TY - JOUR
T1 - Associations of per- and polyfluoroalkyl substances (PFAS) and their mixture with oxidative stress biomarkers during pregnancy
AU - Taibl, Kaitlin R.
AU - Schantz, Susan
AU - Aung, Max T.
AU - Padula, Amy
AU - Geiger, Sarah
AU - Smith, Sabrina
AU - Park, June Soo
AU - Milne, Ginger L.
AU - Robinson, Joshua F.
AU - Woodruff, Tracey J.
AU - Morello-Frosch, Rachel
AU - Eick, Stephanie M.
N1 - We would like to thank our clinical research coordinators for collecting the data and the data analysis teams for helping to enter and compile the data, particularly Aileen Andrade, Cheryl Godwinde Medina, Cynthia Melgoza Canchola, Tali Felson, Harim Lee, Maribel Juarez, Lynn Harvey and Allison Landowski from the CIOB group and Ana Lucic, Shuk Han Ng, Mary Wakefield, Jeni Bushman, Mindy Howe, and Darcie Reckers from the IKIDS group. We also thank the research team in the Eicosanoid Core Lab, including Stephanie Sanchez, Warda Amin, Holly Borntrager, and Sarah Thomas for the analysis of oxidative stress biomarkers. We also thank the study participants who participated in the CIOB and IKIDS studies. Lastly, we would like to thank the DTSC biomonitoring team for the laboratory analysis of PFAS in serum. This work was supported by grants RD83543301 AND RD83543401 from the United States Environmental Protection Agency Children's Environmental Health and Disease Prevention Research Center, P30ES019776, P30ES030284, P01ES022841, P01ES022848 and R01ES02705 from the National Institute of Environmental Health Sciences, and UG3OD023272, UH3OD023272, and 5U2COD023375-05 from the National Institutes of Health Environmental influences on Child Health Outcomes (ECHO) program. Per University of California, San Francisco Institutional Review Board approval, the data that support the findings of this study are restricted for transmission to those outside the primary investigative team. Data sharing with investigators outside the team requires IRB approval. Requests may be submitted to the Program on Reproductive Health and the Environment (PRHE).
This work was supported by grants RD83543301 AND RD83543401 from the United States Environmental Protection Agency Children’s Environmental Health and Disease Prevention Research Center, P30ES019776, P30ES030284, P01ES022841, P01ES022848 and R01ES02705 from the National Institute of Environmental Health Sciences, and UG3OD023272, UH3OD023272, and 5U2COD023375-05 from the National Institutes of Health Environmental influences on Child Health Outcomes (ECHO) program.
PY - 2022/11
Y1 - 2022/11
N2 - Background: Oxidative stress from excess reactive oxygen species (ROS) is a hypothesized contributor to preterm birth. Per- and polyfluoroalkyl substances (PFAS) exposure is reported to generate ROS in laboratory settings, and is linked to adverse birth outcomes globally. However, to our knowledge, the relationship between PFAS and oxidative stress has not been examined in the context of human pregnancy. Objective: To investigate the associations between prenatal PFAS exposure and oxidative stress biomarkers among pregnant people. Methods: Our analytic sample included 428 participants enrolled in the Illinois Kids Development Study and Chemicals In Our Bodies prospective birth cohorts between 2014 and 2019. Twelve PFAS were measured in second trimester serum. We focused on seven PFAS that were detected in >65 % of participants. Urinary levels of 8-isoprostane-prostaglandin-F2α, prostaglandin-F2α, 2,3-dinor-8-iso-PGF2α, and 2,3-dinor-5,6-dihydro-8-iso-PGF2α were measured in the second and third trimesters as biomarkers of oxidative stress. We fit linear mixed-effects models to estimate individual associations between PFAS and oxidative stress biomarkers. We used quantile g-computation and Bayesian kernel machine regression (BKMR) to assess associations between the PFAS mixture and averaged oxidative stress biomarkers. Results: Linear mixed-effects models showed that an interquartile range increase in perfluorooctane sulfonic acid (PFOS) was associated with an increase in 8-isoprostane-prostaglandin-F2α (β = 0.10, 95 % confidence interval = 0, 0.20). In both quantile g-computation and BKMR, and across all oxidative stress biomarkers, PFOS contributed the most to the overall mixture effect. The six remaining PFAS were not significantly associated with changes in oxidative stress biomarkers. Conclusions: Our study is the first to investigate the relationship between PFAS exposure and biomarkers of oxidative stress during human pregnancy. We found that PFOS was associated with elevated levels of oxidative stress, which is consistent with prior work in animal models and cell lines. Future research is needed to understand how prenatal PFAS exposure and maternal oxidative stress may affect fetal development.
AB - Background: Oxidative stress from excess reactive oxygen species (ROS) is a hypothesized contributor to preterm birth. Per- and polyfluoroalkyl substances (PFAS) exposure is reported to generate ROS in laboratory settings, and is linked to adverse birth outcomes globally. However, to our knowledge, the relationship between PFAS and oxidative stress has not been examined in the context of human pregnancy. Objective: To investigate the associations between prenatal PFAS exposure and oxidative stress biomarkers among pregnant people. Methods: Our analytic sample included 428 participants enrolled in the Illinois Kids Development Study and Chemicals In Our Bodies prospective birth cohorts between 2014 and 2019. Twelve PFAS were measured in second trimester serum. We focused on seven PFAS that were detected in >65 % of participants. Urinary levels of 8-isoprostane-prostaglandin-F2α, prostaglandin-F2α, 2,3-dinor-8-iso-PGF2α, and 2,3-dinor-5,6-dihydro-8-iso-PGF2α were measured in the second and third trimesters as biomarkers of oxidative stress. We fit linear mixed-effects models to estimate individual associations between PFAS and oxidative stress biomarkers. We used quantile g-computation and Bayesian kernel machine regression (BKMR) to assess associations between the PFAS mixture and averaged oxidative stress biomarkers. Results: Linear mixed-effects models showed that an interquartile range increase in perfluorooctane sulfonic acid (PFOS) was associated with an increase in 8-isoprostane-prostaglandin-F2α (β = 0.10, 95 % confidence interval = 0, 0.20). In both quantile g-computation and BKMR, and across all oxidative stress biomarkers, PFOS contributed the most to the overall mixture effect. The six remaining PFAS were not significantly associated with changes in oxidative stress biomarkers. Conclusions: Our study is the first to investigate the relationship between PFAS exposure and biomarkers of oxidative stress during human pregnancy. We found that PFOS was associated with elevated levels of oxidative stress, which is consistent with prior work in animal models and cell lines. Future research is needed to understand how prenatal PFAS exposure and maternal oxidative stress may affect fetal development.
KW - Maternal and child health
KW - Mixtures
KW - Oxidative stress
KW - PFAS
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U2 - 10.1016/j.envint.2022.107541
DO - 10.1016/j.envint.2022.107541
M3 - Article
C2 - 36191484
AN - SCOPUS:85138995276
SN - 0160-4120
VL - 169
JO - Environment international
JF - Environment international
M1 - 107541
ER -