Bulletin Board
Archived Bulletin Board
About John
Latest Ideas
Symptoms
Tests and Drugs
Weight Loss Experiment
Hyperthyroidism
Hypothyroidism
Supplement List
Medical Science
Heredity
Other Diseases
Thyroid Physiology
Deeper Studies
Nutrients and Toxics
Hair Analysis
Book Reports
Glossary
Table of Contents | |
PARKINSON'S DISEASE
Study Links Pesticides, Parkinson's
|
|
November 6, 2000
The Associated Press
New research using rats suggests that long-term exposure to a widely
used pesticide kills brain cells and triggers debilitating physical
symptoms associated with Parkinson's disease.
Scientists say the experiment's results strongly indicate what
scientists have suspected for several years - that the most common form
of Parkinson's disease might result from toxins in the environment.
The new study, published in the December issue of Nature
Neuroscience, does not prove that the pesticide used in the test,
rotenone, causes Parkinson's in humans.
But scientists who reviewed the experiment said the results are
powerful and should reinvigorate the search for environmental toxins
that may contribute to Parkinson's, the most common neurological
disorder after Alzheimer's.
"This is more evidence that a class of compounds may increase
the risk of developing Parkinson's," said J. William Langston,
director of the Parkinson's Institute in Sunnyvale, Ca., who was not
involved in the study. "It is not direct evidence that rotenone
causes Parkinson's. The whole puzzle hasn't come together."
More than one million Americans suffer from Parkinson's. Muscle
control ebbs as brain cells in a region called the substantia nigra
produce less dopamine, a hormone vital to normal nerve function. The
illness is marked by small tremors, such as facial tics and shaking
hands. Advanced symptoms include a shuffling gait, speech difficulties
and muscle weakness.
There is no cure, and current drug and surgical therapies tends to
lose effectiveness over time. New therapies involving transplants of
stem cells, the body's master cells from which all tissues grow, have
been slowed by federal funding restrictions on experiments using
embryonic tissues.
In about 10 percent of patients, Parkinson's strikes before age 50.
These rare cases probably are caused by inherited genetic abnormalities.
However, most patients show their first Parkinson's symptoms after
age 60. Researchers believe older patients may have suffered brain
damage from chronic exposure to unspecified toxins. Among the suspects:
pesticides, industrial chemicals and tobacco smoke.
In the experiment conducted at Emory University in Atlanta,
neurologists implanted tiny pumps in the rats to continuously administer
low doses of rotenone through the jugular vein for as long as five
weeks.
Rotenone is an organic product made from extracts of tropical plants.
It is widely used as an agricultural pesticide and to kill unwanted fish
in reservoirs.
People most frequently would be exposed to rotenone by ingesting
residue in food or by handling the compound.
Scientists acknowledged the pump method used in the experiment did
not duplicate rotenone exposure in the real world, but said it was a
more direct and reliable method for research purposes.
"Rats can be picky about what they eat and they might not like
eating rotenone," said J. Timothy Greenamyre, the study's senior
author. "Whether the pesticide would have the same effect in people
via normal routes of exposure is not clear."
Greenamyre said half of the rats gradually showed Parkinson's
symptoms.
Examination revealed that large numbers of dopamine-producing cells
in the rats' brains had died or were damaged. In addition, the cells
showed fibrous protein deposits that closely resemble Lewy bodies,
deposits found in brain cells of Parkinson's patients.
"Together, it's what you see in Parkinson's," Greenamyre
said. How rotenone might have triggered these changes in rat is unclear.
University of Pennsylvania researchers Benoit I. Giasson and Virginia
M.-Y. Lee, who reviewed the Emory experiment, suggest the pesticide
might target the mitochondria, a genetic bundle that generates most of a
cell's energy.
Such damage unleashes rogue molecules known as free radicals that
wreak havoc in cells. Free radicals have been implicated in many
degenerative diseases.
"Neurons are particularly sensitive," Giasson and Lee
noted. Greenamyre said future rotenone experiments with rats would test
new drugs aimed at protecting dopamine-producing cells.
In the meantime, he suggested that farmers and public health agencies
reconsider pesticide usage.
"Pesticides are essential for growing crops, but we may need to
think about minimizing their environmental impact," he said.
|
-
Appl Occup Environ Hyg 2000 Jul;15(7):542-9 |
|
Manganese dioxide exposures and respirator performance at
an alkaline battery plant.
