About

Jodi A. Flaws is a professor in the Department of Bioengineering at the University of Illinois Urbana-Champaign. Her research primarily focuses on understanding the genetic and environmental factors that influence the female reproductive system. Her laboratory investigates key questions such as which genes and hormones regulate the normal development and function of the ovary, the effects of environmental toxicants on ovarian development and function, the mechanisms underlying reproductive toxicants' effects, and the association of environmental exposures with reproductive abnormalities in women. Her work involves exploring how various environmental toxicants, such as phthalates and bisphenol A, impact ovarian health and fertility, with a particular emphasis on the molecular pathways involved. Dr. Flaws has contributed to the scientific understanding of reproductive toxicology through her research, which has been published in numerous scientific journals.

Research topics

• Biology
• Endocrinology
• Chemistry
• Medicine
• Internal medicine
• Physiology
• Genetics
• Ecology
• Psychiatry
• Environmental health
• Biochemistry
• Bioinformatics
• Environmental engineering
• Environmental chemistry
• Environmental science
• Cell biology
• Andrology
• Gerontology
• Immunology

Selected publications

• Isolated and combined exposure to polystyrene nanoplastics and a phthalate metabolite mixture disrupts antral follicle growth and function of mice in vitro

  Toxicological Sciences · 2026-03-18

  article

  Polystyrene nanoplastics (PS-NPs) are small particles derived from plastic degradation that have been detected in several human tissues. Phthalates are ubiquitous plasticizers used to increase flexibility in polymers which act as endocrine disruptors, impacting hormonal homeostasis. Considering that both pollutants have been detected in human follicular fluid, there is increasing concern regarding their potential effects on female reproductive health. This study evaluated the isolated and combined effects of environmentally relevant doses of PS-NPs and a phthalate metabolite mixture (MM) on antral follicle growth, hormone production, and the expression of genes involved in apoptosis, oxidative stress, steroidogenesis, and hormone receptor signaling. Antral follicles from adult CD-1 mice were cultured with vehicle control (DMSO and water), metabolite mixture (0.01, 0.1, 1, and 10 μg/ml), or PSNPs (5, 25, 50, and 100 μg/ml) or MM + PS-NPs (5 µg/ml PS-NPs + 0.01 µg/ml MM; 100 μg/ml PS-NPs + 10 μg/ml MM). Follicle growth was monitored every 24 h for 96 h. PS-NPs and MM were internalized by follicles and they inhibited follicle growth alone and in co-exposure. Both pollutants altered the expression of apoptosis-related (Casp3, Casp8, Bcl2) and oxidative stress-related (Cat, Nrf2, Gpx1) genes without significantly affecting steroid hormone levels. Co-exposure also reduced Esr2 and Ar expression, demonstrating more pronounced effects under low-dose combined exposure. Altogether, these findings indicate that environmentally relevant exposure to PS-NPs and phthalate mixtures impairs antral follicle growth and disrupts molecular pathways essential for ovarian function, highlighting potential pathways and the importance of understanding combined exposures in reproductive toxicity.

  PublisherDOI

• The effects of iodoacetic acid on oxidative stress markers in the mouse ovary

  Biology of Reproduction · 2026-04-03

  articleSenior author

  The incorporation of water disinfectants into the main water supply has significantly decreased the incidence of waterborne diseases. However, the interaction between disinfectants and organic material generates water disinfection byproducts (DBPs) such as iodoacetic acid (IAA). IAA is an ovarian toxicant, but little is known about its mechanisms of toxicity. Thus, we tested the hypothesis that IAA exposure causes ovarian toxicity through oxidative stress pathways. Adult CD-1 mice were dosed with vehicle control (reverse osmosis water) or IAA (2.7- 2,695.7 μM) for 35 days. Then, whole ovaries or isolated antral follicles were collected for measurement of expression of several enzymes that regulate oxidative stress (Gpx1, Gpx2, Gsr, Gss, Gsta1, Gstm1, Gsto1, Gstp1 Gstt1, Sod1, Sod2, and Cat). In other experiments, antral follicles were cultured with vehicle control ± the antioxidant Trolox or IAA (2-15 μM) ± the antioxidant Trolox for 96 hours and follicle growth was measured every 24 hours. Media were collected for estradiol measurements. IAA decreased Cat, Sod1, Gss, Gsta1, Gstp1, and Gstt1 and increased Gstm1 expression in whole ovaries compared to control in vivo. IAA decreased Sod2 and Gpx2 and increased Gstp1 expression in antral follicles compared to control in vivo. IAA increased Gpx1 and Gsto1 expression in antral follicles compared to control in vitro. IAA inhibited follicle growth and reduced estradiol levels, whereas Trolox rescued follicles from IAA-induced inhibition of follicle growth and estrogen levels in vitro. Collectively, these data indicate that IAA exposure causes ovarian toxicity by altering oxidative stress pathways in the mouse ovary.

