DR. BHUSHAN KAMBLE
MODERATOR: DR. ANITA KHOKHAR
DEPT. OF COMMUNITY MEDICINE,
VMMC & SJH
Outline of presentation
Various trace elements
Element: An element is a chemical substance that is made up of a
particular kind of atoms and can not be broken down or
transformed by a chemical reaction into a different element
Trace element: Those elements which occur or function in living
tissues in concentrations most conveniently expressed in μg/l
Trace elements in human nutrition, WHO, 1973
Arbitrarily, the term "trace" has been applied to concentrations of
element not exceeding 250 μg per g of extracellular matrix.
Trace elements in human nutrition and health, WHO, 1996
Trace element*: A naturally occurring, homogeneous, inorganic
substance required in humans in amounts less than 100 mg/day
Bioavailability of minerals are low in vegetarian diet.
Excess amounts are injurious to health
*Department of clinical nutrition, university of Illinois at chicago
Classification (WHO, 1996)
Essential trace elements
Iodine, Zinc, Selenium, Copper, Molybdenum, Chromium,
Trace elements that are probably essential
Manganese, Nickel, Silicon, Boron, Vanadium
Potentially toxic elements with possible essential functions in low
Fluoride, Lead, Cadmium, Mercury, Arsenic, Lithium, Tin,
Body content: 50mg Blood conc: 8-12mcg/dl
Sources of iodine
i. Seafood ii. Vegetables grown on iodine-rich soils
iii. Milk products iv. Eggs
v. Cereal grains vi. Legumes
vii. Green leafy vegetables
Water contains traces of iodine which may contribute to as much
as 10% of total iodine intake
Iodine is an integral component of the thyroid hormones thyroxine
(T4) and tri-iodothyronine (T3).
In foetus and neonate normal protein metabolism in the CNS requires
Requirement of iodine
Age range or state RDA
Infants 50 μg
Children 1-6 years 90 μg
Children 6-12 years 120 μg
Children >12 years & Adults 150 μg
Pregnancy & Lactation 200 μg
Dietary iodine absorbed from the small intestine.
Approximately 30 % used by the thyroid gland for the synthesis
of thyroxine hormone; rest excreted in urine
Vegetables of Brassica group (cabbage, cauliflower and radish)
contain goitrogens -thiocyanates and cynoglycosides.
Consumption of large quantities of these may lead to development
of goiter by making the iodine present in food unavailable to the
Goitrogens inactivated by heating
Spectrum of disorders that result from deficiency of
iodine in body
IDD seen across all ages
Most profound effect of deficiency during periods of
rapid growth: fetus, neonate, infants, pregnancy
Assessment of status of IDD:
Seen in school children
Various levels of prevalence indicate the severity of IDD as a
public health problem
Prevalence of Goitre in
School Age Children
Severity of IDD
Assessment of status of IDD: Indicators
Urinary iodine levels:
School age children
Can be used as an indicator in 2 ways
Median urinary iodine levels to classify severity of IDD
population with median UI levels<100mcg: district endemic
Mean UI levels in mcg Severity of IDD
>= 300 TOXIC
299-200 EXCESSIVE: AT RISK OF TOXICITY
99-50 MILD DEFICIENCY
20-49 MODERATE DEFICIENCY
<20 SEVERE DEFICIENCY
Epidemiological criteria for assessing iodine nutrition
based on median or range in urinary iodine
concentrations of PREGNANT WOMEN
Median UI (g/L) Iodine Intake
150- 249 Adequate
250- 499 Above requirements
Various methods are available for measuring UI.
The method used in ICMR laboratory is Sandell-Kolthoff
method with Ammonium persulfate digestion
Assessment of status of IDD:
Thyroid gland volume:
Measured as proportion of children having thyroid volume
>97 percentiles (2.9 to 4.1 ml)
Measured by USG
Proportion of School Age
Children with thyroid volume>
Severity of IDD
Assessment of status of IDD:
Both children and adults
Thyroglobulin levels indicate the severity of IDD as follows
Median thyroglobulin ng/ml Severity of IDD
Assessment of status of IDD:
Measured as proportion with serum TSH levels >5mU/l
Proportion of neonates with
TSH > 5mU/l
Severity of IDD
Other indicator used: salt iodine
Salt iodine content
Recommended 15ppm at HH level
Can be measured by RAPID test kits: INEXPENSIVE KITS
Method: iodometric titration
100gm loose salt or full packet taken for analysis
50 samples to be collected per month per district
25 rural households
15 urban households
7 rural retailers
3 urban retailers
CONTROL OF IDD
1956-1968: study conducted in Kangra district of Himachal
Pradesh to understand the magnitude of problem in India.
