Details about important trace elements

1. Trace elements
DR. BHUSHAN KAMBLE
MODERATOR: DR. ANITA KHOKHAR
PROFESSOR,
DEPT. OF COMMUNITY MEDICINE,
VMMC & SJH

2. Outline of presentation
 Definitions
 Classification
 Various trace elements
 Body content
 Requirement
 Sources
 Functions
 Deficiency/ Excess
 Control
 Iodine
 Iron
 Zinc
 Selenium
 Copper
 Molybdenum
 Chromium
 Manganese
 Flourine
 Nickel
 Boron

3. Definitions
 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

4.  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

5. Classification (WHO, 1996)
 Essential trace elements
 Iodine, Zinc, Selenium, Copper, Molybdenum, Chromium,
Cobalt, Iron
 Trace elements that are probably essential
 Manganese, Nickel, Silicon, Boron, Vanadium
 Potentially toxic elements with possible essential functions in low
doses
 Fluoride, Lead, Cadmium, Mercury, Arsenic, Lithium, Tin,
Aluminium

6. Iodine

7. Iodine
 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
Functions :
 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
iodine

8. Iodine
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

9. Iodine cont..
 Absorption :
 Dietary iodine absorbed from the small intestine.
 Approximately 30 % used by the thyroid gland for the synthesis
of thyroxine hormone; rest excreted in urine
 Goitrogens :
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
body.
 Goitrogens inactivated by heating
Iodine

10. IODINE DEFICIENCY
DISORDERS
 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
Iodine

11. IDD cont…
Iodine

12. Assessment of status of IDD:
Indicators
 Goitre prevalence:
 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
5.0-19.9% Mild
20.0-29.9% Moderate
>=30% Severe
Iodine

13. Assessment of status of IDD: Indicators
cont..
 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
100-199 ADEQUATE
99-50 MILD DEFICIENCY
20-49 MODERATE DEFICIENCY
<20 SEVERE DEFICIENCY
Iodine

14. 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 Insufficient
150- 249 Adequate
250- 499 Above requirements
 500 Excessive
Various methods are available for measuring UI.
The method used in ICMR laboratory is Sandell-Kolthoff
method with Ammonium persulfate digestion
(spectrophotometric detection)

15. Assessment of status of IDD:
Indicators cont..
 Thyroid gland volume:
 School children
 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>
97th precentile
Severity of IDD
5.0-19.9% Mild
20.0-29.9% Moderate
>=30% Severe
Iodine

16. Assessment of status of IDD:
Indicators cont..
 Serum thyroglobulin
 Both children and adults
 Thyroglobulin levels indicate the severity of IDD as follows
Median thyroglobulin ng/ml Severity of IDD
10-19.9 Mild
20-39.9 Moderate
>=40 Severe
Iodine

17. Assessment of status of IDD:
Indicators cont..
 Serum TSH
 Neonates
 Measured as proportion with serum TSH levels >5mU/l
Proportion of neonates with
TSH > 5mU/l
Severity of IDD
10-19.9% MILD
20-39.9% MODERATE
>=40% SEVERE
Iodine

18. Other indicator used: salt iodine
content
 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
Iodine

19. 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
Iodine

20. 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)

21. Introduction of Iodized Salt in India – study
(1956-62)
42
40 40 40
19
Iodine
15
60
50
40
30
20
10
0
Plain salt Salt + Potassium iodide Salt + Potassium iodate
Goitre prevalence (%)
1956 1962

22.  CONCLUSION FROM KANGRA STUDY:
Iodine
 Iodine supplementation in the form of iodised salt on a
regular and continuous basis reduces goitre
prevalence

23.  In 1962, National Goitre Control Programme (NGCP) was
launched by GOI.
 In 1986, the GOI adopted the policy of Universal Salt
Iodization
Iodine

24. National Goitre Control Programme
(NGCP) 1962
1) Survey to identify endemic areas
2) Production & Supply of iodized salt to endemic areas
3) Impact assessment surveys after five years
Iodine
24

25. 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)
Iodine
25

26. PHASE I: NGCP
 Iodized salt to Endemic districts Only
 Interruptions in the supply of Iodized Salt
 Surveys to find endemic districts
Iodine

27. 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
__________________________________________
Iodine

28. 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
ENDEMIC CRETINISM
 14 Districts, 9 States
 Pooled prevalence
Goitre: 21.1%
Cretinism: 0.7%
Iodine

