University of Nigeria Status, Growth...University of Nigeria Research Publications NWAMARAH, Joy Ugo...
Transcript of University of Nigeria Status, Growth...University of Nigeria Research Publications NWAMARAH, Joy Ugo...
University of Nigeria Research Publications
NWAMARAH, Joy Ugo A
utho
r
PG/Ph.D/02/33558
Title
Iodine Status, Growth and Parasitic infestation of
Primary School Children in Obukpa, a Rural Nigerian Community
Facu
lty
Agricultural Sciences
Dep
artm
ent
Home Science, Nutrition and Dietetics
Dat
e
May, 2006
Sign
atur
e
IODINE STATUS, GROWTH AND PARASITIC INFESTATION OF PRIMARY SCHOOL CHILDREN IN OBUKPA, A RURAL NIGERIAN COMMUNITY
A Thesis
Submitted in Partial Fulfilment of the Requirements For the Award of Doctor of Philosophy Degree in
Human Nutrition
Nwamarah, Joy Ugo PGlPh.Dl02133558
DEPARTMENT OF HOME SCIENCE, NUTRITION AND DIETETICS
UNIVERSITY OF,. NIGERIA, NSUKKA
10th MAY, 2006.
Nwamarah Joy Ugo (MRS), a post graduate student of the Department of Home Science, Nutrition and Dietetics, Registration Number: PGIPh.Dl02133558, has satisfactorily completed the requirements for research work for the degree of Doctor of Philosophy in Human Nutrition. The work embodied in this thesis is original and has not been submitted in part or full for any other Diploma or Degree of this or any other University.
------------ Prof. (MRS.) E. Chinwe Okeke
( ~ u ~ e ~ v i s o r ) (Head of Department)
Prof. M, A . Akpapurrarrs External Examiner
DEDICATION
This thesis is dedicated to my husband, Goodluck Mbamaonyeukwu
Nwamarah and children, Obinna, Chichi and Nenyes.
ACKNOWLEDGEMENT
I am excited and most grateful to the Almighty God, who is Omni-Scientific, my heavenly
Father who made it all possible. He was so gracious to me, and was generous to me
with strength, health and grace throughout the duration of this work.
I wish to express my profound gratitude to my supervisor, Professor (Mrs.)
E.Chinwe Okeke, for her advice, suggestions, frequent prompting and quest for
excellence that helped me to complete this thesis. The advice and concern of Prof. (Mrs) H.
N. Ene-Obong and my other lecturers and colleagues in the Department of Home Science,
Nutrition and Dietetics contributed to the outcome of the quality of the work.
My gratitude also goes to the.headmasters and mistress of Ajuona, Owerre-
Obukpa and Umuorua/Amagu community primary schools, respectively for their
assistance and co-operations. I am most grateful to them for all the sacrifices they made
to make the data collection less stressful and laborious. The cooperation of parents and
all the pupils that took part in the study is highly appreciated.
Again my gratitude goes to Dozie (Lopez) and Nenye Nwamarah, Chukwudi and
Emezie Onuigbo, Onyekachi Uwaomah and Nkechi Nwafor who assisted with data
collection, Safety and Hezekiah laboratories who used their labs for the biochemical
analysis.
I am highly indebted to Dr Agomuo Emmanuel (Associate Dean of Student
affairs) and Mr Ugbor Kalu (Dept of .Economics) for their assistance with statistical . , 4 1 . ' .'> '
analysis. Nenye Nwamarah (Final yr Pharmacy student) and Chichi Nwamarah (Medical
student) who word processed the work.
The last but not the least I appreciate the moral and financial support from my
husband, Nwamarah G.M. (Director MIS Ucit).
The awesome God in His mercies and love bless you and reward you according
to His Word.
TABLE OF CONTENT
PAGES
TITLE PAGE ... ... ... ... ... ... ... ... ... ... ... ... ... .. . CERTIFICATION.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . DEDICATION.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ACKNOWLEDGEMENT.. . . . . . . . . . . . . . , . . . . . . . . . . . . . . . . .
TABLE OF CONTENTS ... ... .. . ... ... ... ... ... ... ... ... LIST OF TABLES.. . . . . .. . .. . .. . .. . .. . .. . .. . .. . .. . .. . .. . LIST OF FIGURES ... ... ... . . . ... ... ... .. . ... .. . ... .. . ABSTRACT. . . , . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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xvi i i
CHAPTER ONE: INTRODUCTION
1 .I Background Information . . . . . . . . . .. . . . . . . . . . . . . . .. . . . . . . . . . . 1
1.2 Statement of the Problem and Justification ... ... ... ... ... ... ... 5
1.3 Objectives of the Study ... ... ... ... ... ... ... ... .. . ... ... .. 6
1.4 Hypotheses.. . . . . . . . . . . . . . . . . . . . . . .. . . .. . . . . . . . . . . . . . . . 6
1.5 Significance of the Study.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 8
CHAPTER TWO: LITERATURE REVIEW
2.1 Iodine an Essential Nutrient.. . .. . .. . .. . ... .. . . . . .. . .. . .. . .. 9
2.1 .I Absorption, Bioavailability, ,Tr&nsp,~fl and Storage of Iodine.. . .. 9
2.1.2 Iodine.. . .. . .. . . . . .. . .. . .. . .. . ... .. . .. . .. . .. . .. . .. . .. . 10
2.1.3 Properties of Iodine., . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
2.1.3.1 Occurrence.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 , I . . 2.1.4 Compounds.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.1.5 Production.. . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . .. . . . . 2.1.6 Uses.. . . . . . . . . . . . . . . . . . . . . . . . . .. .. .. . . . . . . . . . . . . 2.1.7 Functions of Iodine.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.1.8 Inter Relationships . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.2 Parasites.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Intestinal Helminthes
Prevalence among Children . . . . . . . . . . . . . . . . . . . . . . . . . . . . . lntestinal Parasitic Infestation and Growth and Nutritional Status ..
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Morbidity and Mortality
. . . . . . . . . . . . . . . . . . . . . . Share of Children who are Underweight
. . . . . . . . . . . . . . . . . . Toxic Substances and Anti-nutritional Factor
Cassava Toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pathophysiology of Cyanide Intoxication
. . . . . . . . . . . . . . . . . . . . . Goitrogens and Antithyroid Compounds
. . . . . . . . . . . . . . . . . . . . . . . . . . . Sulphur-containing Compounds
. . . . . . Selenium-deficiency-related Thyroid Dyshormonogenesis
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Iodine Deficiency
Prevention of Iodine Deficiency . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Iodine Value or Iodine Number
. . . . . . . . . . . . . . . . . . . . . . . . Diagnosis and Treatment of Goitre
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Causes and Types of Goitre
Micronutrient Malnutrition: a Global Problem . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Vulnerable Groups Affected
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Reasons for Iodine Deficiency
Health Consequences of Iodine Deficiency . . . . . . . . . . . . . . . . . . Solution to Iodine Deficiency Disorder . . . . . . . . . . . . . . . . . . . . . . . .
....... wr. ....... ?>
2.1 1.1 Choice of Strategies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.1 1 .I. 1 Nutrition Education . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.11.1.2 Dietary Diversification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.11.1.3 Dietary Supplementation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
. . . . . 2.1 1.1.4 Food Fortification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.1 2 Hidden Hunger . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.13 Selecting the Right Vehicle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.13.1 Feasibility of Triple . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.14 Food Fortification Gains Support in Africa . . . . . . . . . . . . . . . . . . . . . 2.15 Priority for Child Nutrition Needed . . . . . . . . . . . . . . . . . . . . . . . . . . .
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.16 Correcting Iodine Deficiency
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.17 Monitoring and Evaluation
2.18.1 Assessing Iodine Deficiency Disorders for Public Health
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Programmes
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.18.2 Estimation of Thyroid Size
2.18.3 Estimation of the Consistency of the Thyroid by Palpation ... 2.18.4 Definition of Endemic Goitre as a Public Health Problem . . . . .
. . . . . . . . . . . . . . . . . . 2.18.5 Urine Iodine Excretion Determination
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.19 Sub Clinical IDD
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.19.1 Three Grades of Severity
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.19.2 Iodine in Drinking Water
2.20 Prevention and Eradication of IDD require Continual Vigilance ... . . . . . . . . . . . . . . . 2.20.1 Countries who Successfully Eliminated Iodine
2.21 Adverse Effects Associated with High Nutritional lntakes of
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Iodine
. . . . . . . . . . . . . . . . . . . . . . . . . . . 2.22 Physiological Need for Iodine
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.22.1 Usual Salt Intakes
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.22.2 Other Sources of Iodine
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.22.3 Iodine Availability
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.22.4 Iodine Requirements
. . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.22.5 Required Iodine Levels in Salt
. . . . . . . . . . . . . . . . . . . . . . . . . . 2.22.6 Quality of Available Salt:::' '':.'.''::.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.22.7 Trace Elements
. . . . . . . . . . . . . . . . . . . . . . . . 2.23 Biological Roles of Trace Elements
CHAPTER THREE: MATERIALS AND METHODS
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1 Study Area
3.1 . 1 Study Population . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1.2 Approach to the Local Community . . . . . . . . . . . . . . . . . . . . . . . . 3.1.3 Design and Sampling Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1.3.1 Sample Size Calculation . . . . . . . . . . . . . . . . . . . . . . . .
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3.1.3.2 Sampling Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61
Training of Personnel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62
Data Collection Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62
Basic Data by Questionnaire . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Clinical Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anthropometric Measurements . . . . . . . . . . . . . . . . . . . . . . . . . . .
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Height
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Weight
Growth Monitoring and Velocity Measurement . . . . . . . . . . . .
Urine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Urinary Iodine Excretion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Parasitic Load
Stool . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.6.1.1 Qualitative Direct Wet Smear Technique . . . . . . . . . . . . . . . . .
3.8 Salt Monitoring (spot-test kit) . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.9 Data Analysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.9.1 Questionnaire
3.9.1 . 1 Data on Anthropometric Assessment Analyzed Under
Stunting. Wasting and Underweight . . . . . . . . . . . . . . . . . . . . . . . . . . 66
3.9.2 Worm Load Analysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66
CHAPTER FOUR: RESULTS ' " '"" "'
. . . . . . . . . . . . . . . . . . General Characteristics of the Subjects 68
Socio-demographic Characteristics of the Household
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . of the Subjects 70 .. Socio-economic Characteristics . . . . . . . . . . . . . . . . . . . . . . . 72
Contribution for the Upkeep of Household . . . . . . . . . . . . . . . . 74
Health Facilities and Health Practices . . . . . . . . . . . . . . . . . . . . . . 77
Morbidity and Health History of Children . . . . . . . . . . . . . . . . . . 79
. . . . . . . . . Symptoms Associated with Iodine Deficiency Disease 81
Household Food Security . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81
Respondents' Knowledge of lodized Salt and Iodine Deficiency
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Disorders (IDD) 83
The Result of the Mean Ratings (x) and Standard Deviation of
the Attitude of the Women to Iodized Salt and Iodine Deficiency.. . 85
Results of the Respondents' Practices with Iodized Salt and
Iodine Deficiency Disorders (IDD). . . . . . . . . . . . . . . . . . . . . . . . 87
Anthropometric Measurements . . . . . . . . . . . . . . . . . . . . . . . . . 89
Percentage Distribution of the Nutritional Status of the Children
According to their Weight-for-age, Height-for-age and
Weigh t-for-height.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89
Nutritional Status Classification According to Gender.. . . . . . . . . . . 89
Nutritional Status Classification According to Age-group.. . . . . . . . 89
Mean Weight Velocities for Boys According to School Attended
and in the Different Seasons,,. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93
Mean Height Velocities for Boys According to School Attended
and in the Different Seasons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93
Mean Weight Velocities for Girls According to School Attended
and in the Different Seasons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 95
Mean Height Velocities for Girls According to School Attended
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . and in the Different Seasons 95
Result of T-test Comparing the Weight and Height Velocities of
. the Boys and the Girlsaga Resirlt of the Seasonal Variations.. 99
Comparing Mean Weight, Height Velocities in the Wet and Dry
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Seasons of Boys, Girls and Both 102
Mean W.eight and Height Velocities According to Age Group I! . .
in Different Quarters.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102
Mean Weight-for-age and Height-for-age During the Four
Seasons Pooled together for Boys and Girls Compared to
NCHS-WHO 5oth Percentile.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105
Results for Parasitic Infestation of the Children in the Studied
Communities.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108
Determination of the Existence of any Difference in the Worm
. . . . . . . . . . . . . . . . . . . . . . . . . . . lnfestation of the Boys and Girls
Determination of the Existence of any Differences in the
Hookworm lnfestation of the Pupils According to the Schools
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Attended..
Result for Iodine Status of the Children in the Studied
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Communities
Determination of the Existence of any Difference in the Mean
. . . . . . . . . . . . . of Urine Iodine Level of the Boys and Girls..
Determination of the Existence of any Differences in the Urinary
Iodine Levels of the Pupils According to the Schools Attended
Correlation Coefficient (r) Values Expressing the Relationship
Between the Urinary Iodine ~ e v e l and Underweight, Stunting
and Wasting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Results of Relationship Between the Worm Infestation,
Underweight, Stunting and Wasting.. . . . . . . . . . . . . . . . . . . . . Percentage Frequency of Urinary Iodine Level of the Underweight
and the Normal in Weight-for-age of the Children.. . . Percentage Frequency of Urinary Iodine Level of the Stunted and
the Normal in Height-for-age of the Children.. . . . . . . . . . . . . . Practical Determination of the Iodine Levels of the Salt Used
. * , . I
in the Home and ~a rke t . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
CHAPTER FIVE: DISCUSSION
. . . . . . . . . . . . . . . . . . . . . . 5.1 The Iodine Status of the Children..
... 5.2 The Iodine Levels of the Salt Used in the Homes and Market
5.3 Knowledge, Attitude and Practice (KAP) of Mothers on Iodized
Salt and Iodine Deficiency Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.4 Parasitic lnfestation
5.5 The Anthropometric Status of the Children: Underweight,
Stunting and Wasting.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Seasonal Variations in Growth Velocity of the Children.. . . . . . . . 128
The Relationship Between Parasitic Infestation and
(i) Underweight (ii) Stunting and (iii) Wasting . . . . . . . . . 131
CONCLUSION.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 132
RECOMMENDATIONS ... . . .,. . . . . . .. . . .. . . . . . . . . . . . . . . . . . . .. 134
REFERENCES.. . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136
APPENDICES ... ... ... ... ... ... ... ... ... .... .... ... .... .... 147
Appendix 1 - Table 4.17 Nutritional Status according to
Age-group for fig 1. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147
Appendix II - Table 4.18 for fig. 1 to fig. 3 Nutritional Status
Classification according to Age-group.. . . . . . . . . . . . . . . . . . . . . . . 148
Appendix I11 - Table 4.1 9 for fig. 4: Mean Weight Velocities (kg) for
Boys according to Schools Attended and in the Different Seasons.. 149
Appendix Ill- Table 4.20 for fig. 5: Mean Height Velocities (cm) for
Boys according to Schools Attended and in the Different Seasons. 149
Appendix IV - Table 4.21 for fig. 6: Mean Weight Velocities (kg) for
Girls according to Schools Attended and in the Different Seasons.. 150
Appendix IV - Table 4.22 for fig. 7: Mean Height Velocities (cm) for
Girls according to schools attended and in the different seasons.. . 150
Appendix V - Table for fig. 8: Weight Velocities for Boys and Girls 151
Appendix V - Table for 'fi&gi'~eight Velocities for Boys and Girls.. . 151
Appendix VI - Table for figures 10 and 11: Comparing Weight, Height
Velocities In the Wet and Dry Seasons of the Boys, Girls and Both .. 152
Appendix VI - Table for fig 12: Mean. Weight Velocities according to I I
Age-groups . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 152
Appendix VII - Table for fig 13: Mean Height Velocities according to
Age-groups . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . I53
Appendix VII - Table for fig 14: Mean Weight-for-age (kg) during
The Four Seasons Pooled together for Boys and
Girls (6-1 2yrs 10mths) Compared to NCHS-WHO 1976.. . . . . . . . .. . ..I53
Appendix Vlll - Table for fig. 15: Mean Height-for-age (cm) during the
Four Seasons Pooled together for Boys and
Girls (6-1 2yrs 1 Omths) compared to NCHS-WHO 1976 . . . . . . . . . . . . 154
Appendix IX- Fig. 16: Percentage Hookworm Load Infestation of
Pupils according to Schools Attended.. . . . . . . . . . . . . . . . . . . . . . . . . ... 155
Appendix IX- Fig. 17: Percentage Urinary Iodine Level according to
Sex.. . . . . . .. . . . . . . . . . .. . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . .. . 155
Appendix X- Fig. 18: Percentage Urinary Iodine for the Underweight
and the Normal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . I56
Appendix XI - Table 4.39: Comparing Urinary Iodine Level of the
Normal in Height-for-age with the Stunted Children . ... ... ... ... 157
Appendix XI1 -Table 4.40: Iodine Levels of the Salt Samples
from the Homes of the Pupils in the Three Communities . . . . . . . . . I58
Appendix XI1 - Table 4.41 : Iodine Levels of Marketed and Home
Salt Samples ... ... ... .. . .. . ... ... . . . . . . . . . . . . . . . .. . . . I58
Appendix Xlll -The Questionnaire Used in Collecting Basic Data .. 159
Appendix XIV - Goitre Patient . . . . . . . . . . . . . . . . . . . . . . . . . . . . 171
Appendix XV Height Measurement at Owerre-Obukpa CPS . . . .. . . 172
Appendix XVI Weight Measurement at Ajuona CPS . . . . . .. . . .. . . . 173
. . . X l l l
LIST OF TABLES
Table
Share of Children who are Underweight
Epidemiological Criteria for Assessing Iodine
Nutrition based on Medium Urinary Iodine Concentration
in School-age Children
ICCID-UNICEF-WHO Recommended Levels of Iodine in Salt.
Examples of Desirable Average Levels at Various Points in
the Salt Distribution Chain, Depending on Climate, Salt Intake and Conditions Affecting Packaging and Distribution 5 1
Iodine Trace Elements for Human Nutrition 5 6
Background of the Subjects 67
Socio-demographic Characteristics of Respondents'
Household (parents) 69
Educational Attainment and Occupation of Respondents
Household Heads 7 1
Source of Income, Amount and Expenditure on Food in the
Household 73
Health Facilities and Health Practices in the Three Communities 75
Goitre History 76
Morbidity and History of Children 78
Possible symptoms of Iodine Deficiency as Reported by Mothers 80
Source of Food and Meal Pattern of Respondents 80
Knowledge of lodized Salt and Iodine Deficiency Diseases (IDD) ,, r n 1 7. *
by Respondents 82
Lack of Knowledge of lodized Salt and IDD by Different
Communities Used in the Study 8 2
The Mean Ratings (x) of the Attitude of the Women to lodized
Salt and Iodine Deficiency - 84 Practices Based on Knowledge on lodized Salt and Iodine
Deficiency Disorders by Mothers 86
Comparing the Practices Based on Knowledge on lodized Salt and
Iodine Deficiency Disorders by Mothers of the Three Communities 86 Anthropometric Measurements of Children in the Study 88
Nutritional Status Classification According to Gender 88
Mean Weight and Height Velocities of Children According
Page
2 1
to Season 96
4.24 Result of T-test Comparing the Weight Velocities of the Boys and
Girls during the Seasons 96
4.25 Result of T-test Comparing the Height Velocities of the Boys
and Girls during the Seasons 97
4.26 A Comparison of the Mean Weight and Height Velocities during the
Wet and Dry Seasons 101
4.27 Mean Weight and Height Velocjties of Children According
to Age-group
Percentage Distribution of Intestinal Parasitic lnfestation
of Children
Percentage Distribution of the Intestinal Parasitic lnfestation of
Children According to Sex
Hookworm lnfestation According to School Attended
Result of T-test Comparing the Effect of Parasitic lnfestation
of Boys and Girls
Iodine Status of the Children
Iodine Status of the Children According to Sex
Mean ( S D ) Urinary Iodine Level of Pupils According to Schools
Mean Urinary Iodine Levels According to Sex
Differences in Urinary Iodine Level of the Pupils in the
Different Schools
Correlation Coefficient (r) Values Expressing the Relationship
Between the Iodine Level in the Urine, Worm lnfestation and
Mal-nutritional Status:-{(i) Underweight, (ii) Stunting
and (iii) Wasting}
Comparing Urinary Iodine Level of the Underweight, with the
Normal Weight-for-age Children
, I
LIST OF FIGURES
Figure
Fig 1 Weight-for-height of Children According to Age-groups
Fig 2 Weight-for-age of Children According to Age-groups
Fig 3 Height-for-age of Children According to Age-groups
Fig 4 Seasonal Weight Changes in Boys According to School Attended
Fig 5 Seasonal Height Changes in Boys According to School Attended
Fig 6 Seasonal Weight Changes in Girls According to School Attended
Fig 7 Seasonal Height Change in Girls According to School Attended
Fig 8 Mean Weight Velocities of Boys and Girls According to Season
Fig 9 Mean Height Velocities of Boys and Girls According to Season
Fig10 Weight Velocities of Boys, Girls and Both Combined
in Wet and Dry Seasons
Fig 11 Height Velocities of Boys, Girls and Both Combined
in Wet and Dry Seasons
Fig 12 Mean Weight Velocities by Age-groups in Different Seasons
Fig 13 Mean Height Velocities by Age-groups in Different Seasons
Home Salt Samples
Page
90
90
9 1
92
92
96
96
98
98
ABSTRACT
Recently, iodine deficiency has been recognized as the leading worldwide cause
of preventable intellectual impairment, spontaneous abortions, stillbirth, impaired
fetal development and childhood growth defects. Eliminating iodine deficiency
disorder (IDD) is a global public health priority. Sub-clinical iodine deficiency can
be detected by measuring urinary iodine or assessing thyroid function. Iodine is
an element that directly affects thyroid gland secretions, which themselves to a
great extent control heart action, nerve response to stimuli, rate of body growth
and metabolism. Intestinal disorders, parasitic infestation and nutrient
interactions can impair iodine absorption and utilization. This study was designed
to access the iodine status, growth and the parasitic infestation of primary school
children. The study also tried to ascertain knowledge, attitude and practice (KAP)
of mothers on iodine deficiency disorder and iodized salt utilization, thereby
determining their effect on iodine status growth velocities of the children.
Sampling of the three schools (Ajuona CPS, Owerre-Obukpa CPS and
AmagulUmuorua CPS) was by random sampling using balloting from five
schools in the community, while the children were selected by stratified method
using the class register in each school. Questionnaires were used to elicit basic
information from the children's parents on social and demographic characteristics
of households, health facilities and practices, health records, morbidity, health
status, knowledge, attitude and practice (KAP) of mothers on iodized salts and . ,. , . m , ... ,
iodine deficiency disorder (IDD). The anthropometric measurements of 272
children composing of 154 boys and 146 girls aged 6-12years were taken to
assess their nutritional status using standard procedures. A sub-sample of 33
children was monitored for 12 months to assess their growth velocities; 11
children from each school were randomly selected. Their stools were collected
for assessing the parasitic load, and urine for biochemical analysis of urine iodine
levels. Salt from their homes were tested for iodine content with iodine spot-test
kit. Means, standard deviation, Student t-test, analysis of variance and
correlation coefficient were used where applicable. Anthropometric
measurements of the children revealed that 25% were stunted, 13% were
underweight while 6.3% were wasted. More girls (3.0%) than boys (2.3%) were
wasted. The weight velocities of the children were higher in the dry season
(0.57kg) than in the wet season (0.29kg). Also their height velocities were higher
in the dry season (1.98cm) than in wet season (0.62cm). There were significant
differences in the mean weight velocities of the children in wet and dry seasons
(t= 3.674, P<0.05). There were differences but not significant (t=0.712, P>0.05)
in the mean weight velocities of the boys (0.30kg) and girls (0.26kg), as well as in
the height velocities (t= 1.03, P>0.05) of the boys (0.95cm) and girls (1.00cm).
The weight velocities for boys according to schools attended showed differences
(Ajuona CPS, 0.36kg; Amagu/Umuorua CPS, 0.32kg; and Owerre-Obukpa CPS,
0.30kg; but were not significant, f=3.85, P>0.05) and for height (Ajuona CPS,
0.61cm; AmaguIUmuorua CPS, 1.61cm; and Owerre-Obukpa CPS, 0.65cm; but
were not significant, f=3.89, P>0.05). There were differences in the weight
velocities for girls (Ajuona CPS, 0.46kg; AmaguIUmurua CPS, 0.29kg and
Owerre-Obukpa CPS, 0.23kg; but they were not significant, f=3.77, P>0.05), and
height (Ajuona CPS, 1.14cm; AmaguIUmurua CPS, 1.41 cm and Owerre-Obukpa
CPS, 0.76cm; but were not significant, f=3.95, P>0.05). More than fifty percent
(58.33%) of the children were severely iodine deficient, boys (33.33%) and girls
(25%). The urinary iodine level ranged from about (10 to 650pgIL). The intestinal
parasitic loads were generally low. There were no significant relationships
between worm infestations of children in the various schools and their urine
iodine levels. Wasting in- ~h'ildien'~was positively correlated with the worm
infestation and this was significant (r=0.467, P<0.01). There were positive
relationships between urinary iodine level and stunting (r=0.314, P>0.05) and
underweight (r=0.240, P>0.05) in the children, but were not significant. Low
urinary iodine excretion was more in the stunted children (60.0%) than in the
normal children (21.2%). Most of the salts consumed in the homes were
adequate in iodine. About 91% of marketed salt and 97% of salt brought from
homes were iodized above 3oppm' iodine level. However, there was generally
poor knowledge about iodized salt and iodine deficiency disorders by the
mothers.