Hanley KW, Lenhart SW
National Institute for Occupational Safety and Health, Cincinnati, Ohio,
USA.
Two industrial hygiene studies were conducted at an alkaline battery plant
to evaluate worker exposures to manganese dioxide particulate and the
effectiveness of filtering facepiece respirators. The work areas studied
included the plant's powder-processing tower and press rooms where manganese
was blended, compacted with graphite, and inserted into battery cans.
Full-shift personal breathing zone monitoring was conducted to estimate
manganese dust exposures of press operators, mechanics, and material
handlers. In-facepiece and personal breathing zone air sampling pairs were
also collected using a program protection factor protocol to estimate the
protection provided by the respirators. Particle size evaluations were made
using nylon cyclones and Marple personal multi-stage impactors. All samples
were analyzed for manganese by inductively coupled argon plasma, atomic
emission spectroscopy via NIOSH analytical method 7300 utilizing a modified
acid digestion procedure. Fifty-four, full-shift, time-weighted average (TWA)
exposures to total manganese ranged from 0.1 to 5.4 milligrams per cubic
meter (mg/m3); worker exposures were substantially lower during a follow-up
study due to engineering control improvements. Concurrent area sample
comparisons of total and respirable manganese revealed that the respirable
particulate mass fractions ranged from 6 to 32 percent, and mass median
aerodynamic diameters determined from personal breathing zone air samples
were mostly greater than 10 micrometers. Fifteen respirator performance
evaluations were conducted using Moldex 2200 respirators fitted with 25
millimeter cassettes and light weight sampling probes. Protection factors
ranged from 5 to 220, with a geometric mean and standard deviation of 31 and
2.97, respectively. The 5th percentile protection factor estimate was 5, as
calculated from the protection factor distribution for this sample set. In
1995, the American Conference of Governmental Industrial Hygienists (ACGIH)
lowered the elemental and inorganic manganese dust Threshold Limit Value (TLV)
from 5 mg/m3 to 0.2 mg/m3 to address adverse pulmonary and central nervous
system effects and male infertility. Although most personal breathing zone
concentrations were above 0.2 mg/m3, none of the in-facepiece concentrations
exceeded this concentration. Parkinson's-like symptoms have been reported in
the literature for high manganese dust and fume exposures, but the
importance of low dust exposures for producing neurological effects is
uncertain.
-
Nervenarzt 2000 May;71(5):416-9 |
|
[Follow-up study after enteral manganese poisoning:
clinical, laboratory and neuroradiological findings].
[Article in German]
Degner D, Bleich S, Riegel A, Sprung R, Poser W, Ruther E
Psychiatrische Klinik und Poliklinik, Georg-August-Universitat Gottingen.
Manganese intoxication is an unusual, severe form of intoxication. This
report deals with a patient now 80 years old who accidentally ingested a
solution of potassium permanganate for a period of at least 4 weeks 14 years
ago. Since then, the patient suffers from a mild parkinsonian syndrome and
distally accentuated polyneuropathies. Psychiatric disorders, especially
demential or depressive symptoms, were not observed. Manganese analysis of
his hair still shows a clear increase in manganese concentration. The MRI of
his brain showed no pathological changes, in particular none of those often
described with symmetric signal elevation in T1 in the area of the basal
ganglia. In this study, we present clinical, laboratory, and
neuroradiological findings. Unusual in this case with a short exposition is
the long duration and clinical improvement without L-dopa treatment.
-
J Cell Physiol 2000 Oct;185(1):80-6 |
|
Role of heme oxygenase-1 in the regulation of manganese
superoxide dismutase gene expression in oxidatively-challenged astroglia.
Frankel D, Mehindate K, Schipper HM
Bloomfield Centre for Research in Aging, Lady Davis Institute for Medical
Research, Sir Mortimer B. Davis-Jewish General Hospital, Montreal, Canada.
