000 bodies.
"We don't want dead bodies spewing over our community. What goes up must come down, and we don't want to be breathing it in," … "It's unacceptable, period."

In the Mercola website we read; “Researchers in Northampton have discovered that crematorium workers have twice the level of normal mercury contamination in their bodies.”

“78% of American adults have dental fillings. If there are 200 million American adults that would mean that .78 x 200,000,000 would give us 156 million American adults with dental fillings. If the average American adult has 8 fillings with 800 mg. of amalgam that gives us 3.2 grams of mercury (amalgams are 50% mercury) in their fillings per American adult. 3.2 g x 28g/oz x 156 million = 17,828,571 ounces of mercury x 1/16 (ounces per pound) = 1,114,286 pounds of mercury or 557 tons of mercury stored in our mouths.
This appears to be a much bigger problem than the mercury from the burning of coal.”

Dental offices contribute between 12,000 and 50,000 pounds of mercury to waste water each year in the USA.

Another paper puts a tentative monetary value on Hg polluted food sources in the Arctic, where local, significant pollution sources are limited, and relates this to costs for strategies avoiding Hg pollution …

The cases we studied are relevant for point pollution sources globally and their remediation costs ranged between 2,500 and 1.1 million US dollars kg(-1) Hg isolated from the biosphere. Therefore, regulations discontinuing mercury uses combined with extensive flue gas cleaning for all power plants and waste incinerators is cost effective.

Currently the Australian Dental Association display an interesting position on their website.   It is a paper which they have published in their own journal entitled “The environmental effects of dental amalgam.

The final paragraph states;

“The problem of environmental mercury contamination will not be solved by banning amalgam.  As medical professionals, we should consider the various possibilities that can satisfy both the application of dental amalgam as a restorative material as well as minimizing the environmental effects.  Tackling this problem by the application of simple guidelines for mercury waste handling will reduce the environmental concerns of dental waste to an insignificant level without compromising dental amalgam’s important role in dentistry.”

Clearly these comments do NOT reflect the reality.  Mercury is mercury is mercury!  There are NO safe levels of mercury.  The rest of the world is seriously concerned by the environmental effects of mercury from amalgam.  It appears that the dental associations have NO concern for the environment or our health!

 

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Central Nervous System Diseases and Mercury Exposure

Mercury vapor inhalation inhibits binding of GTP to tubulin in rat brain: similarity to a molecular lesion in Alzheimer diseased brain. Pendergrass JC, Haley BE, Vimy MJ, Winfield SA, Lorscheider FL Neurotoxicology 1997;18(2):315-324

Hg2+ interacts with brain tubulin and disassembles microtubules that maintain neurite structure. Since it is well known that Hg vapor (Hg0) is continuously released from "silver" amalgam tooth fillings and is absorbed into brain, rats were exposed to Hg0 4h/day for 0, 2, 7, 14 and 28 d at 250 or 300 micrograms Hg/m3 air, concentrations present in mouth air of some humans with many amalgam fillings. Average rat brain Hg concentrations increased significantly (11-47 fold) with duration of Hg0 exposure. By 14 d Hg0 exposure, photoaffinity labelling on the beta-subunit of the tubulin dimer with [alpha 32P] 8N3 GTP in brain homogenates was decreased 41-74%, upon analysis of SDS-PAGE autoradiograms. The identical neurochemical lesion of similar or greater magnitude is evident in Alzheimer brain homogenates from approximately 80% of patients, when compared to human age-matched neurological controls. Total tubulin protein levels remained relatively unchanged between Hg0 exposed rat brains and controls, and between Alzheimer brains and controls. Since the rate of tubulin polymerization is dependent upon binding of GTP to tubulin dimers, we conclude that chronic inhalation of low-level Hg0 can inhibit polymerization of brain tubulin essential for formation of microtubules.

Metals and trace elements in plasma and cerebrospinal fluid in normal aging and Alzheimer's disease. Basun H, Forssell LG, Wetterberg L, Winblad B J Neural Transm Park Dis Dement Sect 1991;3(4):231-258

Cerebro-spinal fluid (CSF) and blood levels of aluminium, cadmium, calcium, copper, lead, magnesium, and mercury were studied in 24 subjects with dementia of the Alzheimer type (DAT) and in 28 healthy volunteers. Furthermore, arsenic, bromine, chrome, iron, manganese, nickel, rubidium, selenium, strontium, and zinc were measured only in blood. There were significant changes in the DAT group when compared to the controls. The plasma levels of aluminium, cadmium, mercury and selenium were increased and the contents of iron and manganese were lower in the DAT group as compared to control subjects. In CSF there were low levels of cadmium and calcium and increased content of copper in DAT cases. Iron and zinc levels in blood and calcium in both blood and CSF of DAT patients correlated with memory and cognitive functions. Iron, manganese and strontium levels of DAT sufferers in blood and aluminium in CSF were related with changes in behaviour.

Long-term mercury excretion in urine after removal of amalgam fillings.Begerow J, Zander D, Freier I, Dunemann L Int Arch Occup Environ Health 1994;66(3):209-212

The long-term urinary mercury excretion was determined in 17 28- to 55-year-old persons before and at varying times (up to 14 months) after removal of all (4-24) dental amalgam fillings. Before removal the urinary mercury excretion correlated with the number of amalgam fillings. In the immediate post-removal phase (up to 6 days after removal) a mean increase of 30% was observed. Within 12 months the geometric mean of the mercury excretion was reduced by a factor of 5 from 1.44 micrograms/g (range: 0.57-4.38 micrograms/g) to 0.36 microgram/g (range: 0.13-0.88 microgram/g). After cessation of exposure to dental amalgam the mean half-life was 95 days. These results show that the release of mercury from dental amalgam contributes predominantly to the mercury exposure of non-occupationally exposed persons. The exposure from amalgam fillings thus exceeds the exposure from food, air and beverages. Within 12 months after removal of all amalgam fillings the participants showed substantially lower urinary mercury levels which were comparable to those found in subjects who have never had dental amalgam fillings. A relationship between the urinary mercury excretion and adverse effects was not found. Differences in the frequency of effects between the pre- and the post-removal phase were not observed.

Mercury concentration in the mouth mucosa of patients with amalgam fillings.[Article in German] Willershausen-Zonnchen B, Zimmermann M, Defregger A, Schramel P, Hamm G Dtsch Med Wochenschr 1992 Nov 13;117(46):1743-1747

Mercury concentrations were measured in specimens of oral mucosa taken during oral surgery from 90 patients (53 men, 37 women, mean age 42 +/- 16 years); 30 of the patients had no amalgam fillings. All the mucosal specimens extended for at least 2-3 mm from the epithelium of the gingival margin and were clinically and radiologically normal. Thirteen patients without metallic fillings of any kind had mercury concentrations of 118.4 +/- 83.7 ng/g tissue, and in 17 patients with precious metal fillings but no amalgam the mean mercury concentrations were 144 +/- 290 ng/g tissue. Seventeen patients with 1-3 amalgam fillings had an average of 1975 +/- 4300 ng/g tissue and in 26 patients with 3-6 amalgam fillings the average concentration was 1158 +/- 2500 ng/g tissue. In 17 patients with more than six amalgam fillings the mean mercury concentration was 2302 +/- 5600 ng/g tissue. Although these results demonstrate a considerable degree of transfer of mercury from the amalgam fillings to the oral mucosa, it had not resulted in any clinically detectable mucosal lesions.

Quantitation of total mercury vapor released during dental procedures. Engle JH, Ferracane JL, Wichmann J, Okabe T Dent Mater 1992 May;8(3):176-180

An in vitro method is described in which measurements were made of the total amount of mercury vapor released from three types of amalgam during routine dental procedures. It was found that the greatest amount of mercury was released during dry polishing of one amalgam (44 micrograms). Removal of amalgam from a Class I cavity under water spray and high volume evacuation also generated large amounts of mercury as expected (15-20 micrograms). However, under the more clinically relevant conditions of extending evacuation for one minute to remove residual amalgam and mercury after cutting, this value was reduced by approximately 90%. The total amount of mercury generated during placement (6-8 micrograms), wet polishing (2-4 micrograms) and trituration (1-2 micrograms) were also measured. The study showed that dental procedures associated with amalgam do potentially expose the patient and operator to mercury vapor. However, the total amount of mercury released during any procedure was far below the total exposure level calculated from the daily threshold limits established by regulatory agencies for occupational exposure.

