Dataset Information

Dynamic growth metrics for examining prenatal exposure impacts on child growth trajectories: Application to perfluorooctanoic acid (PFOA) and postnatal weight gain.

ABSTRACT:

Background

Epidemiologic studies investigating prenatal exposures in relation to growth typically rely on cumulative growth measures such as weight or BMI. However, less is known about how prenatal exposure may impact other aspects of growth dynamics, including timing and velocity.

Objectives

To describe and apply a nonlinear growth model previously used in other health science fields to characterize postnatal growth trajectories for use in environmental epidemiology studies.

Methods

We used a double logistic function to model child weight trajectories from birth to 5.5 years using data from the Swedish Environmental Longitudinal Mother and Child, Asthma and Allergy (SELMA) study. From this, we approximated several infant growth metrics: 1) duration of time needed to complete 90% of the infant growth spurt (?t₁), 2) the maximum growth rate in infancy or infant peak growth velocity (PGV), 3) the age at infant PGV (?₁), a measure of growth tempo, and 4) the weight plateau at the end of the infant growth spurt (?₁). We assessed these metrics in relation to prenatal perfluorooctanoic acid (PFOA) exposure among 1334 mother-child pairs, and differences between boys and girls.

Results

Average estimated infant PGV and its timing (?₁) were 0.68 kg/month and 3.4 months, respectively. Mean infant growth spurt duration (?t₁) was 13 months, ending at an average weight plateau (?₁) of 8.2 kg. Higher prenatal PFOA concentrations were related to a longer duration of infant growth (?t₁: 0.06; 95% CI = 0.01, 0.11). PGV was not impacted, but higher prenatal PFOA concentrations were significantly related to delayed infant PGV (?₁: 0.58; 95% CI = 0.17, 0.99) and a higher post-spurt weight plateau (?₁: 0.81; 95% CI = 0.21, 1.41). After adjusting for false discovery, results were only significant for ?₁ and ?₁. We observed a significant interaction by sex for the association with ?₁, and stratified analyses revealed the association was only significant among girls.

Conclusion

Model-derived growth metrics were consistent with published growth standards. This novel application of nonlinear growth modeling enabled detection of altered infant growth dynamics in relation to prenatal PFOA exposure. Our results may help describe how PFOA yields lower birthweights, but higher weight later in childhood. Future applications may characterize adolescent growth or additional metrics of biological interest.

SUBMITTER: Tanner EM

PROVIDER: S-EPMC7027597 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Dynamic growth metrics for examining prenatal exposure impacts on child growth trajectories: Application to perfluorooctanoic acid (PFOA) and postnatal weight gain.

Tanner Eva M EM Bornehag Carl-Gustaf CG Gennings Chris C

Environmental research 20191214

<h4>Background</h4>Epidemiologic studies investigating prenatal exposures in relation to growth typically rely on cumulative growth measures such as weight or BMI. However, less is known about how prenatal exposure may impact other aspects of growth dynamics, including timing and velocity.<h4>Objectives</h4>To describe and apply a nonlinear growth model previously used in other health science fields to characterize postnatal growth trajectories for use in environmental epidemiology studies.<h4>M ...[more]

