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Archives of Environmental Health: An International Journal Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/vzeh20
Status of Mercury and Selenium in Dental Personnel: Impact of Amalgam Work and Own Fillings a
a
a
Ingrid Akesson B.Sc.P.T. , Andrejs Schutz Ph.D. , Robyn Attewell M.Sc. , Staffan a
Skerfving M.D. & Per-Olof Glantz O.D.
b
a
Department of Occupational and Environmental , Medicine University Hospital , Lund, Sweden b
Department of Prosthetics School of Dentistry , University of Lund , Malmo, Sweden Published online: 03 Aug 2010.
To cite this article: Ingrid Akesson B.Sc.P.T. , Andrejs Schutz Ph.D. , Robyn Attewell M.Sc. , Staffan Skerfving M.D. & Per-Olof Glantz O.D. (1991) Status of Mercury and Selenium in Dental Personnel: Impact of Amalgam Work and Own Fillings, Archives of Environmental Health: An International Journal, 46:2, 102-109, DOI: 10.1080/00039896.1991.9937436 To link to this article: http://dx.doi.org/10.1080/00039896.1991.9937436
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http:// www.tandfonline.com/page/terms-and-conditions
Status of Mercury and Selenium in Dental Personnel:
Downloaded by [McGill University Library] at 07:24 07 April 2015
Impact of Amalgam Work and Own Fillings
INGRID AKESSON, B.Sc.P.T. ANDREJS SCHUTZ, Ph.D. ROBYN ATTEWELL, M.k. STAFFAN SKERFVING, M.D. Department of Occupational and Environmental Medicine University Hospital Lund, Sweden PER-OLOF CLANTZ, O.D. Department of Prosthetics School of Dentistry University of Lund Malmo, Sweden
ABSTRACT. Urinary mercury (U-Ha and plasma mercury (P-Hg) levels were higher in 244 dental personnel than in 81 matched referents (U-Hg: 1.8 and 1.1 pmol/mol creatinine, respectively; p < -001; P-Hg: 6.7 and 6.2 nmol/l, respectively; p = .03). The amalgam in the mouth influenced mercury levels in whole blood (B-Hg), plasma, and urine. The association was nonlinear: the more amalgam, the larger the relative increase in mercury levels. The number of amalgam surfaces accounted for more of the variance in blood and urine mercury levels than did the number of fillings (e.g., U-Hg: 44% and 36%, respective ly). The estimated increases in mercury level with rising amalgam load were 3.0%, 2.0%, and 0.8% per filled surface for U-Hg, P-Hg, and B-Hg, respectively (p < .OOO1 in all cases). The impact of occupational exposure on U-Hg in the dental personnel corresponded to approximately 19 amalgam surfaces. Ceramo metallic restorations were associated with higher (319") U-Hg.
OCCUPATIONAL EXPOSURE of dental personnel to elemental mercury (Hg) vapor is well doc~mented.'-~ Even recently, cases of clinical Hg poisoning6 and embryotoxicity' among dental personnel have been published. During recent years, much effort has been directed toward reducing occupational exposure to Hg in dental surgeries. Therefore, examining present exposure in various groups of dental personnel would be of interest. 102
Exposure to inorganic Hg may also occur from amalgam filling^,^^^ the results of which are increased levels of Hg in plasma'of" and Accumulation of Hg in the central nervous system as a result of amalgam exposure has also been ~uggested.'~ Therefore, amalgam may be responsible for much of the "background" Hg exposure in the population. In summary, estimation by biological monitoring of occupational exposure to Hg in dental surgeries should Archives of Environmental Health
take into account the dental amalgam status of the personnel, the impact of which has yet to be sufficiently clarified. Selenium (Se)interacts profoundly with the metabolism of Hg. Moreover, Hg also affects Se metabolism, as has been noted in humans exposed to elemental Hg These findings, however, have not been consistent, and more data are needed. Based on the foregoing, the purpose of this study was to investigate Hg levels in whole blood (B-Hg), plasma (P-Hg), and urine (U-Hg), as well as Se levels in plasma (P-Se), in various groups of dental personnel and matched referents. Special attention was focused on the impact of metallic dental restorations.
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Materials and methods Dental personnel. The eligible study population consisted of 244 dental personnel in the public dental service in the county of Blekinge, Sweden. Subjects who were on leave (except sick leave) were excluded from the study. Eight subjects were on sick leave, and 10 (6.8%) did not wish to participate. The study group consisted of 83 dentists (47 males, 36 females) whose average age was 38 y and who had an average duration of employment of 11 y. Also included were 153 female nurses whose average age was 37 y and who had an average duration of employment of 13 y. Eight dental hygienists were also included (average age, 37 y; average duration of employment, 8.6 y). Referents. After determining sex and age distributions and fish consumption in the dental personnel group, a matched stratified sample (n = 81) was selected from a group of subjects from the same county who had been studied previously.22The referents had no known occupational exposure to Hg. Questionnaire. Information about fish consumption (i.e., frequency of fish meals, species, and origin of the fish), Se tablet intake, smoking habits, general health, and medication was obtained for each subject.22 For dental personnel, job type and duration, clinic size and clinic age, and potential exposure to Hg were assessed. The average number of ”amalgam patients” treated each day was estimated. Personnel whose main duties included dental treatments other than the placement and replacement of amalgam restorations (e.g., prosthetic dentistry, orthodontics, periodontology, oral surgery) were identified and termed “specialists,” and the remainder of personnel were termed “general practitioners.” The method of amalgam preparation (semi-open or incapsulated; mixing, if any; and trituration) and the type of amalgam used (i.e., conventional type or “non-gamma 2 type”) were noted. Dental status. Oral amalgam status was determined using several parameters. (1 .I The number of amalgam restorationdfllings was defined as the total number of observed individual amalgam restorations on one, two, three, or all exposed surfaces of a single tooth. The mean number of fillings for the dental personnel and referents was 14 (range 0-33) and 16 (range = 0-25), respectively.