Rural community based study.
District divided into 3 zones: A B & C
Baseline survey in 1956
Salt distributed to three zones
Zone A : Salt + Potassium iodide
Zone B : Plain salt
Zone C : Salt + Potassium iodate
15 gms of salt/person/day
So as to ensure 200 μg of iodine/person/day
Prevalence of Goitre in Zone A (KI Salt) Prevalence of Goitre in Zone B
(Plain salt till 1962, then KI salt)
Prevalence of Goitre in Zone C (KIO3 Salt)
Introduction of Iodized Salt in India – study
40 40 40
Plain salt Salt + Potassium iodide Salt + Potassium iodate
Goitre prevalence (%)
CONCLUSION FROM KANGRA STUDY:
Iodine supplementation in the form of iodised salt on a
regular and continuous basis reduces goitre
In 1962, National Goitre Control Programme (NGCP) was
launched by GOI.
In 1986, the GOI adopted the policy of Universal Salt
National Goitre Control Programme
1) Survey to identify endemic areas
2) Production & Supply of iodized salt to endemic areas
3) Impact assessment surveys after five years
4 Phases of NGCP
Phase I 1962 – 1980
Phase II 1980 - 1990
Phase III 1990 - 2000
Phase IV 2000 onwards
IN 1992, renamed as National Iodine Deficiency Disorder
Control Programme( NIDDCP)
PHASE I: NGCP
Iodized salt to Endemic districts Only
Interruptions in the supply of Iodized Salt
Surveys to find endemic districts
Phase II: NGCP
1981-1982: pilot surveys: screening of neonates for
hypothyroidism with filter paper techniques
Incidence of NH in Areas with Varying Goitre Prevalence
District Goitre Cretinism Incidence of NH
Prevalence Prevalence (per thousand births)
Deoria 80% 3-5% 133
Gorakhpur 70% 0-5% 85
Gonda 60% 0-4% 75
Delhi 29% Nil 6
PHASE II: NGCP cont..
Such studies established the presence of iodine deficiency in Extra -
Himalayan Regions also.
1983: Ministry of Social Welfare sponsored project for
intensification of NGCP through Nutrition Foundation of India
1984-1986: multiple studies conducted by ICMR
EPIDEMIOLOGICAL SURVEY OF ENDEMIC GOITRE AND
14 Districts, 9 States
Phase II: NGCP cont..
Other NGCP surveys:
Districts surveyed 282
District Endemic: 242
1983 : Iodized salt Production Opened to Private
1984: Policy Decision Universal Salt Iodization (USI)
Compulsory Iodization all Edible Salt in Entire Country
Phase III: NGCP
GOI –Unicef Project : 1992-97
NIDDCP High Priority
Increase in Production of Iodized Salt
National , State and District Levels Advocacy and Trainings
State Plan of Action for Prevention of IDD
Adequate Resources were Provided : Salt Department
1992 :Goiter Control Program (NGCP)
National Iodine Deficiency Disorders Control Program
1997:National ban Notification—Banning Sale of Edible Non-
1996-2000 HNU , AIIMS
17,654 Salt Samples
54 Districts : 9 States and 1 UT
Nil Iodine 3.7%
Less Than 15 ppm 28.5%
15 ppm and more 67.8%
Successful Universal Salt Iodisation Program
PHASE IV: 2000 ONWARDS
Objectives under NIDDCP:
Surveys to assess the magnitude of the Iodine Deficiency
Supply of iodated salt in place of common salt.
Resurvey after every 5 years to asses the extent of Iodine
Deficiency Disorders and the Impact of iodated salt.
