ICMR BULLETIN VOL. 29-No.-8-AUGUST-1999.pdf

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ISSN 0377-4910

August, 1999

Vol. 29, No. 8

RISK OF ALUMINIUM TOXICITY IN THE INDIAN CONTEXT
Aluminium is widely used in the production of
medicines like analgesics, antacids and anti-diarrhoeals
besides finding use as a food additive and water purification
agent. Aluminium also has wide industrial uses. It is
still a metal of choice in the making of various kinds of
household cookware and storage utensils.1 Today, the
. annual production of aluminium amounts to about 22,000
metric tonnes world wide.

Sources of Aluminium Exposure
Environment

The exposure to Aluminium can be through food,
water and airborne dust particles. Aluminium salts such.
as aluminium sulphate are used to flocculate the oganic
matter in water. The higher concentration of aluminium
in vegetables from certain regions is probably due to soil
contamination or acid rains. Certain plants like tea are
known aluminium accumulators.'Normal adults ingest
an average of 2-5 mg Al/day through food and signifi­
cant amounts from drinking water. Recent reports across
the globe indicate that most individuals consume 1-10
mg aluminium/day from natural sources.2

cookers, roasting pans, sauce pans, frozen dinner trays;
foils and wrappers. The usage of aluminium in packag­
ing of food stuffs is on the increase and is becoming a
potential source of contamination. A number of studies
support the leaching of aluminium from cookware and
packaging materials.3 However, the type of aluminium
utensils (new or old), pH, form and composition of the
food, duration of contact with the food during cooking
and presence of salt, sugar and ions such as fluoride,
chloride and carbonate are likely to affect the extent of
leaching of aluminium into the food.
Foods

Aluminium containing food additives are generally
used as buffers, neutralizing agents, dough strengthened,
leavening agents, emulsifying agents for processed cheese,
stabilizers, thickeners, etc* These additives include so­
dium aluminium phosphate, sodium aluminium sulphate
and aluminium silicate. Besides these, aluminium hy­
droxide or aluminium oleate may migrate from paper or
paper board which are used for food packing.5
Medicines

Cookware/Packaging
One of the potential sources of additional dietary
aluminium is aluminium cookware like skillets, pressure

The use of aluminium in over-the-counter drugs such
as antacids, analgesics and anti-diarrhoeals has increased
substantially in recent times. Aluminium containing

Division of Publication & Information, ICMR, New Delhi -110029

antacids are widely used and the most common form of
aluminium in these preparations is aluminium hydrox­
ide.6 Another major use of aluminium in antacids is as
a phosphate binding agent, particularly, administered to
renal patients to lower the elevated serum phosphate levels.
The antacids are estimated to provide between 8005000 mg/day of aluminium to such patients.7

Limits

According to the World Health Organization, the Pro­
visional Tolerable Weekly Intake (PTWI) of aluminium
as a contaminant (including that as an additive) is 7 mg/
kg body weight for adults. For children, the acceptable
daily intake (ADI) of 2 mg is commonly used for risk
assessment.8 The recommendations for the PTWI are,
however, based mostly on short-term toxicity studies and
are therefore, subject to change as and when toxicologi­
cal data from chronic toxicity studies become available.

Toxicity
That aluminium is a potential toxin was known
almost five decades ago. While the neurotoxic potential
of aluminium is undisputed in various animal species,
there is as yet no strong evidence to suggest that
aluminium could be toxic to normal healthy humans.
However, neurotoxicity of aluminium is well documented
in individuals with renal insufficiency in whom
aluminium excretion is compromised. The accumulation
of aluminium in the body is reported to cause disorders
related to bone, blood and brain.13 There is increasing
evidence that Al3* may affect many neurochemical
processes in the central nervous system. These
biochemical alterations are affected by influencing
nuclear, cytoplasmic and cytoskeletal structures, blood
components, membrane integrity, enzyme activities and
neurotransmitter functions which may ultimately lead
to altered memory/behavioural disorders14’16.
A

