Matern Child Health J DOI 10.1007/s10995-011-0940-4 Environments for Healthy Living (EFHL) Griffith Birth Cohort Study: Background and Methods Cate M. Cameron • Paul A. Scuffham • Anneliese Spinks • Rani Scott • Neil Sipe • ShuKay Ng • Andrew Wilson • Judy Searle • Ronan A. Lyons Elizabeth Kendall • Kim Halford • Lyn R. Griffiths • Ross Homel • Roderick J. McClure • Ó Springer Science+Business Media, LLC 2012 Abstract The health of an individual is determined by the interaction of genetic and individual factors with wider social and environmental elements. Public health approaches to improving the health of disadvantaged populations will be most effective if they optimise influences at each of these levels, particularly in the early part of the life course. In order to better ascertain the relative contribution of these multi-level determinants there is a need for robust studies, longitudinal and prospective in nature, that examine individual, familial, social and environmental exposures. This paper describes the study background and methods, as it has been implemented in an Australian birth cohort study, Environments for Healthy Living (EFHL): The Griffith Study of Population Health. EFHL is a prospective, multilevel, multi-year longitudinal birth cohort study, designed to collect information from before birth through to adulthood across a spectrum of eco-epidemiological factors, including genetic material from cord-blood samples at birth, individual and familial factors, to spatial data on the living environment. EFHL commenced the pilot phase of recruitment in 2006 and open recruitment in 2007, with a target sample size of 4000 mother/infant dyads. Detailed Trial Registration Number: ACTRN12610000931077. C. M. Cameron (&) P. A. Scuffham A. Spinks R. Scott S. Ng J. Searle R. J. McClure School of Medicine, Griffith University, Logan Campus, L03 2.45, University Drive, Meadowbrook, QLD 4131, Australia e-mail: [email protected] P. A. Scuffham e-mail: [email protected] A. Spinks e-mail: [email protected] R. Scott e-mail: [email protected] S. Ng e-mail: [email protected] J. Searle e-mail: [email protected] R. J. McClure e-mail: [email protected] C. M. Cameron P. A. Scuffham N. Sipe S. Ng E. Kendall Griffith Health Institute, Griffith University, Southport, QLD 4222, Australia N. Sipe e-mail: [email protected] E. Kendall e-mail: [email protected] A. Spinks Commonwealth Scientific and Industrial Research Organisation (CSIRO) Ecosystem Sciences, Dutton Park, QLD 4102, Australia N. Sipe School of Environment, Griffith University, Nathan, QLD 4111, Australia A. Wilson Faculty of Health, Queensland University of Technology, Kelvin Grove, QLD 4059, Australia e-mail: [email protected] R. A. Lyons School of Medicine, Swansea University, Singleton Park, Swansea SA2 8PP, Wales UK e-mail: [email protected] E. Kendall School of Human Services and Social Work, Griffith University, Meadowbrook, QLD 4131, Australia 123 Matern Child Health J information on each participant is obtained at birth, 12-months, 3-years, 5-years and subsequent three to five yearly intervals. The findings of this research will provide detailed evidence on the relative contribution of multi-level determinants of health, which can be used to inform social policy and intervention strategies that will facilitate healthy behaviours and choices across sub-populations. Keywords Child Cohort studies Longitudinal studies Epidemiology Methods Introduction The health of an individual is determined by the interaction of a number of factors operating at multiple levels [1, 2], including the environment, economic and social context, family interactions, individual behaviours and genetic factors. Figure 1 presents an eco-epidemiological model of health demonstrating the multi-level nature of factors which may influence various health outcomes [3, 4]. These multi-level influences operate throughout the life course, with prenatal and early years of life having a crucial role in later outcomes [5–8]. Public health approaches to improving the health of disadvantaged populations will be most effective if they optimise influences at each of the subordinate levels, particularly in the early part of the life course. Environments and environmental exposures can have profound effects on child development and behaviour. Environmental injury hazards are related to child safety, and spatial relationships between building structures affect opportunities children have for health advancement [9]. There is evidence that certain environments discourage physical activity and encourage excess consumption of food [10]. Characteristics of environments that appear to discourage walking behavior include lack of public K. Halford School of Psychology, University of Queensland, Brisbane, QLD 4072, Australia e-mail: [email protected] L. R. Griffiths Genomics Research Centre, Griffith Health Institute, Griffith University, Southport, QLD 4222, Australia e-mail: [email protected] R. Homel School of Criminology and Criminal Justice, Griffith University, Mt Gravatt, QLD 4122, Australia e-mail: [email protected] R. J. McClure Monash University Accident Research Centre, Monash University, Clayton, VIC 3800, Australia 123 Fig. 1 Ecological model of health across the life course (Nicholson and Sanson 2003 modified with permission from Lynch 2000) reproduced with permission from the Medical Journal of Australia transport and poor ‘walkability/safety’ of urban streets [11]. Proximity to fast food outlets and poor access to fresh fruit and vegetables may contribute to unhealthy eating patterns [11, 12]. Children are considered a specific risk group from environmental night noise exposures with consequences such as skill learning problems, poor memory as well as depression and obesity [13–15]. A lack of social and economic