Manganese superoxide dismutase (MnSOD) is an antioxidant enzyme that reduces
superoxide anion to hydrogen peroxide in cell mitochondria. MnSOD is
overexpressed in normal aging brain and in various central nervous system
disorders; however, the mechanisms mediating the upregulation of MnSOD under
these conditions remain poorly understood. We previously reported that
cysteamine (CSH) and other pro-oxidants rapidly induce the heme oxygenase-1
(HO-1) gene in cultured rat astroglia followed by late upregulation of MnSOD
in these cells. In the present study, we demonstrate that antecedent
upregulation of HO-1 is necessary and sufficient for subsequent induction of
the MnSOD gene in neonatal rat astroglia challenged with CSH or dopamine,
and in astroglial cultures transiently transfected with full-length human
HO-1 cDNA. Treatment with potent antioxidants attenuates MnSOD expression in
HO-1-transfected astroglia, strongly suggesting that intracellular oxidative
stress signals MnSOD gene induction in these cells. Activation of this
HO-1-MnSOD axis may play an important role in the pathogenesis of Alzheimer
disease, Parkinson disease and other free radical-related neurodegenerative
disorders. In these conditions, compensatory upregulation of MnSOD may
protect mitochondria from oxidative damage accruing from heme-derived free
iron and carbon monoxide liberated by the activity of HO-1. Copyright 2000
Wiley-Liss, Inc.
-
J Neurosci Res 1999 Apr 15;56(2):113-22 |
|
Existing and emerging mechanisms for transport of iron
and manganese to the brain.
Malecki EA, Devenyi AG, Beard JL, Connor JR
Department of Neuroscience and Anatomy, College of Medicine, Pennsylvania
State University, Hershey 17033, USA.
The metals iron (Fe) and manganese (Mn) are essential for normal functioning
of the brain. This review focuses on recent developments in the literature
pertaining to Fe and Mn transport. These metals are treated together because
they appear to share several transport mechanisms. In addition, several
neurological diseases such as Alzheimer's Disease, Parkinson's Disease, and
Huntington's Disease are all associated with Fe mismanagement in the brain,
particularly in the striatum and basal ganglia. Similarly, Mn accumulation
in brain also appears to target the same brain regions. Therefore, stringent
regulation of the concentration of these metals in the brain is essential.
The homeostatic mechanisms for these metals must be understood in order to
design neurotoxicity prevention strategies.
-
Arch Neurol 2000 Apr;57(4):597-9 |
|
Manganese intoxication.
Lee JW
Department of Neurology, College of Medicine, The Catholic University of
Korea, Seoul.
Manganese plays an important role as a cofactor in many enzymatic reactions
in humans but in excess amounts can cause irreversible nervous system
damage. Although manganism is a rare condition, it can be the cause of
complex nervous system symptoms, especially in the setting of environmental
exposure. Specifically, manganese is a well-known cause of dystonic
parkinsonism. This article highlights several historical descriptions of the
clinical manifestations, pathological changes, and attempted therapeutic
intervention in manganese intoxication.
-
Rinsho Shinkeigaku 1999 Jul;39(7):693-9 |
|
[Diagnostic utility of positron emission tomography for
parkinsonism after chronic manganese exposure].
[Article in Japanese]
Abe Y, Kachi T, Kato T, Ito K, Yanagisawa N, Sobue G
Department of Neurology, Chubu National Hospital, Obu, Japan.
Positron emission tomography (PET) with [18F] 6-fluoro-L-dopa (18F-FDOPA)
was performed in three South Korean patients with parkinsonism who developed
after chronic manganese exposure. A 51-year-old man (patient 1) suffered
from masked face, marked postural tremor of hands, dystonia in the neck and
the upper extremities, severe retropulsion and lateropulsion which were
typical for chronic manganese intoxication. 18F-FDOPA scan was normal. Other
two patients, a 46-year-old man (patient 2) and a 47-year-old man (patient
3), showed tremor at rest and rigidity predominantly on the right side,
bradykinesia, stooped posture and postural instability; all of these were
typical for Parkinson's disease (PD). There was reduced uptake of 18F-FDOPA
in the striatum, particularly in the posterior putamen predominant on the
left side, in both patient 2 and 3. From these results, patient 1 was
diagnosed as pure manganism, while patient 2 and 3 were primarily as PD,
because loss of nigrostriatal fibers was obvious with asymmetry of affection
in the putamen. PET with 18F-FDOPA provides valuable information for
differentiation between PD and manganism, although it is not clear whether
development of parkinsonian symptoms in patient 2 and 3 was modified by
excessive manganese exposure.
-
J Am Coll Nutr 1999 Oct;18(5):413-23 |
|
Multiple antioxidants in the prevention and treatment of
Parkinson's disease.
Prasad KN, Cole WC, Kumar B
Center for Vitamins and Cancer Research, Department of Radiology, University
of Colorado Health Sciences Center, Denver 80262, USA.