Laboratory monitoring of iodated salt and urinary Iodine
Health education. & Publicity
Production and distribution of iodised salt intensified
Multiple studies conducted by ICMR to study the change after
introduction of iodised salt.
notification banning the sale of non-iodated salt for direct
human consumption in the entire country with effect from 17th
May, 2006 under the Prevention of Food Adulteration Act
Results: district nutrition
PREVALENCE (%) OF GOITRE AMONG CHILDREN
(6-< 12 YEARS)
0 3 6 9 12 15
NORTHERN DISTRICTS EASTERN DISTRICTS SOUTHERN DISTRICT
WESTERN DISTRICT ALL DISTRICTS
2003: National Institute of
E OF GOITRE
SIGNS OF IDD
(> 15 PPM) BY
UIE < 100
13.4 0.67 63.3 3
27.5 0.61 44.8 1
6.1 0.03 77.9 0
10.7 0.62 29.7 4
10.2 0.76 17.9 1
STANDARDS FOR IODATED
Moisture Not more than 6.0% by weight of the sample salt
Sodium Chloride Not less than 96.0 % by weight on dry basis
Matter soluble In water Not more than 1.0% by weight on dry basis
Matter Soluble In water other than Sodium chloride Not more than
3.0 % by the weight on dry basis
IODINE CONTENT AT
a. Manufacturing Level Not less than 30 parts per million (ppm) on dry
b. Distribution Not less than 15 parts per million on dry weight basis.
PACKING OF IODATED SALT
Polyethylene lined jute bags
Retail packing for sale:
500gms or 1 kg packs
Following legends on packet:
Name of manufacturer
Month and year of packing
Iodine content (when packed)
For moderate to severe prevalence of IDD
Mass level programmes carried out in China, South America,
Zaire, Papua New Guinea using iodised oil for injection
Iodised oil can also be given by mouth, but effects last for half
the time as compared to by injection.
Fortification of bread, rice and wheat was also done in various
Rapid Test Kit-Salt iodine
Iodine levels in salt can be measured in the laboratory using a
standard titration test or in the field using a rapid-test kit.
In NFHS-3, interviewers measured the iodine content of
cooking salt in each interviewed household using a rapid-test
The test kit consists of ampoules of a stabilized starch
solution and of a weak acid-based solution and a colour chart
The interviewers were instructed to squeeze two drops of the
starch solution onto a sample of cooking salt obtained from
the household. If the colour changed (from light blue through
dark violet), the interviewer matched the colour of the salt as
closely as possible to a colour chart provided with the test kit
and recorded the iodine level as <15 or >15 ppm.
If the initial test was negative (no change in colour), the
interviewer was required to conduct a second confirmatory
test, adding an acid-based solution in addition to the starch
This test is necessary because the starch solution will not show
any colour change even on iodized salt if the salt is alkaline
or is mixed with alkaline free-flow agents.
If the colour of the salt does not change even after the
confirmatory test, the salt is not iodized.
It is most commonly used quantitative method, still remains the
reference method for determining the iodine concentration in salt
It requires the use of a small laboratory equipped with some basic
instruments, such as precision scale, a burette, glassware, and
titration involves the preparation of four solutions and a standard
solution(Na2S2O3, H2SO4,KI, Starch soln)
The iodine content of salt is determined by liberating iodine from
salt and titrating the iodine with sodium thiosulfate using starch as
an external indicator.
mg/kg (ppm) iodine = titration volume in ml x 21.15 x normality of
sodium thiosulfate x 1000 / salt sample weight in g
ADMINISTRATIVE SET UP
1. The Central Nutrition and IDD Cell at D.G.H.S. is
responsible for the implementation of NIDDCP in the
2. The Salt Commissioner’s Office under the Ministry of
Industry is responsible for licensing, production and
distribution of iodated salt to States/Uts.
3. Each State Government has an IDD Control Cell which
carries out periodic surveys regarding the prevalence of
IDD and reports to D.G.H.S. 31 States/UTs have
established such Cells.
4. A National Reference Laboratory for monitoring IDD at the
Bio-Chemistry & Biotechnology division, NICD, Delhi.
