Oral Concurrent Session 4 - Equity, Public Health, and Public Policy
Oral Concurrent Sessions
Michael D. Jochum, Jr., PhD
Assistant Professor
Baylor College of Medicine
Houston, Texas, United States
Cynthia Shope, MSc
Lab Manager
Baylor College of Medicine
Baylor College of Medicine, Texas, United States
Melissa A. Suter, PhD
Baylor College of Medicine and Texas Children's Hospital
Houston, Texas, United States
Kjersti M. Aagaard, MD, MSCI, PhD
Medical Director, HCA Healthcare and HCA Research Institute
HCA
Houston, Texas, United States
Enrico R. Barrozo, PhD
Assistant Professor
Baylor College of Medicine and Texas Children's Hospital
Houston, Texas, United States
Preterm birth (PTB) is a leading cause of neonatal morbidity and long-term disease risk, yet the role of environmental and dietary exposures in PTB occurrence remains unclear. Toxicants such as polycyclic aromatic hydrocarbons (PAHs) and microplastics accumulate in placentae and are elevated in PTB, but the impact of timing, sources, and dietary modifiers is unknown. We hypothesized that longitudinal urinary analyte measures could predict PTB and that maternal diet would mediate these relationships.
Study Design:
We analyzed dietary data and longitudinal biospecimens from the BaBs cohort (NCT02392650), including 103 PTB and 367 term pregnancies. Mass spectrometry (HHEAR network) quantified 1,230 analytes from maternal urine samples (n=932; ≥2 per participant; median interval first sample-to-delivery: 20.6 weeks). Models integrated clinical and dietary metadata, including 2,129 survey measures. Diet index scores were generated using validated methods.
Results:
Slopes (per-subject rates of change across gestation) for multiple maternal urinary analytes and dietary scores were significantly associated with both dietary quality and PTB. Dietary patterns diverged by PTB status (Fig. 1A), with Mediterranean Diet Score (MDS) declining steeply in PTB (interaction p=0.016). At 28 weeks, PTB pregnancies had lower Alternate Healthy Eating Index (AHEI), fiber adequacy, and MDS (Fig. 1B-D). Unsupervised clustering of analyte slopes revealed three groups, with Cluster 1 defined by a PAH, plasticizer, and metabolite signature. Cluster 1 was associated with a five-week reduction in gestational age (Fig. 2A-C; FDR< 0.05). Higher AHEI, MDS, and dietary diversity increased gestational age by 1.6-3.2 weeks, while increased AHEI and MDS interactions (+6 weeks) offset Cluster 1 risk; higher plastic exposure amplified risk (interaction -6.5 weeks).
Conclusion:
Lower dietary quality and higher toxicant levels were independently and jointly associated with shorter gestational age. These results highlight the need to further evaluate maternal urinary analytes as PTB biomarkers and maternal diet as a modifiable risk factor.