ArticlePDF Available

Parkinson's Disease and Mercury

Authors:
  • Region Jämtland Härjedalen

Abstract

The British physician James Parkinson reported in a publication in 1817 the clinical symptomatology in paralysis agitans or shaking palsy. The name of this disorder today is Parkinson's disease (PD). Parkinsonism is characterized by hypokinesia, rigidity, tremor, symptoms from the vegetative nervous system, and in some cases dementia. Tremor is the most characteristic, and often the first symptom in Parkinson's disease.2 A still more incapacitating symptom is akinesia, which for the patients with the disorder results in augmenting difficulties at every movement. The etiology is known in 25% of the cases of Parkinson's disease (medicaments, poisonings, cerebrospinal meningitis, etc.), and in 75% of the cases the etiology is unknown.1 Cases of unknown etiology are named idiopatic Parkinson's disease. Parkinson's disease has probably a multifactorial etiology involving genetic, environmental, trauma and possibly other factors.
1. Toften 24, N-8610 Grubhei, Norway.
Parkinson's Disease and Mercury
Geir Bjørklund1
The British physician James Parkinson
reported in a publication in 1817 the clinical
symptomatology in paralysis agitans or shak-
ing palsy. The name of this disorder today is
Parkinson's disease (PD).
Parkinsonism is characterized by hypo-
kinesia, rigidity, tremor, symptoms from the
vegetative nervous system, and in some cases
dementia.1 Tremor is the most characteris-
tic, and often the first symptom in Parkin-
son's disease.2 A still more incapacitating
symptom is akinesia, which for the patients
with the disorder results in augmenting dif-
ficulties at every movement.2
The etiology is known in 25% of the cases
of Parkinson's disease (medicaments,
poisonings, cerebrospinal meningitis, etc.),
and in 75% of the cases the etiology is
unknown.1 Cases of unknown etiology are
named idiopatic Parkinson's disease.
Parkinson's disease has probably a multi-
factorial etiology involving genetic, envi-
ronmental, trauma and possibly other fac-
tors.3
The shortage of neuro-transmitters, such
as mono-amines, is well established in the
etiology of Parkinson's disease.2 Studies of
Parkinson patients have demonstrated low
levels of monoamine transmitters encoun-
tered in the basal ganglia, decreased values
of HVA and 5-HIFAA in the cerebrospinal
fluid, and loss of the dark melanin pigment
in the dopaminergic substantia nigra (ergon
= work, niger = black) of the basal ganglia.2
A failure of the neurons in the substantia
nigra result in decreased production of
dopamine and leads secondarily to a loss of
function in the corpus striatum.2 The conse-
quence of this process is the clinical picture
of Parkinson's disease.
Heavy metals, like mercury and copper,
can produce lesions of the basal ganglia,
with symptoms like hyperkinesia.2 Accord-
ing to Komulainen and Tuomisto4 copper
has a significant action on adrenergic neu-
rons.
Researchers at the Henry Ford Hospital in
Detroit, Michigan have studied Parkinson's
disease with respect to heavy metal expo-
sure.5 They have calculated mortality rates
for Parkinson's disease in Michigan counties
for 1986-1988 with respect to potential heavy
metal exposure (iron, zinc, copper, mercury,
magnesium, and manganese) from industry
based on recent census data. The death rates
are statistically significantly higher in coun-
ties with an industry in the chemical, paper,
iron or copper related-industrial categories
(ICs) (p < 0.05) than counties without these
industries.5 The authors concluded: “These
ecologic findings suggest a geographic as-
sociation between PD mortality and the in-
dustrial use of heavy metals.”
Ngim and Devathasan6 have done a case-
control study among the multiethnic popula-
tion of Singapore. They tested the hypoth-
esis that a high level of body burden mercury
is associated with an increased risk of Par-
kinson's disease. In 54 cases of idiopathic
Parkinson's disease and 95 hospital-based
controls, detailed interviews were com-
pleted.6 The two groups were matched for
age, sex and ethnicity, between July 1985
and July 1987. The researchers found that
there was a clear monotonic dose-response
association between blood mercury levels
and Parkinson's disease. The result was ad-
justed for potential confounding factors, in-
cluding dietary fish intake, medications,
smoking and alcohol consumption.6 Scalp
hair mercury was shown to be a poor predic-
tor of the risk of Parkinson's disease after
adjustment.
