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THESIS
l

5523/“ LIBRARY
Michigan State
University

 

 

 

 

This is to certify that the
thesis entitled

Inutero and Perinatal Risk Factors
for Asthma or Wheezing and other

Atopic Manifestations
presented by

Kevin Royd Brooks

has been accepted towards fulfillment
of the requirements for

 

MasteLaflMegrec in Epidemiology

(M M C/fi-v

Major professor

Date (Q/Ze/OZ

0-7639 MS U is an Affirmative Action/Equal Opportunity Institution

 

'v ——~—-.. ..

PLACE IN RETURN Box to remove this checkout from your record.
TO AVOID FINES return on or before date due.
MAY BE RECALLED with earlier due date if requested.

 

 

DATE DUE L DATE DUE DATE DUE
JUL I 0 200

 

 

 

 

 

 

 

 

 

 

 

 

 

 

8/01 clelRCJDatoDUOpBS-p. 15

IN UTERO AND PERINATAL RISK FACTORS FOR
ASTHMA OR WHEEZING AND OTHER ATOPIC MANIFESTATIONS

By

Kevin Royd Brooks

A THESIS
Submitted to
Michigan State University
In partial fulfillment of the requirements
for the degree of
MASTER OF SCIENCE
DEPARTMENT OF EPIDEMIOLOGY

2002

ABSTRACT

IN UTERO AND PERINATAL RISK FACTORS FOR
ASTHMA OR WHEEZING AND OTHER ATOPIC MANIFESTATIONS

By

Kevin Royd Brooks

A better understanding of the etiology of asthma and other atopic disorders may
introduce prevention methods, thus reducing associated outcomes. We tested
the hypotheses, maternal oral contraceptive (00) use before and complications
during pregnancy are risk factors for asthma or wheezing and other atopic
manifestations. These tests were conducted in a follow-up study of 1,720 children
who were part of the Jamaican Perinatal Morbidity and Mortality Survey (n=13,
04810). Mother-infant-pairs were interviewed at birth and babies examined.
Followed-up data at six weeks and at approximately 11 years of age were also
collected. All three datasets were linked using identification number and date of
birth for both mother and child. After controlling for gender, smoking during
pregnancy, birth weight (< 2.5 kg, 2.5kg - 4.0kg, and >=4.0 kg) and other
covariates, adjusted odds ratios (AOR) and their 95% confidence interval (CI)
were estimated by logistic regression analysis. Prevalence of asthma, 00 use
and maternal health complications during pregnancy were 16.8%, 49.9%, and
50.2% respectively. Asthma was more frequently reported for children whose
mothers used OC (AOR_=1.56; 95%Cl 1.04-2.32), and had health complications
during pregnancy, (AOR,=1.75; 95%CI 1.14—2.69). Results suggest that asthma

may be pre-programmed in utero.

DEDICATIONS

This work is specially dedicated to the two most important women in my life; my

wife Valrie and mother Patricia. Also to Jevon Brooks (nephew) for the promise

he represents.

iii

ACKNOWLEDGEMENTS

The planning, designing, implementation and completion of this work is
the result of a team of dedicated individuals. Sincere gratitude to my thesis
advisor, Dr. Wilfn'ed Karmaus, for his foresight, guidance and moral support in
the process of completing this project.

I would also like to thank the other members of my thesis committee, Drs.
Joseph Gardiner and Pramod K. Pathak for taking time from their busy schedule
to provide support during this project.

This project would not be possible without the data provided for analyses.
For this I thank Dr. Maureen Samms-Vaughn and her team for working

acidulously to provide this data.

iv

TABLE OF CONTENTS

LIST OF TABLES ........................................................................................... vi

LIST OF ABBREVIATIONS. .......................................................................... vii
INTRODUCTION ............................................................................................ 1
CHAPTER 1

IN UTERO AND PERINATAL EVENTS AS RISK FACTORS

FOR ASTHMA AND OTHER ATOPIC MANISFESTATIONS ......................... 3
CHAPTER 2

ATOPIC MANIFESTATIONS/DISEASES ....................................................... 6
CHAPTER 3

A REVIEW OF THE ASSOCIATION BETWEEN IN UTERO

AND PERINATAL EXPOSURES AND ATOPIC DISORDERS ..................... 13
CHAPTER 4

THE JAMAICAN PERINATAL MORBIDITY AND MORTALITY SURVEY ....22
CHAPTER 5
METHODS ......... 32
CHAPTER 6

RESULTS ..................................................................................................... 39
CHAPTER 7

DISCUSSION AND CONCLUSION ..................................................................... 52
APPENDIX - A

MAIN QUESTIONNAIRE PERINATAL SURVEY — JAMAICA ...................... 61
APPENDIX — B

FOLLOW-UP QUESTIONNAIRE - SIX WEEK PERINATAL

SURVEY— JAMAICA .................................................................................... 77
APPENDIX — C CHILD HEALTH QUESTIONNAIRE THE JAMAICA
COHORT STUDY ........................................................................................ 84
BIBLIOGRAPHY ........................................................................................... 91

Table 1.

Table 2.

Table 3.

Table 4.

Table 5.

Table 6.

Table 7.

LIST OF TABLES

Association between maternal age at menarche and
occurrence Of atopy in children at 31 years ............................. 18

Comparison characteristics of outcome variables in sub-
population and linked data set ................................................. 39

Comparison characteristics Of exposure variables in main
and linked datasets .................................................................. 41

Proportion of atopic disorders in relation to their in utem risk
factors linked datasets. ............................................................ 43

Proportion of atopic disorders in relation to their perinatal
potential risk factors ............................................................ 46-47

Relationships Of antenatal and perinatal risk factors to asthma
or wheezing, and frequent nighttime or early moming cough. .49

Relationships of antenatal and perinatal risk factors to

eczema, and hay fever or sinus problem or some other
allergy. ..................................................................................... 50

vi

LIST OF ABBREVIATIONS

AD .................................................................................... Atopic Dermatitis
AOR ......................................................................... Adjusted Odds Ratios
AR ....................................................................................... Allergic Rhinitis
CBMC ............... ' ........................................ Cord Blood Mononeucleous cell
Cl ................................................................................. Confidence Interval
F FUQ ........................................................... First Follow-up Questionnaire
lFN-y .............................................................................. Interferon Gamma
lgA ................................................................................ lmmunoglobulin -A
lgE ............................................................................... lmmunoglobulin —E
lgG ............................................................................... lmmunoglobulin -G
lL ................................................................................................. Interleukin
IUD ................................................................................. Intrauterine device
LBW ................................................................................. Low Birth Weight
MQ ............................................................................... Main Questionnaire
MRNA ................................................................. Memory Ribonucleic Acid
00 ................................................................................ Oral Contraceptive
OR .......................................................................................... Odds Ratios
SAS ................................................................... Statistical Analysis System
SF UQ ...................................................... Second Follow-up Questionnaire
TH .......................................................................................... T-Helper Cell
VDRL ............................................... Venereal disease research laboratory

vii

INTRODUCTION

The prevalence of allergies is increasing in many parts of the world, and
asthma has become the most common Chronic disease in childhood. The .
etiology of asthma and allergic disease remains insufficiently understood, despite
considerable research (1 ). Recent studies have expanded to include the study of
novel factors such as in utero and perinatal exposures that may "program" the
initial susceptibility to these disorders (2). Some authors have reported that
maternal health complications during pregnancy and at birth and maternal
estrogen levels are associated with asthma and other atopic manifestations later
in life (3-5).

The current work is based on data of a follow-up study from Jamaica, which
represents a geographic sub-sample of the previously conducted Jamaican
Perinatal Morbidity and Mortality Survey. Offspring Of mothers who participated
in the Jamaican Perinatal Morbidity and Mortality Survey, conducted in
September and October 1986, were re-contacted in 1998. In utero and perinatal
factors were investigated to assess their contribution to the development of
asthma and other atopic manifestations in children 11 to 12 years of age.
Specifically, the association between two risk factors was tested:

(1) Maternal use of oral contraceptives (OC) before pregnancy
(2) Maternal complications during pregnancy
and their influence on the following outcomes:

(3) Asthma or wheezing,

(b) Frequent nighttime/early morning cough,
(0) Eczema, and

(d) Hay fever, sinus problems or other allergy.

Chapter 1

IN UTERO AND PERINATAL EVENTS AS RISK FACTORS FOR ASTHMA AND

OTHER ATOPIC MANISFESTATIONS
In Utero conditions

Although the contribution Of genetics to the atopic phenotype is substantial, the
penetrance of genetic traits is highly dependent on interactions with the
environment. Environmental exposure begins at conception. Because the fetus
contains paternal antigens, it will more likely be rejected by the mother‘s immune
system as a transplanted allograft. In transplantation models, it is thought that
Th-1 lymphocytes are responsible for acute rejection and that Th-2 cells work to
maintain tolerance. During pregnancy, the matemal-fetal interface is an
immunologically active site producing many cytokines. Numerous lines of
evidence point to a dominance of Th-2-type cytokines in the uterine environment.
Fetal cord blood lymphocytes are skewed toward the Th-2 type. Neonatal T cells
produce low levels Of lFN-y and overproduce Th-2 cytokines. Matemal
lymphocytes produce lL-5 in response to normal allogenic placenta, whereas
placentas from abortion-prone pregnancies cause lymphocytes to secrete lL-2
and lFN-y (6). At birth, the immune system of the fetus has been strongly shifted
toward a Th-2 lymphocyte profile (7). In mothers with atopic disease, this effect
may be exaggerated. If this skewed fetal immune response is not rebalanced by
stimuli that restore the normal Th-1/Th-2 balance, the child may become

predisposed to atopic manifestations (6).

Perinatal Events

Perinatal events, focuses on those pertaining to or occurring in the period
shortly before, during or after birth. More specifically, those defined as beginning
with completion of the twentieth to twenty eighth week Of gestation and ending
seven to twenty eight days after birth.

In this period Of development, infants are especially vulnerable to
infections, having no prior exposure to the microbes in the environment at birth.
lgA antibodies are secreted in breast milk and thereby transferred to the gut of
the newborn infant, where they provide protection from newly encountered
bacteria until the infant can synthesize its own protective antibody.

lgA is not the only protective antibody conferred on the infant by 'its
mother. Maternal IgG is transported across the placenta directly into the blood
stream Of the fetus during intrauterine life. Babies at birth have as high a level of
plasma lgG as their mothers, and with the same range of specificities (8). lgG
has the ability to neutralize toxins and vinrses and immobilize bacteria.

T cells are also critical to the pathogenesis Of allergic diseases. It has
been hypothesised that atopy in children represents the persistence Of prenatal
and neonatal allergen specific Th2 responses due to failure Of immune deviation
mechanisms which promote the Th1 state Of the normal adult immune system (9,
10). There is evidence that during pregnancy the maternal immune responSe is of
the Th2 type, as Th1 type cell mediated immune responses are potentially

harmful to the maintenance of pregnancy (10).

Early postnatal factors such as breastfeeding and sites Of antigen
presentation may also affect the neonate's immune response in important ways.
There is evidence to suggest that exposure to maternal allogeneic cells during
breastfeeding leads to donor specific hyporesponsiveness in the neonate (11).

Antibody response to environmental allergens in the perinatal period is
also a concern for atopy. Immune responses to allergens early in life, perhaps
even in utero, may be critical to the pathogenesis Of atopy later in life. Children
produced lgG1 but not lgG4 antibodies against an inhaled allergen between three
and 12 months of age. Data suggest that lgG4 antibodies increase with age
although the majority of the studies were not performed prospectively. Inhaled
allergens are known to stimulate CBMC produced IL-4, IL-5 and lL-9 (mRNA), IL-
6, IL-10, and lL-13 (protein) but very little lFN-y (mRNA or protein). Allergen
specific cytokine production changes with age. Between birth and two years lL-4
mRNA production decreased in non-atopic children but persisted in atopic
children. lFN-y mRNA production increased significantly between birth and six
months in non-atopic children but not in atopic children. Whether absolute levels
of Th1 and Th2 cytokines are significantly different in atopic and non-atopic

children at the age Of two is less clear (10).

Chapter 2
ATOPIC MANIFESTATIONS! DISORDERS

The use Of the term atopy or atopic in designating an allergic reaction implies a
hereditary factor expressed as susceptibility to hay fever, asthma or eczematoid
dermatitis in the families of affected individuals (12). Clinically, it is an immune
disorder, which is manifested as a Type 1 hypersensitivity reaction including
asthma, eczema and/or rhinitis. It is Characterized by a genetic predisposition for
generating lgE antibodies against common environmental allergens. Atopic
individuals may differ from nonatopic individuals in their ability to regulate
production of lgE antibody. The production Of lgE in B—lymphocytes is regulated
by cytokines. lL-12 is one of the important cytokines which down-regulate lgE

production (13).

Astbm

Asthma is the most chronic disease in childhood. In the United States, it is
responsible for frequent admitting diagnosis in children’s hospitals than any other
condition, and results nationally in 5-7 lost school days/yrlchild. As many as 10-
15% of boys and 7-10% of girls may have asthma at some time during childhood.
There is no universally accepted definition of asthma. It may be regarded as a
diffuse, obstructive lung disease with hyperreactivity Of the airways to a variety of
stimuli and/or a high degree Of reversibility Of the Obstructive process, which may

occur either spontaneously or as a result Of treatment (12). Whilst its etiology is

still very ubiquitous, Maddox et al. suggest that it involves the interaction
between genetic factors and environmental stimuli. They also postulated that the
vast majority Of data regarding the pathogenesis Of asthma is concentrated on
Th-1 and Th-2 imbalance between the phenotypes. However, asthma (reversible
airflow Obstruction, persistent airway hyperreactivity, and ainrvay remodeling),
may also occur through nonallergic mechanisms of inflammation. Genetics, the
uterine environment, maternal and infant diet, respiratory infections, and

occupational and environmental exposures all contribute to this delicate balance

(6)-
Occgrrence Of asthma in children

Asthma may have its onset at any age. Approximately 30% of patients are
symptomatic by one year Of age, whereas 80-90% Of asthmatic children have
their first Symptoms before four to five year Of age. The course and severity of ‘
asthma are difficult to predict. The majority of affected children have only
occasional attacks Of slight to moderate severity, which are managed with
relative ease. A minority experience severe, intractable asthma, usually
perennial rather than seasonal. It is incapacitating and interferes with school
attendance, play activity, and day-to—day functioning. The relationship of age of
onset to prognosis is uncertain. Most severely affected children have an onset of
wheezing during the first year of life and a family history Of asthma and other

allergic diseases (particularly atopic dermatitis) (12).