5. Four regional IDD monitoring laboratories
the National Institute of Nutrition Hyderabad South
All India Institute of Hygiene & Public Health, Kolkata East
All India Institutes of Medical Sciences New Delhi west
National Institute for Communicable Diseases, Delhi North
6. Each State has been sanctioned one IDD monitoring laboratory for
the monitoring of iodine content of salt and urine. 21 States/UTs have
established such laboratories.
Total body content of iron: 3-4 gm
1-1.5 gm Hb
2-2.5 gm storage iron
Haem Iron Sources: nonvegetarian sources of iron e.g. meat,
fish and eggs. Milk a poor source of iron but breast milk an
efficient source for the infant.
Non-haem Iron Sources : vegetarian sources, namely cereals,
dark green leafy vegetables, pulses, nuts and dry fruits.
Factors in food that increase absorption of iron:
Factors in food that decrease iron absorption
Absorption varies with type of cereal in the diet
Maximum for rice based diet and minimum for wheat
Dietary iron Absorption varies person to person
Adult men, children and adolescent boys: 3%
Adult women, lactating women, adolescent girls: 5%
Pregnant women: 8%
Basal loss through GI tract , sweat and urine:
Average basal loss across all age groups and gender for India : 14
Requirement of iron
Group Basal loss
Infant 0-2 yrs 14 65 - 79
Children 2-12 14 15 - 29
Adolescent male 14 12 - 26
14 8 8 30
Adult male 14 - - 14
Adult female 14 - 16 30
component of haemoglobin and myoglobin.
constituent of important enzymes like cytochromes, catalase,
important functions in oxygen transport and cellular
involved in cellular immune response for functioning of
Iron deficiency anaemia
Causes of iron deficiency
Increased blood loss or excretion
Defects in release from stores
Signs & symptom:
Lack of concentration
Public Health problem
Categorized as one of the top ten most serious health
problems in the modern world (WHO)
Globally – 41.8% pregnant women and 30.2% of non-pregnant
are anaemic i.e 524 million women worldwide
Prevalence of anaemia in India is among the highest in the
56% Adolescent girls are anaemic
7 out of every10 children age 6-59months are anaemic in
According to a survey conducted by NFHS, the prevalence
of anaemia in young girls aged between 15-24 years is 56%
with higher rates in rural than in urban India
More than 1,000 severely anemic young women die every
week in the perinatal period because of inadequate iron
Who report :1993-2005
Anaemia Testing in NFHS
The HemoCue system (Hb 201+) was used for Anaemia testing in the
This system consists of a battery-operated photometer and a disposable
microcuvette, coated with a dried reagent that serves as the blood-collection
device. The test is performed using a drop of blood taken from
a person’s fingertip.
HemoCue microcuvette :The
microcuvette is a plastic disposable unit that serves as both a reagent vessel and a
The HemoCue Hb 201+ photometer: It measures light absorption and presents the
results on a display. ambient temperature and protect it from direct sunlight. The
HemoCue Hb 201+ analyzer has an internal
The sensitivity and the specificity of Hemocue Hb201+® were 95.1% and 65.3%
National Nutritional Anemia
Launched in 1972 to prevent nutritional anaemia in mothers and children
Pregnant women & nursing mothers with haemoglobin less than 8 gm %
Children 1-5 years with haemoglobin less than 10 gm %
Women acceptors of family planning
Supplementation with iron-folate in the National Nutritional Anaemia prophylaxis
Programme is done as per the following dosage schedule:
For Prevention in “high risk groups”
Pregnant women One big (adult) tablet per day
(100 mg elemental iron and 500 mcg of folate )
For 100 days after first trimester of pregnancy.
If clinically anaemic, 2 such tablets daily to be
given for 100 days
Lactating women & IUD users One big (adult) tablet per day
(100 mg elemental iron and 500 mcg of folate )
For 100 days
Supplementation with iron-folate in the National Nutritional Anaemia Prophylaxis
Programme is done as per the following dosage schedule:
Pre-school children 6-60
One small (paediatric) tablet (20 mg elemental iron
and 100 mcg of folate )
Biweekly throughout the period of 6-60 months
School children 5-10 years 45mg elemental iron + 400 ug folic acid weekly,
throughout the entire period of 5-10 years
Adolescent 10-19 years One big(adult) tablet
(100mg elemental iron +500 mcg of folate)
weekly throughout the entire period of 10-19 years
women in reproductive age
group (15-45 years)
One big(adult) tablet weekly throughout the
(100 mg elemental iron +500 mcg of folate )
12 X 12 INITIATIVE
LAUNCHED ON 23rd APRIL,2007 AT AIIMS ,NEW
Organized by DEPARTMENT OF OBSTETRICS &
GYNECOLOGY OF AIIMS in collaboration with WHO ,
UNICEF AND FOGSI.
