@article{moore_brown_kiederer_calkins_burgess_d'alessandro_davis_fenton_morrison_reh_2023, title={Effective coordination, collaboration, communication, and partnering are needed to close the gaps for occupational PFAS exposure}, url={https://doi.org/10.1002/ajim.23348}, DOI={10.1002/ajim.23348}, journal={American Journal of Industrial Medicine}, author={Moore, Susan M. and Brown, Carol and Kiederer, Meghan and Calkins, Miriam M. and Burgess, Jeffery L. and D'Alessandro, Maryann and Davis, Rick and Fenton, Suzanne E. and Morrison, Patrick and Reh, Christopher M.}, year={2023}, month={May} }
 @article{lakind_verner_rogers_goeden_naiman_marchitti_lehmann_hines_fenton_2023, title={Erratum: Current Breast Milk PFAS Levels in the United States and Canada: After All This Time, Why Don’t We Know More?}, url={https://doi.org/10.1289/EHP12915}, DOI={10.1289/EHP12915}, abstractNote={Vol. 131, No. 3 ErratumOpen AccessErratum: Current Breast Milk PFAS Levels in the United States and Canada: After All This Time, Why Don’t We Know More?is correction ofCurrent Breast Milk PFAS Levels in the United States and Canada: After All This Time, Why Don’t We Know More? Judy S. LaKind, Marc-André Verner, Rachel D. Rogers, Helen Goeden, Daniel Q. Naiman, Satori A. Marchitti, Geniece M. Lehmann, Erin P. Hines, and Suzanne E. Fenton Judy S. LaKind Search for more papers by this author , Marc-André Verner Search for more papers by this author , Rachel D. Rogers Search for more papers by this author , Helen Goeden Search for more papers by this author , Daniel Q. Naiman Search for more papers by this author , Satori A. Marchitti Search for more papers by this author , Geniece M. Lehmann Search for more papers by this author , Erin P. Hines Search for more papers by this author , and Suzanne E. Fenton https://orcid.org/0000-0002-8956-398X Search for more papers by this author Published:17 March 2023CID: 039001https://doi.org/10.1289/EHP12915AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit During the paper editing process, two values in Table 2 were mistakenly modified. Milk:serum concentration ratios from the “Kärrman et al. 2007” study should be 0.01 for PFOS and 0.01 PFNA. This error affects values in Table 2 only. All calculations were performed with the correct values.The authors regret the error.Table 2 Published milk:serum concentration ratios for PFOA, PFOS, PFHxS, and PFNA.StudyCountryPFOAPFOSPFHxSPFNACariou et al. 2015France0.038 (lowercase italic n equals 10n=10)0.011 (lowercase italic n equals 19n=19)0.012 (lowercase italic n equals 8n=8)—Kärrman et al. 2007Sweden0.12 (lowercase italic n equals 1n=1)0.01 (lowercase italic n equals 12n=12)0.02 (lowercase italic n equals 12n=12)0.01 (lowercase italic n equals 2n=2)Kim et al. 2011Korea0.025 (lowercase italic n equals 17n=17)0.011 (lowercase italic n equals 17n=17)0.008 (lowercase italic n equals 17n=17)—Liu et al. 2011China0.11 (lowercase italic n equals 50n=50)0.02 (lowercase italic n equals 50n=50)—0.05 (lowercase italic n equals 50n=50)Mean0.07330.01300.01330.030Note: lowercase italic n equalsn=number of samples with measured milk and serum concentrations within individual studies. —, no data; PFHxS, perfluorohexane sulfonate; PFNA, perfluorononanoic acid; PFOA, perfluorooctanoic acid; PFOS, perfluorooctane sulfonate.FiguresReferencesRelatedDetailsRelated articlesCurrent Breast Milk PFAS Levels in the United States and Canada: After All This Time, Why Don’t We Know More?23 February 2022Environmental Health Perspectives Vol. 131, No. 3 March 2023Metrics About Article Metrics Publication History Manuscript received17 February 2023Manuscript accepted23 February 2023Originally published17 March 2023 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.}, journal={Environmental Health Perspectives}, author={LaKind, Judy S. and Verner, Marc-André and Rogers, Rachel D. and Goeden, Helen and Naiman, Daniel Q. and Marchitti, Satori A. and Lehmann, Geniece M. and Hines, Erin P. and Fenton, Suzanne E.}, year={2023}, month={Mar} }
 @misc{rickard_overchuk_chappell_kemal ruhi_sinawang_nguyen hoang_akin_demirci_franco_fenton_et al._2023, title={Methods to Evaluate Changes in Mitochondrial Structure and Function in Cancer}, volume={15}, ISSN={["2072-6694"]}, url={https://doi.org/10.3390/cancers15092564}, DOI={10.3390/cancers15092564}, abstractNote={Mitochondria are regulators of key cellular processes, including energy production and redox homeostasis. Mitochondrial dysfunction is associated with various human diseases, including cancer. Importantly, both structural and functional changes can alter mitochondrial function. Morphologic and quantifiable changes in mitochondria can affect their function and contribute to disease. Structural mitochondrial changes include