resources has the potential to place children and young people at risk of a number of issues such as developmental problems, [16] school failure, [17] conduct problems [18] and poor physical and mental health [19]. Factors such as maternal depression, family structure and exposure to violence have been found to have a negative impact on child health and development [20]. The mechanisms of the health promoting effects of family, and how they interact within social contexts, are only partially understood, but include promotion of healthier lifestyles, [21] modelling of effective interpersonal skills [22] and affect regulation [22]. Gene-environment interactions are central in any multilevel explanation of health determinants [23, 24]. Studies of attention deficit hyperactivity disorder (ADHD) have suggested a causal interaction between genetic and environmental factors, such as toxins in utero and pregnancy and delivery complications [25]. The foetal environment is considered a key factor in the aetiology of some diseases later in life, including cardiovascular disease, [26, 27] kidney disease, [28] asthma and respiratory functioning [29]. Intrauterine growth is an independent predictor of Matern Child Health J health outcomes both in childhood and throughout life [30] with health behaviours (e.g., nutrition, smoking, alcohol) adopted by parents, important determinants of intrauterine growth [31]. The majority of health behaviours (e.g. health screening, nutrition, alcohol, smoking, physical activity) which have been related to poor health outcomes are differentially distributed by socioeconomic status [32]. Prevention of health inequities therefore requires strategies that not only address individual risk factors but also the fundamental structural and environmental characteristics inherent to poverty [33–35]. It is the structural and environmental characteristics of the community in which an individual lives, that will ultimately influence whether protective health and lifestyle choices are possible. In order to better ascertain the relative contribution of these multi-level determinants of health, there is a need for robust studies, longitudinal and prospective in nature, that examine individual, familial, social and environmental exposures. Empirical studies must quantify the respective causal, and confounding effects of the many covariates involved and account simultaneously for the broad range of biological, social, and behavioural measures operating at the individual and group level. This paper describes the study methods, as it has been implemented in an Australian birth cohort study, Environments for Healthy Living (EFHL): The Griffith Study of Population Health. Australian and New Zealand Clinical Trials Registry ACTRN12610000931077. Methods Study Aim By using a multi-level approach, EFHL aims to investigate social and environmental factors, neighbourhood and family functioning, maternal lifestyle and in utero exposures on child development and health outcomes. A number of health outcomes will be investigated including obstetric complications and birth weight, obesity, child development and quality of life, child injury, oral and dental health, utilisation of health services and all cause morbidity from birth to adulthood. Findings will be used to identify where improvements can be made within the community to make healthy lifestyle choices easier for families. Study Design EFHL is a prospective, multi-level, multi-year longitudinal birth cohort study, designed to collect information from before birth through to adulthood across a spectrum of ecoepidemiological factors, including genetic material from cord-blood samples at birth, individual and familial factors, to spatial data on the living environment. It is anticipated that future sub-studies will be incorporated into the overall design that may include qualitative and interventional components. The EHL Wales study has been designed in collaboration with EFHL to be complementary and is currently in its pilot phase of recruitment [36]. The underlying eco-epidemiological premise for the study design, some outcomes of interest, and branding features of the EFHL are being utilised by EHL Wales. The collaborative nature of the two cohorts will enable international comparisons of several outcomes of interest. Study Setting and Population The study population is the offspring of women residing in the geographically defined Logan/Beaudesert, Gold Coast and Tweed Districts. These districts cover an area of almost 6,000 square kilometres in South East Queensland and Northern New South Wales, Australia and contain an estimated population of over 1,300,000 people or approximately 30% of Queensland’s population. It has one of the fastest rates of population growth in Australia and illustrates the problem of providing effective health promotion in outer metropolitan areas. The region is markedly heterogeneous with respect to age and socioeconomic distribution [37]. Sample Size The target sample size for EFHL is 4000 mother/infant dyads. Sample size calculations have been derived for three key paediatric outcomes of interest—obesity, quality of life and injury, demonstrating that the target sample size will be sufficient for detecting statistically significant and practically important differences in the primary outcomes, if true differences exist. All the sample size calculations are based on significance level of 5% and a two-sided test (Table 1). The sample size calculations for obesity and quality of life are based on an initial cohort of N = 4000 and attrition of 15% per wave of follow-up, resulting in N = 2457 at 5-years. Sample sizes are calculated using GPower 3.1 software [38]. The estimated proportions of obesity and overweight are obtained from a recent study of 1688 children in