Parkinson's disease (PD) is one of the major progressive neurological
disorders for which no preventative or long-term effective treatment
strategies are available. Epidemiologic studies have failed to identify
specific environmental, dietary or lifestyle risk factors for PD except for
toxic exposure to manganese, meperidine (Demerol, the "designer
drug" version of which often contains a toxic byproduct of the
synthesis, 1-methyl-4-phenyl 1,2,3,6 tetrahydropyridine [MPTP]), and some
herbicides and pesticides. The search for genetic risk factors such as
mutation, overexpression or underexpression of nuclear genes in DA neurons
in idiopathic PD has not been successful as yet. Polymorphism in certain
genes appears to be a risk factor, but there is no direct evidence for the
causal relationship between polymorphism and increased risk of PD. In
familial PD, mutation in the alpha-synuclein gene is associated with the
disease, but a direct role of this gene in degeneration of DA neurons
remains to be established. Although mutations in the Parkin gene has been
associated with autosomal recessive juvenile Parkinson's disease, the role
of this gene mutation in causing degeneration of DA neurons has not been
defined. We have reported that in hereditary PD, a mutation in the alpha-synuclein
gene may increase the sensitivity of DA neurons to neurotoxins. We
hypothesize that, in idiopathic PD, epigenetic (mitochondria, membranes,
protein modifications) rather than genetic events are primary targets which,
when impaired, initiate degeneration in DA neurons, eventually leading to
cell death. Although the nature of neurotoxins that cause degeneration in DA
neurons in PD is not well understood, oxidative stress is one of the
intermediary risk factors that could initiate and/or promote degeneration of
DA neurons. Therefore, supplementation with antioxidants may prevent or
reduce the rate of progression of this disease. Supplementation with
multiple antioxidants at appropriate doses is essential because various
types of free radicals are produced, antioxidants vary in their ability to
quench different free radicals and cellular environments vary with respect
to their lipid and aqueous phases. L-dihydroxyphenylalanine (L-dopa) is one
of the agents used in the treatment of PD. Since L-dopa is known to produce
free radicals during its normal metabolism, the combination of L-dopa with
high levels of multiple antioxidants may improve the efficacy of L-dopa
therapy.
-
Neurotoxicology 1999 Apr-Jun;20(2-3):499-507 |
t |
A brief history of the neurobehavioral toxicity of
manganese: some unanswered questions.
McMillan DE
University of Arkansas for Medical Sciences, Little Rock 72205, USA.
McMillanDonaldE@exhange.uams.edu
It was observed by Couper in 1837 that manganese dust produces a
neurological syndrome characterized by muscle weakness, tremor, bent
posture, whispered speech and excess salivation. The similarity of these
symptoms to those of Parkinson's disease were not recognized for many years.
In addition to its Parkinson-like effects, manganese produces behavioral
symptoms in humans including nervousness, hallucinations, memory loss,
cognitive problems, bizarre behaviors and flight of ideas. Despite these
signs and symptoms, there have been few systematic attempts to study the
effects of manganese on behavior using animal models. The need to better
understand the effects of manganese on behavior is becoming more important
due to the potential of increased environmental exposure to manganese due to
its use, or proposed use as a gasoline additive in a number of countries.
However, there is debate as to which manganese compounds should receive
priority for testing, what route of administration should be used in this
testing, what dosing regimens should be used, what species are appropriate
for behavioral testing, and what behavioral tests should be selected.
Research to answer these questions is needed so that the behavioral effects
of manganese can be described comprehensively and the mechanisms underlying
these effects can be understood.
-
Kao Hsiung I Hsueh Ko Hsueh Tsa Chih 1999 May;15(5):297-301 |
|
Rapid progression of parkinsonism associated with an
increase of blood manganese.
Kao HJ, Chen WH, Liu JS
Department of Neurology, Kaohsiung Medical College Hospital, Taiwan,
Republic of China.
In this paper, we report a 72-year-old man whose parkinsonian pictures
accelerated rapidly after an ingestion of unknown herb pills. His serum
manganese and aluminum level increased 2-fold and 5-fold over physiological
level respectively. A reverse of his parkinsonian deterioration was
accompanied with a normalization of these metals. Exclusive heavy metals
have been widely mentioned in parkinsonism. While industrial source of these
metals has extensively been sought, pharmacology is rarely mentioned in this
aspect, especially of herb medicine origin. We suggest that an acceleration
of parkinsonian pictures should raise the need to re-evaluate the
possibility of heavy metal intoxication in parkinsonism. Besides of
industrial contamination, we should be alert for the nonindustrial source in
our population.
