Glyphosate exposure and hormonal disruption in pregnancy: evidence from a birth cohort in Puerto Rico
5 affiliations
- 1Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, MI USA
- 2Department of Environmental Health Sciences, University of Michigan, School of Public Health, Ann Arbor, MI USA
- 3University of Puerto Rico Medical Sciences Campus, Graduate School of Public Heth, San Juan, PR USA
- 4Department of Epidemiology and Biostatistics, University of Georgia, Athens, GA USA
- 5Department of Civil and Environmental Engineering, Northeastern University, Boston, MA USA
Abstract
Background: Glyphosate and its primary metabolite, aminomethylphosphonic acid (AMPA), are widespread environmental contaminants with potential endocrine-disrupting properties. Despite near-universal glyphosate and AMPA exposure, human studies evaluating their association with maternal hormonal regulation during gestation remain scarce.
Objective: To assess associations between urinary glyphosate and AMPA concentrations and repeated measures of maternal hormone levels during pregnancy and explore effect modification by gestational timing and fetal sex.
Methods: We analyzed data from 752 pregnancies in the PROTECT birth cohort in Puerto Rico. Glyphosate and AMPA were measured in up to three urine samples per participant collected at 18 ± 2-, 22 ± 2-, and 26 ± 2-weeks’ gestation. Serum concentrations of sex steroid (estriol, progesterone, testosterone), thyroid (T3, T4, fT4, TSH), and stress-related (CRH) hormones were assessed at two periods. Linear mixed effects models estimated differences in serum hormone levels associated with interquartile range (IQR) increases in urinary glyphosate/AMPA, adjusting for demographic, biological, and technical covariates.
Results: Glyphosate and AMPA were associated with lower estriol concentrations across pregnancy. Each IQR increase in AMPA was associated with 10.6% lower estriol (95% CI: –18.1%, –2.4%), while glyphosate was associated with 8.3% lower estriol (95% CI: –14.6%, –1.4%). AMPA was associated with 4.0% higher T3 (95% CI: 0.9%, 7.0%). In sensitivity analyses, AMPA was linked to 7.9% higher TSH at 26 ± 2-weeks’ gestation (95% CI: 0.5%, 15.9%), while glyphosate was associated with 9.5% higher CRH at this time point (95% CI: 1.5%, 18.2%). Stratified models revealed stronger associations among participants carrying female versus male fetuses.
Significance: This study provides first evidence of associations between prenatal glyphosate and AMPA exposure and disruption of multiple maternal hormonal pathways during pregnancy. Findings suggest these contaminants may interfere with estrogenic, thyroid, and stress hormone systems critical for pregnancy maintenance and fetal development, with implications for understanding mechanisms underlying adverse birth outcomes.
Impact: This study provides the first human evidence that glyphosate and AMPA, ubiquitous environmental contaminants detected in 75–95% of pregnant women, disrupt multiple maternal hormonal pathways during pregnancy. Among 752 participants in a Puerto Rico birth cohort, we demonstrate significant reductions in estriol (8–11% decreases) and alterations in thyroid and stress hormones associated with glyphosate exposure. These findings illuminate potential biological mechanisms underlying previously observed associations between glyphosate exposure and adverse birth outcomes, including preterm birth and altered fetal growth. Given the widespread use of glyphosate-based herbicides globally, our results have significant implications for public health policy and regulatory decision-making. The hormonal disruptions we identified suggest that pregnant populations may be particularly vulnerable to glyphosate exposure, supporting the need for enhanced protective measures and exposure reduction strategies during critical windows of fetal development.