CHAPTER ONE
INTRODUCTION
1 . I BACKGROUND INFORMATION
Iodine deficiency is a condition in which an organism does not take or utilize
enough iodine. Iodine is an element that directly affects thyroid gland secretions,
which themselves to a great extent control heart action, nerve response to
stimuli, rate of body growth, and metabolism (Sofra et a/., 1998). Kennedy et a/.
(2003) defined iodine as an essential mineral required by the body to synthesize
thyroid hormones, the most important of which is thyroxine, a metabolism-
regulating substance.
Iodine deficiency has traditionally been associated with goiter and
cretinism. More recently, iodine deficiency has been recognized as the leading
worldwide cause of preventable intellectual impairment (United Nations, 1993;
Kennedy et a/., 2003). lntellectual and neurologic deficits occur because of a lack
of thyroid hormone during critical phases of brain development. Clinical iodine
deficiency, therefore, is detected by the presence of goiter (swelling of the
thyroid gland) (Kennedy et a/., 2003). . ,. . .I. ..' J
Elimination of iodine deficiency disorder (IDD) is a global publ~c health
priority (Maberly et a/., 1994; Ramalingaswami, 1992; WHO, 1991). In 1990,
seventy-one Heads of State and senior policy-makers from eighty other
countries attended "The World 'Sumriiit for Children" and endorsed "The World
Declaration and 1990-2000 plan of Action on the Survival, Protection and
Development of Children" (UNICEF, 1990). This "plan of Action" included the
virtual elimination of iodine deficiency. Universal access to iodized salt was
recommended as long-term intervention strategy to eliminate IDD, and many
countries set this as a 1995 goal (UNICEF-WHO, 1994).
CHAPTER ONE
INTRODUCTION
1 .I BACKGROUND INFORMATION
Iodine deficiency is a condition in which an organism does not take or utilize
enough iodine Iodine is an element that directly affects thyroid gland secretions.
which themselves to a great extent control heart action, nerve response to
stimuli, rate of body growth, and metabolism (Sofra et a/., 1998). Kennedy et a/.
(2003) defined iodine as an essential mineral required by the body to synthesize
thyroid hormones, the most important of which is thyroxine, a metabolism-
regulating substance.
Iodine deficiency has traditionally been associated with goiter and
cretinism. More recently, iodine deficiency has been recognized as the leading
worldwide cause of preventable intellectual impairment (United Nations, 1993;
Kennedy et a/., 2003). Intellectual and neurologic deficits occur because of a lack
of thyroid hormone during critical phases of brain development. Clinical iodine
deficiency, therefore, is detected by the presence of goiter (swelling of the
thyroid gland) (Kennedy eta/., 2003). ., ,, . ml. 5 : . ,
Elimination of iodine deficiency disorder (IDD) is a global publrc health
priority (Maberly et a/., 1994; Ramalingaswami, 1992; WHO, 1991). In 1990,
seventy-one Heads of State and senior policy-makers from eighty other
countries attended "The World 'Surnriiit for Children" and endorsed "The World
Declaration and 1990-2000 plan of Action on the Survival, Protection and
Development of Children" (UNICEF, 1990). This "plan of Action" included the
virtual elimination of iodine deficiency. Universal access to iodized salt was
recommended as long-term intervention strategy to eliminate IDD, and many
countries set this as a 1995 goal (UNICEF-WHO, 1994).
2
WHO (2001) reported the latest estimates of the global prevalence of
goiter. It indicated that 741million people or 13 percent of the world's population
are affected by goiter (FAO, 2003). Kennedy et a/. (2003) noted that the true
prevalence of iodine deficiency is even more widespread than the numbers of
those affected with goiter would seem to indicate. However, there are no global
estimates for prevalence of low urinary iodine, which is the best sub-clinical
indicator. Sub-clinical iodine deficiency is detected by measuring urinary iodine
or assessing thyroid function (Kennedy et a/., 2003).
Egbuta (2003) showed, that the median urinary iodine excretion for the
sampled population in Nigeria, drawn mostly from IDD-endemic areas, was
14.65ugdl-I. The mean value was 13.39pgdl-I. He reported that Nigeria has
achieved the goal of universal salt iodization and should now focus its attention
on constant monitoring to sustain this iodization level.
The IDD study carried out by Okeke et al. (1997) in Enugu State revealed
that most traders and consumers (94%) had increased knowledge of iodized salt
programme in Nigeria. Fifty-eight percent of families in Nsukka used salts
containing 50ppm of iodine, 33% used salt between 7 and 50ppm iodine and 9%
used non-iodized salts. Most consumers bought salt according to brand name
and cost, even though some salis.d,id.:not contain iodine.
Okeke et a/. (1997) noted that about 23% traders had little knowledge of
iodized salt, and careless handling occured during transportation, storage and
sale of salts.. Okeke et a/. (1997) saw the need for closer monitoring, increased ,, . ..
consumer awareness, systematic evaluation of procurement, marketing,
distribution, consumption, and follow-up of the effects on IDD.
NutriView (1997) reported that intestinal disorders, parasitic infestation
and nutrient interactions can impair iodine absorption and utilization. Furnee et
a/. (1997) in their study with school children reported that intestinal parasitic
3
infestations reduce the efficiency of oral supplementation with iodized ethyl
esters by interfering with absorption.
A common misconception is that IDD primarily affects only remote rural
populations. This belief may have developed because goiter, the most common
visible evidence of iodine deficiency, is usually most prevalent in rural
populations. United Nations (1993) stressed the interactions of low content of
iodine in the local environment with poverty and remoteness. This is as a result
of little contribution of food from outside an iodine-deficient area to the diet; as is
the case with much subsistence agriculture. Poverty, with poor sanitation and
general malnutrition, may worsen the effect of iodine deficiency. Goiter may be
the most common visible evidence of IDD, it is just the 'tip of the iceberg' of the
consequences of IDD, which include lower intelligence quotient (IQ), increased
fetal, infant and child mortality, poorer growth and birth defects (Boyages et a/.,
1989; Hetzel, 1994).
One of the most devastating consequences of iodine deficiency is
reduced mental capacity. Fifty million people worldwide are mentally
handicapped as a result of iodine deficiency (WHO, 2002). International council
for the control of iodine deficiency disorders (ICCIDD, 2002) has estimated that
100,000 children are bohl' edch ybar with irreversible brain damage because
their mothers lacked iodine prior to pregnancy. Maternal iodine deficiencies can
also lead to spontaneous abortions, stillbirth and impaired fetal development. In
infancy and childhood, deficiency is manifested by poor mental development and
growth defects. Persons living in communities with endemic iodine deficiency
may show an intelligence quotient 13.5 points lower than persons from similar
communities with adequate iodine supplies (WHO, 2001).
Growth is the increase in body size and anthropometric measurements of
growth are good indicators of nutritional status of children. With adequate
nutrition and under normal circumstances, a child would grow to its full genetic
potentials. Such conditions are more likely in developed countries. The thyroid
hormones have extensive effects throughout the body. They influence metabolic
rate, protein synthesis, enzyme function, cellular transport, and other
physiological processes. They have specific effects on growth in children: low
levels retard growth, causing stunting and poor development (United Nations,
I 993).
In many developing countries however, children hardly grow to their full
potential as a result of many environmental factors such as malnutrition and
infections (Asworth and Millard, 1986; Scrimahaw et a/., 1968). Children from
poor or less privileged families in those countries are the most affected due to
food insecurity, inadequate facilities, infection and poor general environmental
sanitations. The lack of adequate toilet facilities, water supply, unsanitary
environment, for example, predispose infestation leads to or increases intensity
of malnutrition (UNINigeria Working paper, 1992). Growth faltering is the result of
many factors including inadequate diets, worm infestation, infections and
unsanitary environment. NutriView (1 997) pointed out that poor food hygiene,
inadequate methods of preparation, cooking and storage can reduce the
nutritional content of fdod"~"'cohsiderab1y. Intestinal disorders, parasitic
infestations and nutrient interactions can impair micronutrient absorption and
utilization.
Most of the iodine status ,,monitbring and parasitic studies done are
outside Nigeria. Thus, there is the inadequate documentation on the iodine
status, growth velocity and intestinal parasitic load of the Nigerian school age
children. This group of children is also susceptible to iodine deficiency disorder
and parasitic infection.
5
This study was aimed at assessing the iodine status, growth velocity of
the school children in a rural community and some factors that may influence it.
Such factors may include intestinal parasitic infection, poor knowledge of iodized
salt and iodine deficiency disorders.
1.2 Statement of the problem and justification
There is inadequate documentation on the iodine status and growth pattern of
Nigerian school children. Most lacking is the information on the relationship
between growth, intestinal parasite infection and iodine status. Though not the
most vulnerable, these children are susceptible to iodine deficiency disorder and
infestation, which may result in growth faltering, poor performance at school and
problem in later life. One of the main causes of iodine deficiency disorder in this
group of children is dietary insufficiency and worm infestation (NutriView, 1997).
Adequate and current information on the growth, prevalence and intensity of
parasitic infestation and IDD status of Nigerian school children are necessary for
effective intervention.
Indeed in rural communities it is a common practice for pupils to gather
infected fruits and eat on their way to school. In general, most eat snacks with
soiled hands after work.andlp'tay, 'as there are little or no facilities for washing
hands at school. The lack of adequate toilet facilities and their unhygienic
condition, inadequate water supply (quality and quantity) and poor environmental
sanitation predisposes these child,ren to:intestinal infection (UN-FGN, 1992).
The extent of iodine deficiency in school children is not fully documented.
In Nsukka (a semi urban-town) and the neighbouring villages, not all families
have knowledge of the all celebrated iodized salt. There is also insufficient water
supply (Onofiok, 1998) as such, personal hygiene is poor, coupled with
unsanitary environment.
1.3 Objectives of the study
The general objective of this study was to assess the iodine status, growth and
the parasitic infestation of primary school children in rural Nigerian community
(Obukpa).
The specific objectives were as follows: to
monitor anthropometric status of the children;
determine the variations in growth velocity of the children in different
seasons of the year using established methods;
assess intestinal parasitic load of the children;
determine the iodine status of the children;
ascertain knowledge, attitude and practice (KAP) of mothers, on iodine
deficiency disorder and iodized salt utilization;
determine the iodine levels of the salt used in the homes and sold in the
market.
Hypotheses
The following null hypotheses were tested:
Hol: There is no significant difference (p>0.05) in the effect of seasonal , ,' . * I . "' z
variations on the weight velocities of boys and girls.
Ho2: There is no significant difference (p>0.05) in the effect of seasonal
variations on the height velocities of boys and girls. , I
Ho3: There is no significant difference (p>0.05) in the effect of seasonal
variations on the weight velocities of the pupils according to school
attended.
7
Ho4: There is no significant difference (p>0.05) in the effect of seasonal
variations on the height velocities of the pupils according to school
attended.
Ho5: There is no relationship between the salt iodine level marketed and the
ones brought by the pupils from their homes.
Ho6: There is no relationship between the iodine level in the urine of the
children and
(i) Underweight
(ii) Stunting
(iii) Wasting
Ho7: There is no relationship between the level of worm infestation and
Underweight
(i) Stunting
(ii) Wasting .
Ho8: There is no significant difference (p>0.05) in the effect of urinary excretion
of iodine level on the children with stunted growth and normal growth
children.
Hog: There is no signifiCant4~ifferdhce (p>0.05) in the iodine level of the boys
and the girls.
HolO: There is no significant difference (p>0.05) in the worm load of the boys I f . ..
and the girls.
Ho l I : There is no significant 'difference (p>0.05) of iodine levels of the pupils
according to the school attended.
Ho12: There is no significant difference (p>0.05) in the worm load of the pupils
according to the school attended.
8
1.5 Significance of the study
This study will be useful to the Nigerian Government, National Agency for Food
and Drug Administration and Control (NAFDAC) and UNICEF who are currently
interested in the assessment of the prevalence of micronutrient deficiency and
control in Nigeria (FMHHS, 1992). It will identify some primary school children
who are at high risk of iodine deficiency and parasitic infestation as target for
necessary interventions. Anthropometric measurements are useful indicators in
food and nutrition policy and planning (Nnanyelugo, 1982a.b.c) and their wider
application in clinical and field surveys have been underscored (Nnanyelugo and
Ngwu, 1985). This present study added to the body of information on school
health for long term planning and periodic evaluation of health, educational and
agricultural services and action. The data will be of value to health workers,
groups and organizations concerned with the welfare of children, especially in
the rural areas.
CHAPTER TWO
LITERATURE REVIEW
2.1 Iodine an Essential Nutrient
Iodine is recognized as an essential nutrient for all animal species, including
man. The human body contains about 25 mg of iodine, 10mg of which is in the
thyroid gland. It is an integral component of the thyroid hormones, thyroxine and
triiodothyronine, both of which have important metabolic roles (Price, 1997).
2.1 . I Absorption, bioavailability, transport and storage of iodine
Iodine in foods is primarily in the inorganic iodide (I-) form, which is readily
absorbed from the stomach and upper small intestine. Other forms of iodine in
foods are reduced to iodide before or after absorption. One exception is iodine
in the form of erythrosine (tetraiodofluorescien), a red food dye which is 58%
iodine ("I,). The iodine from erythrosine is only about 2-5% bioavailable.
Absorbed iodine is rapidly cleared from the plasma by the thyroid gland, the
kidney, salivary glands, gastric mucosa cells, and the lactating mammary glands.
Urinary iodine is one means .of assessing iodine status because iodine intake in
excess of requirement is excreted primarily by this route (Pennington, 1993).
Thyrotrophic stimulating hormone (TSH), from the anterior lobe of the
pituitary gland, stimulates the active transport of inorganic iodide from the blood I
I I
into the thyroid gland. Within the thyroid cells, iodide is oxidized to iodine and
combined with tyrosine to form the thyroid hormones. These actions are also
stimulated by TSH. Thyroid hormones are stored in the thyroid gland bound to
thyroglobulin, a glycoprotein. The total amount of iodine in the body is about 10-
50 mg for an adult, and most of this is concentrated in the thyroid gland as
thyroglobulin. Proteolytic enzymes release the thyroid hormones from
thyroglobulin so that the hormones may diffuse into the blood. In the blood,
thyroxine (T4) is found primarily bound to globulin and albumin. The secretion of
thyroid hormones into the blood is regulated by TSH through a biofeedback
system. When dietary iodine is adequate, thyroid hormone is produced in
normal amounts at a low level of TSH; if dietary iodine is limited, TSH secretion
is increased to promote iodine uptake by the thyroid. The thyroid gland stores
enough thyroid hormone to last several months in the event that dietary iodine is
not available (Pennington.,l993).
2.1.2 Iodine
Iodine is a member of a family of non-metal chemical elements called the
halogens. As a solid, iodine is a gray-black crystal with a shiny metallic
appearance. But even at ordinary room temperatures, iodine can change from
solid directly into a purple vapour with a strong irritating odour. The process of
changing from a solid into a gas without first becoming a liquid is called
sublimation (Price, 1997 and Fischer, 1993).
Iodine is very active chemically. It combines easily with other substances
by gaining or losing electrons to form chemical compounds. In fact, iodine is . ,, . * I . r.' .
never found alone in nature. It is always combined with other elements.
A major source of iodine is Chile saltpeter, a mineral that is found in great
quantities in Chile. It was during the processing of saltpeter that the French
manufacturer Bernard Courtois fd'und' i'odine in 181 1. The salty water found
underground near petroleum deposits, called oil-well brine, is another source of
iodine.
Humans need iodine in order to stay healthy. Most people get enough
iodine from the food and water in their diet. Table salt with iodine added can be
used in regions where the food and water do not contain enough iodine, such as
the Alps of South Central Europe and the Great lakes area of the United States
(Price, 1997).
Light sensitive iodine compounds are used in making photographic film.
Other iodine compounds are used in making bread. For a long time, tincture of
iodine - iodine dissolved in alcohol - was used as a disinfectant (germ killer) on
cuts and scratches. Now other forms of iodine less irritating to the skin and
tissues are used as first-aid antiseptics.
Compounds of iodine are also used to treat cancer and other diseases of
the thyroid gland, to locate a variety of tumours, and to trace chemical
substances as they travel through the body.
2.1.3 Properties of iodine
Chemical symbol I
Atomic number 53
Atomic Weight 126,904
Melting point 11 3.5OC (236.3OF)
Boiling point 1 84.35OC (363.83OF)
(The New Encyclopaedia Britannica, 2003) . ,, . n l . 5.' ,
The stable isotope '*'I is the only atomic species in nature, but numerous
radioactive isotopes ranging from l o 9 1 to 14' I have been prepared artificially. The
l3'l, with a'half life of 8 days,. is wildely used as a radioactive tracer. Iodine has
seven electrons in its outermost shell. Its principal oxidation states are + I , +3,
+5 and +7 (The New Encyclopaedia Britannica, 2003; Price, 1997 and Fischer,
1993).
Iodine is only slightly soluble in water, but it does dissolve in organic
solvents such as benzene, carbon disulfide, carbon tetrachloride, chloroform,
and ethyl alcohol. Some iodine solutions are violet and others are brown.
Although iodine is very active chemically, it is generally less active than the other
members of the halogen family - fluoride, chloride and bromine.
2.1.3.1 Occurrence: Iodine is a relatively rare element in that it makes up only a
very small percentage of the earth's crust. Its concentration is low, however the
distribution of the element is widespread. It is found in rocks, soils, underground
brines, minerals and seawater. The concentration of iodine in seawater is low
(about 0.05ppm). Some seaweed, particularly the brown varieties, can extract
and accumulate the element from the sea. Seaweed, laminaria, contains up to
0.45% iodine (dry weight) (Price, 1997 and Fischer, 1993).
2.1.4 Compounds: Iodine forms compounds with all other elements except the
inert gases, sulfur and selenium; however, it does not react directly with carbon,
nitrogen or oxygen and but reacts only at high temperature with platinum. The
most common and important inorganic iodine compound is hydrogen iodide (HI)
a colourless gas that fumes strongly in air. Hydrogen iodide dissolves readily in
water to form hydrodic acid. Potassium iodide (KI) is used in preparing iodides
of other metal. It is also used as the carrier for radioactive iodine, l3'l, when this , . . w , . , * ' . a '
isotope is employed in medicme. Silver iodide (Agl) is a light yellow salt that is
insoluble in water.
Iodine forms several compounds with other halogens, such as iodine i
monochloride (ICI), iodine pentafluoride -(IF,), Iodine heptaflouride (IF5), Iodine
trichloride (IC13) and iodine monobromide (IBr). With Oxygen, iodine forms
several oxides such as lo3, I4O9 and I2O3. Iodine pentaoxide (I2O5) is the most
important and stable of the halogen oxides. It is available commercially and
dissolves in water to form iodic acid (H103). lodic acid and iodates (salts of iodic
acid) are powerful oxidizing agents (Sofra et a/., 1998).
13
The organic compounds containing iodine have a higher density, lower
vapour pressure, greater reactivity and lower stability than the chloro or bromo
analogs, methyl iodide (CH31) is an effective methylating agent and is also used
as a fumigant. Methylene iodide (CH2I2) is utilized in organic synthesis, and
because of its high density, it is also used in separating heavy minerals from light
materials, such as silicates. lodoform (CHI3) is a greenish yellow, crystalline
solid that has been used as a disinfectant. However, recently other germicides
have largely displaced it. Ethyl iodide (CH3CH21) is utilized commercially in the
production of pharmaceuticals and as an intermediate for the preparation of
organic chemicals. lodobenzene (C6H51) is a pale yellow liquid useful in the
synthesis of compounds containing positive iodine.
2.1.5 Production: The first commercial source of iodine was from the ashes of
seaweed. In Japan seaweed still serves as a major source of the element.
However, in the 1840s iodine was discovered in the nitrate deposits in Chile,
mainly in the form of the mineral lautarite (anhydrous Calcium iodate). The
deposits once constituted the world's most important source of iodine.
In the 1920s and 1930s iodides were discovered in the oil well brines in
Louisiana and California and Iaer'in the brine wells of Michigan (USA). Several
processes for the isolation of iodine from brines are currently employed. One
process precipitates the iodine as silver iodide by treatment of the brine with
silver nitrate. The silver iodide is then' converted to ferrous iodide and metallic
silver by subsequent treatment with iron. Iodine is then liberated from the
ferrous iodide by treatment with chlorine (Sofra eta/., 1998).
Iodine is isolated from the Chilean nitrate deposits by extraction, as
sodium iodate, from nitrate-bearing earths called caliche. Treatment of the
sodium iodate with excess sodium bisulfite solution converts the iodate to iodide.
Further treatment of the iodide solution with fresh iodate solution liberates the
free iodine, which is filtered, dried and sublimed in concrete-lined iron retorts.
2.1.6 Uses: The most important uses of iodine are in metabolism and in
medicine as an antiseptic. In metabolism, iodine is necessary for the normal
functioning of the thyroid gland. The element is an important part of the thyroid
hormone thyroxin (Cl5Hl1I4NO4). An iodine deficiency results in a condition
known as endemic goiter. The radioisotope (I3'l) is used in the diagnosis and
treatment of goiter. A solution of Potassium iodide and iodine in alcohol called
tincture of iodine is a widely used and effective topical antiseptic (The New
Encyclopedia Britannica, 1993).
Iodine is utilized in several dyes, the most important being erythrosine,
which serves as an orthochromatic sensitizer for photographic, emulsions and as
a food colouring. Silver iodide is used in photography in negative emulsion and
as a smoke for the seeding of clouds to induce rainfall.
One of the factors affecting the output of thyroid hormones by the thyroid
gland is iodine availability. In the absence of sufficient iodine, the gland attempts
to compensate for the deficiency by increasing its secretory activity and this . ,, . * T . ? ' .'
cause the gland to enlarge. This condition is known as simple or endemic goiter,
(The New Encyclopedia Britannica, 2003). Besides iodine deficiency, certain
environmental agents, both naturally occurring and man-made interfere with
thyroid function. They may cause 'goiter and thyroid dysfunction by acting
directly on the thyroid gland or indirectly by altering its regulatory mechanisms
and thyroid hormone homeostasis. They are thus called goitrogens, or
antithyroid compounds (Vanderpas, 1993).
15
2.1.7 Functions of iodine
The sole function of iodine is for making the iodine-containing hormones
secreted by the thyroid gland, which regulate the rate of oxidation within the
cells. In so doing influence physical and mental growth, the functioning of the
nervous and muscle tissues, circulatory activity, and the metabolism of all
nutrients (Sofra et a/., 1998 and Pennington, 1993).
2.1.8 lnter relationships
Certain foods (especially plants of cabbage family - cabbage, kale, turnips,
cauliflower, rapeseed, and mustard seeds) contain goitrogens, which mterfere
with the use of thyroxin and may produce goiter. Fortunately, goitrogenic action
is prevented by cooking, and an adequate supply of iodine inhibits or prevents it.
lnter relationships: Jointly occurring deficiencies of iodine and vitamin A
are likely to cause a more severe thyroid disorder than lack of iodine alone.
Besides iodine deficiency, certain environmental agents, both naturally
occurring and man-made, interfere with thyroid functions. They may cause
goiter and thyroid dysfunction by acting directly on the thyroid gland or indirectly
by altering its regulatoji 'mechanisms and thyroid goitrogens or anti thyroid
compounds. (The New Encyclopedia Britannica, 2003 and Vanderpas, 1993).
2.2 Parasites
Intestinal parasitic and protozoal infections are common with humans being most
prevalent in poor communities in developing countries (Savioli et a/., 1992).
Many children in developing countries are exposed from birth to intestinal
parasites as a result of crawling, contaminated foods and water, inadequate
16
sanitation and poor personal hygiene (Hall, 1993). The effect of intestinal
parasites on IDD and growth are well documented.
2.2.1 Intestinal helminthes
The most common intestinal helminthes in humans are nematodes: Ascaris
lumbricoides, Tricharis trichiura, and hookworms (Nector americanus and
Ancylostoma duodenal) (Bundy et a/., 1992). Soil is the transmission medium.
Helminth eggs and larvae can live for long periods of time in the soil (Kowal,
1988).
2.2.2 Prevalence among children
Until recently, most of the parasitic studies and target for treatment has been
focused on the preschool child (under 5 years old), while the school-age children
have been neglected (Bundy et a/., 1992). Thus, information on the prevalence
of school-age children is most scanty. However, Tanner et a/. (1987) in
longitudinal study on the health status of children in rural Tanzanian community
observed that the prevalence and incidence of parasitic infection was high and
varied with the specie hookworm (N. americanus), Strongyloides spp. and
Schistosoma haematobiljm weFe f h n d to be highly prevalent In a high annual
incidence rates. Ascaris and Trichuris were of minor importance. They reported
that the prevalence and incidence of parasitic infestation did not differ by sex.
Multiparasitism was reported to be very' frequent and < I 1% of all children were
parasite-free in each year. Bundy etal. (1992), noted that children aged between
5 and 15 years were infected with at least one species of worm. Wan et a/.
(1989), found that the incidence of parasitic infestation of preschool children
particularly by Ascaris lumbricoides and Trichuris trichura was extremely high in
2 villages in Malaysia (70.3% and 41.2%).