-
Brain Res Mol Brain Res 1999 May 7;68(1-2):22-8 |
|
Manganese potentiates nitric oxide production by
microglia.
Chang JY, Liu LZ
Department of Anatomy, Slot 510, University of Arkansas for Medical
Sciences, 4301 W. Markham St., Little Rock, AR 72205, USA.
Manganese toxicity has been associated with clinical symptoms of
neurotoxicity which are similar to the symptoms observed in Parkinson's
disease. Earlier reports indicated that reactive microglia was present in
the substantia nigra of patients with Parkinson's disease. Using N9
microglial cells, the current study was designed to determine whether high
levels of manganese were associated with microglial activation. Results
indicated that manganese significantly increased the bacterial
lipopolysaccharide-induced nitric oxide production. This potent activity of
manganese was not shared by other transition metals tested, including iron,
cobalt, nickel, copper and zinc. Immunohistochemical staining and Western
blot analysis indicated that manganese increased the cellular production of
inducible nitric oxide synthase. Northern blot analysis indicated that
manganese likely increased iNOS gene transcription since this agent
increased the mRNA level of the inducible nitric oxide synthase. In contrast
to other transition metals tested, manganese did not appear to be cytotoxic
to microglial cells. These results suggested that manganese could induce
sustained production of neurotoxic nitric oxide by activated microglial
cells, which might cause detrimental consequences to surrounding neurons.
-
Neurotoxicology 1995 Fall;16(3):511-7 |
|
Effects of calcium-deficient diets on manganese
deposition in the central nervous system and bones of rats.
Yasui M, Ota K, Garruto RM
Division of Neurological Diseases, Wakayama Medical College, Japan.
The presence of both aluminum (Al) and manganese (Mn) in central nervous
system tissues (CNS) has been reported in Parkinson's disease and in
parkinsonism-dementia (PD) on Guam. Epidemiological surveys on Guam have
suggested that low calcium (Ca), magnesium (Mg) and high Al and Mn in
river, soil and drinking water may be implicated in the pathogenesis of
PD. Experimentally, low Ca-Mg diets with or without added Al have been
found to accelerate Al deposition in the CNS of rats and monkeys. Although
excessive deposition of Mn produces similar neurotoxic action to Al in CNS
tissues, the mechanism of Mn deposition coupled with Al loading in the
presence of low Ca-Mg intake is not yet known. In this study, the
deposition and mental-metal interaction of both Al and Mn in the CNS,
visceral organs and bones of rats fed unbalanced mineral diets were
analyzed. Male Wistar rats, weighing 200 g, were maintained for 90 days on
the following diets: (A) standard diet, (B) low Ca diet, (C) low Ca-Mg
diet, (D) low Ca-Mg diet with high Al. Al and Mn content were determined
in the frontal cortex, spinal cord, kidney, muscle, abdominal aorta, femur
and lumbar spine using neutron activation analysis (NAA). Our results
demonstrate that serum Ca levels were decreased in the following dietary
order: C<D<B<A. Serum Mg levels were significantly lower in rats
from Groups C and D, compared with those in Groups A and B, reflecting the
content of Mg and other interacting minerals in the diet. There was no
significant difference in serum Al, zinc and phosphorus levels. Ca and Mg
contents in lumbar vertebrae and the femur were significantly lower and Al
levels significantly higher in rats maintained on the low Ca-Mg diet with
or without added Al. Al content in CNS tissues and visceral organs were
highest in rats fed diets deficient in Ca alone or low in Ca-Mg with or
without added Al. Bone Mn levels significantly increased in rats fed the
low Ca-Mg diet with added Al. Mn content in the frontal cortex
significantly increased in rats fed diets low in Ca-Mg with or without
added Al. But the Mn content of other tissues including the spinal cord,
kidney, muscle and abdominal aorta was unchanged in rats given Ca
deficient diets. Intake of low Ca and Mg with added Al in rats led to the
high concentrations of Mn and Al in bones and in the frontal cortex. We
conclude that unbalanced mineral diets and metal-metal interactions may
lead to the unequal distribution of Al and Mn in bones and ultimately in
the CNS inducing CNS degeneration.