Clinical Manifestations

The onset of an asthma exacerbation may be acute or insidious. Acute
episodes are most often caused by exposure to irritants such as cold air and
noxious fumes (smoke, wet paint) or exposure to allergens or simple chemicals,
for example, aspirin or sulfites. Exacerbations precipitated by viral respiratory
infections are slower in onset, with gradual increases in frequency and severity of
cough and wheezing over a few days. Because airway patency decreases at
night, many children have acute asthma at this time. The Signs and symptoms Of
asthma include cough, which sounds tight and is nonproductive early in the
course Of an attack; wheezing, tachypnea, and dyspenea with prolonged
expiration and use Of accessory muscles of respiration; cyanosis; hyperinflation
of the Chest; and tachycardia and pulsus paradoxus, which may be present to
varying degrees depending on the stage and severity of the attack. Cough may
be present without wheezing, or wheezing may be present without cough.
Tachypnea also may be present without wheezing. Manifestations will vary

depending on the severity of the exacerbation (12).

Coughing

Aspiration of a laryngeal foreign body Often causes a sudden onset of
coughing with choking followed by wheezing. An intermittent, recurrent, dry
cough or a cough productive of clear mucus is consistent with asthma, but a
chronic persistent cough productive of pumlent sputum suggests bronchiectasis

or cystic fibrOsis.

Coughing or wheezing following strenuous exercise may occur in children who
have asthma. Provocation of coughing by laughter, crying, or exposure to smoke
or specific Odors also suggests the bronchial hyperresponsiveness characteristic

Of asthma (14).

Atopic dermatitis or eczema .
Edward D. Perry Of the University Of Colombia coined the term atopy in the early
19203 (15). Wise and Sulzberg clinically characterized the term “atopic
dermatitis” (AD) in 1933 (16). This term was used to describe a skin condition
characterized by intense dryness Of the skin, pruritus, and chronic erythematous
lesions with a relapsing course.

Atopic dermatitis is clearly related to an atopic phenotype in most patients.
The family history is most Often positive, and elevated total lgE antibody levels,
or positive specific IgE antibody to common allergens might be observed (17).
There is conflicting evidence as to whether the level of IgE is related to either the
severity or the extent Of the dermatitis. The concentration Of lgE does, however,
fluctuate with the stage of the disease. The level returns to normal when the
disease has been quiescent for several years. It is not established that AD is
primarily an lgE-mediated allergic disorder. It is difficult to demonstrate
consistently a role for allergens, whether foods or inhalants, in the pathogenesis
of eczema.

Increased concentrations of lgE in atopic dermatitis may be related to a

deficiency of lgE isotype-specific “suppressor” T-ceIl function. Impairment of cell-

mediated immunity in some patients with AD is indicated by (1) absence of the
reactions Of delayed hypersensitivity on intraderrnal Skin testing with certain
antigens; (2) inability to be sensitized with potent contact sensitizers (e.g., poison
ivy, dinitrOchoIorObenzene); (3) diminished proliferative response of lymphocytes
to mitogens such as phytohemagglutinin; and (4) variable phagocytic and
chemotactic defects of monocytes and neutrophils.

Potential primary immune abnormalities for AD include an increased
frequency Of allergen-specific Th2 cells that secrete various interleukins (IL-4, IL-
5, lL-13) and reduced activity of Th1 cells. Th2-type cytokines may initiate the
acute inflammatory response. Allergen-reactive T cells, which expressthe
cutaneous lymphocyte-associated antigen, may migrate to the skin and initiate
disease (12).

Clinical Manifestations

Atopic dermatitis affects 2-10% of children and typically occurs in three
stages with fairly distinctive features. The disease most Often begins in infancy,
usually during the first two to three months of life. The onset is sometimes
delayed until the second or third year. Approximately 60% Of patients are
affected by first year Of age and close to 90% by five year of age. The earliest
lesions are erythematous, weepy patches on the cheeks, with subsequent
extension to the remainder Of the face, neck, wrists, hands, abdomen, and
extensor aspects of the extremities. Involvement Of flexural areas
characteristically appears later, but may occur as popliteal and antecubital

dermatitis in early life.

10

Pruritus is marked. The affected infant makes incessant efforts to scratch
by nibbing the face on bedclothes and against the sides Of the crib. This trauma
to the skin rapidly leads to weeping and ansting. Secondary infection is common
and may be extensive.

The onset Of dermatitis frequently coincides with the introduction of certain
foods into the infant’s diet, especially cow milk, wheat, soy, peanuts, fish, or
eggs. Cutaneous symptoms develop after food challenges in 50-90% Of infants
and children who have dermatitis and high lgE senJm concentrations. Overall,
about 20-30% of patients with eczema have food hypersensitivity to one or more
Of the six common allergens. There is an unequivocal evidence of lgE sensitivity
in certain infants who have urticaria, colic, and a diffuse erythematous flush
following ingestion of the Offending food. The erythematous flush appears to be
accompanied by intense itching, which results in scratching and then in the
appearance of the skin lesions characteristic Of eczema. The major role of
scratching in the production of skin lesions has been demonstrated when one
extremity has been encased in surgical dressings and the other left uncovered.

The lesions Of atopic dermatitis occur only in the uncovered extremity (12).

Hay fever. sinus problem

Allergic rhinitis (AR) or hay fever, sinus problem, is a heterogeneous
disorder, which is characterized by one or more symptoms including sneezing,
itching, nasal congestion, and rhinonhea. Many causative agents have been

linked to AR including pollens, molds, dust mites, and animal dander. AR affects

11

an estimated 20 to 40 million people in the United States alone, and the
incidence is increasing; an estimated 20% of cases are seasonal allergic rhinitis
(SAR); 40% of cases are perennial rhinitis; and 40% of cases are mixed
(1 8).

Pathophysiolggy

Inhaled pollens, mold spores, and animal or mite antigens are deposited
on the nasal mucosa. Water-soluble antigens diffuse into the epithelium and, in
genetically predisposed atopic individuals, initiate the production Of local lgE.
lgE-stimulated release Of mast cell mediators, synthesis of new mast cell
mediators, and subsequent recruitment of neutrophils. eosinophils, basophils,
and lymphocytes are responsible for the early- and late- phase reactions to
inhalant allergens. These reactions result in mucus, edema, inflammation,
pruritus, and vasodilation. Delayed inflammation may contribute to nasal
hyperresponsiveness to specific allergens, a priming effect, and to nonspecific

stimuli such as irritants and strong Odors (12).

Atopic Qisorcfisgosing Notes

In Closing, it is important to note that there is a noticeable proportion of combined
occurrence Of eczema, hay fever and allergic asthma in childhood. Kuehr et al.
support this in a study in a cross-sectional study Of 1376 eight-year-Old pupils

(19).

12

Chapter 3

A REVIEW OF THE ASSOCIATION BETWEEN IN UTERO AND PERINATAL
EXPOSURES AND ATOPIC MANIFESTATIONS.

Aretaeus, Greek physician of Cappadocia, is believed to be the first to attempt to
associate a cause for asthma. In the 2nd or 3rd century AD, he described the
cause to be a coldness and humidity of the spirit (20). Ever since, researchers
have been conducting studies in this area, identifying a plethora of potential
factors involved in the pathogenesis Of asthma and other atopic manifestations.
These factors span three general time-windows; namely, in utero or prenatal,
peripartum or perinatal, and neonatal or postnatal periods.

In the in utero or prenatally time window, maternal smoking, estrogen
levels and infection during pregnancy, are some factors, which may increase the
risk for asthma and atopy. Mode of delivery, neonatal or early childhood illness,
and breast-feeding are all suspected factors during the peripartum or perinatal
period. Postnatally, neonatal or early childhood illness and breast-feeding are
under increasing scrutiny as to their possible role in the development of asthma
(20).

In an attempt to Sort out the complex intenelationships of some of these
potential influences on the development of atopy, this paper will focus on two Of

the three above-mentioned time-windows, namely the in utero and perinatal.

13

Factors associated with the in gtero time-Wm

MattflalsmokLng

Studies investigating the hazardous effects Of contact with tobacco on the
health of the infant can be traced back to as early as 1931. Mgalobeli compared
women who worked in different industries and found that workers in tobacco
factories had a greater infant mortality rate in the age range 1 —3 years (21 ).
Sontag and Wallace in 1935 found a direct impact on the fetus when they
Observed that cigarette smoking during pregnancy increases the human fetal
heart rate (22).

There has been a renewed interest in the association between in utero
cigarette smoke and childhood health outcomes. Oliveti et al. assessed the
relation between in utero risk factors and asthma using a case-control study Of
262 African-American children aged 4-9 years, both asthmatic and nonasthmatic,
all Of whom resided in a poor urban area and received health care at a local
hospital-based clinic. Risk factors were ascertained through review of Obstetric,
perinatal, and pediatric records. They found mothers Of asthmatic children were
more likely to have smoked during pregnancy (50% vs. 27%), than mothers of
nonasthmatic children. Multiple logistic regression showed maternal smoking
during pregnancy (OR = 2.8) to be one Of the strongest independent predictors of
asthma (23).

Though not a universal finding, maternal smoking during pregnancy has
been reported to increase cord blood lgE and lgD levels and to increase

substantially the risk for atopic disease (eg, dermatitis, asthma, or food allergy or

14

intolerance) before 18 months Of age. These effects were most pronounced in
infants Of mothers who had no history of atopic disease. The mechanisms by
which maternal smoking may exert its effects are unknown. However, active
smoking has been Shown to increase the inducibility Of peripheral blood
mononuclear cells to secrete lL-4, an effect that wanes fairly rapidly upon
smoking cessation. It is conceivable that this effect extends beyond maternal
circulating immune cells to placental or fetal cells (20).

Estmgen levels during pregnancy

In an aggregative study, stt et al. performed an assessment of women
using 00 from the Great Britain Population Report Of 1997, and Of children aged
5-14 years who were discharged from the Welsh hospital after being diagnosed
with asthma. They found a geographic trend, which showed asthma prevalence
in children ninning parallel to that of maternal OC use. This Similarity was most
notable during 1970 when and sharp decrease in the rate of increase Of 00 use
was followed by a similar decrease in rate of hospital discharge with a diagnosis
of asthma. Results Of an aggregative (ecological) study, stt et al. deduced
that mother's oral contraceptive use fits well into the geographic and temporal
background of this increase in asthma prevalence (3).

Many studies have presented evidence, which suggest that early age Of
menarche is associated with higher levels Of estrogen in adulthood (24-26). A
geographically defined cohort Of 5188 subjects born in northern Finland was
used to evaluate whether maternal age at menarche is associated with atopy

among offspring at age 31 years. Logistic regression models were used to adjust

15

for maternal age, parity, smoking, season Of birth, parental allergy, and measures
of adiposity and socioeconomic status. Results showed the prevalence of atopy
at 31 years Of age, was lower in children whose mothers reached menarche at a
later age, especially after age 15. Table 1 shows the adjusted odds ratio for

children whose mothers started menarche younger than or at age12, 13, 14 and

Table 1. Association between maternal age at menarche and occurrence of
atopy in children at 31 years (4).

Maternal age at menarche Total no. % Crude OR Adjusted OR“

 

 

(years) (atopic) (95% CI) (95% Cl)

512 694 34.9 1 .49 1 .43
(242) (1.19 to 1.87) (1.12 to 1.83)

13 1181 32.8 1.36 1.29
(387) (1.11 to 1.66) (1.03 to 1.60)

14 1406 30.2 1.21 1.15
(424) (0.99 to 1.47) (0.93 to 1.42)

15 1145 30.0 1.20 1.19
(344) (0.98 to 1.47) (0.95 to 1.48)

216 762 26.4 1.00 1.00

(201)
A p for trend 0.000 0.005

 

' Adjusted variables were defined In the following ways: maternal age s20, 21 -25, 26-30, 31-
35, and 236 years; maternal social classes I + II (professionals with the highest education
and other white collar workers), Ill (skilled workers), IV (unskilled workers) and farmers;
maternal smoking in pregnancy yes or no; parity 0, 1, 2-3 and 24; seasons at birth March-
May, June-August, September-November and December-February; parental allergy yes if
either the father or mother had allergic disorders, otherwise no; current vocational training
In five categories; maternal BMI, ponderal index and current BMI in quintiles (4).

15 years Of age compared to those who started menarche 16 years or over (4).

These results suggest that the intrauterine environment might be important in

later life in terms of development of adult atopy, at least for the mechanism

16

underlying the association Observed (4). This finding supports previous

hypotheses that high maternal estrogen level is a risk factor for atopy.

Maternal infectjon during pregnancy

It has been shown that transplacental sensitization Of the fetus can be
accomplished by maternal immunization during pregnancy. A study of Children,
nine to 16 years Of age, born to mothers infected with Onchocerca volvulus
during pregnancy found higher levels of skin microfilariae than in children Of
uninfected mothers. This correlated with higher production of Th2-type cytokines
in response to onchocercal antigens by peripheral blood mononuclear cells from
these children compared with controls. This Th2-like response is similar to that
observed in models Of neonatal sensitization (20).

Results from a prospective study Of 8088 children of the northern Finland
birth cohort 1985-1986, showed that children had a higher risk of asthma if their
mothers experienced vaginitis and febrile infections during pregnancy, OR =
1.41, (95% CI: 1.08-1.84) and 1.65 (95% CI: 1.25-2.18) respectively. A clear
time trend in risk Of childhood asthma corresponding to the timing of maternal
febrile infections in pregnancy was also seen. Adjusted OR for the first, second,
and third trimesters were 2.08, (95% CI: 1.13-3.82), 1.73 (95% CI: 1.09-2.75) and

1.44 (95% CI: 0.97-2.15) respectively (27).