17
In Nigeria, some researchers (Gilles and Akufo, 1965; Cowper, 1967) had
observed high prevalence of intestinal parasites among children. It is presumed
that children from rural communities or those living in poor sanitary environment
or deprived communities and those of poor socio-economic group would have
high prevalence and incidence of intestinal parasitic infestation (Noor et a/., 1989;
Al-baloa et al., 1993).
However, Hall (1993) in his review on intestinal parasitic infestation
observed that studies which classify children as simply infected or uninfected
were inadequate as the effect of intestinal parasite will depend on the intensity
(worm burden), the worm specie and the nutritional status of the child. He noted
that heavily infected children are most often from deprived and vulnerable
sections of the community.
In Nigeria, the poor economy, high inflation rate, and lack of facilities
would probably make children vulnerable to heavy load of intestinal parasitic
infestation. According to a recent survey, about 66%, 32% and 7% of urban,
semi-urban and rural areas respectively had access to safe pipe-borne water by
1989. Boreholes naturally accounted for 4%, 19% and 15% in urban, semi-
urban and rural areas respectively. Generally, it could be seen that about 70%,
50% and 22% of urbari,"s~mi~urban and rural centers had access to safe water
in Nigeria by 1989 (UN-FGN, 1992). It was also observed that 18% of urban, 3%
of semi-urban and 0% of rural dwellers were using water closet, while the rest
were using pit toilet, dam hill or bush. .'
2.3 Intestinal parasitic infestation and growth and nutritional status
The effect of intestinal parasite depends on the duration of infection before
treatment (Hall, 1993). A long-standing, worm burden would have more effect
on growth than a newly acquired load of similar intensity. This explains why
18
some researchers did not observe any change in growth after treatment (Tanner
et a/., 1987; Noor el a/., 1989).
Blumenthal and Myron (1976) observed that their control group tended to
exceed the infected in percentile of weig ht-for-heig ht, especially the moderate
and heavily infected. They also found that scars of angular stomatitis, (another
sign, associated with adequate riboflavin nutrition) were noted more often in
parasitized children, though the difference was not significant. Tanner et a/.
(1987) reported a high degree of stunting (35-71%) and a substantial proportion
of wasting (3-20%) among rural Tanzania children infected with intestinal
parasites. It was further noted that the anthropometric assessment did not
improve substantially when compared with the untreated group. Gupta (1980)
and Gupta and Urrutia (1982) observed an increased height gain among
Guatemalan pre-school children treated against G. lambia.
In their own contribution, Wan et a/. (1989) reported that Malaysian village
children who were heavily infected with Ascaris and Trichuris were
malnourished. They noted that 28% and 34.3% of children from two villages
were suffering from chronic malnutrition. Blumenthal and Myron (1976) and
Venkatachalam and Patwardhen (1953) shown that ascariasis of moderate to . ,, . .! 3''
severe intensity caused in test ha^ protein loss amounting to about 7% of dietary
protein intake.
Other ways in which intestinal parasite interfere with the host nutrition
includes malabsorption, production-'of antiproteolytic substances and anorexia in
the host (Venkatachalam and Patwardhen, 1953).
Furnee el a/. (1997) in their study with school children indicated that
intestinal parasitic infestations reduce the efficiency of oral supplementation with
iodized esters by interfering with absorption.
2.4 Morbidity and mortality
Most of the deaths and serious illnesses occurring among Nigerians were due to
conditions that are easily preventable or can be treated with simple remedies
(DHS, 1990). Communicable diseases especially those associated with
inadequate environmental sanitation and poor personal hygiene predominate
and are often compounded by malnutrition. While the lack of timely and
appropriate care often increases the risk (UN-FGN, 1992). Nnanyelugo et a/.
(1990) rightly noted that the high mortality rate in two rural communities they
studied was associated with the existing over-all environmental problems.
Although, the cause of death was not usually known, diarrhoea and vomiting
were usually reported to have occurred. The common types of infective and
parasitic diseases in order of occurrence in Nigeria are malaria, dysentery and
diarrhoea1 diseases, measles, pneumonia, gonorrhea, whooping cough,
schistosomiasis, chicken-pox, tuberculosis, meningitis (UN-FGN, 1992).
The five most common causes of death in hospitals in Nigeria according
to national health Policy of 1988 are as follows: Communicable and parasite
diseases, respiratory disease, accidents, poison and violence, disease of the
circulatory system and diseases of the digestive system (UN-FGN, 1992).
According to the World Bank Development Reports (1990) Nigerian infants
mortality rate (IMR) hassdecreasecl steadily from 138 in 1974 to 98 in 1990. It
was also observed that mortality rates are higher for rural than urban areas and
higher for male than female children. Statistics have revealed that infant
mortality .is responsible for almost 50% of all death in the 0-4 years old, whilst, , I
under-five child mortality accounts for 93% of these deaths, 70% of which is
attributed to preventable diseases (FOS, 1984). It was also reported that trend
from 1981 -1 986 for four immunizable diseases namely, measles, tuberculosis,
tetanus and whooping cough showed remarkable decline in incidence within the
12 months of the launching of the expanded Programme of Immunization in
Nigeria (FOS, 1984).
2 0
Although, there is improvement in immunization coverage, other factors
such as nutritional status, health knowledge of mothers, access to health centers
and services, level of household, food security, access to clean water, safe
sanitation and the general environmental conditions of child, which influence
morbidity and mortality need to be improved in Nigeria (UN-FGN, 1992)..
I ne srtuatlon In NSukka (slte ot study) IS not dltterent trom the general
picture described above. Obukpa being a rural community may have high
incidence of child morbidity and mortality.
2.4.1 Share of children who are underweight
The commission on the Nutrition Challenges of the 21St century in its report titled
"Ending Malnutrition by 2020, An Agenda for change in the Millennium", has
pointed out that some 30 million infants are born each year in developing
countries with intrauterine growth retardation, representing about 24% of all new
births in these countries, (Phillip et a/., 2000). Low birth weight (LBW) children
are characterized by mental impairment. Worldwide, there are more than 150
million underweight pre-school children (Table 1) and more than 200 million
stunted children. At current rates of progress in fighting these maladies, about
one billion children will be growing up by 2020 with impaired mental . *l. "' r
development. What wh" be the impact of such a denial to the child of
opportunities for the full expression on its innate genetic potential for mental and
physical development of the intellectual property of a nation? Denying the child
an opportunity for mental and physical development even at the foetal stage is
the cruelest form of inequity. Swaminathan (2000) at the International Congress
on Nutrition Vienna reported that sustained efforts are also needed to eliminate
iodine deficiency disorder.
Table I: Share of Children who were underweight
Country Share Underweight (Percent)
Bangladesh 58
India 53
Ethiopia 48
Vietnam 40
Nigeria 39
Indonesia 34
Source: Gardner and Halwail, 2000
22
2.5 Toxic Substances and Anti-nutritional Factors
Root crops, in common with most plants contain small amounts of potential
toxins and antinutritional factors such as trypsin inhibitors. Apart from cassava,
which contains cyanogenic glucosides, cultivated varieties of most edible tubers
and roots do not contain any serious toxins. Wild species may contain lethal
levels of toxic principles and must be correctly processed before consumption.
These wild species are useful reserves in times of famine or food scarcity. Local
people are aware of the potential risks in their use and have developed suitable
techniques for detoxifying the roots before consumption.
2.5.1 Cassava toxicity: The main toxic principle which occurs in varying
amounts in all parts of the cassava plant is a chemical compound called
linamarm (Nartey, 1981). It often co-exists with its methyl homologue called
Methyl-linamarin or lotaustralin. Linamarin is a cyanogenic glycoside which is
converted to toxic hydrocyanic acid or prussic acid when it comes into contact
with linamarase, an enzyme that is released when the cells of cassava roots are
ruptured. Otherwise linamarin is a rather stable compound which is not changed
by boiling the cassava. If it is absorbed from the gut to the blood as the intact . $ 4 . 1. ..
glycoside it is probably excreteb unchanged in the urine without causing any
harm to the organism. However, ingested linamarin can liberate cyanide in the
gut during digestion (Coursey, 1973).
Hydrocyanic acid or HCN is a.'volatile compound. It evaporates rapidly in
the air at temperatures over 28OC and dissolves readily in water. It may easily
be lost during transport, storage and analysis of specimens. The normal range
of cyanogens content of cassava tubers falls between 15 and 400 mg HCNIkg
fresh weight (Coursey, 1973). The concentration varies greatly between
varieties and also with environmental and cultural conditions. The concentration
23
of the cyanogenic glycosides increases from the center of the tuber outwards
(Bruijn, 1973). Generally, the cyanide content is substantially higher in the
cassava peel. Bitterness is not necessarily a reliable indicator of cyanide
content.
2.5.2 Pathophysiology of cyanide intoxication
Cyanide is detoxicated in the body by conversion to thiocyanide, a sulphur
containing compound with goitrogenic properties. The conversion is catalysed
by an enzyme thiosulphate cyanide sulphur transferase (rhodanase) present in
most tissues in human, and to a lesser extent by mercaptopyruvate cyanide
sulphur transferase which is present in red blood cells (Fielder and Wood, 1956).
The essential substrates for conversion of cyanide to thiocyanate are
thiosulphate and 3-mercaptopyruvate, derived mainly from cysteine, cystine and
methionin, the sulphur-containing amino acids. Vitamin B12 in the form of
hydroxycobalamin probably influences the conversion of cyanide to thiocyonate.
Hydroxycobalamin has been reported to increase the urinary excretion of
thiocyanate in experimental animals given small doses of cyanide (Wokes and
Picard, 1955; Smith and Duckett, 1965). About 60 to 1090 percent of the
injected cyanide in toxic cbf'icetrtration is converted to thiocyanate within 20
hours and enzymatic conversion accounts for more than 80 percent of cyanide
detoxification (Wood and Cooley, 1956). Thiocyanate is widely distributed
throughout body fluids including,,saliv;l, in which it can readily be detected. In
normal health, a dynamic equilibrium between cyanide and thiocyanate is
maintained. A low protein diet, particularly one which is deficient in sulphur-
containing amino acids may decrease the detoxification capacity and thus make
a person more, vulnerable to the toxic effect of cyanide (Oke, 1969; 1973).
24
Excessive consumption of cassava as the sole source of dietary energy and
main source of protein could thus increase vulnerability to cyanide toxicity.
2.5.3 Goitrogens and Antithyroid Compounds
The unique known function of iodine in mammals is its role in the synthesis of
thyroid hormones. The uptake of iodide by the thyroid gland is stimulated by the
hormone, thyrotrophin (TSH), and it can be multiplied 20-40 times in a TSH
stimulated gland. Some goitrogens, such as thiocyanate and isothiocyanate,
interfere with iodide uptake ( Vanderpas, 1993).
After being concentrated by the thyroid gland, iodide is oxidized and
bound to some specific tyrosyl residues of thyroglobulin, forming mono
iodotyrosine (MIT) and diiodotyrosine (DIT); oxidation of iodide and iodination of
selected tyrosyl residues is catalysed by a membrane bound enzyme,
thyroperoxidase (TPO). The same enzyme couples two iodotyrosines to form
thyroxine (T4; four iodine atoms) and triiodothyronine (T3; three iodine atoms).
The ratio of T4 to T3 in thyroglobulin is closely dependent on serum TSH
concentration and iodine supply: in euthyroidism (normal healthy function of
thyroid gland) 85% of the hormonal content of thyroid is represented by T4, while . ,, ."
in the hypothyroid state,"the ratioe~4:T3 is closer to unity. Most of the goitrogens
(Phenol derivatives, dihydrobenzoic acid, flavones, goitrin, disulphides,
polycyclic aromatic hydrocarbons, excess iodine) interfere with TPO activity (
Vanderpas, 1993).
lntrathyroid proteolysis of thyroglobulin results in the release of T4 and T3
in the systematic circulation; this step is inhibited by lithium and excess iodine.
Secreted in the systematic circulation, serum T4 and T3 are bound to albumin,
thyroxine binding-globulin and transthyretin (also named thyroxine-binding
prealbumin). The binding of thyroid hormones to serum proteins is partly
2 5
inhibited by flavonoids resulting in alterations of circulating free hormone
concentrations and adaptation of feedback regulation.
Thiocyanate and cyanide do not occur in the intact plant as free anions.
When the plant is crushed, a thioglucosidase or a glucosidase (such as
linamarase in cassava) is released, which hydrolyses the thioglucoside or the
cyanogenic glucoside, yielding the active goitrogens.
The principal vegetables containing thioglucosides are Kale, cabbage,
sprouts, broccoli, kohlrabi, turnips, Swedes, rapeseed, and mustard. The main
vegetables containing cyanogenic glucosides are bamboo shoots, and sweet
potatoes ( Vanderpas, 1993) .
The inhibitory action of thiocyanate on iodine uptake is due to a
competitive effect of the pseudohalide with the mechanism of iodide
concentration. However, under experimental conditions, rather high plasma
concentration of thiocyanate is required for inhibiting the iodide uptake by the
thyroid gland. In the thiocyanate suppression test, administration of 3 g of
thiocyanate results in serum levels in the range of 8.0 - 15.0 mgdl-I, far
exceeding the levels attained in populations exposed to environmental
thiocyanate overload (around 2.0 mgdl'l). In order to move closer to the
physiological 'coridifions: ' rats were exposed to chronic moderate
supplementation of thiocyanate (0.25 mg per day) and to a low-iodine diet for 11
weeks. This prolonged administration of thiocyanate markedly reduced radio-
labelled pertechnate in the thyroid without change in radioiodine thyroid uptake
(pertechnate is concentrated in the thyroid by the same pathway as iodide, but it
is neither oxidized nor bound to tyrosyl residues by TPO). Decreased iodide
uptake associated with thiocyanate overload, and increased iodide organification
owing to TSH stimulation could explain these discrepancies. The net result is
reduction of circulating thyroxine induced by thiocyanate supplementation in rats
receiving a low-iodine diet ( Vanderpas, 1993).
The role of cassava is the aetiology of endemic goiter in a human
population was first suspected in Nigeria on the basis of geographical overlap of
areas affected by goiter and by tropical neuropathy (presumably resulting from
chronic cyanide poisoning by consumption of poorly processed cassava). A few
years later, extensive studies in eastern and in northern Zaire, have documented
thiocyanate overload resulting from elevated intake of cassava poorly detoxified
through traditional preparation procedures (Sun-drying). The methods of
preparing cassava vary widely from one ethnic group to another; in the ethnic
group with the highest prevalence of goiter, cassava is not soaked; the roots are
peeled, dried in the sun for 1 or 2 days then bruised in a mortar with corn that
has been steeped for 12-24h in water. The flour is eaten as gruel (fuku)
prepared in boiling water (Ermans et al., 1980).
2.5.4 Sulphur-containing compounds
Cabbage has been recognized as a goitrogen in rabbits since 1928. The
antithyroid properties of thiocyanate were shown in 1936 in patients treated for
hypertension with thiocy8hdtk'"as "vasodilator. An important staple food in
tropical countries - cassava - has been recognized to play a major role in the
epidemiology of goiter in central Africa ( Vanderpas, 1993).
Antithyroid sulphur-containing organic identified in vegetable foodstuff can
be divided into two categories according to the way they act on iodine
metabolism:
1. thiocyanate and thiocyanate-derived compounds primarily inhibit the
active concentration mechanism of iodide, and their goitrogenic activitiy
can be overcome by iodine administration.
2. goitrin ( or 1,5-vinyl-2-thiooxazolidone) is analogous to thiourea in its
action, interfering with thyroperoxidase activity and its action cannot
usually be antagonised by iodine ( Vanderpas, 1993).
2.6 Selenium-deficiency-related thyroid dyshormonogenesis
Selenium has been identified as the constitutive compound of 5'deiodinase I, the
main enzyme converting the prohormone thyroxine (T4) to the thyromimetically
active T3 and degrading reverse T3, a further metabolite of T4. The
selenocysteine in the active site is encoded by the amber stop codon, TGA, and
selenium is incorporated in S'deiodinase I enzyme by a specific transfer
ribonucleic acid (tRNA) at the cotranslational level. In vitro, in selenium
deficiency conditions, the level of S'deiodinase I activity is reduced to 10% of the
initial level. In iodine-and selenium-deficient subjects (northern Zaira), Selenium
supplementation in the absence of serum T4 and of serum reverse T3
concentrations; subjects with no loss of thyroid functional capacity (iodine-
deficient, otherwise normal school children), the decrease of serum T4 was not
accompanied by an aggravation of hypothyroidism, as serum Tg and serum TSH
remained stable. In contrast, in subjects with a low thyroid functional capacity
(myxoedematous cretins),'lhZi &crease of serum T4 was accompanied by an
increase of serum TSH and a decrease of serum T3, clearly showing that an
aggravation of hypothyroidism occurred after selenium supplementation in the
absence of sufficient iodine supply, .'According to the results gotten from the
areas which are both iodine and selenium deficient, it is mandatory to correct
iodine deficiency before selenium supplementation; selenium deficiency should
be corrected thereafter too ( Vanderpas, 1993).
2 8
2.7 Iodine deficiency
Iodine deficiency is a condition in which an organism does not take in enough
iodine, an element that directly affects thyroid gland secretions, which
themselves to a great extent control heart action, nerve response to stimuli, rate
of body growth, and metabolism.
Simple goiter (enlargement of the thyroid gland) is the most common form
of iodine deficiency illness and is found particularly in mountainous regions and
areas far from salt water. Lowest incidence of this disease occurs along
seacoasts. When the supply of iodine is moderately deficient, the thyroid gland
works harder to synthesize hormones in normal quantities, but the affected
individual may continue in general good health despite possible presence of
goiter. In case of severe and prolonged deficiency, however, there may be a
deficit of thyroid hormones, resulting in myxedema, a condition characterized by
dry skin, loss of hair, puffy face, flabbiness and weakness of muscles, weight
increase, diminished vigour, and mental sluggishness (The New Encyclopedia
Britannica, 2003 and Mashid and Mason, 1993).
2.7.1 Prevention of iadlrie'd'efl'dieficy
This is most simply accomplished by eating seafood regularly or by use of
iodized table salt. To overcome natural iodine deficits, government health
officials i n Canada and otherllnat&ns have made dietary iodine additives
mandatory.
Sporadic goiter remains a mystery because it occurs in areas where
iodine intake is more than adequate. Foods such as cabbage and turnips
contain a potential dangerous progoitrin substance believed to inhibit normal
29
intake of iodine by body tissues. During the heat of cooking, however, the
offending enzyme usually is destroyed.
A lack of iodine during infancy may cause a condition known as cretinism,
in which mental and physical development is severely impaired. This condition
can be prevented if the mother maintains a diet of foods high in iodine during
pregnancy (The New Encyclopedia Britannica, 2003; Kavishe, 1993 and Hetzel
et a/., 1987).
2.7.2 Iodine value or iodine number
In analytical chemistry, measure of the degree of unsaturation of an oil, fat or
wax. Saturated oils, fats and waxes take up no iodine, therefore, their iodine
value is zero; but unsaturated oils, fats and waxes take up iodine, (unsaturated
compounds contain molecules with double or triple bonds, which are very
reactive toward iodine). The more iodine is attached, the higher is the iodine
values, and the more reactive less stable, softer and more susceptible to
oxidation and rancidification is the oil, fat, or wax. In performing the test, a
known excess of iodine, usually in the form of iodine monochloride, is allowed to
react with a known weight,~f,Jhe,oil, fat, or wax and then the amount of iodine
remaining unreacted is determined by titration (The New Encyclopedia
Britannica, 2003 and Sofra et a/., 1998).
Drying oils used in the paint and vanish industry have relatively high ,I
iodine values (about 190). Semi drying oils, such as soybean oil, have
intermediate iodine values (about 130). Non drying oils, such as olive oil, used
for soap making and in food products, have relatively low iodine values (about
80).
Iodized salt: Table salt with small amounts of iodine added, usually as
potassium iodide, to ensure against dietary deficiency of iodine. Where iodized
30
salt is used, particularly in Switzerland and the United States, endemic goiter has
disappeared.
In United States, iodized salt contains 1 part in 100,000 iodide and in
Switzerland, I part in 200,000. The World Health Organisation recommends 1
part in 100,000 (The New Encyclopedia Britannica, 2003).
2.7.3 Diagnosis and treatment of goitre
The enlargement of the human thyroid gland results into a prominent swelling at
the front of the neck. A normal human thyroid gland weighs 20-30 g (about 0.75
ounce), a goitrous gland as much as 1 kg (more than 2 pounds). A very large or
extensive goiter may produce sensations of choking and can cause difficulty in
breathing and swallowing.
2.7.4 Causes and types of goitre
One class of goiter arises as a result of any of a variety of defects in the thyroid
glands synthesis of thyroid hormone. The gland is unable to secrete sufficient
amounts of that hormone and grow inadequate secretion by producing more.
Other types of goiter occur When the thyroid gland has normally functioning
tissue but enlarges for reasons that have not been exclusively determmed.
Still other types of enlarged gland produces too much hormones
(hyperthyroidism), resulting in the ~onditjPns known as exophthalmic goiter, or
Grave's disease, and toxic multinodular goiter or Plummer's disease.
The most common type of goiter is called simple or endemic goiter and
results from an inadequate intake of iodine, which is one of the two raw materials
necessary to make thyroid hormone. When the body does not receive iodine in
sufficient quantities, the thyroid gland grows larger in an effort to produce an
3 1
adequate amount of hormone. Endemic goitre is five times more common
among women than men. It occurs most frequently in inland or mountainous
regions where the iodine content of drinking water and food is exceedingly low.
It is prevented by the use of iodized salt in one's diet. In the early stages of
endemic goiter, regression of the gland may be complete if iodine is ingested in
adequate amounts. The most effective treatment in more advanced cases is the
administration of thyroid hormone. Surgical removal of the thyroid gland may be
necessary if the gland has grown so large that it is obstructing breathing (Sofra
et a/., 1998).
2.8 Micronutrient malnutrition: a global problem
Chronic diet-related diseases are a public health problem throughout the world.
Despite concerted efforts to reduce poverty, improve nutrition education and
secure access to healthy foods. Blum (1997) reported that more than two billion
people are sick or disabled and million die prematurely each year as a result of
micronutritient deficiencies.
Blum (1997) further noted that the commonest micronutrient deficiencies
of Public health significance are Vitamin A deficiency, Iron deficiency and iodine
deficiency. For proper.fu~ctici'ninQ the body relies on interactions between wide
ranges of nutrients; thus the earlier statement should be considered in isolation.
Hence, food should be provided in adequate and balanced amounts. Even
marginal deficiencies may increape the'risk of poor health.
2.8.1 Vulnerable groups affected
Women of childbearing age, young children and the elderly are the groups most
susceptible to micronutrient deficiencies. In areas where the soil lacks iodine,
deficiencies of this mineral may strike the whole population (NutriView, 1997).
3 2
According to estimates by the World health Organisation (WHO), iodine
deficiency affects one thousand million people worldwide. It is the commonest
cause of preventable mental retardation: 25 million people are affected; 6 million
of them develop cretinism (NutriView, 1997).
Females are consistently more affected than males, because goiter
usually develops in periods when metabolic rate is high, such as during puberty
and pregnancy. It should be noted that not all goiter is simple goiter due to lack
of iodine. Another type of goiter, called Exophthalmic goiter (Grave's disease), is
due to over-activity of the thyroid gland, which is usually but not always,
enlarged.
2.9 Reasons for iodine deficiency
Iodine deficiency disorders (IDD) are endemic in areas where soils have been
depleted of iodine. In mountain regions soils have been leached by glacial
erosion, whereas in tropical areas leaching is due to continuous rainfall. Crops
grown in depleted soils lack iodine. As a result, humans and animals dependent
on these foods become iodine deficient. Only sea foods (fish, shellfish, and 4 T I . 7.'
seaweed) are naturally rich in iodine (NutriView, 1997). Intestinal disorders
parasitic infestation and nutrient interaction can impair iodine absorption and
utilization (NutriView, 1997).
Some vegetables and staple foods (cassava) contain glycosinolates,
which have been shown to interfere with the proper utilization of iodine, further
aggravating iodine deficiency disorders.
33
2.10 Health consequences of iodine deficiency
Iodine deficiency is the World's greatest single cause of preventable brain
damage and mental retardation. Severe iodine deficiency during pregnancy
inhibits fetal growth, increases the risk of stillbirth and impairs the mental
development of the unborn child, resulting in cretinism and permanent mental
retardation. Milder deficiency results in subtle but significant reductions in
cognitive development.
2.1 1 Solution to iodine deficiency disorder:
2.1 1.1 Choice of strategies
International organizations active in micronutrient projects (WHO, UNICEF,
IVACG, INACG) recommend four key strategies to eradicate micronutrient
malnutrition: nutrition education, dietary diversification, dietary supplementation
and food fortification (Nutriview, 1997).
2.11.2 Nutrition education
Food choices are often made on the basis of availability, price, personal
preferences, habits and cultural traditional taboos. A lack of knowledge about . .,, . , l . ..' .
nutrition, and its role In health and disease makes it difficult to introduce
changes. Nutrition education is therefore an essential part of any program.
Knowledge alone, however, is not enough to ensure people eat a balance diet.
They need to have a strong'' motivation to adapt. Activities directed at
encouraging new habits have been termed 'social marketing'. This uses
techniques employed in commercial selling (radio, TV, newspapers, advertising,
competitions, gimmicks, etc) adapted to an ideal rather than a product
(NutriView, 1997).