Australia [39]. Body Mass Index BMI (kg/m2) categories were defined using the International Obesity Task Force age-specific cut-off points for children aged 5-years, BMI [ 19.2 and BMI [ 17.3 for obesity and overweight respectively [40]. The sample size calculations indicate that EFHL has 80% power to detect a difference of 0.015 in the proportion of children who are obese and 0.024 in the proportion of children who are overweight. The estimated mean and standard deviation of child quality of life using the Health Utilities Index Mark 2 123 Matern Child Health J Table 1 Minimum detectable difference in primary outcomes of interest for power of 70, 80 and 90% Outcome of interest Obesitya Overweight a Child quality of lifea Hospitalised injury b Medically treated injuryb a Value SD Minimum detectable difference Power = 70% Power = 80% Power = 90% 0.069c NA 0.014 0.015 0.018 0.219c NA 0.021 0.024 0.028 0.950d 0.072 0.0036 0.0041 0.0047 e 0.066 0.281 0.011 0.012 0.014 0.204e 0.495 0.019 0.021 0.024 Cross-sectional data, at 5 years of age through anthropomorphic assessment and proxy report b Longitudinal data, from birth to 5 years of age through linkage to administrative data c Proportion d Mean e Rate (HUI2) scores are obtained based on the validated Canadian population norms for male and female children [41]. The minimally important difference in HUI2 score is 0.03 [42]. With a sample of 2457 followed up at 5 years, EFHL will be able to detect a difference of 0.004 in mean HUI2 score at 80% power; thus, this study has a sufficient sample size to detect differences in child health-related quality of life. The sample size calculation for paediatric injury is based on linkage to administrative databases to identify medically treated injury and admissions to hospital, with an estimated 95% data obtainment at the 5-year follow-up (i.e. N = 3800). Injury rates were estimated from pilot data from within the study region, [43] which are 0.204 per year for injuries requiring medical treatment and 0.066 per year for hospital treated injuries. A sample of 3800 with complete data at 5 years provides the study with 80% power to detect a difference of 0.021 in medically treated injury rates and 0.012 in hospital treated injury rates. Study Sample, Recruitment and Data Collection Process Eligible participants are the offspring of women who plan to give birth at one of three participating public maternity hospitals (Logan, Gold Coast and The Tweed Hospitals) in South East Queensland and Tweed area. All women waiting for third trimester antenatal clinic appointments (on or after their routine 24 week antenatal visit) at each of the locations, are approached by research trained midwives, provided with a detailed explanation of the study aims and invited to participate in the study. Pregnant women aged less than 16 years or unable to provide informed consent are excluded. Information packages, including the study explanation and aims are provided to participants. Written informed consent is obtained for the release of hospital perinatal data related to the birth of their child, 123 completion of a participant maternal baseline survey and for individual follow-up. Additional and separate consents are sought from each participant for the collection of umbilical cord blood at the time of delivery and for the release of Medicare, Pharmaceutical Benefits (PBS) claims information, and immunisation history related to their child, from Medicare Australia. Consent for release of Medicare Australia data is sought from the calendar month of the child’s birth for a 5-year period inclusively. Women who decline consent to cord blood collection or Medicare Australia data release are not restricted from participation in the study. Figure 2 illustrates the recruitment, consent and data collection processes for EFHL. Following recruitment, expectant mothers complete a baseline questionnaire either at the antenatal clinic or returned by post in a reply-paid envelope. At the time of the birth of the child (Time 00) umbilical cord blood is collected (where consent has been provided). Perinatal data is extracted from the medical records following discharge from hospital. Follow-up questionnaires are sent to the primary carer when the child is 12 months of age (Time 01), 3 years of age (Time 03) and 5 years of age (Time 05). Subsequent follow-ups are planned to occur every 3–5 years until the participant reaches 25 years of age. Multiple strategies have been established to minimise attrition. Routine telephone reminder processes are utilised to prompt questionnaire return rates, however primary carers are also provided with an alternate ‘not this time’ option to decline completing a questionnaire without withdrawing from the entire study. This option enables time poor participants or those with particular limiting circumstances to continue to contribute long term to the study. Concerted efforts are made by the project team to maintain up to date contact records for all participants through the use of the reminder processes for questionnaire Matern Child Health J Fig. 2 Flow diagram of the recruitment and data collection process for EFHL returns; alternate contacts provided by participants to follow up ‘return to sender’ items; and newsletters which are sent to all participants three times a year. EFHL commenced the pilot phase of recruitment in November 2006 and open recruitment in August 2007. The study has a multi-year recruitment approach which has utilised a four-month recruitment period every year since 2006 and is anticipated to continue enrolling new participants until 2013 (Fig. 3). Each of these sub-cohorts is defined by the calendar year of recruitment. One-year (Time 01) and three-year (Time 03) follow-ups have commenced as planned. Medicare Australia data extraction commenced in 2011 when the first cohort of children approached 5 years of age. Ethics Ethical approval for EFHL participant recruitment and follow-up of the birth cohort has been obtained from the Griffith University Human Research Ethics Committee (HREC) (Ref: MED/16/06/HREC, renewed MED/23/11/HREC). Ethical approval for EFHL participant recruitment was also obtained from each of the individual HRECs associated with the three participating public maternity hospitals (Refs: Logan Hospital HREC/06/QPAH/96; Gold Coast Hospital HREC/06/GCH/ 52 and The Tweed Hospital NCAHS HREC 358 N). University and participating hospital ethics approvals have been granted for a maximum 5 and 3 year periods respectively, with renewal applications required at the end of each period. 