  PublisherDOI

• Mechanisms of Phthalate-Induced Accelerated Ovarian Aging in Experimental Models

  Current Environmental Health Reports · 2026-02-13

  articleOpen accessSenior author

  Accelerated ovarian aging is associated with early infertility as well as other adverse health outcomes. Little is known about the factors that accelerate ovarian aging, but several studies indicate that exposure to phthalates accelerates ovarian aging. This is a significant human health concern because humans are ubiquitously and unavoidably exposed to phthalates. Thus, it is imperative to study the mechanisms of phthalate-induced accelerated ovarian aging so that strategies can be developed to prevent phthalate-induced ovarian aging. This review focuses on the mechanisms by which phthalates cause ovarian aging in non-human experimental models and highlights gaps in the literature. Phthalate exposure may accelerate ovarian aging and in turn, accelerate female reproductive aging through several mechanisms. Specifically, phthalates can alter steroidogenesis and folliculogenesis, ultimately dysregulating estrous cyclicity and decreasing fertility. Phthalate-induced disruptions in the brain and gut contribute to these changes. Additionally, phthalate exposures increase ovarian inflammation and oxidative stress, which contribute to accelerated ovarian aging. Phthalate exposure also increases ovarian autophagy, mitochondrial dysfunction, and apoptosis, which ultimately increase follicular atresia and accelerate depletion of the follicle reserve. Phthalates accelerate ovarian aging through numerous interlinked mechanisms that may be used as targets for prevention, inhibition, or reversal of phthalate-induced ovarian aging in patients experiencing infertility. Further studies should investigate the effects of environmentally relevant phthalate exposures on these mechanisms and explore therapies that target these mechanisms.

  PublisherOA PDFDOI

• Gut microbiome influences uterine development in mice

  Reproduction · 2026-01-09

  article

  Diisononyl phthalate (DiNP), a plasticizer increasingly replacing di(2-ethylhexyl) phthalate, is an endocrine-disrupting chemical linked to female reproductive harm. Ingestion is the most common route of DiNP exposure, making the gastrointestinal tract and gut microbiome a direct target for endocrine-disrupting chemical exposure. This study examined the effects of acute DiNP exposure either in the absence or presence of a gut microbiome on uterine development. Female C57Bl/6 germ-free (-microbiome) 40-day-old mice were orally dosed, over 3 days, with either sterile phosphate-buffered (n = 8) to remain germ-free (GF, -microbiome) or with colon contents (n = 10) to develop a gut-microbiome (+microbiome). This was followed by a 10-day period where half of the -microbiome and +microbiome mice were orally dosed with corn oil while half were orally dosed with 200 μg/kg/day DiNP. The control group were specific pathogen-free conventionally housed mice born with a microbiome. Mice were euthanized in diestrus at the end of the 10 days. Uteri were collected for histological analyses. Uterine development was significantly delayed in GF mice, regardless of later microbiome reintroduction or DiNP exposure. Key findings included reduced uterine diameter, stroma area, and gland number, and thinner myometrial layers. Endometrial stromal cell proliferation was also lower in GF mice. DiNP exposure alone showed no significant effects. Estradiol levels and ovarian follicle counts were similar across groups, but GF mice had fewer, smaller litters in fertility tests. The study highlights that the gut microbiome critically influences postnatal uterine development, with its absence leading to persistent structural deficits. DiNP, at the tested dose, did not exacerbate these effects.

  PublisherDOI

• Impact of nanoparticles and nanoplastics on female reproductive health

  Biology of Reproduction · 2026-02-10

  articleSenior author

  Nanomaterials including nanoparticles and nanoplastics are deposited in the environment, resulting in human exposure to nanoparticles and nanoplastics through dermal, oral, and inhalation routes. After exposure, nanoparticles and nanoplastics are absorbed and distributed to many organs in wildlife, animal models, and humans. As a consequence, nanoparticles and nanoplastics have been found in several human tissues including the ovary and brain, raising concern regarding their potential effects on female reproduction. The physicochemical characteristics of nanoparticles and nanoplastics influence their behavior and their toxicity. One of the main challenges in understanding the toxic effects of nanoparticle and nanoplastic exposure is identifying the underlying molecular pathways. This review integrates available data on the effects of nanoparticles and nanoplastics on female reproductive health. Specifically, this review describes recent published data on the effects of nanomaterials on the hypothalamic-pituitary-gonadal axis, folliculogenesis, steroidogenesis, estrous cyclicity, placental function, embryo development, and fertility. This review also highlights the known mechanisms by which nanomaterials exert toxic effects in the female reproductive tract, and it emphasizes the gaps in the literature that need to be addressed to better understand the effects of nanoparticle and nanoplastic exposure on female reproduction and their underlying mechanisms of toxicity.