3 4
2.1 1.3 Dietary diversification
Dietary diversification is seen by many as the ultimate solution to malnutrition.
Eating a variety of nutritious foods is the natural way to obtain the nutrients
needed for health. Dietary diversification requires people to change their eating
habits. It may also involve the need to increase production, distribution and
consumption of micronutrient-rich crops and animal products. Its success is
limited by climatic conditions, the fact that certain foods may be culturally
unacceptable or too expensive, and the lack of effective communication and
motivation programmes (NutriView, 1997).
2.11.4 Dietary supplementation
Administration of supplements is an effective way to rapidly correct existing
deficiencies or avoid their development in high-risk populations. It requires close
contact between health-care workers and the target population, and is mainly
indicated as an emergency strategy because of complicated logistics and high
costs. Supplementation should be replaced by a suitable strategy, such as
dietary diversification or food fortification.
Dietary supplementation has been successfully implemented to reduce
suffering in iodine defickrif'women ki th iodized oil capsules (NutriView, 1997).
2.11.5 Food fortification
Addition of vitamins, mineralslland .trace elements to stable foods has been
practiced in numerous industrialized countries for many years with considerable
success. This method has long proven its value as an effective public health
measure to correct nutritional deficiencies in whole populations or specific
segment at risk. Food fortification does not require the active participation of the
customer. If a suitable food vehicle can be identified, traditional food
3 5
consumption patterns can be maintained; technology is available for a wide
variety of foods. Costs are negligible compared with the medical and public
health costs associated with malnutrition. In many cases, fortification costs can
be recovered by a small price increase at the retail level. Fiscal measures such
as sales tax reductions can be used as an incentive to promote fortification
(NutriView, 1997). The earliest example of fortification is the iodization of a table
salt in Switzerland since 1923 to prevent goiter and cretinism which was
widespread throughout the alpine region until then (NutriView 1997).
2.12 Hidden hunger
Micronutrient malnutrition is also called "hidden hunger", because people have
no innate appetite or hunger for these essential vitamins or minerals. It poses a
threat to 2 billion people across the globe and affects 1 billion of them, mostly,
but not exclusively in developing countries. Most people suffering from the
condition may get enough food to eat - the problem is shortages of important
vitamins and minerals in their food. Besides iodine, iron and vitamine A,
deficiencies of zinc, folic acid, the B vitamins and vitamin D also cause concern
(Roche, 1997).
Iodine deficiencjl L4Sb'ine'?.6 billion people in 95 countries are at risk of
iodine deficiency, especially those living in mountainous or flood-prone areas,
where the soil lacks iodine. Lack of iodine can permanently lower the IQ of
children by at least 10 points. Some.655 million people suffer goiter, a swelling
of thyroid gland in the neck caused by a lack of iodine. It is also the most
common cause of preventable mental retardation. Today, there are 43 million
cases of mental retardation and 6 million cases of cretinism (Roche, 1997).
2.13 Selecting the right vehicle
To select a suitable vehicle for fortification, certain criteria have to be met.
Above all, the food must be consumed regularly by the target population in
appropriate amounts; fortification should supply optimal amounts of the required
nutrients without changing the characteristics of the food or increasing its price
substantially. In this regard, instant noodles emerged as the ideal candidate, in
Asia (Asia, 1996).
Report shows that lnstant noodles were consumed by 15-49 year old
Thais of both sex and from all socio-economic levels. Nineteen ninety three,
annual per capita consumption was equivalent to 30 packs (Asia, 1996). lnstant
noodles have acceptable sensory characteristics and good shelf stability. Their
shelf life at room temperature is at least six months.
To combat the problem in endemic area, potassium iodated solution has
been added to the drinking water supplies of households, communities and
schools for many years. Since 1994 table salts have been fortified with 50ppm
of potassium iodated or potassium iodide (Nutrition Division, 1996).
2.13.1 Feasibility of triple fortification
In late 1994, the ministetial'committee agreed that a study should be undertaken
to test if triple fortification of instant noodles with iodine, iron and vitamin A is
feasible. The committee and the manufacturers of instant noodles agreed to
fortify the seasoning powder, because this need only little additional cooking
before consumption and it is well protected in a separate bag within the package.
The project is being conducted on a voluntary basis, and representatives from
the manufacturers are working jointly with the committee members (Chavasit
and Tontisirin, 1998).
3 7
For the feasibility study, data on the fortificants to be used, and the
sensory acceptability, cost and shelf stability of the fortified products were
evaluated. A premix (20 mg per package of instant noodle) containing
potassium iodide, encapsulated iron and vitamin A palmitate was used for
fortification. The fortification dosage were set at 50 pg for iodine, 5 mg for iron,
and 267 pg for vitamin A (Chavasit and Tontisirin, 1998).
Judged mainly by appearance, most of the fortified seasoning powders
have a shelf life of about three months. The incubated seasoning powders from
each period were later analyzed for micronutrient content at the Institute of
Nutrition. The results showed that the added micronutrients are stable under
accelerated incubation conditions. There were no significant differences in
sensory qualities between the original and the fortified products. Fortification has
only a minimal effect on the cost of the product.
2.14 Food fortification gains support in Africa
Several African countries have recently started staple food fortification or are at
an advanced stage of preparation. Others are considering fortification of sugar
(Lesotho, Madagascar, and Malawi) and/or maize flour (Kenya, Lesotho, Malawi,
Tanzania). In additiori,"aWvari& of fortified commercial products (lemonade
powder in Tanzania, Malted and instant chocolate beverages in Nigeria,
Complementary Foods for infants in several countries) are being sold (NutriView,
2001/1).
It is apparent that an increasing number of donors, national governments
and food manufacturers are committed to this strategy for reducing the health
burden due to malnutrition. A major challenge is to sustain activities, secure
more top-level commitment, and establish effective measures of legislation and
monitoring.
2.15 Priority for child nutrition needed
Proper nutrition throughout childhood is the foundation for healthy life as well as
for human development. Addressing the nutritional problems among Asian
children, both Professor Aree Valyasevi (President of the Congress of Peadiatric
Nutrition held in Chiang Mai, Thailand, on November 28 - December 1, 2000)
and Professor Keyou Ge (Director of the Institute of Nutrition and Food Hygiene
Chinese Academy of Preventive medicine) stressed the importance of
implementing the solutions urgently.
Due to inadequate food intake, poor nutrition knowledge and infections
there are still too many undernourished children in many Asian countries.
Under-nutrition during pregnancy leads to intrauterine growth retardation
(IUGR) and low birth weight (LBW) (NutriView, 200112).
NutriView, (200112) recommendations for intellectual development in Nigeria:
to access the effects of early nutrition on growth and intellectual
development, Ab~doye conducted a retrospective survey of 285, approximately
10 year old primary school children in Nsukka, Nigeria. Less than a third of the
pupils had normal weight for height or height for age. Current nutritional status
significantly affected sctiob14peffoiri7ance.
The main factors affecting later school performance were the level of
maternal education and occurrence of complications in pregnancy and childbirth.
There seemed to be no relationship betiveen performance and duration of breast
feeding, frequency of feeding during preschool years or anaemia (found clinically
in 39% of the pupils).
To improve nutritional status and academic performance status, Abidoye
(2000) recommends establishing a clear policy that includes compulsory free
education to secondary school level for girls, a ban on marriage before age 18,
promotion of exclusive breastfeeding up to 6 months of age, subsidized school
feeding and health programs.
A recent hypothesis also suggests that increased oxidative stress in
micronutrient deficient individuals precipitates genetic changes in viruses,
making them more virulent (King, Black and Doyle, 2001).
In the light of the multiple factors, constraints and deficiencies, multiple
approaches may be the only effective way to combat micronutrient deficiencies.
Among the other suggestions for the way forward in Africa made during the
International congress of Nutrition (NutriView, 200014):
Provide practical nutrition education including food preparation. People must understand the importance of eating micronutrient-rich foods. A major problem of local foods is their high content of absorption inhibitors. Methods to improve micronutrient availability, such as soaking should be taught and encouraged.
Promote multiple micronutrient supplementation and small-scale multiple micronutrient fortification. A multiple micronutrient approach through supplementation could be facilitated through government or regional efforts to support local manufacture.
2.16 Correcting iodine deficiency:
The occurrence of cretinisrh,"'chdracterized by physical and mental retardation,
increases significantly when the mother's daily intake of iodine falls below 20pg
(the normal daily intake for adults being 80-150pg). Simple public health
measures can be taken to prevent iodine deficiency and the birth of children
disable in this way (Hetzel and Orley, 1985).
Iodine deficiency also causes swelling of the thyroid gland, termed simple
goiter; compression in the neck may result but this is not a major public health
problem. Goiter, however, especially when it affects more than 50% of an adult
population, is a reliable indicator of sufficiently severe iodine deficiency to cause
frequent births of disabled children.
Maternal iodine deficiency is also associated with increased incidences of
other congenital abnormalities, stillbirth, abortion and low birth weight, which are
reduced by iodine supplementation. Past studies in Papua New Guinea and
Indonesia (Hetzel, 1983) have demonstrated a coordination defect in otherwise
normal children exposed to iodine deficiency in pregnancy; isolated deaf, mutism
and mental deficiency also occur, probably reflecting a less severe iodine
deficiency at a foetal stage. In china, partial correction of iodine deficiency
disorders has been reported in children with relatively mild handicaps (Ma et a/.,
1982).
Iodine deficiency probably also has some effect on the mental functioning
of older children and adults, because of a reduced level of circulating thyroxine.
In the foetus, on the other hand, a low level of circulating iodine seems more
likely to be the critical factors. In a small highland village in Bolivia where goiter
was very prevalent, a double-blind control study was conducted on the effect of a
single dose of oral iodized oil in 100 school children. Observations made 22
months after treatment revealed a reduction in goiter size and improved
intellectual performance, particularly in girls (Bautista et a/., 1982).
Iodine deficiency often occurs in isolated mountainous areas where the 4 . l ..'
iodine has been leached from the soil. Affected populations are usually poor and
politically weak, with little prospect of pressurizing governments into tackling the
problem; technical difficulties also hinder iodine supplementation. As outside
influences grow, foods containing iobine are introduced and deficiency is
reduced. In some parts of the world, action programmes have been mounted
involving either the addition of an iodide or an iodate to salt or other food
products, or the administration of iodine to individuals, typically by injecting
iodized oil, which can be effective for up to five years. Unfortunately, salt does
not always return added iodine, especially if it becomes damp. In many areas,
4 1
legal enforcement of the use of iodized salt, which may be marginally more
expensive than non-iodized salt, is necessary. Where a community obtains salt
from several sources, however, it is difficult to enforce or control iodization. The
injection of iodized oil may only be necessary for women of childbearing age,
although this is not always acceptable to other members of a population. The
treatment of a whole population in this way is about 20 times more expensive
than the use of iodized salt. However, the cost can be considerably reduced by
restricting the provision of iodized oil to those most in need. Syringes are a
major component in the expense of injection, and consequently work is
proceeding on the development of a cheap and stable oil formulation capable of
giving long lasting protection after oral administration. Iodine supplementation
for a woman must be given before pregnancy so that the developing fetus is
protected during the first trimester (Bautista etal., 1982).
2.17 Monitoring and evaluation
The most direct method of assessing success or failure in correcting iodine
deficiency is by determining urinary iodine as in the initial situation analysis. This
can in due course be supported by evidence of regression of goiter rates and the
prevention of cretinism." '"if'" labbratory services permit, determining blood
thyroxine in adults or neonatal thyroxine in cord blood samples will also indicate
whether iodine deficiency has been corrected.
Monitoring and evaluation are' essential for iodization programmes,
particularly because of the need to ensure quantitative correction of iodine
deficiency in order to reduce foetal damage and impaired mental function in
children. As already indicated there should be more use of prescriptive
measures for quantitative correction and hence prevention and control of IDD.
The availability of iodized oil with a follow-up of iodized salt makes elimination of
IDD a feasible goal (May eta/., 1997).
2.18.1 Assessing iodine deficiency disorders for public health programmes
In public health programmes carrying out iodine supplementation, the problem is
to assess a population or group living in an area or region that is suspected of
being iodine-deficient. The data required include the following (Stanbury and
Hetzel, 1980):
The total population including the number of children under 15 years of
age (in which the effects of iodine deficiency are so important);
The goiter rate, including the prevalences of palpable or visible goiter
classified according to accepted criteria;
The rates of cretinism and 'cretiniodism' in the population;
Urinary iodine excretion;
The level of iodine in the drinking water;
The level of serum thyroxine (T-4) in various age groups. Particular
attention is now focused on the levels in the neonate because of the
importance of the. X-4hl.evel.f~r early brain development.
2.18.2 Estimation of thyroid size
A slight modification of the system of Perez et a/. (1960) is recommended. I1
Stage 0 No goiter
Stage 1 a Goitre detectable
Stage 1 b Goitre is palpable and visible only, when the neck is fully
extended. This stage also includes nodular glands, even, if
not goitrous;
common even when all known environmental factors are controlled (United
Nations, 1993).
2.18.5 Urine Iodine excretion determination
The difficulties associated with the collection of 24 hour samples made Follis
(1963) originally suggest casual samples collection for determination of iodine
from a group of 30 subjects (Thrilly eta/., 1980). The iodine levels are expressed
mcglg of creatinin excretion and the range plotted out as a histogram. This
provides a reference point for the level of iodine excretion which is also a good
index of the level of iodine nutrition.
2.19 Sub- clinical IDD
Until the 1990s total goiter prevalence (TGP) was the recommended indicator for
assessing population iodine status. Today, however, urinary iodine (UI) and
goiter are the most common indicators of iodine status. UI is thus the preferred
indicator for monitoring and evaluating salt iodization programmers. The current
global and regional prevalence of iodine deficiency has been estimated based on
the most representative UI data available to WHO in June 2003 from surveys
carried out among school-age children between 1993 and 2003 iodine deficiency . , 4 1 . : . > .
is considered to be a public health problem in populations of school-age children
(6-12 years) where median U1 concentration is below 100 p11
(ICCIDDIUNICEFNVHO, 2001). The severity of iodine deficiency is assessed for
each country using criteria baskd on-median UI.
common even when all known environmental factors are controlled (United
Nations, 1993).
2.18.5 Urine Iodine excretion determination
The difficulties associated with the collection of 24 hour samples made Follis
(1963) originally suggest casual samples collection for determination of iodine
from a group of 30 subjects (Thrilly et a/., 1980). The iodine levels are expressed
mcglg of creatinin excretion and the range plotted out as a histogram. This
provides a reference point for the level of iodine excretion which is also a good
index of the level of iodine nutrition.
2.19 Sub- clinical IDD
Until the 1990s total goiter prevalence (TGP) was the recommended indicator for
assessing population iodine status. Today, however, urinary iodine (UI) and
goiter are the most common indicators of iodine status. UI is thus the preferred
indicator for monitoring and evaluating salt iodization programmers. The current
global and regional prevalence of iodine deficiency has been estimated based on
the most representative UI data available to WHO in June 2003 from surveys
carried out among school-age children between 1993 and 2003 iodine deficiency . ,' 4 .1 ,.' r
is considered to be a public health problem in populations of school-age children
(6-12 years) where median UI concentration is below 100 pl1
(ICCIDDIUNICEFNVHO, 2001). The severity of iodine deficiency is assessed for
each country using criteria based on me'aian Ul.
Table 2: Epidemiological Criteria for Assessing Iodine Nutrition Based on Medium Urinary Iodine Concentration in School-age Children
Median Urinary Iodine intake Iodine nutrition iodine (vg11)
Insufficient Severe Iodine deficiency
Insufficient Moderate Iodine deficiency
50-99 Insufficient Mild Iodine deficiency
100-299 Optimal Optimal
>= 300 Excessive Risk of adverse health consequences (iodine- induced hyperthyroidism, autoimmune thyroid disease)
Source: Adapted from WHOIUNICEFIICCIDD (2001)
2.19. I Three grades of severity
It has been suggested that there are three grades of severity of iodine deficiency
in a population that may be determined by urinary excretion (Querido et a/.,
1974). These are as follows:
Grade I: Goitre endemias with an average urinary iodine excretion of more than
50 mcglg of creatinine: At this level, a thyroid hormone supply adequate
for normal mental and physical development can be anticipated. This
group could be described as suffering from 'mild IDD'.
Grade 2: Goitre endemias with an average urinary iodine excretion of between
25 and 50 mcglg of creatinine: In these circumstances, adequate thyroid
hormone, formation may be impaired. This group is at risk of
hypothyroidism but not of overt cretinism (moderate IDD)'
Grade 3: Goitre endemias with an average urinary iodine excretion below 25
mcglg of creatinine: Endemic creatinism is a serious risk in such a
population (severe IDD).
2.1 9.2 Iodine in drinking water
The level of iodine in drinking water indicates the level of iodine in the soil which
in turn determines the ley,et.af ,i~dine in the crops and animals in the area. Iodine
levels of water in iodine-deficient areas are usually below 2 mcgllitre (2ppm)
(United Nations, 1993).
Severity of IDD Provide the Indication for an lodization Programme ,I
The gradation of severity of IDD provides the indications for an iodization
programme.
Mild IDD (Grade I): With urinary iodine (median) more than 50 mcglg of
creatinine, requires iodized salt (or possibly economic development alone) for
the correction and the prevention of goiter.
47
Moderate ID0 (Grade 2): With urinary iodine (median) in the range 25-
50 mcg/g creatinine, may be prevented by an effective iodized-salt programme;
often iodized oil may be necessary in addition to produce a quantitative
correction for the more severely iodine-deficient groups.
Severe ID0 (Grade 3): With urinary iodine (median) less than 25 mcglg
of cretinine, requires iodized oil for quantitative correction. Iodized salt might be
used as a follow-up measure if economic development permits; but if substitute
agriculture continues, administration of iodized oil needs to be continued (United
Nations, 1993).
2.20 Prevention and eradication of IDD require continual vigilance
It should be emphasized that prevention and eradication of IDD require continual
vigilance through regular feedback of epidemiological data including: estimates
of iodine content of salt; iodine content of urine in the vulnerable population
(especially school children who are readily accessible through school
attendance); goiter prevalence; and levels of T-4 including neonates if possible
(Hetzel, 1987).
2.20.1 Countries who sllc1c~sSfuIly eliminated iodine deficiency disorder
In the last 50 years, many countries in the America, Asia, Europe and Oceania
have successfully eliminated IDD, or made substantial progress in their control,
largely as a result of salt iodization kith potassium iodide or potassium iodate
and through dietary diversification. For example in Switzerland, where salt
iodization began in 1922, cretinism has been eliminated and goiter has
disappeared, while there has been negligible evidence of any adverse effects
from iodine intake.
48
Universal salt iodization (is defined as fortification of all salt for human and
animal consumption) has been endorsed in numerous international fora by
heads of state, senior government officials, and representatives of international
intergovernmental and non-governmental organizations. The most important of
these forums are the World health assembly, in resolutions WHA39.31 (1986)
and WHA 43.2 (1990), the World Summit for Children (UNICEF, 1990), the
Policy Conference on ending Hidden Hunger (Montreal, 1991) and the
International Conference on Nutrition (Rome, 1992). Nevertheless, WHO
continues to receive queries from national health authorities and others seeking
reassurance about the safety of providing iodized salt to non-deficient
population. As with all preventive public health measures, the decision to ensure
universal salt iodization will be made by weighing the potential risk of excess
intake for the few against the well-documented risk of mental and physiological
impairment for the many if a deficiency is uncorrected.
2.21 Adverse effects associated with high nutritional intakes of iodine
Since iodine, when ingested in large amounts, is easily excreted through the
kidneys into the urine, iodine intakes even at very high levels (milligram , ,, 4 R l . ..'
amounts) can be consumed safely. However, the following adverse effects,
though rare, have been reported:
Allergic reactions to iodine in food: skin rashes and acne have
occasionally been attributed to iodized salt. Such reports are extremely
rare, however, and thus these conditions are unlikely to occur following
salt iodization. For example, among 20,000 children in USA suffering
from allergy during the period 1935-1974, not a single case was reported
of allergic hypersensitivity to iodine in food. Following publication in
Annals of allergy of a request for notification of allergy to iodine, not a
49
single report was recorded between 1974 and 1980 (Stanbury and Hetzel,
1980)
High intakes of dietary iodine and thyroid diseases: Through adaptive
mechanisms, normal people exposed to excess iodine remain euthyroid
and free of goiter. In certain susceptible individuals, iodide goiter and
Hashimoto thyroiditis with hypothyroidism have been observed after
iodine intakes of 500-3000pglday. The prevalence of susceptible
individuals in different countries is not fully known. It has been suggested
that high nutritional intake of iodine substantiated by urinary iodine of
1000-10,00Opg/litre - as observed in one country in up to 2% of the
population - could have an adverse effect in susceptible individuals and in
patients with pre-existing abnormalities of the thyroid gland (Stanbury and
Hetzel, 1980). In this small proportion of the population, chronic excess
intake might contribute to the development of Hashimoto thyroiditis, iodide
and colloid goiter, and thyroid carcinoma. However, the incidence of
follicular thyroid cancer, a more severe form of cancer, is lower in iodine-
sufficient than in iodine-deficient areas. There is little indication that
iodine in the amounts noted influences the development of any of these
thyroid diseases. " ' "" '" ' '
In Japan, where dietary iodine-intakes are high, it has been shown that:
normal people who are not iodine-deficient can maintain normal thyroid
function states even at intakes of several milligrams of dietary iodine per
day;
the incidence of non-toxic diffuse goiter and toxic nodular goiter is
markedly decreased by high dietary iodine intake;
5 0
the incidence of Grave's disease and Hashimoto disease does not appear
to be affected by high intakes of dietary iodine.
However, high intakes of dietary iodine may induce hypothyroidism in auto-
immune thyroid diseases and may inhibit the effects of thionamide drugs (WHO,
1 994).
2.22 Physiological need for iodine
Based on studies of balance and excretion over 24 hour period, a safe daily
intake of iodine has been estimated to be between a minimum of 5019 and a
maximum of at least 10001g (WHO, 1991 and Stanbury and Hetzel, 1980). A
generally accepted desirable adult intake is 100-300pglday. At all intake levels,
a proportionate amount of iodine is excreted in the urine, which is the
biochemical basis for assessing iodine status (Dunn et a/., 1993).
2.22.1 Usual salt intakes
Average daily intakes vary from country to country. Usually, consumption levels
are within the 5-15gldayWlrange for children and adults. No increase in salt
consumption is called for. Rather, the recommended level of salt iodization
should be adjusted to provide approximately 150pg of iodine per day. Actually
consumed, taking into account usual climatic factors like heat and humidity,
which can affect retention of this element. The recommended quantities of
iodate to be added to salt under different conditions are provided in Table 3
(ICCIDDIUNICEFNVHO, 1993). Although potassium iodide was first used in salt
iodization, the use of iodate is now recommended since it is more stable than
iodide under varying climatic conditions. Because iodate, on ingestion is very
rapidly reduced to iodide, its use in iodinated salt is equivalent to iodide.
Table3: ICCID-UNICEF-WHO recommended levels of iodine in salt. Examples of desirable average levels at various points in the salt distribution chain, depending on climate, salt intake and conditions affecting packaging and distribution
Parts of iodine per million parts of salt, i.e micrograms per gram, milligrams per
kilograms or grams per tone
Climate and Requirement of Requirement of Requirement at retail Requirement at daily salt factory outside factory inside the sale (shoplmarket) household level
consumption the country country (glperson) Packaging
Bulk Retail Bulk Retail pack Bulk (sack) Retail (sack) pack (Sack) (<2kg) pack
(<2kg) (<2kg) Warm Moist %I 100 80 90 70 80 60 50 109 50 40 45 35 40 30 25
Warm dry or cool moist 34 90 70 80 60 70 50 45 109 45 35 40 30 35 25 22.5 Cool dry 59 80 60 70 50 60 45 40 1 og 40 30 35 25 30 22.5 20
Source: Adapted from World Summit for Children mid-decade goal: Iodine deficiency disorders (Geneva, 1994).
UNICEF-WHO Joint Committee on health Policy, document JCHPSSl9412.7 and
reference 5.
N.B: 168.6 mg of K103 contains 100mg of iodine . ,, 4 -1 . ,!'
N.B: These are indicative i n i t i a l h l s , which should be adjusted in the light of
urinary iodine measurement.
2.22.2 Other sources of iodine
Poultry and eggs from animals that consume fish flour as part of their feed
and iodoform in water that is used as a disinfectant.
- Cow's milk and dairy products from animals fed seaweed, producing an
iodine content
- Breed and baked goods through the iodates used as oxidants in dough
conditioners and cleaning agents for bakery equipment
The iodine-containing colouring agents added to some drugs including
many multivitamins, minerals, and antacids as a creating or colouring
agent), beverages, foods including some brands of dry cereal that contain
as much as 850 pg of iodine per 209 of product) and cosmetics.
2.22.3 Iodine availability
The iodine content of food actually consumed is not necessarily equivalent to
that of raw food since some iodine is lost during cooking. For example, losses of
about 20% occur in the iodine content of fish by frying or grilling and as much as
58% by boiling. Iodine consumed in food is generally well absorbed, with the
possible exception of people suffering from protein-energy malnutrition, which is
of particular concern in lhigh.:.prwalence, endemic goiter areas of developing
countries.
