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Research Article
TheScientificWorldJOURNAL (2003) 3, 281-290
ISSN 1537-744X; DOI 10.1100/tsw.2003.22
Neurophysiological Effects of Chronic Indoor
Environmental Toxic Mold Exposure on Children
Ebere C. Anyanwu
1,
*, Andrew W. Campbell
2
, and Aristo Vojdani
3
1
Cahers Neurosciences Research, 8787 Shenandoah Park Drive, Suite 122, Conroe, TX
77385;
2
Center for Immune, Environmental and Toxic Disorders, 2501 Oakhurst, Suite 200,
Spring, TX 77386;
3
Immunosciences Laboratory, Inc., 8693 Wilshire Boulevard, Suite 200,
Beverly Hills, CA 90211
E-mail: ebereanyanwu@msn.com
Received March 19, 2003; Revised April 4, 2003; Accepted April 6, 2003; Published April 28, 2003
The phenomenon of building-related diseases is attracting much research interest
in recent years because of the extent to which it affects people with compromised
immune systems, especially children. In this study, we reported the neurological
findings in children who attended our Center because of chronic exposure to toxic
molds. Clinical neurological and neurobehavioral questionnaires were
administered with the cooperation of the children’s parents. The children then
underwent a series of neurophysiological tests including electroencephalogram
(EEG), brainstem evoked potential (BAEP), visual evoked potential (VEP), and
somatosensory evoked potential (SSEP). The results showed high levels of
abnormalities in the analysis of the subjective responses derived from the
questionnaires. The EEG examination was abnormal in seven out of ten of the
patients compared to the controls with only one in ten with episodes of
bihemispheric sharp activity. In all the patients, there was frontotemporal theta
wave activity that seemed to indicate diffuse changes characteristic of metabolic
encephalopathies. Also, there was highly marked 1 to 3 Hz delta activity that was
asymmetrical in the right hemisphere of the brain in three out of ten patients. The
waveforms of BAEP showed abnormalities in 90% of the patients with both 15’
and 31’ check sizes compared to none in the controls. There were significant
delays in waveform V in a majority of the patients representing dysfunctional
cognitive process and conductive hearing loss in both ears. VEP showed clear
abnormalities in four in ten of the patients with P100 amplitudes and latencies
decreased bilaterally. In all the patients, there was slowing of conduction in the
right tibial at an average of 36.9 ms and there was significant decrease in
amplitude of response at the proximal stimulation site. Sensory latencies obtained
in the median, ulnar, and sural nerves bilaterally showed abnormalities in five out
of ten compared to none in the controls. The median, ulnar, and sural sensory
potentials were abnormal in six out of ten patients. There was prolongation of the
median distal sensory latencies bilaterally at an average of 4.55 ms on the right
and an average of 6.10 ms on the left as compared to the ulnars of 2.55 ms
bilaterally. There was no abnormality in the controls. These findings represent
evidence of diffuse polyneuropathy to which three patients demonstrated
*Corresponding author.
©2003 with author.
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Anyanwu et al.: Environmental mycotoxicity in children TheScientificWorldJOURNAL (2003) 3, 281–290
borderline slow motor conduction at an average of 41.1 ms. Overall, the objective
neurophysiological measurements (EEG, BAEP, VEP, and SSEP) were abnormal,
indicating significant neurological deficits in all the patients. Our findings
revealed the extent to which toxic molds can affect the neurological and
behavioral status of children. Further work should be encouraged in this regard.
KEYWORDS: sick building syndrome, molds, mycosis, mycotoxins, neuropediatric
effects, U.S.
DOMAINS: child health and human development, atmospheric systems, neuronal
function, sensation & perception, neurology, behavior, medical care
INTRODUCTION
Building-related diseases are defined by the manifestations of symptomatic illnesses due to poor
indoor environmental air quality and pollutant exposures. According to the WHO definition, it is
characterized by irritations of mucosa, vegetative complaints such as headache and fatigue, as
well as mental health impairment, depression, and irritability[1,2].