Ngim and Devathasan6 listed the follow-
ing factors that could contribute to the body
burden of mercury: dietary fish intake, eth-
nic over-the-counter medications, occupa-
tional exposures and dental amalgam fill-
ings.6
Tremor is a classical symptom among vic-
tims of inorganic mercury poisoning, as well
as among methyl mercury poisoning vic-
tims. “Tremor Mercurialis” has been known
since antiquity.2 The tremor of methyl mer-
cury poisoning is different from physiologi-
147
Journal of Orthomolecular Medicine Vol. 10, No. 3 & 4, 1995
148
cal tremor and other pathological tremors in
frequency and amplitude.7
According to Störtebecker a possible ex-
posure to mercury should be considered in
the etiology of “Shaking Palsy” (Parkinson's
disease).2 He asks: “... why shouldn't a daily
release of small amounts of mercury from
dental amalgam fillings be capable of pro-
ducing similar neurological symptoms.”
Dental amalgams are the predominant
source of inorganic mercury and mercury
vapour in the general population.8 There is
found a direct correlation between the
number and surfaces of dental amalgam fill-
ings and the amount of mercury in the brain.9
Mercury vapour has no toxic threshold.10 No
exposure to mercury can therefore be con-
sidered totally harmless.
In light of these facts, the possible role of
dental mercury in etiology of Parkinson's
disease should be further studied.
References
1. Hamre HJ: Amalgam og sykdom. Oslo:
Vidarforlaget, 1993.
2. Störtebecker P: Neurology for barefoot
doctors in all countries. Correct Diagnosis by
simple methods. Täby/Stockholm: Störte-
becker Foundation for Research, 1988.
3. Semchuk KM, Love EJ, Lee RG: Parkinson's
disease: a test of the multifactorial etiologic
hypothesis. Neurology 43: 1173-80, 1993.
4. Komulainen H, Tuomisto J: Effects of heavy
metals on dopamine, noradrenaline and
serotonin uptake and release in rat brain
synaptosomas. Acta Pharmacol Toxicol 48:
199-204, 1981.
5. Rybicki BA, Johnson CC, Uman J, Gorell
JM: Parkinson's disease mortality and the
industrial use of heavy metals in Michigan.
Mov Disord 8: 87-92, 1993.
6. Ngim CH, Devathasan G: Epidemiologic
study on the association between body burden
mercury level and idiopathic Parkinson's
disease. Neuroepidemiology 8: 128-41, 1989.
7. Yamanaga H: Quantitative analysis of tremor
in Minamata disease. Tohukv J Exp Med 141:
13-22, 1983.
8. Clarkson TW, Friberg L, Nordberg GF, Sager
PR editors: Biological monitoring of toxic
metals. New York: Plenum Press, 1988.
9. Nylander M, Friberg L, Lind N: Mercury
consentrations in the human brain and kidneys
in relation to exposure from dental amalgam
fillings. Swed Dent J 1987; 11:179-87.
10.World Health Organization. Environmental
Health Criteria 118: Inorganic Mercury.
Geneva: World Health Organization, 1992.
... N,N'-dimethyl-4,4'-bipyridine dichloride), maneb, and manganese ethylene-1,2-bisdithiocarbamate, polymer has been associated with an increased risk of PD [17][18][19][20][21][22]. In addition to pesticides, dozens of other commonly encountered environmental toxicants have been implicated in PD, such as metals, solvents, and other pollutants [23][24][25]. ...