29. Phase II: NGCP cont..
 Other NGCP surveys:
 Districts surveyed 282
 District Endemic: 242
 1983 : Iodized salt Production Opened to Private
Sectors
 1984: Policy Decision Universal Salt Iodization (USI)
Iodine
Compulsory Iodization all Edible Salt in Entire Country

30. Phase III: NGCP
 GOI –Unicef Project : 1992-97
 NIDDCP High Priority
 Increase in Production of Iodized Salt
Iodine
 National , State and District Levels Advocacy and Trainings
 State Plan of Action for Prevention of IDD
 Adequate Resources were Provided : Salt Department

31.  1992 :Goiter Control Program (NGCP)
Re-named
National Iodine Deficiency Disorders Control Program
 1997:National ban Notification—Banning Sale of Edible Non-
Iodized salt
Iodine

32.  1996-2000 HNU , AIIMS
17,654 Salt Samples
54 Districts : 9 States and 1 UT
Results:
 Nil Iodine 3.7%
 Less Than 15 ppm 28.5%
 15 ppm and more 67.8%
Successful Universal Salt Iodisation Program
Iodine

33. PHASE IV: 2000 ONWARDS
Objectives under NIDDCP:
 Surveys to assess the magnitude of the Iodine Deficiency
Disorders.
 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
excretion.
 Health education. & Publicity
Iodine

34.  Production and distribution of iodised salt intensified
Iodine
 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
1954.

35. Results: district nutrition
project
PREVALENCE (%) OF GOITRE AMONG CHILDREN
0.04
0.92
(6-< 12 YEARS)
1.56
3.6
4.46
9.86
0.15
0.2
0.78
8.56
12.95
0.13
4.78
0.02
31.02
0.02
0 3 6 9 12 15
BADAUN
MAINPURI
BARAMULLA
MANDI
LAKHIMPUR KHERI
SRINAGAR
BIKANER
DEHRADUN
BISHNUPUR
NAGAON
GAYA
PATNA
DIBRUGARH
MEHBOOB NAGAR
RAIGARH
ALL DISTRICTS
35
NORTHERN DISTRICTS EASTERN DISTRICTS SOUTHERN DISTRICT
WESTERN DISTRICT ALL DISTRICTS
Iodine

36. 2003: National Institute of
Nutrition
REGION PREVALENC
E OF GOITRE
(%)
PREVALENCE
OF OTHER
SIGNS OF IDD
(%)
SALT IODINE
(> 15 PPM) BY
SPOT TEST
Iodine
NO. OF
DISTRICTS
WITH MEDIAN
UIE < 100
mcg/l
Northern
(8 districts)
13.4 0.67 63.3 3
Eastern
(8 districts)
27.5 0.61 44.8 1
North
Eastern
(8 districts)
6.1 0.03 77.9 0
Central
(8 districts)
10.7 0.62 29.7 4
Southern
(8 districts)
10.2 0.76 17.9 1

37. STANDARDS FOR IODATED
SALT
 Moisture Not more than 6.0% by weight of the sample salt
 Sodium Chloride Not less than 96.0 % by weight on dry basis
Iodine
 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
weight basis.
 b. Distribution Not less than 15 parts per million on dry weight basis.

38. PACKING OF IODATED SALT
 BULK PACKING
 50kg bags
 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)
Net weight
Batch number
Iodine

39. Iodine
 Iodised oil
 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
trials.

40. Rapid Test Kit-Salt iodine
detection
 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
kit.
 The test kit consists of ampoules of a stabilized starch
solution and of a weak acid-based solution and a colour chart

41.  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
solution.
 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.

43. Titration Method
 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
pipettes
 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

44. ADMINISTRATIVE SET UP
1. The Central Nutrition and IDD Cell at D.G.H.S. is
responsible for the implementation of NIDDCP in the
country.
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.

45. 4. A National Reference Laboratory for monitoring IDD at the
Bio-Chemistry & Biotechnology division, NICD, Delhi.
5. Four regional IDD monitoring laboratories
Lab Region
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.

46. Iron

47. Iron
 Total body content of iron: 3-4 gm
 1-1.5 gm Hb
 2-2.5 gm storage iron
Sources:
 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.