Maternal complications during prpgnancy

There is a paucity of studies on the relationship between maternal

 

complications during pregnancy and the risk of having asthma or any atopic

17

disorders. Nafstad et al. conducted a population-based, four-year, cohort study
involving 2531 children (28). Information was collected on matemally-
(hyperemesis, hypertension, and preeclampsia) and uterus- (antepartum
hemorrhage, preterm contractions, insufficient placenta, and restricted growth of
the uterus) related complications in pregnancy. Asthma was assessed at age
four years. After controlling for potential confounders, they found that uterus-
related complication increased the risk Of having asthma (AOR, 3.0; 95% CI, 1.8-
5.4) and allergic rhinitis (AOR, 2.9; 95% CI, 1.6-5.2).

Complications, which occur in the perinatal period and their relation to
asthma, was also addressed by Annesi-Maesano et al. (5). Using a large British
birth cohort Of 4065 natural children of 2583 mothers, from the National Child
Development Study. Maternal complications during pregnancy was defined as
any complication which had needed medical supervision apart from routine
checks and hospital admissions at any time during pregnancy before labor
began. After adjusting for relevant confounders, they found maternal
complications during pregnancy to be a risk factor Of asthma (OR, 2.01; 95% CI,
1.52-2.67) in the offspring. To assess the possibility that this association was not
purely due to a specific complication, independent analyses were conducted to
test the association between each specific complication and asthma. Only early
or threatened labor and malposition and malpresentation Of the fetus at birth
(namely, breech, transverse lie, and face presentation) was found to have

significantly increased the risk of asthma for the child.

Factprs associated with the perinatal time-window

18

Mode of delivenl

The relation between factors associated with parturition, and their
influence on the pathogenesis of atopy is Uncertain. In a prospective birth cohort
born in northern Finland in 1966, Xu et al. evaluated the relationship of
caesarean section to the risk of asthma in adulthood. lnfonnation on current
doctor-diagnosed asthma and other allergic disorders was Obtained from 1953
subjects by a self-administered questionnaire and skin prick test. Results showed
that caesarean section had a strong effect on current doctor-diagnosed asthma
in adulthood with an adjusted Odds ratio (OR) Of 3.23 (95% Cl 1.53, 6.80).
However, no substantial effects were Observed for atopy, hay fever, and atopic
eczema (29).

AnneSi-Maesano et al. challenged this finding using the afore mentioned
cohort from the National Child Development Study. Analyses were adjusted for
potential confounders. It was found that delivery by emergency caesarean was
not significantly related to childhood asthma. Adjusted OR =0.92; 95% Cl 0.44,
1.86) (5).

Later, McKeever et al. supported findings of Xu et al. In a birth cohort of
24 690 children who contributed to the West Midlands General Practice
Research Database they assessed whether the way in which babies were born
has an impact on their subsequent risk of allergic disease. After controlling for
potential confounders (sex, prematurity, consulting behavior of the child, parental
atopy, year Of birth, general practice, maternal age, and parental smoking) they

found that being born by forceps or vacuum extractor delivery was associated

19

with an increased risk of developing eczema, incidence rate ratio [(IRR) 1.21;
95% CI, 1.11-1.31]. Similarly, there was an increased risk of asthma with a
caesarean birth (IRR 1.09; 95% CI, 1.01-1.18). They concluded that this did not
provide an association strong enough to suggest that babies born by caesarean,
forceps, or breech delivery had an increased risk of developing allergic disease
(30).

Neonatal and early childhood illness

Whilst there are numerous studies addressing the specific association
between childhood infection and atopy, there is but one to my knowledge that
assesses the non-specific childhood illness atopy relationship. This area was
one examined in the previously mentioned study by Annesi-Maesano et al. The
exposure “childhood illness” was based on whether the child had any illness or
complication during the first week of life. They found child illness or health
complications during the first week of life to be a risk factor for asthma at age 33

years (AOR =1.35; 95% CI 1.01—1.82) (5).

Breast-feeding
Since Gmlee and Sanford in 1936 (11), first reported that breastfeeding

protects against infantile eczema, the relation between breastfeeding and
Childhood atopic disorders have been conflicting.

The relation between breastfeeding and the prevalence Of asthma among
a childhood population was tested in a population-based case-control study. The
study population included 2,315 students with asthma and 21,513 controls all -

from public elementary and junior high schools in Tokorozawa, Japan (age

20

range, 6—1 5 years). After adjusting for age, gender, parental smoking status,
and parental history Of asthma, a significantly higher prevalence Of asthma was
noted among children who had been breastfed (adjusted OR = 1.198; 95% CI:
1.05, 1.36). Results from this study suggest that breastfeeding in infancy may be
related to a higher prevalence Of asthma during preadolescence (11).

After conducting a systematic review Of prospective studies that evaluated
the association between exclusive breast-feeding during the first 3-months after
birth and asthma, Gdalevich et al. found the Opposite to be true. They found
summary Odds ratio (OR) for the protective effect of breast-feeding to be 0.70
(95% Cl 0.60, 0.81 ). Their conclusion was that exclusive breast feeding during
the first months after birth is associated with lower asthma rates during childhood

(31).

21

Chapter 4

THE JAMAICAN PERINATAL MORBIDITY AND MORTALITY SURVEY

For this project, preexisting datasets from the Jamaican Perinatal
Morbidity and Mortality Survey were used. These datasets provided the
exposure variables whilst the outcome variables came from the follow-up study

conducted when the children were approximately 11 years Old.

Background and Rationale

The motivating factors, which lead to the development Of the Jamaican
Perinatal Morbidity and Mortality Survey is based on the results of the Child
Mortality Study Of 1972 that clearly demonstrated the extent Of under-reporting Of
early infant deaths. Following these results, the research team submitted a
project proposal with draft questionnaires in December 1984 and funding
approved in June 1985. It was agreed that the study would be implemented
through the University Of the West Indies’ Child Health Department, although the
principal investigators were full time employees of the Ministry Of Health.
Preparatory work for implementation of the study was initiated in December

1985.

22

Aims and Objectives

The overall aim of this study was to provide information that will help
improve the maternal and Childcare services and reduce perinatal morbidity and

mortality in Jamaica.
Objectives specific to this study

Morbidiy

1. TO identify the infants who get ill in the neonatal period and determine the
causes Of neonatal morbidity.

2. To identify maternal, environmental and clinical characteristics predictive of
serious neonatal morbidity.

3. TO determine whether criteria used to identify pregnancies at high risk of

mortality also adequately identify those at high risk Of major morbidity.

Low birth weight

1. TO identify the birthweight distribution and birthweight-specific mortality and
morbidity rates.

2. TO determine maternal, environmental and clinical factors associated with: (a)
low birthweight associated with short gestation; (b) low birthweight associated

'with growth retardation.

Methodology

In order to achieve the Objectives of the study, Observation periods of
different lengths were required in order to attain adequate sample sizes. The

survey was divided into four components: (a) main cohort study (2 months), (b)

23

neonatal morbidity (6 months), (0) perinatal mortality (12 months) and (d) service

evaluation to run concurrent with the cohort study.

Organization and administration Of t_he stfly

 

A 15 member Steering Committee was established in January 1986 to act as an
advisory body, providing the necessary input advice and critique in the
organization and implementation of the study. This included Obstetricians,
pediatricians, pathologists and midwives.

game

There were two full-time professional members Of staff employed on the study -
the Study Administrator and the Pediatric Research Officer.

At the field level, each parish had a coordinator with responsibility for
managing study activities and supervising the team Of interviewers. The eight
larger parishes also had an assistant coordinator. Full-time interviewers were
assigned to the hospitals and a core Of district midwives (field interviewers) were
selected to interview mothers delivering at home. A nominal cash incentive of
two Jamaican dollars, equivalent to $USO.36, was Offered to other members Of
the primary health care team who brought the occurrence Of a delivery tO the

attention Of the field interviewers.
The main cohort

In this phase, all pregnant women were included who had a live birth, or stillbirth
Of 500 g or more, during the two-month period September 1, 1986 to October 31,
1986, regardless of the place Of delivery. These women were interviewed and

their babies examined, usually within the first 48 hours after delivery. Between

24

six weeks and three months after delivery mothers and their infants were again
interviewed and examined at postnatal clinics. Those persons who went to
private doctors or who failed to Show up for their clinic appointments were visited

at home to facilitate completion of the follow-up questionnaire.

Morbid'fl commnent

All babies with major illnesses admitted to any Of the neonatal care units in any Of
the eight hospitals with pediatric consultants were included in the morbidity study.
Each case had a neonatal admission questionnaire completed by the attending
pediatrician and the mother was interviewed. The survivors were followed up at

six weeks.
Service evaluation

In order to measure the potential impact of services on outcome, an evaluation of
institutional and domiciliary services was undertaken.

(i) Institutions (public hospitals and maternity centers) were assessed by
direct observation of the practice Of Obstetrical care on randomly selected days
during the two months Of the main cohort study. An inventory Of basic equipment
and supplies used for obstetric and newborn care and the staff complement were
also included.

(ii) For the field domiciliary evaluation, a 25% sample of district midwives was
interviewed to assess the knowledge and practice Of domiciliary midwifery and

the availability of basic supplies and equipment.

25

Training and sensitization

The project manager received training in perinatal epidemiology, two Of the
pathologists spent one and two weeks undergoing instruction in perinatal
pathology. Parish coordinators, their assistants and interviewers were trained in
the two months prior to implementation Of the study.

A series of briefing meetings were held between the study team and
members Of staff Of each parish Health Department (primary care), Obstetric and
pediatric units and other relevant staff at all hospitals (private and. government),
members Of the Association Of general practitioners, Pediatric Association Of
Jamaica, Medical Association Of Jamaica and the Association of Obstetricians
and Gynecologists. The Heads of the Departments Of Pathology and
Microbiology at the University of the West Indies were also briefed and their help

and cooperation solicited.

Management

The island (Figure 1) was divided into four regions along the major migratory
routes Of patients in search of medical care. Coordinators could therefore come
in contact with persons in adjacent parishes where a mother may have had
antenatal care or been delivered.

Coordinators would visit hospitals daily in the first phase (September and
October 1986) and at least twice weekly in the second phase (November 1986 to
August 1987) to keep track Of deliveries, neonatal admissions and deaths, collect
completed questionnaires and ensure their submission to the national Office. The

mail service was not to be used, as this can sometimes be unreliable With long

26

delivery delays. All material was to be transferred by messenger or by the
coordinators themselves.

Each parish coordinator was provided with a supervisor's manual setting
out guidelines for completion and preliminary processing Of the questionnaires as
well as administrative procedures and the maintenance of a register Of all
deliveries and deaths in the parish during the study period.

Interviewers were also provided with manuals, which outlined basic
interviewing techniques and took them through each question on the relevant
questionnaires. Administrative procedures were also outlined.

Hospitals participating in the morbidity survey Were provided with neonatal
admission forms and newborn nursery charts to guarantee the collection of
uniform basic information on the neonate. The neonatal admission
questionnaires were for completion on discharge (or death) Of the infant.

Each mother who attended between six weeks and three months post-
delivery was presented with a certificate on which was included her child’s study
number. At one year of age the infants were sent birthday cards. These were
used in the hope that they will facilitate subsequent follow-up studies Of the

cohort.

27

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28

Questionnaires relevant t9_t_his stt_rgy

Three questionnaires were developed, pre-tested and finally used in the study; all
but the pathology questionnaire were pre-coded.
1. The main questionnaire contained information on past Obstetric history, social
and environmental factors, the antenatal period, labor and delivery. Infants were
examined and supplementary information from institutional record included.
Antenatal, intrapartum and postpartum data were supplemented by other
hospital, clinic or doctor’s records as necessary. Often this entailed collaboration
between parish coordinators, especially where antenatal records were required.
2. The follow-up questionnaire contained sections relating to the postnatal
status Of the mother and the infant. The questionnaire was completed by
interviewing the mother, and examining both mother and infant.
3. The neonatal admission form was completed by the attending pediatrician or
study research pediatrician for each newborn admitted to newborn nurseries
before the age Of 28 days.

Prior to the implementation of the study-a standardized newborn nursery
chart was introduced in all nurseries to facilitate completion of the neonatal

admissions questionnaire.

Data Processing

Questionnaires were checked by the clerical staff and reviewed by the Study
Administrator, the pediatrician and a small team Of reviewers. These
questionnaires were then microfilmed prior to being coded and the data were put

on transcription sheets. These sheets were then transferred to a private data

29

processing company for data entry and computer editing (range and logic tests).
This was supervised by the statistician at the Health Information Unit Of the

Ministry Of Health.
Preliminarv resulfi

There were 10,310 births during the main cohort study, 8,956 (87%) Of these
were followed up in the postnatal period. A total Of 393 deaths were identified in
the main cohort giving a perinatal mortality rate Of 38.1 per 1000 total births.

There were 1,405 neonatal admissions to specialist units during the 6-
month study period.

A total Of 1,855 fetal and early neonatal and 73 late neonatal deaths were
identified during the 1-year study. Postmortem examinations were undertaken
on 1,021 Of the 1,855 perinatal deaths yielding an overall postmortem rate Of
55%.

A total Of 78 midwives were interviewed for the domiciliary service
evaluation. Observations were done at all public hospitals and maternity centers.
Information for this section (I' he Jamaica Perinatal Morbidity Mortality Survey) to
this point was taken from the publication on the preliminary work of this survey
(32).

Follow-up of 11 to 12 year Old children.

Subsequent to the completion Of the first follow-up at six weeks Of age, the
11 to 12 year old children follow-up was initiated. This aspect of the study was
conducted chiefly in the parish Of Kingston and St. Andrew in the island Of

Jamaica. These parishes are the two most highly urbanized Of the fourteen and

30

function as a single political unit. Approximately 27% Of the island’s population
lives in Kingston and St. Andrew. It is only in this sub-population that the health
questionnaire was administered. This instmment was used to Obtain information
on early childhood development, past medical illnesses, and current medical
concerns (33). The current work is responsible for merging datasets from the
Jamaica Perinatal Morbidity and Mortality Survey and the follow-up study for the

first time.

31

Chapter 5

METHODS

Study Population and Desigp

The Jamaican Perinatal'Morbidity and Mortality Survey was aimed at all pregnant
women who had a live birth or stillbirth during the two-month period from
September 1, 1986 to October 31, 1986. A face-tO-face interview was conducted
with these women and their babies examined, usually within the first 48 hours
after delivery. A standardized questionnaire was used to get at data during the
antenatal, labor and delivery, and perinatal periods. This questionnaire is
referred to as the main questionnaire (MQ). Overall, 10,310 (94 %) of the births
in the two-month period were identified and included in the study (main cohort
study) (34).