Diseases Caused by High Intake of Aluminium
Absorption
Aluminium is mostly absorbed through the oral route,
though a certain amount is also suspected to be absorbed
through the pulmonary route. The mechanism of intesabsorption of aluminium is fairly complex and not
y**! fully elucidated. This is because of different types of
aluminium chemical speciation, depending on pH, ionic
strength and presence of complexing agents and other
ions like iron2* zinc2*, calcium2* or magnesium2* in the
intestine.9 In more acidic solutions (pH < 5.0), aluminium
exists as the octahedral hexahydrate [A1(HLO)63*], largely
represented as Al3*. Successive deprotonations yield
Al(OH)2*and A1(OH)22*, with increasing pH. In neutral
solutions, aluminium precipitates as amorphous A1(OH)3
and slowly begins to redissolve and forms tetrahydral
A1(OH)4". Ions such as fluoride, lactate, etc., form soluble
complexes with aluminium and thus prevent precipita­
tion of aluminium and increase absorption.10,11 There is
evidence to show that aluminium interacts with the gas­
trointestinal calcium transport system and also with trans­
ferrin mediated iron uptake. There is consistent evidence
that absorption of aluminium increases in the presence
of citrate through formation of soluble aluminium cit­
rate complex-.12 There are some data suggesting that
aluminium absorption increases after fasting. The alu­
minium levels in the blood of healthy, occupationally
unexposed humans are reported to be around 5 pg/1. The
highest levels are fourtd in tissues such as bone, liver
and lung.

86

Dialysis dementia (Aluminium dialysis encephalopathy)
This neurological syndrome was first described in pa­
tients who had had long-term haemodialysis for chronic
renal failure. This disorder is clinically characterized by
changes in the electroencephalogram (EEG) followed by
speech disorders, development of psychosis, progressive
dementia, convulsions, loss of memory, moverhent disor­
ders, myoclonicjerks and seizures followed by death within
a yqgr. A number of epidemiological studies from Europe
recognised that in geographical areas where patients with
dialysis dementia were detected, there was a high incidence
of osteomalacia leading to fractures. It was also seen that
the municipal water used in haemodialysis in renal patients
contained high concentration of aluminium.17’19
(
Bone diseases
Bone is the major accumulator of aluminium in the
body and consequently there are several bone diseases
associated with increased plasma aluminium concentra­
tions. The most common aluminium-induced bone dis6- ,
eases are renal osteodystrophy (low turnover osteoma­
lacia), aplastic bone disease and bone disease associated
with toal parenteral nutrition.20’22.

Microcytic anaemia

This condition has been known to occur m renal
patients with increased plasma aluminium levels, however,

^without iron deficiency. Reports show that reduced
A haemoglobin levels, preceded by microcytosis, result as
a specific toxic manifestation of aluminium exposure23.

(iii)

Other neurological disorders such as epilepsy, Par­
kinsonism, amyotropic lateral sclerosis and diseases
predisposing to multiinfarct dementia are not asso­
ciated with increased concentrations of aluminium
in drinking water.

(iv)

Chelation of aluminium by desferrioxamine lowers
the body and brain aluminium content and retards
the progression of AD.

Senile dementia of the Alzheimer's type (SDAT)
Dementia* is the most common disorder of the
elderly and nearly 46% of the population over the
age of 85 years meet the diagnostic criteria for
dementia. The most common form of dementia is re’ ported to be that of the Alzheimer’s disease (AD) type.
It is a progressive neurodegenerative disorder with the
clinical features of rapid loss of memory, inability to
perform simple intellectual tasks, reduced flexibility, dis­
orientation, speech problems, mental deterioration and
emotional instability.24,25

After the appearance of the first symptoms, the
disease slowly progresses leading to death in 4-12 years.
* AD has been recognised as the main cause of
neurodegeneration in the developed countries and ac­
counts for nearly 75% of all dementias in the aged26. Five
percent of the population aged above 65 years is estimated
to be affected by Alzheimer’s disease.
In India, no epidemiological survey has been carried
out regarding dementia and dementing illness and
therefore, data are scanty. However, AD is present in
India although the'age related prevalence rates are not
available to permit comparisons with .the West. It is
reported that 30-38% of cases of dementia in India were
in the group of senile and presenile dementia of the
Alzheimer’s type27. Due to the changing demographic
pattern, as longevity increases, the incidence ofAD could
well go up in the Indian population. Certain experimental
and epidemiological evidences suggest that aluminium
exposure is a risk factor in the etiopathogenesis of AD
in humans. Though the evidence regarding the role of
Al in the etiology of AD is equivocal, it must still be
regarded as a possible risk factor in the pathogenesis of
the disease. The focal accumulation of aluminium in
brains of AD patients and its possible role in the senile
plaques and neurofibrillary tangles cannot be ruled out.
There are strong epidemiological evidences28 which
indicate a positive role ofalumiaium in AD. These include-