OBJECTIVE---Ensuring every child at least 12gm%
Hemoglobin by 12 yrs of age.
GOALS --- 1)To determine the prevalence of anemia in
adolescence to ensure healthy parenthood.
2)To increase awareness among adolescents
regarding anemia and appropriate nutrition.
Hb testing camps at various cities/towns of India under the banner
of 12X12 initiatives.Program coverage
The camps are conducted in schools for the student’s of 5th to 7th
level primarily focusing girl child.
formal presentation on anaemia (giving focus on importance of Hb
Lab technicians performs the Hb testing on students.
A Health card is maintained for each student .
a literature on anaemia is also provided to each student.
The students with low Hb (<11.5 gm) are provided 5-10 days
course of Orofer XT tablets or suspension.
Till now we have conducted such camps in 40 cities/towns of India
and covered a population of over 100,000 students.
NATIONAL INSTITUTE OF NUTRITION,Hyderabad showed that simple
addition of ferric ortho-phosphate or ferrous sulphate with sodium
bisulphate was enough to fortify salt with iron.
Commercial production of iron fortified salt was started in 1985.
In 2005, NIN, Hyderabad evolved the concept of fortification of iodized
salt with iron (double fortified salt, DFS) for controlling IDD and IDA as
'one intervention controlling two problems'
The Prime Minister's Office on April 2011 issued instructions for the
introduction of DFS in ICDS, MDM and PDS in phased manner
DFS is being supplied at Orissa in the open market and in MDM
programmes of Karnataka, Chhattisgarh, Jharkhand & Haryana
Iron Fortified Wheat Flour (Atta) and Rice: Doubts have been raised
about bio-availability of iron from wheat 'atta’ because of high phytate
(inhibitor of absorption) content.
Zinc is present in small amounts in all tissues of the body.
Total content of the body is 1.4 to 2.3 g.
Zinc absorbed mainly from jejunum
Absorption affected by
Phytates in diet
Proteins in diet
Total zinc content
Calcium and other divalent ions in diet
Chronic iron supplementation decreases zinc absorption
Fermentation of food digests phytates: zinc availability
ADULT MALE 15mg
ADULT FEMALE 12mg
Part of over 100 enzymes
Protein and carbohydrate metabolism,
Immune response and gene expression.
Structural constituent of leucocytes
Role in the synthesis of nucleic acids
Lymphoid tissue contains zinc.
Efficient storage of insulin in pancreas.
The principal clinical features of severe zinc deficiency in humans are
A delay in sexual and skeletal maturation
The development of orificial and acral dermatitis
A failure of appetite/ affects voluntary food intake
Appearance of behavioural changes.
An increased susceptibility to infections (reflects the development of
defects in the immune system)
Delayed wound healing
Restricts utilization and storage of vitamin A
STATUS OF ZINC
DEFICIENCY IN INDIA
Very little data available
Study done from 2005-2007 in 6-60 month old children in 5
states by Prof Umesh Kapil & Prof. S. N. Dwivedi (AIIMS)
M.P. Orissa U.P. Total
Other studies conducted in 1998- 2004 suggested
that a 10- to 14-day therapy of zinc treatment can
considerably reduce the
1. Duration and severity of diarrhoeal episodes,
2. Decrease stool output, and
3. Lessen the need for hospitalization.
4. May also prevent future diarrhea episodes for up to
next three months.
WHO and UNICEF recommend daily 20 mg zinc supplements
for 10–14 days for children with acute diarrhoea, and 10 mg
per day for infants under six months old
Government adopted policy of use of Zinc in treatment of
diarrhoea in National Rural Health Mission in children < 5
years from the year 2008.