At the first follow-up, at six weeks Of age, information on breastfeeding
and the infant’s health were ascertained using another standardized
questionnaire during a face-tO-face interview. For the benefit of this project this
questionnaire will be referred to as the first follow-up questionnaire (FFUQ).

A geographic sub-sample of 1,720 eleven to twelve year Old children,
representing those born in Kingston and St. Andrew, was selected for a second
follow-up. In a cross-sectional survey of these children, data on health outcomes
were collected from the parent or guardian and recorded using the second follow-

up questionnaire (SFUQ).

32

All three datasets were carefully linked using a unique identification
number and date of birth for both mother and child for the analysis proposed in

this project.

Q_u_e_st_jonnaires armfinitjon of variables
- Copies of questiOnnaires are provided in the appendix.

The primary goals of the Jamaica Perinatal Morbidity and Mortality Survey
was to assess a more precise estimate Of perinatal mortality, to identify causes Of
death and to determine the maternal, social and environmental factors predictive
of fetal and early infant deaths in Jamaica. TO this end standardized
questionnaires adapted in part from the First British Perinatal Mortality Survey
(34) were developed. Questions enabling us to determine in utero and perinatal
exposures were included. Using the MQ, the gender Of the child was recorded.
This questionnaire was also use to get at lnfonnation on past Obstetric history
was Obtained by asking mothers:

1. Have you ever been pregnant at any time before this pregnancy?

2. Total number Of pregnancies—

3. Have you ever used a contraceptive? If yes, which methods have you
used? I will go through a list: a). Intrauterine device (IUD) or coil, b). Depo
provera or injection, c). Contraceptive pill, d), Sperrnicidal cream, e).
Diaphragm, f). Vaginal foam, g). Condom, h). Rhythm method, i).
Withdrawal, j). Other if yes please describe

Questions pertaining to the mother during pregnancy were:

1. Did you smoke tobacco regularly at any time during this pregnancy?

33

Did you have vaginal bleeding in the first 28 weeks of pregnancy?

Did you have vaginal bleeding after 28 weeks (7 months)?

Have there been any other complications, disorder or serious illness
during this pregnancy?

After starting antenatal care, were you referred during pregnancy for any
reason?

Were you admitted to hospital or nJral matemity center during this

pregnancy but before labor?

Additional information from the antenatal records were used to answer the

following questions for this section:

1.

99"!"

Was the mother referred to the medical officer during pregnancy for any
reason?

Did the mother have vaginal bleeding in the first 28 weeks Of pregnancy?
Did the mother have vaginal bleeding after 28 weeks of pregnancy?

Did she have a vaginal discharge or infection during this pregnancy?

Did the mother have any Of the following during this pregnancy: a). Urinary
tract infection, b). Tuberculosis, c). Rubella (German measles), d).
Gonorrhea, e). Syphilis, f) Genital sores or blisters during pregnancy?
Indicate results and dates of venereal disease research laboratory (VDRL)

test.

. Was the mother diagnosed as having hypertension, pre-eclampsia or

eclampsia during this pregnancy?

34

8. Did the mother have any of the following during this pregnancy; epilepsy,
eclamptic fits or heart disease and lastly, any other complications, disorder
or serious illness during this pregnancy?

Responses from these questions allowed the creation Of the “maternal
complications during pregnancy” and “maternal infections during pregnancy”
variables. Whether delivery was induced or by any other method was
ascertained by asking: How did labor start? [1] spontaneously [2] after induction
[3] no labor (elective CS) or [4] in other way. Information relating to whether
analgesic or anesthetic was given during labor was extracted from hospital
delivery notes. Additionally, the midwife was interviewed where necessary.

The variable “Maternal health complications during labor and delivery" was
defined as a positive answer to any of the following questions from the labor,
delivery and postpartum section Of the MQ:

1. Did the mother have eclamptic fits?

Did She haemorrhage?
Was labor Obstructed?

+5919

Did the uterus rupture?
Was mother transferred during labor?
Did the cord prolapse?

Was there meconium in the liquor?

9°.‘ISI’S’I

Were there any other complications?

35

Child’s birth weight was also recorded in the labor, delivery and postpartum
section of the MO. To facilitate analyses in this study, this variable was
categorized into <2.5kg, 2.5-4.0 kg and >40 kg.

At the first follow-up, when the child was four to six weeks Of age, the
following questions were asked from the first follow-up questionnaire (FFUQ):

1. Was the baby referred to a medical Officer?

2. Was the baby admitted to hospital or special care baby unit?

3. Were any abnormal symptoms noted in the baby?

A positive response to the abovementioned, in addition to hospital notes at
birth and questions from the SF UQ were used to create the variable “child’s
illness or health problems in first week of life".

1. Current status of baby — [1] Alive, healthy [2] Alive, ill [3] dead [4] NK.

2. Since birth until 28 days Old, did the baby have any Of the following:

a. Jaundice

b. Convulsions I twitching

0. Persistent vomiting

d. Diarrhea (3 or more loose stools)
e. Sticky or discharging eyes

f. Cord infection

9. Other infection

h. Other problems

36

3. Had the baby beenadmitted to hospital in the first 28 days of life
At the 11 to 12 year follow-up, parents were asked, “Has your child ever
had...:
1. Asthma or wheezing?
2. Frequent night time or early morning cough?
3. Eczema?
4. Hay fever, sinus problem or some other allergy?”
Children were defined as experiencing any Of the above if their parents gave a
positive response to the respective outcome.
The dependent variables of interest (asthma/wheezing, coughs, eczema

and hay fever) were captured as binary variables.

Statistical analysis

Prevalence Of the four atopic manifestations for the different ante- and
perinatal exposures were tabulated. Adjusted Odds ratios (AOR) and their 95%
confidence intervals (95% Cl) were estimated by logistic regression analysis. All
calculations were carried out using SAS software, release 8.2 (35).

Lpgiitic Regression

Logistic regression is an adaptation to dichotomous outcomes Of the
classical linear regression model for continuous outcomes. It is primarily used to
describe the relationship to the outcome of a primary exposure after adjusting for
the effects Of other (independent) variables that may influence both the outcome

and exposure.

37

Formally, in formulating a logistic model let Y (0 or 1) denoting the

dichotomous outcome of interest with Y =1 labeling the presence of the condition

under study. Then the logistic model for P[ Y=1 I X1, X2...X.,] is written simply as

P(X) where X is a shortcut for X1 through X, The model formula is given by

1

P(X')=1+e-(0I+El3ixi)

 

in which or and B. is representing unknown

 

parameters to be estimated based on the Observed exposure variables X1
through XI, and the outcome variable Y. The coefficients [31 through 8., can be
interpreted as adjusted log-odds ratios. For example, if X1 is the primary
exposure, mded X1 = 1 for “exposed” and X1 =0 for “not exposed”, then
assuming the variables X2 through XI, do not include X1, the AOR is given by
exPlBil-

The proposed hypotheses were tested in a model with gender, maternal
infection during pregnancy, maternal hospital admission during pregnancy,
induced labor, analgesic or anesthetic given during labor, maternal health
complications during labor or delivery, smoking during pregnancy, feeding
(breast only, breast and formulae, formulae only), birth weight (<2.5kg, 2.5 —
4.0kg and >4.0kg), and child’s illness or health problems in first week of life as

covariates.

38

Chapter 6

RESULTS

From the three data sets, we were able to successfully link 1040 (60.4%) of the
1720 mother-child pairs from the Kingston or St. Andrew sub-cohort. One child
was deceased. Table 2 shows the prevalence Of the outcome variables from the
total subpopulation compared to those from the linked data set. Approximately
17% of the children at approximately 11 years suffered from asthma or wheezing
while 20% experienced hay fever sinus problem or some other allergy. Frequent
nighttime or early morning cough was found in approximately 5% Of the children

while approximately 6% had eczema.

Table 2. Comparison characteristics of outcome variables in
sub-population and linked data set.
Sub-population data Linked maternal Child pairs

 

 

(%) M)
N 1163 1040
Factors
Asthma or Wheezing 17.0 17.3
Frequent night time or
early morning cough 4.8 5.3
Eczema 6.5 6.7
Hay fever Sinus problem 19.6 20.0

or some other allergy

Prevalence for each exposure variable is prevented in Table 3. Male gender
accounted for 47% Of the cohort. There was a 50% prevalence Of both maternal

00 use, and complication during pregnancy. The proportion Of mothers who had

39

infection during pregnancy, and who were admitted to hospital during pregnancy
was approximately 25.7% and 12.3 % respectively. Labor was induced for
approximately 7% Of the mothers while approximately 23% were given analgesic
or anesthetic during labor. There were 14.5% of mothers who experienced
health complications during labor or delivery while 7.5% smoked during
pregnancy. Report on breastfeeding showed 35% of the children were breastfed
exclusively, 59% had both breast and formulae feed while 6.4% were exposed to
formulae only. The proportion of children born low birth weight (<2.5 kg) was
12.2%, normal birth weight (2.5 kg - 4.0 kg) was 83.4% while 4.4% were born
weighing over four kilogram. Of the children in the study, 20.3% were ill or had

health complications in the first four weeks of life.

40

 

 

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41

The proportion of atopic disorders in relation to their in utero potential risk
factors is presented in Table 4. There was no difference in the proportion of
asthma in females vs. male gender. The prevalence for asthma or wheezing,
frequent nighttime or early morning cough, eczema, and hay fever, sinus problem
or some other allergy for children of female gender vs. those of male gender did
not present significant variation. Children of mothers, who used, compared to
those who did not use 00 before pregnancy, had a higher prevalence of asthma
(20% vs. 13.4%), frequent nighttime or early morning cough (7.4% vs. 3.6%) and
eczema (7.4% vs. 5.5%). Asthma (19.3% vs. 14.3%), frequent nighttime or early
morning cough (6% vs. 4.6%), eczema (7.4% vs. 5.3%), and hay fever, sinus
problem or some other allergy (22.2% vs. 18%) were more common in those
children whose mothers had complications during pregnancy than in those who
did not. Reports of asthma or wheezing, frequent nighttime or early morning
cough, and hay fever sinus problem or some other allergy for children of mothers
who had infections during pregnancy were to those who did not. The proportion
asthma or wheezing, frequent nighttime or early morning cough, and eczema
were not significantly different for children born to mothers who were and those
who were not admitted to hospital during pregnancy. When compared to children
whose mothers did not smoke during pregnancy, the proportion of mothers who

smoked during pregnancy were similar.

42

 

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5:050... Aocmcmma 582%: 50:00
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.9300: .2055. .0890... .80 .0E0fiS.
.0E0.0.>.

 

.8208 0.0... 0003 E :05 8 5.5.0.. :. 20200.0 0.00.0 “—0 53309.5 .0 0.00...

43

Table 5 shows perinatal risk factors and the proportion of their related
atopic disorders. Children who were delivered by induced labor reported having
a higher prevalence of asthma or wheezing (18.6% vs. 16.7%), eczema (11.4%
vs. 6%), and hay fever sinus problem or some other allergy (20.3% vs. 20.1%)
when compared to those who were delivered otherwise. Mothers who received,
when compared to those who did not receive analgesic or anesthetic during
labor, reported having children with a higher prevalence of asthma or wheezing
(18.3% vs. 16.6%), eczema (12.2% vs. 4.7%), and hay fever sinus problem or
some other allergy (28.8% vs. 17.2%). Children of mothers who had
complications during labor or delivery had a greater proportion of asthma or
wheezing (18% vs. 16.6%), frequent nighttime or early morning cough (8.1% vs.
4.8%), eczema (7.3% vs. 6.2%), and hay fever sinus problem or some other
allergy (21.5% vs. 19.9%). Of the feeding groups “breast only", “breast and
formulae”, and “formulae only”, asthma or wheeze (14.8%, 18.7% and 17.4%),
and frequent nighttime or early morning cough (5.9%, 6% and 4.6%) were more
frequently reported for those who were fed breast and formulae. There was a
higher proportion of hay fever sinus problem or some other allergy for those who
were fed formulae only, (16.5%, 20.6% and 24.4%) whilst frequent nighttime or
early morning cough was more frequently reported for the “breast only” group
(5.9%, 6% and 4.6%). Children who were born with LBW (<2.5kg) compared to
those born 2.5kg — 4 kg, and >4 kg had more frequent nighttime or early morning
cough (8.1%, 5.1%, and 4.4%) respectively. Asthma or wheezing (17.7% vs.

16.6%), frequent nighttime or early morning cough (5.8% vs. 5.2%), eczema

(10.5% vs. 5.3%) and hay fever sinus problem or some other allergy (27.4% vs.
18.3%) were more common for children who had illness or health problems in

their first week of life.

45

 

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46

 

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47

Adjusted odds ratios for asthma or wheeze, and frequent nighttime or
eafly morning cough are reported in Table 6. Maternal 0C use before pregnancy
and maternal complications during pregnancy were significantly associated with
asthma in the offspring, (AOR: 1.56 [95% Cl 1.04 - 2.321) and (AOR: 1.75 [95%
Cl 1.14 - 2.69]) respectively. Additionally, maternal OC use before pregnancy
was also significantly associated with frequent nighttime or early morning cough
(AOR: 2.28 [95% Cl 1.17 - 4.461), while maternal complications during
pregnancy was significantly associated with hay fever sinus problem or some
other allergy (AOR: 1.77 [95% Cl 1.17 - 2.701).

Table 7 shows odds ratios for eczema and hay fever, sinus problem or
some other allergy. Surprisingly, analgesic or anesthetic given during labor and
child’s illness or health problems in first week of life were both significantly
associated with eczema, (AOR: 2.27 [95% Cl 1.17 - 4.421) and (AOR: 2.30 [95%
Cl 1.11 - 4.721) respectively. Analgesic or anesthetic given during labor was
also significantly associated with hay fever, sinus problem or some other allergy
(AOR: 1.73 [95% Cl 1.10 - 2.711). The effect of maternal OC use before
pregnancy was stronger for girls (AOR: 1.98 [95% Cl 1.13 — 3.451) than the effect
for boys (AOR: 1.18 [95% Cl 0.65 — 2.141) in the association with asthma.
Smoking during pregnancy (in utero smoking) was not significantly associated to

childhood asthma (5.2% in asthmatic vs. 8.1% in others; NS).