123 Matern Child Health J Fig. 3 Multi-year recruitment and longitudinal follow-up design of EFHL Data Sources and Instruments ups are planned to occur every 3–5 years until the participant reaches 25 years of age. Questionnaires Umbilical Cord Blood All questionnaires are self-administered. The maternal baseline questionnaire consists of 48 questions and takes approximately 30 min to complete. Items include maternal and family demographics, socioeconomic status, household income, family structure, Kessler 6 psychological distress scale [44], neighbourhood and community connectedness [45], short form of the Family Environment Scale [46], maternal smoking and drinking behaviour, gestational medical conditions and injuries, the usage of health supplements as well as recreational substances during pregnancy. The first follow-up contact with participants occurs when the child reaches 12 months of age (Time 01) and again at 3 years of age (Time 03). The primary carer, who is predominantly the mother, is mailed a questionnaire eliciting details on familial, social and environmental exposures as well as child health and developmental outcomes. The questionnaires consist of a range of self-report and proxy child measures and take approximately 40 min to complete. Items include infant feeding practices and child nutrition [47], sun exposure, sleep patterns [48], developmental milestones, [49] child temperament [50], Spence Children’s Anxiety Scale (SCAS-P) Parent Form [51] and Modified Checklist for Autism in Toddlers (M-CHAT) at 3 years, [52] child height and weight measurements, child injury and child medical conditions. Primary carer items include the Kessler 6 psychological distress scale, [44] adult attachment style, [53] EuroQOL five dimensions (EQ-5D) health status measure, [54] as well as household income, structure and social support, neighbourhood and community connectedness, [45] short form of the Family Environment Scale [46] and Life Events Stress Scale [55]. The questionnaire for 5-year follow-up (Time 05) is currently under construction. Web development is also underway to enable an online option for participants to complete and submit questionnaires. Subsequent follow- 123 Umbilical cord blood is collected by the midwife present at the time of delivery. Approximately 10–12 ml of cord blood is collected in two labelled vacutainers which are then couriered to the Griffith University Genomics Research Centre to be stored at -80°C until required for analysis. This comprehensive birth cohort study will provide a valuable resource to study the development of disorders in this population enabling an assessment of genetic and environmental contributors to disease. Future plans include conducting analyses to investigate genetic risk factors relating to the causes of common chronic diseases such as cardiovascular disease, obesity, diabetes, hypertension, mental health and various types of cancer. The collection of cord blood samples and the assessment of longitudinal medical information will allow us to investigate the interplay of genetic and environmental factors in disease susceptibility. For these studies we will undertake DNA extraction in-house using established kit based methods (e.g. Qiagen) and investigate genetic variants in relation to disease development. Because the technology for genetic analysis is developing at a rapid pace, with for example, whole genome sequencing becoming much less expensive, the method finally used for genetic analysis of cohort samples will be selected at the time of analysis. In addition, biochemical analyses can also be undertaken to investigate exposure to or levels of various chemicals or toxins, such as heavy metals and selenium, as well as to investigate disease biomarkers. Perinatal Data Collection Perinatal data is extracted from the medical records following discharge from hospital. The data is obtained from the Queensland and New South Wales Perinatal Data Matern Child Health J Collection completed by the hospital midwives. Data items include previous pregnancies, maternal conditions, obstetric care and complications, delivery information and baby information such as gender, plurality, gestational age, birth weight, APGAR (Appearance, Pulse, Grimace, Activity, Respiration) scores at birth and any complications. Comparisons will be made to Queensland and New South Wales Health local area population perinatal data. of participants, home safety assessments, ongoing participant/proxy completed questionnaires and linkage to administrative databases to access health and education records. It is anticipated that future sub-studies will be incorporated into the overall design that may include focus studies, qualitative or interventional components. Data Linkage The analytic strategy for this study incorporates two dimensions. The first of these relates to the level at which the exposure factors are situated within the conceptual model (Fig. 1). A multi-level modelling (MLM) approach will be used to determine the effects of the various