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March/April1991 [Vol. 46 (No. 2)]
(2.) The number of restored surfaces was defined as the total number of observed tooth surfaces with an amalgam restoration or part of such a restoration (dental personnel 29 [range = 0-591, referents = 32 [range = 0-541). (3.) The total amalgam surface area was defined as the total estimated area of the observed amalgam restorations (dental personnel = 941 mmz [range = 0-2 395 mmz], referents = 985 mmz [0-2 067 mmz]). For these calculations, the areas of the teeth were calculated according to W0elfe1*~ and the relative areas of the various types of amalgam restorations according to Milleding.24 (4.) The total surface area o f the mechanically active part of amalgam restoration/fillings was defined as the total estimated occlusal areas of all observed amalgam restorations/fillings (dental personnel = 444 mmz [range = 0-1 078 mmz], referents 434 mm2 [range = 0-706 mm2]). The occlusal areas of the teethz3and the relative occlusal areas of the types of amalgam restorat i o n were ~ ~ ~determined. (5.)The surface area of the mechanically inactive part of the restoration was calculated as the difference between the total area and area of mechanically active amalgam. Restorations other than amalgam ones were also recorded. Sampling. Samples of blood (4 x 10 ml) were obtained from the cubital vein and put in four metal-free tubes containing heparin (VacutaineP ). The plasma was separated soon after sampling. The samples were kept frozen at -20 “C until analysis. A morning spot sample of urine was collected in metal-free tubes (2 x 10 ml) on the same day the blood samples were obtained. The subjects were instructed to void the urine sample directly into the tubes. The urine samples were kept frozen at -20 “C until analysis. Mercury analysis. The Hg content of blood and urine was determined in wet-digested samples by “cold vapor” atomic absorption technique; automatic equip ment was Samples of plasma (1.0 g) and whole blood (0.5 g) were digested overnight with nitric and perchloric acids at 65 0C.26Urine samples (0.5 ml) were digested with potassium permanganate and sulfuric acid at room temperature.” The detection limit was 0.5 nmol/l in plasma, 1.1 nmol/l in whole blood, and 1.0 nmolll (approximately 0.1 pmollmol creatinine) in urine. All samples were analyzed in duplicate. The precision, as calculated from the duplicate analyses, was 13% (coefficient of variation) for plasma samples in the 1.0-8.0 nmol/l range (mean 5.1 nmolll; n = 192) and 7% in the 8.1-60 nmol/l range (mean 11.8 nmol/l; n = 133). For whole blood, the precision was 8% for samples in the range of 5.8-16.0 nmolll (mean 12.7 nmol/l; n 143) and 6% for samples in the range of 16.1-69 nmol/l (mean = 22.2 nmolll; n = 182). For urine, the precision was 9% in the 1.0-25 nmol/l range (mean = 14.5 nmol/l; n = 164) and 7% in the 26-125 nmol/l range (mean = 45 nmol/l; n = 155). Accuracy was checked by analyses in each series of reference samples. For lyophilized serum (“Seronorm,” Nycomed AS, Diagnostics, Oslo), the reference value
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was 5.6 nmol/l, and our results in different series averaged 5.8 nmolll (standard deviation [SD] = 0.1 1; range = 5.1-7.2; n = 27). For lyophilized whole blood (Behring Institute, Marburg, Federal Republic of Cermany) the reference value was 52 nmol/l, and our average was 52 nmolll (SD = 1.6, range = 48-55; n = 54). For lyophilized urine ("Lanonorm," Behring Institute), the assigned value was 50 nmolll (confidence range = 42-57 nmol/l), and our results averaged 49 nmolll (SD = 2.5, range = 44-60; n = 51). Selenium analysis. Selenium was determined by a fluorimetric method2' (detection limit = 0.03 pnolll). All samples were analyzed in duplicate. The precision, as calculated from the duplicate analyses, was 3.2%. Accuracy was checked by including a reference sample ("Seronorm," Nycomed AS, Diagnostics, Oslo) containing 1.14 prnolll (value certified by IUPAC; SD = 0.08). The results obtained by the method used in this study averaged 1.15 pmolll (SD = 0.03, range = 1.12-1.20 pmolll; n = 10). Creatinine analysis. Creatinine in urine was determined by a modified kinetic method of Jaff. (Lustgarten and Wenk,29 modified by P. Masson, Department of Clinical Chemistry, University Hospital, Lund). The precision was 5.9% and was calculated from duplicate analyses of 93 samples in the 4-31 mmol/l range (mean = 12.9 mmol). Results were not available for six of the subjects. Statistics. We used multiple linear regression to study the relationships between Hg (and Se) levels and occupational, dental, and other factors. We performed separate regressions for €3-Hg, P-Hg, U-Hg, and P-Se. Consideration of the skewness of the distributions and examination of the residual plots confirmed that log transformation was necessary for each Hg variable, but not for Se. Therefore, geometric means are used as the descriptive statistic for the Hg variables and are quoted as ordinary arithmetic means for Se. Several different regression models were fitted according to which of the five measures of amalgam status (Table 1) was being considered (Models 1-5) and according to whether all 325 subjects were included in the analyses (Models 1-5) or just the 244 dental personnel (Model 6). The results of the different regression models are expressed according to whether a factor has been treated as a continuous variable (e.g., surface area, employment duration) or a categorical variable (e.g., sex, occupational status) and whether the log transformation has been applied to the dependent variable. Thus, the incremental increases in Hg for each continuous variable are expressed as percentages (e.g., percentage increase per mm2) and as absolute increments for Se. However, we have summarized the differences between subgroups identified by categorical variables by calculating the adjusted means (e.g., for sex, the mean values for males and females are presented, corrected for all other factors in the model, and calculated at the mean value of each factor). Geometric means are presented for Hg levels, whereas arithmetic means are presented for Se levels. For those Hg models where logarithmic transformation was used, the effect of the different factors is multiplicative. This also results in the 104
Table 1.-Factors Included in Different Regression Models For Mercury and Selenium levels Model no.