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BibTeX
@article{valentincortes2026glyphosate,
title = {{Glyphosate exposure and hormonal disruption in pregnancy: evidence from a birth cohort in Puerto Rico}},
author = {Mislael A. Valentín-Cortés and Amber L. Cathey and Haley M. Jenkins and Jennifer Fernandez and Zaira Rosario Pabón and Carmen M. Vélez Vega and José F. Cordero and Akram Alshawabkeh and Deborah J. Watkins and John D. Meeker},
journal = {Journal of Exposure Science \& Environmental Epidemiology},
year = {2026},
month = jun,
doi = {10.1038/s41370-026-00902-6},
url = {https://doi.org/10.1038/s41370-026-00902-6},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Glyphosate exposure and hormonal disruption in pregnancy: evidence from a birth cohort in Puerto Rico
AU - Mislael A. Valentín-Cortés
AU - Amber L. Cathey
AU - Haley M. Jenkins
AU - Jennifer Fernandez
AU - Zaira Rosario Pabón
AU - Carmen M. Vélez Vega
AU - José F. Cordero
AU - Akram Alshawabkeh
AU - Deborah J. Watkins
AU - John D. Meeker
PY - 2026
DA - 2026/06/15
JO - Journal of Exposure Science & Environmental Epidemiology
DO - 10.1038/s41370-026-00902-6
UR - https://doi.org/10.1038/s41370-026-00902-6
AB - Background: Glyphosate and its primary metabolite, aminomethylphosphonic acid (AMPA), are widespread environmental contaminants with potential endocrine-disrupting properties. Despite near-universal glyphosate and AMPA exposure, human studies evaluating their association with maternal hormonal regulation during gestation remain scarce. Objective: To assess associations between urinary glyphosate and AMPA concentrations and repeated measures of maternal hormone levels during pregnancy and explore effect modification by gestational timing and fetal sex. Methods: We analyzed data from 752 pregnancies in the PROTECT birth cohort in Puerto Rico. Glyphosate and AMPA were measured in up to three urine samples per participant collected at 18 ± 2-, 22 ± 2-, and 26 ± 2-weeks’ gestation. Serum concentrations of sex steroid (estriol, progesterone, testosterone), thyroid (T3, T4, fT4, TSH), and stress-related (CRH) hormones were assessed at two periods. Linear mixed effects models estimated differences in serum hormone levels associated with interquartile range (IQR) increases in urinary glyphosate/AMPA, adjusting for demographic, biological, and technical covariates. Results: Glyphosate and AMPA were associated with lower estriol concentrations across pregnancy. Each IQR increase in AMPA was associated with 10.6% lower estriol (95% CI: –18.1%, –2.4%), while glyphosate was associated with 8.3% lower estriol (95% CI: –14.6%, –1.4%). AMPA was associated with 4.0% higher T3 (95% CI: 0.9%, 7.0%). In sensitivity analyses, AMPA was linked to 7.9% higher TSH at 26 ± 2-weeks’ gestation (95% CI: 0.5%, 15.9%), while glyphosate was associated with 9.5% higher CRH at this time point (95% CI: 1.5%, 18.2%). Stratified models revealed stronger associations among participants carrying female versus male fetuses. Significance: This study provides first evidence of associations between prenatal glyphosate and AMPA exposure and disruption of multiple maternal hormonal pathways during pregnancy. Findings suggest these contaminants may interfere with estrogenic, thyroid, and stress hormone systems critical for pregnancy maintenance and fetal development, with implications for understanding mechanisms underlying adverse birth outcomes. Impact: This study provides the first human evidence that glyphosate and AMPA, ubiquitous environmental contaminants detected in 75–95% of pregnant women, disrupt multiple maternal hormonal pathways during pregnancy. Among 752 participants in a Puerto Rico birth cohort, we demonstrate significant reductions in estriol (8–11% decreases) and alterations in thyroid and stress hormones associated with glyphosate exposure. These findings illuminate potential biological mechanisms underlying previously observed associations between glyphosate exposure and adverse birth outcomes, including preterm birth and altered fetal growth. Given the widespread use of glyphosate-based herbicides globally, our results have significant implications for public health policy and regulatory decision-making. The hormonal disruptions we identified suggest that pregnant populations may be particularly vulnerable to glyphosate exposure, supporting the need for enhanced protective measures and exposure reduction strategies during critical windows of fetal development.
SN - 1559-0631
SN - 1559-064X
ER -