Acute zinc poisoning:
after ingestion of 4-8 g of zinc.
nausea, vomiting, diarrhoea, fever and lethargy
Long-term exposure to high zinc intakes result in interference
with the metabolism of other trace elements.
Copper utilization is especially sensitive to an excess of
Copper/zinc interaction may cause copper deficiency::
deliberately exploited to control copper accumulation in
Wilson disease .
Changes in serum lipid patterns and immune response have
also been associated with zinc supplementation
It is present in all body tissues except fat.
Sources : Meat, fish, nuts and eggs are good
sources. vegetarians and vegans may be at risk of
Selenium is an integral part of over 30
selenoproteins; the most important of which are
glutathione peroxidases and iodothyronine
Requirements : Recommended daily intake is 70 μg
Infants 6-12 mcg
Children 20-30 mcg
Its deficiency is associated with increased coronary artery
Keshan disease (endemic cardiomyopathy) in China
Kashin Beck syndrome, an osteo-arthropathy in children of 05-
13 years age is seen in selenium deficient areas
The major histopathological feature of Keshan disease is a
multifocal myocardial necrosis.
Coronary arteries unaffected.
Membranous organelles, such as mitochondria or
sarcolemma, affected earliest.
Once the disease is established, selenium is of little or no
Treatment generally follows the standard procedures
employed in cases of congestive heart failure.
Kashin-Beck disease: an endemic osteoarthropathy linked
with low selenium status.
Primarily affects children between the ages of 5 and 13 years
living in certain regions of China
Advanced cases of the disease are characterized by
enlargement and deformity of the joints.
The principal pathological change is multiple degeneration and
necrosis of hyaline cartilage tissue.
Some studies have suggested that selenium may prevent
Kashin-Beck disease, but this work needs further confirmation
Chronic selenium poisoning
loss of hair and changes in fingernail morphology.
skin lesions (redness, blistering)
nervous system abnormalities (paresthesia, paralysis,
In animals, particularly rats, liver damage is a common feature
of chronic selenosis but evidence less convincing in humans .
An essential trace element:
component of many metallo-enzyme systems
Role in iron metabolism
The amount of copper in the adult body is estimated to be 80 -
Sources : Meat, nuts, cereals and fruits are good sources
Functions : Many metalloenzymes contain Copper.
RDA of copper :
Deficiency : Copper deficiency is rare.
Hypocupraemia : serum copper level <= 0.8mcg/ml
in patients with nephrosis
Wilson’s disease and
protein energy malnutrition.
Neutropaenia - commonest abnormality of copper deficiency.
Infants, especially premature, may develop copper deficiency
usually presenting as chronic diarrhoea. Neutropaenia and
later anaemia develop and they do not respond to iron.
Copper deficiency may be a risk factor for coronary heart
disease as it has been associated with raised plasma
cholesterol levels and heart-related abnormalities
Requirement 25 μg/day in adults
The three principal molybdenum-containing enzymes
A reduced tissue activity of xanthine oxidase has been associated with
a genetic defect characterized by a low output of uric acid and high
concentrations of xanthine and hypoxanthine in blood and urine.
Clinical manifestations: renal calculi formed or deposition of xanthine and
hypoxanthine in muscles resulting in a mild myopathy
Other enzyme, sulfite oxidase,
responsible for the conversion of sulfite into inorganic sulfate,
Genetic "deficiency" of sulfite oxidase have been detected in early
human infancy and have a lethal outcome at the age of 2-3 years.
The lesion results in severe neurological abnormalities, mental
retardation and ectopy of the lens.
A nutritional deficiency of molybdenum leading to decreased
activity of sulfite oxidase reported in those on prolonged total
The clinical symptoms included irritability followed by
tachycardia, tachypnoea and night blindness. Severe cases, coma
may be seen.
The clinical symptoms of molybdenum deficiency were totally
eliminated by supplementation with 300 μg of ammonium
molybdate (147 μg of molybdenum) daily.
Molybdenum intoxication is accompanied by a secondary
deficiency of copper.
Typical features of molybdenosis include
defects in osteogenesis leading to skeletal and joint deformities,
spontaneous fractures, and mandibular exostoses .