Factors (a) Occupational exposure (dental personnel/ referents) (b) Amalgam surface area (total mm') (c) Ceramometallic crowns (yeslno) (d) Cold crowns (yeslno) (e) Sex ( M l n (0 Age (Y) (g) Smoking status (neverledcurrent) (h) Fish meals per week ( 6 y) (d) Clinic size (< 6 dentists/, 6 dentists) (e) Employment duration (y) (0 Average number of amalgam patients treated per day (g) Amalgam surface area (total mm') (h) Ceramometallic crowns (yeslno) (i) Cold crowns (yeslno) (j) Sex (Mln (k) Age (y) (I) Smoking status (neverlexlcurrent) (m) Fish meals per week ( 28 pmol/mol ~reatinine).~’ The levels found in subjects who had no occupational exposure were even lower. Health significance of exposure in this range is not known. In one study, no association was seen between symptoms and amalgam statu~.~’ However, considerable variation in susceptibility probably exists. Therefore, Hg is an allergen.32Also, considering the extreme variation in susceptibility of different rodent strains to Hg,33low uptakes might be of interest-especially when large populations are exposed. Despite the small numbers of subjects, dental personnel who used amalgam capsulae had significantly lower U-Hg levels than the other. This indicates a way to reduce exposure. We found that females had higher U-Hg levels than males, which i s in accordance with an earlier study.* 108
Perhaps males and females metabolize Hg differently, as has been described in animals.34 Associations with age were also seen. The decrease in U-Hg as age increased has been reported elsewhere.’ Surprisingly, B-Hg increased with age. These findings suggest an as-yet-unexplored variation in Hg metabolism with age. This relationship, however, was not o b served in regressions performed solely on the referents. Fish consumption was associated with B-Hg. This duplicates earlier findings” and obviously results from the methylmercury content of fish. Methylmercury in blood i s mainly found i n the cells, and little is present in plasma or urine.3oFish intake was also associated with an increase in P-Se, which reflects the importance of fish as a selenium source in the diet.35,36 Dental personnel had higher P-Se than referents. Perhaps this results from varying Se dietary intake among dental personnel and referents (although, fish intake and Se tablet consumption were allowed for). Another possibility is that a metabolic interaction exists between Hg and Se. The present pattern may agree with similar findings in earlier studies of Hg-exposed s u b j e ~ t s ~but ~ ~not ’ ~ ~with ~ ’ the increase in Se excretion in another.17 The mechanism is not clear. However, it may result from a combined binding of Hg and Se in plasma proteins.
********** This study was supported by a grant from the National Swedish Environmental Protection Agency. Support was also given by the County Council of Blekinge. Valuable assistance was given by Dr. Carl-Cunnar Lingstrom, chief dental officer; Ms. Vivi Svensson; Ms. Kerstin Wijk; Ms. Ulla Persson; Ms. Anita Nilsson, R.N.; Ms. Catharina Mattsson; Ms. Wiveka Larsson; Ms. Vivian Sturesson; Mr. Peter Ohrbring; Ms. Cudrun Karlsson; Ms. Agneta Bohlin; Ms. Anna Akantis; Mr. Lars Lindgren; Mr. Anders Ekholm; Dr. Bengt Akesson, D.M.Sci.; Mr. Cert-Ake Hansson, M. Eng; Mr. Mark Olson, B.A.; Dr. Krister Nilner, O.D.; Dr. Lennart Roslund; Ms. Cudrun Persson; and Dr. Erik Strandman, senior consultant. Requests for reprints should be sent to: Ms. Ingrid Akesson, B.Sc. P.T., Department of Occupational and Environmental Medicine, University Hospital, 5221 85 Lund, Sweden.
********** References 1. 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;13:235-43. 2, Cundersen N, Lie A. Mercury exposure in dental surgeries. An epidemiological cross-sectional study. Norsk Tannl Form Tid /in Norwegian) 1981;91:219-26. 3. Smart ER. The hazards of mercury in dentistry. Rev Environ Health 1985;1:59-86. 4. Nilsson B, Nilsson B. Mercury in dental practice. I. The working environment of dental personnel and their exposure to mercury vapor. Swed Dent J 1986a;101-14. 5. Nilsson B, Nilsson B. Mercury in dental practice. 111. Urinary mercury excretion in dental personnel. Swed Dent J 1986b;1022132. 6 Hryhorczuk DO, Meyers L. Chen C. Treatment of mercury intoxication in a dentist with N-acetyl-D, L-penicillamine. J Toxicol Clin Toxicol 1982;19:401-08. 7 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;59:551-57.