factors on child health and development including obesity, injury and quality of life. MLM recognises the existence of hierarchies in the data by allowing for residual components for each level analysed. Levels in the analyses include individual child characteristics (e.g. child temperament [50]), proximal social environments (e.g. family environment scale [46]), and distal social environments (e.g. the purpose built neighbourhood characteristics database). In addition, longitudinal data, where individual’s responses over time are correlated with each other, can be accounted for in MLM. Thus, the multi-level regression models can be used to quantify the relationships between determinants (risk factors) and outcomes whilst controlling for confounders and covariates. This approach overcomes common methodological barriers associated with conventional regression analysis. The second dimension underpinning the analytic strategy is the use of the multi-year recruitment design to facilitate the identification of possible ‘cohort effects’. Cohort effects are defined as the ‘‘variation in health status that arises from the different causal factors to which each birth cohort in the population is exposed as the environment and society change’’ [58]. Cohort effects will be analysed by comparing changes in exposures and outcomes between each of the sub-cohorts for any given age. These differences in risk will be interpreted in the context of changes in the population exposure to area level risk factors or macro environmental factors, over the time period. Medicare Australia data is retrospectively sought from the calendar month of the child’s birth for a 5 year period inclusively. Medicare data includes claims for listed items on the Medicare benefits schedule (MBS), Pharmaceutical benefits schedule (PBS) and the childhood immunisation register. The Medicare data will be matched to the EFHL cohort on date of birth, names and Medicare number. Those data contain item numbers and dates for General Practitioner (GP) consultations, fees paid by the MBS to the GP, cost to the patient, pharmaceutical records (including medications prescribed, date of prescription and cost to the PBS), and full immunisation records. Hospital inpatient data will be obtained through linkage with Queensland Health and New South Wales Health Admitted Patients Data Collection and Morbidity and Mortality System databases. Environmental Level Data All participant residential information is geo-coded using ArcGIS software [56] and will be linked to community profile information at the appropriate scale. Much of these data have been collected as part of the Australian Bureau of Statistics [57] census which is conducted every 5 years (2001, 2006, 2011). These socio-demographic data are available at various scales ranging from the census collection district CD (approximately 200 households) to statistical local areas SLAs (suburbs) to local government areas. Within the EFHL study region there are 64 SLAs and 1,257 CDs based on the 2006 ABS census [57]. These data will be supplemented with land use and transport data (available from public and private databases) to build the neighbourhood characteristics database. The land use and transport data is an important part of the database as it will provide information on a household’s accessibility to essential services including medical facilities, shopping, schools and other key social services. Future Data Collection Future data collection methods are projected to include face to face interviews and anthropometric measurements Analytic Strategy Discussion EFHL is a multi-level, multi-year longitudinal birth cohort recruiting pregnant mothers in South East Queensland, Australia, with the intention of following their children for up to 25 years. The main outcome measures, obesity, injury and quality of life were selected as a diverse range of outcomes to cover a spectrum of common health states in children. The long-term consequences of obesity are a 123 Matern Child Health J serious public health concern, since they are associated with psychological morbidity [59] and the development of chronic disease in later life [60]. Injury is one of the most prevalent serious problems in childhood [61] and is an outcome of behavioural and environmental factors; and quality of life captures general health and wellbeing across all health conditions. While EFHL has features similar to existing birth cohort studies, such as the pre-natal recruitment of participants in order to collect in utero exposures and cord blood samples at birth for genetic analyses [62, 63], it differs from existing birth cohorts in a number of ways. This study will measure changes in individuals as well as their environments over time. Based on an eco-epidemiological framework, EFHL offers a robust study design to understand the various micro to macro factors that contribute to overall health and wellbeing of populations. In addition to genetic samples and individual survey data, EFHL includes the collection of geographic and area level data to enable spatial analysis of the effects of neighbourhood characteristics such as safety, transport and services availability on lifestyle choices, physical activity and health service use. This is a contemporary study, addressing current issues such as obesity, an emerging disease of the modern era, which has not been typically addressed in older cohort studies. There are few studies that have examined risk factors for child health outcomes across multiple levels [64]. For example, obesity studies tend to focus either on physical activity or nutritional behaviours and less frequently consider both determinants within one analysis [65]. There are no longitudinal analyses relating obesogenic social and physical environments to obesity