alterations in cristae morphology, mitochondrial DNA integrity and quantity, and dynamics, such as fission and fusion. Functional parameters related to mitochondrial biology include the production of reactive oxygen species, bioenergetic capacity, calcium retention, and membrane potential. Although these parameters can occur independently of one another, changes in mitochondrial structure and function are often interrelated. Thus, evaluating changes in both mitochondrial structure and function is crucial to understanding the molecular events involved in disease onset and progression. This review focuses on the relationship between alterations in mitochondrial structure and function and cancer, with a particular emphasis on gynecologic malignancies. Selecting methods with tractable parameters may be critical to identifying and targeting mitochondria-related therapeutic options. Methods to measure changes in mitochondrial structure and function, with the associated benefits and limitations, are summarized.}, number={9}, journal={CANCERS}, author={Rickard, Brittany P. P. and Overchuk, Marta and Chappell, Vesna A. A. and Kemal Ruhi, Mustafa and Sinawang, Prima Dewi and Nguyen Hoang, Tina Thuy and Akin, Demir and Demirci, Utkan and Franco, Walfre and Fenton, Suzanne E. E. and et al.}, year={2023}, month={Apr} }
 @article{timmermann_avenbuan_romano_braun_tolstrup_vandenberg_fenton_2023, title={Per- and Polyfluoroalkyl Substances and Breastfeeding as a Vulnerable Function: A Systematic Review of Epidemiological Studies}, url={https://doi.org/10.3390/toxics11040325}, DOI={10.3390/toxics11040325}, abstractNote={Milk formation in the breast during breastfeeding is a complex hormonally regulated process, potentially sensitive to the effects of endocrine-disrupting chemical exposures. The environmental chemicals, per- and polyfluoroalkyl substances (PFAS) are known endocrine disruptors. PFAS exposure have been associated with insufficient mammary gland development in mice and reduced breastfeeding duration in humans. The aim of this review was to gather the epidemiological evidence on the association between PFAS exposure and breastfeeding duration. Using PubMed and Embase, we performed a systematic literature search (on 23 January 2023) to identify epidemiological studies examining the association between maternal PFAS exposure and breastfeeding duration. Animal studies, reviews, and non-English studies were excluded. The risk of bias was assessed using the risk of bias in non-randomized studies of exposures tool. Estimates describing the association between PFAS exposure and the duration of breastfeeding were identified, and the data were synthesized separately for each type of PFAS and for the duration of exclusive and total breastfeeding. Six studies with between 336 and 2374 participants each were identified. PFAS exposure was assessed in serum samples (five studies) or based on residential address (one study). Five out of six studies found shorter total duration of breastfeeding with higher PFAS exposure. The most consistent associations were seen for perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA), and perfluorononanoic acid (PFNA). The finding of a potential causal association between PFAS exposure and breastfeeding duration is in agreement with findings from experimental studies.}, journal={Toxics}, author={Timmermann, Amalie and Avenbuan, Oyemwenosa N. and Romano, Megan E. and Braun, Joseph M. and Tolstrup, Janne S. and Vandenberg, Laura N. and Fenton, Suzanne E.}, year={2023}, month={Mar} }
 @article{lakind_naiman_verner_lévêque_fenton_2023, title={Per- and polyfluoroalkyl substances (PFAS) in breast milk and infant formula: A global issue}, url={https://doi.org/10.1016/j.envres.2022.115042}, DOI={10.1016/j.envres.2022.115042}, abstractNote={Per- and polyfluoroalkyl substances (PFAS) are transferred from mother to infants through breastfeeding, a time when children may be particularly vulnerable to PFAS-mediated adverse health effects. Infants can also be exposed to PFAS from infant formula consumption. Our recent literature-based scoping of breast milk levels reported that four PFAS often exceeded the United States Agency for Toxic Substances and Disease Registry (ATSDR) children's drinking water screening levels in both the general population and highly impacted communities in the U.S. and Canada. This work presents a comparison of global breast milk and infant formula PFAS measurements with the only reported health-based drinking water screening values specific to children.We focused on four PFAS for which ATSDR has developed children's drinking water screening values: PFOA (perfluorooctanoic acid), PFOS (perfluorooctanesulfonic acid), PFHxS (perfluorohexanesulfonic acid), and PFNA (perfluorononanoic acid). Published literature on PFAS levels in breast milk and infant formula were identified via PubMed searches. Data were compared to children's drinking water screening values.Breast milk concentrations of PFOA and PFOS often exceed children's drinking water screening values, regardless of geographic location. The limited information on infant formula suggests its use does not necessarily result in lower PFAS exposures, especially for formulas reconstituted with drinking water containing PFAS. Unfortunately, individuals generally cannot know whether their infant's exposures exceed children's drinking water screening values. Thus, it is essential that pregnant and lactating women and others, especially those having lived in PFAS-contaminated communities, have data required to make informed decisions on infant nutrition. An international monitoring effort and access to affordable testing are needed for breast milk, drinking water and infant formula to fully understand infant PFAS exposures. Currently, our understanding of demonstrable methods for reducing exposures to emerging PFAS is limited, making this research and the communications surrounding it even more important.}, journal={Environmental Research}, author={LaKind, Judy S. and Naiman, Josh and Verner, Marc-Andre and Lévêque, Laura and Fenton, Suzanne}, year={2023}, month={Feb} }
 @article{kay_cardona_rudel_vandenberg_soto_christiansen_birnbaum_fenton_2022, title={Chemical Effects on Breast Development, Function, and Cancer Risk: Existing Knowledge and New Opportunities}, url={https://doi.org/10.1007/s40572-022-00376-2}, DOI={10.1007/s40572-022-00376-2}, abstractNote={Abstract}, journal={Current Environmental Health Reports}, author={Kay, Jennifer E. and Cardona, Bethsaida and Rudel, Ruthann A. and Vandenberg, Laura N. and Soto, Ana M. and Christiansen, Sofie and Birnbaum, Linda S. and Fenton, Suzanne E.}, year={2022}, month={Aug} }
 @article{lakind_verner_rogers_goeden_naiman_marchitti_lehmann_hines_fenton_2022, title={Current Breast Milk PFAS Levels in the United States and Canada: After All This Time, Why Don’t We Know More?}, url={https://doi.org/10.1289/EHP10359}, DOI={10.1289/EHP10359}, abstractNote={Background: Despite 20 y of biomonitoring studies of per- and polyfluoroalkyl substances (PFAS) in both serum and urine, we have an extremely limited understanding of PFAS concentrations in breast milk of women from the United States and Canada. The lack of robust information on PFAS concentrations in breast milk and implications for breastfed infants and their families were brought to the forefront by communities impacted by PFAS contamination. Objectives: The objectives of this work are to: a) document published PFAS breast milk concentrations in the United States and Canada; b) estimate breast milk PFAS levels from maternal serum concentrations in national surveys and communities impacted by PFAS; and c) compare measured/estimated milk PFAS concentrations to screening values. Methods: We used three studies reporting breast milk concentrations in the United States and Canada We also estimated breast milk PFAS concentrations by multiplying publicly available serum concentrations by milk:serum partitioning ratios for perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), perfluorohexane sulfonate (PFHxS), and perfluorononanoic acid (PFNA). Measured and estimated breast milk concentrations were compared to children’s drinking water screening values. Discussion: Geometric means of estimated breast milk concentrations ranged over approximately two orders of magnitude for the different surveys/communities. All geometric mean and mean estimated and measured breast milk PFOA and PFOS concentrations exceeded drinking water screening values for children, sometimes by more than two orders of magnitude. For PFHxS and PFNA, all measured breast milk levels were below the drinking water screening values for children; the geometric mean estimated breast milk concentrations were close to—or exceeded—the children’s drinking water screening values for certain communities. Exceeding a children’s drinking water screening value does not indicate that adverse health effects will occur and should not be interpreted as a reason to not breastfeed; it indicates that the situation should be further evaluated. It is past time to have a better understanding of environmental chemical transfer to—and concentrations in—an exceptional source of infant nutrition. https://doi.org/10.1289/EHP10359}, journal={Environmental Health Perspectives}, author={LaKind, Judy S. and Verner, Marc-André and Rogers, Rachel D. and Goeden, Helen and Naiman, Daniel Q. and Marchitti, Satori A. and Lehmann, Geniece M. and Hines, Erin P. and Fenton, Suzanne E.}, year={2022}, month={Feb} }
