Abstracts: ISEE 21st Annual Conference, Dublin, Ireland, August 25-29, 2009: Symposium Abstracts
*Mount Sinai School of Medicine, New York, NY, United States; and †Centers for Disease Control and Prevention, Atlanta, GA, United States.
Background and Objective:
Prenatal exposure to phthalates has been associated with reproductive toxicity and neurodevelopmental consequences in offspring. Fetal exposure is typically estimated by prenatal maternal urinary biomarker levels; however, the extent to which fetuses are directly exposed to metabolites in amniotic fluid has not been established.
A pilot study to estimate the correlation between urine and amniotic fluid concentrations of phthalate metabolites, and their relations with placental expression of imprinted genes was performed (n = 11). This study was nested within the Study of Advanced Reproductive Age and Environmental Health (SARAEH), which enrolled 97 women who were undergoing amniocentesis at the Mount Sinai Medical Center as a part of their routine prenatal care. Women were enrolled on the day of their procedure, and a sample of their urine was obtained immediately following the amniocentesis. At delivery, placental biopsies were obtained for RNA collection. Phthalate concentrations were normalized by specific gravity.
Women were predominantly white (n = 10), with a mean age of 36 years. Eleven phthalate metabolites were detected in most prenatal urines. Few amniotic fluid samples had measureable phthalate metabolites, with the exception of mono(2-ethyl-5-carboxypentyl) phthalate (MECPP), an oxidative metabolite of di(2-ethylhexyl) phthalate, which was detectable in all samples. Amniotic fluid concentration of MECPP ranged from 0.7–2.1 ug/L (med 1.1, sd = 0.23). Urine concentration of MECPP ranged from 4.2–359 ug/L (med 81.6, sd = 105.8). There was no correlation between amniotic fluid and urinary concentrations of MECPP. Among other associations, placental expression of IGF2 was increased with increasing urinary concentration of high molecular weight metabolites.
Direct fetal exposure to phthalate metabolites in amniotic fluid appears to be minimal, and limited to MECPP. Disruption of placentally imprinted genes may be an alternative mechanism linking phthalate exposure to effects in offspring.