(i)

About eight studies conducted in five countries sug­
gest a statistically significant association between the
concentration of aluminium in drinking water and
the number of AD cases.

(ii)

At least ten laboratories from four continents have
reported elevated levels of aluminium in brain tis­
sue from AD patients.

However, the precise pathogenic role of aluminium
in AD is still controversial and highly debated as the studies
in this area still fail to extrapolate the experimentally
induced neurological changes in animals to the human
situation.

Effect on respiratory tract
Historically, pulmonary fibrosis has been associated
with various types of occupations within
cIlmh
industry. Occupational aium;/.
cxFvduie is reported
to cause pathological lung functions, abnormal chest
X-rays, development of intestinal fibrosis29, etc.

Effect of Nutrients and Dietary Factors
Recent evidences indicate that absorption of alu­
minium is much higher when certain organic acids such
as citrate; lactate and ascorbate are present in the diets.
It is reported that afuminium absorption increases sev­
eral fold both in humans and other animals when it is
ingested in small amounts (<5 mg) as compared to the
absorption involving phaimaceutical doses (1 -3 g). Chronic
nutrient deficiencies of certain divalent metals have been
shown to induce an abnormal metabolism leading to the
accumulation of non-essential elements. In addition, alu­
minium is reported to have a slow turnover in the body
and therefore might accumulate in tissues over a long
period of time3031.

Sub-populations at Risk
Aluminium toxicity has been reported to develop over
weeks or months in patients with chronic renal failure
when dialysis fluids or parenteral solutions contained
aluminium, or when higher aluminium was ingested
through aluminium containing oral phosphate binders.
The increased aluminium content in brains of patients
with renal failure seems to be major etiological factor in
the development of dementia32.

The development of a specific form of osteomalacia
and of microcytic, hypochromic anaemia is attributed to
87

aluminium. It has been demonstrated that aluminium
absorption is modified by the presence of minerals such
as iron, calcium and zinc in the medium. Iron deficiency
is shown to be widely prevalent and the calcium intakes
are sub-optimal in most of the Indian population, espe­
cially in children and pregnant and lactating women.
Hence, these groups are at risk due to aluminium ab­
sorption. It. is important to note that because of the wide
use of aluminium cookware and storage vessels, the in­
take of aluminium by Indian population could be much
higher than what has been reported for the West.

Table I. Aluminium content of cooked food (rng/100 g)

Food commodities

No.

Type of vessel used for cooking

Stainless
steel

New
Old
aluminium aluminium

Vegetables

6

1.26
(0.66-2.71)

1.45
(0.97-2.75)

1.80
(1.3-2.81)

Leafy vegetables

4

7.36
10.73
(3.79-11.07) (4.39-21.70)

13.37
(4.85-30.7)

Pulses (Rqjgram)

5

3.41
(0.94-6.65)

2
2

1.57
1.08

4.80
1.46

4.80
1.68

2

0.32

0.50

0.85

9.24
4.06
(0.97-7.23) (1.93-22.2)