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8. Clarkson 1w,Friberg L, Hursh JB, Nylander M. The prediction of intake of mercury vapor from amalgams. In: Biological monitoring of toxic metals. New York: Plenum Press, 1988;247-60. 9. Berglund A, Pohl L, Olsson S, Bergman M. Determination of the rate of release of intra-oral mercury vapor from amalgam. J Dent Res 1988;671235-242. 10. Molin M, Marklund S, Bergman 6, Bergman M, Stenman E. Plasma-selenium, glutathione peroxidase in erythrocytes and mercury in plasma in patients allegedly subject to oral galvanism. Scand J Dent Res 1987;95:328-34. 11. Molin M, Bergman 6, Marklund SL, Schutz A, Skeking S. Mercury, selenium and gluthathion peroxidase after amalgam removal in man. Acta Odont Scand (in press). 12. Olstad ML, Holland RJ, Wandel N, Hensten Pettersen A. Correlation between amalgam restorations and mercury concentrations in urine. J Dent Res 1987;66:1179-82. 13. Langworth S, Elinder CG, ikesson A. Mercury exposure from dental fillings. I. Mercury concentrations in blood and urine. Swed Dent J 1988;12:69-70. 14. Nylander M, Friberg L, Lind 6. Mercury concentrations in the human brain and kidneys in relation to exposure from dental amalgam fillings. Swed Dent J 1987;11:179-87. 15. Kosta L, Vyrne AR, Zelenko V. Correlation between selenium and mercury in man following exposure to inorganic mercury. Nature 1975;254238-39. 16. Rossi L, Clemente C, Santaroni G. Mercury and selenium distribution in a defined area and in its population. Arch Environ Health 1976;31: 16065. 17. Alexander J, Thomassen Y, Aaseth 1. Increased urinary excretion of Selenium among workers exposed to elemental mercury vapor. Appl Toxicol 1983;3: 143-45. 18. Hongo T, Suzuki T, Himeno S, Watanabe C, Satoh H, Shimada Y. Does mercury vapor exposure increase urinary selenium excretion? Ind Health 1985;23:163-65. 19. Suzuki T, Himeno S, Hongo T, Watanabe C. Mercury-selenium interaction in workers exposed to elemental mercury vapor. J Appl Toxicol 1986;6:149-53. 20. Nylander M, Weiner 1. Relation between mercury and selenium in pituitary glands of dental staff. Br J Ind Med 1989;46:751-52. 21. BarreGrd L, Thomasen Y, Schijtz A, Marklund SL. tevels of selenium and oxidative enzymes following occupational exposure to inorganic mercury (in press).
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22. Svensson BG, Bjornham A, Schutz A, Lettevall U, Nilsson A, Skerfving S. Acidic deposition and human exposure to toxic metals. Sci Tot Environ 1987;67101-15. 23. Woelfel JB. Dental anatomy. Philadelphia, PA: Lea & Febinger, 1984;369-70. 24. Milleding P. Preparation techniques 1 (in Swedish). Stockholm: Almqvist & Wiksell, 1973; 45-100. 25. Einarsson 0, Lindstedt G, Bergstrom TA. A computerised automatic apparatus for determination of merculy in biological samples. J Autom Chem 1984;6:74-79. 26. Skare I. Micrcdetermination of mercury in biological samples. H I . Automated determination of mercury in urine, fish and blood samples. Analyst 1972;97148-55. 27. Lindstedt G. A rapid method for the determination of mercury in urine. Analyst 1970;95:264-71. 28. La Londe L, Jean Y, Roberts KD, Chapdelaine A, Bleau G. Fluorometry of selenium in serum or urine. Clin Chem 1982;28 172-74. 29. Lustgarten JA, Wenk RE. Simple, rapid kinetic method for serum creatinine measurement. Clin Chem 1972;18:1419-22. 30. Skerfving S, Berlin M. Inorganic mercury. Arbete & Halsa (in Swedish) 1985201-80. 31. Ahlqwist M, Bengtsson C, Furunes 8, Hollender L, Lapidus L. Number of amalgam tooth fillings in relation to subjectively experienced symptoms in a study of Swedish women. Community Dent Oral Epidemiol 1988;16:227-31. 32. Stenman E, Bergman M. Hypersensitivity reactions to dental materials in a referred group of patients. Sand J Dent Res 1989;9776-83. 33. Hultman P. Enestram S. The induction of immune complex deposits in mice by peroral and parenteral administration of mercuric chloride: strain dependent susceptibility. Clin Exp lmmunol 1987;2:283-92. 34. Magos L, Webb M, Butler WH. The effect of cadmium pretreatment on the nephrotoxic action and kidney uptake of mercury in male and female rats. Br J Exp Pathol 1974;55:589-94. 35. Ringstad I, Fdnnebh V. The Tromd heart study: serum in a lowrisk population for cardiovascular disease and cancer and matched controls. Ann Clin Res 1987;19:351-54. 36. Thorngren M, lkesson 6. Effect of dietary fish on plasma selenium and its relation to haemostatic changes in healthy adults. Int J Vit Nutr Res 1987;57:429-35.