Article
Genetic background accounts for only 5 to 10% of the reported cases of Parkinson's disease (PD), while the remaining cases are of unknown etiology. It is believed that environmental factors may be involved in the causality of a large proportion of PD cases. Several PD genes are activated by xenobiotic exposure, and a link between pesticide exposure and PD has been demonstrated. Many epidemiological studies have shown an association between PD and exposure to metals such as mercury, lead, manganese, copper, iron, aluminum, bismuth, thallium, and zinc. This review explores the biological effects, the pathogenetic processes, genetic susceptibilities to metals as well as examining future strategies for PD treatment, such as chelation therapy.
Book
This document is the result of a conference on "Biological Monitoring of Metals" held in Rochester, June 2-6, 1986, organized jointly by the Environmental Health Sciences Center of the School of Medicine and Dentistry of the University of Rochester, NY, and the Scientific Committee on the Toxicology of Metals within the International Commission on Occupational Health (ICOH) at the Karolinska Institute and the National (Swedish) Institute of Environmental Medicine and the University of Umea, Sweden. The aim of the Conference was to define and evaluate the scientific basis for the biological monitoring of metals. The conference was co-sponsored by the World Health Organization through its International Program on Chemical Safety and received substantial encouragement and support from the Swedish Work Environmental Fund and the United States Environmental Protection Agency. This was the second conference organized jointly by the Scientific Committee on the Toxicology of Metals and The Toxicology Division of the University of Rochester. The previous joint conference was held in 1982 on the Reproductive and Developmental Toxicity of Metals. In addition, conferences have been organized by each group (see Appendices A and B). Several of these conferences are specially relevant to the topic of the current conference. These include the joint conference mentioned above and the conferences on dose-effect and dose-response relationship held in Tokyo in 1974 and on accumulation of metals held in Buenos Aires in 1972.
Article
The effects of some heavy metals on the initial high affinity uptake and spontaneous release of tritiated dopamine (3H-DA), noradrenaline (3H-NA) and 5-hydroxytryptamine (3H-5-HT) were studied in vitro in rat striatal, cortical and hypothalamic synaptosomes, respectively. As uptake inhibitors, metals were quite inactive in these conditions. At 10 μM Cu2+ was most potent, inhibiting 3H-DA and 3H-5-HT uptake nearly completely while inhibition of 3H-NA uptake varied. 3H-DA uptake was in addition inhibited slightly by Zn2+, sometimes by Sn2+ but never by Co2+, Hg2+ or Mn2+. Unexpectedly Pb2+ and Cd2+ tended to increase the synaptosomal 3H-DA uptake. 3H-5-HT uptake was affected least while that of 3H-NA showed some diversity. Zn2+, Pb2+ and Sn2+ induced inhibition of 3H-NA uptake possibly by direct interference with 3H-NA. As to the spontaneous release of tritiated amines during short incubation from preloaded synaptosomes, Cd2+ decreased that of 3H-DA at high concentrations but Hg2+, Pb2+, Sn2+ and Zn2+ were ineffective. The results suggest that in vitro the uptake and the release of 3H-DA are more affected than those of other amines. The inhibitory mechanisms of monoamine uptake may include both direct effects on synaptosomes and indirect ones by interference with the amines themselves.
Article
A case-control study was conducted among the multiethnic population of Singapore to test the hypothesis that a high level of body burden mercury is associated with an increased risk of Parkinson's disease (PD). Selected factors investigated that could contribute to the body burden of mercury included dietary fish intake, ethnic over-the-counter medications, occupational exposures and possession of dental amalgam fillings. Detailed interviews were completed in 54 cases of idiopathic PD and 95 hospital-based controls, matched for age, sex and ethnicity, between July 1985 and July 1987. After adjusting for potential confounding factors, including dietary fish intake, medications, smoking and alcohol consumption, there was clear monotonic dose-response association between PD and blood mercury levels. The odds ratios (OR) and 95% confidence intervals (CI) for the approximate subject tertiles based upon blood mercury levels were 8.5 (CI = 2.2-33.2) and 9.4 (CI = 2.5-35.9), relative to the tertile with lowest blood mercury levels (less than 5.8 ng Hg/ml). Similar associations were revealed using scalp hair and urinary mercury levels. However, only the comparisons between the highest and lowest tertiles were statistically different from unity (p less than 0.05). When the body burden mercury indicators were mutually adjusted in addition to the four confounding factors, blood and urinary mercury levels showed ORs of 21.00 and 18.65, respectively. These ORs were statistically different from unity (p less than 0.05, 2-sided test). After adjustment, scalp hair mercury was shown to be a poor predictor of PD risk.
