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8/13/2019 Lauter Bach
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2008;139;138-145 J Am Dent Assoc
Woods and Timothy DeRouenBrenda Townes, Gail Rosenbaum, James S.Helena Amaral, Jorge Leitão, Michael D. Martin,Castro-Caldas, Mario Bernardo, Henrique Luis,Martin Lauterbach, Isabel P. Martins, Alexandre
randomized trialSeven years of longitudinal observations in awithout amalgam-related mercury exposure:Neurological outcomes in children with and
jada.ada.org ( this information is current as of December 14, 2009 ):The following resources related to this article are available online at
http://jada.ada.org/cgi/content/full/139/2/138
found in the online version of this article at:including high-resolution figures, can beUpdated information and services
dental restorations. Controversyexists, however, as to whether detri-
mental effects on brain develop-ment in children occur as a function
of low-level exposures to mercuryfrom amalgam.1,2 In two recent long-
term, randomized, controlled clin-ical trials of elementary school chil-
dren, investigators found nosignificant differences in neuro-
behavioral performance betweenchildren who received amalgamrestorations and those who received
only resin-based compositerestorations.3,4
The nervous system and thekidney are the two main sites in
which any toxic effects of mercurymight be expected to occur, accord-
ing to results from studies of high-level mercury exposure.1,5 The neu-
rological examination provides one
ABSTRACT
Dr. Lauterbach is a neurologist/researcher, Laboratorio de Estudios de Linguagem, Faculty of Medicine, University of Lisbon, Portugal.Dr. Martins is a neurologist and the director, Laboratorio de Estudios de Linguagem, Faculty of Medicine, University of Lisbon, Portugal.Dr. Castro-Caldas is a professor, Department of Neurology, Faculty of Medicine, University of Lisbon, Portugal.Dr. Bernardo is an associate professor and the chairperson, Department of Preventive Dentistry, Faculty of Dental Medicine, University of Lisbon, Portugal.Mr. Luis is an assistant professor, Dental Hygiene Program, Faculty of Dental Medicine, University of Lisbon, Portugal.Ms. Amaral is a patient care coordinator, Faculty of Dental Medicine, University of Lisbon, Portugal.Dr. Leitão is a cathedratical professor, Institute of Health Sciences, Portuguese Catholic University, Lisbon, Portugal.Dr. Martin is an associate professor, Department of Oral Medicine, School of Dentistry, University of Washington, UW Health Sciences Building, 1958 PacificNortheast, Room B316, Seattle, Wash. 98195-6370, e-mail “[email protected]”. Address reprint requests to Dr. Martin.Dr. Townes is a professor emeritus, Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle.Ms. Rosenbaum is a psychometrist supervisor, Neuropsychology Laboratory, University of Washington, Seattle.Dr. Woods is a research professor, Department of Environmental and Occupational Health Sciences, University of Washington, Seattle.Dr. DeRouen is the executive associate dean for academic affairs and research, School of Dentistry, and a professor, Department of Dental Public Health Sciences,School of Dentistry, University of Washington, Seattle.
Neurological outcomes in children with andwithout amalgam-related mercury exposureSeven years of longitudinal observations in a randomized trial
Martin Lauterbach, MD; Isabel P. Martins, MD, PhD; Alexandre Castro-Caldas, MD, PhD;Mario Bernardo, DMD, PhD; Henrique Luis, MS; Helena Amaral, BS; Jorge Leitão, MD;Michael D. Martin, DMD, MPH, MA, MSD, PhD; Brenda Townes, PhD; Gail Rosenbaum, MS;James S. Woods, PhD; Timothy DeRouen, PhD
JADA, Vol. 139 http://jada.ada.org February 2008 139
method of assessing the integrity of the central
nervous system. In children, it includes observa-tions of neurological hard signs (NHSs) and neu-
rological soft signs (NSSs). NHSs indicatedamage to specific neural structures and, in clin-
ical practice, are used to localize the site of lesionor dysfunction—for example, right homonymoushemianopsia as a sign for left occipital lobe lesion.