PMID: 31874421

Similar Datasets

Project description:BackgroundPregnant women are ubiquitously exposed to per- and polyfluoroalkyl substances (PFAS). Prenatal exposure to PFAS has been associated with lower birth weight but also with excess adiposity and higher weight in childhood. These mixed findings warrant investigation of the relationship between PFAS and dynamic offspring growth.ObjectivesTo investigate the association between prenatal PFAS exposure and early-life growth trajectories during the first 2 y.MethodsPregnant women (n=3,426) were recruited from 2013 to 2016 from the Shanghai Birth Cohort (SBC) Study, and their children were followed up from birth to 2 y of age. Seven PFAS congeners were quantified in pregnant women's serum during the first trimester. Our study population was restricted to 1,350 children who had five repeated measurements for at least one anthropometric measure. Four anthropometric measures, including weight, length/height, weight-for-length, and head circumference, were evaluated at birth, 42 d, 6 months, 12 months, and 24 months, and standardized into z-scores using the World Health Organization reference. Trajectories of each measure were classified into five groups using group-based trajectory modeling. Multinomial logistic regression was used to estimate odds ratio (OR) and 95% confidence interval (CI) for trajectory groups according to log2-transformed PFAS concentrations, and the moderate-stable group was selected as the reference group for all measures.ResultsHigher prenatal exposure to PFAS was associated with elevated odds for the low-rising weight-for-age z-score (WAZ) trajectory, and the high-rising length-for-age z-score (LAZ) trajectory. Meanwhile, PFAS levels were associated with decreased odds for the low-rising and high-rising weight-for-length z-score (WLZ) trajectories. In addition, the associations of PFAS with growth trajectory groups differed by sex, where males had greater odds for the low-rising and low-stable WAZ trajectories and for the high-stable and low-rising WLZ trajectories. In contrast, inverse associations were consistently observed with trajectories of the high-stable, low-stable, and low-rising head-circumference-for-age z-score (HCZ) in relation to most individual PFAS congeners. PFAS mixtures analysis further confirmed the above findings.DiscussionTrajectory analysis approach provided insight into the complex associations between PFAS exposure and offspring growth. Future studies are warranted to confirm the present findings with trajectory modeling strategies and understand the clinical significance of these trajectory groups. https://doi.org/10.1289/EHP9875.

Project description:BackgroundThe exposure-response association between prenatal and postnatal household air pollution (HAP) and infant growth trajectories is unknown.ObjectivesTo evaluate associations between prenatal and postnatal HAP exposure and stove interventions on growth trajectories over the first year of life.MethodsThe Ghana Randomized Air Pollution and Health Study enrolled n=1,414 pregnant women at ≤24wk gestation from Kintampo, Ghana, and randomized them to liquefied petroleum gas (LPG), improved biomass, or open fire (control) stoves. We quantified HAP exposure by repeated, personal prenatal and postnatal carbon monoxide (CO) and, in a subset, fine particulate matter [PM with an aerodynamic diameter of ≤2.5μm (PM2.5)] assessments. Length, weight, mid-upper arm circumference (MUAC) and head circumference (HC) were measured at birth, 3, 6, 9, and 12 months; weight-for-age, length-for-age (LAZ), and weight-for-length z (WLZ)-scores were calculated. For each anthropometric measure, we employed latent class growth analysis to generate growth trajectories over the first year of life and assigned each child to a trajectory group. We then employed ordinal logistic regression to determine associations between HAP exposures and growth trajectory assignments. Associations with stove intervention arm were also considered.ResultsOf the 1,306 live births, 1,144 had valid CO data and anthropometric variables measured at least once. Prenatal HAP exposure increased risk for lower length [CO odds ratio (OR)= 1.17, 95% CI: 1.01, 1.35 per 1-ppm increase; PM2.5 OR= 1.07, 95% CI: 1.02, 1.13 per 10-μg/m3 increase], lower LAZ z-score (CO OR= 1.15, 95% CI: 1.01, 1.32 per 1-ppm increase) and stunting (CO OR= 1.25, 95% CI: 1.08, 1.45) trajectories. Postnatal HAP exposure increased risk for smaller HC (CO OR= 1.09, 95% CI: 1.04, 1.13 per 1-ppm increase), smaller MUAC and lower WLZ-score (PM2.5 OR= 1.07, 95% CI: 1.00, 1.14 and OR= 1.09, 95% CI: 1.01, 1.19 per 10-μg/m3 increase, respectively) trajectories. Infants in the LPG arm had decreased odds of having smaller HC and MUAC trajectories as compared with those in the open fire stove arm (OR= 0.58, 95% CI: 0.37, 0.92 and OR= 0.45, 95% CI: 0.22, 0.90, respectively).DiscussionHigher early life HAP exposure (during pregnancy and through the first year of life) was associated with poorer infant growth trajectories among children in rural Ghana. A cleaner-burning stove intervention may have improved some growth trajectories. https://doi.org/10.1289/EHP8109.

