About
Rebecca Fry is the Carol Remmer Angle Distinguished Professor and Associate Chair at the University of North Carolina School of Public Health. Her research focuses on understanding how environmental exposures are associated with human disease, with a particular emphasis on genomic and epigenomic perturbations. Using environmental toxicogenomics and systems biology approaches, her lab aims to identify key molecular pathways that link environmental exposure to disease outcomes. A current research focus involves studying prenatal exposure to various metals, including arsenic, cadmium, and lead. Her work seeks to understand the molecular mechanisms by which early exposures to these metals are associated with long-term health effects in humans. Specifically, she examines DNA methylation profiles in humans exposed to metals during the prenatal period to identify gene and epigenetic biomarkers of metal exposure. These biomarkers can serve as targets for further study to unravel potential molecular bases for metal-induced disease. Ultimately, her research aims to identify mechanisms of metal-induced disease and the basis for inter-individual disease susceptibility.
Research topics
- Medicine
- Biology
- Internal medicine
- Environmental health
- Bioinformatics
- Genetics
- Immunology
- Computer Science
- Physiology
- Demography
- Chemistry
- Environmental chemistry
- Evolutionary biology
- Cell biology
- Gerontology
- Psychology
- Statistics
- Anesthesia
- Psychiatry
- Biochemistry
- Geography
- Endocrinology
- Pediatrics
- Organic chemistry
Selected publications
Prenatal over-the-counter acetaminophen use and birth outcomes in the ECHO cohort
American Journal of Epidemiology · 2026-05-20
articleOpen accessSenior authorAcetaminophen is among the most common over-the-counter medications used during pregnancy. Given inconsistent findings from both experimental and epidemiological studies on associations between use and adverse health outcomes, further research is warranted. To address this, our objective was to assess the relationship between prenatal acetaminophen use and birth outcomes. We studied 8957 mother-infant pairs from 36 pediatric study sites participating in the Environmental influences on Child Health Outcomes (ECHO) program. After imputation and inverse probability weighting, we used regression models to examine the relationship between acetaminophen during pregnancy and the following outcomes: (1) preterm birth, (2) birthweight, (3) small-for-gestational age (SGA), and (4) large-for-gestational-age (LGA). Approximately 59% of mothers reported using acetaminophen at any point during their pregnancy (n = 5257). After adjustment for relevant covariates, prenatal acetaminophen use was associated with lower odds of LGA (adjusted odds ratio (aOR): 0.87; 95% CI: 0.79, 0.96). Prenatal acetaminophen use was not associated with preterm birth (aOR: 0.99; 95% CI: 0.86, 1.14), birthweight (aβ: -7.52 g; 95% CI: -27.80, 12.77) or SGA (aOR: 1.02; 95% CI: 0.88, 1.18). Based on these findings, future research should test for dose-response, trimester-specific exposures, and factors affecting individual responses.
Invited Perspective: Toxic Metals and Hypertensive Disorders of Pregnancy
UNC Libraries · 2025-07-25
articleOpen accessSenior authorThe worldwide prevalence of gestational hypertension and preeclampsia is estimated at 10% and 2%–8%, respectively. In the United States alone, the incidence of preeclampsia—a leading cause of maternal mortality—increased by 25% between 1987 and 2004. Despite the prevalence and severity of these conditions, definitive causes remain elusive, hindering risk reduction interventions. There has been increasing attention to the role of environmental chemicals, including toxic metals, in the development of gestational hypertension and preeclampsia (together termed hypertensive disorders of pregnancy). The recent study by Borghese et al. significantly contributes to the growing literature establishing associations between toxic metal exposure and these disorders.