It is also defined as an increased occurrence of nonspecific symptoms among populations in
determined buildings and this definition differs from those of other medical syndromes in that it
refers to a system (a building inclusive of its population) rather than to a clinical state in a single
individual[3,5]. Such a definition has made the term “sick building syndrome” (SBS) impossible
to use as a diagnosis applied to individual persons[3,4,5]. Hence, we prefer to call this
phenomenon “indoor environmental related diseases (IERD)”. The syndrome has apparently
become one of the common health concerns in the world, especially in the developed countries
where industrially related environmental pollutions favor the growth of opportunistic toxic molds.
DISTRIBUTION OF TOXIC MOLDS
In recent years, climatic changes have dramatically ensued from extreme cold to extreme heat,
from sporadic lack of rainfall to geographically devastating floods. All these conditions favor the
rapid growth of molds, some of which are saprophytically opportunistic and toxic to humans.
Although the adverse health effects of toxic molds on humans are still emerging and not fully
understood, some of the etiological factors may include extreme conditions of the indoor
environmental conditions such as dampness, moldy air, temperature, and humidity. Visible
condensation on windows, high air humidity in the bathroom, moldy odor, and water leakage of
the residential homes, are the sources of toxic mold–related illnesses and all indicators of
dampness are related to an increase in all types of symptoms, significant even when adjusted for
age, gender, population density, type of ventilation system, and ownership of the building[6]. In
fact, both toxic and nontoxic molds are everywhere and under favorable conditions, grow
luxuriantly and cause diseases. Hence, more and more people throughout the country are having
mold-related medical problems. Homes are being bulldozed in Houston, schools are closing in
Arizona, and buildings are being shut down in Florida due to toxic mold.
SOURCES OF INDOOR TOXIC MOLD EXPOSURE IN CHILDREN
Sources of indoor toxic mold exposures in children include contaminated schools, home
environments, and cereals. When indoor environmental conditions are rife, the toxic mold release
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their spores and volatile organic chemicals such as methanol, ethanol, methane, and other toxic
compounds into the air. People inside the schools or homes breathe in the polluted air. Children
are the most vulnerable. The children readily inhale the polluted air and become ill especially if
their immune systems are not yet competent to handle the antigenic effects of toxicity. Several
cases of this nature have been reported globally. [7,8]
In the U.S., there had been concerns about health and indoor air quality (IAQ) in homes and
schools in which toxic molds were isolated from swab samples of visible growth under wet
carpets, on wet walls, or behind vinyl wall coverings and the associations with adverse health
effects observed among the children exposed to such environments. Jarvis et al.[9,10]
investigated a cluster of cases of pulmonary hemosiderosis in infants in Cleveland, OH and found
that Stachybotrys atra and two isolates of a related toxigenic mold, Memnoniella echinata, were
responsible for the adverse health effects on infants. M. echinata produces two cytotoxic
trichothecene mycotoxins, trichodermol (1a) and trichodermin (1b), as well as several
griseofulvins[9]. Alternaria alternata, Aspergillus spp., Bipolaris spicifera, Curvularia lunata,
Epicoccum nigrum, and Fusarium solani were isolated repeatedly from groups of patients among
96 diagnosed patients with allergic fungal sinusitis[11]. E. nigrum was obtained consistently from
four patients, one of whom yielded mycelial masses consistent in morphology with E. nigrum. Of
the predominant toxic molds recovered from air samples from selected patients' residences, 15
included the same species isolated from the mucin of its inhabitants[11].
CLINICAL MANIFESTATIONS OF TOXIC MOLDS
The adverse effects of toxic molds were first identified more than 60 years ago following an
epidemic of stomatitis, rhinitis, conjunctivitis, pancytopenia, neurological disorders, and death in
horses[12]. Since then, several toxic molds including Stachybotrys, Fusarium, and Aspergillus
have been identified in patients and in their homes. Toxic molds are particularly important
because they produce mycotoxins that are biologically active and can produce a variety of
physiological and pathologic changes in humans, including modulation of inflammation and
altered alveolar surfactant phospholipid concentrations[12].
In this study, all the toxic mold–exposed children continued to suffer from multiple illnesses.
These included frequent symptomatic headaches, fatigue, earache, abdominal and joint pains,
mood swing, persistent coughs, nosebleeds, hyperactivity, memory loss, and allergic reactions.
Their previous surgical history was negative of mycosis and family history was also
noncontributory with the exception of corresponding time frames for similar illnesses among
family members residing in the same homes. According to their medical records, they were all in
excellent health conditions before the toxic mold exposures that predicated frequent doctor’s
visits with reports of evidence of flu-like illnesses and upper respiratory problems.