Alkaline phosphatase activity decreases.
Due to copper deficiency: anaemia, cardiac hypertrophy, and
achromotrichia arising from the development of defects in melanin
synthesis in hair
Chromium is an essential nutrient that potentiates insulin
action and thus influences carbohydrate, lipid and protein
Processed meats, whole grain products, pulses and spices
are the best sources of chromium
while dairy products and most fruits and vegetables
contain only small amounts
Deficiency occurs if diets contain predominantly refined foods
Deficiency also associated in infants with PEM
Requirement: 33 μg/day
Deficiency produces a state similar to diabetes mellitus
So far seen only in patients on long term parentral nutrition
impaired glucose tolerance and glucose utilization
elevated plasma free fatty acids,
depressed respiratory quotient
abnormalities in nitrogen metabolism.
All symptoms alleviated by chromium supplementation
Toxicity not seen with excess intake of trivalent chromium.
Hexavalent chromium is much more toxic than the trivalent
oral administration of 50 μg/g diet has been found to induce
growth depression together with liver and kidney damage in
Not seen in humans so far
Diets high in unrefined cereals, nuts, leafy vegetables and
tea will be high in manganese;
diets high in refined grains, meats and dairy products will
Functions: both an activator and a constituent of several
Activates: hydrolases, kinases, decarboxylases and
transferases, glycosyltransferase and xylosyltransferase.
Mn is a constituent of arginase, pyruvate carboxylase,
glutamine synthetase, and manganese superoxide
Manganese deficiency has been produced in many species of
animals, but not, so far, in humans.
Signs of manganese deficiency include
disturbed or depressed reproductive function
ataxia of the newborn
defects in lipid and carbohydrate metabolism
Manganese among the least toxic
The major signs in animals: depressed growth, depressed
appetite, impaired iron metabolism and altered brain function
Cases of human toxicity few.
Chronic inhalation of airborne manganese in mines, steel
mills and some chemical industries.
Signs of toxicity in Chilean manganese miners
severe psychiatric abnormalities, hyperirritability, violent
acts and hallucinations (manganic madness).
As the disease progresses, permanent crippling
neurological disorder of the extrapyramidal system similar
to Parkinson disease
Plant sources contain more nickel than animal sources
Approximately half the total daily intake of nickel is usually
derived from the consumption of bread and cereals
Milk, coffee, tea, orange juice, ascorbic acid depress absorption
Requirement : 100 μg/day.
Safe upper limit of consumption: 600 μg/day
four nickel-containing enzymes : urease, hydrogenase,
methylcoenzyme M reductase and carbon-monoxide
Deficiency rare in humans
Growth and haematopoiesis depressed, especially in those
with a marginal iron status.
Iron utilization impaired
Foods of plant origin especially fruits, leafy vegetables,
nuts and legumes are rich sources.
Wine, cider and beer are also high in boron.
Meat, fish and dairy products are poor sources.
Requirement:0.75 mg/ day
Affects steroid harmone metabolism
Studies suggest role in metabolism of other minerals like
aluminium and magnesium
Dietary boron affects plasma and organ calcium and magnesium
concentrations, plasma alkaline phosphatase, and bone calcification.
Boron deficiency causes
elevated urinary excretion of calcium and magnesium
depressed serum concentrations of lipo-estradiol and ionized calcium
lower plasma ionized calcium and serum 25-hydroxycholecalciferol
higher serum calcitonin and osteocalcin
Two infants whose pacifiers were dipped into a preparation of borax and
honey over a period of several weeks exhibited scanty hair, patchy dry
erythema, anaemia and seizure disorders
It is found in combined forms
96% of fluorides in the body found in bone and teeth.
An essential for normal mineralisation of bones and formation of
Drinking water : Fluorine in the drinking water is 0.5 mg per ltr.
Excess of fl > 3mg causes flourosis.