48

 

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49

 

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50

Further analysis was conducted on the specific complications used to define the
“maternal complications during pregnancy covariate”. A parsimonious model
was produced by allowing only variables which had p<0.10 to remain in the
model. After adjusting for potential confounders, only “have there been any
other complications, disorder or serious illness during this pregnancy?” conferred

a significantly increased risk for asthma in the child.

Additionally, it is well established that “All that wheezes is not asthma” (36)
therefore, the variables asthma or wheezing and frequent night time or early
morning cough were combined to create one outcome variable. The association
between maternal 00 use before pregnancy and this variable was then
assessed in a full model. This did not change the association significantly (AOR:

2.7, 95% CI 1.1 — 6.9).

51

Chapter 7

DISCUSSION AND CONCLUSION
Discussion

Findings for this study support the hypothesis that children whose mothers
used OC before pregnancy, may be predispose to a higher risk for developing
asthma or wheezing at age 11 to 12 year of age. Results also support the
hypothesis that maternal complication during pregnancy is a risk factor for
asthma and wheezing in the offspring, as well as for eczema, ‘hay fever, sinus
problem, or some other allergies’. These associations persisted after adjusting
for known confounders.

Surprisingly, we found analgesic or anesthetic given during labor to be
statistically significantly associated with eczema, and ‘hay fever, sinus problem,
or some other allergies”. Additionally, child illness or health problems in the first
week of life were statistically significantly associated with eczema.

The study showed that children whose mothers used 00 before
pregnancy were 1.5 times, more likely to have asthma (AOR: 1.56 [95% Cl 1.04
- 2.321) than those whose mothers did not use 00 before pregnancy. This
finding is in concordance with those of stt who, based on aggregative data on
00 sales and hospital discharge data, was the first to hypothesize that maternal
use of 00 is a risk factor for asthma in the offspring. (3) To the best of my
knowledge, this is the first study to assess the association between, maternal OC

use and asthma or wheeze in offspring, using individual data.

52

The most popularly 00 in Jamaica during the study period was the Pearl. Active
components were Ethinyloestradiol (30 pg) and Levonorgestrel (150 pg), an
estrogen and progesterone respectively. stt suggested, that estrogen might
alter the activity of Th2 type cytokines (3) predisposing the fetus to atopic
disorders later in live. In agreement with this assumption, Xu et al. reported that
atopy in adults was more common among those whose mothers experienced an
early age of menarche (4). A likely explanation for the atopy - age at menarche
association are findings that early age of menarche is associated with higher
levels of estrogen in adult women (24-26, 37). Hence, the fetus of women with an
early age at menarche may experience a higher exposure to estrogens.
Regarding 00 use, it has been suggested that women who used OC have
higher estrogens levels after discontinuing its use (38), however, the evidence is
less convincing (26). Michel et al. reported that lgE levels in the cord blood were
significantly increased among neonates whose mothers had taken progesterone
during pregnancy (39). Furthermore, it is assumed that progesterone can also
function as a potent inducer of the production of the Th2 type cytokines (40).
These endocrine effects during pregnancy may play a role in immunologic
development as progesterone seems to promote the preferential development of
Th2-type cells (41, 42). The proposed mechanism may explain the OC - atopy
association, as T-helper (Th) cells are thought to be important in the
development of allergy. Th cells of the Th2 type produces large quantities of
interleukin (lL)—4, IL-5, and lL-13 which promote the production of lgE and
eosinophil infiltration in the airways and ultimately orchestrate the development of

allergy and asthma (43-45).

53

To our knowledge, there is no data whether use of CC is associated with a
different progesterone response in the luteal phase after discontinuing 00 use.

The effect of 00 use, however, may be independent of estrogen or
progesterone level after stopping. There are two other possible scenarios, which
may explain this association. Either maternal exposure to estrogen via 00 use
may trigger a programmed change in the Th1 I Th2 activity. A persistent change
in Th2 activity during pregnancy thus predisposes the fetus to a higher risk of
developing atopy later in life, a Th2-mediated disorder (46) (44, 47). Alternatively,
women who used 00 continuously, discontinuing before becoming pregnant,
may have created an environment of higher estrogen or progesterone levels.
This higher level, in turn, may result in an increased Th2 activity impacting the
fetus transplacentally.

Children born to mothers who had complications during pregnancy were at
a 1.7-fold increased risk of having asthma compared to their counterpart (AOR:
1.75 [95% Cl 1.14 - 2.69]). It might be that complications during pregnancy is
reflective of other underlying factor such as a threatened pregnancy which will
alter the Th1 I Th2 balance. Hence, we speculate that not specific diseases but a
general threat of miscarriage may be responsible for the association. For
instance, data from this study showed that not specific complications but among
the variables comprising the “maternal complications during pregnancy" variable,
only “have you had any other complication or disorder during this pregnancy“
was found to be significantly associated with asthma in the offspring.

Child’s illness or health problem in the first week of life was found to be

significantly associated with eczema (AOR: 2.30 [95% Cl 1.11 - 4.72]). Since

54

the present analysis adjusted for birth weight, which can be used as an indicator
of prematurity, it would be prudent to suggest that child’s illness or health
problem in the first week of life might be a risk factor for asthma. The actual role
of child illness or health problems in the first week of life is a topic worth
investigating further.

A number of studies have suggested that some analgesics and
anesthetics may be associated with an increased risk and severity of asthma (48-
51). However, to-date, there has not been any studies addressing the effect of
analgesics administered during delivery and allergies in offspring. A succinct
explanation of the mechanistic explanations of the analgesics or anesthetic —
eczema, and “hay fever or sinus problems or some other allergy" association
found in this study is not readily clear. It is beyond the scope of the present study
to address the independent association between anesthetic and asthma.
However, the thought that a single exposure to anesthetic during delivery is
associated to asthma would be rejected on the grounds of weak biological
plausibility. The logical supposition then is that the association is purely due to
analgesics. In an effort to explain the association between analgesics and
asthma, one would first postulate that analgesics given during delivery might be
an indication of a low pain threshold in the mother. It is pmdent to assume that if
there is a low maternal threshold for pain, then the mother may also have been
exposed to analgesics during and before pregnancy. It has been shown that
allergens, in this case analgesic (52, 53) (54), may cross the fetal membranes
where the maternal (decidua) and fetal tissues are in intimate contact (47).

There is evidence to suggest that immune response to allergen may begin in

55

utero (46). It is clear to see how fetal T cell responses may be initiated before
birth via the transplacental transfer of low levels of analgesics to which the
mother is exposed during pregnancy.

Following along the trend of thought that “analgesics given during delivery
might be an indication of a low pain threshold in the mother“, another possible
explanation may be that analgesic, acting as an allergen, may have activated an
existing dormant allergic disorder in the mother. This then triggers a chain of
immunologic reaction, which includes the modification of lFN-y activity. lFN-y
production in neonates with a family history of atopic disease is noticeably
decreased when compared to normal neonates (55, 56). This reduction has
been shown to be a risk factor for allergic diseases (47, 57, 58). Lastly, one
cannot ignore the fact that if the mother has the tendency of using more
analgesics than is usually expected, due to a low pain threshold, this would
suggest that her offspring would also have greater access and thus be more
exposed. This may lead to higher analgesic use in the offspring, resulting in
atopic disorders independent of allergen transfer via the placenta. lnfonnation on
analgesic use in the offspring is not available in this study thus testing this latter
supposition is not possible.

Given that Xu (29) found a positive association between mode of delivery
and asthma while both Annesi-Maesano et al. (5) and McKeever et al. (30) were
unable to support this finding, it is well advised that further studies be conducted.
The primary purpose of these suggested studies would be to assess the possible

role anesthetic and or analgesics may play in the mode of delivery — asthma

56

association since it is practical to suppose that anesthetic and analgesics given
during delivery are both highly correlated with mode of delivery.

The strengths of the current investigation are in its prospective design,
being derived from a large population based cohort, with all the exposure .
information collected during pregnancy, at birth and four weeks after. This
presents a clear time-order, as outcomes were not assessed until approximately
11 years after. This also reduces the effect of recall bias. Additionally,
controlling for a broad range of confounders reduced the possibility of these
findings occurring purely by chance.

The findings should be interpreted with some caution as they may be
influenced by selection bias, as follow-up rate was 60.4%. However as shown in
tables 3 and 4 no significant difference were found between the characteristics of
the variables from the main and sub-cohort when compared with those of the
linked dataset. Another limitation is that information on how long before
pregnancy 00 was used and if it was the last method of birth control used. This
may impact the serum levels of maternal estrogen during pregnancy and hence
significantly alter our association.

The definition or measurement of asthma or wheezing may also be of
concern as wheezing is a heterogeneous disorder (59) and not all that wheezes
is asthma (36). The impact this misclassification may have was assessed by
combining the variables asthma or wheezing and frequent night time or early
morning cough to create one outcome variable.

The association between this new variable and maternal OC use before

pregnancy was assessed and results showed did not reflect a significant change

57

the positive association previously found (AOR: 2.7 [95% CI 1.1 — 6.91). Also
since all the children in the cohort would have had equal chance of been
misdiagnosed, this would result in non-differential misclassification and thus

would not alter our findings significantly.

58

Conclusion

The present work provides results of a follow-up study of 11 to 12 year old
children. These results are in support of previous findings that maternal 00 use,
and complications during pregnancy are important in the development of asthma.
Further studies are hereby encouraged to corroborate with these results. This
will not only provide a better understanding of these reported findings, but more

effective preventive strategies could also be developed.

59

APPENDICES

60

APPENDIX - A
Main Questionnaire
Perinatal Survey - Jamaica

61

PERINATAL SURVEY - JAMAICA
MAIN QUESTIONNAIRE

A1. TobeoompletedanallwomenwhomddiverinSephanbeandOdObelmmrwhogivebhthtoanmfantwhoia
hosplhlicedpriorhozsdaysoflifefiept1966—May1987)orwhooeinfantiutillbomordieainthefim28daysof
life (September 1986-September 1987).

A2. Motha’ename

 

mmame first middle pet name
A3. Mother's date ofbirth / - /19
A4. Mother’s home address (usual maidenoe)

 

 

 

A5. landmaranotaneadaddm)
A6. Nextofktnhume)
A7. Nortofkinhddm)
A8. Surnameofchild
A9. Placedddiverr- EWM
El nualmaunityoaMcpedfy
E hedthm-pedfy
El wmmm-pedfy
E mmmm
E ownhome IE nothiown
El 06mm
A10. Dateddelivery '/ /198..
A11. Sexofbaby E male E female E m E mam
E notkmwn
A12. Cmmdmodier E mummy E mm
[2 dead‘ E] notknown
A13. Ctmmtatatuaofbahy E alivehalthy E 11mm
E dead“ E ”known

 

 

 

 

 

 

 

 

 

 

 

AILIftnf-ntm. E mum-mangled:
(E mmmnmmm
El mmmmummmw
E madmittedto WW

 

 

 

 

 

 

HWaWbWflNmy,WUHWLCRflWTmWaMSLAm’aM,
mpleteNmNATALADmONQUEHONNAmB

’CompleheMA‘l'ERNALDEATl-IQUETIONNAIRB E W E notcompleted
"mmmmmmommoumomm

62

nutnfamationinthefollowingaecflmistobe
.coflectedbyhua'vtewtngflwmofliedorwrtofldnifa
matemaldeathhaaoccurred).

B. THEPARENTS. Madonpduabackguund

informaflonouthepamntsandslmldnotbe

midaedasbdngaskedforanyotherm

Bl. Whatkfiwnameoffiuecommufltymwhflyw
live?

 

Areanyolthefollowingaavloeaavallablewidtin
l-Zmileswalldngdiatamofwhaeyoultve.

Bank myeamnomNK
PrimarySchool Eye-EnoENK
PoatOffioe ENEMENK
HealthCenhe EyaEmENK
PolioeStation EysEnoENK
TotalScore (names)

35. l-Iovvmanyadultaandchfldmhdudmgymaelf,
compooeymnrhandnoldandeatbgefia‘!

adults

 

children 0—10 yuan
rhildren 11-18 years

 

 

36. Anymtlwmajuwageeamer?
III yea Lil no

B7.Whatbd1eactualjobofthemajorwagem?

 

IfyeatoB6,goontoB9.

38a. Ifyouarenotmemjorwageeama,ueym
mallyemployed?

m yes [2' limbomewife E nomnemployed

b.1fyeswhatdoyoudo -
ePleaaedeaa-befltereladomhtpbetweenymmefland
themjorwageearner:

Em Emu Ema”
Emuammm
-Enoumed

 

 

 

32. Hawwouldyoudeacrbethelelafimshtpyouhave
withyourchfld’a fame/pants (union status).

E mmmw E mutated
E notltvingwifiicommonlawpam
E “havspedfy

 

33. Howbmtuveyoubeenaaaodatedvdflithehtlu
ofyourd'dld ya.

84. Whatwaathehlgluteducaflonlevdcompleted.

E mformaleduaflon m primary

 

63

 

B9. Howmudiiaapentwadfyforbods

BIO. Doyouorywrfanulyownormthelnmem
whichyoulive?

E omen-.pleaaedeaa'ibe

BllmWhattypeoftollethdlifieaareavaflableboflie
W

m mdoaetflmhtype)

E pitlauine E none
E dimpleaaedeaaibe
b. Amthetoflethdflfiamedadndvdybyflte

family?
Era Em ENK

812. Whatistheaourceofwawmedbydue
W?

E puhflcptpedhmdwamg
El mmmm
E maximum
E Wm notptped
[31 Mica-raw
E adapts-seam

 

ENK

 

ENK

 

BlSIHowmanyroomahithehmarewedfor
Win87

 

'l‘hianortaectioncontainaqueafimaonpast
Wifany,.anduaeofhmfiy'plamdng.

C. PAS'I‘OBSTETRICIflSl'ORY
C1. Haveymeverbeai-pmgnantatanydmebqfwc

WW?
Em ENK

El ya
Ifm,gotoquestion08.