outcomes [66, 67]. Developed in collaboration with EHL Wales [36], the planned multi-level analysis is a design element that sets these studies apart from the traditional risk-outcome analyses that characterise epidemiological cohort studies. This study has a major advantage compared with other cohort studies by including linkage of the socio-demographic survey data with administrative healthcare databases, including hospital inpatient, emergency department, GP, immunisation and pharmaceutical data. Historically, data linkage was not available and only few recent cohort studies have incorporated individual consents for record linkage [68]. The use of administrative data circumvents issues arising from attrition and provides a robust data source that is not limited by self or proxy recall biases. The ‘multi-year’ longitudinal study design of EFHL enables potential analysis of cohort effects by comparing data between each of the sub-cohorts from different recruitment years. This design will provide a rare opportunity to assess and quantify the impact of structural or environment changes and health policy implementations 123 during the cohort period. In addition, the research design allows for a series of nested studies to be developed, with the opportunity to examine complex exposures and outcomes. The study is not without its limitations. The EFHL sample is likely to include fewer low birth-weight, low gestational age babies or multiple births than in the general population. This is mostly because the women are recruited from only public maternity units and are not approached for inclusion until approximately 24 weeks gestation at routine clinics, with a significant proportion of women approached closer to 36 weeks, by which time most pregnancies have ended for babies at risk for low birth weight. However, this is unlikely to have a significant effect on outcomes at 5 years of age and beyond. Further limitations common to most cohort studies, are related to the amount of information that is feasible to collect, bias from self or proxy administered surveys, and attrition. The length of the self-administered surveys is kept to a minimum and additional data obtained from linkage with administrative sources at the individual and local area level, will provide externally validated data with no participant burden and as previously stated, will minimise self-report bias. A number of other strategies are also implemented that aim to minimise participant loss to follow-up, including regular mailed newsletters–often be returned by post if the participant has moved house, the use of alternative phone contacts supplied at enrolment, and telephone options for questionnaire completion provided at reminder follow-ups. Limitations and constraints also pertain to the use of linked administrative data [69, 70]. Administrative errors exist with regards to data entry and name discrepancies increasing matching errors. Recording of any non-mandatory data fields may not be complete or the quality may be questionable. Diagnostic information is reliant on physicians who code the clinical visits and a lag time also exists between the events occurrence and the information becoming accessible in the different data sources. However, despite these inherent problems with the reliability of data from large databases these techniques are cost efficient and allow for a large amount of data to be collected prospectively on a large sample size with minimal attrition, which is a clear strength of the study. The findings of this research will provide detailed evidence on the relative contribution of multi-level determinants of health, which can be used to inform social policy and intervention strategies that will facilitate healthy behaviours and choices across sub-populations. Acknowledgments The research reported in this publication is part of the Griffith Study of Population Health: Environments for Healthy Living (EFHL) (Australian and New Zealand Clinical Trials Registry: ACTRN12610000931077). Core funding to support EFHL is provided by Griffith University. We are thankful for the crucial Matern Child Health J contributions of the Project Manager Rani Scott and the current and past Database Managers. We gratefully acknowledge the administrative staff, research staff, hospital antenatal and birth suite midwives of the participating hospitals for their valuable contributions to the study. Expert advice has been provided by Associate Investigators throughout the project. Dr Cameron was supported by a Public Health Fellowship (ID 428254) from the National Health and Medical Research Council (NHMRC) Australia and Professor Scuffham was supported by a Career Development Award (ID 401742) also from the NHMRC. Conflict of interest interests. The authors declare there are no competing References 1. Lynch J (2000) Income inequality and health: expanding the debate. Social Science & Medicine 51(7), 1001–1005; discussion 9–10. 2. Frenk, J., Bobadilla, J. L., Stern, C., et al. (1991). Elements for a theory of the health transition. Health Transition Review, 1(1), 21–38. 3. Nicholson, J. M., & Sanson, A. (2003). A new longitudinal study of the health and wellbeing of Australian children: how will it help? Medical Journal of Australia, 178(6), 282–284. 4. Lynch, J. W. (2000). Social epidemiology: Some observations on the past, present and future. Australasian Epidemiologist, 7, 7–15. 5. Eriksson, J. G. (2007). Epidemiology, genes and the environment: Lessons learned from the Helsinki Birth Cohort Study. Journal of Internal Medicine, 261(5), 418–425. 6. Shaheen, S. O., Newson, R. B., Smith, G. D., et al. (2010). Prenatal paracetamol exposure and asthma: Further evidence against confounding. International Journal of Epidemiology, 39(3), 790–794. 