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Archives of Environmental Health: An International Journal Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/vzeh20
Status of Mercury and Selenium in Dental Personnel: Impact of Amalgam Work and Own Fillings a
a
a
Ingrid Akesson B.Sc.P.T. , Andrejs Schutz Ph.D. , Robyn Attewell M.Sc. , Staffan a
Skerfving M.D. & Per-Olof Glantz O.D.
b
a
Department of Occupational and Environmental , Medicine University Hospital , Lund, Sweden b
Department of Prosthetics School of Dentistry , University of Lund , Malmo, Sweden Published online: 03 Aug 2010.
To cite this article: Ingrid Akesson B.Sc.P.T. , Andrejs Schutz Ph.D. , Robyn Attewell M.Sc. , Staffan Skerfving M.D. & Per-Olof Glantz O.D. (1991) Status of Mercury and Selenium in Dental Personnel: Impact of Amalgam Work and Own Fillings, Archives of Environmental Health: An International Journal, 46:2, 102-109, DOI: 10.1080/00039896.1991.9937436 To link to this article: http://dx.doi.org/10.1080/00039896.1991.9937436
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http:// www.tandfonline.com/page/terms-and-conditions
Status of Mercury and Selenium in Dental Personnel:
Downloaded by [McGill University Library] at 07:24 07 April 2015
Impact of Amalgam Work and Own Fillings
INGRID AKESSON, B.Sc.P.T. ANDREJS SCHUTZ, Ph.D. ROBYN ATTEWELL, M.k. STAFFAN SKERFVING, M.D. Department of Occupational and Environmental Medicine University Hospital Lund, Sweden PER-OLOF CLANTZ, O.D. Department of Prosthetics School of Dentistry University of Lund Malmo, Sweden
ABSTRACT. Urinary mercury (U-Ha and plasma mercury (P-Hg) levels were higher in 244 dental personnel than in 81 matched referents (U-Hg: 1.8 and 1.1 pmol/mol creatinine, respectively; p < -001; P-Hg: 6.7 and 6.2 nmol/l, respectively; p = .03). The amalgam in the mouth influenced mercury levels in whole blood (B-Hg), plasma, and urine. The association was nonlinear: the more amalgam, the larger the relative increase in mercury levels. The number of amalgam surfaces accounted for more of the variance in blood and urine mercury levels than did the number of fillings (e.g., U-Hg: 44% and 36%, respective ly). The estimated increases in mercury level with rising amalgam load were 3.0%, 2.0%, and 0.8% per filled surface for U-Hg, P-Hg, and B-Hg, respectively (p < .OOO1 in all cases). The impact of occupational exposure on U-Hg in the dental personnel corresponded to approximately 19 amalgam surfaces. Ceramo metallic restorations were associated with higher (319") U-Hg.
OCCUPATIONAL EXPOSURE of dental personnel to elemental mercury (Hg) vapor is well doc~mented.'-~ Even recently, cases of clinical Hg poisoning6 and embryotoxicity' among dental personnel have been published. During recent years, much effort has been directed toward reducing occupational exposure to Hg in dental surgeries. Therefore, examining present exposure in various groups of dental personnel would be of interest. 102
Exposure to inorganic Hg may also occur from amalgam filling^,^^^ the results of which are increased levels of Hg in plasma'of" and Accumulation of Hg in the central nervous system as a result of amalgam exposure has also been ~uggested.'~ Therefore, amalgam may be responsible for much of the "background" Hg exposure in the population. In summary, estimation by biological monitoring of occupational exposure to Hg in dental surgeries should Archives of Environmental Health
take into account the dental amalgam status of the personnel, the impact of which has yet to be sufficiently clarified. Selenium (Se)interacts profoundly with the metabolism of Hg. Moreover, Hg also affects Se metabolism, as has been noted in humans exposed to elemental Hg These findings, however, have not been consistent, and more data are needed. Based on the foregoing, the purpose of this study was to investigate Hg levels in whole blood (B-Hg), plasma (P-Hg), and urine (U-Hg), as well as Se levels in plasma (P-Se), in various groups of dental personnel and matched referents. Special attention was focused on the impact of metallic dental restorations.
Downloaded by [McGill University Library] at 07:24 07 April 2015
Materials and methods Dental personnel. The eligible study population consisted of 244 dental personnel in the public dental service in the county of Blekinge, Sweden. Subjects who were on leave (except sick leave) were excluded from the study. Eight subjects were on sick leave, and 10 (6.8%) did not wish to participate. The study group consisted of 83 dentists (47 males, 36 females) whose average age was 38 y and who had an average duration of employment of 11 y. Also included were 153 female nurses whose average age was 37 y and who had an average duration of employment of 13 y. Eight dental hygienists were also included (average age, 37 y; average duration of employment, 8.6 y). Referents. After determining sex and age distributions and fish consumption in the dental personnel group, a matched stratified sample (n = 81) was selected from a group of subjects from the same county who had been studied previously.22The referents had no known occupational exposure to Hg. Questionnaire. Information about fish consumption (i.e., frequency of fish meals, species, and origin of the fish), Se tablet intake, smoking habits, general health, and medication was obtained for each subject.22 For dental personnel, job type and duration, clinic size and clinic age, and potential exposure to Hg were assessed. The average number of ”amalgam patients” treated each day was estimated. Personnel whose main duties included dental treatments other than the placement and replacement of amalgam restorations (e.g., prosthetic dentistry, orthodontics, periodontology, oral surgery) were identified and termed “specialists,” and the remainder of personnel were termed “general practitioners.” The method of amalgam preparation (semi-open or incapsulated; mixing, if any; and trituration) and the type of amalgam used (i.e., conventional type or “non-gamma 2 type”) were noted. Dental status. Oral amalgam status was determined using several parameters. (1 .I The number of amalgam restorationdfllings was defined as the total number of observed individual amalgam restorations on one, two, three, or all exposed surfaces of a single tooth. The mean number of fillings for the dental personnel and referents was 14 (range 0-33) and 16 (range = 0-25), respectively.