Screening for NHSs, consists of a brief neurolog-ical examination, including the evaluation of
mental status, cranial nerves, gross motor andsensory function.6,7
NSSs, on the other hand, are subtle signs of cen-tral nervous system dysfunction that have no local-
izing value—that is, they may merely point toimmature sensory-motor skills and not to any
structural damage or localization in the brain,
such as showing clumsiness in rapid sequences of fine finger movements. In healthy children, theirfrequency and severity tend to decrease with age,along with central nervous system maturation.8-10
In addition, their prevalence is increased in anumber of conditions, such as low birth weight,
mental or cognitive disturbances, emotional distur-bances, low IQ, attention-deficit/hyperactivity dis-
order, obsessive-compulsive disorders and schizo-phrenia.11-16 Although the physiopathology of NSSs
is not fully understood, the fact that they are asso-ciated with or might be predictive of certain disor-
ders makes them useful as nonspecific probes fordisturbances of neurological development.
In previously reported findings, our research
team found no significant differences in neuro-behavioral performance or nerve conduction
velocity (the primary study endpoints) betweenchildren who received only amalgam restorations
and children who received only resin-based com-posite restorations.4,17 This article reports additional
findings on secondary endpoints from systematicneurological examinations of the same cohort of 507
children, randomly assigned to receive dental treat-
ment with either amalgam or resin-based com-posite for posterior restorations (and composite for
all anterior restorations) and studied across aseven-year follow-up period. The aim of the neuro-
logical examination was to identify evidence of focallesions or diffuse dysfunction of the nervous system
to determine whether dental restoration withamalgam has a deleterious effect on neurological
development. The presence of tremor was specifi-cally recorded, in addition to the results of the rou-
tine neurological examination, because it is one of the common manifestations of mercury toxicity.2,3,5
PARTICIPANTS, METHODS ANDMATERIALS
Participants. The study participants were 507children from the Casa Pia school system in
Lisbon, Portugal, who were 8 to 12 years old at thetime of enrollment in the study, which began inJanuary 1997. Inclusion criteria for the study
were having at baseline at least one carious lesionin a permanent tooth, no previous exposure to
amalgam treatments, urinary mercury level lessthan 10 micrograms per liter, blood lead level less
than 15 µg per deciliter, IQ equal to or greaterthan 67 as obtained with the Comprehensive Test
of Nonverbal Intelligence18 and no interfering health condition, such as progressive neurological
disease or renal insufficiency. Participants were
randomly assigned to receive either dentalamalgam for posterior restorations (and resin-based composite restorations elsewhere) or resin-based composite restorations only. The study
design has been described in detail previously.4,17,19
Institutional review board (IRB) approval was
obtained at both the University of Washington,Seattle, and the University of Lisbon, Portugal.
( Author’s note: Please see a note at the end of this article regarding this IRB approval.) We
obtained parental or guardian consent, as well asassent from each child (although assent was not
required). Neurological examinations were ob-tained before the beginning of dental treatmentat baseline and at yearly follow-up examinations
for seven subsequent years.The table shows the number of participants in
each of the randomly assigned groups who under-went neurological examinations at baseline
(before receiving dental treatment) and at follow-up years 1 through 7, together with their sex, eth-
nicity and age. Similar to what was reported pre-viously for the neurobehavioral endpoints,4
among those with neurological examinations
there were no significant differences between thetwo randomized groups in sex, ethnicity or mean
age at the study’s inception.The number of participants who received a
neurological examination in a given year some-times is less than the number for whom we had
data at primary endpoints because the neurolog-
ABBREVIATION KEY. IRB: Institutional review
board. NHS: Neurological hard sign. NSS: Neurologi-cal soft sign.
140 JADA, Vol. 139 http://jada.ada.org February 2008
TABLE
Demographic data for subjects who received neurologicalexaminations.CHARACTERISTIC SUBJECTS’ DATA AT EACH MEASUREMENT POINT, ACCORDING TO RESTORATION TYPE
Baseline Year 1
Amalgam
Resin-Based Composite
Year 2 Year 3 Year 4 Year 5 Year 6 Year 7
No. of Children
Sex Male
Female
Ethnicity (No. [%])White
Nonwhite
Age (Years)Mean
Standard deviation (SD)
Amalgam SurfacesPresent (Mean No.)
No. of Children
Sex Male
Female
Ethnicity (No. [%])WhiteNonwhite
Age (Years)Mean
SD
Amalgam SurfacesPresent (Mean No.)