48. Absorption and
bioavailability
 Factors in food that increase absorption of iron:
Vitamin C
Amino Acids
 Factors in food that decrease iron absorption
 Phytates
 Oxalates
Tannins
 Phosphates
IRON

49. IRON
 Absorption varies with type of cereal in the diet
 Maximum for rice based diet and minimum for wheat
based diet
 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
mcg/kg/day

50. Requirement of iron
Group Basal loss
Mcg/kg
Growth
Mcg/kg
Menstrual loss
Mcg/kg
Total
requirement(m
cg/kg/day)
Infant 0-2 yrs 14 65 - 79
Children 2-12 14 15 - 29
Adolescent male 14 12 - 26
Adolescent
14 8 8 30
female
Adult male 14 - - 14
Adult female 14 - 16 30
Pregnant
14
46
-
60
Lactating
14
16
-
30
IRON

51. Functions :
 component of haemoglobin and myoglobin.
 constituent of important enzymes like cytochromes, catalase,
peroxidase,etc.
 important functions in oxygen transport and cellular
respiration.
 involved in cellular immune response for functioning of
phagocytic cells
IRON

52. Iron deficiency anaemia
 Causes of iron deficiency
 Inadequate ingestion
 Increased requirement
 Inadequate absorption
 Inadequate utilization
 Increased blood loss or excretion
 Defects in release from stores
Signs & symptom:
 fatigue
 Headache
 Weakness
 Lack of concentration
 Irritation
dizziness
IRON

53. 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
world
 56% Adolescent girls are anaemic
 7 out of every10 children age 6-59months are anaemic in
india
 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
status
Who report :1993-2005

54. *NFHS REPORT 2005-06

56. Iron deficiency anaemia: current
status
35
15
NFHS-2 NFHS-3
2
52
39
16
2
IRON
56
Mild Moderate Severe Any anaemia

58. Anaemia in adolescent girls
56
90
56
100
90
80
70
60
50
40
30
20
10
0
NFHS2 (1998-99) NFHS 3 (2005-06) ICMR (2003)
Percentage
IRON

59. Anaemia Testing in NFHS
 The HemoCue system (Hb 201+) was used for Anaemia testing in the
NFHS-3.
 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.

60. HemoCue microcuvette :The
microcuvette is a plastic disposable unit that serves as both a reagent vessel and a
measuring device
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
electronic “SELFTEST”.
The sensitivity and the specificity of Hemocue Hb201+® were 95.1% and 65.3%
respectively.

61. National Nutritional Anemia
Prophylaxis Program
IRON
61
Launched in 1972 to prevent nutritional anaemia in mothers and children
Beneficiaries:
 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

62. IRON
62
Supplementation with iron-folate in the National Nutritional Anaemia Prophylaxis
Programme is done as per the following dosage schedule:
Pre-school children 6-60
months
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
reproductive period
(100 mg elemental iron +500 mcg of folate )

63. 12 X 12 INITIATIVE
 LAUNCHED ON 23rd APRIL,2007 AT AIIMS ,NEW
DELHI
 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.

64. SPECIFIC ACTIVITES
 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.

65. IRON FORTIFICATION
 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.

67. Zinc
 Zinc is present in small amounts in all tissues of the body.
 Total content of the body is 1.4 to 2.3 g.
 Sources :
 Meat
Whole grains
 Legumes.
Nuts

68. Absorption and
Bioavailability
 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
increases
Zinc

69. RDA- ZINC
RDA
ADULT MALE 15mg
ADULT FEMALE 12mg
PREGNANCY 15mg
LACTATION 20mg
INFANT 5mg
CHILDREN 10mg
Zinc

70. Zinc
Functions :
 Part of over 100 enzymes
 Protein and carbohydrate metabolism,
 Bone metabolism
 Oxygen transport.
 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.
 Powerful antioxidant.

71. Zinc- deficiency
 The principal clinical features of severe zinc deficiency in humans are
 Growth retardation
 A delay in sexual and skeletal maturation
 The development of orificial and acral dermatitis
 Diarrhoea
 Alopecia
 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)
 Altered taste
 Delayed wound healing
 Restricts utilization and storage of vitamin A

72. STATUS OF ZINC
DEFICIENCY IN INDIA
 Very little data available
Zinc
 Study done from 2005-2007 in 6-60 month old children in 5
states by Prof Umesh Kapil & Prof. S. N. Dwivedi (AIIMS)
Gujarat Karnat
aka
M.P. Orissa U.P. Total
Zinc-deficient
156
(44.2)
129
(36.2)
111
(38.9)
177
(51.3)
152
(48.1)
725
(43.8)
Non-zinc
deficient
197
(55.8)
227
(63.8)
174
(61.1)
168
(48.7)
164
(51.9)
930
(56.2)
Total
(%)
353
(100)
356
(100)
285
(100)
345
(100)
316
(100)
1655
(100)

73. 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.
Zinc

74. Zinc
 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.

75. Zinc
Zinc toxicity
 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
zinc.
 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

76. Selenium

77. Selenium
 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
deficiency.
Functions :
 Selenium is an integral part of over 30
selenoproteins; the most important of which are
glutathione peroxidases and iodothyronine
deiodinases.