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March/April1991 [Vol. 46 (No. 2)]
(2.) The number of restored surfaces was defined as the total number of observed tooth surfaces with an amalgam restoration or part of such a restoration (dental personnel 29 [range = 0-591, referents = 32 [range = 0-541). (3.) The total amalgam surface area was defined as the total estimated area of the observed amalgam restorations (dental personnel = 941 mmz [range = 0-2 395 mmz], referents = 985 mmz [0-2 067 mmz]). For these calculations, the areas of the teeth were calculated according to W0elfe1*~ and the relative areas of the various types of amalgam restorations according to Milleding.24 (4.) The total surface area o f the mechanically active part of amalgam restoration/fillings was defined as the total estimated occlusal areas of all observed amalgam restorations/fillings (dental personnel = 444 mmz [range = 0-1 078 mmz], referents 434 mm2 [range = 0-706 mm2]). The occlusal areas of the teethz3and the relative occlusal areas of the types of amalgam restorat i o n were ~ ~ ~determined. (5.)The surface area of the mechanically inactive part of the restoration was calculated as the difference between the total area and area of mechanically active amalgam. Restorations other than amalgam ones were also recorded. Sampling. Samples of blood (4 x 10 ml) were obtained from the cubital vein and put in four metal-free tubes containing heparin (VacutaineP ). The plasma was separated soon after sampling. The samples were kept frozen at -20 “C until analysis. A morning spot sample of urine was collected in metal-free tubes (2 x 10 ml) on the same day the blood samples were obtained. The subjects were instructed to void the urine sample directly into the tubes. The urine samples were kept frozen at -20 “C until analysis. Mercury analysis. The Hg content of blood and urine was determined in wet-digested samples by “cold vapor” atomic absorption technique; automatic equip ment was Samples of plasma (1.0 g) and whole blood (0.5 g) were digested overnight with nitric and perchloric acids at 65 0C.26Urine samples (0.5 ml) were digested with potassium permanganate and sulfuric acid at room temperature.” The detection limit was 0.5 nmol/l in plasma, 1.1 nmol/l in whole blood, and 1.0 nmolll (approximately 0.1 pmollmol creatinine) in urine. All samples were analyzed in duplicate. The precision, as calculated from the duplicate analyses, was 13% (coefficient of variation) for plasma samples in the 1.0-8.0 nmol/l range (mean 5.1 nmolll; n = 192) and 7% in the 8.1-60 nmol/l range (mean 11.8 nmol/l; n = 133). For whole blood, the precision was 8% for samples in the range of 5.8-16.0 nmolll (mean 12.7 nmol/l; n 143) and 6% for samples in the range of 16.1-69 nmol/l (mean = 22.2 nmolll; n = 182). For urine, the precision was 9% in the 1.0-25 nmol/l range (mean = 14.5 nmol/l; n = 164) and 7% in the 26-125 nmol/l range (mean = 45 nmol/l; n = 155). Accuracy was checked by analyses in each series of reference samples. For lyophilized serum (“Seronorm,” Nycomed AS, Diagnostics, Oslo), the reference value
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was 5.6 nmol/l, and our results in different series averaged 5.8 nmolll (standard deviation [SD] = 0.1 1; range = 5.1-7.2; n = 27). For lyophilized whole blood (Behring Institute, Marburg, Federal Republic of Cermany) the reference value was 52 nmol/l, and our average was 52 nmolll (SD = 1.6, range = 48-55; n = 54). For lyophilized urine ("Lanonorm," Behring Institute), the assigned value was 50 nmolll (confidence range = 42-57 nmol/l), and our results averaged 49 nmolll (SD = 2.5, range = 44-60; n = 51). Selenium analysis. Selenium was determined by a fluorimetric method2' (detection limit = 0.03 pnolll). All samples were analyzed in duplicate. The precision, as calculated from the duplicate analyses, was 3.2%. Accuracy was checked by including a reference sample ("Seronorm," Nycomed AS, Diagnostics, Oslo) containing 1.14 prnolll (value certified by IUPAC; SD = 0.08). The results obtained by the method used in this study averaged 1.15 pmolll (SD = 0.03, range = 1.12-1.20 pmolll; n = 10). Creatinine analysis. Creatinine in urine was determined by a modified kinetic method of Jaff. (Lustgarten and Wenk,29 modified by P. Masson, Department of Clinical Chemistry, University Hospital, Lund). The precision was 5.9% and was calculated from duplicate analyses of 93 samples in the 4-31 mmol/l range (mean = 12.9 mmol). Results were not available for six of the subjects. Statistics. We used multiple linear regression to study the relationships between Hg (and Se) levels and occupational, dental, and other factors. We performed separate regressions for €3-Hg, P-Hg, U-Hg, and P-Se. Consideration of the skewness of the distributions and examination of the residual plots confirmed that log transformation was necessary for each Hg variable, but not for Se. Therefore, geometric means are used as the descriptive statistic for the Hg variables and are quoted as ordinary arithmetic means for Se. Several different regression models were fitted according to which of the five measures of amalgam status (Table 1) was being considered (Models 1-5) and according to whether all 325 subjects were included in the analyses (Models 1-5) or just the 244 dental personnel (Model 6). The results of the different regression models are expressed according to whether a factor has been treated as a continuous variable (e.g., surface area, employment duration) or a categorical variable (e.g., sex, occupational status) and whether the log transformation has been applied to the dependent variable. Thus, the incremental increases in Hg for each continuous variable are expressed as percentages (e.g., percentage increase per mm2) and as absolute increments for Se. However, we have summarized the differences between subgroups identified by categorical variables by calculating the adjusted means (e.g., for sex, the mean values for males and females are presented, corrected for all other factors in the model, and calculated at the mean value of each factor). Geometric means are presented for Hg levels, whereas arithmetic means are presented for Se levels. For those Hg models where logarithmic transformation was used, the effect of the different factors is multiplicative. This also results in the 104
Table 1.-Factors Included in Different Regression Models For Mercury and Selenium levels Model no.