253
137
116
178 (70)
75 (30)
10.2
0.98
0.0
253*
141
112
180 (71)
73 (29)
10.1
0.94
0.0
235
129
106
164 (70)
71 (30)
11.3
1.01
8.3
231
131
100
164 (71)
67 (29)
11.1
0.99
0.0
230
126
104
163 (71)
67 (29)
12.3
1.03
8.1
222
130
92
155 (70)
67 (30)
12.2
1.00
0.0
197
109
88
137 (70)
60 (30)
13.3
1.06
7.7
185
102
83
134 (72)
51 (28)
13.2
1.02
0.0
197
111
86
137 (70)
60 (30)
14.3
1.07
8.0
193
104
89
132 (68)
61 (32)
14.1
1.05
0.0
194
101
93
145 (75)
49 (25)
15.3
0.99
8.9
200
111
89
141 (71)
59 (29)
15.1
0.99
0.0
146
78
68
98 (67)
48 (33)
16.2
0.94
9.7
144
79
65
96 (67)
48 (33)
16.0
0.93
0.0
136
69
67
95 (70)
41 (30)
17.2
0.98
10.7
142
80
62
99 (70)
43 (30)
16.9
1.03
0.0
* Data from the neurological examination are missing for one subject in the resin-based composite group.
ical examinations took place in schools and thechildren sometimes could not leave their class-
rooms at the time the neurological evaluationswere scheduled. The number of participants was
not uniform across study years because of dropouts and missed appointments.
The table also shows the average numbers of
surfaces filled with amalgam that were present atthe time of each neurological examination for
those in the amalgam group. The overall averagenumber of amalgam surfaces filled during the
study was previously reported,4 but the numberspresented here are specific to those who under-
went neurological examinations at each year. Asis shown, those in the amalgam group had a rela-
tively large number of surfaces treated withamalgam in the first year and maintained during
follow-up, so that those in the amalgam groupwho had neurological examinations averaged
between 7.7 and 10.7 surfaces of amalgam presentduring the seven years of follow-up neurological
examinations. The resin-based composite group,on the other hand, did not have any exposure to
amalgam. (Technically, two participants in thecomposite group received amalgam restorations
through inadvertent protocol violations. Although
those two participants originally were included inthe composite group as called for in intent-to-treat
analyses, the results presented here, for purposesof clarity, do not include any outcomes from those
two participants after they received the erroneousamalgam restorations. Their inclusion or exclu-
sion did not change the results of the analysis.)
Methods. One of two neurologists (either
I.P.M. or M.L.) performed neurological exami-nations for NHSs at baseline and annually for the
seven years of follow-up. A category for recording adventitious movements (including tremor) was
JADA, Vol. 139 http://jada.ada.org February 2008 141
added to the examination midway through year 1
of follow-up. We introduced screening for NSSs infollow-up year 2 and continued it throughout the
remaining five years of the study. NSS severityscores were added starting in follow-up year 3.
The neurologists performed the complete neuro-logical examination at one visit, and all exami-nations took place at the participants’ school.
At any point in the study, the difference betweenthe youngest and the oldest children of the sample
was four years. The children were examined onceper year, with an interval of approximately one
year between the follow-ups. During the course of the study, the sample became smaller because of
dropouts and because not all subjects were able toundergo every follow-up examination owing to
incompatibility with their school schedules. The
loss of participants throughout the seven-yearperiod, however, was in the acceptable range forsufficient statistical power.
The neurological examination was performed
according to standard practice.7 It included a brief evaluation of mental status (consciousness; lan-
guage; and orientation to person, time and place),observation of the function of the 12 cranial
nerves, gross motor function (muscle strength andtone and deep tendon reflexes), plantar responses,
cerebellar functions (including limb and gait coor-dination), touch, joint position and vibration
senses and recording of involuntary movements(such as athetosis or chorea). The neurologistsscored NHSs in eight different categories. They
evaluated the presence of tremor separately fromthe other NHSs. For analysis purposes, they
denoted NHSs (including tremor) as present if any were present or absent if none were present.
Because of the relationship of positional or kinetictremor to mercury toxicity, its presence or
absence also was reported separately.We introduced screening for NSSs in follow-up
year 2. We adapted the NSS evaluation from the
examination described by Peters and colleagues.
