The Western Australian preterm birth prevention initiative: a whole of state singleton pregnancy cohort study showing the need to embrace alternative models of care for Aboriginal women.

BACKGROUND: Preterm birth (PTB) is the greatest cause of mortality and morbidity in children up to five years of age globally. The Western Australian (WA) PTB Prevention Initiative, the world's first whole-of-population whole-of-state program aimed at PTB prevention, was implemented across WA in 2014. METHODS: We conducted a prospective population-based cohort study using pregnancy data for singleton births in WA from 2009 to 2019. Logistic regression using the last full year before the Initiative (2013) as the reference, and run charts were used to examine changes in PTB rates compared to pre-Initiative levels, by gestational age group, hospital type, low and high risk of PTB in mid-pregnancy, and onset of labour (spontaneous/medically initiated). Analyses were stratified by Aboriginal and non-Aboriginal maternal ethnicity. RESULTS: Amongst non-Aboriginal women, there was initially a reduction in the PTB rate across the state, and in recent years it returned to pre-Initiative levels. Amongst Aboriginal women there was a small, non- significant reduction in the state-wide PTB rate in the first three years of the Initiative, followed by a rise in recent years. For non-Aboriginal women, the reduction in the rate of PTB at the tertiary centre was sustained and improved further for women of all risk levels and onsets of labour. This reduction was not observed for Aboriginal women giving birth at the tertiary centre, amongst whom there was an increase in the PTB rate overall and in all subgroups, with the exception of medically initiated PTB. Amongst Aboriginal women the PTB rate has also increased across the state. At non-tertiary hospitals there was a large increase in PTB amongst both Aboriginal and non-Aboriginal women, largely driven by medically initiated late PTB. Maternal risk factors cannot account for this increase. CONCLUSIONS: The reduction in PTB rates amongst non-Aboriginal women at the state's tertiary hospital demonstrates that with the right strategies, PTB can be reduced. A sustained collaborative model is required to realise this success in non-tertiary hospitals. The series of interventions was of limited use in Aboriginal women, and future efforts will need to be directed at strategies more likely to be successful, such as midwifery continuity of care models, with Aboriginal representation in the healthcare workforce.

Associations between Prenatal Exposure to Phthalates and Features of the Metabolic Syndrome in Males from Childhood into Adulthood.

Phthalate metabolites are detectable within the majority of the population. Evidence suggests that a prenatal exposure to phthalates may be associated with the subsequent risks of obesity and elevated blood pressure. We hypothesised that a prenatal exposure to phthalates would lead to an increase in adverse cardiometabolic parameters through childhood and adulthood. The maternal serum phthalate measurements from the stored samples taken from Gen1 mothers at 18 and 34 weeks gestation were examined in relation to the cardiometabolic measures in 387 male offspring from the Raine Study. Data from the Gen2 follow-ups between 3 and 27 years were used. The primary outcomes were analysed longitudinally using linear mixed models for the repeated measures. Non-alcoholic fatty liver disease (NAFLD) was assessed at 17 years using logistic regression. A consistent positive relationship was observed between a prenatal exposure to mono-carboxy-iso-octyl phthalate (MCiOP) through adolescence into adulthood with systolic blood pressure. There were no other consistent cardiovascular associations. Mid-levels of prenatal exposures to Mono-n-butyl phthalate (MnBP) were associated with a greater incidence of NAFLD. Detectable Mono-3-carboxypropyl phthalate (MCPP) was associated with a lower serum HDL-C through late childhood into adulthood, while a higher prenatal exposure to mono-iso-butyl phthalate (MiBP), was associated with a higher LDL-C at 22 years of age. A mid-level prenatal exposure to mono-2-ethylhexyl phthalate (MEHP) metabolites was associated with higher insulin in adulthood, while a higher prenatal exposure to the sum of the Di-(2-ethyl-hexyl) phthalate (DEHP) and Di-iso-nonyl phthalate (DiNP) metabolites was associated with higher fasting serum glucose in adulthood. In conclusion, our study demonstrated that higher prenatal phthalate exposures to some phthalate metabolites was associated with some adverse metabolic profiles through adolescence into adulthood, although the consistent themes were limited to a few metabolites and the outcomes of systolic blood pressure, fasting insulin and glucose.

Associations between Prenatal Exposure to Phthalates and Timing of Menarche and Growth and Adiposity into Adulthood: A Twenty-Years Birth Cohort Study.

Phthalates are ubiquitous environmental chemicals with endocrine disrupting properties and potentially obesogenic effects. We hypothesised that antenatal phthalate exposure may influence growth and adiposity patterns in girls through childhood into adolescence. Among 1342 Raine Study singleton females, 462 had maternal serum and at least one outcome available up to 20 years of age. Individuals' maternal serum collected at 18 and 34 weeks gestation was pooled and analyzed for concentrations of 32 metabolites of 15 phthalate diesters. Cox regression and linear models were used to determine associations between maternal phthalate levels and age at menarche, change in height and weight z-scores between birth and two years, height from birth to 20 years, BMI from two to 20 years, deviation from mid-parental height at age 20 and DEXA scan measures at age 20. Weak negative associations were detected with some phthalate metabolites and change in height and weight z-score during infancy. Weak positive associations between some of the high molecular weight phthalate metabolites and height z-score were detected during childhood. While still within the normal range, age at menarche was slightly delayed in girls with higher prenatal exposure to the higher molecular weight phthalate metabolites. We derived some associations between prenatal phthalate exposure with early growth patterns and age at menarche.