The uptake of radioactive iodine by an individual thyroid is dependent on
the amount of stable, i.e. non-radjoactive, iodine in the diet. This is the basis for
using radioactive iodine to evaluate thyroid function. Studies from Chernoby
following the nuclear reactor accident in 1986 indicate high thyroid cancer rates,
especially among young children. It is postulated that the thyroids of children in
this iodine-deficient area experienced an unusual uptake of radioactive iodine
released into the atmosphere following the accident. It has been estimated that,
53
in general, iodine prophylaxis, e.g. use of iodized salt, should reduce by two fold
to three fold the risk of thyroid irradiation resulting from a nuclear accident
(Rubery and Samles, 1990).
Daily iodine intakes of up to Img, i.e. IOOOpg, appear to be entirely safe.
lodization of salt at a level that assures an intake of 150-300pglday thus keeps
intakes well within a safe daily range for all populations, irrespective of their
iodine status. Daily consumption of log of salt containing 50 parts per million of
iodine would add a maximum of only 500pg of iodine. Thus the likelihood of
exceeding an iodine intake of Imglday from iodized salt is quite small.
In susceptible individuals - a minority of adults, usually over 45 years of
age, who may or may not have nodular goiters - transient side-effects have
been reported at usual intakes exceeding 500-3000pglday. The benefits to be
derived from universal salt iodization by the more than 1500 million people
estimated to be at risk or deficient, and the absence of significant adverse effects
among others in the same areas that are not iodine-deficient, far outweigh any
risk of excess intake for a small minority (Rubery and Samles, 1990).
2.22.4 Iodine requirements
90pg for children (2~8,yeim of'age)
120 pg for school children (7-12 years of age)
150 pg for adults (beyond 12 years of age)
200 pg for pregnant and lactqting Women (WHOINUT, 1996).
2.22.5 Required Iodine levels in Salt
Taking into account the following revised assumptions, which are based on new
information:
iodine lost from salt is 20% from production site to household,
another 20% is lost during cooking before consumption,
- average salt intake per capita is IOgIday,
In order to provide 150 pglday of iodine concentration in salt at the point
of production should be within the range of 20-40mg of iodine (or 34-66mg
potassium iodate) per kg of salt, when all salt used in processed food is iodized,
the lower limit (20mg) is recommended. Under these circumstances, median
urinary iodine levels will vary from 100-200 pgll (WHOINUT, 1996).
2.22.6 Quality of available Salt
(WHOINUT, 1996) reported that in many situations in developing countries,
however, despite improvements in salt production and marketing technology, the
quality of available salt is poor, or salt that has been correctly iodized
deteriorates due to excessive or long term exposure to moisture, light, heat and
contaminants. Under these circumstances, iodine losses can be 50% or more
from the moment salt is produced until it is actually consumed, and median
urinary iodine levels could thus fall below the recommended range (100-200
pgll). In addition, salt consumption is sometimes considerably less than
10glpersonlday. All these factors should be taken carefully into account,
particularly when establi~h7rig"the initial level of iodine in salt.
2.22.7 Trace elements are those elements of the periodic table that occur in the
body in pglg amounts or less. They may be essential (i.e. indispensable for
growth and health), or they may be non-essential, fortuitous reminders of our
geochemical origins or indicators of environmental exposure. All that trace
elements are potentially toxic when intake is excessive. Trace elements known
to be essential to humans are chromium, cobalt, copper, iodine, iron,
molybdenum, selenium, zinc and possibly boron.
5 5
An element is considered nutritionally essential if an organism can neither
grow nor complete its life cycle in the absence of the element (Nielson, 1991).
An element is nutritionally essential if a dietary deficiency consistently
results in a suboptimal biological function that is preventable or reversible by
physiological amounts of the element. In this definition, physiological is
construed as those quantities usually found in biological material.
2.23 Biological roles of trace elements
Trace elements have four known roles in living organisms.
1. In close association with enzymes, some trace elements are an integral
part of the catalytic centers at which the reactions of biological chemistry
occur. Working in concert with a protein, and frequently with other
organic coenzymes, the trace element attracts substrate molecules that
facilitate their conversion to a specific end product.
2. Some trace elements donate or accept electrons in reactions of reduction
or oxidation. These redox reactions are of primary importance in the
generation and utilization of metabolic energy through the "burning" of
foods in cells. Chemical transformations of molecules frequently involve
redox reactions:' '.' '" '
3. Some race elements (especially iron), bind, transport and release oxygen
in the body
4. Some trace elements ,,have:structural roles, i.e imparting stability and
three-dimensional structure to important biological molecules (Nielson,
1991).
Table 4.0: Iodine -trace elements for human nutrition
Trace Adult Recommended Daily Essential Biological function element human daily intake sources status for
body human content
Iodine I lgm 150 IJS @ Iodized salt, Essential Component of thyroid sea food, food from high-iodine soils
hormones, thyroxine (T4) and triiodothyronine (T3)
(a) Recommended dietary allowance established by the National Academy of Sciences (Nielson, 1991).
The most common manifestation of iodine deficiency is goiter, or
enlargement of the thyroid gland. With severe and prolonged iodine deficiency
hypothyroidism, or myxedema, occurs. Myxedema is characterized by reduced
metabolic rate and the accumulation of a jellylike substance, mucin, in the body;
these in turn, cause a great number of their characteristic abnormalities. A
deficiency of iodine during pregnancy, infancy or early childhood may result in
cretinism. Cretinism is characterized by mental retardation, retarded growth,
deafness, deaf mutism, delayed psychomotor development, and various
neurological abnormalities.
Excessive intake of iodine may cause hyperthyroidism (thyrotoxicosis).
The symptoms are hyperthyroidism, goiter, bulging eyes, rapid heart beating,
fatigue, weakness, increased appetite and weight loss. Iodine intakes of 2000
pglday have been suggested as being excessive.
Both iodine deficiency and toxicity are practical nutritional concerns.
However, iodine deficiency seldom occurs in the United States because of the
use of iodine-containing compounds in the dietary and baking industries salt.
iodine deficiency continues to be a significant problem in some mountainous,
third world countries found in the Andes Chain, parts of Africa, and south-east
and central Asia. G'oit&''occurs as a consequence of large intakes of dietary
iodine in Japan and other Oriental countries were seaweed containing high
mounts of iodine is commonly eaten.
Urinary iodine excretion is.'the most appropriate outcome indicator for
iodine (Pardede, 1998). Iodine deficiency is the leading cause of mental
impairment and has serious effects on the physical development of children, on
young child mortality and on the reproductive performance of women as
indicated by increased rates of abortion, stillbirth and congenital abnormalities,
(Hetzel, 1983). The most notable clinical sign of iodine deficiency is goiter.
5 8
Iodine deficiency, which is the primary cause of preventable mental
retardation in children, remains a major global public heath problem. There has
been widespread mobilization in the international community over the last
decade in support of eliminating iodine deficiency disorders (IDD). Most
countries where IDD is a public health problem have taken measures to control
iodine deficiency mainly through universal salt iodization programmes.
In May 2002, the United Nations General assembly in its special session
on children endorsed the goal of IDD elimination by 2003. The World Health
Organisation (WHO) continually updates its Global Database on IDD as part of
its mandate to track progress made by countries in meeting this goal, to follow
trends and to monitor the sustainability of implemented salt iodisation
programmes. Updated global estimates of iodine deficiency were recently
released (De Benoist, Anderson, Egli and Takkouche, 2003).
CHAPTER THREE
3.0 MATERIALS AND METHODS
3.1 Study Area
The study was carried out in Obukpa in Nsukka Local Government Area of
Enugu State, which is a town of Northern lgbo culture area. Seven towns helm
Obukpa in. In the south are Nsukka and Ero-Uno; in the east are Orba and
Ovoko; in the north are Iheakpu-Awka and Ibagwa-Aka; and flanked in the west
by Ibagwa-Ani and the small settlement Okpaligo (Ugwu, 1987). Obukpa was
selected because it is a typical rural community and one of the catchment
communities to the University of Nigeria Teaching Hospital (UNTH). Not much in
terms of research has been documented about it.
Obukpa community is divided into three quarters, namely: Ajuona, Owerre
and Obige. Each quarter is made up of sub-quarters which have several
kindreds (Ugwu, 1987). There are at least seven community primary schools:
sited at Ihe, Owerre, Ajuona, Amagu Umuora, Ime-Okpe, Ugbagu and Central
School Obukpa at Eluagu. There is one community secondary school at
Ochikum. ., ,, . 9 .r, ,:' , . ..:,a '
As in most rural communities, there is no pipe borne water except the
borehole sited at Eluagu. Almost all of the villages are electrified. In each set up,
women and children fetched water from the borehole or University borehole or , I
from local stream and/or harvested rainwater. There is a UNTH Comprehensive
Health Centre at Umuekwu. Obukpa holds two small markets at "Nkwo" and
"Eke" (native market days) every four days. The inhabitants are mostly farmers
and traders on food items.
The community has two main seasons namely: dry (November to March)
and wet (April to October). Petty farming is practiced in the wet season. The
60
main staple includes cassava (Manihot esculenta), maize (Zea mays), cocoa
yam (Colocasia spp), pigeon pea (Cajanus cajan), and sweet potatoes (Ipomoea
batatas). Obukpa has a population of 210, 1800 (FOS, 1992).
3.1.1 Study population
The subjects consist of primary school children aged 6-12 years. The ages of
the children were derived from the school registers or available information
possible to ascertain their ages.
3.1.2 Approach to the local community
The names and population. of all the schools in the community were collected
from the Local Primary Education Board at Nsukka town. A letter of introduction
and approval from the Chief of the Obukpa community was presented to the
headmaster of each school. Mothers were addressed at their monthly meetings
and their consent and cooperation were solicited.
3.1.3 Design and sampling procedure
The study was longitudinal lasting from March 2004 to February 2005. Three out . " 1 . ..'
of the seven primary schools in fhe community were randomly selected for study.
3.1.3.1 Sample size calculation
The sample size was calculated using the formula:
Where N = total number of children required
p = proportion of the subjects assumed to have subnormal iodine urine
excretion and nutritional status.
6 1
p = 28%
IlTA (2004) reported that 27.5% of the children suffered various degrees of
iodine deficiency
W = required precision level or probability level for the study
W = 0.05(5%)
In order to make up for drop outs, this figure approximated to 330. The
sub-sample for determining casual urinary iodine excretion, stool biochemistry
and anthropometric measures were obtained using 10% of the total sample as
follows:
3.1.3.2 Sampling Procedure: The sampling frame comprised all school
children from class one to five.
The source of sample frame was obtained from the school register.
This was done by stratified systematic random sampling and simple random
sampling. The three schools constituted the three strata. The total sample size
was three hundred and thirty children.
The procedure for systematic random sampling is given below:
The population sampled was obtained from the school registers; the count of
units was known i.e. 330. The total number of the units in the sampling frame
(N) i.e. (children population) was, divided by the required number of units in the
sample (n) to obtain the sampling interval (K)
K=N/n
The first unit from the population was selected randomly using some method of
simple random selection. The rest of the units were chosen systematically by
selecting every Kth unit on the list.
3.2 Training of personnel
Two research assistants from the community were trained on carrying out the
interview schedule, and filing of questionnaire plus collection of urine, stool
samples and taking anthropometric measurements. The researcher tested the
salt samples using the test kit and supervision of the work.
3.3 Data Collection: - Methods
Basic data by questionnaire
A validated and pretested questionnaire were used to gather basic information
from the mothers on social demographic characteristics of the household, health
facilities, health records and practices, morbidity and health status, IDD and
health status, food intake, 24-hour dietary recall and KAP of mothers on iodized
salt ADD. The questionnaire will be filled with the assistance of field workers.
3.3 Clinical examination
Each pupil in the sub-sample was clinically examined in detail for iodine
deficiency disorders. To avoid bias, the visible goiter (Grade II) was used for
estimating the level of 10d; 'shce the contour of the neck, and the fat pad of the
neck especially girls, might give a false impression of Grade I thyroid swelling.
3.4 Anthropometric measur;ements
General initial anthropometric measurements were made on all the units in the
sample size to determine their nutritional status. The measurements were
carried out every month on a sub-sample of ten percent of the sample size for a
year to determine growth velocity (rate). Anthropometric measurements
included height and weight
3.4.1 Height: The heights of the subjects were measured without shoes and
stockings with microtoise anthropometer. In measuring the height, the subjects
were made to stand on a horizontal platform with feet parallel to each other. The
back and knee were made straight. The subjects stretched upwards to the fullest
extent by applying a gentle traction by holding the subject's head at each side
over the mastoid process (just behind the ear). Then the head piece lowered by
a second person and the reading taken to the nearest centimeter and recorded.
The subject's heels matched to make sure that they did not leave the ground
while the traction was being applied (WHO, 1986; Lohman et a/., 1988).
3.4.2 Weight: weight of children would be obtained on a scale (C.M.S.
Weighing Equipment Ltd), with a capacity of 100kg and accuracy of 59. The
children would be weighed wearing only shorts or minimum clothing. All
measurements would be made according to standardized procedure (Lohman et
a/., 1988).
3.4.3 Growth monitoring and velocity measurement: longitudinal monthly
monitoring of weight ahB h"eGht for one year by anthropometric measurements
would assess growth. Changes in weight (kg) and height (cm) during the one-
year period would represent the weight and height velocities per year or the
annual growth rate for each child. Mean monthly and quarterly velocities were
calculated.
3.5 Urine: Samples of urine were collected from the pupils in sterilized clean
containers marked, numbered and distributed to the children on the day of
collection. The samples transported in an ice pack to the laboratory and were
64
analysed immediately, with the help of a biochemist, using "method H", as
recommended by IDD Newsletter ( I 998).
3.5.1 Urinary iodine excretion
Casual urine samples were collected from the subject (the school children) to
determine the urinary iodine excretion using "method H". The currently
recommended technique is "method H" (IDD Newsletter, 1998). Small samples
of urine (250-500 microlitres) were digested with ammonium per sulfate at 90-
1 looF degrees; arsenious acid and uric ammonium sulfate were then added. The
decrease in yellow colour over a fixed time period was measured by a
spectrophotometer and plotted against a curve constructed from standards with
known amounts of iodine, ran in the same assay. This method required a heating
block and a spectrophotometer, and plotted against a curve constructed from
standards with known amounts of iodine, ran in the same assay.
Frequency distribution curves are necessary for full interpretation,
because urinary iodine values from population are usually not normally
distributed; therefore, the median value should be used rather than the mean. An
indicator for iodine deficiency elimination was a median iodine concentration of 4 * I ..'
100 microgrammes iodhe per litre, that was, 50% of the samples should be
above 100microgrammes iodine per litre. Urine and not more than 20% of
samples should be below 50 microgrammes per litre. The urinary iodine
concentration was currently the most practical biochemical marker for iodine
nutrition. It assessed iodine nutrition only at the time of measurement, whereas
thyroid size reflected iodine nutrition over months or years. Therefore,
populations may have attained iodine sufficiency by median urinary iodine
concentration, yet goiter may persist in children.
65
3.6 Parasitic load
3.6.1 Stool: Containers were marked, numbered and distributed to children a
day to the day of collection. Instruction on how to collect a small sample the
following morning was given to the children. Collection was done in batches of
eleven samples per day. The samples were transported in an ice pack to the
laboratory and analyzed immediately by a pathologist.
3.6.1 .I Qualitative direct wet smear technique
The method was used to detect protozoa e.g. flagellates, Entamoeba and their
cyst.
Method
About 29 of stool was taken and emulsified in 5mls of normal saline.
About 2 loopful of the emulsified stool were taken unto a slide.
Then slide was covered with the cover slip.
And viewed with XI 0 Objective and confirmed with x40 and for details.
3.8 Salt monitoring (spot-test kit): The iodine content of the salt sample
collected from the pupils"was'"estimated with the spot-test kit from UNICEF,
Enugu.
3.9 Data analysis: Statistical pack&e for the social sciences (SPSS) was
used.
3.9.1 Questionnaire
Data on questionnaires were analyzed using frequencies, percentages, and
correlation of information gathered on KAP.
Data for the iodine deficiency information statements formulated to elicit the
attitudes of the respondents were all given above-average mean ratings (> 3.00)
on a 5-point Likert type scale. The five points on the Likert type scale were
weighed in order of degree of agreement: Strongly agree (SA) = 5; Agree (A) =
4; Undecided (UD) = 3; Disagree (D) = 2 and Strongly Disagree (SD) = 1. The
overall level of agreement with the eight iodized salt and iodine deficiency
statements was determined by dividing the grand mean score by eight .
3.9.1.1 Data on anthropometric assessment was analyzed under stunting, wasting and underweight
Stunting = Height -for-age at <-2 standard deviations (SD) of the mean value of
NCHSNVHO Standard. Severe stunting is defined as <-3 SD.
Wasting = Weight-for-height at <-2 standard deviations (SD) of the mean value
of NCHSNVHO standard. Severe wasting was defined as <-3 SD.
Underweight = Weight-for-age at <-2 standard deviations (SD) of the Mean
value of NCHSNVHO standard.
3.9.2 Worm load analysis
Mean and correlation analysis. were used to correlate variables, such as:
Worm load and Iodine in urine
Worm load and stunting
Worm load and underweight , I . ..
Worm load and wasting
Iodine in urine and stunting
Iodine in urine and underweight
Iodine in urine and wasting
CHAPTER FOUR
Result
Table 4.1 Background of the subjects
Parameter No %
School Community primary 112 37.3 School (C.P.S.) Ajuona
Community primary 101 School (C.P.S.) Owerre Obukpa
Community primary 87 29.0 School (C.P.S.) Amagul Umuorua Total 272 100.0 Sex Male 154 51.3 Female 146 48.7 Total 272 100.0 Age group 6-7 years I I months 68 22.7 8-9 years I I months 98 32.6 10-1 1 years I I months 90 30.0 12-1 2 years I I months 44 14.7 Total 272 100.0
4.1 General characteristics of the subjects
Table 4.1 showed that 37.3% were from community primary school (C.P.S)
Ajuona; 33.7% from community primary school (C.P.S) Owerre-Obukpa and
29.0% from community primary school (C.P.S) AmaguIUmuorua. In age group,
32.6% were within 8-9 years I lmonths, 22.7% were within 6-7years I Imonths
and 14.7% were within 12-12years I Imonths. Of this number, 51.3% were boys
and 48.7% were girls.
Table 4.2: Socio - demographic characteristics of respondents' household (parents).
Parameter No Percent Headship of household Male Female Total Gender of respondents Male Female Total Family size 1-5 6-1 0 17-15 Total Religion Christian Muslim Traditionalist Total Marital status Married Single Divorced Separated Widow Total Community or kindred Ajuona Owerre Obukpa Amagu/Umuoru . ,* ...
70
4.2 Socio- demographic characteristics of the household of the subjects
Most subjects (64.0%) said they were not heads of their household while
(36.0%) were heads (Table 4.2). The total respondents were female, two
hundred and seventy two in number.
Most households (61.8%) had 6 to 10 members, while (31.3%) had 1 to 5
members. Almost ninety percent (89.7%) were Christians, while (10.3%) were
traditionalists.
The marital status of the respondents showed that most of them were
married (76.9%) while a few (14.0%) were widowed.
The respondents from Owerre-obukpa and Amagu/Umuoru were slightly
more in number (33.8%) than respondents from Ajuona (32.4%) (Table 4.2).
Table 4.3: Educational attainment and occupation of respondents and household heads
Respondents Household heads
Parameter No % No %
Education None
Primary school Uncompleted
lo school Completed
2' school Uncompleted
2' school Completed
Post 2' school
University
Total Occupation Trading
Farming
Skilled work
Unskilled work
Civil servant
Full timelhome- Makers
Total 272 99.9 272 99.9
72
4.3: Socio- economic characteristics
Most of the mothers and the household heads had little or no formal education
(41.2% and 35.0%) respectively. About nineteen percent (1 9.1 %) of respondents
and (23.9%) of household heads completed primary school. Those who were
unable to complete primary schools were 15.4% and 17.6% respectively. A few
had secondary school, post secondary schools, and university education: 11.4%
and 9.6%, 6.6% and 5.9% 4.4% and 7.4% respectively, (Table 4.3).
Petty trading was the major occupation of the respondents (46.3%), while
farming was the major occupation of the family heads (32.75). Twenty-nine
percent of respondents engaged in farm work and a few in teaching (5.9%) and
civil service (5.1%). A few family heads (24.6%) engaged in trading, civil service
(23.5%) and (15.1%) in skilled work (Table 4.3).
Table 4.4: Sources of income, amount and expenditure on food
Expenditure (N) No % 500-3,500 73 26.8 3,501 -6,5000 108 39.7 6,501-9,500 40 14.7 9,501-1 2,500 29 10.7 12,501-13,000 22 8.1 Total 272 100.0 Contributions from relatives per month
Response No % Yes 7 3 26.8 No 199 73.2 Total 272 100.0 Amount per month No % N 500 - 1,500 31 42.47 PC 1,501 - 2,500 28 38.36 N 2,501 - 3,500 4 5.48 Above N 3,501 10 13.70 Total 272 100.0 Sources of Income Parameter No % Salary 52 19.1
Sales from farm proceeds 130 47.8 Trading 84 30.9 Others specify 6 2.2 Total 272 100.00
One pound sterling = N240 at time of sunley One dollar = N133.5 at time of study
4.4 Contribution for the upkeep of household
Above fourty percent (39.7%) of families spent from 443,501 to 446,500 on food
per month followed by (26.8%) who spent 44 500 - 3,500 on food per month.
About (33.5%) spent between 81 6,501 to 81 13,000 on food per month as shown
in Table 4.4.
Data from Table 4.4 revealed that most families (73.2%) did not receive
financial assistance for the upkeep of their household from other relatives, while
(26.8%) did. About (43.0%) of those who received financial assistance got
between 44500 - 44 1,500 per month. Then followed by (38.36%) of families
received 441,501- 442,500 and about fourteen percent (13.7%) received above 44
3,501; while five percent (5.48%) received 442,501 - 3,500 monthly. In Obukpa
community most households (47.8%) depended on sales of farm produce as
source of income, while 30.9% obtained their income from trading, (Table 4.4).
Table 4.5: Health facilities and health practices in the three communities Number of available health facilities No %
Health centreslhospitals
None One Two Three Source of drinking water
Public tap Borehole RiverslSpring Tankers Rain water Other specify (combination of sources) Water Treatment None Filtering Bo~ling Boiling and filtering Addition of Milton Addition of alum Washing of pots Once a week Twice a week Thrice a week Daily Once a month Once a while Toilet Facilities Bucket Pit Bush Water closet Times mothers ensure hand washing by children After toileting After back from school. Before eating After play All of the above No time . , I . * I . r t ' +
After toilet and before eating No. of woman with goiter Yes No Treatment received by goiter patients Operation Iodine salt , I
Oil iodine injection Nothing Herbal Last time children were de-wormed 1-3 months ago 4-6 months ago A year ago 1 -2years Never Total 272 100.1
Table 4.6: Goiter History
No %
Women with goiter
Yes 28 10.3
No
Total
Treatment received by goiter
patients
Operation
Iodine salt
Oil iodine injection
Nothing
Herbal
Total 28 100.0
4.5 Health facilities and health practices
Modern health centers/hospitals were sited at least one (85.3%) in Obukpa
community to meet with the health needs of the people (Table 4.5).
There were combined sources (82.0%) of drinking water for the people of
Obukpa: rain water during rainy season, borehole, tankers and spring water
during dry seasons. Drinking water were rarely treated (72.4%), while 14.3%
filter their drinking water (5.5%) boiled, (5.5%) boiled and filtered and (2.2%)
added alum to water (Table 4.5). With regards to cleaning water pots 28.3% did
so once a while, 23.9% twice a week, 19.1% thrice a week, 18.8% once a week,
9.6% daily and 0.4% once a month.
Precisely 57.7% of the surveyed households had pit toilet and 37.9%
defecate in the bush (Table 4.3, while 4.4% had water closet.
Sixty point seven percent of mothers ensured hand-washing before
meals (Table 4.5) 14.3% did ensure hand-washing after toileting and before
eating, while 6.3% did not bother. Table 4.5 showed that most children (49.3%)
were last de-wormed 4-6months ago. Eleven percent of mothers reported they
never de-wormed their children.
Ten percent (10.3%) of respondents had history of goiter. Subsequently
67.9% of goiter patients did not treat their goiter while 25.0% had the goiter
operated upon and 7.1% hw'he'rbal treatment (Table 4.6).
Table 4.7: Morbidity and health history of children
Parameters No Oh
Common ailments
FeverJmalaria 125 46 Diarrhea 48 17.6 Nothing 19 7.0 Measles 27 9.9 Coughkatarrh 33 12.1 Hepatitis 2 0.7 Typhoid fever 5 1.8 Worm 13 4.8 Total 272 99.9 Reasons for hospitalization Malaria 86 31.6 Diarrhea 37 13.6 Cough 23 8.5 Measles 23 8.5 Hepatitis - - Typhoid fever 4 1.5 No hospitalization 99 36.4 Total 272 100.1
4.6 Morbidity and health history of children
The commonest ailments reported by the mothers included malarialfever
(46.0%), diarrhea (17.6%), coughlcatarrh (12.1%), measles (9.9%) (Table 4.7).
Ailments that led to the hospitalization of children were malaria /fever
(31.6%), diarrhea (13.6%), measles (8.5%) and cough (8.5%) as shown in
(Table 4.7).