AIM OF THE STUDY
The aim of this study therefore, was to assess the neurophysiological effects of chronic indoor
environmental toxic mold exposures on children.
MATERIALS AND METHODS
The Study Population
The study population was made up of ten children aged between >18 months and =/>15 years old,
six (60%) female and four (40%) male, and ten sex- and age-matched controls. A majority of the
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children came from families that bought their homes 2 to 8 years prior to this study. They moved
into their homes before renovating them, then pulled off old wallpaper and carpets that were
soaked with urine and stains. Some moved from homes that tested positive for molds and thus
carried with them mold-contaminated furniture and household wares. Less than 30% of the
children were either born in homes that were already exposed to toxic molds or lived in homes
that were not previously known to be toxic mold–exposed but were later flooded, moist, damp,
and humid. All the homes were extensively tested by certified environmental science laboratories
and found positive for toxic mold contamination. The predominant toxic molds found were
Stachybotrys, Aspergillus, Cladosporium, and Penicillium. The controls, on the other hand, had
no known history of chronic toxic mold exposures either at home or school.
Electrophysiological Tests
Carefully designed neurological questionnaires were first administered with the cooperation of
the children’s parents. Then, all the patients and controls underwent clinical neurophysiological
tests including electroencephalogram (EEG), brainstem auditory evoked potential (BAEP), visual
evoked potential (VEP), somatosensory evoked potential (SSEP), and nerve conduction velocity
using Biologic CEEG Graph 4 Model 810 Version 5.71 with Biologic EP Explorer. All tests were
carried out according to the standard methods. The EEG examination included hyperventilation
and intermittent photic stimulation (IPS) using Biologic PS2 photostimulator at intensity 1363
cd/m
2
. International electrode placement 10-20 system was used. The photostimulator was
positioned at a distance of 18 in. (45.72 cm) from subjects’ eyes at a visual angle of 25º and was
given first with the eyes open for 5 s, then 5-s eye closure, and another 5 s with the eyes closed.
Both the patients and the controls were asked to sit at a distance of 170 cm from the stimulus
source with their eyes fixated on the red spot at the center of the monitor.
Brainstem auditory response testing was carried out by stimulating each ear independently
with rarefaction clicks at a rate of 4 to 8 Hz. After taking proper consideration to the patients’
comfort, the stimulus intensity was adjusted to 70 to 80 dB. Although, this sound range might
seem relatively high, it was the range to which the patients were perceptive and comfortable. The
recording electrodes were placed at the vertex (Cz of the International 10-20 System) and both
earlobes. That is, the BAEPs were recorded between Cz and Ai, with a second channel, Cz-Ac.
This was because this channel placement aided in the identification of waves IV and V, which
may be fused in the channel 1 waveform. BAEPs were carried out within 0.3 ms on two repeats.
This was necessary to achieve a check size of 15’ and 31’. Nerve conduction velocity was
carried out using TECA Synergy Multimedia EMG with multisync color SVGA monitor and
Delux stimulator probe (TECAsynergy, Oxford Instruments Medical, Inc.). VEP test was
performed with corrective lenses if needed. However for SSEP, adequate pretest measures were
taken to avoid dispensing too noxious stimuli. For the reliability and reproducibility of tests,
repeats were performed.
Data Analysis
Data generated from the questionnaire were analyzed using power formula analysis[13] to
calculate the number required to detect a difference between the mean score of the patients
(abnormal) and controls (normal) responses. Values from power analysis formula for n to detect a
20% difference was 0.05 for abnormal; 0.05 for normal. Power (P) was 95% and the constant (K)
was 3.29. Neurological response differences in mean change were assessed using
an analysis of
variance (ANOVA) model. Paired t-test comparisons
between outcomes in each were conducted
using least squares means from the above
model. Confidence intervals of 95% for effect-exposure
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differences were computed
on the basis of the least squares means from the ANOVA model.
For
binary measures, such as the percentage of neurological abnormalities, comparisons were
conducted
using Chi-square test. Unadjusted p values are reported. To assess symptom severity at
endpoint relative to an unaffected population, we analyzed scores on the primary outcome
measure
as t scores. All statistical analyses were performed using StatiBot 2000–2002
software[14,15,16].