Project description:BackgroundPerfluorooctanoic acid (PFOA or C8) has hepatotoxic effects in animals. Cross-sectional epidemiologic studies suggest PFOA is associated with liver injury biomarkers.ObjectivesWe estimated associations between modeled historical PFOA exposures and liver injury biomarkers and medically validated liver disease.MethodsParticipants completed surveys during 2008-2011 reporting demographic, medical, and residential history information. Self-reported liver disease, including hepatitis, fatty liver, enlarged liver and cirrhosis, was validated with healthcare providers. Alanine aminotransferase (ALT), ?-glutamyltransferase (GGT) and direct bilirubin, markers of liver toxicity, were obtained from blood samples collected in the C8 Health Project (2005-2006). Historically modeled PFOA exposure, estimated using environmental fate and transport models and participant residential histories, was analyzed in relation to liver biomarkers (n = 30,723, including 1,892 workers) and liver disease (n = 32,254, including 3,713 workers).ResultsModeled cumulative serum PFOA was positively associated with ALT levels (p for trend < 0.0001), indicating possible liver toxicity. An increase from the first to the fifth quintile of cumulative PFOA exposure was associated with a 6% increase in ALT levels (95% CI: 4, 8%) and a 16% increased odds of having above-normal ALT (95% CI: odds ratio: 1.02, 1.33%). There was no indication of association with either elevated direct bilirubin or GGT; however, PFOA was associated with decreased direct bilirubin. We observed no evidence of an effect of cumulative exposure (with or without a 10-year lag) on all liver disease (n = 647 cases), nor on enlarged liver, fatty liver, and cirrhosis only (n = 427 cases).ConclusionResults are consistent with previous cross-sectional studies showing association between PFOA and ALT, a marker of hepatocellular damage. We did not observe evidence that PFOA increases the risk of clinically diagnosed liver disease.CitationDarrow LA, Groth AC, Winquist A, Shin HM, Bartell SM, Steenland K. 2016. Modeled perfluorooctanoic acid (PFOA) exposure and liver function in a Mid-Ohio Valley community. Environ Health Perspect 124:1227-1233;?http://dx.doi.org/10.1289/ehp.1510391.

Project description:BackgroundPerfluoroalkyl substances (PFAS) are ubiquitous synthetic chemicals with long half-lives and are known to cross the placenta during pregnancy. We examined the influence of maternal PFAS levels on in utero fetal growth trajectories and assessed whether maternal stress modified these associations.MethodsBlood serum concentrations of five PFAS (PFOS, PFHxS, PFNA, PFOA, PFDA) were measured in 335 prenatal specimens (mean gestational age (GA): 21±9 weeks) in the MADRES cohort. Fetal growth outcomes (head circumference (HC), abdominal circumference (AC), biparietal diameter (BPD), femur length (FL), and estimated fetal weight (EFW)) were abstracted from ultrasound medical records and measured at the 3rd trimester study visit (N = 833 scans, GA range 10-42 weeks, mean 2.4 scans/participant). Adjusted linear mixed models with a GA quadratic growth curve were used for each PFAS exposure and growth outcome. PFOS and PFHxS were modeled continuously (100% sample detection), while PFOA, PFNA, and PFDA were modeled categorically (57-70% sample detection). Scores on the Perceived Stress Scale (PSS) measured in pregnancy were dichotomized at the median (<13 vs. ≥ 13) in stratified models.ResultsParticipants were on average 29±6 years old and predominately Hispanic (76%). Median serum concentrations of PFOS, PFHxS, PFNA, PFOA and PFDA were 1.34, 1.10, 0.07, 0.12, and 0.04 ng/mL, respectively. Participants with detected PFOA concentrations had fetuses with -2.5 mm (95% CI -4.2, -0.8) smaller HC and-0.7 mm (95% CI -1.3, -0.2) smaller BPD on average for a fixed GA than those without detected PFOA concentrations. In models stratified by PSS level, the effects of PFOA on fetal growth parameters were stronger and only significant in participants with higher stress levels (HC: β= -3.5, 95% CI -5.8, -1.4; BPD: β = -0.8, 95% CI -1.6, -1.1).ConclusionsPrenatal PFOA exposure adversely impacted fetal head biometric parameters in participants experiencing higher stress during pregnancy.

Dataset Information

Dynamic growth metrics for examining prenatal exposure impacts on child growth trajectories: Application to perfluorooctanoic acid (PFOA) and postnatal weight gain.

Background

Objectives

Methods

Results

Conclusion

Publications

Dynamic growth metrics for examining prenatal exposure impacts on child growth trajectories: Application to perfluorooctanoic acid (PFOA) and postnatal weight gain.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets