180-LB: Associations of Phthalate Metabolites with Glycemic Parameters and Fetal Growth in Type 1 Diabetes (T1D) Pregnancies

Abstract

Background: The risk of delivering a large for gestational age (LGA) infant is higher in pregnant individuals with T1D compared to individuals without diabetes, despite advances in managing T1D in pregnancy. Exposure to endocrine disrupting chemicals (e.g., phthalates) can affect both glucose homeostasis and fetal growth. Objective: To estimate associations of urinary phthalate metabolite levels with continuous glucose monitoring (CGM) data in pregnancy and birthweight. Methods: We analyzed urinary levels of 14 phthalate metabolites and derived trimester-specific CGM summary measures in 32 pregnant women with T1D. We estimated associations of log2-transformed urinary metabolite levels with continuous CGM outcomes and infant weight (GROW percentile) using linear regression, and estimated associations between metabolite levels and odds of LGA (GROW percentile ≥90) vs. AGA (<90) using logistic regression. Models were adjusted for maternal age and gestational week of study visit. Results: Participants were primarily white (85%), nulliparous (53%), with a mean age of 33 years, and 50% had LGA infants. Concentrations of mono-benzyl phthalate (mBzP) and mono-carboxy octyl phthalate (mCNP), were associated with glycemia in the 3rd trimester. Specifically, each doubling of mBzP and mCNP concentration was associated with 8.5 mg/dL (95% CI: 1.4, 15.6) and 8.9 mg/dL (-1.3, 19.0) higher average glucose, -6.0% (-10.9, -1.0) and -8.9% (-15.1, -2.7) less time spent in range (63-140mg/dL), and 5.9% (0.7, 11.2) and 7.4% (0.3, 14.5) more time spent above range (>140 mg/dL). Phthalates were not associated with continuous GROW percentile. Conclusion: Exposure to certain phthalates in later pregnancy may affect glycemic control in pregnant individuals with T1D. However, effects of phthalate exposure on birthweight are unclear. Future studies may disentangle the extent to which phthalate exposure and its effects on glycemic control may impact fetal growth. Disclosure E. V. Preston: None. F. M. Brown: Other Relationship; Dexcom, Inc. G. A. Hansbury: None. J. C. O'connell: None. D. Wolfs: None. J. Dreyfuss: None. S. Wolpowitz: None. Z. Wang: None. T. James-todd: None. E. M. Isganaitis: None. Funding National Institute of Environmental Health Sciences; National Institute of Diabetes and Digestive and Kidney Diseases