Table 4.8: Possible symptoms of iodine deficiency as reported by mothers
Parameter No YO Deafnesslhard hearing Yes 6 2.5 No 266 97.8 Muteness Yes No 272 100% Slow to understanding Yes 10 3.7 No 262 96.3 Poor performance at school Yes 7 0 25.7 No 202 74.3 Abnormally short Yes No 272 100 Goiter swelling Yes No 272 100 Abnormal behavior Yes 3 1.1 No 269 98.9 Congenital abnormalities ,
Yes 2 0.7 No 270 99.3 Squint Yes 2 0.7
Table 4.9: Source of food and meal pattern of respondents
Sources No YO Mostly home produced 57 21 .O Partly home produced and Partly purchase
, ,, .nl 3.' r
21 5 79.0 Mostly purchased Meals children eat in the day Break fast only 17 6.3 Lunch only 17 6.3 Super only 15 5.5 Breakfast, lunch and super 125 46.0 Bread fast and lunch 16 5.9 Breakfast and supper 37 13.6 Breakfast, lunch, supper and occasional 4 5 16.5 snacks 24hr Dietary recall Carbohydrate 147 54 Protein 79 29 Oil and fats 5 1.8 Fruits and vegetables 41 15.1
4.7 Symptoms associated with iodine deficiency disease
Table 4.8 showed that mothers observed the following symptoms of iodine
deficiency in their children: deafnesslhard hearing (2.5%), slow in understanding
(3.7%), poor performance at school (25.7%), abnormal behavior (1.1%),
congenital abnormalities (0.7%), and squint (0.7%) (Table 4.8).
4.8 Household food security
Table 4.9 showed that (79.0%) of the household foods were partly home
produced and partly purchased, while (21.0%) mostly produced their foods at
home.
The meals children eat in a day about (46.0%) ate breakfast/lunch/supper,
16.5% ate breakfast/lunch/supper and occasional snacks; and (13.6%) had
breakfast and supper only. About (5.9%) had breakfast only or lunch only, while
5.5% had supper only (Table 4.9).
Table 4.10: Knowledge of iodized salt and iodine deficiency diseases (IDD) by respondents
Had knowledge Had no knowledge
Variable No 1 Knowledge of iodized salt 36 2 Causes of goiter 25 3 Iodine deficiency causes goiter 26 4 Other consequences of iodine deficiency 6 5 Iodized salt in container with tight lid is 10
better preserved 6 Iodine in salt may evaporate when 26
exposed for a long period under the sun 7 High temperature causes loss of iodine 28
from iodized salt 8 Knowledge of the banning of non-iodized 22
salt
Table 4.1 1 Lack of knowledge of iodized salt and ID0 by different communities used in the study
Variable Ajuona Owerre- Amagul Total p-value (No) Obukpa Umuorua (No)
(No) (No)
Had knowledge of iodised salt 55 80 69 204 17.281NS P>0.05
Causes of goiter 58 86
The awareness that iodine deficiency 57 81 causes goiter
Other consequences of iodine deficiency .,+ 63 .. ,, 4 m l , 7 1
Iodized salt in container with tight lid is 62 69 better preserved
Iodine in salt may evaporate when 42 64 exposed for a long period under the sun ,,
High temperature causes loss of iodine 65 89 from iodised salt
The awareness of the banning of non- 81 77 iodized salt
d.f.= 4 NS=Not significant
4.9 Respondents' knowledge of Iodized salt and iodine deficiency disorders (IDD)
Entries in Table 4.10 revealed that majority (86.8%) did not have the knowledge
of what iodized salt was, while (13.2%) had knowledge of it.
The table also showed that 90.8% of the respondents had no knowledge of what
caused goiter, while 9.2% knew the cause.
The knowledge that goitre was due to iodine deficiency was shown by
9.6% of the respondents, while 90.4% did not have the knowledge that goitre
was due to iodine deficiency. More respondents (97.8%) were not aware of other
consequences of iodine deficiencies, while 2.2% were aware. On better
preservation of iodized salt in container with lid, only 3.7% of the respondents
knew about it while 96.2% did not.
Majority (90.4%) of the respondents had no knowledge that exposure of
salt under the heat of the sun for a long period cause evaporation of the iodine,
while 9.6% had this knowledge. Majority of the respondents (89.7%) did not
know that high temperature caused loss of iodine from iodized salt, while 10.3%
knew about it. Awareness of the banning of non-iodized salt was another point
raised but majority (91.9%) of the respondents were not aware of the banning
order by the Federal Government of Nigeria of non-iodized salt as indicated in
Table 4.1 0.
In the relationship of the mothers' lack of knowledge of the iodized salt . , 1 . . > '
and IDD to their different communities, majority of the mothers who lacked
knowledge were from Amagu/Umuorua community followed by Owerre-Obukpa.
Using Chi-square analysis in Table 4.1 1 showed that there were no significant
differences in the relationships between the variables of knowledge on iodized
salt and IDD and the three communities of the mothers at (p>0.05).
Table 4.12: The mean ratings of the attitude of the women to iodized salt and iodine deficiency
Iodized Salt and Iodine Deficiency Mean Standard Rating Information Statement Importance in creating IDD awareness I could be a source of creating awareness Should encourage iodized salt productionlmarketing Prevent iodine vaporising from iodised salt Iodine deficiency causes goiter in patients Waterlmoisture should not come in contact with iodized salt Avoids goitre patients
Ratings 3.86 3.64
3.63
3.53
3.48
3.32
3.00
Deviation k0.97 k0.96
k0.91
k0.82
k0.82
k0.995
kl.178
Position 1 2nd
3rd
4'h
5'
6'"
7'h Favours banning of non-iodized salt 1.74 k0.93 8th
Grand mean score = 26.2
Level of agreement with iodized salt and iodine deficiency information statements = 3.28
On a 5-point Likert scale
4.10 The result of the mean ratings and standard deviation distribution of the attitude of the women to iodized salt and iodine deficiency
Attitude to iodized salt and iodine deficiency
Data in Table 4.12 showed that statement no.1 "importance in
creating IDD awareness", received the highest mean rating of 3.86 * 0.97. The
statement no. 2 "1 could be a source of creating awareness" had a mean rating of
3.64 k 0.96. The statement no. 4 "should I encourage iodized salt
productionlmarketing" took the 3rd rating position with a mean of 3.63 * 0.91.
Statement no. 5 "Do not allow iodine vaporizes from iodized salt" had 41h position
with mean rating 3.53 k 0.82. No. 3 statement "iodine deficiency causes goitre in
patients" took the 5th position with mean rating 3.48 k 0.82. "Waterlmoisture
should not come in contact with iodized salt" is the No.6 statement with 61h
position having mean rating 3.32 k 0.995. Statement no. 8 "Avoids goitre
patients" took the penultimate position 71h with mean rating 3.00 k 1.178 and the
81h position with mean rating 1.74 k 0.93 is the statement "favours banning of
non-iodized salt".
Table 4.13: Practices based on knowledge on iodized salt and iodine deficiency disorders by mothers
Practice based on No Practice Iodized salt and iodine deficiency knowledge
disorder indices No % No YO Creating IDD awareness 34 12.5 238 87.5
Recommending iodized salt to goitre 36 13.2 236 86.76 patients
Iodized salt container covered 37 13.6 235 86.4
Table 4.14: Comparing the practices based on knowledge on iodized salt and iodine deficiency disorders by mothers of the three communities
Indices Ajuona Owerre- Amagul Total p-value Obukpa Umurua
(No) (No) (No) (No)
Creating IDD awareness 68 67 69 203 1.817~' p>0.05
Recommending iodized 67 5 5 72 194 18.525~' salt to goitre patients - " '"'. "' " ' p>0.05
Iodized salt container 68 56 7 1 195 8.098~' covered p>0.05
d.f.=4 NS=Not significant
4.11 Results of the respondents' practices with iodized salt and iodine deficiency disorders (IDD)
Table 4.13 showed that majority (87.5%) of the respondents did no practice,
"creating IDD awareness and recommending iodized salt to goitre patients while
12.5% did.
Iodized salt as a therapy for goiter patients as shown in Table 4.13
revealed more respondents (86.76%) did not practice "recommending iodized
salt to goitre patients" and 13.21% did recommend it.
Container for iodized salt covered, was not practiced by 86.4% of the
respondents while 36.6% practiced it.
Table 4. I 4 Using chi-square analysis there were no significant differences
as regards the relationship of the mothers from different communities and their
lack of practice of iodized salt and IDD (p>0.05).
Table 4.15 Anthropometric measurements of children in the study
-
Nutritional WIA HiA WIH
status No % No % No %
(Low) 39 13.0 75 25.0 16 6.3
(Normal) 258 86.0 221 73.7 271 90.3
(High) 3 1.0 4 1.3 13 4.3
Table 4.16: Nutritional status classification according to gender
Boys Girls Weig ht-for- N O/O N O/O
age < -2SD 20 6.7 19 6.3 -2 to +2SD 131 43.7 127 42.3 >+2 SD 3 1 .O - - Total 154 51.3 146 48.7 Heig ht-for- age < -2SD 4 1 13.7 34 11.3 -2 to +2SD 11 1 37 110 36.7 >+2 SD 2 0.7 2 0.7 Total 154 51.3 146 48.7 Weig ht-heig ht N % N YO < -2SD * ,, 7d. .,. . a 2.3 9 3.0 -2 to +2SD 139 46.3 132 44.0 >+2 SD 8 2.7 5 1.7 Total 154 51.3 146 48.7
<-2SD = LOW -2 to +2SD = nol'tnal. -. >+2SD - - above normal
Low indicated underweight, stunting and wasting depending on the indicator. Z-scores of <- 2.0 standard deviation from NCHS median value was used as cut -off. W/A - Weight -for - age
H/A - Height - for -age W/H - Weight - for - height
4.12 Anthropometric Measurements
Percentage distribution of the nutritional status of the children according to their weight-for-age, height-for-age and weight-for-height
In Table 4.15 using weight-for-age thirteen percent (1 3.0%) of the surveyed
population were underweight, while 86.0% were normal and 1.0% overweight.
Using height-for-age, 25.0% were stunted, while 73.7% were normal and (1.3%)
too tall. Using weight-for-height, 5.3% were wasted, while 90.3% were normal
and 4.3% obese.
4.13 Nutritional status classification according to gender
Table 4.16 showed that more girls (3.0%) than boys (2.3%) were wasted while
more boys (2.7%) than girls (1.7%) were above normal. For normal weight-for
height there were more boys (46.3%) than girls (44%).
4.14: Nutritional status classification according to age-group
Table 4.17 showed that more of age-group 6 to 9years I lmonths (3.3%) than of
age-group 10 to 12yea~~~ll.montt;ts (2.0%) were wasted.
(-2 to *2SD) N2SD
Ntritional status
fig1 Weight-torheight of ohildren aooording to age-roups
Nutritional status
67yrsllmth 89yrllmth 10-llyrllrnth o 12-12yrllmth
Fig. 2 Weight-for-age of children according to agelgroups
<-2SD (-2 to +2SD) >+2SD
Nutritional status
I 6-7ynl1 mth ~3'-95/r1 rffith' 10-1 l y r l 1 mth o 12-12yr11 mth I Rg. 3 Height-mr-age of children according to age-groups
LRS Seasons as LDS
I --Ajuona CPS -0werre Obukpa CPS AmagulUmrua CPS /
Fig. 4: Seasonal weight changes in boys according to school attended
ERS LRS EDS Seasons
LDS
/ + Ajuona CPS - h e r r e Obukpa CPS - -An-~g JUrmorua CPS
Fig. 5: Seasonal height charges in boys according to school attended
ERS- early rainy season, LRS- late rainy season, EDS- earty dry season, LDS- late dry season
4.15 Mean weight velocities for boys according to school attended and in the different seasons
Fig.4 showed that Ajuona had the highest weight velocity (0.57kg) in late rainy
season (LRS) as compared to other boys from other schools, Owerre-Obukpa
(0.42kg) and Amagu/Umuorua (0.22kg). In early dry season (EDS)
Amagu/Umuorua boys had the highest weight velocity (0.44kg) than Ajuona (-
0.02) and Amgu/Umuorua (-0.06kg). Ajuona and Owerre-Obukpa had the same
weight velocities (0.54kg) than Amagu/Umuorua (0.29kg) in late dry season
(LDS). In Table 4.19 using ANOVA in comparing the weight velocities of the
boys from the three schools with the degree of freedom (d.f.) 2,69 and p-value
3.851 (p>0.05) there was no significant difference.
4.16 Mean height' velocities for boys according to school attended and in the different seasons
Fig. 5 compared the height velocities of the boys in the three schools during the
various seasons. Owerre-Obukpa boys had the highest height velocity (0.69cm)
in LRS than Ajuona (0.51cm) and Amagu/Umuorua (0.46cm). In EDS the boys of
Owerre-Obukpa had the highest height velocity (0.33cm) than Amagu/Umuorua
(0.28cm) and Ajuona (0.26cm). Amagu/Umuorua boys had the highest height . , 4 7 . ,, , . I
velocity (4.08cm) compared to Ajuona (1.06cm) and Owerre-Obukpa (0.92cm) in
LDS. In Table 4.20 using ANOVA in comparing the height velocities of the boys
from the three schools with the degree of freedom (d.f.) 2,69 and p-value 3.878 ' I '
(p>0.05) there was no significant difierence.
ERS LRS EDS LDS seasons
-Ajuona CPS Owerre Obukpa CPS - -ArnagulUmrorua CPS --
Fig. 6: Seasonal weight changes in girls according to school attended
I.J , 0 I I
ERS LRS EDS LDS Seasons
+ Ajuona CPS - Owerre Obukpa CPS - -AmagulUrnuorua CP
Fig. 7: Seasonal heighi changes in girls according to school attended
ERS- early rainy season, LRS- late rainy seeson, EDS- early dry season, LDS- late dry season
4.17 Mean weight velocities for girls according to school attended and in the different seasons
Fig. 6 showed that in LRS season, Ajuona C.P.S. girls had the highest (0.67kg)
mean weight velocity than Owerre-Obukpa C.P.S (0.24kg) and Amagu/Umuorua
C.P.S (0.lOkg). In LDS Ajuona C.P.S. girls also had a higher mean weight
velocity (0.63kg) followed by Amagu/Umuorua C.P.S. (0.57kg) and Owerre-
Obukpa C.P.S. (0.38kg). In EDS, Amagu/Umuorua C.P.S had the highest mean
weight velocity (0.21kg) than Owerre-Obukpa (0.09kg) and Ajuona C.P.S.
(0.08kg). In Table 4.21 ANOVA was used to compare the mean weight velocities
of the girls from the three schools with the degree of freedom (d.f.) 2,73, p-value
3.770 (p>0.05) there was no significant difference.
4.18 Mean height velocities for girls according to school attended and in the different seasons
Fig.7 revealed that LDS season had the highest mean height velocity for
Amagu/Umuorua, Ajuona and Owerre-Obukpa C.P.S. girls (3.00cm, 1.47cm and
1.32cm) respectively. In sea season Ajuona had the highest (1.04cm) mean
height velocity than Amagu/Umuorua (0.85cm) and Owerre-Obukpa (0.81cm). ., ,, .. . .v, w , ,,.v> '
Ajuona C.P.S. girls had the highest mean weight velocity (0.92cm) followed by
Amagu/Umuorua (0.38cm) and Owerre-Obukpa C.P.S. (0.15cm) in EDS. In
Table 4.22 using ANOVA to compare the mean height velocities of the girls from
the three schools, with degree 'bf figedom (d.f.) 2,73, p-value 3.951 (p>0.05)
there was no significant difference.
Table 4.23 Mean weight and height velocities of children according to season
Seasons Weight velocity 95% CI Height velocity 95% CI kg (SE) cm (SE)
LRS 0.83 (0.1 9) 0.35 to 1.32 0.87 (0.18) 0.41 to 1.33
EDS 0.78 (0.25) . 0.14 to 1.43 0.70 (0.25) 0.046 to 1.35
LDS 1.18 (0.21) 0.66 to 1.71 1.10 (0.16) 0,70 to 1.54
SE = Standard error LRS = Late rainy season EDS = Early dry season LDS = Late dry season d.f. = degree of freedom
S = significant
Table 4.24: Result of t-test comparing the weight velocities of the boys and girls during the seasons
Sex N Mean Standard Degree Observed Critical Remarks deviationv.. .. o f (calculated) (Tabulated) (decision) (SD) freedom t value T value
- (d.0
Boys 72 8.44 5.28 0 . ..
Girls 76 7.86 4.79
Not
.712 1.645 Significant
p>O. 05
Table 4.25: Result of t-test comparing the height velocities of the boys and girls during the seasons
Sex N Mean Standard Degree Observed Critical Remarks deviation of (calculated) (Tabulated) (decision) (so) freedom t value t value
- (d.0
Boys 72 8.40 8.31
Girls 76 7.11 7.04
Not
Significant
at p O . 05
ERS LRS EDS
Seasons
LDS
gl Boys u Girls L Fig. 8 Mean weight velocitiesof boys and girls according to season
ERS LRS EDS LDS
Seasons
la Boys o Girls I Fig. 9 Mean height velocities of boys and girlsaccording to season
ERS- early rainy season, EDS- early dry season
LRS- late rainy season, LDS late dry season
4.19: Result of t-test comparing the weight and height velocities of the boys and girls as a result of the seasonal variations
Fig. 8 compared the weight velocities of the boys and girls of the study groups in
the various seasons. The boys had higher weight velocities throughout the
seasons. The result from the data in Table 4.18a showed that there was no
statistical significant difference that existed between the weight velocities of the
boys and girls as a result of seasonal variations. At p>0.05 level of significance
within 146 degrees of freedom the observed (calculated) t value of 0.712 was
found less than the critical (tabulated) t value of 1.645.This showed that the
seasonal variations did not affect the weight velocities of the boys differently to
that of the girls.
For height velocities in fig. 9 the girls had higher velocities in the LRS and
EDS while in LDS the boys had higher velocity. Statistically in Table 4.18b
showed that no significant difference existed between the height velocities of the
boys and girls as a result of skasonal variations. At p>0.05 level of significance
within 146 degrees of freedom the observed (calculated) t value of 1.03 was
found less than the critical (tabulated) t value of 1.645 respectively. This showed
that the seasonal variations did not affect the height velocities of the boys and .,,..... y..r.... ..v1 '
girls differently.
!AM season
Vlkt season Dryseason
Dry season
Seasons Boys r!l Girls o Both combined
Seasons
Fig 11 : Height velocities of boys, girls and both combined in wet am dry seasons
a Boys Girls a Both combine Fig 10 Weight velocities of boys, girls and both combined in wet
and dry seasons
Table 4.26 A Comparism of the mean weight and height velocities during
the wet and dry seasons
Season N Mean d.f p=value
(SE)
Wet season 2 2(.58) 4 -3.674'
P<0.05
Dry season 2 . 5(.58)
SE= standard error
d. f= degree of freedom
S= significant difference
Table 4.27 Mean weight and height velocities of children according to age- group
Age-group N Weight 95% CI Height velocity 95% CI
velocity Mean (SE)
Mean (SE) - ,. . , I .. .1
6-7,11 yrs 18 5.00(2.517) -5.83 to 15.83 6.67 (2.333) -3.37 to 16.71
8-9,11 yrs 51 5.33(2.186) -4.07 to 14.74 7.33 (1.453) 1.08 to 13.58
10-1 I , I lyrs 64 5.00 (.577) ' 2.52.to 7.48 6.00 (3.055) -7.14 to 19.14
12-12,l Iyrs 15 6.33 (1.333) 0.60 to 12.07 6.00 (2.517) -4.83 to 16.83
df 3,144 p>0.05 df 3,144 p >0.05
p=value 0. 1 2oN" p=value 0.070 ' I S
NS=Not Significance
4.20 Comparing mean weight, height velocities in the wet and dry seasons of boys, girls and both
During the dry season in fig.10 the boys had the highest weight velocity (0.60kg)
than girls (0.53kg), both had (0.57kg). Again the dry season had a higher
(0.50kg) weight velocity as compared to the wet season (0.29kg).
The height velocities followed the same trend. Dry season had a higher
velocity (1.98cm) than wet season (0.62cm) and the girls had (0.69cm) higher
than boys (0.55cm) in wet season, while in dry season boys had a higher
(2.02cm than girls (1.93cm height velocities). Statistically there were significant
differences at pc0.05, d.f 4 and p=value -3.674; using t-test analysis for mean
weight velocity.
4.21 Mean weight and height velocities according to age group in different quarters
Fig. 12 showed that in the 3rd quarter (July-September 2004), age group 6 to
7years I lmonth had the highest mean weight velocity (0,57kg), followed by 8 to
9years I lmonths (0.50kg), 12 to 12years I 1 months (0.25kg and 10 to I lyears
I lmonths (0.24kg). In the 4'h quarter (October-December 2004), 6 to 7years
I 1 months and 8 to 9years I lmonths had reductions in weight velocities (-0.33kg
and -0.03kg) respectkely;'T2 ta 12years I 1 months and 10 to I 1 years I 1 months
had (0.25kg and 0.24kg) respectively. Statistically in Table 4.27 there was no
significant difference ( p>0.05) comparing the mean weight velocities of the four
age-groups with the degree of freedo;m (d.0 3,144 and p-value 0.120.
Fig. 1 1 revealed that age group 12 to 12years I I months had the highest
height velocity (1.08cm) than 8 to 9years I 1 months, 6 to 7years I 1 months and
10 to I I years I I months (0.93cm, 0.73cm and 0.1 I cm) respectively, in the 3rd
quarter (July-September 2004). In the 4'h quarter (October-December 2004), the
highest height velocity was in age-group 8-9years I I months (0.47cm) followed
103
by 10-1 I years I I months, 6-7years I I months and 12-1 2years I I months
(0.37cm, 0.20cm and 0.09cm) respectively. In the lS' quarter (January- March
2005) 10 to I I years I I months had the highest height velocity (2.57cm) than
6years to 7years I I months, . ( I .33cm), 8 to 9years I I months (1.21 cm) and
12years to 12years Ilmonths (1.03cm). Statistically in Table 4.27 there was no
significant difference ( p>0.05) comparing the mean weight velocities of the four
age-groups with the degree of freedom (d.9 3,144 and p-value 0.070.
Y
I
Aprilto June2004 Jldyto Sql2004 Jan to March ZOC5 Quarterly intervals
Rg. 12 Man weight wkciies by agegoups in d i i ren t seasons
April to Jure 2004 July to Sept 2004 Od to Dec 2004 Jan t o March 2(
Quarterly intervals
I t 6-7,l lyrs -- 8-9,l lyrs 10-1 l,l lyrs + 12-12.1 1yn /
Fig. 13 Mean height velocities by age-groups in different seasons
4.22 Mean weight-for-age and height-for-age during the four seasons pooled together for boys and girls compared to NCHS-WHO 5oth percentile ,
Fig. 14 and 15 compared the mean weight-for-age, height-for-age of the boys
and girls with their reference NCHS-WHO 5oth percentile. Fig.14 showed that the
entire age-groups of the boys fell below the NCHS-WHO reference 50Ih
percentile. There were fluctuations in weight as the ages increased but from
10years on there was a steady increase.
Fig. 14 showed that the girls in the age-groups also fell below their
NCHS-WHO reference 501h percentile, even though the girls had a steady
appreciation in weight as the ages increased.
All the boys in the age-groups fig. 15 had height growth rate below their
NCHS-WHO reference 5oth percentile, at 9-9years Ilmonths they had a
reduction in height.
In fig. 15 unlike the boys, girls of age-groups 6-6years I lmonths grew
above, and 8-8years I lmonths fell below their NCHS-WHO references followed
appreciations in heights which were not up to the reference age-groups.
Age ranges
-+- NCHS-WHO Boy i- BOYS NCHS-WHO Girls + Girls
Fig. 14: Mean weight-for-age during the four seasons pool together for boys and girls compared to NCHS-WHO 197€
I +- NCHSWHO Boy - Boys NCHS-WHO Grb -w-- Girk (
flg 16: Mean helght-torsgo durlng the tour seasons pooled together tor boys and glrls compared to NCHS-WWO 1976
Table 4.28: Percentage distribution of intestinal parasitic infestation of children
Intestinal parasite No %
Hookworm 20 13.5
Entamoebic hystolytica 4 2.7
Intestinal flagellet 4 2.7
No parasite 120 81.1
Total 148 100.0
Table 4.29: Percentage distribution of intestinal parasitic infestation of children according to sex
Intestinal Parasites Boys Girls Total
Hookworm 12 8.1 8 5.4 20 13.5
Entamoeba histolytica 4 2.7 - - 4 2.7
Intestinal flagellet - - 4 2.7 4 2.7
No parasite -'56-"57:8“ 64 43.2 120 81.1
Total 72 48.6 76 51.3 148 100.0
4.23 Result for parasitic .infestation of the children in the studiec communities
Table 4.28 showed that 13.5% of the surveyed children had hookworm, 2.79
had Entamoeba histolytica and intestinal flagellate respectively while 81 .I % ha(
no parasites. Table 4.29 showed more boys (8.1%) than girls (5.4%) ha(
hookworm, and boys (2.7%) than girl (0%) had Entamoeba histolytica. Howeve
more girls (2.7%) than boy (0%) had intestinal flagellet. More girls (43.2%) that
boys (37.8%) had no parasitic infestation.
Table 4.30 Hookworm infestation according to school attended
N Mean %
Ajuona CPS . I2 1.75 32
Owerre-Obukpa CPS 12 2.00 36
Amagu/Umuorua CPS
Table 4.31 : Result of t-test. comparing parasitic infestation of boys and girls
Worm No Mean d.f 0 bsewed Critical Remarks
infestations calculated t (tabulated) t (decision)
of value value
Boys 72 3.39 146 -1.397 1.645 Not significant
., ,.. ..6 r? , ..'a '
Girls 76 3.63
Level of significance pO.05 ,I . ..