C2. Pleaaehelpuslisttheaepnvlouapregnandeem
order,h1dudingmlscardages,terminatlomand
mmmfiwmumam
mammmmmwe
pregnandea-whichmayaothaveresulhedina
Iivebirth. .

dam—l—lw

 

 

 

 

 

 

 

 

 

 

 

 

 

 

111
Macrame

211d date..__l__'_/19
31d dau__/__/19
4th date..__..l——/l9
5th date._/_/19
6th date__;.l_./l9
7111 11m__/__/19
81h 111111__/___/19
9111 date—.J—IIQ
10111 date___/__/19
11111 daue__/__/19
12111 dm___/__/19
13111 date—l—ll9
14111 aau_l__../19
15111 date—l—lw

 

(3a. Tohlnnmberofpmgnanda .
b. Howmanydtheplevmpregnandesmltedina

11111111111131
c. Howmmyweremmiaged
d. Howmnyoftheaeweretwinaoru'lpleu
e. Howuuyatmbirthamflm
f. Howmyinfantabomaflquiedmflnfimtweekt
g. Hw'mymhmbanafivgdhdhuandawhat

‘89

 

 

 

 

 

 

l1. Howmyarealiv'emw
i. Howmanydtfldmerdudmgthianewbaby,do A
ywhaveforymucumtparmer?

 

C4. Howmyotlupamhaveywhad

 

C5. i-lowoldwereyouwhmyoubecamepregnantfor
thefircttime

 

C6. lnanypreviouapregnancy,didyouhaveanyof
thefdlowing

LCaaareanaection ENEMENK

b.3dampticfita EyaEMENK

chdive-ry ENEMENK

d.A111eputum EqunbENK
haunt-these

ePoctpartum EyaEmENK
We

£de EyaEnOENK

gPreedampsiacr EyaEmENK
hypertension

116311111111: EqunoENK

LOtha'oomplicaficna EyaEnoENK

MM

 

 

C7a. Whatwasthewtcomeoffinepregmmy
immediatelybefiorethbone

E fulltermlivebirth
E] mmfiwbtrth
E 111111111111

E 11111111111131

E termination

b. Whatwdiedateofdelivu'yofdielutpreytancy‘

beforedliapregnancy
/ /19

c. Ifyourlastpregmncywaaalivebimdidyw

Weed? .
mm ENK

Elves

d. Hymforluwlongdldheastfeedingoondmae?
months

 

Q.Atthetimeyoubecamepregnant,wereywu'ymg
11151111111511.1112
E no

Eyes
Em

C9. Atwhatagedidymatarthavingaemalrelatiom
——-—Y”~

C10. Have you ever used contraception?

EwEmENK

Ifno,gotoaectionD.

@htdiffemnt

C11. Hymwhidmethodsluveyouuaed?

Iwillgothroughalist
a.lUDorcoil EyaEMENK
b.0epoprovera‘orh1jecflon
ENEMENK
eC'Elnu-aceptive ENEMENK
iSpa'micida] EyeaEnoENK
eDiaphragm GREENE“
vam EyaEnoENK
sCondo-n Eye-EMENK
lLRhythmmethod EyegEnoENK‘
LMthdr-awal EyaEnoENK
101111-1- EyaEmENK
Pleaaedeaaibe ..

 

C1211. Ondieoccasionywbemntepregrnnnwereym
usingamntracepfivemetlwd? -
E yes no E NK

b. Hyamleaaegivemethodhwolved

 

 

Mnextaecdonaabquauonsonaalvfieaandhealfii
mdurlngdnsamupmaney.

D. THE MOTHER-DURING PREGNANCY

Dla. Doyoulmowmedateofthefiratdayofyourlast.

menatrualperlod?

E mummy

E yabutdoubtful

[E noper'lodhnmediate'lybeforepregnancy

E1111

1). Hymwhatwasflwdateofthefirstdayolya'rrlast
menstnnlperiod?

/ 11.9

 

 

02a. Didywamoketohaccoregularlyatanytime
duringthispregnancy.Andif.}a,what did-you

smoke?
E no E new E NK
E mac-n E map.

E media-,pleaeedeaaibe

 

b. Hyu,hoivmany(orhowofien)perdaydidyou
emote?

 

03a. Didyouamokeganjaatanytimedmingthis
W

E no E yesapedfymethod

E NK
b. Ifyes,howoftenperweekdidyouamoke?_

0411. Didyoudrlnkanyalcohoflcdrinbdurtng

W7 .
Eyes ENK

b. Hya,llownunydrh1bperweekdidyouhave_

05a. Howwereyouapendmgywrdayaataroundthe
timedquickenlnflwhenthebabyanrtedto
mapprozdmalaelySmcnfiu) '
E N1<

E unnamepddrob
E inpart-flmepakljob
E helpingwithfamtlybuahneu
E looflngaftaownfandly,houaewife
Eothermleaaedeealbe-

 

 

b. Whatwereywactu'allydoing

 

 

06. lfinapbmtwhatweekofpregnancydidyouetop
working?

07. Whatwaaymn'weightattheetartof
mm————_ E NK

 

65

In; Didymhavennyvagimlbloedingluthcfimzs
weebofpregmmy?
E NK.

Eyes

 

Hympleuedena-nae

 

b.01dyouhnvemyuginflbleedhgafiazsweeksa

mouths)
E you E no E NK
[implanting-the

 

 

D9. Eveduebemmyofimamplbflau,
Wammnwdumm

W
Eyes Em ENK

Ifya,pleuedeucribe

 

 

DIOa. Didyoumendumuldinic?

Eye- Eno ENk

b. Hymwhaedidyouamd?
E healthomhgspedfy

 

EhoupiuL-Pedfv

 

 

E macaw-pew
E 03"!wa

 

D11. Howmyweehmntmyouaty’ourfirot
visit?

 

012. Howmymmlvubdflyoumke?
a. mmmmuwb)
b. oeoondhinuterflZ-zswb)

 

c. mmmmémm

 

‘Dl3. Howmydfiuevhitsm
a. atfilchoalthoentre

 

 

b. hospital

c. mam

m4. Didyouhaveantenatalmanywhaeehe?
E ye- E no E NK
flquhere‘!

 

66

D15; AMMnganfiauhlo-mwereyourefened
dufingpregnnncyfounymson?
E yes E no ' E NK
“variance“
b. Raooufotrdunl
c. Diagtosinmde
d. ngm
e. WhenawMedimlOffioer

 

 

 

 

 

016:. memgimaMabemalRaoordCard?

E ye- E no E NK
b.1fhhoopthDidywbm-ingittohoopital?

E yes E no E NK
cMayIseeit‘t’Isducudoanplemdmduptodm?

Dl7. Wmmyhudidomlmediafimothome
renwdieflegbushteafltakendmingd‘is
W7

E Y” E no E NK
lfya,p|easeduuibewhatwuhkmmd
mwhyulnm.

 

 

 

018. Wmmyofmefollowingmedhdomhkm
“newsman-my?
napkin E yes E no E NK

b.unibioda.EyaEMENK
specify

 

cOtha'pteaabed Eyes Em ENK
WWW

 

 

¢deerovu~fiwootmterm yang no.5] NK
meditationsflpedfy .

 

 

eFolicacid Eye- Eno ENK

Llron

Eye- Emf ENK

g. “yahowmyfimapadnymthehm
heatmenthken

 

h. thowmynnnfiudflumncydidym
hhedueimnheatmmt?

019a. memadmflhedcohospitnlornml
meanitycmuedmingfilkpregnmcyhat

b'eiuugoinghtohbom'?
b.1fyes,pluaeglve:
Dated NM: Hooper Rmfo:

Adm. days RMC Admission

lat

 

 

 

 

2nd
3rd _-_
020:. Didwaedsadatanytimeduringyour
Pregnancy?
E yel E no
b.1fya,whm? E mums
E M E end
cmwhandidyoudmduefedmgs?
E partner [2] doctor
E name/midwife E other,npedfy

 

m1. mmmmflywwm
dWhGMW

E yes E no
Ifyesmrho?’
E mocha [E m/dtfid'shtha'

E ndshbmn E mend E other
D22. Hmoftatpaweekmywhaflngmfl
intercourse?
a. mudduefimeofquichning
(Smooth!)
b. {nthehstweekbefomddivcry

 

mmmdd‘emkwhuafewqum
mktingtodtetimeyouwentinmhbourqmddivay
andtheimnudhhepoat-partumpaiod.

 

E. WOMANDKBTPARTUM

Bl. Doymknowwhatfimymmmmhgof
mushuptmedorbroke?

hr min Dun.
DP-m-

Date / /19

 

an. mammw
E-mmnlybefmhbm E NK
E dew
B] My
E atCaau-lanoecdm
E3; Howdidlab'mn-mrt?
E] spontaneously E afterinducticn
E mhbmmeaiveCS) E NK
E honay,plenedeaaibe

 

84. “WmaHMwmymgmmw
wholdlnunedhhelyafisddivay?

E Y3 [2 no E NK
MapplhblflCneat-hnncum)
m Wawpnmmmnuymww
E yes E no E NK
I mw(mm

86. Whnhaveywleuntfinmuhfimnmgmof
youth-W?

tam E E E
holder: E E E
ckundioe E E E
dlnfedion E E E
eBCGvacdne E E E
Lomm E E E
samnyphmms E E E
nonumpecify E E E E]

 

E7. Whaedoyouphntogoforyourweekpost
mhlvidt?

E Mmm
E WM
E pdvatedoaompecifywpaednmdm
1mm,
E 06%wa
hadnotplannedbogo

 

 

 

 

E NK
mudghtofmodter: fL—ins.__.._

as. deluofnwdtéafiadelivery
(Pk-”N810 “In

 

 

mmwmwmmdmmtm
halthcenheandgivehenpnmpldet’fllUS‘l‘HADA
BABY".

Ankmoduhpermisaimbobdeflymmhwha
We)andmpletesecfionG-MBABYN1HB
FIRSI‘QHOURS.Complcteaseparateaheetf0tead1
inhntinthemeofnufltiplebirfluAlSOborrowfiu
wwmmmplebeumuchofm
H-fitpplanmmAnmulW-ak
possible.

 

ENDOFINTEKVIEW

 

mmhbbecomplehedbymddnghospml
dellverymhuandifmryjpmiewlngthe
hddwifewhodidtheadualdelivery.

Fla. Howdidfiuemanbmnemptme?

E Wybefmhbom

E Wdflfifigm

E wad-11y

E «Wm E'NK

b. ‘I‘imcofdelivay.

Dun. [3pm

lus___..x'nins

 

c. Wasthaeanabmrmalammtdflquor?
m metacavemydnnudoa)
E yesvaymtwoasohydnm)
E3] nomomulamovmt E NK.

68

E nolabom-(electiveCS) NK
E Mod-amy,pleasedesafiae

 

Ifmduced,'pleue give:

hm
amethod

 

 

Fa. Whatwudxepresenntiou?
E mama-1am» E breech
E mpoomwl’) [,5] NK
E mAathuwn
E campusedaawe

 

 

Ma. Wmfiumemodddefivay?
E heeded-action E vamumextnctim
E fetcepammmewhethalow.
midorhlgh
E Cam ' Mahdi”
campkuedaaibe

 

 

 

b. IfdelivaedbyCaaarhnndimpleueglvem

 

 

F5. Howlongdidlahomhst
a. usage Mange

m Wumouymgc'gimdmgw
E mmvvedms
[2] an E NK

F7. Wumanflgdc/ngdmw
[1| mphsesivetypem
[Z] no E NK’
m Wmmyofludmgsglm?
E rev-pedfymdsivem
E no E NK

 

 

 

 

Dunmcunounmoomvm
P9a. Dldthemothahnveedampficfits?
E ya E no E NK
b. 014mm?
E ya E no E NK
c. Didahehaemouhage?
E yea E no E NK
1!”,de
W

 

when

 

m

 

d. Wuhbmn'obau'ucbed?
E yes E no E NK

If ya, plane deco-nae

 

 

e. Diddteutausmptme?

Eyes Eno ENK

f. Wmdmmynbnormalitiesinfoetalhmtmte?

E yapleuedeaa-Ibe

 

Eno ENK

3. Wumoduhandeneddmhlgw
E yea,glvereason

 

 

Eno ENK

Wherewupnfienttnmfandhom?

 

 

h. Dldtheoordpmhpoe?

E ye- E'no E NK
i. Wuthaemeoonhnnintheflquor?

E yea E no E NK
LWumepuooomygivm?

E ya E no E NK
. k. Werethenperimalm?

Eyes Eno ENK

l. Wmfimmyofluoompflcafiom?

Eyes Eno ENK

 

[tympleuelist

 

 

FlOa. Wamoxytodcgivmtonwfiunfiadelimy?

E molaseapedfydms

E no E NK

b. Weemyothadmgpgivmhomemotherafter
delivery?

E yesnpedfydms
moon— E no E NK

m. Whoactuallydidmedeliva'y?
E am E midwife E mm

WM
E mfludedflnlwspihl)
E Nam E self-delive-yfiiotinhospihl)

F12. Wuficmodu’sbloodpfiumhkeninhbmfl
E yea E no E NK

Hyampedfyfilebloodprmcmdhtgwith
thehighestdiasbofic.

 

 

 

 

 

I

F133. Wuhnnflxa’surhwteuedfotproednin
labour?

Eyes Eno ENK

b. “gagivemlt

 

F14. Wuoedmpmeminlabo‘n-‘IE yes,givedtes

Eno ENK

F154. Washemoglobmmeusuredhtfilelshotmafier
delivery?

E ya E no E NK
Hympleuegive

 

hmult
cmethod

 

 

msmmum

Flea. hmefimwhomsufwdenvaydidfiemouu
hayeedmpflcfim?

Eye! Eno ENK

b. Diddlemoduhaveapostpamhumordme?
E mifyn,giveo¢mt ml:

 

69

c. Wumytnmfusionglven? ENDOFMATERNALWAIRE

 

 

E yalfya,howmuch ml:
Elm E] NK WM— Phaempknednwpdtheflmmeomu
WWWTALQUBSTIONNARB
d. Dldthcmotherhavemyofiuooinpfladau? mflngmbmddwhdfity/hdflfiawhidt
E y!!! E no [2] NK provideunmulmmmenwflu.
Ifympleuelist I Goontommimfltehfammmdcomplehefin

 

mmmmammnmmauoumm
ficaseofmflfipkbirfiunupumdwetmbe
completedfocudunhnt.

 

 

 

aWumothcu-andqredmhoaphloflomotha
haspihlnflerdelivay?

m mphueglvcm

 

 

mofwhl
Eno, ENK

 

7O

mmmmmwm

roancowmmnonmuvmmsmummsamounnmms
NmofMother DateofDdiva-y / [19
mam BabyE 3.1ny aabyE magnesium-y-

 

 

 

demmawmflmdfiuhbyumamdufimdfiumhmw
Wamuflmmumpkmdhudlbabyandathchdbflummdmm.

