Trace elements

DR. BHUSHAN KAMBLE

MODERATOR: DR. ANITA KHOKHAR

PROFESSOR,

DEPT. OF COMMUNITY MEDICINE,

VMMC & SJH

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

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

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,

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

Iodine

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

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

Requirement of iodine

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

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

IDD cont…Iodine

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

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

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)

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

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

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

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

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

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

(1956-62)

40 40 4042

19

15

0

10

20

30

40

50

60

Plain salt Salt + Potassium iodide Salt + Potassium iodate

Goitre

pre

vale

nce (

%)

1956 1962

Iodine

CONCLUSION FROM KANGRA STUDY:

Iodine supplementation in the form of iodised salt on a

regular and continuous basis reduces goitre

prevalence

Iodine

In 1962, National Goitre Control Programme (NGCP) was

launched by GOI.

In 1986, the GOI adopted the policy of Universal Salt

Iodization

Iodine

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

24

Iodine

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)

25

Iodine

PHASE I: NGCP

Iodized salt to Endemic districts Only

Interruptions in the supply of Iodized Salt

Surveys to find endemic districts

Iodine

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% 133Gorakhpur 70% 0-5% 85Gonda 60% 0-4% 75Delhi 29% Nil 6__________________________________________

Iodine

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

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)

Compulsory Iodization all Edible Salt in Entire Country

Iodine

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

Iodine

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

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

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

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

1954.

Iodine

Results: district nutrition project

0.04

0.92

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

NORTHERN DISTRICTS EASTERN DISTRICTS SOUTHERN DISTRICT

WESTERN DISTRICT ALL DISTRICTS

35

PREVALENCE (%) OF GOITRE AMONG CHILDREN

(6-< 12 YEARS)

Iodine

2003: National Institute of NutritionREGION PREVALENC

E OF GOITRE

(%)

PREVALENCE

OF OTHER

SIGNS OF IDD

(%)

SALT IODINE

(> 15 PPM) BY

SPOT TEST

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

Iodine

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

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.

Iodine

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

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.

Rapid Test Kit-Salt iodinedetection

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

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.

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

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.

4. A National Reference Laboratory for monitoring IDD at the

Bio-Chemistry & Biotechnology division, NICD, Delhi.

5. Four regional IDD monitoring laboratories

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.

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

Iron

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.

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

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

Requirement of iron

Group Basal lossMcg/kg

GrowthMcg/kg

Menstrual lossMcg/kg

Total requirement(mcg/kg/day)

Infant 0-2 yrs 14 65 - 79

Children 2-12 14 15 - 29

Adolescent male 14 12 - 26

Adolescent female

14 8 8 30

Adult male 14 - - 14

Adult female 14 - 16 30

PregnantLactating

1414

4616

--

6030

IRON

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

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

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

*NFHS REPORT 2005-06

Iron deficiency anaemia: current status

35

15

2

52

39

16

2

56

Mild Moderate Severe Any anaemia

NFHS-2 NFHS-3

IRON

Anaemia in adolescent girls

56

90

56

0

10

20

30

40

50

60

70

80

90

100

NFHS2 (1998-99) NFHS 3 (2005-06) ICMR (2003)

Perc

enta

ge

IRON

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.

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 internalelectronic “SELFTEST”.The sensitivity and the specificity of Hemocue Hb201+® were 95.1% and 65.3% respectively.

National Nutritional Anemia Prophylaxis Program

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

61

IRON

Launched in 1972 to prevent nutritional anaemia in mothers and childrenBeneficiaries: 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:

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 )

62

IRON

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.

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.

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.

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

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

RDA- ZINC

RDA

ADULT MALE 15mg

ADULT FEMALE 12mg

PREGNANCY 15mg

LACTATION 20mg

INFANT 5mg

CHILDREN 10mg

Zinc

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.

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

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)

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)

Zinc

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

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.

Zinc

Zinc

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

Zinc toxicity

Selenium

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.

SELENIUM

Requirements : Recommended daily intake is 70 µg (WHO)

ICMR recommends:

RDA

Infants 6-12 mcg

Children 20-30 mcg

Adult 50mcg

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

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

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

SELENIUM TOXICITY

Chronic selenium poisoning

loss of hair and changes in fingernail morphology.

skin lesions (redness, blistering)

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 .

SELENIUM

Copper

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

Copper

Functions : Many metalloenzymes contain Copper.

RDA of copper :

RDA

Infants 80mcg/kg/day

Children 40mcg/kg/day

Adults 30mcg/kg/day

Copper

Copper Deficiency

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

Copper

Molybdenum

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

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.

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.

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

Chromium

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

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

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

MANGANESE

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.

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

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

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

NICKEL

Nickel deficiency:

Deficiency rare in humans

Growth and haematopoiesis depressed, especially in those

with a marginal iron status.

Iron utilization impaired

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

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

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

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

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

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