Factors (a) Occupational exposure (dental personnel/ referents) (b) Amalgam surface area (total mm') (c) Ceramometallic crowns (yeslno) (d) Cold crowns (yeslno) (e) Sex ( M l n (0 Age (Y) (g) Smoking status (neverledcurrent) (h) Fish meals per week ( 6 y) (d) Clinic size (< 6 dentists/, 6 dentists) (e) Employment duration (y) (0 Average number of amalgam patients treated per day (g) Amalgam surface area (total mm') (h) Ceramometallic crowns (yeslno) (i) Cold crowns (yeslno) (j) Sex (Mln (k) Age (y) (I) Smoking status (neverlexlcurrent) (m) Fish meals per week ( 28 pmol/mol ~reatinine).~’ The levels found in subjects who had no occupational exposure were even lower. Health significance of exposure in this range is not known. In one study, no association was seen between symptoms and amalgam statu~.~’ However, considerable variation in susceptibility probably exists. Therefore, Hg is an allergen.32Also, considering the extreme variation in susceptibility of different rodent strains to Hg,33low uptakes might be of interest-especially when large populations are exposed. Despite the small numbers of subjects, dental personnel who used amalgam capsulae had significantly lower U-Hg levels than the other. This indicates a way to reduce exposure. We found that females had higher U-Hg levels than males, which i s in accordance with an earlier study.* 108
Perhaps males and females metabolize Hg differently, as has been described in animals.34 Associations with age were also seen. The decrease in U-Hg as age increased has been reported elsewhere.’ Surprisingly, B-Hg increased with age. These findings suggest an as-yet-unexplored variation in Hg metabolism with age. This relationship, however, was not o b served in regressions performed solely on the referents. Fish consumption was associated with B-Hg. This duplicates earlier findings” and obviously results from the methylmercury content of fish. Methylmercury in blood i s mainly found i n the cells, and little is present in plasma or urine.3oFish intake was also associated with an increase in P-Se, which reflects the importance of fish as a selenium source in the diet.35,36 Dental personnel had higher P-Se than referents. Perhaps this results from varying Se dietary intake among dental personnel and referents (although, fish intake and Se tablet consumption were allowed for). Another possibility is that a metabolic interaction exists between Hg and Se. The present pattern may agree with similar findings in earlier studies of Hg-exposed s u b j e ~ t s ~but ~ ~not ’ ~ ~with ~ ’ the increase in Se excretion in another.17 The mechanism is not clear. However, it may result from a combined binding of Hg and Se in plasma proteins.
********** This study was supported by a grant from the National Swedish Environmental Protection Agency. Support was also given by the County Council of Blekinge. Valuable assistance was given by Dr. Carl-Cunnar Lingstrom, chief dental officer; Ms. Vivi Svensson; Ms. Kerstin Wijk; Ms. Ulla Persson; Ms. Anita Nilsson, R.N.; Ms. Catharina Mattsson; Ms. Wiveka Larsson; Ms. Vivian Sturesson; Mr. Peter Ohrbring; Ms. Cudrun Karlsson; Ms. Agneta Bohlin; Ms. Anna Akantis; Mr. Lars Lindgren; Mr. Anders Ekholm; Dr. Bengt Akesson, D.M.Sci.; Mr. Cert-Ake Hansson, M. Eng; Mr. Mark Olson, B.A.; Dr. Krister Nilner, O.D.; Dr. Lennart Roslund; Ms. Cudrun Persson; and Dr. Erik Strandman, senior consultant. Requests for reprints should be sent to: Ms. Ingrid Akesson, B.Sc. P.T., Department of Occupational and Environmental Medicine, University Hospital, 5221 85 Lund, Sweden.
********** References 1. 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;13:235-43. 2, Cundersen N, Lie A. Mercury exposure in dental surgeries. An epidemiological cross-sectional study. Norsk Tannl Form Tid /in Norwegian) 1981;91:219-26. 3. Smart ER. The hazards of mercury in dentistry. Rev Environ Health 1985;1:59-86. 4. Nilsson B, Nilsson B. Mercury in dental practice. I. The working environment of dental personnel and their exposure to mercury vapor. Swed Dent J 1986a;101-14. 5. Nilsson B, Nilsson B. Mercury in dental practice. 111. Urinary mercury excretion in dental personnel. Swed Dent J 1986b;1022132. 6 Hryhorczuk DO, Meyers L. Chen C. Treatment of mercury intoxication in a dentist with N-acetyl-D, L-penicillamine. J Toxicol Clin Toxicol 1982;19:401-08. 7 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;59:551-57.