4.24 Determination of the existence of any difference in the worm infestation of the boys and girls
Table 4.30 showed that Owerre-Obukpa C.P.S the highest percentage worm
load infestations (36%) than Ajuona and Amagu/Umuorua C.P.S. (32%) each.
However, statistically there was no significant differences d.f=2,33 and p-
value=1.83 (p>0.05). Table 4.31 showed that there was no significant
difference in mean ratings of stool analysis for worm load infestation of the boys
and the girls (P>0.05) with d.f 146, p-value -1.397.
4.25: Determination of the existence of any differences in the hookworm infestation of the pupils according to the schools attended
There was no significant difference in hookworm infestation of the pupils in
different schools (Table 4.31).
Table 4.32: Iodine status ofthe children
Iodine in urine No % ( ~ 2 0 pg/L severe iodine deficiency) 21 58.33
20 - 49 pg/L (moderate iodine deficiency) 2 5.56
50 - 99 pg/L (mild iodine deficiency)
100 - 199 pg/L (optimal)
200 - 299 pg/L (more than adequate)
>300 pg/L (possible excess)
Total
Table 4.33: Iodine status of the children according to sex
Boys Girls Total
Iodine level in urine N % N % N %
Total
Notec2Opg/L - Severely iodine deficient 20 - 49pg/L - Moderately iodine deficient 50 - 99 pg/L - Mild iodine deficient 100 - 199 pg/L - Optimal iodine 200 - 299 pg/L - More than adequate >300 pg/L - Possible excess
4.26 Result for iodine status of the children in the studied communities
Table 4.32 revealed that majority (58.33%) of the children had c20pgIL iodin
This denotes severe iodine deficiency. About 13.89% had 50-99pgIL (mild iodir
deficiency), and 11.1 1% had >300pg/L (possible excess). On the other han
8.33% 5.56% and 2.78% had 100-199pgIL (optimal), 20-49pglL (modera
iodine deficiency) and 200-299pglL (more than adequate) respectively. Tak
4.33 showed that more boys (33.33%) than girls (25%) had C20pglL (seve
iodine deficiency level) and more girls (13.89%) than boy (0%) had 50-99pg
(mild iodine deficiency). More girls (5.56%) than boys (2.78%) had 100-199pg
(optimal) iodine in urine. However, only girls (2.78%) had 200-299pglL (mo
than adequate) and more boys (8.33%) than girls (2.78%) had >300pg
(possible excess) iodine.
Table 4.34 Mean (fSD) urinary iodine level of pupils according to schools
School attended N Mean Std. Deviation Ajuona C.P.S 13 93.92~glL 234.48
Owerre Obukpa 12 56.07pgIL
C.P.S
AmaguIUmuorua 11 164.48pglL
C.P. S
Total 36 102.2OpglL 186.49
Note<2OpgL - severely iodine deficient d.f 2,33 20 - 49pg/L - Moderately iodine deficient F= 3.32 NS p>0.05 50 - 99 pgL - Mild iodine deficient 100 - 199 pg/L - Optimal iodine 200 - 299 pgk - More than adequate >300 pgL - Possible excess NS - Not Significant
Table 4.35: Mean urinary iodine levels according to sex
Urine No Mean) d.f Observed Critical Remarks
iodine level . . ., ,. .. -6 -1' ...... :..' ' .
(calculated) t (tabulated) t (decision) in value value
Boys 17 128.20 34 .787 1.697 Not
significant . I! . ..
Girls 19 78.93
Level of significance: p > 0.05
Table 4.36: Differences in urinary iodine level of the pupils in the different schools
Source d.f Sum of Mean F Observed F Critical Remarks
squares square (calculated) (tabulated) (decision)
Between 2 71361.68 35680.84
groups
Within 33 1 145950 34725.75
groups
Total 35 1217311
Not
Significant
Level of significance: p > 0.05
4.27: Determination of the existence of any difference in the mean of urine iodine level of the boys and girls
Table 4.34 showed that Amagu/Umuorua CPS had the highest (164.48pglL
k210.11) mean urinary iodine level followed by Ajuona CPS (93.92plL k234.48)
and Owerre-Obukpa (56.OpgIL k65.75).
Table 4.35 showed that there was no significant difference between the
mean ratings of iodine level of the boys and girls. The calculated t-value 0.787
was less than the tabulated t-value of 1.697.
4.28: Determination of the existence of any differences in urinary iodine levels of pupils according to schools attended
Table 4.36 showed that the result of One-way classification analysis of variance
(ANOVA) f-test to determine the existence of any difference in the urinary iodine
level of the pupils in the different schools had no significant difference in urinary
iodine levels on growth rate of the pupils according to the schools attended (p>
0.05).
Table 4.37: Correlation coefficient (r) values expressing the relationship between the iodine level in the urine, worm infestation and mal- nutritional status: {(i) underweight, (ii) stunting and (iii) wasting)
Iodine level in
Variables Underweight Stunted Wasted urine Worm Underweight 1 .351(*) -.I10 ,240 -.222
N 36 36 36 36 36 Stunted .351(*) 1 -.398(*) ,314 -.316
N Wasted
N Iodine level in urine
N Worm
Correlation is significant at 0.05 level (2-tailed). '* Correlation is significant at 0.01 level (2-tailed).
4.29: Correlation coefficient (r) values expressing relationship between the Urinary iodine level and underweight, stunting and wasting
Table 4.37 showed that the correlation coefficient (r) of relationship between
urinary iodine level of the pupils and the underweight and stunted had positive
values (r = 0.240) and (r = 0.314) respectively and the wasted had negative
value (r = -0.179). The relationship was stronger among stunted children and
urinary iodine level (r = 0.314). However, it was generally weak with other
nutritional status.
Stunted children'had the highest urinary iodine correlation coefficient (r
=0.314) level. This relationship could be regarded as below average within the
degree range of 0 to 1.
Table 4.37 showed ' a correlation coefficient (r) (r =0.351) between
underweight and stunting as being significant (Pc0.05). There was a negative
relationship (r =-0.398) between wasted and stunted and was significant
(P<0.05).
4.30: Results of relationship among worm infestation, underweight, stunting and wasting
Table 4.37 showed that the correlation coefficient (r) values were both negative
and positive. There,+Ww a'-negative relationship (r = -0.222) between
underweight and hookworm infestation as well as stunted and hookworm
infested children (r =-0.316). Wasted and hookworm infestation had a positive
relationship (r =0.467) which was , significant . . (P<0.01).
Table 4.37 showed that there was a positive (r=0.351) between
underweight and stunted nutritional status. The correlation was significant (P<
0.05). Stunted and wasted had a negative correlation coefficient (r =-0.398)
which was significant (P< 0.05). There was least negative (r =-0.110) between
wasted and underweight.
Table 4.38: Comparing urinary iodine level of the underweight with the normal weight-for-age children
Iodine level in urine -3 to -1SD (Underweight) -1 to +lSD (Normal)
Total 20 60.6 13 39.4
Note<POpg/L - Severely iodine deficient 20 - 49pgL - Moderately iodine deficient 50 - 99 pgL - Mild iodine deficient 1 00 - 199 pg/L - Optimal iodine
200 - 299 pgL - More than adequate >300 pgL - Possible excess
4.31: Percentage frequency of urinary iodine level of the undetweight and the normal in weight- for- age of the children
Table 4.38 showed that more underweight (36.4%) than normal (21.2%) children
were severely iodine deficient (<20pg/L). However, only 6.1 % of underweig ht
were moderately iodine deficient (20-49pgIL). Mild iodine deficiency (50-99pglL)
was, more underweight (9.1 %) than normal (6.1 %). Underweight and normal
(3.0%) each had optimal iodine (100-199pgIL). Only normal (3.0%) were more
than adequate (200-299pglL). Underweight and normal (6.1%) each had
possible excess (>300pg/L) urinary iodine.
(-1 to +lsD)
Height-for-age nutritional status
- ~
Fig. 19 Percentage distribution of urinary iodine level of the stunted and the normal in height-for-age of the children
4.32: Percentage frequency of urinary iodine level of the stunted and the normal in height- for- age of the children
Table 4.39 and (fig. 19) showed that there were more stunted (39.4%) than
normal (18.2%) children who were severely iodine deficient (<20pg/L). There
were more stunted (6.1%) than normal (0%) that were moderately iodine
deficient (20-49uglL). More stunted (12.12%) than normal (3.03%) children had
mild iodine deficiency (50-99~gIL). The optimal (100-199pglL) iodine deficient
children were stunted and normal (3.0%) each. However, the children that had
more than adequate (200-299~gIL) urinary iodine level were normal (3.0%) than
stunted (0%) pupils. More normal (9.1%) than stunted (3.0%) children had
(>300pg/L) possible excess urinary iodine level. Table 4.39 appears to suggest
that more stunted pupil had low urinary iodine level.
Table 4.39 showed that there was equal value between calculated value
(1.67) and the tabulated (1 .,697). This indicated that the levels of urinary iodine of
the stunted and normal children were the same (P>0.05). There was no
difference between the urinary iodine level of the stunted and the normal children
(P>0.05).
Ajuona Owerre-Obukpa A magulUmuorua
Communities
Above 30pprn iodine level 13 30ppm iodine level IN no iodine
Fig.20 Iodine spot-test kit result of the salt samples from the homes
Marketed salt Homesalt I t . ..
Sources
I 0 Above 30 ppm iodine leuel 130ppm iodine level 0 No iodine I Fig. 21 Spot-test kit result of iodine leml of marketed and home salt
samples
4.33 Practical determination of the iodine levels of the salt used in the home and market
Table 4.40 and (fig 20) showed the results of iodine content of salts pupils
brought from homes. About 96.83% of these salts had over 30ppm iodine, some
had (1.90%) 30ppm iodine and others (1.27%) had no iodine. The non-iodized
salts were those of pupils from AmagulUmuorua C.P.S.
Table 4.41 and (fig 21) showed that (90.76%) of the salt samples
marketed had over iodine 30ppm and 9.23% had 30ppm iodine. The salt
samples namely - cassava salt, royal salt, Dangote, Uncle palm, Super power
king salt and E-Nuel table salt, and some unidentified salt samples being sold
with measuring cups were among those tested.
CHAPTER FIVE
DISCUSSION
5.1 The iodine status of the children
The 58.33% severe iodine deficiency (<20pg/L), 5.56% moderate iodine
deficiency (20-49pg/L), and 13.89% mild iodine deficiency (50-99 yg/L) were
observed in this survey. Kennedy et a/. (2003) also noted that the true
prevalence of iodine deficiency is even more widespread than the number of
those affected with goitre would seem to indicate; however, he reported that
there were no global estimates for prevalence of low urinary iodine, which is the
best sub-clinical indicator. The study agreed with Kennedy et a/. (2003) that sub
clinical iodine deficiency was detected by measuring urinary iodine which was an
indication of low iodine intake and/or utilization. The low urinary iodine level
reported in this study may be an indication of poor utilization of iodine consumed.
The market survey showed that all the salt samples were iodized and the salt
samples from the homes were almost iodized; but this study did not get into the
area of utilization of iodine. NutriView (1997) pointed out that food hygiene;
inadequate methods'*&.pl;eparation, cooking and storage can reduce the
nutritional content of foods considerably. Furnke et a/. (1997) in their study with
school children reported that intestinal parasitic infestations reduce the efficiency
of oral supplementation with iodized ethyl esters by interfering with absorption. I' . .
United Nations (1993) stressed the interactions of low content of iodine in the
local environment with poverty and remoteness, when there is little contribution
of food from outside an iodine-deficient area to the diet; as is the case of
subsistence agriculture
Low urinary iodine level of the stunted children was observed in this
study. Stunting may be the effect of low iodine utilization, although there are
other predisposing factors, such as infections and poor nutrition that could give
rise to stunting. Sofra et a/. (1998) defined iodine as an essential mineral
required by the body that directly affects thyroid gland secretions, which
themselves to a great extent controls heart action, nerve response to stimuli, rate
of body growth and metabolism estimates for prevalence of low urinary iodine,
which is the best sub clinical indicator.
5.2 The iodine levels of the salt used in the homes and market
The high level iodized salt in these communities agreed with Egbuta (2003) who
reported that Nigeria in general terms, had achieved the goal of universal salt
iodization and should now focus its attention on constant monitoring in order to
sustain this iodization level. The IDD study carried out by Okeke et a/. (1997) in
Enugu State revealed that 58% of families in Nsukka used salts containing
50ppm of iodine, 33% used salt between 7 and 50ppm iodine and 9% used non-
iodized salts. This study therefore has revealed an upward trend in the use of
iodized salt in Nigeria, indicating success of the IDD programme of the nation.
Okeke et a/. (1997) stated that most consumers bought salt according to brand
name and cost. This study ,however revealed that most mothers bought salt - < ,. .. 1.1. 4' , . . . . . I >
based on what was available in the market. A survey in late 2002 found 98% of
the salt at production and market was adequately iodized. Of households 88.6%
consumed adequately iodized salt, another 9.7% used poorly iodized and only
1.7% received no iodine from kalt ( I ~ D Newsletter, 2004). Even though most
mothers lacked the awareness of iodized salt and iodine deficiency disorders,
they bought and used iodized salt based on it's availability in the market. Most
semi-rural community mothers did not know the brand names but bought the
ones measured out to them. This study was not extended to preferences of
cheapness or brand names, but majority bought salt measured out with cups. It
was noted that the 2.0% non-iodized salt samples were observed to have come
from Amagu/Umuorua community primary school. The market salt test were
carried out on salts sold in the city market not on the ones in rural market were
there could be the possibilities of selling locally moulded baked salts that were
not iodized.
5.3 Knowledge, attitude and practice (KAP) of mothers on iodized salt and iodine deficiency disorders
The low mean knowledge of mothers (8.24%) on iodized salt and iodine
deficiency disorders in this study could possibly be as a result of lack of
awareness creation in the rural and semi-rural communities. In rural communities
there may be poor communication gaps or poor access to news media as to
have a glimpse of NAFDAC'S jingles on iodization of salt. Some may be unable
to purchase radios and television set due to their poverty level. Okeke et a/.
(1997) reported that about 94% traders and consumers had knowledge of
iodized salt programme in Nigeria. The attitudes of the mothers to iodized salt
and iodine deficiency disorders were above average rating; there is a positive
attitude towards iodization programme. The low practical application of the
knowledge of iodized salt and iodine deficiency disorders was an indication of
the consequences of poor, knowledge of same. None educational (41.2%) - . , a '..!;*'.. .... :.> '
background level of the mothers could have contributed to their lack of
knowledge of IDD. Again activities by mothers in taking care of large size
families (6-10 persons) could affect their social lives especially in acquiring
current knowledge on iodization of kalt. dkeke et a/. (1 997), reported the need for
closer monitoring, increased consumer awareness, systematic evaluation of
procurement, marketing, distribution, consumption and follow-up of the effect of
IDD.
127
5.4 Parasitic infestation
The study revealed that 19.4% of the surveyed children had hookworm,
Entamoeba histolytica (2.7%) and intestinal flagellate (2.7%). The low
prevalence was not in agreement with earlier study conducted in Obimo, Nsukka
(Onofiok, 1998) and lloputeife (2004) who reported a higher load of worm
infestations. Onofiok observed 62.9% infestation with hookworm, Trichuris and
ascariasis among children. The low incidence of parasitic infestation reported in
this present study may be due to the influence of the modern health
centrelhospitals cited in each of the three communities. Again most mothers
(89.6%) reported de-worming their children once a year. Majority of the mothers
(49.3%) did de-worm every four to six months. The common ailments reported
by mothers, worm infestation (4.8%) is low compared to others reported. Hall
(1993) noted that the effect of intestinal parasite depended on the duration of
infection before treatment. A longstanding worm burden would have more effect
on growth than a newly acquired load of similar intensity.
Generally, intestinal parasitic infestations persist and flourish where there
is poverty (Tanner et a/., 1987), unsanitary condition, insufficient health care and
overcrowding (Compton and Savioli, 1993; Bundy et al., 1992). In this study, only
a few families use bush"fo!'defecation the rest made use of pit toilet and water
closet which reduces the infection of the green vegetables consumed with ova of
helminths. Drinking water was derived from combined sources: mainly
boreholes, harvested rain water,. tankers and local streamlspring. Mothers
ensured hand washing before eating. The faecal-oral transmission of
geohelminths in these communities was reduced.
5.5 The anthropometric status of the children: underweight, stunting and wasting
The 25.0% stunting, 13.0% underweight and 6.3% wasting observed in this
survey agreed with those of Granthan-McGregor et a/., (1989) who observed that
globally stunting is much more prevalence. The FGNIUNICEF (1994) study
observed more stunting (36-52%) and underweight (27-45%) than wasting (5-
12%). On the other hand, the magnitude of stunting and wasting observed in the
present study was lower than that of Nnanyelugo et a/. (1990). They observed
50.0% stunting and 70.0% wasting. Onofiok, (1998) reported 43.0%
underweight, (33.0%) stunting and (1 8.6%) wasting.
The explanation for the differences might be that the previous studies
were conducted in rural farmland communities who depended heavily on
cassava consumption. Obukpa community is a semi-urban who consumed a lot
of mixed cereals, legumes and vegetables dishes. These foods are rich in
nutrients and essential amino acids which are more energy dense than cassava.
The community is very close to the University of Nigeria Teaching Hospital,
coupled with improved maternal literacy.
The causes of the recent malnutrition might be attributed to inadequate
dietary intake, anaemia, inadequate iodine utilization, worm infestation, infection . ,, 4 * , 1 7 ' I *
and general ill health.
5.6 Seasonal variations in growth velocity of the children
The mean weight velocity of 1.5kg p& year reported in this study was lower,
while the mean height velocity of 5.96cm per year was higher than that reported
by Onofiok (1998). Onofiok had mean weight of 2.3kglyear and mean height
velocity 4.38cmlyear. Other researchers have reported a higher rate in other
countries (Spurr et a/., 1983). There are many factors that could contribute to
impaired growth rate in the present study such as maternal illiteracy and socio-
129
economic factors. In the present inflation rate, cost of food items is very high,
only 39.7% of the families spent up to about 813,501 to 81 6,500 monthly for
feeding a family of more than five persons. Again about 46.0% of the children ate
up to three meals per day with poor diets and high disease load. About 93% of
the children reported one common ailment or the other while hospitalization
(63.7%) was as a result of one or more common ailment. Karlberg et a/. (1994)
reported that impaired growth is associated with many factors such as socio-
economic strata, maternal illiteracy, overcrowding, high disease load, improper
diets and their interaction. Attributing impaired growth to a particular cause in
developing countries is therefore misleading.
The seasonal and quarterly effects on weight and height velocity were
not contrary to expectation. Generally, growth rate was better in dry season than
in the wet season. The period of highest growth in late dry season (January-
March) contrary to other researcher who observed highest growth in October to
December (Onofiok, 1998). In this study highest growth corresponded to post
harvest of major staples like yam, cocoyam, pigeon pea and sweet potatoes. It is
also a period when some beans species and some other food-stuffs are
relatively cheaper than the preceding months. It should be noted that increase in
height gave the histov'of past'adequate nutritional intake.
The highest mean weight and height growth velocities corresponded with
the period food was in abundance before farming period. Staple foods like yam,
cocoyam, pigeon pea and sweet pdtatoes were harvested. It was also the time
where rice, cowpea and other foodstuffs were relatively cheaper than the
' preceding months. The weight velocity also reflected current nutritional status of
the children. The period of least growth was in October to December (early dry
season), this observation was not in agreement with the findings of other
researchers for example Onofiok, (1998) reported that in Obimo Nsukka the
130
period of least growth was in (April-June). Again, in this study the initial
measurements commenced in the month of April, this could also explain there
was no record of growth velocities. Also the observation in this present study
could be explained as a result of the fluctuations in the cost of fuel in the country
that affect the cost of transportation which subsequently hike up cost of food
items. But it should be noted that early and late dry seasons pooled together
was the highest weight and height velocities. While the least mean growth
velocity was in the wet season which was the planting period during which food
items were expensive and scarce. Children at this time were involved in some
levels of farming activities both at home and schools. Most households at this
period were food secure. This is supported by the possible lower energy and
protein intakes by the children at this period of the year. Nnanyelugo et a/. (1985)
reported that in Nsukka, food items were scarce and expensive in the wet
season. In Gambia, the weight and height gains of infants were reported lowest
in rainy season (June-November) but increased in December when it was dry
season (Waterlow, 1994).
The mean weight velocity for boys and girls were the same while there
was higher mean height velocity in girls (l.lOcm/quarter) than in boys
(0.95cmlquarter). Onofiok,.$(1$98) ported that girls had a higher (2.68kgIyr)
mean weight and mean height (4.71cmlyr) velocities than boys (2.03kglyr and
4.14cmlyr respectively). The present study did not indicate preferential treatment
in work allocation and care of girls over boys. The explanation could be that girls
grow taller than boys at this stage of adolescence. Later the boys overtake them
(Eke, 2004 ).
5.7 The relationship between parasitic infestation and (i) underweight (ii) stunting and (iii) wasting
The study revealed that 19.4% of the surveyed children had hookworm,
Entamoeba histolytica (2.7%) and intestinal flagellate (2.7%). The low
prevalence was not in agreement with earlier study conducted in Obimo, Nsukka
(Onofiok, 1998). Onofiok observed 62.9% infestation with hookworm, Trichuris
and Ascariasis among children. The low incidence of parasitic infestation
reported in this study may be due to health education received from modern
health centre cited in each of the three communities. Again most mothers
(89.6%) reported de-worming their children once a year. Majority of the mothers
(49.3%) did de-worm every four to six months. The common ailments reported
by mothers, worm infestation (4.8%) was low compared to others reported. Hall
(1993) noted that the effect of intestinal parasite depended on the duration of
infection before treatment. A longstanding worm burden would have more effect
on growth than a newly acquired load of similar intensity.
Generally, intestinal parasitic infestations persist and flourish where there
is poverty (Tanner eta/., 1987), unsanitary condition, insufficient health care and
overcrowding (Compton and Savioli, 1993; Bundy et al., 1992). In this study, only
a few families use bush for defecation the rest made use of pit toilet and water . , ' IJ
closet. Drinking water was derived from combined sources: mainly boreholes,
harvested rain water, tankers and local streamlspring. Mothers ensured hand
washing before eating. The faecal-oral transmission of geohelminths in these
communities was reduced.
CONCLUSION
The following interesting highlights have been synthesized from this study based
on the anthropometric measurements, urine iodine tests and stool analysis done.
The study indicated a higher prevalence of stunting than underweight and
low hookworm infestations. The existence of stunting, underweight and
wasting in the school children in the semi-rural community may have
serious implications in the general well being of the children and their
achievement and attainment later as adults.
There were evidences of the influence of seasonal variation and possible
less hookworm infestation in the growth velocity of the children.
There was evidence of the intakelutilization of inadequate iodine as
evidence in the urinary output. Urinary iodine is one of the means of
assessing iodine status because iodine intake in excess of requirement is
excreted primarily by this route (Kennedy eta/., 2003).
Although, the urinary iodine was low, the parasitic infestation was also
low. The later was an evidence of the influence of the primary health
centres situated in the communities and mothers1 awareness of de-
worming their ~hildrpp. ,,
Generally, the actual knowledge, attitudes and practices (KAP) of mothers
towards iodized salt and iodine deficiency disorders were inadequate.
However, it was &pected .to appreciate with the recent (NAFDAC)
promotions of iodized salt and iodine deficiency disorders, programmes
on the news media.
The salts consumed were adequate but there seemed to be utilization
interferences by possible goitrogens in both sexes.
A very important finding of this study is that it provided information on the
relationship between growth, parasitic infestation and iodine deficiency.
133
This has also provided significant information on the nutritional status of
Obukpa rural school children which can be extrapolated to
underprivileged children in similar circumstances.
The study has provided baseline information needed for this particular
community, which can be extrapolated to other rural communities in the
whole Federation for the purpose of intervention programmes, such as
eradication of micronutrient deficiency.
The study also can be used as a guide on the nature of creating
awareness programme that is on-going by FGNIUNICEF on food
fortification strategy for Nigeria perhaps for the control of iodine
deficiency.
The study has also shown evidence of multi-factors of malnutrition as
related to growth retardation lending support to multi-directional approach
for appropriate intervention progrmmes with particular reference to
environmental, hygienic and low urinary iodine.
Lastly this study contradicts some previous studies on poor iodization of
marketed salt and also revealed low urine iodine level despite
consumption of iodized salt. . ,, ..'.,' I >
The most devastating consequences of iodine deficiency is reduced
mental capacity, and fifty million people worldwide are mentally handicapped as
a result of iodine deficiency. WHO (2002) had estimated that 100,000 children
were born each year with irreversible brain damage because their mothers
lacked iodine prior to pregnancy; these reaffirms the need to continue to pursue
systematic iodization of salt and iodine deficiency disorders promotion activities.
Therefore, taking the overall, there is good reason to expect that activities
would improve the growth and health (mental and physical) of children
134
particularly in the developing countries. Taken together, they constitute one of
the most cost-effective interventions that can be carried out in the area of public
health care.