Roots & Tubers*

NIN Studies
Aluminium content of cookedfoods
Extensive data are available.from the western litera­
ture regarding the risk of aluminium toxicity, while it is
scanty from India. As aluminium vessels are the most
commonly’used cookware in rural and semi-urban In­
dia, a study was undertaken to assess the contribution of
aluminium cooking utensils to the total daily intake of
aluminium. In addition, several commonly consumed food
items were analysed for their aluminium content. The
study revealed that the major contribution of aluminium
from Indian foods are through consumption of vegetables,
spices and pulses. Cereals, milk and milk products con­
tribute negligible amounts. Green leafy vegetables and
sambar (a popular legume and gravy-based preparation)
contribute significantly to the total daily aluminium in­
take. Usage of aluminium utensils significantly contrib­
utes to the total daily aluminium intake and the type of
food preparation determines the extent of leaching of
aluminium from the vessels. More acidic food prepara­
tions containing green leafy vegetables, tomato contain­
ing dhal (split pulse)/sa/n5aF, etc., cause greater leach­
ing of aluminium into food from the utensils. It appears
that the daily intake of aluminium in certain populations
where aluminium utensils are regularly used could be
much higher when compared to those who use stainless
steel cookware. New aluminium vessels contribute greater
amounts of aluminium when green leafy as well as other
vegetables and legume preparations are cooked in them
(Table I).

Effect ofCd/Fe deficient diets on aluminium absorption
\Aluminium has been implicated in diseases of the
brain, bone and blood. Recent evidences suggest that
certain nutrient deficiencies like iron and calcium
deficiencies might enhance aluminium absorption and
hence its toxicity33.

88

Yam
Potato
Cereals (rice)*

* Average of twn observations

Studies conducted on experimental rats showed that
dietary factors such as citrate and nutritional deficien­
cies of essential minerals such as calcium and iron can
significantly enhance aluminium absorption and tissue
accumulation especially over a long period. The effects
of long-term feeding of aluminium rich diets on age-as­
sociated degenerative changes, as reflected by alterations .
in specific parameters of neuronal function, were inves­
tigated. It was found that some of the direct effects of
aluminium observed in vitro could be produced in vivo
through dietary aluminium feeding in both iron deficient
and calcium restricted rats. These include inhibition of
brain hexokinase (glucose utilization), mitochondrial
respiration (cerebral oxidative metabolism), choline acetyl
transferase activity (cholinergic function) and depletion
of intra-synaptosomal free calcium levels. Attempt was
made to corroborate these biochemical changes with
lesions in the cytoskeletal architecture, if any, to arrive
at definite conclusions regarding neurodegenerative
changes in experimental rats, attributable to aluminium.
The results showed that the reduction in the brain pro­
tein kinase C (PKC) activity and also cytoskeletal ab­
normalities as revealed by increase in microtubule.asso ­
ciated protein - tubulin associated unit (MAP -Tau) and
neurofibrillary protein, (NF-200), and the tangle bear­
ing neurons were found only in calcium restricted rats
on moderately high aluminium diet (Table II). These
observations suggest that aluminium-calcium interactions
are perhaps more important in the development’of cha­
racteristic neuropathology in chronic age associated alu­
minium toxicity state when compared to aluminium-iron
interactions. Thus.it appears that, aluminium is able to

exert a greater toxicity in states of calcium restriction.
It was also found that anaemic individuals have higher
circulating aluminium levels perhaps due to higher intestinal absorption and binding to transferrin, which has
more number of sites unsaturated in iron deficiency.
Table II. Effect of iron and calcium deficiency on parameters
related to neuronal function in the brain of experimental
rats.
Parameters

Aluminium levels

Fe deficiency
+ high Al

Ca restriction
+ high Al

T

t

t'
i
r
T

—
—

—•

Hexokinase
Oxidation of succinate
Succinate dehydrogenase
Oxidation of malate

Malate dehydrogenase
Choline acetyl transferase
Membrane PKC
Cytosolic PKC
Synaptosomal membrane fluidity
Synaptosomal (Ca2*),
Neurofibrillary tangles
Taii:no.of cells
NF-200
intensity
no.of cells

—
—

1
—
—

T
T

—

T
T

The changes in Fe deficiency or Ca restriction were compared with
respective normal Fe and Ca sufficient groups receiving some levels
of aluminium. There were no significant changes in Na+, K*-ATPase,
Mg2*-ATPase, acetylcholine esterase, Tau-intensity and gross histo­
logy.
Tau: Tubulin Associated Unit; PKC: Protein Kinase C;
NF: Neurofibrillary protein
t :Significantly increased ; 4- : Significantly decreased •;
- : Change is statistical not significant.