The relationship between mercury from dental amalgam and mental health. Siblerud, Robert L American Journal of Psychotherapy, Oct 1989 v43 n4 p575(13)

In the last century, hat makers who were exposed to mercuric nitrate often exhibited symptoms of mental illness, which included irritability, excitability, and shyness, earning them the name ''Mad Hatters.'' Since that time, the relationship between mercury toxicity and health problems, both physical and mental, has been well documented. Dental amalgam, or ''silver fillings,'' is used to fill 80 percent of the dental cavities in the world. This substance contains up to 50 percent mercury. Thus, it was hypothesized that there may be a relationship between dental fillings and mental health. It was also theorized that mercury in this form may enter the brain in cumulatively toxic levels through inhalation and by absorption into the cranial veins. One hundred one subjects were studied to determine the relationship between the presence of mercury amalgam fillings and mental health status. Half of the group had amalgam, while 51 had no fillings. The hair and urine of the subjects was monitored for the presence of mercury, and the subjects were given two questionnaires regarding levels of stress tolerance, physical health, and emotional or psychological symptoms such as anger or depression. Those in the amalgam group were found to have twice as much mercury in their urine and 26.5 percent more in their hair samples as the nonamalgam group. In addition, the subjects with fillings rated their reading comprehension significantly lower, and had significantly more episodes of sudden anger, depression, and irritability. In a separate, uncontrolled questionnaire given to dental patients who had their fillings removed, 67 percent claimed to have improved psychological status. Mercury has been related to stress, fatigue, premenstrual syndrome, and loss of short term memory. It is recommended that psychotherapists consider the possibility of mercury toxicity as a causative factor in disorders ranging from mild stress-related complaints to schizophrenia. (Consumer Summary produced by Reliance Medical Information, Inc.)

Regional brain trace-element studies in Alzheimer's disease. Thompson CM Markesbery WR Ehmann WD Mao YX Vance DE Neurotoxicology (1988 Spring) 9(1):1-7

Alzheimer's disease (AD) brain trace-element imbalances in the amygdala, hippocampus and nucleus basalis of Meynert (nbM) are found in most cases to be consistent with those previously reported in samples derived principally from AD cerebral cortex (Ehmann et al., 1986). The elevation of mercury in AD nbM, as compared to age-matched controls, is the largest trace-element imbalance observed to date in AD brain. In addition to the general confirmation of imbalances for Cs, Hg, N, Na, P, and Rb noted previously in cerebral cortex samples, imbalances for Fe, K, Sc, and Zn were observed in two regions and one region also exhibited imbalances for both Co and Se. Persistent imbalances for the univalent cations Na, K, Rb and Cs support arguments for a membrane abnormality in AD. The data presented here also provide the first comprehensive simultaneous multi-element determinations in both control and AD nbM.

Mercury accumulation in tissues from dental staff and controls in relation to exposure. Nylander M Friberg L Eggleston D Bjorkman L Swed Dent J (1989) 13(6):235-43

Samples, mainly from occipital cortex and pituitary gland, but also from rental cortex, olfactory bulbs, thyroid gland and liver were collected from autopsies of 8 dental staff cases and 27 controls. These samples were analysed for total mercury content using radiochemical neutron activation analyses. The results revealed high mercury concentrations (median 815, range 135-4,040 micrograms Hg/kg wet weight) in pituitaries from the dental staff cases compared to controls (N = 23, median 23 range 6-1, 170 micrograms Hg/kg). In occipital cortex, the cases had a median of 17, range of 4-300 micrograms Hg/kg and the controls (N = 20) had a median of 10, range 2-29 micrograms Hg/kg. A few samples from olfactory bulbs show low mercury concentrations for both cases and controls. Renal cortex was analysed from three cases and contained clearly higher concentrations (945, 1,545, 2,110 micrograms Hg/kg) compared to controls (N = 12, median 180, range 21-810 micrograms Hg/kg). There is no control material for the other analysed samples, but one thyroid sample had an extremely high concentration of 28,000 micrograms Hg/kg.

Mercury concentrations in the human brain and kidneys in relation to exposure from dental amalgam fillings. Nylander M Friberg L Lind B Swed Dent J (1987) 11(5):179-87

Samples from the central nervous system (occipital lobe cortex, cerebellar cortex and ganglia semilunare) and kidney cortex were collected from autopsies and analysed for total mercury content using neutron activation analyses. Results from 34 individuals showed a statistically significant regression between the number of tooth surfaces containing amalgam and concentration of mercury in the occipital lobe cortex (mean 10.9, range 2.4-28.7 ng Hg/g wet weight). The regression equation y = 7.2 + 0.24x has a 95% confidence interval for the regression coefficient of 0.11-0.37. In 9 cases with suspected alcohol abuse mercury levels in the occipital lobe were, in most cases, somewhat lower than expected based on the regression line. The observations may be explained by an inhibition of oxidation of mercury vapour. The regression between amalgams and mercury levels remained after exclusion of these cases. The kidney cortex from 7 amalgam carriers (mean 433, range 48-810 ng Hg/g wet weight) showed on average a significantly higher mercury level than those of 5 amalgam-free individuals (mean 49, range 21-105 ng Hg/g wet weight). In 6 cases analysis of both inorganic and total mercury was carried out. A high proportion (mean 77% SD 17%) of inorganic mercury was found. It is concluded that the cause of the association between amalgam load and accumulation of mercury in tissues is the release of mercury vapour from amalgam fillings.

Could Mercury Fillings Influence Manic Depression? Journal of Orthomolecular Medicine (1998) 13:31

Amalgam fillings, which contain mercury, a potent neurotoxin, have become increasingly controversial in recent years. Most dentists insist that amalgam is safe, but a small group of self-styled "nontoxic" dentists claim that amalgam is harmful. A new study hints that amalgam fillings may play a role in bipolar disorder.

The researchers studied 20 men and women with manic depression. Eleven chose to have their amalgam fillings removed and replaced with ceramic fillings. The nine others opted to have either real or placebo plastic sealants placed over their fillings.

Before the study and eight months after the amalgam removal or sealant placement, the participants had their bipolar symptoms assessed using standard psychological tests. Compared with both sealant groups, the amalgam-removal group registered significant symptom improvement.

The researchers concluded that amalgam fillings may play a role in manic depression, and urged additional studies to clarify what is certain to be a controversial finding.

Cognitive Deficit in 7-Year-Old Children With Prenatal Exposure to Methylmercury.” Grandjean, P; Weihe, P; White, RF; Debes, F; Araki, S; Yokoyama, I; Murata, K; Sorensen, N; Dahl, R; Jorgensen, PJ. Neurotoxicol Teratol., 19(6):417-28, Nov-Dec 1997.

ABSTRACT: A cohort of 1022 consecutive singleton births was generated during 1986-1987 in the Faroe Islands. Increased methyl mercury exposure from maternal consumption of pilot whale meat was indicated by mercury concentrations in cord blood and maternal hair.

At approximately 7 years of age, 917 of the children underwent detailed neurobehavioural examination. Neuropsychological tests included Finger Tapping; Hand-Eye Coordination; reaction time on a Continuous Performance Test; Wechsler Intelligence Scale for Children-Revised Digit Spans, Similarities, and Block Designs; Bender Visual Motor Gestalt Test; Boston Naming Test; and California Verbal Learning Test (children).

Clinical examination and neurophysiological testing did not reveal any clear cut mercury related abnormalities. However, mercury related neuropsychological dysfunctions were most pronounced in the domains of language, attention, and memory, and to a lesser extent in visuospatial and motor functions. These associations remained after adjustment for covariates and after exclusion of children with maternal hair mercury concentrations above 10 micrograms (50 nmol/g).

The effects on brain function associated with prenatal methyl mercury exposure therefore appear widespread, and early dysfunction is detectable at exposure levels currently considered safe.

Bio Probe COMMENT: This publication of the widely discussed Faroe Islands study should have dramatic impact on evaluation of mercury exposure to unborn babies. Obviously, the adverse effect is not detectable at birth, and shows a dramatic impact on quality of life for the affected individuals. It should be kept in mind that methyl mercury and mercury vapour are the two forms of mercury that readily penetrate cell membranes and accumulate in tissues of unborn babies. Methyl mercury is derived primarily from consumption of fish and seafood, whereas the primary contributor of mercury vapour to human body burdens comes from dental fillings.

Increased blood mercury levels in patients with Alzheimer's disease. Hock C, Drasch G, Golombowski S, Muller-Spahn F, Willershausen-Zonnchen B, Schwarz P, Hock, U, Growdon JH, Nitsch RM J Neural Transm 1998;105(1):59-68

Alzheimer's disease (AD) is a common neurodegenerative disorder that leads to dementia and death. In addition to several genetic parameters, various environmental factors may influence the risk of getting AD. In order to test whether blood levels of the heavy metal mercury are increased in AD, we measured blood mercury concentrations in AD patients (n = 33), and compared them to age-matched control patients with major depression (MD) (n = 45), as well as to an additional control group of patients with various non-psychiatric disorders (n = 65). Blood mercury levels were more than two-fold higher in AD patients as compared to both control groups (p = 0.0005, and p = 0.0000, respectively). In early onset AD patients (n = 13), blood mercury levels were almost three-fold higher as compared to controls (p = 0.0002, and p = 0.0000, respectively). These increases were unrelated to the patients' dental status. Linear regression analysis of blood mercury concentrations and CSF levels of amyloid beta-peptide (A beta) revealed a significant correlation of these measures in AD patients (n = 15, r = 0.7440, p = 0.0015, Pearson type of correlation). These results demonstrate elevated blood levels of mercury in AD, and they suggest that this increase of mercury levels is associated with high CSF levels of A beta, whereas tau levels were unrelated. Possible explanations of increased blood mercury levels in AD include yet unidentified environmental sources or release from brain tissue with the advance in neuronal death.