 @article{rickard_rizvi_fenton_2022, title={Per- and poly-fluoroalkyl substances (PFAS) and female reproductive outcomes: PFAS elimination, endocrine-mediated effects, and disease}, volume={465}, ISSN={["0300-483X"]}, url={https://doi.org/10.1016/j.tox.2021.153031}, DOI={10.1016/j.tox.2021.153031}, abstractNote={Per- and poly-fluoroalkyl substances (PFAS) are widespread environmental contaminants frequently detected in drinking water supplies worldwide that have been linked to a variety of adverse reproductive health outcomes in women. Compared to men, reproductive health effects in women are generally understudied while global trends in female reproduction rates are declining. Many factors may contribute to the observed decline in female reproduction, one of which is environmental contaminant exposure. PFAS have been used in home, food storage, personal care and industrial products for decades. Despite the phase-out of some legacy PFAS due to their environmental persistence and adverse health effects, alternative, short-chain and legacy PFAS mixtures will continue to pollute water and air and adversely influence women's health. Studies have shown that both long- and short-chain PFAS disrupt normal reproductive function in women through altering hormone secretion, menstrual cyclicity, and fertility. Here, we summarize the role of a variety of PFAS and PFAS mixtures in female reproductive tract dysfunction and disease. Since these chemicals may affect reproductive tissues directly or indirectly through endocrine disruption, the role of PFAS in breast, thyroid, and hypothalamic-pituitary-gonadal axis function are also discussed as the interplay between these tissues may be critical in understanding the long-term reproductive health effects of PFAS in women. A major research gap is the need for mechanism of action data - the targets for PFAS in the female reproductive and endocrine systems are not evident, but the effects are many. Given the global decline in female fecundity and the ability of PFAS to negatively impact female reproductive health, further studies are needed to examine effects on endocrine target tissues involved in the onset of reproductive disorders of women.}, journal={TOXICOLOGY}, publisher={Elsevier BV}, author={Rickard, Brittany P. and Rizvi, Imran and Fenton, Suzanne E.}, year={2022}, month={Jan} }
 @article{rickard_tan_fenton_rizvi_2022, title={Select Per- and Polyfluoroalkyl Substances (PFAS) Induce Resistance to Carboplatin in Ovarian Cancer Cell Lines}, volume={23}, ISSN={["1422-0067"]}, url={https://www.mdpi.com/1422-0067/23/9/5176}, DOI={10.3390/ijms23095176}, abstractNote={Per- and polyfluoroalkyl substances (PFAS) are ubiquitous environmental contaminants associated with adverse reproductive outcomes including reproductive cancers in women. PFAS can alter normal ovarian function, but the effects of PFAS on ovarian cancer progression and therapy response remain understudied. Ovarian cancer is the most lethal gynecologic malignancy, and a major barrier to effective treatment is resistance to platinum-based chemotherapy. Platinum resistance may arise from exposure to external stimuli such as environmental contaminants. This study evaluated PFAS and PFAS mixture exposures to two human ovarian cancer cell lines to evaluate the ability of PFAS exposure to affect survival fraction following treatment with carboplatin. This is the first study to demonstrate that, at sub-cytotoxic concentrations, select PFAS and PFAS mixtures increased survival fraction in ovarian cancer cells following carboplatin treatment, indicative of platinum resistance. A concomitant increase in mitochondrial membrane potential, measured by the JC-1 fluorescent probe, was observed in PFAS-exposed and PFAS + carboplatin-treated cells, suggesting a potential role for altered mitochondrial function that requires further investigation.}, number={9}, journal={INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES}, publisher={MDPI AG}, author={Rickard, Brittany P. and Tan, Xianming and Fenton, Suzanne E. and Rizvi, Imran}, year={2022}, month={May} }