Biomonitoring

Hazards to neurological development and brain func­
tion from exposure to aluminium have been identified
through animal studies. However, aluminium has not
been demonstrated to pose a health risk to healthy nonoccupationally exposed humans. Aluminium has a very
low absorption rate (1%) and also slow turnover in the
body. Therefore, the risk of aluminium toxicity is probr
ably due to prolonged chronic exposure. A single analy­
sis of blood or urinary aluminium at one time point does
not indicate aluminium toxicity. Hence, keeping in view
the epidemiological evidence ofhigh aluminium in drink­
ing water with the incidence of SDAT along with ex­
perimental evidence from animal studies, reduction/control

in the intake of aluminium by patients with renal failure
and aged persons is advisable. Meanwhile, regular moni­
toring of plasma aluminium levels in haemodialysed pa­
tients and those at risk for aluminium toxicity should be
made mandatory. The use of aluminium cookware should
be limited. While they are safe to use for most cereal
preparations, their use for the preparation of acidic foods
such as tomato/tamarind containing dhal/sambar and green
leafy vegetables should be avoided, since leaching ofalu­
minium from the vessel into food preparations occurs in
greater proportions.

Conclusions
Aluminium is among the most plentiful elements in
the earth’s crust. * Experimental evidence suggests that
aluminium is a potent neurotoxin. Human exposure to
aluminium has increased markedly and in the present
scenario, man is more prone to absorb higher amounts
of aluminium. Several disorders of the nervous system
such as dialysis dementia, senile dementia of the
Alzheimer’s type, Parkinson’s dementia besides
osteodystrophy and dialysis associated arthropathy have
been associated with increased ingestion of aluminium.
Dietary factors like citrate and sub-optimal intake of
nutrients like iron and calcium are shown to enhance the
gut absorption of aluminium. Investigations also revealed
that chronic exposure ofrats to high aluminium on calciumrestricted diets resulted in neurodegenerative changes in
ageing rats, as identified by formation of neurofibrillary
tangles and abnormal accumulation ofMAP-Tau and NF200 proteins along with impairment in certain
physiologically important biochemical functions in the
brain. Being a metal of very slow turnover, there is perhaps
no escape from the aluminium load in the body making
it necessary to minimize chronic exposure to high levels
of aluminium, especially through diet and water.

References
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21.

Parkinson,' I.S., Feest, T.G., Ward; M.K, Fawcett, R.W.P. and
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Walker, G.S., Aaron, J.E., Peacock, M., Robinson, P.J.A. and
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*
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30.

This write-up has been contributed by Dr. Neelam, Research
Associate, Dr. P. Uday Kumar and Dr. M. Kaladhar, Sr. Research
Officers, National Institute of Nutrition, Hyderabad.
?"

ABSTRACTS
Some Research Projects Completed Recently
Cellular manifestations of p53 and bcl-2 genes in ovarian
carcinoma

expression of apoptosis regulatory genes p53 and hel-2 as

The study was carried out to determine the extent of
apoptosis in various ovarian tumours and correlate it to the

defined by the expression of the proliferating cell nuclear

90

well as the total proliferative compartment of the tumour
antigen (PCNA). Patients (138) with various histopathological

types, stages and grades of ovarian carcinoma were included
in the study. Of these, 24 patients had benign cystadenomas
and were grouped as controls. The malignant tumours were
further sub-divided to include 51 patients with serous, 26
with mucinous, 18 with endometroid, 6 with clear cell and
13 with undifferentiated carcinomas.

Expression of p53 and bcl-2 oncogenes were analysed
by immunocytochemistry and Western blot assay. The levels
of mutant p53 was estimated using a mutant specific p53
ELISA. Apoptosis was evaluated by analysing the presence
of nucleosomes by ELISA and further confirmed by the
TUNEL (Tdt-mediated dUTP biotin nick end labelling) assay.
The bcl-2 gene was found to be expressed predominantly
in benign cystadenomas. It was also expressed by
Endometroid carcinomas. However, it was mostly absent
in'serous tumours, clear cell carcinomas and undifferentiated
carcinomas. None ofthe benign lesions expressed p53 while
most of the undifferentiated (77%) and serous carcinomas
(59%) expressed the protein. ELISA results for mutant p53
closely correlated with the immunocytochemistry data. The
tumour proliferative compartment analysed by PCNA
expression was also maximum in undifferentiated carcinomas
and serous tumours The presence of p53 protein and
expression ofPCNA were significantly correlated, supporting
a major role of p53 in the regulation of cell proliferation in
ovarian tissue. The lack of correlation between bcl-2 and
PCNA suggested that bcl-2 is not a major regulator of cell
proliferation. Higher levels of apoptosis were seen in
mucinous carcinoma compared to the other tumour subtypes.
Mucinous carcinoma also had lower levels of bcl-2
expression. There was an increased apoptosis and bcl-2
expression in benign cystadenomas.