20
Six items of that examination have shown a high
correlation with cognitive performance and schoolachievement10; therefore, we selected them for our
study. All of these items were motor signs thathad a better interrater and test-retest reliability
than did sensory tasks21: the presence of mirrormovements, synkinesias, clumsiness of fine finger
movements, clumsiness of heel-to-toe walking (tandem gait), motor impersistence and restless-
ness or hyperactivity. The neurologists scoredeach item from 0 (absent) to 3 (maximum devia-
tion) points, depending on the degree of deviation
observed. There were two scores: one for the pres-ence or absence of any NSSs and an overall NSS
score calculated by summing the score of the sixindividual items. The latter ranged from 0 to 18
points, with higher scores corresponding to thepresence of more, or more evident, NSSs thanlower scores. (A detailed description of NSS
scoring is reported in the supplemental data sec-tion of the online version of this article, available
at “http://jada.ada.org”.)
Statistical analyses. We recorded for each
year the proportions of patients in the two treat-ment groups who exhibited NHSs, tremor or any
NSSs. We also computed means and standarddeviations of the NSS severity scores within each
treatment group for follow-up years 3 through 7.
We made comparisons between treatment groupsusing the Fisher exact test for proportions and thetwo-sample Student t test for mean severityscores (using SPSS, Version 15, SPSS, Chicago).
We report P values for each univariate test,without adjustment for multiple comparisons.
RESULTS
As is demonstrated in Figure 1, the percentage of participants exhibiting any NHSs before receiving
dental treatment was 2.4 percent in the resin-based composite group and 3.6 percent in the
amalgam group. Across time, there were slightdifferences between the two treatment groups inthe percentages exhibiting any NHSs, but the
directions of the differences were not consistentfrom year to year, and the differences were not
statistically significant in any of the years. Therewas an overall slight increase in the percentage of
participants exhibiting NHSs in both of thegroups during the last three years, as high as 8.9
percent to 14.1 percent.We report every NHS registered in follow-up
year 7 to illustrate the above-mentioned increase
in NHSs. Among the 31 children with NHSs, 13showed either kinetic tremor in the finger-nose
test or postural tremor in the outstretched-armtest. Two children had congenital decreased
auditory acuity, two had congenital nystagmus,and one child was blind in the right eye as a
result of surgery at the age of 7 months. Theneurologists observed one case of decreased level
of tendon reflexes of the lower limb (present onlyin follow-up year 7) and four cases of loss of
olfactory discrimination because of sinus disease.Two children showed an abnormal mental status
144 JADA, Vol. 139 http://jada.ada.org February 2008
population ranges between 2 and 5 percent. The
prevalence of essential tremor shows a bimodaldistribution, with a peak in the second and sixth
decades.22-25 Although not all of the children in thesample will develop essential tremor, the remark-
able increase of tremor seems to be related toessential tremor. Furthermore, the severity of
physiological tremor is influenced by emotionaltension or stress and may increase during a med-
ical examination, becoming more obvious to the
observer. Another 13 incidences of NHSs were first
observations or reflected transient pathologicalconditions, such as decrease of olfactory discrimi-
nation owing to constipation or occasionally lowtendon reflex level caused by insufficient relax-ation or low environmental temperature. The
eight first observations of a NHS in follow-up year7 were related to adverse life events such as
traumas or surgical interventions, changes of visual acuity or changes of mood as a symptom of
a possible first manifestation of a psychiatric ill-ness. At baseline, approximately 3 percent of the
children demonstrated NHSs that were scoredcontinuously throughout the study. As children
became older, the probability of their showing
manifestations of chronic diseases increased. Fur-thermore, teenagers are more inclined to demon-strate risky behavior, thus increasing their risk of injury.
The incidence of NSSs decreased across thecourse of the study. This is consistent with matu-
ration of the nervous system and the fact thatNSSs tend to diminish or disappear with
increasing age.9,10 In addition, the severity of NSSs decreased steadily across time in the whole
group of participants and within each treatmentgroup, reflecting progressive neural development
and maturation with time. A large 2005 study of 1,663 adults examined
the relationship of mercury from dental amalgam
exposure to neurological function and found thatthere were no associations between amalgam
exposure and neurological signs (including tremor) or clinically evident peripheral neu-
ropathy.26 These findings are consistent withthose among the children in our study.