RESULTS
The subjective neurological findings based on the clinical questionnaire and case histories are
presented in Table 1. With a threshold of 0.05, n = 2646, ny = 20, Ch
2
= 692, p < 0.0001. A low p
value means that the result was statistically significant. Hence, the neurological manifestations
found among the patients were related to chronic mold exposures compared to the controls.
Fatigue, headache, dizziness, cough, and nosebleeds were the most frequent (100%) occurrences.
TABLE 1
Subjective Neurologic Responses with Parental Cooperation
Neurological Responses No. (%) (n = 2 x 10)
Patient Control
Fatigue 10(100) 0(0)
Headache 10(100) 0(0)
Dizziness 10(100) 0(0)
Feeling sick (nausea) 7(70) 3(30)
Cough 10(100) 0(0)
Shortness of breath without physical exercise 9(90) 1(10)
Feeling of general exhaustion 9(90) 1(10)
Heart fluttering (palpitations) 5(50) 0(0)
Bright light 9(90) 3(30)
Burning eyes 7(70) 0(0)
Ringing in your ears 5(50) 0(0)
Ear discharges 4(40) 0(0)
Hearing loss 6(60) 0(0)
Problems with balance 4(40) 0(0)
Runny nose 8(80) 2(20)
Nosebleeds 10(100) 1(10)
Poor appetite 6(60) 0(0)
Abdominal pains 4(40) 1(10)
Weakness of you arms and legs 9(90) 0(0)
Numbness in the limbs 9(90) 0(0)
Tingling in arms or legs 5(50) 0(0)
The EEG Examination
The EEG examination was abnormal in seven out of ten of the patients compared to the controls
with only one in ten with episodes of bihemispheric sharp activity. It was later found that this
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particular control subject had had seizures of unknown etiology in the past. There was
frontotemporal theta wave activity that seemed to indicate diffuse changes characteristic of
metabolic encephalopathies. There was scattered and slowing of the alpha rhythm with
subsequent appearance of theta and delta activity. This wave activity was enhanced by
hyperventilation. There was certainly undefined triphasic wave activity in a majority of the
patients that consisted of a minor positive potential preceded and followed by another smaller
negative waves. In three out of ten patients in particular, there was highly marked 1- to 3-Hz delta
activity that was asymmetrical in the right hemisphere of the brain. Sharp synchronous bilateral
theta activity of 4 Hz was also observed and there were no such wave activity in the controls.
BAEP Examination
The waveforms of BAEP showed abnormalities in 90% of the patients with both 15’ and 31’
check sizes compared to none in the controls. There were significant delays in waveform V in a
majority of the patients. This may represent dysfunctional cognitive process and conductive
hearing loss in both ears since the waveform V is known to be very sensitive in both patients and
in normal subjects[17]. Although the interpeak latencies were symmetrical and bilaterally well
developed in all the patients, probably because of their age however, the amplitudes were
diminished and the latencies were prolonged in a majority of the cases.
VEP Examination
Visual evoked response testing was carried out stimulating each eye independently with pattern
shift stimulus. Although the waveforms were well developed bilaterally in all the patients, the
VEP showed clear abnormalities in four in ten of the patients compared to one in ten of the
controls. Four in ten of the patients’ P100 amplitudes and latencies were decreased bilaterally.
The mean full-field pattern reversal for P100 latency was OS 120.17:OD 119.19 ms in the
patients compared to OS 93.79:OD 93.63 ms in the controls. The mean P100 amplitude was OS
6.82:OD 5.19 µV compared to OS 21.42:OD 20.18 µV for the controls.
On hemifield testing there was also a definite prolongation of the latencies bilaterally in all
the patients during stimulation. These findings may represent evidence of bilateral optic nerve
dysfunction. One of the patients (8 years old) had visual disturbances with a visual acuity of
20/30 in the right eye. It was not possible to verify the visual acuity of the left eye due to
nystagmus in that eye. Note the waveforms were well developed with right eye stimulation and
less developed with left eye stimulation. The P100 latency was markedly prolonged with left eye
stimulation at 143.62 ms and the amplitude of response was decreased at 1.26 µV. The P100
latency and amplitudes were well within normal limits with the right eye stimulation. This is an
evidence of left optic nerve dysfunction.