M. Radhakrishna Pillai
Division of Laboratory
Medicine and Tumour Biology
Regional Cancer Centre
Thiruvanantapuram.
Serodiagnosis of invasive aspergillosis.

The study was carried out to identify and purify
immunodominant antigens from circulating antigens ofAs­
pergillusfumigatus present in invasive aspergillosis as also
to evaluate the purified immunodominant antigens in anti­
body and antigen detection tests for the diagnosis of inva­
sive aspergillosis in experimentally infected mice and in
patients suffering from invasive aspergillosis. Crude anti­
gens of the two strains used in the study (standard strain
Aspergillus fumigatus ATCC 13077 and clinical isolate
A.fumigatus MCC LS 77,0010) were prepared and rabbit
hyperimmune sera raised against the respective crude an­
tigens (CF-73, MYC-73 and C-10) were used for detection

of circulating antigens. Acute invasive aspergillosis was
established in cyclophosphamide treated adult Swiss albino
mice. After infection 100% mortality was observed in mice
within four days of infection.

After the establishment of experimental animal model
of acute invasive aspergillosis circulating antigens were
detected by Western blotting. Prominant protein bands were
found at 18 kDa position using anti CF-73 antibody.
Prominant bands at 44 kDa regions were seen with anti
C-10 antibody. Similarly anti-MYC-73 antibody produced
prominant bands at 89 kDa region. These three
immuno4pminant antigens (18,44 and 89 kDa) were chosen
for purification and further studies.
The 18 kDa antigen was purified using sepharose CL6B gel filtration and Sephadex G-50 column chromatography.
The 44 and 89 kDa proteins were purified by gel
electrophoresis.

Various serological procedures were evaluated for the
detection of antigen and antibody in experimental murine
model of acute invasive aspergillosis as well as in patients
of acute aspergillosis. The latex agglutination test and ELISA
were used for antigen detection. Latex agglutination showed
a sensitivity of 55% and specificity of 100% whereas ELISA
showed 72% sensitivity and 96.6% specificity. Sensitivity
of Pastorex latex agglutination was found to be 70%. The
18 kDa antigen detection ELISA in patients had a sensi­
tivity of 77% in the immunosuppressed and 71.4% in the
non-immunosuppressed patients.
Antibody detection was carried out by gel diffusion
and ELISA. Overall, lower sensitivity and 100% specific­
ity was observed in gel diffusion against all the three pu­
rified antigens. The highest sensitivity of 29% was found
against 44 kDa antigen. The immunosuppressed patients
had a sensitivity of 18.7-25% while the non-immunosuppressed patients 28.5-51.1%. The ELISA showed 80%
sensitivity against 44 kDa antigen and 71 % against 18 kDa
and 89 kDa antigens. The specificity was 96.6% against all
the 3 antigens. The highest sensitivity of 85.7% was ob­
served against the 44 kDa antigen in the non-immunosup­
pressed patients and 75% against 89 kDA antigen in the
immunosuppressed patients.

It is concluded that the ELISA for antigen detection
against 18 kDa antigen is a better diagnostic test as compared
to latex agglutination and amongst the antibody detection
tests the ELISA using 44 kDa antigen is promising as
compared to gel diffusion.

A; Chakrabarti
Department of Medical Microbiology
Postgraduate Institute of
Medical Education and Research
Chandigarh.