  PublisherDOI

• Effects of Phthalate Metabolite Mixture Exposure on Mouse Oocyte Development

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-05-22

  article

  Phthalates are pervasive endocrine-disrupting chemicals widely used in consumer products. The wide use of many phthalates results in chronic human exposure to complex mixtures rather than single compounds. Despite extensive studies on individual compounds, the combined effects of phthalate metabolites on oogenesis remain poorly understood. Here, we developed a precise microinjection-based single-oocyte toxicological assay to examine the impact of a defined phthalate metabolite mixture on meiotic progression. Phthalate mixture exposure markedly impaired oocyte maturation, as most oocytes failed to extrude the first polar body. Mechanistic analyses revealed severe meiotic defects, including disrupted spindle morphology, chromosome misalignment, disorganized actin cytoskeleton, and impaired mitochondrial function, accompanied by excessive reactive oxygen species (ROS) accumulation and DNA damage. Single-cell transcriptomic profiling further identified differentially expressed genes enriched in biological processes related to exocytosis, secretory pathway regulation, and cytoskeletal organization, as well as in MAPK, JAK-STAT, cGMP-PKG, and GnRH signaling pathways that are essential for follicular development and oocyte maturation. Together, these findings demonstrate that combined phthalate exposure directly compromises female gamete quality and underscore the importance of evaluating mixture effects when assessing risks to women's reproductive health.

  PublisherDOI

• Epidemiologically relevant phthalate mixture and mono(2-ethyl-5-hydroxyhexyl) phthalate exposure alter cell energy metabolism in primary mouse granulosa cells

  Reproductive Toxicology · 2025-05-03 · 3 citations

  articleOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• Effects of phthalate exposure on human ovarian extracellular matrix composition: insights from a 3D spheroid model

  Environmental Research · 2025-05-08 · 2 citations

  articleOpen access
  PublisherOA PDFDOI

• Prenatal Exposure to Imidacloprid Affects Cognition and Anxiety-Related Behaviors in Male and Female CD-1 Mice

  Toxics · 2025-10-27 · 1 citations

  articleOpen access

  Neonicotinoid pesticides, including imidacloprid (IMI), are widely used in agriculture and as household insecticides. IMI displays strong affinity for insect nicotinic acetylcholine receptors (nAChRs); however, neonicotinoids still partially bind to mammalian nAChRs. Relatively little is known about how neonicotinoid exposure alters learning, memory or mood, even though nAChRs play a role in these mechanisms. We tested the hypothesis that developmental exposure to IMI impairs performance on memory tasks, and anxiety- and depressive-like behavior. We orally dosed pregnant CD-1 mice from gestation day 10 to birth with vehicle or IMI at 0.5 mg/kg/day or 5.7 mg/kg/day. When exposed animals were adults, we examined cognitive and emotional behaviors and we examined the effect of IMI on α7 and α4 nAChR subunit mRNA expression using qPCR. For both sexes, IMI exposure was associated with impaired striatal-dependent procedural learning task and hippocampal-dependent spatial learning but had no effect on hippocampal-dependent working memory. Males, but not females, displayed increased anxiety-like behavior, with low dose subjects displaying more pronounced effects, suggesting a non-linear dose response. In males, we found lower α7 subunit mRNA expression in the hippocampus and amygdala and lower α4 mRNA expression in the striatum compared to controls. Thus, exposure to IMI during a critical period is associated with disruptions to cognitive and anxiety-like behaviors. Additionally, in males, IMI exposure is associated with reduced expression of nAChR subunits in relevant brain regions.

  PublisherOA PDFDOI

• Content and Volume Overview

  Elsevier eBooks · 2025-02-04

  book-chapter1st authorCorresponding
  PublisherDOI

Recent grants

• NIH Grant U01ES020835

  NIH · $464k · 2017

• NIH Grant R01HD038955

  NIH · $950k · 2005

• NIH Grant R01ES012893

  NIH · $1.1M · 2010

• Phthalate Exposure and Female Reproductive Aging

  NIH · $543k · 2022–2027

• Phthalates and Ovarian Toxicity

  NIH · $1.8M · 2018–2024

Frequent coauthors

• Howard A. Zacur

  Johns Hopkins University

  103 shared

• Susan R. Miller

  Keck Hospital of USC

  92 shared

• Lisa Gallicchio

  National Cancer Institute

  83 shared

• Jonathan L. Tilly

  Northeastern University

  70 shared

• Gloria I. Perez

  Michigan State University

  68 shared

• Harry B. Greenberg

  Stanford University

  64 shared

• Andrea Jurisicova

  Sinai Health System

  64 shared

• Keith E. Latham

  Michigan State University

  64 shared

Awards & honors

• Fellow of the Academy of Toxicological Sciences, 2013-curren…
• Pfizer Animal Health Award for Research Excellence, 2009
• University Scholar, 2009-2012