 

cu’uumubyamméruipm
E finale E mum E NK
E mum E mmm
E mum E mpleb3rdbom
L—Z] mudaunknown hiplet,o/u

G2. Wintwasfitetimofbhfilofdthbaby.

hr min: Damme.

ca. Howddwasthebabywhmmmhudfoflhb
W?
hrs

 

G4. Whatwutheoumomeofdthddiveryl
E Wuhan-MW
E inducedabaflon E stillbirth
E diedafterdelivu'ymgeatdeadt
hrs E alivenow,healthy
E NK E alivemwmdmlttedho
1‘08?“ E dimple-sedated»

 

camammemamubabyz
E male E tame E inferno:

E mum E NK
66. Givetheblrtl'mdghtofflliababy
lbs on! gnu)

 

G7. Whatbfimaown—heellengthoflhebnby
indie-lam
GB. Whathtluheaddramfemnce
int/am
G93. Haemoizeofbabfsbmam
fight—._.mm left

 

b. Haaeducribenippla:
E barelyvidble E flatmla
E mm E NK

610.1’1medena'naesolem
Eno-um Ema-mud ENK
Ema-thirds Ehedamapment

Gll. Heatedeauibem
E noretum E downturn
E Mandarin E NK

Glzneuedau'lbem
Enouppnauew
Emma Eingmin
E finned: E inaaotum E NK

(:13. Plenuedenqibehbh
El] manna-Memo» El NK
D] m>n§°n E minions
union E mjaa>minon
E mammal:

cu. Diddcbnbycryimmedhtelynfierbirfix

Eyes Eno ENK

(:15. Whntwuduenpgatm
tatlmin___b.at5min

cm. mmmmwmwymm
E hunt-fed l2 glucosewater—botflefed
E fornmhbottlefed E our,“
tie-cube '
E untmliablehbvdied) E NK

b. Atwhatagedidbahyhavethefirufeed___-
hrs

 

71

(:17. Did the baby have any convulsion?

E Y6 E an E NK
6181. Wufiubobyjaundioed?
E16 E no E NK
“ample-seam
b. ageatomet hrs

c. WNW)—
d. pmbdalecause

e. beautifully

 

619a. Was the babfs haemoglobin measured?

 

 

E] Y“ E no E NK
“gammy“:
1). result date‘ / /
c. methodused

 

GZO.Waethefollowinggivm: .
mdlvernitnu: Eyes Eno ENK

1:.va Eye- Euo ENK
Wm)

cBCGvuccin: Eyes Eno ENK

(321. mammwmm

deluhamydficmhgml

ahawdgmohbmfityorcongerdhl
malfmdon.

Ifyes,pleuedescdbe.

LSKIN EnoEyes____ENK
cEARS EmEya—ENK
(tm EmEyes—ENK
e.MOUTH mmEya—ENK
LPALA'IB EmEyes___ENx

72

gibNTANELLB

asurumzs EnoEyes___‘Em(
nsxuu.

SHAPE EMEyes—_ENK

LNUTRI'HONAL

STATUS EmEyeI—_J:INK
yum».-
EnoEyes__—ENK

may
kHEART EnoEyes—ENK
LABDOMEN Em'Eya____[:INK

mummus EmEya_____l:|NK

umus EnoEyu—ENK
Immuno-

q.SKELETAL

r. -clavide EmEyes.__—.J:INK
3.4-tips EmEya—JZINK
L-feet EmEyes—_J:INK
n.0'l'HER Emmy—Em

Plenaedeoaibeanyoflheaboveflnflu‘ifmry.

 

 

 

622. Wmmyofiumnesesowabmumlaympboms
mmmw
E NK

E yel E no
liyapleuelist

 

 

 

(:23. Wuflxebabyréaredtoamedhlofflca?
E ye E no E NK

Kymglvemforrdmfl

 

 

 

024a. Wasthebabyadmittedtohospitalorspedal
ambabyunit?

Eyes Eno ENK

b. [Immgvemmedhospital

 

 

c. Rmonfortnnsfu'

 

COMPLETION OF QUBTIONNAIRE

I’IEASECI-IKZK'I'HATEVERYQUESI'IONHAS
BEENANSWERED.

COMPLETE IDEN'IIHCATION INIDRMA‘I'ION ON
SUPPLEMENTARY AN'I'ENATAL QUE'I'IONNAIRE.

IF BABY HAS DIED, PLEASE ALSO FILL IN A
SHLLBHU'H/WFANT DEATH QUESTIONNAIRE.

IF THE MOTHER DIED, PLEASE ALSO FILL IN A
MATERNAL DEATH QUESTIONNAm.

IF THE BABY HAS BEEN ADMIITED T0 VII-I
NURSERY, BUSTAMANTE, UHWI, cm.
MANDEVILLE, SPANISH IOWN, sr. ANN’S BAY,
PLEASE ALSO GET A NEONATAL ADMISSION
QUESTIONNAIRE COMPLETED BY ma
PAEDIATRICIAN OR' PAEDIATRIC HOUSE
OFFICER.

‘I'HISQUE'I'IONNAIRE WAS COMPLETED BY

Name:

 

Position:

 

Date:

 

CHECICEDBY:

Name:

 

Date:

 

NEW-Summarymmflmblbmkmbempkudmmwm

73

WWWWMyWJMMbeMWEeWWthMEM
mmeMAMNALRmDCARDWbeanBm

mam—

HealthCelme/Hospihl

'I'
Manhatdtfinm

 

Parishanmhlcuetemived

 

DahofDellva'y
PukhofDelivu'y
PhoedDdivery
Study

Number: DUE] DUDE] E]

 

 

 

 

mmumbempwmuumnukmnsdmmmmmmmm
MATERNALRmDCARDbpndMMMMMWMEW

mL-Bloodmandkhofmother
E Aposiflve E Anegative
E 3905“" E Bnegatiw
E Oposifive Omegadve E NK

b. letsofCoombotestGorbloodgxmpmfibodies)

Epoamve Eng-ave .notdonc
ENE

m. Didflumhnvemyblooddisuderduflng
WW
E mmwmm E no
E micklecelltnith) E NE
E mddh.ASor$mthwn
E yaw
E modumpleuedencribe

 

Han. Wuthehnamgloflnmeddmhgmy

MM?
E ye- E no E NI<
nymph-Begin:

b. Numberofmdings

 

c. Wreadhg_date / ll?

d. Method

 

74

e. Wuanyuuunmtgivenfionmda?

E MAXI! E “when
E yuanlhmandfiolkadd
E ”8.th E NK

E ”Mum
E madmplemdaa-Ibe

 

 

f. Hbremluafla‘mm
4m / ‘ [19

 

H4O. HowmnyfimowufieVDRLdmdmingthb
m

b. Indian-Manda”
E neg [2] po- / I19
[:1 neg E pen I I19
E] neg CZ] poo I I19
HS. Wuhmmwmm
E ”.mmbmm
E mdmdfi-m
El mwhmyhmmed
H6O. Howmyflmumflnmodu’sbbod
11‘3““me
notatall
b. Whatmsthefintmdhgmded
___../..._ date I l

c. Whatwuflnmdingwflhlhehww
dau+ / /

 

 

 

 

ENK

_._.._/__

d. Whatmsthemdingwflhthelflgtuuywic?
due I I

 

._._.../__

H7. Didthemotha'hvedhbemdmtngfifis
mum?

 

Ewmm
Eno ENK

HBa. Howmanyfinumsurhtemdforprotdn
duringthispregmncy?
notatall

b. Ifnon-lnfectivepmtdnufiawufo‘udwhatmsme
high-«level
I!!!

data /

 

H9a. Whatmsfiwmotlm’sweightatfiustutof
W———lb°/k9

b. Whatwuthenwtha’swdgluatfinfiutmmhl
visit lbs/kg!

c. Howmyweehgahflonwufitis

H10. Whatwufiunwtha’smflmnmwdgludumg
fidsmuncy
___1ba/kgsdate

I /

 

H11. Wacedmnomddmhgmymww?
E MPWSMW

 

 

describe

 

Eno ENK

HIZLWuthqmotIu'diagnooedashnving
predampdaoredampdn
“1118th

E] ya [El no IE! NE

b. “’15,thme

 

 

 

cAthowmnyweeksgahfionmsfidsfiI-st

 

diagnosed
1113a. Wufiteumrefandtothemedialdflca

 

 

demqformyn-m?
[:1 yes [2 no E NK
b. mum
c. Dhgmdamade

dTmtmmtgivm

 

END OF MA'IERNAL RECORD CARD
INKJRMA‘I'ION

75

H14. Didthemothahnvemyvaginflbleedinghme
“28de

E yapleuedescrlbe

 

 

Eno

at whgeatafion
E NK
H15. Didduhavemyvaginflbleedingaflanweeks

“W
E mphmdeaann

 

 

weeksgatadm EM

at

ENE

 

H16. Didahchnveavaginaldbdurgeorinfecfion
deW
E Y‘apleasedeaaibetlumgim_
andt‘ypeofhfecdmflfknown)

ENE

 

E no
1117. MMWMMWW
from:

Eyes

mahmuulwdghtlou

Eno ENE

1:.me
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76

APPENDIX - B
F ollow-up Questionnaire — Six Week
Perinatal Survey - Jamaica

77

PERINATL SURVEY - JAMAICA
NK — not known F OLOW-UP QUESTIONNAIRE

DATE OF DELIVERY

 

PARISH OF DELIVERY

 

FOR OFFICE USE ONLY

 

Al. StudyNo.:[ 11 l 11]"! C]

To be completed between 6 weeks and 3 months after delivery. Data to be collected by
interviewing the mother and checking the notes at post-partnum clinic visit, if made.
Otherwise, attempts must be made to locate mother and baby before 3 months of age.

A2. Name of mother

 

Surname first middle pet name

A3. Mother’s date of birth

 

A4. Mother’s home address: Parish

 

 

A5. Date of delivery

 

A6. Place of delivery:

 

A7. Full name of child:

 

Surname first middle

A8. Sex of baby E] male Cl female 1:] intersex
E] undetermined E] NK

A9. Is this baby E] a single Cl 1St twin Cl 2"d twin
Cl 1m triplet Cl 2'“1 triplet E] 3rd triplet

A10. Names of hospital to which bay admitted (if at all)
Date /19
Date /19

 

 

 

 

A11. Motherseen Dyes Dno DNK
Babyseen Dyes Duo DNK

A12. Mother interviewed at 6 wk clinic El yes Cl no [I NK
Mother interviewed at home after [I yes C] no U NK

 

 

6 weeks
A13. Date of interview / 19
A14. Current status of mother
a alive, healthy [:1 alive, ill ' D dead. a NK
Current status of baby
a alive, healthy [3 alive, ill [I dead” a NK

78

[EDIE]

 

[DIED
EDI!

 

DC]
ICICJ

 

A15. If infant ill, [:1 ill at home, diagnosis

 

D ill, being treated at health center, diagnosis

 

EJ ill, being treated at hospital outpatient, diagnosis
D ill, admitted to hospital, specify
diagnosis
Ifadmitted or transferred to VJH Nursery, UHWI, Bustarnante, CRH,
Spanish Town, Mandeville, St. Ann’s Bay, complete NEONATAL
ADMISSION QUESTIONNAIRE

[I] completed E] not completed

 

; If death afier discharge from hospital, a MATERNAL DEATH
} QUESTIONNAIRE must be completed] completed El not completed Cl NA

** If death after discharge, an INFANT DEATH QUESTIONNAIRE must
be completed and if possible, a post mortem arranged

D questionnaire completed I] not completed [1 NA

Postmortem arranged El yes [I] no El infant already buried U NA

79

DEEII

DU

 

NK — not known F OLOW-UP QUESTIONNAIRE, CONTINUED
MATERNAL HISTORY
DATE OF DELIVERY
PARISH OF DELIVERY
FOR OFFICE USE ONLY
StudyNo,;I II I II I

11. Since delivery of the baby has the mother had any of the following

 

 

 

 

 

 

 

 

 

 

 

 

 

 

a. postpartum hemorrhage yes no NK
b. Anemia yes no NK
c. Mastitis yes no NK I:
(1. Breast engorgement yes no NK D
e. Puerperal depression yes no NK D
f. Infected lochia yes no NK D
g. High blood pressure yes no NK :1
h. Other disorder yes no NK 8
specify [:1
If yes to any of the above, please describe
12. Was the mother admitted to hospital at all during the period since the D
birth of the baby? yes no NK [:I
If yes, give dates of and reason for admission and treatment given:
Date No. days in Reason Treatment given I:I
admitted hospital
i __/__/19____
ii _/_/19_
[EDIE]
I3 Has menstruation returned? yes no NK
if yes, date returned / /19 69%
14a. Have you felt sad since your delivery? yes no NK [D] [[13]]
14b. If yes, With whom have you shared these feelings D m
partner doctor other, specify
relative midwife ,NK D
C]
15a. Has anyone been particularly helpful 0 kind to you since you have '
had your baby?
yes no NK
, C]
b. If yes, whom: mother partner neighbor
friend other, specify
NK
L__l

 

80

FOLLOW-UP QUESTIONNAIRE, CONTINUED
EXAMINATION OF THE MOTHER

 

 

 

 

 

 

 

 

DATE OF DELIVERY

NK - not known PARISH or DELIVERY
FOR OFFICE USE ONLY
Study No.: IJ I I I I1

J I. Date of examination /19

J 2. Hb. level Method

J3. Blood pressure

J4. Weight kg/lb

J 5a. Is the mother using a contraceptive method at the moment?

yes no NK

EXAMINATION OF THE BABY

Kl. Hb. level K2. Weight kg/lbs

Method K3. Crown-heel length cm.
K4. Head circumference cm.
K5. What is baby currently being fed? Breast breast &
formula formula only other, please describe NK
K6. Ifnot breast fed how is feed given bottle cup & spoon

other, specify

K7 a. If the babay is presently receiving breast milk, how often per

24 hr period? feeds per 24 hrs.

b. I If yes, which method? Pill injection (Depo Provera)
IUD diaphragm condom Spermicidals Sterilization

 

other, specify NK
c. When did she start using this method after delivery
/ 19
d. Ifno, is she planning to do so in the future? yes no
NK

e. If yes, please give proposed method

 

(if infant was stillborn, interview ends here).