91

ICMR NEWS
The XI meeting of the Directors of the ICMR Institutes/Centres located in different parts of India was held
at New Delhi on August 4, 1999.
***

♦**

♦**

The following meetings of various technical groups/
committees of the Council were held :
Meetings of the Expert Groups (EGs)/Scientific
Advisory Group (SAG)/Task Force (TF)/Project
Review Committee (PRC) held:
EG on Phase III Clinical Trial
July 14, 1999
on “Risug” (Styrene maleic anhydride (at New Delhi)
dissolved in DMSO) as injectable
intravasal male contraceptive

EG on Phase II Clinical Trial on
Praneem

EG on Infertility and Assisted
Reproductive Technologies

SAG of the Division of
Epidemiology and Communicable
Diseases

August 5-6, 1999
(at New Delhi)

PRC on Mental Health, Neurology
Orthopaedics, Environmental
Hygiene and Biomedical
Engineering

August 9, 1999
(at New Delhi)

TF on Feasibility of Using
Syndromic Approach for
Diagnosis and Treatment of
RTI/STD at PHC Level

August 10-11, 1999
(at Calcutta)

Participation of ICMR Scientists in Scientific Events :

Dr. A.K. C?upta, Assistant Director, National Insti-

July 23, 1999
(at New Delhi)
and
August 10, 1999
• (at Mumbai)

tute of Virology, Pune, participated in the XI International Congress of Virology at Sydney (August 9-13,
1999).

July 31.August 1, 1999
(at Mumbai)

ICMR participated in the fifth Delhi Book fair,
organised at Pragati Maidan, New Delhi (August 14-22,
1999)

9)

Book Fair

ICMR AIDED SYMPOSIA/SEMINARS/WORKSHOPS/COURSES/CONFERENCES
Symposium/Seminar/Workshop/
Course/Conference

Date & Place

Contact Address

International Symposium on Atraumatic Restorative
Treatment

August 12-14, 1999;
(at Chennai)

Dr. S. Balagopal, Organising Secretary of the
Symposium, SHIRAZ-47,3rd East Street, Kamraj ml
Nagar, Chennai-600041.
W

Biennial National Conference of the Association of
Gerontology on Challenges of Ageing in the 21st
Century

August 20-21, 1999;
(at Hyderabad)

Sh. K.R. Gangadharan, Organising Secretary of
the Conference, c/o Heritage Medical Centre,
7-1-59/4 & 8, Ameerpet, Hyderabad-500016.

Symposium on Cardiology for the Next Millenium

September 10-12,1999;
(at Chennai)

Dr. S. Thanikachalam, Director, Cardiac Care
Centre, Porur, Chennai-600016.

Symposium on Research in Molecular Biology and
Biotechnology in India: Challenges in the Next Millenium

September 13-14,1999;
(at Calcutta)

Dr. A.N. Bhaduri, Indian Institute of Chemical
Biology, Jadavpur, Calcutta-700032.

International Seminar on Disability Caused by Mental
Disorders
v

September 15-17,1999;
(at Chennai)

Dr. R. Thara, Organising Secretary of the Semi­
nar, Schizophrenia Research Foundation, R/7A,
North Main Road, West Anna Nagar Extn.
Chennai-600101.

XXI Biennial Conference of Indian Association of
Leprolpgists

September 17-19,1999;
(at Chandigarh)

Dr. Bhushan Kumar, Organising Secretary of the
Conference, Department of Dermatology, Venere­
ology and Leprology, Postgraduate Institute of
Medical Education pnd Research, Chandigarh160012.

92

Symposium/Seminar/Workshop/
Course/Conference

Date & Place

Contact Address

National Symposium and Update on Problem1 Areas
in Diagnostic Oncopathology

October 8-10,1999;
(at Sevagram)

IntematiQnal Conference on Man, Environment and
Nature

November 26-28,1999;
(?t Calcutta)

Prof. Sunirmal Chanda, Convenor, of the Con­
ference, Centre for Study of Man and Environ­
ment, Parivesh Kendra, CK-11, Sector-2, Salt Lake
City, Calcutta-700091.

International Symposium on Chemotherapy: Problem
and Perspectives in 21st Century

November 28-29,1999;
(at Lucknow)

Dr. R.C. Saxena, Head, Department of Pharma­
cology, K.G. Medical College, Lucknow-226003.

