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Importance of trace elements in Public Health

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Importance of trace elements in Public Health

  2. 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. 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. 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. 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. 6. Iodine
  7. 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. 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. 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. 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. 11. IDD cont… Iodine
  12. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 22.  CONCLUSION FROM KANGRA STUDY: Iodine  Iodine supplementation in the form of iodised salt on a regular and continuous basis reduces goitre prevalence
  23. 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. 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. 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. 26. PHASE I: NGCP  Iodized salt to Endemic districts Only  Interruptions in the supply of Iodized Salt  Surveys to find endemic districts Iodine
  27. 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. 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. 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. 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. 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. 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. 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. 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.
  36. 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. 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. 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. 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. 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. 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.
  42. 42. 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
  43. 43. 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.
  44. 44. 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.
  45. 45. Iron
  46. 46. 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.
  47. 47. 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
  48. 48. 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
  49. 49. 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
  50. 50. 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
  51. 51. 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
  52. 52. 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
  53. 53. *NFHS REPORT 2005-06
  54. 54. Iron deficiency anaemia: current status 35 15 NFHS-2 NFHS-3 2 52 39 16 2 IRON 56 Mild Moderate Severe Any anaemia
  55. 55. 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
  56. 56. 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.
  57. 57. 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.
  58. 58. 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
  59. 59. 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 )
  60. 60. 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.
  61. 61. 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.
  62. 62. 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.
  63. 63. 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
  64. 64. 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
  66. 66. 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.
  67. 67. 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
  68. 68. 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)
  69. 69. 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
  70. 70. 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.
  71. 71. 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
  72. 72. Selenium
  73. 73. 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.
  74. 74. SELENIUM  Requirements : Recommended daily intake is 70 μg (WHO)  ICMR recommends: RDA Infants 6-12 mcg Children 20-30 mcg Adult 50mcg
  75. 75. 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
  76. 76.  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
  77. 77. 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
  78. 78. 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 .
  79. 79. Copper
  80. 80. 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
  81. 81. Copper  Functions : Many metalloenzymes contain Copper.
  82. 82.  RDA of copper : RDA Infants 80mcg/kg/day Children 40mcg/kg/day Adults 30mcg/kg/day Copper
  83. 83. 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
  84. 84. Molybdenum
  85. 85. 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
  86. 86. 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.
  87. 87. 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.
  88. 88. 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
  89. 89. Chromium
  90. 90. 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
  91. 91. 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
  92. 92. 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
  93. 93. MANGANESE
  94. 94. 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.
  95. 95. 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
  96. 96. 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
  97. 97. 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
  98. 98. NICKEL  Nickel deficiency:  Deficiency rare in humans  Growth and haematopoiesis depressed, especially in those with a marginal iron status.  Iron utilization impaired
  99. 99. 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
  100. 100. 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
  101. 101. 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
  102. 102.  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
  103. 103. 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
  104. 104. Thank you

Notes de l'éditeur

  • 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.