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8. Clarkson 1w,Friberg L, Hursh JB, Nylander M. The prediction of intake of mercury vapor from amalgams. In: Biological monitoring of toxic metals. New York: Plenum Press, 1988;247-60. 9. Berglund A, Pohl L, Olsson S, Bergman M. Determination of the rate of release of intra-oral mercury vapor from amalgam. J Dent Res 1988;671235-242. 10. Molin M, Marklund S, Bergman 6, Bergman M, Stenman E. Plasma-selenium, glutathione peroxidase in erythrocytes and mercury in plasma in patients allegedly subject to oral galvanism. Scand J Dent Res 1987;95:328-34. 11. Molin M, Bergman 6, Marklund SL, Schutz A, Skeking S. Mercury, selenium and gluthathion peroxidase after amalgam removal in man. Acta Odont Scand (in press). 12. Olstad ML, Holland RJ, Wandel N, Hensten Pettersen A. Correlation between amalgam restorations and mercury concentrations in urine. J Dent Res 1987;66:1179-82. 13. Langworth S, Elinder CG, ikesson A. Mercury exposure from dental fillings. I. Mercury concentrations in blood and urine. Swed Dent J 1988;12:69-70. 14. Nylander M, Friberg L, Lind 6. Mercury concentrations in the human brain and kidneys in relation to exposure from dental amalgam fillings. Swed Dent J 1987;11:179-87. 15. Kosta L, Vyrne AR, Zelenko V. Correlation between selenium and mercury in man following exposure to inorganic mercury. Nature 1975;254238-39. 16. Rossi L, Clemente C, Santaroni G. Mercury and selenium distribution in a defined area and in its population. Arch Environ Health 1976;31: 16065. 17. Alexander J, Thomassen Y, Aaseth 1. Increased urinary excretion of Selenium among workers exposed to elemental mercury vapor. Appl Toxicol 1983;3: 143-45. 18. Hongo T, Suzuki T, Himeno S, Watanabe C, Satoh H, Shimada Y. Does mercury vapor exposure increase urinary selenium excretion? Ind Health 1985;23:163-65. 19. Suzuki T, Himeno S, Hongo T, Watanabe C. Mercury-selenium interaction in workers exposed to elemental mercury vapor. J Appl Toxicol 1986;6:149-53. 20. Nylander M, Weiner 1. Relation between mercury and selenium in pituitary glands of dental staff. Br J Ind Med 1989;46:751-52. 21. BarreGrd L, Thomasen Y, Schijtz A, Marklund SL. tevels of selenium and oxidative enzymes following occupational exposure to inorganic mercury (in press).
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22. Svensson BG, Bjornham A, Schutz A, Lettevall U, Nilsson A, Skerfving S. Acidic deposition and human exposure to toxic metals. Sci Tot Environ 1987;67101-15. 23. Woelfel JB. Dental anatomy. Philadelphia, PA: Lea & Febinger, 1984;369-70. 24. Milleding P. Preparation techniques 1 (in Swedish). Stockholm: Almqvist & Wiksell, 1973; 45-100. 25. Einarsson 0, Lindstedt G, Bergstrom TA. A computerised automatic apparatus for determination of merculy in biological samples. J Autom Chem 1984;6:74-79. 26. Skare I. Micrcdetermination of mercury in biological samples. H I . Automated determination of mercury in urine, fish and blood samples. Analyst 1972;97148-55. 27. Lindstedt G. A rapid method for the determination of mercury in urine. Analyst 1970;95:264-71. 28. La Londe L, Jean Y, Roberts KD, Chapdelaine A, Bleau G. Fluorometry of selenium in serum or urine. Clin Chem 1982;28 172-74. 29. Lustgarten JA, Wenk RE. Simple, rapid kinetic method for serum creatinine measurement. Clin Chem 1972;18:1419-22. 30. Skerfving S, Berlin M. Inorganic mercury. Arbete & Halsa (in Swedish) 1985201-80. 31. Ahlqwist M, Bengtsson C, Furunes 8, Hollender L, Lapidus L. Number of amalgam tooth fillings in relation to subjectively experienced symptoms in a study of Swedish women. Community Dent Oral Epidemiol 1988;16:227-31. 32. Stenman E, Bergman M. Hypersensitivity reactions to dental materials in a referred group of patients. Sand J Dent Res 1989;9776-83. 33. Hultman P. Enestram S. The induction of immune complex deposits in mice by peroral and parenteral administration of mercuric chloride: strain dependent susceptibility. Clin Exp lmmunol 1987;2:283-92. 34. Magos L, Webb M, Butler WH. The effect of cadmium pretreatment on the nephrotoxic action and kidney uptake of mercury in male and female rats. Br J Exp Pathol 1974;55:589-94. 35. Ringstad I, Fdnnebh V. The Tromd heart study: serum in a lowrisk population for cardiovascular disease and cancer and matched controls. Ann Clin Res 1987;19:351-54. 36. Thorngren M, lkesson 6. Effect of dietary fish on plasma selenium and its relation to haemostatic changes in healthy adults. Int J Vit Nutr Res 1987;57:429-35.
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