7. Stettler, N., & Iotova, V. (2010). Early growth patterns and longterm obesity risk. Current Opinion in Clinical Nutrition and Metabolic Care, 13(3), 294–299. 8. Freisthler, B., Gruenewald, P. J., Ring, L., et al. (2008). An ecological assessment of the population and environmental correlates of childhood accident, assault, and child abuse injuries. Alcoholism, Clinical and Experimental Research, 32(11), 1969–1975. 9. Liu, G. C., Wilson, J. S., Qi, R., et al. (2007). Green neighbourhoods, food retail and childhood overweight: Differences by population density. American Journal of Health Promotion, 21(4 Suppl), 317–325. 10. Giles-Corti, B., Timperio, A., Bull, F., et al. (2005). Understanding physical activity environmental correlates: Increased specificity for ecological models. Exercise and Sport Sciences Reviews, 33(4), 175–181. 11. Sallis, J. F., & Glanz, K. (2006). The role of built environments in physical activity, eating, and obesity in childhood. Future Child, 16(1), 89–108. 12. Wakefield, J. (2004). Fighting obesity through the built environment. Environmental Health Perspectives, 112(11), A616–A618. 13. Bistrup, M. L., Hygge, S., Keiding, L., et al. (2001). Health effects of noise on children and perception of the risk of noise. Copenhagen: National Institute of Public Health, Denmark. 14. Stansfeld, S. A., Berglund, B., Clark, C., et al. (2005). Aircraft and road traffic noise and children’s cognition and health: A cross-national study. Lancet, 365(9475), 1942–1949. 15. WHO (2009) Night noise guidelines for Europe. Copenhagen. 16. BrooksGunn, J., & Duncan, G. J. (1997). The effects of poverty on children. Future of Children, 7(2), 55–71. 17. Bradley, R. H., Convyn, R. F., Burchinal, M., et al. (2001). The home environments of children in the United States part II: Relations with behaviorial development through age thirteen. Child Development, 72(6), 1868–1886. 18. Battin-Pearson, S., Newcomb, M. D., Abbott, R. D., et al. (2000). Predictors of early high school dropout: A test of five theories. Journal of Educational Psychology, 92(3), 568–582. 19. Durlak, J. A., & Wells, A. M. (1997). Primary prevention mental health programs for children and adolescents: A meta-analytic review. American Journal of Community Psychology, 25(2), 115–152. 20. Westbrook, T. R., & Harden, B. J. (2010). Pathways among exposure to violence, maternal depression, family structure, and child outcomes through parenting: A multigroup analysis. American Journal of Orthopsychiatry, 80(3), 386–400. 21. Youngblade, L. M., Theokas, C., Schulenberg, J., et al. (2007). Risk and promotive factors in families, schools, and communities: A contextual model of positive youth development in adolescence. Pediatrics, 119(Suppl 1), S47–S53. 22. Van Voorhees, B. W., Paunesku, D., Kuwabara, S. A., et al. (2008). Protective and vulnerability factors predicting new-onset depressive episode in a representative of US adolescents. Journal of Adolescent Health, 42(6), 605–616. 23. Kishi, R., Sata, F., Yoshioka, E., et al. (2008). Exploiting geneenvironment interaction to detect adverse health effects of environmental chemicals on the next generation. Basic & Clinical Pharmacology & Toxicology, 102(2), 191–203. 24. Romao, I., & Roth, J. (2008). Genetic and environmental interactions in obesity and type 2 diabetes. Journal of the American Dietetic Association, 108(4 Suppl 1), S24–S28. 25. Linnet, K. M., Dalsgaard, S., Obel, C., et al. (2003). Maternal lifestyle factors in pregnancy risk of attention deficit hyperactivity disorder and associated behaviours: Review of the current evidence. American Journal of Psychiatry, 160(6), 1028– 1040. 26. Barker, D. J. (2002). Fetal programming of coronary heart disease. Trends in Endocrinology and Metabolism, 13(9), 364–368. 27. Hocher, B. (2007). Fetal programming of cardiovascular diseases in later life: Mechanisms beyond maternal undernutrition. Journal of Physiology, 579(Pt 2), 287–288. 28. Ojeda, N. B., Grigore, D., & Alexander, B. T. (2008). Intrauterine growth restriction: Fetal programming of hypertension and kidney disease. Advances in Chronic Kidney Disease, 15(2), 101–106. 29. Alati, R., Al Mamun, A., O’Callaghan, M., et al. (2006). In utero and postnatal maternal smoking and asthma in adolescence. Epidemiology, 17(2), 138–144. 30. Barker, D. J. P. (1998). Mothers, babies and health in later life (2nd ed.). Edinburgh: Churchill Livingstone. 31. Kramer, M. S. (1987). Determinants of low birth weight: methodological assessment and meta-analysis. Bulletin of the World Health Organization, 65(5), 663–737. 32. Barkley, G. S. (2008). Factors influencing health behaviours in the National Health and Nutritional Examination Survey, III (NHANES III). Social Work in Health Care, 46(4), 57–79. 33. Adler, N. E., & Ostrove, J. M. (1999). Socioeconomic status and health: What we know and what we don’t. Annals of the New York Academy of Sciences, 896, 3–15. 34. Laflamme, L., Hasselberg, M., & Burrows, S. (2010). 20 years of research on socioeconomic inequality and children’s-unintentional injuries understanding the cause-specific evidence at hand. International Journal of Pediatrics, 2010. doi:10.1155/2010/ 819687. 35. Orleans, C. T. (2000). Promoting the maintenance of health behaviour change: Recommendations for the next generation of research and practice. Health Psychology, 19(1), 76–83. 123 Matern Child Health J 36. Hill, R. A., Brophy, S., Brunt, H., et al. (2010). Protocol of the baseline assessment for the environments for healthy living (EHL) Wales cohort study. BMC Public Health, 10, 150. 37. Queensland Health (2007) South Area Health Service Profile. Queensland Government. 38. Faul, F., Erdfelder, E., Buchner, A., et al. (2009). Statistical power analyses using G*Power 3.1: Tests for correlation and regression analyses. Behavior Research Methods, 41(4), 1149– 1160. 