Article
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.
Article
Applying the techniques of power spectrum and pulse correlation, we carried out a quantitative analysis of tremor in normal subjects, patients with methyl mercury poisoning (Minamata disease) and patients with other diseases. We found that tremor of methyl mercury poisoning was different from physiological tremor and the other pathological tremors in frequency and amplitude.
Article
We studied the relative etiologic importance upon the development of Parkinson's disease (PD) of occupational exposure to herbicides and other compounds, ionizing radiation exposure, family history of PD and essential tremor, smoking, and history of various viral and other medical conditions. We identified patients (n = 130) with neurologist-confirmed idiopathic PD through contacts with Calgary general hospitals, long-term care facilities, neurologists, the Movement Disorder Clinic, and the Parkinson's Society of Southern Alberta, and selected two matched (by sex and age +/- 2.5 years) community controls for each case by random digit dialing. We obtained lifetime work, chemical, radiation, medical, and smoking exposure histories and family histories of PD and essential tremor by personal interviews, and analyzed the data using conditional logistic regression for matched sets. After controlling for potential confounding and interaction between the exposure variables, using multivariate statistical methods, having a family history of PD was the strongest predictor of PD risk, followed by head trauma and then occupational herbicide use. Cases and controls did not differ in their previous exposures to smoking or ionizing radiation; family history of essential tremor; work-related contact with aluminum, carbon monoxide, cyanide, manganese, mercury, or mineral oils; or history of arteriosclerosis, chicken pox, encephalitis, hypertension, hypotension, measles, mumps, rubella, or Spanish flu. These results support the hypothesis of a multifactorial etiology for PD, probably involving genetic, environmental, trauma, and possibly other factors.
Article
Parkinson's disease (PD) mortality rates in Michigan counties for 1986-1988 were calculated with respect to potential heavy metal exposure (iron, zinc, copper, mercury, magnesium, and manganese) from industry based on recent census data. Individuals were counted as a PD death if the diagnosis was listed as an "underlying" or "related" cause of death on the death certificate. Counties with an industry in the paper, chemical, iron, or copper related-industrial categories (ICs) had statistically significantly (p < 0.05) higher PD death rates than counties without these industries. Significant correlations of chemical (rs = 0.22; p = 0.05), paper (rs = 0.22; p = 0.05) and iron (rs = 0.29; p = 0.008) industry densities with PD death rates were also present. Counties were divided into high (> 15/100,000 individuals 45 years old and over) and low (< = 15/100,000) PD death rate counties by cluster analysis. Geographically, counties with high PD mortality were located mainly in the southern half of the lower peninsula and eastern half of the upper peninsula; low PD death rate counties formed two distinct clusters in the western edge of the upper peninsula and the north-central portion of the lower peninsula. Other possible risk factors that may explain the varied distribution of PD death rates in Michigan were examined. Those significantly correlated with PD mortality included population density (rs = 0.31; p = 0.005), farming density (rs = 0.25; p = 0.02), and well water use (rs = -0.24; p = 0.03). These ecologic findings suggest a geographic association between PD mortality and the industrial use of heavy metals.
Neurology for barefoot doctors in all countries. Correct Diagnosis by simple methods. Täby/Stockholm: Störtebecker Foundation for Research
  • P Störtebecker
Störtebecker P: Neurology for barefoot doctors in all countries. Correct Diagnosis by simple methods. Täby/Stockholm: Störtebecker Foundation for Research, 1988.
Amalgam og sykdom. Oslo: Vidarforlaget
  • Hj Hamre
Hamre HJ: Amalgam og sykdom. Oslo: Vidarforlaget, 1993.