 @article{cope_blake_love_mccord_elmore_harvey_chappell_fenton_2021, title={Latent, sex-specific metabolic health effects in CD-1 mouse offspring exposed to PFOA or HFPO-DA (GenX) during gestation}, volume={7}, url={https://doi.org/10.1016/j.emcon.2021.10.004}, DOI={10.1016/j.emcon.2021.10.004}, abstractNote={Perfluorooctanoic acid (PFOA) is an environmental contaminant associated with adverse metabolic outcomes in developmentally exposed human populations and mouse models. Hexafluoropropylene oxide-dimer acid (HFPO-DA, commonly called GenX) has replaced PFOA in many industrial applications in the U.S. and Europe and has been measured in global water systems from <1 to 9350 ng/L HFPO-DA. Health effects data for GenX are lacking.Determine the effects of gestational exposure to GenX on offspring weight gain trajectory, adult metabolic health, liver pathology and key adipose gene pathways in male and female CD-1 mice.Daily oral doses of GenX (0.2, 1.0, 2.0 mg/kg), PFOA (0.1, 1.0 mg/kg), or vehicle control were administered to pregnant mice (gestation days 1.5-17.5). Offspring were fed a high- or low-fat diet (HFD or LFD) at weaning until necropsy at 6 or 18 weeks, and metabolic endpoints were measured over time. PFOA and GenX serum and urine concentrations, weight gain, serum lipid parameters, body mass composition, glucose tolerance, white adipose tissue gene expression, and liver histopathology were evaluated.Prenatal exposure to GenX led to its accumulation in the serum and urine of 5-day old pups (P = 0.007, P < 0.001), which was undetectable by weaning. By 18 weeks of age, male mice fed LFD in the 2.0 mg/kg GenX group displayed increased weight gain (P < 0.05), fat mass (P = 0.016), hepatocellular microvesicular fatty change (P = 0.015), and insulin sensitivity (P = 0.014) in comparison to control males fed LFD. Female mice fed HFD had a significant increase in hepatocyte single cell necrosis in 1.0 mg/kg GenX group (P = 0.022) and 1.0 mg/kg PFOA group (P = 0.003) compared to control HFD females. Both sexes were affected by gestational GenX exposure; however, the observed phenotype varied between sex with males displaying more characteristics of metabolic disease and females exhibiting liver damage in response to the gestational exposure.Prenatal exposure to 1 mg/kg GenX and 1 mg/kg PFOA induces adverse metabolic outcomes in adult mice that are diet- and sex-dependent. GenX also accumulated in pup serum, suggesting that placental and potentially lactational transfer are important exposure routes for GenX.}, journal={Emerging Contaminants}, publisher={Elsevier BV}, author={Cope, Harlie A. and Blake, Bevin E. and Love, Charlotte and McCord, James and Elmore, Susan A. and Harvey, Janice B. and Chappell, Vesna A. and Fenton, Suzanne E.}, year={2021}, pages={219–235} }
 @article{fenton_boyles_2021, title={Looking for Proof in the Wrong Generation?}, volume={30}, url={https://doi.org/10.1158/1055-9965.EPI-21-0475}, DOI={10.1158/1055-9965.EPI-21-0475}, abstractNote={Abstract}, number={8}, journal={Cancer Epidemiology, Biomarkers & Prevention}, publisher={American Association for Cancer Research (AACR)}, author={Fenton, Suzanne E. and Boyles, Abee L.}, year={2021}, month={Aug}, pages={1459–1461} }
 @article{rock_gillera_devarasetty_horman_knudsen_birnbaum_fenton_heather_2019, title={Sex-specific behavioral effects following developmental exposure to tetrabromobisphenol A (TBBPA) in Wistar rats}, volume={75}, ISSN={["1872-9711"]}, url={https://doi.org/10.1016/j.neuro.2019.09.003}, DOI={10.1016/j.neuro.2019.09.003}, abstractNote={Tetrabromobisphenol A (TBBPA) has become a ubiquitous indoor contaminant due to its widespread use as an additive flame retardant in consumer products. Reported evidence of endocrine disruption and accumulation of TBBPA in brain tissue has raised concerns regarding its potential effects on neurodevelopment and behavior. The goal of the present study was to examine the impact of developmental TBBPA exposure, across a wide range of doses, on sexually dimorphic non-reproductive behaviors in male and female Wistar rats. We first ran a pilot study using a single TBBPA dose hypothesized to produce behavioral effects. Wistar rat dams were orally exposed using cookie treats to 0 or 0.1 mg TBBPA/kg bw daily from gestational day (GD) 9 to postnatal day (PND) 21 to assess offspring (both sexes) activity and anxiety-related behaviors. Significant effects were evident in females, with exposure increasing activity levels. Thus, this dose was used as the lowest TBBPA dose in a subsequent, larger study conducted as part of a comprehensive assessment of TBBPA toxicity. Animals were exposed to 0, 0.1, 25, or 250 mg TBBPA/kg bw daily by oral gavage starting on GD 6 through PND 90 (dosed dams GD 6 - PND 21, dosed offspring PND 22 - PND 90). Significant behavioral findings were observed for male offspring, with increased anxiety-like behavior as the primary phenotype. These findings demonstrate that exposure to environmental contaminants, like TBBPA, can have sex-specific effects on behavior highlighting the vulnerability of the developing brain.}, journal={NEUROTOXICOLOGY}, publisher={Elsevier BV}, author={Rock, Kylie D. and Gillera, Sagi Enicole A. and Devarasetty, Pratyush and Horman, Brian and Knudsen, Gabriel and Birnbaum, Linda S. and Fenton, Suzanne E. and Heather, Patisaul B.}, year={2019}, month={Dec}, pages={136–147} }