Because ours was a large-scale, randomizedtrial, the exposure to mercury from all sources
besides dental amalgam should have been equiva-
lent between the two treatment groups. The pri-mary outside source would be dietary, so we per-
formed a dietary survey and analyses of seafoodsamples eaten by the children to examine the con-
tribution of dietary mercury27 to total mercuryexposure and found that dietary mercury was not
a significant source of mercury exposure in thestudy population. A second source of mercury
exposure in children is vaccines. All children inthe study received the routine series of vaccines
used in Portugal, which is similar to that used inthe United States, so there was no difference
Amalgam ban reported in Norway
Norway has acted to discontinue the use of
dental amalgam, the American Dental Associa-tion reported in an eGram sent Jan. 4 to more
than 75,000 members who have provided theire-mail addresses to the Association.
The eGram noted that Norway acted on
amalgam shortly after the new year as part of asweeping effort to restrict the use of mercury—
action reportedly taken chiefly for environ-mental reasons and with some limited excep-
tions that still allow amalgam to be used.It is possible, the eGram also stated, that
Sweden may have taken similar action,although this could not be verified at the time
the eGram was prepared.
The ADA noted, too, that no new scientificstudies or other new data have been cited ascalling for this action, which is not likely tohave an economic impact in these countries
because of their national health care systems.
INFORMATION ON AMALGAM
For information about amalgam, dentists can
visit the ADA’s Web site, ADA.org, at “www.ada.org/prof/resources/topics/amalgam.asp”.
Patients seeking credible information onamalgam can visit the public side of ADA.org at
“www.ada.org/public/topics/fillings.asp”.
NEW PATIENT BROCHURE
The ADA also has posted a new, free-of-chargepatient education brochure on dental restora-
tive materials that dentists may wish to down-load and have available for patients. Visit
Dental Fillings Facts (abstract) at “www.ada.org/prof/resources//topics/materials/dental_
fillings_facts_abstract.pdf” or Dental Filling Facts (full) at “www.ada.org/prof/resources/
JADA, Vol. 139 http://jada.ada.org February 2008 145
between groups for this source either.
Studies of neurological parameters in dentalpersonnel exposed to mercury from both occupa-
tional sources and amalgam restorations in theirmouths have been performed as well, and investi-
gators have not found that clinically evident neu-rological findings (including those examined inour study) have been present.28,29
CONCLUSION
Because there are concerns that both develop-mental and psychiatric disorders may result from
environmental toxic exposures (such as to mer-cury), it is important to understand the possible
effect of such exposures on NSSs. This study failsto show that exposure to mercury in childhood as
a consequence of treatment with amalgam resto-
rations is associated with a higher frequency of NSSs in childhood and adolescence.
From a prognostic point of view, the decrease of the NSS scores observed in this study group could
serve as a baseline for comparison with singlesubjects in a clinical arena. The persistence of
NSSs may correlate with diverse negative neu-robehavioral and emotional outcomes, but in our
large longitudinal randomized trial, we found noindication that it is associated with exposure to
mercury from dental amalgam. ■
This project was funded by the National Institute of Dental and
Craniofacial Research Cooperative Agreement grant U01 DE11894. Additional funding was provided by Center grant P30ES07033 and bySuperfund Program Project grant P42ES04696 to the University of Washington from the National Institute of Environmental HealthSciences.
Clarification: In a 2006 review, the Office of Human Research Protec-tion of the U.S. Department of Health and Human Services said thatthe University of Washington institutional review board (IRB) shouldhave required more discussion of the risk associated with both dentalmaterials being studied in the consent forms that were approved at thebeginning of the study in 1996 (P.J. McNeilly, PhD, Office for HumanResearch Protections, U.S. Department of Health and Human Services,written communication, Dec. 13, 2006). The University of Washington’sresponse was that its IRB exercised due diligence at the time in con-cluding that the consent form satisfied federal requirements for pro-cedures that were standard of care and in routine use, but that it wouldimplement a new IRB process for explicitly addressing risks associated
with all procedures for future studies comparing two or more standard-of-care protocols (J.M. Cheek, PhD, Office of Research, University of Washington, written communication, March 8, 2007).
The authors wish to acknowledge the assistance of Peter Slade, PhD,of Expert Data Analysis for Doctors & Others, West Kirby, Wirral,England, and Tessa Rue, MS, of the University of Washington, Seattle,with the statistical analyses.
1. Brownawell AM, Berent S, Brent RL, et al. The potential adversehealth effects of dental amalgam. Toxicol Rev 2005;24(1):1-10.
2. Trask CL, Kosofsky BE. Developmental considerations of neuro-
ical and renal effects of dental amalgam in children: a randomized clin-ical trial. JAMA 2006;295(15):1775-83.
