ESPE Abstracts (2014) 82 P-D-1-3-94

ESPE2014 Poster Presentations Sex Development (11 abstracts)

Prenatal Exposure to Phthalates and Phenols in Relation to Anogenital Distance at Birth in Male Infants

Benjamin G Fisher a , Ajay Thankamony a , Ken K Ong b , David B Dunger a , Ieuan A Hughes a & Carlo L Acerini a


aDepartment of Paediatrics, University of Cambridge, Cambridge, UK; bMRC Epidemiology Unit, Institute of Metabolic Science, Cambridge, UK


Introduction: Increasing incidence of male reproductive disorders may be due to fetal exposure to putative endocrine disruptor chemicals (EDCs), such as phthalates and phenols. Anogenital Distance (AGD) is a biomarker of fetal androgen action in animals, and has recently been linked to testicular dysgenesis syndrome in humans.

Objective: To examine the relationship between prenatal phthalate and phenol exposure and birth AGD in male infants.

Method: Serum samples were collected from pregnant women between 10 and 12 weeks of gestation as part of a larger prospective study (n=334). 27 EDCs (16 phthalate monoesters, and nine phenols) were measured using liquid chromatography/tandem mass spectrometry. Statistical analyses excluded EDCs detectable in <45% of mothers. Birth AGD in males (measured from centre of anus to base of scrotum) was recorded (n=151).

Results: Six phthalate monoesters (MEP, MiBP, MnBP, MEHP, MECPP, and MCiOP) and three phenols (BPA, TCS, and BP-3) were detectable in ≥45%; median concentrations were 1.57, 3.77, 1.30, 1.17, 0.52, 0.19, 1.78, 0.75 and 0.30 μg/l, respectively. Summed levels were calculated for di(2-ethylhexyl)phthalate metabolites (ΣDEHPm), dibutylphthalate isomer metabolites (ΣMBP(i+n)), and all phthalate metabolites (Σall.phth.m). Mean±S.D. birth AGD was 19.5±5.5 mm. AGD was negatively correlated with ΣDEHPm (ρ=−0.188, P=0.021) and Σall.phth.m (ρ=−0.203, P=0.012), but no other EDCs. In a multiple regression model, potential confounding factors (maternal age, BMI, gestation, birth weight, and birth length) explained 4.5% of variance in birth AGD; entry of EDC levels (MEP, ΣMBP(i+n), ΣDEHPm, MCiOP, BPA, TCS, and BP-3) explained an additional 7.1%. In this model, only ΣDEHPm (β=−0.210, P=0.019) and BMI (β=0.177, P=0.043) were significant. In a separate analysis, Σall.phth.m explained an additional 4.5% of variance in AGD when potential confounders were controlled for (β=−0.213, P=0.014).

Conclusion: These results suggest that exposure to phthalates during the first trimester (specifically DEHP, and possibly others in combination), but not phenols, adversely affects male reproductive development.

Volume 82

53rd Annual ESPE (ESPE 2014)

Dublin, Ireland
18 Sep 2014 - 20 Sep 2014

European Society for Paediatric Endocrinology 

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