The influence of prenatal exposure to phthalates on subsequent male growth and body composition in adolescence.

Phthalates are ubiquitous environmental chemicals with predominantly anti-androgenic, and potentially obesogenic effects. We hypothesised that antenatal phthalate exposure may influence subsequent boy's growth and body composition through childhood and adolescence. Among 1399 singleton males from the Raine Study, 410 had maternal serum and at least one height, BMI or DEXA outcome available after birth and up to 20 years of age. Maternal serum collected at 18 and 34 weeks' gestation was pooled, and analyzed for concentrations of 32 metabolites of 15 phthalate diesters. Their serum concentrations were categorized into undetectable/detectable levels or tertiles. Linear mixed models were used to determine associations between maternal serum phthalate levels and longitudinal height and body mass index (BMI) z-scores in boys from birth to 20 years of age (n = 250 and n = 295 respectively). Linear regression was used to determine associations between maternal phthalate levels and deviation from mid-parental height (n = 177) and DEXA scan outcomes (n = 191) at the 20 year follow-up. Weak positive associations of participants height z-score increase were detected with exposure to some phthalate metabolites in particular to the lower molecular weight phthalate metabolites. Less consistent findings, by mixed model analyses, were detected for BMI and body composition, by dual energy X-ray absorptiometry (DEXA), with some positive associations of phthalate metabolites with BMI and some negative associations with DEXA fat tissue measures, although no consistent findings were evident. In conclusion, we derived some associations of childhood growth with prenatal phthalate exposure, particularly with respect to the lower molecular weight phthalate metabolites.

Rates of neonatal morbidity by maternal region of birth and gestational age in New South Wales, Australia 2003-2016.

INTRODUCTION: Research suggests that neonatal morbidity differs by maternal region of birth at different gestational ages. This study aimed to determine the overall and gestation-specific risk of neonatal morbidity by maternal region of birth, after adjustment for maternal, infant and birth characteristics, for women giving birth in New South Wales, Australia, from 2003 to 2016. MATERIAL AND METHODS: The study utilized a retrospective cohort study design using linked births, hospital and deaths data. Modified Poisson regression was used to determine risk with 95% confidence intervals (95% CI) of neonatal morbidity by maternal region of birth, overall and at each gestational age, compared with Australian or New Zealand-born women giving birth at 39 weeks. RESULTS: There were 1 074 930 live singleton births ≥32 weeks' gestation that met the study inclusion criteria, and 44 394 of these were classified as morbid, giving a neonatal morbidity rate of 4.13 per 100 live births. The gestational age-specific neonatal morbidity rate declined from 32 weeks' gestation, reaching a minimum at 39 weeks in all maternal regions of birth. The unadjusted neonatal morbidity rate was highest in South Asian-born women at most gestations. Adjusted rates of neonatal morbidity between 32 and 44 weeks were significantly lower for babies born to East (adjusted relative risk [aRR] 0.65, 95% CI 0.62-0.68), South-east (aRR 0.76, 95% CI 0.73-0.79) and West Asian-born (aRR 0.93, 95% CI 0.88-0.98) mothers, and higher for babies of Oceanian-born (aRR 1.11, 95% CI 1.04-1.18) mothers, compared with Australian or New Zealand-born mothers. Babies of African, Oceanian, South Asian and West Asian-born women had a lower adjusted risk of neonatal morbidity than Australian or New Zealand-born women until 37 or 38 weeks' gestation, and thereafter an equal or higher risk in the term and post-term periods. CONCLUSIONS: Maternal region of birth is an independent risk factor for neonatal morbidity in New South Wales.

Rates of stillbirth by maternal region of birth and gestational age in New South Wales, Australia 2004-2015.

BACKGROUND: Research suggests that in Australia, maternal region of birth is a risk factor for stillbirth. AIMS: We aimed to examine the relationship between stillbirth and maternal region of birth in New South Wales (NSW), Australia from 2004 to 2015. METHODS: Adjusted logistic regression was used to determine odds of stillbirth by maternal region of birth, compared with Australian or New Zealand-born (AUS/NZ-born) women. Intervention rates (induction or pre-labour caesarean) by maternal region of birth, over time, were also examined. Interaction terms were used to assess change in relative odds of stillbirth, over two time periods (2004-2011 and 2012-2015). RESULTS: There were 944 457 singleton births ≥24 weeks gestation that met the study inclusion criteria and 3221 of these were stillbirths, giving a stillbirth rate of 3.4 per 1000 births. After adjustment for confounders, South Asian (adjusted odds ratio (aOR) 1.42, 95% CI 1.24-1.62), Oceanian (aOR 1.45, 95% CI 1.17-1.80) and African (aOR 1.46, 96% CI 1.19-1.80) born women had significantly higher odds of stillbirth that AUS/NZ-born women. Intervention rates increased from the earlier to the later time period by 13.1% across the study population, but the increase was larger in African and South Asian-born women (18.1% and 19.6% respectively) than AUS/NZ-born women (11.2%). There was a significant interaction between ethnicity and time period for South Asian-born women in the all-births model, with their stillbirth rates becoming closer to AUS/NZ-born women in the later period. CONCLUSION: South Asian, African and Oceanian maternal region of birth are independent risk factors for stillbirth in NSW.