Developmental Trajectories of Autistic Social Traits in Youth Born Extremely Preterm
Journal of the American Academy of Child & Adolescent Psychiatry · 2025-12-01 · 2 citations
articleOpen accessResearch Square · 2025-12-15
preprintOpen accessSenior authorClinical Epigenetics · 2025-11-25
articleOpen accessSenior authorBACKGROUND: Several maternal exposures such as acetaminophen during pregnancy have been previously associated with altered placental CpG methylation. Epigenetic gestational age measures biological aging using DNA methylation from gestational tissues such as placenta and cord blood. We hypothesize that placental epigenetic gestational age (eGA) could serve as a biomarker for maternal exposures or pathological processes that influence placental development. To investigate relationships between maternal exposures and placental eGA, we evaluated prenatal medication use (antibiotics, acetaminophen, aspirin, and ibuprofen) in relation to placental epigenetic gestational age acceleration (eGAA) using the Robust Placental Clock (RPC). We also examined associations between these four exposures and the methylation levels of the 558 individual CpGs comprising the RPC. Using data from the Extremely Low Gestational Age Newborns (ELGAN) study (N = 408), we ran linear mixed-effects regression models that accounted for multiple births to the same mother. We further stratified by infant sex assigned at birth to assess effect measure modification. RESULTS: We observed a positive association between prenatal aspirin use and eGAA at borderline significance (β: + 0.35 weeks gestation; 95% CI: - 0.01, 0.72). When stratified by sex, this finding was significant among females (β: + 0.63 weeks gestation; 95% CI: 0.10, 1.17) but not males (β: - 0.05 weeks gestation; 95% CI: - 0.60, 0.49). Prenatal aspirin use in female pregnancies was further associated with ten differentially methylated RPC CpGs, mapping to genes including Retinoid X Receptor Alpha (RXRA), a nuclear receptor that can function as transcription factor and thereby influence multiple processes critical to placental development. CONCLUSION: These findings highlight that prenatal aspirin use is associated with placental eGAA in a sex-dependent manner, and RPC CpG methylation is sensitive to maternal medication exposures. Additional research is required to validate these eGAA observations, and future research should investigate the mechanisms underlying these relationships and their potential long-term clinical implications in the infant.
Archives of Toxicology · 2025-06-12 · 2 citations
articleMaternal one carbon metabolism and arsenic methylation in a pregnancy cohort in Mexico
UNC Libraries · 2025-08-09
articleOpen accessThe interplay between environmental exposures and COVID-19 risks in the health of children
UNC Libraries · 2025-05-20
articleOpen accessDiscrimination exposure and DNA methylation of stress-related genes in Latina mothers
UNC Libraries · 2025-08-30
articleOpen accessEpigenomics · 2025-07-16 · 1 citations
reviewThe placenta is a dynamic organ that serves numerous purposes for fostering a successful pregnancy and the delivery of a healthy infant in humans. It performs critical functions in nutrient and oxygen transport, immune modulation, and hormonal regulation. DNA methylation, a key epigenetic mechanism of transcriptional regulation, plays a key role in the underlying etiologies of placenta-related health complications. Therefore, assessing placental DNA methylation is essential for understanding how adverse prenatal exposures may impact both short-term and long-term health outcomes in women and children. In this review, we summarize current knowledge on the effects of prenatal exposures on placental DNA methylation and their implications for maternal and child health, focused on human population studies. We also outline five critical directions for human placental DNA methylation research: (1) Investigating sex-specific DNA methylation patterns, (2) Assessing cell type-specific DNA methylation signatures, (3) Applying causal inference methods, (4) Integrating multi-omics approaches, and (5) Using DNA methylation as a biomarker for environmental exposures and developmental outcomes. Advancing research in these areas will enhance our understanding of the biological underpinnings of the developmental origins of health and disease (DOHaD) hypothesis and maximize the potential of placental samples to inform DOHaD-related research.
Recent grants
Placental Epigenome and Brain Dysfunction after Preterm Birth
NIH · $2.6M · 2017–2023
Genetic underpinning of diabetes associated with arsenic exposure
NIH · $3.3M · 2019–2024
Developmental windows for arsenic-associated diabetes
NIH · $456k · 2018–2023
Environment, Epigenetics, Neurodevelopment & Health of Extremely Preterm Children
NIH · $4.5M · 2016–2023
Environment, Epigenetics, Neurodevelopment & Health of Extremely Preterm Children
NIH · $5.7M · 2016–2025
Frequent coauthors
- 146 shared
T. Michael O’Shea
- 134 shared
Lisa Smeester
University of North Carolina at Chapel Hill
- 129 shared
Julia E. Rager
University of North Carolina at Chapel Hill
- 100 shared
Karl Kuban
- 93 shared
Hudson P. Santos
- 66 shared
Robert M. Joseph
- 65 shared
Jean A. Frazier
- 58 shared
Lauren A. Eaves
University of North Carolina at Chapel Hill
Labs
Education
- 2005
Ph.D., Environmental Sciences and Engineering
University of North Carolina at Chapel Hill
- 2001
M.S., Environmental Sciences and Engineering
University of North Carolina at Chapel Hill
- 1999
B.S., Environmental Sciences and Engineering
University of North Carolina at Chapel Hill
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