SSEP Examination
SEEP was performed by stimulating each posterior tibial nerve independently while recording at
popliteal fosse lumbar point, cervical point, and scalp. There was prolongation of lumbar point to
the scalp interpeak latency with left posterior tibial stimulation in five in ten of the patients. There
was also evidence of a central conduction delay from lumber point with left posterior stimulation.
This could represent sensorimotor polyneuropathy. In all the patients, there was slowing of
conduction in the right tibial at an average of 36.9 ms and there was significant decrease in
amplitude of response at the proximal stimulation site.
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Sensory latencies obtained in the median, ulnar, and sural nerves bilaterally showed
abnormalities in five out of ten compared to none in the controls. There was mild prolongation of
the left median distal sensory latency at 3.5 ms and both ulnar distal sensory latencies at 3.15 ms
on the left and 3.10 ms on the right. The mean parametric median nerve somatosensory
measurements in both the patients and the controls are presented in Table 2. There were
significant differences between the readings from the patients and the controls (p < 0.001).
TABLE 2
Mean Parametric Median Nerve Somatosensory Measurements in Both the Patients
and the Healthy Control
PARAMETER PATIENTS CONTROLS X SD MIN MAX
Left Right Left Right
Absolute latency (peak in ms)
EP 10.03 9.95 9.56 9.72 9.7 0.76 7.9 11.2
N13 12.32 12.64 12.32 12.64 13.5 0.92 11.5 15.6
N19 18.09 18.25 17.22 17.62 19.0 1.02 16.7 21.2
P22 20.78 20.86 19.67 20.22 22.0 1.29 19.1 25.2
Interwave latency (ms)
EP-N13 2.29 2.69 2.76 2.92 3.8 0.45 2.7 4.5
EP-N19 8.06 8.30 7.66 7.90 9.3 0.53 7.8 10.4
EP-P22 10.75 10.91 10.11 10.50 12.3 0.86 10.0 15.0
N13-N19 5.77 5.61 4.90 4.98 5.5 0.42 4.7 6.8
L/R latency difference (ms)
EP 0.08 0.16 0.2 0.20 0.0 0.9
EP-N13 0.40 0.16 0.2 0.17 0.0 0.6
EP-N19 0.24 0.24 0.2 0.21 0.0 0.8
EP-P22 0.16 0.39 0.3 0.24 0.0 1.1
N13-N19 0.16 0.08 0.3 0.25 0.0 1.1
Amplitude (
µς
)
EP 2.55 1.67 1.88 0.78 3.0 1.86 0.5 8.6
N13 2.52 2.20 0.99 9.67 2.3 0.87 0.8 4.4
N19 2.62 1.63 0.54 1.51 1.0 0.56 0.1 2.7
P22 1.79 1.97 1.12 1.55 2.2 1.10 0.5 5.5
L/R amplitude difference (
µς
)
N19 0.99 0.97 41.7 33.14 0.0 144.4
P22 0.18 0.33 25.7 21.23 0.0 80.4
Stimulation rate = 4.7 ms.
Nerve Conduction
Nerve conduction velocity studies were carried out in both upper and lower extremities. The
median, ulnar, peroneal, and tibial nerves were evaluated with regard to motor conductions
bilaterally. There was prolongation of the median nerve distal motor latencies bilaterally on the
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right and on the left of the patients, markedly low readings on the right and left of the ulnars. The
median, ulnar, and sural sensory potentials were abnormal in six out of ten patients. There was
prolongation of the median distal sensory latencies bilaterally at an average of 4.55 ms on the
right and an average of 6.10 ms on the left as compared to the ulnars of 2.55 ms bilaterally. There
was no abnormality in the controls. These findings represent evidence of diffuse polyneuropathy
to which three patients demonstrated borderline slow motor conduction at an average of 41.1 ms.
DISCUSSION
Unlike household allergens typically found indoors, the allergens from toxic molds such as
Aspergillus, Stachybotrys, Cladiosporium, etc., are conceivably ubiquitous in homes and in
schools that are exposed to dampness and dusty air. Homes with poor indoor air quality (IAQ) are
also found to be frequently susceptible to toxic surface fungal contamination. Such molds can
grow on building materials such as wallpaper, drywall,
and ceiling tiles, particularly after water
damage has occurred[18]. It was found that condensation on windows, high air humidity in the
bathroom, moldy odor, and water leakage exposed children to fungal infection[6] leading to the
neurophysiological effects such as ocular, nasal, throat, dermal symptoms, cough, headache, and
tiredness. The prevalence of pulmonary hemorrhage/hemosiderosis due to indoor toxic mold
exposures among children still remains valid[19,20,21,22,23,24].