78. SELENIUM
 Requirements : Recommended daily intake is 70 μg
(WHO)
 ICMR recommends:
RDA
Infants 6-12 mcg
Children 20-30 mcg
Adult 50mcg

79. Deficiency :
 Its deficiency is associated with increased coronary artery
disease.
 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
SELENIUM

80.  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
therapeutic value.
 Treatment generally follows the standard procedures
employed in cases of congestive heart failure.
SELENIUM

81. Selenium
 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

82. SELENIUM TOXICITY
 Chronic selenium poisoning
 loss of hair and changes in fingernail morphology.
 skin lesions (redness, blistering)
SELENIUM
 nervous system abnormalities (paresthesia, paralysis,
hemiplegia)
 In animals, particularly rats, liver damage is a common feature
of chronic selenosis but evidence less convincing in humans .

83. Copper

84. Copper
 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 -
100mg.
 Sources : Meat, nuts, cereals and fruits are good sources

85. Copper
 Functions : Many metalloenzymes contain Copper.

86.  RDA of copper :
RDA
Infants 80mcg/kg/day
Children 40mcg/kg/day
Adults 30mcg/kg/day
Copper

87. Copper Deficiency
 Deficiency : Copper deficiency is rare.
Copper
 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

88. Molybdenum

89. Molybdenum
 Requirement 25 μg/day in adults
 RDA: 500μg/day
 The three principal molybdenum-containing enzymes
 xanthine dehydrogenase
 aldehyde oxidase
 sulfite oxidase
 A reduced tissue activity of xanthine oxidase has been associated with
xanthinuria,
 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

90. MOLYBDENUM
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.

91. Molybdenum deficiency
 A nutritional deficiency of molybdenum leading to decreased
activity of sulfite oxidase reported in those on prolonged total
parenteral nutrition.
 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.

92. Molybdenum toxicity
 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

93. Chromium

94. Chromium
 Chromium is an essential nutrient that potentiates insulin
action and thus influences carbohydrate, lipid and protein
metabolism.
 Sources
 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

95. Chromium deficiency
 Deficiency produces a state similar to diabetes mellitus
 So far seen only in patients on long term parentral nutrition
 Symptoms include:
 impaired glucose tolerance and glucose utilization
 weight loss
 Neuropathy
 elevated plasma free fatty acids,
 depressed respiratory quotient
 abnormalities in nitrogen metabolism.
 All symptoms alleviated by chromium supplementation

96. Chromium toxicity
 Toxicity not seen with excess intake of trivalent chromium.
 Hexavalent chromium is much more toxic than the trivalent
form
 oral administration of 50 μg/g diet has been found to induce
growth depression together with liver and kidney damage in
experimental animals
 Not seen in humans so far

97. MANGANESE

98. Manganese
 Sources:
 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
be low.
 Functions: both an activator and a constituent of several
enzymes.
 Activates: hydrolases, kinases, decarboxylases and
transferases, glycosyltransferase and xylosyltransferase.
Mn is a constituent of arginase, pyruvate carboxylase,
glutamine synthetase, and manganese superoxide
dismutase.

99. Manganese deficiency
 Manganese deficiency has been produced in many species of
animals, but not, so far, in humans.
 Signs of manganese deficiency include
 impaired growth
 skeletal abnormalities
 disturbed or depressed reproductive function
 ataxia of the newborn
 defects in lipid and carbohydrate metabolism

100. Manganese toxicity
 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

101. Nickel
 Sources:
 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
 Function:
 four nickel-containing enzymes : urease, hydrogenase,
methylcoenzyme M reductase and carbon-monoxide
dehydrogenase

102. NICKEL
 Nickel deficiency:
 Deficiency rare in humans
 Growth and haematopoiesis depressed, especially in those
with a marginal iron status.
 Iron utilization impaired

103. Boron
 Sources:
 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
 Functions:
 Affects steroid harmone metabolism
 Studies suggest role in metabolism of other minerals like
aluminium and magnesium

104. BORON
 Boron deficiency:
 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
 Boron toxicity:
 Osteoporosis
 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

105. Fluoride
 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
dental enamel
 Source:
 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
teeth
 Skeletal fluorosis: severe pain and stiffness in joints , stiffness in
neck and backbone, bow legs

106.  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,
CHATTISGARH,
 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

107. References
 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

108. Thank you