Motor neuron uptake of low dose inorganic mercury. Pamphlett R Waley P J Neurol Sci (1996 Jan) 135(1):63-7

In animals, inorganic mercury can bypass the blood brain barrier and enter motor neurons. We sought to determine the lowest injected dose of mercury that could be detected in mouse motor neurons. Mice were injected intraperitoneally with mercuric chloride in doses from 0.05 to 2 micrograms/g body weight and studied between 5 days and 18 months after injection. After formalin fixation, 7 microns sections of cerebrum, cerebellum, brain stem, spinal cord and kidney were stained with silver nitrate autometallography. Five days after injection, mercury granules were detected at doses from 0.2 microgram/g upwards in the cell bodies of spinal and brain stem motor neurons, more granules being seen at the higher doses. Mercury granules were also seen in 5% of posterior root ganglion neurons. At doses from 0.05 microgram/g upwards mercury was detected 5 days later in renal tubule cells. Mercury was still present in motor neurons 6- 11 months after injection, but by this time mercury had been cleared from the kidneys. Low doses of inorganic mercury are therefore selectively taken up and retained by motor neurons, making this neurotoxin a good candidate for a cause of sporadic motor neuron disease.

Recovery from Amyotrophic Lateral Sclerosis and from Allergy after Removal of Dental Amalgam Fillings. Redhe, O; Pleva, J. J. Risk Safety Medicine. (1994): 4, 229-236.

An evaluation of 100 cases of poisoning and immunological effects in dental amalgam patients, documented in clinical practice. The patient had suffered for a long period from neurological problems. In 1984, following a complete neurologic evaluation, a diagnosis of amyotrophic lateral sclerosis (ALS) was made at the department of neurology of the University Hospital in Umea, Sweden. It is of unknown etiology and considered to be 100% fatal. No further visit to the clinic was proposed, as the disease is pernicious and there is no known therapy for ALS.

A dentist recognised the symptoms as those familiar in the patient group with health problems attributable to dental amalgam fillings. Patient history revealed the onset or exacerbation of neurologic symptoms following placement of amalgam dental fillings. The patient had 34 tooth surfaces filled with amalgam, most of which were shallow and of moderate extent.

With the consent of the patient, all amalgams were removed and replaced with alternative material. Treatment was completed in March 1984. Removal of the amalgam in the first tooth that had originally given post-operative problems resulted in an exacerbation of symptoms, with a continued recurrence of exacerbation following each subsequent replacement.

Following the replacement of the last DA, the patient's entire condition rapidly improved. Six weeks following the final replacement, the patient was able to go up stairs without experiencing back pain. Pains in the mouth also receded and the sore throat, present during the whole history of the disorder, recovered. Five months after completion of the DA removal , the patient returned to the same University Hospital at Umea for a week- long follow-up investigation, after which the following notation was placed in her record: "The neurologic status is completely without comment . Hence, the patient does not show any motor neuron disease of type ALS. She has been informed that she is in neurological respect fully healthy."

Recovery from amyotrophic lateral sclerosis and from allergy after removal of dental amalgam fillings. Redhe O & Pleva J Int J Risk & Safety in Med 4:229-236 (1994)

CITATION FROM THE TEXT FOLLOWS: "...Five months after the completion of DA removal (29 August 1984) the patient was called for a week-long investigation at the same University clinic where the diagnosis ALS had been made. She felt now extraordinarily healthy and her health status was also confirmed by the words in her record: "The neurologic status is completely without comment. Hence, the patient does not show any motor neuron disease of type ALS. She has been informed that she is in neurological respect fully healthy." ...At the time of writing (early 1993), 9 years have elapsed since removal of the DA fillings, and the patient continues to enjoy good health ... "

Metallothionein in ALS Motor Neurons. Kasarskis, EJ. FEDRIP Database, National Technical Information Service (NTIS).

ABSTRACT: Amyotrophic Lateral Sclerosis (ALS) is a chronic neurodegenerative disease, recognized clinically by its relentless progression of muscle atrophy, weakness, and eventual fatal outcome due to respiratory insufficiency. The illness has no effective treatment. The pathological hallmark of ALS is a selective death of motor neurons in the spinal cord and motor cortex. These features of ALS, however, fail to provide insight into its etiology with the result that several theories of etiopathogenesis have been advanced.

Our research focus is upon the potential involvement of toxic trace metals in causing the death of motor neurons. Heretofore, studies of toxic metals have only considered the possibility of excessive accumulation of a metal in the brain and spinal cord. Our work advanced the notion that mercury is present to excess in ALS patients when compared to age-matched controls based on a multi-element analytical study using neutron activation analysis of several types of tissue. Further studies have suggested that mercury may be localized within spinal motor neurons using photoemulsion histochemistry. Thus it appears that mercury accumulates within the very cells which degenerate in ALS, suggesting that mercury may be a necessary precondition for ALS-type degeneration to occur.

OBJECTIVE: To investigate one aspect of mercury detoxification in ALS. As a prelude, we have ascertained the distribution of metallothionein (MT) in spinal cord by immunocytochemical methods using a polyclonal antibody to a defined epitope present in all forms of human MT. The Mts are a family of structurallysimilar, soluble, cysteine-rich, 6-7 kD proteins which detoxify heavy metals by sequestration and also regulate copper and zinc homeostasis.

In control subjects, we found MT immunoreactivity localized to the nucleus, cytoplasm, and axonal extensions of spinal motor neurons. In ALS spinal motor neurons, MT immunoreactivity was absent (or greatly reduced) in the nucleus. These findings open the possibility that abnormalities of MT may be involved in the pathogenesis of ALS. According to this formulation, MT may be structurally altered in ALS, greatly reduced in amount, or diverted from its normal nuclear localization as a result of toxic metal exposure.

PLAN and METHODS: The overall goal of this study is to isolate and sequence the Mts from the spinal cord of controls and compare the results to ALS patients to determine if Mts are altered in composition in ALS. The issue is a complicated one because: a) 6 MT isoforms have been sequenced from human tissues; b) 11 separate, but closely-related MT genes have been found; and c) MT has not been characterized from human spinal cord. To date, we have partially purified MT from bulk samples of control human spinal cord. Methods are in place to complete the purification of MT isoforms and determine their sequence.

After dissection of the anterior horn region and subcellular fractionation, we propose to isolate and identify the nuclear-associated MT isoform in control spinal cord. Strategies have been developed to deal with collateral issues such as the newly described MT-related protein, GIF. Guided by the results in controls, we will isolate the nuclear-associated MT(s) from ALS spinal cord. As a final test of the hypothesis, we will compare MT isoforms in motor cortex, the other region in which motor neuron degeneration occurs in ALS.

The results of these studies will evaluate the hypothesis that MT is altered in ALS . Finding an abnormality in MT would give considerable support to the concept tnat toxic metals are involved in the patnogenesis of ALS.

LOU GEHRIG'S DISEASE (ALS) THE MERCURY CONNECTION! BIOPROBE VOLUME 9 Issue 5 Sept. 1993

It cannot yet be said that mercury has been absolutely proven to be a causative factor in the development of ALS (Amyotrophic Lateral Sclerosis; " Lou Gehrig's Disease"); but recently published research definitely points to that probability.

As early as the mid 1950's, it had been established that the clinical features of chronic mercury intoxication at times mimic motor neuron disease. Subsequently, a number of case studies of ALS-like neuropathies caused by various forms of mercury have been documented.

Recent studies from the Departments of Neurology, Chemistry, Toxicology, Pathology and the Sanders-Brown Center on Aging of the University of Kentucky and the Veterans Administration Medical Center of Lexington, Kentucky further implicate mercury in the development of ALS. The following information is extracted from these studies. [It may be noted that some of the authors of these studies are recognizable as having published findings relating mercury to Alzheimer's Disease.]

Trace Element Imbalances In Amyotrophic Lateral Sclerosis Khare, SS; Ehmann, WD; Kasarskis, EJ; Markesbery, WR. Neurotoxicology. 11: 521-32. 1990.