-
J Neurol 1999 Mar;246(3):198-206 |
|
Parkinsonism, pyramidal signs, polyneuropathy, and
cognitive decline after long-term occupational solvent exposure.
Hageman G, van der Hoek J, van Hout M, van der Laan G, Steur EJ, de Bruin
W, Herholz K
Department of Neurology, Medical Spectrum Twente, Hospital Enschede, The
Netherlands.
It is well known that exposure to manganese, solvents, or carbon monoxide in
an occupational setting may lead to central nervous system damage and
parkinsonism. The most important solvents in this respect are methanol,
toluene, carbon disulfide, and n-hexane. We describe three patients who had
been exposed to various solvents for more than 20 years (25, 34, and 46
years). They presented with parkinsonism, pyramidal signs, mild cognitive
decline, and unresponsiveness to levodopa. Two patients had a predominantly
axonal and sensory polyneuropathy of the lower legs with fasciculations in
one of them. Parkinsonian features were progressive, even after the patients
had stopped work. We present clinical data, neuropsychological findings, and
results of brain computed tomography or magnetic resonance imaging,
electroneuromyography, evoked potentials, single photon emission computed
tomography, and positron-emission tomography. There is growing evidence that
various organic solvents give rise to a parkinsonism syndrome with pyramidal
features in susceptible individuals.
-
Mov Disord 2001 May;16(3):565-8 |
|
Parkinsonism after glycine-derivate exposure.
Barbosa ER, Leiros Da Costa MD, Bacheschi LA, Scaff M, Leite CC.
Divisao de Clinica Neurologica, do Hospital das Clinicas da Faculdade, de
Medicina da Universidade, de Sao Paulo, Sao Paulo, Brazil.
This 54-year-old man accidentally sprayed himself with the chemical agent
glyphosate, a herbicide derived from the amino acid glycine. He developed
disseminated skin lesions 6 hours after the accident. One month later, he
developed a symmetrical parkinsonian syndrome. Two years after the initial
exposure to glyphosate, magnetic resonance imaging revealed hyperintense
signal in the globus pallidus and substantia nigra, bilaterally, on
T2-weighted images. Levodopa/benserazide 500/125 mg daily provided
satisfactory clinical outcome.
-
Scand J Work Environ Health 1994 Aug;20(4):301-5 |
|
Parkinsonism after chronic exposure to the fungicide
maneb (manganese ethylene-bis-dithiocarbamate).
Meco G, Bonifati V, Vanacore N, Fabrizio E.
Department of Neurosciences, La Sapienza University, Rome, Italy.
Permanent parkinsonism was observed in a man with chronic exposure to the
fungicide maneb (manganese ethylene-bis-dithiocarbamate). Symptoms developed
at 37 years of age, two years after exposure had ceased. To our knowledge,
this is the second report on parkinsonism associated with exposure to maneb.
Manganese is a well-known parkinsonigen toxin in humans. More recently, it
has been shown that dithiocarbamates can also induce extrapyramidal
syndromes. The biochemical effects of manganese and dithiocarbamates are
reviewed and their possible neurotoxic mechanisms are discussed. Both of
these components may have played a role in this case.
-
: Neurology 1988 Apr;38(4):550-3 |
|
Chronic exposure to the fungicide maneb may produce
symptoms and signs of CNS manganese intoxication.
Ferraz HB, Bertolucci PH, Pereira JS, Lima JG, Andrade LA.
Department of Neurology and Neurosurgery, Escola Paulista de Medicina, Sao
Paulo, Brazil.
Manganese (Mn) poisoning, a well-known hazard in miners and industrial
workers, shares many features with Parkinson's disease. Two young
agricultural workers with a parkinsonian syndrome, who mentioned exposure to
the fungicide maneb (manganese ethylene-bis-dithiocarbamate), led us to
investigate a new possible source of Mn intoxication. Fifty male rural
workers with occupational exposure to maneb were compared with 19 rural
workers without fungicide exposure. We noted significantly higher prevalence
of plastic rigidity with cogwheel phenomenon, headache, fatigue,
nervousness, memory complaints, and sleepiness in the exposed group. In
addition, we saw other neurologic signs, such as postural tremor, cerebellar
signs, and bradykinesia, although without statistical significance. The data
suggest that occupational exposure to pesticides containing Mn is a possible
source of Mn intoxication of the CNS.
|