 

 

 

 

 

 

 

 

b. If the baby is not currently receiving breast milk, at what age
did the baby stop receiving breast milk days.

c. Ifreceiving bottle, at what age was it introduce _days/weeks

d. Ifbeing fed by cup and spoon, at what age were they introduce
_days/weeks

 

81

 

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ED]

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ED

[EDIE]

Cl
ICE

 

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[CED

CECE
":1

 

[II
CD

CD

 

FOLLOW-UP QUESTIONNAIRE, CONTINUED
DATE OF DELIVERY
PARISH OF DELIVERY
FOR OFFICE USE ONLY
Study No.:
NK — not known

K8. What drinks and foods were given to the baby in the first 28 days?
a. Glucose water yes no NK
b. Bush tea, specify yes no NK

c. Cow’s milk yes no NK
d. Formula yes no NK
e. Fruit Juice yes no NK
f. Porridge yes no NK
g. Other, please describe yes no NK

 

K9. Please describe below, in detail, what the baby was given to eat and
drink in the past 24 hours ending at midnight last night.

Time (24 Quantity (if breast Food/drink given
Hr clock) Milk, state length
of time on breast)
K10. Since birth until 28 days old, did the baby have any of the
following?
a. J aundice yes no NK
b. Convulsions/twitching yes no NK
c. Persistent vomiting yes no NK
(1. Diarrhea (3 or more yes no NK
Loose stool)
e. Sticky or discharging eyes yes no NK
f. Cord infection yes no NK
g. Other infection yes no NK
Ifyes, please describe
h. Other problems yes no NK
Please describe

 

DDDDDDDD

IEDJEDD]
[EIIDZID]
JIDDZID]
:EIICDED

 

 

K11. Examine the anterior fontanelle. Check all that apply. Is it
Open Closed ‘ Depressed

Bulging Normal NK

82

.l._ J ..l JLLJLLI

D DDDDDDD

 

FOLLOW-UP QUESTIONNAIRE, CONTINUED
DATE OF DELIVERY
PARISH OF DELIVERY
FOR OFFICE USE ONLY
K12. On examination of the infant, were any of the following systems
found to be abnormal or show congenital malformation.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

a. Skin no yes NK
b. Eyes no yes NK
c. Ears no yes NK
d. Nose no yes NK
e. Mouth no yes NK
f. Palate no yes NK
g. F ontanelle & sutures no yes NK
h. Skull shape no yes NK
i. Nutritional status no yes NK
j. Respiratory system no yes NK
k. Heart no yes NK
1. Abdomen no yes NK
m. Umbilicus no yes NK
n. Anus no yes NK
0. Genitalia no yes NK
p. Neurological no yes NK
Skeletal
q. — clavicle no yes NK
r. — hips no yes NK
5. — feet no yes NK
t. Other no yes NK
K13. Had the family been admitted to hospital in the first 28 days of life
no yes NK
if yes, give details below
Name of hospital Date Reason Treatment
admitted

_/___/19_

_/_/19_

_/___/ l 9__

__/_/1 9_

Kl4a. Is the baby living with the mother no yes NK

b. If no, who is caring for the child
Other relative, describe
Non-relative, describe
Foster care or adoption
K15. Is father supporting the child no yes not applicable NK
This questionnaire was filled in by

 

Position Date /19

83

 

 

Cl

APPENDIX - C
Child Health Questionnaire
The Jamaica Cohort Study

84

Child’sIDNo. I__II II II II II II II I
Mother’s ID No.[_][_][_] [_][_]LJLJ L_I

(As recorded in Perinatal Survey)

Interviewer ID [_][_]
Date of interview [_]L_] L_][__] [1][9][9][_]

(day) (month) (year)

THE JAMAICAN COHORT STUDY

CHILD HEALTH QUESTIONNAIRE
(To be administered to the study child's mother/mother figure or father/father figure)

A. IDENTIFICATION
1 Child's Surname F orenarnes

2. Sex: [1] M ale [2] Female

3. Child'sDateofbirth[ ][ ][ ][ ][1][9][9]Lj
(daY) (month) (year)

B. DEVELOPMENTAL MILESTONES
4. Before your child was 3 years old, were you ever concerned that he/ she

a. Began to walk later than other children? [I] Yes [2] No [3] Don't remember [9] N K
b. Began-to talk later than other children? [I ] Yes [2] No [3] Don't remember [9] N K

5. At what age did your child first take a few steps without any help? UL] mths.
(Probe: If you-had to take a guess, what would you say?)

6. At what age did your child first say his/her first word? UL] mths
(e. g."ma-ma", "da-da" to call you)

7. At what age did your child first put two or three, words together? [__]L_] mths

8. At what age was your child toilet trained? [_]L] mths
(Exclude night-time bed-wetting.)

9. At what age did your child stop bed wetting at night? [_][_] mths

10. As a baby under the age of six months did your child have any of the following
difficulties?
a) Excessive crying [I] Yes [2] No [9] Not know
b) Frequent feeding problems. [1] Yes [2] No [9] Not know

c) Frequent sleeping difficulty at night [1] Yes [2] No [9] Not know

85

C. GENERAL HEALTH
11. At present, how would you rate your child's health?

[1] Excellent [2] Good [3] Fair [4] Poor

12. a) Has your child ever been so sick that you thought that he/she might die?
[1] Yes [2] No [3] Not known

b) If yes, how old was your child when this happened? I II I yrs I II ]mths.
c) What was his/her diagnosis?

13. a) Has your child ever been admitted to hospital overnight or longer or had an
operation as a day case? (Remember to enquire about circumcision, grommets,

hernia, squint op.) [I ]Yes [2] No [3] Don‘t know

b) If yes, please give details below of each admission:

 

Admission 1 2 3 4 5
Age at
admission

No. of nights
Reason for
admission
Operations or
procedures
Hospital name
(If child has had more than 5 admissions, please continue on back page)

 

 

 

 

 

 

 

 

 

 

 

 

 

14. Has this child attended a hospital outpatient or specialist clinic or attended a
specialist privately for any condition?

[I] Yes [2] No [3] Don't know

b) Ifyes, please give details below of each condition or illness resulting in
attendance?

Condition/Illnes
s
first visit

Total no. visits

 

Treatment
(If child has 'h6d more than 5 conditions, please continue on back page)

86

15. Has this child ever suffered any of the following?***

a) Accidental swallowing of medicines or poisons“ [1] Yes [2] No [3] Not know
b) Burns or scalds [1] Yes [2] No [3] Not know
c) Involvement in a motor-vehicle accident [1] Yes [2] No [3] Not know
(Include pedestrian, cycle or vehicle accidents)
d) Injury to the head, other than in 0) above [I] Yes [2] No [3] Not know
e) Broken bones or fractures" [1] Yes [2] No [3] Not know
f) Any other accident [1] Yes [2] No [3] Not know
Please give tails of each accident below:

 

Accident 1 2 3 4 5

 

Age (yrs)

 

Place (home,
school, road)

 

What happened?

 

Injuries received
(burn, fracture,
cut, LOC)

 

Treatment
facility
(hosp., clinic,
pvt. doctor,
home)

 

Treatment

 

 

 

 

 

 

 

 

(If more than 5 accidents, please continue on back page)

* If ingestion, please give name of substance ** Indicate site of fracture

"*Please check that all accidents resulting in admission or outpatient attendance are
also documented at q. 13 and I4.

16. During the past 6 months, do you think that your child has had any emotional or
behavioral problems?
[1] Yes [2] No [3]Not known

17. During the past 6 months, do you think that your child has had any difficulty
learning or remembering things?

[I]Yes [2]No [3]Not known
18. Has your child ever received care from any of the following?
a) Speech therapist [I] Yes [2] No [3]Not known
b) Occupational therapist [I] Yes [2] No [3]Not known
c) Physiotherapist [1] Yes [2] No [3]Not known
d) Family counselor [1] Yes [2] No [3]Not known

e) Child psychiatrist/psychologist [1] Yes [2] No [3]Not known

If yes, give details below: Age, Reason, Where treated:

87

19.

I am going to read to you a list of sicknesses or conditions that some children
have. For each one can you tell me whether or not your child has ever had it?

Has your child ever had:
a. Frequent sore throats [] Yes []No []Don’t known
b. Frequent ear infections (Number =) [] Yes [] No []Don’t known
c. Hay fever sinus problem or some other allergy [] Yes [] No []Don’t known
(1. Asthma or wheezing [] Yes [] No []Don’t known
e. Rheumatic fever [] Yes [] No []Don’t known
f. Other heart condition [] Yes [] No []Don’t known
g. Arthritis or rheumatism (other than rheumatic fever)[]Yes[]No []Don’t known
h. Fits with fever [] Yes [] No []Don’t known
i. Fits without fever/Epilepsy [] Yes [] No []Don’t known
j. Cerebral palsy/Stiff limbs [] Yes [] No []Don’t known
k. Slow development in any area [] Yes [] No []Don’t known
1. Mental retardation [] Yes [] No []Don’t known
m. Muscular dystrophy or other muscle disease) [] Yes [] No []Don’t known
n. Abnormality of spine (e.g.Spina bifida, scoliosis) [] Yes [] No []Don’t known
0. Missing fingers, hands, arms, toes, feet or legs [] Yes [] No []Don’t known
p. Any stiffiress or deformity of the foot, leg, fingers

arms or back [] Yes [] No []Don’t known
q. A condition since birth such as club foot or

clefi palate [] Yes [] No []Don’t known
r Paralysis or weakness of any kind [] Yes [] No []Don’t known
8. Regular severe headaches [] Yes [] No []Don’t known
t. Any difficulty with coordination or clumsiness [] Yes [] No []Don’t known
11. Sickle cell disease or trait [] Yes [] No []Don’t known
v. Diabetes [] Yes [] No []Don’t known
w. Eczema [] Yes [] No []Don’t known
x. Frequent night, time or early morning cough [] Yes []No []Don’t known

y. Urinary tract infection (infection in urine/kidney) [] Yes [] No []Don’t known
2. Other condition, please specify [] Yes [] No []Don’t known

If yes to any of the above, and condition not already documented above, please give
details below (Age at illness, Diagnosis, Where treated, Treatment, Outcome)

20. Has your child had any of the following childhood illnesses?
a) Measles [] Yes [] No []Don’t known If yes, age [_][_]yrs.
b) Mumps [] Yes [] No []Don’t known Ifyes, age [_][_]yrs.
c) Chicken Pox [] Yes [] No []Don’t known If yes, age [_][_]yrs.
(I) Whooping cough [] Yes [] No []Don’t known If yes, age [_]Uyrs.
e) German measles [] Yes [] No []Don’t known If yes, age [_][_]yrs.

21. Please list all medication taken by your child in the last seven ays.

N_ame Rea_son taken

 

 

 

 

88

22. What immunizations has this child received to date? (Verify from immunization record.)

a) BCG [1] [2] e)Measles [I] [2] [3] h) HepatitisB [l] [2][3]
b)DPT [1] [2] [3H4] f) MMR [1] [2] [3] 1) HIB [1] mm
C) UT [1] [2] [3H4] g)Tetanus [1] [2] [3] 1') Other, Specify____

4) OPV [1] [2] [3] [4]

 

Immunization record not seen [9]

23. Where does your child usually receive medical care?
[1] Hospital [3] Family/ general doctor [5] Other, specify
[2] Clinic [4] Pediatrician

24. How often does your child visit the dentist?

[1] Never [3] Occasional check-ups [5]Other,

specify
[2] Only when tooth trouble [4] Regular check ups 6-12 mths. [9] Not knoWn

D. FUNCTIONAL ABILITY
I WILL NOW ASK YOU A FEW QUESTIONS ABOUT YOUR CHILD'S VISION
HEARING. SPEECH AND MOVEMENT.

 

Vision:
25. a) Is your child unable to see from one or both eyes?

 

[I] Yes, one eye only
[2]. Yes, both eyes
[3]. No
b) Ifyes, how long has he/she had this problem? [_]L] yrs. [_][_] mths

26. a) Does your child wear prescribed glasses or contact lenses?
[1] Yes [2] No

b) If yes, how long has he/she been wearing these? [_][_] yrs. L][_] mths

27. a) Does your child have any difficulty reading regular printed words?
[I] Yes [2] No [9] Not known

b) If yes, how long has he/she had difficulty seeing words? [_][_] yrs. [_]L] mths

89

Hearing
28. a) Is your child unable to hear from one or both ears?

[1 ]. Yes, one year only

[2]. Yes, both ears

[3]. No

b) If yes, how long has he/she had this problem? [_][_] yrs. [_]L] mths
29. a) Does your child wear a hearing aid ?
[1] Yes [2] No

b) If yes, how long has he/she been wearing this? [_][_] yrs. [_][_] mths

30. a) Does your child have any difficulty hearing regular conversation?

[I] Yes [2] No [9] Not known
b) If yes, how long has he/she had difficulty hearing? [_][_] yrs. [_]L] mths
Speech
31. a) Is your child unable to communicate at all using words or speech?
[1] Yes [2] No
b) If yes, how long has he/she had this problem? [_][_] yrs. UL] mths

32. a) Does your child starnmer, lisp or have difficulty being understood by others?
[1] Yes [2] No [9] Not known

b) If yes, how long has he/she had difficulty speaking? [_][_] yrs. [_][_] mths

Movement
33. a) Does your child need any assistance to move around (e. g. a person or artificial
aid)? [1] Yes [2] No *
b) If yes, what does he/she use to get around?
[1]. A wheelchair [I] Yes [2] No
[2]. Artificial limbs or braces [I] Yes [2] No
[3]. Cane or crutches [I] Yes [2] No

[4]. Other, specify

 

c) If yes, how long has he/she had this problem? [_][_] yrs. [_][_] mths

34. a) Does your child need any assistance using his hands and fingers, e.g., eating,
dressing, using the toilet?
[I] Yes [2] No
b) If yes, how long has he/she had this problem? [_][_] yrs. [_]L] mths

THANK RESPONDENT FOR PARTICIPATING IN THE S UR VE Y AND REMIND HER
THAT THE INF ORMA T ION WILL BE KEPT CONFIDENTIAL.

90

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91

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