ABSTRACT: Concentrations of 15 elements were determined by instrumental neutron activation analysis in brain, spinal cord, blood cells, serum and nails of Amyotrophic Lateral Sclerosis (ALS) patients and appropriately matched control subjects. Several significant imbalances were detected in trace element levels in ALS samples compared to control samples. Some of these changes are probably secondary to the loss of tissue mass, especially in spinal cord. However the widespread changes observed in Hg and se levels in ALS tissues deserve special attention. The significance of these alterations in trace element levels in relation to the pathogenesis of ALS is discussed.

The authors stated: "The changes observed in Hg concentration and the interactions of Hg and se are worthy of special comment and may possibly be relevant to the pathogenesis of ALS. Although an exact mechanism of Hg neurotoxicity has not yet been elucidated, Hg is known to have a high affinity for the sulfhydryl groups of proteins and may subsequently inactivate a protein or an enzyme. This could lead to total inhibition of the cellular function and to cell death."

BIO-PROBE COMMENT: The authors also discussed the significance of the selenium depletion, particularly in light of its established importance in the detoxification of mercury and protection against the adverse effects of mercury. This subject is discussed in detail in the following, more recent and comprehensive publication, which also addressed other important topics such as why ALS may develop in some individuals exposed to harmful agents (such as mercury) but not others.

Trace Metals In Human Neurodegenerative Diseases Kasarskis, EJ; Ehmann, WD; Markesberry, WR. Essential and Toxic Trace Elements in Human Health and Disease: An Update. Pg. 299-310. Wiley-Liss, Inc. 1993.

INTRODUCTION

Several examples of trace metal neurotoxicity causing recognizable classic syndromes have now been established. These have been documented resulting from subacute or sustained chronic exposure to a toxic metal from an identified environmental source or by intentional poisoning.

Implicating toxic metals in the etiology or pathogenesis of chronic neurodegenerative diseases is more challenging for several reasons:

1. Dating the onset of the human neurodegenerative disease is uncertain, thereby making the identification of the source of exposure by epidemiologic study difficult. As a further complication of this factor, a significant degree of neuronal loss must occur before clinical dysfunction is apparent. In the case of ALS, it has been shown that 50% of spinal motor neurons will have degenerated before the typical features of the disease are noticed. Therefore, the exposure to a harmful neurotoxin could have occurred many years preceding the clinical onset of the disease.

2. Neurodegenerative disorders are caused by the death of select neurons, rather than wholesale destruction of tissue. The neurotoxin could therefore be very specific in its action and effective at a low dose, making systemic toxicity less likely.

3. Biopsy material is not usually available until post-mortem, which is at the end-stage of the disease. At this point, trace metal analysis of brain and spinal cord may not accurately reflect the biochemical condition when the disease process was set in motion.

THE PATHOLOGY OF ALS

Amyotrophic Lateral Sclerosis is a chronic neurodegenerative disease. It is characterized clinically by progressive atrophy and weakness of skeletal muscle and small local involuntary muscular contractions visible under the skin. Although clinical variants and familial forms of ALS occur, the classical disease is readily identified by physical findings and electrophysiological studies.

Pathologically, ALS is characterized by atrophy and degeneration of selective motor neurons in the ventral spinal cord and the motor cortex.

The etiology and pathogenesis of ALS are unknown. Viral inclusions have not been found, but study of the 5-10% of patients with a familial pattern suggest that a genetic defect may render motor neurons more susceptible to other secondary insults, such as exposure to an exogenous toxin.

THE INVOLVEMENT OF TOXIC METALS IN ALS

The toxic trace element theory of the pathogenesis of ALS has received considerable support and derives its attractiveness from three sources:

1. Epidemiologic considerations indicate that long-term exposure to heavy metal is more common among ALS patients compared to controls.

2. An ALS-like syndrome has been linked to chronic intoxication with mercury and lead.

3. Environmental factors have been implicated in the etiology of a related motor neuron disorder; ie, ALS/Parkinson' s/Dementia in Guamanian subjects.

To date, most studies have examined a very basic hypothesis, that ALS may be caused by chronic, low-level exposure to toxic metals. If this hypothesis is true, then one should be able to analyze tissue from ALS patients and demonstrate that the concentration of toxic metals is higher in ALS compared to age-matched controls.

RESULTS

We began our studies of ALS in this traditional mode by analyzing several tissues (brain, spinal cord, serum, blood cells, and nails) from patients and controls for 15 elements by instrumental neutron activation analysis (INAA). The most important finding was a significant elevation of mercury in brain, blood cells, and serum in ALS patients compared to age- matched controls. The elevation of mercury in ALS could reflect a true excess of body burden of mercury, altered turnover, or perhaps binding to unusual intracellular ligands.

The results of our study also indicated that selenium was reduced in the serum and blood cells of ALS patients. The data were more striking when the ratio of mercury:selenium was computed for each sample in order to study both elements concurrently. This approach not only considered the accumulation of a toxic metal, but also evaluated the integrity of potential detoxification mechanisms. The results of our work indicated that mercury was present to excess relative to selenium in ALS blood cells, serum, and brain.

We have considered that mercury accumulation in motor neurons may be a necessary precondition for ALS-type degeneration to occur. This hypothesis predicts that mercury should be enriched in spinal motor neurons of normal spinal cords and that additional factors would impinge on motor neurons to cause their degeneration in ALS. Our formulation is specific in proposing:

1. Mercury accumulation by neurons is a prerequisite for subsequent neurodegenerative changes to ensue.

2. The ALS phenotype develops either by excessive mercury accumulation or inadequate mercury detoxification.

If mercury is, in fact, an etiologic factor in the pathogenesis of ALS, then one would predict the mercury would accumulate in precisely those neurons which ultimately degenerate in ALS. In order to evaluate this hypothesis, the analysis of mercury must be investigated on a cell-by- cell basis.

Because LAMMS (Laser-Activated Microprobe Mass Analysis) did not provide the requisite sensitivity to detect mercury under our conditions, the mercury-specific photoemulsion histochemical (PH) method described by Moller-Madsen and Danscher in 1986 was adapted to human postmortem spinal cord. Mercury was found localized primarily to the nucleus of motor neurons with lesser amounts seen in the cytoplasm. Mercury was also found associated with spinal motor neurons in normal humans. These data, together with the results of the buLk tissue analyses, indicate

that spinal motor neurons have an avidity [ED: Strong affinity] for mercury which could possible render them more susceptible to other neurotoxic agents, thereby conferring a selective vulnerability to neuronal degeneration.

Metallothionein in als: some speculations and direction for future research.

Metal detoxification may be the more critical factor in the pathogenesis of ALS because it appears unlikely that ALS results from a simple, environmental-type exposure based upon population studies.

The metallothionein (MT) family of proteins has not been investigated in ALS. The rationale for studying MT in ALS receives support from the detailed understanding of MT from human and animal studies.

Our preliminary data implies that at least part of the accumulated mercury may be bound to MT in motor neurons. It is premature to seriously speculate on potential mechanisms, although MT could directly detoxify mercury. Alternatively, mercury could conceivably divert MT from its function in copper and zinc homeostasis.

Our findings suggest a potential mechanism to explain the selective death of spinal motor neurons in ALS, namely an imbalance between mercury accumulation and detoxification of mercury. Our hypothesis considers that inadequate mercury detoxification by MT might occur in ALS spinal and cortical motor neurons leading to neuronal death. Impaired detoxification could result from an aberrant MT isoform within spinal motor neurons or altered MT gene expression following mercury exposure.

BIO-PROBE COMMENT: This presentation is dramatic and compelling. The credentials of the investigators, institutions, and publications are impressive. The techniques, investigative protocols and rationale are beyond reproach.

It should be obvious to even the most biased, that continued acceptance of doctrines and rationales that permit human chronic low-level exposure to mercury, are totally without scientific support, and cannot be condoned any longer.

Inorganic mercury is transported from muscular nerve terminals to spinal and brainstem motoneurons. Arvidson B. Muscle Nerve. 15(10):1089-1094, Oct 1992.

ABSTRACT: The distribution of mercury within the brainstem and spinal cord of mice was investigated with the autometallographic technique after intramuscular administration of a single dose of mercuric mercury (HgCl2). Deposits of mercury were localized to motor neurons of the spinal cord and to brainstem motor nuclei; i.e., neurons with their peripheral projections outside the blood-brain barrier. Unilateral ligation of the hypoglossal nerve prior to the injection of HgCl2 prevented the accumulation of mercury deposits in the ipsilateral hypoglossal nucleus. The selective accumulation of mercury in spinal and brainstem motoneurons is most probably due to a leakage of metal-protein complexes from capillaries in muscle into myoneural junctions, followed by uptake into nerve terminals and retrograde axonal transport. The possible link between this process and the development of motor neuron degeneration in ALS is discussed.