Indo-European Seminar-cum-Workshop on Advances
in Human Cytogenetics

December 6-9,1999;
(at Lucknow)

Dr. S.S. Agarwal, Head, Department of Medi­
cal Genetics, Sanjay Gandhi Postgraduate Insti­
tute of Medical Sciences, Lucknow-226014.

Dr. N. Gangane, Organising Secretary of the Sym­
posium, Department of Pathology, Mahatma
Gandhi Institute of Medical Sciences, Sevagram,
Wardha-442102.

COUNCIL’S TRAINING PROGRAMMES FOR 1999-2000
Leprosy

Laboratory Animal Technology

At the Central JALMA Institutefor Leprosy, Agra:

At the National Centre for Laboratory Animal Science,
National Institute ofNutrition, Hyderabad:

•

Training Course for Medical Officers Working under
the National Leprosy Eradication Programme (Sep­
tember, 1999).

•

Training Course for Laboratory Animal Supervisors
(September 1-November30,1999).

Reproductive Biology

MediCal Entomology:

At the Institutefor Research in Reproduction, Mumbai:

At the Vector Control Research Centre, Pondicherry:

•

Training Course in Molecular Techniques in Ovarian
Function (September 27-October 2,1999).

•

Training Course on Cytological Detection of Repro­
ductive Tract Infections (December 13-17,1999).

Endocrinology

•

Biomedical Statistics

At the National Institute ofEpidemiology, Chennai:

•

At the National Institute ofNutrition,, Hyderabad:
'•

Annual Certificate Course on Endocrinological
Techniques and their Application (August 1 September 15,1999).

•

M.Sc. in Applied Nutrition (June 1,1999-February28,
2000).

•

Postgraduate Certificate Course in Nutrition (Decem­
ber 1, 1999-February28,2000).

Training Course in Field Epidemiology (November,
1999).

Haematology
At the Institute of Immunohaematology, Mumbai:

•

Training Course in Transfusion Medicine for Blood
Bank Medical Officers (August 31 -October29,1999).

•

Training Course in Blood Group Serology and Blood
Bank Methodology for Blood Bank Technicians
(August 31-September 30,1999).

•

Training Course in Advanced Haematology and
Immuno-haematology (October 11-29,1999).

Nutrition

At the National Institute of Nutrition, Hyderabad:

Postgraduate Diploma Course in Medical Entomology
(from July 1999).

93

ICMR ON INTERNET
http://www.icmr.iiic.in
A web site of ICMR has been developed inhouse and is hosted from a server located
at the National Informatics Centre (NIC), New Delhi. The site contains detailed information
about the activities of ICMR.

The welcome section gives general information like address and phone numbers of
Chiefs of Divisions in the ICMR Hqs., Profile of the Director General, Highlights of
activities, Achievements, History of the ICMR, Details of ICMR Awards and Prizes,
Guidance for international collaboration, etc.
\
Information is available about Council’s training programmes, meetings, ICMR aided
Seminars/Symposia/Workshops and other announcements under ‘News’.

General information 'on various funding schemes for Research & Development
implemented by the ICMR is found under ‘Grants’. Application forms for various schemes
can be downloaded from the site. Information on extramural projects ever funded by
ICMR can be searched from the dynamic web pages using search keys.
Issues of ICMR Bulletin, current and one year old are accessible under ‘Publications’.
The list of ICMR publications is also available.

An informative write-up on each of the ICMR Institutes/Centres is available under
‘Institutes’. A searchable list of ICMR scientists is also available. It is planned to publish
research results and results of epidemiological surveys, etc. of ICMR Institutes on the
web.
Any comments/suggestions regarding the web site from readers of ICMR Bulletin
are welcome. These may be sent to the ICMR (provision has been made on the homepage).

EDITORIAL BOARD
Chairman

Members

Dr. N.K. Ganguly
Director-General

Dr. Padam Singh
Dr. Lalit Kant
Dr. Bela Shah
Sh. N.C. Saxena
Dr. V. Muthuswamy

Editor
Dr. N. Medappa
Printed and "Published by Shri J.N. Mathur for the Indian Council of Medical Research, New Delhi
at the ICMR Offset Press; New Delhi-110 029
KN. 21813/71

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