For Nigeria to contribute effectively to achieving the goal of reducing the
prevalence of iodine deficiency disorders, as proposed by the World Summit for
children in "Ending Hidden Hunger" by year 2000, which has come and past. The
above problems should therefore be given serious considerations.
5.9 RECOMMENDATIONS
The following are recommended for future action:
1. This study revealed high incidence of low urinary iodine in the children.
Thus it is recommended that steps be taken to improve iodine utilization
by studying goitrogenic factors that can hinder the utilization of iodine
since there is high percentage iodization of salt.
2. There were incidences of stunting and underweight amongst the children.
Stunting indicates history of past malnutrition at the vulnerable years of
childhood, the outcome of which manifests later in life. Priority therefore . , , ..., ? ' t >
should be given to the feeding of this group of children.
3. Food and nutrient intakes were significantly affected by seasons. Efforts
should be made to improve and expand storage facilities in rural
communities to reduce 'the adverse impact of seasonal fluctuations on
food supply. Possibilities for farming all year round through irrigation are
also recommended as a long-term solution.
4 Education level and economic status of mothers are known to have
significant influence on the nutritional status of children. The mothers in
this study had little or no education and this explains the low nutritional
135
status of the children. It is therefore recommended that efforts be made to
improve education and economic empowerment of rural women in
general. This could be achieved through adult education and skill
acquisition opportunities and health talks.
5. There is still serious gap in knowledge of iodized salt and iodine
deficiency disorders which influence growth velocity. In view of this,
further studies in this area are recommended. Such studies could assess
the different food consumed and their iodine levels with their effects on
the height velocity and the extent to which worm infestation and iodine
intake contribute to iodine deficiency disorder
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APPENDICES
Appendix 1
Table 4.17 Nutritional status according to age-group for fig 1
Weight-height 6-9yrs I I mths 10-12yrs I lmths
Total 166 55.3 1 34 44.7
Appendix I I
Table 4.18 for fig.1 to fig.3 Nutritional status classification according to age -group
Weight- 6-7yrs -7yrs 8-9yrs I I mths 10-llyrs 12-1 3yrs height I I mths I I mths Ilmths
N % N % N % N %
<-2sd
-2 to +2SD
>+2SD
Weig ht-for- age
<-2sd
-2 to +2SD
>+2SD
Height- for-age <-2sd
-2t0 +2SD
>+2SD
Appendix 4 11
Table 4.19 for fig.4: Mean weight velocities (kg) for boys according to schools attended and in the different seasons
ERS LRS EDS LDS
Ajuona CPS Mean . 20.44 22.17 22.33 24.50 Change - 1.73 .O. 16 2.17 Velocity - 0.57 -0.02 0.54
Owerre-Obukpa Mean 24.50 25.75 25.58 27.75 CPS
Change - 1.25 -0.17 2.17 Velocity - 0.42 -0.06 0.54
AmagulUmuorua Mean 27.33 28.00 29.33 30.50 CPS
Change - 0.67 1.33 1.17 Velocity - 0.22 0.44 0.29
ERS- early rainy season, LRS- late rainy season, EDS- early dry season, LDS- late dry season Using ANOVA d.f 2,69 p-value 3.851 NS p>0.05
Table 4.20 for fig. 5: Mean height velocities for boys according to schools attended and in the different seasons
ERS LRS EDS LDS
Ajuona
CPS
Owerre
Obukpa
CPS
Amagu
Umuorua
CPS
Mean
Change
Velocity
Mean
Change
Velocity
Mean
Change
Velocity
ERS- early rainy season, LRS- late rainy season, EDS- early dry season, LDS- late dry season Using ANOVA d.f 2, 69 p-value 3.878 NS p>0.05
Appendix 1V
Table 4.21 for fig. 6: Mean weight velocities (kg) for girls according to schools attended and in the different seasons
ERS LRS EDS LDS
Ajuona CPS Mean Change Velocity
Owerre-Obukpa Mean CPS
Change Velocity
AmagulUmuorua Mean CPS
Change Velocity
ERS- early rainy season, LRS- late rainy season, EDS- early dry season, LDS- late dry season Using ANOVA d.f 2,73 p-value 3.770 NS p>0.05
Table 4.22 for fig. 7: Mean height velocities (cm) for girls according to schools attended and in the different seasons
ERS LRS EDS LDS
Ajuona CPS Mean 120.88 124.00 126.75 132.63 Change - 3.13 2.75 5.88 Velocity . ,. . .. ,,. - p 1 .04 0.92 1.47
Owerre-Obukpa Mean 124.57 127.14 127.57 132.86 CPS
Change ' - 2.57 0.43 5.29 Velocity - 0.81 0.15 1.32 \
AmagulUmuorua Mean 127.94 . 130.50 131.63 143.63 CPS
Change - 2.56 1.13 12.00 Velocity - 0.85 0.38 3.00
ERS- early rainy season, LRS- late rainy season EDS- early dry season, LDS- late dry season Using ANOVA d.f 2.73 p-value 3.951 NS p>0.05
Appendix V
Table for fig 8: Weight velocities for boys and girls Seasons ERS LRS EDS LDS
Boys Mean 24.08 25.3 1 25.74 27.58
Change - 1.23 0.43 1.84
Velocity 0.3 1 0.14 0.46
Girls Mean 24.73 25.75 26.04 27.76
Change - 1.02 0.29 1.72
Velocity - 0.26 0.10 0.43
ERS- early rainy season, LRS- late rainy season, EDS- early dry season, LDS- late dry season
Table for fig 9: Height velocities for boys and girls
Seasons ERS LRS EDS LDS
Boys Mean 126.05 128.26 129.13 137.20
Change - 2.2 1 0.87 8.07
Velocity - 0.55 0.29 2.02
Girls Mean 124.46 127.2 1 128.65 136.47
Change - 2.75 1.44 7.72
Velocity - 0.69 0.48 1.93
ERS- early rainy season. LRS- late rainy season, EDS- early dry season, LDS- late dry season
Appendix V l
Table for figures 10 and 11: Comparing weight, height velocities in the wet and dry seasons of the boys, girls and the pupils
Weight velocities Height velocities
Wet season Dry season Wet season Dry season
Boys 0.31 0.60 0.55 2.02
Girls 0.26 0.53 0.69 1.93
Pupils 0.29 0.57 0.62 1.98
Table for fig 12: Mean weight velocities according to age groups April-June July-Sept 2004 Oct-Dec 2004 Jan-March
2004 2005
6yrs - 7yrsllmonths Mean 18.6 20.3 20.55 21.40 Change - 1.70 -0.1 1 .OO Velocity - 0.57 -0.33 0.25
* , . . . , * .'
8yrs - 9yrsl lmonths Mean 20.91 22.42 22.33 24.54 Change - 1.5 -0.08 2.2 1 Velocity 0.5 -0.03 0.55
I I
lOyrs - l lyrs llmonths Mean 28.73 29.47 30.20 32.07 Change 0.73 0.73 1.87 Velocity - 0.24 0.24 0.47
12yrs - 12yrsllmonths Mean 28.75 29.50 30.25 32.5 Change - 0.75 0.75 2.25 Velocity - 0.25 0.25 0.56
Appendix V11
Table for fig 13: Mean height velocities according to age-groups April-June July-Sept 2004 Oct-Dec 2004 Jan-March
2004 2005 6yrs - 7yrs llmonths Mean 115.8 118.0 1 18.6 123.9 Change 2.2 0.6 5.3 Velocity - 0.73 0.20 1.33
8yrs-9yrsl1 months Mean 1 17.33 120.13 121.54 126.38 Change 2.79 1.42 4.83 Velocity - 0.93 0.47 1.21
l0yrs-llyrsllmonths Mean 130.69 132.81 133.91 144.19 Change 2.13 1.09 10.28 Velocity 0.1 1 0.37 2.57
12yrs - 12yrsll months Mean 13 1.75 135.00 135.25 139.38 Change 3.25 0.25 4.13 Velocity 1.08 0.09 1.03
Table for fig 14: Mean weight-for-age (kg) during the four seasons pooled together for boys and girls (6-12years IOmonths) compared to NCHS-WHO 1976, .
6-6yrs 7-7yrs 8-8yrs 9-9yrs 10-1 Oyrs I 1-1 I yrs 12-1 2yrs 1Omths 1Omths 10mths 10mths 1Omths 1Omths 1Omths
NCHS- 24.7 26.9 , 29.4 32.9 38.8 41.7 W HO(B0ys) 1, . ,
Boys 20.3 22.7 20.8 25.3 28 30.8
NCHS- 20.7 23.6 26.6 31.8 34.2 39.5 42.5 WHO(Girls)
Girls 18 20 22.5 25 25.8 29 30.5
Appendix Vlll
Table for fig. 15: Mean height-for-age (cm) during the four seasons pooled together for boys and girls (6-12years 10months) compared to NCHS-WHO 1976
6-6yrs 7-7yrs 8-8yrs 9-9yrs 10- I 1-1 I yrs 12-1 2yrs IOmths IOmths IOmths IOmths 1Oyrs IOmths IOmths
1 Omths
NCHS- 123.9 131.3 134.3 139.8 148.2 152.2 WHO(Boys)
Boys 1 18 123.1 119.5 129.3 134.4 135.1
NCHS- 117.9 121.7 129.2 137.3 140.7 149.8 153.3 WHO(Girls)
Girls 120.5 124.8 116.7 128 131.4 137.8 144.4
Appendix I X
Ajuona CPS m Ow erre-ObukpaCPS AmgulLkrwrua CPS
Fig. 16:Petcentage hookworm load inkstation of pupils accodng to schools attended
% Boys % Girls
Gender
<2O uglL 0 20-49uglL .50-99ugIL 0 ao-199uglL .20@299ug/L rn ~300ugIL m
Rg.17 Percentage urinary iodine kvel according to sex
Appendix X
% underw eight D 96 normal I
4 0 uglL 20-49uglL 50-99uglL QO-199uglL 200- >300uglL
Urinary iodine l e ~ l 299uglL
3fg 18 Pertentlge rlinlty iodine fot the rnlmbGight and the normal
Appendix X I
Table 4.39: Comparing urinary iodine level of the normal in height-for-age with the stunted children
Iodine level in urine -3 to -lSD (Stunted) -1 to +1SD (Normal)
200-299pgIL - - 1 3 . 0
>3OOpg/L 1 3 . 0 3 9 .1
Total 21 63.6 12 36.4
Note<POpgL - Severely iodine deficient d.f=33 p-value=l. 6YS p>0.05 20 - 49pg5 - Moderately iodine deficient 50 - 99 pg5 - Mild iodine deficient 100 - 199 pgYL - Optimal iodine
200 - 299 pg5 - More than adequate >300 pg5 - Possible excess
NS - Not Significant
158
Appendix X I I
Table 4.40 iodine levels of the salt samples from the homes of the pupils in the three communities
Community Above 30ppm 30ppm iodine No Total
iodine level level iodine
Ajuona 1 17 37.02 3 0.94 - - 120 37.96
Owerre-Obukpa 97 30.69 3 0.94 - - 100 31.63
Total 306 96.82 6 1.88 4 1.26 316 99.96
Table 4.41 Iodine levels of marketed and home salt samples
Sources Above 30pprn iodine 30ppm iodine No iodine
level level
N , Yo N % N %
Market 43 90.,76 : 2 9.24 - -
Home 306 96.83 6 1 .90 4 1.27
Total 349 93.80 8 5.57 4 0.64
Appendix X I 11
UNIVERSITY OF NIGERIA, NSUKKA DEPARTMENT OF HOME SCIENCE, NUTRITION AND DIETETICS
IODINE STATUS, GROWTH AND PARASITIC INFESTATION OF PRIMARY SCHOOL CHILDREN IN RURAL NIGERIAN COMMUNITY OBUKPA
The Questionnaire used in collecting basic data
INSTRUCTION: To be filled by mothers or care-giver of primary school children. Tick (V) or fill in the appropriate answer. All information will be kept confidential.
SECTION A: General Characteristics
Respondent's Code [ ]
Are you the head of your household: (a) Yes [ ] (b) No 1 1
Sex of Respondent (a) Male [ ] (b) Female [ ]
No. of people in the Household (people who live and eat from the same pot):---
Religion: (a) Christianily'["] @) Muslim [ ] (c) Traditional religion [ ]
What is your marital status? Married [ I Single [ ] Divorced [ ] Separated [ Widow [ ]
,I
SECTION B: Socio-economic Characteristics
10. Educational attainment of respondent. a. None [ ] b. Primary uncompleted [ ] c. Primary completed [ ] d. Secondary uncompleted [ ] e. Secondary completed [ ] f. Post Secondary School [ ] g. University [ 1
11. Educational Level of household (if difference from 10 above) [ ]
a. None [ ] b. Primary uncompleted [ ] c. Primary completed [ ] d. Secondary uncompleted [ ] e. Secondary completed [ ] f. Post Secondary School [ ] g. University [ ]
Occupation of respondentlmother; a. Trading [ ] B. farming[ ] c. hair dressing [ ] d. Teaching [ ] e. Sewing f. Civil servant [ ] g. House wife [ ] h. others (specify)
Occupation of head of household: a. trading [ ] b. farming [ ]c. Skilled work [ ] d. unskilled work [ ] e. civil servant f. house wife [ I g. others (specify)
How much do you spend on food per month? a. less than N500 [ ] b. N500-N1000 [ ] c. N100-N1,500 [ I d. N1,500-N2000 [ ] e. N2,000-N3,000 [ ] f. N3,000-N4000 [
Does any other person earn income or contribute to he up keep of the household? a. Yes [ ] b. No [ ]
If yes, about how much is earned or contributed monthly by such person(s)? a. Less than N500 [ ] b. N500-1000 [ ] C. N1,000-N2000 [ ] d. N2,000-N3,000 [ ] e. Above N3,000 1 -
What are the sources of income in your household? a. Salary [ ] b. Sales from farm proceeds [ ]
c. Trading [ ] d. . Others (specify) II . .
SECTION C: HEALTH FACILITIES AND HEALTH RECORDS AND PRACTICES 18. How many modern centers/hospitals do you have in this
village/community a. None [ ] b. One [ ] c. Two [ ] d. Three[ ]
19. Are there herbal centers in this area? a. Yes [ ] b. No [ ]
Which of the health centers do your family members attend frequently? a. Modern health centerlhospital [ ] b. Traditional healing homes [ ] c. Prayer houses [ ]
What are your major reasons for attending modern health1 hospital services? a. cheaper [ ] b. More expensive [ ]c. short distance[ ] d. receives better treatment [ ] e. save times [ If. family likes it [ ]
What are your major for attending berbal centres? a. cheaper [ ] b. close to the house [ ]c. receive better
treatment [ ] d. saves time[ ] e. our family likes it[ ] f. Any other (specify)
How do you usually get to the clinic? a. walk [ ] b. bus [ ] c. motor-cycle[ ] d. bicycle [ ] f. Others
(specify)
Do you have1 had goiter before? Yes [ ] No[ 1
How are you treatingltreated it? A. Operation [ ] b. Iodine salt [ ] c. Oil Iodine injection [ ] d. Nothing e. State others please -
How many miscarriages had? a. None[ ] b. One [ ] c. Two [ ] d. Three[ ] e. More than three [ ]
Have you still births? A. None [ ] b. One [ ] c. two [ ] d. three [ ] e. more than three [ ]
How many surviving children do you have? a. None [ ] b. One [ ] c. Two [ ] d. Three [ ] e. Four [ ] f. More than Four [ ]
How many children died in the first year of life? a. None [ ] b. One L, 1. . c. Two [ ] d. Three [ ] e. Four [ ] f. Five [ ] g. More than five [ ]
What was the cause of death? a. convulsions [ ] b. diarrhea [ ] c. vomiting [ ] d. fevers [ ] e. measles [ ] f. Pneumonia [ ] g. others please specify
How many children dies after 5 years of age?
a . None [ ] b. One [ ] c. Two [ ] d. Three [ ] e. Four [ ] f. Five [ ] g. More than five [ ]
How many abnormally behaved children do you have? a . None [ ] b. One [ ] c. Two [ ] d. Three [ ] e. Four [ ] f. Five [ ] g. More than five [ ]
How many dwarfed children do you have? a . None [ ] b. One [ ] c. Two [ ] d. Three [ 1 e. Four [ ] f. Five [ ] g. More than five [ ]
What are the sources of drinking water for member of your family? a. Public tap [ ] b. borehole [ ] c. Rivers, spring [ I d. tanker [ ] e. rain-water [ ] f. Others (specify)
What treatment do you normally give your drinking water? a. None [ ] b. filtering [ ] c. boiling [ ] d. boiling &filtering [ ] e. addition of Milton [ ] f. addition of alum [ ] g. alum & filtering [ ]
How often do you clean your water pot? a. Once a week [ ] b. Twice a week [ ] c. Thrice a week [ ] d. Daily [ ] e. Once a month [ ] f. Once a while [ ]
Which toilet facility do have? a. Bucket [ ] b. Pit [ ] c. Bush [ ] d. Others (specify)
Do you ensure that children wash their hands? a. Yes [ ] b. No [ ]
" $. 4 * i r. 1.-
If yes, when? a. after using the toilet [ ] b. after coming back from school [ I c. before eating [ ] d. after play [ ] e. no time [ ]
SECTION D: MORBIDITY AND HEALTH STATUS
40. When last did you give them worm medicine?
41. Has any of your children suffered from any of the following diseases in the last 3 months? (children 6-15 years only). Start with the youngest.
SIN
1
2
3
4
5
6
7
8
9
Disease
FeverlMalaria
Diarrhea
Vomiting
Measles
Coughlcatarrh
Hepatitis
Typhoid fever
Worm . ,.
Others (specify)
Age
4 . I . \.
Child 2 Child 4 Child 1
+
Child 3 Child 5
42. Which of these children have been admitted into the hospital in the last 3 months and why?
43. Is any of your children aged 6-15 years on drug (medicine)? If so, which and what type of drug?
Children
Child 1
Child 2
Child 3
Child 4
Child 5
None
44. Has any of your children any of the following problem I I
Malaria
Others (specific)
r
SIN
1
2
3
4
5
6
Hepatitis
SECTION E: IDD STATUS
SIN
1
2
3
4
Typhoid fever
Diarrhea
Children
Child 1
Child 2
Ch~ld 3
Child 4
Child 5
None
Problem
Deafness
Muteness
Slow to understanding
Doesn't do well at school
Cough
Panadol
* ,. 4
Measles
Age
Malaria drug
<.' .v I >
No. of Children
Antibiotic Multivite
6 I Goitre
5 Abnormally short
Food intake
45. Is your food
7
8
9
(a) Mostly home-product ( )
(b) Partly home-produced, partly purchased ( )
(c) Mostly Purchased ( )
(d) Others (Please' Specify)
Abnormal Behaviour
Congenital Abnormalies
Squint
School Children response
46. Which of the meals do you take in a day? (Please indicate below) I
24-Hour Dietary Recall
47 Which of these food items did you eat yesterday?
Breakfast
A. Cereals: (i) Rice ( ) (ii) Bread (iii) Maize ( ) (iv) pap ( )
(v) Others (Please Specify)
B. . Roots and tubers: (i) ,;Yams1 ) (ii) Sweat potatoes ( ) (iii) Plantain ( ) (iv) Garri ( ) (v) Coco Yams ( ) (vi) Cassava (fufu) ( )
Snack
C. Legumes: (i) Soya beans ( ) (ii) Cowpea ( ) (iii) Groundnut ( )
(iv) Pigeon pea ( ) (v) African yam bean (Nkikisi) ( )
(vi) Bambara groundnut (Okpa) ( )
(vii) Others (Please Specify)
Lunch Snack Supper Snack
D. Vegetables: (i) Okro ( ) (ii) Dark green Vegetables ( ) (iii)
Tomatoes ( ) (iv) Pepper ( ) (v) Carrot ( ) (vi) Others
(Please specify)
E. Fruits: (i) Mango ( ) (ii) Orange ( ) (iii) Pawpaw ( ) (iv)
Pineapple ( ) (v) Sausop ( ) (vi) Avacado pear ( ) ( vii)
Coconut ( ) (viii) Cashew ( ) (xi) Guava ( ) (x) Velvet
tamarind (Ichekwu) ( ) (xi) Local apple (udara) ( ) (xii)
Banana ( )
(xiii) Others (specify)
F. Fish and Meat: (i) Dried fish ( ) (ii) Frozen fish ( ) (iii) Chicken ( )
(vi) Egg ( ) (v) Goat meat ( ) (vi) Beef ( ) (vii) Liver ( )
(viii) Stock fish ( ) (ix) Crayfish ( ) (x) Snail ( )
(xi) Turkey meat ( )
(xii) Others (Please specify)
G. Oilloil seeds: (i) Palm oil ( ) (ii) Groundnut oil ( ) (iii) Butter ( )
(iv) Melon seed (egusi) ( ) (v) Dikanut (Ogbono) ( )
(vi) Others (please specify)
, ,. . 4 . r . ... ?'
H. Beverages: Cow's milk ( ) (ii) Palm wine ( ) (iii) Breast milk ( )
(iv) Beer ( ) (v) Tea ( ) (vi) Cocoa drinks ( )
(vii)Others (please specify) . I . ..
I. Snacks: (i) Roasted groundnut ( ) (ii) Akara ( ) (iii) Roasted corn ( )
(iv) Pop corn (v) Okpa ( ) (vi) Moimoi ( ) (vii) Bread ( )
(viii) Boiled Groundnuts ( ) Others (please specify)
J. Seasoning/Condiments: (i) Fermented oil bean (ukpaka) ( ) (ii)
Fermented melon seed (Ogiri) ( ) (iii) Onoin ( ) (v) Nchuanwn ( )
(vi) Curri ( ) (vii) Garlic ( ) (viii) Thyme ( ) (ix) Salt ( )
(x) Others (Please specify)
48 How do you use palm oil?
(i) Bleached ( . ) (ii) Normal form ( ) (iii) Others (Please
specify
49. Do you have any food taboo (food@) that your culture or religious
forbids)? If yes please list
50. Which foods serve as your favourite foods? (Please name the
food)
SECTION E: KNOWLEDGE ATTITUDE AND PRACTICE (KAP) OF MOTHER ON IODIZED SALTllDD
I 51. Question
1
2
3
4
Response
Do you Know what is Iodized salt?
Do you Know what causes goiter?
Do you Know That goiter is due to Iodine deficiency?
Are you aware of other. consequences of IDD?
5
[ 8 Are you aware of the order banning non-iodine salt? I I
Do you know that stored iodized salt with lead is better preserved?
6
7
No Response Yes
Are you aware that iodine in salt evaporates when expased for a long period?
Do you also know that high temperature causes loss of iodine from salt?
No
52. ATTITUDE
SA = Strongly Agreeable; A = Agreeable; NR =No Response; DA = Disagreeable;
SD = Strongly Disagreeable
D A
- 1
2.
3.
4.
5.
6. -
7.
8.
PurchAsing of Iodized Salt
54. The salt you buy is it a. iodized [ ] b. non-iodized [ ]
c. I don't know [ ]
56. Do you buy salt
a. Packaged [ ] b. Unpackaged [ ]
SD S A Question
Creation of awareness of IDD is
Sources of awareness could be me
Giotre Patients are Iodine deficient
Iodized salt productionlmarketing should be encouraged
Iodine from salt should not be allowed to evaporize.
Waterlmoisture should not get in touch with iodized salt
Are you in favour of banning non- iodized salt?
Do you avoid goitee patients?
53. PRACTICE
A
I
NR
Question
1
2.
Response
I help to create the awareness of iodine deficiency dosprders. . ,. . I -
Goiter patients should be given well iodized salt1 foods
Yes
3. 1 I cover my iodized salt
No No Response
I 1
Storage of Salt
Do you store your salt near the fireplace? Yes [ ] No [ ]
Do you store your salt in an open space? Yes [ ] No [ ]
Do you store your salt in a damp place? Yes [ ] No [ ]
Do you store salt purchased salt more than six months? Yes [ ] (state
how long please)
Do you purchase salt exposed to Sunlight? Yes [ ] No [ ]
Do you purchase salt to moisture? Yes [ ] No [ ]
What type of container do you store salt? A. Plastic [ ] b. Class [ ]
c. Wood [ ] d. Clay [ ] e. Metal [ ] f. state others please
Is the container with well-fitting lid? Yes [ ] No [ ] No lid at all [ ]
Adding salt in food
65. Do you add salt in food (a) Before cooking [ ] b. During cooking [ ] c.
After cooking [ ]
66. Do you wash salt before use to remove impurityldirt Yes [ ] No [ ]
Anthopometric measurement
Sex: Male [ ] Female [ ] ,,
Weigh (kg)
Height (cm)
Arm
Circumference
(cm)
Enlargement on the neck
Seen
Squint
Deafness
Muteness
Abnormal behaviour
Congenital
No seen
Tool Analysis
Ascaris Lumbrocoides
Trichuris triciura I
Hook worm
Entamoeba histlytica
Giardis
Flagelettes
, ,. 4 . . 0' $ +
Mean Urinary Iodine (uglL)
Salt test
Severe Iodine Deficiency C 20
(With rapid test Kit)
Moderate Iodine deficiency 20-49
Mild iodine deficiency 50-99
Optimal Iodine . deficiency ' 100-199
More than adequate
200-299
Possible excess
> 300
Appendix XIV
---
Goitre Patient
Appendix XV
neight Measurement at Owerre-Obukpa C.P.a
Appendix XVI
weight Measurement at Ajuona C.P.S
Appendix XVll
Weight Measurement at Owerre-Obukpa C. P.S