39. Goris, J. M., Petersen, S., Stamatakis, E., et al. (2010). Television food advertising and the prevalence of childhood overweight and obesity: A multicountry comparison. Public Health Nutrition, 13(7), 1003–1012. 40. Cole, T. J., Bellizzi, M. C., Flegal, K. M., et al. (2000). Establishing a standard definition for child overweight and obesity worldwide: International survey. BMJ, 320(7244), 1240–1243. 41. Saigal, S., Feeny, D., Furlong, W., et al. (1994). Comparison of the health-related quality of life of extremely low birth weight children and a reference group of children at age eight years. Journal of Pediatrics, 125(3), 418–425. 42. Drummond, M. (2001). Introducing economic and quality of life measurements into clinical studies. Annals of Medicine, 33(5), 344–349. 43. McClure, R., Cameron, C. M., & Scott, R., et al. (2007). The griffith study of population: Environments for healthy living. School of Medicine, Griffith University. 44. Furukawa, T. A., Kessler, R. C., Slade, T., et al. (2003). The performance of the K6 and K10 screening scales for psychological distress in the Australian National Survey of Mental Health and Well-Being. Psychological Medicine, 33(2), 357–362. 45. Homel, R., Freiberg, K., & Lamb, C., et al. (2006). The pathways to prevention project: The first five years 1999–2004. Griffith University. 46. Moos, R., Moos, B. (1994). Family environment scale manual: Development, applications, research (3rd ed.). P. Alto (Ed). CA: Consulting Psychologist Press. 47. Cade, J. E., Frear, L., & Greenwood, D. C. (2006). Assessment of diet in young children with an emphasis on fruit and vegetable intake: using CADET: Child and diet evaluation tool. Public Health Nutrition, 9(4), 501–508. 48. Agras, W. S., Hammer, L. D., McNicholas, F., et al. (2004). Risk factors for childhood overweight: A prospective study from birth to 9.5 years. Journal of Pediatrics, 145(1), 20–25. 49. QueenslandHealth. Child, Youth and Family Health. 26 Week Assessment; 12 Month and 18 Month Assessments.: Gold Coast Health Service District. 50. Hegvik, R. L., McDevitt, S. C., & Carey, W. B. (1982). The middle childhood temperament questionnaire. Journal of Developmental and Behavioral Pediatrics, 3(4), 197–200. 51. Nauta, M. H., Scholing, A., Rapee, R. M., et al. (2004). A parentreport measure of children’s anxiety: Psychometric properties and comparison with child-report in a clinic and normal sample. Behaviour Research and Therapy, 42(7), 813–839. 52. Robins, D. L., Fein, D., Barton, M. L., et al. (2001). The modified checklist for autism in toddlers: An initial study investigating the early detection of autism and pervasive developmental disorders. Journal of Autism and Developmental Disorders, 31(2), 131–144. 123 53. Bartholomew, K., & Horowitz, L. M. (1991). Attachment styles among young adults: A test of a four-category model. Journal of Personality and Social Psychology, 61(2), 226–244. 54. Dolan, P., Gudex, C., Kind, P., et al. (1996). The time trade-off method: Results from a general population study. Health Economics, 5(2), 141–154. 55. Holmes, T. H., & Rahe, R. H. (1967). The social readjustment rating scale. Journal of Psychosomatic Research, 11(2), 213–218. 56. ESRI. (2010). ArcGIS software package (Version 9). Redlands, CA: ESRI. 57. ABS. (2006). 2006 census. Canberra: Australian Bureau of Statistics. 58. Last, J. M., Abramson, J. H., International Epidemiological Association. (1995). A dictionary of epidemiology (3rd ed.). Oxford, NY: Oxford University Press. 59. Schwimmer, J. B., Burwinkle, T. M., & Varni, J. W. (2003). Health-related quality of life of severely obese children and adolescents. JAMA, 289(14), 1813–1819. 60. Srinivasan, S. R., Myers, L., & Berenson, G. S. (2002). Predictability of childhood adiposity and insulin for developing insulin resistance syndrome (syndrome X) in young adulthood: The Bogalusa Heart Study. Diabetes, 51(1), 204–209. 61. Ameratunga, S. N., & Peden, M. (2009). World report on child injury prevention: A wake-up call. Injury, 40(5), 469–470. 62. Jaddoe, V. W., Mackenbach, J. P., Moll, H. A., et al. (2006). The generation R study: Design and cohort profile. European Journal of Epidemiology, 21(6), 475–484. 63. Olsen, J., Melbye, M., Olsen, S. F., et al. (2001). The Danish National Birth Cohort–its background, structure and aim. Scandinavian Journal of Public Health, 29(4), 300–307. 64. Hawkins, S. S., Cole, T. J., & Law, C. (2009). An ecological systems approach to examining risk factors for early childhood overweight: Findings from the UK millennium cohort study. Journal of Epidemiology and Community Health, 63(2), 147–155. 65. Hawkins, S. S., & Law, C. (2006). A review of risk factors for overweight in preschool children: A policy perspective. International Journal of Pediatric Obesity, 1(4), 195–209. 66. Davison, K. K., & Lawson, C. T. (2006). Do attributes in the physical environment influence children’s physical activity? A review of the literature. The International Journal of Behavioral Nutrition and Physical Activity, 3, 19. 67. van der Horst, K., Oenema, A., Ferreira, I., et al. (2007). A systematic review of environmental correlates of obesity-related dietary behaviours in youth. Health Education Research, 22(2), 203–226. 68. Tate, A. R., Calderwood, L., Dezateux, C., et al. (2006). Mother’s consent to linkage of survey data with her child’s birth records in a multi-ethnic national cohort study. International Journal of Epidemiology, 35(2), 294–298. 69. Roos NP, Black CD, Frohlich N, et al. (1995). A populationbased health information system. Medical Care 33(12 Suppl): DS13–20. 70. Kelman, C. W., Bass, A. J., & Holman, C. D. (2002). Research use of linked health data–a best practice protocol. Australian and New Zealand Journal of Public Health, 26(3), 251–255.
© Copyright 2026 Paperzz