BIO-PROBE COMMENT: It is time that the medical profession took cognizance of the fact that some Amyotrophic lateral sclerosis (ALS) patients improve or become symptom free after amalgam replacement. Animal and human research studies are providing the scientific basis and support to ALS patient case histories reflecting amelioration or cure of this "incurable" disease.

Motor Neuron Uptake of Low Dose Inorganic Mercury. Pamphlett, R; Waley, P.J Neurological Sciences, 135:63-7,1996.

ABSTRACT: In animals, inorganic mercury can bypass the blood brain barrier and enter motor neurons. We sought to determine the lowest injected dose of mercury that could be detected in mouse motor neurons. Mice were injected intraperitoneally with mercuric chloride in doses from 0.05 micrograms/g body weight and studied between 5 days and 18 months after injection. After formalin fixation, 7 micrometer sections of cerebrum, cerebellum, brain stem, spinal cord and kidney were stained with silver nitrate autometallography. Five days after injection, mercury granules were detected at doses from 0.2 micrograms/gram upwards in the cell bodies of spinal and brain stem motor neurons, more granules being seen at the higher doses. Mercury granules were also seen in 5 % of posterior root ganglion neurons. At doses from 0.05 micrograms/gram upwards mercury was detected 5 days later in renal tubule cells. Mercury was still present in motor neurons 6-11 months after injection, but by this time mercury had been cleared from kidneys. Low doses of inorganic mercury are therfore selectivel taken up and retained by motor neurons, making this nurotoxin a good candidate for cause of sporadic motor neuron disease.

BIO-PROBE COMMENT: This new study should be of great interest to scientists who have already connected exposure to mercury to motorneuron diseases such as Amyotrophic Lateral Sclerosis (Lou Gehrig's Disease). Previous research, dating back to the 1960's, has demonstrated that inorganic mercury (Hg 2+ does penetrate the blood-brain barrier, but at a low rate. Mercury vapor, the form released from dental amalgam fillings penetrates the blood-brain barrier far more readilly. We must also consider that the above findings represent findings from just a single dose, whereas patients with amalgam fillings receive thousands of doses of mercury vapour every day.

Editor's Report

(This is followed by the abstract of the paper)

IN FOCUS NEURO REPORT 0959-4965 & Lippincott Williams & Wilkins Vol 12 No 4 26 March 2001 A23

Mercury induced growth cone collapse:

Owen Hamill

Physiology and Biophysics,

UTMB, Galveston, TX, USA

Cases where exposure to heavy metals in the domestic and work environment have contributed to human disease extend back to antiquity with the use of lead in water pipes and wine storage vessels. It has been proposed that pandemic lead poisoning, resulting in mental incompetence and declining birth rate, especially amongst the ruling class, contributed to the fall of Rome [1] (see [2] for another view). More recent lead poisoning in the general population has arisen from lead-based paints and lead- additives in petrol. A well-documented case of occupational poisoning arose in workers of the 19th century felt hat industry due to the use of mercury as a stiffener of rabbit fur. Increased irritability, mood swings, tremulous- ness, ataxia and impairment in intellectual capacity characterize Mad Hatter's disease [3]. Currently there is ongoing public health debate on whether low level chronic exposure to mercury due to dental repair work results in subclinical behavioral changes associated with CNS damage (see [4] for review). For example, in the USA the most common material used in dental fillings is a mercury/silver mixture (amalgam) in which an estimated 70 000 kg is used in 100 million fillings/year. Furthermore, evidence indicates that mercury vapor is continuously released from tooth fillings where it is breathed in by the lungs and converted into mercuric ions. Although there is no debate on the toxic effects of high concentrations of mercury (i.e. associated with urinary concentrations .50 ìg/l), a challenge exists to demonstrate more subtle, preclinical effects associated with chronic low level mercury exposure in the general population with fillings. At least consistent with this notion is the study published in this issue [5] showing that exposure to mercury concentrations of ,0.1 ìM results in rapid (i.e. within 10 min) retraction of growth cones in snail neurons and is correlated with disruption of microtubules. Interestingly, the authors point out that similar disruption of microtubules is associated with Alzheimer's disease. These recent findings give added impetus for the development and implementation of alternative materials for fillings and may provide parents with added ammunition in teaching their children to floss.

REFERENCES

Woolley DE. Neurotoxicity 5, 353±361 (1984).
Scarborough J. J Hist Med Allied Sci 39, 469±475 (1984).
O'Carroll RE, Masterton G, Dougall N et al. Br J Psychiatry 167, 95±98 (1995).
Lorscheider FL, Vimy MJ and Summers AO. FASEB J, 9, 1499±1500 (1995).
Leong CCW, Syed NI and Lorscheider FL. Neuroreport, 12, 733±737.
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Abstract

TITLE: Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury

JOURNAL: NeuroReport VOLUME: 12 ISSUE: 04 PAGES: 0733-0737

RECEIVED: 6 December 2000

ACCEPTED: 21 December 2000

AUTHOR: Christopher C. W. Leong*, Naweed I. Syed†, Fritz L. Lorscheider‡

ADDRESS: *Faculty of Medicine, Department of Physiology and Biophysics, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, Canada T2N 4N1; †Faculty of Medicine, Department of Physiology and Biophysics, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, Canada T2N 4N1; ‡Faculty of Medicine, Department of Physiology and Biophysics, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, Canada T2N 4N1

Inhalation of mercury vapor (Hg0) inhibits binding of GTP to rat brain tubulin, thereby inhibiting tubulin polymerization into microtubules. A similar molecular lesion has also been observed in 80% of brains from patients with Alzheimer disease (AD) compared to age-matched controls. However the precise site and mode of action of Hg ions remain illusive. Therefore, the present study examined whether Hg ions could affect membrane dynamics of neurite growth cone morphology and behavior. Since tubulin is a highly conserved cytoskeletal protein in both vertebrates and invertebrates, we hypothesized that growth cones from animal species could be highly susceptible to Hg ions. To test this possibility, the identified, large Pedal A (PeA) neurons from the central ring ganglia of the snail Lymnaea stagnalis were cultured for 48 h in 2 ml brain conditioned medium (CM). Following neurite outgrowth, metal chloride solution (2 ml) of Hg, Al, Pb, Cd, or Mn (10–7 M) was pressure applied directly onto individual growth cones. Time-lapse images with inverted microscopy were acquired prior to, during, and after the metal ion exposure. We demonstrate that Hg ions markedly disrupted membrane structure and linear growth rates of imaged neurites in 77% of all nerve growth cones. When growth cones were stained with antibodies specific for both tubulin and actin, it was the tubulin/microtubule structure that disintegrated following Hg exposure. Moreover, some denuded neurites were also observed to form neurofibrillary aggregates. In contrast, growth cone exposure to other metal ions did not effect growth cone morphology, nor was their motility rate compromised. To determine the growth suppressive effects of Hg ions on neuronal sprouting, cells were cultured either in the presence or absence of Hg ions. We found that in the presence of Hg ions, neuronal somata failed to sprout, whereas other metalic ions did not effect growth patterns of cultured PeA cells. We conclude that this visual evidence and previous biochemical data strongly implicate Hg as a potential etiological factor in neurodegeneration.

KEYWORDS: Mercury, Microtubules, Neurite growth cone, Neurodegeneration, Neurofibrillary aggregates, Tubulin

 

   

 

Mercury Has Profound Effects on Cardiac Function

There is a vast body of research which demonstrates the effect that mercury has on the heart. One of the ways that this may be mediated is that cardiac function relies strongly on the use of selenium.  Mercury specifically binds selenium.

Marked Elevation of Myocardial Trace Elements in Idiopathic Dilated Cardiomyopathy Compared With Secondary Dysfunction

Frustaci, A., Magnavita, N., Chimenti, C., Caldarulo, M., Sabbioni, E., Pietra, R., Cellini, C., Possati, G.F. and Maseri, A. Department of Cardiology, Department of Occupational Medicine, and Department of Cardiac Surgery, Catholic University, Rome Italy and CEC 4Environmental Institute Joint  Research Center Ispra, Rome, Italy  Journal of the American College of Cardiology Vol. 33, No. 6, 1999, pp. 1578-1583

Objectives: We sought to investigate the possible pathogenic role of myocardial trace elements (TE) in patients with various forms of cardiac failure.

Background: Both myocardial TE accumulation and deficiency have been associated with the development of heart failure indistinguishable from an idiopathic dilated cardiomyopathy.

Methods: Myocardial and muscular content of 32 TE has been assessed in biopsy samples of 13 patients (pts) with clinical, hemodynamic and histologic diagnosis of idiopathic dilated cardiomyopathy (IDCM), all without past or current exposure to TE. One muscular and one left ventricular (LV) endomyocardial specimen from each patient, drawn with metal contamination-free technique, were analyzed by neutron activation analysis and compared with 1) similar surgical samples from patients with valvular (12 pts) and ischemic (13 pts) heart disease comparable for age and degree of LV dysfunction; 2) papillary and skeletal muscle surgical biopsies from 10 pts with mitral stenosis and normal LV function, and 3) LV endomyocardial biopsies from four normal subjects.

