Maternal bisphenol urine concentrations, fetal growth and adverse birth outcomes: A population-based prospective cohort

Abstract

Background Exposure to bisphenols may affect fetal growth and development. The trimester-specific effects of bisphenols on repeated measures of fetal growth remain unknown. Our objective was to assess the associations of maternal bisphenol urine concentrations with fetal growth measures and birth outcomes and identify potential critical exposure periods. Methods In a population-based prospective cohort study among 1379 pregnant women, we measured maternal bisphenol A, S and F urine concentrations in the first, second and third trimester. Fetal head circumference, length and weight were measured in the second and third trimester by ultrasound and at birth. Results An interquartile range increase in maternal pregnancy-averaged bisphenol S concentrations was associated with larger fetal head circumference (difference 0.18 (95% confidence interval (CI) 0.01 to 0.34) standard deviation scores (SDS), p-value< 0.05) across pregnancy. When focusing on specific critical exposure periods, any detection of first trimester bisphenol S was associated with larger second and third trimester fetal head circumference (difference 0.15 (95% CI 0.05 to 0.26) and 0.12 (95% CI 0.02 to 0.23) SDS, respectively) and fetal weight (difference 0.12 (95% CI 0.02 to 0.22) and 0.16 (95% CI 0.06 to 0.26) SDS, respectively). The other bisphenols were not consistently associated with fetal growth outcomes. Any detection of bisphenol S and bisphenol F in first trimester was also associated with a lower risk of being born small size for gestational age (Odds Ratio 0.56 (95% CI 0.38 to 0.74) and 0.55 (95% CI 0.36 to 0.85), respectively). Bisphenols were not associated with risk of preterm birth. Conclusions Higher maternal bisphenol S urine concentrations, especially in the first trimester, seem to be related with larger fetal head circumference, higher weight and a lower risk of being small size for gestational age at birth.

Association of Pentachlorophenol with Fetal Risk of Prolonged Bradycardia: A Systematic Review and Meta-Analysis

“…The epididymal sperm density was decreased. In 2002, Bemard et al fed 2 generations of SD rats with PCP, and reproductive toxicity tests showed that high-dose (60 mg/(kg.d)) feeding caused delayed sexual maturation, reduced sperm number, reduced prostate and testes, reduced embryo implantation capacity, and reduced litter production [ 28 ].…”

“…The limitations of this study are as follows: incorporating observational studies in the study is limited, the follow-up varies from 3 to 36 months, making the evaluation of long-term complications, the publication bias analysis is only qualitative and large personal factors, and the two techniques described in this study contain multiple surgical procedures, which may increase the bias of the article. Since the assessments were all based on a small number of studies [ 26 – 28 ], the results must be interpreted with caution. As the accumulated evidence grows, our conclusions may either be supported or overturned.…”

Bisphenol S Impairs Invasion and Proliferation of Extravillous Trophoblasts Cells by Interfering with Epidermal Growth Factor Receptor Signaling

“…In this study, the lowest BPS dose that exerted a significative effect on cell invasion was 100 ng/mL BPS, a dose within the urinary BPS concentration range observed in the U.S. (0.07 to 211.9 ng/mL; [ 10 ]). While in vivo exposure to BPS can result in cell fusion defects in an ovine model [ 23 ], effects of BPS in human pregnancies have been associated with both higher [ 56 ] and lower [ 57 ] birth weight and birth length. Thus, whether BPS can interfere with EGF signaling, in vivo, in humans, resulting in poor pregnancy outcomes remains to be determined.…”

Prenatal Exposure to Nonpersistent Chemical Mixtures and Fetal Growth: A Population-Based Study

“…2019 ; Santos et al. 2021 ; Sol et al. 2021 ) but used different model structures, exposure and outcome parameterizations, and covariate sets based on the research questions of each study.…”

“…Second, we created single-pollutant regression models to estimate the individual chemical biomarker associations with fetal growth parameters. These estimates have been previously published (Ferguson et al 2019;Santos et al 2021;Sol et al 2021) but used different model structures, exposure and outcome parameterizations, and covariate sets based on the research questions of each study. Thus, we replicated those analyses here with the same primary model structure (i.e., averaged biomarkers over pregnancy in association with growth measurements at each time point) and with the same covariates included in our primary model for more direct comparison with our results.…”