Foods: Sea fish, cheese, Tea
Dental fluorosis : chalky white teeth, transverse yellow bands on
Skeletal fluorosis: severe pain and stiffness in joints , stiffness in
neck and backbone, bow legs
Public health problem:
Fluorosis affects 25 million people and 66 million are at risk
Endemic in 275 districts of 20 states in india : AP, MP, ORRISA , BIHAR,
National Programme for Prevention & Control of Fluorosis:2008-9
Preventive measures: providing defluoridated water, rain water
harvesting , restrict intake of fluorine rich items: tobacco, supari, black
tea and black salt, use of fluoride rich casmetics/drugs
WHO Technical Research Series no. 580, 1996
WHO Technical Research Series no. 532, 1973
Recommended Dietary Intakes for Indians. Report of an Expert
Group,Final Draft . ICMR, New Delhi, 2010.
Nutrition India, NFHS 3 Report, 2005-06.
Park K, Textbook of Preventive and Social Medicine, 20th edition
Taneja D K, Health Policies and Programmes in India, 12th edition
Revised Policy Guidelines on National Iodine Deficiency Disorder Control
Programme, Ministry of Health & Family Welfare, 2006
Kapil Umesh, et al. Process of implementation of National Iodine
Deficiency Disorders Control Programme activities in Himachal Pradesh,
India, Indian J Public Health. 1995 Oct;39(4):172-175
trace elements can be defined as those comprising less than 0.01% of total body weight or more appropriately those which are needed in a concentration of less than 1ppm
25 samples per month/ district sent to state idd Casual 5 ml sample In 15-20 ml bottle screw capped Layer of toluene
10% samples to state idd cell
Provided that table Iodated salt may contain aluminum silicate as an anti caking agent to an extent of 2.0% by weight.
Provided further that the total matter insoluble in water in such cases shall not exceed 2.2% and sodium chloride content on dry basis shall not be less than 97.0% bye weight.
Infants cant utilize zinc from heterologous milk
A zinc intake of as little as 50 mg/day has been shown to influence copper status, as indicated by a decline in erythrocyte copper-zinc superoxide dismutase activity . Low plasma copper and plasma caeruloplasmin levels and anaemia have been observed after higher intakes of zinc (450-660 mg/day).
Glutathione peroxidase has an important role in the detoxification of peroxides and free radicals. Its antioxidant action might be protective against certain cancers especially prostate, lung, colon and non-melanoma skin cancers. It may also be helpful in delaying the aging process. It is also involved in the production of tri-iodothyronine from thyroxine. It also contributes to antibody responses, the production of eicosanoids as well as cytotoxicity of natural killer cells
Keshan disease categorized clinically into four types depending on its severity, namely acute, subacute, chronic and insidious.
The biochemical mechanisms of selenium toxicity have not been clearly established. Some features of its deleterious effects reflect the chemical form of the particular selenium compound to which exposure has been excessive selenite is a potent catalyst for the oxidation of sulfhydryl groups, and this may be the basis of its inhibitory effect on protein biosynthesis. selenomethionine can be incorporated as such into proteins by mimicking methionine and can thereby increase the susceptibility of certain proteins to denaturation by heat or treatment with urea
Menke’s disease, a rare hereditary defect of copper absorption is invariably fatal.
Urinary outputs of sulfite, thiosulfate and S-sulfo-L-cysteine all increase and urinary sulfate decreases . These pathological changes may result either from the accumulation of toxic concentrations of sulfite in some critical organs or from inadequate production of the sulfate required for synthesis of sulfolipids, proteins and sulfate-conjugates
A reduced intake of protein and sulfur-containing amino acids alleviated the symptoms, whereas they were exacerbated by infusion of sulfite. Tissue sulfite oxidase activity was low, thiosulfate excretion increased 25-fold, sulfate output declined by 70% and plasma methionine increased markedly.
Apparemment, vous utilisez un bloqueur de publicités qui est en cours d'exécution. En ajoutant SlideShare à la liste blanche de votre bloqueur de publicités, vous soutenez notre communauté de créateurs de contenu.
Vous détestez les publicités?
Nous avons mis à jour notre politique de confidentialité.
Nous avons mis à jour notre politique de confidentialité pour nous conformer à l'évolution des réglementations mondiales en matière de confidentialité et pour vous informer de la manière dont nous utilisons vos données de façon limitée.
Vous pouvez consulter les détails ci-dessous. En cliquant sur Accepter, vous acceptez la politique de confidentialité mise à jour.