However, the fact that molds can produce lethal mycotoxins is apparently becoming well
established[25,26]. Nevertheless, the neurophysiological effects of chronic toxic mold exposure
in children are emerging. In our patients, there were frontotemporal theta wave activities that
seemed to indicate diffuse changes characteristic of metabolic encephalopathies. There was
scattered and slowing of the alpha rhythm with subsequent appearance of theta and delta activity
that was enhanced by hyperventilation. There was certainly undefined triphasic wave activity in a
majority of the patients that consisted of a minor positive potential preceded and followed by
smaller negative waves. These triphasic wave activities were previously thought to be specific for
hepathic encephalopathy but are now believed to be in fact metabolic encephalopathy[25,26]. Our
findings suggest that children who are chronically exposed to toxic mold may manifest either
hypo- or hyperglycemia, hypo- or hyperthyroidism, or myexedema because of the low voltage
record in which alpha activity was preserved with intermix of theta. There was also the presence
of 4 Hz paroxysmal bilaterally synchronous generalized focal theta activities probably suggesting
probably lesions to cortex. Although most of the activity varied with age, the presence of delta
rhythms in a majority of the children was probably indicative of a destructive lesion of the cortex
such as demyelination, infarction, or abscess.
The waveforms V of BAEP were abnormally delayed in all the patients. When the latency of
P100 is outside 95 to 99% of normal boundaries or when there is unusual prolongation or absence
of N75 of P100, or when there is an absence of VEP such as we have found in our study, there is
no doubt that mycosis has a new dimension in neurologic science. It could be interpreted that not
only did the children have dysfunctional cognitive process and conductive hearing loss, but also
had some lesional disturbances in occipito- or paratemporal regions of the brain function. In this
case, visual evoked response gave serious indications of clear abnormalities with possible optic
nerve dysfunction. Nerve conduction study showed abnormalities that were consistent with
neurological damage.
CONCLUSIONS
Toxic molds can affect the nervous system in children who are chronically exposed. Common
neurological symptoms are headaches, fatigue, sleep disturbance, confusion, mood swings,
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nosebleeds, and cough. High levels of sensorimotor dysfunction and the related disorders in
children means that toxic mold exposure should be regarded as a serious neurological health
concern in children indeed. Children can develop agitation and poor performance in school,
which is sometimes misdiagnosed as hyperactivity. There are neurological tests that can help
determine what has been damaged in the body of the children due to toxic mold exposures and
how severely. Overall, the results seem to indicate that children are neurophysiologically
vulnerable, especially those under 10 years of age. Although, further work in this topic is
ongoing, further research investigations at other centers are encouraged.
ACKNOWLEDGMENTS
We thank Ms. Nina Immers for her management support and invaluable administrative input in
the execution of this research.
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This article should be referenced as follows:
Anyanwu, E., Campbell, A.W., and Vojdani, A. (2003) Neurophysiological effects of chronic indoor environmental
toxic mold exposure on children. TheScientificWorldJOURNAL 3, 281–290.
Handling Editors:
Hatim A. Omar, Associate Editor and Joav Merrick, Principal Editor for Child Health and Human Development — a
domain of TheScientificWorldJOURNAL.
BIOSKETCH
Ebere C. Anyanwu is a Clinical Neurophysiologist and the Director of Cahers Neurosciences
Research Inc., Houston. Dr. Anyanwu is also an Adjunct Professor of Anatomy and Physiology at
the North Harris and Montgomery Colleges in Houston and the Woodlands, TX.
Andrew W. Campbell is an Expert Medical Scientist in Immunotoxicology and the Medical
Director and Chief Executive of the Center for Immune, Environmental and Toxic Disorders,
Houston, TX.
Aristo Vojdani is a Professor of Immunochemistry and the Chief Executive of the
Immunosciences Laboratory, Inc., Beverly Hills, CA. Dr. Vojdani is also Board Certified in
Medical Laboratory Technology.
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