ArticleThe Science of the total environment2021
Prenatal phthalate exposure measurement: A comparison of metabolites quantified in prenatal maternal urine and newborn's meconium.
Article in The Science of the total environment, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 17 citations in OpenAlex.
- An assessment of measurement error when using maternal urinary phthalates as proxies for placental tissue levels in the estimation of the association of prenatal phthalates and infant anogenital distance.Journal of exposure science & environmental epidemiology · 2026Article
- Article
- Disrupted Prenatal Metabolism May Explain the Etiology of Suboptimal Neurodevelopment: A Focus on Phthalates and Micronutrients and their Relationship to Autism Spectrum Disorder.Advances in nutrition (Bethesda, Md.) · 2024Review
- The Relationship between Phthalates and Diabetes: A Review.Metabolites · 2023Review
- The associations between prenatal phthalate exposure measured in child meconium and cognitive functioning of 12-month-old children in two cohorts at elevated risk for adverse neurodevelopment.Environmental research · 2022Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Phthalates are chemicals suspected to adversely affect fetal neurodevelopment, but quantifying the fetal exposure is challenging. While prenatal phthalate exposure is commonly quantified in maternal urine, the newborn's meconium may better capture cumulative prenatal exposure. Currently, data on phthalates measured in meconium is sparse. We measured phthalate metabolites in 183 maternal second and 140 third trimester (T2, T3) urine, and in 190 meconium samples collected in an autism enriched-risk pregnancy cohort of 236 mothers. Eleven and eight metabolites were detected in over 90% of urine and meconium samples, respectively. Hydrophilic and hydrophobic metabolites were detected in both biosamples. Most urine phthalate metabolite distributions were similar between T2 and T3. Among metabolites detected in both biosamples, those of di(2-ethylhexyl) phthalate displayed a similar pattern in magnitude across metabolite type. Specifically, T2 creatinine adjusted distribution [median (25%, 75%)] of urine measured mono(2-ethylhexyl-carboxypentyl) (MECPP), mono(2-ethyl-5-hydroxyhexyl) (MEHHP), and mono(2-ethyl-5-oxohexyl) phthalate (MEOHP) were 18.8(11.9, 31.4), 11.8(7.2, 19.1), and 8.9(6.2, 14.2) ng/mg. In meconium these were 16.6(10.9, 23.7), 2.5(1.5, 3.8), and 1.3(0.8, 2.3) ng/g, respectively. Metabolite-to-metabolite correlations were lower in meconium than urine, but patterns were similar. For example, correlation (95% CI) between mono(2-ethylhexyl) phthalate and MECPP was 0.73 (0.66, 0.78), and between MEOHP and MEHHP was 0.96 (0.95, 0.97) in urine as compared to 0.10 (-0.04, 0.24) and 0.31 (0.18, 0.43) respectively in meconium. Correlations between same metabolites measured in urine and meconium were low and differed by metabolite and trimester. Correlation between MEHHP in urine and meconium, for example, was 0.20 (0.008, 0.37) at T3, but 0.05 (-0.12, 0.21) at T2. Our study provides evidence of general population-level prenatal phthalate exposure in a population at high risk for neurodevelopmental disorders and supports the utility of meconium to measure prenatal phthalate exposure but provides little evidence of correlation with exposure measured in prenatal maternal urine.
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