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

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 (Delta t(1)), 2) the maximum growth rate in infancy or infant peak growth velocity (PGV), 3) the age at infant PGV (delta(1)), a measure of growth tempo, and 4) the weight plateau at the end of the infant growth spurt (alpha(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 (delta(1)) were 0.68 kg/month and 3.4 months, respectively. Mean infant growth spurt duration (Delta t(1)) was 13 months, ending at an average weight plateau (alpha(1)) of 8.2 kg. Higher prenatal PFOA concentrations were related to a longer duration of infant growth (Delta t(1): 0.06; 95% CI = 0.01, 0.11). PGV was not impacted, but higher prenatal PFOA concentrations were significantly related to delayed infant PGV (delta(1) : 0.58; 95% CI = 0.17, 0.99) and a higher post-spurt weight plateau (alpha(1): 0.81; 95% CI = 0.21, 1.41). After adjusting for false discovery, results were only significant for delta(1) and alpha(1). We observed a significant interaction by sex for the association with delta(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.