Results: A large increase (>10,000 times for mercury and antimony) of TE concentration has been observed in myocardial but not in muscular samples in all pts with IDCM. Patients with secondary cardiac dysfunction had mild increase (<5 times) of myocardial TE and normal muscular TE. In particular, in pts with IDCM mean mercury concentration was 22,000 times (178,400 ng/g vs. 8 ng/g), antimony 12,000 times (19,260 ng/g vs. 1.5 ng/g), gold 11 times (26 ng/g vs. 2.3 ng/g), chromium 13 times (2,300 ng/g vs. 177 ng/g) and cobalt 4 times (86.5 ng/g vs. 20 ng/g) higher than in control subjects.

Conclusions: A large, significant increase of myocardial TE is present in IDCM but not in secondary cardiac dysfunction. The increased concentration of TE in pts with IDCM may adversely affect mitochondrial activity and myocardial metabolism and worsen cellular function.

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Effects of mercury on the isolated heart muscle are prevented by DTT and cysteine.

Vassallo DV, Moreira CM, Oliveira EM, Bertollo DM, Veloso TC Department of Physiological Sciences, Federal University of Espirito Santo, Vitoria, ES, Brazil. Toxicol Appl Pharmacol 1999 Apr 15;156(2):113-8

The protective effects of dithiothreitol (DTT, 50 &mgr;M) and cysteine (CYS, 100 &mgr;M) against toxic effects of HgCl2 (1, 2.5, 5, and 10 &mgr;M) were studied in isolated, isometrically contracting rat papillary muscles. Force reduction promoted by Hg2+ was prevented by both DTT and CYS. Also, after both treatments, no significant changes in dF/dt were observed. A progressive reduction in the time to peak tension was observed when increased concentrations of HgCl2 were used after CYS and DTT treatment. This was an indication that the enhancement of calcium release from the sarcoplasmic reticulum produced by mercury was not affected by DTT and CYS. Tetanic contractions were also studied. After treatment with DTT or CYS tetanic tension did not change. No significant reduction of tetanic tension was observed during treatment with 1 &mgr;M Hg2+ but its reduction was observed after 5 &mgr;M Hg2+. Myosin ATPase activity was also affect by Hg2+, being completely blocked by 1 &mgr;M Hg2+ and reduced by 50% with 0.15 &mgr;M Hg2+. Full activity was restored by using 500 nM DTT. These findings suggest that several but not all toxic effects of Hg2+ on the mechanical activity of the heart muscle are prevented by protectors of SH groups such as DTT and CYS. The enhancement of the Ca2+ release from the sarcoplasmic reticulum by Hg2+ during activation was not affected by prior treatment with DTT and CYS, suggesting that interactions with SH groups may not be important for the activation of the Ca2+ channel of the sarcoplasmic reticulum. Copyright 1999 Academic Press.

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The chamber exposure of laboratory rats to metal oxides originating from metal producing industry.

Kovacikova Z, Chorvatovicova D    Physiol Res 1997;46(1):41-5

Institute of Preventive and Clinical Medicine, Slovak Academy of Sciences, Bratislava, Slovak Republic.

Laboratory rats were exposed to the inhalation of dust from an agglomeration unit which is the greatest contributor to dust pollution in the vicinity of a mercury producing plant. The exposure lasted for 6 months (4 hours daily, 5 days per week), the concentration of aerosol in the chamber was 10 mg x m(-3). After finishing the exposure, the animals were examined and compared with the controls which were held under standard laboratory conditions. The number of alveolar macrophages was highly elevated (P< 0.001) in the exposed animals, Mg2+ ATPase activity in the heart muscle was decreased. The alanine aminotransferase activity in the serum was not changed, the aspartate aminotransferase was slightly enhanced. No differences in the frequency of abnormal sperm and in the frequency of polychromatic erythrocytes in bone marrow were detected.

***********************

Mercury effects on the contractile activity of isolated heart muscle.

Oliveira EM, Vassallo DV, Sarkis JJ, Mill JG Toxicol Appl Pharmacol 1994 Sep;128(1):86-91 Department of Biochemistry, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.

The toxic effects of HgCl2 (1, 2.5, 5, and 10 microM) were studied in isolated, isometrically contracting rat papillary muscles and frog ventricular strips. In rat papillary muscles 1 microM Hg2+ produced a small increase in the force of contraction. Higher concentrations of HgCl2 produced a dose-dependent decrease in contractile force. The rate of force development was affected differently, increasing at 1 and 2.5 microM Hg2+ and decreasing to control levels at 5 and 10 microM Hg2+. This was the result of a progressive reduction in the time to peak tension observed when HgCl2 concentrations increased. This effect probably reflects the binding of Hg2+ to SH groups inducing Ca2+ release from the sarcoplasmic reticulum. The relative potentiation of postrest contractions was used as an index of sarcoplasmic reticulum activity. It was measured after pauses of increasing duration and was reduced at concentrations of 1 microM Hg2+ when compared to that of the control. A further decrement in the relative potentiation was observed with higher Hg2+ concentrations, indicating that the activity of the sarcoplasmic reticulum was depressed by mercury in a dose-dependent manner. Tetanic contractions were also studied in the rat myocardium. The tetanic tension did not change during treatment with 1 microM Hg2+ but decreased with 5 microM Hg2+, suggesting a toxic effect on the contractile proteins only at high Hg2+ concentrations. Frog ventricular strips were studied using the same HgCl2 concentrations and no effects on either force or relative potentiation were observed. These findings suggest that Hg2+ promotes dose-dependent toxic effects on heart muscle via actions on the sarcolemma, the sarcoplasmic reticulum, and contractile proteins.

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Mercury compounds: lipophilicity and toxic effects on isolated myocardial tissue.

Halbach S   Arch Toxicol 1990;64(4):315-9

Gesellschaft fur Strahlen- und Umweltforschung, Institut fur Toxikologie, Neuherberg, Federal Republic of Germany.

Lipophilicity is suggested to modulate the diffusion and the cytotoxic effects of mercury compounds. To investigate this, the positive inotropic effect of four Hg compounds (HgCl2, CH3HgCl, chlormerodrin, bromomercurihydroxypropane) was studied in catecholamine-depleted isolated heart muscle preparations. The rate of development of the positive effect was inversely correlated to the concentration in the case of HgCl2 and chlormerodrin, i.e. the product of concentration (c) and time to half-maximal effect (t50) remained constant. This was in accordance with the assumption of a permeation-controlled rate of action, as was shown earlier for p-chloromercuriphenyl-sulfonic acid. In addition, the c X t50 values of the individual mercurials decreased hyperbolically with the increase in lipophilicity as measured by the octanol/water partition. The results support the view that the toxicity of mercurials increases with their lipid solubility. In conjunction with the previously reported negative inotropic effect of Hg compounds, a model is proposed allocating thiol groups responsible for the negative inotropic action to lipid compartments within the cell membrane, while SH groups conveying the increase in contraction force are thought to be situated at the internal surface of the sarcolemma.

***********************

The relationship between mercury from dental amalgam and the cardiovascular system.

Siblerud RL Sci Total Environ 1990 Dec 1;99(1-2):23-35

Department of Physiology, College of Veterinary Medicine and Biological Sciences, Colorado State University, Fort Collins 80523.

The findings presented here suggest that mercury poisoning from dental amalgam may play a role in the etiology of cardiovascular disorders. Comparisons between subjects with and without amalgam showed amalgam-bearing subjects had significantly higher blood pressure, lower heart rate, lower hemoglobin, and lower hematocrit. Hemoglobin, hematocrit, and red blood cells were significantly lower when correlated to increased levels of urine mercury. The amalgam subjects had a greater incidence of chest pains, tachycardia, anemia, fatigue, tiring easily, and being tired in the morning. The data suggest that inorganic mercury poisoning from dental amalgam does affect the cardiovascular system.

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Hemodynamic and electrophysiological effects of mercury in intact anesthetized rabbits and in isolated perfused hearts.

Rhee HM, Choi BH Exp Mol Pathol 1989 Jun;50(3):281-90

Department of Pharmacology, Oral Roberts University School of Medicine, Tulsa, Oklahoma 74171.

Using intact anesthetized rabbits and isolated perfused hearts, the hemodynamic and electrophysiological effects of mercury (Hg) were examined in order to assess the role of cardiovascular dysfunction in Hg intoxication. The most consistent and prominent cardiovascular effect was a significant reduction in blood pressure. This cardiodepressive action was probably brought about by the primary action of Hg on the heart rather than by altered sympathetic activity, as evidenced by normal renal nerve activity at times when the hemodynamic actions of Hg were clearly manifest. Although the principal target organ for the toxic actions of inorganic Hg is the kidney, chronic exposure to both inorganic and organic Hg frequently results in signs and symptoms of CNS dysfunction. The profound hemodynamic effects of Hg that we have observed emphasize the potential importance of Hg cardiotoxicity and indicate the need to differentiate between the primary and the secondary effects of Hg intoxication on CNS tissues for evaluation of the toxic effects of Hg compounds.

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Cardiovascular homeostasis in rats chronically exposed to mercuric chloride.

Carmignani M, Boscolo P Arch Toxicol Suppl 1984;7:383-8

Two groups of male Sprague-Dawley rats received from weaning 50 micrograms/ml of mercury as mercuric chloride (HgCl2) in drinking water for 320 and 350 days. Hg exposure increased cardiac inotropism, without chronotropic changes, in both groups, and induced arterial hypertension in the rats exposed for 350 days. In the exposed rats, cardiovascular responses to the stimulation of peripheral alpha and beta adrenoceptors were decreased and increased, respectively, possibly through a reduced intracellular availability of calcium ions for contractile mechanisms. Hg exposure did not affect either vagal or sympathetic activity or cardiovascular reactivity to several physiological agonists. On the other hand, Hg exposure induced baroreflex hyposensitivity and produced a drastic alteration of the levels of copper and zinc in brain and kidney.

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Mechanisms in cardiovascular regulation following chronic exposure of male rats to inorganic mercury.

Carmignani M, Finelli VN, Boscolo P Toxicol Appl Pharmacol 1983 Jul;69(3):442-50

In this study we verified the possibility that chronic exposure to inorganic mercury may induce hemodynamic changes in the rat by affecting some neurogenic and/or humoral mechanisms regulating cardiovascular function. For this reason, aortic blood pressure, maximum rate of rise of the left ventricular pressure, heart rate, and electrocardiogram were monitored under pentothal anesthesia in rats which received 50 micrograms/ml of mercury (as HgCL2) in drinking water for 320 days and in control rats. No pressor or electrocardiographic changes were found in mercury-treated animals, which showed increase of cardiac inotropism and decrease of the pressor and inotropic responses to bilateral carotid occlusion. Cardiovascular responses to bilateral vagotomy and iv hexamethonium under vagotomy were unchanged in the mercury-exposed rats. In these animals both pressor and inotropic responses to iv norepinephrine and to higher doses of epinephrine were reduced, while the vascular beta-adrenergic response to 0.125 micrograms/kg of iv epinephrine was potentiated. Cardiovascular responses to acetylcholine, angiotensin I, angiotensin II, bradykinin, histamine, and serotonin did not differ in the two groups of rats. These results indicated that chronic mercury exposure affects cardiovascular function by interfering with the baroreflex mechanisms and/or the reactivity to catecholamines. Higher amounts of mercury were found in kidney, but the metal was significantly accumulated also in urine, blood, and brain. Mercury exposure greatly increased the levels of copper and zinc, but not that of iron, in brain and kidney. The increased accumulation of copper and zinc in tissues may be related in part to the mercury-induced synthesis of metallothionein, a protein able to bind these essential metals. It may be suggested that zinc and copper interact with mercury in inducing cardiovascular changes.

 

   

 

The danger of mercury from amalgam is well known to the manufacturers of this substance.
All one needs to do is to read their Material Safety Data Sheets

______________________________________

Latest Research
Linking Mercury To Autism

B.E. Haley/Medical Veritas 2 (2005)
Mercury toxicity: Genetic susceptibility and synergistic effects
Boyd E. Haley, PhD
Professor and Chair Department of Chemistry University of Kentucky

Abstract
Mercury toxicity and intoxication (poisoning) are realities that every American needs to face. Both the Environmental Protection Agency and National Academy of Science state that between 8 to 10% of American women have mercury levels that would render any child they gave birth to neurological disorders. One of six children in the USA have a neurodevelopmental disorder according to the Centers for Disease Control and Prevention. Yet our dentistry and medicine continue to expose all patients to mercury. This article discusses the obvious sources of mercury exposures that can be easily prevented. It also points out that genetic susceptibility and exposures to other materials that synergistically enhance mercury and ethyl-mercury toxicity need to be evaluated, and that by their existence prevent the actual determination of a "safe level" of mercury exposure for all. The mercury sources we consider are from dentistry and from drugs, mainly vaccines, that, in today's world are not only unnecessary sources, but also sources that are being increasingly recognized as being significantly deleterious to the health of many.

From the Conlusion:

... If certain infants are more susceptible to mercury toxicity due to their inability to excrete mercury then it seems plausible that, since this is a genetic susceptibility, older individuals may suffer from the inability to excrete mercury also. Based on the ability of mercury to mimic many of the biochemical aberrancies found in AD brain and to produce aspects of the pathological diagnostic hallmarks of AD it seems plausible that AD is a disease related to mercury toxicity. The published decrease of mercury in the nail tissue of AD versus normal age-matched individuals seems to support this possibility.
Finally, the synergistic effects of other heavy metals, diet, antibiotics, etc. on mercury toxicity make it impossible to define a "safe level of mercury exposure." Therefore it is imperative that we try to eliminate all exposure to mercury; and removal from dentistry and medicines is most important and critical for human health.

---

On 7 January 2003, the Superior Court in San Francisco
approved the warnings on dental amalgam mercury
that are required under California's Proposition 65

"Warning on dental amalgam,
used in many dental fillings,
causes exposure to mercury,
a chemical known to the state of California to cause
birth defects or other reproductive harm."

---

Swedish Government report of 2003 states:

"With reference to the fact that
mercury is a multipotent toxin
with effects on several levels of the
biochemical dynamics of the cell,
amalgam must be considered to be
an unsuitable material for dental restoration.
This is especially true since fully adequate
and less toxic alternatives are available."

______________________________________

 

 

Mercurial Effects on Women's Health

Dental amalgam fillings are made from an alloy of silver, copper, zinc and tin which is powdered and mixed in the surgery with an EQUAL amount of mercury.  Amalgams are a mixture of metals not an alloy.  The word amalgam is defined as a mixture of one or more metals with mercury.  Mercury leaks continuously from these fillings at a rate which is higher than the OSHA standards allowable for industrial exposure!   Mercury is very toxic and is stored mainly in the Brain, Kidney and Liver. It has profound effects on the health of women, foetus and newborn.

Many countries have recommended that mercury amalgam should NOT be used in pregnant women, women of child bearing age and in children.  It should also not be used for people with kidney diseases.  Not only is this official policy for such organizations as the NHMRC, it is also clearly stated by the manufacturers.  The dental profession in Australia simply ignores these warnings.

Mercury crosses the placenta and enters the body of the developing foetus.  High levels of mercury can be found in fetal tissues.  In 1994, it was found that the levels of mercury in the tissues of foetuses and newborns was directly proportional to the number of amalgams in the mother's mouth.

Mercury leaks continuously from amalgam fillings!

"The average absorbed daily dose for an individual with 8 amalgam fillings is estimated
to be 10 mcg / day, with a range that may exceed 100 mcg / day"3

The affects of mercury on women's health have been known for a long time:

 

"Effects and Use of Inorganic Drugs" H. Schulz, Dept of Pharmacology, Univ. of Greifswald. G. Theime, Leipzig 1907.........Over 80 years ago.
“In women there will be inflammations of the outer genitals, vaginal catarrhs and disturbances of menstruation That there is a tendency to miscarriage during chronic mercurialism is well known from the toxicology of mercury.”

 

 

 

 

Environmental Protection Agency
“Women chronically exposed to mercury vapour experienced increased frequencies of menstrual disturbances and spontaneous abortions.” “A high mortality rate was observed among infants born to women who displayed symptoms of mercury poisoning.” EPA Mercury Health Effects update Health Issue Assessment. 1984 EOA- 600/8-84f. USEPA

 

 

World Health Organization

In 1991 the World Health Organization published it's report on Environmental Mercury (Criteria 118). They concluded that the single greatest source of mercury exposure for the general population is Dental Amalgam.

This is up to ten times more than from all other dietary and environmental sources combined.2 The WHO also state that there is NO SAFE LEVEL of mercury vapor. This means that mercury vapour from fillings in your mouth and the vapour found in dental surgeries where amalgam is used can be absorbed into your body and can potentially have an effect on your health.

In all publications put out by the official bodies such as the ADA in Australia and America, no mention is ever made of WHO report (Criteria 118.)

Sweden and Germany

In Sweden the use of Dental amalgam will be outlawed by 1997. A number of years ago the phase out program was initiated. When the phase out program was initiated the first group to be protected were women and children. If, as the ADA suggest, that this is purely for environmental reasons, we should ask: Why are the first groups in society, to be protected, those groups who are most sensitive to mercury poisoning?

                                                          

 

In April 1995 the German Government issued the following directive;

"Since foetuses will be exposed to mercury from the mother's amalgam fillings, on the basis of preventive health protection, there should be no placement or no additional amalgam fillings placed, respectively, during pregnancy. Alternative materials should, if possible, be the preferred choice. Since removal of amalgam will cause an additional exposure to mercury, no clinically faultless amalgam restorations should be removed during pregnancy especially."

Mercury Crosses the Placenta and Breast Milk

Animal Studies

Many animal studies have demonstrated that mercury will cross the placenta and be absorbed by the developing child. In 1991 a landmark study was published which studied the effects of amalgam fillings in pregnant sheep. The study conclusively showed that Mercury from dental amalgam not only crossed the placenta and was detected in the foetus WITHIN 48 HOURS of the fillings being placed in the sheep teeth, but that it was also stored in many tissues of the foetus especially the

Kidney, Liver and Brain (in particular the Pituitary Gland). The researchers were also able to demonstrate that mercury from the amalgam was found in the breast milk.3,4,5,6,7,8,

Human Studies

A 1994 German study showed similar findings in humans. Deceased foetuses, newborns and young children were examined for tissue levels of mercury. What was found was that the levels of mercury in the Brain, Liver and Kidney tissues were in direct proportion to the number of amalgam fillings in the mother's mouth.

This research supports the findings of the earlier animal models!

Dental Amalgam Warning Labels

The Australian Dental Association has recently claimed19 that mercury is only dangerous if it is in a form which is 'BIO-AVAILABLE'. No scientific research has been offered in support of this claim.  The documented facts are that mercury vapour coming off dental amalgam is just as toxic as mercury vapour from any other source. All Mercury Vapour is Bio-Available and is Toxic! In fact, in California the warning label that comes with dental amalgam includes the following:

"WARNING: This product contains a chemical known to the State of California
to cause birth defects and other reproductive harm."

Auto-Immune Diseases

It has been shown conclusively that mercury from dental amalgam can cause a number of Auto- Immune diseases.9,10

Infertility & Birth Defects

Many studies have shown that exposure to mercury was associated with a demonstrable increase in the rate of birth defects, infertility and miscarriage.12,13,14,15,16 Concerns have been raised with the observations that the placenta does not protect the foetus from mercury accumulation during chronic exposure. It has been stated in the scientific literature that "Pregnant women should not be exposed to mercury vapour at all."17, 18

The dental professions assurances of safety are ironic when one of these studies has even been cited by the Environmental Protection Agency as well as the American Dental Journal. 17,18

 

 

Alternatives: Safe and Effective

Modern technologies have given us materials and techniques which make the alternatives to amalgam both safe and effective as a long term filling material. These include gold, porcelain and composite resins. Composite resins do not contain Formaldehyde, even though the Australian Dental Association imply that they do.19

Quintessence International, a popular and widely read dental journal, recently published an editorial (Volume 26, Number 3 / 1995) by Richard J. Simonsen, the Editor-in-Chief who wrote;

"Amalgam should never be used as a restorative material in pediatric dentistry. Why?
Because better materials are available."

"Amalgam should never be used as a first time restorative material. Why?
Because better alternatives are available."

"Move Over Amalgam - At Last

References:

1- Vimy, Lorscheider - FASEB J. Vol 7 #15 pp1432-1433 1993

2- World Health Organisation. Environmental Mercury. Criteria 118 Geneva 1991

3- Toxic Teeth: The Chronic Mercury Poisoning of Modern Man. Vimy Chemistry & Industry 2 January 1995 17

4- Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Vimy MJ Takahashi Y. Lorscheider FL. Am J Physiol (1990 Apr) 258(4 Pt 2):R939-45

5- Amalgam Hazards in your Teeth; Mats Hanson Department of Zoophysiology University of Lund, Helgonavägen 3B Sweden

6- Friberg L, Vostal J, eds. Mercury in the environment: an epidemiological and toxicological appraisal. Cleveland, Ohio: CRC Press, 1972.

7- Braunwald E, Isselbacher KJ, Petersdorf RG, Wilson JD, Martin JB, Fauci AS, eds. Harrison's principles of internal medicine. 11th ed. New York: McGraw-Hill, 1987.

8- Last JM. Public health and preventive medicine. 12th ed. Norwalk, Connecticut: Appleton-Century Crofts, 1986.

9- Drasch G Schupp I Hofl H Reinke R Roider G Mercury burden of human fetal and infant tissues. Eur J Pediatr (1994 Aug) 153(8):607-10

10- Kubicka-Muranyi, M; Behmer, O; Uhrberg, M; Klonowski, H; Bister, J; Gleichmann, E. Murine Systemic Autoimmune Disease Induced by Mercuric Chloride (HgC12): Hg-Specific Helper T-Cells React to Antigen Stored in Macrophages. Int J

Immunopharmacol. 1993,Feb. 15(2):151-61.

11- Hultman, P; Johansson, U; Turley, SJ; Lindh, U; Enestrom, S; Pollard, KM. Adverse Immunological Effects and
Autoimmunity Induced by Dental Amalgam and Alloy in Mice. FASEB J. (1994): 8, 1 183-1190.

12- Ziff. Infertility and Birth defects. 1987

13- Gordon - Pregnancy in Female Dentists- a Mercury hazard. Proceedings of Intl. Conference on Mercury Hazards in Dental Practice Sept. 2-4 Glasgow 1981

14- Lee, L.P. and Dixon. Effects of Mercury on Spermatogenisis J Pharmacol Exp Thera 1975: 194(1); 171-181.

15- Till et al. Zahnarztl. Welt/reform 1978:87;1130-1134

16- Koos et al., Mercury toxicity in pregnant women, fetus and newborn infant. Am J Obstet And Gynecol., 1976:126;390-409

17- EPA mercury Health Effects Update Health Issue Assessment. Final report 1984 EOA-600/8-84f. USEPA,

18- By Irwin Mandel DDS. Dean of School of dental and Oral Surgery, Colombia University. Published JADA Vol. 122 August 1991

19- ADA Media Conference Feb 1995, Australian Dental Association News Bulletin April 1995.

 

 

This is a transcript of a lecture delivered to the Proceedings of the First World Congress on Cancer by Professor W Kostler (President of Austrian Society of Oncology, Austria.)   Sydney 1984

Professor W Kostler

Glutadione Peroxidase and Selenium

The glutadione peroxidase is detoxifying peroxides to water and glutadione. We try to improve the scavenging activity by applying selenium. There is a correlation between the level of glutadione peroxidases in the blood and the plasma selenium. A study was made in the US, on AIDS patients and patients with AIDS related complexes, using a control group. A direct correlation was found between the plasma selenium level and glutadione peroxidase activity in the blood. It is very important to supply this selenium, because glutadione peroxidase is one of the most effective scavengers.

Excessive intake of selenium (2,000 to 5,000 micrograms a day) is said to produce poisoning. But it is not true in a way - we know that women m Venezuela take 5,000 micrograms a day and don't suffer from breast cancer. The optimal intake is in comparison to the sub-optimal intake- sub-optimal means 50 to 200 micrograms a day and optimal intake is 250 to 300 per day. Optimal means you have some reserve, for example, for radiotherapy or chemotherapy, with agents that activate radicals in your body.

The normal level of selenium should be 80 to 130 micrograms per litre of blood. We check the levels of selenium in different cancer patients at their first consultation in our office - most of them suffer from a big deficiency in selenium. One patient had a level of 49 micrograms-a very low level in a person with advanced bladder cancer.

Effects of Mercury in Dental Amalgam

1 want to emphasise that there is a very strong interaction between some trace elements, and I'll focus on mercury and selenium. A surplus of mercury causes a diminution of selenium. Why is that important?

Most of our cancer patients have a lot of amalgam dental fillings. 1 remember a study we made few years ago at the University of Vienna. One group of students with amalgam fillings had to chew a chewing gum for twenty minutes, and the other group had to drink hot lemon juice for twenty minutes. We wanted to know what happens with the mercury level in their blood. By chewing the gum, with dental fillings of amalgam, or by drinking hot and acid juices, there was always a big mercury intake in the blood.

In the same way, the level of selenium was lowered, because a lot of selenium was needed to detoxify the mercury to mercury Selenite, and therefore it was not available any longer. What we didn't expect was that the immune status showed us a small decrease in the immune-competent cells after this test-after 20 minutes of chewing gum or drinking hot juice

Therefore, we usually try to remove the dental fillings made out of amalgam, and use chelation therapy to bring out the mercury, leaving the selenium free for the glutadione peroxidase activity again. Such a patient can have normal mercury levels in the blood, but after the injection DMPS there is a large amount of mercury over the next 24 hours, going out with the urine. The mercury is deposited in the brain and the central nervous system, mostly in the hypophysis, and causes a lot of problems with hormonal regulation.