4. DeRouen TA, Martin MD, Leroux BG, et al. Neurobehavioraleffects of dental amalgam in children: a randomized clinical trial.JAMA 2006;295(15):1784-92.
5. Bleecker ML. The role of the quantitative neurological examinationin clinical neurotoxicology. Clin Neurobehav Toxicol 2003;18(3):563-78.6. Martins IP, Castro-Caldas A, Townes BD, et al. Age and sex differ-
ences in neurobehavioral performance: a study of Portuguese elemen-tary school children. Int J Neurosci 2005;115(12);1687-709.
7. DeMeyer WE. Technique of the neurological examination. Interna-tional ed. New York: McGraw-Hill; 1994.
8. Denckla MB. Minimal brain dysfunction and dyslexia: beyonddiagnosis by exclusion. In: Blaw ME, Rapin I, Kinsbourne M, eds.Topics in child neurology. New York: Spectrum; 1977:243-61.
10. Martins IP, Fernandes T. Avaliação cognitiva e neurológica numapopulação recém- escolarizada. Psychologica 2003;34:187-214.
11. Mandelbaum DE, Stevens M, Rosenberg E, et al. Sensorimotorperformance in school-age children with autism, developmental lan-guage disorder, or low IQ. Dev Med Child Neurol 2006;48(1):33-9.
12. Breslau N, Chilcoat HD, Johnson EO, Andreski P, Lucia VC. Neu-rologic soft signs and low birthweight: their association and neuropsy-
chiatric implications. Biol Psychiatry 2000;47(1):71-9.13. Foodman A, McPhillips K. ADD and soft signs. J Am Acad Child
Adolesc Psychiatry 1996;35(7):841-2.14. Dickstein DP, Garvey M, Pradella AG, et al. Neurologic exami-
nation abnormalities in children with bipolar disorder or attention-deficit/hyperactivity disorder (published correction appears in Biol Psy-chiatry 2006;60[4]:418). Biol Psychiatry 2005;58(7):517-24.
15. Bachmann S, Bottmer C, Schroder J. Neurological soft signs infirst-episode schizophrenia: a follow-up study. Am J Psychiatry2005;162(12):2337-43.
16. Pine D, Shaffer D, Schonfeld IS. Persistent emotional disorder inchildren with neurological soft signs. J Am Acad Child Adolesc Psychi-atry 1993;32(6):1229-36.
17. Townes BD, Martins IP, Castro-Caldas A, et al. Repeated testscores on neurobehavioral measures over an eight year period in asample of Portuguese children. Int J Neurosci (in press).
19. DeRouen TA, Leroux BG, Martin MD et al. Issues in design andanalysis of a randomized clinical trial to assess the safety of dentalamalgam restorations in children. Control Clin Trials 2002;23(3):301-20.
20. Peters JE, Romine JS, Dykman RA. A special neurological exami-nation of children with learning disabilities. Dev Med Child Neurol1975;17(1):63-78.
21. Pine DS, Scott MR, Busner C, et al. Psychometrics of neurologicalsoft signs. J Am Acad Child Adolesc Psychiatry 1996;35(4):509-15.
22. Tan EK, Lum SY, Prakash KM. Clinical features of childhoodonset essential tremor. Eur J Neurol 2006;13(12):1302-5.
23. Louis ED, Ottman R. Study of possible factors associated with ageof onset in essential tremor. Mov Disord 2006;21(11):1980-6.
24. Louis ED, Dure LS 4th, Pullman S. Essential tremor in childhood:a series of nineteen cases. Mov Disord 2001;16(5):921-3.
26. Kingman A, Albers JW, Arezzo JC, Garabrant DH, Michalek JE. Amalgam exposure and neurological function. Neurotoxicology 2005;
26(2):241-55.27. Evens CC, Martin MD, Woods JS, et al. Examination of dietarymethylmercury exposure in the Casa Pia Study of the health effects of dental amalgams in children. J Toxicol Environ Health A 2001;64(7):521-30.
28. Nilsson B, Gerhardsson L, Nordberg GF. Urine mercury levelsand associated symptoms in dental personnel. Sci Total Environ1990;94(3):179-85.
29. Bittner AC Jr, Echeverria D, Woods JS, et al. Behavioral effectsof low-level exposure to Hg0 among dental professionals: a cross-studyevaluation of psychomotor effects. Neurotoxicol Teratol 1998;20(4):429-39.